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NBME 22 Answers

Block 1/Question#1
A 66-year-old man develops worsening shortness of breath and ...
Dilution of serum sodium due to ADH (vasopressin) secretion

Block 1/Question#2
A 28-year-old man has recurrent pancreatitis associated with ...
Decreasing VLDL

Block 1/Question#3
Parenterally administered cholera vaccines consisting of ...
Inability of the vaccine to elicit secretory antibody at the epithelial surface

Block 1/Question#4
A 48-year-old man begins furosemide therapy for pedal edema ...
Decreases the luminal permeability to Na+ in the collecting duct

Block 1/Question#5
A 10-month-old girl is brought to the emergency department ...
Naloxone

Block 1/Question#6
A 2-month-old boy is brought to the physician because of a ...
Human papillomavirus

Block 1/Question#7
Two patients, a 54-year-old man (Patient X) and a 76-year-old ...
Loading dose

Block 1/Question#8
A 16-year-old girl has pain and tingling in her left hand ...
Cervical rib

Block 1/Question#9
A 54-year-old man has an aneurysm in the distal portion of ...
2.4

Block 1/Question#10
A 25-year-old woman is admitted to the hospital because of ...
Streptococcus pneumoniae

Block 1/Question#11
A 6-month-old boy has recently been diagnosed with ...
Sphingomyelin degradation

Block 1/Question#12
During the first week of life, a male newborn has vomiting, ...
21-Hydroxylase

Block 1/Question#13
A 13-year-old girl is brought to the physician by her mother ...
Ask the mother to leave the room before asking the patient any questions

Block 1/Question#14
A 57-year-old woman comes to the physician because of ...
Trigeminal neuralgia

Block 1/Question#15
A 35-year-old woman has weakness and fever. When she was 25 ...
Acute myelocytic leukemia

Block 1/Question#16
An Rh-negative woman, gravida 3, para 2, has had an ...
O, Rh-negative

Block 1/Question#17
A 27-year-old man is brought to the emergency department ...
Eversion

Block 1/Question#18
A 13-year-old boy is brought to the physician for a ...
Reassurance

Block 1/Question#19
An 11-year-old boy has had pain in his right mid-thigh for 2 ...
Ewing sarcoma

Block 1/Question#20
A 49-year-old man comes to the physician because of ...
Avascular necrosis

Block 1/Question#21
A 30-year-old man comes to the physician because of a 2-day ...
Polycystin

Block 1/Question#22
A previously healthy 6-year-old boy is brought to the ...
Does anyone else in the family have an itchy rash like this?

Block 1/Question#23
A patient in the early stages of hemorrhagic shock is most ...
A weak pulse due to decreased stroke volume

Block 1/Question#24
A 48-year-old man with renal artery stenosis undergoes stent ...
Testicular artery

Block 1/Question#25
During an experiment, a 22-year-old man receives an infusion ...
Arteriolar resistance: decreased;
Capillary hydrostatic pressure: increased;
Capillary filtration rate: increased


Block 1/Question#26
A 42-year-old man comes to the physician because of a 1-month ...
Hydrochlorothiazide

Block 1/Question#27
During a clinical study, 15 patients with renal allografts ...
Azathioprine

Block 1/Question#28
A 48-year-old man comes to the physician because of fatigue, ...
Transferrin saturation and serum ferritin measurements

Block 1/Question#29
A 28-year-old man comes to the emergency department because ...
Jejunum

Block 1/Question#30
A 42-year-old woman is brought to the emergency department by ...
Temporal lobe

Block 1/Question#31
A 60-year-old woman comes to the physician because of a ...
Lung cancer

Block 1/Question#32
A 17-year-old boy is brought to the emergency department 45 ...
Hypokalemia

Block 1/Question#33
A 32-year-old woman begins to hyperventilate and then ...
Cerebral blood flow

Block 1/Question#34
A 15-year-old girl is brought to the physician by her mother ...
First-degree burn

Block 1/Question#35
A 35-year-old man is brought to the hospital after a diving ...
Alteration of the thermostatic set point

Block 1/Question#36
A 67-year-old woman comes to the physician because of a ...
Idiopathic pulmonary fibrosis

Block 1/Question#37
A 28-year-old woman is brought to the physician because of a ...
Area labeled ‘C’ (Abducens nucleus, right)

Block 1/Question#38
A newborn born at 26 weeks' gestation has respiratory ...
Dipalmitoyl lecithin

Block 1/Question#39
A 23-year-old woman develops multiple red, papulovesicular ...
Processing of antigen by Langerhans cells, leading to activation of CD4+ T cells

Block 1/Question#40
A 45-year-old man with chronic pancreatitis caused by alcohol ...
Pancrelipase

Block 1/Question#41
A 21-year-old man is brought to the emergency department 1 ...
Gender and body habitus

Block 1/Question#42
An 18-year-old woman develops sepsis after an abortion. ...
Decreased plasma fibrinogen concentration

Block 1/Question#43
A 13-year-old girl is brought to the emergency department 15 ...
C1 inhibitor

Block 1/Question#44
A 52-year-old man with a history of alcoholic cirrhosis is ...
Superior rectal

Block 1/Question#45
A 16-year-old girl is brought to the physician because of ...
Diuretics

Block 1/Question#46
A 12-year-old girl is referred to the emergency department by ...
Conversion disorder

Block 1/Question#47
A 25-year-old woman comes to the physician because of easy ...
Immune thrombocytopenic purpura

Block 1/Question#48
A 1-year-old boy is found to have an impairment of the ...
Staphylococcus aureus

Block 1/Question#49
A 17-year-old primigravid woman at 16 weeks' gestation has a ...
Azithromycin

Block 1/Question#50
A 9-year-old boy is brought to the physician by his mother ...
Protein structure

Block 2/Question#1
A 29-year-old woman is brought to the emergency department 1 ...
Avulsion of hepatic veins from the inferior vena cava

Block 2/Question#2
A 65-year-old man starts using topical fluorouracil for ...
Thymidylate synthase

Block 2/Question#3
A previously healthy 28-year-old man comes to the physician's ...
Nephrolithiasis

Block 2/Question#4
A previously healthy 60-year-old woman is admitted to the ...
Increased central venous pressure

Block 2/Question#5
A 74-year-old man with emphysema and lung cancer is brought ...
Negative nitrogen balance

Block 2/Question#6
A 52-year-old man is brought to the emergency department 1 ...
4 Months

Block 2/Question#7
A 66-year-old man comes to the physician because of a 2-month ...
Libido: decreased;
Nocturnal erections: normal


Block 2/Question#8
A 73-year-old man has difficulty urinating and frequent ...
Area labeled ‘E’

Block 2/Question#9
A 26-year-old woman develops hypotension and hemoglobinuria ...
Antibody, complement C5-9

Block 2/Question#10
A 56-year-old man with a palpable hard nodule on the prostate ...
Pelvic parasympathetic nerves

Block 2/Question#11
A 52-year-old man comes to the physician because a lump in ...
Sensation from the anterior surface of the scrotum

Block 2/Question#12
A 42-year-old woman with frequent heartburn has relief of ...
cAMP

Block 2/Question#13
A 5-year-old boy who lives on a farm has had diarrhea, ...
Yersinia enterocolitica

Block 2/Question#14
A previously healthy 12-year-old boy is brought to the ...
Glucose and sodium

Block 2/Question#15
A 62-year-old woman comes to the physician 3 days after ...
Carcinoma of the breast

Block 2/Question#16
A 60-year-old man is brought to the emergency department ...
Prostate adenocarcinoma

Block 2/Question#17
Ten healthy human subjects are given a new oral drug and ...
Phase 1

Block 2/Question#18
A 32-year-old man comes to the physician because of a 2-week ...
Reverse transcriptase

Block 2/Question#19
A 50-year-old man comes to the physician 3 days after his ...
Calcium

Block 2/Question#20
A 26-year-old nulligravid woman comes to the physician ...
Hypothalamus

Block 2/Question#21
A newborn has cyanosis, tachypnea, and retractions of the ...
Respiratory acidosis and metabolic acidosis

Block 2/Question#22
A 35-year-old man comes to the physician because of a 3-year ...
Adenylyl cyclase

Block 2/Question#23
A 32-year-old woman comes to the physician because of a 1-day ...
Reduviid bug

Block 2/Question#24
A 72-year-old man is given ketorolac for pain control after ...
Acute renal failure

Block 2/Question#25
A 37-year-old woman undergoes excision of a 1-cm, painless, ...
Angiogenesis

Block 2/Question#26
A randomized controlled trial is conducted to assess the ...
(194/2371) – (123/2365)

Block 2/Question#27
A 50-year-old man who has smoked 2 packs of cigarettes a day ...
Increased blood HCO3−

Block 2/Question#28
A 65-year-old man comes to the physician for a follow-up ...
Ulnar and tibial

Block 2/Question#29
A 79-year-old man is brought to the emergency department by ...
Insertion of transvenous pacemaker

Block 2/Question#30
A 40-year-old woman comes to the physician because of a ...
Multifactorial

Block 2/Question#31
An unimmunized 1-year-old boy is admitted to the hospital ...
Phase variation

Block 2/Question#32
A 54-year-old man who works in a delicatessen comes to the ...
Schwann cells

Block 2/Question#33
A 29-year-old woman comes to the physician because of a ...
Thyroid-stimulating hormone: decreased;
Free thyroxine: decreased;
Free triiodothyronine: increased


Block 2/Question#34
A 30-year-old man and a 24-year-old woman (indicated by the ...
1 in 600

Block 2/Question#35
A 45-year-old man with Li-Fraumeni syndrome agrees to ...
Decreased binding of RNA polymerase

Block 2/Question#36
Which of the following drug effects is the most common reason ...
Anticholinergic

Block 2/Question#37
A 63-year-old man has had progressive stiffness over the past ...
Area labeled ‘D’

Block 2/Question#38
Following a stroke, a patient is hoarse and cannot detect ...
Lateral medulla

Block 2/Question#39
A 22-year-old woman comes to the office because of a 3-day ...
Cardiomyopathy

Block 2/Question#40
A previously healthy 7-year-old girl is brought to the ...
Serum potassium concentration

Block 2/Question#41
A 12-year-old boy is swimming in a mountain stream. He is ...
Central blood volume: increased;
Serum ADH (vasopressin): decreased;
Serum atrial natriuretic peptide: increased


Block 2/Question#42
A 75-year-old woman has taken 12 over-the-counter ...
Plasma renin activity

Block 2/Question#43
A 20-year-old man comes to the physician because of tingling ...
Area labeled ‘C’

Block 2/Question#44
A 3-day-old full-term male newborn is brought to the ...
Hepatic UDP-glucuronosyltransferase activity

Block 2/Question#45
An 86-year-old man who lives in a skilled nursing care ...
Dextromethorphan

Block 2/Question#46
A 62-year-old man is being evaluated for rectal bleeding. An ...
Greater mucosal surface area

Block 2/Question#47
A 22-year-old woman who is at 16 weeks' gestation has ...
Down syndrome

Block 2/Question#48
Clostridium perfringens-α toxin affects cells and facilitates ...
Splitting lecithin to phosphorylcholine and diglyceride

Block 2/Question#49
A physician is unable to communicate "bad news" to a patient ...
Countertransference

Block 2/Question#50
An 18-month-old boy is admitted to the hospital because of ...
Tuberous sclerosis complex

Block 3/Question#1
A 35-year-old man comes to the physician because of a 6-week ...
C7 nerve root

Block 3/Question#2
A 30-year-old man is brought to the emergency department 30 ...
Increased serum angiotensin II concentration

Block 3/Question#3
An obese 45-year-old woman with type 2 diabetes mellitus, ...
Diarrhea

Block 3/Question#4
A 29-year-old woman has an inflammatory disease involving her ...
Immune complex-mediated cytotoxicity

Block 3/Question#5
A 72-year-old man with multiple myeloma agrees to participate ...
Unrearranged immunoglobulin gene

Block 3/Question#6
A 50-year-old man is admitted to the hospital because of ...
Intracellular [Na+]: increased;
Intracellular [K+]: decreased;
Intracellular [Ca2+]: increased


Block 3/Question#7
A 50-year-old man who is a college professor has had an ...
It must be difficult for you to accept this diagnosis when you feel healthy.

Block 3/Question#8
A 38-year-old man who lives at sea level flies to a mountain ...
pH: increased;
HCO3-: increased;
Volume: increased


Block 3/Question#9
Microelectrode injection of antibodies to α-actinin results ...
Area labeled ‘C’

Block 3/Question#10
A 50-year-old man comes to the physician for follow-up ...
Yes; the patient may wish to consider the money's influence on the physician's recommendation

Block 3/Question#11
A 38-year-old man with Down syndrome is brought to the ...
Contact adult protective services

Block 3/Question#12
An 82-year-old woman has been bedridden since surgical repair ...
Carboxylation of precursor proteins

Block 3/Question#13
A previously healthy 26-year-old woman comes to the physician ...
Acute retroviral infection

Block 3/Question#14
A 57-year-old woman comes to the physician 2 weeks after ...
Intercostal

Block 3/Question#15
An 18-year-old man comes to the physician 10 days after ...
C8

Block 3/Question#16
A 27-year-old woman comes to the physician because of ...
Antiphospholipid antibodies

Block 3/Question#17
A 50-year-old man with chronic gastritis is diagnosed with a ...
Helicobacter pylori

Block 3/Question#18
An 85-year-old woman is diagnosed with a fracture of the ...
Morphine is metabolized to active metabolites that accumulate

Block 3/Question#19
A 42-year-old man comes to the physician because of numbness ...
Sensory neuropathy

Block 3/Question#20
A 43-year-old man is brought to the emergency department ...
Fibularis (peroneus) brevis

Block 3/Question#21
A screening test for cancer is developed and applied to 500 ...
Data point labeled ‘A’

Block 3/Question#22
A study is conducted to assess the prevalence of hypertension ...
Chi-square test

Block 3/Question#23
A 45-year-old woman comes to the physician for a follow-up ...
25%

Block 3/Question#24
An 84-year-old woman comes to the physician because of a ...
Downregulation of E-cadherin

Block 3/Question#25
A 3-month-old girl is brought to the physician by her mother ...
Motor: normal;
Social: delayed;
Verbal and cognitive: delayed


Block 3/Question#26
A study is conducted to assess the extent of cardiac valvular ...
Type I error: No change;
Type II error: decreased


Block 3/Question#27
A 45-year-old man with poorly controlled type 2 diabetes ...
Enterococcus faecalis

Block 3/Question#28
A 12-year-old girl who recently immigrated to the USA from ...
Praziquantel

Block 3/Question#29
A 45-year-old man with end-stage renal failure is brought to ...
Bicarbonate

Block 3/Question#30
Which of the following is required for the synthesis of ...
Glutamine

Block 3/Question#31
A 35-year-old man is admitted to the hospital because he has ...
Absorption of nitrogenous products from the gastrointestinal tract

Block 3/Question#32
A 25-year-old woman comes to the physician because of a ...
Fasting insulin: increased;
Testosterone: increased;
Luteinizing hormone: increased


Block 3/Question#33
A 22-year-old man comes to the physician because of ...
47,XXY

Block 3/Question#34
The risk for hemorrhagic stroke from drug X is investigated ...
Case-control study

Block 3/Question#35
A 4-year-old boy is brought to the physician by his parents ...
Interstitial inflammation

Block 3/Question#36
A 62-year-old man comes to the physician's office for ...
Alternative treatments

Block 3/Question#37
A 35-year-old man with bronchial asthma starts taking ...
Increase in cAMP

Block 3/Question#38
A 73-year-old man comes to the physician with his wife ...
Blood pressure

Block 3/Question#39
A 52-year-old man with stable angina pectoris begins ...
Headache

Block 3/Question#40
A 49-year-old man has had the gradual onset of numbness and ...
Essential thrombocythemia

Block 3/Question#41
A 56-year-old man develops brief episodes of ventricular ...
CL x Css

Block 3/Question#42
A 62-year-old man comes to the physician for a follow-up ...
Inorganic phosphorus: increased;
Parathyroid hormone: increased;
Calcitriol: decreased


Block 3/Question#43
A 53-year-old woman shows evidence of adrenal failure. On CT ...
Autoimmune adrenalitis

Block 3/Question#44
A 35-year-old man comes to the physician because of an itchy ...
Prescribe permethrin for the patient and his family

Block 3/Question#45
A 28-year-old man who is seropositive for HIV has numerous ...
Slit-like vascular spaces with plump spindle-shaped stromal cells

Block 3/Question#46
A 54-year-old woman with hypertension and bilateral renal ...
Vasodilating prostaglandins at the afferent arteriole

Block 3/Question#47
A 10-year-old boy receives a renal transplant from a living, ...
Lymphocytes infiltrating tubular epithelium

Block 3/Question#48
A 2-year-old boy is brought to the physician because of fever ...
Bruton agammaglobulinemia

Block 3/Question#49
A 42-year-old man is brought to the emergency department ...
Dopaminergic neurons in the substantia nigra

Block 3/Question#50
A 56-year-old woman is brought to the emergency department by ...
Herpes encephalitis

Block 4/Question#1
A 2-day-old full-term female newborn suddenly develops ...
Superior mesenteric

Block 4/Question#2
Thirty minutes after taking 2 aspirin tablets for a tension ...
Acetaminophen

Block 4/Question#3
A 60-year-old man comes to the physician because of ...
Alveolar macrophage

Block 4/Question#4
A 24-year-old man who is comatose is admitted to the hospital ...
25 mL/cm H2O

Block 4/Question#5
A new virus has been isolated that causes encephalitis. The ...
Single-stranded positive-sense

Block 4/Question#6
A population of vegetarians is surveyed to investigate the ...
t-Test

Block 4/Question#7
A 27-year-old man comes to the physician for a routine ...
Ask the patient to identify the pros and cons of smoking cessation

Block 4/Question#8
A 6-year-old boy who recently emigrated from Russia is ...
Vitamin E

Block 4/Question#9
A 5-year-old boy is brought to the physician because of a ...
Interruption of erythrocyte production

Block 4/Question#10
An 81-year-old man comes to the physician for ongoing ...
Atherosclerosis

Block 4/Question#11
A 26-year-old woman comes to the physician 5 weeks after the ...
Sertraline

Block 4/Question#12
A 73-year-old woman dies 7 years after the onset of ...
Hydrocephalus ex vacuo

Block 4/Question#13
A 36-year-old woman comes to the physician because of a ...
Cytosol with translocation into the nucleus

Block 4/Question#14
In patients with adenosine deaminase deficiency, there is a ...
Ribonucleotide reductase

Block 4/Question#15
A 24-year-old woman, gravida 1, para 1, comes to the ...
Release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes

Block 4/Question#16
A 4-month-old boy is brought to the office by his parents ...
Maxillary and medial nasal prominences

Block 4/Question#17
A 62-year-old man with dyslipidemia is brought to the ...
Gemfibrozil

Block 4/Question#18
A 10-year-old girl has a slightly painful 2-mm subcutaneous ...
Granuloma

Block 4/Question#19
A 76-year-old man with a 1-month history of a pulsatile ...
Anomalous origins of multiple renal arteries to each kidney

Block 4/Question#20
During a study of symptomatic proximal deep venous ...
Open-label clinical trial

Block 4/Question#21
A previously healthy 45-year-old woman has had fever, ...
Thrombotic thrombocytopenic purpura

Block 4/Question#22
A 37-year-old man comes to the physician for a follow-up ...
Hyperplastic arteriolosclerosis

Block 4/Question#23
A 57-year-old woman comes to the office because of a 5-week ...
Autoimmune downregulation of Ca2+ channels of the presynaptic terminal

Block 4/Question#24
A 39-year-old woman with rheumatoid arthritis comes to the ...
Tumor necrosis factor-α

Block 4/Question#25
A healthy 25-year-old man eats a meal consisting of 60% ...
Fusion of an intracellular vesicle with the plasma membrane

Block 4/Question#26
A 60-year-old woman comes to the physician because of a ...
Meningioma

Block 4/Question#27
A 78-year-old man comes to the physician because of a 3-month ...
Metastatic carcinoma

Block 4/Question#28
A 48-year-old man comes to the emergency department because ...
Splenic vein

Block 4/Question#29
A 45-year-old man who is HIV positive comes to the physician ...
Disruption of the pathogen cell membrane

Block 4/Question#30
A 27-year-old man who is a construction worker is brought to ...
Splenic flexure

Block 4/Question#31
A 65-year-old man comes to the emergency department because ...
Crackles

Block 4/Question#32
A case-control study is conducted to assess the relationship ...
Cannot be determined from the data given

Block 4/Question#33
A 38-year-old single woman with a history of chronic ...
Displacement

Block 4/Question#34
A 17-year-old boy comes to the physician because of a 1-week ...
B lymphocyte

Block 4/Question#35
Nicotinic acid acts at which of the following labeled sites ...
Pathway labeled ‘C’

Block 4/Question#36
A 38-year-old man is admitted to the hospital after ...
Acute-phase response

Block 4/Question#37
A 53-year-old woman with a long history of fibromuscular ...
Tubular atrophy

Block 4/Question#38
Patients with mucolipidosis II (I-cell disease) lack the ...
Secreted from the cells

Block 4/Question#39
A 5-year-old boy is brought to the physician because of pain ...
Retinal cells

Block 4/Question#40
A 5-year-old boy with mental retardation is grossly obese and ...
Maternal origin of both chromosomes 15

Block 4/Question#41
A 65-year-old woman with a 20-year history of osteoarthritis ...
L-3 to 4

Block 4/Question#42
A 31-year-old man comes to the physician because of concerns ...
Dihydrotestosterone

Block 4/Question#43
A 44-year-old man comes to the physician because of fever and ...
Tricuspid insufficiency

Block 4/Question#44
A 10-year-old boy has bruised easily since swallowing some of ...
Prolonged prothrombin time

Block 4/Question#45
An 1814-g (4-lb) male newborn is delivered in the hospital at ...
Endodermal cells

Block 4/Question#46
A 39-year-old woman comes to the physician because of ...
Hemoglobin

Block 4/Question#47
A 56-year-old woman comes to the physician for a follow-up ...
Maintenance of basement membrane integrity

Block 4/Question#48
An 8-year-old boy is brought to the physician by his parents ...
Calorie consumption that exceeds energy expenditure

Block 4/Question#49
A 52-year-old man with metastatic oat cell carcinoma begins ...
Ensure that the patient receives enough medication to control his pain

Block 4/Question#50
A 31-year-old woman in the second trimester of pregnancy is ...
Hematopoietic stem cells

Recent comments ...

... meningitis made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
 +8  upvote downvote
submitted by meningitis(121)

I also thought the same as @bubbles, but now trying to "justify" this tricky NBME question: I think this revolves on the fact that the patient has a HIGH blood pressure meaning we should focus on an answer that explains both increased BP and Hypovolemia (i.e: increased ADH which vasoconstricts and also absorbs free-water, both of which increase BP and cause hypovolemia).

Maybe if this patient were decompensated with LOW BP, one could think more about ANP.

I still think this question is TOO tricky.

meningitis  Sorry, hyponatremia* right?
... bubbles made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
 +1  upvote downvote
submitted by bubbles(26)

This question confused me a lot because so many questions have drilled me on the importance of the ANP escape mechanism in times of fluid overload (as in CHF).

I thought ANP was a huge player in the loss of Na in circumstances of volume overload as in this patient (which is why you see euvolemic hypOnatremia in patients with SIADH or overactivity of the RAAS as in CHF).

Why is ADH now being named as the responsible agent?

jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong.
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha.
... imgdoc made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
 +3  upvote downvote
submitted by imgdoc(18)

I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

... moloko270 made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
 +1  upvote downvote
submitted by moloko270(29)

https://www.ncbi.nlm.nih.gov/pubmed/7058822

"syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli"

hayayah  Apparently, in chronic CHF you see hyponatremia. Because CHF causes a decrease in cardiac output and circulating blood volume, which in turn triggers a compensatory response aimed at preserving blood pressure. This stimulates the body to retain both water and sodium.
seagull  i agree with Hayayah... the RAAS system is activated due to poor perfusion to the kidney due to decomp heart failure.
... dr.xx made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
 +1  upvote downvote
submitted by dr.xx(35)

CHF patients often display signs and symptoms of increased vasopressin secretion.

hyperfukus  if all else fails i hope i just drill this one statement in my brain and it comes out in the right way on test day thank u!!!
... fuckster made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
... nwinkelmann made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
 +1  upvote downvote
submitted by nwinkelmann(60)

From UpToDate: PATHOGENESIS

Like most other causes of hyponatremia, heart failure impairs the ability to excrete ingested water by increasing antidiuretic hormone levels. When cardiac output and systemic blood pressure are reduced, "hypovolemic" hormones, such as renin (with a subsequent increase in angiotensin II formation), antidiuretic hormone (ADH), and norepinephrine, respond [1-3]. Although edematous patients with heart failure have increased plasma and extracellular fluid volumes, the body perceives volume depletion (reduced effective arterial blood volume) since the low cardiac output decreases the pressure perfusing the baroreceptors in the carotid sinus and the renal afferent arteriole. The degree of neurohumoral activation is generally related to the severity of cardiac dysfunction, as assessed by left ventricular ejection fraction or functional class [2]. The neurohumoral changes limit both sodium and water excretion in an attempt to return perfusion pressure to normal. ADH release directly enhances water reabsorption in the collecting tubules, whereas angiotensin II and norepinephrine limit distal water delivery (and thereby water excretion) by lowering the glomerular filtration rate (due to a marked reduction in renal perfusion) and by increasing proximal sodium and water reabsorption [4]. In addition, both the low cardiac output and high angiotensin II levels are potent stimuli to thirst, leading to enhanced water intake.

https://www.uptodate.com/contents/hyponatremia-in-patients-with-heart-failure#H2

... fuckster made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
... fuckster made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
... lauri made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
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submitted by lauri(0)

I CANNOT VIEW THE ENTIRE QUESTION. IS THIS NORMAL?

trichotillomaniac  Hi Lauri, this is normal. We can't post the whole question due to copy right laws but you can almost always find the question you are looking for and the answer to by going to the form and then Ctrl + find -ing the age of the patient and other key words or the answer!
drdoom  HI LAURI. THANK YOU FOR DEMONSTRATING YOUR PROFICIENCY WITH ALL-CAP COMPOSITION!
... hello made a comment on nbme22/block1/q#1 (A 66-year-old man develops worsening shortness of...)
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submitted by hello(51)

There has to be a better explanation for why ANP is wrong?

... armymed88 made a comment on nbme22/block1/q#2 (A 28-year-old man has recurrent pancreatitis...)
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submitted by armymed88(13)

Shouldn't the treatment for hyperTG be a fibrates? Which would indicate the answer to be increasing HDL (FA.2017 p306)

I see decreasing VLDL as a function of niacin, which serves to decrease hepatic VLDL..

keycompany  Fibrates inhibit VLDL secretion (by inhibiting 7-a Hydroxylase) and they increase HDL. However, this patient has chronic pancreatitis, which decreases enzymes that allow for fat absorption. Because a large portion of HDL is synthesized in enterocytes from newly absorbed fat, HDL content is unlikely to increase in patients with chronic pancreatitis from any of the lipid-lowering agents. Hope this helps!
mr_haib  fibrates cause decreased VLDL as well as niacin. They increase the activity of LpL by activating PPARa causing increase catabolism of VLDL and chylomicrons. since VLDL are rich in triglycerides, this is how they decrease triglycerides.
lordxrequiem  but fibrates also decrease bile acid production by inhibiting 7alpha hydroxylase, which is how they cause increased cholesterol gallstones.
... gh889 made a comment on nbme22/block1/q#2 (A 28-year-old man has recurrent pancreatitis...)
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submitted by gh889(32)

The answer is due to an exception outlined here where niacin is used in pts w/o diabetes who have refractory hypertriglyceridemia at high risk or has a hx of pancreatitis.

I agree that fibrates are first line (and so does that article) but NBME was honing in on a specific exception that niacin can also be used since VLDL and TGs are high in hypertriglyceridemia.

The "clue" they had was "recurrent pancreatitis" which is supposedly a lead towards niacin.

I also put increase HDL....

wutuwantbruv  Correct, you would not want to give fibrates to someone with recurrent pancreatitis since fibrates increase the risk of cholesterol gallstones due to inhibition of cholesterol 7α-hydroxylase.
kernicterusthefrog  FYI @gh889 can't follow your link w/o an NYIT username and password, unless there's a more tech-savvy way around that.. I appreciate the info, though. Niacin rx for familial hypertriglyceridemia w/ recurrent pancreatitis. Now I know..
impostersyndromel1000  Great points, very in depth knowledge taking place here. Also, familial hypertriglyceridemia (per FA 2019 pg 94) has hepatic overproduction of VLDL so picking this would have been the easiest answer (in retrospect)
hyperfukus  @impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while
... dr.xx made a comment on nbme22/block1/q#2 (A 28-year-old man has recurrent pancreatitis...)
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submitted by dr.xx(35)

Fibrates decrease triglycerides by reducing the production of VLDL.

... hyperfukus made a comment on nbme22/block1/q#2 (A 28-year-old man has recurrent pancreatitis...)
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submitted by hyperfukus(5)

so I think if you forget actual drugs on the market that we know of and how they work, the question is purposely not asking you that specifically...If you flip it in your head to think what the problem is that leads to inc TG its because of VLDL therefore they said administering a DRUG with which of the following EFFECTS is MOST appropriate--->DECREASING VLDL b/c that's the culprit

Although drugs we know of have the other characteristics, for this guy, we would be looking for the effect of VLDL everything else is a side thing that doesn't directly address his condition

... fleurmuxlin made a comment on nbme22/block1/q#2 (A 28-year-old man has recurrent pancreatitis...)
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submitted by fleurmuxlin(0)

First Aid Page 94

Type 4 -hypertriglyceridemia is caused by Hepatic overproduction of VLDL. If we just consider the primary issue, then it is easy to see why decreasing VLDL would be the answer.

(full disclosures, I also was think about the types of medication that should be used)

... upstairs_bumblebee made a comment on nbme22/block1/q#3 (Parenterally administered cholera vaccines...)
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submitted by upstairs_bumblebee(7)

The question asks about parenteral administration of the vaccine (meaning, not using the oral route). Non-oral vaccines will not strongly elicit IgA response. Non-oral vaccines not super helpful in combating a gut mucosal infection such as V. cholera, where IgA is more salient. Not sure if this is the actual correct reasoning, but it led to the right answer.

aesalmon  I totally skipped over the word "parentally" when taking this - ugh!
... biliarytree220 made a comment on nbme22/block1/q#4 (A 48-year-old man begins furosemide therapy for...)
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submitted by biliarytree220(5)

Should use a potassium-sparing diuretic (FA 591). Triamterene and amiloride work by blocking ENaC channels.

... just_1more made a comment on nbme22/block1/q#4 (A 48-year-old man begins furosemide therapy for...)
 +1  upvote downvote
submitted by just_1more(1)

I got that it needed to be a potassium sparing diuretic. Is there a reason it cannot be an aldosterone antagonist? I chose blocks basolateral K+ channels as these decrease the basolateral K+/Na+/ATPase because the wording of the correct answer did not make sense to me -- assuming they were going for an ENaC blocker (and that decreased luminal permeability indicates that Na+ would be remaining in the lumen, not remaining in the principal cell as I originally thought).

luckeroo  I think the reason it’s a potassium-sparing diuretic rather than an aldosterone antagonist has less to do with why the aldosterone antagonist cannot be used and more to do with the fact that a potassium-sparing diuretic would be more of a “first-line” adjunctive diuretic treatment.
luckeroo  As for the answer choice, potassium sparing diuretics achieve their overall anti-aldosterone effect by competitively inhibiting aldosterone receptors on the interstitial side (decreasing the Na/K-ATPase effect of shunting Na into the blood), thereby decreasing the gradient for sodium to enter the cell from the luminal aspect, blocking ENaC.
yotsubato  There is no such thing as "Basolateral K Channel" there is only basolateral Sodium Potassium Pumps which are controlled by aldosterone. FA pg 573
nwinkelmann  @yotsubato LOL.... why didn't I think of it that what?! (by the way, that LOL is for me). The only basolateral K channel is the nephron (based on the first aid picture) is in the thick ascending limb of the loop of henle.
hello  Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase, so I'm not sure what @luckeroo is referring to. Spironolactone and aplerenone are both ALDO antagonists. Na/K ATPase is found on the basolateral membrane. None of the answer choices fit with this. Amiloride and triamterene are also potassium-sparing diuretics; their mechanism is to block ENaC channels on the luminal membrane, this is choice "B."
... hello made a comment on nbme22/block1/q#4 (A 48-year-old man begins furosemide therapy for...)
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submitted by hello(51)

Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase. Na/K ATPase is on the basolateral membrane. None of the answer choices fit with this.

Amiloride and triamterene are also potassium-sparing diuretics. The mechanism is to block ENaC channels on the luminal membrane, this is choice "B."

... dr.xx made a comment on nbme22/block1/q#5 (A 10-month-old girl is brought to the emergency...)
 -1  upvote downvote
submitted by dr.xx(35)

Normal respiratory rate for a 10 month old > 50 breaths per minute.

Naloxone should be given in the presence of respiratory depression and may require repeated dosing.

https://www.ncbi.nlm.nih.gov/pubmed/28506439

... d_holles made a comment on nbme22/block1/q#5 (A 10-month-old girl is brought to the emergency...)
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submitted by d_holles(31)

This question confused me bc I thought loperamide could not cross the BBB and therefore could not cause respiratory depression (mu-opioid agonism at the brainstem results in CNS/respiratory depression, 1). But @dr.xx is correct in noting that ↓ RR and CNS depression in the Pt should call for an mu-opioid antagonist rather than bethanchol (cholinomimetic) to treat constipation.

  1. https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2675905
nwinkelmann  http://medresearch.in/index.php/IJPR/article/view/782/1271 This explains a case in an infant. "Respiratory depression and coma after overdosage have been shown to be reversible by injection of naloxone [6]. Owing to its structural similarity to opioid, loperamide toxicity can be reversed by using Nalaxone which is a specific opioid antagonist acts competitively at opioid receptors. Naloxone hydrochloride is usually given intravenously for a rapid onset of action which occurs within 2 minutes."
yb_26  FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression
whoissaad  Also maybe because the blood brain barrier in a baby is not developed as well as in an adult.
... seagull made a comment on nbme22/block1/q#6 (A 2-month-old boy is brought to the physician...)
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submitted by seagull(355)

True vocal cords are often damaged in singing or yelling. THis allows HPV to enter the underlying nucleated cells. HPV 16 and 18 are common subtypes that may cause SCC.

meningitis  Out of all of the virus', HPV has a predilection for stratified squamous epithelium and there is no indication of vesicles(HSV) or linear ulcers (CMV)in the question stem. But with HPV you usually get a big/small (depending on time) unilateral nodule. You are correct to say singing and yelling can cause nodules but these would be bilateral in the and would appear differently. So if a question stem could easily have included that as an option: maybe irritation or something like that.
... chosened made a comment on nbme22/block1/q#6 (A 2-month-old boy is brought to the physician...)
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submitted by chosened(1)

Correct me if I m wrong but I think it's laryngeal papillomatosis. Papillomas can develop anywhere along the respiratory tract, but most often affect the larynx and the vocal cords (laryngeal papillomatosis). Not sure how HY this is but heres More info: https://rarediseases.org/rare-diseases/recurrent-respiratory-papillomatosis/

hyperfukus  yes you are definitely correct i think its a common wtf q that pops up bc there's one on uworld that asks if its true or false vocal cords and i had to hunt my prof down to figure it out...
hyperfukus  also i think they love anything that compromises the airway
... keycompany made a comment on nbme22/block1/q#7 (Two patients, a 54-year-old man (Patient X) and a...)
 +1  upvote downvote
submitted by keycompany(105)

Loading Dose is the only answer that is independent of drug clearance.

nwinkelmann  I totally get this and understand it... but at the same time, couldn't loading dose differ due to renal function if patient has nephrotic syndrome so had less plasma proteins, because it would change the Vd of the drug, right? Per wiki: Volume of distribution may be increased by renal failure (due to fluid retention) and liver failure (due to altered body fluid and plasma protein binding). Conversely it may be decreased in dehydration.
... usmleuser007 made a comment on nbme22/block1/q#7 (Two patients, a 54-year-old man (Patient X) and a...)
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submitted by usmleuser007(86)

Someone care to explain why [time to steady-state concentration] is not the correct answer?

omerta  In pharmacokinetics, steady state refers to the situation where the overall intake of a drug is fairly in dynamic equilibrium with its elimination. In practice, it is generally considered that steady state is reached when a time of 4 to 5 times the half-life for a drug after regular dosing is started. The time to reach steady state is defined by the elimination half-life of the drug. So in a patient with renal dysfunction, the plasma half-life is going to be prolonged and the time to reach steady state will increase proportionally.
belleng  loading dose is independent of the concentration of the drug in the plasma and the dose frequency...this is why you give a patient who is seizing a huge dose of anti-seizure meds in order to reach a theraputic range on the first dose despite the high risk of toxicity and side effects...primary objective when seizing is stoping the seizure so you want to increase the dose response curve with a massive load
belleng  loading dose is independent of DOSE (should have said dose, not concentration in plasma) & FREQUENCY
... amitgrewal990 made a comment on nbme22/block1/q#7 (Two patients, a 54-year-old man (Patient X) and a...)
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submitted by amitgrewal990(1)

its in first aid 2019. Loading dose is unchanged in liver or renal dx. (FA 2019 pg233)

... mcl made a comment on nbme22/block1/q#8 (A 16-year-old girl has pain and tingling in her left...)
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submitted by mcl(169)

Homegirl got some cervical outlet syndrome and should probably take some stuff out of her backpack or get one of those lil roller ones.

mcl  Whoops, my bad, THORACIC outlet syndrome
dr.xx  Stretching, occupational and physical therapy are common non-invasive approaches used in the treatment of TOS. The cervical rib can be surgically removed.
... pparalpha made a comment on nbme22/block1/q#8 (A 16-year-old girl has pain and tingling in her left...)
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submitted by pparalpha(13)

According to BnB:

Cervical rib is an anomalous extra rib from the 7th cervical vertebrae. People with this are at risk for thoracic outlet syndrome (aka compression of nerves and vessels that leave the thorax. This occurs above the first rib and behind the clavicle).

Clinical features include:

1) brachial plexus injury (such as Klumpke palsy, which is a lower plexus injury)

2) Venous compression

3) Arterial compression

*An important anatomical correlate the scalene triangle (anterior scalene, middle scalene, above the first rib)

... keycompany made a comment on nbme22/block1/q#9 (A 54-year-old man has an aneurysm in the distal...)
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submitted by keycompany(105)

Flow Rate = Velocity x Cross-Sectional Area

2 cm^2 x 20 cm/sec x 60 sec/min x 1 L/1,000 cm^3 = 2.4 L/min

1,000 cm^3 = 1 L

seagull  Well, I missed this one. I don't even feel bad.
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L
hello  @keycompany how did you edit your original comment to fix your typo?
... kernicterusthefrog made a comment on nbme22/block1/q#9 (A 54-year-old man has an aneurysm in the distal...)
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submitted by kernicterusthefrog(17)

Just in case that lovely little equation provided by @keycompany wasn't quite enough for you, here's a link to a more complete explanation by Kahn Academy. Helped me, when I looked at the equation and said, whaaaa?

... nwinkelmann made a comment on nbme22/block1/q#9 (A 54-year-old man has an aneurysm in the distal...)
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submitted by nwinkelmann(60)

I've never been good at converting units :( lol so had to ask my brother. He told me that distance x distance = distance^2 = area, and distance x distance x distance = distance^2 x distance = distance^3 = volume. Gotta love public school for never been taught that... geesh (obviously I've done the equations and stuff, just never been told it that way/that simple before). Knowing that makes figuring out the equation much easier.

Flow rate = velocity x CSA = 20 cm/sec * 2cm^2 = 40cm^3/sec. To convert to L/min, just multiply: 40cm^3/sec X 60 sec/min X 1L/100cm^3 = 240 L/100 min = 2.4 L/min

Hope this helped!

impostersyndromel1000  to all my public school peeps out there (and not the nice public schools in rich areas, the real public schools)... we made it!
angelaq11  Thankfully I was taught how to convert units, but let me tell you that I was SO lost on this one. It's USELESS to know how to do it if you (I, I mean I) don't know the damn formula xD. Obviously got this one wrong, but it's good to know that if it ever comes up again (and I know it won't) I already know it.
... seagull made a comment on nbme22/block1/q#10 (A 25-year-old woman is admitted to the hospital...)
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submitted by seagull(355)

Splenectomy patients are vulnerable against encapsulated organisms. Which commonly include Strep Pneumo, Niesseria, H. Influenza.

... atstillisafraud made a comment on nbme22/block1/q#11 (A 6-month-old boy has recently been diagnosed with...)
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submitted by atstillisafraud(39)

Niemann-Pick Disease presents with mental retardation, lipid laden (foam cells) in bone marrow and cherry red spot on macula. No sphingomyelinase results in buildup of sphingomyelin which builds up in macrophages.

meningitis  "Pick your **Big** **Foamie** **Zeibra** nose with your Sphinger" Choose options with the letter I. SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells
... meningitis made a comment on nbme22/block1/q#11 (A 6-month-old boy has recently been diagnosed with...)
 +1  upvote downvote
submitted by meningitis(121)

"Pick your Big, Foamie, Zeibra nose with your Sphinger"

Choose options with the letter I.

SpIngomyelin, Sphingomyelinase, bIgorgans (hepatomegaly etc), zeIbra bodies, Foam cells

... dr.xx made a comment on nbme22/block1/q#12 (During the first week of life, a male newborn has...)
 +0  upvote downvote
submitted by dr.xx(35)

Congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia_due_to_21-hydroxylase_deficiency

wutuwantbruv  Can't be 17α-hydroxylase because this would present with hypertension and some sort of ambiguous sexual presentation (males) or lack of secondary sexual development (females). Can't be 11β-hydroxylase because this would present with the opposite of the kid's presentation due to the production of 11-deoxycorticosterone (similar effects to aldosterone but not nearly as potent). The other two would not really make sense since there are increased levels of 17-hydroxyprogesterone.
... wutuwantbruv made a comment on nbme22/block1/q#12 (During the first week of life, a male newborn has...)
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submitted by wutuwantbruv(2)

Can't be 17α-hydroxylase because this would present with hypertension and some sort of ambiguous sexual presentation (males) or lack of secondary sexual development (females). Can't be 11β-hydroxylase because this would present with the opposite of the kid's presentation due to the production of 11-deoxycorticosterone (similar effects to aldosterone but not nearly as potent). The other two would not really make sense since there are increased levels of 17-hydroxyprogesterone

... organicmechanic made a comment on nbme22/block1/q#13 (A 13-year-old girl is brought to the physician by...)
 -2  upvote downvote
submitted by organicmechanic(1)

Hereditary (or acquired) angioedema = C1 inhibitor deficiency. Patient has a 9-year Hx of soft tissue swelling, especially of the face. It's Autosomal Dominant if inherited, or can be acquired through multiple mechanisms.

https://www.ncbi.nlm.nih.gov/pubmed/11532278

dr.xx  wrong question?
... dr.xx made a comment on nbme22/block1/q#13 (A 13-year-old girl is brought to the physician by...)
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submitted by dr.xx(35)

During this initial encounter, we establish what the parents' concerns are, obtain a family history, and ask about previous medical problems. This begins the transition from parent to teen as the medical historian. We next ask parents to wait in the waiting room so that we can speak privately with the adolescent. We interview the adolescent alone, perform a physical examination with a chaperone, and then invite the parents back into the room at the conclusion of the visit to discuss our findings.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1070800/

... atstillisafraud made a comment on nbme22/block1/q#15 (A 35-year-old woman has weakness and fever. When she...)
 +4  upvote downvote
submitted by atstillisafraud(39)

Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts).
seagull  CML has blasts too but they tend to favor mature forms.
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company
sweetmed  Procarbazine is alkylating as well.
... d_holles made a comment on nbme22/block1/q#15 (A 35-year-old woman has weakness and fever. When she...)
 +2  upvote downvote
submitted by d_holles(31)

Goljan stresses the Boards giving the leukemia questions away based on the age given in the question stems.

ALL = 0-14

AML = 15-39; 40-59

CLL = 60+

CML = 40-59

https://forums.studentdoctor.net/threads/goljan-on-leukemias.303605/

impostersyndromel1000  thanks for the reminder, often overlooked are the simple demographic hints. helps you make an educated guess
hyperfukus  also a key thing to remember in general is a person who undergoes chemo is a big demographic hint to later developing AML regardless of the clues :) and yes the AGE!!!
... sweetmed made a comment on nbme22/block1/q#15 (A 35-year-old woman has weakness and fever. When she...)
 +1  upvote downvote
submitted by sweetmed(28)

Procarbazine side effect is leukemia. FA 2018 page 428

... keycompany made a comment on nbme22/block1/q#16 (An Rh-negative woman, gravida 3, para 2, has had an...)
 +2  upvote downvote
submitted by keycompany(105)

O, Rh-negative blood is the universal donor for blood plasma.

keycompany  Edit:: Blood RBCs***
... usmleuser007 made a comment on nbme22/block1/q#16 (An Rh-negative woman, gravida 3, para 2, has had an...)
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submitted by usmleuser007(86)

Mother is Rh-neg --> she will generate RH-antibodies 1) fetus affected by Anti-Rh if it is Rh-positive 2) even if O-Rh-Positive is given, then still mother's Rh-antibodies will attack transfused blood due to its cells containing Rh+ 3) therefore, O-Rh-negative is best

... _pusheen_ made a comment on nbme22/block1/q#17 (A 27-year-old man is brought to the emergency...)
 +0  upvote downvote
submitted by _pusheen_(1)

How can you tell that the ankle fracture is eversion?

lnsetick  Because there is avulsion fracture on medial side from deltoid ligament and fibular fracture on oppostie side, this is classic for an eversion.
... seagull made a comment on nbme22/block1/q#17 (A 27-year-old man is brought to the emergency...)
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submitted by seagull(355)

https://singaporeosteopathy.com/2015/05/23/ankle-injuries-sprain-strains-and-fractures/

Figure 2. although figure 1 looks shockingly similar

... pitaziki made a comment on nbme22/block1/q#17 (A 27-year-old man is brought to the emergency...)
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submitted by pitaziki(0)

Why is the answer fibularis brevis and not fibularis tertius? How do you distinguish between the two from this vignette?

gainsgutsglory  tertius is an anterior muscle and overlays the dorsum of foot as it fans out to the toes. Does not relate to the lateral malleolus.
... moloko270 made a comment on nbme22/block1/q#18 (A 13-year-old boy is brought to the physician for a...)
 +1  upvote downvote
submitted by moloko270(29)

increased amount of estrogen compared to androgen activity is physiologic in puberty

... meningitis made a comment on nbme22/block1/q#18 (A 13-year-old boy is brought to the physician for a...)
 +4  upvote downvote
submitted by meningitis(121)

Tanner stages start at TEN years old

Stage I:

  • I is flat, as in flat chest;
  • I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

  • 2 balls (testicular enlargement)
  • 2 hairs (pubic hairs now appearing)
  • 2 breast buds form

Stage III (3): starts at 13 y/o

  • If you rotate 3, it looks like small breasts (Breast mounds form);
  • If you squiggle the III they look like curly+coarse pubic hair
  • Increased penis length and size can be represented by: II --> III
    (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

  • First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
    MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
  • The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

  • V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
  • 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

meningitis  Sorry about the format, it came out wrong but I hope his helps.
drdoom  looks good to me!
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from?
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions.
endochondral1  stage 3 breast mound is for females not males btw
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females
angelaq11  this is just too funny, I LOVE it! xD
... dr.xx made a comment on nbme22/block1/q#18 (A 13-year-old boy is brought to the physician for a...)
 +1  upvote downvote
submitted by dr.xx(35)

Pubertal gynecomastia is thought to be a physiological phenomenon, and is most commonly seen in midpuberty with Tanner stage 3–4 pubic hair and testicular volumes of 5 to 10 mL bilaterally.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706045/

... impostersyndromel1000 made a comment on nbme22/block1/q#18 (A 13-year-old boy is brought to the physician for a...)
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submitted by impostersyndromel1000(4)

so its reassurance bc some boys can have mild breast development at 13? I've never heard or seen this before can someone please clarify. Basically reassuring that this is (relatively) normal?

... mcl made a comment on nbme22/block1/q#19 (An 11-year-old boy has had pain in his right...)
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submitted by mcl(169)

Ewing sarcoma is the second most common bone malignancy in children. Histology is usually described as a small cell tumor with high N:C ratio.

praderwilli  Also the concentric layers of reactive bone sounded like "onion skin" to me!
... meningitis made a comment on nbme22/block1/q#19 (An 11-year-old boy has had pain in his right...)
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submitted by meningitis(121)

Ewing sarcoma cells look like small blue hypercromatic cells because they are neuroectodermal origin (PNET) and are therefore undifferentiated with high N:C ratio.

Also remember 22+11 translocation (EWS gene on chromosome 22 and the FLI-1 gene on chromosome 11)

Yeah, I thought the same @praderwilli (about the concentric layers)

... link981 made a comment on nbme22/block1/q#19 (An 11-year-old boy has had pain in his right...)
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submitted by link981(24)

Important to know here is location. Apart from learning the histologic descriptions (which are boring as shit), neoplasia in the diaphysis is consistent with Ewing sarcoma. Osteosarcoma location is at the Metaphysis.

... usmleuser007 made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by usmleuser007(86)

(A) Risk factors for developing avascular necrosis include:

1) Trauma = Injuries, such as hip dislocation or fracture, can damage nearby blood vessels and reduce blood flow to bones.

2) Steroid use= Use of high-dose corticosteroids, such as prednisone, is a common cause of avascular necrosis. The reason is unknown, but one hypothesis is that corticosteroids can increase lipid levels in your blood, reducing blood flow.

3) Excessive alcohol use = Consuming several alcoholic drinks a day for several years also can cause fatty deposits to form in your blood vessels.

4) Bisphosphonate use = Long-term use of medications to increase bone density might contribute to developing osteonecrosis of the jaw. This rare complication has occurred in some people treated with high doses of these medications for cancers, such as multiple myeloma and metastatic breast cancer.

5) Certain medical treatments = Radiation therapy for cancer can weaken bone. Organ transplantation, especially kidney transplant, also is associated with avascular necrosis.

(B) Medical conditions associated with avascular necrosis include:

Pancreatitis Diabetes Gaucher's disease HIV/AIDS Systemic lupus erythematosus Sickle cell anemia

... usmleuser007 made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by usmleuser007(86)

Causes

1) Avascular necrosis occurs when blood flow to a bone is interrupted or reduced. Reduced blood supply can be caused by:

2) Joint or bone trauma. An injury, such as a dislocated joint, might damage nearby blood vessels. Cancer treatments involving radiation also can weaken bone and harm blood vessels.

3) Fatty deposits in blood vessels. The fat (lipids) can block small blood vessels, reducing the blood flow that feeds bones.

4) Certain diseases. Medical conditions, such as sickle cell anemia and Gaucher's disease, also can cause diminished blood flow to bone.

For about 25 percent of people with avascular necrosis, the cause of interrupted blood flow is unknown.

... fuckster made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by fuckster(-44)

[special]

... fuckster made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by fuckster(-44)

[special]

... meningitis made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by meningitis(121)

I think the small dark area on the left head of femur and the darkened neck are the avascular sites.

Neck: http://img.medscapestatic.com/pi/meds/ckb/15/19515tn.jpg

Head: (obvious lesion on the RT femur, but similar discrete lesion on the left as seen on the practice NBME) http://radsource.us/wp-content/uploads/2005/11/1a.jpg

... seagull made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by seagull(355)

maybe someone can explain why this is avascular necrosis and not sepsis. It doesn't mention fever or absence of fever. The MRI has a small amount of hypodensity but to get avascular necrosis seems odd/

someduck3  Pg 455 of F.A. mentions that alcoholism can be a cause of avascular necrosis.
meningitis  I think the small dark area on the left head of femur and the darkened neck are the avascular sites. Neck: http://img.medscapestatic.com/pi/meds/ckb/15/19515tn.jpg Head: (obvious lesion on the RT femur, but similar discrete lesion on the left as seen on the practice NBME) http://radsource.us/wp-content/uploads/2005/11/1a.jpg
yotsubato  He wouldnt be playing golf if he had septic arthritis. Avascular necrosis is a more chronic condition that has a slow onset.
... aerrow3 made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by aerrow3(-1)

What are we supposed to be seeing on the MRI? Or do you just base it off the patient being an alcoholic with hip problems? I would’ve assumed avascular necrosis would’ve shown something on the X-ray but the x-ray showed no abnormalities so idk if the MRI is showing something?

skinnynomore  alcoholic in the hx should point you towards avascular necrosis when there is an “atraumatic” complaint
... dr.xx made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by dr.xx(35)

MRI is highly sensitive, specific, and accurate in the detection of AVN.

T1-weighted images: AVN most often presents with a crescentic, ring-like or well defined band of low signal within the superior portion of the subchondral femoral head bone marrow. This band is thought to represent the reactive interface between the necrotic and reparative zones, and typically extends to the subchondral plate.

http://radsource.us/avn-of-the-hip/

... warbyparker1 made a comment on nbme22/block1/q#20 (A 49-year-old man comes to the physician because of...)
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submitted by warbyparker1(0)

I thought it was septic arthritis bc pain with weight bearing + mri, but 2 months with septic arthritis come on, it was an easy question and I missed it.

warbyparker1  Evolution time is key
... usmleuser007 made a comment on nbme22/block1/q#21 (A 30-year-old man comes to the physician because of...)
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submitted by usmleuser007(86)

1) ADPKD = polycystins (PC2)

2) ARPKD = fibrocystin /polyductin (FPC) -- similar to polycystins

FPC protein is found on the primary cilia of epithelia cells of cortical and medullary collecting ducts and cholangiocytes of bile ducts

FPC interacts with ADPKD protein PC2 and may also participate in this regulation pathway of the mechanosensory function of the primary cilia, calcium signaling, and PCP.

... fuckster made a comment on nbme22/block1/q#21 (A 30-year-old man comes to the physician because of...)
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submitted by fuckster(-44)

[special]

... dr.xx made a comment on nbme22/block1/q#21 (A 30-year-old man comes to the physician because of...)
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submitted by dr.xx(35)

The most common and severe form of autosomal dominant polycystic kidney disease (ADPKD) results from mutations in PKD1, encoding polycystin-1 (PC1)..

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4348948/

yotsubato  Here we thank FA for failing us yet again. Giving us PKD1, but not polycystin. I got the question right but I just guessed it because nothing else made sense.
usmleuser007  Autosomal dominant polycystic kidney disease 1) occurs in patients with mutations in the gene (PKD1) encoding polycystin-1 (PC1). 2) PC1 is a complex polytopic membrane protein expressed in cilia that undergoes autoproteolytic cleavage at a G protein–coupled receptor proteolytic site (GPS). 3) A quarter of PKD1 mutations are missense variants, though it is not clear how these mutations promote disease. 4) GPS cleavage is required for PC1 trafficking to cilia. 5) A common feature among a subset of pathogenic missense mutations is a resulting failure of PC1 to traffic to cilia regardless of GPS cleavage. 6) Missense mutation in the gene encoding polycystin-2 (PC2) that prevented this protein from properly trafficking to cilia. 
... welpdedelp made a comment on nbme22/block1/q#22 (A previously healthy 6-year-old boy is brought to...)
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submitted by welpdedelp(64)

It was scabies, which is transmitted person-operon.

welpdedelp  **person-person lol
... atstillisafraud made a comment on nbme22/block1/q#23 (A patient in the early stages of hemorrhagic shock...)
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submitted by atstillisafraud(39)

Ambiguous question but in because it is early shock, there is not enough time to activate the RAAS to increase kidney perfusion.

... dr.xx made a comment on nbme22/block1/q#23 (A patient in the early stages of hemorrhagic shock...)
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submitted by dr.xx(35)

Hypovolemia is a direct loss of effective circulating blood volume leading to:

  • A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia
  • Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction
  • Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis
  • Hypothermia due to decreased perfusion and evaporation of sweat
  • Thirst and dry mouth, due to fluid depletion
  • Cold and mottled skin (Livedo reticularis), especially extremities, due to insufficient perfusion of the skin

https://en.wikipedia.org/wiki/Shock_(circulatory)

... moloko270 made a comment on nbme22/block1/q#24 (A 48-year-old man with renal artery stenosis...)
... endochondral1 made a comment on nbme22/block1/q#24 (A 48-year-old man with renal artery stenosis...)
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submitted by endochondral1(4)

is this question asking what we physically pass through or by?

impostersyndromel1000  no, basically the question is testing if you know the branches of the abdominal aorta and which is closest to the renal (in this case, inferior to the renal arteries)
impostersyndromel1000  what you are passing by would better answer your question actually
... atstillisafraud made a comment on nbme22/block1/q#25 (During an experiment, a 22-year-old man receives an...)
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submitted by atstillisafraud(39)

Histamine causes capillary arteriolar dilation (decrease resistance)(increased pressure in the capillary because efferents remain the same size) Histamine also increases capillary permeability.

... moneysacs made a comment on nbme22/block1/q#25 (During an experiment, a 22-year-old man receives an...)
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submitted by moneysacs(0)

Histamine causes a decrease in hydrostatic pressure (get this, it’s a vasodilator) but then causes an increase in capillary hydrostatic pressure? (Okay, this is how it causes edema, I guess.) Does anyone get how this actually works?

its_raining_jimbos  Not 100% sure on this one, but here’s how I approached it: histamine causes arterial dilation (decreased arteriolar resistance), but all of that blood has to go somewhere since you now have more blood flowing through the arteries and that somewhere is the capillaries (increased capillary hydrostatic pressure). Histamine causes increased permeability of the post-capillary venules (one of Dr. Sattar’s favorite facts) so you’d have increased capillary filtration rate.
... its_raining_jimbos made a comment on nbme22/block1/q#25 (During an experiment, a 22-year-old man receives an...)
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submitted by its_raining_jimbos(8)

Not 100% sure on this one, but here’s how I approached it: histamine causes arterial dilation (=decreased arteriolar resistance), but all of that blood has to go somewhere since you now have more blood flowing through the arteries and that somewhere is the capillaries (increased capillary hydrostatic pressure). Histamine causes increased permeability of the post-capillary venules (one of Dr. Sattar’s favorite facts) so you’d have increased capillary filtration rate.

... link981 made a comment on nbme22/block1/q#25 (During an experiment, a 22-year-old man receives an...)
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submitted by link981(24)

Histamine causes arteriole vasodilation, causing a buildup of blood in the capillaries. The increased blood in the capillaries will cause the pressure there to rise. Filtration is dependent on pressure, the higher the pressure, the more the filtration.

Remember blood flow: veins to venules to capillaries to arterioles to arteries

yb_26  agree in all, except the blood flow - it is right the opposite [https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/]
link981  I stand corrected @yb_26. Brainfart moment 🙈
... alexb made a comment on nbme22/block1/q#25 (During an experiment, a 22-year-old man receives an...)
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submitted by alexb(10)

What they mean by filtration...

Fluid comprised of water and electrolytes, with a very small amount of protein and other macromolecules, normally leaves capillaries and small postcapillary venules by a process called filtration. Filtration is primarily driven by the capillary hydrostatic pressure, and the amount filtered per unit time is additionally influenced by the permeability of the vessel wall (endothelium and basement membrane). The fluid that filters into the tissue flows within the intercellular space (the interstitium) and most of it is reabsorbed at the venular end of capillaries where the hydrostatic pressure is lower. Some of the filtered fluid is taken up by lymphatic vessels and returned to the circulation.

... asapdoc made a comment on nbme22/block1/q#26 (A 42-year-old man comes to the physician because of...)
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submitted by asapdoc(17)

Patient has nephrogenic Diabetes Insipidus. One of the treatments is Hydrochlorthiazide.

meningitis  hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely. Also you shouldn't have chosen Desmopressin because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct. On that note, Amiloride is used for Lithium induced nephrogenic DI.
... meningitis made a comment on nbme22/block1/q#26 (A 42-year-old man comes to the physician because of...)
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submitted by meningitis(121)

hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely.

Desmopressin is incorrect because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct.

On that note, Amiloride is used for Lithium induced nephrogenic DI.

hello  Where in Pathoma? I couldn't find it.
... gh889 made a comment on nbme22/block1/q#26 (A 42-year-old man comes to the physician because of...)
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submitted by gh889(32)

according to uptodate thiazides cause a mild hypovolemic state thus your PCT will see more Na and H2O --> by principle that the PCT always reabsorbs 60% of what it sees, it will reabsorb more water and Na.

... link981 made a comment on nbme22/block1/q#27 (During a clinical study, 15 patients with renal...)
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submitted by link981(24)

Page 36 of FA 2018. Purine antagonist drugs are:

6-MP(Azathioprine is a prodrug of 6-MP), Mycophenolate, ribavirin.

sbryant6  I forgot what the MP stood for in 6-MP, so I chose methylprednisolone. Silly mistake.
... lamhtu made a comment on nbme22/block1/q#28 (A 48-year-old man comes to the physician because of...)
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submitted by lamhtu(26)

Hemochromatosis associated with HLA-A3, but the appropriate screening test is serum transferrin saturation and ferritin levels

... keycompany made a comment on nbme22/block1/q#28 (A 48-year-old man comes to the physician because of...)
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submitted by keycompany(105)

While this question stem is vague, the most likely diagnosis is Hereditary Hemochromatosis.

... usmleuser007 made a comment on nbme22/block1/q#29 (A 28-year-old man comes to the emergency department...)
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submitted by usmleuser007(86)

Intussusception is generally caused by a blockage in the GI tract caused by a tumor, polyp, diverticulum, or just immobility at part of the tract.

1) My thought was that the patient had a Meckel diverticulum yes it happens in 2 feet from the ileocecal valve; but that is in about %2 of the population

... mcl made a comment on nbme22/block1/q#29 (A 28-year-old man comes to the emergency department...)
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submitted by mcl(169)

These images are useful in combination.

... iviax94 made a comment on nbme22/block1/q#29 (A 28-year-old man comes to the emergency department...)
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submitted by iviax94(5)

CT shows mass on the left side of his abdomen and you’re told it’s intussusception. Asks which part of the GI tract is most likely to cause the pain. I immediately looked for ileocecal junction ... not an answer choice. Why is the answer jejunum (vs. duodenum)?

liverdietrying  The picture is key here. You’re right that ileocecal is most common, but ileo-ileal and jejuno-jejunal are the next most common (I think I might just know this from having done clerkships already, not sure). Ileo-ileal isn’t an answer, so that rules that out. Look at where the arrows are pointing in the picture as well. Its on the L, ruling out appendix and cecum. And the slice is not at the level of the duodenum, ruling out that answer. So by process of elimination based on the picture you could get this one too.
dr.xx  Duodeno-duodenal intussusception is a rare because of the retroperitoneal fixation of the duodenum. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4529645/
... lnsetick made a comment on nbme22/block1/q#29 (A 28-year-old man comes to the emergency department...)
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submitted by lnsetick(28)

How are you able to tell that the CT slice is not at the level of duodenum?

zelderonmorningstar  I think the small intestine narrows as you go along, so jejunum would most likely intuss into the duodenum.
yotsubato  Duodenum is fixed to the retroperitoneal wall, and also has lots of named vessels attached to it, along with the pancreaticobiliary duct and ampulla. It cant really intussuscept.
gh889  You should also know that the duodenum is almost purely on the right side of the body
... wolvarien made a comment on nbme22/block1/q#29 (A 28-year-old man comes to the emergency department...)
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submitted by wolvarien(0)

I have answered this question with this method the CT is showing a mass on the left appendix is on the right so this choice is wrong Ceacum is on the right so this choice is wrong stomach is on the middle so this choice is wrong duodenum intussusception never heard of it so the only thing left is Jejunum

... hello made a comment on nbme22/block1/q#29 (A 28-year-old man comes to the emergency department...)
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submitted by hello(51)

Please help - how are you able to tell that the CT image is not at the level of duodenum?

I don't know what I'm looking for to compare and contrast a CT at the level of the duodenum vs the CT given in this Q.

... moloko270 made a comment on nbme22/block1/q#30 (A 42-year-old woman is brought to the emergency...)
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submitted by moloko270(29)

FA p.547 - burning rubber smell hallucination occurs as an aura for temporal lobe epilepsy

... atstillisafraud made a comment on nbme22/block1/q#31 (A 60-year-old woman comes to the physician because...)
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submitted by atstillisafraud(39)

Weight loss - think cancer Hyponatremia - SIADH from small cell lung cancer Edema + JVD - SVC syndrome

... moloko270 made a comment on nbme22/block1/q#32 (A 17-year-old boy is brought to the emergency...)
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submitted by moloko270(29)

loss of fluid triggers aldosterone production, so patient will have hypernatremia and hypokalemia as a result

... iviax94 made a comment on nbme22/block1/q#32 (A 17-year-old boy is brought to the emergency...)
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submitted by iviax94(5)

I was between hypokalemia (due to diarrhea) and hypercalcemia/hyperuricemia (since sweat is hypotonic and would cause hyperosmotic volume contraction). I didn’t have a great way to decide between hyperCa/hyperuricemia so I figured they wanted hypoK. Is there a better rationale for why the hyper answers are incorrect?

liverdietrying  I think you over-thought this one a little bit with the hypercalcemia/hyperuricemia. Good fact to commit to memory: you lose bicarb in the stool (hence why diarrhea causes nonanion gap metabolic acidosis), and especially lose potassium with laxative abuse (as mentioned in the question stem). https://www.uptodate.com/contents/acid-base-and-electrolyte-abnormalities-with-diarrhea
w7er  Basically they are asking about electrolyte distrubance that cause collapse mainly due to hypokalemia from laxative abuse because diarreha cause hypokamlemia and also cause incrase in renin angiotensin sytem which will further cause hypokalemia resuling cardiocascular colapse :)
hyperfukus  i thought the hyperuricemia thing too but i wasn't smart enough to think they wanted hypokalemia like u :(
... liverdietrying made a comment on nbme22/block1/q#32 (A 17-year-old boy is brought to the emergency...)
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submitted by liverdietrying(20)

Good fact to commit to memory: you lose bicarb in the stool (hence why diarrhea causes nonanion gap metabolic acidosis), and especially lose potassium with laxative abuse (as mentioned in the question stem). https://www.uptodate.com/contents/acid-base-and-electrolyte-abnormalities-with-diarrhea

sbryant6  I'm going to go take a big bicarbonate poop now.
... keycompany made a comment on nbme22/block1/q#33 (A 32-year-old woman begins to hyperventilate and...)
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submitted by keycompany(105)

Hyperventilation decrease PaCO2. Central chemoreceptors respond to low PaCO2 by vasoconstricting cerebral blood vessels.

A) Arterial Blood Oxygen Concentration: Blood Oxygen Concentration is directly related to Hb concentration and saturation (SaO2) FA2019, p. 653. Via the Bohr Effect, decreased PaCO2 will increase SaO2, thus increasing blood oxygen concentration.

B) Arterial Blood PO2: PaO2 changes in response to decreased PAO2, PIO2, or diffusion. There would be no change in PaO2 during hyperventilation (theoretically).

C) Aterial Pressure: Decreased PaCO2 is associated with vasoconstriction, which would increase blood pressure.

E) Cerebral Tissue pH would increase due to respiratory alkalosis.

keycompany  EDIT: Via the **Haldane Effect**, not the Bohr Effect.
impostersyndromel1000  excellent response
... seagull made a comment on nbme22/block1/q#33 (A 32-year-old woman begins to hyperventilate and...)
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submitted by seagull(355)

https://en.wikipedia.org/wiki/Reflex_syncope

Vasovagal Syncope. Much easier

... usmleuser007 made a comment on nbme22/block1/q#34 (A 15-year-old girl is brought to the physician by...)
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submitted by usmleuser007(86)

1) Superficial (first-degree) = Epidermis ~ presents as red skin without blisters

2) Superficial partial thickness (second-degree) = Extends into superficial (papillary) dermis ~ Presents with redness with clear blister & blanches with pressure

3) Deep partial thickness (second-degree) = Extends into deep (reticular) dermis ~ presents as yellow or white skin with less blanching. May be blistering.

4) Full thickness (third-degree) = Extends through entire dermis ~ presents as stiff and white/brown skin. No blanching.

5) Fourth-degree = Extends through entire skin, and into underlying fat, muscle and bone ~ presents as black skin; charred with eschar

endochondral1  what is rhus dermis?
endochondral1  nvm its urshiol
btl_nyc  Allergic contact dermatitis because of contact with poison ivy.
... keycompany made a comment on nbme22/block1/q#35 (A 35-year-old man is brought to the hospital after a...)
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submitted by keycompany(105)

Alteration of the thermostatic set point is a hypothalamic process mediated by prostaglandins and is independent of the sympathetic nervous system.

B, C, D, and E all require sympathetic nerves to ellicit a response.

... gribear made a comment on nbme22/block1/q#35 (A 35-year-old man is brought to the hospital after a...)
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submitted by gribear(0)

Can someone explain why when you transect the spinal cord superior to the level of sympathetic outflow -- and you get a systemic infection -- the response is alteration of the thermostatic set point?

its_raining_jimbos  So I chose that one because set point is controlled by the hypothalamus (PGE2 and IL-1 mediate fever in the hypothalamus) and the rest of the answer choices involved something below the level that has been transected. Not 100% sure if that’s accurate though.
noselex  Agreed with @its_raining_jimbos -- Fever is mediated by altering set point in hypothalamus. All the other choices, as far as I can tell, involve sympathetic nerves and their effects at target organs.
... gh889 made a comment on nbme22/block1/q#35 (A 35-year-old man is brought to the hospital after a...)
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submitted by gh889(32)

From ShoryukenHadooken on reddit:

What the question is getting at is the sympathetic chain was spared. It was a terrible way of wording it.

Your anterior hypothalamus is responsible for cooling features and is under parasympathetic control. A lesion would cause hyperthermia.

Your posterior hypothalamus is responsible for heating when you're cold and to generate the Fever response and is under sympathetic control. A lesion would cause hypothermia.

In this question it is simply asking a person gets sick, hypothalamus was spared, what happens.

Answer: hypothalamus will still be able to elevate set body temperature to battle infection.

Hint: IF they give a question similar to this but reworded to include a lesion of the sympathetic fibers or of the hypothalamus, you would in turn NOT be able to generate a fever response to infection. The hypothalamus would be entirely under parasympathetic control

This adds more context to the fact the Q states that the sympathetics was spared

... imgdoc made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
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submitted by imgdoc(18)

I think its the right MLF (area C), not the right abducens nucleus that is lesioned on the cross section. If the abducens nucleus were lesioned she wouldn't have abduction in her left eye. The MLF mediates cross talk between the abducens nucleus on both sides to the MLF on the opposite side (2 abducens nuclei, 2 MLF one on each side). In her case, her right MLF wasn't functioning hence why she was gazing left but her right middle rectus wasn't contacting to mediate leftward gaze.

This picture helps: http://what-when-how.com/wp-content/uploads/2012/04/tmp15F9_thumb.jpg

imgdoc  *medial rectus
... drdoom made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
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submitted by drdoom(166)

Nice schematic of how horizontal gaze is coordinated through the abducens/MLF/oculomotor pathway:

https://n.neurology.org/content/neurology/70/17/e57/F1.large.jpg

In the diagram, the system is coordinating gaze toward pt’s left, which (conveniently) is the same as in the stem.

Source article: https://n.neurology.org/content/70/17/e57

... drdoom made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
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submitted by drdoom(166)

Here’s another very nice one that superimposes the pathway onto a simplified brainstem drawing (nice for the anatomical relations):

https://webeye.ophth.uiowa.edu/eyeforum/cases-i/case252/Fig2-INO-LRG.png

Source article:

https://webeye.ophth.uiowa.edu/eyeforum/cases/252-internuclear-ophthalmoplegia.htm

To see even more, try google image search on “medial longitudinal fasciculus”:

https://www.google.com/search?q=medial+longitudinal+fasciculus&tbm=isch

endochondral1  what is A and B in this pic? i knew it was dorsal pons ipsilateral but i just didn't know what part that was on the pic?
nwinkelmann  A and B are the superior cerebellar peduncles.http://what-when-how.com/wp-content/uploads/2012/04/tmp15F2.jpg
... pppro made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
... lnsetick made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
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submitted by lnsetick(28)

This is internuclear ophthalmoplegia. In INO you would see impaired adduction during horizontal gaze due to a lesion of the ipsilateral MLF. However, since the MLF is not involved in convergence, the affected eye is still able to converge normally.

... ahd_ve made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
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submitted by ahd_ve(0)

This imagen is a transverse section through the pons at the level of trigeminal nuclei: A and B: Superior Cerebellar peduncle. C and D: Medial longinutidinal fasciculus. E and F: Bundles of corticospinal and cortinuclear fibers.

... hyperfukus made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
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submitted by hyperfukus(5)

so the lesion is in the Right MLF right? If so I'm just about to memorize the eye see SAME MiLF lol its the MLF on the same side of the eye keep it simple i hope that's what yall are saying lol

... hello made a comment on nbme22/block1/q#37 (A 28-year-old woman is brought to the physician...)
... atstillisafraud made a comment on nbme22/block1/q#38 (A newborn born at 26 weeks' gestation has...)
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submitted by atstillisafraud(39)

Premie has no surfactant

Angiotensin II - generated in hypovolemia

Dipalmitoyl lecithin aka dipalmitoylphosphatidylcholine lung surfactant

Phosphatidylinositol 4,5-bisphosphate aka PIP2 Gq receptor pathway

Phosphatidylserine -involved in intrinsic apoptosis when exposed on extracellular surfaces

Sphinogmyelin - composes myelin and also has roles in signal transduction, apoptosis. Lecithin: Sphingomyelin ratio >2 indicates mature fetal lungs.

endochondral1  how are we supposed to know that dipalmitoyl lecithin is the same thing as dipalmitorylphosphatidylcholine
... mcl made a comment on nbme22/block1/q#39 (A 23-year-old woman develops multiple red,...)
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submitted by mcl(169)

Poison ivy triggers a type IV hypersensitivity (mediated by T cells); only one of the answer choices mentions T cells.

... impostersyndromel1000 made a comment on nbme22/block1/q#39 (A 23-year-old woman develops multiple red,...)
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submitted by impostersyndromel1000(4)

would anyone be able to clarify what the others would be? A) Allergen mediated vasoconstriction, leading to ischemic tissue injury: Type I B) Binding of antigen to IgE on the surface of mast cells leading to mast cell degranulation: Type I C) deposition of antigen-antibody complexes within postcapillary venules, leading to activation of complement: Not sure D) Phagocytosis of antigen by neutrophils, leading to oxidant mediated tissue damage: Type III?

sunny  i think C is type III
sunny  i think C is type III
... yotsubato made a comment on nbme22/block1/q#40 (A 45-year-old man with chronic pancreatitis caused...)
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submitted by yotsubato(214)

Pancrealipase is basically "Pancreatic Enzymes" in fancy pants NBME world

... moloko270 made a comment on nbme22/block1/q#40 (A 45-year-old man with chronic pancreatitis caused...)
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submitted by moloko270(29)

low amount of fecal elastase is common in pancreatic insufficiency (FA 375) - use pancrelipase (combo of lipase, protease and amylase enzymes) to remove malabsoprtion

... its_raining_jimbos made a comment on nbme22/block1/q#41 (A 21-year-old man is brought to the emergency...)
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submitted by its_raining_jimbos(8)

Everywhere I found (UpToDate and several papers) said the smoking is the biggest risk factor for spontaneous pneumothorax, with body habitus and gender being a lesser risk. Am I just completely misunderstanding the question?

imresident2020  Yes smoking is a risk factor but not the best option among the choices given. Check FA, it says that it occurs more in tall thin young males. Smoking isn’t even mentioned. Tall & thin males are more at risk because they have more negative intrapleural pressure. Check Uworld for this.
drdoom  You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about this patient?” Said a different way: Given a CONDITION [spontaneous pneumo], what other finding is most likely to be the case? Still other words: Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them? In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN. If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? The latter.
cocoxaurus  Rupture of pulmonary blebs are a common cause of spontaneous pneumothorax in young adult males that are tall and thin. I know it's also associated with smoking, but gender and body habitus seemed like the more likely answer here since the patient is a young male.
... drdoom made a comment on nbme22/block1/q#41 (A 21-year-old man is brought to the emergency...)
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submitted by drdoom(166)

You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about that person?” Or you can phrase it these ways:

  • Given a CONDITION (spontaneous pneumo), what other finding is most likely to be the case?
  • Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them?

In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN.

If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.

someduck3  Is this the best approach to all of the "strongest predisposing risk factor" type questions?
drdoom  There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer."
drdoom  There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].)
impostersyndromel1000  this is WILD! thanks guy
belleng  beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies.
drdoom  @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P
hyperfukus  @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom!
... drdoom made a comment on nbme22/block1/q#41 (A 21-year-old man is brought to the emergency...)
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submitted by drdoom(166)

If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.

... seagull made a comment on nbme22/block1/q#41 (A 21-year-old man is brought to the emergency...)
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submitted by seagull(355)

Why spontaneous? He's engaging in an active sport with an increased risk of Traumatic injury. So we really just assume hes not injured because the stem doesnt directly say he's injured? These questions lead to too many assumptions. (in my opinion)

nc1992  Spontaneous pneumothorax, as a condition, is significantly more likely than a traumatic pneumothorax from just about anything but a car crash (ok maybe if he was in a fight). The car crash or a stabbing is also more probable overall but there's no point in inferring something that isn't provided
nwinkelmann  I picked the traumatic injury also. After reading these comments I looked into it further. Traumatic pneumos occur because of blunt or penetrating chest trauma, and I found that the MCC form of blunt trauma (>70%) is motor vehicle acidents that cause significant trauma (i.e. rib fractures) or even blast trauma. Although it didn't say there were no chest wall fractures, at the same time it didn't indicate any rib fractures, which would be most like to cause the traumatic injury pneumo in the patient's case.
drdoom  The stem makes no mention of trauma.
hyperfukus  i guess the issue is that you have to assume what they mean by "strongest predisposing risk factor for this patient's condition" I think this is dumb bc the answer is completely different based on what you consider this patient's "CONDITION" to be? either way he has a pneumothorax so if you wan to know what caused that its prob him being active or bumping into someone but if you consider the etiology of the pneumothorax then its the bleb and that is from him being a skinny dude/smoker i went to this b/c he's also only 5/10 that's not tall in my head they could have been nicer and made him 6'1 at least...also i feel like i saw a lot of q's back in the day when i first learned this with a presentation of the person like tripping or something dumb but they already had the bleb and then got the pneumothorax
... cocoxaurus made a comment on nbme22/block1/q#41 (A 21-year-old man is brought to the emergency...)
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submitted by cocoxaurus(22)

Rupture of pulmonary blebs are a common cause of spontaneous pneumothorax in young adult males that are tall and thin. I know it's also associated with smoking, but gender and body habitus seemed like the more likely answer here since the patient is a young male.

... nwinkelmann made a comment on nbme22/block1/q#41 (A 21-year-old man is brought to the emergency...)
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submitted by nwinkelmann(60)

Here's some epidemiology information about spontaneous pneumos: There are two kinds, primary spontaneous pneumos (PSP) and secondary (SSP). PSPs occur in people aged 20-30 years, with a peak incidence is in the early 20s, is rarely observed in people older than 40 years, with a male to female ratio of 6.2:1, and most frequently occurs in tall, thin men, though smoking increases risk even further. SSPs occur in patients with underlying lung conditions, such as COPD/older patients. If the patient's demographic was older and had history of lung disease, but that wasn't an option, then I think smoking would be the appropriate choice because smoking is the biggest risk factor for underlying lung conditions.

Regarding the trauma, traumatic injury pneumos most commonly occur due to motor vehicle acidents where there is injury (i.e. fracture) to chest wall, and with blast injuries. Although the question didn't specify the chest wall was void of fractures, it also didn't say fractures were present, so I think it would be safe to assume that the collision injury didn't have enough force to cause the pneumo, especially with keeping in mind the epidemilogy of primary spontaneous pneumos.

At least, this is my thought process having researched it more, now.

... hello made a comment on nbme22/block1/q#41 (A 21-year-old man is brought to the emergency...)
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submitted by hello(51)

Patient has a hemithorax + CXR shows trachea deviates towards the hemithorax --> most likely diagnosis is spontaneous pneumothorax.

Epidemiologically, spontaneous pneumothorax is most associated with thin males

hello  Wait, maybe this is wrong logic? Please correct me regarding the exam findings if needed.
hello  Can confirm that this explanation is INCORRECT regarding trachea. Disregard this explanation.
... dr.xx made a comment on nbme22/block1/q#42 (An 18-year-old woman develops sepsis after an...)
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submitted by dr.xx(35)

Severe, rapidly evolving disseminated intravascular coagulation (DIC) causes thrombocytopenia, depletion of plasma coagulation factors and fibrinogen, and bleeding.

https://www.msdmanuals.com/professional/hematology-and-oncology/coagulation-disorders/disseminated-intravascular-coagulation-dic

... dr.xx made a comment on nbme22/block1/q#43 (A 13-year-old girl is brought to the emergency...)
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submitted by dr.xx(35)

Hereditary angioedema. Type I and II are caused by a mutation in the SERPING1 gene that makes the C1 inhibitor protein.

https://en.wikipedia.org/wiki/Hereditary_angioedema

... link981 made a comment on nbme22/block1/q#43 (A 13-year-old girl is brought to the emergency...)
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submitted by link981(24)

FA 2018 page 107

C1 esterase inhibitor deficiency: Causes hereditary angioedema due to unregulated kvllikrein activation, which leads to increased bradykinin.

... bobson150 made a comment on nbme22/block1/q#44 (A 52-year-old man with a history of alcoholic...)
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submitted by bobson150(2)

The wording of this question confused me. This is asking "which of these vessels is the high pressure system" right? So the high pressure superior rectal is causing increased pressure into the inferior rectal?

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360
nc1992  Superior rectal not superior mesenteric. Took me a minute
hyperfukus  ugh am i ever gonna get these right EVER
... usmleuser007 made a comment on nbme22/block1/q#45 (A 16-year-old girl is brought to the physician...)
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submitted by usmleuser007(86)

This more likely to be diuretics rather than laxatives b/c

the lab study shows a renal dysfunction (BUN & Creatinine are elevated)

Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis

endochondral1  would laxatives also have the low potassium?
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken?
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis.
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis.
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue.
... presidentdrmonstermd made a comment on nbme22/block1/q#45 (A 16-year-old girl is brought to the physician...)
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submitted by presidentdrmonstermd(5)

Dec. NaCl - general volume loss Dec. K+ - Diuretic (most diuretics, except K+ sparing ones, cause hypoK+) Inc. HCO3-& pH - Volume loss -> RAAS -> aldosterone causes K+ & H+ wasting -> metabolic alkalosis; She may be vomiting as well, which is another possible cause of met. alk. Inc PaCO2 - respiratory compensation for met. alk.

hello  Patient has normal Na.
hello  Lab data indicates serum bicab not ABG bicarb.
hello  oops! just realized bicarb is never given as an ABG haha
... yotsubato made a comment on nbme22/block1/q#45 (A 16-year-old girl is brought to the physician...)
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submitted by yotsubato(214)

Why cant this be laxatives? Both would cause metabolic alkalosis with hypokalemia... ?

sup  Laxatives would cause an anion gap metabolic acidosis due to loss of bicarbonate in the stool. You would see hypokalemia though as seen in this question.
... alexb made a comment on nbme22/block1/q#45 (A 16-year-old girl is brought to the physician...)
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submitted by alexb(10)

Is the part with "constant studying" just supposed to support that she has a psych disorder related to perfectionism, which is why she's going to extremes to control her weight?

rrasha2  No, the constant studying is to trick you into thinking shes abusing amphetamines.Amphetamines decrease appetite so a lot of people abuse them for weight loss. That combined with increased concentration to study all day errrday.. #onehellofadrug
rrasha2  forgot to mention, another side effect of amphetamines would be increased BP due to the increased catecholamines..don't forget to keep an eye out for that
... dr.xx made a comment on nbme22/block1/q#46 (A 12-year-old girl is referred to the emergency...)
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submitted by dr.xx(35)

Inability to walk cannot be explained by medical evaluation. ==> Conversion disorder

... sbryant6 made a comment on nbme22/block1/q#46 (A 12-year-old girl is referred to the emergency...)
... dr.xx made a comment on nbme22/block1/q#47 (A 25-year-old woman comes to the physician because...)
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submitted by dr.xx(35)

The hallmark of ITP is isolated thrombocytopenia.

https://emedicine.medscape.com/article/202158-workup

jboud86  Refer to page 419 in FA2019.
hello  @dr.xx Compared to what?
... atstillisafraud made a comment on nbme22/block1/q#48 (A 1-year-old boy is found to have an impairment of...)
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submitted by atstillisafraud(39)

Question is asking about encapsulated organisms infecting CGD patients. E.coli is also encapsulated. Can anyone expand on this?

keycompany  Step pneumonia is the most common pathogenic organism in CGD, and the most common cause of pneumonia, otitis media, meningits, and sepsis. While CGD are at an increased risk of encapsulated E. coli infections, however, they are at MOST risk for S. pneumo. This is kind of just a memorization fact that you need to know about S. pneumo.
keycompany  Sorry english is clearly not my shit, but you get the point
biliarytree220  CGD is susceptible against catalase-positive organisms (FA 109), of which S. aureus is the one to look out for. It's not about encapsulated organisms, like I had it confused in my head.
.ooo.   You are completely right about E.Coli being encapsulated and is also a CAT+ organism and patients with CGD would have an increased risk of infection for both S. Aureus and E. Coli. How you narrow down the two is the most common infections are S. Aureus and Aspergillus (FA 109 like mentioned above) and also using the pneumonic "Cats Need PLACESS to Belch their Hairballs" (FA 128) Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, Staphylococci, Serratia, B cepacia, H pylori
... usmleuser007 made a comment on nbme22/block1/q#48 (A 1-year-old boy is found to have an impairment of...)
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submitted by usmleuser007(86)

Note: the questions stated "respiratory burst" suggesting an URT infection.

1) this rules out anything but respiratory infection (non rep infection: E. coli, E. faceium)

2) G6PD deficiency more susceptible to catalase positive organisms -- this rules out (all strep organisms)

3) Left with H. influenzae & Straph. aureus (BOTH are catalase positive)

4) Encapsulated organism are most concerning when there is asplenia.

imnotarobotbut  Respiratory burst has nothing to do with a respiratory infection. It describes the process of phagocytosing a bacteria and using NADPH oxidase/ROS to lyse it
belleng  Aspergillus is still in the running, it is catalase positive as well...but not a choice
... rogeliogs made a comment on nbme22/block1/q#48 (A 1-year-old boy is found to have an impairment of...)
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submitted by rogeliogs(1)

This Question its about respiratory burst

Patients with NADPH deficiency=chronic granulomatous disease (CGD)

Even though patients with CGD can't make Superoxide, they can use it from the bacterias and convert it to bleach HCLO and kill the bacterias.

BUT bacterias with catalase enzymes neutralize their own superoxide and thats why the CGD patient can't kill them.

Catalase positive bacterias: S. aureus - Aspergillus

... rogeliogs made a comment on nbme22/block1/q#48 (A 1-year-old boy is found to have an impairment of...)
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submitted by rogeliogs(1)

This Question its about respiratory burst

Patients with NADPH deficiency=chronic granulomatous disease (CGD)

Even though patients with CGD can't make Superoxide, they can use it from the bacterias and convert it to bleach HCLO and kill the bacterias.

BUT bacterias with catalase enzymes neutralize their own superoxide and thats why the CGD patient can't kill them.

Catalase positive: S. aureus - Aspergillus

... hello made a comment on nbme22/block1/q#48 (A 1-year-old boy is found to have an impairment of...)
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submitted by hello(51)

please help -- If catalase-positive bacteria neutralize their own superoxide, why isn't it the case for catalase-positive bacteria to infections in everyone?

I'm not understanding the connection to NADPH oxidase deficiency.

hello  to cause** infections in everyone
... medstudied made a comment on nbme22/block1/q#49 (A 17-year-old primigravid woman at 16 weeks'...)
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submitted by medstudied(2)

Why is it azithromycin not doxycycline? According to sketchy, you treat chlamydia with macrolides/doxy +ceftriaxone. You treat neisseria gonorrhea with ceftriaxone+azithromycin+doxycycline.

​Not sure what this question is testing -- is it wanting us to know that gonorrhea has to be treated as well? In that case, doxy would work for both according to sketchy ... Any other reasonings appreciated!

dr_salface  The patient in the stem is pregnant! The question wants to see if you know that doxy is a teratogen. Tetracyclines in general like to bind to fetal bone/teeth which can impair development.
dr_salface  As a side note, treating chlamydia alone only requires macrolides or doxy. Treating gonorrhea alone only requires ceftriaxone or macrolides. The reason sketchy includes all three is because you usually treat one infection and co-treat the other.
yotsubato  Theres a crow in the chlamydia sketchy. You can use Macrolides, OR Ceftriaxone, OR Doxycycline. Most doctors in real life just give the azithromycin z pack (which kicks ass cause its one drug 5 doses thats it)
... organicmechanic made a comment on nbme22/block1/q#50 (A 9-year-old boy is brought to the physician by his...)
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submitted by organicmechanic(1)

Increased sweat and Na+ concentration should point to cystic fibrosis (CF). The problem with CF is not that the gene is being transcribed less, but that the protein that the gene codes for is altered, which leads to the CF channel being degraded due to mis-folding --> less CF receptors on cell surface --> phenotypic CF.

ls3076  why not membrane receptor?
a1913  delF508 is a 3 base pair deletion of phenylalanine at amino acid position 508. Mutation causes impaired post-translational processing of CFTR (improper folding) which rough ER detects. Sends mutant misfolded CFTR to the proteasome for degradation, preventing it from reaching cell surface. So problem is not malfunctioning CFTR channels in the surface; problem is complete absence of CFTR on cell surface (since they keep getting misfolded and sent to proteasome to be trashed). Source of primary problem: error in protein structure
angelaq11  @Is3076 because the CFTR is a channel not a receptor.
... a1913 made a comment on nbme22/block1/q#50 (A 9-year-old boy is brought to the physician by his...)
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submitted by a1913(0)

delF508 is a 3 base pair deletion of phenylalanine at amino acid position 508. Mutation causes impaired post-translational processing of CFTR (improper folding) which rough ER detects. Sends mutant misfolded CFTR to the proteasome for degradation, preventing it from reaching cell surface. So problem is not malfunctioning CFTR channels in the surface; problem is complete absence of CFTR on cell surface (since they keep getting misfolded and sent to proteasome to be trashed). Source of primary problem: error in protein structure

... haliburton made a comment on nbme22/block2/q#1 (A 29-year-old woman is brought to the emergency...)
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submitted by haliburton(74)

apparently this is a common sequelae of abdominal trauma.

(from link below) Twenty-two of the 25 deaths were caused by blood loss. Two patterns of hepatic venous injury appeared to predominate: avulsion of the trunk of the right hepatic vein from the inferior vena cava and avulsion of the upper branch of the right hepatic vein.

https://www.ncbi.nlm.nih.gov/pubmed/2300894

... monoloco made a comment on nbme22/block2/q#1 (A 29-year-old woman is brought to the emergency...)
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submitted by monoloco(49)

Anyone else figure out how a surgeon gets his hand inside the patient deep enough to avulse the hepatic veins from the IVC during a LAPAROTOMY? Baffles me.

mesoform  I think this one was pretty easy if you just know the regional anatomy. That was the only answer choice that could remotely have that presentation, so I think it was just testing your knowledge of the structures listed relative to the description.
kimcharito  aorta is also behind of liver...
... thepromise made a comment on nbme22/block2/q#1 (A 29-year-old woman is brought to the emergency...)
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submitted by thepromise(11)

Guessed on this one but if you look into pg 354-355 FA 19, you'l notice the structure of the IVC compared to the liver 1:IVC is retroperitoneal 2: if transected, (similar to an abdominal aorta) blood accumulates behind the peritoneum and causes severe hypovolemia 3: all other answers are either too far, or within the peritoneum

... alexb made a comment on nbme22/block2/q#1 (A 29-year-old woman is brought to the emergency...)
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submitted by alexb(10)

It's also just the only option that's "behind" the liver.

... angelaq11 made a comment on nbme22/block2/q#1 (A 29-year-old woman is brought to the emergency...)
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submitted by angelaq11(0)

I think besides knowing basic anatomy (I suck BIG time on anatomy), we could more or less easily rule out most of the options. She is in pain, but she is awake and with stable vital signs (even after 6 hours) so I think arterial damage would definitely lead to a more rapid deterioration. That leaves us with the portal vein and the hepatic veins. The portal vein (if knowing zero anatomy) brings much more blood to the liver than the hepatic artery (if I'm not mistaken), and so that leaves you with only the hepatic veins.

... usmleuser007 made a comment on nbme22/block2/q#2 (A 65-year-old man starts using topical fluorouracil...)
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submitted by usmleuser007(86)

Two major mechanisms of action have been elucidated:

1) Flucytosine is intrafungally converted into the cytostatic fluorouracil which undergoes further steps of activation and finally interacts as 5-fluorouridinetriphosphate with RNA biosynthesis thus disturbing the building of certain essential proteins.

2) Flucytosine also undergoes conversion into 5-fluorodeoxyuridinemonophosphate which inhibits fungal DNA synthesis.

3) Thymidylate synthetase is an enzyme that catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP).

Thymidine is one of the nucleotides in DNA.

With inhibition of TS, an imbalance of deoxynucleotides and increased levels of dUMP arise. Both cause DNA damage.

(WIKI)

link981  Just look at page 36 of FA 2018 and memorize that shitty diagram o De novo pyrimidine and purine synthesis they ask so much about. No need for scientific explanations for this one unless you like to waste time.
... hopsalong made a comment on nbme22/block2/q#3 (A previously healthy 28-year-old man comes to the...)
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submitted by hopsalong(2)

This question has a lot of answer options, and you arrive at Nephrolithiasis by throwing out all the other options by what is missing.

A, B - Cortical Necrosis and Papillary Necrosis almost always occur in the setting of ischemia. Previously healthy 28 year old man has no evidence of significantly decreased renal perfusion.

C - Acute Tubular Necrosis is what you should think of with Salicylate (NSAID) toxicity. There are many other nephrotoxic drugs that cause ATN, but think of ATN as drug induced kidney damage.

D - Cystitis - Flank pain is related to kidney injury, not bladder damage. Cystitis could be possible in ascending UTI, but the patient has no fever and is male (much less common in males).

E - Glomerulonephritis - This gets into nephrotic/nephritic syndromes. The stem mentions that he has blood in the urine which may lead you down the nephritic pathway, but he does not have any of the other associated symptoms.

F - Hypernephroma - Another word for Renal Cell Carcinoma. No weight loss or other cancer related symptoms (fatigue etc.)

G - Interstitial Nephritis - This is often a drug induced IMMUNE mediated nephrotoxicity. This is a type IV hypersensitivity reaction that occurs weeks to months after the start of medication (like NSAIDs). ATN is more associated with drug overdose while Interstitial is more associated with immune reaction. Intersitial Nephritis will have WBC casts in urine.

I - Pyelonephritis - Caused by ascending UTI but no fever is present.

This leaves Nephrolithiasis (H) as the correct answer. 85% of Nephrolithiasis is associated with hypoactive bowel sounds. The pain for nephrolithiasis can relapse and remit, and occasionally the pain can travel from the kidney (flank pain) to the scrotum as the stone moves through the ureter.

whoissaad  Great explanation. Always found it hard to differentiate between ATN and AIN due to NSAID use. This made it clear. Thanks!
hyperfukus  yasss
... nwinkelmann made a comment on nbme22/block2/q#4 (A previously healthy 60-year-old woman is admitted...)
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submitted by nwinkelmann(60)

This article explains the pathophysiology well: https://www.ncbi.nlm.nih.gov/books/NBK431048/.

The right ventricle is primarily supplied by the RCA which also supplies the SA node and AV node (90% of hearts because they are right dominant), leading to loss of contractility of the right side, and thus fluid buildup causing elevated central venous pressure. Elevated pressures in the liver and portal system would lead to hepatomegaly and free fluid accumulation in the peritoneum.

henoch280  Hellppp. pls why is it not decreased capillary oncotic pressure?
whoissaad  @ henoch280 Because there is no change in the levels of protein in the blood.
... keycompany made a comment on nbme22/block2/q#5 (A 74-year-old man with emphysema and lung cancer is...)
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submitted by keycompany(105)

Nitrogen balance is a measurement of protein metabolism in the body. A negative nitrogen balance indicates muscle loss, as increased amounts of amino acids are being metabolized to produce energy. This increases the amount of nitrogen secreted from the body. Because the amount of nitrogen you are taking in is less than the amount of nitrogen you are secreting, you have a negative nitrogen balance.

This man is malnourished, edematous, cachetic, and has hypoalbuminemia. These clinical findings point to protein malnutrition (Kawashkior Disease), which causes edema due to decreased serum oncotic pressure. Low oncotic pressure in this case is due to protein loss, and hence a negative nitrogen balance.

drdoom  Nice!
... pparalpha made a comment on nbme22/block2/q#5 (A 74-year-old man with emphysema and lung cancer is...)
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submitted by pparalpha(13)

Can someone please explain why it would not be glycogen depletion? I thought the question was talking about the Warburg phenomenon... so why not breakdown of glycogen to glucose?

I guess it would not explain the edema?

hello  Glygocen stores are depleted within 24h. This person has signs and symptoms of longterm nutritional deficiences.
... welpdedelp made a comment on nbme22/block2/q#6 (A 52-year-old man is brought to the emergency...)
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submitted by welpdedelp(64)

It was just asking the lifespan of RBCs (120 days)

haliburton  If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking.
link981  The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh
... iviax94 made a comment on nbme22/block2/q#6 (A 52-year-old man is brought to the emergency...)
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submitted by iviax94(5)

I figured they were trying to get at the life expectancy of an RBC, but wouldn’t supplemental O2 technically replace the CO bound to RBCs? FA even mentions that CO binds competitively to RBCs, and isn’t that the whole point of giving hyperbaric/100% O2?

nc1992  First aid has a lot of errors
yotsubato  Thats not an error though. Thats the actual reason behind giving hyperbartic O2 for CO poisoning...
... link981 made a comment on nbme22/block2/q#6 (A 52-year-old man is brought to the emergency...)
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submitted by link981(24)

The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask the RBC lifespan in weeks or in hours, who knows? smh

... mattnatomy made a comment on nbme22/block2/q#7 (A 66-year-old man comes to the physician because of...)
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submitted by mattnatomy(21)

Answer = Decreased libido; normal nocturnal erections

I believe what they were trying to indicate in this question was Psychological Sexual Dysfunction (aka - Performance Anxiety).

In this case, it wasn't so much the performance that worried the man, but he may be so focused on his health issues (post stroke), that he is unable to perform adequately. Therefore, his natural libido would be decreased. However, because it's psychogenic & not physiologic, he should still have normal nighttime erections.

... iviax94 made a comment on nbme22/block2/q#7 (A 66-year-old man comes to the physician because of...)
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submitted by iviax94(5)

There have been a couple of questions about this topic on the newer exams. I’ve been answering by equating libido to testosterone levels and nocturnal erections to health of vasculature (atherosclerosis or not). Is this correct?

liverdietrying  When you’re thinking of libido, don’t just equate it to testosterone -- make sure you’re always considering depression! Depression following stroke is common, especially with residual physical disability, so this would decrease his libido. Nocturnal erections equate to “does it actually work?” not just the vasculature but the neural input as well. For example, during prostatectomy damage to the pelvic plexus (nerves) can lead to impotence. There’s nothing to suggest that he has vascular or neurologic erectile dysfunction here, which is why his nocturnal erections are intact.
_pusheen_  @liverdietrying Was it premature to assume he has trouble with erections because of neural damage from the stroke? I put low libido, low nocturnal erections. Is it because the stroke resulted in hemiparesis and not autonomic dysfunction or something like that?
liverdietrying  @pusheen Correct, you won’t classically get impotence after a hemiplegic stroke. His inability to achieve an erection is much more likely to be 2/2 psychosocial effects than organic disease. If this vignette instead said that this had gotten a prostatectomy with resulting damage to the pelvic nerves that allow for erection, then it’d be a more safe choice to put no nocturnal erections.
fast44  Is there a video or somewhere that explains these sexual dysfunctions? This seems to be a topic that keeps repeating on the new exams.
forerofore  well, i though that because he had a stroke he would be likely to have atherosclerosis, which would keep libido high and reduce nocturnal erections, i kinda ignored the whole "he´s depressed" part of the vignette despite understanding the mechanism well. but from a clinical depression point of view, if his arteries are intact, and he is depressed, then libido would be low, and erections present at night.
... nwinkelmann made a comment on nbme22/block2/q#7 (A 66-year-old man comes to the physician because of...)
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submitted by nwinkelmann(60)

So, I thought this question was super vague and not great... that being said, having gotten it wrong and not really having a good explanation for the answer, I did a little research and found this article: https://www.ahajournals.org/doi/pdf/10.1161/01.STR.30.4.715

This was the main conclusion: "The results of the present study, aimed at assessing the effects of stroke on sexual functioning, reveal a significant decline in libido, coital frequency, sexual arousal, and satisfaction with sexual life in both stroke patients and their spouses. The present results also demonstrate that disorders of sexual functions are most significantly associated with various psychosocial factors, such as patients’ general attitude toward sexuality, fear of impotence, and ability to discuss sexuality, as well as with the degree of poststroke functional disability. Moreover, sexual dysfunction was related to the presence and degree of depression, diabetes mellitus, and cardiovascular medication. The etiology or location of the stroke and the gender or marital status of the patients were not associated with changes in poststroke sexuality in patients in the present study."

Looking at the question again, I'm guessing the "fatigue and difficulting sleeping and concentrating" statement was supposed to be a clue for depression, especially since it started after his stroke. Also, no physical abnormalities suggest functioning is intact and thus nocturnal erections would be preserved normally. This is just stupid.

ls3076  appreciate this kind of effort to look up journal articles but honestly this is not really what nbme answers is for... we should be able to get the answer from process of elimination/basic science concepts and not from looking up studies as we obviously can't do this on the test
... ls3076 made a comment on nbme22/block2/q#7 (A 66-year-old man comes to the physician because of...)
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submitted by ls3076(5)

Is decreased nocturnal erections not possible due to the incongruity between onset of symptoms and stroke (2 mos versus 3)? Agree that these questions are very vague and frustrating. Not sure where to get a good grasp on this material.

... pppro made a comment on nbme22/block2/q#8 (A 73-year-old man has difficulty urinating and...)
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submitted by pppro(5)

Patient has BPH. Give alpha one antagonist to reduce smooth muscle contraction and relieve difficulty urinating.

d_holles  lol i thought it was some kind of urinary retention problem and put H.
sbryant6  How is H wrong? Oxybutinin or tolterodine treat urinary incontinence by blocking M3 muscarinic acetylcholine receptors --> urinary retention. We're just supposed to assume they are talking about BPH here because he is old?
jaxx  I agree. I picked "H" for that same logic. Does anyone know where we should have come to the conclusion that this was BPH?
forerofore  they are telling you he's having "difficulty urinating", one of the clinical criteria for BPH is reduced urinary flow rate. this is not incontinence because they are not telling you he leaks at all, just that he pees "a lot"
... seagull made a comment on nbme22/block2/q#8 (A 73-year-old man has difficulty urinating and...)
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submitted by seagull(355)

So alpha was the answer so my fatigued mind put "A"...well done. You're going to be a doctor. lol

impostersyndromel1000  hope you dont have to write a prescription for me one day lol
... enbeemee made a comment on nbme22/block2/q#8 (A 73-year-old man has difficulty urinating and...)
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submitted by enbeemee(3)

would an acetylcholinesterase inhibitor work as well to relieve the symptoms? but just because he's 73yo, we're supposed to assume it's due to BPH and give an a1 inhibitor?

yb_26  acetylcholinesterase inhibitors are used in treatment of urinary retention, not urinary frequency
... mattnatomy made a comment on nbme22/block2/q#9 (A 26-year-old woman develops hypotension and...)
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submitted by mattnatomy(21)

Diagnosis: Acute Hemolytic Transfusion Reaction

Pathogenesis:

Type II hypersensitivity reaction. Intravascular hemolysis (ABO blood group incompatibility) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs).

Presentation:

Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria (intravascular hemolysis), jaundice (extravascular). Within 1 hour.

... potato_for_brains made a comment on nbme22/block2/q#9 (A 26-year-old woman develops hypotension and...)
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submitted by potato_for_brains(1)

This is acute hemolytic transfusion reaction, I believe. Type II HSR so she’s forming antibodies against the ABO groups on the blood cells. Complement is induced by antibodies.

kfratta1  But with hypotension in the stem I thought more of anaphylaxis due to IgA def. Why would a T2 HSR give you hypotension?
2ndmedschool  I think the hemoglobinuria is the key. As I’m looking at it it seems that anaphylaxis would cause hypotension, urticaria, itching, wheezing. ABO incompatibility is the only one that mentions hemoglobinuria.
hyperfukus  abo incompatibility and rh incompatibility with mom blood rxns are gonna TYPE 2 no matter what it looks like
... mattnatomy made a comment on nbme22/block2/q#10 (A 56-year-old man with a palpable hard nodule on the...)
... mattnatomy made a comment on nbme22/block2/q#11 (A 52-year-old man comes to the physician because a...)
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submitted by mattnatomy(21)

I believe they're referring to compression of branches of the Ilioinguinal Nerve (possibly the Anterior Scrotal Nerves.

Source: https://en.wikipedia.org/wiki/Anterior_scrotal_nerves

armymed88  Ilioingual covers part of the medial thigh, base of penis and anterior scrotum Posterior scrotal nerves are a branch of pudendal and cover said area Doral nerves cover the dorsum of the penis which are also from the pudendal
meningitis  I thought it was the Genitofemoral nerve because the genital branch supplies the cremaster and scrotal skin, but I looked it up and: The genital branch passes through the *deep inguinal ring* and enters the inguinal canal; also, Ilioinguinal wraps around the spermatic cord just like the question stem says.
... saifshaikh made a comment on nbme22/block2/q#11 (A 52-year-old man comes to the physician because a...)
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submitted by saifshaikh(4)

I think this picture explains it well:

http://www.groinpainclinic.co.uk/data/images/nervesaffected.jpg

hello  Adding to this... The Q is describing the GENIOFEMORAL nerve, which runs EXTERNAL TO of spermatic cord at the superficial inguinal ring This Q is NOT referring to ilioinguinal nerve, which exits THROUGH the superficial inguinal canal
... meningitis made a comment on nbme22/block2/q#11 (A 52-year-old man comes to the physician because a...)
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submitted by meningitis(121)

Actually, I correct myself: I looked closer and the Genito femoral has an external Spermatic branch and a Lumboinguinal branch. I thought it was the Genitofemoral nerve because the genital branch passes through the deep inguinal ring, enters the inguinal canal, goes to spermatic cord and supplies the cremaster and scrotal skin.

Heres the image: https://upload.wikimedia.org/wikipedia/commons/e/e4/Gray824.png

Correct me if I am wrong please.

gh889  I think you're right, FA2019 pp444 even states that sensory to the scrotum is via the Genitofemoral nerve
... d_holles made a comment on nbme22/block2/q#11 (A 52-year-old man comes to the physician because a...)
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submitted by d_holles(31)

I got this one via process of elimination. Not sure how you are supposed to remember all that shit.

... hello made a comment on nbme22/block2/q#11 (A 52-year-old man comes to the physician because a...)
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submitted by hello(51)

The Q is describing the genitofemoral nerve, which runs on the external surface of the spermatic cord at the superficial inguinal ring

This Q is NOT referring to ilioinguinal nerve -- the ilioinguinal nerve exits THROUGH the superficial inguinal canal whereas this Q is asking about a nerve that is EXTERNAL to the superficial inguinal canal.

See http://www.groinpainclinic.co.uk/data/images/nervesaffected.jpg

... haliburton made a comment on nbme22/block2/q#12 (A 42-year-old woman with frequent heartburn has...)
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submitted by haliburton(74)

ranitidine blocks H2 receptor, which is Gs. Gs activates adenylyl cyclase -> +cAMP.

q: HAVe 1 M&M => H1, alpha1, V1, M1, M3 i: MAD 2 => M2, alpha2, D2 s: (everything else) => beta1, beta2, V2, D1 H2

I think this is from FA.

... pppro made a comment on nbme22/block2/q#13 (A 5-year-old boy who lives on a farm has had...)
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submitted by pppro(5)

Yersinia thrives in cold temperatures and can be obtained from poor sanitated milk. (Check sketchy sketch)

forerofore  growth in cold temperatures seems to be the method of isolation of yersinia enterocolitica https://www.ncbi.nlm.nih.gov/pmc/articles/PMC275385/ https://jcm.asm.org/content/2/6/559
... jfny21 made a comment on nbme22/block2/q#13 (A 5-year-old boy who lives on a farm has had...)
 +0  upvote downvote
submitted by jfny21(0)

Here's a way for me to remember: Y. enteroCOLDitica. Hope it helps.

... armymed88 made a comment on nbme22/block2/q#14 (A previously healthy 12-year-old boy is brought to...)
 +1  upvote downvote
submitted by armymed88(13)

Glucose is co-transported into enterocytes of SI via sodium

... gunnersinchrome made a comment on nbme22/block2/q#14 (A previously healthy 12-year-old boy is brought to...)
 +2  upvote downvote
submitted by gunnersinchrome(2)

Easiest way to think of this is that this is Gatorade. Sure everyone thinks that sports drinks have glucose for the energy (which is also true) but they also contain sugar because the Na/Glucose co-transporter in the small intestine helps drive electrolyte intake. Without glucose, you don’t pull in sodium nearly as efficiently in the gut and the first makers of the Gatorade formula at UF found that once they gave glucose and electrolytes instead of just water to the football team during practice, they didn’t get as dehydrated and their electrolyte balance was a lot more stable.

... partybrockk made a comment on nbme22/block2/q#14 (A previously healthy 12-year-old boy is brought to...)
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submitted by partybrockk(1)

Kid probably had cholera -- giving Na+ and glucose takes advantage of sodium-glucose cotransporter thereby replenishing electrolytes and energy.

hipster_do  To add on to the diarrhea kid -- SGLT1 is the Na-glucose symporter and it facilitates movement of water into the enterocytes. Water loves to follow sodium around, I think sodium over other electrolytes purely because sodium is generally the highest concentration electrolyte.
... hello made a comment on nbme22/block2/q#14 (A previously healthy 12-year-old boy is brought to...)
 +0  upvote downvote
submitted by hello(51)

The patient is dehydrated. Need to give water to rehydrate.

Water follows solute. If sodium is added to the solution, water will follow the sodium. Now, enterocyte uptake of sodium is mediated by Sodium-Glucose transporter. Hence, the solution needs to contain sodium and glucose in order to have the enterocytes take up the sodium.

... usmleuser007 made a comment on nbme22/block2/q#15 (A 62-year-old woman comes to the physician 3 days...)
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submitted by usmleuser007(86)

Per Pathoma:

Most common in postmenopausal women:

1) fibrocystic changes, intraductal papilloma, Fibroadenoma

More likely in postmenopausal women: 1) phyllodes tumor (fibroadenoma-like tumor) 2) Breast cancers increased risk d/t 1) increased age, duration of estrogen throughout life (early menarche, late menopause, obesity) 2) Atypical hyperplasia 3) First degree relatives

Question states presents it as: a) 2cm firm, nontender mass b) no axillary lymphadenopathy or nipple discharge c) extremly radiodense mass with irregular margins clustered irregular microcalcifications

so what can it be: 1) DICS = does not usually produce mass

2) Comedo type = high- grade cells with necrosis & dystrophic calcifications at center of duct

3) Paget Disease = involves the skin of the nipple (underlying carcinoma)

4) IDC = a) forms duct-like structures (>80% of cases) b) mass detected by physical examination (check) c) usually 1cm or greater (check) d) Desmoplastic stroma = connective tissue growing with tumor (supports tumor) ~~~ (check -- irregular margins) e) Medullary Carcinome (IDC) = mimics fibroadenoma

5) LCIS & ILC = DO NOT produce calcifications or mass a) ILC - cells have "single-file pattern" think of a beaded necklace and you cut it in middle (lack E-cadherin)

usmleuser007  correction Most common in premenopausal women: 1) fibrocystic changes, intraductal papilloma, Fibroadenoma
... airhead5 made a comment on nbme22/block2/q#15 (A 62-year-old woman comes to the physician 3 days...)
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submitted by airhead5(1)

The answer is carcinoma of the breast. I get that, but I’m having trouble figuring out which Carcinoma of Breast it is. I’m stuck between DCIS, and Invasive Ductal Carcinoma. I’m leaning towards Invasive Ductal Carcinoma, just because it’s (1) most common and (2) the mass with irregular margins in clusters sounds like it could be ‘stellate infiltration’, seen in Invasive Ductal Carcinoma. But I’m not sure. Can anyone help?

liverdietrying  There is not enough information in the question stem to determine what kind of cancer it is. You would need a biopsy and histology information to determine that. However, this is definitely not DCIS since there *is* a mass. DCIS usually just shows up as small microcalcifications on XR (I’d google an image so you can see it). All the words they use here describe an invasive cancerous scary mass -- what kind of cancer can’t be known until they biopsy it!
... oznefu made a comment on nbme22/block2/q#15 (A 62-year-old woman comes to the physician 3 days...)
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submitted by oznefu(7)

What are the words that point to Carcinoma rather than Fibrocystic or Fibroadenoma or Fat Necrosis (not an answer)?

Those can have masses and calcifications right? Is it only the irregular margins?

mnemonia  Fibrocystic changes doesn’t technically encompass sclerosing adenosis, which is the one where you would get calcifications. Cysts and fibrosis don’t usually present with calcifications. Fat necrosis I’m sure they would give history of trauma in the stem.
mnemonia  Calcifications = fat necrosis, sclerosing adenosis, and DCIS/IDC. Microcalcifications specifically I would venture to say is a buzzword ductal carcinoma specifically. Either way, of these 3, only cancer is an answer choice.
... seagull made a comment on nbme22/block2/q#15 (A 62-year-old woman comes to the physician 3 days...)
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submitted by seagull(355)

The mass is in the outer upper quadrant, this is why it want DCIS. Nice and simple

seagull  *wasn't
... joker4eva76 made a comment on nbme22/block2/q#15 (A 62-year-old woman comes to the physician 3 days...)
 +1  upvote downvote
submitted by joker4eva76(10)

Could also use the patient's age to make the differential. Age is a risk factor related to breast cancer (common in post-menopausal women, unless there's a history of breast cancer in the family).

Fibrocystic changes and fibroadenomas are usually common in premenopausal women.

No discharge noted, so it's not an intraductal papilloma.

yotsubato  Intraductal papillomas are also under the areola
... cocoxaurus made a comment on nbme22/block2/q#16 (A 60-year-old man is brought to the emergency...)
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submitted by cocoxaurus(22)

Almost got tricked by this one because osteosarcoma also causes osteoblastic lesion. Osteosarcoma most commonly metastasizes to lungs though.

impostersyndromel1000  This was in pathoma, he said prostate cancer causes osteoblastic lesions and "the board examiners really want you to know that". also following the potential site of mets helps choose the answer
... armymed88 made a comment on nbme22/block2/q#17 (Ten healthy human subjects are given a new oral drug...)
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submitted by armymed88(13)

Phase 1- small # of healthy people. Is the drug safe? Phase 2- smell # with disease. Does it work? Phase 3- large #, some with new drug, some with old. Is is good or better? Phase 4- Postmarket watch. Can it stay?

... johnthurtjr made a comment on nbme22/block2/q#17 (Ten healthy human subjects are given a new oral drug...)
 +2  upvote downvote
submitted by johnthurtjr(43)

FA2019 p256 "SWIM"

  • 1 - small, healthy group or volunteers w/ disease- Is it S afe
  • 2 - moderate-sized group w/ disease - Does it W ork
  • 3 - large group w/ disease/RCT - Is it an I mprovement compared to currently available treatment
  • 4 - Surveillance after approval - Can it stay on the M arket?
... lamhtu made a comment on nbme22/block2/q#18 (A 32-year-old man comes to the physician because of...)
 +2  upvote downvote
submitted by lamhtu(26)

It appears that although NRTIs are phosphorylated by thymidine kinase, resistance is actually due to mutations in the actual reverse transcriptase rather than thymidine kinase itself.

forerofore  mutations in thymine kinase are more frequent in herpes drugs
... adisdiadochokinetic made a comment on nbme22/block2/q#18 (A 32-year-old man comes to the physician because of...)
 +1  upvote downvote
submitted by adisdiadochokinetic(7)

This question is so annoying but this explanation is supported by several papers.

... hopsalong made a comment on nbme22/block2/q#19 (A 50-year-old man comes to the physician 3 days...)
 +0  upvote downvote
submitted by hopsalong(2)

This question gets at whether or not you can recognize Trousseau's Sign or Chvostek's Sign in kind of an unusual presentation. Basically you get muscle twitches in the setting of Hypocalcemia. Hypoxemia further exacerbates the sign and can cause twitches randomly throughout the body.

Chvostek's Sign is tapping on the facial nerve of the face that illicits a facial muscle spasm.

Trousseau's Sign is when you put a blood pressure cuff on a patient. This causes cells in the arm to not recieve blood -> No O2 -> No oxidative phosphorylation -> decrease in ATP available -> Na+/K+ pump fails without ATP -> Increased intracellular Na+ -> Increased Ca+ because of increased Na+/Ca2+ exchanger -> decreased SERUM Ca2+ -> Flexion of hand.

Trousseau's Sign is more sensitive for Hypocalcemia, but both are diagnostic. Other tips in this question - Tingling around the mouth, hands, and feet can be another sign of Hypocalcemia. Both generalized tonic-clonic or focal motor seizures can occur with hypocalcemia.

... mguan1993 made a comment on nbme22/block2/q#20 (A 26-year-old nulligravid woman comes to the...)
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submitted by mguan1993(2)

can someone explain why the answer is not adrenal gland? I feel ike if adrenal gland was the issue there would also be decreased concentrations of FSH, LH, and estrogen right?

mguan1993  ^nvm had a brain fart and go adrenal gland mixed up with anterior pituitary lmao
nor16  ovaries are #1 estrogen producer no estrogen no lubricant = dyspareunia no estrogen and no fsh/lh --> there must be a "higher" problem, up there in the brain
... armymed88 made a comment on nbme22/block2/q#21 (A newborn has cyanosis, tachypnea, and retractions...)
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submitted by armymed88(13)

A little math here.. pH is low --> acidosis pCO2 is high --> respiratory Normal compensation should be roughly a 1 (acute) to 4(chronic) increase in bicarb per every 10 increase in pCO2.. Its lower here, so clearly not compensated and indicated additional drop in bicard --> add on metab acidosis

hello  Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb?
kateinwonderland  How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis??
yb_26  normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis
... privwill made a comment on nbme22/block2/q#21 (A newborn has cyanosis, tachypnea, and retractions...)
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submitted by privwill(3)

Step by step:

  1. pH = low = acidosis
  2. HCO3 = low = acidosis
  3. CO2 = high = acidosis

So, what I've learned is that, in essence, metabolic acidosis always takes priority in these scenarios. It's evident that the person is not compensating, but you want to calculate anyway by using Winter = 1.5 (HCO3) + 8 .
If you calculate you will see that the expected is 30.5.

  1. If CO2 is higher than expected = concomitant respiratory acidosis
  2. If CO2 is lower than expected = concomitant respiratory alkalosis

Here it is higher than expected (65) so concomitant respiratory acidosis.

I guess if you wanted to start with the respiratory acidosis you would've taken into consideration that bicarbonate should've gone up to compensate. It didn't so it's uncompensated. Not sure if there's a formula to calculate the other stuff

... hayayah made a comment on nbme22/block2/q#22 (A 35-year-old man comes to the physician because of...)
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submitted by hayayah(345)

Growth hormone releasing hormone acts via G-coupled receptors. G coupled receptors need GTP to become activated and GTPase to become inactivated.

No GTP-ase --> chronically active growth hormone releasing hormone receptor --> constant activation of adenylyl cyclase / cAMP pathway and release of growth hormone.

mcl  This figure is useful https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png
mcl  [link](https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/a025a0e224d366e987bc15edd0f7764ef5611e0d/4-Figure3-1.png)
meningitis  How did you knkow it was GHRH and not GH perse?
meningitis  nevermind; I just read down below. Thank you
... goldenwakosu made a comment on nbme22/block2/q#22 (A 35-year-old man comes to the physician because of...)
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submitted by goldenwakosu(2)

Why is the answer adenylyl cyclase? I looked in FA and I saw that GH uses the JAK2/STAT pathway and that IGF-1 uses the MAP Kinase pathway. Not sure how adenylyl cyclase plays into this.

pug_sheen  I think they are talking about the GHRH receptor on somatotrophs, which works through the cAMP pathway.
staygoodpupper  I don’t know how it relates to GH/IGF-1 in particular, but the question said there was a mutation in the alpha subunit of Gs, which activates adenylyl cyclase.
kash1f  I agree the patient does have Acromegaly, but in the question it talked about how the patient had a mutation that prevented the GTPase activity of Gas. So Gs would be overactive --> excess adenylyl cyclase
hyperfukus  ugh i was so excited too bc i thought i remembered jak stat epicfail
... fuckster made a comment on nbme22/block2/q#23 (A 32-year-old woman comes to the physician because...)
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submitted by fuckster(-44)

[special]

... biliarytree220 made a comment on nbme22/block2/q#23 (A 32-year-old woman comes to the physician because...)
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submitted by biliarytree220(5)

Chagas disease, trypomastigote on blood smear; cardiomyopathy, predominantly found in South America

... usmleuser007 made a comment on nbme22/block2/q#23 (A 32-year-old woman comes to the physician because...)
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submitted by usmleuser007(86)

Arthropod infections

a. Trypansoma cruzi = reduviid bug

b. Trypanosoma brucei = Tsetse fly

c. Malaria = Anopheles mosquito

d. Flavivirus Group (West Nile Virus, Dengue) = Aedes mosquito

e. Microfilariae = black fly

f. Leishmania braziliensis = sand fly

g. Borrelia & Babesia =Ixodes tick

h. Rickebsia rickebsii & Francisella tularensis = Dermacentor tick

i. Rikebsia prowazekii = lice

j. Loa loa (African eye worm) = deer fly

k. Wuchereria bancrofti = mosquitoes

... usmleuser007 made a comment on nbme22/block2/q#23 (A 32-year-old woman comes to the physician because...)
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submitted by usmleuser007(86)
16. Arthropod infections a. Trypansoma cruzi = reduviid bug b. Trypanosoma brucei = Tsetse fly c. Malaria = Anopheles mosquito d. Flavivirus Group (West Nile Virus, Dengue) = Aedes mosquito e. Microfilariae = black fly f. Leishmania braziliensis = sand fly g. Borrelia & Babesia =Ixodes tick h. Rickebsia rickebsii & Francisella tularensis = Dermacentor tick i. Rikebsia prowazekii = lice j. Loa loa (African eye worm) = deer fly k. Wuchereria bancrofti = mosquitoes
... gh889 made a comment on nbme22/block2/q#24 (A 72-year-old man is given ketorolac for pain...)
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submitted by gh889(32)

Ketorolac is a reversible NSAID given IV, all NSAIDs have a risk of interstitial nephritis, renal ischemia, gastric ulcers, and aplastic anemia.

the best answer is renal failure b/c it is given IV and has less of a chance of causing gastric ulcers

... armymed88 made a comment on nbme22/block2/q#25 (A 37-year-old woman undergoes excision of a 1-cm,...)
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submitted by armymed88(13)

Wound healing inflammatory for up til 3 days (clots, PMNs, macros) Proliferative 3days til weeks- granulation tissue, new vessels, new epithelium, contraction (repair and regeneration) Remodel 1wk til 6m- replace collagen III with I, increase strength (up to 60-70% original strength possible)

... usmleuser007 made a comment on nbme22/block2/q#25 (A 37-year-old woman undergoes excision of a 1-cm,...)
... btl_nyc made a comment on nbme22/block2/q#25 (A 37-year-old woman undergoes excision of a 1-cm,...)
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submitted by btl_nyc(9)

Proliferative phase of wound healing. FA 2019 pg 217

... adisdiadochokinetic made a comment on nbme22/block2/q#26 (A randomized controlled trial is conducted to assess...)
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submitted by adisdiadochokinetic(7)

Absolute risk reduction = (Risk in control) - (Risk in experimental). In this case, the risk in the control group is calculated by the number who had an infarction (194) divided by the total (194/2371). Likewise, for the experimental group, (194/2365). This is answer choice B.

adisdiadochokinetic  Whoops, second parenthesis should be 123/2365, sorry!
... armymed88 made a comment on nbme22/block2/q#27 (A 50-year-old man who has smoked 2 packs of...)
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submitted by armymed88(13)

emphysema leads to CO2 trapping leading to increase paCO2 in the blood, which gives you a respiratory acidosis Proper renal compensation will increase bicard reabs and decrease excretion- giving you increased bicarb in the blood

meningitis  Increased blood HCO3 could have easily been interpreted as increased blood pH aswell. FOllowing your explanation, since the pt had acidosis, the increased HCO3 will just make it a normal pH. Another way to think of the question is: if there is decreased exhalation due to COPD --> increased CO2 --> increased CO2 transported in blood by entering the RBC's with Carbonic Anhydrase and HCO3 is released into blood stream. So increased CO2 -> increased HCO3 seeing as this type of CO2 transport is 70% of total CO2 content in blood.
... yotsubato made a comment on nbme22/block2/q#28 (A 65-year-old man comes to the physician for a...)
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submitted by yotsubato(214)

Interosseous muscles are innervated by the ulnar nerve.

Flexion of the foot is innervated by tibial nerve

... mattnatomy made a comment on nbme22/block2/q#29 (A 79-year-old man is brought to the emergency...)
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submitted by mattnatomy(21)

A Pacemaker is the correct treatment for 3rd degree AV block. Makes it so the atria and ventricles beat in sync.

... nbmessuck made a comment on nbme22/block2/q#30 (A 40-year-old woman comes to the physician because...)
... alexb made a comment on nbme22/block2/q#30 (A 40-year-old woman comes to the physician because...)
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submitted by alexb(10)

It seems like a lot of the systemic autoimmune diseases are multifactorial. Is there a general rule for this?

ls3076  Really good observation
... yotsubato made a comment on nbme22/block2/q#31 (An unimmunized 1-year-old boy is admitted to the...)
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submitted by yotsubato(214)

In biology, phase variation is a method for dealing with rapidly varying environments without requiring random mutation. It involves the variation of protein expression, frequently in an on-off fashion, within different parts of a bacterial population. As such the phenotype can switch at frequencies that are much higher (sometimes >1%) than classical mutation rates. Phase variation contributes to virulence by generating heterogeneity. Although it has been most commonly studied in the context of immune evasion, it is observed in many other areas as well and is employed by various types of bacteria, including Salmonella species.

https://www.wikiwand.com/en/Phase_variation

whoissaad  is it the same thing as antigenic variation?
dorsomedial_nucleus  No, antigenic variation involves genomic rearrangement Phase variation can be thought of as MORE or LESS of something. An on/off switch. No DNA is being rearranged, just under or overexpressed in response to the environment.
... bhangradoc made a comment on nbme22/block2/q#32 (A 54-year-old man who works in a delicatessen comes...)
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submitted by bhangradoc(9)

Schwann cells: they are supposed to degrade residual myelin sheath during the neuronal degeneration. Without that degeneration, I guess you can’t re-innervate properly. Not totally sure.

... lodododo made a comment on nbme22/block2/q#32 (A 54-year-old man who works in a delicatessen comes...)
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submitted by lodododo(1)

There’s a UWorld question on this. Once the healthy axon retracts and the distal (injured) axon degenerates, there’s a bunch of myelin debris in the way that remains there for a long time. This blocks regeneration of the axon.

alacran763  Reinnervation *is* assisted by schwann cells, but the process is very delicate. After Wallerian degeneration, the schwann cells basically have to line up perfectly along where the nerve is supposed to grow, but it does not happen perfectly and the schwann cell disorganization often prevents proper reinnervation.
dantescuttlefish  I thought the Uworld question said that in the CNS myelin debris is there for months even years....the PNS it gets cleared much quicker.
... armymed88 made a comment on nbme22/block2/q#32 (A 54-year-old man who works in a delicatessen comes...)
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submitted by armymed88(13)

Of these options available, Schwann cells would be the only cells present in the PNS. Astrocytes, microglia and oligos are all CNS cells Satellite cells are in the muscle and serve to aid in muscle repair and regeneration

yb_26  Thats myosatellite cells. Satellite cells are also glial cells that form around damaged nerve cells and lie close to neuron bodies in the CNS
... usmleuser007 made a comment on nbme22/block2/q#32 (A 54-year-old man who works in a delicatessen comes...)
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submitted by usmleuser007(86)

Neuroregeneration in the peripheral nervous system (PNS) occurs to a significant degree.[5][6] After an injury to the axon, peripheral neurons activate a variety of signaling pathways which turn on pro-growth genes, leading to reformation of a functional growth cone and regeneration. The growth of these axons is also governed by chemotactic factors secreted from Schwann cells. Injury to the peripheral nervous system immediately elicits the migration of phagocytes, Schwann cells, and macrophages to the lesion site in order to clear away debris such as damaged tissue which is inhibitory to regeneration. When a nerve axon is severed, the end still attached to the cell body is labeled the proximal segment, while the other end is called the distal segment. After injury, the proximal end swells and experiences some retrograde degeneration, but once the debris is cleared, it begins to sprout axons and the presence of growth cones can be detected. The proximal axons are able to regrow as long as the cell body is intact, and they have made contact with the Schwann cells in the endoneurial channel or tube. Human axon growth rates can reach 2 mm/day in small nerves and 5 mm/day in large nerves.[4] The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, but the endoneurium remains. In the later stages of regeneration the remaining endoneurial tube directs axon growth back to the correct targets. During Wallerian degeneration, Schwann cells grow in ordered columns along the endoneurial tube, creating a band of Büngner (boB) that protects and preserves the endoneurial channel. Also, macrophages and Schwann cells release neurotrophic factors that enhance re-growth.

(wiki)

... usmleuser007 made a comment on nbme22/block2/q#32 (A 54-year-old man who works in a delicatessen comes...)
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submitted by usmleuser007(86)

Central nervous system regeneration

Unlike peripheral nervous system injury, injury to the central nervous system is not followed by extensive regeneration. It is limited by the inhibitory influences of the glial and extracellular environment. The hostile, non-permissive growth environment is, in part, created by the migration of myelin-associated inhibitors, astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia. The environment within the CNS, especially following trauma, counteracts the repair of myelin and neurons. Growth factors are not expressed or re-expressed; for instance, the extracellular matrix is lacking laminins. Glial scars rapidly form, and the glia actually produce factors that inhibit remyelination and axon repair; for instance, NOGO and NI-35.The axons themselves also lose the potential for growth with age, due to a decrease in GAP43 expression, among others.

usmleuser007  (wiki)
... bubbles made a comment on nbme22/block2/q#33 (A 29-year-old woman comes to the physician because...)
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submitted by bubbles(26)

Just to be crystal clear (because I've gotten more thyroid axis questions wrong than I should):

T4 --> T3 is possible but T3 --> T4 isn't?

meningitis  Exactly. I know there are papers saying there is some conversion of T3 to T4 but I try to keep it simple and think of it as once you break it apart (T4->T3), you cant put it back together. Only thyroglobin etc can put another I on it, so any T3 cant become T4 because you need it to be done in thyroid.
angelaq11  I honestly don't know about this, but the way I reasoned this was: she is taking a whole lot of T3, so on top of already having hypothyroidism, she is just making things worse, so TSH is going to be decreased because of feedback inhibition, and hence T4 (Which is the main one produced by the thyroid) is also going to be decreased. I think the high T3 is the exogenous T3.
... oznefu made a comment on nbme22/block2/q#33 (A 29-year-old woman comes to the physician because...)
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submitted by oznefu(7)

I get she doubled her levothyroxine dose because of fatigue. I get that TSH is decreased. But why is free T4 decreased and free T3 increased? Wouldn’t both free T4 and free T3 be increased?

lnsetick  she doubled her triiodothyronine not levothyroxine, so she took a bunch of T3 -> feedback inhibition of TSH and therefore decreased T4
oznefu  D’oh didn’t even read that just assumed it was levothyroxine. Thanks!
... keycompany made a comment on nbme22/block2/q#34 (A 30-year-old man and a 24-year-old woman (indicated...)
 +2  upvote downvote
submitted by keycompany(105)

Mandelian Genetics:

Man has 2/3 chance of being a carrier. (He does not have the disease). Woman carrier risk must be calculated with p^2 + 2pq + q^2. q^2 = 1/40,000 q = 1/200, p is roughly = 1 2pq = 1/100 = Carrier frequency .

Risk of having a child thus equals 2/3 x 1/100 x 1/4 = 1/600 Because: 2/3 = Man Carrier risk 1/100 = Female Carrier Risk 1/4 = Chance they each pass on the recessive gene to their offspring.

hello  See my explanation if you need more words to explain this explanation
... beastfromtheastx made a comment on nbme22/block2/q#34 (A 30-year-old man and a 24-year-old woman (indicated...)
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submitted by beastfromtheastx(0)

The probability of the father being a carrier is 2/3 since it is known that he doesn’t have the disease. Then the probability of him passing it on to his kid is:

1/2 * 2/3 = 1/3

With the Hardy-Weinberg Principle, you can figure out the probability of the mother being a carrier:

q = sqrt(1/40,000) = 1/200

So, 2pq = 2 * 1/200 * 199/200, which approx is 1/100, and the probability of the child getting this allele is 1/100 * 1/2 = 1/200

Thus:

1/200 * 1/3 = 1/600

brill45  You did this right but I think made it a bit more complicated than needed to be. To figure out the likelihood of a random person in the population passing on a recessive allele, you just need to do squareroot(q2) to get to q. And just use that q to multiply with the 1/3 you got earlier. The q value tells you the allele frequency in the population, whether the person is a carrier or homozygous recessive both. You still got it, but just letting you know the easier route in case you see it again!
... drdoom made a comment on nbme22/block2/q#34 (A 30-year-old man and a 24-year-old woman (indicated...)
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submitted by drdoom(166)

Calculations for dad. The probability of the father being a carrier is 2/3 since it is known that he doesn’t have the disease. Then the probability of him passing it on to his kid is 1/2, thus:

  • Probability of dad being carrier = 2/3
  • Probability of dad passing on disease allele = 1/2

Calculations for mom. With the Hardy-Weinberg Principle, you can figure out the probability of the mother being a carrier:

q = sqrt(1/40,000) = 1/200

So, 2pq = 2 * 1/200 * 199/200, which is approx 1/100.

For the child to get the allele from mom, two things need to happen: (1) mom must be a carrier [“heterozygote”] and (2) mom must pass the allele to child:

  • Probability of mom being carrier = 1/100
  • Probability of mom passing on disease allele = 1/2

Puting it all together. Now, combine all together:

= (probability of dad being carrier) * (probability of dad passing on disease allele) * (probability of mom being carrier) * (probability of mom passing on disease allele)

= 2/3 * 1/2 * 1/100 * 1/2
= 1 in 600

kernicterusthefrog  To quote Thorgy Thor, drag queen: "ew, Jesus, gross"
niboonsh  This question makes me want to vomit
drdoom  lol
... hello made a comment on nbme22/block2/q#34 (A 30-year-old man and a 24-year-old woman (indicated...)
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submitted by hello(51)

This the same as @keycompany's explanation with more explanation those that need it...

The patient is unaffected by the particular autosomal recessive disease and his brother has the autosomal recessive disease --> this means each of their parents carries the AR allele. Now, for the patient to be unaffected given that both his parents have the AR allele, it means that the patient has a 2/3 chance that he is simultaneously unaffected and a carrier.

The patient's partner is unaffected and normal Hardy-Weinberg genetics (as stated in the problem)..when this is specifically mentioned, you are to assume that the partner has a carrier frequency for the AR allele, which equal to 2pq.

The disease has a frequency in the population of 1/40000. This is q^2 --> q^2 = 1/40000. Solving for q, you get q = 1/200.

Carrier frequency is 2pq. However, for a rare disease, 2pq ≈ 2q. So, the carrier frequency for the partner = 2q = 2 * 1/200 = 1/100.

Now, the Q asks about an offspring of the patient and his partner being affected, so to have an affected child, there is a 1/4 chance of having an affected child (becasuse the patient and the partner both have a 1/2 chance of passing the allele --> you multiple these together 1/2 * 1/2).

So, multiply 2/3 * 1/100 * 1/4 = 1/600. This is P(patient being a carrier) * P(partner being a carrier) * P(having an affected offspring together).

... yotsubato made a comment on nbme22/block2/q#35 (A 45-year-old man with Li-Fraumeni syndrome agrees...)
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submitted by yotsubato(214)

p53 is mutated and cant bind the TATA box, so what happens to transcription of inhibitory proteins?

Is basically what this question is trying to ask...

So no TATA box promoter => Decreased binding of RNA polymerase

link981  You said it, they are "trying" to ask. Should use better grammar.
... dantescuttlefish made a comment on nbme22/block2/q#35 (A 45-year-old man with Li-Fraumeni syndrome agrees...)
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submitted by dantescuttlefish(1)

Why is this not increased binding of DNA polymerase?

This mutation should cause cellular division ie DNA replication and cause increased binding to origin replication sequences ie TATA by DNA polymerase.

brise  It's talking about mutations on the transcription of genes that inhibit the cell division. Also RNA polymerase binds to the promoter region.
nwinkelmann  Also, the question specifically (though in a very wordy, convoluted way) asked what the effect of the mutation on transcription was. DNA pol is not used in transcription, it is used in replication. RNA pol is used in transcription. In terms of increased or decreased binding, argining is polar/positively charged and proline is neutral/nonpolar, so there are fewer H-bonding sites, and thus decreased binding of the RNA pol.
medn00b  Could this convoluted question also mean.......... that since the gene to make p53 is messed up due to the hydrogen bonds, RNA polymerase will not be able to bind to make the mRNA ... So there will be cancer? Because P53 is a tumor suppressor... lemme know thanks guys
... seagull made a comment on nbme22/block2/q#35 (A 45-year-old man with Li-Fraumeni syndrome agrees...)
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submitted by seagull(355)

Did anyone need to read that last sentence like 50 times because the author refuses to use better grammar. Just frustrating.

link981  Author rationale: "What is grammar?"
... pipter made a comment on nbme22/block2/q#35 (A 45-year-old man with Li-Fraumeni syndrome agrees...)
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submitted by pipter(3)

Does anyone have any specific idea on the mechanism of the p53 mutation question regarding the TATA box (the one with the single amino acid conversion and the different hydrogen bonding)?

I chose the decreased binding of RNA polymerase on the TATA sequence of genes that inhibit cell division based solely on the fact that p53 is a tumor suppressor (aka mutated p53->less inhibition of division->multiple divisions).

joha961  From a random paper I found, “Arguably p53’s most important function is to act as a transcription factor that directly regulates perhaps several hundred of the cell’s RNA polymerase II (RNAP II)-transcribed genes.” So normally it increases RNA pol binding; a mutation would decrease it.
estsosa  The TATA box is part of the promoter region site where RNA polymerase II and other transcription factors bind to DNA. A defect would therefore decrease binding of RNA polymerase.
mnemonia  Also you can reason it out (I got this wrong because you have to be really meticulous) since we know that loss of p53 = cancer. Cancer = want more cell division = don’t want inhibitory gene = less transcription of said gene.
... fenestrated made a comment on nbme22/block2/q#35 (A 45-year-old man with Li-Fraumeni syndrome agrees...)
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submitted by fenestrated(5)

For this one I think what you had to know is that Transcription (DNA-->RNA) is performed by RNA polymerase. It was not DNA polymerase because this one replicates (DNA-->DNA)

fenestrated  between increased or decreased binding I picked decreased because it was a mutation which affected the hydrogen bonds which is how nucleotides bind to each other
... d_holles made a comment on nbme22/block2/q#35 (A 45-year-old man with Li-Fraumeni syndrome agrees...)
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submitted by d_holles(31)

This is a good picture of an experiment showing this:

https://www.nature.com/articles/1210296/figures/1

Oncogene volume 26, pages 2212–2219 (2007)

... hello made a comment on nbme22/block2/q#35 (A 45-year-old man with Li-Fraumeni syndrome agrees...)
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submitted by hello(51)

The grammar of the actual Q was confusing.

To make better sense, it should say "Which of the following is the most likely result on the transcription of genes that inhibit cell division and that contain the consensus sequeence TATA..."

So, the Q is asking about the tp53 gene and specifically about the tp53 gene promoter region.

Promoter regions have a TATA box (obviously, meaning rich in A-T base pairs). A-T base pairing has 2 hydrogen bonds, which makes them easier to cleave --> allows for DNA transcription to occur more easily. RNA Pol does transcription of DNA into RNA.

The entire Q-stem talks about how Li-Fraumeni is due to a mutation in tp53 gene, leading to a lack of tumor suppression activity.

So, if the promoter region TATA box of the tp53 gene is mutated, then the tp53 gene will not get transcribed --> this is why there will be decreased RNA Pol binding. RNA Pol will have a reduced ability to bind tp53 --> less tumor supressor gene transcription --> less tumor suppression.

... seagull made a comment on nbme22/block2/q#36 (Which of the following drug effects is the most...)
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submitted by seagull(355)

Which of the following reasons is why this question is bull?

1) Using the word "cyclic" instead of tricyclic for clarity

2) Knowing all of epidemiology of all drugs

3) having to reason out that anticholinergic effects are probably the worst over alpha1 or H1 effects to no certainty.

4) The crippling depression of studying for days-to-weeks on end to probably do average on the test.

nlkrueger  yo, re-fucking-tweet
aesalmon  I agree, I picked H1 because such a common complaint for those on TCAs is Sedation, I figure it might be so commonly seen as to be the "most common" reason for noncompliance. I suppose the "hot as a hare...etc" effects would be more severe/annoying, but I didn't think they were more common.
fcambridge  I just like to pretend that there's a reason this question is now in an NBME and no longer being used for the test. Hopefully they realized the idiocy of this question like we all do
link981  Since it said cyclic, I thought of using, discontinuing, then using again. These people who write these questions need take some English writing courses so they can write with CLARITY. Cyclic is not the same as Tricyclic.
... niboonsh made a comment on nbme22/block2/q#36 (Which of the following drug effects is the most...)
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submitted by niboonsh(57)

tri-CyCliC antidepressent - anti C holinergic, C ant stand up (a1 block), C ardiotoxic (prolong qt by messing w na channels)

... kard made a comment on nbme22/block2/q#36 (Which of the following drug effects is the most...)
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submitted by kard(3)

Tricyclic and tetracyclic antidepressants, also called cyclic antidepressants. The peripheral anticholinergic complaints of dry mouth, constipation, ocular side effects and urinary hesitancy are described and specific clinical guidelines for their effective management are provided.

So, most common reason for noncompliance with cyclic antidepressant therapy is its anticholinergic effect.

https://www.ncbi.nlm.nih.gov/pubmed/3290996 https://www.mayoclinic.org/diseases-conditions/depression/in-depth/antidepressants/art-20046983

Note: Please if im mistaken, or my approach is mistaken, correct me... Thank you

... mcl made a comment on nbme22/block2/q#37 (A 63-year-old man has had progressive stiffness over...)
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submitted by mcl(169)

This image is useful. Note that the stain used makes myelin appear dark.

Vignette is typical for Parkinson's disease. Area D is the substantia nigra.

oznefu  Oh nice! Thanks!
... oznefu made a comment on nbme22/block2/q#37 (A 63-year-old man has had progressive stiffness over...)
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submitted by oznefu(7)

does anyone know what A, B, C and E are pointing to? I figured D is substantia nigra since it's the correct answer.

upstairs_bumblebee  A/B - i think both of these are just thalamic nuclei; C -> STN; D -> substantia nigra; E -> hippocampus
... moloko270 made a comment on nbme22/block2/q#38 (Following a stroke, a patient is hoarse and cannot...)
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submitted by moloko270(29)

this is Wallenberg syndrome - stroke caused by obstruction of PICA - so thats why we get symptoms of dysphagia, hoarseness, absent gag reflex (p. 502 FA)

armymed88  dysphagia from hit of nucleus ambiguus (CN IX/X/XI) Sensation changes due to hit of lateral spinothalamic tract and spinal trigeminal Check out rule of 4s if you haven't already
theecohummer  Yup, lateral meduallary syndrome or Wallenburg Syndrome. Whatever you want to call it. The hemifacial analgesia is from damage to the spinal trigeminal nucleus/tract, and you get the hoarseness from damage to the vagus and the body loss is from the spinal thalamic tract. You can also get Horner’s syndrome with this.
dr.xx  Lateral medullary syndrome = Wallenberg's syndrome
... pppro made a comment on nbme22/block2/q#39 (A 22-year-old woman comes to the office because of a...)
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submitted by pppro(5)

Pregnancy can cause dilated cardiomyopathy causing systolic dysfunction.

... kobeandming23 made a comment on nbme22/block2/q#40 (A previously healthy 7-year-old girl is brought to...)
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submitted by kobeandming23(1)

DKA (acidosis) > Potassium shifts out of the cell > hyperkakemia

FA 2019, pg 578

... yotsubato made a comment on nbme22/block2/q#41 (A 12-year-old boy is swimming in a mountain stream....)
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submitted by yotsubato(214)

What happens when you go into cold water? You pee.

How does this happen.

Vasoconstriction of vessels to preserve heat, pulls water into vasculature due to decreased hydrostatic pressure in vessels. Volume goes up, ADH goes down, ANP goes up due to increased volume.

... usmleuser007 made a comment on nbme22/block2/q#41 (A 12-year-old boy is swimming in a mountain stream....)
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submitted by usmleuser007(86)

This question has nothing to do with temperature (the vignette doesn't address the temperature of the water - so don't assume)

This is how you get the answer:

1) Being in outer-space or in a swimming pool up to the neck will:

a. Increases Central blood volume (more blood returns to the right side of heart = increased preload)

b. Increases ANP = increased dilation of ventricles ~ compensatory mechanism to reduce volume overload

c. Decreased ADH & Renin-aldo-system = body is in state of volume overload & needs to reduce systemic volume

usmleuser007  correction: yea it does address the water temp but the main take away is increased preload
... bubbles made a comment on nbme22/block2/q#41 (A 12-year-old boy is swimming in a mountain stream....)
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submitted by bubbles(26)

Wouldn't constriction of peripheral vessels also trigger sphlancnic vasoconstriction, which simulates renal ischemia and causes increased RAAS activity?

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process!
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome?
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort"
... keycompany made a comment on nbme22/block2/q#41 (A 12-year-old boy is swimming in a mountain stream....)
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submitted by keycompany(105)

Answer: Increased Central Blood Volume (CBV), Decreased ADH, Increased ANP.

The physiological response to hypothermia is vasoconstriction of peripheral vessels (i.e. the ones in your extremities) in an effort to keep your core body temperature normal, and thus your organs functioning properly. Peripheral Vasoconstriction will increase CBV. Increased CBV will cause an increase in preload, and thus cause an increase in ANP/BNP. ANP/BNP has inhibitory effects on the Renin-Angiotensin-Aldosterone System, resulting in decreased ADH.

... medstudied made a comment on nbme22/block2/q#41 (A 12-year-old boy is swimming in a mountain stream....)
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submitted by medstudied(2)

I missed this as well because I completely overthought it since they had to add (vasopressin) instead of just saying ADH which made me think of its role in constriction of smooth muscle, but the point is that there will be pooling of the blood volume in the viscera and vital organs which will increase ANP release from the atria and since ANP is released with higher blood volume/atrial stretch, you can draw the conclusion that ADH will be low because ANP is signaling to the kidneys that there is an abundance of volume. Also, since the viscera is going to get more blood flow compared to the extremities since he is going to be hypothermic, you should also get increased flow to the kidneys or at least preservation (to a certain extent) and this would not promote the release of ADH which is only released when the body senses an increase in blood osm.

... littletreetrunk made a comment on nbme22/block2/q#42 (A 75-year-old woman has taken 12 over-the-counter...)
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submitted by littletreetrunk(9)

I think the increase in plasma renin activity with NSAIDs has to do with inhibition of efferent artery dilation by prostaglandins (PGE2), since that's what NSAIDs do by inhibiting COX. This decreased renal blood flow leads to RAAS activation to conserve water and ultimately renin increases.

htballer55  Afferent artery dilation*
link981  There is decreased afferent renal artery dilation (less blood flow) leads to increased renin release from the juxtaglomerular cells (located near the afferent artery) to try to increase blood flow. I got it wrong but after reviewing saw my idiotic mistake.
... lilamk made a comment on nbme22/block2/q#42 (A 75-year-old woman has taken 12 over-the-counter...)
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submitted by lilamk(4)

I am so confused! The only logic I could come up w is that NSAIDs decrease dilation of afferent arteriole so this more constricted arteriole is interpreted as decreased blood flow and Renin increases? My issue w this is that when I google it and search UW for this renin affect nothing comes up only article I could find actually contradicts it and says renin would DECREASE from NSAIDs leading to the hyperkalemia we sometimes see ...

Any thoughts would be helpful! Thanks geniuses.

generic_login  I used that reasoning to pick C, but in looking it up now it seems like you are right ... There appear to be a bunch of mistakes on this test, and it’s not giving me a lot of confidence for the real thing.
mee48  I think it is because NSAIDs inhibit the local prostaglandin (PGE2) in afferent arteriole —-> less AA dilation —-> stimulation renin release. I think my reasoning came from sketchy pharm nsaid video but I can’t 100% remember
keycompany  NSAIDs constrict the afferent arteriole. ​ A. GFR would decrease due to decreased renal blood flow. B. Renal Blood flow would decrease. C. Renin would increase due to renal hypoperfusion. D & E. PGE2 and TXA would decrease (by MOA of NSAIDs).
... privwill made a comment on nbme22/block2/q#42 (A 75-year-old woman has taken 12 over-the-counter...)
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submitted by privwill(3)

Step by Step:

  1. NSAIDs block prostaglandins which normally dilate the afferent arteriole
  2. Constriction = decreased blood flow to glomerulus (decreased GFR; decreased RPF)
  3. Decreased blood flow leads to activation of RAAS system
  4. Activation of RAAS leads to increased renin

Why not the other ones:

A. GFR will be decreased due to constriction of the afferent
B. Renal blood flow will be decreased due to vasoconstriciton of the afferent
D & E. Production blocked by NSAID so wouldn't even be around

... medstudied made a comment on nbme22/block2/q#43 (A 20-year-old man comes to the physician because of...)
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submitted by medstudied(2)

Can someone please explain why the answer to this is injury to the posterior cord rather than the radial nerve?

pipter  because raising the arm above the shoulder suggests abduction which would mean the axillary nerve is also involved. the lesion would be more proximal.
kchakhabar  I thought "up to the shoulder" is done by deltoid muscle (aka axillary nerve) and above is done by trapezius.
forerofore  as far as i can find, abduction ranges of motion, per first aid are: 0-15° = supraspinatus 15-90° = Deltoid 90° = trapezius 100° (over the head) = serratus anterior in this question, they are directly telling you its not the serratus (long thoracic), because no option compromises it. Also, trapezius is innervated by cranial nerve XI, which is not a part of the brachial plexus, so, even though its worded weirdly, you can assume they are talking about deltoid disfunction. so deltoid disfunction (axillary) + radial disfunction = posterior cord
... hello made a comment on nbme22/block2/q#43 (A 20-year-old man comes to the physician because of...)
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submitted by hello(51)

Patient cannnot extend wrist, which is innervated by radial nerve

Patient has been on crutches, which would affect axillary nerve --> this affects deltoid muscle, which does arm abduction 15-100º (so it can normally move arm above shoulder)

The only location in the given diagram to effect all of these nerves would be location "C"

Note: normally, arm movement above the horizontal is associated with serratus anterior muscle/long thoracic nerve. However, none of the diagram locations allow for inclusion of SALT. Since the patient has been on crutches for weeks, it suggests axillary nerve involvement --> deltoid is affected

... dantescuttlefish made a comment on nbme22/block2/q#44 (A 3-day-old full-term male newborn is brought to the...)
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submitted by dantescuttlefish(1)

Babies don't have mature activity of this enzyme when first born...Tx with phototherapy...not same mechanism as enzyme but makes bilirubin more soluble

... ilikecheese made a comment on nbme22/block2/q#44 (A 3-day-old full-term male newborn is brought to the...)
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submitted by ilikecheese(7)

There is a high indirect bilirubin concentration (8 mg/dl out of the total 10 mg/dl) so there must be a problem with conjugation. the enzyme needed for conjugation is UDP-gluronosyltransferase.

In this case, this is physiological neonatal jaundice. due to immature enzyme that resolves without treatment in 1-2 weeks. pg 387 FA 2019

... calcium196 made a comment on nbme22/block2/q#45 (An 86-year-old man who lives in a skilled nursing...)
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submitted by calcium196(6)

How is a synthetic opioid (dextromethorphan) that you can find with a 2 second google search as causing constipation the correct answer? Is it just because tiotropium wouldn’t treat the cough?

moneysacs  Tiotropium would cause constipation bc it’s an anticholinergic. Don’t have any insight into why dextromethorphan is the right answer though, other than process of elimination and diphenhydramine wouldn’t treat his symptoms.
upstairs_bumblebee  I thought it was dextromethorphan because it would bind NMDA receptors and have weaker opioid effect = less constipation? Idk though :/
dr_salface  I agree. I mainly went by way of elimination but even DXM made me think of opiod-induced constipation. Though, all the other answer choices had obvious anticholinergic effects. At least, that was my reasoning for picking dxm.
... noselex made a comment on nbme22/block2/q#45 (An 86-year-old man who lives in a skilled nursing...)
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submitted by noselex(4)

Dextro vs Codeine: Both are antitussives, but dextro is more of NMDA agonist that also has opioid agonist activity. Dextro is often abused to get a similar out of body feeling due to its NMDA agonist effect. Codeine on the other other is a full-on opioid agonist. It’s also used as anti-diarrheal, so constipation is very common adverse effect.

Tiotropium is wrong because it’s not an antitussive. Also, it’s an anticholinergic which is (1) contraindicated in elderly unless really indicated, (2) a well-documented anticholinergic effect is constipation.

pparalpha  According to Sketchy and Amboss: dextromethorphan is a weak opioid receptor AGONIST and NMDA receptor ANTAGONIST (it's not an agonist).
... calcium196 made a comment on nbme22/block2/q#45 (An 86-year-old man who lives in a skilled nursing...)
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submitted by calcium196(6)

NBME 20 has a question with a guy taking over the counter cough medication and now he has constipation. Want to guess the answer? It was dextro! -> https://nbmeanswers.com/exam/nbme20/458

So I’m pretty sure the NBME 22 question is just straight up wrong.

rockediny  No, not so. Dextro *is* the correct answer here. From the choices given, dextro is the least likely to cause constipation since its main mechanism of action is NMDA antagonism w/ *some* opioid activity -- it can cause constipation but the other choices are MUCH MORE likely to. As for diphenhydramine = it is not appropriate for elderly patients and it isn’t an antitussive.
surely_not_a_robot_  Agreed with @rockediny. Dextro would be the best to prescribe because it has the least amount of constipation out of the drugs that you could prescribe + Anti-cholinergics in the elderly have much more morbidity and risk of mortality.
keycompany  The only way to wrap your head around this is to conclude that Dextro is the "least wrong". I thought a lot about this, and I can't think of any drugs that can suppress cough without also causing constipation, so it makes sense that Dextro is the answer because it is the "least likely" to cause significant constipation. This is probably just a clinical correlate that will be learned during rotations/years in practice.
... rockediny made a comment on nbme22/block2/q#45 (An 86-year-old man who lives in a skilled nursing...)
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submitted by rockediny(5)

Dextro is the correct answer here. From the choices given, dextro is the least likely to cause constipation since its main mechanism of action is NMDA antagonism w/some opioid activity -- it can cause constipation but the other choices are MUCH MORE likely to. As for diphenhydramine = it is not appropriate for elderly patients and it isn’t an antitussive.

forerofore  diphenhydramine and other Gen 1 antihistamines are good choices for chronic cough in allergy and patients with posterior draining and post viral chronic cough (careful with the elderly). That being said, apparently it also causes constipation, so dextro is still the correct answer.
... surely_not_a_robot_ made a comment on nbme22/block2/q#45 (An 86-year-old man who lives in a skilled nursing...)
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submitted by surely_not_a_robot_(0)

Per first aid. Dextromethorphan = “Antitussive (antagonizes NMDA glutamate receptors). Synthetic codeine analog. Has mild opioid effect when used in excess.”

I guess the key is that the opioid effect is mild. Seems like they’re asking which would treat the symptoms and reduce the side effects, not necessarily get rid of the side effects completely. Agree that it is a challenging one for Step 1.

... hayayah made a comment on nbme22/block2/q#46 (A 62-year-old man is being evaluated for rectal...)
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submitted by hayayah(345)

X in the image is the small intestine. Its characteristic feathery appearance after a barium meal is due to permanent circular folds and villi. The villi give the small intestine a great mucosal surface area.

nwinkelmann  Yes. The appearance of the mucosal folds depends upon the diameter of the bowel, and when they fold they appear feathery. Mucosal folds are largest and most numerous in the jejunum and tend to disappear in the lower part of the ileum.
... sweetmed made a comment on nbme22/block2/q#46 (A 62-year-old man is being evaluated for rectal...)
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submitted by sweetmed(28)

PLica circularis: muscosal folds that extend from distal duodenum to proximal ileum FA2018 pg 356

... armymed88 made a comment on nbme22/block2/q#47 (A 22-year-old woman who is at 16 weeks' gestation...)
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submitted by armymed88(13)

Down syndrome 2nd trimester screen (usually around 16-18wks) shows decreased AFP, estriol and increased hCG and inhibin A.

Of trisomy 13/18/21, Down Syndrome is the only to have an eleveted hCG

... adisdiadochokinetic made a comment on nbme22/block2/q#48 (Clostridium perfringens-α toxin affects cells and...)
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submitted by adisdiadochokinetic(7)

The clostridium perfringens alpha toxin is a lecithinase which cleaves lecithin to phosphorylcholine and diglyceride. Essentially, alpha toxin mimics phospholipase C. This means it has a vaguely similar effect of the phospholipases seen in Bacillus Cereus and Listeria Monocytogenes. The end result of the toxin activation is activation of second messenger systems through diglyceride (AKA diacylglycerol), which activates several pathways, most notably in this case Arachidonic acid metabolism and IL-8, with the net effect of increased vascular permeability leading to edema.

... bubbles made a comment on nbme22/block2/q#50 (An 18-month-old boy is admitted to the hospital...)
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submitted by bubbles(26)

Can someone could explain to me how this is unequivocally tuberous sclerosis despite NF-1 and Sturge-Weber also presenting with skin lesions, hypopigmented macules, and seizures?

And considering the negative family history, I would have assumed that a sporadic mutation (like SW) would be more likely...

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off.
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out
... armymed88 made a comment on nbme22/block2/q#50 (An 18-month-old boy is admitted to the hospital...)
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submitted by armymed88(13)

Hypopigmented lesions refer to Ash-leaf spots, CNS lesions likely hamartomas . TS also associated with seizures.

fcambridge  How is Tuberous Sclerosis the most likely given that it is an AD disorder and there is no family history of "seizure disorder or major medical illnesses"?
d_holles  @fcambridge variable expressivity of TSC allows for many different phenotypes.
... d_holles made a comment on nbme22/block2/q#50 (An 18-month-old boy is admitted to the hospital...)
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submitted by d_holles(31)

This video explains the pediatric neurocutaneous disorders well.

https://www.youtube.com/watch?v=Lom7tnK8HCk

Basically the key here is hypopigmented macules. NF1 has cafe au liate spots (hyperpigmented macules) while TSC has ash leaf spots (hypopigmented macules). This is a decode the buzzword style question. I felt like I didn't really understand these orders until I watched the above video.

... welpdedelp made a comment on nbme22/block3/q#1 (A 35-year-old man comes to the physician because of...)
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submitted by welpdedelp(64)

So I think that issue of wrist extension and/or finger drop would be more radial nerve. However, there was more proximal weakness, so it would be C7.

"7-8 lay them straight", the pt couldn't "lay them straight" so it would be C7 root

welpdedelp  *As an addition, median nerve involvement would have leaned more toward C8 than C7.
meningitis  Do you have anymore useful mnemonics for brachial plexus?
henoch280  FA pg 494 for mnemonics
... obliviondo made a comment on nbme22/block3/q#1 (A 35-year-old man comes to the physician because of...)
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submitted by obliviondo (1)

According to FA 2019 Tricep Reflex is mediated by C6, yes C6 NOT C8, and C7 [In BOLD, implying it is more important].

... mcl made a comment on nbme22/block3/q#1 (A 35-year-old man comes to the physician because of...)
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submitted by mcl(169)

Pronator teres and quadratus are both supplied by median nerve (C5/C6/C7/C8/T1, so that's not super helpful.) Extension of the forearm is radial nerve (also C5-T1, also not helpful). This does tell us is it can't be isolated median or radial. Triceps tendon reflex is C7/C8, which narrows it down to these two.

Can anyone explain why it's C7 over C8?

joha961  Same question. How could you determine between the specific nerve roots (C7 vs. C8)?
mcl  Someone I was talking to (and post below) was saying that first aid mentions triceps is C7, so that's what should've been the big thing for us.
... magrufnis made a comment on nbme22/block3/q#1 (A 35-year-old man comes to the physician because of...)
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submitted by magrufnis(1)

I’m confused about this one. Weakness of extension and pronation of the right forearm, with a decreased triceps muscle stretch reflex. The answer was C7 nerve root, but how are you able to localize to C7 and not C6 or C8? I figured that extension is radial, C5-T1, and pronation is median, also C5-T1. Triceps reflex is C7-C8 (FA2019 says C6-C7). How would you narrow down to just C7 damage?

txallymcbeal  My FA2018 has “C7” bolded, meaning it is the main nerve root. But I also got this one wrong so I can’t be much help besides that.
mnemonia  Honestly just a guess but I have this vague understanding that intrinsic hand muscles are C8-T1 so we might’ve expected more hand motor findings as well with a C8 lesion.
theecohummer  I narrowed it down to C7 using the fact that the C7 myotome is elbow extension. I also learned that the C7 nerve root was the main contributor to the triceps DTR so I just went with that.
mchu21  They also mentioned that the person had weakness pronating the right forearm which is performed by the biceps. Biceps is innervated by the musculocutaneous nerve which is C5-C7 and that's what helped me pick C7 > C8.
mcl  Sorry, I thought the biceps was a supinator of the forearm?
henoch280  yes.. its the supinator not pronator
... nwinkelmann made a comment on nbme22/block3/q#1 (A 35-year-old man comes to the physician because of...)
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submitted by nwinkelmann(60)

Per Wikipedia: The triceps reflex, a deep tendon reflex, is a reflex as it elicits involuntary contraction of the triceps brachii muscle. It is initiated by the Cervical (of the neck region) spinal nerve 7 nerve root (the small segment of the nerve that emerges from the spinal cord). The reflex is tested as part of the neurological examination to assess the sensory and motor pathways within the C7 and C8 spinal nerves.

Also, from a different website: The triceps reflex is mediated by the C6 and C7 nerve roots, predominantly by C7. https://informatics.med.nyu.edu/modules/pub/neurosurgery/reflexes.html.

... paulm made a comment on nbme22/block3/q#1 (A 35-year-old man comes to the physician because of...)
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submitted by paulm(0)

Per UWorld (ID 15553)

The C7 root is the most frequently affected nerve root in patients with cervical radiculopathy, resulting in deficits across the median and radial nerve distributions.

"tingling sensation of fingers" → median nerve

"triceps muscle reflex is decreased" → radial nerve

... bubbles made a comment on nbme22/block3/q#2 (A 30-year-old man is brought to the emergency...)
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submitted by bubbles(26)

Just as clarification, capillary hydrostatic pressure would decrease because of systemic vasoconstriction in response to aortic rupture/systemic hypotension?

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA.
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible
... jboud86 made a comment on nbme22/block3/q#2 (A 30-year-old man is brought to the emergency...)
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submitted by jboud86(1)

Page 576 of FA2019. This is the renin-angiotensin-aldosterone system working. A decrease in BP is sensed by the renal baroreceptors causing a release of renin.

... bubbles made a comment on nbme22/block3/q#3 (An obese 45-year-old woman with type 2 diabetes...)
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submitted by bubbles(26)

Sorry if I'm being dense...why does this woman have diarrhea due to statins, diet, and exercise? I didn't really understand what they were asking for here to be honest.

.ooo.   I believe they were asking what the most common effect of statins, which is GI upset (including diarrhea). Rarely you can have hepatotoxicity and myopathy but neither of these are a side effect in the answer choices. Hopefully this helps!
niboonsh  Theyre asking about the most common side effect of Orlistat - which is really fatty diarrhea
... aaaaaaa made a comment on nbme22/block3/q#3 (An obese 45-year-old woman with type 2 diabetes...)
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submitted by aaaaaaa(2)

orlistat is used for weight loss (its not a statin as some people thought in the comments here). its in FA 2019 pg 294, m/c side effects are GI including diarrhea

imnotarobotbut  Thanks! It's actually page 394
... welpdedelp made a comment on nbme22/block3/q#4 (A 29-year-old woman has an inflammatory disease...)
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submitted by welpdedelp(64)

This was SLE. https://step1.medbullets.com/msk/112039/systemic-lupus-erythematosus

Think: 1,2,3= S-L-E

Using ACID: Type III is for Immune Complexes

... airhead5 made a comment on nbme22/block3/q#4 (A 29-year-old woman has an inflammatory disease...)
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submitted by airhead5(1)

Does anyone know the disease they are talking about? I was thinking lupus which makes sense with the answer, but i can’t find anything on anterior chamber of eye and choroid plexus.

liverdietrying  It's lupus, all the symptoms listed are classic especially the serositis. Anterior chamber of the eye = uveitis. Choroid plexus = cerebritis. For a great overview, check out this (free) video: https://onlinemeded.org/spa/rheumatology/lupus/acquire
in_a_pass_life  I think this was reactive arthritis, not lupus. Choroid plexus not just in the brain, also in eye (can’t see, can’t pee, can’t climb a tree). Mechanism of reactive arthritis is immune complex deposition, per UWorld, which was correct answer.
trichotillomaniac  The inside of the eye is divided into two chambers: the anterior chamber and the posterior chamber. Both chambers contain fluid, and when there’s inflammation in the eye, a specialist can often see inflammatory cells in the fluid. https://www.hss.edu/conditions_eye-problems-lupus.asp
trichotillomaniac  I agree that this is Lupus after doing some more research!
nwinkelmann  I find this article describing the SLE ocular manifestations, including uveitis and cerebritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908056/ Also this talks about the lupus cerebritis (choroid plexus inflammation): https://en.wikipedia.org/wiki/Cerebritis
medulla  every time I read about Lupus there is something new!!
... welpdedelp made a comment on nbme22/block3/q#5 (A 72-year-old man with multiple myeloma agrees to...)
... david_bball made a comment on nbme22/block3/q#5 (A 72-year-old man with multiple myeloma agrees to...)
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submitted by david_bball(3)

The way I thought about this question was that in MM there is a TON of antibodies being made, so the VDJ segment is being broken up/selected/rearranged many times and has been shortened to 1.5kb. As for the T Cells, that region isn’t being used (since there is no clonal expansion or selection) so it’s still got the full 6kb length untouched.

d_holles  T cells still undergo VDJ recombination to form their TCRs.
... sacredazn made a comment on nbme22/block3/q#5 (A 72-year-old man with multiple myeloma agrees to...)
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submitted by sacredazn(20)

The concept is a convoluted way of asking if you knew how VDJ recombination works, which is that it is actually an example of altering the DNA of the B/T lymphocyte.

Southern blot technique: So when they use a probe against some region, and outputting a size of 1.5 kb or 6 kb, this is telling you the size of the DNA fragment in each cell (doesn’t matter if they say J probe or constant region probe, they’re just saying they’re targeting some nucleotide sequence found in the Ig locus/TCR beta chain locus respectively for B/T cells).

I think the confusing part could be wondering how you know whether you’re partly through rearrangement (answer choices B thru D) or if it hasn’t occurred at all yet (correct answer). Here, the concept is that B cells undergo V(D)J rearrangement in the bone marrow, while T cells do it in the thymus, and it all happens at once. So a plasma cell in the blood like in Multiple Myeloma would have fully undergone recombination, while a T cell in the blood could either be fully educated (and have finished VDJ recombination) or immature (hasn’t started VDJ).

Since the T cell gene was 6 kb and definitely bigger than the 1.5 kb gene, the T cell hasn’t undergone recombination yet.

trichotillomaniac  very nice explanation!
nwinkelmann  This was awesome! Made so much sense and hopefully I will be able to think that critically about questions in the future (because I NEVER would have come up with this on my own, hah).
... sam1 made a comment on nbme22/block3/q#5 (A 72-year-old man with multiple myeloma agrees to...)
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submitted by sam1(0)

While T cells do use the VDJ recombination, the T cell receptor chains are different genes from the B cell's heavy and light chains. Since they used a B cell J-region probe, the T cell's band will be much larger as this area of its DNA (the B cell heavy or light chain genes) have not been rearranged -- instead its T cell receptor genes have been rearranged.

... oznefu made a comment on nbme22/block3/q#6 (A 50-year-old man is admitted to the hospital...)
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submitted by oznefu(7)

I get that the answer is correct for a reversible injury where there is cell swelling because of the increased intracellular Na+ and Ca2+ due to impaired Na/K and sarcoplasmic reticulum activity ...

But if there are increased cardiac enzymes in the blood indicating cell death and membrane damage, wouldn’t the intracellular electrolytes be low since they are released into the blood?

lord_voss  troponin = irreversible injury and membrane damage -> high extracellular concentration of Na+ and Ca++ causes both to move into cell through damaged membrane and high intracellular K+ leaves the cell
rogeliogs  Question is asking about the changes in the myocardiocytes and my second interpretation was that they are asking the changes before they "rupture" and liberate their content in the blood producing increase enzymes in the patient. Therefore because is a ischemic process = reduction of O2 = low ATP = impairment of Na/K ATPase = increase Na-decrease K intracellular = block Ca/Na exchanger = increase Ca intracellular. the same effect as digoxin
... sbryant6 made a comment on nbme22/block3/q#6 (A 50-year-old man is admitted to the hospital...)
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submitted by sbryant6(17)

If you know the MOA of digoxin you should be able to get this question right.

... imnotarobotbut made a comment on nbme22/block3/q#7 (A 50-year-old man who is a college professor has had...)
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submitted by imnotarobotbut(22)

Acknowledge the patient's difficulty. I hate these questions

nwinkelmann  Me too... also, he's had cough that's worsening for 6 months plus hemoptysis for 1 week... I didn't interpret that as "feeling healthy." The correct answer was my first choice just because it was the least "dick-ish" but to me, he didn't sound like he "felt health," so I didn't go with it.
nor16  if he didnt feel healthy, why would he say something like that then... but i agree, these (especially this) question(s) are often XYZ123!
... mcl made a comment on nbme22/block3/q#8 (A 38-year-old man who lives at sea level flies to a...)
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submitted by mcl(169)

Since you're losing all your bicarb into your pee, you would expect the pH to be more alkaline. Also, since there is decreased Na+/H+ antiport, there is less sodium reabsorbed and therefore increased loss of free fluid to the urine.

mcl  useful figure http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-036-f002.jpg
joker4eva76  Why wouldn't this be similar to a Type 2 RTA where urinary pH <5.5?
mcl  I can't remember exactly what the question was asking off the top of my head, I think it was asking about relative to normal? But I think you're right in that the alpha intercalated cells (AIC) can still dump H+ into the urine and acidify it to an extent. And, like in RTA2, I don't know that the action of the AIC would be able to overcome the bicarb and acidify the urine enough for it to be the usual pH, so the urine should still be more alkaline compared to baseline. Kinda sucks, pH less than 5.5 should technically be acidic but it's alkaline for pee.
mcl  JK, normal urine pH is around 4-8, but I guess they consider closer to 5.5 on the more alkaline side...? I guess I would go more off that the alpha intercalated cells can't completely compensate for the amount of bicarb in the pee due to the CA inhibitor, not so much the actual pH.
meningitis  Anhydrase inhibitors also affect the anhydrase inhibitors that are used in the AIC in order to excrete the H+. Here is a link:**http://pedclerk.bsd.uchicago.edu/sites/pedclerk.uchicago.edu/files/uploads/distal_0.png**
mcl  ohhhhhhhhhhhhhhhhhhhhhhh my god duh yes thank you <3
meningitis  Lol yw!!
... yotsubato made a comment on nbme22/block3/q#8 (A 38-year-old man who lives at sea level flies to a...)
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submitted by yotsubato(214)

Its a diuretic, so volume is increased.

HCO3 is increased because acetazolamide reduces reabsorption of HCO3.

pH is increased, because HCO3- is a weak base, so it sucks up stray hydrogen ions in the urine.

... meatus made a comment on nbme22/block3/q#8 (A 38-year-old man who lives at sea level flies to a...)
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submitted by meatus(1)

I'm sorry but what am I missing here... I thought the whole point of diuretics is to correct volume overload by diuresis? How would total volume be increased??

niboonsh  the question is asking what would happen to the URINARY ph, bicarb, and volume. dont worry, i misread the question too -_-
link981  Also misread the question, thought about the lab volumes of the BLOOD smh
hyperfukus  yooooo me too!!! this is the second NBME i did this on they purposely don't write urine on the arrow categories to mess u up i swear!!! AHHHHHH
medulla  missed this question for the same reason .. still pissed
... yotsubato made a comment on nbme22/block3/q#9 (Microelectrode injection of antibodies to α-actinin...)
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submitted by yotsubato(214)

Area C is where the gap junctions between cardiac myocytes are. Gap Junctions are found on the plasma membrane of the cardiac myocyte.

The question is basically asking where the plasma membrane is with a bunch of biochem mumbojumbo you dont have to understand.

... usmleuser007 made a comment on nbme22/block3/q#9 (Microelectrode injection of antibodies to α-actinin...)
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submitted by usmleuser007(86)

Actinin is a microfilament protein. α-Actinin is necessary for the attachment of actin filaments to the Z-lines in skeletal muscle cells,[1] and to the dense bodies in smooth muscle cells.[2] The functional protein is an anti-parallel dimer, which cross-links the thin filaments in adjacent sarcomeres, and therefore coordinates contractions between sarcomeres in the horizontal axis.

The non-sarcomeric α-actinins, encoded by ACTN1 and ACTN4, are widely expressed. ACTN2 expression is found in both cardiac and skeletal muscle, whereas ACTN3 is limited to the latter. Both ends of the rod-shaped α-actinin dimer contain actin-binding domains.

Mutations in ACTN4 can cause the kidney disease focal segmental glomerulosclerosis (FSGS).

(WIKI)

... moloko270 made a comment on nbme22/block3/q#9 (Microelectrode injection of antibodies to α-actinin...)
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submitted by moloko270(29)

Myofibrils are composed of smaller structures called myofilaments. There are two main types of filaments: thick filaments and thin filaments; each has different compositions and locations. Thick filaments occur only in the A band of a myofibril. Thin filaments attach to a protein in the Z disc called alpha-actinin and occur across the entire length of the I band and partway into the A band.

https://opentextbc.ca/biology/chapter/19-4-muscle-contraction-and-locomotion/

meningitis  isn't letter C the intercalated disc where the gap junctions are?
... omerta made a comment on nbme22/block3/q#9 (Microelectrode injection of antibodies to α-actinin...)
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submitted by omerta(9)

I thought this image was helpful.

https://doctorlib.info/physiology/medical/49.html

... gh889 made a comment on nbme22/block3/q#9 (Microelectrode injection of antibodies to α-actinin...)
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submitted by gh889(32)

The area labeled C is the spot desmosomes between two myocytes and where actin filaments insert on the sarcolemma

LINK

... nwinkelmann made a comment on nbme22/block3/q#9 (Microelectrode injection of antibodies to α-actinin...)
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submitted by nwinkelmann(60)

This link has a labeled electron microscope image of cardiac myocytes like the question next to a cartoon image, so it's really helpful. There is also a good description. Scroll all the way down to the last figure.

https://www.researchgate.net/publication/318173841_Overview_of_the_Muscle_Cytoskeleton/figures?lo=1

... sunny made a comment on nbme22/block3/q#10 (A 50-year-old man comes to the physician for...)
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submitted by sunny(0)

WHY NOT YES,and then share the money with the patieny so he doesn't doubt your motives.

... usmleuser007 made a comment on nbme22/block3/q#11 (A 38-year-old man with Down syndrome is brought to...)
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submitted by usmleuser007(86)

In cases of child or adult abuse

1) if there is clear evidence such as if a child states that parents punish by hitting, child is showing fear of parent ---- call child protection right away ( don't need to wait and ask)

2) same thing goes for the adult but call the adult protection services

... angelaq11 made a comment on nbme22/block3/q#11 (A 38-year-old man with Down syndrome is brought to...)
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submitted by angelaq11(0)

I hate Qs like this. They make me feel all kinds of sadness.

... sup made a comment on nbme22/block3/q#12 (An 82-year-old woman has been bedridden since...)
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submitted by sup(1)

Why not PGI2 by way of ASA? Especially given other answer choices of proteins C + S: doesn't warfarin also suppress these?

imnotarobotbut  Protein C and S are ANTI-thrombotic, so although Warfarin does decrease them, they wouldn't decrease the patient's risk for thrombosis
epr94  the question ask "suppression" of which one will decrease risk of thrombosis if you suppress C and S which and anti-thrombotic you get thrombotic
... haliburton made a comment on nbme22/block3/q#12 (An 82-year-old woman has been bedridden since...)
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submitted by haliburton(74)

warfarin inhibits the synthesis of factors II, VII, IX, X, C, and S by blocking reduction of oxidized vitamin K. The enzyme Epoxide Reductase is inhibited by warfarin. The reduced (active) form of vit. K is a cofactor for gamma-glutamyl carboxylase.

link981  So factors II, VII, IX, and X are precursor proteins? GTFO
... bubbles made a comment on nbme22/block3/q#13 (A previously healthy 26-year-old woman comes to the...)
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submitted by bubbles(26)

For the peeps who got confused on this question bc of UWorld's weird question on HIV viral load:

acute HIV-1 infection: HIGH viral load, low Ab HIV-2 infection: LOW viral load, low Ab (bc standard HIV assays detect p24, which is not present on HIV-2)

Kinda annoyed I missed an easy immunology concept question :/

... ilikecheese made a comment on nbme22/block3/q#14 (A 57-year-old woman comes to the physician 2 weeks...)
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submitted by ilikecheese(7)

If you want to think of this simply, the ribs are connected posteriorly to the vertebral column. and the intercostal veins run between them, so they are the closest to the vertebral column.

... mcl made a comment on nbme22/block3/q#14 (A 57-year-old woman comes to the physician 2 weeks...)
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submitted by mcl(169)

Intercostal veins drain into the azygous/hemiazygous veins, which run right next to the vertebral column. Another useful diagram showing left and right intercostal veins.

... pitaziki made a comment on nbme22/block3/q#14 (A 57-year-old woman comes to the physician 2 weeks...)
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submitted by pitaziki(0)

Why is it that the intercostal vein provides the most direct pathway for metastatic breast cancer cells to spread to vertebral column? I thought it was internal thoracic (mammary) and I couldn’t find much searching online, besides wikipedia saying that internal thoracic vein drains the breast.

gainsgutsglory  Intercostal vein → Azygos → Batson vertebral plexus → infection of inner vertebral body
realmedicmd  The internal thoracic drains into the subclavian, intercostal drains into the azygos system which is a more direct path to the vertebral drainage.
... d_holles made a comment on nbme22/block3/q#14 (A 57-year-old woman comes to the physician 2 weeks...)
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submitted by d_holles(31)

Goljan mentioned this (not sure what lecture -- might have been the endo one).

... monoclonal made a comment on nbme22/block3/q#14 (A 57-year-old woman comes to the physician 2 weeks...)
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submitted by monoclonal(3)

http://i.imgur.com/3fZ2AaE.png

This image shows the multiple veins which drain breast tissue. easy visual. (to easy to miss it, but i did)

yb_26  this one is the best, thank you!
canyon_run  very nice!
... haliburton made a comment on nbme22/block3/q#15 (An 18-year-old man comes to the physician 10 days...)
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submitted by haliburton(74)

https://geekymedics.com/nerve-supply-to-the-upper-limb/

a nice review of myotome and dermatome / reflexes

... mcl made a comment on nbme22/block3/q#15 (An 18-year-old man comes to the physician 10 days...)
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submitted by mcl(169)

To expand on this, contraction of flexor digitorum profundus muscle results in flexion at the DIPs and PIPs. The tendon attaches at the tip of the finger, in contrast to flexor digitorum superficialis (attaches at the PIPs). Recall innervation of the forearm muscles is mostly from the median nerve, except for 1.5 muscles (ulnar half of flexor digitorum profundus and the flexor carpi ulnaris, both supplied by ulnar which makes it ez to remember yay).

But also if you got this wrong like me go read that link because it's a really nice review.

... zup made a comment on nbme22/block3/q#15 (An 18-year-old man comes to the physician 10 days...)
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submitted by zup(3)

Flexor Digitorum Profundus Action: Flexes distal phalanges at distal interphalangeal joints of medial four digits; assists with flexion of hand Innervation: Medial part: ulnar nerve (C8 and T1); Lateral part: anterior interosseous branch of median nerve (C8 and T1) https://rad.washington.edu/muscle-atlas/flexor-digitorum-profundus/

... hayayah made a comment on nbme22/block3/q#16 (A 27-year-old woman comes to the physician because...)
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submitted by hayayah(345)

Pregnancy + Hx of thrombosis --> think antiphospholipid syndrome

The PT and PTT are prolonged d/t interference from the antibodies to phospholipids. Thrombin time normal.

Had to find research articles about it so take it from here and don't waste your time...

monoloco  yeah, i’ve never heard of antiphospholipids increasing PT time ...
goldenwakosu  Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis)
johnthurtjr  I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies.
link981  No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it
yb_26  UWorld mentioned "prolong aPTT (and sometimes PT)" in APS
... usmleuser007 made a comment on nbme22/block3/q#17 (A 50-year-old man with chronic gastritis is...)
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submitted by usmleuser007(86)

1) EBV = Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, 1° CNS lymphoma (in immunocompromised patients)

2) HBV & HCV = Hepatocellular carcinoma

3)HHV-8 = Kaposi sarcoma

4) HPV= Cervical and penile/anal carcinoma (types 16, 18), head and neck cancer

5) H. pylori = Gastric adenocarcinoma and MALT lymphoma

6) HTLV-1 = Adult T-cell leukemia/lymphoma

7) Liver fluke (Clonorchis sinensis) = Cholangiocarcinoma

8) Schistosoma haematobium = Bladder cancer (squamous cell)

some0217710  Aren’t both H.pylori and EBV associated with gastric lymphoma?
... haliburton made a comment on nbme22/block3/q#17 (A 50-year-old man with chronic gastritis is...)
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submitted by haliburton(74)

FA 2017: H pylori is associated with gastric adenocarcinoma and MALT lymphoma

seagull  I might be mistaken but I also thought Epstein Bar Virus was also implicated in gastric lymphomas?
... link981 made a comment on nbme22/block3/q#17 (A 50-year-old man with chronic gastritis is...)
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submitted by link981(24)

Marginal zone lymphoma is caused by CHRONIC INFLAMMATION. H-Pylori can cause chronic inflammation in the stomach.

Epstein barr virus is associated with BURKITT lymphoma, the JAW lesion in Africa.

Got it wrong because I thought H-Pylori only caused gastric cancer.

... moloko270 made a comment on nbme22/block3/q#18 (An 85-year-old woman is diagnosed with a fracture of...)
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submitted by moloko270(29)

Morphine is metabolized in the liver to morphine-6-glucuronide and morphine-3-glucuronide, both of which are excreted by the kidneys. In the setting of renal failure, these metabolites can accumulate, resulting in a lowering of the seizure threshold. Morphine should therefore be used with caution with mild renal impairment and be avoided in the setting of renal failure.

source: https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/morphine-6-glucuronide

they gave a hint of increased creatinine level, plus older age can give a slowed down metabolism and CNS symptoms

... medstudied made a comment on nbme22/block3/q#18 (An 85-year-old woman is diagnosed with a fracture of...)
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submitted by medstudied(2)

can someone explain how morphine is degraded into active metabolites that accumulate? I couldn't find any sources that state this fact. Isn't it metabolized through the P450 system and excreted in urine?

staygoodpupper  Morphine mostly undergoes phase II metabolism and is then excreted renally. Some of the metabolites are metabolically active, and her creatinine was a little elevated, so renal clearance could have been impaired.
... k_tron_3000 made a comment on nbme22/block3/q#19 (A 42-year-old man comes to the physician because of...)
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submitted by k_tron_3000(8)

The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).

As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities

D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.

So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral).
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function.
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative?
link981  Great explanation guys
... niboonsh made a comment on nbme22/block3/q#20 (A 43-year-old man is brought to the emergency...)
... sweetmed made a comment on nbme22/block3/q#20 (A 43-year-old man is brought to the emergency...)
... wolvarien made a comment on nbme22/block3/q#20 (A 43-year-old man is brought to the emergency...)
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submitted by wolvarien(0)

I am trying to figure this out from the links provided. Can someone please explain the rational behind this question ?

p4p4y4  I believe it's that this muscle everts the foot + runs over the lateral malleolus .. But the phrasing on the question is odd
angelaq11  I didn't actually know this one. I just ruled out everything except the fibularis muscles, and then to be quite honest, I think I had never heard before of the tertius one, so...I chose brevis.
... seagull made a comment on nbme22/block3/q#21 (A screening test for cancer is developed and applied...)
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submitted by seagull(355)

This is a likelihood ratio. LR+= Sens/1-Specif

Any value greater than 10 (per first aid) indicated "usefulness of diagnostic test" which is comparable to PPV (ruling in a dz). Point "A" is the closest mark to where 10 should be on the Y axis.

brise  The question is asking what point would be the most likely to rule in cancer, and high specificity when positive rules in cancer. The highest specificity value is A, bc the the X axis shows (1-specificity)!
hello  brise is correct. Knowing the LR+ value = 10 does not help in this situation because estimating where "10" should fall on an axis is arbitrary. The way to approach this Q is to know that a high specificity is will mean that a positive result is very very likely to be a true positive. In theory, suppose that the specificity was 0.99. This is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculating 1-specificity = 1 - 0.99 = 0.1. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A."
... hello made a comment on nbme22/block3/q#21 (A screening test for cancer is developed and applied...)
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submitted by hello(51)

Knowing the LR+ value = 10 does not help to solve this Q because estimating where "10" should fall on an axis is arbitrary. Also, the data points are coordinates -- they have an X-value and a Y-value (X, Y).

The way to approach this Q is to know that a high specificity means that a positive result is very, very likely to be a true positive.

Suppose that the specificity is 0.99 -- this is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculate 1-specificity = 1 - 0.99 = 0.10. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A."

You don't even need to know a specific specificity value to solve this problem. All you need to do is understand that if the specificity is extremely high, you will need to find a datapoint that is closest to the origin -- at least for the value in the X-axis in the coordinate of the data point -- because the X-axis corresponds to a calculation of "1-specificity".

link981  Excellent explanation but a minor typo. 1-0.99 = 0.01 not 0.10 :)
... brise made a comment on nbme22/block3/q#21 (A screening test for cancer is developed and applied...)
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submitted by brise(17)

The question is asking what point would be the most likely to rule in cancer, and high specificity when positive rules in cancer. The highest specificity value is A, bc the the X axis shows (1-specificity)!

sbryant6  SPin and SNout. Specificity in, sensitivity out.
... adisdiadochokinetic made a comment on nbme22/block3/q#21 (A screening test for cancer is developed and applied...)
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submitted by adisdiadochokinetic(7)

How many people didn't see that it was 1-specificity and picked E like me :(

jfny21  Here
... alexb made a comment on nbme22/block3/q#21 (A screening test for cancer is developed and applied...)
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submitted by alexb(10)

The words "most effectively" confused me. I thought to myself "even if it has the highest specificity, it's not very effective if it's got super low sensitivity -- since it will miss a lot of the true +ve's (failing to rule in cancer for the ones that get missed)." That was a story I told myself about their use of the words "most effectively" lol.

... usmleuser007 made a comment on nbme22/block3/q#22 (A study is conducted to assess the prevalence of...)
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submitted by usmleuser007(86)

Just remember:

1) T-test (tea for two) = looks at the mean values of 2 groups

2) ANOVA (analysis of variance) ~ like t-test but = looks at mean values of 3 or more groups

3) Chi-square = looks at the (%) or proportions between 2 or more groups.

so, just look for how many groups being addressed and what values they are using (% or means)

... usmleuser007 made a comment on nbme22/block3/q#22 (A study is conducted to assess the prevalence of...)
... usmleuser007 made a comment on nbme22/block3/q#22 (A study is conducted to assess the prevalence of...)
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submitted by usmleuser007(86)

1) Analysis of variance is a procedure used for comparing sample means to see if there is sufficient evidence to infer that the means of the corresponding population distributions also differ.

2) Where t-test compare only two distributions, analysis of variance is able to compare many. • What does the one-way part mean? It is one dependent variable (always continuous) and exactly one independent variable (always categorical). A single independent variable can have many levels.

... mcl made a comment on nbme22/block3/q#22 (A study is conducted to assess the prevalence of...)
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submitted by mcl(169)

Despite a numeric value (blood pressure) being measured, patients would be designated either hypertensive or normotensive. To my understanding, the best test for comparing categorical variables across groups is a chi square test.

In contrast, a t-test is used to compare between the means of two groups (measured variable must be quantitative).

... medstudied made a comment on nbme22/block3/q#22 (A study is conducted to assess the prevalence of...)
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submitted by medstudied(2)

Why is the correct answer chi-square test? I get that it’s used for categorical variables but we’re comparing prevalence percentages. Is that considered categorical?

liverdietrying  You’re looking at two categorical variables, Caucasian vs. AA and HTN versus normotensive. So you’re still using Chi2 to analyze.
... d_holles made a comment on nbme22/block3/q#22 (A study is conducted to assess the prevalence of...)
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submitted by d_holles(31)

I was never taught what t-test vs Chi-squared was. Going off of the FA table didn't help. This video below explained the concept really well.

https://www.youtube.com/watch?v=Tda29m0SKYE

For the Q refer to @mc1's comment.

... bubbles made a comment on nbme22/block3/q#23 (A 45-year-old woman comes to the physician for a...)
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submitted by bubbles(26)

Can someone explain properly how we know that this trait follows Mendelian genetics and is autosomal recessive and furthermore how the parents were heterozygous?

I guessed a lot on this question and got lucky :(

niboonsh  Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected.
nwinkelmann  Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)?
impostersyndromel1000  we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend
... its_raining_jimbos made a comment on nbme22/block3/q#23 (A 45-year-old woman comes to the physician for a...)
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submitted by its_raining_jimbos(8)

Tamoxifen has to be metabolized via first pass metabolism to an active metabolite (endoxifen). The patient has decreased concentrations of the metabolized product indicating that the patient’s pair of cytochrome P450 alleles aren’t metabolizing tamoxifen correctly. The question is asking what the chances are the sister has the same genotype, which would be 25% --> 1/2 * 1/2 = 1/4

medschul  How do we know the parents are not homozygous
yotsubato  Chances are they are not unless they had or are incestuous
... g8427 made a comment on nbme22/block3/q#23 (A 45-year-old woman comes to the physician for a...)
 +0  upvote downvote
submitted by g8427(0)

If some one can help me understand bc im a bit confused. I understand the thought process and I realized that this was an AR disease and I also got the 1/4 affected, 1/2 carrier and 1/4 unaffected. But I chose 0% bc I figured if it was an AR disease the 1 child already diseased was homozygous affected (1/4 affected). Which lead me to think that the other sister was either a carrier or not affected at all. Am I just over thinking this or am I not fully understanding whats going on?

rush  you have to think about each child individually, doesn't matter what the siblings have. The question states what are the odds of the child getting the disease. So regardless of the other siblings it still is Mom (1/2) dad (1/2) which makes it 1/4 AR
... naughtyegg made a comment on nbme22/block3/q#24 (An 84-year-old woman comes to the physician because...)
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submitted by naughtyegg(1)

Downregulating E-cadherin is the first step cancer takes toward metastasis because low E-cadherin helps invade the basement membrane -> eventually leads to spread of cancer elsewhere. Laminin is also involved but according to pathoma, cancer will actually attach to laminin in order to destroy the basement membrane. Idk if receptor up/downregulation happens, that might be a stretch.

nwinkelmann  It makes sense that a tumor cell would increase their laminin, as opposed to decreasing, if attaching to laminin is what allows the cells to destroy the basement membrane. The more laminin, the more destruction possible.
... rajkamal17 made a comment on nbme22/block3/q#24 (An 84-year-old woman comes to the physician because...)
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submitted by rajkamal17(1)

Pretty sure I’m missing something basic here. This was SCC invading basement membrane facilitated by what? The answer is downregulation of E-cadherin but I thought that’s for metastastses (FA 18 says so too.) I ticked decreased laminin receptors (incorrect) coz laminin was found in basement membrane. At least that was my reasoning. Any help appreciated. Thanks!

naughtyegg  Downregulating E-cadherin is the first step cancer takes toward metastasis because low E-cadherin helps invade the basement membrane -> eventually leads to spread of cancer elsewhere. Laminin is also involved but according to pathoma, cancer will actually attach to laminin in order to destroy the basement membrane. Idk if receptor up/downregulation happens, that might be a stretch.
nuket0wn  per medbullets, there are increased laminin and integrin receptors. Also upregulated MMPs (matrix metallo-proteinases) to breakdown the basement membrane.
nwinkelmann  It makes sense that a tumor cell would increase their laminin, as opposed to decreasing, if attaching to laminin is what allows the cells to destroy the basement membrane. The more laminin, the more destruction possible.
... imnotarobotbut made a comment on nbme22/block3/q#24 (An 84-year-old woman comes to the physician because...)
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submitted by imnotarobotbut(22)

UWorld Question ID 1084 has a great explanation of this

... d_holles made a comment on nbme22/block3/q#24 (An 84-year-old woman comes to the physician because...)
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submitted by d_holles(31)

This is a Pathoma Ch3 Q (p28).

Tumor invasion and spread

  1. Epithelial tumor cells are attached to one another by E-cadherin (cellular adhesion molecule). Downregulation of E-cadherin → dissociation of attached cells.
  2. Cells attach to laminin and destroy basement membrane via collagenase.
  3. Cells attach to fibronectin in the ECM and spread locally.
  4. Entrance into vascular or lymphatic spaces allows for metastasis.

https://imgur.com/a/FD16HiB

... princesskrafna made a comment on nbme22/block3/q#24 (An 84-year-old woman comes to the physician because...)
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submitted by princesskrafna(0)

According to Uworld.... 1.Tumor cells detach from the surrounding cells when adhesion molecule E-cadherin is low 2.Tumor cells adhere to basement membrane by increasing lamin 3.Tumor cells invade basement membrane by increasing proteolytic enzymes like metalloprotease

... tissue creep made a comment on nbme22/block3/q#25 (A 3-month-old girl is brought to the physician by...)
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submitted by tissue creep(22)

Lifting head while prone: 1 month Social smile: 2 months Cooing: 2 months

... _pusheen_ made a comment on nbme22/block3/q#26 (A study is conducted to assess the extent of cardiac...)
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submitted by _pusheen_(1)

No change in type 1 error and decrease in type 2 error? Can someone please explain why?

bhangradoc  The P-value is basically the type 1 error, and they keep the p-value the same (at <.05) in both versions of the experiments. By increasing number of patients in the group, they increase power of the study, which reduces type II error.
... bhangradoc made a comment on nbme22/block3/q#26 (A study is conducted to assess the extent of cardiac...)
 +8  upvote downvote
submitted by bhangradoc(9)

The P-value is basically type 1 error, and they keep the p-value the same (at <.05) in both versions of the experiments. By increasing number of patients in the group, they increase power of the study, which reduces type II error.

jfny21  Thank you
... sam1 made a comment on nbme22/block3/q#26 (A study is conducted to assess the extent of cardiac...)
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submitted by sam1(0)

If anyone needs a refresher on these statistical concepts, Khan has a brilliant video:

https://www.khanacademy.org/math/ap-statistics/tests-significance-ap/error-probabilities-power/v/introduction-to-type-i-and-type-ii-errors

... presidentdrmonstermd made a comment on nbme22/block3/q#27 (A 45-year-old man with poorly controlled type 2...)
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submitted by presidentdrmonstermd(5)

Question said "Nonhemolytic, Catalase -ve, Gram +ve cocci"

Enterococcus fits description

Listeria: ROD

Staph. aureus: Cat +ve

Staph. epidermidis: Cat +ve

Strep. pneumo: alpha/partial hemolysis

... mcl made a comment on nbme22/block3/q#28 (A 12-year-old girl who recently immigrated to the...)
 +1  upvote downvote
submitted by mcl(169)

CDC recommended treatment of schistosoma mansoni is praziquantel.

... skraniotis made a comment on nbme22/block3/q#29 (A 45-year-old man with end-stage renal failure is...)
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submitted by skraniotis(5)

Undialyzed renal failure leads to metabolic acidosis, and as a result bicarb gets depleted as it tries to buffer the accumulation of organic acids.

bubbles  Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca).
nwinkelmann  From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well. https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212
hyperfukus  why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd
hyperfukus  does uremia potentially have to do with this?
medulla  ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic
angelaq11  @medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection.
... medulla made a comment on nbme22/block3/q#29 (A 45-year-old man with end-stage renal failure is...)
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submitted by medulla(1)

Renal Failure: MAD HUNGER Met Acidosis Dyslipidemia Hyperkalemia Uremia (inc BUN etc) Na/water retention (HF, pulmonary edema, HTN) Growth retardation and developmental delay Erythropoietin failure (anemia) Renal osteodystrophy

... meningitis made a comment on nbme22/block3/q#30 (Which of the following is required for the synthesis...)
 -1  upvote downvote
submitted by meningitis(121)

Process of elimination on this one.

  • I eliminated Carbomyl phosphate, Arginine due to urea cycle.
  • I eliminated ATP because ATP alone wouldn't change F6P into glucosamine
  • NAG I got lucky and I eliminated it due to its use in ECM and collagen so I didn't think it was relevant and I kind of remembered it being in urea cycle.
dr.xx  you mean, pure luck? :)
impostersyndromel1000  lol pretty sound logic here mate
nor16  same here, Glutamine is a NH3 (-amin) donor, so guessing made sense
... mcl made a comment on nbme22/block3/q#30 (Which of the following is required for the synthesis...)
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submitted by mcl(169)

The question is referring to the hexosamine pathway.

Carbamoyl phosphate and arginine are involved in the urea cycle. So is n-acetylglutamate (NAG) (regulates production of carbamoyl phosphate).

... seagull made a comment on nbme22/block3/q#30 (Which of the following is required for the synthesis...)
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submitted by seagull(355)

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not
nlkrueger  i did not lol
ht3  you're definitely not alone lol
yotsubato  no idea
yotsubato  And its not in FA, so fuck it IMO
niboonsh  i didnt
epr94  did not
link981  I guessed it because the names sounded similar :D
d_holles  i did not
yb_26  I also guessed because both words start with "glu")))
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
jaxx  Not a clue. This was so random.
wolvarien  I did not
ls3076  no way
hyperfukus  no clue
... redvelvet made a comment on nbme22/block3/q#30 (Which of the following is required for the synthesis...)
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submitted by redvelvet(4)

If you want to take a look for the clinical importance of the hexosamine pathway & products: https://www.sciencedirect.com/topics/neuroscience/hexosamines

... yotsubato made a comment on nbme22/block3/q#31 (A 35-year-old man is admitted to the hospital...)
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submitted by yotsubato(214)

What do you use to treat Hepatic Encephalopathy? Lactulose. What does that do, it acidifies NH3 in the GI tract into NH4+ and promotes loss of the nitrogenous products that cause encephalopathy. This is how you remember this process.

... dr.xx made a comment on nbme22/block3/q#31 (A 35-year-old man is admitted to the hospital...)
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submitted by dr.xx(35)

The most important waste product is ammonia (NH3). This small molecule crosses the blood–brain barrier and is absorbed and metabolised by the astrocytes, a population of cells in the brain that constitutes 30% of the cerebral cortex. Astrocytes use ammonia when synthesising glutamine from glutamate. The increased levels of glutamine lead to an increase in osmotic pressure in the astrocytes, which become swollen. There is increased activity of the inhibitory γ-aminobutyric acid (GABA) system, and the energy supply to other brain cells is decreased. This can be thought of as an example of brain edema of the "cytotoxic" type.

https://en.wikipedia.org/wiki/Hepatic_encephalopathy#Causes

... d_holles made a comment on nbme22/block3/q#31 (A 35-year-old man is admitted to the hospital...)
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submitted by d_holles(31)

Can portal HTN contribute to hepatic encephalopathy?

... mcl made a comment on nbme22/block3/q#32 (A 25-year-old woman comes to the physician because...)
 +1  upvote downvote
submitted by mcl(169)

Patient likely has PCOS. PCOS is associated with elevated levels of LH from the pituitary, which stimulates ovaries to produce increased amounts of sex steroids (including androgens --> hirsutisim). Androstenedione is converted to estrone in adipocytes, which results in still further increased release of LH. Obesity and insulin resistance is associated with PCOS.

... bubbles made a comment on nbme22/block3/q#33 (A 22-year-old man comes to the physician because of...)
 +1  upvote downvote
submitted by bubbles(26)

Has anybody found a good explanation for this histology? I genuinely have no idea what I'm looking at.

meningitis  This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around)
... aesalmon made a comment on nbme22/block3/q#33 (A 22-year-old man comes to the physician because of...)
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submitted by aesalmon(33)

Leydig cell hyperplasia, should also see fibrosis and hylinazation of the tubules but i'm not seeing it... ¯_(ツ)_/¯

meningitis  I think its there.. I thought it was the lighter red/pink material (hyaline material) And I thought the white streaks were the fibrosis like "streaked ovaries"in Turners.
... bubbles made a comment on nbme22/block3/q#34 (The risk for hemorrhagic stroke from drug X is...)
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submitted by bubbles(26)

So...case-control studies compare a group of people with the disease and a group of people without the disease. I'm not sure I understand why you can call people randomly and call that a control group. What if among those called randomly, some of them have also had hemorrhagic strokes?

impostersyndromel1000  this is one of those Qs where you just dont over think it and focus on your first point, that they are comparing a group with the disease vs (potentially) one without it. Thats what i took from it at least (sorry fi this is too late)
... sunny made a comment on nbme22/block3/q#34 (The risk for hemorrhagic stroke from drug X is...)
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submitted by sunny(0)

why is this not a cross sectional survey? ... since we are asking at a particular time

drdoom  As Aristotle once quipped, “A ‘single-point in time’ doth not a cross-sectional study make.” The design of a cross-sectional study would not define “ahead of time” two cohorts (two groups); said another way, a cross-sectional design would not “split people into two groups.” In the design of a cross-sectional study there is only “one group”, and then you ask all members of that group some question (“Do you have asthma?”). At the end of a cross-sectional study, the authors will be able to make a statement like this: “We called 10,000 phone numbers with area code 415 at random and asked ‘Do you take Drug X?’ 500 responded ‘I don’t know’, 633 responded ‘Yes’, and 8,867 responded ’No’.”
... bobson150 made a comment on nbme22/block3/q#35 (A 4-year-old boy is brought to the physician by his...)
 +1  upvote downvote
submitted by bobson150(2)

Is this saying there is vesicoureteral reflux? I could have sworm this same image was on form 20 or 21 and the answer was Wilms tumor

hello  Yes, it was. I think in both vignettes, the picture was basically irrelevant. Or another possible clue -- but definitely not needed to answer the Q.
presidentdrmonstermd  My school uses old "retired" NBME questions for exams and I've also seen this exact same picture multiple times...w/ different scenarios I think. I tried remembering what the questions were but I guess it's mostly irrelevant.
hyperfukus  SAME
hyperfukus  I also put wilm's tumor bc it felt really familiar wtf
... keycompany made a comment on nbme22/block3/q#35 (A 4-year-old boy is brought to the physician by his...)
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submitted by keycompany(105)

Urinary tract infections are the most common acquired cause of Vesicouteric Reflux (VR) in children. VR can lead to Reflux Nephropathy, which is characterized by chronic tubulointerstitial inflammation with fibrosis and scarring, leading to renal failure.

lancestephenson  Can someone please explain what's going on in this picture? This is the SAME PICTURE used in NBME 20 and 21 with one of them being a 66 y/o with urothelial cell carcinoma and the other being tubular atrophy. I just don't know anymore
spacepogie  I'd be happy to send them a gift card to purchase more stock images of kidneys for use in future exams...
... gainsgutsglory made a comment on nbme22/block3/q#35 (A 4-year-old boy is brought to the physician by his...)
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submitted by gainsgutsglory(4)

Why is this Intersitial Inflammation? I understand this is a VUR causing hydronephrosis.

skinnynomore  this kid has chronic pyelonephritis due to recurrent UTIs (VUR/hydronephrosis is a risk factor). And -itis = inflammation. That was my take on it.
... nwinkelmann made a comment on nbme22/block3/q#35 (A 4-year-old boy is brought to the physician by his...)
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submitted by nwinkelmann(60)

I HATED this picture, just like everyone else, lol, so I did some more digging. Everyone below is correct, that the presentation is suggesting an infectious process. UTIs can cause acute pyelonephritis, and if chronic, progresses to chronic. Pyelonephritis is a tubulointerstitial disease. I found this information regarding it, and in the last part, it describes the gross pathology of chronic pyelonephritis. From my interpretation, it sounds like what the picture is showing, but I wasn't able to find a better/just as good one online yet, so I don't know for sure.

Acute Tubulointerstitial Nephritis: Acute inflammation of tubules and interstitium can cause ARF, and if the inflammatory process persists this can evolve into chronic tubulointerstitial nephritis and chronic interstitial fibrosis and tubular atrophy with risk of progression to end-stage kidney disease. Two major categories of acute tubulointerstitial nephritis are acute pyelonephritis and acute hypersensitivity tubulointerstitial nephritis.

Acute pyelonephritis: Caused by bacterial infection most commonly E. coli infection. Hypersensitivity tubulointerstitial nephritis: Caused by an allergic response, for example, to a drug or other substances that are ingested, such as herbal remedies.

By far the most common route of infection in acute pyelonephritis is an ascending infection in the urinary tract, for example, derived from a bacterial bladder infection. Acute pyelonephritis = extensive influx of PMNs within the interstitium, tubules (tubulitis), and lumens of tubules (WBC casts) (http://bit.ly/2JiPyBD).

With persistence or recurrence of acute pyelonephritis, the disease process evolves into chronic pyelonephritis, which usually is accompanied by marked erosion of the papillary tip resulting in dilation of the adjacent calyx (caliectasis).

The most characteristic pathologic features of chronic pyelonephritis are the gross changes in the kidney with broad-based scars in the parenchyma overlying areas of cortical and medullary atrophy with adjacent caliectasis. Also, the presentation suggests hydronephrosis, and from my research, hydronephrosis, when chronic/sever, can contribute to the marked loss of cortex and scars/fibrosis of the medulla (https://webpath.med.utah.edu/RENAHTML/RENAL007.html) and caliectasis (which I think is present on this picture). This is the closest picture with description I could find that matches the stem presentation (i.e. hydroureter and hydronephrosis, suggesting vesicoureteral reflux leading to infection from "a long standing obstruction (probably congenital)" so likely from a child) https://webpath.med.utah.edu/RENAHTML/RENAL008.html.

Also, to mention on the other comments expressing frustration that the same picture was used for tumors and tubular atrophy, from what I read, that gross pathology, is the general appearance of hydroureter due to obstructive uropathy (i.e. tubular atrophy, fibrosis/scarring, caliectasis/calyx dilation, and thin cortical rim due to atrophy. Pathologyonline.com says that the caliectasis is exaggerated in less severe cases/partial obstruction since GFR is not suppressed https://www.pathologyoutlines.com/topic/kidneyobstructive.html).

Hope this helps everyone! It sure helped me, but took WAY too long to understand, lol.

nor16  nice job, but i dont think you need all this for these questions
... usmleuser007 made a comment on nbme22/block3/q#36 (A 62-year-old man comes to the physician's office...)
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submitted by usmleuser007(86)

The process of informed consent occurs when communication between a patient and physician results in the patient’s authorization or agreement to undergo a specific medical intervention. In seeking a patient’s informed consent (or the consent of the patient’s surrogate if the patient lacks decision-making capacity or declines to participate in making decisions), physicians should:

(a) Assess the patient’s ability to understand relevant medical information and the implications of treatment alternatives and to make an independent, voluntary decision.

(b) Present relevant information accurately and sensitively, in keeping with the patient’s preferences for receiving medical information. The physician should include information about:

The diagnosis (when known) The nature and purpose of recommended interventions The burdens, risks, and expected benefits of all options, including forgoing treatment (c) Document the informed consent conversation and the patient’s (or surrogate’s) decision in the medical record in some manner. When the patient/surrogate has provided specific written consent, the consent form should be included in the record.

In emergencies, when a decision must be made urgently, the patient is not able to participate in decision making, and the patient’s surrogate is not available, physicians may initiate treatment without prior informed consent. In such situations, the physician should inform the patient/surrogate at the earliest opportunity and obtain consent for ongoing treatment in keeping with these guidelines.

AMA Principles of Medical Ethics: I, II, V, VIII

... nwinkelmann made a comment on nbme22/block3/q#36 (A 62-year-old man comes to the physician's office...)
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submitted by nwinkelmann(60)

FA 2019 page 264: A process (not just a document/signature) that requires: Disclosure: discussion of pertinent information (using medical interpreter, if needed), Understanding: ability to comprehend, Capacity: ability to reason a nd make one's, own decisions (distinc t from competence, a legal determination), Voluntariness: freedom from coercion and manipulation.

Patients must have an intelligent understanding of their diagnosis and the risks/benefits of proposed treatment and alternative options, including no treatment.

... mcl made a comment on nbme22/block3/q#37 (A 35-year-old man with bronchial asthma starts...)
 +0  upvote downvote
submitted by mcl(169)

Beta-2 receptors are coupled to Gs proteins, which activate adenylyl cyclase and increase cAMP. Cyclic AMP then increases activity of protein kinase A, which phosphorylates myosin light chain kinase, ultimately resulting in smooth muscle relaxation. Albuterol, a B2 agonist, is therefore useful in treating bronchospasm.

impostersyndromel1000  are you able to clarify that phosphorylated myosin light chain kinase from cAMP/PKA and dephosphorylated myosin light chain from cGMP both cause smooth muscle relaxation? saw this on another Q with the nitrates causing headache so now im confused
... welpdedelp made a comment on nbme22/block3/q#38 (A 73-year-old man comes to the physician with his...)
 -4  upvote downvote
submitted by welpdedelp(64)

Increased intracranial pressure that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia. Thus, high CO2 induces cushing triad and if you give PP then it will reduced CO2, and then down regulate the sympathetic vasoconstriction. Originally the brain had so much CO2 that it spazzed out and tried to increase the BP in order to push more oxygenated blood to the brain.

https://pbs.twimg.com/media/CK3J5kZUsAAqSf-.jpg:large

lispectedwumbologist  "Bradycardia" 84 bpm lol
lispectedwumbologist  The hypertension in obstructive sleep apnea is due to increased sympathetic tone not increased intracranial pressure lmao
meningitis  @lispectedwumbologist : Be mature enough to correct him/her and move on, not laugh at him/her.
... noselex made a comment on nbme22/block3/q#38 (A 73-year-old man comes to the physician with his...)
 +1  upvote downvote
submitted by noselex(4)

I understand sleep apnea would cause hypoxia and increase in SNS activity. So treatment would reduce BP and Heart Rate. I was stuck between the two options. Why was the answer blood pressure and not HR? I googled around a bit and found studies that show drop in both HR and BP. I guess BP drops more? Can someone please explain.

madeforupvoting2  CPAP increases intrapleural pressure as the elevated airway pressure is transmitted to other things in the cavity (lung pushes on pleural space/cavity which can then push on other structures). This can lead to compression of veins, including the vena cava -> decreased venous return -> decreased bp (from decreased preload). This is similar to what happens during valsalva (exertion phases) though the positive pressure is provided by a machine pump instead of abdominal muscles/diaphragm. I think heart rate likely increases instead of decrease as a compensatory response. Here’s one site that explains it well (the “free” content is enough and probably already exceeds the depth one might need to know) https://thoracickey.com/extrapulmonary-effects-of-mechanical-ventilation/
apolla24  I guess since changes in HR are such a transient phenomenon and you only have sustained increase in HR when exercising or like acutely experiencing some medical emergency vs BP that can be elevated for long periods of times with no effects. Therefore an improvement in BP is more important. That’s my take.
... madeforupvoting2 made a comment on nbme22/block3/q#38 (A 73-year-old man comes to the physician with his...)
 +2  upvote downvote
submitted by madeforupvoting2(6)

CPAP increases intrapleural pressure as the elevated airway pressure is transmitted to other things in the cavity (lung pushes on pleural space/cavity which can then push on other structures). This can lead to compression of veins, including the vena cava -> decreased venous return -> decreased bp (from decreased preload). This is similar to what happens during valsalva (exertion phases) though the positive pressure is provided by a machine pump instead of abdominal muscles/diaphragm. I think heart rate likely increases instead of decrease as a compensatory response.

Here’s one site that explains it well (the “free” content is enough and probably already exceeds the depth one might need to know) https://thoracickey.com/extrapulmonary-effects-of-mechanical-ventilation/

... meningitis made a comment on nbme22/block3/q#38 (A 73-year-old man comes to the physician with his...)
 +3  upvote downvote
submitted by meningitis(121)

Although it’s about PPV, this researching helped me understand basic phys, I hope this helps everyone in some way.

Takeaway: During PPV, venous return decreases, cardiac output decreases, and heart pressures decrease in the right side of the heart.

Why does PPV decrease venous return?

  • intrathoracic pressure compresses heart, causing blood not to return

Causes for decreased left ventricular output during ventilation:

  • Shifting of intraventricular septum to Left due to increased RV volume
  • Decreased venous return
  • Changes in hearts ability to contract due to positive pressure
  • lack of O2 to heart

Normal compensatory mechanisms for maintaining CO and BP during PPV?

  • increased HR to compensate for decreased SV
  • increased SVR to maintain BP

Other Physiologic responses:

  • Decreased cerebral perfusion pressure (body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels)
  • Decreased renal perfusion (Increased ADH, RAAS, and Patient has renal problems so increased creatinine and uric acid)
  • Possible malnutrition (increased glucose via gluconeogenesis etc.)
meningitis  sorry about the formatting, they were supposed to be bullets not italic.
drdoom  looks good to me! ;) instead of asterisks try using the plus sign for unordered lists; the system gets confused sometimes because the asterisk is also for italics 😊
meningitis  Yeah, I noticed :s Oh, I didnt know the + sign did that! Very much appreciated, I will try that next time.
... marbledoc made a comment on nbme22/block3/q#39 (A 52-year-old man with stable angina pectoris begins...)
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submitted by marbledoc(0)

What is this medication being described here? Can someone chime in.

thatyummyslice  Nitrates i believe! NO --> increased cGMP in vessel smooth muscle --> myosin light chain dephosphorylate --> vascular smooth muscle RELAX --> Dilate (primarily in venous) AKA more venous capacitance --> LOWER preload and workload for heart.
marbledoc  Thanks! Thought it was nitrates too from the Q stem. But had no clue it was notorious for headaches (only thought of hypotension, dizziness, etc) so doubted it all together. But you’re absolutely right apparently it’s the most common side effect!
dr.xx  Previously, Ferid Murad et al. described that organic nitrates, such as nitroglycerine, induce vasodilation by release of nitric oxide, activating soluble guanylyl cyclase and subsequent cyclic guanosine monophosphate formation.7 These discoveries rendered Robert Furchgott, Louis Ignarro, and Ferid Murad the Nobel Prize in Physiology or Medicine in 1998. https://anesthesiology.pubs.asahq.org/article.aspx?articleid=2085806
... nwinkelmann made a comment on nbme22/block3/q#39 (A 52-year-old man with stable angina pectoris begins...)
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submitted by nwinkelmann(60)

I found this when trying to understand why increased NO caused headaches: Nitrates/nitrites are a very common headache and migraine food triggers (WebMD) and raise nitric oxide levels. High levels of nitric oxide are associated with migraine (Study). Headaches and migraines are also very common in medications that boost nitric oxide, such a viagra (study), but it is unclear why this happens. The original hypothesis was that nitric oxide increases blood vessel size and triggers a migraine, but the viagra study and others disproved this. Newer studies on nitric oxide shows that it increases the peptide (CGRP) that is considered responsible for triggering migraines (Study) after increases in inflammation. Because nitric oxide is associated neurogenic inflammation diseases, it's likely that headaches and migraines from nitric oxide are a warning sign of this inflammation (Study).

The research is basically stating that nitrates raise nitric oxide levels and high nitric oxide levels increase inflammation and headaches and migraines. However, the exact reason why this happens is unknown.

https://www.quora.com/Why-do-nitrates-cause-headaches

... bubbles made a comment on nbme22/block3/q#40 (A 49-year-old man has had the gradual onset of...)
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submitted by bubbles(26)

Take a look at that massive platelet count -- over a million per mm3! That should point you towards a myeloproliferative disorder of some sort since this fella isn't bleeding out as far as we can tell from the blood panel (which would put reactive thrombocytosis on the ddx).

Now let's look at those erythrocytes. Normal -- so it's not polycythemia vera, and considering the lack of leukocytosis, probably not CML or myeloid metaplasia.

So our answer must be essential thrombocythemia!

... haliburton made a comment on nbme22/block3/q#40 (A 49-year-old man has had the gradual onset of...)
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submitted by haliburton(74)

FA 2017: Characterized by massive proliferation of megakaryocytes and platelets. Symptoms include bleeding and thrombosis. Blood smear shows markedly increased number of platelets, which may be large or otherwise abnormally formed. Erythromelalgia may occur.

... link981 made a comment on nbme22/block3/q#40 (A 49-year-old man has had the gradual onset of...)
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submitted by link981(24)

Per First Aid 2018 (pg 421) & Merck Manual

a) CML is not the answer because in CML you have HIGH WBCs & Platelets. In the stem there is only high platelets. b) Is the answer because in Essential Thrombocythemia we have normal WBCs and RBCs, just high platelets. c) Myeloid metaplasia refers to well a metaplasia in myeloid cells which are basophils, eosinophils, etc. d) In Polycythemia Vera we have HIGH RBCs, WBCs, and Platelets. e) Reactive thrombocytosis- is a elevated platelet count that occurs secondary to another disorder like:

-Chronic inflammatory disorders (eg, rheumatoid arthritis, inflammatory bowel disease, tuberculosis, sarcoidosis, granulomatosis with polyangiitis) -Acute infection

-Hemorrhage

-Iron deficiency

-Hemolysis

-Cancer

-Splenectomy or hyposplenism

impostersyndromel1000  perfect response right here
... joha961 made a comment on nbme22/block3/q#41 (A 56-year-old man develops brief episodes of...)
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submitted by joha961(13)

Maintenance dose = (Css * CL * t) / F

... where t is elapsed time between doses (not relevant here since it’s continuous infusion) and F is bioavailability (which is 100% or 1.0 here because it’s given IV).

​Contrast with loading dose:

(Css * Vd) / F

... where Vd is volume of distribution.

yotsubato  So do we just have to memorize this...
gh889  yep
... bubbles made a comment on nbme22/block3/q#42 (A 62-year-old man comes to the physician for a...)
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submitted by bubbles(26)

Chronic renal insufficiency:

1) poor phosphate clearance --> high serum inorganic phosphorous

2) high serum phosphate --> complexes with divalent cation Ca --> Ca falls

3) Ca falls --> triggers PTH axis

4) kidney failure --> decreased activity of 1-hydroxylase at the kidney --> less calcitriol

... sne made a comment on nbme22/block3/q#42 (A 62-year-old man comes to the physician for a...)
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submitted by sne(10)

Since she has celiac spruce --> fat vitamin malabsorption, thus Vit. D is decreased Low vit. D = low calcitriol, low absorption of phosphate from intestine, and low absorption of Ca2+ causing an increase PTH

... biliarytree220 made a comment on nbme22/block3/q#43 (A 53-year-old woman shows evidence of adrenal...)
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submitted by biliarytree220(5)

Primary renal insufficiency; chronic cause; Addison disease (FA 332)

... seagull made a comment on nbme22/block3/q#43 (A 53-year-old woman shows evidence of adrenal...)
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submitted by seagull(355)

THis question is just critical thinking. The adrenals are bilaterally and symmetrically small. All other answer choices are not likely to be even bilaterally. Cancer won't equally spread in perfect symmetry nor infectious causes while maintaining the adrenal architecture.

slim23shady  Will TB be the answer if they'd mentioned the patient from developing world?
... mcl made a comment on nbme22/block3/q#44 (A 35-year-old man comes to the physician because of...)
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submitted by mcl(169)

Scabies likes to burrow in the areas between the fingers and toes (FA 2019 161) and causes itching. Could also potentially be lice (groin involvement), but treatment for either overlaps -- gotta use permethrin.

kchakhabar  If only one person is there to see the doctor, why would the doctor prescribe medicine even for his family members who are not there?
mcl  Unfortunately, both of these are pretty contagious conditions. FA mentions that scabies spreads via skin to skin contact, and goes on to mention that you're supposed to treat close contacts. I think in this scenario it's ok to give permethrin to the family members who are not present but affected (it's also non-prescription in some cases, I believe.) Slightly related note, similar to why you would treat the sexual partner of someone with chlamydia/gonorrhea, or close contacts of someone with n. meningitides infection.
... d_holles made a comment on nbme22/block3/q#44 (A 35-year-old man comes to the physician because of...)
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submitted by d_holles(31)

Damn I feel like NBME fucking loves scabies or some shit.

... usmleuser007 made a comment on nbme22/block3/q#45 (A 28-year-old man who is seropositive for HIV has...)
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submitted by usmleuser007(86)

my list of spindle type cells and conditions:

  • a. NF-1
  • b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies
  • c. Leiomyoma (uterus & esophagus)
  • d. Mesothelioma (cytokeratin positive)
  • e. Anaplastic Thyroid cancer (biphasic & along with giant cells)
  • f. Medullary Thyroid cancer (can also have polygonal cells)
  • g. Primary cardiac angiosarcoma (malignant vascular spindle cells)
  • h. Osteosarcoma (bone cancer) (pleomorphic cells)
  • i. Meningioma
  • j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells
drdoom  @usmleuser007 to make lists display correctly, try using the plus sign (+) for each "bullet point"; that should work
mcl  I love this and I love you
usmleuser007  LOL thanks, had to ddo a lot of digging since "spindle cells" are commonly tested
... haliburton made a comment on nbme22/block3/q#45 (A 28-year-old man who is seropositive for HIV has...)
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submitted by haliburton(74)

kaposi sarcoma. HHV8. violaceous (purple) lesions. advanced HIV CD4 < 200 (WHO).

yotsubato  Yeah thats the easy part. But the histology is whats hard
... mcl made a comment on nbme22/block3/q#45 (A 28-year-old man who is seropositive for HIV has...)
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submitted by mcl(169)

To expand on this, pathologyoutlines describes the histology of kapowsi sarcoma as "spindle cells forming slits with extravasated red blood cells"

mcl  lul i don't know why i spell kaposi like that, my b
bubbles  This site is super helpful. Thanks for sharing :)
mcl  yesssssss ofc <3 I love path outlines
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells
... enbeemee made a comment on nbme22/block3/q#45 (A 28-year-old man who is seropositive for HIV has...)
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submitted by enbeemee(3)

sketchy says that kaposi's has infiltrating lymphocytes, so why would large aggregates of atypical lymphocytes be incorrect?

... imnotarobotbut made a comment on nbme22/block3/q#46 (A 54-year-old woman with hypertension and bilateral...)
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submitted by imnotarobotbut(22)

Prostaglandins vasodilate the afferent arteriole and increase GFR. NSAIDs inhibit prostaglandin synthesis (FA 2019 pg 577)

... mcl made a comment on nbme22/block3/q#47 (A 10-year-old boy receives a renal transplant from a...)
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submitted by mcl(169)

page 119 FA Patient is presenting months after the transplant, which means it can't be hyperacute unless he stopped taking his immunosuppressants. Acute/chronic/GVH disease are mediated by T cells for the most part (I think), so this would mean lymphocytic infiltrates.

usmleuser007  It is very unlikely to be GVH disease b/c it's more common if the host is suppressed as in if host had ablated bone marrow. (FA states that it's more common with bone marrow & liver transplants)
usmleuser007  any one care to explain why fibrous scars with plasma cells not a good option?...
... niboonsh made a comment on nbme22/block3/q#47 (A 10-year-old boy receives a renal transplant from a...)
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submitted by niboonsh(57)

This is a case of acute transplant rejection. weeks to months after the transplant, recipient cd8 and/or cd4 t cells are activated against the donor (a type 4 HSR) and the donor starts making antibodies against the transplant. This presents as a vasculitis with dense interstitial lymphocytic infiltrates. (FA2018 pg 119)

ls3076  Actually was confused about this due to a UW explanation. UW said acute txp rejection has two types - humoral and humoral and cellular. Humoral has Neutrophilic infiltrate + necrotizing vasculitis while cellular has lymphocytosis. Can anyone simplify/explain this please?
... nwinkelmann made a comment on nbme22/block3/q#47 (A 10-year-old boy receives a renal transplant from a...)
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submitted by nwinkelmann(60)

Hyperacute = minutes to hours, host preformed Ab against graft endothelial cell Ag = compliment activation, endothelial damage, inflammation (within the tissue, NOT interstitium), clotting cascade, ischemic necrosis and thrombosis. https://tpis.upmc.com/tpislibrary/kidney/KHAcuRej.html

Acute = weeks to months = graft Ag activates host CD4 and CD8 T cells leading to parenchymal cell damage, interstitial lymphocytic infiltration, and endotheliaitis. https://tpis.upmc.com/tpislibrary/kidney/KARejMod.html

Chronic = months to years, chronic DTH (type IV hypersensitivity) reaction in vessel wall leading to intimal smooth muscle cell proliferation and vessle occlusion, with biopsy showing narrowed vascular lumen and extensive smooth muscle.

GVHD = graft cells (most typically bone marrow transplants) recognize host cells as self/foreign and lead to destruction of host tissue leading to rash, jaundice, diarrhea, and GI hemorrhage (this occurs because most bone marrow transplant patients have undergone full radiation which attacks the rapidly providing cells most (i.e. skin, GI mucosa, hair, hepatocytes) so graft destruction of host cells in those areas leads to symptoms).

https://tpis.upmc.com/

... adisdiadochokinetic made a comment on nbme22/block3/q#47 (A 10-year-old boy receives a renal transplant from a...)
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submitted by adisdiadochokinetic(7)

Can anyone explain why Fibrous scars with plasma cells is not the correct answer?

... haliburton made a comment on nbme22/block3/q#48 (A 2-year-old boy is brought to the physician because...)
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submitted by haliburton(74)

no tonsilar tissue is a huge clue here. total lack of Ig which causes recurrent infections after 6mo (maternal IgG is gone). LN and tonsils are minor/non-existent. (FA 2017).

angelaq11  I totally hated this Q! I almost completely overlooked the "no tonsillar tissue", and thank God I didn't because that's the clue that made me change my answer. I had CGD (yeah, I know, S. pneumoniae not catalase +), but it said that he had muuultiple infections since birth. And I took to heart that "since birth" thing, because, isn't Bruton supposed to present with infections from around 6moa? I hope I don't screw this up next week
... yotsubato made a comment on nbme22/block3/q#49 (A 42-year-old man is brought to the emergency...)
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submitted by yotsubato(214)

"MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a prodrug to the neurotoxin MPP+, which causes permanent symptoms of Parkinson's disease by destroying dopaminergic neurons in the substantia nigra of the brain. It has been used to study disease models in various animal studies." Wiki

ilikecheese  pg 508 FA 2019
sbryant6  I thought this was testing "lead pipe rigidity" aka Neuroleptic Malignant Syndrome and its connection to dopamine. Had no clue what MPTP was and got it right still. Probably wrong train of thought though.
... sunny made a comment on nbme22/block3/q#49 (A 42-year-old man is brought to the emergency...)
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submitted by sunny(0)

FA pg 508 (19) mptp causes parkins..................................................

... imnotarobotbut made a comment on nbme22/block3/q#50 (A 56-year-old woman is brought to the emergency...)
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submitted by imnotarobotbut(22)

Although there are no specific herpes indicators, a CSF panel with mostly leukocytes indicates a viral infection (as well as the normal glucose). So you can rule out TB, neurosarcoidosis and bacterial. Brudzinski/kernig sign are related to meningitis, but even if you don't know what those are, the question says that there is an abnormality in the TEMPORAL lobe (meningitis = meninges). Encephalitis would be the best answer, especially because Herpes Encephalitis affects the temporal lobe.

... yotsubato made a comment on nbme22/block4/q#1 (A 2-day-old full-term female newborn suddenly...)
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submitted by yotsubato(214)

Celiac: doesnt make sense, it comes out of the root of the aorta and ends instantly. Thats not getting caught up in the volvulus alone.

Left/right colic: thats all IMA branches, thats uninvolved in the situation.

Umbilical: that getting occluded is physiologic after birth.

Whats left is SMA: which goes right above the duodenum, so i would imagine a duodenal volvulus would involve the SMA easily.

... mattnatomy made a comment on nbme22/block4/q#1 (A 2-day-old full-term female newborn suddenly...)
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submitted by mattnatomy(21)

I believe this is referring to midgut malrotation. Due to improper positioning of bowel (on the right side). Ladds bands connect the large intestine to the liver.

Can lead to:

  1. Volvulus

  2. Duodenal obstruction

3. SMA Occlusion -- I'm guessing based on the answer to the question

meningitis  Yes, the question clicked for me when I realized the ligament was on the RT side instead of LT so I thought of Volvulus. Image of ligament of treitz: https://media.springernature.com/original/springer-static/image/chp:10.1007/978-3-642-13327-5_17/MediaObjects/978-3-642-13327-5_17_Fig3_HTML.gif
hyperfukus  So Volvulus regardless in baby or adult is gonna cause SMA prob + Duodenal Obstruction: d/t Ladd bands im gonna go back and remember those associations :)
... moloko270 made a comment on nbme22/block4/q#1 (A 2-day-old full-term female newborn suddenly...)
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submitted by moloko270(29)

just know probably that anatomically SMA runs above third part of duodenum. so if we have a ligament pulling over that side it can obstruct both duodenum (was mentioned in stem) and SMA that lies over it

in GI section they also describe SMA syndrome - when SMA obstructs the duodenum itself so its stuck between SMA and aorta. guessing from there

... nwinkelmann made a comment on nbme22/block4/q#1 (A 2-day-old full-term female newborn suddenly...)
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submitted by nwinkelmann(60)

This is a good animation video of abnormalities of gut rotation (MUSIC IS WEIRD, lol): https://www.youtube.com/watch?v=gT85dJTT2QE and part 1 if you want to see a good animation of the normal gut rotation (also weird music, i.e. is the same, lol): https://www.youtube.com/watch?v=49awxUGZvdY

... alexb made a comment on nbme22/block4/q#1 (A 2-day-old full-term female newborn suddenly...)
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submitted by alexb(10)

There is a decent UWorld question explaining how this works. Only reason I remembered it.

hyperfukus  i had notes from forever ago but i totally forgot lol
... gainsgutsglory made a comment on nbme22/block4/q#2 (Thirty minutes after taking 2 aspirin tablets for a...)
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submitted by gainsgutsglory(4)

Why is acetaminophen the correct answer other than process of elimination. NSAIDs can be used for tension HA and she’s too old for Reye Syndrome (i mean technically shes a child since shes <17, but not a classic picture at all). I’m confused.

zelderonmorningstar  My reasoning was that aspirin and the other 3 are all NSAIDs, and she had an adverse reaction. Acetaminophen is not an NSAID, so she probably won’t have the reaction.
gainsgutsglory  @zelderon But what’s the pathophys here?
generic_login  This is aspirin-intolerant asthma. Acetaminophen only inhibits COX within the CNS, so doesn't cause the leukotriene shunting that characterizes that disease.
... generic_login made a comment on nbme22/block4/q#2 (Thirty minutes after taking 2 aspirin tablets for a...)
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submitted by generic_login(6)

This is aspirin-intolerant asthma. Acetaminophen only inhibits COX within the CNS, so doesn’t cause the leukotriene shunting that characterizes that disease.

... welpdedelp made a comment on nbme22/block4/q#3 (A 60-year-old man comes to the physician because of...)
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submitted by welpdedelp(64)

It was a Ferruginous bodies--> asbestosis. Ferruginous bodies are believed to be formed by macrophages that have phagocytosed and attempted to digest the fibers.

... menacingmegalodon made a comment on nbme22/block4/q#4 (A 24-year-old man who is comatose is admitted to the...)
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submitted by menacingmegalodon(0)

How do you know that respiratory system compliance is 25 ml/cm h2o?

alwaysanonymous  His tidal volume was 500 mL. End-expiratory was +5 cm and end-inspiratory was +25. We were supposed to use the difference in airway pressure, and not the end-inspiratory pleural pressure (+20). Compliance = ΔV/ΔP = 500 / 20 = 25 mL/cm H2O
... alwaysanonymous made a comment on nbme22/block4/q#4 (A 24-year-old man who is comatose is admitted to the...)
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submitted by alwaysanonymous(12)

His tidal volume was 500 mL. End-expiratory was +5 cm and end-inspiratory was +25. We were supposed to use the difference in airway pressure, and not the end-inspiratory pleural pressure (+20).

Compliance = ΔV/ΔP = 500 / 20 = 25 mL/cm H2O

some-zheimers  Great explanation. In general, also a great idea to pay attention to the units. I studied Physics in undergrad and have got one or two questions based purely on following the units, when the formula slips.
endochondral1  is that equation in FA?
redvelvet  yes @endochondral1, at page 651 in 2019FA
... welpdedelp made a comment on nbme22/block4/q#5 (A new virus has been isolated that causes...)
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submitted by welpdedelp(64)

Ok, so RNA dependent DNA polymerase is for reverse transcriptase... single stranded + use RNA dependent RNA polymerase. Can someone explain?

hyoid  The only thing I can think of is that HIV is a (+)-sense single-stranded RNA virus that relies on an RNA dependent DNA polymerase (reverse transcriptase) to synthesize DNA.
haliburton  according to [medbullets link](https://step1.medbullets.com/step1-microbiology/104196/rna-viruses_) ns ss RNA must carry RNA dependent RNA polymerase (so that is out). also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this.
some0217710  Can’t think of any retroviruses outside of HIV and HTLV and they’re both +ssRNA
... haliburton made a comment on nbme22/block4/q#5 (A new virus has been isolated that causes...)
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submitted by haliburton(74)

according to medbullets link ns ss RNA must carry RNA dependent RNA polymerase (so that is out).

also, according to medbullets there are very few ds RNA viruses, so "most likely" will be ss. Also, RNA-dependent DNA polymerase = Reverse Transcriptase. Since HIV is a ss ps RNA virus with RT, they've described an HIV cousin. not sure beyond this.

nc1992  negative stranded can't be read by a translator so it needs to be transcribed into + first. Only then can it be used for protein. + is basically mRNA already. There's only one double stranded RNA family as far as I know- Reovirus so no encephalitis
... hipster_do made a comment on nbme22/block4/q#5 (A new virus has been isolated that causes...)
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submitted by hipster_do(2)

I think this was referring to reverse transcriptase, and the only two viruses I knew that used them were HepB and HIV/retroviruses. Given the context I picked HIV/retroviruses which are SS + sense. This was kind of weird though since the virus was “new” ... but I’ve learned that “new” usually means very little on these tests.

yotsubato  "New" means made up fantasyland virus
yotsubato  Also Hep B is a ssDNA virus that goes to RNA, then is reverse transcribed to dsDNA
... niboonsh made a comment on nbme22/block4/q#5 (A new virus has been isolated that causes...)
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submitted by niboonsh(57)

My guess is that they are referring to Retrovirus (HIV/HTLV)- a single stranded positive sense linear RNA. Retroviruses are known to carry reverse transcriptase (RNA-dependent DNA-polymerase). The encephalitis is what threw me off cuz I automatically thought of the many negative sense RNA viruses that cause encephalitis (like arenavirus or bunyavirus). Apparently there have been a few causes of HTLV causing encephalitis... maybe this is what they were trying to get at? Idk but i just spent way too much time on this damn question https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5878187/

... meddeku made a comment on nbme22/block4/q#5 (A new virus has been isolated that causes...)
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submitted by meddeku(0)

Japanese encephalitis virus according to Dr. Google (ncbi)

Google

... dr.xx made a comment on nbme22/block4/q#6 (A population of vegetarians is surveyed to...)
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submitted by dr.xx(35)

The t test is one type of inferential statistics. It is used to determine whether there is a significant difference between the means of two groups.

https://researchbasics.education.uconn.edu/t-test/

... marbledoc made a comment on nbme22/block4/q#7 (A 27-year-old man comes to the physician for a...)
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submitted by marbledoc(0)

Why would you ask the patient to identify the pros and cons? I don’t get the approach here!

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize.
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit...
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives.
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx.
... someduck3 made a comment on nbme22/block4/q#8 (A 6-year-old boy who recently emigrated from Russia...)
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submitted by someduck3(15)

Fat soluble vitamins are A,D,E,K. So both D & E could be decreased in this pt. But you have to know that Vitamin E deficiency is associated with demyelination & has been associated with posterior column demyelination. Also Vit E can be given with Alzheimer patients as it helps with free radicals..?

aesalmon  I actually thought that the posterior column findings were likely due to B12 deficiency - "subactue combined degeneration", due to malabsorption, as we see in this pt (. Turns out vitamin E can also cause symptoms which look like subacute combined degeneration: https://www.ncbi.nlm.nih.gov/pubmed/9012278, as does Copper (TIL): https://www.ncbi.nlm.nih.gov/pubmed/15249607
jooceman739  Vitamin E deficiency causes posterior column findings and hemolytic anemia :)
nwinkelmann  The way I think about it is that essentially, vitamin E is an anti-oxidant. Vitamin E deficiency = LOTS of oxidation, i.e. free radicals, which are toxic to most cells in the body (particularly myelination and RBCs). That's why it can be used with Alzheimer's patients.
... alexb made a comment on nbme22/block4/q#8 (A 6-year-old boy who recently emigrated from Russia...)
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submitted by alexb(10)

I think there's a UWorld question describing how cystic fibrosis can cause fat soluble vitamin deficiency and how a Vit E def in that context might manifest similarly to B12 def. (Also in first aid)

... its_raining_jimbos made a comment on nbme22/block4/q#9 (A 5-year-old boy is brought to the physician because...)
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submitted by its_raining_jimbos(8)

Our little friend has a Parvovirus infection, which infects erythroid precursors, causing interruption of erythrocyte production. This is the same way it causes hydrops fetalis in unborn babies and aplastic anemia in sickle cell, etc.

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest?
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced.
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed.
yotsubato  He can drop from 11 to 10 hgb easily
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts??
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :)
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia.
... hello made a comment on nbme22/block4/q#9 (A 5-year-old boy is brought to the physician because...)
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submitted by hello(51)

Patient has red lacy rash- this fits more with HHV-6 (Roseola virus), not Parvovirus.

HHV-6 causes deformation of erythoblasts, leading to anemia.

hyperfukus  Hey so i just looked in first aid and it says "diffuse Macular Rash for Roseola" and usually you have a super high fever and febrile seizures are almost always mentioned...I found in my notes from uworld that i mustve filled in a long time ago for Parvo: Infects Erythroid precursors + Replicates in BM Face/cheek rash followed by LACY Reticular rash on body...May get Rash from IC deposition...and then again i wrote replicates in erythrocyte progenitors causing reticulocytopenia which makes sense why dec Hb and dec Hct
... keycompany made a comment on nbme22/block4/q#10 (An 81-year-old man comes to the physician for...)
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submitted by keycompany(105)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290806/

Osler Sign is a low-sensitivity, low-specficity finding of Mockenberg Arteriolosclerosis (MA) characterized by "a palpable although pulseless, radial artery while the BP cuff is inflated above systolic pressure".

It is possible that either: a) The low-specificity of this test means it is also applicable to atherosclerosis (not just MA) b) The NBME incorrectly implies that MA is interchangable with atherosclerosis.

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse."
... catacholamine16 made a comment on nbme22/block4/q#10 (An 81-year-old man comes to the physician for...)
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submitted by catacholamine16(1)

what is happening in this stem? unable to occlude the radial artery ? Can someone please explain?

lilamk  I chose atherosclerosis because they said “radial artery is non-pulsatile but remains palpable even as the cuff is inflated”--> my reasoning was that normally you can’t feel the artery anymore once you overflate the cuff bc this occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally a hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!)
mnemonia  I think athero is just a subtype of arteriosclerosis. Also my thought process was (like Lila) if something were to not be palpable then it would have to collapse and athero prevents this from happening.
yb_26  FA 2019, page 299: types of Arteriosclerosis: arteriolosclerosis and Mockenberg sclerosis. then on page 300: Atherosclerosis - form of arteriosclerosis caused by buildup of cholesterol plaques.
... yb_26 made a comment on nbme22/block4/q#10 (An 81-year-old man comes to the physician for...)
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submitted by yb_26(28)

FA 2019, page 299: types of Arteriosclerosis: arteriolosclerosis and Mockenberg sclerosis.

then on page 300: Atherosclerosis - form of arteriosclerosis caused by buildup of cholesterol plaques.

... mattnatomy made a comment on nbme22/block4/q#11 (A 26-year-old woman comes to the physician 5 weeks...)
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submitted by mattnatomy(21)

I thought initially we were dealing with post-partum psychosis, but on re-reading, this looks more like either Generalized Anxiety Disorder or OCD or both. Either way, treatment should be an SSRI (Sertraline).

seagull  OCD for sure
... dr.xx made a comment on nbme22/block4/q#12 (A 73-year-old woman dies 7 years after the onset of...)
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submitted by dr.xx(35)

The four types of hydrocephalus are communicating, noncommunicating, ex vacuo, and normal pressure. Diagnosis is typically made by physical examination and medical imaging.

Hydrocephalus ex vacuo also refers to an enlargement of cerebral ventricles and subarachnoid spaces, and is usually due to brain atrophy (as it occurs in dementias), post-traumatic brain injuries and even in some psychiatric disorders, such as schizophrenia. As opposed to hydrocephalus, this is a compensatory enlargement of the CSF-spaces in response to brain parenchyma loss; it is not the result of increased CSF pressure.

https://en.wikipedia.org/wiki/Hydrocephalus#Type

... ilikecheese made a comment on nbme22/block4/q#13 (A 36-year-old woman comes to the physician because...)
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submitted by ilikecheese(7)

corticosteroids - steroid bind to receptor located in nucleus or cytoplasm --> transformation of receptor to expose DNA-binding protein etc pg 332 FA 2019

... haliburton made a comment on nbme22/block4/q#14 (In patients with adenosine deaminase deficiency,...)
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submitted by haliburton(74)

this image shows lymphocytic toxicity.

this image shows that the buildup of dATP inhibits RNR (ribonucleotide reductase), which inhibits the rest dNTP synthesis.

bonus image shows RNR is the target of hydroxyurea.

... coolcatac made a comment on nbme22/block4/q#14 (In patients with adenosine deaminase deficiency,...)
... hayayah made a comment on nbme22/block4/q#15 (A 24-year-old woman, gravida 1, para 1, comes to the...)
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submitted by hayayah(345)

This is a patient case of postpartum thyroiditis. Can arise up to a year after delivery and has lymphocytic infiltrate.

... liverdietrying made a comment on nbme22/block4/q#15 (A 24-year-old woman, gravida 1, para 1, comes to the...)
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submitted by liverdietrying(20)

This one was a little tricky. For this one the key is the low radioiodine uptake. This patient has high T4 and low TSH which makes sense in a hyperthyroid patient, perhaps your first thought is that this patient has Grave’s disease. However, in Grave’s your thyroid is being stimulated to make more thyroid hormone from scratch and as such would have an increased radioiodine uptake because the thyroid is bringing in the required (now radiolabeled) iodine. This is why it is not Graves (“release of thyroid hormone from a thyroid stimulated by antibodies”).

So if its not Grave’s what could it be? For this you’d have to know that Hashimoto’s Thyroiditis (also known as Chronic Lymphocytic Thyroiditis and is often referred to as such on board exams to throw you off) has three phases - first they are hyperthyroid, then euthyroid, then the classic hypothyroid that you would expect with low T4 and high TSH. This was the key to this question. The reason for this is that antithyroid peroxidase antibodies in Hashimoto’s cause the thyroid to release all of its stored thyroid hormone making the patient hyperthyroid for a short period of time. After this massive release of thyroid hormone, the antibodies make them unable to make new TH and therefore they become euthyroid for a short period and then hypothyroid which you would expect! Since they can’t make new TH, the thyroid will not take up the radioiodine and therefore there will be low radioiodine uptake. Hence, “release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes.” aka “Lymphocytic (hashimotos) thyroiditis”.

I think “release of thyroid hormone from a lymphomatous thyroid gland” is referring to some kind of thyroid cancer in which case you would expect them to be describing a nodule on radioiodine uptake.

​Summary video here and also a great site in general: https://onlinemeded.org/spa/endocrine/thyroid/acquire

aesalmon  pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first
hyperfukus  yep that was the key! Goiter is "HOT" but the remaining answer choices were still kind of bleh D was distracting the hell out of me i spent so long to convince myself to pick C and move on
hello  Pasting nwinkelmann's comment as an addition: Choice "D" is wrong b/c "lymphomatous thyroid gland" = primary thyroid lymphoma (typically NHL, which is very rare) or Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. Both of these present with hypothyroidism with low T4 and high TSH (opposite of this patient).
... seagull made a comment on nbme22/block4/q#15 (A 24-year-old woman, gravida 1, para 1, comes to the...)
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submitted by seagull(355)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/

According to this paper, Postpartum Thyroiditis presents with anti-TPO antibodies. The answer choice uses lymphocytes. So this is a transient Hashimotos Hyperthyroidism. Good Luck with that one!

seagull  EDIT: Lymphocytes are also present in this as well. My bad
... niboonsh made a comment on nbme22/block4/q#15 (A 24-year-old woman, gravida 1, para 1, comes to the...)
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submitted by niboonsh(57)

Can someone explain the difference between C. (release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes) and D. (Release of thyroid hormone from a lymphomatous thyroid gland.

drdoom  @niboonsh, ending a comment with a question mark will make it appear on the "comments seeking answers" lists
nwinkelmann  A lymphomatous thyroid gland can either be due to primary thyroid lymphoma (which is almost always NHL, but is very rare) or due to Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. These, I believe, would still present with hypothyroidism, and thus would have low T4 and high TSH (opposite of this patient).
... nwinkelmann made a comment on nbme22/block4/q#15 (A 24-year-old woman, gravida 1, para 1, comes to the...)
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submitted by nwinkelmann(60)

The explanation by liverdietrying plus the explanation in the article posted below (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/) are the best, just need to be combined :). The differential diagnosis table 1 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/table/OM-10-0041-SLTB1/?report=objectonly) specifically identifies the condition in this question as postpartum thyroiditis.

Ultimately, if you know that hypothyroidism has a transient hyperthyroidism phase (due to autoimmune destruction of the cells which already had preformed TH and so it was released upon destruction) before hypothyroidism (nonfunctioning cells so can't take up iodine) and that hypothyroidism is a lymphocytic infiltrating thyroiditis, you will know the answer. I had a hard time understanding this at first because we evaluate/diagnose based on the presence of anti-TPO Ab, but the underlying pathogenesis of the thyroid destruction is cell-mediated (type IV hypersensitivity) not Ab mediated (type II hpyersensitivity) like graves. Hashimoto's = lymphocytic infiltration wiht germinal centers (which can transform to B cell lymphoma) with hurthle cells (pinker cytoplasm cells).

... hyperfukus made a comment on nbme22/block4/q#15 (A 24-year-old woman, gravida 1, para 1, comes to the...)
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submitted by hyperfukus(5)

I think that since they're asking for an explanation of the patient's current SSx which shows that she's in the state of Transient Hyperthyroidism: which is due to C: Release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes

... aesalmon made a comment on nbme22/block4/q#16 (A 4-month-old boy is brought to the office by his...)
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submitted by aesalmon(33)

FA pg. 607 - failure of fusion of the maxillary and merged medial nasal processes (formation of primary palate)

meningitis  I think Cleft palate could also be due to failure of fusion of lateral and medial nasal prominences.. but since the baby had lip involvement and the lateral nasals can be seen, I went with failure of Maxillary and medial nasal fusion. Someone correct me if im wrong.
... luckeroo made a comment on nbme22/block4/q#17 (A 62-year-old man with dyslipidemia is brought to...)
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submitted by luckeroo(2)

why was this gemfibrozil and not niacin? I was lucky and guessed, but I thought niacin combined could also trigger myopathy?

.ooo.   Gemfibrozil is a CYP450 inhibitor causing an increase drug concentration of statin which would lead to the adverse side effect of myopathy. Not sure about niacin in combination with statin but believe this would be more likely to occur. Hope this helps!
yb_26  yes, it can be seen with niacin and esetemibe as well, according to UWorld. But first choice in such questions is always fibrates.
nor16  number one no-go combi is statin+fibrate here
... bobson150 made a comment on nbme22/block4/q#18 (A 10-year-old girl has a slightly painful 2-mm...)
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submitted by bobson150(2)

Is the grey supposed to be a suture? If not why would this not be wound healing therefore granulation tissue?

asapdoc  If you look at the picture you can see the epithelioid and giant cells. I only picked granuloma because I remember seeing a similar picture in Uworld.
... seagull made a comment on nbme22/block4/q#18 (A 10-year-old girl has a slightly painful 2-mm...)
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submitted by seagull(355)

The authors went out of their way to find thew worst photo of a granuloma they could. The threw on a stem that suggests that it would be granulation tisue. But little did we know...

amorah  I was between granulation tissue and granuloma. Then ruled out granulation tissue because this is a 10 week old wound. Assuming normal wound healing, granulation tissue would be replaced by type III collagen/resolution by 10 weeks.
sbryant6  Got this right because the exact same question is in Uworld.
... kard made a comment on nbme22/block4/q#18 (A 10-year-old girl has a slightly painful 2-mm...)
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submitted by kard(3)

Might be this way, correct me please if my approach is mistaken. So in the Stem we have a Painful nodule, (Due to 10weeks ago Sutures) So im thinking on Suture granuloma, that forms a lesion (Painful Nodule) arround the non-absorbable suture material.

... aesalmon made a comment on nbme22/block4/q#19 (A 76-year-old man with a 1-month history of a...)
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submitted by aesalmon(33)

Those arteries go wherever they want - off the Aorta, common iliacs, wherever. Only 2 ureters tho

... niboonsh made a comment on nbme22/block4/q#19 (A 76-year-old man with a 1-month history of a...)
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submitted by niboonsh(57)

https://www.ncbi.nlm.nih.gov/pubmed/15599631 The horseshoe kidney was detected before surgery in 12 patients (80%) by ultrasonography, angiography, computed tomography (CT) or excretory urography. Angiography revealed multiple or anomalous renal arteries in 8 of 12 patients studied preoperatively

... nwinkelmann made a comment on nbme22/block4/q#19 (A 76-year-old man with a 1-month history of a...)
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submitted by nwinkelmann(60)

Can someone explain how to rule out the other answer choicers?

warbyparker1  you can r/o SMA because as kidneys ascend they get stuck low in the INFERIOR MA (L3 level). So I guess there should be no problem w SMA
hello  I think friability of vascular tissue would indicate in inflammatory process (the one I can think of is strawberry cervix) -- so i think that's why you can rule out choice C.
... aesalmon made a comment on nbme22/block4/q#20 (During a study of symptomatic proximal deep venous...)
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submitted by aesalmon(33)

Clinical trial - compares therapeutic benefits of 2+ treatments (warfarin vs. dalteparin) Open-label - both the health providers and the pt are aware of the drug being given

... niboonsh made a comment on nbme22/block4/q#20 (During a study of symptomatic proximal deep venous...)
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submitted by niboonsh(57)

I am confusion. why wouldnt this be a cross over study?

shokay  there is no washout period and the order of drugs given isn't switched
... hello made a comment on nbme22/block4/q#20 (During a study of symptomatic proximal deep venous...)
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submitted by hello(51)

Why isn't this a cohort study?

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem.
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one.
... jboud86 made a comment on nbme22/block4/q#21 (A previously healthy 45-year-old woman has had...)
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submitted by jboud86(1)

FA 2019 page 419. Pt's PC is low and BT is increased. TTP presents with the triad (thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury), fever, and neurologic symptoms.

... mattnatomy made a comment on nbme22/block4/q#22 (A 37-year-old man comes to the physician for a...)
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submitted by mattnatomy(21)

Severe hypertension often leads to hyperplastic arteriolosclerosis (onion-skin appearance). Also see proliferation of smooth muscle cells.

meningitis  and explains the flame hemorrhages (Goljan) caused by malignant HTN
... welpdedelp made a comment on nbme22/block4/q#23 (A 57-year-old woman comes to the office because of a...)
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submitted by welpdedelp(64)

This is Lambert-Eaton, which improves with movement as compared to Myesthenia gracias whichh worsens with movement

sbryant6  Lambert-Eaton is typically associated with Small Cell Lung Cancer. Since there was no mentino of that, I was thrown off. Such is the difference between UWorld and NBME I guess.
... trichotillomaniac made a comment on nbme22/block4/q#23 (A 57-year-old woman comes to the office because of a...)
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submitted by trichotillomaniac(13)

antibodies form against the presynaptive Ca2+ channels at the NMJ-most commonly seen in patients with small cell lung cancer

... trichotillomaniac made a comment on nbme22/block4/q#23 (A 57-year-old woman comes to the office because of a...)
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submitted by trichotillomaniac(13)

antibodies form against the presynaptive Ca2+ channels at the NMJ-most commonly seen in patients with small cell lung cancer

... seagull made a comment on nbme22/block4/q#24 (A 39-year-old woman with rheumatoid arthritis comes...)
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submitted by seagull(355)

Im also convinced blocking IL-2 is also a treatment? WHy is TNF-alpha the better answer here?

amorah  FA P120-122. Immunosuppressants for RA are calcineurin inhibitor (cyclosporine and tacrolimus), 6MP, and TNFa inhibitors (adalimumab,infliximab, etanercept). It is important to distinguish that calcineurin inhibitors block t cell activation by preventing IL-2 transcription, not necessarily block IL-2 action. Sirolimus(rapamycin) blocks IL-2 action but it is used for kidney transplant rejection prophylaxis specifically.
... dr.xx made a comment on nbme22/block4/q#25 (A healthy 25-year-old man eats a meal consisting of...)
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submitted by dr.xx(35)

The β-cells have evolved a mechanism to detect the amount of insulin stored and secreted and adjust insulin synthesis accordingly. A granule transmembrane protein called islet cell autoantigen 512 (ICA512), is a crucial part of this feedback control. Insulin granules travel a long distance on tubulin tracks before arriving at the peripheral actin network [125]. Before becoming linked to the cytoskeleton, insulin granules are anchored to actin cortex via ICA512 and β2-synthrophin. Upon activation, the granule membrane fuses transiently to the cell membrane to release insulin. Elevated Ca2+ levels in the meantime activate the protease μ-calpain to cleave away a cytosolic fragment from ICA512. The free ICA512 cytosolic fragment then moves to the nucleus and binds to the tyrosine-phosphorylated transcriptional factor STAT5 to prevent STAT 5 from dephosphorylation, which in turn upregulates insulin transcription [127]. Nuclear free ICA512 cytosolic fragments also bind to sumoylating enzyme PIASγ. The sumoylation of ICA512 by PIAS γ reverses the binding of ICA512 to STAT5 [127]. Hence, the release of insulin from secretory granules is communicated to the nucleus, which serves as a positive feedback mechanism to initiate insulin translation for maintaining an adequate amount of stored insulin.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3934755/

... trichotillomaniac made a comment on nbme22/block4/q#25 (A healthy 25-year-old man eats a meal consisting of...)
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submitted by trichotillomaniac(13)

basically glucose stimulates Beta cells to exocytos insulin. An process involving exocytosis involves fusion od an intracellular vesicle with the plasma membrane.

... trichotillomaniac made a comment on nbme22/block4/q#25 (A healthy 25-year-old man eats a meal consisting of...)
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submitted by trichotillomaniac(13)

basically glucose stimulates Beta cells to exocytose insulin. Any process involving exocytosis involves fusion of an intracellular vesicle with the plasma membrane.

... natuwalrien made a comment on nbme22/block4/q#26 (A 60-year-old woman comes to the physician because...)
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submitted by natuwalrien(0)

meningiomas count as enhancing lesions? (this comment needs to be more than 50 characters apparently.)

goldenwakosu  I think it’s because meningiomas are able to calcify (aka sometimes they have psamomma bodies). I got this question wrong too but I totally did not completely register that the tumor was in the dura (interhemispheric fissure + central sulcus). Hope that helps!
pipter  the only reason I got this right was because they described the tumour as being near the falx cerebri.
fcambridge  Other hints include being described as round and seen in a female. Both indicative of Meningioma
niboonsh  also meningiomas typically present with seizures or focal neurological signs
... fallenistand made a comment on nbme22/block4/q#26 (A 60-year-old woman comes to the physician because...)
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submitted by fallenistand(5)

This is meningioma because its in the interhemispheric fissure its not infiltrating the brain. All the other ones are within the brain tissue

... fallenistand made a comment on nbme22/block4/q#26 (A 60-year-old woman comes to the physician because...)
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submitted by fallenistand(5)

This is meningioma because its in the interhemispheric fissure its not infiltrating the brain. All the other ones are within the brain tissue

... nor16 made a comment on nbme22/block4/q#26 (A 60-year-old woman comes to the physician because...)
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submitted by nor16(3)

one important aspect not mentioned: the " long " 1 year "benign" history of the symptoms... not likely for malginant lymphomas, astros or metastasis to stay that calm

of course in addition to all other mentioned here "not brain infiltrating etc."

... oznefu made a comment on nbme22/block4/q#27 (A 78-year-old man comes to the physician because of...)
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submitted by oznefu(7)

I’m having trouble understanding why this is a better choice than Paget disease, especially with the increased ALP?

zelderonmorningstar  Paget’s would also show some sclerosis.
seagull  ALK is increased in bone breakdown too. Prostate loves spreading to the lumbar Spine. It's like crack-cocaine for cancer.
aesalmon  I think the "Worse at night" lends itself more towards mets, and the pt demographics lean towards prostate cancer, which loves to go to the lumbar spine via the Batson plexus. I picked Paget but i think they would have given something more telling if they wanted pagets, histology or another clue
fcambridge  @seagull and aesalmon, I think you're a bit off here. Prostate mets would be osteoblastic, not osteolytic as is described in the vignette.
sup  Yeah I chose Paget's too bcz I figured if it wasn't prostate cancer (which as @fcambridge said would present w/ osteoblastic lesions) they would give us another presenting sx of the metastatic cancer (lung, renal, skin) that might point us in that direction. I got distracted by the increased ALP too and fell for Paget :(
kernicterusthefrog  @fcambridge, not exactly. Yes, prostate mets tends to be osteoblastic, but about 30% are found to be lytic, per this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768452/ Additionally, the night bone pains point to mets, and Paget's is much more commonly found in the cranial bones and appendicular skeleton, than axial. This could also be RCC mets!
sweetmed  I mainly ruled out pagets because they said the physical examination was normal. He would def have other symptoms.
... notadoctor made a comment on nbme22/block4/q#27 (A 78-year-old man comes to the physician because of...)
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submitted by notadoctor(47)

Metastatic disease is more common than primary bone tumors.

... mattnatomy made a comment on nbme22/block4/q#28 (A 48-year-old man comes to the emergency department...)
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submitted by mattnatomy(21)

Most common cause of splenic vein thrombosis is chronic pancreatitis, caused by perivenous inflammation.

Source: https://www.ncbi.nlm.nih.gov/pubmed/14502405

hyperfukus  great link! helps answer other qs too thank you :)
... k_tron_3000 made a comment on nbme22/block4/q#28 (A 48-year-old man comes to the emergency department...)
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submitted by k_tron_3000(8)

Just a random factoid (as far as I know), in patients with pancreatitis the most likely vessel for thrombosis is the splenic vein due to close “anatomic ties” with the pancreas. This would also cause gastro-splenic varices, explaining the vomiting of blood.

meningitis  Also explains the splenomegaly. If you have thrombosed splenic vein, the blood will pool in the spleen, can also cause expansion of red pulp of spleen.
... aesalmon made a comment on nbme22/block4/q#28 (A 48-year-old man comes to the emergency department...)
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submitted by aesalmon(33)

When in doubt its probably the Splenic Vein ("play odds" - Goljan)

... haliburton made a comment on nbme22/block4/q#29 (A 45-year-old man who is HIV positive comes to the...)
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submitted by haliburton(74)

pathogen: cryptococcus

Treatment options: Ampho B: binds ergosterol -> pores in fungal membrane -> leaks contents. can add Flucytosine: converted to 5-FU to inhibit nucleic acid synthesis

https://step1.medbullets.com/microbiology/104161/flucytosine https://step1.medbullets.com/microbiology/104158/amphotericin-b

... johnthurtjr made a comment on nbme22/block4/q#30 (A 27-year-old man who is a construction worker is...)
... meningitis made a comment on nbme22/block4/q#30 (A 27-year-old man who is a construction worker is...)
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submitted by meningitis(121)

I thought: lower pole then cant be suprarenal nor stomach which are higher""

Duodenum and Body of pancreas (except tail) are retroperitoneal and midline

... praderwilli made a comment on nbme22/block4/q#30 (A 27-year-old man who is a construction worker is...)
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submitted by praderwilli(19)

I crossed out all of the other ones and all of the sudden that was all that was left 🤘

... sweetmed made a comment on nbme22/block4/q#30 (A 27-year-old man who is a construction worker is...)
... mattnatomy made a comment on nbme22/block4/q#31 (A 65-year-old man comes to the emergency department...)
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submitted by mattnatomy(21)

Crackles either indicates chronic bronchitis or consolidation (from pneumonia or pulmonary edema).

Given that there's only a 1 day history of SOB, I'm leaning more towards lobar pneumonia. Maybe that's also what's causing the S3 at the LLSB? If it's Staph Aureus, I guess we could be looking at acute endocarditis + pneumonia? Or Q Fever? But that's just speculation. Could also just be that the lung consolidation is altering blood flow, leading to the back up into the Right Atrium & Ventricle.

brise  Patient has CHF from the S3 heart sound and has MR. You hear fine crackles in early congestive heart failure. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4518345/
usmleuser007  No Infection - normal temps ; Q-fever presents with A patient with exposure to waste from farm animals who develops: a. nonspecific illness (myalgias, fatigue, fever [>10 days], b. retroorbital headache) c. normal leukocyte count d. Thrombocytopenia e. increased liver enzymes
... usmleuser007 made a comment on nbme22/block4/q#31 (A 65-year-old man comes to the emergency department...)
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submitted by usmleuser007(86)

Just note why other answers are not correct:

  1. Egophony is an increased resonance of voice sounds heard when auscultating the lungs, often caused by lung consolidation and fibrosis.

    • a. It is due to enhanced transmission of high-frequency sound across fluid, such as in abnormal lung tissue, with lower frequencies filtered out.
  2. Whispered pectoriloquy refers to an increased loudness of whispering noted during auscultation with a stethoscope on the lung fields on a patient’s torso.

    • a. Usually spoken sounds of a whispered volume by the patient would not be heard by the clinician auscultating a lung field with a stethoscope.

    • b. However, in areas of the lung where there is lung consolidation, these whispered spoken sounds by the patient (such as saying ‘ninety-nine’) will be clearly heard through the stethoscope.

    • c. This increase in sound exists because sound travels faster and thus with lower loss of intensity through liquid or solid (“fluid mass” or “solid mass,” respectively, in the lung) versus gaseous (air in the lung) media.

    • d. Whispered pectoriloquy is a clinical test typically performed during a medical physical examination to evaluate for the presence of lung consolidation, which could be caused by cancer (solid mass) or pneumonia (fluid mass).

... meningitis made a comment on nbme22/block4/q#32 (A case-control study is conducted to assess the...)
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submitted by meningitis(121)

A case control study cant assess the prevalence of a disease but a cross sectional study can.

  • A case control study is that you are setting the margins in the 2 by 2 table therefore you're deciding how many cases and controls you want to have in your study and the calculation of incidence / prevalence in this scenario would be biased.
meningitis  the prevalence of the exposure and the health outcome are measured at the same time. You are basically trying to figure out how many people in the population have the disease and how many people have the exposure at one point in time. Case Control would determine ODDS ratio Cohort would determine Relative Risk
... dr_trazobone69 made a comment on nbme22/block4/q#32 (A case-control study is conducted to assess the...)
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submitted by dr_trazobone69(1)

Why wasn’t the table enough to determine prevalence in the general population?

sacredazn  For the case control question, it’s taking that principle that you can’t use case control studies to calculate relative risk and applying it to prevalence. Basically with case control studies we start by saying okay, I’m going to find 200 people with sinusitis and 400 without. Then, you go back and look at the number exposed/unexposed and calculate the odds ratio. So you can’t use case controls to calculate prevalence because it all depends on how many cases you picked in the first place. Might make more sense to think about it with a rare cancer like craniopharyngioma or something- let’s say you chose 10 cases and 10 controls and wanted to look at how many people smoked. It wouldn’t make sense to then say the prevalance of craniopharyngioma is 10/20 = 50%.
dr_trazobone69  Thank you, that makes a lot of sense! So we can use relative risk (cohort studies) to calculate prevalence?
sacredazn  @trazobone Hmm I think the wording would be key, you could use a prospective cohort to calculate incidence, but you wouldn’t be able to find prevalence of the gen population unless you had more info. I think the concept is that really to calculate prevalence you need a proper ecologic study looking at population-level data. The way it was worded in the question was tricky though lol since when has “cannot be determined from the info given” ever been a right answer.
nwinkelmann  @sacredazn thank you! this was the best explanation to use the rare disease comparison. Made everything make so much sense and hopefully I'll actually just remember it now, instead of learning the factoid and failing to recall it all the time.
hyperfukus  i guess this makes sense but i don't understand why we are asked to calculate it from tables like this then? is there more info in those?
hello  @hyperfukus The table was given because that a 22 table is typically what you do see regarding data for case-control studies. If the 22 table wasn't include, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers. The difference in including the data-table is that 1. again, you need to report a 22 table because that is typically what you will see regarding data for a case-control study and 2. by including the 22 table, it actually tests if the test-taker realized that the data in the 2*2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence.
... gatoruiz1 made a comment on nbme22/block4/q#32 (A case-control study is conducted to assess the...)
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submitted by gatoruiz1(0)

Formulat for prevalence is as follows:

Prevalence = Incidence x Disease Duration

Disease duration was not given in the vignette.

... gatoruiz1 made a comment on nbme22/block4/q#32 (A case-control study is conducted to assess the...)
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submitted by gatoruiz1(0)

Formula for prevalence is as follows:

Prevalence = Incidence x Disease Duration

Disease duration was not given in the vignette.

... gatoruiz1 made a comment on nbme22/block4/q#32 (A case-control study is conducted to assess the...)
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submitted by gatoruiz1(0)

Formula for prevalence is as follows:

Prevalence = Incidence x Disease Duration

Disease duration was not given in the vignette.

... hello made a comment on nbme22/block4/q#32 (A case-control study is conducted to assess the...)
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submitted by hello(51)

For people asking why the data table was even included if it was not needed to answer this Q, here is a useful explanation:

The table was given because a 2x2 table is typically what you do see regarding data for case-control studies.

If the 2x2 table wasn't included, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers.

The difference in including the data-table is that:

  1. Again, you need to report a 2x2 table because that is typically what you will see regarding data for a case-control study

and

  1. by including the 2x2 table, it actually tests if the test-taker realized that the data in the 2x2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence.
hello  I also want to add that the Q is asking about sinusitis in the GENERAL population, meanwhile the Q-stem discusses a case-control study that is studying the relationship of smoking (an exposure) to development of sinusitis. To then ask "what is the prevalence of sinusitis in the general population" totally disregards taking into account the exposure of smoking which was the entire reason for the study. In other words, asking prevalence would be very non-sensical.
... kernicterusthefrog made a comment on nbme22/block4/q#33 (A 38-year-old single woman with a history of chronic...)
 +3  upvote downvote
submitted by kernicterusthefrog(17)

"she feels happier and more relaxed" after starting kickboxing: this is a MATURE defense mechanism (classic textbook sublimation, as has been said). This question is just plain wrong. It's not displacement, because it's a healthy, socially acceptable outlet that improves her emotional state; punching bags are meant to be punched (thus it is actually NOT neutral). Displacement to an object would be punching a hole in her wall, or breaking her vase (I just like that imagery). Both of those would be better than punching her family, or breaking their car window, which is why it's displacement (unconscious redirection of an emotion to a safer object). However, kickboxing is LITERALLY an example in several psych textbooks for sublimation. Thank you for coming to my TED Talk.

jaxx  Meanwhile, I thought everything was wrong so I went with another Mature defense mechanism.
... borborygnoramus made a comment on nbme22/block4/q#33 (A 38-year-old single woman with a history of chronic...)
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submitted by borborygnoramus(3)

As best as I could tell, it was displacement because the other choices were definitely wrong, not b/c displacement was a good choice. Felt like there were lots of this type of question on this exam.

diffuseaxonalinjury  I ended up choosing displacement bc sublimation wasn't there + in the beginning of the question, it said "she's angry at her family for not helping her" so my thought was she's displacing her anger about her child's illness on her family (a neutral 3rd party). wack question regardless.
... joha961 made a comment on nbme22/block4/q#33 (A 38-year-old single woman with a history of chronic...)
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submitted by joha961(13)

Like others have said, I think sublimation would have been better, but displacement from first aid says that it is, “redirection of emotions or impulses to a neutral person or object” so she’s kicking her family by kicking the bag.

... dr.xx made a comment on nbme22/block4/q#34 (A 17-year-old boy comes to the physician because of...)
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submitted by dr.xx(35)

Epstein-Barr virus (EBV) is carried by most humans. It can cause several types of cancer. In healthy infected people, EBV persists for life in a "latent" state in B cells.

https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004906

... mattnatomy made a comment on nbme22/block4/q#35 (Nicotinic acid acts at which of the following...)
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submitted by mattnatomy(21)

Answer = C. (Decreased hepatic VLDL synthesis)

Nicotinic acid = Niacin. Niacin works by:

  1. Inhibiting lipolysis (hormone sensitive lipase) in adipose tissue)

  2. Reducing hepatic VLDL synthesis

johnthurtjr  Well color me surprised. I was completely thrown off here.
... usmleuser007 made a comment on nbme22/block4/q#35 (Nicotinic acid acts at which of the following...)
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submitted by usmleuser007(86)

1) label D (VLDL -->ILD --> LDL) = anything that increased LPL = Fibrates which use PPAR-alpha (Rx) are good at reducing [VLDL]; therefore, less VLDL means more ILD.

2) VLDL --> fatty acid oxidation = using fats (TAGs) for energy production Here PPAR-gamma plays a role= which are Thiazolidinediones (also called glitazones) are a class of medicines that may be used for the treatment of type 2 diabetes. They are also good at reducing serum TAGs

Note VLDL are very rich in TAGs

... gh889 made a comment on nbme22/block4/q#35 (Nicotinic acid acts at which of the following...)
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submitted by gh889(32)

Could someone please explain which drugs (if any) are at D and E?

usmleuser007  1) label D (VLDL -->ILD --> LDL) = anything that increased LPL = Fibrates which use PPAR-alpha (Rx) are good at reducing [VLDL]; therefore, less VLDL means more ILD. 2) VLDL --> fatty acid oxidation = using fats (TAGs) for energy production Here PPAR-gamma plays a role= which are Thiazolidinediones (also called glitazones) are a class of medicines that may be used for the treatment of type 2 diabetes. They are also good at reducing serum TAGs Note VLDL are very rich in TAGs
... btl_nyc made a comment on nbme22/block4/q#35 (Nicotinic acid acts at which of the following...)
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submitted by btl_nyc(9)

A: cholestryramine and other bile acid resins prevent the reuptake of bile acids from the gut. B: Statins inhibit HMG-CoA reductase, preventing the liver from making mevalonic acid, a precursor to cholesterol. C: Niacin (nicotinic acid) reduces hepatic VLDL synthesis and also inhibits lipolysis in adipose tissue by inhibiting hormone sensitive lipase. D&E: Fibrates upregulate lipoprotein lipase (LPL), increasing triglyceride clearance (VLDL and chylomicrons are full of triglycerides) and also activate peroxisome proliferator-activated receptor- alpha (PPAR-alpha) to induce HDL synthesis.

... btl_nyc made a comment on nbme22/block4/q#35 (Nicotinic acid acts at which of the following...)
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submitted by btl_nyc(9)

A: cholestryramine and other bile acid resins prevent the reuptake of bile acids from the gut.

B: Statins inhibit HMG-CoA reductase, preventing the liver from making mevalonic acid, a precursor to cholesterol.

C: Niacin (nicotinic acid) reduces hepatic VLDL synthesis and also inhibits lipolysis in adipose tissue by inhibiting hormone sensitive lipase.

D&E: Fibrates upregulate lipoprotein lipase (LPL), increasing triglyceride clearance (VLDL and chylomicrons are full of triglycerides) and also activate peroxisome proliferator-activated receptor- alpha (PPAR-alpha) to induce HDL synthesis.

... aesalmon made a comment on nbme22/block4/q#36 (A 38-year-old man is admitted to the hospital after...)
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submitted by aesalmon(33)

pg. 213 of FA - Acute phase reactants up-regulated during systemic manifestations: "More FFiSH in the C" Ferritin, Fibrinogen, Serum amyloid A, Hepcidin, C-reactive protein.

... haliburton made a comment on nbme22/block4/q#37 (A 53-year-old woman with a long history of...)
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submitted by haliburton(74)

fibromuscular dysplasia in the left renal a. causes low flow resulting in low GFR. Chronic low GFR causes tubular atrophy. (excerpt and reference below).

Tubular atrophy is a general term that describes several patterns of chronic tubular injury with thickened tubular basement membranes, and clinically manifests as chronic kidney disease with decreased glomerular filtration rate. Increased extent of tubular atrophy and accompanying interstitial fibrosis correlates with worse prognosis. Proteinuria is variable, depending on cause.

https://www.ajkd.org/article/S0272-6386(16)30033-6/fulltext

... lala123 made a comment on nbme22/block4/q#37 (A 53-year-old woman with a long history of...)
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submitted by lala123(4)

found the explanation of question id 453 in uworld helpful

... keycompany made a comment on nbme22/block4/q#37 (A 53-year-old woman with a long history of...)
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submitted by keycompany(105)

wouldn’t chronic hypertension of the L-renal artery induce RAAS activation, and hence tubular hypertrophy with cortical atrophy?

fcambridge  I had a similar thought regarding mesangial hypercellularity. I missed a UW question on a similar topic. Unilateral renal artery stenosis results in hyperplasia of modified smooth muscle cells (JG cells) due to reduced RBF. The hyperplasia is intended to correct the supposed deficiency via increased production of renin.
... keycompany made a comment on nbme22/block4/q#37 (A 53-year-old woman with a long history of...)
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submitted by keycompany(105)

Why would deposition of fibrinoid deposits (i.e. fibrinoid necrosis/malignant HTN) be wrong?

amorah  Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN.
... mattnatomy made a comment on nbme22/block4/q#38 (Patients with mucolipidosis II (I-cell disease) lack...)
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submitted by mattnatomy(21)

I-cell disease (inclusion cell disease/mucolipidosis type II)—inherited lysosomal storage disorder; defect in N-acetylglucosaminyl-1-phosphotransferase ; failure of the Golgi to phosphorylate ; mannose residues (mannose-6-phosphate) on glycoproteins --> proteins are secreted extracellularly rather than delivered to lysosomes. Results in coarse facial features, gingival hyperplasia, clouded corneas, restricted joint movements, claw hand deformities, kyphoscoliosis, and high plasma levels of lysosomal enzymes. Often fatal in childhood.

... jooceman739 made a comment on nbme22/block4/q#39 (A 5-year-old boy is brought to the physician because...)
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submitted by jooceman739(11)

Retinoblastoma:

The physician said the boy is unlikely to develop any other neoplasms, so he doesn't have the inherited Rb mutation.

In this case, he has the sporadic retinoblastoma. Sporadic retinoblastoma requires two somatic mutations of Rb in the same retinal cell.

Just as a side note: Inherited retinoblastomas tend to be bilateral. Sporadic are unilateral.

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child?
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything.
kernicterusthefrog  I had the same struggle and thought process.
... haliburton made a comment on nbme22/block4/q#40 (A 5-year-old boy with mental retardation is grossly...)
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submitted by haliburton(74)

Prader Willi = Paternal deletion (partial or full). Noted for imprinting. Cousin to Angelmann (opposite deletion).

FA 2017: 25% of cases due to maternal uniparental disomy (two maternally imprinted genes are received; no paternal gene received).

... rogeliogs made a comment on nbme22/block4/q#40 (A 5-year-old boy with mental retardation is grossly...)
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submitted by rogeliogs(1)

Fact: 75% are due to a deletion in the long arm of the chromosome 15.

Input: This question tricked me up because when I saw a deletion in the chr15 as an option I though "I got it" but actually I did not because it is not in the short arm is in the long arm.

... seagull made a comment on nbme22/block4/q#41 (A 65-year-old woman with a 20-year history of...)
 +1  upvote downvote
submitted by seagull(355)

Couple ways to get the answer. 1. sensation of the anterior thigh and medial leg are by branches of the femoral nerve (L3, L4, L5). 2. Since the anterior thigh is affected the platellar reflex is likely affected which is a branch of L4.

medschul  Isn't the femoral nerve innervated by L2-4?
... sbryant6 made a comment on nbme22/block4/q#41 (A 65-year-old woman with a 20-year history of...)
... gh889 made a comment on nbme22/block4/q#42 (A 31-year-old man comes to the physician because of...)
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submitted by gh889(32)

answer is leading you to finasteride - 5alpha-reductase inhibitor for BPH and male patterned baldness - it blocks the conversion of testosterone into DHT

... pppro made a comment on nbme22/block4/q#43 (A 44-year-old man comes to the physician because of...)
 +2  upvote downvote
submitted by pppro(5)

IV drug abuse + R heart failure symptoms (congested liver): think tricuspid insufficiency

... mattnatomy made a comment on nbme22/block4/q#44 (A 10-year-old boy has bruised easily since...)
 +4  upvote downvote
submitted by mattnatomy(21)

You can basically think of Dicumarol as warfarin. MOA: Depletes vitamin K stores Since Vitamin K is involved in gamma carboxylation of factors 2, 7, 9, & 10, you can use the Prothrombin Time to measure the response. Prothrombin time measures the extrinsic pathway of coagulation, which is mainly mediated via Factor 7.

... seagull made a comment on nbme22/block4/q#44 (A 10-year-old boy has bruised easily since...)
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submitted by seagull(355)

If you don't know what Dicumarol does like any normal human. The focus on what aspirin doesn't do, namely it's doesn't affect PT time and most pills don't increase clotting (especially with aspirin). This is how I logic to the right answer.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT?
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets.
... zpatel made a comment on nbme22/block4/q#44 (A 10-year-old boy has bruised easily since...)
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submitted by zpatel(3)

Can anyone tell the effect of aspirin on a blood lab value (i.e PT,PTT,Fibrin product)?

... dr.xx made a comment on nbme22/block4/q#45 (An 1814-g (4-lb) male newborn is delivered in the...)
 +2  upvote downvote
submitted by dr.xx(35)

As part of embryonic development, the pancreas forms as two buds from the foregut, an embryonic tube that is a precursor to the gastrointestinal tract. It is therefore of endodermal origin.

https://en.wikipedia.org/wiki/Pancreas#Development

gh889  nice! I reasoned it as that most of the GI system is of endodermal origin
... sup made a comment on nbme22/block4/q#46 (A 39-year-old woman comes to the physician because...)
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submitted by sup(1)

Somehow I was able to convince myself that increased testosterone --> decreased estrogen --> decreased negative feedback on LH/FSH secretion --> increased FSH. Does anyone care to explain why this logic is wrong? Thanks :)

btl_nyc  The increased testosterone is metabolized by granulosa cells to estrogen and by adipose tissue into estrone. Both feed back on the hypothalamus to inhibit FSH & LH secretion, but FSH is much more sensitive to feedback inhibition than LH, causing an increased LH/FSH ratio.
impostersyndromel1000  @sup, i did the same thing. Had no idea testosterone and androgens can increase epo
... oznefu made a comment on nbme22/block4/q#46 (A 39-year-old woman comes to the physician because...)
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submitted by oznefu(7)

how do you narrow down that testosterone increased hemoglobin concentration? just a random fact to know? i put alkaline phosphatase because i figured increased testosterone will increase bone growth and ruled out prostate-specific antigen bc it’s a woman.

hysitron  I guessed this one cause men have a higher hemoglobin than women.
notadoctor  High levels of testosterone will result in amenorrhea. I guessed that since she's not menstruating she will not be losing blood and therefore hemoglobin. Therefore her hemoglobin levels will be higher than expected.
meningitis  It kinda makes sense knowing testosterone causes catabolism so I was in between Alkaline phosphatase and hemoglobin...
enbeemee  isn't testosterone anabolic?
... johnthurtjr made a comment on nbme22/block4/q#46 (A 39-year-old woman comes to the physician because...)
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submitted by johnthurtjr(43)

here's a google

johnthurtjr  FTR I had no idea this was a thing, and was pretty disappointed in myself when the google search had it in big bold letters right in my face.
drdoom  via @johnthurtjr link: "Testosterone and other androgens have an erythropoietic stimulating effect that can cause polycythemia, which manifests as an increase in hemoglobin, hematocrit, or red blood cell count." https://www.medscape.com/viewarticle/773465
meningitis  I guess that's another reason for steroids and doping up.
... johnthurtjr made a comment on nbme22/block4/q#46 (A 39-year-old woman comes to the physician because...)
... nwinkelmann made a comment on nbme22/block4/q#46 (A 39-year-old woman comes to the physician because...)
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submitted by nwinkelmann(60)

I interpreted the patient to have PCOS (hirsutism, amenorrhea, ovarian mass) though the super elevated testosterone is more concerning for ncer (per this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1069067/). If the patient has PCOS, she is likely obese and at higher risk for NAFLD which can be associated with elevated alkaline phosphatase, lipid accumulation, and elevated testosterone, but not DUE to androgenic effects ("serum androgen levels were not associated with the presence of NALFD. This is indirectly confirmed with our result on phenotypes. Namely, there is no difference in NAFLD prevalence between hyperandrogenic, and non-hyperandrogenic or reproductive PCOS phenotypes. NAFLD is considered a hepatic component of metabolic syndrome with a central pathogenic role of insulin resistance that also affects the hypothalamo-pituitary-ovarian axis in subjects with PCOS... Hyperandrogenic state may be due to insulin resistance." http://bit.ly/2FWKGjy).

Then, as said by @btl-nyc, elevated testosterone in a female is converted to estrogen and estrone and feedback inhibits the hypothalamus leading to decreased FHS and LH levels, but FSH is inhibited more, so there is an increased LH:FSH ratio.

Finally, regarding PSA (which does occur in women, who knew? lol), the correlation between testosterone and PSA in men is still pretty week (in this study, there was only a correlation and a weak one at that, after multivariate analysis adjusting for several things https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436005/) so there is definitely not a correlation in women. However, per this study (https://www.ncbi.nlm.nih.gov/pubmed/9062481/) there may be an association between certain androgens (not testosterone) and PSA in women.

... alexb made a comment on nbme22/block4/q#46 (A 39-year-old woman comes to the physician because...)
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submitted by alexb(10)

First Aid 2019 page 622 stimulatory growth effects of testosterone include red blood cells. I think they expect us to know this.

... rogeliogs made a comment on nbme22/block4/q#46 (A 39-year-old woman comes to the physician because...)
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submitted by rogeliogs(1)

My mind went this way: in Men Andropause = less testosterone = less bone density in Women more testosterone = more bone density = more alkaline phosphatase. Hemoglobin was my second option because I don't hear too much about anemia in post menopause or post andropause, but bonds density is a big deal there.

blah.

... bubbles made a comment on nbme22/block4/q#47 (A 56-year-old woman comes to the physician for a...)
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submitted by bubbles(26)

Basement membrane integrity is the determinant of full lung recovery following pulmonary insult.

Summary:

(1) loss of basement membrane integrity is critical in determining the “point of no return,” and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis;

(2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis;

(3) transforming growth factor-β is necessary, but not entirely sufficient, to promote permanent fibrosis;

(4) persistent injury/antigen/irritant is critical for the propagation of fibrosis;

(5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an “antigen(s),” chronic inflammation, and fibrosis; and

(6) unique cells are critical cellular players in the regulation of fibrosis.

citation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/

endochondral1  any FA or pathoma or uworld correlation?
endochondral1  or was this a random?
... drdoom made a comment on nbme22/block4/q#47 (A 56-year-old woman comes to the physician for a...)
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submitted by drdoom(166)

You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the normal architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be disorganized healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.)

drdoom  by "restorative" i mean healing which restores the previous (and normal) tissue architecture. for that to happen, you need an intact basement membrane!
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/
... shaydawn88 made a comment on nbme22/block4/q#47 (A 56-year-old woman comes to the physician for a...)
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submitted by shaydawn88(3)

I would think resolution involves the stem cells (type II pneumocytes). Is the intact basement membrane the answer because it limits spread?

aesalmon  I would also like to know if anyone can answer this question - I saw it as a Sattar "one day, one week, one month" kind of question. Its probably very simple but I still don't get it
bubbles  I posted a new comment explaining: basement membrane integrity is the strongest determinant of full fx recovery following pulmonary insult :)
drdoom  You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the *normal* architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be *disorganized* healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.)
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/
... ls3076 made a comment on nbme22/block4/q#47 (A 56-year-old woman comes to the physician for a...)
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submitted by ls3076(5)

can anyone explain why (D) metaplasia is incorrect?

angelaq11  because metaplasia would be a transformation of the normal architecture of the respiratory epithelium to one that does not belong there, in response to chronic irritation. This woman had pneumococcal pneumonia that was correctly (and I dare say promptly) treated, so she suffered an acute rather than a chronic insult.
... jotajota94 made a comment on nbme22/block4/q#48 (An 8-year-old boy is brought to the physician by his...)
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submitted by jotajota94(11)

I think the key to understanding this question is that the boy has above average height. Leptin stimulates the release of GH (https://www.ncbi.nlm.nih.gov/pubmed/12122085) Children with Cushing syndrome have short stature https://www.ncbi.nlm.nih.gov/pubmed/16675933) insulin inhibits GH secretion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC425166/) I think that both a high caloric diet in fats and glucose can make you fat so you can eliminate those answer choices.

... aesalmon made a comment on nbme22/block4/q#48 (An 8-year-old boy is brought to the physician by his...)
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submitted by aesalmon(33)

I feel dumb for asking but can someone explain this? If his parents are of close to normal BMI and are concerned about his weight why would they be allowing his calorie consumption to exceed his energy expenditure? ( AKA letting the kid eat too much and not exercise enough)

meningitis  That's a modern day mystery.
drdoom  The prompt is only asking "what's the likely cause of obesity?" It's not that they're "allowing" him to eat more than exercise. (Few parents can monitor their kids that closely!) The prompt is only asking what's the most likely explanation for his 95th percentile weight and BMI (given that he otherwise appears normal); in the United States, the most likely explanation is eating way more than you expend.
niboonsh  aka 'merica #firstworldproblems
... rogeliogs made a comment on nbme22/block4/q#48 (An 8-year-old boy is brought to the physician by his...)
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submitted by rogeliogs(1)

My approach to this question was more just focusing in the info they are giving. None of the other option makes sense because there is not evidence to talk about them. I was very tempted to pick the "decrease leptin production" but I remembered Dr Goljan saying "Think simple, think cheap, they are not trying to trick you." So, chubby parents = chubby kids.

... dr.xx made a comment on nbme22/block4/q#49 (A 52-year-old man with metastatic oat cell carcinoma...)
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submitted by dr.xx(35)

Medication dosages should be titrated promptly to achieve effective pain control.

https://www.aafp.org/afp/2000/0201/p755.html

... sweetmed made a comment on nbme22/block4/q#49 (A 52-year-old man with metastatic oat cell carcinoma...)
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submitted by sweetmed(28)

The patient is in hospice care. according to Conrad fischer ethics example, a man with COPD in hospice can be given high dose opiates even though there is a risk of respiratory depression becuase the intent to relieve suffering is the highest priority.

... seagull made a comment on nbme22/block4/q#50 (A 31-year-old woman in the second trimester of...)
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submitted by seagull(355)

This is an incomplete hydatidiform mole. They contain incomplete fetal parts including stem cells which are trisomy and give rise to unstructured tissue.

kard  Can someone explain why the other choices are incorrect?, Thanks
... nwinkelmann made a comment on nbme22/block4/q#50 (A 31-year-old woman in the second trimester of...)
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submitted by nwinkelmann(60)

I know that complete moles do not contain fetal tissue (i.e. only chorionic villus, cytotrophoblast, and syncyciotrophoblasts) and partial mole as fetal tissue, chorionic villus, cytotrophoblast, and syncyciotrophoblast. Obviously hematopoietic stem cells are fetal parts as they turn into blood cells, but what is the overall definition of fetal parts?

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