Diabetics get peripheral neuropathy from glucose damaging Schwann cells. For what I believe is an unconfirmed reason, T2DM patients tend to see parasympathetic autonomic neuropathy before sympathetic.
The hypogastric nerve carries sympathetic innervation to the posterior urethra and is responsible for ejaculation.
Inferior rectal nerve is a branch of the pudendal nerve that innervates the external anal sphincter and provides sensation below the pectinate line. A peripheral nerve problem with this nerve would cause the sphincter to remain relaxed and cause incontinence, not constipation.
Pelvic splanchnic nerves are parasympathetics (craniosacral outflow). If he is constipated, his rest and digest (parasympathetic) system is not working.
Perineal nerve is a branch of the pudendal nerve. It has both motor and sensory, is involved in the external anal sphincter, urethral sphincter, and is responsible for conscious sensation of the need to urinate.
Sacral sympathetic inhibits peristalsis, and contracts internal anal sphincter to maintain continence.
Another way to think of this: She has a strong family history, so we are thinking she probably does indeed have this mutation (probably a True Positive). Our fear, would be we do the wrong test and aberrantly tell her that she is in the clear (False Negative). Having a high False Negative would be deleterious to this patient, and plugging this into a 2x2 table gives a low sensitivity (TP/ TP +FN).
B: Distal to the vestibule → respiratory region/nasal airway proper pic
C: Inferior to the hiatus semilunaris → uncinate process pic
D: Posterior to the middle concha → sphenoid sinus pic
E: Proximal to the fusion of the hard and soft palate → horizontal plate (of palatine bone) pic
F: Superior to the superior concha → sphenoethmoidal recess pic
*I was really conflicted on what this could be referring to. Ultimately, I thought angular artery aligned the best with being anterior to the nasolacrimal duct, but I'm not 100% sure.
Breast cancers are one of the most common malignancies to be associated with hypercalcemia. Most often the hypercalcemia is due to osteolytic metastases and hence portends a bad prognosis. A significant number of the patients with breast cancers (up to 15%) show hypercalcemia in the absence of metastasis.
Hypercalcemia is relatively common in patients with cancer, occurring in approximately 20 to 30 percent of cases. It is the most common cause of hypercalcemia in the inpatient setting.
Beck's triad: muffled heart sounds, jugular vein distension, and electrical alternans. This patient has cardiac tamponade. The fluid has to be removed.
A pericardial window is a cardiac surgical procedure to create a window from the pericardial space to the pleural cavity. The purpose of the window is to allow a pericardial effusion (usually malignant) to drain from the space surrounding the heart into the chest cavity.
I'd seen a Question just like this one on Amboss and still managed to get this one wrong. So basically a ganglion on the VOLAR (palmar) surface of the wrist could potentially compress the structures within the carpal tunnel (i.e the median nerve, the flexor pollicis longus, the flexor digitorum profundus and superficialis tendons) and cause weakness/paresthesias if it kept growing. A DORSAL ganglion, on the other hand, is a lot less likely to compress on anything, and is more likely to remain asymptomatic and regress spontaneously. P.S. Carole did it.
To diagnose hypertension, there must be a hypertensive emergency >180/120, evidence of hypertension related end organ disease if greater than 160/100, or measurements in the office showing bp of greater than 130/80 at least three times. The measurements must be spaced over a period of weeks to months.
Osmotic diuresis caused by glucosuria is one of the most common causes of excessive renal salt and water loss.
In 85 percent of patients with latent TB, the chest radiograph is normal.
Bone marrow examination is generally not required for the initial evaluation in most cases of unexplained isolated thrombocytopenia in children. This child has pancytopenia and therefore requires a bone marrow aspiration.
Deficiency of calcium, magnesium, or phosphorus may be related to decreased intake, malabsorption, or renal losses. Calcium deficiency may also be secondary to magnesium or vitamin D deficiency. This patient's magnesium was low. Calcium, magnesium, and phosphorus levels should be checked in all patients with an alcohol use disorder or heavy alcohol use.
Retinal vein occlusion is the second most common cause of visual loss in older adults throughout the world. The first is diabetic retinopathy. Age, HTN, and diabetes are risk factors. This patient is a diabetic and the retinal veins are dilated (clear giveaway).
The pt presents with IBD sxs
sulfalazine= combo antibacterial and anti-inflammatory that is used in IBD and is assoc w/ orange discoloration of body fluids
The pt has sarcoidosis via the classic demographic association and the b/l hilar adenopathy
in sarcoid you get increased ACE and you also get hypercalcemia due to increased 1-alpha-hydroxylase (via acitvated macrophages) which leads to increased vitamin D
FA2020 pg 676
Inhalant intoxication= slurred speech, disturbed gait, drowsiness
Inhalant withdrawal= headaches and irritability
usually will present with rash around nose and mouth too
FA2020 pg 570
increased PTT + hemarthroses + easy bruising = Hempophillia A which is a deficiency of Factor 8 and is XL recessive (ie why the mom's brothers have it)
The prednisone will induce T cell apoptosis (FA2020 pg 120)
Holosystolic murmur--> think mitral or tricuspid regurg Based on the location (APTM) the murmur is heard over the "T" area
furthermore, murmurs that increase in intensity upon inspiration due to increased venous return to the RH are RIGHT SIDED
FA pg 290 and 291
Asplenic and sickle cell pts are susceptible to encapsulated organisms such as strep pneumo.
Knight is holding the sickle in the sketchy!
FA 2020 pg 425
Porphyria cutanea tarda-- defect in UROD in the heme synthesis pathway that causes photosensitivity and blistering
late onset CAH w/ 21 hydroxylase defiency--> excess androgens (increased facial hair and irregular menses, etc), salt wasting (low BP), increased 17-hydroxyprogesterone is key
11B problem= HTN and excess androgens 17a problem= HTN and decreased androgens 5a reductase converts testosterone to DHT 3B-hydroxysteroid dehydrogenase is involved in steroid synthesis earlier in the pathway
First aid 2020 pg 511-- brain lesion in the subthalamic nucleus = contralateral hemiballismus
Of all the things they can test us on, they're testing our fucking Gadar??
Great figure with all the lysosomal storage diseases!
A= Caudate ( flanks Lateral Ventricle) B= Internal Capsule, between Thalamus and Lentiform Nucleus( Putamen, GP) C= Thalamus( Flanks 3rd Ventricle D= Temporal Lobe E= Occipital Lobe
To get bilateral hydroureter/hydronephrosis there needs to be an obstructive mass of some type at the level of the bladder or FURTHER downstream. Cervical CA is the only reasonable option of those listed (highly unlikely to have bilateral CA in the others)
So we already know the answer is either 11- or 21- Betahydroxylase. How to determine which one?
Question stem cells "dry mucous membranes". He is dehydrated.
We already know that he can't make aldosterone since the lack of either of these enzymes would block that pathway. However, if he is able to make a molecule that ACTS like aldosterone, he would not have dry mucus membranes. He could save water.
Do we have such a molecule? YES! 11-deoxycorticosterone.
Now, if he has 11-beta hydroxylase deficiency, there would be a buildup of 11-deoxycorticosterone. Hence, it has to be the other option.
Petrolatum is a compound found in sunscreen.
He started working outdoors AKA getting sunburns (if left unprotected, lower lips are one of the prime locations where people can develop squamous cell cancer later on). He should really use sunscreen, which is a barrier (absorbs the UV rays so the skin does not-- rather than deflecting the sun rays.)
It doesn't matter which potassium-sparing diuretic you use. You can still get to this answer. Aldosterone normally upregulates Na/K ATPase in the principal cells of the CD, decreased Na+ intracellularly, which leads to increased ENaC activity. Spironolactone/eplerenone will inhibit this upregulation of ENaC, leading to decreased permeability to Na+ in the CD.
Obv amiloride and triamterene will block principal cell ENaC. It's all in the same class so they will all lead to this effect :)
FA 2019 pg 573
Anybody know why fatty acid degradation doesn't play a role?
So I think where I got tripped up is that she does, indeed, have multiple myeloma (so there will be increased serum IgG), but the thing that is actually causing her bones to show the osteoclastic lesions shown in the image is IL-1 (osteoclast activating factor). Weird wording. Thanks NBME.
Amniotic fluid phospholipid analysis is used for testing fetal lung maturity via measuring surfactant production.
Fetal echocardiography would reveal any congenital heart defects if present, but would not be diagnostic of Downs syndrome
Fetal ultrasound First-trimester ultrasound commonly shows increased nuchal translucency and hypoplastic nasal bone. But I feel this is used more commonly in older women who might have chromosomal dysgenesis as the cause of downs syndrome
Fetal biopsy Pretty invasive technique, when we have a lesser invasive and more specific test available.
The subcutaneous tissue is highly vascularized and has larger blood vessels than the dermis, leading to a higher risk of metastasis and worse prognosis (TNM staging system)
Oxygen can compete CO to bind Hb but i think not all CO-Hb can be removed. Notice " ALL" the C0-binding RBC so go with CO-Hb RBC die. though i spent a lot of time for this question too
Can someone clarify why Prostacyclin was wrong? I knew the CHALK thing but for some reason had trouble ruling out prostacyclin since it's a vasodilator
Wouldn't chronic alcoholism also reduce available NAD and thus inhibit pyruvate decarboxylation by PDH?
You're just going to diss the son like that right in front of him?
all fine and dandy except bicarbonate isn't constant with flow rate
They love picking these cases right on the border. Just barely outside of that sexually active age range
this is clearly another one of those trap questions for overthinkers
This is where the hernia begins but ultimately where it bulges out varies depending on how far down the inguinal canal the hernia goes. It could pop out well below the inguinal ligament. The wording is crap, they should have just shown a picture of the patient.
The incorrect labeling of the gross pecimen makes this question a bona fide piece of garbage.
You should find out whether or not she wants her parents to know first
I ruled out most of them because of no evidence of person-to-person transmission and only people with pre-existing conditions were affected. The rest would probably also affect children or other attendees or spread to others in the nursing home.
Looked this up. Starvation causes GH resistance. Never heard of this, unfortunately fell into the trap of thinking increased GH would increase IGF-1. Punished for overthinking.
I don't think you're going to find any evidence for this one. It's just the test-writers' opinion
this question was utter BS, but the way I justified "same epitopes" was that it said "in the context of anti-serum X," i.e., which epitopes would have been developed in the context of the antibodies present. It's unlikely that anti-X antibodies would bind to epitopes on Y that aren't on X. But you could argue there are theoretical epitopes on Y that could be bound by another antibody that doesn't exist in this scenario.
Very drawn out and took me 5 minutes to actually figure out on the test, honestly a waste of time in my opinion, but there you go.
Couldn't the answer also be IL-2? Why can't you use cyclosporine in this patient with RA?
Drugs that act on microtubules may be remembered with the mnemonic "Microtubules Get Constructed Very Poorly":
M: Mebendazole (antihelminthic)
G: Griseofulvin (antifungal)
C: Colchicine (antigout)
V: Vincristine/Vinblastine (anticancer)
P: Palcitaxel (anticancer)
I thought that the cognitive impairment could be the manifestation of neurosyphilis. In addition, the doctor should talk directly to the patient to check for sexual abuse.
The patient asks about the most effective treatment. FA 2019 page 642: Copper IUD = long-acting reversible contraception, most effective emergency contraception. Although FA refers to emergency situations, maybe the word most effective is the clue.
about 70% of the circulating thyroid is bound to thyroid-binding globulin (tbg). the remainder of the bound protein is attached to thyroxine-binding prealbumin (transthyretin) and albumin. Large variations in tbg do not normally affect the free form. a rare congenital deficiency or excess of tbg drastically alters the bound fraction but because the free fraction is normal, the individuals are all euthyroid.
I was stuck on this one for a long time but maybe my super round about way will help someone?
you know this person has chronic bronchitis (especially cause they have cyanosis which is blue bloater vs pink puffer of emphysema). The distinguishment of pink vs blue is b/c in emphysema you have destruction of both the alveoli with the associated vasculature. Therefore there is no V/Q mismatch (pink). But in chronic bronchitis the damage is further up from the alveoli. All the other answers were in the alveoli so that's how I chose pseudostratified columnar epithelial cells.
Or maybe i'm just dum as hell and this level of overthinking is why i'm losing points on other questions
Damn everyone out here looking at the eyes when my dumbass was thinking the girl was missing a nasal bridge or something lol fml
For people who generally had trouble reading the two charts:
First chart: We separated the entire population into two smaller populations to test for the cookies affect. In Population A (drank milk) there was an odds ratio of 6 (typo in the actual chart). In Population B (did not drink milk) there was an odds ratio of 6. Since the odds ratios are not 1, we can conclude that the cookies have an effect regardless of the population (ie drank milk people versus didn't drink milk people).
Second chart: New set of populations to test for the effect of milk. In Population C (ate cookies) there was an odds ratio of 1. In Population D (did not eat cookies) there was also an odds ratio of 1. This means that milk did not have an effect ever and didn't contribute to the disease.
"Only cookies are independently associated with E. coli cases" means that only the cookies cause the disease without the effects of something else.
The pedigree presents us with Male-to-Male transmission. There are two modes of inheritance where Male-to-Male transmission is impossible: 1) X-linked recessive 2) Mitochondrial inheritance
Formation of granulation tissue (Day 3-7 of healing): Fibroplasia leads to the synthesis and deposition of type III collagen. Growth factors (ie- VEGF) from fibroblasts and epithelial cells promote angiogenesis. (Credit- Amboss)
Mixed up cytoscopy with culposcopy so I put HPV. Insert upsidedownsmileyface.jpg
I think something not mentioned yet is the fact that odds ratio can be used to estimate relative risk in RARE diseases as per the Rare Disease Assumption (where disease prevalence is <10%). Although the cancer in this question is described as "common," (common relative to other cancers), the cancer is still probably rare overall.
This question is not good. The math is simple, sure. But the PDA (which is most of the time a branch of the RIGHT coronary artery) supplies 2/3 posterior walls of the ventricles (FA 2019 p.281) which I'm sure is a significant portion of the left ventricle. The LAD specifically does not account for the entirety of the oxygen supply to the left ventricle, but about 45-55% according to wiki. If the question asked, "How much oxygen is delivered to the left ventricle by the LAD" it would have been acceptable.
https://www.youtube.com/watch?v=VsMw7DwwSPU This video explains it really well!
Anyone else got thrown off by their use of HNPCC rather than Lynch syndrome?
How come melanocytes:basal keratinocytes don't also have a desmosomal connection (in addition to their E-cadherin link)?
So I hate this question because you can't tell what the parent's genotypes are. This enzyme defect isn't something that you can tell photogenically so we can't just assume the parents are heterogeneous.
It honestly does't even matter if it is autosomal recessive or not since we only have to worry about homozygous off springs. Here is the math.
Parents possible genotypes:
A - Normal; a - abnormal.
Mom: Aa Dad: Aa (what the question is assuming)
Mom: Aa Dad: aa
Mom: aa Dad: Aa
Mom: aa Dad: aa (who is to say this isn't possible?)
(Mom AA or Dad AA is impossible since the offspring can't be aa)
From those genotype possibilities we can calculate better probabilities.
Since it's possible for parents to have any of these 4 genotypes we just assume that each possibility is 1/4.
Mom: Aa + Dad: Aa -> offspring aa = 1/4 (multiply this by 1/4 since we're assuming equal possibility for other genotypes) -> 1/16
Mom: aa + Dad: Aa -> offspring aa = 1/2 -> 1/2*1/4 = 1/8
Mom: Aa + Dad: aa -> offspring aa = 1/2 -> 1/2*1/4 = 1/8
Mom: aa + Dad: aa -> offspring aa = 1 -> 1*1/4 = 1/4
Then we add all the probabilities together 1/16 + 1/8 + 1/8 + 1/4 = 9/16
I know the question's answer is 25%... so I guess put 25% on the test. BUT if you want to actually understand, this is a better approximation. The only problem is we don't know the gene distribution of the alleles or I can give better math :P
Sorry it's long and confusing
I think one giveaway in this question for Adenovirus versus Coxsackie virus is the shortness of breath when lying down (orthopnea). That can be a sign of dilated cardiomyopathy, which is most common after viral myocarditis with Coxsackie B infection (as per Sketchy).
The question stem describes that the drug is "newly marketed", so it's likely in Phase IV drug trials.
From FA 2019 pg. 256, Phase IV = "Postmarketing surveillance of patients after treatment is approved." Phase IV is for detecting rare side effects that weren't picked up during the smaller clinical trials or long-term effects. Phase IV determines if the drug can stay on the market.
The drug is approved and is appropriate to use in patients without side effects, but the drug is still being monitored by the FDA so any new, previously unreported side effects need to be filed with the FDA.
I would like to include here that it can not be B (Decreased leptin production) because leptin levels increase in obesity. Leptin is secreted by adipocytes, which become significant in obesity. High levels of leptin may also desensitize the satiety centers in the hypothalamus, which is why many obese people have trouble limiting their food intake.
Aldo is primarily regulated by ATII. Cortisol is primarily regulated by ACTH. However, since cortisol can also activate aldo secondarily, it works. However, I believe that ADH should not have been answer choice however since no lung biopsy findings were reported so we can't really distinguish between SCC vs. NSCLC
Pyridostigmine is an acetylcholineserase inhibitor used long term for MG (Sketchy). Put pyridostigmine as my answer because it does treat MS. But yes baclofen is a classic anti-spasm drug.
Can't histamine also cause swelling or is it just not involved in the pathology of gout?
strawberry hemangioma: capillary hemangioma consist on thin walled blood vessels filled with blood and separated by conective tissue. cavernous hemangioma: LARGE dilated vascular spaces this is the difference
to me, this is a process of elimination question.
Fasciotomy and bosentan don't make sense.
Clopidogrel and aspirin kinda make sense, Except Treatment of DVT is not part of their clinical use. (Clopidogrel 429 and aspirin 475 of FA 2019).
So we're left w Embolectomy.
PS. Thrombolytics and Direct Factor Xa inhibitors are used for DVT
Renin concentration will be increased because feedback mechanism of renin release is due to angiotensis II (Ang II) on angiotensin type 1 receptor (AR1). That is, Ang II acting on AR1 will cause a negative feedback on the RAAS pathway. Since AR1 is blocked by ARB, this negative feedback is no longer active, triggering an increase in renin and increasing Ang II production (correct answer). Blocking AR1 will inhibit downstream actions (release of aldosterone and Ang II-mediated increase in sympathetic activation, triggering norepinephrine). Therefore, aldosterone and norepinephrine will be reduced.
theres a uworld question like this ... ,, rivoraxaban and other factor Xa inhibitors prolong pt and aPTT but they dont affect thrombin time ... while direct thrombin inhibitors prolong PT aPTT and Thrombin time , also unfractionated heparin prolongs aPTT and Thrombin Time (Theoreticallly it should prolong PT too but in the test the PT reagent contains heparin neutralizers that minimize this effect ) . sorry if this veered off course a little
Per boards and beyond, in the lateral pons is there is the spinal V nucleus which carries contralateral pain and temperature. Knowing that + CN V arises it in the pons, I went with pons. The only other option I had left not crossed out was cerebral hemisphere but that seemed to broad.
Calcium is low while PTH is high. It’s primary hyperparathyroidism (not secondary). Ans is branch of IJV.
The inferior thyroid artery (branch of the thyrocervical trunk) irrigates the posterior thyroid, including the parathyroid hormones.
Any good material for this and lymph node drainage in general? Is this common knowledge or low yield stuff?
confused why this is not autonomic dysfunction or hyponatremia due to sweating and why is this orthostatic hypotension?
Myeloperoxidase is the only one actually involved in making free radicals. Catalase makes H2O2 into water, Superoxide dismutase eliminates oxygen radicals, LDH makes lactate (no role in bacterial killing), and NO synthase, makes NO.
No need for MUDPILES here. Bad kidneys = Can't reabsorb HCO3 "base" > Metabolic Acidosis. Compensation is Resp Alkalosis. Based on that: PH less than 7.4 HCO3 Less than 24 Pco2 less than 40 Only answer is A
Perifollicular hyperkeratosis and hemorrhage are seen with corkscrew hairs, that juicy buzz word for Vit. C deficiency. Hydroxylation of proline in collagen synthesis cannot occur without vitamin c
not sure if this is right but the way I thought about it was that after family a surrogate decision maker can be a close friend and the neighbor has cooking for him and running errands for the last 5 years since his wife died so I believe that the close friend surrogate designation may apply
Fragile X syndrome X-linked dominant inheritance. Trinucleotide repeat in FMR1 gene = hypermethylation = Increased expression.
Most common inherited cause of intellectual disability (Down syndrome is the most common genetic cause, but most cases occur sporadically).
Findings: post-pubertal macroorchidism (enlarged testes), long face with a large jaw, large everted ears, autism, mitral valve prolapse, hypermobile joints.
Trinucleotide repeat expansion [(CGG) n ] occurs during oogenesis.
Larva currens (Latin for racing larva) is an itchy, cutaneous condition caused by infections with Strongyloides stercoralis. It is caused by the intradermal migration of strongyloides and distinguished from cutaneous larva migrans (caused by hookworms Ancylostoma and Necator) by its rapid migration, perianal involvement and wide band of urticaria.
HHV8 belongs to Herpesviridae family. Is it true that all members of this family have multinucleate cell with intranuclear inclusion body? HSV and VZV(cowry type A inclusion), EBV and CMV(owl-eye internuclear inclusion) certainly have them. Did anyone pick E for this reason?
From the UW ID 666 explanation, although type II pneumocytes normally differentiate into type I pneumocytes after proliferation, they do not differentiate in idiopathic pulmonary fibrosis due to altered cell signals and altered basement membrane, which is why type II pneumocytes are increased.
explanation by @benwhite_dotcom is incorrect
If you are making fatty acid, you should not burn it simultaneously.
Men generally have a higher RBC mass (hematocrit, hemoglobin, etc) and it is thought to be attributed to higher testosterone levels. She has high testosterone so you can assume the same for her. This is in Zanki, so it must be in FA or Pathoma.
Why high PTH 200pg/ml (normal <60)? it should be primary hypoparathyroidism!
reaction formation "in psychoanalytic theory, a defense mechanism in which unacceptable or threatening unconscious impulses are denied and are replaced in consciousness with their opposite. For example, to conceal an unconscious prejudice, an individual may preach tolerance [...]"
"The drainage pathways are as follows: (a) upper rectum: through the superior rectal nodes to the inferior mesenteric nodes, (b) lower rectum: from the lower rectum through the middle rectal nodes to the internal iliac nodes, and (c) anal canal: through the mesorectal (also known as inferior rectal) nodes to the inguinal and femoral nodes."
A mnemonic I use:cohoRt - R for risk case serIes - I for intervention case contrOl - O for outcome
"Cohort study A study in which a defined group of people (the cohort) is followed over time, to examine associations between different interventions received and subsequent outcomes.
Case series Observations are made on a series of individuals, usually all receiving the same intervention, before and after an intervention but with no control group."
Case control "[...] an outcome of interest is first defined and then subjects are selected with (cases) and without (controls) the designated outcome. The investigator then looks back in time to compare the two groups for a risk factor or other exposure or treatment of interest. Therefore, the case-control study design is inherently retrospective."
In cellular ischemia, the Na+/K+ ATPase pump stops working due to decreased ATP levels. Consequently, sodium is not pumped out and potassium is not pumped into the cell, leading to an accumulation of sodium in the cell and potassium outside the cell. Furthermore, the sarcoplasmic reticulum Ca-ATPase pump fails, which leads to an increase in calcium in the cell.
Bottom line, ischemic tissue: there is a buildup of sodium and calcium in the cell.
Pathoma gives the three major causes of galactorrhea as nipple stimulation, prolactinoma of anterior pituitary, and drugs (see 16.1 - Breast Pathology). Only drug effect is an answer choice for this question.
To put another way - before you try to go through every answer choice, asking yourself "would this cause galactorrhea?" Instead, ask yourself, "What are the causes of galactorrhea?" According to Dr. Sattar, they are "nipple stimulation, prolactinoma of anterior pituitary, and drugs."
The question doesn't say anything that would point you toward nipple stimulation, like "it only seems to appear when she puts on a shirt/plays sports/runs/etc."† So you can rule out nipple stimulation.
It also makes no mention of bitemporal blindness (which would point you to an anterior pituitary tumor), so you can rule out prolactinoma. The only option left is drug effect.
†I've never seen anything like this on a question but I assume the NBME would word it in some convoluted way like that.
I initially wrote this as a subcomment, but I feel like it deserves its own comment. I was never really satisfied with any of the explanations for this problem, and I finally arrived at one that makes the most sense to me.
In India, our nurses are smart enough to perform PV and even to deliver the neonate!!!
I am crying due to my 60usd loss!!!!