Huntington Disease is a neurological disorder characterized by a classic triad of choreiform movement (in this case the bilateral writhing motions of the upper extremities), dementia/depression, and behavioural changes (aliens).
Per UW, evaluation of fetal demise includes fetal autopsy, gross and microscopic examination of placenta, membranes, cord, and karyotype and genetic analysis. Evaluation of fetal demise on moms side includes kleihauer betke test for fetomaternal hemmorhage, antiphospholipid antibodies and coag studies.
Nobody has answered this question through the lens of a learning objective quite yet so here's my 2 cents: Km is INCREASED bc this patient has an enzyme with an overall LOWER affinity (can be corrected to normal after an increase in substrate) which is characteristic of COMPETITIVE inhibition, which is why the line of the pt. is one of competitive inhibition on a LB plot
This isn't the scenario in this question, but I was wondering what would happen if you had told the parents the diagnosis and they didn't want their child to know?
Alcohol withdrawal - - > increased catecholamines - - > increased insulin (via B2) - - > cellular uptake of K+ - - > hypokalemia
This question might be tricky because the mutation of interest here is inherited from the dad side (paternal) but affects the mitochondria.
That is, the mutation is not a mutation of the mitochondrial DNA.
In their explanation, the NBME says, “
Mitochondrial diseases are strictly inherited through the mother” but that is incorrect; it would be more correct for them to have said: Mitochondrial DNA mutations are strictly inherited through the mother.
In other words, the stem does not describe a "
mitochondrial disease" in the way the NBME defines it.
Yes, mitochondria are affected but the mutation is in nuclear DNA that govern the maintenance of "healthy mitochondria". The mutation affects the function and operation of mitochondria but the mutation itself is in the nuclear DNA (which control something about the "quality" of mitochondria but what exactly is not yet understood).
This explains why dad and dad's brother show the same “proximal muscle weakness of the lower extremities”.
Am I crazy, or does the question stem imply that this was inherited paternally?
Why couldn't this be branching enzyme impairment? They both cause cardiac symptoms (according to Amboss at least)
Both histoplasmosis and blastomycosis are associated with living in Ohio and can cause pulmonary disease. Histoplasmosis is more associated with hilar lymphadenopathy and can cause cavitations (recall from Sketchy that it can resemble Tb) - another association to note with Histo is hepatosplenomegaly. Blastomycosis is uniquely associated with extra-pulmonary involvement in the bone, prostate, and skin
I got this right because I thought of the cavernous sinus which has CN 3, CN4, CN V1 & V2. Out of all of all the options V2 is the only one that controls upper lip. For option C, pupillary reflex is controlled by CN 2 and 3, and if there is a fracture to the orbital floor the closest to the sinuses to be injured is CN5 (V2). Idk I could be wrong but if you guys agree let me know pls.
Mom and her daughter have the same sequence of FBN1. What is special is that compared to a “normal” (wild-type) FBN1, mom and daughter have one little tiny mutation in their sequence: a single nucleotide (A,T,G,C) that is different than most other folks.
(Interestingly, this nucleotide difference does not alter the amino acid encoded by this part of the gene; that makes Choice D (
change the folding of the protein) and Choice E (
truncated protein) very unlikely.)
Back to our question. Even though mom and daughter have the same mutation, mom shows no signs of Marfan syndrome; this eliminates Choice A (
disease-causing mutation in the patient and her mother).
You might think this is an example of variable expressivity (not an option but a good guess), and it might be.
In the stem they say:
The same nucleotide change is found in 15 of 200 individuals without Marfan syndrome.
Interesting! This means that in a “normal” sample of people (who have no signs of Marfan), 15 out of 200 still have this mutation.
(They don't say anything about how many Marfan people have the mutation but we don't need that information to answer the question.)
When a gene can be found in multiple “versions”, we call the gene polymorphic (literally,
So the best response is Choice B (
The graft is placed below the renal arteries and above the aortic bifurcation, which contains the IMA. IMA supplies the hindgut (distal 1/3 of transverse colon to to upper portion of the rectum).
FA 2019 pg. 357
So are we just not going to talk about how an NBME question writer just sketched this real quick and put it on a question
I always remember locus caeruleus as Marcus Aurelius (if anyone has seen the movie Gladiator) its about action and being hopped on up Nor epi would recommend
My two Leishmania questions were literally back to back lol
I don't believe this question is addressing hereditary angioedema (which is definitely a manifestation of C1-INH deficiency), but rather just overactive complement (since its inhibitor is deficient). Remember that byproducts of the complement cascade include C3a, C4a, and C5a, which are all anaphylatoxins. "Episodes of cutaneous urticaria and occasional episodes of laryngospasm" describes an allergic reaction that can be mediated by the anaphylatoxins produced in the cascade. The other answer choices would lead to decreased complement activity and therefore release of fewer anaphylatoxins.
can someone explain why it's not degranulation of eosinophils?
How would we rule out antithrombin deficiency?
So I thought about the "tombstone" picture on p.207 of Pathoma where the desmosomes are defective. The cells in the basal layer stay attached to the basement membrane, but the cells above get disconnected. So that made me think of breaking the connection between cells in the basal layer and cells above the basal layer (suprabasal).
honestly fuck them. increased direct should point you to another dx.
^ Important read, if you have the time.
Tacrolimus has the same MOA as cyclosporine
This question is describing what is literally called "Head Out Water Immersion." The pressure that the water exerts on the body is greater than the pressure that air exerts on the body. This hydrostatic pressure pushes the water in the limbs up into the central cavity (the rib cage protects from this hydrostatic pressure). Because there's more blood in the central cavity, the heart experiences an increase in volume. This is why you often need to pee more often when standing in the pool.
In summation: water pushes blood into center cavity -> increased blood volume in central cavity -> blood stretches heart -> increase in ANP
"clear-fluid-filled, tense blisters" and "subepthelial blister" with "autoantibodies" scream bullous pemphigoid, but I thought BP blisters were itchy>>painful. Contrast with pemphigus vulgaris in which pain>>itch.
This Q stem was confusing to me because I thought pain>>itch for shingles. Any thoughts?
"In addition to slightly decreased platelet count..." — why are plts slightly low in EBV infection/mono?
totally buy the answer of K+ being increased, but can somebody explain why her extreme dehydration (decreased skin turgor, excess urine output) wouldn't lead to an increase in serum [Na+]?
Pt shows classical signs of lack of platelet ADHESION. ADHESION is mediated by vWF. Platelet AGGREGATION studies test for AGGREGATION, which is mediated by fibrinogen, thus they have normal results on lab testing as they are not testing a pathway that uses vWF (very miniscule detail I know, very annoying).
Because it is a straight downward slope, you can also tell that Y and X are bound in similar ways by antibodies. What differentiates the two, then, isn't epitope binding capability, but the concentration. All else equal with binding sites, more Y with an unchanging amount of X will lead to less X bound, in a 1:1 manner.
Don't need to know this is FAP to get it right.
Father and Grandfather had it, so can assume an AD mutation in this patient. Assuming her partner is homozygous without the mutation, the risk of her AD train going to her child is 50%
Can anyone help explain what the other options would entail?
RIPE: Rifampin, Isoniazid (INH), Pyrazinamide, Ethanbutol.
RIPE treats TB.
Dirty Medicine has a great mnemonic to memorize these diseases:
Compression of the C5/C6 spinal nerves would mean the axillary nerve is compressed.
(Use the mnemonic: 5 Muskateers Assassinated 5 Rats 5 Mice, and 2 Unicorns; assassinated would be C5/C6 and axillary sounds like assassinated)
The axillary nerve innervates the deltoid muscle which abducts the upper extremity.
Bacterial vaginosis is also very common in women/people with vaginas who have sex with women/people with vaginas, and more common in that population vs gen pop.
One 2005 study of 12K vagina-owners found 45% prevalence in folx who'd had at least one partner with a vagina, vs 29% rest of study population.
(Sorry no link, just sharing from "Lesbian Health" by Dibble & Robertson.)
Hydronephrosis causes tubular atrophy from compression of the tubules by urine. Two common causes of hydronephrosis in infants and young children include pelvic-urethral obstruction and vesicourethral reflux.
Reflex erection--> somatic tactile stimuli to penis Can still happen if a spinal-cord transection occurs cranial to T10/T12.
Sympathetic--> psychogenetic erection Males with cord transections above T9 are unable to achieve psychogenic erections.
Anyone else jump to phenylephrine as a drug that would clear the sinus congestion and also happens to cause constipation? Just me... cool
Was it wrong to see blood tinged sputum, and automatically assume its cancer? since none of the others would have caused blood tinged sputum?
This probably has to do with Barr Bodies (FA 2021, pg 61). To paraphrase FA, penetrance and severity of diseases in XX individuals can be impacted. DMD is included in their list.
Due to its pink staining, I thought B was smooth muscle surrounding the corpus cavernosum. But I suppose that the cells composing the CC are contractile by themselves? And my assumption would make the penis a giant muscle — which it most certainly is not...
Pneumococcal conjugate vaccines are strongly immunogenic in infancy due to both B and T cell recruitment. They provide higher, longer-lasting antibody titers relative to pneumococcal polysaccharide vaccines. The pneumococcal polysaccharide vaccine is poorly immunogenic in infants due to their relatively immature humoral antibody response.
Why is the T normal in this patient? I would have predicted underlying infection — ie, fever — before even "early" septic shock. I selected septic shock purely for the intractable low SVR despite fluids but want to understand more about the absence of fever... Thanks!
The glomerular filtration rate (GFR) depends on the interplay of hydrostatic and oncotic pressures in the glomerular capillaries and Bowman's space. The GFR increases with higher glomerular hydrostatic pressure and decreases with increasing Bowman's capsule hydrostatic pressure or higher glomerular capillary oncotic pressure. Acute ureteral obstruction increases hydrostatic pressure proximal to the constriction. This pressure rise is transmitted back to the Bowman's space, resulting in decreased GFR.
• This patient with alcohol withdrawal most likely developed acute hypokalemia due to stress-related beta-adrenergic hyperactivity, which causes potassium to shift intracellularly. • Severe physiologic stress (eg, myocardial infarction, head injury) results in significant endogenous catecholamine (eg, norepinephrine, epinephrine) release. Epinephrine activates the beta-2 receptor, leading to increased activity of the sodium-potassium ATPase pump and the sodium-potassium-2-chloride cotransporter, both of which transport potassium intracellularly. Adrenergic activity also stimulates the release of insulin, which further promotes intracellular potassium shifting.
just as a general question, would there be low levels of 1 25-(OH)2 ?
I agree that Serum K decrease is the better answer, but wouldn't Urine K also decrease once blood sugar goes down with insulin treatment (i.e. osmotic diuresis would lessen)?
Case-fatality rate (CFR): Measure of the severity of a disease/condition. It is calculated as the # of fatal cases (deaths/mortality) from a disease divided by the # of cases (incidence) of the same disease.
CFR% = (Deaths/Cases) x 100
In this question: CFR% = (6/15) x 100 = 40%
No such thing as hypoallergenic dogs!!
The major dog allergen, Can f 1, is responsible for allergies in most people who are allergic to dogs. Hypoallergenic breeds of dogs were promoted because it was thought they would produce lower concentrations of Can f 1, and therefore cause less (or even no) allergic symptoms in people with a dog allergy. Examples of dog breeds that have previously been labeled as hypoallergenic include Poodles, Labradoodles, and Yorkshire terriers. There is no scientific proof these breeds truly produce lower amounts of Can f 1; these dogs were simply labeled as hypoallergenic because of the false assumption that dog breeds that do not shed hair must release less allergen.
(Nicholas CE, Wegienka GR, Havstad SL, Zoratti EM, Ownby DR, Johnson CC. Dog allergen levels in homes with hypoallergenic compared with nonhypoallergenic dogs. Am J Rhinol Allergy. 2011;25(4):252–256. doi:10.2500/ajra.2011.25.3606)
But i was thinking back and chest are protected by clothese and Scalp protected by hat or hair and Palm not much exposed. So I chose forehead.
No one talks about AR? That's much more unlikely in this case than XR
I think this question was asking about the anger that she expresses toward her family for not helping out more, which is really displacement of her stress related to caring for an ill child. The kickboxing is a second coping mechanism(Sublimation).
Diaphragmatic Hernia: Abdominal structures enter the thorax; may occur due to congenital defect of pleuroperitoneal membrane or from trauma. Commonly occurs on left side due to relative protection of right hemidiaphragm by liver.
FA 2020 p.370
Late or terminal complement deficiency (C5-C9): Increased susceptibility to recurrent Neisseria Bacteremia (in this px, cultures grow oxidase-positive, gram-negative diplococcus = Neisseria)
The crypts of Lieberkühn contain stem cells that replace enterocytes/goblet cells and Paneth cells. These are present all throughout the small and large intestine.
FA 2020 p. 362
I understand that feedback inhibition isn't working and is why ACTH is undetectable/low (and why there is no change after dexamethasone), but wouldn't cortisol levels increase after dexamethasone? Or does dexamethasone not count as cortisol when quantifying serum levels? pls help
It's stupid but it helps:
Bad boobs cut pulm
Breast, bladder, colon, prostate to lungs
The medial aspect of the primary motor cortex and the primary somatosensory cortex (this px has weakness and decreased sensation) is irrigated by the Anterior Cerebral Artery. According to the Homunculus, the medial aspect would affect the lower extremities.
So thromboxane A2 has two roles: Promote aggregation (from granule release) and cause vasoconstriction.
I'm thinking we'd see decreased adherence because you're inhibiting vasoconstriction and platelets would be less likely to adhere to vWF. The increased aggregation seen with TXA2 is due to the granule release, which then goes on to activate the platelets. So while you technically do decrease the activity of the GP2b3a receptors, it's from a decreased release of ADP and not from a direct inhibitor of the receptors.
Patients are allowed to let themselves die. You're just not allowed to kill anyone (murder).
All anticholesterol agents will upregulate the LDLR one way or another.
Hypersensitivity pneumonitis (inflammatory interstitial pneumonitis) is a hypersensitivity reaction following exposure to environmental allergens. It is associated with inflammatory interstitial lung disease. Chronic inflammatory pneumonitis leads to destruction of Type I pneumocytes, an increase in Type II pneumocytes to serve as progenitor cells to replace alveolar cells, and an increase in fibroblast proliferation.
This 36-year-old patient with protruding abdomen has fluid collection in the omental bursa (lesser sac) on CT imaging. The omental bursa (lesser sac) is the cavity in the abdomen that is formed by the lesser and greater omentum. It is connected with the greater sac via the omental foramen.
The omental bursa is a complex and important anatomical region. It serves as a barrier to block pathological processes, but it is also a channel for disease spread in the abdominal cavity. It is a large recess of the peritoneal cavity formed by a double-layered fold of serous peritoneum situated inferiorly to the liver, posteriorly to the lesser omentum and the stomach and anteriorly to the pancreas.
Under physiological conditions the omental bursa is poorly visualized, both because it is situated deeply in the abdomen and because the cavity is merely a potential one containing only a small amount of liquid, which acts as a lubricant. However, the omental bursa may become clearly visible in the presence of disease.
The pathological conditions of the omentum are varied, and findings may range from fluid collection to widespread infiltration. Ascites (regardless of the cause), pancreatic necrosis during and after acute pancreatitis, chronic pancreatitis, surgery involving the pancreas or trauma may cause peripancreatic fluid collections. The omental bursa may therefore present noninflammatory or inflammatory fluid collections in different phases, pancreatic pseudocysts and hematoma.
The patient is presenting with headache, myalgia, fatigue, sudden onset of high fever and chills, unilateral swollen and tender lymph nodes, and buboes containing malodorous pus discharge has the bubonic plague and must be treated with aminoglycosides which interfere with ribosomal assembly. The bubonic plague is caused by Yersinia pestis – a small facultative intracellular gram-negative bacilli. It is transmitted from rodents to fleas to humans. Reservoirs include rats, squirrels, and prairie dogs of the southwest US. The bubonic plague presents with hot, red swollen lymph nodes (especially in the inguinal regions), and skin hemorrhages with black discoloration.
Alternatively, this patient may be infected by Francisella tularensis – another small gram-negative coccobacillus that is facultative intracellular within macrophages. The organism enters at site of infection, then travels in macrophages to reticuloendothelial organs where it produces caseating granulomas. It is transmitted from wild animals to Dermacentor tick/deer flies to humans. Ulceroglandular Tularemia is one of the presentations and presents with black skin ulcer at the site on infection, swollen, red lymph nodes; all of which closely resembles the bubonic plague.
Both Francisella tularensis and Yersinia pestis infections can be treated with an aminoglycoside
But i was thinking TUMOR NECROSIS (factor, TNF).And fact that rapid growing tumor alwasy get necrosis due to deficient blood supply(eg. GBM). And Burkitt is definitely rapid growing(High ki-67) Please correct me thx
The key is when her legs up, Bp normal and symptoms free. In contast, When standing up(running), low Bp and syncope. And Low volume is surly the MMC. It's just so weird. "retrospective posture change"??
GLUT3 is in the brain/neurons. If there is glucose, the brain will be able to use it.
Only GLUT4 is insulin-dependent, seen in muscle and fat.
For those choosing puppies: Puppies, New pet-----Toxocara canis Pet feces(eg puppies)---Yersinia
FA2021 p276 "Thank the patient for being patient and apologize for any inconvenience. Stay away from efforts to explain the delay." So it's another ugly FA-copying Qs
Even i got it wrong, then searched google and got this from Harrison (FOBT has low sensitivity and better methods are now available for screening) : https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623689/all/COLORECTAL_CANCER - PREVENTION : Early detection of colon carcinoma may be facilitated by routine screening of stool for occult blood (Hemoccult II, ColonCare, Hemosure); however, sensitivity only ∼50% for carcinoma; specificity for tumor or polyp ∼25–40%. Newer tests (e.g., Cologard) incorporating detection of blood and mutated genes are more sensitive and specific. False positives for occult blood: ingestion of red meat, iron, aspirin; upper GI bleeding. False negatives: vitamin C ingestion, intermittent bleeding. Genetic testing is unaffected by these factors.
So, to rule OUT a disease (Sen-Out/snout), screening test should have high sensitivity. Vice versa, to rule IN a disease (Spec-In/specin), confirmatory test should have high specificity.
I still don't understand how we rule out NPV and PPV from the answers since we're specifically talking about the 'at-risk' population group only and these values are used for that itself.
COPII vesicles: RER to Golgi COPI vesicles: Golgi to RER Clathrin : Golgi to Cell Membrane
Great diagram to refer - https://ars.els-cdn.com/content/image/1-s2.0-S0092867410005660-fx1.jpg
If anybody wants to see roughly the names of diseases COPII mutation causes
Also I'm pretty sure that you're getting the referred pain from irritation of the genitofemoral nerve which is right next to the ureter. Correct me if I'm wrong.
Anyone else get this right because they get them so often from absolutely uncontrolled stress?
The key here is to know that desmosomes connect keratinocytes to other keratinocytes. Remember that in PV you get the "tombstone" look at the basement membrane.
I don't think they expect us to know all of these connections here, just where are desmosomes and where are hemidesmosomes.
Urethral injury: Occurs almost exclusively in males. Presents with blood at urethral meatus, hematuria, difficulty voiding. Urethral catheterization is relatively contraindicated. Anterior urethral injury—perineal straddle injury disruption of bulbar (spongy) urethra scrotal hematoma. If Buck fascia is torn, urine escapes into perineal space. Posterior urethral injury—pelvic fracture disruption at bulbomembranous junction, urine leakage into retropubic space and high-riding prostate. FA2021 page 651
Credits - Reddit : @Colden_Haulfield 7 months ago D. Multiple myeloma is due to plasma cell proliferation, which only have secretory antibodies and do not have membrane bound antibodies. An anti-idiotypic antibody would only bind the secreted antibodies by the plasma cells, but would not target the cell itself. Need to target the cell to kill it.
Best given on page 303 FA 2021, MUST SEE.
I got this right because of the presentation, but in two days this girl has used multiple tampons and multiple pads.... That would mean at the least one tampon and one pad per day, so no tampon in longer than 24 hours. Maybe she forgot about one from the first day.
Her mom has high CK because her X inactivation is likely imbalanced to have more mutated X expressed. But note that a high CK does not equal full-blown Duchennes. It's similar to Hemophilia--women can have increased bleeding but not full hemophilia because of this phenomenon.
Her mother has some Duchenne phenotype, but we could just as easily see no phenotype in a carrier.
Further, if this woman is a carrier, her child has a 25% chance of developing DMD (50% chance of a boy, 50% of the bad X).
This woman likely has a 50% chance of being a carrier, she doesn't have DMD based on her CK and age and gender.
Schistosoma: Liver and spleen enlargement ( A shows S mansoni egg with lateral spine), fibrosis, inflammation, portal hypertension Chronic infection with S haematobium (egg with terminal spine B ) can lead to squamous cell carcinoma of the bladder (painless hematuria) and pulmonary hypertension Snails are intermediate host; cercariae penetrate skin of humans in contact with contaminated fresh water (eg, swimming or bathing). Tx: Praziquantel FA2021 160
PCOS: Hyperinsulinemia and/or insulin resistance hypothesized to alter hypothalamic hormonal feedback responseLH:FSH,androgens (eg, testosterone) from theca interna cells,rate of follicular maturationunruptured follicles (cysts) + anovulation. Common cause offertility in females. Enlarged, bilateral cystic ovaries A ; presents with amenorrhea/oligomenorrhea, hirsutism, acne, fertility. Associated with obesity, acanthosis nigricans.risk of endometrial cancer 2° to unopposed estrogen from repeated anovulatory cycles. Treatment: cycle regulation via weight reduction (peripheral estrone formation), OCPs (prevent endometrial hyperplasia due to unopposed estrogen); clomiphene (ovulation induction); spironolactone, finasteride, flutamide to treat hirsutism. FA2021 669
Always specifically address what the patient is concerned with. Even if another option sounds nice, you can't just ignore what the patient says.
Most petroleum jelly today is used as an ingredient in skin lotions and cosmetics, providing various types of skin care and protection by minimizing friction or reducing moisture loss (from wiki)
This guy is having internal bleeding hemorrhoids secondary to cirrhosis of the liver. The path that internal hemorrhoids take is:
This cannot be superior mesenteric vein although it also drains to the portal vein by combining with the splenic vein. Back up of portal venous pressure is occurring here but it doesn't drain the anal canal which is where the bleeding is happening.
The inferior rectal vein hemorrhoid is called an external hemorrhoid and it usually causes painful bleeding below the dentate line. Internal hemorrhoids are present above the dentate line, and don't have somatic sensation so they are painless.
Lastly it is asking for where the "varicosities" or dilated veins are present specifically, and they are located in the superior rectal vein, not the inferior mesenteric vein.
Guys, there are two ways to go about this question:
You recognize this guy has familial hypertriglyceridemia.
You recognize that chylomicrons and VLDL are the only two triglyceride molecules in this entire list. This narrows it down to 1 answer, decreasing VLDL, because the other answer choice was to increase chylomicrons. Boom, this is one way of answering it.
You recognize that we give fibrates for hypertriglyceridemia. They have 1 MOA, which is to active peroxisome proliferator activator alpha, and that increases HDL levels, decreases VLDL levels, and upregulates Lipoprotein lipase. This also narrows it down to two options, increase in HDL and decrease in VLDL levels. Whats the function of HDL? it leads to CETP upregulation and decreases cholesterol levels. It isn't useful in the reduction of triglycerides. Boom, your answer is still decreasing VLDL.
There is literally a UW question on this, this young lady is having a panic attack, as a result she is hyperventilating and decreasing her PaCO2, leading to hypocapnia, this stimulates vasoconstriction-> decreased cerebral blood flow -> decrease in ICP.
I like to think that unless this is ADHD, Alcohol withdrawl, Schizophrenia, Bipolar, or Tourettes. You basically shove an SSRI down their throat. lololol
Chondrosarcoma occurs in the hip or axial skeleton. I'd imagine that it is specifically located in one region rather than multiple lesions throughout the vertebra. Thats why I ruled this out.
I ruled out osteosarcoma and ewing sarcoma based on age alone. These tumors are seen in 15-25 year olds, and the clinical manifestations don't match up.
Paget's disease has an elevated Alkaline phosphatase level, but there would definitely be a sclerotic phase of bone deposition, rather than multiple osteolytic lesions. Besides, on a clinical vignette they would talk about enlarging head size, CN 8 impingement, fractures, etc. Even if you did go this route, paget's disease causes osteosarcoma, not multiple lytic lesions.
This left me with metastatic carcinoma.
When you hear reverse transcriptase (RNA dependent DNA polymerase) you should immediately be thinking HIV or Hep. B. In this case, Hep B. isn't amongst the answer choices, it is a partially double stranded circular DNA virus, not a fully double stranded DNA virus.
This leaves HIV, single stranded positive sense RNA virus. Another clue is that this is causing encephalitis, which immediately clued me into HIV associated encephalitis with microglial proliferation. HIV has tropism in the CNS for macrophages (microglia). Hep B. infects hepatocytes, and I'm unaware that it can spread to the CNS at all.
FFiSHH Pee in the C (sea) Ferritin Fibrinogen Serum Amyloid A Procalcitonin CRP
FA2021 page 214
You rule out tiotropium and diphenhydramine because both are anticholinergics which would cause constipation folks. Diphenhydramine can be further ruled out because it's part of Beer's criteria of medications you don't give to the elderly, it can provoke delirium in this patient group.
Codeine and morphine are FULL opioid agonists and would cause constipation.
Dextromethorphan is a NMDA receptor antagonist and a weak opioid agonist. Yes you can give it for this patients cough and expect decreased risk for constipation, that doesn't mean it is completely risk free of constipation. But out of all the answer choices this one is the "best". That's why there's confusion over this in NBME 20.
5 days after px was treated with ciprofloxacin, they present with watery diarrhea and abdominal cramping, This is C. Difficile infection, often secondary to antibiotic use. It is diagnosed by PCR or antigen detection of one or both toxins in the stool.
FA 2018 pg. 138
Acute laryngotracheobronchitis also called croup. Caused by parainfluenza viruses. Virus membrane contains hemagglutinin (binds sialic acid and promotes viral entry) and neuraminidase (promotes progeny virion release) antigens. Results in a “seal-like” barking cough and inspiratory stridor. Narrowing of upper trachea and subglottis leads to characteristic steeple sign on x-ray. Severe croup can result in pulsus paradoxus 2° to upper airway obstruction. FA2020 page 170
E. coli isn't an inflammatory diarrhea, Shigella is (think back to the flames in the Sketchy video). That alone is enough to rule out E. coli from answer choices.
Atrophy: in tissue mass due toin size (cytoskeleton degradation via ubiquitin-proteasome pathway and autophagy;protein synthesis) and/or number of cells (apoptosis). Causes include disuse, denervation, loss of blood supply, loss of hormonal stimulation, poor nutrition. FA2020 page 206
AD tubulointerstitial kidney disease: Also called medullary cystic kidney disease. Causes tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; smaller kidneys on ultrasound. Poor prognosis. FA2020 page 602
Can someone explain why cardiac output is high in septic shock?
Heparin-induced thrombocytopenia (HIT) type 2—development of IgG antibodies against heparin-bound platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets thrombosis and thrombocytopenia. Highest risk with unfractionated heparin. HIT type 1 characterized by nonimmunologic milder drop in platelet count, usually asymptomatic. FA2020 page 436
Ureteropelvic junction (UPJ) obstruction is when part of the kidney is blocked. Most often it is blocked at the renal pelvis. This is where the kidney attaches to one of the ureters (the tubes that carry urine to the bladder). The blockage slows or stops the flow of urine out of the kidney. Urine can then build up and damage the kidney.