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 +2  (free120#19)

Subacute combined degeneration never produces exagerated reflexes. It's one of the causes of babinski + with absent ankle reflex.


 +0  (nbme24#5)

Just adding on- Xray of large muscle groups would help in diagnosis of cysticercosis since cysts are calcified, in trichinella they are not. I think i'm the only one who got this wrong :/


 +0  (nbme24#42)

IRT is measured in routine heel-prick blood taken for biochemical screening of all newborn infants born in the UK. This test is one of a number of completed in newborn screening (the "Guthrie Test"). In Australia it is known 94% of those with eventual diagnosis of CF have a positive IRT on newborn screen. Samples with a raised IRT (defined as highest 1% of values) are then screened for common CF gene mutations. Each centre has a slightly different gene panel; currently 40-50 of the most common genes are sequenced. However, there are more than 2000 known mutations, so gene panel testing does miss occasional CF patients

If gene testing finds one mutation they will then have a sweat test to help confirm the diagnosis. Sweat testing is more likely to be equivocal in infants and typically not attempted in those under 5kg. If sweat test is positive more expansive gene testing is considered. If two mutations are found they are diagnosed with CF.

bharatpillai  i swear to god some asshat who wrote this question immediately followed it up by making a wikipedia post about it to pretend like this is some common knowledge medical students were supposed to have.

 +0  (nbme24#6)

One way to look at this would be to go back to pathogenesis of fatty streaks. They are most commonly found at the aortic bifurcation, so basically the lower down you go down the abdominal aorta, more turbulent the flow, causing higher potential for atherosclerosis and stenosis of branch vessels. Also, renal artery stenosis is well described which is given off after the celiac trunk so safe to say celiac trunk is spared in any kind of atherosclerotic stenosis.


 +0  (nbme21#24)

am i the only one who chose mesothelioma? didnt that look like a pleural plaque posteriorly to anyone?

brotherimodu  That's what I thought too.




Subcomments ...

While E coli is normal gut flora, your body would prefer it stay intraluminal.

tallerthanmymom  Just remember that E.Coli and Bacteriodes Fragilis (sp?) are the 2 main gutys that cause intraperitoneal infections from the gut. +2  
bharatpillai  Why not citrobacter though? +  


IRT is measured in routine heel-prick blood taken for biochemical screening of all newborn infants born in the UK. This test is one of a number of completed in newborn screening (the "Guthrie Test"). In Australia it is known 94% of those with eventual diagnosis of CF have a positive IRT on newborn screen. Samples with a raised IRT (defined as highest 1% of values) are then screened for common CF gene mutations. Each centre has a slightly different gene panel; currently 40-50 of the most common genes are sequenced. However, there are more than 2000 known mutations, so gene panel testing does miss occasional CF patients

If gene testing finds one mutation they will then have a sweat test to help confirm the diagnosis. Sweat testing is more likely to be equivocal in infants and typically not attempted in those under 5kg. If sweat test is positive more expansive gene testing is considered. If two mutations are found they are diagnosed with CF.

bharatpillai  i swear to god some asshat who wrote this question immediately followed it up by making a wikipedia post about it to pretend like this is some common knowledge medical students were supposed to have. +  


submitted by hopsalong(15),

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! +2  
hyperfukus  yasss +  
dubywow  "occasionally writhes in pain" -- as a guy who has had a kidney stone, writhing in pain definitely hits the mark. Picture yourself knees on the ground, face on the couch, screaming incoherently while the paramedics are there because you can't control your own body movement and don't know if you're dying or whatnot from the canonball sized hole that (may or may not be) in your flank. Then imagine one of the paramedics is your premed study buddy. Never forget writhing and nephrolithiasis and premed study buddies. You will forever get this question correct in the future. +2  
bharatpillai  i swear to god ive done a similar question on the usmlerx qb and they answer was renal papillary necrosis. which is why i got it wrong :( +  
targetmle  i also remember that uw ques which got me this ques wrong. i think in that ques,patient sibling or he himself had sickle cell +  


submitted by qfever(13),

Pathoma 2018 edition page 4 chapter 1 - Cellular Injury - III. Reversible & irreversible cellular injury - B.1.

I had difficulty trying to figure out what hydropic change means though...

bharatpillai  i swear i've done the same question before on uworld/ one of the previous NBMEs and the answer to that was intracellular Ca accumulation. +  


submitted by celeste(49),

Sounds like a hypertrophic scar. "Hypertrophic scars contain primarily type III collagen oriented parallel to the epidermal surface with abundant nodules containing myofibroblasts, large extracellular collagen filaments and plentiful acidic mucopolysaccharides." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022978/

johnthurtjr  I think it may actually be a keloid, not a hypertrophic scar, as it expands beyond the borders of the original incision. +2  
thepacksurvives  I believe this is a keloid; a hypertrophic scar does not extend past the borders of it's original incision, while a keloid does. regardless, the answer to this question is the same :) +  
breis  First AID pg 219 Scar formation: Hypertrophic vs. Keloid +  
charcot_bouchard  They give granulation tissue is a option which is type 3 collagen. so if it was hypertrophic scar it would be ap problem since its only excessive growth of Type 3. while keloid is excessive growth of both 1 and 3 +3  
bharatpillai  I literally ruled put collagen synthesis defect since this is not a collagen synthesis defect at all ( EDS, Scurvy) :/ hate these kind of questions +  


submitted by mbourne(18),

I think that if they had something like "statin therapy" as an answer choice, we would have an argument for that as it would decrease mortality by helping prevent ANOTHER heart attack. However, I think that anti-depressant therapy will do a LOT to prevent suicide, while omega-3 fatty acids (healthy as they are) wouldn't do AS MUCH to prevent a heart attack.

The question is basically asking, "You can only prescribe one of these to keep this dude alive as long as possible. Which one will have the best chance at accomplishing that?"

Therefore, the answer should be anti-depressant therapy.

bharatpillai  why antidepressant therapy though? there are not enough features given to suggest MDD. He's 56 years old, not an elderly single male so not at the highest "classical" population at risk of suicide? the question is so ambiguous... Given MI, wouldn't chronic alcoholic intake predispose him to dilated cardiomyopathy? +  
neovanilla  I don't believe it's that he has MDD by the clinical definition. It's more that his QoL has probably changed drastically since the MI and MIs are strongly associated with decreased outlook on life, especially considering how common it is to get a second MI soon after the first. I don't know the stats on suicide post-MI, but helping the patient's depression to make him more pro-active to help himself prevent another MI would be better than "a diet high in omega 3 FAs" (at least, this was my justification, as mbourne was saying) +  
drzed  First sentence of the stem: he has a 6-week history (e.g. >2 weeks) of depression (1), difficulty sleeping (2), fatigue (3), decreased appetite (4), and poor memory/concentration (5) For a diagnosis of MDD, you need a 2 week history of 5 of the SIGECAPS symptoms which he meets (he is only missing suicidal ideation and interest in activities). Thus he meets the diagnostic criteria for a major depressive episode, which means that treatment is indicated with an SSRI. +  


What makes this coxsackie virus over Adenovirus? Both cause myocarditis which would be seen on autopsy? Is it just more common to get coxsackie?

drdoom  the general consensus appears to be that Coxsackie is more common than Adenovirus, but i haven’t come across any papers or textbooks that would agree (they only mention “Coxsackie” and “Adenovirus” as associations with myocarditis) +1  
bharatpillai  there specifically is a question on uworld in which a young woman gets viral myocarditis with sore throat and the answer to that is adenovirus. i think thats why many people (including me) got it wrong :( +  


submitted by usmle11a(36),

legionella : very common in advanced age, COPD, immunosuppressed patients and " going back from a residence hall" which probably had a contaminated AX system (basically fits every one in the Q)

adeno X : would present with conjunctivitis, throat pain ... flu virus: not everyone got the disease RSV: no children strep pneumo: would target a larger population of healthy people as well.

bharatpillai  why would they say that the only people who didnt get affected by the disease were people on steroids (lupus nephritis and severe asthma) couldnt have been rsv since it causes croup in children. strep pneumo would cause fever and other systemic signs. i went for adenovirus because uworld says most common causes of copd excacerbation are viral infections... +1  
brbwhat  I went for adeno forr the same reason. I guess the MAIN HINT is that this is not a copd exacerbation. Since people without prexesting copd also had pneumonia, also people with copd exacerbation will have different presenting symptoms, here it was told, that we are told that dx was penumonia. People with copd exacerbation wouldn’t be diagnosed with pneumonia if it was an adenovirus infections. +1  


submitted by hayayah(603),

Notice, the stem says "precorsors in the skin"

D3 (cholecalciferol) from exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants.

D2 (ergocalciferol) from ingestion of plants, fungi, yeasts.

Both converted to 25-OH D3 (storage form) in liver and to the active form 1,25-(OH)2 D3 (calcitriol) in kidney.

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +2  
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +3  
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +2  
bharatpillai  7 dehydrocholesterol +2  
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +1  
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +  
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +  


submitted by hayayah(603),

Notice, the stem says "precorsors in the skin"

D3 (cholecalciferol) from exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants.

D2 (ergocalciferol) from ingestion of plants, fungi, yeasts.

Both converted to 25-OH D3 (storage form) in liver and to the active form 1,25-(OH)2 D3 (calcitriol) in kidney.

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +2  
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +3  
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +2  
bharatpillai  7 dehydrocholesterol +2  
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +1  
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +  
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +