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 +0  (nbme23#39)

This question makes no sense to me. She has an extremely low opening pressure yet has signs of increased intracranial pressure. Did they mean to put 32 cm H20?????????

uslme123  Standard lab values are incorrect, way to go NBME.
wutuwantbruv  I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg.
alexb  I lost a bit of time wondering about that ugh lol
mjmejora  I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high.

 -4  (nbme21#20)

very stupid question. The virus was inhaled -- bats hang upside when they sleep and drool. So it spreads to the brain directly from the olfactory system via retrograde transport through nerves.

niboonsh  yea, aeresol transmission via bat poop in caves

 +0  (nbme21#35)

AVF's = increased cardiac output. BUT this isn't new for this person? I view this as a heart that has finally begun to fail -- decreased effective circulatory volume --> increased SVR.

But i guess you can't have B before A -- whatever --\





Subcomments ...

Why would it not be anemia of chronic disease with decreased serum transferrin concentration?

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +7  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +  
loftybirdman  I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency +8  
seagull  maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well. +  
vshummy  Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me... +  
gonyyong  It's a B12 deficiency Ileum is where B12 is reabsorbed, folate is jejunum The blood smear is showing enlarged RBCs Methionine synthase does this conversion, using cofactor B12 +  
uslme123  Anemia of chronic disease is a microcytic anemia -- I believe this is why they put a lymphocyte on the side -- so we could see that it was a macrocytic anemia. +  
yotsubato  Thanks NBME, that really helped me.... +  
keshvi  the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption. +2  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  


submitted by lsmarshall(191),

"Probenecid and high-dose salicylates inhibit reabsorption of uric acid in proximal convoluted tubule (also inhibits secretion of penicillin)." - First Aid 2019

uslme123  so ............... +3  
adisdiadochokinetic  So probenecid is the best answer here because they only specified acetylsalicylic acid, not the dosage, and low-dose acetylsalicylic acid has the opposite effect. +  


submitted by welpdedelp(75),

when a follicle doesn't rupture (aka anovulation) then it will form a cyst.

uslme123  n premenopausal women, simple adnexal cysts (image 1) that are <3 cm in diameter typically represent normal follicles or may be a corpus luteal cyst (these may appear simple or complex) and may be considered a normal finding. Even when up to 5 cm in diameter, these simple cysts are so commonly due to normal menstrual physiology that the Society of Radiologists in Ultrasound (SRU) does not recommend follow-up when asymptomatic +1  


submitted by keycompany(115),

Can somebody please explain how nonionizing radiation has an ionizing effect.

uslme123  "technically non-ionizing, can produce photochemical reactions that are damaging to molecules by means other than simple heat. Since these reactions are often very similar to those caused by ionizing radiation, often the entire UV spectrum is considered to be equivalent to ionization radiation in its interaction with many systems (including biological systems)." -- https://en.wikipedia.org/wiki/Non-ionizing_radiation#Near_ultraviolet_radiation I'm guessing NBME reads wiki lmao? +1  


submitted by sympathetikey(303),

Mad at myself for changing my answer.

Faulty logic made me wonder if hitting your head would caused increased ICP so, like a cushing ulcer, you would get increased Vagus nerve activity and maybe bradycardia + hypotension. But I guess the RAAS system would have counteracted that and caused vasoconstriction over 24 hours, so Hypovolemic shock is definitely the best choice.

Always should go with the obvious answer :)

seagull  I had the idea that this was a neurogenic shock and increasing intracranial pressure could affect the vagus too. I think the question really wants us to go that direction. +1  
uslme123  The Cushing reflex leads to bradycardia! +1  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +1  
littletreetrunk  apparently, there's a thing called sympathetic escape that can happen after a while (i.e. he's been out for 24 hours): Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion. +  
littletreetrunk  also also if he hit his head he could have loss of sympathetic outflow from a hypoxic medulla which could lead to vasodilation, which further reduces arterial pressure, but this was a hard one for me lol. I also put increased ICP wah. +  
catch-22  Any lack of sympathetic outflow/increased vagal outflow should reduce HR, not increase it. Further, you would expect brainstem signs if there was hypoxia to the brainstem. For example, if you had damage to the solitary nucleus, you wouldn't be able to regulate your HR in response to reduced BP. Since this patient has reduced BP and increased HR, this indicates that the primary disturbance is likely the reduced BP. He's also been in a desert for 24+ hours so. +1  
charcot_bouchard  In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out! Plus Absent Bradycardia rules it out +  


submitted by hayayah(399),

Femfibrozil is a fibrate, used for lowering TG levels.

mousie  I also chose Gemfibrozil too because its the best TG lowering drug listed but I can see where there might be some red flags for this drug in the way they asked the question... 40 year old obese woman with some upper abdominal pain ..... HELLO GALL STONES which is a common adverse outcome of Fibrates. +2  
uslme123  Well I didn't wanna give a fat, forty, female, that smokes a fibrate. So a statin, for me, was the best next option. +2  
whoissaad  Used same reasoning to choose statins. Fibrates are the main drug of choice for hypertriglyceridemia but given her symptoms, statins made more sense. Why do they do this to us... +  
roaaaj  what a tricky question! there are multiple factors should be taken in consideration.. she has triglyceridemia which put her in risk of pancreatitis, and most importantly atherosclerotic disease, and all of that would outweigh the risk of giving her gallstone. +  


submitted by joker4eva76(10),

The question stem is describing a mitochondrial disease, which commonly present with lactic acidosis. There is an increase in anaerobic forms of energy production (glycolysis). The mitochondria are faulty, so they can’t use the end product of glycolysis (pyruvate) in TCA. Instead pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate pyruvate.

Aside: Recall that LDH uses NADH and generates NAD+. Deficiency of LDH can lead to loss of regeneration of NAD+ and inhibits glycolysis.

drdoom  ... pyruvate is shunted over and is used by LDH (lactate dehydrogenase) to generate lactate*. +  
chris07  It's hinted in the answer, but I would like to clarify: max O2 consumption is decreased because O2 is consumed in the Electron Transport Chain, which occurs in the mitochondria. With the mitochondria not working, the ETC cannot work, and thus there is less demand for Oxygen. +6  
masonkingcobra  Mitochondria are the powerhouse of the cell +12  
uslme123  Apparently ragged red fibers are the result of coarse subsarcolemmal or intermyofibrillar mitochondrial accumulations.. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/mitochondrial-myopathy +  


submitted by uslme123(9),

This question makes no sense to me. She has an extremely low opening pressure yet has signs of increased intracranial pressure. Did they mean to put 32 cm H20?????????

uslme123  Standard lab values are incorrect, way to go NBME. +1  
wutuwantbruv  I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg. +2  
alexb  I lost a bit of time wondering about that ugh lol +  
mjmejora  I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high. +  


submitted by sajaqua1(202),

Gynecomastia, spider angiomata, and hypogonadism (as well as palmar erythema) are all signs of excess estrogen. The liver in patients with hepatic disease is impaired and so cannot clear estrogen sufficiently. Six 12 oz beers daily (72 oz, or half a gallon) is too much, and is destroying his liver.

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +1  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +2  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +  


It’s acute alcohol consumption so fatty change more likely. Cellular swelling indicates alcoholic hepatitis which requires chronic alcohol consumption (See FA 2019 pg 385). At least that’s the logic I used to pick fatty change.

seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +11  
nc1992  I think it's just a bad question. It should be "on weekends" +5  
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +1  
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +  
sympathetikey  @seagull I agree! +  
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +  
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +  


It’s acute alcohol consumption so fatty change more likely. Cellular swelling indicates alcoholic hepatitis which requires chronic alcohol consumption (See FA 2019 pg 385). At least that’s the logic I used to pick fatty change.

seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +11  
nc1992  I think it's just a bad question. It should be "on weekends" +5  
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +1  
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +  
sympathetikey  @seagull I agree! +  
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +  
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +  


My thought was that this is endemic typhus from louse [on a cruise, rash only on the trunk, arthralgia]

Thoughts?

Honestly, even if it is dengue was the same answer shrug emoji

uslme123  I did too ... but It looks like the timing fits better for denge. +  


submitted by liltr(11),

I choose MVP too, but this patient’s main symptom is cough only during exercise. This is more indicative of exercised associated asthma. You could see shortness of breath in MVP during exercise, but choosing MVP leaves the cough unaccounted for.

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +6  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +3  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +1  
cienfuegos  Just noticed that he has FHx, game changer. +  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +  


submitted by liltr(11),

I choose MVP too, but this patient’s main symptom is cough only during exercise. This is more indicative of exercised associated asthma. You could see shortness of breath in MVP during exercise, but choosing MVP leaves the cough unaccounted for.

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +6  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +3  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +1  
cienfuegos  Just noticed that he has FHx, game changer. +  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +  


I get that this answer choice is the most amicable answer.

But honestly the way they asked the question "it is most appropriate for the physician to address the issue of a feeding tube in which of the following manners"

My reasoning was: well...before the family can even begin to argue what do do don't you have to propose a medical treatment/management strategy? which is why I went with "recommend a tube..."

home_run_ball  Like what is the learning objective of this question? On first aid if you go by the Surrogate decision maker priority: you do spouse first...so like wtf nbme? +6  
uslme123  I think it's because there isn't a legally appointed health care surrogate in this case. The family hierarchy is only an "ethical suggestion." +  
nala_ula  According to first aid, there is an order to who makes decisions when the patient is not able to and hasn't left any directives. My issue was the same as home_run_ball, since they specifically asked about the feeding tube and not "who is supposed to make decisions now" even though that is also warped since the spouse has precedence. +1  


submitted by hayayah(399),

Case of arteriolosclerosis.

Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')

  • Consequence of malignant hypertension (>180/120 w/ acute end-organ damage)
  • Results in reduced vessel caliber with end-organ ischemia
  • May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure (ARF) with a characteristic 'flea-bitten' appearance
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +5  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +7  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +2  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


submitted by hayayah(399),

Renovascular disease is the most common cause of 2° HTN in adults. Can be d/t ischemia from renal stenosis or microvascular disease. Can hear renal bruits lateral to umbilicus.

Main causes of renal artery stenosis:

  • Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers.

  • Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females.

Lab values based off:

  1. Stenosis decreases blood flow to glomerulus.
  2. Juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin I.
  3. Angiotensin I is converted to angiotensin II (ATII) by angiotensin converting enzyme (ACE --in lungs)
  4. ATII raises blood pressure by (1) contracting arteriolar smooth muscle, increasing total peripheral resistance and (2) promoting adrenal release of aldosterone, which increases reabsorption of sodium (where Na+ goes H2O will follow) in the distal convoluted tubule (expanding plasma volume). Can lead to hypokalemia (seen in the labs for this question)
  5. Leads to HTN with increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary hypertension
uslme123  So both causes would result in increased aldo and MR is the only way to differentiate the two? +1  
hello  @USMLE123 I think both are causes of renal artery stenosis and that could be seen via MR angiography. It is asking what could help DIAGNOSE this patient -- and her most likely cause of the findings is fibromuscular dysplasia. So, yes, MR angiography would look different for the 2 different etiologies and thus could can be used to differentiate the two from one another. However, epidemiologically, we are looking to diagnose her with the suspected most probable cause. +1  
yotsubato  @USLME123 I think measuring Aldosterone is an incorrect answer because you already know its increased due to low K. Knowing she has high Aldosterone wouldnt provide you evidence for a final diagnosis. +2