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Comments ...

 +0  (nbme18#3)

the pulsatile mass gave it away for me but looking back this patient has all the risk factors for AA - male smoker with HTN + deep chest pain and pulsatile mass = AA all day long


 +0  (nbme18#31)

Read pathoma...... chapter 1 p 5 on "cell death" Liquefactive necrosis occurs in brain infarct ( proteolytic enzymes from microglial cells liquify the brain) & Abscess (proteolytic enzymes from neutrophils liquify tissue [in this case pulmonary parenchyma]) & pancreatitis (same thing)


 +1  (nbme23#42)

Why not urothelial carcinoma? Or how did you rule it out? I was thinking radiation would increase risk for future CA...


 +3  (nbme23#48)

Why no sweating? I mean I get Ecstasy is probably the drug of choice before an all night dance party (lol) but don't understand why there would be cold extremities and no sweating when is FA it says hyperthermia and rhabdo????

sympathetikey  FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism. Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome." So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though.
amorah  I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv.
yotsubato  Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore?
fulminant_life  you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol
monkd  Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :)
usmleuser007  Why not LSD?
d_holles  @usmleuser007 LSD doesn't cause HTN and ↑ HR.
sbryant6  @fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION.
dashou19  Take a look at why the patient has pale and cold extremities. "Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008716/

mousie  Caudal = Bottom of the SC = failure to close = spina bifida and Rostral = top of SC = failure to close = Anencephaly

 +0  (nbme23#15)

why does treatment of hypothyroid (with levothyroxine I'm assuming) increase risk for myopathy? I chose it simply bc its a common adverse effect of statins but I don't really understand how treating hypothyroidism at the same time would have anything to do with it ??? help please!

yb_26  They are just asking about side effect of statins, not about treatment of hypothyroidism
mjmejora  Hypothyroidism is just a red herring.
ususmle  statins cause both hepatotoxic and mypopathy so I want for hepatotoxic:( I thought usmle expects different stuff

 +8  (nbme23#33)

My understanding if BC>AC this is abnormal = conductive hearing loss = otosclerosis VS Sensoryneural hearing loss will have normal AC>BC = loss of hair cells

dentist  VS: progressive unilateral hearing loss, doesn't affect Rinne Test, associated with NF2 and actor Mark Ruffalo Otoslcerosis is (usually....) progressive bilateral hearing loss, BC > AC. source

 +4  (nbme23#23)

Your pituitary lactotrop cells hypertrophy during pregnancy to produce increasing amounts of prolactin - part of the pathophysiology of Sheehan's syndrome... increased blood loss during delivery can cause ischemic necrosis of pituitary

tinydoc  I thought the elevated Estrogen and progesterone depress the function of Prolactin until delivery. I guess you needed to know that it decreases its function by downregulating receptors or something as opposed actually decreasing the prolactin production. I picked gonadotrophs. This was a fair question but I reasoned it out and arrived at the wrong conclusion.
maxillarythirdmolar  Specifically, the estrogen is stimulating lactotrophs as progesterone is preventing the prolactin from actually working on the breasts. So it's the estrogen that is stimulating the lactotrophs to grow, and you would see the effects of this growth if it weren't for the progesterone preventing the action of prolactin (their secretory product) on the breasts.

 +0  (nbme23#37)

help with this one please.... is this because he has hyperTG AND Cholesterol AND chylomicrons.. only LL deficiency would explain all of these findings? I chose LDL R deficiency because I guess I though it would cause all of them to increase but is this type of deficiency only associated with high LDL?

sympathetikey  First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL. Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if it's not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to.
davidw  There is much easier way go to page 94 in first aid. This kid has Type 1 Hyper-Chylomicronemia which is I) Increased Chylomicrons, Increase TG and Increased Cholesterol. It can be either Lipoprotein Lipase or Apolipoprotein CII Deficiency
bulgaine  The video sympathetikey referred to only mentions pancreatitis in type IV but according to page 94 of FA 2019 it is also present in type I Hyper-chylomicronemia which is what the question stem is referring to with the abdominal pain, vomiting and increased amylase activity
dentist  thats not the only difference in that video....

 +4  (nbme23#5)

Cholera = Fecal oral /Legionnaires = Legonalla pneumo = NO person to person only by inhalation of bacteria contaminated water /Lyme = tick bite /Meningiococcal = sharing respiratory and throat secretions (saliva or spit). Generally, it takes close (for example, coughing or kissing) or lengthy contact to spread these bacteria (CDC) /RMSF = tick bite

smc213  Also, when Meningococcal meningitis is treated ... close contacts are also treated prophylactically whereas the others typically are not. There's also a subunit vaccine for n. meningitis due to high infectivity rate especially in crowded establishments.
dentist  So, Cholera is also p2p but Mening is more likely?

 +2  (nbme23#34)

Organophosphate poisoning = Antidote = Atropine (Airway M receptor blocker) = dilation of bronchioles


 +9  (nbme23#8)

Marfanoid habitus + Mucosal neuromas + Neck mass = MEN 2B (PMM) Pheo, Medullary thyroid CA (Calcitonin secreting), mucosal neuromas


 +2  (nbme23#26)

I chose PAN for this one, saw the renal a. aneurysms and went right for it but PAN would have more systemic findings (fever, weight loss, head ache) and usually effects middle age MEN vs Women in FMD.


 +1  (nbme23#3)

Can someone please explain this to me? I don't understand why starting the other drug would not count as exclusion criteria?

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s
dr.xx  Where does the question mention "intention-to-treat"?
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet)
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx
yex  I agree with @notadoctor !!
ergogenic22  i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group.

 +0  (nbme23#33)

Not sure I am understanding this question - the patient got an NSAID for RA and this decreased her prostaglandins so she developed GERD... Doc added Misoprostol to counteract the decreased Prostaglandins I the gut and an adverse reaction of Misoprostol is diarrhea .. Correct?

chris07  Yes. Diarrhea is a side effect of misoprostol.

 +1  (nbme23#10)

Analasmosis Phagocytophilum carried by Ixodes scapularis tick similar to babesia (Babesiosis)and borrelia(Lyme dz) where Rickettsia Rickettsia is carried by ectoparasites such as fleas, lice, mites, and ticks. as per the CDC


 +4  (nbme23#27)

A hemangioma is a type of benign (non-cancerous) tumor in infants. This abnormal cluster of small blood vessels appears on or under the skin, typically within one to three weeks after birth. - www.childrenshospital.org Hemangioma is a BV/capillary birthmark

sympathetikey  Probably a Strawberry Hemangioma since she's a baby
meningitis  Can anyone explain what is option A?
redvelvet  bc, it's a benign "capillary" hemangioma, we can see "thin-walled blood vessels with narrow lumens filled with blood and separated by connective tissue". It sounds similar to "arterioles in a fibrous stroma" but it's capillary.

 +1  (nbme23#11)

An epitope, also known as antigenic determinant, is the part of an antigen that is recognized by the immune system, specifically by antibodies, B cells, or T cells. For example, the epitope is the specific piece of the antigen to which an antibody binds. - Wiki - Because the amount of Labeled X bound is unchanged by the addition of Y- they are independent of each other i.e. share no epitopes


 +1  (nbme24#33)

A Teen with injection of both conjunctiva = weed could also be abusing other drugs Is 12 years old and four months just too old and too long of a time for it to be impetigo? I narrowed it down to these two and guessed but... I wasn't sure I could eliminate it.

medskool123  I picked impetigo because of the gold stippling... I guess I took that as honey crusted lesions. F*ck NBME.
yotsubato  Huffing gold spray paint. A la the chrome huffers in Mad Max
subclaviansteele  LOL I think that might be what they were going for here. Gold spray paint.
et-tu-bromocriptine  Anyone know what may be causing his weight loss and unwillingness to eat? I thought too much into it and put "mercury poisoning", since I thought the heavy metal's abdominal symptoms may have caused him to not want to eat. ¯_(ツ)_/¯

 +0  (nbme24#6)

looking back at this Q I notice that the patient also has hypertension ...could that have been a clue to include the SMA bc its so close to the renal arteries (Renal a stenosis)?

nwinkelmann  I didn't know how to approach this either, but now this is my thought process: Patient has pain after eating. If it's not due to an ulcer (which is the only thing I could come up with because I didn't know what else it was talking about), why would eating cause pain? Well... eating causes increased GIT activity which means increased blood flow. As you pointed out, the patient has HTN and CAD, indicating likely extensive atherosclerosis. This is important because why would eating leading to increased blood flow cause pain, when usually it doesn't? Well... atherosclerosis in the heart leads to stable angina. This presentation sounds like a "stable angina" of the abdomen.

 +3  (nbme24#36)

"dronates" are Bisphosphonates, commonly used to prevent/treat osteoporosis. Most common adverse effects are Esophagitis (patients should take with water and be upright for at least 30minutes), Osteonecrosis of the jaw, and atypical femoral stress fractures. -taken right from FA 2018 pg 471


 +1  (nbme24#13)

is this subacute endocarditis associated Membrano-proliferative GN?

jus2234  The question describes how he had a strep infection 15 days ago, and now this is poststreptococcal glomeruloneprhitis, which can also be described as proliferative glomerulonephritis
seagull  The question would be too fair if it just said PSGN. Instead we need to smell our own farts first.
yotsubato  And they used terminology NOT found in FA
water  who said they were limited to FA?
nbmehelp  FA uses the common nomenclature and the fact most of our other resources use the same nomenclature for this, I think we can agree that is is the accepted terms. If they're gonna decide not to use the nomenclature that most medical students are taught then they should provide their own study materials at that point for us to use. The test shouldn't be this convoluted for no reason.

 +1  (nbme24#6)

Is 45 minutes too long to be anaphylactic and would the absence of rash (urticaria, pruritus) RO anaphylactic?

hayayah  Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours. (pg 114 of the 2019 FA has a list of them ordered by time)
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus)
seagull  The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer.
charcot_bouchard  Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm.
soph  I saw hypotension and though anaphylaxis........ -.-
usmile1  Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis.

 +0  (nbme24#31)

if your CO falls ... wouldn't that cause vasoconstriction in the lung vasculature? hypoxia induced vasoconstriction?

ug123  My take on this----His respirations are high-22/min--that will cause c02 washout---so actually lung has high oxygen---pulmonary vasodilation. Dont know if its right.
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel




Subcomments ...

Trihexphenidyl and Benztropine are antimuscarinics that can treat the resting tremor and rigidity of parkinsonism.

mousie  haloperidol induced Parkinson's... ? adding a anticholinergic can counter these adverse effects of the antipsychotic .. ? +1  
fulminant_life  @mousie yeah it balances the dopamine-cholinergic imbalance caused by the antipsychotics +  
kai  +So antipsychotics induce Extrapyramidal side effects which is drug induced Parkinson = low Dopamine High Ach, and you would treat this with anticholinergic (Benztropine).This is neurologic. +Antipsychotics also produce non-neurologic, systemic anti-cholinergic effects like dry mouth, sedation, hypotension etc +  


submitted by step420(18),

Ritonavir inhibits CYP450! So you can use it to boost the concentration of the other Protease inhibitors by preventing their metabolism by CYP450!

mousie  who knew +1  
sympathetikey  Right on (thanks sketchy) +3  
mguan1993  MAGIC RACKS is a good mnemonic ive heard for 450 inhibitors (macrolides, amiodarone, grapefruit, cimetidine, RITONAVIR, alcohol (chronic), cipro, ketoconazole, sulfa +1  
criovoly  "CRACK AMIGOS" Cimetidine Ritonavir Amiodarone Ciprofloxacion Ketoconazole Acute alcoholism Macrolides Isoniasid Grapefruit juice Omeprazole Sulfonamides +2  


submitted by sakbarh(4),

She has many cardiovascular risk factors and likely suffered a stroke of the basilar artery causing locked in syndrome. According to FA this can cause a lesion at the pons, medullar, or lower midbrain -- however anatomically the basilar artery runs right on top of the pons so proximity most likely makes it the right answer.

mousie  The Boards and Beyond video of SC strokes was really helpful at explaining this if you are a video kind of person! +  
yotsubato  What pushed me away from pons was "dysarthric speech" which implied she still could speak to some degree.... which made me pick medulla. +1  
mimi21  I think FA may be misleading. Primarily it will effect the Pons because that is where the majority of the Basilar Artery is located. and I guess it could effect the other locations? but everywhere I have looked Locked-in syndrome is an issue with the Pons. But someone please continue to clarify, cause I was a bit tripped up at first with this question +  
cbrodo  Although FA says it can be pons, medulla, or lower midbrain, "locked-in" syndrome generally arises from BL pons lesions. Another way you can rule out medulla and midbrain in this question is the ocular movement findings. Since the patient has impaired horizontal gaze BL, you can conclude that the Abducens nuclei are involved on both sides. The abducens nuclei are located in the pons. +7  
gh889  USMLE secrets also states that it is most commonly in the pons Bates states that locked-in syndrome preserves consciousness but these patients have limited speaking ability +  


The most important hints to the question are as follows, with #2 being the most specific:

1) patient reports pain with overhead motion and reports recurrent overhead motion during work. Overhead motion can damage the supraspinatus muscle due to impingement by the acromion.

2) Pain is worst with internal rotation of the shoulder - this is consistent with the findings of the empty-can test, which indicates a supraspinatus injury.

mousie  I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right +  
sympathetikey  Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense. +1  
charcot_bouchard  IDK WTF i picked Trapezius +6  
ls3076  why would injury to supraspinatus cause weakness with internal rotation though? +3  
targetusmle  yeah coz of that i picked subscapularis +  
maddy1994  ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis +1  
darthskywalker306  I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me. +  


mousie  Caudal = Bottom of the SC = failure to close = spina bifida and Rostral = top of SC = failure to close = Anencephaly +4  


submitted by beeip(63),

The best I can understand, they're describing endometrial hyperplasia, a result of excess estrogen, a steroid hormone that translocates to the nucleus and binds its transcription factor.

mousie  My exact thinking also! +2  
sympathetikey  Ditto. +  
meningitis  My thought as well but the answer says: "Binding of ligand to Nuclear transcription factor" and I thought to myself: "Estrogen Receptors aren't transcription factors.. they are receptors with Transcription Factor function that bind to the ER Element and recruit more Transcription Factors". Can anyone explain what I am missing? Am overthinking things? +  
criovoly  You are overthinking it, Steroid hormones receptor is found intracellular in the cytoplasm then they are translocated to the nucleus where they regulate gene transcription. HOPE THIS HELPS +  


What are we supposed to be looking at? I see multinucleated giant cells. I also see infiltrate (can’t tell if this is mononuclear or not).

methylased  Young child following URI with TCP is pretty classic ITP. Sometimes they throw in extra stuff on purpose, but I didn’t see much on the bone marrow aspirate either. +1  
mousie  I was also thinking ITP but the bone marrow image kind of threw me off too, not sure what I'm supposed to see but still think ITP is best choice ... +  
meningitis  It also almost threw me off, but then I remembered he had low platelet count and I guessed those multinucleated cells were Megakaryocytes (I looked for Megakaryocyte Bone Marrow Biopsy in google and they are the same). +1  
what  Bone marrow shows increased megakaryocytes -> ITP +  


The patient has ATN secondary to renal ischemia. Due to tubular necorsis, the patient will have an elevated FeNa. The patient's urine will also be dilute, but this will be reflected by the low urine osmolality, not the FeNa

mousie  Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia? +1  
sympathetikey  I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself. +  
ajo  This might help clarify why the pt. has ATN rather than pre renal azotemia. The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong. +11  
ajo  In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption! +6  
gh889  Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN +  
sugaplum  for anyone who wants to see it: FA 2019 pg591 +1  


Patient has a fracture to the inferior orbit. This can dmg V2 or entrap the IR muscle. Only IR entrapment would impair vision.

nlkrueger  if this isn't a globe rupture than idk what is tbh +2  
mousie  the air in the center of the globe made me think rupture too ..... +  
sajaqua1  There may be some global rupture, but impairment of one of the ocular muscles causing diplopia would still be the best explanation for this patient's double vision. +1  
catch-22  Globe rupture leads to entrapment of the IR muscle which causes diplopia. The question is asking what is causing his visual complaints, which is diplopia, not loss of vision. +  


Envelopes benefit the virus in that the virus will look like the host, facilitating fusion. However, an enveloped virus is generally less stable than a naked icosahedral virus (naked viruses are generally icosahedral).

docred123  So do these patients have h.Flu? What was the giveaway? Thanks +  
mousie  I chose Enveloped simply bc it said dies when heated, not sure if there where any other clues to narrow this down or make me feel more confident in my choice but I went with it anyway +3  
eclipse  I don't think they expected us to narrow down the answer to a specific virus. Enveloped viruses tend to be less stable (?) than the non-enveloped ones and don't survive as well under harsher environments (outside human's body, heat, etc.) +  


submitted by seagull(437),

i'm still convinced this is irritable bowel syndrome. Change my mind.

mousie  haha I picked this too bc she's 44.... isn't celiac something that would present much younger?? but I don't think IBS would cause an iron deficiency anemia is the hint they were trying to give us. +  
sympathetikey  If it was IBS, they would have mentioned something about them having abdominal pain, different stool frequency, and then relief after defecation, me thinks. +  
aknemu  I was between celiac sprue and IBS but what pushed me towards celiac's was a few things: 1. The Iron deficency anemia (I think that would be unlikely in IBS) 2. Steatorrhea (which would also be unlikley in IBS) 3. Osteopenia- I was think vitamin D deficency 4. Lack of a psychiatric history +4  
catch-22  IBS is a diagnosis of exclusion. If you haven't excluded Celiac (and this can't be excluded based on epidemiology alone), you can't diagnose IBS. +4  


submitted by docred123(3),

Can someone please further explain this question? What biostatistical analysis should I be thinking about?

vshummy  I got this wrong but best I could come up with was this was about Bradford Hill Criteria for establishing causality. And of the 9 included, F has the most that are actually included in the information given to us. I chose D but I think since we don't know about other study results, we can't include it as directly answering the question about *this* study. https://en.m.wikipedia.org/wiki/Bradford_Hill_criteria Someone double check me here: A: biologic plausibility is a weak point in the criteria, according to the wiki. Also probably not true in regards to this study. B: Sensitivity is not part of the criteria C: " " D: We don't know about consistency E: " B " +5  
mousie  Found this ... still confused about why A and D are wrong though... https://stats.stackexchange.com/questions/534/under-what-conditions-does-correlation-imply-causation +1  
2zanzibar  The three criteria for causality are: 1) empirical association (i.e. strength of association; a change in independent variable correlates or is associated with a change in dependent variable), 2) time order (i.e. temporal relationship; the independent variable must come before change in the dependent variable, or plainly stated, cause must come before effect). and 3) nonspuriousness (i.e. dose-response gradient; the relationship between 2 variables is due to a direct relationship between the two, not because of the actions of changes in a third variable... this can be evinced by a dose-dependent response). +5  


submitted by ferrero(18),

A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +11  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +1  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +13  
cr  the main difference between the 2 cases is that in this case the patient has high BP +  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +  
asteroides  I think they may be talking about the myogenic compensatory mechanism: https://www.ncbi.nlm.nih.gov/books/NBK53445/figure/fig4.1/?report=objectonly "Increased arterial or venous pressure also induces myogenic constriction of arterioles and precapillary sphincters, which raises arteriolar resistance (thereby minimizing the increase in capillary pressure) and reduces the microvascular surface area available for fluid exchange. For example, because vascular smooth muscle in arterial and arteriolar walls contracts when exposed to elevated intravascular pressures, this myogenic response increases precapillary resistance and protects capillaries from a concomitant rise in their intravascular pressure." +  


submitted by seagull(437),

This is a type II Renal Tubular Acidosis. My Medical School Never taught this to me. Did you also go to poverty med school? I'm surprised they even gave us toilet paper.

mousie  haha mine didn't either. But they usually leave out most high yield info so, to be expected I guess. +1  
yotsubato  I didnt have physiology in my medical school. None, zip, zero, none. Nor did I have biochem. They said "you learned all this shit in undergrad, youll memorize it again for step 1 and forget it promptly" and then just moved on. +2  


submitted by hayayah(416),

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 docred123(3),

Hey can someone please explain this! I am not sure how to do the math, I keep getting tripped up.

mousie  Equation is Maintenance dose = (concentration at steady state) * (Clearance) if you convert all the units to what it wanted them in (mg/kg/day) you'll get 25.92 like weird-in said above I didn't think to round 0.09 to 0.1 of course so I guessed 2.5 assuming I must have done a conversion wrong and was off by a tenth .... BOO bad Q +4  
hyperfukus  OMG ME TOO!!!!! +  


Hey can someone explain the renal findings? Physio is definitely not my strong suit.

Is it because he has fluid/Na+ retention that his specific gravity and Na+ are so low? Is there a reason for those specific BUN/creatinine over the others?

brolycow  He has heart failure which leads to a decrease in renal blood flow and prerenal azotemia. In prerenal azotemia BUN/Cr ratio is >= 20; Activation of the RAAS system due to the prerenal azotemia means that the spec grav is high at 1.025 and he is holding onto sodium so urinary sodium will be low (<20, FENa <1%). +5  
mousie  Agree with above, HF and not taking meds would increase or activate RAAS = increase ATII and Aldosterone which leads to body retaining Na and H2O so the urine concentration of Na will be low and the urine will be very concentrated i.e. high SG. I didn't think about the BUN:Cr > 20 but this would have also narrowed it down! +2  


submitted by hayayah(416),

Coloboma is an eye abnormality that occurs before birth. They're missing pieces of tissue in structures that form the eye.

  • Colobomas affecting the iris, which result in a "keyhole" appearance of the pupil, generally do not lead to vision loss.

  • Colobomas involving the retina result in vision loss in specific parts of the visual field.

  • Large retinal colobomas or those affecting the optic nerve can cause low vision, which means vision loss that cannot be completely corrected with glasses or contact lenses.

mousie  thanks for this explanation! +  
macrohphage95  can any one explain to me why not lens ? +  
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss +1  


submitted by docred123(3),

Hi guys can someone please elaborate on these findings. I understand she has lung cancer that's impeding her trachea. But how is this representative of an obstructive disorder? Aren't lung cancers restrictive if anything? Thanks

nlkrueger  I agree that it's confusing but I looked at it as a physical *obstruction* since it's impinging on the airway.... but yeah idk this is weird +  
ferrero  Doesn't the trachea have cartilage rings so it wouldn't collapse which makes it seem less like a typical obstructive disorder? I'm really not sure why FVC would change because I don't see how total lung capacity or residual volume would change because those are static conditions where there is no airflow at all. I understand FEV1, peak expiratory flow, peak inspiratory flow etc. +  
mousie  Agree this is a really tough Q but I also think I really over thought it... I eliminated all with a normal Ratio bc something obstructing would obviously produce an obstructive pattern although I don't know why FVC would be decreased. I wasn't sure about both peak expiratory and inspiration flow being decreased can someone help me with this or tell me I'm totally overthinking again.. are they both decreased simply bc theres an obstruction ..? +1  
mimi21  Yea I got confused on this question. But I guess they wanted us to look at it as a obstructive disease . If this were the case all of those function tests would dec. ( See FA ) +  
gh889  Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology. +2  
charcot_bouchard  FVC here dec same way it dec in Obstructive lung disease. Read the concept of Equal pressure point of BnB. There he says in bronchitis we have onstructive pattern because inflammed airways gen more resistance. so EPP comes early. I guess here due to tracheal narrowing pressure inc downstream. which collapses smaller airway. result in air trapping. +  


submitted by trazabone(7),

Kidney makes 1-25, hydroxy vitamin D. (calcitriol) 25-hydroxy vit D (calcidiol) is made in the liver, and hypoparathyroidism would not decrease its levels as it acts to increase 1-alpha hydroxylase in the kidney to increase calcitriol concentrations --> Ca/phosphate reabsorption from the bone and small intestine.

queezyfish  I'm confused about the phosphate level in questions like these. Decreased calcitriol would decrease phosphate absorption while PTH decrease lowers phosphate excretion. I'm assuming that the PTH decrease has the greater effect with serum phosphate levels? +1  
mousie  PTH = "Phosphate trashing hormone" if PTH is high Phosphate must be low - they are always opposite (unless d/t renal failure then Phosphate will be high - kidneys will be unable to get rid of phosphate) So low Ca d/t low PTH does not effect 25 H. Vit D ... only 1,25 H Vit D (active Calcitriol)? +4  
haliburton  Clarification because I was confused: PTH stimulates kidney to produce 1,25-(OH)2 D3 (calcitriol) via 1α-hydroxylase in proximal convoluted tubule. Therefore, without parathyroid glands, low PTH, 25,D is not converted and therefore not down (normal or up). phosphate "trashed" by PTH as eloquently stated above. +  
zbird  Here the primary defect is high up from the parathyroid gland, there is decresed or no PTH which normally trashes phosphate but not in this case so serum PHOSPHATE INCREASES and the serum calcium is low because PTH should have prevented the urine calcium so there is calciuria and no resorption from bone-LOW CALCIUM, Vitamin-D is independent of PTH so stays NORMAL +  


submitted by neonem(263),

This is acute hemolytic transfusion reaction, a type II hypersensitivity where pre-formed IgM antibodies bind to incompatible ABO antigens on donor RBCs, which causes intravascular hemolysis. Rh incompatibility, like colonelred_ said, comes more into play with Rh-compatibility of pregnancy and it is due to IgG antibodies, which more often cause extravascular hemolysis since splenic macrophages have those Fc-gamma-R receptors to bind whatever IgG has caught. Extravascular doesn't cause that hypotension, fever, flank pain associated with hemoglobinuria since the macrophages hold on to the degraded RBCs and convert it to biliverdin, which can safely be excreted by the liver.

mousie  Could you help me with understanding why this isn't a Type I HSR? I understand that ABO incompatibility is Type II HSR but I don't know how to tell the difference between a patient who is IgA deficient and having a Type I Reaction to an infusion vs ABO incompatibility .... +1  
sympathetikey  @mousie - https://imgur.com/QH5rCEX Basically, think of Type 1 HS like a normal allergic reaction (itchy, wheezing, etc.). Whereas, with ABO incompatibility you get the question's presentation. +2  
medpsychosis  When it comes to Acute hemolytic transfusion reactions, they are Type II hypersensitivity and divided into Intravascular (ABO) and Extravascular (host Ab against foreign antigen on donor RBC). The differentiating factor between them is simple. Intravascular (ABO) will present with hemoglobinuria alongside all the other common symptoms (fever,hypotension, tachypnea etc.) Extravascular hemolysis will stand out with Jaundice as one of the presenting symptoms. Hope this helps! +2  


submitted by brethren_md(44),

Requires knowing how to calculate an anion gap - look it up. In this case, it is a normal anion gap metabolic acidosis. Know the mneumonics MUDPILES and HARDASS. Renal Tubular acidosis is the only answer choice that is an example of a normal anion metabolic acidosis.

mousie  Anion Gap: Na - (Cl + HCO3) = normally around 10-12 +1  
seagull  good to know. I keep looking up the urine values but all it said was "varies", then I threw my computer and yelled "does that vary Mother F****ers. I do feel better now. +14  
_yeetmasterflex  glad I wasn't the only one who got very pissed off at the urine values +1  
fulminant_life  Usually the first thing I look at is whether or not the Cl- is high. Generally if the Cl- is high its going to be a normal gap +1  
henoch schonlein  i think they gave you the urine values bc you can calculate the URINE anion gap which is (Na + K - Cl). In this case the Urine Anion Gap is positive (5). Boards and Beyond mentions that a positive UAG is due to Renal Tubular Acidosis Type 1 (inability of alpha intercalated cells to secrete hydrogen ions). just another approach to answer this q +6  
270onstep1  Actually diarrhea is the "D" in "HARDASS"(reason why I was stuck between Chron's and RTA). Ended up getting it right with RTA.. +  


submitted by neonem(263),

Since this patient is a non-smoker, it is less to be small cell carcinoma, squamous cell carcinoma, or large cell carcinoma of the lung. Besides small cell carcinoma being from neuroendocrine origin, the one major lung cancer described by nests of well-differentiated, "regular" cells is a carcinoid tumor. Additionally, rosettes are histological features of carcinoid tumors (fun fact: rosettes also in neuroblastomas/ependymomas (in CNS), retinoblastomas, granulosa cell tumors (ovarian cancer))

mousie  When ever I hear Rosettes I always think NE tumors .... and I agree non smoking kind of RO small cell, squamous cell, or lg cell +2  
charcot_bouchard  I thought it was Hamartoma & pick chondrocyte! Can lung even have hamartoma? Pardon me it was the laast ques of whole nbme +  
drmomo  @charcot_bouchard i thought the same. uworld gave a question on coin lesion in the lungs as classically hamartoma +  


submitted by neonem(263),

I think the reason you need to inject gonadotropins in this case is because you need FSH and LH to produce sperm. FSH stimulates the sertoli cells, which line the seminiferous tubules and help the spermatogonia produce spermatocytes. Testosterone is a product of Leydig cells when they're stimulated by LH, so injecting testosterone would bypass that step but it wouldn't really help with spermatogenesis. However, injecting GnRH also doesn't doesn't really help because you need that pulsatile GnRH at night to make LH and FSH whereas long-acting GnRH analogs actually decrease LH and FSH production.

m-ice  Adding on to the answer above. I was stuck between the gonadotropin injections and clomiphene. But, clomiphene acts to increase activity of GnRH which then exerts its effects on the pituitary. The man in this question had his pituitary removed because of an adenoma. So, he needs the FSH and LH directly. +7  
mousie  agree! Removal of the pituitary would case a deficit in Gonadotropins (LH, FSH) and therefore nothing to simulate the testes to make sperm... replacing the T with a patch would not stimulate the testes to make sperm and if his axis was intact (although its not) this would further down regulate the production of sperm. I eliminated Clomiphene because if he dosent have T to induce negative influence on the hypothalamus he will have increased GnRH and further increasing it with Clomiphene would not correct the deficit in Gonadotropins. +2  
neonem  Oh duh... that makes much more sense. Thanks! P.s. I thought clomiphene was more of a fertility drug for women, since it blocks negative feedback of estrogen on the hypothalamus/pituitary. But in men the system is under feedback due to testosterone, not estrogen. +4  


Can anybody explain this one? I put repeated tests because I assumed an 83-year-old woman is an unusual demographic for syphilis.

m-ice  83 might seem an uncommon age, but we don't know for sure her sexual history. She only recently (8 months ago) started showing some signs of mild cognitive impairment. She has all these results implying that she has syphilis, so the most likely answer is that she has syphilis, so we should speak to her privately about her sexual history. The tests don't necessarily means she got syphilis very recently, it's possible she's had syphilis for a while and never got treated. +2  
mousie  I understand that she could possibly have syphilis but I also put repeat tests because I know there are a few things that can cause false positive VRDLs but if she also has a + RPR does this make a FP less likely? And also if she has mild cognitive impairment you still discuss with her not her daughter correct ...? +2  
m-ice  This definitely could be a false positive, but before we want to consider it to be a false positive, we should talk to the patient about it privately. Assuming that it's a false positive before asking the patient about it could delay treatment of her syphilis. There's a chance she didn't want to disclose her sexual history in front of her daughter or maybe she was embarrassed or didn't think it was important to mention. And you're absolutely right, she only has mild cognitive impairment, so we most definitely should talk to the patient alone without her daughter first. +  
seagull  She has dementia. She doesn't have the capacity to determine her own care (23/20 MME). I feel the daughter should have the word on the care since Grandma likely doesn't have the capacity to understand her actions. +1  
sajaqua1  From what I remember, dementia is typically a combination of impaired memory *and* impaired thought processes. There is nothing to indicate that the patient has impaired thought processes, and the memory impairment is only mild. The patient can still reasonably said to be competent, and so her private information should be discussed with her alone. +6  
yotsubato  Elder care homes or elderly communities actually have a high rate of STDs. Turns out, when you put a bunch of divorced/widowed adults together in a community they have sex. +3  
yotsubato  Additionally, you should respect the privacy of a competent adult with "Mild memory" impairment. I know I could have mild memory impairment considering the crap I forget studying for step 1 +5  
drdoom  @seagull dementia ≠ absence of competence -- the two are separate concepts and have to be evaluated independently. see https://meshb.nlm.nih.gov/record/ui?ui=D003704 and https://meshb.nlm.nih.gov/record/ui?ui=D016743 +1  
wowo  also important to note, d) repeated tests is also incorrect as the microhemagglutination assay is a confirmatory treponemal test (along the same lines as FTA-ABS) https://www.uofmhealth.org/health-library/hw5839 +1  
sunshinesweetheart  also.... I think we can assume that "repeated tests" means repeat VRDL, not "additional tests to rule out false positives" +  


submitted by sattanki(31),

Does anyone have any idea on this question? Thought it was ALS.

ankistruggles  I thought it was ALS too (and I think it still could be?) but my thought process was that a lower motor neuron lesion would be the more specific answer. +  
sattanki  Yeah makes sense, just threw me off cause ALS is both lower and upper motor neuron problems. Corticospinal tract would have been a better answer if they described more upper motor neuron symptoms, but as you said, they only describe lower motor neuron symptoms. Thanks! +1  
mousie  Agree I thought ALS too but eliminated Peripheral nerves and LMN because I guess I thought they were the same thing ....??? Am I way off here or could someone maybe explain how they are different? Thanks! +  
baconpies  peripheral nerves would include motor & sensory, whereas LMN would be just motor +6  
seagull  Also, a LMN damage wouldn't include both hand and LE unless it was somehow diffuse as in Guil-barre syndrome. It would likely be specific to part of a body. right??? +  
charcot_bouchard  No. if it was a peri nerve it would be limited to a particular muscle or muscles. but since its lower motor neuron it is affecting more diffusely. Like u need to take down only few Lumbo sacral neuron to get lower extremity weakness. but if it was sciatic or CFN (peri nerve) it would be specific & symptom include Sensory. +  


mousie  http://www.sparknotes.com/biology/cellreproduction/cellcycle/section3/page/2/ +2  
fahmed14  Cyclins help regulate cell cycle phases. They help with checkpoints before progression to the next phase of a cell cycle. Therefore the checkpoint before mitosis would be in G2 and probably where mitotic specific cyclins are synthesized +5  
artist90  https://en.wikipedia.org/wiki/Cyclin . 4 types of Cyclins and when they rise and fall. +