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 +0  (nbme18#29)

Anyone have an idea on how to approach this question?

gdupgrant  So the thing i think they tried to catch people on was that the SMV Joins with the splenic to become the portal vein and the IMV feeds into the splenic vein. And they want you to know that cecum is midgut, so drained by the SMV. so my approach was automatically eliminate any answer that included IMV or Splenic vein and that left me with only Ileocolic → superior mesenteric → portal → right hepatic branch of the portal

 +0  (nbme24#6)

Cholestasis will present with elevated conjugated bilirubin, Alkaline phosphatase, GGT. Depending on the cause for cholestasis it can present with pale stools and dark urine.


 +1  (nbme20#10)

Prosthetic valves are one of the causes of extravascular hemolysis so suspect this in a patient that has symptoms of anemia such as fatigue, pallor, jaundice. Further supporting evidence in this patient is the increased indirect bilirubin. Also, look for elevated LDH, decreased haptoglobin.

nephroguy  All of this is correct except its intravascular hemolysis, not extravascular. Also look for hemosiderinuria, hemoglobinuria and schistocytes on blood smear

 +0  (nbme20#29)

Tetracyclines most common adverse effects are nausea/vomit/diarrhea and photosensitivity. Can affect bones and teeth of newborn if given to pregnant women. Also this drug class covers GAS, GBS, +/- MRSA, respiratory flora and intracellular.

Why Cipro is not the answer: Macrolide covers GNR + Pseudo, therefore not a treatment for acne (skin flora). And common adverse effects are C.Diff infection, QT prolongation, tendon rupture, teratogenic effects.



 +0  (nbme20#8)

Take a look at FA pg.623 for tanner stages of sexual development.


 +0  (nbme20#16)

I was thinking along the lines of facial sensation which is mediated by the trigeminal nerve and the fact that the trigeminal nerve is located in the pons.


 +0  (nbme22#44)

I had the same question regarding this. I know that external hemorrhoids rarely bleed and internal hemorrhoids present as painless bleeding so in my mind I knew I was being asked about internal hemorrhoids. However, superior rectal--> inferior mesenteric vein--> portal vein, can anyone tell me why the answer was superior rectal and not inferior mesenteric?

dubywow  Because the wording sucks. It's a confusing way to word the question. I too was confused what direct tributaries was referring to and chose Inferior mesenteric because I suck and also because this question sucks. Really its asking where are the hemorrhoids? They are on/from the superior rectals even though those veins feed to Inferior mesenteric.
drdoom  Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them).




Subcomments ...

submitted by sugaplum(80),

the deeper the melanoma goes the worse the prognosis

wishmewell  isn't the basement membrane the deepest? +  
wishmewell  nvm! lol +  
lilyo  I also picked basement membrane but unlike you I haven't had a "nvm" moment. Help please. +  


submitted by vshummy(65),

I think more generally, protein folding happens at the RER and the stem says the protein doesn’t fold properly. Specifically, the most common CF mutation is a misfolded protein and the protein is retained in the RER and not transported to the cell membrane - FA 2019 pg 60.

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +  
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +1  
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +2  
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +  
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +  
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +  


The disease here is fructose bisphosphatase deficiency. In it, IV glycerol or fructose doesn’t help because both enter the gluconeogenesis pathway below fructose bisphophatase. Galactose on the other hand enters above it. I don’t think you really need to know this to choose the correct answer since the clinical picture of fasting hypoglycemia that is corrected w/ some sort of sugar that can enter the gluconeogenesis pathway should clue you into the right answer.

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +9  
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +11  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +1  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +  


submitted by lm4(6),

in the exocrine pancreas, gallbladder, and liver pathology section of pathoma, sattar mentions that the epithelium lining biliary tract has alkaline phosphatase so when they are damaged it releases this, increasing serum alk phos.

lilyo  Cholestasis will present with elevated conjugated bilirubin, Alkaline phosphatase, GGT. Depending on the cause for cholestasis it can present with pale stools and dark urine. This patient has cholestasis due to choledocolithiasis. Look at FA 2019 page 390. +  


submitted by urachus(3),

not EPO bc it's asking what's made from the bone marrow. EPO is from kidney

lilyo  Thanks, I was wondering why EPO was not correct. So EPO synthesis would be stimulated in case of blood loss? its just wrong becase they ask specifically what is going to be produced in the bone marrow? +  


submitted by m-ice(145),

This girl has Mono caused by Epstein-Barr Virus. The symptoms are relatively vague, but lymphadenopathy like this would be common for Mono. The CBC shows elevated lymphocytes, implying this is not a bacterial illness, so viral is likely. Combined with the lymphadenopathy, this makes us worry about Mono. The Mono-Spot test for EBV is what the question is referring to when describing the sheep erythrocytes agglutinating. From there, this question requires that you know that in EBV infection, EBV infects B cells, but does not cause them to become abnormal. Instead, CD8 cells, which are actively trying to kill the B cells, become abnormal.

medskool123  NBME does trick now and then.. when they zig you zag. then when you think they are going to zag, they zig just to destroy yourself confidence. +5  
kylemax  The abnormal T-cells are known as Downey type II cells (Sketchy) +2  
haliburton  I was recognized EBV, then knew EBV infects Bc, and the atypical lymphocytes are Tc. Then I said CD8 are MHC1 for virii, and bingo bango, boom. +  
trichotillomaniac  congrats you played yourself +2  
lilyo  Soooooooo EBV infested B- cells is not considered atypical WTFF?? +  
med4fun  They are atypical b/c usually you do not see a super high amount of CD8+ in peripheral blood. Now there are a ton to try to stop the infected cells. +  


submitted by hayayah(512),

Statins can have a side effect of rhabdomyolysis.

lilyo  Statins have an increased risk of myopathy, specially when combined with other medications like Fibrates. This patient presents with muscle pain along with an elevated CK and + myoglobin test in urine. Consistent with myopathy. +1  


submitted by xxabi(125),

This is a thyroglossal duct cyst. The tyroglossal duct may persist and result in a thyroglossal duct cyst (occurring in midline near hyoid bone or at the base of the tongue), thus will classically move up with swallowing or tongue protrusion.

The foramen cecum (of the tongue) is the normal remnant of the thyroglossal duct

lilyo  I got it wrong though because the question clearly asks what does this structure (thyroglossal duct) DEVELOP from, not this structure eventually develops to form which structure. If it asked that then I would have picked option A but because it didnt that was the first option I crossed out. +3  


submitted by hello(108),

Patient's symptoms began 30 min after mowing lawn (i.e. after doing physical activity). He has severe chest pain and is cool, clammy, diaphoretic. He has increased pulmonary artery pressure and increased left atrial pressure. Taken altogether, this is cardiogenic shock.

Cardiogenic shock is a heart pump problem -- the LV isn't working.

When the LV, isn't working, it causes a back up in the direction opposite to how blood normally flows. Therefore, blood will back up in the lungs.

This causes increased capillary hydrostatic pressure --> this drives more fluid into the interstitium --> this causes increased interstitial hydrostatic pressure --> there is now more fluid than normal in the interstitium --> this affects the protein ratio within the interstitum --> this causes decreased interstitial oncotic pressure.

targetusmle  awesomely explained :) +  
lilyo  This was amazingly explained Thank you @Hello! +  


submitted by chandlerbas(26),

Legend:

OB = osteoblastic

OC = osteoclastic/osteolytic

P=prostate, B=breast, K=kidney, T=thyroid, L=lung

my mneumonic: Lead Kettle

P------------B-------------K--------------T------------L

OB-------OB/OC------OC------------OC--------OC/OB

lilyo  @chandlerbas is this pneumonic in order of most common to least common, as in is prostate cancer the most common cause of metastasis to the bone regardless of wether the patient presents with osteoclastic or osteoblastic lesions? +  


submitted by cyrus_em(0),

I don't know why I feel the correct answer is 100%. The ques states, "what is the chance that offsprings will EVENTUALLY develop cancer?, not inherit the mutation"

Prophylactic colectomy or else 100% EVENTUALLY progress to CRC.

lilyo  I also chose 100% with that same reasoning!!! +  
lilyo  @usmlecrasher, Yes it does so which is why if they inherited they have 100% chance of developing colon cancer later in life and the question was confusing because it didnt ask what is the percentage that this patient will have children with this mutation? It might be my language barrier but I don't know. +  
diegolc26  Its a little tricky bk they want you to think the probability of developing cancer IF the offspring HAS the mutation, which is 50%. I mean, he has 50% chances of inheriting the cancer developing mutation. Thats how I think they want to trick us. +  
mbourne  @cryus_em, you're putting way too much emphasis on the word "eventually". Either way the question and answer makes sense. It's an AD disease, so the chance of the offspring inheriting it would be 50% (and if they inherit it, they WILL develop adenocarcinoma of the colon, so the answer is still 50%). +  


submitted by cyrus_em(0),

I don't know why I feel the correct answer is 100%. The ques states, "what is the chance that offsprings will EVENTUALLY develop cancer?, not inherit the mutation"

Prophylactic colectomy or else 100% EVENTUALLY progress to CRC.

lilyo  I also chose 100% with that same reasoning!!! +  
lilyo  @usmlecrasher, Yes it does so which is why if they inherited they have 100% chance of developing colon cancer later in life and the question was confusing because it didnt ask what is the percentage that this patient will have children with this mutation? It might be my language barrier but I don't know. +  
diegolc26  Its a little tricky bk they want you to think the probability of developing cancer IF the offspring HAS the mutation, which is 50%. I mean, he has 50% chances of inheriting the cancer developing mutation. Thats how I think they want to trick us. +  
mbourne  @cryus_em, you're putting way too much emphasis on the word "eventually". Either way the question and answer makes sense. It's an AD disease, so the chance of the offspring inheriting it would be 50% (and if they inherit it, they WILL develop adenocarcinoma of the colon, so the answer is still 50%). +  


submitted by monoloco(75),

As a rule of thumb, if you give someone an ACE inhibitor and they get a problem, they had renal artery stenosis (usually bilaterally, or so we were taught at our med school). Probably has to do with decreased GFR thanks to decreased Angiotensin II–selective vasoconstriction of the efferent arteriole => decreased sodium delivery to macula densa => increased renin release.

lilyo  Vasoconstriction of the EFFERENT arteriole actually leads to increased GFR. It selective VASODILATION of the efferent arteriole effect of ACE inhibitors since they undo Angiotensin II actions. This patient already has rescued renal blood flow due to bilateral renal artery stenosis, the addition of an ACE inhibitor further decrease GFR prompting an increase in renin due to loss of negative feedback. +1  


submitted by xxabi(125),

Terminal Complement (C5-C9) Deficiencies increase susceptibility to recurrent Neisseria bacteremia. Patients most often present with recurrent meningitis.

lilyo  FA 2019 P. 107 Early and Terminal complement deficiencies. +  


submitted by strugglebus(86),

So you know that 65% of the data will fall within 1SD of the mean. So if you subtract 100-65 you will get 35. Which means that about 16% will fall above and 16% will fall below 1 SD. They are asking for how many will fall above 1 SD. I'm sure there is a better way of doing this, but thats how I got it lol.

sympathetikey  Same! +  
sympathetikey  Except according to FA, it's 68% within 1 SD, so 34%, which split in half is 17%. +2  
amirmullick3  Sympathetikey check your math :D 100-68 is 32 not 34, and half of 32 is 16 :) +3  
lilyo  Can anyone explain why we subtract 68 from 100? This makes me think that we are saying its 35% of the data that falls within 1SD as opposed to 65. HELLLLLLP +  
sallz  @Lilyo If you consider 1 SD, that includes 68% of the population (in this case, you're saying that 68% of the people are between 296 and 196 (1SD above and 1 below). This leaves how many people? 32% outside of that range (100-68=32); half of those would be above 296 and the other half below 296, so 16% +1  


Itraconazole requires the acidic environment of the stomach to be absorbed. Omeprazole inhibits the H+/K+ pump of the stomach, thereby decreasing the acidity of the stomach. So when the patient takes Omeprazole and Itraconazole together, Itraconazole won't be absorbed into the body. That's why it has no effect.

It's recommended to take medications at least 2 hours prior to taking an antacid.

necrotizingfasciitis  Just adding support to the above explanation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671798/ +1  
pakimd  do all azoles or just itraconazole only requires an acidic environment to be absorbed? +1  
chandlerbas  just itraconazole and posaconazole +1  
lilyo  @chandlerbas, where did you find this information? I was looking over this on FA but they do not mention it and I would like a bit more information. Thanks! +  
chandlerbas  haha no stress! the article above submitted by @necrotizingfasciitis does a descent job explaining it, however its not good enough, I looked into a bit more on uptodate but wasn't fruitful in my endeavours. goodluck! +  


submitted by hayayah(512),

He has fecal incontinence so his external sphincter is damaged, which is innervated by the pudendal n. (S2-S4). The pelvic splanchnic nerves, which mediate the erection process, are also S2-S4.

thomasburton  Why could this not be dysuria? +  
lilyo  I think that you are thinking about urinary incontinence. If we damage the pudendal nerve S2-S4, you can exhibit urinary and fecal incontinence since this nerve innervates both the urethral and the external anal sphincters. However since the pelvic splanchnic nerves also have roots that originate in S2-S4 a patient with pudendal nerve damage will also have impotence since these control the erection reflex. He wouldn't have dysuria which is painful urination. Most likely caused by a urethral infection or a blockade of the urinary tract. He would have urinary incontinence. I hope this helps. +3  


submitted by bobson150(4),

The wording of this question confused me. This is asking "which of these vessels is the high pressure system" right? So the high pressure superior rectal is causing increased pressure into the inferior rectal?

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360 +7  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +3  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +1  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +