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Comments ...

 +1  (nbme22#9)

Some extra thoughts on distinguishing between Roseola/Parvo. I was a little thrown off by the:

  • fever since 1 week
  • rash since 4-days
  • my brain → rash after 3 day fever = Roseola


However, if I had read more carefully:

  • rash did not spare face
  • no mention that fever was gone after 3 days, might still have fever
  • 5-year old boy; Roseola usually in 6m-2year old.

 +0  (nbme22#1)

Newly born → ligament of Treitz on the wrong side → something went wrong with rotation...

In the 10th week the midgud rotates 270 degrees counterclockwise around the superior mesenteric artery (FA2019 pg352).

 +0  (nbme22#49)

Countertransference (FA2019 pg. 542) = doctor projects feelings about formative or other important persons onto patient (e.g. Epstein didn't kill himself).

 +1  (nbme22#15)

Finger flexion done by:

  • FDP = flexor digitorum profundus (flexes DIP)
  • FDS = flexor digitorum superficialis (flexes PIP)



  • FDS 2/3/4/5 by median (C5-T1)
  • FDP 2/3 by median (C5-T1)
  • FDP 4/5 by ulnar (C8-T1)


Our patient can't flex DIP of ring finger → FDP4 → ulnar → C8-T1.

Only possible answer we can pick is C8.

 +0  (nbme22#28)

Iron accumulation causes free radical damage in organs:

  • liver → dysfunction / ascites / cirrhosis
  • pancreas → glucose intolerance (diabetes)
  • heart → cardiac enlargement (LVF can leads to prominent pulmonary vasculature)

Also notice patient + older brother are >40, which is when total iron body accumulates enough to cause symptoms.

 +0  (nbme22#30)

Primary olfactory cortex is located in the temporal lobe.


 +0  (nbme22#45)

Our patient has a metabolic alkalosis with (partial) compensatory respiratory acidosis.


Metabolic alkalosis → H+ loss or HCO3- gain:

  • vomiting: lose H+ (and lose K+/Cl-)
  • loop diuretics: lose H+ (and K+)


Metabolic acidosis, possible causes in this context:

  • diarrhea/laxatives → lose HCO3- (and K+) ; Cl- compensatory increase (normal anion gap)
  • acetazolamide → lose HCO3- (and K+) ; H+ also decreases but not enough to overcome the alkalosis caused by HCO3- loss
  • spironolactone

 +0  (nbme22#32)

You mostly lose HCO3- and K+ in stool.

Loss of HCO3- leads to a normal anion gap metabolic acidosis (FA2019 pg. 580 'HARDASS'), in which we also see a compensatory increase in Cl-.

 +0  (nbme22#1)

Here we go:

  • decreased LV contractility (bilateral crackles)
  • decreased cardiac output
  • activate RAAS → ADH
  • increase sympathetic activity → more RAAS → more ADH

 +0  (nbme22#47)
  • DIC, unlikely: PT/PTT normal; wouldn't just see gum bleeding
  • hypersplenism: would cause anemia
  • iron deficiency: anemia
  • vitamin C deficiency: wouldn't cause thrombocytopenia
  • von Willebrand disease: mixed platelet/coagulation disorder → would cause deep joint bleeding instead of mucosal membrane bleeding. Inherited (Autosomal Dominant), would see symptoms before. PTT can be normal/high.

 +0  (nbme23#37)

I tried to calculate it more precise, and messed up the answer...

Here is why:

  • 99.7% CI = 3 SD
  • However: 99.0% CI is actually 2.5 SD (or 2.57 if you want to be more precise)

1 SD = 1.5 mmHg → 2.5 SD = 3.75 mmHG

This results in a 99% CI of 109.25 (113-3.75) to 116.75 (113+3.75)

Closer to answer C than B.

 +0  (nbme23#26)

Case = Middle-aged female with severe hypertension (180/120 mmHg), and an aneurysm.

(1) Main cause of renovascular diseae in middle-aged females = fibromuscular dysplasia (FA2019 pg. 592).

(2) Also notice the -classic- 'string-of-beads' appearance of the artery: EXAMPLE

Subcomments ...

submitted by seagull(432),

If you don't know what Dicumarol does like any normal human. The focus on what aspirin doesn't do, namely it's doesn't affect PT time and most pills don't increase clotting (especially with aspirin). This is how I logic to the right answer.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +2  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +  
drmohandes  Because dicumarol does not decrease platelet count either. +  

submitted by armymed88(15),

emphysema leads to CO2 trapping leading to increase paCO2 in the blood, which gives you a respiratory acidosis Proper renal compensation will increase bicard reabs and decrease excretion- giving you increased bicarb in the blood

meningitis  Increased blood HCO3 could have easily been interpreted as increased blood pH aswell. FOllowing your explanation, since the pt had acidosis, the increased HCO3 will just make it a normal pH. Another way to think of the question is: if there is decreased exhalation due to COPD --> increased CO2 --> increased CO2 transported in blood by entering the RBC's with Carbonic Anhydrase and HCO3 is released into blood stream. So increased CO2 -> increased HCO3 seeing as this type of CO2 transport is 70% of total CO2 content in blood. +8  
drmohandes  I thought you could never fully compensate, so your pH will never normalize. Primary problem = respiratory acidosis → pH low. Compensatory metabolic alkalosis will increase blood HCO3-, but not enough to normalize pH, it will just be 'less' low, but still an acidosis. +