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Welcome to peteandplop’s page.
Contributor score: 13

Comments ...

 +0  (nbme20#48)

Can anyone explain why it's not anxiolytic? My logic was this dude has a bum ticker from previous MI, and his HR was 104/min--which can't be good for the old heart. I went w/a anxiolytic to bring his HR and anxiety under control.

Would an antidepressant do the same, thus, is it a better answer, or cover a wider range of symptoms?

 +2  (nbme19#0)

The above is correct in terms of MoA, however I believe the stem states it is PT (prothrombin) prolongation, not PTT (Partial Thromboplastin). I did not have any idea what dicumarol was.. but here was my logic:

  1. Patient had aortic valve replacement, she's 80, probably put on an anti-coagulant
  2. I know Warfarin is sold under the brand name Coumadin
  3. Remind yourself that Warfin was discovered in 1927 (10,9,2,7) and inhibits Vit K dependent clotting factors (vit K deficiency-like state)
  4. Pronounce the drug not in FA as diCOUMarol, and you shall hopefully now know it also inhibits epoxide reductase, and pseudo guess your way to victory.
rina  Yes it was PT! Personally I forgot that PT detects changes in I, II (thrombin), V, VII, & X. Vit. K affects II (thrombin), VII, IX & X so there is significant overlap. +

 +1  (nbme19#41)

FA2019 p490, patient presents with UMN lesion of face. Motor is anterior to central sulcus, sensory is posterior (C vs F); face location via homonculus diagram. Motor UMN facial lesion will present ipsilateral lower 2/3 dysfunction.

FA2019 p520, forehead is spared in UMN face lesion due to bilateral UMN innervation.

 +4  (nbme19#0)

This patient is presenting with with STEMI (FA2019 p301), thus the entire vessel must be occluded. Coronary vasospasm via a1 stimulation (increased smooth muscle contraction) would lead to these findings.

As far as the nitro aspect, I think this could be referring to pt history of ischemic heart disease, and the scenario of coronary steal, however I don't think you would need that to answer this question (and I could be going down an unnecessary rabbit hole of misery).

Other helpful pages are FA2019 p238, a1 sympathetic stimulation results in increased vascular smooth muscle contraction.

Last, big ups to the brother for setting arguments aside and still taking his hermano to the emergency department. Perhaps they were arguing at who responded to COVID-19 and medical education worse: USMLE or Prometric.

 +1  (nbme19#39)

While not traditionally discussed, the kidneys' contributions to maintaining glucose homeostasis are significant and include such functions as release of glucose into the circulation via gluconeogenesis, uptake of glucose from the circulation to satisfy their energy needs, and reabsorption of glucose at the level of the proximal tubule.

FA2019 p78 - [Gluconeogensis] occurs primarily in the liver; serves to maintain euglycemia during fasting. Enzymes also found in kidney, intestinal epithelium.

... seems like a silly thing to test... shrugs shoulders laughs in NBME

Subcomments ...

submitted by yotsubato(836),
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djjix  Non sense ... you can hide the amputation from her +15  
charcot_bouchard  Just show her one leg twice. +4  
pg32  I picked "request that an oncologist..." because I figured it would be better to have someone with more knowledge of next steps and prognosis discuss the disease with the family as compared to someone working in the ED... why is that wrong? +2  
ibestalkinyo  @pg32: Referring to another physician is almost never an answer for NBME/USMLE questions. Plus, I feel like this would be hiding the patient's problem from her and the patient's parents. +3  
dunkdum  I think the reason that you requesting the oncologist isnt the most correct answer here is because... even if more tests needed to be done... you would still discuss with your patient about that fact and say "Hey these results came back suggesting that you might have this disease, we will need to do more testing to make sure we can get it taken care of if you in fact have this disease." and you'd probably do that before you go and get the oncologist. +2  
peteandplop  @pg32 I was kind of with you, but I went with the correct answer because it says STRONGLY suggestive. If you're giving me a powerful word to really emphasize this is osteosarcoma, there's no need to delay passing that information to patient, and in this case of a minor, her parents. +  

submitted by cassdawg(610),

This is normal menopause (FA2020 p636). Average age of onset is 51 years (our woman is 52). Hot flashes are a common symptom.

In menopause, the ovaries stop secreting estrogen (17beta-estradiol is an estrogen) due to a decline in the number of ovarian follicles with age. FSH is increased because the feedback inhibition is removed. The source of estrogen after menopause becomes peripheral conversion of androgens.

peteandplop  FA2019 p622 +1  
cheesetouch  FA2018 P617 +  

submitted by cassdawg(610),

I don't like how they are asking this, but I think what they are getting at is that after the stent placement ("subsequent to the stent placement") there will be reperfusion injury to the myocardial tissue which occurs through free radical injury and therefore membrane lipid peroxidation is the best answer (FA2020 p210 mentions membrane lipid peroxidation as a mechansism of free radical damage and lists reperfusion injury after thrombolytic therapy as a type). Elevations in the cardiac enzymes I assume are because of the injury to the cells.

zalzale96  Created an account just to up vote this answer +1  
cheesetouch  1998 journal via google " Myocardial injury after cardiac surgery with cardiopulmonary bypass may be related to free oxygen radical-induced lipid peroxidation" +  
peteandplop  "Evidence suggests that reactive oxygen species (ROS) may play important roles in the pathogenesis in myocardial infarction [2]. Following ischemia, ROS are produced during reperfusion phase [3, 4]. ROS are capable of reacting with unsaturated lipids and of initiating the self-perpetuating chain reactions of lipid peroxidation in the membranes" ( +1  
mittelschmerz  Honestly the wording got me on this one. Great answer +  
acerj  Also, you can rule out a few of the options to help justify this. Post MI you expect necrosis, not apoptosis. Remember, apoptosis is suicide, and necrosis is MURDER! Cell swelling is a sign of cellular injury, not cell shrinkage. The heart will undergo coagulative necrosis, not liquefactive necrosis. Also, protease inactivation by cytoplasmic free calcium is kind of nonsensical to me. Free calcium is more likely to cause cell injury via caspases (a form of proteases amongst other things), which is why calcium is usually bound up inside healthy cells. +  

I think that this is osteogenesis imperfecta based on the hx of several fractures that occurred during birth.

From FA2019, pg. 51: Manifestations can include--multiple fractures with bone deformities and minimal trauma; may occur during the birth process

OI is caused by gene defects in COL1A1 and COL1A2; most common form is autosomal dominant with decreased production of normal type 1 collagen.

cheesetouch  OI does have macrocephaly +1  
cheesetouch  FA2018 P 51 +  
peteandplop  If you've ever seen Unbreakable, the main villain (Mr. Glass) has OI and is born with many broken bones--memorable scene to remember this disease (; Other memory device, OI = bONEs for Collagen Type ONE +3