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Welcome to jackie_chan’s page.
Contributor score: 7


Comments ...

 +0  (nbme15#22)

Hey Peter

Go sincerely fuck yourself with a 10 foot pole.

Love

Med students

jackie_chan  50$ a month when all content is contributed by the community, wheres my cut? +
jackie_chan  Wheres every contributor's cut? +

 +2  (nbme22#19)

I found an easier way to just logic through this is the complaints are basically muscle spasms, tetany, hyperreflexia.

  • Abnormalities in bicarbonate give metabolic acidosis/alkalosis, nothing in stem gives us reason to think theres acid/base balance.
  • calcium, hypocalcemia textbook fits with tetany, hyperreflexia
  • abnormal chloride not much clinically significant
  • potassium abnormalities can have tetany but also arrhythmia, no signs of cardiac involvement
  • sodium, hyponatremia can have seizures, hypernatremia have irritability and signs unlikely to be ongoing for entire month.
nootnootpenguinn  Thank you so much for the potassium explanation! It was totally a "D'oh!" moment, haha! +1

 +1  (nbme22#20)

If estrogen is low and FSH/LH high, the problem at ovaries. FSH/LH both low so problem with the pituitary gland releasing FSH/LH or even higher up with GnRH in the hypothalamus. Best answer hypothalamus


 +0  (nbme21#12)

I approached this question because man with rather extreme HTN and abdominal bruit is quite often renal stenosis

ALso captopril renal radionuclide scan's function is literally to assess renal stenosis (looked it up, but i did not know that when i answered)


 +3  (nbme20#37)

Cystic fibrosis patient --> consider fat soluble vitamin deficiencies Presentation is neurologic with ataxia, mostly likely Vit E

A deficiency- visual, infections D- calcium low K- bleeding, coagulopathy

Folic acid- anemia, not given B6- anemia also (heme synthesis defect/ALA synthase)





Subcomments ...

submitted by cassdawg(580),

Hormone sensitive lipase (HSL) is the enzyme which degrades triglycerides stored within adipocytes (FA2020 p93). Thus, it makes sense that it is activated in times of fasting and suppressed in the fed state.

Insulin would inhibit HSL, as insulin is a fed state enzyme secreted by the pancreas and would want to trigger storage of triglycerides.

In contrast glucagon is secreted in response to hypoglycemia by the pancreas and will trigger fasted state activation. In terms of the fed/fast state I always think of glucagon and epinephrine kind of like a superhero and their side kick, because they usually work together in the fasting state on similar targets to ensure the body has enough energy (this helps me remember that epinephrine and glucagon are fasting state hormones). Here though is epinephrine's big action away from glucagon, where glucagon has minimal effect and epinephrine has the big action of activating HSL! Glucagon has a minor role and other catecholamines and ACTH can also serve to activate HSL as well.

Another example of the synergistic work of glucagon and epinephrine is in glycogen breakdown (FA2020 p85). Both will trigger cAMP increase and protein kinase A activation which will phosphorylate glycogen phosphporylase and activate it (FAST PHOSPHORYLATE! Hormone sensitive lipase is actually phsophorylated to activate it as well).

FUN FACT: Hormone sensitive lipase actually got its name because it was sensitive to epinephrine!

flapjacks  In Type 1 DM, the glucagon response to hypoglycemia is not functional and these individuals are reliant on the epinephrine-stimulated hepatic glycogenolysis. I recall this by remembering you can administer glucagon to these patients if they're having a hypoglycemic episode. They can respond to it, but they aren't releasing it. +  
passplease  How did you eliminate thyroxine? As it also plays a role in lipolysis. I was thrown off my the low blood pressure and therefore did not select epinephrine. Why would they still have a low blood pressure? +  
jackie_chan  ^ they have low blood pressure because DKA causes a lot of dehydration (vomiting, diuresis due to osmotically active glucose in urine) so low BP Thyroxine I eliminated because remember that thyroxine is unique in that it functions similar to a steroid hormone and acts in the nucleus to upregulate expression of many genes. I figured hormone-sensitive lipase needs to be activated, not stimulated to upregulate expression, so I thought about EPI and beta-3 stimulation. fuckPeter +  


Hey Peter

Go sincerely fuck yourself with a 10 foot pole.

Love

Med students

jackie_chan  50$ a month when all content is contributed by the community, wheres my cut? +  
jackie_chan  Wheres every contributor's cut? +  


Hey Peter

Go sincerely fuck yourself with a 10 foot pole.

Love

Med students

jackie_chan  50$ a month when all content is contributed by the community, wheres my cut? +  
jackie_chan  Wheres every contributor's cut? +  


MDMA is the only hallucinogen that has sympathetic activity as it is derived from methamphethamines ( look at its name) ... that explains everything.

tyrionwill  Yes, good point to remember. In the category of FA stimulants, 2 agents has sympathetic activity: 1)MDMA; 2)PCP +  
jackie_chan  Basically how I solved it, all the other drugs are downers +  
jackie_chan  Even tho ketamine has sympathomemetic effects, they would be widly tripping, they dont call it falling into a K-hole for nothing. +  


MDMA is the only hallucinogen that has sympathetic activity as it is derived from methamphethamines ( look at its name) ... that explains everything.

tyrionwill  Yes, good point to remember. In the category of FA stimulants, 2 agents has sympathetic activity: 1)MDMA; 2)PCP +  
jackie_chan  Basically how I solved it, all the other drugs are downers +  
jackie_chan  Even tho ketamine has sympathomemetic effects, they would be widly tripping, they dont call it falling into a K-hole for nothing. +  


submitted by usmle11a(66),

spironolactone acts as an aldosterone antagonist which means decreasing Na+ permeability

j000  i think they're referring to triamterene and amiloride, not spironolactone spironolactone doesn't actually decrease Na+ permeability +  
jackie_chan  @j000 It doesnt matter, spiro and triamterene/amiloride have a common effect of messing with ENaC. Aldosterone upregulates ENaC, spiro would inhibit that so in effect would decrease luminal permeability to Na in duct due to fewer ENaC channels; triamterene would block the channel directly, same effect. http://tmedweb.tulane.edu/pharmwiki/doku.php/potassium_sparing_diuretics +  


submitted by aesalmon(79),
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liinClac tairl - ecopsrma aeittecpuhr fteiensb of 2+ reatnttesm anfrarw(i v.s a-nle)pOnlabpdtela ier - htbo the tlheha rrvodpies nda het pt rae reawa of het durg bngei veign

jackie_chan  How are we supposed to know in the question the patients and providers are aware that they know what they are being given? +  
haydenelise  I went back and forth about it, but in the end figured that they were aware since one regimen involved subQ injection + oral med and the other was subQ injection alone with no oral placebo. +2  


submitted by adong(82),

hit the kidney so retroperitoneal. leaves only the duodenum and splenic flexure. kidneys are more lateral structures so splenic flexure (at turn of descending colon)

jackie_chan  Basically how I reasoned too; left kidney is close to tail, not body, of pancreas so that was out, duodenum is right side, stomach is not retroperitoneal, supraadrenal gland is superior to kidney, not immediately anterior; thus leaves splenic flexure (and its also left side) +  


submitted by seagull(1112),
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fI uyo otn'd nwko thwa raiclmuoD sedo ikle nay nmloar anu.hm Teh cfous on wath iisparn oedtns' d,o emaynl ti's e'ndtso acfeft TP tiem adn otms lilps 'notd neiesrca lctntogi seelalci(py wtih )sp.riina Tish si woh I lcogi to hte rgith wrs.nae

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +11  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +4  
drmohandes  Because dicumarol does not decrease platelet count either. +  
krewfoo99  @usmleuser007 Because the answer choice says decrease in PTT. If you take a heparin like drug then the PTT will increase. Drugs wont increase PTT (that would be procoagulant) +3  
pg32  I think usmleuser007 and is3076 were working form the perspective of not knowing what dicumerol was. If you were unsure what dicumarol was, there really wasn't a way to get this correct, contrary to @seagull's comment. You can't really rule out any of these as possible options because aspirin doesn't do any of them. +2  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +3  
jackie_chan  Not true, the logic works. You gotta know what aspirin does at least, it interferes with COX1 irreversibly and inhibits platelet aggregation (kinda like an induced Glanzzman), all it does. PT, aPTT are functions of the coagulation cascade and the test itself is not an assessment of platelet function. Bleeding time/clotting time is an assessment of platelet function. A- decreased plasma fibrinogen concentration- not impacted B- decreased aPTT/partial- DECREASED, indicates you are hypercoaguable, not the case C- decreased platelet count- aspirin does not destroy platelets D- normal clotting time- no we established aspirin impacts clotting/bleeding time by preventing aggregation E- prolonged PT- answer, aspirin does not impact the coagulation factor cascades in the test +1  
teepot123  di'coumarin'ol +  


submitted by gh889(89),
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arcoKtloe is a vesrebriel DSNAI ginve ,IV all sSDIAN aveh a rski fo ttinelatiirs rpnthie,si aelnr ,hisameic srciatg sc,leru nad acltpias .emania

the sbet wnrsea is nlrea fraelui /bc ti is gveni VI dan has ssle fo a canceh fo saucing rctaisg uscler

tiredofstudying  I would also take into account that this patient has had HTN and T2DM for 20 years. His kidneys are probably shot. +5  
jackie_chan  @tiredofstudying 100%, thats probably why the mentioned it, if you didn't know wtf ketorolac was (I didnt) but i saw a long 20 year history of HTN, DM I assumed his kidney def could not be fully functional +  


submitted by hungrybox(791),
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ugjular ovuens iteinosntd = felt erath alfruie

rynpluamo eeamd = trghi rtahe lruefia

croFm-urbeha niiatdlo si eht smot klyiel n.erasw

threO sreaswn:

  • cmsiAeyrts atespl yehy,rhrpotp arolmaydic s:draaiyr teseh ear othb sicscla snfngiid in hhptipyoercr apyyohoaicrmtd )HM(C
  • ardenlicdoa eborsatiosf:ils a rrae iesvrttcrie yhcpaoimryadto esen ni ftanhnnisercidl/
  • chypclyimot norfainiltti fo eht mmoircuy:da enes in varil )unumte(oima yiimcts.rdao A eucsa fo dlieadt ,aymycrhiodpaot but rehte asw on temonin fo a iecpegdnr ailvr .isslnel
meningitis  I think you meant: Jugular venous distention = LT HF Pulmonary edema = RT HF +4  
hungrybox  woops yea I meant Jugular venous distention = RIGHT HF, Pulmonary edema = LEFT HF +10  
jackie_chan  What threw me off the picking 4-chamber dilatation was it seemed like that would be a major cardiac/ventricular remodeling and the vignette gave a somewhat acute 2 week onset +