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They really had mercy here by not also including Transference as an option.... phew.
If I'm reading this right, this is just a tricky dicky question. I think CO binds 200x stronger than O2. But if an O2 cycles through binding / unbinding 200 times before a CO gets kicked off, this should still clear the CO from that cell sooner or later. strange to think it is 1. essentially permanently trapped in a cell, and 2. doesn't kill you and can be treated with O2 to resolution within a few hours or a day. They must just be thinking, until that last RBC dies, you've got original CO in a circulating cell. but just a fraction (because you didn't die). not sure how that CO isn't just passed on during recycling, based on this line of thinking.
The question while stupidly written, asks how long the RBC's that carry the CO take to be removed from the circulation, not how long the CO takes to be removed from the RBC. Just asking the lifespan of RBCs in an stupidly complicated way. As we know, RBC's life span is about 120 days and then they are removed from our circulation. 120 days is about 4 months. Next time they will probably ask weeks or in hours, who knows? smh
If that's what they're looking for why cant the NBME people just ask "How long does it take for RBCs to turn over?" Ridiculous.
This question is likely not important for two reason:
They're both Trypansomastigotes, so of course they look almost the same.
You can differentiate these two species clinically as they have very little clinical similarity in patient presentation.
For these reasons there's little to no reason you would be expected to differentiate these two species by histology alone
Does Chagas have recurrent fever? Because that's what pointed me to African Sleeping Sickness.
The history of travel to the Amazon is what pointed me to Cruzi over Brucei but agree it's a tough distinction to make here. In the absence of that detail I would have probably picked Tsetse fly.
That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea?
Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...?
@pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :)
salt and sugar, that's all the kid needs when ill simple
you're definitely not alone lol
And its not in FA, so fuck it IMO
I guessed it because the names sounded similar :D
I also guessed because both words start with "glu")))
same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
Not a clue. This was so random.
this made me feel a lot better.
also, no fucking clue
My immediate thought after reading this was "why would i know this and how does this make me a better doctor?"
Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess.
yea, I mature 30k anki cards to see this bs
I literally shouted wtf in quiet library at this question.
Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol
Is it biochemistry? Then I do not know it.
I Ctrl+F'd glucosamine in FA and it's not even there lol
i definitely guessed, for some reason got it down to arginine and glutamine
I did not
Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic.
+1 no idea!
troponin = irreversible injury and membrane damage -> high extracellular concentration of Na+ and Ca++ causes both to move into cell through damaged membrane and high intracellular K+ leaves the cell
Question is asking about the changes in the myocardiocytes and my second interpretation was that they are asking the changes before they "rupture" and liberate their content in the blood producing increase enzymes in the patient. Therefore because is a ischemic process = reduction of O2 = low ATP = impairment of Na/K ATPase = increase Na-decrease K intracellular = block Ca/Na exchanger = increase Ca intracellular.
the same effect as digoxin
What will happen to Na and ca conccentration when there is an irreversible injury?
@allodynia Pathoma pg. 4 has a really good summary of this. In short, Na+ and Ca2+ both increase intracellularly in an irreversible injury.
Aren’t both H.pylori and EBV associated with gastric lymphoma?
So do we just have to memorize this...
@yotsubato Not necessarily. I can't remember a formula to save my life. The Css is the amount you want in the blood. The clearance is the fraction removed per unit time. Since we want to maintain a steady state, we only need to replace what is removed.
Thus, maintenance dose = amount present * fraction removed.
I remember CLoCk Time as in check the clock time to give the next dose
Cl = clearance, C = concentration and T = half life. I have never had to use F.
This is on p. 233 in FA 2019.
Also look for Kluver-Bucy like symptoms in the stem
I agree with everything but normal glucose. Glucose here is NOT normal.
to quote wiki
"The glucose level in CSF is proportional to the blood glucose level and corresponds to 60-70% of the concentration in blood. Therefore, normal CSF glucose levels lie between 2.5 and 4.4 mmol/L (45–80 mg/dL)."
NBME reference table gives normal CSF glucose to be 40-70 mg/dL. As far as I'm concerned, for the purposes of the exam the reference table is probably a better source than wiki.
For more, FA 2019 p. 262 goes over Type I and II errors.
Alcohol withdrawal sx (p. 554 FA 2018)
Time from last drink:
3–36 hr: tremors, insomnia, GI upset,
diaphoresis, mild agitation
6–48 hr: withdrawal seizures
12–48 hr: alcoholic hallucinosis (usually visual) 48–96 hr: delirium tremens (DTs)
there is a delayed onset hemolytic transfusion reaction which should be evaluated with direct cooms test.
takess longer due to slow destruction by RES
Dang, I didn't know that was the same thing as a direct Coombs test. I guess it makes sense in hindsight. Thanks!
(This is the right page for FA 2019)
FA2019 p. 581. Fanconi syndrome causes a type 2 (proximal) renal tubular acidosis
I had narrowed it down to that and the correct answer. I think the difference is that esophageal spasm tends to present with pain and dysphagia. FA 2019 p. 371, right at the top of the page.
Relating the phrase "diffuse painful contraction" to esophageal spasm has helped me remember the associated descriptions they go to.
FA2020 P497(Sleep physiology): Changes in narcolepsy: decrease REM latency.
p. 485 for us plebs still using FA 2019
Mechanism of opioid-induced rhinorrhoea, lacrimation, stomach cramps and diarrhoea is actually muscarinic receptor effects, rather than alpha adrenergic blockade caused by cocaine, causing nasal vasoconstriction.
Symptoms of Opioid Withdrawal can be remembered with the phrase "anxious, hot, and moist" per SketchyPharm Opiods. Rhinorrhea is one way people can be "moist" during opioid withdrawal, but they can also sweat excessively and lacrimate too.
agreed! more specifically damage to the VPL
Pg. 403 FA 19.
Both commenters above got the page wrong; it's FA 2019 p. 503.
what were the odd of both being wrong
winter's formula is to look at the compensation to see if it is appropriate.
PCO2 = 1.5[HCO3-] + 8 +/- 2
In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25
Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis
in other words, winter's formula is not necessary for this question
@ergogenic22 Someone might use Winter's formula to rule out choice A.
Isn't the low pCO2 enough to rule out A?
Understood, but is there anything in the question that rules out BPH specifically? I honed in on the words "most likely" and saw he was 60. I guess I overthought it but I'd appreciate any insight as to what if anything in the Q makes that definitively wrong.
I think the question stem, with the trauma and fractures, points you in the direction of membranous urethral trauma. Pelvic fractures are more associated with urethra damage than prostate damage, although they're right next to each other, and I can see why someone would choose prostate hypertrophy. Also, I'm not sure if bleeding is associated with BPH.
can remember it as wearing a pearl necklace (upper 2/3 of throat-ish)
Patient is also a heavy smoker and drinker. In the absence of GERD this should raise suspicion for SCC of esophagus over Adenocarcinoma.
Deltoid only does abduction from 15 to 90 degrees. So not overhead.
With that logic, supraspinatus only does abduction form 0-15
the positive empty can test is the biggest thing "pain and weakness with abduction, particularly with simultaneous shoulder internal rotation" - that tells you it has to be one of the SITS muscles (supraspinatus, infraspinatus, teres minor, subscapularis), not the deltoid.
tenderness in the right deltoid region tells you it's the supraspinatus which is right underneath the deltoid muscle
Alpha receptors are also G-coupled and are another potential site of action for Epinephrine (at high doses according to SketchyPharm Sympathomimetics)