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FA says, "euphoria, disinhibition, hyperactivity, distorted sensory and time perception, bruxism.
Lifethreatening effects include hypertension, tachycardia, hyperthermia, hyponatremia, serotonin syndrome."
So I think they wanted you to see Sinus Tachy and jump for MDMA. Idk why Ketamine couldn't also potentially be correct though.
I picked ketamine because it said no diaphoresis. But if you need to find a reason, I guess the half life of ketamine might rule it out. Remember from sketchy, ketamine is used for anaesthesia induction, so probably won't keep the HR and BP high for 8 hrs. In fact, its action is ~10-15 mins-ish iv.
Because the NBME is full of fuckers. The guy is probably dehydrated so he cant sweat anymore?
you wouldnt see tachycardia with ketamine. It causes cardiovascular depression but honestly i saw " all-night dance party" picked the mdma answer and moved on lol
Ketamine acts as a sympathomimetic but oh well. NBME hasn't caught on to ketamine as a drug of recreation :)
@usmleuser007 LSD doesn't cause HTN and ↑ HR.
@fulminant_life FALSE. KETAMINE CAUSES CARDIOVASCULAR STIMULATION.
Take a look at why the patient has pale and cold extremities.
"Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation."
@sbryant6 you're both saying the same thing. Ketamine has a direct negative inotropic effect on the heart, but it is also a sympathomimetic. You are both correct.
@drzed Can you please site that? As far as I understand ketamine has a sympathomimetic effect on the CV system --> increased chronotropy and BP. I also don't see how they're saying the same thing. One person said "stimulation" and the other said "depression"
People tend to drink a lot of water on MDMA. I just guessed the confusion was a result of hyponatremia (too much free water) but no idea if there's any data saying that people tend to become hyponatremic due to water over-consumption on MDMA lol.
Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN.
I ruled out selection A since it is involving the interlobar artery. Renal artery stenosis involves the "renal artery" and the stem gives you fibromuscular dysplasia with renal artery stenosis.
I was between granulation tissue and granuloma. Then ruled out granulation tissue because this is a 10 week old wound. Assuming normal wound healing, granulation tissue would be replaced by type III collagen/resolution by 10 weeks.
Got this right because the exact same question is in Uworld.
Got baited... took my eye off the ball (and onto that worst photo ever) and missed the Ten week part. Granulation for the "L".
Anytime they go out of their way to mention sutures, my mind goes right to granulomas
there are multinucleated cells(minimum 4). this helped me to choose granuloma over granulation tissue
FA P120-122. Immunosuppressants for RA are calcineurin inhibitor (cyclosporine and tacrolimus), 6MP, and TNFa inhibitors (adalimumab,infliximab, etanercept). It is important to distinguish that calcineurin inhibitors block t cell activation by preventing IL-2 transcription, not necessarily block IL-2 action. Sirolimus(rapamycin) blocks IL-2 action but it is used for kidney transplant rejection prophylaxis specifically.
in addition to the above responses, IL 1 antagonists (Anakinra) can be used to treat RA. Anakinra is a recombinant human IL 1 receptor anatagonist but less effective than other treatment modalities.
Prednisone is a glucocorticoid (which inhibits IL-2 synthesis) is already being used with no effect. So TNF-alpha is the next option.
DMARDs: methotrextate, sulfasalazine, hydroxychloroquine, leflunomide, TNF inhibitors, Anti- IL6 (Tocilizumab), JAK inhibitor (Tofacitinib), Rituximab.
You can use cyclosporine and tacrolimus to treat RA, but those aren't first line treatments. DMARDs are used the long term treatment of RA and methotrexate is often started first, and the other drugs are prescribed if methotrexate does not sufficiently control symptoms. None of the other choices listed are a part of DMARD therapy.
Can you please explain how gastrin relates to the physical exam findings in the patient?
I believe the logic behind it is patient has pain and black stool, suggesting peptic ulcer with bleeding. Since pain is not relieved by antiacid and H2 blockers, it suggests ectopic source to stimulate the excessive acid. Among all, gastrin by ZE syndrome fits the most.
Also has hypotension and light headedness with blood loss due to a bleeding ulcer. The sweating is likely from sympathetic activation due to hypotension