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:
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.
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.
https://www.ncbi.nlm.nih.gov/pubmed/22559853
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
"physicians should always encourage healthy minor-guardian communication."
Also you're going to do some serious things to cure this girl's disease, leading up to amputation. You cant hide that from her.
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.
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.
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.
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?