This is how I narrowed it down:
It is on the left. Not cecum, appendix, or stomach (it’s the way left on CT and small).
This leaves jejunum and duodenum. It is cut in cross section which means it would have to be retroperitoneal (2nd portion of duodenum). You can see the kidneys and descending colon way behind it. Likely not retroperitoneal.
This leaves jejunum.
For all wondering why testosterone doesn’t cause an increase in alk phos, I found this article that basically says men with low testosterone have high alkaline phosphatase and weak bones.
Without knowing what MTPT did (p. 520 in 2020FA) I reasoned through it like this:
Cholinergic in Nucleus Basalis of Meynert=ACh. Possibly but disease here causes alzheimers/huntingtons even though it is increased in parkinsons. Dopaminergic in neostriatum= Didn’t know so I just kinda ignored it 😂 Dopaminergic in substantia nigra = Parkinsons so it sounded like a good choice. Serotonergic in dorsal raphe nuclei = serotonin. A lack or excess here wouldn’t cause this. Serotonergic in locus ceruleus = norepinephrine. Same as last.
Ultimately chose dopaminergic in Sub. Nigra because of the rigidity on exam and feeling frozen in ice.
FA 2020 p. 684
SCC: Hilar mass arising from bronchus; cavitation, cigarettes, hypercalcemia.
FA 2020 p. 525.
Ash-leaf spots are pretty pathognomonic for TSC. The subependymal nodules add further support for TSC
Methotrexate would be a drug of choice for psoriasis refractory to topical creams and light therapy; inhibits dihydrofolate reductase in order to decrease skin cell proliferation and reduce inflammatory response.
First Aid 2019 page 622 stimulatory growth effects of testosterone include red blood cells. I think they expect us to know this.
ranitidine blocks H2 receptor, which is Gs. Gs activates adenylyl cyclase -> +cAMP.
q: HAVe 1 M&M => H1, alpha1, V1, M1, M3 i: MAD 2 => M2, alpha2, D2 s: (everything else) => beta1, beta2, V2, D1 H2
I think this is from FA.
bronchus obstruction traps oxygen in alveoli no nitrogen able to enter (atmospheric air entering body (78% nitrogen and 21% oxygen, nitrogen is so important nitrogen bc it is a poorly absorbed gas and thus is in charged of keeping alveoli inflated) oxygen in the alveoli is absorbed into the blood reducing the volume of the alveoli alveolar collapse absorption atelectasis
Acute MI and mitral regurg (from the murmur) leads to LV failure and backflow of blood into the lungs.
This leads to increased pulmonary hydrostatic capillary pressure. This will lead to excess volume leaking from the pulmonary capillaries into the interstitial and this will manifest as pulmonary edema (crackles).
Pulmonary edema will interfere with gas exchange leading to hypoxemia.
here are partial clinical manifestations of the right oculomotor nerve palsy: the right pupil is 6 mm and nonreactive to light, and adduction of the right eye is impaired. The oculomotor nerve exits midbrain through the interpeduncular fossa and goes between the beginning of the posterior cerebral and superior cerebellar arteries. Rapture of an aneurysm in the posterior communicating artery near the beginning of the posterior cerebral artery may compress the oculomotor nerve and affect its function
I struggled with why this couldn’t be essential HTN for a while. I think what it comes down to is this, and someone help me out if I’m incomplete/wrong.
In bilateral RAS, ACE inhibitors will decrease the GFR from dilation of efferent arteriole and they can’t increase the GFR further because they’re already maxed out on afferent dilation to keep up GFR in the first place.
In essential HTN, yes ACE inhibitors decrease GFR from dilation of efferent arterioles, however they’re able to maintain GFR through autoregulation because they haven’t touched their afferent arteriole. So this means that renin won’t actually increase.
TL;DR: Bilateral RAS is unable to use autoregulation to correct the decrease in GFR where essential is able to.