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yep, I also chose C. Relatively easy question, but a bit misleading picture.
no, decreased CO => peripheral vasoconstriction => SVR will be increased
No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs )
Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI?
@snafull: my initial thought is that we would see pulmonary vasoconstriction because of the relatively low oxygen tension (that results from the low cardiac output).
Vasodilation of the skin is under sympathetic control as well -- beta-2 receptors when stimulated cause vasodilation (via increase of cAMP in vascular smooth muscle). The key is recognizing that stimulation of a GANGLION of the pns will lead to release of NOREPINEPHRINE, which preferentially stimulates alpha-1 receptors. Those receptors will cause vasoconstriction.
If the question asked what happens when you stimulate the adrenal medulla, the answer would be (potentially) vasodilation. This is because the adrenal medulla releases EPINEPHRINE which preferentially stimulates beta-1/2 receptors.
@drzed Awesome explanation except I think sympathetic response induces vasoconstriction in the skin though vasodilation in the muscles!
@jesusisking yes you are correct!
α1: vasoconstriction in skin and intestine ;
β2: vasodilation in skeletal muscle (transmitter: only epinephrine!)
@charcot The patient is young and doesn't have any risk factors for weak bones. Also, disc herniation is a common problem in the young. The disc gets fibrosed and stiff in the elderly so they have less chance for disc herniation.
So basically age was the key to answering this question.
you are genius! thank you! :)
As the poster indicates, the described patient has a defect in the urea cycle, specifically an ornithine transcarbamylase deficiency.
Added for clarity to future readers.
For orotic aciduria, From FA 2019 p. 412, "Orotic acidura is inability to convert orotic acid to UMP (de novo pyrimidine synthesis pathway) because of defect in UMP synthase. Aut recessive. Presents in children as failure to thrive, developmental delay, and megaloblastic anemia refractory to folate and B12 (supplementation). NO hyperammonemia (vs. ornithine transcarbamylase def. which as increased orotic acid with hyperammonemia."
Also it's not Carbamoylphosphate synthetase (I) deficiency because there would be only hyperammonemia, increased glutamine and decreased BUN but no orotic acid increase since carbamoyl phosphate isn't getting made and then shunted to pyrimidine synthesis pathway to get acted on by carbamoyl phosphate synthetase II as is the cause of increased orotic acid seen in OTC deficiency.
If there is isolated elevated orotic acid and no urea defects or hyperammonemia then it's Orotic aciduria due to UMP synthase deficiency.
If there if hyperammonemia and orotic acid increase then OTC deficiency.
If there is hyperammonemia with no orotic acid increase then carbamoyl phosphate synthetase I deficiency.
I think it's also because he has an infection (since he was prescribed antibiotics) boosting the immune system is more important than increasing platelet count E) or RBC count A)
the question stem states a "a scent vaginal discharge" is that a distractor in the question.
Could you elaborate? Is this related to: less "preload" from mother circulation causes lowered HR?
Or backflow of blood and causes a Reflex Bradycardia? still confused on this question.
So I think the subtle difference in choice E is that there would be a negative CHRONOTROPIC effect, no inotropic effect (contractility).
if anything, inotrophy could go UP not down as diastole prolongs and LVEDV increases --> Starling equation bullshit
Im pretty sure so is strept pneumoniae
COPD is also exacerbated by Viral infection: Rhinovirus, influenza, parainfluenza; and Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus.
however, the questions gives a hint that it may be legionella = "weekend retreat" which may be associated with this infection
From FA 2017 pg 139: Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in **chronic lung disease.**
I also believe that the other attendees showed signs of pontiac fever, which is another hint they tried to get at.
i did it wrong and chose influenza virus since it is most common infection in COPD but the clue in the Question is that the other attendee didnt get sick since in legionella there is no person to person transmission
but in Uworld s. pneumo is one of the most common bacterial exacerbation of COPD legionella wasn't even mentioned. How do we rule out s. pneumo ?
maybe because in children s.pneumo causes otitis media?
Another hint made in the Q stem is the location being rural Pennsylvania.... Legionnaires disease was first discovered by the outbreak in 1976 at a convention held in Philadelphia, Pennsylvania. Not sure why I know this fact...
Biggest hint towards legionella to me was that they all were at a residence hall... i.e. where there'd be air conditioners and such.