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nbme24/Block 2/Question#26

A 35-year-old man is brought to the emergency ...

Catecholamine-mediated intracellular shifts of K+

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 +4  upvote downvote
submitted by fallot4logy(4),

in the other hand , urine potassium is high enough , so if seizures =>rhabdomyolysis => myoglobinuria => ATN => high potassium excretion , why not?





 +2  upvote downvote
submitted by medstruggle(6),

Can someone explain why does this patient have hypokalemia?

colonelred_  Catecholamines activate the Na/K pump, which will drive K inside. +5  
trazabone  Read online that catachelamines are released following tonic clonic seizures. Besides that, BP of 180/100 could indicate that catecholamines are circulating. +  
fulminant_life  This mechanism is why giving albuterol for hyperkalemia works +3  
nbmehelp  Why does this guy have increased catecholamines tho +  
johnson  His SNS activity is seriously increased --> increased catecholamines. +  
nbmehelp  Why is his SNS activity increased? Is the BP literally the only hint? +  
youssefa  Alcohol withdrawal creates a hyper- catecholaminergic state + Seizures do that as well. +1  
water  My best guess is that withdrawal puts the body in a state of stress (same for seizures) and with stress you have release of catecholamine which we'll see in the BP and the hypokalemia. +  




 +1  upvote downvote
submitted by paszw0red(1),

Emedicine says: Delirium tremens (DTs) is the most severe form of ethanol withdrawal, manifested by altered mental status (global confusion) and sympathetic overdrive (autonomic hyperactivity), which can progress to cardiovascular collapse.

Also ref. https://pubs.niaaa.nih.gov/publications/aa05.htm

I assume the patient has Delerium tremens, had a seizure, and now is hypertensive because of the "sypathetic overdrive", with excess secretion of catecholamines, thus the hypokalemia.