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NBME 24 Answers

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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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.

Can someone explain why does this patient have hypokalemia?

colonelred_  Catecholamines activate the Na/K pump, which will drive K inside. +6  
trazabone  Read online that catachelamines are released following tonic clonic seizures. Besides that, BP of 180/100 could indicate that catecholamines are circulating. +1  
fulminant_life  This mechanism is why giving albuterol for hyperkalemia works +4  
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. +2  
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  

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submitted by rolubui(4),

1) Alcohol withdrawal --> seizure

2) Seizure --> increased release of catecholamines (https://www.ncbi.nlm.nih.gov/pubmed/6538024), also BP of 180/100 indicates high levels of catecholamines

3) Major hormones that shift K+ intracellularly are insulin & beta-2-adrenergic agonists (e.g. epinephrine (http://www.clinicalguidelines.scot.nhs.uk/media/1286/fig1picu007.png)

4) Also they are asking why serum K+ is low, NOT why urine K+ is high

osler_weber_rendu  Point 4) above helps you RULE OUT MUSCLE BREAKDOWN. It will cause initial hyperkalemia. Hypokalemia, if at all happens weeks later in ATN. +  

I was trying to figure out how are the catecholamines cause the K shift into the cells. I was not seeing the connection at first. normally in old NBMEs and Uworld questions- Insulin is causing K+ to enter the cells. then I remember seeing the sketchy band camp and in the far right of the sketch there is B2 activation = beta 2 tuba or something.. anyway beta 2 is found on pancreatic beta cells, catacholamines activate beta 2 on pancreatic beta cells which will cause insulin to be released. insulin released causes K to be driven inside the cells, causing the hypokalemia


-FA 2019 pg 238 Beta 2 --> increase in insulin release and increase cellular K+ uptake.

-Linda S. Costanzo's physiology text:image showing insulin and beta agonist driving K+ into the cells

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

krewfoo99  True but hypokalemia would occur in the recovery phase. So weeks after the inciting phase. +  

This maybe to late for anyone but here was my train of thought Catecholamine : 1. increases insulin release --> glu and K will enter cells. Causing hypokalemia in the plasma 2. Can trigger the beta 1 receptor causing the release of Renin---> Angiotensin 2 (can be contributing / causing an increase in BP)--> aldosterone --> you waste K in the urine.