GI/Hepatology Flashcards
what labs do you need for liver transplant?
PETH, hepatitis labs, ceruloplasmin, AFP, stress echo, PFTs, ANA, AMA, CA 19-9, CBC, CMP, PT/INR, alpha-1 antitrypsin Ab, fibrinogen, CMV, HIV, varicella, EGD (varices), colonoscopy, PPD, U/S + doppler, cancer screenings in general (pulm CT if needed, mammogram, Pap smear, etc…)
AST/ALT < 1
inflammatory hepatocellular injury (viral hepatitis, fatty liver dx, extrahepatic cholestasis)
AST/ALT >1
necrotic hepatocellular injury (alcoholic hepatitis, fulminant necrotic hepatitis, decompensated cirrhosis, hepatocellular carcinoma, muscle damage, MI)
AST
located in mitochondria of hepatic cells (so if really increased AST, there is a good chance there is severe hepatocellular injury). AST also in heart, erythrocyte, and muscle cells, so dont be fooled if elevated w/ other pathology present
2 labs indicating cholestasis
ALP and GGT (impaired bile production or secretion leads to increase in Dbili and induces production of ALP and GGT)
most common cause of albumin elevation
dehydration
vitamin K protocol
10 g IV vit K given for 3 days
criteria of SBP
- chronic underlying cirrhosis
- ascites neutrophil count >250
- exclusion of secondary bacterial peritonitis
why might you see a decrease in phosphate in a cirrhotic patient who is receiving optimal treatment?
as the liver recovers and is able to participate in gluconeogenesis and create more ATP, this will consume more phosphate within the body
liver decompensation due to alcohol will have an AST in what range?
usually the 200-300s (if way higher than this, most likely something else also going on)
ALF is characterized by rapid progression (within ___ weeks) and severe liver injury, which is impairment of coagulopathy and enceph in an individual _____ (with/without) previous hepatic dx
within 26 weeks
without
what is the most common cause of ALF?
tylenol (acetaminophen) overdose
in ALF, what is the typical INR you would see?
> 1.5
treatment for ALF 2/2 acetaminophen
N-acetylcysteine (antioxidant that restores hepatic glutathione)
why does hyponatremia develop in cirrhosis?
either hypovolemia (in setting of diuretic use), or hypervolemia (third spacing causes kidneys to waste sodium)
the development of NASH is driven by
increased insulin resistance (hepatic cells uptake more fatty acids due to increased peripheral lipolysis, and this can lead to swelling of cells, damage, and leads eventually to cirrhosis, though majority of patients are asymptomatic)
