Fatty Liver Disease Flashcards
T/F histologically, alcohol and non alcohol FLD looks the same
T –> can only differentiate based on hx and enzymes
Spectrum of alcohol liver disease
fatty liver –> hepatitis –> cirrhosis
How much alcohol is too much?
maximally 1-2 units of wine/day
Risk factors for alcohol liver disease
alcohol consumption, alcoholism, diet/nutrition, coinfection, genetic
Normal alcohol metabolism
alcohol (+ADH)–> acetaldehyde +NADH (+ALDH) –> acetate + NADH
Binge alcohol metabolism
Excess alcohol is converted to NADP+ and O2- by MEOS–> free radicals
Pathogenesis of alcohol fatty liver
increase nadh –> increase fatty acid synthesis/decrease beta oxidation –> accumulation in hepatic cytoplasm –> esterification and storage as TG –>FATTY LIVER
When does alcohol/alcohol fatty liver cause liver damage?
ROS damage, lipid peroxidation, kupffer cell activation + cytokine release (TNFalpha and TGFbeta and superoxide)
How does alcohol cause fibrosis?
steallate cells activated by acetaldehyde, ROS, products of peroxidation, TGF beta –> produce collagen
T/F fatty liver is reversible
T
T/F alcohol hepatitis and cirrhosis are reversible
F
Findings in fatty liver
mild to moderate increase in AST/ALT, malaise, tenderness
Tx of fatty liver
discontinue EtOH
Findings in alcohol hepatitis
after years of drinking –> weakness, anorexia, nausea, vomiting, portal hypertension findings, jaundice, palmar erythema, increase prothrombin time, asterixis, ascites, 2:1 AST:ALT, increase bilirubin
Histologic findings of alcohol hepatitis
poly infiltrates, mallory bodies, ballooning degeneration
Prognostic factors in alcohol hepatitis
maddrey discriminant function, continued alcohol use
Tx of alcohol hepatitis
stop etoh, nutrition, steroids/pentoxifylline, tx for infection
NAFLD
looks like alcohol liver injury w/ no history of alcohol
Major etiologic factor in NAFLD
obesity –> manifestation of metabolic syndrome –> insulin resistance + oxidative stress of hepatocytes
Pathogenesis of NAFLD
hyperinsulinemia –> increased lipolysis, increased glycolysis, and decrased apoB production for FA transport in VLDL –> increased FFA –> accumulation of FFA –> ROS production –> lipid peroxidation
How do we differentiate between NASH and alcohol liver disease?
NASH = more women, more diabetes/obesity, fewer symptoms, lower AST:ALT ratio, less fibrosis/cirrhosis
Tx of NAFLD
lose weight! –> improves insulin resistance, reverse steatosis, reverse injury/inflammation/fibrosis
- can use insulin sensitizing agents (rosiglatazone, metformin) + antioxidants (VitE)
