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22 Cards in this Set

  • Front
  • Back
NAFLD is a spectrum of dz containing 3 major conditions. What are they?
1. Simple steatosis (fat in hepatocytes)
2. Non-EtOH steatohepatitis (fat + inflammation)
3. Cirrhosis (diffuse bridging fibrosis; fat and inflammation may DISAPPEAR)
What is the principle finding in NAFLD?
Macrovesicular steatosis (cytoplasm replaced by a large bubble of fat that displaces the nucleus to the edge of the cell)
There are 2 general theories by which steatosis can progress to steatohepatits. What are they?
1. Lipotoxicity theory -- Fat can beget inflammation by itself
2. 2-hit hypothesis -- Excess Fe, EtOH, endotoxin (from gut), etc. are metabolized forming free radicals that damage hepatocytes.
What are the major histological findings of steatohepatitis?
LOOKS LIKE CHICKEN WIRE
1. Macrovesicular steatosis
2. Cytologic ballooning
3. MALLORY BODIES (eosinophilic concretions w/in balooned hepatocytes)
4. Scattered lobular inflammation
True or False: Progression from NASH to Cirrhosis occurs in 80% of pts.
False! It occurs in 20% of pts
What are the cures available for liver failure resulting from the NASH-->Cirrhosis progression?
liver transplant is the only curative option.
Briefly discuss the epidemiology of NAFLD.
It's on the rise!
1. 1/3 of Americans have steatosis
2. u/s data estimates prevalence around 50%
3. Incidence rising in step w/ rates of obesity, DM, and laziness
What pattern of LFTs is pathognomonic for NAFLD?
There isn't one! But in general, ALT > AST and rarely higher than 5x ULN (usually in the 100-200 range)
What's the gold standard for diagnosing NAFLD?
Liver bx demonstrating steatosis +/- inflammation and fibrosis
1. Bx not always needed for clinical dx
2. Imaging may suffice if shows fatty infiltrate.
How is the dx of NAFLD made?
Pts have negative screening tests (HBV, HCV, ANA, AMA, ASMA, Fe, etc.) with echogenic U/S
Besides a liver bx, what non-invasive method is useful for determining severity of NAFLD?
NAFLD Fibrosis Score which is based on routing blood work.
What is the cut-off for low vs. high risk of dz severity using the NAFLD Fibrosis Score?
<= -1.455 --> Low risk
> -1.455 --> High risk
How is NAFLD managed?
DIET & EXERCISE, Diet & Exercise, diet & exercise!!! Vitamin E might be helpful.
True or False: EtOH liver disease is usually the pts only medical problem?
False! Often co-morbid w/ HCV, polysubstance abuse, etc.
Which enzyme on a LFT panel is raised by EtOH?
GGT
What does the liver panel look like in a pt w/ EtOH liver dz?
AST:ALT ratio of 2:1-3:1 (AST rarely exceeds 300-400)
Elevated GGT
AP may be normal

Extrahepatic labs may show macrocytosis, folate/B12 def, low BUN, thrombocytopenia
How do you establish the severity of alcoholic hepatitis?
By using a discriminant function:
4.6 x (PT-control) + bilirubin
What is the cut-off for treatment of alcoholic hepatitis based on the discriminant function and what is the therapy?
Score > 32 benefit from Rx
Prednisolone 40mg qd x 1 month
Pentoxifylline 400mg TID x 1 month (anti-TNFa)
What drugs are notorious for causing liver injury?
1. MTX
2. Tylenol
3. Statins
What drugs cause a subclinical DILI? What is the course of the dz?
statins, NSAIDs, some abx
asymptomatic rise in transaminases that fall when drug removed
What drugs are usually implicated in acute DILI (10% of all acute hepatitis)? What's the course of the dz?
Tylenol, augmentin
May be acute hepatits form (ALT/AST elevated) or cholestatic form (GGT, AP, bili elevated)
What drugs are usually implicated in chronic DILI?
minocycline, NSAIDs (both cause an AI picture); amiodarone and tamoxifen (cause NAFLD picture); MTX (cirrhosis)
Note that all these eventually lead to cirrhosis and scarring