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29 Cards in this Set
- Front
- Back
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NAFLD
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Non-Alcoholic Fatty Liver DIsease. Spectrum of disease includes: Simple steatosis, non-alcoholic steatohepatitis, cirrhosis
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Simple Steatosis
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fat in hepatocytes; centrilobular hepatocytes affected first.
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NASH
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fat + inflammation
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Cirrhosis
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fibrosis (fat + inflammation may disappear)
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Simple Steatosis - microvesicular
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cytoplasm replaced by bubbles of fat that don't displace nucleus
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SImple Steatosis - macrovesicular
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Cytoplasm replaced by a large bubble of fat that displaces the nucleus to the edge of the cell. **key finding in NALFD
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Simple steatosis progression
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some pts progress to steatohepatitis
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Steatohepatitis - histology
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macrovesicular steatosis, cytologic ballooning, mallory bodies, scattered lobular inflammation. Alcoholic is indistinguishable from non-Alcoholic.
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Mallory Bodies
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eosinophilic clumped cytoskeletal filaments w/in ballooned hepatocytes. typically well-formed in alcoholic disease, less so in non-alcoholic.
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Importance of monitoring Steatohepatitis
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20% go on to develop cirrhosis/ESLD/HCC. Need liver transplant.
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NAFLD epidemiology
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increasing prevalence as rates of obesity, DM, physical inactivity increase
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Dx NAFLD
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AST:ALT <1; (ALT > AST and rarely higher than 5x ULN). Must exclude other causes and have convincing evidence of negligible ETOH consumption.
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Imaging of fatty liver
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Steatosis/steatohepatitis can be visualized w/ US, MRI, CI, but can't distinguish btw 2. fatty liver looks darker than spleen in CT. (usually brighter than spleen) and may be enlarged.
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gold standard for dx
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liver biopsy demonstrating steatosis +/- inflammation and cirrhosis. Often not practical/needed for clinical dx
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Dx and evaluation algorithm
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Confirm LFT's, then do screening tests/imaging: Viral Hep serology, iron levels, auto AB, etc.
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assessing severity
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liver biopsy (gold standard, more risks), transient elastography (noninvasive, poor negative predictive value for mild disease) or NAFLD score
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NAFLD scores
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Greater than -1.455 means increased risk, needs further investigation/eval/management
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NAFLD Management
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Vitamin E may be beneficial, insulin sensitizers and lipid lowering drugs, diet, exercise, Coffee. Target dyslipidemia, obesity, insulin resistance, oxidative stress
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ETOH Liver Disease
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acute and chronic toxicity; alcoholism is often comorbid w/ other liver-related illness.
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pathogenesis of alcoholic FLD
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heavy O2 consumption to metabolize alcohol means centrilobular hepatocytes are more susceptible to injury. Increased endotoxin absorption activates kuppfer cells to release cytokines hat cause hepatocyte death. alcohol metabolites stimulate immune-mediated injury and formation of mallory bodies
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Dx ETOH Liver Disease
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CAGE; AST:ALT ratio 2:1 - 3:1 and AST rarely exceeds 400 on its own.
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alcoholic hepatitis presentation
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low fever, leukocytosis, hepatomegally, AST:ALT 2.1-3.1
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discriminant function equation
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4.6 x (PT - control) + bili
treat above 32 |
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AFLD vs NAFLD
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AFLD: AST: ALT >2; mallory bodies well-formed; NAFLD: AST:ALT <1; mallory bodies poorly formed, rare.
**tough to distinguish histology, but clinical signs and hx are key |
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DILI - notorious offenders
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methotrexate, tylenol, statins
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most common offenders
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AB, NSAIDS
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DILI - sublinical
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asx elevations in transaminases; seen in statins, NSAIDS, some AB. Labs normalize when drug is stopped
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DILI - acute
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tylenol, amoxicillin-clav acid; may look like acute hepatitis or cholestatic form.
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DILI - chronic
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may mimic autoimmune disease or NAFLD; ultimately may lead to fibrosis and cirrhosis
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