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30 Cards in this Set
- Front
- Back
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AST
Normal value? Significance? |
3-40 U/L
Increase indicates hepatocyte lysis/damage. Elevated in all liver dz and in MI. |
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ALT
Normal value? Significance? |
10-50 U/L
High conc in hepatocytes; increase means hepatocyte lysis/damage. Elevated in all liver dz; more liver-specific than AST which is also found in cardiac tissue. |
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Bilirubin (total)
Normal value? Significance? |
0.1-1.2 mg/dL
Bili = breakdown of hemoglobin; conjugated to glucuronide. Indicates liver's ability to conjugate and eliminate broken down HgB |
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GGT
Normal value? Significance? |
M: <95 U/L
F: <70 U/L AP + GGT elevation = liver dz but just GGT elevation not really dx for anything. |
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Alkaline Phosphatase
Normal value? Significance? |
30-130 U/L
Found in liver and bone; elevation means bone dz or liver damage (usu biliary obstruction) |
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Albumin
Normal value? Significance? |
3.5 to 5g/dL
Albumin made EXCLUSIVELY by liver --> indicates synthetic ability Albumin long t1/2 so you'll see changes about ~20d after damage occurs. |
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ProTime
Normal value? Significance? |
10-15 sec
Elevated PT = longer bleeding time = problems with synthesizing clotting factors. Best indicator of liver's synthetic ability! |
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NH3
Normal value? Significance? |
10-80ug/dL, ideally <48umol/L
Indicates liver's ability to convert NH3 --> urea. High NH3 suggestive of hepatic encephalopathy. |
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Fibrosis
Pathology? Hallmarks? Causes? |
precedes cirrhosis; formation of fibrous, nonfunctional scar tissue.
MTX, Vit A overdose |
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Vascular Lesions
Pathology? Hallmarks? Causes? |
due to clots, veno-occlusive disease, portal hypertension
estrogens, azathioprine, 6-thioguanine |
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Tumors
Pathology? Hallmarks? Causes? |
adenomas, hepatocellular carcinomas (gene muation, oncogene activation, etc.)
estrogens, anabolic steroids** |
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Hepatocellular necrosis
Pathology? Hallmarks? Causes? |
direct toxic effect/poisoning of liver cells. Will see zonal necrosis around portal triad.
APAP overdose, CCl4 exposure |
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Cholestasis
Pathology? Hallmarks? Causes? |
obstruction of bile flow. elevated GGT, Alk Phos
estrogen, amox-clav, piroxicam, erythromycin |
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Hepatitis (acute/chronic)
Pathology? Hallmarks? Causes? |
inflammation of the liver; may lead to fibrosis/cirrhosis
halothane, isoniazid, methyldopa, phenytoin, viruses |
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Fatty Liver disease
Pathology? Hallmarks? Causes? |
Accumulation of fat droplets in the liver (apparent on microscopic examination of biopsy)
ethanol (!), corticosteroids, tetracycline |
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Sample Case 2: what type of liver disease?
AST 280 ALT 200 Alk Phos 160 Bili 4.2 Alb 2.2 PT 18s |
Alcoholic Liver disease.
Note AST > ALT, hallmark of alcoholic liver dz |
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Sample case 3: what type of liver disease?
ALT 110 AST 120 AlkPhos 700 Bili 7.8 Alb 3.4 PT 18 seconds |
Cholestatic liver disease.
++Alk Phos, Bili, GGT |
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Sample case 4: dx and prognosis? Measurements taken 4d apart
ALT 2200 --> 700 AST 3100 --> 800 AlkPhos 130 --> 140 Bili 15 --> 29 Alb 3.6 --> 3.2 PT 23 --> 38s |
Acute viral hepatitis. This pt is dying.
Note the very high AST and ALT, classic sign of acute hepatitis. |
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Sample Case 2: what type of liver disease?
AST 2200 ALT 3100 Alk Phos 130 Bili 1.4 Alb 4.0 PT 14 sec |
Acute viral hepatitis.
ALT and AST in the thousands is indicative of acute viral hep. Note also ALT > AST. This is true of most dz except alcoholic cirrhosis. |
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Drugs to avoid in liver disease?
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-sedating meds
-nephrotoxic agents -IM injections -anything with an anticoagulant effect. |
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Why avoid sedating meds in DILD pt?
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won't know if a coma is due to high drug conc or from liver going to hell
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Why avoid nephrotoxic agents in DILD pts?
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Don't burn your only bridge.
Your liver's shot, your kidneys are pretty much the only way for you to eliminate drugs. Treat them nicely. |
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Why avoid anticoagulant meds in DILD pts?
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Pt already can't make clotting factors. Don't want to risk making them hemorrhage
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Why avoid IM injections in DILD pts?
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Can't make clotting factors --> get large hematoma around injection site.
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Main complications of ESLD (end stage liver disease)?
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ascites
esophageal varices (from portal HTN) hepatic encephalopathy (brain is poisoned by NH3) hepatorenal syndrome (kidneys fail in that pt but still functional) |
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Clincal presentation of liver disease?
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Palmar erythema
Scleral Icterus, Jaundice Ascites, Peripheral pitting edema Spider angioma pt is red, yellow, and bloated. |
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Factors of Child-Turcotte-Pugh scoring system?
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QOL aspects:
encephalopathy? ( + or - ) ascites (degree of severity) Lab values: albumin, bili, PT (considers both prognosis and QOL but potentially unfair b/c includes subjective data) |
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Factors considered in MELD staging system?
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creatinine
bilirubin INR **only uses lab values; no consideration of QOL. Considered fairer bc uses only objective data |
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Prognoses/categories of liver disease according to Child-Turcotte-Pugh?
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Childs A: 80-90% 10 year survival rate
Childs B: 60-80% 5 year survival rate Childs C: <50% 2 year survival rate |
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Chronic Viral Hepatitis vs. Acute Viral Hepatitis (lab value differences)
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Acute will have huge increases in pretty much everything but albumin and PT won't have had much time to change.
Chronic will have smaller changes BUT a larger drop in albumin and increase in PT because the liver's been messed up for so long. |
