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GI > LFT's - GI > Flashcards

LFT's - GI Flashcards

1
Q

Liver Function Tests

A
  • Biochemical tests useful in the evaluation and management of hepatic dysfunction
  • Screen for liver disease
  • Confirm suspected liver disease
  • Assist in differential diagnosis of liver disease
  • Monitor the progression of liver disease
  • Monitor the progress of specific therapies
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2
Q

Shortcomings

A
  • Lack of sensitivity (may be normal in cirrhosis or HCC-Hepatocellular Carcinoma)
  • Lack of specificity (aminotransferase levels may be elevated in musculoskeletal or cardiac disease)
  • Results suggest general category of liver disease, not a specific diagnosis such as hepatocellular or cholestatic
  • To increase both the sensitivity and the specificity it is best to use LFT as a battery of tests and repeat them over time
  • Probability of liver disease is high when more than one test is abnormal or the findings are persistently abnormal on serial determinations
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3
Q

Tests based on detoxification & excretory functions

A
  • Serum bilirubin
  • Urine bilirubin
  • Blood ammonia

Serum enzymes :

  • Enzymes that reflect damage to hepatocytes: AST, ALT
  • Enzymes that reflect cholestasis: GGT, 5’Nucleotidase,ALP
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4
Q

Tests that measure Biosynthetic function of liver

A
  • Serum Albumin
  • Serum Globulins
  • Prothrombin time
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5
Q

Serum Bilirubin

A
  • A break down product of porphyrin ring of heme – containing proteins
  • Normal: 0.3 – 1.3 mg/dl

2 Fractions

  • Unconjugated (indirect)- insoluble in water
  • Normal: 0.2 – 0.9 mg/dl
  • Elevated rarely due to liver disease
  • Conjugated (direct)- soluble in water
  • Normal: 0.1 – 0.4 mg/dl
  • Elevation almost always implies liver or biliary tract disease
  • In liver disease conjugation ability usually remains intact and therefore see a predominance of conjugated bili and not unconjugated
  • ↑ in obstruction, cholestasis, cirrhosis, hepatitis, primary biliary cirrhosis, etc.
  • No elevation until liver loses >50% excretory capacity
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6
Q

Unconjugated hyperbilirubinemia

A

-Indirect bilirubin fraction > 85% of total bilirubin

Problem outside of the liver usually having to do w/ the blood

Increased production due to:

  • hemolysis
  • ineffective erythropoiesis : folate or Vit B12 def
  • resolution of hematoma
  • Defects in hepatic uptake/conjugation
  • Physiologic neonatal jaundice
  • Gilbert’s syndrome: absence of enzyme that converts bilirubin
  • Crigler-Najjar syndrome
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7
Q

Conjugated hyperbilirubinemia

A
  • Dubin-Johnson syndrome: is due to altered hepatocyte excretion of bilirubin into the bile ducts
  • Rotor syndrome: is due to defective hepatic reuptake of bilirubin by hepatocytes
  • Benign recurrent intrahepatic cholestasis(BRIC)
  • Progressive familial intrahepatic cholestasis (FIC)
  • Bile duct obstruction
  • Primary sclerosing cholangitis
  • Intrahepatic cholestasis of pregnancy
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8
Q

Urine Bilirubin

A
  • Unconjugated bilirubin – binds to albumin in serum & not filtered by kidneys
  • Any bilirubin in urine is conj. bilirubin, the presence of bilirubinuria implies liver disease.
  • Undiagnosed febrile illness , bilirubinuria implies hepatitis
  • In acute viral hepatitis – bilirubin appears in urine before urobilinogen/ jaundice.
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9
Q

Blood Ammonia

A
  • Produced during normal protein metabolism and by intestinal bacteria in colon
  • Liver – detoxifies it by converting into urea which is excreted by kidneys.
  • Striated muscle also detoxifies ammonia by combining it with glutamic acid to form glutamine.
  • Patients with adv.liver disease with significant muscle wasting contributes to hyperammonemia
  • Used for detecting hepatic encephalopathy or for monitoring hepatic synthetic fn.
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10
Q

Aspartate Aminotransferase (AST)

A
  • Previously known as SGOT (Serum glutamic oxaloacetic transaminase)
  • Normal: 12 -38 U/L
  • AST found in liver , cardiac muscles, skeletal muscle, kidneys, brain, pancreas, lungs, leucocytes, RBC in decreasing order of concentration
  • 2 Iso enzymes- cytoplasmic, mitochondrial
  • Mild degree of tissue injury – cytoplasmic form in serum
  • Severe injury – mitochondrial type in serum
  • Significant elevation – MI
  • Mod .elevation – liver disease
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11
Q

Alanine Aminotransferase(ALT)

A
  • Previously known as SGPT (Serum glutamic pyruvic transaminase)
  • Normal: 7-41 U/L
  • ALT found primarily in liver, more specific indicator of liver injury than AST
  • Minimal ALT elevations in asymptomatic patients rarely indicate severe liver disease
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12
Q

Aminotransferases (ALT & AST) combined

A

-Up to 300U/L – nonspecific , any type of liver disorder(CLD…cirrhosis /malignancy)

> 1000U/L – extensive hepatocellular damage (viral hepatitis, ischemic liver injury , toxin /drug induced liver injury )

  • The ratio of AST to ALT is sometimes useful in differentiating between causes of liver damage
  • Acute hepatocellular disease – ALT >AST
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13
Q

Aminotransferase in Alcoholic LD

A
  • AST in alcoholic LD is rarely > 300 U/L
  • ALT is often normal (due to alcohol induced def of pyridoxal phosphate)
  • AST:ALT - >2:1- suggestive of alcoholic LD
  • AST:ALT - >3:1 –highly suggestive of alcoholic LD
  • AST:ALT- < 1 – suggestive of Chronic viral hepatitis and non alcoholic steatohepatitis (NASH)
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14
Q

Medications causing elevation of aminotransferases

A
  • Acetaminophen
  • Amoxicillin-clavulanic acid
  • HMGCoA reductase inhbtrs (Statins)
  • INH
  • NSAIDS
  • Phenytoin
  • Valproate
  • Herbs/alt. medicines
  • Illicit drugs
  • Toxins
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15
Q

Serum Enzymes – that reflect cholestasis - something wrong with the ducts

A

-Alkaline Phosphatase found near the bile canalicular membrane—more specific for cholestasis

  • 5’Nucleotidase found near the bile canalicular membrane—more specific for cholestasis
  • Gamma glutamyl transpeptidase: located in the endoplasmic reticulum and in bile duct

-GGT and alkaline phosphatase are most widely used

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16
Q

Alkaline Phosphatase

A
  • Normal :40 – 125 U/L
  • found in the liver, bone, placenta, small intestine

Isoenzymes:

  • Alpha -1 ALP – epithelial cells of biliary canaliculi , increased in obs.jaundice.
  • Alpha-2 heat labile ALP – hepatic cells , increased in hepatitis
  • Alpha -2 heat stable ALP – placental origin, normal pregnancy
  • Pre Beta ALP – bone origin , increased in bone ds
  • Gamma ALP – Intestinal cells, increased in Ul colitis
  • Leucocyte ALP – Increase – lymphoma, decrease – cml, pnh .
  • Elevation of liver derived ALP is not totally specific for cholestasis .
  • < 3 fold rise can be seen in many types of liver disease ( infective, alcoholic hepatitis, HCC )
  • > 4 times – cholestatic liver disease, infiltrative liver disease such as cancer, bone disease with rapid bone turnover .
  • In absence of jaundice or elevated aminotransferases – elevated ALP of liver, often indicates early cholestasis and less often infiltrative hepatic disease.
  • Not helpful in distinguishing b/w intrahep & extrahep cholestasis
17
Q

Gamma glutamyl transpeptidase

A
  • Normal: 9 -58 U/L
  • 11 isoenzymes
  • Seen in liver, kidney, pancreas, intestinal cells, prostate
  • Slightly high, normally in males due to prostate
  • GGT is sensitive for detecting hepatobiliary disease, but its usefulness is limited by its lack of specificity.
  • Mod rise – inf.hepatitis, prostate Ca, pancreatic disease, myocardial infarction, renal failure, chronic obstructive pulmonary disease, diabetes mellitus, alcoholism, anorexia nervosa, hyperthyroidism, myotonic dystrophy, and obesity

-High rise - patients taking medications such as phenytoin and barbiturates.

18
Q

5’Nucleotidase

A
  • Normal: 0 – 11 U/L
  • Moderately elevated – hepatitis
  • Highly elevated – biliary obstruction
  • Rarely elevated in conditions other than liver disease
19
Q

Serum Albumin

A
  • Tests that measure Biosynthetic function of liver
  • Synthesized exclusively by hepatocytes
  • Normal: 3.5 – 5.5 g/dl
  • Long half life: 18 -20 days
  • Because of slow turnover S. Albumin is not a good indicator of acute/mild hep. dysfn.
  • < 3 g/dl in hepatitis – possibility of Chr.liver disease

Hypoalbuminemia- not specific for liver disease can be caused by:

  • Chr.liver disorders ( cirrhosis )
  • Ascites: synthesis of albumin may be normal or even increased, but blood levels become low because of the increased volume of distribution.
  • Protein malnutrition,
  • Nephrotic syndrome
  • Chronic infections
20
Q

Serum Globulins

A 
-Normal: 2.0 – 3.5 g/dl
> 4 g/dl  - Chronic liver disease
-Gamma globulins – B lymphocytes
-Alpha , beta globulins – hepatocytes
-Increased gamma globulins indicate Chr. Liver Disease:  increased in CLD, due to the increased synthesis of antibodies against intestinal bacteria, which are normally cleared by the liver.

Elevation of specific Isotypes

  • Increase in IgG – Auto immune hepatitis
  • Increase in IgM – Primary biliary cirrhosis
  • Increase in Ig A – Alcoholic liver disease
21
Q

Prothrombin Time (INR)

A

-Normal: 12.7 – 15.4 sec
-Prolongation of PT by 2 sec / more – Abnormal
-PT measures factors II,V, VII, X
-Half life of Fac VII is 6 hrs, fibrinogen is 5 days
-Rapid turnover – best measure of hep.syn.fn
& helpful for diagnosis of ac.parenchymal liver disease.
-PT prolonged – hepatitis, cirrhosis, vit K def ( obs. jaundice, fat malabsorption )

GI (14 decks)

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