Hepatobiliary Testing Flashcards

1
Q

AST (Aspartate Aminotransferase)

A

aka SGOT

Reference Range: 5 – 40 IU/L

AST is an intracellular enzyme; cellular damage causes enzyme to leak into plasma

Found in liver cells, cardiac muscle, skeletal muscle, renal cells, brain cells, pancreas, WBCs & RBCs

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2
Q

AST Clinical use

A

Primarily for the evaluation of hepatocellular injury/necrosis

Previously used for detection of cardiac ischemia or myocardial infarction

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3
Q

AST Increased levels implications

A

Liver disease
Heart disease
Skeletal muscle disease/injury

Acute hemolytic anemia
Acute pancreatitis
Acute cholangitis

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4
Q

AST Decreased levels implications

A

Acute renal disease
Chronic renal dialysis

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5
Q

ALT (Alanine Aminotransferase)

A

Reference Range: 5 – 53 IU/L

Intracellular enzyme that is more specific than AST for liver

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6
Q

Clinical Uses for ALT

A

Diagnose and monitor hepatocellular injury or necrosis

Aid in diagnosis of jaundiced patient

Viral hepatitis
Alcoholic hepatitis

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7
Q

Mild ALT increase implications

A

Myositis
Pancreatitis

Myocardial infarction
Infectious mononucleosis

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8
Q

Moderate ALT increase implications

A

Moderate Increase

Cirrhosis
Cholestasis
Hepatic tumor

Obstructive jaundice
Severe burns
Muscle trauma

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9
Q

Severe ALT increase implications

A

Severe Increase

Hepatitis, hepatic necrosis/ ischemia

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10
Q

LDH (Lactic Dehydrogenase)

A

Reference Range: 90 – 190 IU/L

Intracellular enzyme in many body tissues

Total LDH elevation is relatively nonspecific; LDH isoenzymes offers more specificity

LDH 1 – myocardium, RBCs, brain, kidney
LDH 2 – myocardium, RBCs, brain, lung
LDH 3 – brain, kidney, lungs
LDH 4 – liver, skeletal muscle, brain, kidney
LDH 5 – liver, skeletal muscle, kidney

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11
Q

Clinical Uses for LDH

A

Important diagnostic tool for hepatic dysfunction
Hemolysis and transfusion reactions

Specific injury patterns
LDH 1:2 “Flip” – cardiac necrosis

LDH 4 & 5 ⇑ - hepatitis, cirrhosis

LDH 5 ⇑ - hepatocellular disease/injury or skeletal muscle disease/injury

LDH 2, 3, 4, 5 ⇑ - lung and liver abnormality

All fractions ⇑ - multi-organ dysfunction or failure

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12
Q

ALP (Alkaline Phosphatase)

A

Reference Range: 42 – 128 U/L

Enzyme originating mainly in the bone, liver and placenta

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13
Q

Clinical use for ALP

A

Detection of bone diseases
Detection of liver diseases
Obstructive biliary diseases/conditions

Metastatic liver cancer
More specific ALP isoenzymes can help differentiate between liver & bone disease

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14
Q

Implications of Increased levels of ALP

A

Cirrhosis
Biliary obstruction
Liver cancer

Normal pregnancy
Growing children
Bone mets

Intestinal ischemia
Hyperthyroidism
Hyperparathyroidism

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15
Q

Implications of Decreased levels of ALP

A

Malnutrition
Hypothyroidism
Pernicious anemia

Magnesium deficiency
Celiac sprue

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16
Q

GGT (Gamma-Glutamyltransferas)

A

Reference Range: <45 yrs = 5-27 U/L ; >45 yrs = 8-38 U/L

Highest concentrations in liver & biliary tract

17
Q

Clinical Uses of GGT

A

Sensitive indicator of hepatocellular disease or biliary obstruction

Elevations parallel ALP ⇑ but more sensitive
Indicate heavy & chronic alcohol use – elevations in chronic drinkers 75% of the time

18
Q

Implications of Increased levels of GGT

A

Liver disease
Pancreatic disease
Many cancers

ETOH
Phenytoin, barbituates
DM
Obestity

19
Q

Common patterns in liver disease

A
20
Q

Billirubin source and excretion

A

Breakdown of RBCs in RES releases Hgb + globin portion from the RBCs; heme is converted to biliverdin → bilirubin

Bilirubin initially is unconjugated (indirect)
Unconjugated bilirubin conjugates with glucuronide in the liver to form a conjugated (direct) form of bilirubin
Direct bilirubin is excreted from liver cells to hepatic ducts → common bile duct → bowel

21
Q

Bilirubin testing organization

A

Differentiation between direct & indirect to determine etiology of defect

Protect sample from light (>1 hr exposure can decrease bilirubin levels

22
Q

Clinical uses of bilirubin

A

Hepatocellular/Biliary tract disease/dysfunction
Evaluation of jaundice in adult patients

Evaluation of jaundice in newborns
Interference of testing methods with hemolysis and lipemic specimens

23
Q

Implications of increased indirect bilirubin

A

(pre-hepatic)

Erythroblastosis fetalis
Transfusion reaction
Sickle cell, pernicious, & hemolytic anemia

Large volume blood transfusion
Hepatitis, cirrhosis

Neonatal hyperbilirubinemia
Crigler-Najjar syndrome, Gilbert syndrome

24
Q

Implications of increased direct bilirubin

A

⇑ Levels of Direct (posthepatic)

Extrahepatic duct obstruction
Extensive metastatic liver cancer
Congenital defects in enzyme quantity

25
Q

Implications of increased levels of both indirect and direct bilirubin

A

⇑ Levels with both Direct & Indirect (hepatic)
Hepatocellular disease
Hepatotoxins
Hepatoma

26
Q

Markers of Hepatic Synthesis

A

The liver is largely responsible for coagulation factor and protein synthesis

Albumin – decreased levels indicate a chronic condition & are useful for monitoring progression of disease

Prothrombin time (PT) – in pts with chronic & severe hepatocellular injury, the PT is markedly prolonged (PTT is usually prolonged as well)

27
Q

Ammonia source hepatic implication

A

Ammonia is a breakdown product of protein catabolism which is converted to urea in liver & excreted by kidneys

In severe hepatocellular dysfunction it cannot be catabolized into urea

28
Q

Clinical uses of Ammonia

A

Specimen should be drawn in a green top tube and placed on ice immediately

Monitoring of severe liver disease and diagnosis or follow-up of hepatic encephalopathy

29
Q

Implications of increased Ammonia

A

*Hepatic encephalopathy
*Hepatocellular disease

Portal hypertension
GI bleeding

Obstruction with mild liver disease