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ANOOP'S LFT

Date post: 07-Apr-2018
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    LIVER FUNCTION TESTS

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    Some example of liver dysfunction

    Hepatocellular disease Cholestastic disease

    Cirrhosis of the liver

    Hepatitis Jaundice

    Liver cancer

    Fatty Liver

    Genetic Disorders

    Hemochromatosis (iron storage)

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    LFT :TB 4 mg/dl [0.3-1 mg/dl] DB 1 mg/dl [0.1-0.3 mg/dl]

    AST 250 U/L [0-35 U/L] ALT 220 U/L [0-35 U/L]

    ALP 100 U/L [30-120 U/L]

    Case 112/F Presented With RUQ Pain ,

    Icterus

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    LFT :TB 2 mg/dl [0.3-1 mg/dl] DB 1.5 mg/dl [0.1-0.3 mg/dl]

    AST 1000 U/L [0-35 U/L] ALT 1300 U/L [0-35 U/L]

    ALP 180 U/L [30-120 U/L]

    U/S : bile duct dilatation with gall stone

    Case 234/M Presented with RUQ pain ,

    Indigestion

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    LFT :TB 3 mg/dl [0.3-1 mg/dl] DB 0.2 mg/dl [0.1-0.3 mg/dl]

    AST 30 U/L [0-35 U/L] ALT 30 U/L [0-35 U/L]

    ALP 100 U/L [30-120 U/L]

    alb 4 g/dl [3.5-5.5 g/dl] glob 3 g/dl [1.5-3.5 g/dL]

    Case 3 6y/m presented with increasing jau

    ndice during illnesses with self remission

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    General categories of LFTs

    Transport organic anions & metabolize drugs Bilirubin, ICG

    Hepatocyte injury

    AST, ALT, LDH Cholestasis

    ALP, GGT

    Biosynthetic capacity Albumin, cholesterol, PT, clotting factor

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    Liver Function Test

    Liver chemistry test Clinical implication of abnormality

    ALT Hepatocellular damage

    AST Hepatocellular damage

    Bilirubin Cholestasis, impair conjugation, or biliary obstruction

    ALP Cholestasis, infiltrative disease, or biliary obstruction

    PT Synthetic function

    Albumin Synthetic function

    GGT Cholestasis or biliary obstruction

    Bile acids Cholestasis or biliary obstruction

    5`-nucleotidase Cholestasis or biliary obstruction

    LDH Hepatocellular damage, not specific

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    Liver Function Test

    Mild

    (times)

    Moderate

    (times)

    Marked

    (times)

    AST 20

    ALT 20

    ALP 5

    GGT 10

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    Bilirubin

    Production/hepatic removal Overproduction

    Uptake, conjugation, excretion

    Regurgitation

    Uncomplicated hemolysis < 3-5 mg/dL

    Parenchymal liver dis, Calculi < malignant obstruction

    Clay color stool: usually cholestatic, hepatocellular possible,not hemolytic

    Dark urine: direct hyperbilirubinemia, usually cholestatic

    30-50 mg/dL : renal failure

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    Unconju. Conjugated

    Van den Bergh reaction Indirect Direct

    Water solubility - +

    Lipid solubility + -

    Albumin attachment + +

    Icteric urine - +

    Bile - +

    Brain affinity + -

    Hemolysis ++ +/-

    Obstructive/hepatocellular + +++

    Unconjugated & conjugated bilirubin

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    Urinary bilirubin

    Unconjugated bilirubin Tightly albumin bound

    Not filtered not present in urine

    100% of serum bilirubin by new precise methods

    Unconjugated bilirubin

    Both healthy & Gilbert syndrome

    Urinary bilirubin +

    Conjugated bilirubinemia Hepatobiliary disease

    Low renal threshold

    Normal serum bil level, no jaundice

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    Aminotransferase (transaminase)

    Liver cell injury AST (SGOT), ALT (SGPT)

    Present in serum in low concentration: source?

    AST: liver, cardiac m., skeletal m.,kidney, brain,

    pancreas, lung, WBC, RBC No tissue specific isoenzyme

    Damage or permeability

    Clearing AST > ALT

    By RES

    Not biliary or urinary excretion

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    AST ALTcatalyze transfer aminogroups to form pyruvate catalyze transfer aminogroups to form oxaloacetatecytosol (20%) and

    mitochondria (80%) cytosol

    T1/2 17 hr. (cytosol)

    87 hr. (mitochondria) T1/2 47 hr.liver, cardiac muscle,

    skeletal muscle, kidneys,brain, pancreas, lungs,leucocytes, and RBC

    low concentration in other

    tissues

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    AST/ALT ratio

    Location ALT: cytosol

    AST: cytosol most circulating AST in healthy

    mitochondria 80% of activity in the liver

    ALT: more sensitive & specific

    ALT < 300 IU, AST/ALT ratio >2 or >3: ALD

    Noninvasive indicator of cirrhosis

    Very specific (94-100%) but Not sensitive (44-75%)

    AST/ALT < 1 : viral hepatitis, NASH

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    Alkaline phosphatase

    Function, degradation site? Canalicular membrane of hepatocyte, osteoblast,

    brush border of intestine, Proximal convolutedtubules, placenta, WBC

    Half life: 7 days

    Higher in older & men (15-50 years old)

    Normally elevated in adolescents & late pregnancy

    Elevation: hepatobiliary disease, bone orpregnancy > intestine > kidneys

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    0

    10

    20

    30

    40

    50

    60

    70

    80

    90

    alcoholic post necrotic

    cirrhosis

    chronic

    hepatitis

    obstructive

    jaundice

    viral hepatitis

    AST/ALT >1

    AST/ALT >2

    AST/ALT ratio

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    Aminotransferases levels

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    Principal diagnostic value

    75% of prolonged cholestasis pts > 4 WNL No difference between extra and intrahepaticobstruction

    Isolated elevation

    Partial bile duct obstruction: stone, tumor Infiltrative disease: sarcoidosis, abscesses, Tb,

    metastatic carcinoma

    Elevation in cancer patients

    Bone or hepatic metastasis

    Tumor secretion / leakage of hepaticphosphatase

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    Principal diagnostic value II

    Elevation < 4 WNL Nonspecific

    Viral hepatitis, CH, LC, infiltrative disease

    Moderate elevations Hodgkins disease, CHF, myeloid metaplasia,

    intraabdominal infections, osteomyelitis

    Familial

    Extremely low level

    Wilson disease with hemolysis

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    -Glutamyl Transpeptidase

    Cell membrane in kidney, pancreas, liver, spleen,heart, brain, seminal vesicle; not in bone

    Normally exist in serum (0-30 IU/L)

    No change during pregnancy

    Clinically elevated in disease of liver, biliary tract,pancreas

    Clinical value: DDx of elevated ALP, alcohol abuse

    Not elevated in bone disease

    Not elevated in childhood & pregnancy

    GGT/ALP > 3: alcohol, drug

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    -Glutamyl Transpeptidase

    Isolated elevation of GGT Medication: barbiturate, phenytoin,

    anticonvulsant, warfarin

    Alcohol

    Induction of hepatic microsomal GGT by EtOH ordrugs

    Leakage from hepatocyte by alcohol

    Fatty liver disease

    Insulin resistance, visceral fat, fatty liver

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    Albumin

    300-500 g in body fluids Synthesize 15 g/d

    Half life: 20 days

    4% degraded daily

    Regulation of synthesis: Nutrition, osmotic pressure,systemic inflammation, hormone

    AA, corticosteroid, thyroid hormone

    Alcohol, inflammation Chronic liver disease, heavy alcohol ingestion,

    chronic infection, malnutrition, protein loosingenteropathy, nephrotic syndrome

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    Prothrombin time

    I, II, V, VII, IX, X, XII, XIII Half life < 24h

    Congenital, consumption, warfarin, Vitamin Kdeficiency, parenchymal liver disease

    Vitamin K 5- 10 mg parenteral injection

    Improves 30% within 24 hours

    Not sensitive but highly prognostic

    Alcoholic steatonecrosis, hepatocellular disease,acetaminophen overdose

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    Diagnostic approach in elevated serum bilirubin

    elevated bilirubin

    History and PE

    unconjugated bilirubin

    normal ALP, ALT, AST

    conjugated bilirubin

    normal ALP, ALT, AST abnormal ALP, ALT, AST

    Rotors syndrome AST, ALT ALP

    Dubin-Johnson syndrome predominate predominatehemolysis studies,review medications

    as elevated

    ALT evaluation U/S

    ERCP as elevated ALT evaluation

    review medications

    AMA, ERCP, liver biopsy

    present absent

    //

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    Thank You


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