Liver Function Tests

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LIVER FUNCTION TESTS:

LIVER FUNCTION TESTS DR. RAFIA TABASSUM ANAESTHETIST,DEPARTMENT OF ANAESTHESIA & SICU,PMCH NAWABSHAH, SIND

THE LIVER:

THE LIVER Both a metabolic and excretory organ Has “double” blood supply 1- Hepatic artery – oxygenated blood 2-Portal vein – nutrient rich blood Unique anatomic structure 1- Series of plates of hepatocytes that radiate from a central vein 2- Hepatocytes in contact with bloodstream on one side and bile canaliculi on the other 3- Between plates are vascular spaces (sinusoids) Kupffer cells – phagocytic macrophages

LIVER FUNCTIONS:

LIVER FUNCTIONS Metabolic Storage Excretory/Secretory – bile excretion Protective Circulatory – large blood storage organ Coagulation – production of clotting factors

METABOLIC FUNCTIONS:

METABOLIC FUNCTIONS Carbohydrate metabolism 1- Gluconeogenesis 2- Glycogenolysis and glycogenesis Hormone metabolism Lipid Metabolism 1- Synthesis of fatty acids, cholesterol, lipoproteins 2- Ketogenesis Drug Metabolism

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Protein Metabolism 1- Synthesis of plasma proteins Distribution of fluid Carrier molecules Antibodies Endocrine system Coagulation Source of nutrients for cellular repair Enzymes 2-Urea synthesis

STORAGE FUNCTION:

STORAGE FUNCTION Glycogen All fat-soluble vitamins (A, D, E, K) and some water soluble vitamins (B12) Iron

PROTECTIVE FUCTIONS:

PROTECTIVE FUCTIONS Detoxification – converts noxious or insoluble compounds into less toxic or more water soluble forms Kupffer cells ingest bacteria or other foreign material from blood

LABORATORY TESTS:

LABORATORY TESTS May measure synthetic function May measure excretory function May indicate damage to cells: determination of specific enzymes may be used to show the location of liver damage

USES OF LFTS:  :

USES OF LFTS: To establish a diagnosis. Monitor response to Rx or surgery. For prognosis. For screening. Performed by Automatic biochemistry analyzer

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The true liver function tests (LFT's) include albumin, bilirubin, PT, and glucose. More specifically, AST, ALT, and alkaline phosphatase are called the liver enzymes and they typically are used to detect damage or injury to the liver (not its function).

LFT’S INCLUDE;:

LFT’S INCLUDE; Alanine aminotransferase.( ALT). Aspartate aminotransferase.(AST) Alkaline phosphatase.(ALP) Gamma-glutamyltransferase (GGT) Albumin. Bilirubin. Prothrombin time (PT) 5’nucleotidase

ALANINE TRANSAMINASE (ALT):  :

ALANINE TRANSAMINASE (ALT): Also called Serum Glutamic Pyruvate Transaminase (SGPT) or Alanine aminotransferase (ALAT) Normal value 5-40 U/L It is an enzyme present in hepatocytes (liver cells). When a cell is damaged, it leaks this enzyme into the blood, where it is measured. ALT rises dramatically in acute liver damage, such as viral hepatitis or paracetamol (acetaminophen) overdose.

ASPARTATE TRANSAMINASE (AST):  :

ASPARTATE TRANSAMINASE (AST): Also called Serum Glutamic Oxaloacetic Transaminase (SGOT) or aspartate aminotransferase (ASAT) Found in many sources, including liver, heart, muscle, intestine, pancreas Not very specific for liver disease Normal range: 8-20 U/L Often follows ALT to a degree AST:ALT RATIO > 2 Consider alcoholic liver disease

HEPATIC CAUSES OF AST ELEVATION:    :

HEPATIC CAUSES OF AST ELEVATION: Alcoholic liver disease. Ch. Hep B Ch. Hep c Autoimmune hep Fatty liver Cirrhosis Hemochromatosis Wilson’s disease A1 –antitrypsin deficiency Drug-induced liver disease Congestive hepatopathy Acute viral hep (EBV,CMV) Celiac disease.

ALKALINE PHOSPHATASE :

ALKALINE PHOSPHATASE Produced by biliary epithelial cells -Non-specific to liver: bone, intestine,Kidney, placenta Normal range: 20-70 U/L

CAUSES OF HIGH ALP: :

CAUSES OF HIGH ALP: Elevations Biliary duct obstruction Primary biliary cirrhosis Primary sclerosing cholangitis Infiltrative liver disease- i.e sarcoidosis, lymphoma Hepatitis/cirrhosis Medications In growing children Elderly patients with Paget's disease.

G-GLUTAMYL TRANSFERASE (G-GT): :

G-GLUTAMYL TRANSFERASE (G-GT): Normal values 3-17 U/L(M), 2-13 U/L(F) Elevated GGT: 1-Hepatic neoplasm 2-Obstructive jaundice 3-Hepatitis 4-Alcohol toxicity (acute and chronic)

TESTS OF PROTEIN METABOLISM  :

TESTS OF PROTEIN METABOLISM Serum total protein (TP),albumin (A) and globulin (G) The normal range of TP, A and G is 60-80g/L, 40-55g/L and 20-30 g/L respectively. The normal ratio of A to G (A/G) is 1.5-2.5 : 1 Increased G and decreased A (reversed A/G) can be seen in chronic hepatitis, cirrhosis, hepatic neoplasm Composition/ Electrophoresis 1- Albumin 2- α -1 globulin 3- α -2 globulin 4- β -globulin 5- g-globulin

ALBUMIN:

ALBUMIN It is synthesized exclusively by the liver. Half life is 20 days Rapidly decreases after trauma and surgery Prealbumin has half life of 1.5 days, thus more useful in assessing acute liver disease Dehydration can cause high albumen level.

CAUSES OF HYPOALBUMINEMIA:  :

CAUSES OF HYPOALBUMINEMIA: Malnutrition Malabsorption Malignancy Inflammation ( acute, chronic) Increased loss: Nephrotic syndrome Protein losing enteropathy Burns Exudative skine disease Intravenous fluids Rapid hydration Overhydration Cirrhosis Pregnancy. Ch. Liver disease

TESTS OF BILIRUBIN METABOLISM:

TESTS OF BILIRUBIN METABOLISM Bilirubin is a breakdown product of heme (a part of haemoglobin in red blood cells). The liver is responsible for clearing the blood of bilirubin. It does this by the following mechanism: bilirubin is taken up into hepatocytes, conjugated (modified to make it water-soluble), and secreted into the bile, which is excreted into the intestine. Bilirubin: two primary sources 1- Indirect (unconjugated): 2- Liver “adds” glucuronic acid, making these cells water soluble for excretion into the intestine ; now called direct (or conjugated) Normal range: less than 0.8 mg/dL (0.3-1.5 mg/dL)

Increased total bilirubin causes jaundice, and can signal a number of problems:  :

Increased total bilirubin causes jaundice, and can signal a number of problems: Prehepatic: Increased bilirubin production. This can be due to a number of causes, including hemolytic anemias,Malaria, Gilbert Syndrome, Neonatal juandice and internal hemorrhage.

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2. Hepatic: Problems with the liver, which are reflected as deficiencies in bilirubin metabolism (e.g. reduced hepatocyte uptake, impaired conjugation of bilirubin, and reduced hepatocyte secretion of bilirubin). Examples would be; Cirrhosis, Pregnancy,Oral contraceptives, Sepsis and Viral hepatitis.

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3. Posthepatic : Obstruction of the bile ducts, reflected as deficiencies in bilirubin excretion. (Obstruction can be located either within the liver or in the bile duct.)

PROTHROMBIN TIME (PT) & INR:  :

PROTHROMBIN TIME (PT) & INR: PT: It will be normal until 80% of liver’s synthetic function is impaired. It is useful in acute liver disease {short half life of coagulation factors related to PT (hours) than albumin (3 wks) }.

CAUSES OF HIGH PT: :

CAUSES OF HIGH PT: Vit K deficiency Liver disease ( to differentiate between vit K deficiency & liver disease , give 10 mg vit K subcutaneously , decrease in PT of at least 30 % within 24 hrs suggest vit K deficiency). Warfarin Factor VII deficiency (rare) False +ve result (high hematocrit).

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INR: The liver is responsible for the production of coagulation factors. The international normalized ratio (INR) measures the speed of a particular pathway of coagulation, comparing it to normal. If the INR is increased, it means it is taking longer than usual for blood to clot. The INR will only be increased if the liver is so damaged that synthesis of vitamin K-dependent coagulation factors has been impaired: it is not a sensitive measure of liver function.

5' NUCLEOTIDASE (5'NTD)  :

5' NUCLEOTIDASE (5'NTD) 5' nucleotidase is another test specific for cholestasis or damage to the intra or extrahepatic biliary system, and in some laboratories, is used as a substitute for GGT. If there is isolated increase in ALP.The high ALP is either hepatobiliary or bone origin. So to differentiate 5’nucleotidase is done.

OTHER TESTS:  :

OTHER TESTS: Serum glucose: The liver's ability to produce glucose (gluconeogenesis) is usually the last function to be lost in the setting of fulminant liver failure. Lactate dehydrogenase (LDH) Lactate dehydrogenase is an enzyme found in many body tissues, including the liver. Elevated levels of LDH may indicate liver damage.

DYE INTAKE & EXCRETION:

DYE INTAKE & EXCRETION Bromosulphthalin & Indocyanine green retention rate (ICGR): 15 min: < 10% -chronic hapatitis: 15-20% -cirrhosis : 35% Radioactivelly labelled colloid : To assess Kupffer cell function

HEPATIC NEOPLASM MARKERS:

HEPATIC NEOPLASM MARKERS Alpha fetoprotein (AFP): < 25ug/ L , > 500 ug /L : primary hepatocellular carcinoma Carcinoembryonic antigen (CEA): 0-5 ug /L Increased CEA: liver metastatic carcinoma or other carcinomas of the gastrointestinal system Abnormal prothrombin (APT): < 20 ug/L, Increased APT : primary hepatocellular carcinoma

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SUMMARY

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ALT & AST ------------rises in heptocyte damage Or necrosis of liver cells( hepatic picture) ALP (with GGT) ------------------rises with obstruction of bile flow ( cholestatic picture) Bilirubin ( total/direct + indirect) -------- rises with excess Hb breakdown or failure to excrete bile. Albumin & PT --------- low Albumin & increased PT ( synthesis is affected)

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THANKS