Cirrhosis 1
Cirrhosis 1
Cirrhosis 1
CIRRHOSIS :
1. PROTEIN:
A:G WILL GO DOWN THIS WILL CAUSE EDEMA.
2. CLOTTING FACTORS:
THESE FACTORS WILL ALSO GO DOWN AND IT WILL CAUSE BLEEDING.
PLATELET COUNT INCREASED.
• DECREASED METABOLISM:
1. ESTROGEN:
PALMAR ERYTHEMA,SPIDER ANGIOMA,GONADAL ATROPHY.
2. AMMONIA:
SE CROSSES BLOOD BRAIN BARRIER RESULTS IN. HEPATIC
ENCEPHALOPATHY
PORTAL HYPERTENSION
CIRRHOSIS
PORTAL HYPERTENSION
LEADS TO:
1. ASCITES
2. CAPUT MEDUSAE
3. CONGESTIVE SPLENOMEGALY
CLASSIFICATION :
1. MICRONODULAR CIRRHOSIS:
NODULE SIZE > 3MM.
CAUSES :
PRIMARY BILIARY
CIRRHOSIS.
INDIAN CHILDHOOD
CIRRHOSIS.
ALCOHOL LIVER DISEASE .
HEMOCHROMATOSIS.
2.MACRONODULAR CIRRHOSIS:
NODULE SIZE <3MM
CAUSES:
ALCOHOL LIVER DIESEASE
WILSON DISEASE
VIRAL HEPATITIS.
CAUSES OF CIRRHOSIS:
• ALCOHOL LIVER DISEASE.
• AUTO IMMUNE HEPATITIS.
• CRYPTOGENIC CIRRHOSIS (NALD).
• BILIARY DISEASE.
• ENZYME DEFICIENCY ALPHA 1 ANTITRYPSIN DEFICIENCY.
• HEPATITIS.
• HEMOCHROMATOSIS.
• WILSON DISEASE.
• DRUG INDUCED.
LCOHOLIC LIVER DISEASE :
HEALTHY LIVER
STEATOSIS/FATTY LIVER
STEATOHEPATITIS
LAENNEC CIRRHOSIS
STEATOSIS (FATTY LIVER)
DIABETES MELLITUS.
HYPERTENSION.
NON ALCOHOLIC STEATOHEPATITIS
CIRRHOSIS OF LIVER
CIRRHOSIS IN ALPHA-1 ANTITRYPSIN
DEFICIENCY
• THIS ENZYME IS PRESENT ON CHROMOSOME 14.
• IT IS AN AUTOSOMAL RECESSIVE DISORDER.
• AAT IS A GLYCOPROTEIN NORMALLY SYNTHESISED IN THE
ROUGH ENDOPLASMIC RETICULUM OF THE HEPATOCYTES AND IS
THE MOST POTENT PROTEASE INHIBITOR (PI).
• GENOTYPE PI MM=NORMAL PI ZZ= DISEASE PI MZ=CARRIER
• PI ZZ WILL CAUSE LIVER OR LUNG DISEASE.
CIRRHOSIS IN HEMOCHROMATOSIS
ALSO CALLED AS BRONZE DIABETES
• GENETIC CAUSE: HFE GENE (CHR 6)
• ACQUIRED CAUSE:IN BLOOD TRANSFUSION.
IN THALASSEMIA
• BANTU SIDEROSIS:
AFRICAN IRON OVERLOAD IN INDIVIDUALS OF AFRICAN
DESCENT WHO HAVE A GENE, FERROPORTIN, THAT PREDISPOSES
THEM FOR IRON OVERLOAD (EARLIER CALLED BANTU SIDEROSIS
AFFECTING SOUTH AFRICAN BANTU TRIBALS WHO CONSUME
LARGE QUANTITIES OF HOME-BREW PREPARED IN IRON VESSELS.)
TRIAD
LIVER
PANCREAS. SKIN
PIGMENTATION/BRONZE
BETA CELL FUNCTION (DECREASE)
INSULIN (DECREASE)
DIABETES MELLITUS.
• IRON CAN ALSO GO INTO THE HEART AND CAN CAUSE
CARDIOMYOPATHY.
• IRON CAN ALSO GO INTO THE PITUITARY GLAND,CAUSE
CIRRHOSIS IN WILSON DISEASE (CU
OVERLOAD)
INHERITANCE: AUTOSOMAL RECESSIVE
GENE : ATP7B
NORMALLY, COPPER SO ABSORBED THROUGH THE STOMACH AND
DUODENUM IS TRANSPORTED TO THE LIVER WHERE IT IS
INCORPORATED INTO ALPHA2-GLOBULIN TO FORM
CERULOPLASMIN, WHICH IS EXCRETED BY THE LIVER VIA BILE
NORMALLY. MOST OF THE PLASMA COPPER CIRCULATES AS
CERULOPLASMIN. ONLY MINUTE AMOUNT OF COPPER IS
EXCRETED IN THE URINE NORMALLY
• IN PATHOLOGICAL CONDITION DUE TO MUTATION OF ATP7B
GENE,COPPER ACCUMULATES IN LIVER RATHER THAN EXCRETION.
• AS THE CAPACITY OF HEPATOCYTES TO STORE COPPER IS EXCEEDED AND
COPPER IS RELEASED INTO CIRCULATION WHICH THEN GETS DEPOSITED
IN EXTRAHEPATIC TISSUES SUCH AS THE BRAIN, EYES AND OTHERS
TRIAD
LIVER
4. SKIN PIGMENTATION.
2.PRIMARY SCLEROSING CHOLANGITIS:
CHRONIC PROGRESSIVE CONDITION CHARACTERIZED BY
INFLAMMATION AND SCARRING OF INTRAHEPATIC AND
EXTRAHEPATIC BILE DUCT.
CAUSES:
1. IMMUNE MEDIATED
2. GENETIC PREDISPOSITION
3. BACTERIAL INFECTIONS.
SIGNS AND SYMPTOMS:
FATIGUE, PRURITUS, JAUNDICE,FEVER.
DIAGNOSIS
1. ULTRASOUND
2. LIVER FUNCTION TEST. (AST/SGOT=4-17 IU/L,ALT/SGPT=3-15
IU/L)
3. LIVER ELASTOGRAPHY.
4. LIVER BIOPSY.
5. CT SCAN.
6. UPPER G.I ENDOSCOPY.
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