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L20 cirrhosis sr

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  • Pressure exceeding greater than 22 mm Hg in the portal vein or a pressure difference between the portal vein and the hepatic vein of greater than 12 mm Hg will result in portal hypertension. Measuring portal pressure involves inserting a catheter into the portal vein. The internal jugular, femoral, or medial antecubital vessels are the best way to access the hepatic and portal veins.
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    • 1. Liver Cirrhosis Lecture 19 Dr Mohammad Manzoor Mashwani BKMC Mardan
    • 2. Yellowish brown color Tawny
    • 3. Introduction• The term cirrhosis was first used by Rene Laennec (1781-1826) to describe the abnormal liver color of individuals with alcohol induced liver disease. • Derived from Greek word Kirrhos means Yellowish brown color. Cirrhosis is among the top 10 causes of death in the Western world.
    • 4. Definition • Cirrhosis is defined as a diffuse (not focal) involvement of most or all of the liver. It involves the entire liver. • process characterised by fibrosisand the conversion of normal liver architecture into structurally abnormal nodules containing a mix of senescent and replicating (often stem/progenitor cell-derived) hepatocytes..
    • 5. Common Causes 1. Chronic alcoholism & NASH 2. Chronic hepatitis B& C 3. Biliary disease 4. Hemochromatosis (Iron oveload) 5. Cryptogenic 10% 6. Wilson's disease, 7. Alpha-1 anti-trypsin deficiency.
    • 6. Causes of Liver Cirrhosis • Obesity • Autoimmune hepatitis • Diseases that damage or destroy bile ducts. • Inherited diseases • Drugs, toxins & toxins
    • 7. Types of Cirrhosis • 1. Alcoholic Cirrhosis (Laennec) • 2. Post necrotic Cirrhosis (macronodular) • 3. Billiary Cirrhosis • 4. Cardiac Cirrhosis
    • 8. Pathogenesis 1. Hepatocellular death 2. Regeneration 3. Progressive fibrosis 4. Vascular reorganization Three processes are central to the pathogenesis of cirrhosis: •death of hepatocytes, •extracellular matrix deposition, and •vascular reorganization.
    • 9. Pathophsiology : Liver insult due to alcohol ingestion, viral hepatitis, exposure to toxin Hepatocyte damage Liver inflammation - ↑WBCs, nausea, vomiting, pain, fever, anorexia, fatigue Alteration in blood and lymph flow
    • 10. Cont.. Liver necrosis →liver fibrosis and scarring → portal hypertension - Ascities, edema, - Spleenomegaly ( thrombocytopenia, leucopenia) - Varices (esophageal varices, hemorrhoids, anemia) ↓ billirubin metabolism – hyperbilirubinemia, jaundice
    • 11. Cont.. • ↓ bile in gastrointestinal tract – light colored stool • ↑ urobilinogen – Dark Urine • ↓ vit K absorption- bleeding tendency • ↓ metabolism of protein, carbohydrate, fats→ hypoglycemia, • ↓ plasma protein- ascites and edema • ↓androgen and estrogen detoxification(↓ hormone metabolism)- ↑ estrogen and androgens hormone – Gynecomastia, loss of body hair, menstrual dysfunction, spider angioma, palmer erythema, testicular atrophy
    • 12. Cont.. • ↓ Aldesterone metabolism so ↑ levels – sodium and water retention-- edema • Biochemical alteration - ↑ AST, ALT levels, ↑ bilirubin, low serum albumin, prolong prothombin time, elevated alkaline phosphatase. • Liver failure • Hepatic encephalopathy • Hepatic coma • Death
    • 13. Morphology • Its three main morphologic characteristics are: • 1.Bridging fibrous septa (delicate fibrous bands/broad scars) • 2. Parenchymal nodules- micro (<3mm) & macro (>1cm) • 3. Disruption of the architecture of the entire liver. 4. It occurs following hepatocellular necrosis of varying etiology so that there are alternate areas of necrosis and regenerative nodules. However, regenerative nodules are not essential for diagnosis of cirrhosis since biliary cirrhosis and cirrhosis in haemochromatosis have little regeneration.
    • 14. Clinical manifestations Early manifestations • No symptoms • GI disturbances: anorexia, dyspepsia, flatulence, weakness, fatigue, nausea, vomiting, weight loss, abdominal pain, bloating, diarrhea, constipation • Abdominal pain, dull and heavy feeling • Fever, lassitude, weight loss, enlargement of liver and spleen.
    • 15. Clinical manifestations Cont… Later manifestations: Results from liver failure and portal hypertension • Jaundice • Peripheral edema • Ascites • Others: Skin lesion, hematological disorders, endocrine disturbances, and peripheral neuropathy • Advanced stage: small and nodular liver
    • 16. Clinical Manifestations
    • 17. Complications • The ultimate mechanism of deaths in most cirrhotic patients is • (1) progressive liver failure, • (2) a complication related to portal hypertension, or • (3) the development of hepatocellular carcinoma.
    • 18. Complications Portal hypertension • The nodules and scar tissue can compress hepatic veins within the liver. • This causes the blood pressure within the liver to be high, a condition known as portal hypertension. • Portal venous pressure is more than 15mmHg or 20 cm of water (normal 5-10mm Hg)
    • 19. Cont… • Is characterized by ↑venous pressure in the portal circulation, spleenomegaly, large collateral vein, ascites, systemic hypertension, and esophageal varices. • The common area to form collateral channels are in the lower esophagus( the anastomosis of the left gastric vein and azygos vein), the parietal peritoneum, rectum. • High pressures within blood vessels of the liver occur in 60% of people who have cirrhosis.

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