Cirrhosis Pathophysiology PDF

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 8: Altered Fluid and Electrolyte Balance Module 3: Clinical Models Cirrhosis MPAT12001 Medical Pathophysiology Lecture S...

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 8: Altered Fluid and Electrolyte Balance Module 3: Clinical Models Cirrhosis MPAT12001 Medical Pathophysiology Lecture Series Copyright © 2017 Wolters Kluwer Health | Lippincott Williams & Wilkins  Cirrhosis Clinical Diagnostic Pathophysiology Treatment manifestations criteria  Cirrhosis Pathophysiology Cirrhosis and chronic liver disease: leading cause of mortality Cirrhosis: end-stage liver disease Frequent cause (not always) Viral hepatitis Liver damage from alcohol (alcoholic hepatitis) 1. Interference with local blood flow 1. Exacerbates hypoxia of the hepatocytes and result in further cell death 2. Causes blood and bile to back up into the liver resulting further injury and inflammation 3. Obstructs blood flow from portal circulation 2. Widespread hepatocyte damage, fibrosis, scarring 3. Liver failure and death may result  Cirrhosis Pathophysiology Common complication: ascites (accumulation of fluid in peritoneal cavity) 85% ascites is caused by cirrhosis Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby; 2011 Altered fluid balance Fluid loss to 3rd space Unavailable to use it in ICF and ECF  Cirrhosis Pathophysiology Ascites is result of the combination of Increased hydrostatic pressure Hepatic vein obstruction Congestive heat failure Decreased colloid osmotic pressure Malnutrition Nephrotic syndrome Increased capillary permeability Malignancy Bacterial peritoneal infection  Cirrhosis Pathophysiology 1. Chronic inflammation lead to hepatocyte damage, fibrosis, scarring 2. Liver sinusoids become increasingly disordered, blood flow obstructed 3. Obstruction leads to increased vascular resistance to blood flow in liver a) Elevation in hepatic (portal) pressure develops (portal hypertension) b) Increased pressure promotes fluid out of capillaries (hydrostatic pressure) c) Fluid movement exceeds lymph ability to recirculate fluid into systemic circulation d) Fluid accumulates, ascites develops 4. Increased vascular resistance triggers release of vasodilators to increase blood flow (dilation) a) Dilation will eventually lead to decreased blood flow, drop in blood pressure b) Compensation triggered to maintain arterial blood pressure c) Sodium and water retention, expanding plasma volume d) Contribute to ascites 5. Advanced stage: decline in albumin production, decrease oncotic pressure a) Sodium and water retention, expanding plasma volume b) Contribute to ascites Adapted from Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby; 2011  Cirrhosis Pathophysiology Progressive pathology may lead to renal impairment Impaired water excretion (water retention) Dilutional hypernatremia Renal vasoconstriction Hepatorenal syndrome (renal failure caused by severe renal vasoconstriction)  Cirrhosis Clinical Manifestations The clinical signs and manifestations are related to the severity of ascites Ascites can be described based on volume of fluid in the peritoneum Moderate to large volume 500ml is detectable Moderate to severe abdominal discomfort Increased abdominal girth Increased weight Severe sodium retention Dilutional hyponatremia (due to water retention) Renal failure  Cirrhosis Diagnostic Criteria History taking and Physical exam Changes in body weight Abdominal girth/circumference measurement Liver, renal and cardiac function: to determine systemic damage/dysfunction Laboratory analysis Ascitic fluid analysis 1. Serum-ascetic albumin gradient (SAAG) >1.1g/dL: portal hypertension or transudative ascites