Manifestations of

- – Elevated AST, ALT Liver, Gall Bladder, – Steatosis – Enlarged Liver and Pancreatic Disease • • Functional – Jaundice – Lowered albumin (and other proteins) • – Scarring – Small liver

Hepatitis Hepatitis

• Alcohol • Symptoms • Hepatitis – A,B,C,D,E,G – Latent: 30% HBV, 80% HCV – 44% Hep B (present in all secretions, STD) – Acute Phase: 1 – 4 months – 37% Hep A (oral-fecal route) • Malaise, anorexia, fatigue, NV, abd pain • Fever, H/A, Icterus (optional) – 19% Hep C (percutaneous) – Convalescence: 2 – 4 months – Liver damage – Immune mediated – Chronic – Systemic effects – Type III reaction • Uncommon for HAV • Most common HCV – Fulminant Hepatitis

Hepatitis Tests Portal Vein System

• LFTs – AST, ALT (SGOT, SGPT) – Albumin – Globulins • Specific – Antibodies: surface and core, IgM, IgG • e.g., HBcIgM, HBcIgG – Antigens: surface and core • e.g., HBsAg, HBcAg Portal Hypertension Pathophysiology

• Etiology • Blood backs up – Intrahepatic – Mesenteric veins – Spleen (splenomegaly) • Thrombosis – Collateral circulation • Inflammation • (varices) • Fibrosis (cirrhosis) • Abdominal wall (caput medusa) – Posthepatic • () • Splanchnic artery dilation • Cardiac insufficiency – Drop in blood pressure – Prehepatic – RAAS activation, epinephrine • Narrowing of portal vein • Ascites • Increased splanchnic artery vasodilation •

Splenomegaly

• Premature erythrocyte removal Splanchnic Artery Dilation

• Inappropriate dilation of gut arteries – Lowers systemic BP • Increased Epi and Norepi • Increased RAAS • Even though fluid overloaded, at risk for hypotension – Increased Portal Pressure • Worsens portal hypertension • Increases ascites

Ascites

• Transudate • Accumulation of • Increased portal hydrostatic pressure • Decreased oncotic pressure • Manifestations – Distended – Fluid wave – Respiratory distress – Electrolyte imbalance • Treatment – Underlying cause – Paracentesis Paracentesis Other Hepatic Manifestations

• Jaundice – Excess bilirubin – Liver cannot conjugate bilirubin – Liver cannot excrete conjugated bilirubin – Icterus include yellowing of sclera • Decreased liver function – Decreased plasma • Edema, increased bleeding, increased infection – Decreased removal of waste • Drug levels become toxic • Increased ammonia levels

Hepatic Encephalopathy Gall Bladder Diseases

• Ammonia buildup from protein • Cholecyst • Manifestations – fills from – Changes in personality – Stores and secretes bile into the common bile – Memory, confusion duct – Asterixis (Hand flapping) • Cholelithiasis/ – Stupor, Coma – Genetic component • Treatment – High fat diets – Low protein diet – Cholecystectomy – Lactulose • Requires diet modification

Acute

• Ranges from mild edema to necrosis • Pathophysiology – Autodigestion: lipase, , trypsin – May resolve completely or • Clinical Manifestations – Become chronic/episodic – Pain…unbelievable pain • Etiology • Worse with eating • Patient often writhes – Biliary tract disease (most common in women) – Other – (most common in men) • Fever, leukocytosis • Hypotension, tachycardia, jaundice – Trauma, surgery, drugs, – Complications • , pancreatic abcess Acute Pancreatitis

• Eval • Progressive inflammatory replacement of parenchyma with fibrous tissue – Amylase and lipase levels – Chronic obstructive pancreatitis – Various radiographic tests • Gall bladder disease – Chronic calcifying pancreatitis • Treatment • Alcholic – PAIN management • Eval: Same – Antispasmodics • Tx: – NPO – Dietary/alcohol modification – Cholecystecomy – Support blood pressure – Pancreatic Enzymes – Surgery – Treat flares like acute pancreatitis