Liver Cirrhosis and Complications Year 4 Internal Medicine

Year 4 Internal Medicine study notes: Liver Cirrhosis and Complications. Full notes on OmpathStudy. Free notes for medical students worldwide.

Liver Cirrhosis and Complications Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / I MED BEAUTIFUL NOTES / GIT -- ● Objectives: ● To understand Cirrhosis definition, causes and complications ● To know the pathophysiology of Cirrhosis complications ● To know how to approach patients with Cirrhosis and its complications\n\n [ Color index: ​Important​ ​Notes ​ ​Extra​ ]\n[​ ​Editing file​ ​ ​ ​Feedback​ ​ ​Share your notes​ ​ ​Shared notes​ ​ ​Twitter​ ] ● Resources: ● 435 slides.\n\n● Done by:​ ​Lina alshehri & Khalid AlNaeem ● Team sub-leader:​ ​Jwaher Alharbi ● Team leaders:​ ​Khawla AlAmmari & Fahad AlAbdullatif ● Revised by: ​Luluh Alzeghayer \n\n Liver cirrhosis\n\n Cirrhosis: ​Late stage of chronic liver inflammation and fibrosis, in which liver parenchyma is\ndistorted and replaced by fibrous tissue and regenerating nodules​ ​(if no nodules present no\ncirrhosis is there)​. ​fibrous tissue replaces damaged or dead hepatocytes \n● Chronic liver injury (Chronic hepatitis) → Compensated Cirrhosis → Decompensated\nCirrhosis → Death or liver transplantation \nChronic hepatitis is a spectrum depends on how aggressive is the etiology. Some people progress faster\nto cirrhosis and some remains years and then develop very minimal fibrosis (Genetic predisposition) \nCompensated cirrhosis the liver has the ability to regenerate and maintains normal function \nPathophysiology: \nThe distortion of liver anatomy causes (Cirrhosis): \nA- ​Decreased sinusoidal blood flow through the live​r\n(vasoconstriction)​ ​→ high resistance in portal circulation\n(portal hypertension) → this lead widespread\nmanifestations, including (ascites, peripheral edema,\nsplenomegaly, and varicosity of veins). \nB- ​Hepatocellular failure that leads to impairment of\nbiochemical function​s, such as decreased albumin\nsynthesis and decreased clotting factor synthesis. \nAetiology: \nCauses Notes Viral hepatitis (B and C) The ​most common​ cause worldwide Alcoholic Steatohepatitis The most common cause in the western world\nLike all drugs causing liver disease gives a ​greater elevation in AST\ncompared to ALT Non-alcoholic Steatohepatitis Associated with Obesity, Diabetes, Hyperlipidemia, Corticosteroid use \nCirculating auto-antibodies (antinuclear, smooth muscle, soluble liver Autoimmune hepatitis antigen, Liver/kidney microsomal antibodies) ( ​ASMA​ ) ​(ANA)\n“Hypergammaglobulinemia” \n● Progressive destruction of ​intrahepatic bile ducts​ causing Primary Biliary Cirrhosis cholestasis eventually leading to cirrhosis. (autoimmune) ● Affects women in 40s or 50s\n● Presents with pruritis with or without jaundice. In advanced\ndisease there is ​xanthelasma​ (due to secondary\nhypercholesterolemia)\n● The most accurate blood test is Antimitochondrial antibody\n(AMA) \n\nPrimary Sclerosing Cholangitis ● Progressive obliterating fibrosis of ​intra and extra hepatic (autoimmune) ducts eventually leading to fibrosis\n● More common in male than female\n● 75% or more occurs ​in association with IBD\n● The ​most accurate test is ​Endoscopic retrograde\ncholangiopancreatography​ not liver biopsy! Alpha 1 antitrypsin deficiency Combination of liver disease and emphysema in young patient (under\n40) who is non smoker Wilson's disease ● Disorder of abnormally ​decreased copper excretion​ from the\nbody because of a decrease in ceruloplasmin. Copper builds up\nin the liver, Kidney, Red blood cells and nervous system\n● Presents with: ​Neurological symptoms​, coombs negative\nhemolytic anemia and renal tubular acidosis Hemochromatosis ● Genetic disorder leading to ​over-absorption of iron​ in the\nduodenum\n● Presents with: Fatigue and joint pain, Erectile dysfunction in\nmen and Amenorrhea in women, Skin darkening, Diabetes,\nRestrictive cardiomyopathy Vascular Budd-Chiari syndrome, Heart failure, portal vein thrombosis\nHypoxic damage and necrosis of hepatocyte Biliary Sclerosing Cholangitis Drugs methotrexate, acetaminophen toxicity\n\n 1. Clinical manifestations (Signs and symptoms)\n● No symptoms (Most patients in early cirrhosis)\n● Symptoms of cirrhosis (sometimes nonspecific\nsymptoms)\n● Symptoms of ​decompensations​ (when liver start to\nfail):\n1. Neurological disorientations (Hepatic\nencephalopathy)\n2. Ascites\n3. Dilated veins on abdomen and Variceal\nhemorrhage\n4. Hepatocellular carcinoma\n5. Pulmonary (Hepatopulmonary\nsyndrome/Portopulmonary HTN) \n\n2. Investigations\n\n Lab Test \nLFTs​: \n● Moderately​ elevated aminotransferases (often with an AST:ALT ratio 1)\n● Elevated ALP (2 to 3 times the ULN1) \nCBC: \n● Thrombocytopenia ​(platelets will be low due to hypersplenism)\n● Leukopenia/neutropenia\n● Anemia \nLiver function: \nProlonged prothrombin time/elevated INR​ and Low serum albumin ​(are the best indicators\nof liver function With advanced disease\n\n Hyperbilirubinemia / Hyponatremia / Elevated serum creatinine ​( with severe liver disease)\n\n Radiology\n\n Mild to moderate disease With advanced disease\n\
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