HEPTOLOGY

Information about HEPTOLOGY

Published on March 19, 2014

Author: drmustansar

Source: authorstream.com

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PowerPoint Presentation: Diseases of the Liver & Biliary System PowerPoint Presentation: If individual hepatocytes are destroyed but the architecture of the lobule is not destroyed, the remaining hepatocytes will totally regenerate the liver parenchyma. Liver regeneration PowerPoint Presentation: If whole lobules are destroyed, the remaining lobules will expand. They will function normally, though bile may not be drained quite so well. PowerPoint Presentation: Of course, if scar tissue alters the flow of blood through the liver (i.e., cirrhosis has occurred), regeneration will only produce less-than-fully-perfused nodules of liver cells. (This will disappoint well-read problem drinkers who understood that their hepatocytes had unlimited capacity to regenerate....) PowerPoint Presentation: NORMAL CT SCAN PowerPoint Presentation: Blood enters the liver from the hepatic artery and the portal vein and leaves the liver from the hepatic vein . The blood from the artery carries oxygen while the portal vein carries nutrients from the intestine. Liver blood supply PowerPoint Presentation: The portal vein is formed by the junction of the splenic & superior mesenteric veins. Within the liver, the hepatic artery & portal vein come together with the bile ducts & lymphatics. The branches of all of these vessels extend into the liver into the central lobular vein Functional anatomy PowerPoint Presentation: The acinus make up the primary functional unit of the portal tract which contains branches of the hepatic artery, bile ducts, branches of the portal vein. Hepatocytes (liver cells) are in the ascini. They contain glycogen. Each cell abuts the sinusoids. The bile canaliculi run between the liver cells forming a network which end up in the bile ducts. Functional anatomy PowerPoint Presentation: Inside the two lobes is a network of tubes, also called the biliary tree that carries bile from the liver to the intestine. Bile is a substance that helps carry away wastes and is needed for the breakdown and absorption of dietary fats. Hepatic Ducts PowerPoint Presentation: Each tube is called a duct. Smaller ducts connect to larger ducts. The larger ducts join to form the hepatic duct . This duct network allows bile to drain out of the liver. PowerPoint Presentation: Concentrate & conduct the 1-1.5L of bile produced by the liver to the intestine Fasting diversion of bile into the gall bladder for storage & concentration Food intake  releases CCK to relax sphincter of Oddi for delivery of bile into the intestine Gallbladder PowerPoint Presentation: Bile acids & detergents  cholesterol & phospholipids to the intestine. Also solubilizes dietary fat & promotes its digestion & absorption PowerPoint Presentation: The liver has multiple functions: Making bile to help digest foods Bile acid synthesis & secretion Stopping cuts from bleeding (coagulation) Responsible for the synthesis of prothrombin, factor VII, IX, and X from vitamin K absorption . What Does the Liver Do? PowerPoint Presentation: Killing germs, helping keep the body healthy Filtering toxic chemicals from the body Remove waste products of nutrient breakdown Biotransformation, detoxification & excretion of various endogenous & exogenous compounds PowerPoint Presentation: Helps with disposing of bilirubin excretes bilirubin into the small bowel so that bowel bacteria can change it into the safe green colored biliverdin. Break down the major nutrients in foods (protein, fats and carbohydrates) Role of Liver (cont) PowerPoint Presentation: Helping to build muscles/ proteins Plasma protein synthesis Lipid & lipoprotein synthesis Glucose homeostasis PowerPoint Presentation: Albumin is synthesized exclusively in the liver albumin is essential for carrying molecules (and drugs), and for keeping fluid in the blood vessels. Hypoalbuminemia causes fluid shift into tissue and patient will show signs of edema. albumin decreases in malabsorption & tumor necrosis, or any form of chronic liver disease. Role of the liver (cont) PowerPoint Presentation: Storing energy Store vitamins A, D, E and K, & B12 Role of the liver (cont) Fate – Soluble Vitamins Vitamin Function A Visual pigments, normal development of bones D Absorption of Ca ++ E Antioxidant, stability of cell membranes K Prothrombin synthesis (clotting) PowerPoint Presentation: Bilirubin is the primary waste product of heme metabolism -degradation of hemoglobin (RBC’s). Unconjugated bilirubin is transported in the plasma bound to albumin . The liver is the major site of metabolism of bilirubin & ammonia Liver Physiology PowerPoint Presentation: The metabolism of carbohydrate in the liver is regulated by insulin, glycogen, catecholamines, corticosteroids, & thyroxine Most drugs are metabolized by the liver, microsomal enzymes such as cytochrome p450 system and rendered water soluble Hepatic Physiology (cont.) PowerPoint Presentation: Liver Function Hepatic Test Jaundice Biliary Tract Disease Cholelithiasis-Choledocholithiasis Cholecystitis-Cholangitis Biliary tract obstruction Disorders PowerPoint Presentation: Hepatic Disease Hepatitis Acute & Chronic A/B/C/D/E, ETOH/drug Cirrhosis Hepatic Failure Neoplasm (later section) PowerPoint Presentation: Functions of the Liver and Manifestations of Altered Function Function Manifestations of Altered Function Production of bile salts Malabsorption of fat and fat-soluble vitamins Elimination of bilirubin Metabolism of steroid hormones Elevation in serum bilirubin and jaundice Sex hormones Disturbances in gonadal function, including gynecomastia in the male Glucocorticoids Signs of increased cortisol levels (i.e., Cushing’s syndrome) PowerPoint Presentation: Function Manifestations of Altered Function Aldosterone Signs of hyperaldosteronism (e.g., sodium retention and hypokalemis) Metabolism of drugs Decreased drug metabolism Decreased plasma binding of drugs owing to a decrease in albumin production Carbohydrate metabolism Hyperglycemia may develop when glycogenolysis and gluconeogenesis are impaired Stores glycogen and synthesizes glucose from amino acids, lactic acid, and glycerol Abnormal glucose tolerance curve may occur because of impaired uptake and release of glucose by the liver PowerPoint Presentation: Fat metabolism Formation of lipoproteins Conversion of carbohydrates and proteins to fat Impaired synthesis of lipoproteins Synthesis, recycling, and elimination of cholesterol Formation of ketones from fatty acid Protein metabolism Deamination of proteins Altered cholesterol levels Formation of urea from ammonia Elevated blood ammonia levels PowerPoint Presentation: Synthesis of plasma proteins Decreased levels of plasma proteins, particularly albumin, which contributes to edema formation Synthesis of clotting factors (fibrinogen, prothrombin, factors V, VII, IX, X) Bleeding tendency Storage of mineral and vitamins Signs of deficiency of fat-soluble and other vitamins that are stored in the liver Filtration of blood and removal of bacteria and particulate matter by Kupffer’s cells Increased exposure of the body to colon bacilli and other foreign matter PowerPoint Presentation: Clinical Manifestations of Liver Disease Sign/Symptom Pathogenesis Liver Disease Constitutional Fatigue, anorexia, malaise, weight loss Liver dysfunction Acute or chronic hepatitis Cirrhosis Fever Hepatic inflammation or infection Liver abscess Alcoholic hepatitis Viral hepatitis Fetor hepaticus Sulfur compounds, produced by intestinal bacteria, not cleared by the liver Acute or chronic liver failure PowerPoint Presentation: Sign/Symptom Pathogenesis Liver Disease Cutaneous Spider telangiectasias, palmar erythema Altered estrogen and androgen metabolism with altered vascular physiology Cirrohsis Jaundice Diminished bilirubin excretion Biliary obstruction Severe liver disease Pruritus Uncertain Biliary obstruction Xanthomas and xanthelasma Increased serum cholesterol Biliary obstruction / cholestasis PowerPoint Presentation: Endocrine Gynecomastia, testicular atrophy, di-minished libido Altered estrogen and androgen metabolism Cirrohsis Hypoglycemia Decreased glycogen stores and gluconeogenesis Acute liver failure Alcohol binge with fasting PowerPoint Presentation: Gastrointestinal Right upper quandrant abdominal pain Liver swelling, infection Acute hepatitis Hepatocellular carcinoma Liver congestion (heart failure) Acute cholecystitis Liver abscess Abdominal swelling Ascites Cirrhosis, portal hypertension Gastrointestinal bleeding Esophageal varices Portal hypertension PowerPoint Presentation: Hematologic Decreased red cells, white cells, and/or platelets Hypersplenism Cirrhosis, portal hypertension Ecchymoses Decreased synthesis of clotting factors Liver failure Neurologic Altered sleep pattern subtle behavioral changes, somnolence, confusion, ataxia, asterixis, obtundation Hepatic encephalopathy Liver failure, portosystemic shunting of blood History: History FHx: Hx of jaundice or liver disease. Social Hx-Recent travel. Exposure to alcohol , Exposure to individuals or animals with liver or parasitic disease. Exposure to alcohol . Multiple sex partners. IV drug use. Exposure to alcohol . PowerPoint Presentation: General: fever & weight loss Cutaneous: spider angiomas, telangiectasias, palmar erythema, jaundice, xanthomas & xanthelasma Endocrine: gynecomastia, testicular atrophy, hypoglycemia Physical exam PowerPoint Presentation: G.I.: RUQ pain, abdominal swelling/ascites, heptosplenomegaly, G.I. Bleed Hematological: pale skin/mucous membranes, ecchymoses Neuro: Ataxia, somnolence, confusion, asterixis & obtundation PowerPoint Presentation: Ascites PowerPoint Presentation: Telangiectatic Lesions PowerPoint Presentation: Xanthelasma PowerPoint Presentation: Xanthomata on the abdomen PowerPoint Presentation: Splinter hemorrhages PowerPoint Presentation: Spider angioma PowerPoint Presentation: Serum albumin (or prealbumin levels): multipurpose serum protein synthesized in the liver. It is decreased when disease is prolonged enough to deplete the blood levels. Albumin is the protein of the highest concentration in plasma. Tests of liver function PowerPoint Presentation: Albumin transports many small molecules in the blood (for example, bilirubin, calcium, progesterone, and drugs). It is also of prime importance in maintaining the oncotic pressure of the blood (that is, keeping the fluid from leaking out into the tissues). PowerPoint Presentation: This is because, unlike small molecules such as sodium and chloride, the concentration of albumin in the blood is much greater than it is in the extracellular fluid. Because albumin is synthesized by the liver, decreased serum albumin may result from liver disease. PowerPoint Presentation: It can also result from kidney disease, which allows albumin to escape into the urine. Decreased albumin may also be explained by malnutrition or a low protein diet.  The normal range is 3.4 to 5.4 g/dL. PowerPoint Presentation: Prothrombin time (PT)- Prolongation of the PT is one of the most sensitive prognosticators of severe liver disease . Tests capacity for protein synthesis It measures the function of the livers clotting ability of factors I (fibrinogen), II (prothrombin), V, VII, and X. Tests of Liver Function PowerPoint Presentation: When any of these factors is deficient, the PT is prolonged. Coumadin or vitamin K deficiency impair the function PowerPoint Presentation: Plasmalogen PowerPoint Presentation: The normal PT range is 11 to 15 seconds ("normal" varies somewhat in different labs). The normal value for the INR is 1.0 Also used for oral anticoagulant monitoring following venous thromboembolism, myocardial infarction, atrial fibrillation or rheumatic heart disease PT (prothrombin time) & INR (international normalized ratio) PowerPoint Presentation: For a person on full anticoagulant therapy, the PT should be 2 to 3 times the laboratory "control" value. INR 2.0-3.0 For oral anticoagulant monitoring for those with mechanical heart valves: INR 2.5-3.5 PowerPoint Presentation: Transaminases Aspartate- AST (SGOT) & Alanine- ALT (SGPT) : LFT’s/Transaminases PowerPoint Presentation: AST (SGOT) is normally found in a diversity of tissues including liver, heart, muscle, kidney, and brain. It is released into serum when any one of these tissues is damaged. For example, its level in serum rises with heart attacks and with muscle disorders. It is therefore not a highly specific indicator of liver injury. PowerPoint Presentation: ALT (SGPT) is, by contrast, normally found largely in the liver. This is not to say that it is exclusively located in liver but that is where it is most concentrated. It is released into the bloodstream as the result of liver injury. It therefore serves as a fairly specific indicator of liver PowerPoint Presentation: status.released into the circulation following hepatocyte injury or death. The ratio of AST:ALT can be helpful AST:ALT > 2:1 suggesting alcoholic liver disease AST:ALT < 1:1 suggesting viral hepatitis. AST/ALT PowerPoint Presentation: They are sensitive, but non-specific for liver damage. Need isoenzymes The normal range of values for AST (SGOT) is from 5 to 40 units per liter of serum (the liquid part of the blood). The normal range of values for ALT (SGPT) is from 7 to 56 units per liter of serum. Normal range can vary according to a number of factors, including age and gender. PowerPoint Presentation: The highest levels of AST and ALT are found with disorders that cause the death of numerous liver cells (extensive hepatic necrosis ). Although, the precise levels of these enzymes do not correlate well with the extent of liver damage or the prognosis AST/ALT PowerPoint Presentation: This occurs in such conditions as acute viral hepatitis A or B, pronounced liver damage inflicted by toxins as from an overdose of acetaminophen (Tylenol), and prolonged collapse of the circulatory system (shock) when the liver is deprived of fresh blood bringing oxygen and nutrients PowerPoint Presentation: Derived from liver, intestines, bones & placenta. Released causing high levels during liver damage, particularly necrosis, cholestasis/ bile duct obstruction, neoplastic, infiltrative & granulomatous liver disease. Need isoenzymes Serum Alkaline Phosphatase- (Alk Phos) PowerPoint Presentation: Alk Phos PowerPoint Presentation: Alk Phos PowerPoint Presentation: Alk Phos PowerPoint Presentation:   Property Examined Significance of Abnormal Result Tests of Hepatic Function (Normal Values) Serum albumin (3.5-5.5 mg/dl) Protein synthetic capacity (over days to weeks) Decreased synthetic capacity Protein malnutrition Increased protein loss (nephritic syndrome, protein-losing enteropathy) Increased extracellular fluid volume Prothrombin time (10.5-13 sec) Protein synthetic capacity (hours to days) Decreased synthetic capacity (especially factors II and VII) Vitamin K deficiency Consumptive coagulopathy PowerPoint Presentation:   Property Examined Significance of Abnormal Result Screening Tests of Hepatobiliary Disease Tests of Biliary Obstruction or Impaired Bile Flow     Serum bilirubin (0.2-1.0 mg/dl) (3.4-17.1 mol/L Extraction of bilirubin from blood conjugation and excretion into bile Hemolysis Diffuse liver disease Cholestasis Extrahepatic bi,e duct obstruction Congenital disorders of bilirubin metabolism PowerPoint Presentation:   Property Examined Significance of Abnormal Results Serum alkaline phosphatase (also 5’-nucleotidase and γ-glutamyl transpeptidase) (56-176 U/L) Increased enzyme synthesis and release Bile duct obstruction Cholestasis Infiltrative liver disease (neoplasms, granulomas)Bone destruction/remodeling Pregnancy PowerPoint Presentation:   Property Examined Significance of Abnormal Results Tests of Hepatocellular Damage Aspartate Aminotransferase (AST, SGOT) (10-30 U/L) Release of intracellular Enzyme Hepatocellular necrosis Cardiac or skeletal muscle necrosis Alanine aminotransferase (ALT, SGPT) (5-30 U/L) Release of intracellular enzyme Same as AST; however, more specific for liver cell damage PowerPoint Presentation: Characteristic Patterns of Liver Function Tests Disorder Bilirubin Alkaline Phosphatase Aspartate Aminotransferase Alanine Aminotransferase Prothrombin Time Albumin Gilbert’s syndrome (abnormal bilirubin metabolism) ↑ NL NL NL NL NL Bile duct obstruction (pancreatic cancer) ↑↑↑ ↑↑↑ ↑ ↑ ↑-↑↑ NL Acute hepatocellular damage (toxic, viral hepatitis) ↑-↑↑↑ ↑-↑↑ ↑↑↑ ↑↑↑ NL-↑↑↑ NL-↓↓ Cirrhosis NL-↑ NL-↑ NL-↑ NL-↑ NL-↑↑ NL-↓↓ NL = normal; ↑ = increased; ↓ = decreased (arrows indicate extent of change; ↑-↑↑↑=slight to large) PowerPoint Presentation: Liver biopsy- U/S or CT guided. Valuable in the histological differential, diagnosis & treatment of diffuse or localized parenchymal disease. Generally safe. Must check coagulation values and platelets before procedure secondary to risk of severe hemorrhage. LFT’s/ Diagnostic Tests PowerPoint Presentation: Serum bilirubin- Balance between bilirubin production and its conjugation & excretion into bile by the liver. Elevated level is not specific for any etiology of liver disease Tests for biliary obstruction/cholestasis &/or hepatocellular damage PowerPoint Presentation: Direct bilirubin (already conjugated by the liver): elevated in intra- or extra hepatic obstruction. Indirect bilirubin (Unconjugated , insoluble): elevated when hemolysis releases it from red blood cells (RBC’s) or in rare genetic deficiencies in conjugating enzymes. PowerPoint Presentation: Jaundice - yellow/green appearance to the skin & eyes (Icterus) produced by increased serum bilirubin. Usually given in a direct/total relationship Normal Bilirubin ranges 0.5 to 1.0 mg/dl. Levels >3.0 mg/dl to be clinically jaundiced. Newborn period is the exception Approach to Jaundice PowerPoint Presentation: Red cells (Heme) break down forming biliverdin (bile pigment). This is unconjugated (indirect bilirubin). It is transported by albumin & is not soluble. (No Bilirubin in the urine). Bilirubin Metabolism PowerPoint Presentation: (i.e., Binding Bilirubin (" indirect", unconjugated ) to plasma albumin.) The bile pigment is converted to conjugated (Direct bilirubin) by the Kupffer cells of the liver. PowerPoint Presentation: In the liver, the bilirubin is conjugated with UDPglucuronate, making it water-soluble Bilirubin diglucuronide, i.e. ("direct" conjugated bilirubin).    This is soluble & only shows up in blood & urine with obstruction in the system. PowerPoint Presentation: In the terminal ileum the bilirubin is converted to stercobilinogen & urobilinogen by natural bacteria. Conjugated bilirubin is excreted into the bile and passed into the intestine where it is further metabolised: urobilinogen ->urobilin-> stercobilin , which colors the feces brown . Bilirubin conjugation PowerPoint Presentation: Some is reabsorbed and returned to the liver. Some urobilinogen is found in the urine. If excretion of conjugated bilirubin is hindered, it is excreted by the kidney. PowerPoint Presentation: A. Normal process of conjugation of bilirubin by the liver, which promotes excretion through the bile. B. With increased destruction of red blood cells, large amounts of unconjugated bilirubin are released and the liver is unable to conjugate all that comes to it. Increased bilirubin in the blood results, which leads to bilirubinemia and jaundice. PowerPoint Presentation: Pre-hepatic jaundice Hemolytic disease Post hepatic jaundice Hepatitis Drug induced hepatitis Cirrhosis Bilirubin Metabolism PowerPoint Presentation: Notes: Obstruction of biliary system prevents production of urobiligen & stercobilinogen Stool is light and urine is dark showing bilirubin PowerPoint Presentation: Diseases that elevate blood levels of bilirubin fall into one of these four categories of disorder: 1. Increased bilirubin production 2. Decreased bilirubin uptake by the liver 3. Impaired conjugation in the liver 4. Decreased excretion of bilirubin into the bile (cholestasis) Hyperbilirubinemia PowerPoint Presentation: The first 3 types listed are unconjugated (indirect)= normal stool and urine color. The 4 th (decreased excretion/ cholestasis) shows increased conjugated bilirubin (direct) with dark urine and light stool color. PowerPoint Presentation: Due to overproduction, decreased hepatic uptake or decreased conjugation of bilirubin Unconjugated (Indirect) hyperbilirubinemia PowerPoint Presentation: 1. Overproduction 2 0 hemolysis (autoimmune), ineffective erythropoiesis (megablastic anemia), increase RBC fragility/turnover (2,3 DPG deficiency) 2. Impaired hepatic uptake : Gilbert’s syndrome & certain drugs such as rifampin, anesthetics & radiographic dyes PowerPoint Presentation: 3. Impaired conjugation : Hepatocellular disease, drug inhibition such as chloramphenicol, anabolic steroids, genetic disorders such as Gilbert’s syndrome or Crigler- Najjar syndrome (decreased UDP-glucuronyl transferases). Unconjugated (Indirect) hyperbilirubinemia PowerPoint Presentation: The most common cause of jaundice is neonatal jaundice They do not have a significant quantity of glucouronyl transferase (the enzyme used for conjugation), due to enzyme immaturity, but kicks in within a few weeks. Unconjugated (Indirect) hyperbilirubinemia PowerPoint Presentation: Bilirubin is very toxic to the neonatal brain ( kernicterus ), UV light is used to isomerize the bilirubin, which prevents it from crossing the blood-brain barrier. PowerPoint Presentation: Common causes of neonatal jaundice Rh disease/ABO incompatibility is hemolytic and also impaired hepatic intake. Kernicterus: is a type of brain damage that causes athetoid cerebral palsy and hearing loss. It also causes problems with vision and teeth and sometimes can cause mental retardation. PowerPoint Presentation: 4. Due to Altered biliary drainage, impaired hepatic excretion of bile, or extra hepatic obstructions : A. Altered biliary drainage of bile (TPN, cholestasis, drugs), hepatocellular disease, cirrhosis. Conjugated (Direct) hyperbilirubinemia PowerPoint Presentation: May occur in setting of cholestasis with impaired formation or excretion of all components of bile or hepatocellular injury independent of cholestasis. May indirectly cause increase in unconjugated also if severe enough **You will have change in color of stool and urine** PowerPoint Presentation: B. Impaired hepatic excretion : intrahepatic cholestasis- Dubin-Johnson syndrome & all disorders in the transport of conjugated bile from the hepatocytes to intrahepatic bile ducts. Drug-induced cholestasis-phenothiazines, OCP’s & methyltestosterone. Conjugated (Direct) hyperbilirubinemia PowerPoint Presentation: C. Extra hepatic : Gallstones, pancreatic/biliary obstructive tumors, strictures & biliary atresia ** Dark brown or green urine implies conjugated hyperbilirubinemia PowerPoint Presentation: Cholestatic jaundice- -Increased alk phos to 3-4 times normal. Hypercholesterolemia, pruritus, malabsorption of fat & fat-soluble vitamins. Minimal or marked evidence of liver cell damage. Causes of Conjugated (Direct) hyperbilirubinemia PowerPoint Presentation: Determine mechanism involved: Hx : pale stools & pruritus--> cholestasis. & nausea--> gallstones = biliary obstruction. Inquire about drugs & alcohol use, risks for viral hepatitis & pre-existing liver disease. Diagnosis of conjugated hyperbilirubinemia PowerPoint Presentation: Laboratory : biliary obstruction : <5-10 fold increase in transaminases & >2-3x normal alk phos . Hepatocellular disease : >10-15 fold increase in transaminases & < 2-3x normal alk phos. PowerPoint Presentation: Sepsis - mainly gram-negative organisms. Mildly elevated serum alk phos Disorders of the Biliary System PowerPoint Presentation: Post-op jaundice- - 1-10 days post-op. 15% incidence following heart/ 1% elective abdominal surgery. Increased alk phos & minimally elevated levels of transaminases. Secondary to anesthesia side effects PowerPoint Presentation: Hepatocellular disease (hepatitis, cirrhosis ) elevated transaminases, prolonged PT, hypoalbuminemia & clinical features of hepatic dysfunction. Extrahepatic biliary obstruction– obstruction of extra hepatic bile ducts--gallstones, neoplasias, bile duct strictures, chronic pancreatitis. Clay-colored stools . PowerPoint Presentation: Extra hepatic obstruction : CT or U/S to determine stone or bile duct dilation. Bile duct dilation : endoscopic retrograde cholangiography (ERCP) for management & treatment. Liver biopsy : for determining cause of intrahepatic cholestasis. Special diagnostic procedures in cholestatic jaundice PowerPoint Presentation: " HOT L iver": H emolysis O bstruction T umor L iver disease Hyperbilirubin Mneumonic PowerPoint Presentation: Prehepatic (Excessive Red Blood Cell Destruction) Hemolytic blood transfusion reaction Hereditary disorders of the red blood cell Sickle cell anemia Thalassemia Spherocytosis Causes of Jaundice PowerPoint Presentation: Acquired hemolytic disorders Hemolytic disease of the newborn Autoimmune hemolytic anemias PowerPoint Presentation: Intrahepatic Decreased bilirubin uptake by the liver Gilbert’s disease Decreased conjugation of bilirubin Hepatocellular liver damage Hepatitis Cirrhosis Cancer of the liver Drug-induced cholestasis PowerPoint Presentation: Posthepatic (Obstruction of Bile Flow) Structural disorders of the bile duct Cholelithiasis Congenital atresia of the extrahepatic bile ducts Bile duct obstruction caused by tumors PowerPoint Presentation: Predominantly Unconjugated Hyperbilirubinemia Overproduction Hemolysis (e.g., spherocytosis, autoimmune disorders) Ineffective erythropoiesis (e.g., megaloblastic anemias) Decreased hepatic uptake Gilbert’s syndrome Drugs (e.g., rifampin, radiographic contrast agents) Neonatal jaundice Classification of Jaundice PowerPoint Presentation: Decreased conjugation Gilbert’s syndrome Crigler-Najjar syndrome types I and II Neonatal jaundice Hepatocellular disease Drug inhibition (e.g., chloramphenicol) PowerPoint Presentation: Predominantly Conjugated Hyperbilirubinemia Impaired hepatic excretion Familial disorders (Dubin-Johnson syndrome, Rotor syndrome, benign recurrent cholestasis, cholestasis of pregnancy) Hepatocellular disease Drug-induced cholestasis Primary biliary cirrhosis Sepsis Postoperative PowerPoint Presentation: Extrahepatic (“mechanical”) biliary obstruction Gallstones Tumors of the head of the pancreas Tumors of bile ducts Tunors of the ampulla of Vater Biliary strictures (postcholecystectomy, primary sclerosing cholangitis) Congenital disorders (biliary atresia) PowerPoint Presentation: OBSTRUCTIVE JAUNDICE VERSUS CHOLESTATIC LIVER DISEASE SUGGESTS OBSTRUCTIVE JAUNDICE SUGGESTS CHOLESTATIC LIVER DISEASE History Abdominal pain Fever, rigors Prior biliary surgery Older age Anorexia, malaise, myalgias, suggestive of viral prodrome Known infectious exposure Receipt of blood products, use of intravenous drugs Exposure to known hepatotoxin Family history of jaundice PowerPoint Presentation: Physical examination High fever Abdominal tenderness Palpable abdominal mass Abdominal scar Ascites Stigmata of liver disease (e.g., prominent abdominal veins, gynecomastia, spider angiomata, Kayser-Fleischer rings) Asterixis, encephalopathy PowerPoint Presentation: Laboratory Studies Predominant elevation of serum bilirubin and alkaline phosphatase Elevated serum amylase Prothrombin time which is normal or normalizes with vitamin K administration Predominant elevation of serum transaminases Prolonged prothrombin time which does not correct with vitamin K administration Blood tests indicative of specific liver disease PowerPoint Presentation: Approach to the patient with cholestatic jaundice PowerPoint Presentation: The word "hepatitis" means inflammation of the liver. It can be caused by a number of agents, including bacteria, drugs, toxins and excess alcohol , but of serious concern is hepatitis that results when any one of several hepatitis viruses infect the liver. Hepatitis PowerPoint Presentation: 1. Virus A. Hepatitis A (HAV) B. Hepatitis B (HBV) C. Hepatitis C (HCV) D. Hepatitis D (HDV) E. Hepatitis E (HEV) F. Cytomegalic (CMV) G. Epstein-Barr (EBV) Hepatitis Causes PowerPoint Presentation: 2. Toxins 3. Alcohol 4. Other diseases a. Wilson’s disease b. Leukemia c. Lymphoma PowerPoint Presentation: **Hepatitis E & A are fecal-oral (f E c A l –oral) **While Hep B,C,D are blood borne (parenteral) “ C oming in the B ack D oor” PowerPoint Presentation: Viral Hepatitis Hepatitis A virus Hepatitis B virus Hepatitis C virus Hepatitis D virus (“delta agent”) Hepatitis E virus Epstein-Barr virus PowerPoint Presentation: Cytomegalovirus Alcohol Toxins Amanita phalloides mushroom poisoning Carbon tetrachloride Drugs Acetaminophen PowerPoint Presentation: Isoniazid Halothane Chlorpromazine Erythromycin Other Wilson’s disease Herbs PowerPoint Presentation: Hepatitis A virus Hepatitis B virus Hepatitis C virus Hepatitis E virus Yellow fever virus Epstein-Barr virus (infectious mononucleosis) PowerPoint Presentation: Lassa, Marburg, and Ebola viruses Rubella virus Herpes simplex virus Cytomegalovirus Enteroviruses other than hepatitis A virus Leptospires (leptospirosis) Entamoeba histolytica (amebic hepatitis) PowerPoint Presentation: Hepatitis can be defined as a constellation of signs & symptoms resulting from inflammation & hepatic cell necrosis In a previously asymptomatic individual the term “ acute ” is applied Acute Hepatitis PowerPoint Presentation: Virus is the most common cause of hepatitis . Only occasionally can bacterial infections like syphilis or TB be considered Most cases of acute hepatitis are sub-clinical & usually undiagnosed PowerPoint Presentation: The different types of hepatitis cannot be distinguished clinically & their distinction depends upon serological testing Acute Hepatitis PowerPoint Presentation: Histologically they are all the same: Classically the histological appearance of acute hepatitis is liver damage & necrosis in the centrilobular area Mild edema occurs in the portal tracts with some degree of cholestasis causing jaundice, depending on the degree of obstruction PowerPoint Presentation: The hepatic cells undergo degeneration with some scarring Most cases only have minimal damage & go on to complete recovery Some cases progress to liver failure and death Acute Hepatitis PowerPoint Presentation: Symptoms of Hepatitis Malaise Vomiting Nausea Diarrhea Anorexia Low grade fever Fatigue Rash Arthralgias PowerPoint Presentation: Tenderness of the liver Hepatomegally on occasion Dark urine Jaundice Clinical findings of Hepatitis PowerPoint Presentation: Bilirubin elevated SGPT (ALT) (very specific for liver) SGOT ( AST) (not as specific) Alkaline phosphatase (alk phos) Nonspecific- represents obstruction of liver Can be elevated in bone ds. or child growth PT,PTT (elevated c ~55% liver destruction) Hypoglycemia Laboratory Tests (LFT’s) PowerPoint Presentation: Serum markers for viral hepatitis Anti-HAV (IgM-IgG) HBsAg   HBeAg Anti-HBc (IgM-IgG)   Anti-HBe Anti-HBs   Anti-HCV Anti-HDV   Monospot, Heterophile   (also do Urinalysis)   PowerPoint Presentation: 1. Massive hepatic necrosis (1%) Usually in B,C,D,E 2. Chronic Hepatitis 3. Cholestatic Hepatitis Syndrome Pruritis Dark urine Light stools Hyperbilirubinemia Alk phos elevation Complications of Hepatitis PowerPoint Presentation: Don’t complain about the seating arrangements PowerPoint Presentation: Age: 15-25 yo “ Kissing Disease” Symptoms: Fever Hepatosplenomegally Malaise** Lymphadenopathy* Loss of appetite Sore throat** Nausea/Vomiting Rash (maculopapular) Fatigue Abd pain Jaundice Headache** **Most common symptoms Mononucleosis Epstein-Barr Virus (EBV) PowerPoint Presentation: Maculopapular rash: NEVER GIVE AMPICILLIN FOR SORE THROAT TO MONO PATIENT  causes rash Mononucleosis (EBV) PowerPoint Presentation: Key Signs: Fever Exudative Pharyngitis Lymphadenopathy Splenomegaly Mononucleosis (EBV) PowerPoint Presentation: Labs 1. CBC shows a relative lymphocytosis Atypical lymphocytes Reduction in platelet count 2. Mono spot test Heterophile 3. EBV specific serology IgM specific IgG confirms prior illness 4. Transaminase elevated slightly (AST/ALT) Mononucleosis Epstein-Barr virus PowerPoint Presentation: Complications- Bacterial pharyngitis Upper airway obstruction Bells palsy Ruptured spleen Mononucleosis (EBV) PowerPoint Presentation: Treatment- Supportive therapy Tylenol for fever and malaise Antibiotic if bacterial pharyngitis is present Avoid ampicillin (RASH) Steroids for severe pharyngitis & fever 40-60 mg of prednisone/day Activities reduced- no contact sports for 6 weeks Mononucleosis (EBV) PowerPoint Presentation: Similar to EBV in many ways No pharyngitis or respiratory symptoms Atypical lymphocytes Abnormal liver function studies Diagnosis made by CMV titers Transmitted in same manner as mono more common in transplant and AIDS patients. **If mono test neg  due CMV titer Cytomegalic Virus PowerPoint Presentation: Approximately 25% of all cases of hepatitis Less morbidity & mortality Contact by fecAl-oral route Incubation period 2-6 weeks (shortest) Hepatitis A PowerPoint Presentation: Symptoms: (more severe sx than mono) Malaise Abd pain Fever Jaundice Hepatosplenomegally(25%) Diarrhea Anorexia ** h/o eating clams, out of country travel, etc. PowerPoint Presentation: Duration: 4 weeks Complications: rare (no chronic type) Lab: SGOT  , SGPT  , Bilirubin  , HAV IgM, HAV IgG Treatment: Good nutrition No alcohol Hepatitis A (cont) PowerPoint Presentation: Prophylaxis: Administration of Gamaglobulin effective in prevention (prior to exposure) Post exposure: is recommended for household & sexual contacts within two weeks, plus Hepatitis A vaccine Hepatitis A (cont) PowerPoint Presentation: Travelers: recommended in normal dose for 2 mo stay, and triple dose for 4-6 mo stay Hepatitis A vaccine given 15 days prior to travel, followed by 6 mo later PowerPoint Presentation: Incubation: 1-6 months Symptoms: same as Hep A, but even more severe Contact: Parenteral inoculation, sexual (blood or mucus membrane) Hepatitis B PowerPoint Presentation: Course: 90% recover 10% develop chronic hepatitis (with HBsAg carrier state) A small amount go onto chronic progressive hepatitis which goes on to cirrhosis 1% develop a fulminate course Hepatitis B PowerPoint Presentation: Lab tests: SGPT (ALT) & SGOT (AST) rise with symptoms Bilirubin & alk phos PT, PTT **(all these labs are higher than in HAV) PowerPoint Presentation: Serological tests : HBcAg : disappears soon after the peak of ALT HBeAg : Positive in acute HBV HBsAg : positive in acute & chronic Hepatitis B (Lab continued) PowerPoint Presentation: Anti-HBs : + in late acute HBV and immunized (protective) HBeAb : appears when antigen decreased HBcAb : IgM marker for acute infection. IgG chronic HBV & carrier PowerPoint Presentation: HBsAg: First virologic marker detectable in serum in acute HBV infection ; precedes elevations of liver enzymes and clinical symptoms. Serologic Markers: PowerPoint Presentation: Usually detectable 4 weeks after infection and typically disappears at 6 months after active infection. Persistence of HBsAg beyond 6 months implies chronic HBV infection . PowerPoint Presentation: Anti-HBs : Appears shortly after HBsAg disappears from serum and persists indefinitely in patients who have recovered from acute infection . Serologic Markers: PowerPoint Presentation: Anti-HBs is felt to be the protective antibody against HBV infection; thus, vaccine consists of nonglycosylated HbsAg particles that are safe and highly immunogenic, thereby inducing active immunity. PowerPoint Presentation: HBcAg : Not detectable in serum Serologic Markers: (cont) PowerPoint Presentation: Anti-HBc : IgM appears at 1 to 2 weeks after the appearance of HBsAg ; its detection in serum is indicative of acute HBV infection . It is the only marker of acute HBV during the window period between the disappearance of HBsAg and the appearance of anti-HBs in serum . Serologic Markers: (cont) PowerPoint Presentation: IgM predominates for the first 6 months following acute infection but may persist up to 2 years. PowerPoint Presentation: IgG predominates after 6 months and generally persists indefinitely in patients who have recovered from HBV infection. Present in virtually all patients who have ever been exposed to HBV PowerPoint Presentation: HBeAg: Considered to be a marker of active virus replication and infectivity ; also correlates with detection of HBV DNA in serum. Usually appears with or after the appearance of HBsAg in serum and disappears shortly after peak elevations in serum aminotransferase activity in acute infection. PowerPoint Presentation: In chronic infection, HBeAg may persist for years prior to seroconversion to anti-HBe ; its presence is indicative of the replicative stage of HBV infection, which represents a time of maximal infectivity and liver injury. PowerPoint Presentation: Likelihood of perinatal transmission correlates with presence of HBeAg: ~90% of HBeAg-positive mothers transmit HBV to their offspring but only 10-15% of anti-HBe positive mothers do so. PowerPoint Presentation: In a small subset of patients with acute HBV infection, HBeAg is not detected because of a viral mutation; in such patients, HBV DNA levels are elevated, representing the replicative stage of the virus. PowerPoint Presentation: Anti-HBe: Appears after seroconversion of HBeAg to anti-HBe. Its presence in chronic HBV infection signals the onset of the nonreplicative phase , where HBV DNA becomes undetectable in serum and liver injury tends to subside. Serologic Markers: (cont) PowerPoint Presentation: Generally exists in serum indefinitely unless seroconversion back to HBeAg occurs. PowerPoint Presentation: HBV DNA: Probably the most reliable indicator of active viral replication . Can be detected by hybridization methods or PCR. Recovery from acute HBV infection is accompanied by the disappearance of HBV DNA from serum ; however, very low levels may remain detectable by PCR. Serologic Markers: (cont) PowerPoint Presentation: Persistence of HBV DNA implies chronic infection . Useful in predicting response to interferon therapy ; high pretreatment HBV DNA levels > 200 pg/ml by hybridization assay are predictive of poor response to interferon. Also, clearance of HBV DNA is used as an endpoint in assessing response to treatment. PowerPoint Presentation: HBsAg Anti-HBs Anti-HBc HBeAg Anti-HBe Interpretation + – IgM + – Acute HBV, high infectivity + – IgG + – Chronic HBV, high infectivity + – IgG – + Late-acute or chronic HBV infection, low infectivity + + + + /– + /– Heterotypic anti-HBs with HBsAg; usually indicates chronic HBV carrier state PowerPoint Presentation: HBs Ag Anti- HBs Anti- HBc HBe Ag Anti- HBe Interpretation – – IgM +/– +/– Acute HBV (anti-HBc window) – + IgG – +/– Recovery from HBV infection – – IgG – +/– Low-level HBsAg carrier or remote past infection – + – – – Immunization for HBV (HBsAg) PowerPoint Presentation: Screening for acute viral hepatitis: anti-HAV IgM HBsAg anti-HBc IgM anti-HCV Screening PowerPoint Presentation: Screening for chronic viral hepatitis: HBsAg anti-HCV if + HBsAg then check HBeAg +/- HBV DNA. PowerPoint Presentation: Chronic hepatitis B is characterized by the persistent presence of HBV DNA and usually HBeAg in the serum; remissions are characterized by the disappearance of HBV DNA and HBeAg from serum despite the persistence of HBsAg. PowerPoint Presentation: Treatment: After exposure: give hepatitis B immunoglobulin (IG) + active immunization with HBV vaccine (Combivax) in any patient who is: Stuck by a needle Within 14 days of sexual exposure An infant born to a mother HBsAg positive Hepatitis B PowerPoint Presentation: Preventative to: Health care workers Homosexual men Household & sexual contacts of HBsAg carriers PowerPoint Presentation: Follow up: Recheck in 3 months if tests are normal A liver biopsy if patient appears to have chronic hepatitis Keep in mind patients with chronic hepatitis B can develop hepatocellular carcinoma Hepatitis B PowerPoint Presentation: (Blood) Parenteral Associated with transfusion in 85% of the time inoculation from drug abuse 50-70% go onto chronic hepatitis which can lead to cirrhosis of the liver 20% of the time Incubation is 5-10 weeks Anti-HCV (antibody to the C virus) is 70% accurate Hepatitis C account for 80-90% of the Non A, Non B hepatitis Hepatitis C PowerPoint Presentation: New serologic test for Hep C Anti-HCV if present indicates the presence of viremia (80%) + HCV plus  ALT (SGPT) is confirmatory A second generation recombinant immunoblot assay (RIBA) is used for confirmation. Polymerase chain reaction (PCR) is used in equivocal cases, but is not + for at least 6-8 weeks (this is a test to specifically find the HCV RNA virus) Hepatitis C PowerPoint Presentation: Treatment: The patient is given alpha interferon for the chronic infection 3 x’s/ wk for 6 months What is interferon: 30% of circulating lymphocytes are B cells & 70% are T cells Hepatitis C PowerPoint Presentation: B cells produce immunoglobulins that produce antibodies T cells produce cytokines (hormone like proteins) that bind to the target cells. There are many kinds, one of which is interferon which limit viral replication. PowerPoint Presentation: The latest treatment is 6-12 mo of combination therapy using a-2b interferon plus ribavirin The cure rate varies around 40% with no HCV detectable 6 mo after cessation of treatment Do not use if the patient is depressed or on alcohol (must be off ETOH x 6 mo) Hepatitis C treatment (cont) PowerPoint Presentation: Recommendations: Treatment is worth considering on selective basis on some patients with mild liver disease Patients with geno type 2 or 3; treatment is stopped at 6 mo. Cure rate 50-70% to 90% Patients with geno type 1 is less responsive with overall cure rate of 27% Hepatitis C PowerPoint Presentation: Toxicity: Ribavirin can cause hemolytic anemia Interferon causes depression PowerPoint Presentation: Requires HBV for its replication Incubation 4-6 weeks Can accelerate chronic hepatitis B to cirrhosis Anti-HDV become positive in 12-15 weeks Hepatitis B vaccine is preventative Treatment poor. Interferon can be tried **Must have B to get D** Hepatitis D PowerPoint Presentation: Found mostly in India, Asia, Mexico, Africa Usually water borne (fEcal- oral) Incubation 2-9 weeks All cases in US have been imported by immigrants HEV antibodies found in blood Hepatitis E PowerPoint Presentation: Comparative Features of the Common Forms of Viral Hepatitis Hepatitis A Hepatitis B Hepatitis C Genome RNA DNA RNA Incubation period 3-6 weeks 6 weeks to 6 months 7-8 weeks Transmission Oral Parenteral Parenteral Blood No Yes Yes Feces Yes No No PowerPoint Presentation: Hepatitis A Hepatitis B Hepatitis C Vertical No Yes ? Fulminant hepatic necrosis Very rare Yes Yes Chronic hepatitis No 10% 50% Carrier state No Yes Yes Liver cancer No Yes Yes PowerPoint Presentation: Characteristics of Common Causative Agents of Acute Viral Hepatitis Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Hepatitis G Causative agent 27-nm RDA virus 42-nm DNA virus; core and surgace components Flavivirus-like RNA agent 36-nm hybrid particle with HBsAg coat 27-34 nm non enveloped RNA virus Single strand RNA virus Trans mission Fecal-oral; waterborne or foodborne Parenteral inoculation or equivalent; direct contact Similar to HBV Similar to HBV Similar to HAV Parenteral PowerPoint Presentation: Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Hepatitis G Incubation period 2-6 wk 4 wk-6 mo 5-10 wk Similar to HBV 2-9 wk 2-4 wk Period of infectivity 2-3 wk in late incubation and early clinical phase During HBsAg positivity (occasionally only with anti-HBc positivity) During anti-HCV positivity During HDV RNA or anti HDV positivity Similar to HCV Unknown Massive hepatic necrosis Rare Uncommon Uncommon Yes Yes Unclear PowerPoint Presentation: Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Hepatitis G Carrier state No Yes Yes Yes No Unknown Chronic hepatitis No Yes Yes Yes No Possible; viremia per-sistent but hepatitis uncertain PowerPoint Presentation: Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Hepatitis G Prophylaxis Hygiene, immune serum globulin, vaccine Hygiene, hepatitis B immune globulin, vaccine Hygiene Hydiene, HBV vaccine Hygiene, sanitation Hygiene PowerPoint Presentation: Agent Marker Definition Significance Hepatitis A virus (HAV) Anti-HAV IgM type IgG type Antibody to HAV Current or recent infection or convalescence Current or previous infection; conferring immunity Hepatitis B virus (HBV) HBsAg HBeAg HBV surface antigen e antigen; a component of the HBV core Positive in most cases of acute or chronic infection Transiently positive in acute hepatitis B May persist in chronic infection Reflection of presence of viral replication, whole Dane particles in serum, and high infectivity PowerPoint Presentation: Agent Marker Definition Significance Anti-HBe Antibody to e antigen Transiently positive in convalescence Possibly persistently present in chronic cases Usually a reflection of low infectivity Anti-HBc (IgM or IgG) Antibody to HBV core antigen Positive in all acute and chronic cases Reliable marker of infection, past or current IgM anti-HBc a reflection of active viral replication Not protective PowerPoint Presentation: Agent Marker Definition Significance Anti-HBs Antibody to HBV surface antigen Positive in late convalescence in most acute cases Conferring immunity Hepatitis C virus (HCV) Anti-HCV Antibodies to a group of recombinant HCV peptides (C22-3, C200) Positive on average 15 wk after exposure; not protective Persistent in chronic infection Hepatitis D virus (HDV) Anti-HDV (IgM or IgG) Antibody to HDV antigen Acute or chronic infection; not protective PowerPoint Presentation: An acute or chronic illness involving the liver with necrosis, inflammation & scarring 95% develop a fatty liver which is a reversible process Encephalopathy & death 20% 30% go on to cirrhosis within 6 mo 50% of those abstaining for 6 mo recover completely Alcoholic Hepatitis PowerPoint Presentation: Most patients are symptomatic. The most common complaints are: Anorexia, nausea, vomiting Abdominal pain (RUQ) Fever (due to infection or inflammation of liver) Weight loss due to anorexia Jaundice is usually mild Diarrhea which is due to portal hypertension Alcoholic Hepatitis Symptoms PowerPoint Presentation: Jaundice Spider angiomas Palmar erythema Clubbing of fingers Gynecomastia Hepatomegaly Alcoholic Hepatitis Physical Findings PowerPoint Presentation: Splenomegaly Pruritis Ascites Edema Caput medusa Testicle atrophy Dark urine, light stool PowerPoint Presentation: Hepatic insufficiency: which is responsible for the following: Coma Jaundice Ascites Anemia Hemorrhagic tendency Ankle edema Alcoholic Hepatitis Damage to liver causes PowerPoint Presentation: Hyperestrinism: which is responsible for: Spider nevi Alopecia Gynecomastia Palmar erythema Testicle atrophy Alcoholic Hepatitis Damage to liver causes PowerPoint Presentation: Portal Hypertension: causes the following: Esophageal varices Splenomegaly Caput medusa Ascites Alcoholic Hepatitis Damage to the Portal System PowerPoint Presentation: Hypersplenism: causes the following: Anemia Leukopenia Thrombocytopenia Alcoholic Hepatitis Damage to the Portal System PowerPoint Presentation: A. Laboratory Test: The SGOT (AST) 2-10x’s normal SGPT (ALT) is less elevated Bilirubin mild to moderate Alk phos is usually 2-3x’s normal Alcoholic Hepatitis Diagnostic Studies PowerPoint Presentation: Globulins elevated with reverse A/G ratio Prothrombin time elevated (poor prognosis) Leukocytosis Blood NH3 (Ammonia) level PowerPoint Presentation: B. Ultrasound C. Liver Biopsy To be done early, but not to be done if PT/PTT are elevated Microscopic exam confirms the diagnosis Alcoholic Hepatitis Diagnostic Studies PowerPoint Presentation: Findings of biopsy Hepatocellular necrosis Inflammatory exudates Fibrosis Fatty infiltration Cholestasis Hemosiderosis (iron accumulation in the lungs) PowerPoint Presentation: 1. Mortality of 10-15% 2. Worsening of symptoms in early recovery program 3. Complication: Varices gastritis Peptic ulcer coagulopathy Kidney infection lung infection Peritonitis Acute Hepatitis Course PowerPoint Presentation: 4. Seizures with withdrawal Use of benzodiazepines are helpful Can also cause encephalopathy PowerPoint Presentation: 5. Hepato-renal syndrome Development of Acute Renal Failure Renal functions are excluded There is an intense intra-renal vasoconstriction and distribution of blood flow, causing oliguria PowerPoint Presentation: A. Supportive therapy with bed rest Stop the BOOZE B. Diet Multiple vitamins: folic acid & thiamine Magnesium, calcium, phosphate, & glucose are carefully monitored 2500 calories at least. Low protein if encephalopathy is present. Vegetable protein & milk are acceptable. Acute hepatitis Therapy PowerPoint Presentation: C. Benzodiazepines if Alcohol withdrawal Seizures- delerium tremons Encephalopathy may occur D. Steroids: Used with encephalopathy Minimal value in less severely ill patients Acute Hepatitis Therapy (cont) PowerPoint Presentation: Wernicke Encephalopathy Ophthalmoplegia Ataxia Nystagmus Acute Hepatitis Nutritional Complications PowerPoint Presentation: Korsakoff Syndrome Loss of new memory Disorientation to time & place Confabulation **Treatment: large doses of thiamine Hcl PowerPoint Presentation: 1. Pathology: hepatocellular necrosis similar to virus (cholestatic reaction) 2. Diagnosis: usually established by history of drug use 3. Lab: similar to viral disease Drug Related Hepatitis PowerPoint Presentation: 4. Cholestatic reaction: impairment of bile secretion by hepatocytes (BC pills) 5. Hepatocellular reaction: very similar to viral hepatitis ( acetominophen, isoniazid, methyldopa) Drug Related Hepatitis: Drug Related Hepatitis 6. Symptoms: Arthralgias Fever Rash Eosinophilia Treatment: Removal of offending agent PowerPoint Presentation: Classification of Drug-Induced Liver Disease Category Examples Predictable hepatotoxins with zonal necrosis Acetaminophen Carbon tetrachloride Nonspecific hepatitis Aspirin Oxacillin Herbs (chaparral, germander) Viral hepatitis-like Reactions Halothane Isoniazid Phenytoin Cholestasis Estrogens Noninflammatory 17  -Substituted steroids Chlorpromazine Antithyroid agents PowerPoint Presentation: Category Examples Fatty liver Large droplet Ethanol Corticosteroids Small droplet Amiodarone Allopurinol Chronic hepatitis Methyldopa Nitrofurantion Tumors Estrogens Vinyl chloride Vascular lesions 6-Thioguanine Anabolic steroids Herbs (senna, comfrey) Methotrexate Fibrosis Methotrexate Granulomas Allopurinol Sulfonamides PowerPoint Presentation: Chronic Hepatitis PowerPoint Presentation: Refers to inflammation, necrosis & fibrosis for at least 6 months. Varying from benign process to death. Groups: Viral Autoimmune Chronic Hepatitis PowerPoint Presentation: Alcoholic Primary biliary cirrhosis Drug induced liver disease Wilson’s disease Anti-trypsin deficiency Hemochromatosis Sclerosing cholangitis PowerPoint Presentation: Viral Hepatitis B Hepatitis B with superimposed hepatitis D Hepatitis C Drugs and Toxins Methyldopa Nitrofurantoin Causes of Chronic Hepatitis PowerPoint Presentation: Amiodarone Isoniazid Autoimmune Genetic and Metabolic Disorders Wilson’s disease α1- Antitrypsin deficiency Nonalcoholic steatohepatitis PowerPoint Presentation: Forms: A. Chronic Active Hepatitis : Refers to the form of CH were the liver test & histology are compatible with active & progressive inflammation & necrosis Chronic Hepatitis PowerPoint Presentation: B. Chronic Persistent Hepatitis : Refers to the mild & histological non progressive CH where the inflammation is confirmed only to the portal tracts. The enzymes are normal or only moderately elevated. PowerPoint Presentation: Mainly a disease of young women Most have hypergamaglobulinemia & ANA positive Chronic Hepatitis Autoimmune Hepatitis PowerPoint Presentation: Patients have multisystem disease which include: Arthritis kidney involvement Colitis heart Thyroiditis portal hypertension Pulmonary fibrosis PowerPoint Presentation: Diagnosis: Consider any young female with elevated liver function studies without course with hepatitis for greater than 6 months Positive ANA Elevated GG =means chronic Liver biopsy showing chronic inflammation Chronic Hepatitis Autoimmune Hepatitis PowerPoint Presentation: Treatment: Steroids Decrease in symptoms Prognosis: is good. About 50% live more than 15 years from the time of diagnosis PowerPoint Presentation: Inherited Chronic Liver Disorders A. Wilson’s disease B. Hemachromatosis C. Alpha 1-antitrypsin deficiency D. Reye syndrome Other causes of Chronic Hepatitis PowerPoint Presentation: Pathogenesis: a rare treatable genetic disorder of copper metabolism. There is an abnormal accumulation of copper in the hepatocytes. This is a metabolic disorder affecting basal ganglia, eyes, & kidney. Wilson’s Disease PowerPoint Presentation: The defect is in the ceruloplasm which carries the copper. The serum ceruloplasm & copper are both low (copper low b/c it can’t be carried) PowerPoint Presentation: Diagnosis: Made by seeing neurological, psychiatric, hepatitis, cirrhosis in a young person . Liver disease with the Kayser-Fleischer ring in the eyes in the young is characteristic Wilson’s disease (cont) PowerPoint Presentation: Kayser – Fleischer Ring PowerPoint Presentation: Pathogenisis : A group of disorders with excessive absorption of iron. The iron is layed down in liver, heart, pancrease, kidney, & skin (bronze diabetes) Primary cause unknown Haemochromatosis PowerPoint Presentation: Secondary- Iron overload : anemias cirrhosis Dietary Diagnosis : Lethargy, weakness in men 40-60 yo Skin hyperpigmentation Diabetes 30-60% of pt’s arthopathy PowerPoint Presentation: In children associated liver disease In teenagers & adults, a progressive liver disease with pulmonary manifestations Pathogenesis: Alpha 1-trypsin is a potent protease inhibitor found in the serum, body fluids, & tissues Alpha 1-Antitrypsin Deficiency PowerPoint Presentation: It is synthesized by the liver to protect from tissue injury resulting from protease like trypsin PowerPoint Presentation: An illness seen in the pediatric age group associated with the flu Symptoms: Nausea, vomiting, hyperactivity, confusion, seizures, & coma, Increasing drowsiness, Belly Pains Reye’s Syndrome PowerPoint Presentation: On liver biopsy there are fatty infiltration Chemistry: elevated liver enzymes, NH3 ***NEVER give Aspirin to children with varicella infection (chicken pox), or during flu sx.*** PowerPoint Presentation: only happens in kids less than 15 years old. The cause is unknown, but it is strongly associated with Aspirin use during flu's. The liver becomes inflamed and destroyed for unknown reasons. REYE'S SYNDROME PowerPoint Presentation: It is important because Reye's syndrome kills about half of kids who get it. NEVER give aspirin containing medications to your kids under 15 years old for fever control. Use Acetaminophen/ Ibuprofen instead. PowerPoint Presentation: May result from: A. Slow deterioration as part of a chronic progress B. Rapid worsening after repeated injuries C. catastrophic event such as massive necrosis Hepatic (Liver) Failure PowerPoint Presentation: Causes : 1. Functional liver failure without overt necrosis Reye’s syndrome, tetracycline toxicity 2. Chronic liver disease Chronic active hepatitis Cirrhosis PowerPoint Presentation: 3. Fulminate failure : refers to acute severe impairment of liver function with encephalopathy & coma in patients who have had liver disease for less than 8 weeks PowerPoint Presentation: Management of Selected Problems in Fulminant Hepatic Failure Complications Pathogenesis Management Hepatic encephalopathy Liver failure Search for treatable causes, i.e., hypoglycemia, drugs used for sedation, sepsis, gastrointestinal bleeding, electrolyte imbalance, decreased PO 2, increased PCO 2 ; lactulose Cerebral edema Unknown Elevate head of bed 20-30 degrees; hyperventilate (PCO 2 25-30 mm Hg); mannitol, 0.5-1 g/kg IV bolus over 5 min; pentobarbital infusion; urgent liver transplantation PowerPoint Presentation: Complications Pathogenesis Management Coagulopathy and gastrointestinal hemorrhage Decreased synthesis of clotting factors Gastric erosions Vitamin K; fresh-frozen plasma if actively bleeding and for prevention of bleeding; IV H2-antagonist prophylaxis Hypoglycemia ↓ Gluconeogenesis Insulin degradation IV 10% dextrose, monitor every 2 hours; 30%-50% dextrose may be needed Agitation May be due to: Encephalopathy ↑ Intracranial pressure Hypoxemia Search for treatable causes (i.e., ↓ PO2, skin ulcersl lacerations, or abscesses); soft restrains; if severely agitated and a concern of injury, consider sedation along with mechanical ventilation to protect airway PowerPoint Presentation: Clinical features: Jaundice Hypoalbuminemia Hyperestrogenism which causes Testicular atrophy Gynecomastia Palmar erythema Spider angiomas Hepatic Failure (cont) PowerPoint Presentation: Hepatorenal Syndrome Fetor odor Coagulopathy PowerPoint Presentation: CLAPS : C lubbing L eukonychia A sterixis P almar erythema S cratch marks Liver failure (chronic): signs of found on the arms Mneumonic PowerPoint Presentation: Complications of hepatic failure PowerPoint Presentation: Hepatic encephalopathy : A metabolic disorder of the CNS system & neuromuscular system with slight changes in the brain (edema) Hepatic Failure (cont) PowerPoint Presentation: Clinical Features : Confusion Flapping tremor (asterixis) Drowsiness Coma  death Caused by elevated levels of NH3 (ammonia) PowerPoint Presentation: HEPATICS : H emorrhage in GIT/ H yperkalemia E xcess protein in diet P aracentesis A cidosis/ A nemia T rauma I nfection C olon surgery S edatives Hepatic encephalopathy: precipitating factors Mneumonic PowerPoint Presentation: Treatment: Remove precipitating causes (drugs/ETOH) Decrease enteric toxins (BUN-NH3) Gut enema Low protein diet Neomycin 1-2 gms Q 2 hrs PO Hepatic failure (cont). Hepatic Encephalopathy PowerPoint Presentation: Lactulose 50 ml orally Q 2hrs until diarrhea ensues. Then reduce dosage until there are two stools per day Transplantation: Any young patient with progressive disease Metabolic disease: wilson’s, alpha antitrypsin def. PowerPoint Presentation: Etiology: triad 1. necrosis 2. regenerating nodules 3. fibrosis Categories: Major Alcoholic (#1 cause in western world) Post necrotic Cirrhosis PowerPoint Presentation: Minor Wilson’s disease Haemochromatosis Biliary Chronic hepatic congestion PowerPoint Presentation: Budd-Chiari syndrome uncommon condition induced by thrombotic or nonthrombotic obstruction to hepatic venous outflow Cardiac Right sided heart failure Tricuspid insufficiency PowerPoint Presentation: HEPATIC : H emochromatosis (primary) E nzyme deficiency (alpha-1-anti-trypsin) P ost hepatic (infection + drug induced) A lcoholic T yrosinosis I ndian childhood (galactosemia) C ardiac/ C holestatic (biliary)/ C ancer/ C opper (Wilson's) Causes of hepatic cirrhosis Mneumonic PowerPoint Presentation: Common causes are ABC : A lcohol B (Hepatitis) C (Hepatitis) Cirrhosis: differential: common and rarer Mnoumonic PowerPoint Presentation: · Rarer are also ABC : A utoimmune B iliary cirrhosis C opper (Wilson's) PowerPoint Presentation: Cirrhosis PowerPoint Presentation: Cirrhosis resulting from chronic viral hepatitis PowerPoint Presentation: Budd-Chiari syndrome. Therombosis of the major hepatic veins has caused extreme blood retention in the liver. PowerPoint Presentation: Biliary Cirrhosis: One of the more common causes of nonalcoholic liver disease Pathology is destruction of the intrahepatic bile ducts 90% are found in middle age females Most common symptoms are fatigue & pruritis Antimitochondrial antibodies (90%) Order after all hepatitis profile excluded Cirrhosis (cont) PowerPoint Presentation: Complications of cirrhosis: Spontaneous bacterial peritonitis (SBP) which occurs in 10% of alcoholic cirrhosis (E. coli) Cirrhosis (cont) PowerPoint Presentation: Ascites : Refers to the accumulation of excessive volumes of fluid within the peritoneal cavity Always a poor prognostic sign Ultrasound & CT scans are best method of detection of small amounts of fluid. Flat plate has ground glass look. PowerPoint Presentation: Ascites (cont) Diagnosis of ascites: Bulging flanks Umbilical hernia Shifting dullness Scrotal edema Right sided pleural effusion Cirrhosis (cont) PowerPoint Presentation: Paracentesis: 50cc of fluid removed, look at color CBC, WBC, protein, LDH, glucose, amylase, albumin Gram stain, AFB, fungus cultures, cytology PowerPoint Presentation: Clinical and Laboratory Features of Cirrhosis Clinical Laboratory Hepatocellular Dysfunction Jaundice Hyperbilirubinemia Spider angiomas Edema Palmar erythema Low serum blood urea nitrogen Gynecomastia Prolonged prothrombin time Loss of body hair Hyperammonemia Testicular atrophy Thrombocytopenia Dupuytren’s contracture Leucopenia Muscle wasting ─ PowerPoint Presentation: Clinical and Laboratory Features of Cirrhosis Clinical Laboratory Hypoalbuminemia Low serum albumin Bruising ─ Signs of hepatic encepha-lopathy ─ Fetor Hypertension Splenomegaly ─ Ascites ─ Caput medusae ─ Variceal bleeding ─ PowerPoint Presentation: Pathophysiology: Alteration of hepatic blood flow causing portal hypertension. Reduction in liver function: Reduction in synthesis of albumin & coagulation proteins Reduction in detoxification of bilirubin, ammonia, & drugs Ascites (cont) PowerPoint Presentation: Ascites PowerPoint Presentation: Complications of ascites: Dyspnea vomiting Decreased cardiac output hydrothorax Anorexia scrotal edema Reflux esophagitis Ascites (cont) PowerPoint Presentation: Treatment: Improve hepatic function Restrict sodium & fluid intake Aldactone which inhibits aldosterone Paracentesis (removal of fluid with addition of IV albumin) PowerPoint Presentation: Shunts Abstain from alcohol Diuretics Aldactone Lasix PowerPoint Presentation: Treatment (cont): Supportive Nutrition high calories, low protein with encephalopathy Minerals & vitamins Sodium restriction Copper restriction if wilson’s disease Ascites treatment (cont) PowerPoint Presentation: Neomycin & Lactulose if NH3 elevated Liver Transplants PowerPoint Presentation: Classification: Portal vein (prehepatic) Intrahepatic (sinusoids) Hepatic (posthepatic) (Budd Chiari- us

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20. 11. 2014
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LIPO PROTEINS

LACTATION
21. 03. 2015
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LACTATION

Dietary Plan for Diabetes
29. 03. 2015
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Dietary Plan for Diabetes

tissue processing
17. 03. 2015
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tissue processing

dr mustansar lahore
03. 07. 2015
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dr mustansar lahore

SOCIAL MEDIA USEAGE
29. 03. 2016
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SOCIAL MEDIA USEAGE