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Alcoholism and Hepatitis

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Alcoholism and Hepatitis put together by Alex Yartsev: Sorry if i used your images or data and forgot to reference you. Tell me who you are. [email protected] Alcoholism and Hepatitis History of Presenting Illness - Anorexia - Nausea and Vomiting - - - Weight loss Malaise Yellow eyes - - - Fever Diarrhoea Itching - - - Generalized Abdominal Pain Ankle swelling Bruising - - Abdomen distension Black tarry stools - ASK ABOUT: JAUNDICE - Tattoos - The eyes are first to go. - Blood trasnfusions - ASK ABOUT THE COLOUR OF URINE AND STOOL: Needlestick injury - Injecting drug use JAUNDICE WITHOUT DARK URINE OR PALE STOOL - Sexual practices means HAEMOLYSIS (unconjugated bilirubin released - recent contacts @ circulation, thus not water soluble and cannot be - Travel excreted by kidneys) - MEDICATIONS ( see below) JAUNDICE WITH DARK URINE AND PALE STOOLS Differential Diagnoses means OBSTRUCTIVE JAUNDICE Nonalcoholic steatohepatitis (NASH) Acute fatty liver of pregnancy Drug-induced liver disease Metabolic liver disease and inborn (valproic acid, tetracycline, errors of metabolism antiviral agents such as zidovudine) Reye syndrome Viral hepatitis Congestive Heart failure Examination - Tender Hepatomegaly (80-90% of cases) - Jaundice Acute fatty liver of pregnancy - Ascites Metabolic liver disease and inborn - Splenomegaly errors of metabolism Reye syndrome - Spider naevi Congestive Heart failure Epidemiology Alcoholic Hepatitis seen in 33% of chronic alcoholics Tests and Investigations FBC + blood microscopy: looking for macrocytic anaemia of alcoholism alpha-fetoprotein: very specific marker of hepatocellular carcinoma LIVER FUNCTION TESTS: ALT = the necrosis enzyme AST = alcoholic heptitis enzyme AST to ALT ratio = 2:1 SAP/ALP = cholestasis enzymes (with GGT) GGT =induceable acoholism enzyme Bilirubin: Conjugated = hemolysis or liver dysfunction Unconjugated = biliary obstruction or liver failure SERUM ALBUMIN will be low; trying to explain ascites PROTHROMBIN Time low due to reduced rate of cloting factor synthesis Thiamine =low mainly due to malnutrition RBC Folate (alcohol inhibits the gut tranbsporter of folate) HEPATITIS VIRUS SEROLOGY: HBsAg -earliest ACUTE marker, may persist chronically HBeAg -ACTIVE INFECTION, virus is replicating (25% don’t have this) HBV DNA Ascites Fluid Aspiration: Looking for malignant cells Abdominal ultrasound Looking for cysts, focal lesions, biliary tree stones etc. Abdominal CT scan Looking for masses, enlarged lymph nodes, vascular malformations Liver Biopsy: only way to objectively diagnose alcoholic liver disease MANAGEMENT: Limit progression to cirrhosis: Stop drinking. Antiviral drugs: - nucleoside analogue lamivudine for hepatitis B - interferon-alpha plus ribavirin for hepatitis C Immune suppression may work for autoimmune disease Control lipid vitamin deficiencies: A, D, E, K For ascites: - salt restriction, - aldosterone antagonist (first choice) - loop diuretic (second choice) diuretics control variceal bleeding by means of endoscopic surgery (banding or adrenaline injection) by reducing portal pressure pharmacologically (eg by somatostatin analogues (octreotide) and b-adrenergic blocking agents). Screen for hepatocellular carcinoma LOOK FOR LIVER TRANSPLANT DONOR Survival rates are about 80% in adults and 90% in children An Occupational Hazard 7.10 by Eleanor Curtin Problem summary Seok Kim is a 52-year-old importer. He migrated to Australia with his family from Korea in 1995.Mr Kim has noticed dark urine and yellow eyes for the past three weeks. For about three months he has noticed a poor appetite and decreasing energy . He is known to have a history heavy alcohol intake and hypertension. He has a past history of hepatitis. There is no history of blood transfusion, tattoos or injecting drug use but his mother had liver disease. Diagnosis & defn PROLONGED ALCOHOL INTAKE and infection with HEPATITIS B VIRUS resulted in damage to the liver parenchyma, inflammation, fatty infiltration and cirrhosis. Hepatitis B Virus DEFINITION A. Hepadna virus B. Small double-stranded DNA genome, viral DNA polymerase (DNAP) C. envelope (SURFACE), protein coat (CORE) Incubation : 1-5 months (~ 2m) Transmission : blood**, vertical**, sexual*, saliva Replication : @ HEPATOCYTE, salivary glands, pancreas, testis (1) ATTACHMENT: unknown receptor (2) UNCOATING: core released, DNAP makes DNA circular - CCC DNA ( covalently closed circular DNA) (3) NUCLEUS ENTRY: CCC DNA very stable → PERSISTS for life of cell, may also integrate in host DNA (4) VIRAL PROTEIN SYNTHESIS : ENVELOPE encodes surface antigen HBsAg CAPSID encodes core antigen HBcAg (not found in blood) encodes circulating peptide HBeAg Host response : THIS CAUSES THE MOST DAMAGE!!!! A. Innate immune response INDUCES APOPTOSIS to clear infxd cells. T-CELL MEDIATED RESPONSE: HBcAg induces cytotoxic Tcell response → FIBROSIS (worse with alcohol) ***if impaired T-cell immunity → less damage to liver but virus never clears & higher cancer risk (high level replication) B. three antibodies: anti-HBs , anti-HBc , anti-HBe . Durable & highly infectious Stable to temperature, dryness, anti-septics Inactivated by: glutaraldehyde, formulin, urea INITIAL ACUTE PHASE LATER ACUTE HPI ~~ MOSTLY ASYMPTOMATIC A. TYPICAL ACUTE INFXN a. FATIGUE, HEADACHE b. FEVER (low grade) B. GIT a. NAUSEA A. GIT RESOLVES b. ANOREXIA c. DISTASTE FOR CIGS d. DIARRHOEA C. ABDO PAIN (right upper quad) 3-6 →peritoneum stretches over big liver WEEKS PHYS EXAM A. JAUNDICE → SCLERAL RESOLUTION A. TENDER LIVER → DARK URINE B. CERVICAL LYMPH NODES (advancing) → PALE STOOLS C. SPLENOMEG (esp. children) → PALPABLE LIVER D. “SERUM SICKNESS ∆” (10%) circulating Ag-Ab complexes deposited a. ARTHRALGIA b. RASH c. FEVER CHILDHOOD INFXN → ASYMPTOMATIC → flares in adulthood → SEVERE CHRONIC LIVER DISEASE (high prevalence pattern) ADULT / OLDER CHILD INFXN → ACUTE HEPATITIS →RECOVERY (low prevalence pattern) DIAGNOSIS HISTORY A. SEROLOGY - !!GOLD STANDARD!! RISK FACTORS Antigens: A. IV drug user HBsAg -earliest ACUTE marker, may persist chronically B. HOMOSEXUAL (male) HBeAg -ACTIVE INFECTION , virus is replicating (25% don’t have this) C. CLOSE CONTACT with infxd individuals HBV DNA 1. mother DNA polymerase 2. regular sexual partners Antibodies: D. HAEMODIALYSIS HBsAb -previous Hep B INFECTION + IMMUNITY E. HEALTHCARE worker or VACCINATION + IMMUNITY F. TRAVEL 1. Asia HBcAb -CONVALESCENCE: core window as surface Ag cleared by surface Ab 2. Pacific Islands HBeAb -earliest Ab, LOW INFECTIVITY: predicts Hep B resolution 3. Eskimo LIVER FUNCTION TESTS 4. India * ALBUMIN normal 5. Sub-Saharan Africa * BILIRUBIN-URIA early →perists to convalescence 6. Haiti FBC G. TATTOO’S / ACUPUNCTURE *WCC high EPIDEMIOLOGY PREVALENCE: DIFFERENTIAL DIAGNOSES Persistent HBV ~ 300 million worldwide A. ALCOHOLIC HEPATITIS -ENDEMIC sub-Saharan Africa, China, SE Asia B. MEDICATIONS (different viral genotypes) C. ISCHAEMIA →vertical transmission (at birth) D. BILIARY TRACT ∆ →chronic liver disease 5-20% acute hep B rare, 10-20% adults are carriers , most non-carriers are immune -LOW prev: →acute hepatitis →sexual transmission, IV drugs -AUSTRALIA: 1-2% carriers ACUTE HEPATITIS IMMUNE RESPONSE CAUSES CELL DAMAGE!! (immuno-suppressed & neonates →asymptomatic infection) a. immune response against viral Ag’s damages virus-infxd hepatocytes A. cytotoxic T-cells react to virus Ag’s or virus-modified cell membrane Ag’s → CELL LYSIS B. antibody-dependent cytoxicity → circulating immune complexes containing viral Ag’s and Ab’s can cause POLYARTHRITIS, VASCULITIS, GLOMERULO-NEPHRITIS b. strength of immune response determines clinical expression PROMPT response → cell injury & virus clearance – ACUTE HEPATITIS ACCELERATED & EXCESSIVE response → fulminant liver necrosis → total clearance – FULMINANT HEPATITIS WEAK response →persistence of antigenic hepatocytes →continued low-level destruxn – CHRONIC HEPATITIS FAILED response →virus perpetuates, no liver damage – CARRIER STATE INCUBATION ACUTE –preicteric ACUTE –icteric CONVALESCENCE DNA Viral replication Immune response causing liver cell Bile canaliculi obstruction & Viral replication stops, LIVER destruction damage → cholestasis architecture restores, inflammatory exudate clears asymptomatic usually mild illness Non-specific symptoms intensify Clinical & chemical recovery in 12- SYMPTOMS (or cessation = “anicteric”) 16wks → malaise, nausea, anorexia →high fever, chills, headache → “serum sickness” →abdo pain PHYS EXAM → tender LIVER → big, tender LIVER → jaundice → pale stools (cholestasis) → pruritis (bile salt irritation) ↑ ALT, AST ↑ Bilirubin (conjugated) → serum → urine DARK (late stage) HBsAg early acute markers HBsAg, HBeAg as acute phase ends, HBcAb (1) HBcAb (2) HBeAb rises and e Ag falls (3) HBsAb (gives immunity) antigens no longer detectable NORMAL LIVER Central vein Councilman body Portal tract Ballooning degeneration ACUTE HEP B – LIVER (micro) HISTOLOGY – ACUTE HEPATITIS GROSS A. enlarged ACUTE HEP B – LIVER (low power) B. pigmented: red , greenish (if cholestasis) A. portal MONONUCLEAR INFLAMM EXUDATE: MICRO limited to hepatocyte plate – “PIECEMEAL NECROSIS” A. CELL INJURY – lobular disarray BALLOON DEGENERATION : cytoplasm swelling ( E.R. , MITO ) B. NECROSIS – single cells / sml clusters (1) Cytolysis: cells “disappear” from framework (2) Apoptosis : condensation & fragmentation → COUNCILMAN BODIES C. INFLAMMATORY ∆’S (1) KUPFFER CELL HYPERTROPHY (2) MONONUCLEAR INFLAMMATORY INFILTRATE from portal region D. BILE DROPLETS @ ballooned cells, Kupffer cells, within canaliculi E. REGENERATION
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