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Alcoholic hepatitis
- 1. ALCOHOLIC HEPATITIS NUR IZZATULNAJWA - 36
- 2. OBJECTIVES • Know thebrief components of alcoholic liver disease • Know the threshold developing ALD • Know the pathophysiology • Know the clinical syndrome specifically on alcoholic hepatitis • Know the investigation • Describe the prognosis • Describe the management of alcoholic hepatitis
- 3. INTRODUCTION According to theWHO, alcohol consumption accounts for 3.8% of the global mortality and 4.6% of DALYs. Liver disease represents 9.5% of alcohol-related DALY’s worldwide, while individual rates vary in different regions. Alcohol is the main cause of liver-related death in Europe with highest mortality rates reported from France and Spain (approximately 30 deaths per 100,000 per year). There is a possibility of underestimation of mortality due to legal issues of documenting alcohol as primary cause of death. The lack of specificity of the national survey questionnaires also fails to allow accurate classification of liver diseases. Today, even in Asian countries like India, alcohol is emerging as the commonest cause of chronic liver disease 11.
- 4. INTRODUCTION • Chronic andexcessive ingestion of alcohol can cause liver disease : – Fatty liver – Alcoholic hepatitis – Alcoholic cirrhosis
- 6. THRESHOLD FOR DEVELOPINGALD • THE VALUE MIGHT VARIES, BECAUSE THERE’S NO LINEAR RELATIONSHIP BETWEEN DOSE AND LIVER DAMAGE INTAKE OF >60-80 G/DAY FOR 10 YEARS IN MEN INTAKE OF >20-40 G/DAY FOR 10 YEARS IN WOMEN
- 7. RISK FACTOR • Drinkingpattern – continous drinkers • Gender - women • Genetics • Nutrition
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- 11. 2) ALCOHOLIC HEPATITIS (STEATOHEPATITIS ) • Most asymptomatic • Fever, rapid onset of jaundice, abdominal discomfort and proximal muscle wasting • Hepatomegaly • Features of CLD ; spider angiomata, palmar erythema, chapped lips, gynaecomastia • Severe cases ; portal hypertension, ascites and variceal bleeding occur without cirrhosis • Non hepatic manifestation ; polyneuropathy, cardiomyopathy • AST and ALT elevated two to seven fold, but usually <400 IU • AST : ALT ratio > 2 • Elevated bilirubin • Mild increase in alkaline phosphatase • Reduced albumin • Leucocytosis, elevated c-reactive protein • POTENTIALLY REVERSIBLE BUT MANY PROGRESS TO CIRRHOSIS!
- 12. PATHOLOGICAL FEATURES • Lipogranuloma •Neutrophil infiltration • Mallory’s hyaline • Pericellular fibrosis
- 14. INVESTIGATION • LAB FINDINGS •LIVER BIOPSY
- 15. PROGNOSIS • High mortalityin severe hepatitis • Poor prognostic factors include : – Prothrombin time > 5 sec of control – Anaemia – Albumin < 2.5g/dL – Bilirubin > 8mg/dL – Renal failure – Presence of ascites
- 17. MANAGEMENT • Complete abstinencefrom alcohol • Treatment for complication such as ; variceal bleeding, encephalopathy and ascites • Good nutrition • Drugs : – Corticosteroids – Pentoxifylline • Liver transplantation (poorer outcome if patients still not abstinent)
- 18. • If Glasgowscore > 9 • Side effect of sepsis • Contraindicated in sepsis and variceal hemorrhage • If bilirubin has not fallen in 7 days, then it should be stopped
- 19. DRUG AND TOXIN INDUCEDHEPATITIS
- 20. OBJECTIVES • KNOW THERISK FACTORS FOR DRUG INDUCED HEPATITIS • KNOW THE BRIEF PATHOPHYSIOLOGIC MECHANISM • KNOW THE DRUGS AND ITS PATTERN OF ACTION • KNOW HOW TO DIAGNOSE • KNOW THE TREATMENT
- 21. INTRODUCTION • Liver isthe primary site of drug metabolism • Liver disease may affect the capacity of liver to metabolise drugs, thus unexpected toxicity may occur
- 22. RISK FACTOR • AGE •SEX • ALCOHOL INGESTION • LIVER DISEASE • GENETIC FACTORS • OTHER COMORBIDITIES • DRUG FORMULATION
- 23. PATHOPHYSIOLOGIC MECHANISM • DISRUPTIONOF THE HEPATOCYTE • DISRUPTION OF TRANSPORT PROTEIN • CYTOLYTIC T-CELL ACTIVATION • APOPTOSIS OF HEPATOCYTE • BILE DUCT INJURY
- 24. MECHANISM • Two majormechanism of chemical hepatotoxicity : DIRECT TOXIC • PREDICTABLE •DOSE RELATED TOXICITY •SHORT LATENT PERIOD •ABSENCE OF EXTRA-HEPATIC MANIFESTATION IDIOSYNCRATIC •UNPREDICTABLE •MOSTLY DOSE- INDEPENDENT TOXICITY •VARIABLE LATENT PERIOD •PRESENCE OF EXTRA- HEPATIC MANIFESTATION ; FEVER, RASHES, ARTHRALGIA, EOSINOPHILIA
- 25. CLINICAL MANIFESTATION • Themanifestations of drug-induced hepatotoxicity are highly variable : – ranging from asymptomatic elevation of liver enzymes to fulminant hepatic failure.
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- 27. 1) CHOLESTASIS – Conditionwhere bile cannot flow from the liver to the duodenum – Pure cholestasis ( high concentrations of estrogen, 50mcg/day) – Cholestatic hepatitis due to inflammation and canalicular injury 2) HEPATOCYTE NECROSIS – Inflammation does not always happen but does accompany necrosis in liver injury
- 28. 3) STEATOSIS – Microvesicularhepatocyte fat deposition, due to direct effects on mitochondrial beta- oxidation – Macrovesicular hepatocyte fat deposition 4) VASCULAR/ SINUSOIDAL LESION – Damage the vascular endothelium and lead to hepatic venous outflow obstruction – Damage of sinusoids can trigger local fibrosis and result in portal hypertension ( overdose of vit A) 5)HEPATIC FIBROSIS
- 31. TREATMENT • Withdrawal ofthe suspected agent • Supportive therapy as in viral hepatitis
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