Hepatic Disease Normal Anatomy andPhysiology. Hepatic: Normal Anatomy 1. Biliary system 2. Portal system 3. Reticulo-endothelial system 4. Hepatic parenchyma:

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Presentation transcript:

Hepatic Disease Normal Anatomy andPhysiology

Hepatic: Normal Anatomy 1. Biliary system 2. Portal system 3. Reticulo-endothelial system 4. Hepatic parenchyma: syntheticmetabolic

Liver : Biliary Portal RES Parenchyma

Hepatic: Normal physiology 1. Secretion of bile for fat absorption 2. Short term sugar storage (glycogen) 3. Aged RBC breakdown and excretion of bilirubin 4. Synthesis of coagulation factors 5. Synthesis of albumin 6. Drug metabolism

Hepatitis Hepatitis : Inflammation of the liver Causes: alcoholic and viral (A,B,C,D,E) (others: mononucleosis, syphillis, TB, methotrexate, ketoconazole) Acetaminophen overdose

Hepatitis Hepatitis : Acute symptoms Abdominal pain, nausea, vomiting, fever, malaise Jaundice Hepatomegaly and splenomegaly In recovery phase: persistent hepatomegaly and abnormal LFTs

Hepatitis Hepatitis : Chronic symptoms May be asymptomatic for 10 to 30 years Nonspecific signs: fatigue, weight loss,itchiness, right upper quadrant pain

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Hepatitis A Hepatitis BHepatitis C Transmission : Fecal-oral percutaneous/percutaneous permucosal Sources : Water, shellfish blood and bloodblood and blood restaurants products (dirty products needles, sex, etc)

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Hepatitis A Hepatitis BHepatitis C High risk groups: 40% of US health care workersIV drug users population shows SE Asian immigrants transfusion serological hemodialysis patientsrecipients prior evidence IV drug usersto 1992 of infection transfusion recipients unprotected sex with multiple partners Incubation : 15 to 50 days 45 to 180 days14 to 180 days

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Hepatitis A Hepatitis BHepatitis C Risk : Typically 6 to 30 % risk with 2 to 8% risk with epidemic needle stick needle stick Carrier state :: None 5 to 10% risk of 80 to 90% risk becoming carrier becoming carrier with increased riskwith increased risk of hepatocellular of hepatocellular carcinoma and carcinoma and cirrhosiscirrhosis

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Hepatitis A Hepatitis BHepatitis C Immunization : Vaccine Vaccine No active or and immuno- and immuno-passive immuni- globulin available globulin availablezation available

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Other Hepatitis viruses: D and E Hepatits D: occurs as a co-infection with hepatitis B transmitted both sexually and parenterally Hepatitis E: resembles hepatitis A (fecal / oral)

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Dental Management: Difficult to identify all patient through history Many acute cases of Hep B and C are mild MUST use universal precautions for all Screening recommended for patients from high risk groups

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Guidelines for blood exposure From patients with Hepatitis B: 1. Determine the titre of anti-HBs in the health care professional 2.If adequate: no treatment is needed 3.If inadequate give Hepatitis B Immunoglobulin

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Guidelines for blood exposure From patients with Hepatitis C 1.Exposed professional gets baseline and follow up testing for anti-HCV and liver enzymes

Viral Hepatitis Viral Hepatitis : A,B,C,D,E Guidelines for blood exposure From patients with Unknown 1.Ask for serological testing of the patient (this can be ordered by the Medical Officer)

Alcoholic Liver Disease: 1.Definition of an alcoholic … estimate: 170 to 200 out of 2000 patients 2.Problem drinking: male > 12 oz. / week female > 9 oz. / week 3. During history taking: double it

Alcoholic Liver Disease: 1.10 to 15% of alcoholics develop cirrhosis 2.Early change: fatty liver 3.Second stage: alcoholic hepatitis 4.Final stage: cirrhosis with parenchymal damage and scarring leading to portal hypertension

End-stage Liver Disease: (regardless of cause) 1.Loss of Synthetic function: Vit K dependant coagulation factors (II, VII, IX, X) hypoalbuminemia (edema) 2.Portal hypertension esophageal, umbilical, hemorroidal varices ascites (abdominal fluid build-up) splenomegaly (thrombocytopenia) 3.Loss of de-toxification function: ammonia poisoning: encephalopathy and dementia

End-stage Liver Disease: (regardless of cause) 4. Bone marrow toxicity: anemia, leukopenia and thrombocytopenia (decrease HgB, WBC and platelets on CBC) 5.Endocrine disturbances: testicular atrophy and gynecomastia 6.Esophagitis / gastritis 7.Elevated Liver enzymes: AST / ALT

End-stage Liver Disease: (regardless of cause) 8. Elevated bilirubin: causing Jaundice 9. Elevated INR: causing bleeding 10. Decreased albumin: causing edema and ascites 11. Altered drug metabolism: unpredictable Drug effect can be Up or Down

End-stage Liver Disease: (regardless of cause) 11. Altered drug metabolism (cont’d): unpredictable Decreased drug effect due to induction of hepatic microsomal enzymes and accelerated metabolism of the drug Increased drug effect due to loss of hepatic function and slowed metabolism of the drug Increased drug effect due to decreased plasma protein (albumin) binding and therefore increased unbound (active) drug

Liver Disease: treatment 1.In acute hepatitis: supportive, steroids 2.In chronic hepatitis: interferon 3. In failure or end stage disease: transplant

Liver Disease: management 1.Beware of second addictions (narcotics, etc) 2.Unpredictable drug metabolism 3.Caution or avoid hepatically metabolized drugs: NSAIDs, narcotics, acetaminophen, benzodiazepines, metronidazole, local anaesthetics 4. Bleeding tendencies (CBC, PTT, INR): may require vit K, FFP or platelets

Questions????