Hepatic DiseaseHepatic Disease

Normal AnatomyNormal Anatomy

and and

PhysiologyPhysiology

Hepatic: Normal Anatomy

1. Biliary system1. Biliary system

2. Portal system 2. Portal system

3. Reticulo-endothelial system3. Reticulo-endothelial system

4. Hepatic parenchyma:4. Hepatic parenchyma:

synthetic synthetic

metabolicmetabolic

Liver:

Biliary

Portal

RES

Parenchyma

Hepatic: Normal physiologyHepatic: Normal physiology

1. Secretion of bile for fat absorption2. Short term sugar storage (glycogen)3. Aged RBC breakdown and

excretion of bilirubin4. Synthesis of coagulation factors5. Synthesis of albumin6. Drug metabolism

HepatitisHepatitis: Inflammation of the liver

Causes: alcoholic and viral (A,B,C,D,E)

(others: mononucleosis, syphillis, TB, methotrexate, ketoconazole)

Acetaminophen overdose

HepatitisHepatitis: Acute symptoms

Abdominal pain, nausea, vomiting, fever, malaise

Jaundice

Hepatomegaly and splenomegaly

In recovery phase: persistent hepatomegaly and abnormal LFTs

HepatitisHepatitis: Chronic symptoms

May be asymptomatic for 10 to 30 years

Nonspecific signs: fatigue, weight loss, itchiness, right upper quadrant pain

Viral HepatitisViral Hepatitis: A,B,C,D,E

Hepatitis A Hepatitis B Hepatitis C

Transmission:

Fecal-oral percutaneous/ percutaneous permucosal

Sources:

Water, shellfish blood and blood blood and blood restaurants products (dirty products

needles, sex, etc)

Viral HepatitisViral Hepatitis: A,B,C,D,E

Hepatitis A Hepatitis B Hepatitis C

High risk groups:

40% of US health care workers IV drug userspopulation shows SE Asian immigrants transfusion serological hemodialysis patients recipients priorevidence IV drug users to 1992of infection transfusion recipients

unprotected sex with multiple partners

Incubation:

15 to 50 days 45 to 180 days 14 to 180 days

Viral HepatitisViral Hepatitis: A,B,C,D,E

Hepatitis A Hepatitis B Hepatitis C

Risk:

Typically 6 to 30 % risk with 2 to 8% risk withepidemic needle stick needle stick

Carrier state::

None 5 to 10% risk of 80 to 90% risk becoming carrier becoming carrier with increased risk with increased risk of hepatocellular of hepatocellular carcinoma and carcinoma and cirrhosis cirrhosis

Viral HepatitisViral Hepatitis: A,B,C,D,E

Hepatitis A Hepatitis B Hepatitis C

Immunization:

Vaccine Vaccine No active orand immuno- and immuno- passive immuni-globulin available globulin available zation available

Viral HepatitisViral Hepatitis: A,B,C,D,E

Other Hepatitis viruses: D and E

Hepatits D:

occurs as a co-infection with hepatitis Btransmitted both sexually and parenterally

Hepatitis E:

resembles hepatitis A (fecal / oral)

Viral HepatitisViral 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 fromhigh risk groups

Viral HepatitisViral 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 HepatitisViral 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 HepatitisViral 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: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: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: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 hypertensionesophageal, umbilical, hemorroidal varicesascites (abdominal fluid build-up)splenomegaly (thrombocytopenia)

3. Loss of de-toxification function: ammonia poisoning: encephalopathy and dementia

End-stage Liver Disease: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 andgynecomastia

6. Esophagitis / gastritis

7. Elevated Liver enzymes: AST / ALT

End-stage Liver Disease: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:End-stage Liver Disease:(regardless of cause)

11. Altered drug metabolism (cont’d): unpredictable

Decreased drug effect due to induction of hepaticmicrosomal enzymes and accelerated metabolismof the drug

Increased drug effect due to loss of hepatic function and slowed metabolism of the drug

Increased drug effect due to decreased plasmaprotein (albumin) binding and therefore increasedunbound (active) drug

Liver Disease: Liver Disease: treatmenttreatment

1. In acute hepatitis: supportive, steroids

2. In chronic hepatitis: interferon

3. In failure or end stage disease: transplant

Liver Disease: Liver Disease: managementmanagement

1. Beware of second addictions (narcotics, etc)

2. Unpredictable drug metabolism

3. Caution or avoid hepatically metabolized drugs:NSAIDs, narcotics, acetaminophen, benzodiazepines, metronidazole, localanaesthetics

4. Bleeding tendencies (CBC, PTT, INR):may require vit K, FFP or platelets

Questions????