LIVER – Dra.

Cham  Categories forms:  Maybe acute event or asymptomatic

 HBe Ag (+)  chemoTx and immunosuppressive are at
Hepatitis A  HBe Ag (-) risk
 HBs Ag carrier state
 RNA virus Diagnosis
 Fecal-oral route Phases of Chronic Infection
 IP: 2-6 weeks  HBs Ag
 (-) chronic and carrier stage  Immune tolerant - General marker of infxn

st
 <1% fulminant hepa Immune clearance - 1 marker to appear
 5% in pedia; 70-80% in adult  Residual or inactive  HBc Ag
 Self limitng  Reactivation - Nucleocapsid that encloses the viral
 Dx: anti HAV (IgM) – acute; (IgG) – DNA
Immune tolerant phase  HBeAg
immunity
 Rx: supportive  Young, asymptomatic
- Rapid viral replication
 Anti HBs
 (+) HBsAg, (+) HBeAg
Hepatitis B - Protective immunity
 High HBV-DNA (>2,000,000-20,000,000
- Recovered from natural infection or
 Small DNA virus, Partially double stranded IU/ml)
vaccinated
 Parenteral, STD’s, *perinatal  ALT normal, no clinicopathological changes
 AntiHBe
 IP: 1-6 mo
Immune Clearance Phase - Produced in response to HBeAg
 10%  chronic carrier - Slow viral replication
 (+) !% fulminant  ↑ ALT ↓HBV-DN - (+) after cleared from HBeAg
 Chr infection = <5% adults, >90% infants  Eventually followed by seroconversion of  Anti HBc (IgM)
 HBe Ag  anti HBe - Acute or recent infection
Genotypes A-H:
 For undetectable HBV-DNA - Maybe (+) in low tites in 15-20% of
 B and C – Asia Pacific Regions acute flares of chronic infection
Residual or Inactive Phase
 A and D – Europe and Mediterranean  Anti HBc (IgG)
 B<C – progression of liver disease - Current or past infection
 After seroconversion
 C>B – risk of HCC - Found in recovery
 Preceded by marked ↑HBV-DNA, Normal
 A and C – more severe liver disease ALT, resolution of liver necroinflam’n Treatment
- Greater disease progression  Mostly remain (+) HBeAg for lifetime
 IFN or PEG IFN alpha 2a
Chronic Hepatitis B Reactivation Phase  Antiviral drugs
 Persistent infection=/> 6mos - Lamivudine
 Reappearance of necroinflam’n of the liver
 (+) HBsAg with chr inflam’n, necrosis and - Entecabir
 ↑ALT, (+) HBV-DNA, (+/-) HBe Ag
fibrosis of the liver - Adefovir
 Approx. 50% may reactive
- Telbivudine
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 - Tenofovir Hepatitis G  Entecavir
 Lifestlye – prevent transmission thru sex, - Immunomodulator
blood, spill, perinatal  RNA virus  IFN
 Alcohol abstinence  Parenteral  Glucocorticoids
 Contacts – vaccination  15% non-A, non-B, non-C cases of chronic  Thymosin alpha 1
hepa
 Ribavirin
Hepatitis C  Associated with fulminant hepatitis
 IL 2 and 12
 RNA virus Pathology  HCV infection treatment:
 90% post BT 1. IFN A 2a – 3 MU tiw x 12mo
 Parenteral, perianal, STD’s  Mononuclear cell infiltration 2. IFN A 2b – 3-6 MU tiw x 12 mo

 IP: 2 weeks – 6 mos  Cellular ballooning and necrosis 3. Lymphoblastoid IFN – 3 MU tiw x 6

 30-50%n chronic and cirrhosis, CA  Condensed cytoplasm with pyknotic nuclei mo

(acidophilic bodies) 4. IF A 2b 3MU tiw + Ribavirin
Treatment: 1000mg/d
Clinical Features ***decompensated liver cirrhosis
 PEG IFN  liver transplantation
 Malaise, anorexia, fatigue
 Ribavirin
 Arthritis and urticaria (common in HB) Complications
Response to Rx: - due to circulating immune complexes
 influenza like syndrome in HA  Fulminant hepatitis
 Genotypes 2>3>4>1  50% jaundice  Chronic persistent hepatitis
 Hepatomegaly and tenderness  Chronic active hepatitis
Hepatitis D
 20% hepatomegaly  Chronic carrier state
 Delta hepatitis  Cholestatic hepatitis
 Small, defective RNA virus
Diagnosis  Aplastic anemia
 Infectious if (+) Hep B infection  Malignancy
 Serology
 Relies on HB proteins for replication  LFT Fulminant Hepatitis
 Gen has chronic, severe infection  Hepatitis profile
 2-7.5% fulminant hepatitis  Rare in HA
Treatment  Occurs in 1-2% of Hb and HC
Hepatitis E
 Common in delta agent superinfection with
 Supportive  acute
 Small RNA virus CHB
 Chronic active Hepa B:
 Short IP  Progressive jaundice, hepatic enceph and
- Nucleoside analogues
 Probably water borne ascites
 Lamivudine
 10-20% MR in pregnant  Common hepatorenal syndrome
 Famciclovir
 90-100% MR in 60yo and increase
 Adefovir
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 Chronic Persistent Hepatitis Risk Factors - ↑ glucose
- (-) viral markers
 After HB, HC and HG  Obesity - (-) autoantibodies
 Increase transaminase > 6 mos  Hyperglycemia – insulin resistant - US= fatty liver
 (-) fibrosis  Hypercholesterolemia = stigmata of Postal HPN (unusual)
 Mostly asymptomatic
***2/3 are >45yo have NIDDM, obese and increase
 Some have fatigue, abdominal pains,
anorexia triglyceride
 Liver bx: periportal lymphocytic Etiology
infiltrates but (-) extension beyond the
portal triad  Drugs and toxins
 Benign course - Ex. Methotrexate, amiodarones,
diltiazem, estrogen, hydralazine,
Chronic Active Hepatitis coumarin, tamoxifen, steroids
 Metabolic abnormality
 Complication of HB and Hc
 Acquired – DM, IBD, severe anemia
 Increase transaminase >6 mo
 Congenital – wilson’s disease,
 May lead to cirrhosis
galatosemia, abetalipoprotein
 No consistent Rx
 Trials of IFN and antiviral agents Pathogenesis
 Liver Bx: (+) inflammation, necrosis and
 Maultifactorial Treatment
fibrosis bridging the portal areas
- Amino acid imbalance
Define risk factors for NAFLD
Chronic Carrier state - Hyperglycemia
- X’sive circulating level of anabolic (FBS, lipid profile, BMI evaluation, meds)
 (+) HBs Ag
(insulin) compare to catabolic (leptin)
 (+) Anti HBe Controlled weight loss
hormones and endothermia
 Normal ALT
 Health carrier state  (-) cirrhosis Clinical features Rx DM and Hyperlipidemia
(-) hepatoma
 Often asymptomatic Dic toxic meds and alc
Non Alcoholic Fatty Liver Disease  Hepatomegaly – common
 Splenomegaly in some
 Form of chronic hepa but no tx of
 Portal HPN (unusual) Monitor lab results, wt clin Rx trials
alcoholism
 Lab findings
 Middle age obese women Lipid levels
- ↑transaminase
 Macrovesicular steatosis
- ↑alkphos
 Directly proportional to body weight - ↑chol and triglycerides (common)\
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Alcoholic Liver Disease 3. Liver Cirrhosis Clinical features

Normal Liver - Long term alc is tosic to the testes   Hepatomegaly

testicular atrophy  impotence  Hepatic bruit
90-100% Alc ↑peri levels of estrogen 
-  Bloody ascites
Fatty liver
gynecomastia, spider angiomas, palmar  Abdominal pains
erythema  Anorexia
10-35% 8-20% - Irreversible  Weight loss

Complications of ALD Diagnosis

Alcoholic hepatitis cirrhosis 1. Ascites  Liver Biopsy

2. GI he – from varices  AFP
40% 3. Encephalopathy  LFT
4. Hypoalbuminemia
 Grp of liver disease due to chr alc  Gallium scan (filling defect)
5. Hypoprothrombinemia
 Alc> 80g/d in men; >40g/d in women  CT Scan
6. Liver cirrhosis  hepatoma
1. Fatty liver Treatment
Hepatoma
- Hepatomegaly (+/-)  No effective Rx
 Occurs 5x in men
- Gen asymp - Surgery
 Peak age incidence: 40-80 yo
- ↑ transaminase and alk phos - RFA
 Unknown etiology - chemoRx
- Histo: large fat droplet in liver
- Reversible - liver transplant
Risk Factors:
- chemoembolization
2. alcoholic hepatits  Alcoholism
 Hepatitis B and C
- In heavy alcohol consumption
 Aflatoxin
- Most have >100g/d for >1yr
 Cirrhosis of the liver
- Fever, jaundice, hepatomegaly, tender liver
- Abn LFT  Hematochromatosis
- Liver bx: liver fat droplets  Wilson’s disease
PMN infiltration  NIDDM type (w/ obesity  NAFLD)
Alc hyaline bodies (Mallory bodies)
- RX: supportive, alcohol abstinence
- Reversible

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