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HEPATITIS - A Complete Medical Education Module

Based on Goldman-Cecil Medicine (22e), Harrison's Principles (22e), Park's Preventive Medicine, Yamada's Gastroenterology, Washington Manual, Tintinalli's Emergency Medicine, and current AASLD/EASL 2024-2025 Guidelines

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QUICK ORIENTATION

Hepatitis in one sentence: Inflammation of the liver - caused most commonly by viruses - that can range from a brief illness that heals completely, to a silent chronic infection that quietly destroys the liver over decades.

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SECTION 1 - DEFINITION

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SECTION 2 - CAUSES & RISK FACTORS

Causes

• D - Drugs (paracetamol, isoniazid, statins, halothane)
• A - Autoimmune hepatitis
• V - Viruses (HAV, HBV, HCV, HDV, HEV - the "hepatitis alphabet")
• I - Ischaemic (shock liver, cardiac failure)
• D - Direct toxins (alcohol, industrial chemicals)
• 'S - Steatohepatitis (NAFLD/NASH - non-alcoholic fatty liver disease)
• W - Wilson's disease (copper accumulation)
• A - Alpha-1 antitrypsin deficiency
• I - Infections (CMV, EBV, HSV, leptospirosis)
• S - Storage disorders (haemochromatosis)
• T - Total parenteral nutrition, pregnancy-related

The 5 Hepatitis Viruses at a Glance

Risk Factors

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SECTION 3 - CLASSIFICATION / TYPES

By Duration

• Acute hepatitis - < 6 months; usually symptomatic; often self-limiting
• Chronic hepatitis - > 6 months; often asymptomatic; requires treatment

By Cause

1. Viral (most common worldwide) - HAV, HBV, HCV, HDV, HEV
2. Alcoholic - fatty change → alcoholic hepatitis → cirrhosis
3. Drug-induced (DILI) - paracetamol (#1 cause of acute liver failure in the West), INH, statins
4. Autoimmune - autoimmune hepatitis (AIH), predominantly women, positive ANA/ASMA
5. Metabolic - NAFLD, NASH, Wilson's disease, haemochromatosis
6. Ischaemic - "shock liver" from hypoperfusion

By Severity

• Asymptomatic - abnormal LFTs only; found incidentally
• Symptomatic/icteric - jaundice, malaise, RUQ pain
• Fulminant hepatitis - acute liver failure developing within 8 weeks of onset of jaundice - life-threatening emergency

By Histology (Grading and Staging)

• Grade = activity/inflammation (1-4 scale)
• Stage = fibrosis (0 = none, 4 = cirrhosis)
• These are assessed by liver biopsy or non-invasive fibrosis scores (FIB-4, APRI)

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SECTION 4 - RELEVANT ANATOMY & PHYSIOLOGY

The Liver - Why It Matters

• Portal vein (75%) - carries nutrients from the gut
• Hepatic artery (25%) - carries oxygenated blood

What Hepatocytes Do (Normal Functions)

How Bilirubin Works (Simplified)

Old RBCs → Haemoglobin → Unconjugated bilirubin (water-insoluble)
          ↓ [Liver conjugates it with glucuronide]
Conjugated bilirubin (water-soluble) → Bile → Gut → Stercobilin (brown stool)
                                                   ↓ Some reabsorbed → Urobilinogen → Urine (yellow)

• Conjugated bilirubin leaks into blood → dark urine (bilirubin in urine)
• Less bile reaches the gut → pale/clay-coloured stools
• Bilirubin deposits in skin/sclera → jaundice

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SECTION 5 - PATHOPHYSIOLOGY (Step-by-Step)

General Mechanism

VIRUS ENTERS BODY
       ↓
Infects hepatocytes (liver cells)
       ↓
Immune system recognises infected cells
       ↓
CD8+ T-cells & NK cells attack infected hepatocytes
       ↓
HEPATOCYTE NECROSIS & INFLAMMATION
       ↓
[Three possible outcomes]
    ↙          ↓           ↘
Clearance   Chronic      Fulminant
(recovery)  infection    failure

Key insight: The liver damage in viral hepatitis is NOT caused by the virus directly killing cells - it is caused by the immune response attacking infected cells. This is why immunosuppressed patients may have less inflammation but worse chronic infection.

Why Does HBV Become Chronic in Newborns?

Progression to Cirrhosis (Chronic Hepatitis)

Chronic inflammation (years to decades)
         ↓
Repeated cycles of hepatocyte necrosis
         ↓
Stellate cell activation → collagen deposition
         ↓
HEPATIC FIBROSIS (Stage 1→4)
         ↓
CIRRHOSIS (Stage 4 fibrosis = bridging + nodules)
         ↓
Portal hypertension → varices, ascites, splenomegaly
         ↓
Hepatocellular Carcinoma (HCC) risk

Specific Virus Pathobiology

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SECTION 6 - CLINICAL FEATURES

The Typical Four Phases of Acute Viral Hepatitis

Symptoms - with Explanations

Signs

Chronic Hepatitis - Often Asymptomatic!

Clinical Pearl: Most patients with chronic hepatitis B or C have NO symptoms for years or even decades. The disease progresses silently until cirrhosis or its complications develop. This is why screening is so important.

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SECTION 7 - HISTORY TAKING

Questions to Ask - and Why They Matter

• Duration and onset of symptoms?
• Any confusion or drowsiness? (encephalopathy - emergency)
• Any bleeding, bruising easily? (coagulopathy)
• Any weight loss - how much, over how long?
• Colour of urine and stools?

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SECTION 8 - DIFFERENTIAL DIAGNOSIS

"My Patient Has Jaundice and High LFTs - What Else Could It Be?"

The Hepatocellular vs. Cholestatic Pattern

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SECTION 9 - INVESTIGATIONS

Basic Tests (Order for EVERY patient with suspected hepatitis)

Specific Serological Tests - The "Hepatitis Screen"

Understanding the HBV Serology Panel - A Roadmap

Scenario                    HBsAg   Anti-HBc   Anti-HBs   HBeAg   Interpretation
─────────────────────────────────────────────────────────────────────────────────
Acute HBV infection           +      IgM +        -          +      Acute infection
Chronic HBV (active)          +      IgG +        -         +/-     Chronic; may replicate
Resolved infection            -      IgG +        +          -      Past; now immune
Vaccinated                    -        -           +          -      Protected; no prior infection
Window period              -/+      IgM +        -           -      Anti-HBc only positive

Clinical Pearl: In the "window period" of acute HBV, HBsAg may have cleared but Anti-HBs not yet appeared. Anti-HBc IgM is the only positive marker - do NOT miss this!

Imaging

LFT Interpretation - A Practical Guide

Raised ALT/AST (>10x ULN) + Normal ALP = Hepatocellular damage
  → Viral hepatitis, drugs, ischaemia, alcohol (if AST:ALT >2)

Raised ALP (>3x ULN) + Mildly raised ALT = Cholestatic
  → Obstruction, PBC, drugs (e.g. co-amoxiclav)
  
Mild raise in all = Non-specific
  → NAFLD, chronic disease, muscle disease (check CK)

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SECTION 10 - DIAGNOSIS

Diagnostic Criteria

1. Clinical syndrome: fatigue, jaundice, RUQ pain
2. ALT/AST > 10x ULN (often 200-3000 IU/L)
3. Positive serology (anti-HAV IgM, HBsAg + anti-HBc IgM, HCV RNA, etc.)
4. Exclusion of other causes

• HBsAg positive for > 6 months
• HBV DNA detectable
• ± elevated ALT
• Liver biopsy or non-invasive fibrosis staging

• Anti-HCV positive (screening)
• HCV RNA positive (confirms active infection)
• HCV genotyping (guides treatment duration and DAA choice)

• Jaundice + encephalopathy within 8 weeks of symptom onset
• INR > 1.5
• No prior liver disease

Diagnostic Approach Flowchart

PATIENT WITH JAUNDICE / RAISED LFTs
              ↓
        HISTORY + EXAM
              ↓
    BLOODS: LFTs, FBC, INR, U&E, glucose
              ↓
    HEPATITIS SCREEN (full serology panel)
              ↓
        ULTRASOUND ABDOMEN
              ↓
    ┌─────────────────────────────┐
    ↓                             ↓
VIRAL SEROLOGY +ve          All markers -ve
    ↓                             ↓
Identify virus          Think: alcohol (AST:ALT >2)
and manage                   drug (recent medication)
accordingly                  autoimmune (ANA/ASMA/IgG)
                             metabolic (ferritin, caeruloplasmin)
                             biliary (dilated ducts?)

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SECTION 11 - COMPLICATIONS

Acute Complications

Chronic Complications

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SECTION 12 - RED FLAGS & EMERGENCIES

Danger Signs - Never Miss These

⚠️ ADMIT IMMEDIATELY if any of the following:

□ Confusion, drowsiness, asterixis → Hepatic encephalopathy
□ INR > 1.5 → Acute liver failure (coagulopathy)
□ Bilirubin rapidly rising
□ Hypoglycaemia (glucose < 3.5 mmol/L)
□ Haematemesis (vomiting blood) → Variceal bleed
□ Signs of sepsis → May be SBP
□ Rapid clinical deterioration
□ HEV in pregnancy (3rd trimester) → 20-25% mortality

Admission Criteria

• Signs of acute liver failure: encephalopathy, INR > 1.5, jaundice deteriorating rapidly
• Inability to maintain oral hydration
• Clinical signs suggesting cirrhosis complications
• Severe alcoholic hepatitis (Maddrey's Discriminant Function > 32)
• Pregnant woman with acute hepatitis E

Referral Criteria

• Gastroenterology/Hepatology referral:
  • All confirmed chronic hepatitis B or C (for treatment)
  • Uncertain aetiology
  • Abnormal LFTs persisting > 6 months
  • Advanced fibrosis or cirrhosis
• Urgent transplant centre referral:
  • Acute liver failure (King's College Criteria)
  • Decompensated cirrhosis

King's College Criteria for Liver Transplant in Acute Liver Failure

• pH < 7.3 after resuscitation, OR
• All three: INR > 6.5, creatinine > 300 μmol/L, grade III-IV encephalopathy

• INR > 6.5, OR
• Any 3 of: age <10 or >40, aetiology (non-A non-B hepatitis, drug reaction), jaundice-to-encephalopathy interval >7 days, INR >3.5, bilirubin >300 μmol/L

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SECTION 13 - MANAGEMENT

Treatment Goals

Non-Drug Treatment (ALL patients)

• Rest - physical rest until symptoms improve; LFTs guide return to normal activity
• Avoid alcohol - strictly forbidden; worsens liver damage
• Avoid hepatotoxic drugs - paracetamol, NSAIDs (especially in cirrhosis), statins (caution)
• Adequate nutrition - small frequent meals; high carbohydrate, moderate protein; avoid high-fat meals (worsens nausea)
• Hydration - maintain oral fluid intake; IV fluids if necessary
• Avoid sexual contact until partner is vaccinated (HBV) or infection resolved
• No blood donation
• Alcohol abstinence - lifelong in alcoholic hepatitis

Drug Treatment - Overview

• Fulminant hepatitis
• Severe or prolonged course
• Immunosuppressed patient

1. Tenofovir disoproxil fumarate (TDF) 300 mg/day
2. Tenofovir alafenamide (TAF) 25 mg/day (preferred if renal/bone concerns)
3. Entecavir (ETV) 0.5 mg/day
4. Pegylated interferon alfa-2a 180 mcg/week SC x 48 weeks (finite treatment option)

• Sofosbuvir/Velpatasvir (Epclusa) - pan-genotypic; 12 weeks; 95%+ SVR
• Sofosbuvir/Ledipasvir (Harvoni) - genotypes 1, 4, 5, 6; 8-12 weeks
• Glecaprevir/Pibrentasvir (Maviret) - pan-genotypic; 8 weeks for non-cirrhotic
• Sofosbuvir/Velpatasvir/Voxilaprevir (Vosevi) - for retreatment failures

• New agent: Bulevirtide (EMA approved 2020, EU) - entry inhibitor; promising

• Corticosteroids (prednisolone 40 mg/day x 28 days) if Maddrey's score > 32
• Lille score at day 7 to assess response; if < 0.45 = continue; if > 0.45 = poor prognosis
• Pentoxifylline no longer recommended (STOPAH trial 2015)
• Nutritional support (enteral feeding if not eating)

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SECTION 14 - PHARMACOLOGY OF IMPORTANT DRUGS

1. Tenofovir Disoproxil Fumarate (TDF) - Hepatitis B

2. Tenofovir Alafenamide (TAF) - Hepatitis B

3. Entecavir (ETV) - Hepatitis B

4. Pegylated Interferon Alfa-2a (Pegasys) - HBV and HCV

5. Direct-Acting Antivirals (DAAs) for HCV - Sofosbuvir/Velpatasvir (Epclusa)

6. Ribavirin - HCV (adjunctive) and HEV

Drug Summary Table

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SECTION 15 - TREATMENT ALGORITHM

Acute Viral Hepatitis

ACUTE VIRAL HEPATITIS SUSPECTED
            ↓
    Confirm diagnosis (serology + LFTs)
            ↓
    ┌───────────────────────────────┐
    ↓                               ↓
MILD/MODERATE                   SEVERE/FULMINANT
(no encephalopathy,             (encephalopathy / INR > 1.5
INR < 1.5, tolerating           / rapid deterioration)
oral intake)                            ↓
    ↓                           ADMIT TO ICU
Outpatient management                   ↓
    ↓                           IV fluids, glucose monitoring
Rest, diet, no alcohol                  ↓
Monitor LFTs 1-2 weekly         Check for transplant criteria
    ↓                           (King's College Criteria)
HAV/HEV → supportive only               ↓
HBV (acute) → supportive       Tenofovir or entecavir for HBV
HCV (acute) → consider          Contact transplant centre
PEG-IFN or DAA (50-80% risk
of chronicity)

Chronic Hepatitis B

Confirmed Chronic HBV (HBsAg +ve > 6 months)
                ↓
    Stage fibrosis (Fibroscan / FIB-4)
                ↓
    Assess HBeAg, HBV DNA, ALT
                ↓
┌──────────────────────────────────────────────────┐
↓                                                  ↓
TREATMENT INDICATED                      NO TREATMENT NOW
(HBV DNA > threshold                     (immune-tolerant phase,
+ ALT > 2x ULN                           low viral load, normal ALT)
OR cirrhosis, regardless                         ↓
of ALT)                                  Monitor 6-monthly
    ↓                                    6-monthly AFP + USS (if cirrhotic)
FIRST LINE:
TDF 300mg/d OR TAF 25mg/d
OR Entecavir 0.5mg/d
    ↓
HBeAg-positive: treat until HBeAg
seroconversion + 6 months extra
    ↓
HBeAg-negative: at least 1 year;
often indefinite
    ↓
Cirrhosis: LIFELONG treatment

Chronic Hepatitis C

Confirmed Chronic HCV (anti-HCV + HCV RNA positive)
                ↓
    HCV Genotype testing
    Assess for cirrhosis (Fibroscan/FIB-4)
    Check for drug interactions
                ↓
    Pan-genotypic DAA regimen:
    Sofosbuvir/Velpatasvir 12 weeks
    OR Glecaprevir/Pibrentasvir 8 weeks (non-cirrhotic)
                ↓
    Check HCV RNA at end of treatment
                ↓
    SVR12 (undetectable RNA at 12 weeks post-treatment)
    = CURE (~95-99%)
                ↓
    If cirrhotic: continue HCC surveillance (6-monthly
    AFP + USS) even after cure - HCC risk persists

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SECTION 16 - REAL-WORLD CLINICAL APPROACH

OPD (Outpatient) Approach

1. Jaundice + fatigue + dark urine = hepatocellular jaundice until proven otherwise
2. Ask: travel? IV drugs? blood transfusions? medications? alcohol? contacts?
3. Examine: confirm jaundice, check liver size + tenderness, look for signs of chronic disease
4. Order: LFTs, FBC, INR, hepatitis screen, ultrasound abdomen
5. While waiting for results: advise rest, no alcohol, no hepatotoxic drugs, contact precautions for HAV
6. Review results and adjust management

Emergency Approach

ABCDE assessment → this is TIME-SENSITIVE
    ↓
Check blood glucose IMMEDIATELY (hypoglycaemia = treat)
    ↓
IV access, blood tests: LFTs, INR, ammonia, FBC, U&E, blood cultures
    ↓
Check for asterixis (flapping tremor = grade II-III encephalopathy)
    ↓
Treat precipitating factors:
  - Infection? → Blood cultures + empirical antibiotics
  - GI bleed? → Urgent endoscopy
  - Constipation? → Lactulose (reduces ammonia production)
  - Dehydration? → IV fluids cautiously
    ↓
Lactulose 30-50 mL TDS (titrate to 2-3 soft stools/day)
    ↓
Rifaximin 550 mg BD for recurrent/persistent encephalopathy
    ↓
AVOID: sedatives, opioids, benzodiazepines (worsen encephalopathy)
    ↓
Contact hepatology/transplant unit

Common Clinical Mistakes - Do Not Make These!

Clinical Pearls

Pearl 1: HCV is the "silent epidemic." Most patients have no symptoms until cirrhosis develops decades later. Screen all adults born 1945-1965 (birth cohort) and anyone with risk factors.

Pearl 2: In Asia and Africa, chronic HBV is usually acquired perinatally (mother to child), not through IV drug use as in Western countries. Always ask about maternal HBV status.

Pearl 3: A patient can have both HBV AND HCV - check for both in all cases of chronic liver disease.

Pearl 4: HCC can develop in HBV carriers even WITHOUT cirrhosis - this is unique to HBV. All HBsAg-positive patients need 6-monthly surveillance regardless of fibrosis stage.

Pearl 5: The AST:ALT ratio > 2 strongly suggests alcoholic liver disease. An ALT > AST ratio favours viral hepatitis or NAFLD.

Pearl 6: In severe acute hepatitis, the INR is a better marker of synthetic function than albumin (albumin has a half-life of 21 days; clotting factors have half-lives of hours-days).

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SECTION 17 - PRESCRIPTION EXAMPLES

Example 1: Acute Hepatitis A (Outpatient)

Patient: 25-year-old female, confirmed acute HAV (anti-HAV IgM +ve), 
mild disease, tolerating oral intake

Rx:
1. Paracetamol 500 mg - 1g oral PRN (for fever/myalgia) - BUT avoid if liver severely impaired
   [Note: Use lowest effective dose; monitor LFTs]
2. Promethazine (Phenergan) 10 mg oral TDS PRN for nausea
   [Or: Metoclopramide 10 mg oral TDS PRN - avoid sedating antiemetics in severe disease]
3. Oral rehydration sachets (ORS) - maintain hydration

Advice:
- Rest at home until LFTs improving
- STRICT hand hygiene; separate utensils for 2 weeks
- No alcohol for at least 6 months
- No school/work during infectious period (up to 1 week after jaundice onset)
- Report to public health (notifiable disease)
- Review in 1 week with repeat LFTs

Follow-up: LFTs in 1 week; if worsening (INR rising, encephalopathy) → ADMIT

Example 2: Chronic Hepatitis B - Starting Treatment

Patient: 40-year-old male, HBsAg +ve >6 months, HBeAg negative, 
HBV DNA 8,000 IU/mL, ALT 85 U/L (3x ULN), Fibroscan F2 fibrosis

Rx:
TENOFOVIR DISOPROXIL FUMARATE (Viread) 300 mg oral ONCE DAILY
- Take on an empty stomach or with food
- Do NOT miss doses; do NOT stop without specialist advice
- Long-term therapy required

Monitoring:
- LFTs + HBV DNA at 3 months, then 3-6 monthly
- Renal function (creatinine, phosphate, eGFR) at 3 months, then 6-monthly
- Bone density (DEXA scan) if used >5 years or risk factors

Vaccinate household contacts and sexual partners for HBV if not already immune.

Example 3: Chronic Hepatitis C - DAA Treatment

Patient: 55-year-old male, anti-HCV +ve, HCV RNA 1.2 million IU/mL, 
Genotype 1a, Fibroscan F1 (mild fibrosis), no cirrhosis

Rx:
SOFOSBUVIR/VELPATASVIR (Epclusa) 400/100 mg - ONE tablet oral ONCE DAILY with food
Duration: 12 weeks

Drug interactions to CHECK before prescribing:
- Stop PPIs or take simultaneously (at same time as Epclusa)
- Check for rifampicin, carbamazepine, phenytoin - AVOID (reduce drug levels)
- Check for amiodarone - AVOID with sofosbuvir (fatal bradycardia)

Monitoring:
- HCV RNA at 4 weeks (on-treatment virological response)
- HCV RNA at 12 weeks after completing treatment (SVR12 = CURE)
- LFTs at 12 weeks post-treatment

Counsel: "This medication can CURE your hepatitis C in 12 weeks. 
Take every day without missing a dose. No alcohol during treatment."

Common Prescribing Errors

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SECTION 18 - PREVENTION

Hepatitis A

• Vaccine: Two-dose inactivated vaccine (Havrix/Vaqta); 6-18 months apart; > 95% protective
• Indications: Travellers to endemic areas, MSM, IV drug users, chronic liver disease patients, food handlers, childcare workers
• Post-exposure prophylaxis: Single-dose vaccine OR immunoglobulin 0.1 mL/kg IM within 2 weeks of exposure
• Hygiene: Handwashing, safe water, proper food preparation; boiling water kills HAV

Hepatitis B

• Vaccine: Three-dose recombinant vaccine (0, 1, 6 months); universal infant vaccination recommended by WHO
• Immunogenicity: >95% of healthy adults develop protective anti-HBs; check anti-HBs titre 4-8 weeks after third dose
• Non-responders: Repeat full course; if still no response → check HBsAg (may already be infected)
• Post-exposure prophylaxis:
  • Unvaccinated: HBV immunoglobulin (HBIG) 0.06 mL/kg IM within 96 hours PLUS start vaccine series
  • Known vaccinated responder (anti-HBs ≥10 mIU/mL): no treatment needed
• Perinatal prevention: HBIG + HBV vaccine within 12 hours of birth to infants born to HBsAg-positive mothers; highly effective (>90% protection)
• Screening: Screen pregnant women for HBsAg; high-risk groups; healthcare workers (EASL 2025 guidelines advocate population-based screening)

Hepatitis C

• No vaccine available (quasi-species variability prevents development)
• Prevention: Harm reduction for PWID (clean needles, needle exchanges); safe medical practices; blood product screening; avoid sharing personal items (razors, toothbrushes)
• Treatment = prevention: Cure reduces transmission and prevents disease progression

Hepatitis E

• Vaccine: Hecolin (approved in China); not widely available globally
• Prevention: Safe water and food, sanitation, handwashing; especially important in pregnant women travelling to endemic areas
• No effective post-exposure prophylaxis

Hepatitis D (Delta)

• Prevention by HBV vaccination - HBV vaccine is also HDV vaccine
• Screen HBsAg-positive patients for HDV

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SECTION 19 - PROGNOSIS

By Virus Type

Factors Determining Prognosis in Chronic Hepatitis

• Older age at infection
• Male sex (men progress faster to cirrhosis than women)
• Alcohol use (synergistic liver damage)
• HIV co-infection
• High HBV/HCV viral loads
• HBV genotype C > A (faster progression)
• Advanced fibrosis at diagnosis
• Failure to respond to treatment

• Early diagnosis and treatment
• Achievement of SVR (HCV) or viral suppression (HBV)
• Abstinence from alcohol
• Regular HCC surveillance catches early, resectable tumours

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SECTION 20 - PATIENT COUNSELLING

What to Tell the Patient (in Plain Language)

"Your liver is inflamed because of a viral infection. The good news is that this type of hepatitis almost always gets better on its own within 4-8 weeks. You don't need any special medicines. Here's what you need to do:

• Rest as much as you can
• Drink plenty of fluids
• Eat small, frequent meals - try to avoid fatty food
• Absolutely no alcohol - for at least 6 months, because your liver is still recovering
• This infection can spread to others through your stools - wash your hands very thoroughly after using the toilet
• Come back immediately if you feel confused, drowsy, or your urine gets much darker or you stop urinating - those are danger signs"

"You have a chronic infection of the liver with hepatitis B virus. The virus has been in your body for more than 6 months. Most people with this infection feel completely normal for years, but the virus is slowly damaging your liver.

• We need to start you on tablets [e.g., tenofovir] that will suppress the virus - they won't cure it, but they'll prevent serious liver damage
• You must take the tablet every single day - missing doses can cause the virus to become resistant
• Never stop the tablet without telling your doctor - stopping suddenly can cause a dangerous flare
• Don't drink alcohol - it speeds up liver damage
• You cannot donate blood
• Your household contacts and sexual partner need to be tested and vaccinated
• We will check your blood tests every 3-6 months and do a liver ultrasound every 6 months to look for early signs of liver cancer"

"You have hepatitis C - a virus that's been quietly infecting your liver, possibly for many years. The great news is that we now have medicines that can COMPLETELY CURE hepatitis C in 8-12 weeks with just one tablet a day. More than 95 out of 100 people are cured.

• Once cured, the virus is gone from your blood permanently
• Your liver can even recover some of the damage
• However, if you already have scarring (cirrhosis), you'll still need regular scans to check for liver cancer even after cure
• No alcohol during or after treatment
• Don't share needles, razors or toothbrushes with anyone"

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QUICK REFERENCE SUMMARY

The "10 Questions" Framework Applied to Hepatitis

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MNEMONICS SUMMARY

• Clubbing, Ascites, Flapping tremor (asterixis), Encephalopathy
• Spider naevi, Anaemia, Palmar erythema, Splenomegaly

• DNA > threshold (>2000 IU/mL HBeAg-neg; >20,000 HBeAg-pos)
• ALT elevated (>2x ULN)
• Liver biopsy showing active inflammation
• Threat of cirrhosis (any stage in cirrhosis = treat)

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• Goldman-Cecil Medicine, 22nd Edition, Chapters 134, 135, 328 (Antivirals)
• Harrison's Principles of Internal Medicine, 22nd Edition (2025)
• Park's Textbook of Preventive and Social Medicine, 26th Edition
• Yamada's Textbook of Gastroenterology, 7th Edition
• Washington Manual of Medical Therapeutics (Post-Exposure Prophylaxis)
• Tintinalli's Emergency Medicine, 9th Edition (Acute Liver Failure)
• Basic Medical Biochemistry - Marks, 6th Edition (Pathophysiology)
• AASLD/IDSA Practice Guideline on Treatment of Chronic Hepatitis B (2024)
• EASL Clinical Practice Guidelines on the Management of Hepatitis B (May 2025)

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What Was Covered - Module Summary

Key Teaching Points Highlighted:

1. Definition - Hepatitis is liver cell inflammation with specific patterns (hepatocellular vs. cholestatic) that guide your diagnosis.
2. The "Hepatitis Alphabet" - HAV and HEV spread fecal-orally and never (rarely) become chronic; HBV, HCV, HDV spread parenterally/sexually and CAN become chronic with cirrhosis/HCC risk.
3. Pathophysiology Core Insight - Liver damage in viral hepatitis is caused by the IMMUNE SYSTEM attacking infected cells, not the virus directly. This explains why neonates get chronic HBV (immature immunity) and why immunosuppressed patients can have worse viral loads but less inflammation.
4. The Window Period - In acute HBV, HBsAg may clear before anti-HBs appears. Only anti-HBc IgM is positive - a classic exam and clinical trap.
5. HCV is Now Curable - DAAs (sofosbuvir/velpatasvir, glecaprevir/pibrentasvir) achieve >95% cure in 8-12 weeks. This is one of medicine's greatest achievements.
6. Treatment Thresholds for HBV - Treat when HBV DNA + ALT both exceed thresholds, or any patient with cirrhosis.
7. Red Flags - Rising INR + encephalopathy = acute liver failure = emergency. HEV in pregnancy has 20-25% mortality.
8. Never stop HBV antivirals abruptly - risk of life-threatening rebound hepatitis flare.