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GI core conditions > ACUTE & CHRONIC HEPATITIS > Flashcards

ACUTE & CHRONIC HEPATITIS Flashcards

1
Q

Acute hepatitis is defined as…

A

Acute parenchymal liver damage that resolves within 6 months, or can progress to chronic hepatitis and rarely acute hepatic failure

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2
Q

Chronic hepatitis is defined as…

A

Hepatitis lasting longer than 6 months. Chronic viral hepatitis is the main cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma.

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3
Q

Who does Hep A (notifiable disease in UK) commonly affect and how does it spread?

A

Children & young adults. Faecal-oral route and arises from contaminated water and food.

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4
Q

Clinical features of Hep A & E (only acute infection)

A

Non-specific symptoms ie nausea and anorexia prior to jaundice. Many recover at this stage, commonly children.

After 1-2 weeks, jaundice occurs with dark urine and pale stool. Enlarged liver, splenomegaly. Recovers within 3-6weeks.

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5
Q

What are the investigation (biochemistry, blood test and serology) results in Hep A?

A

Biochem: Raised AST & ALT precedes jaundice
Bilirubin reflects degree of jaundice. AST reaches maximum 1-2 days after jaundice

Bloods: Leukopenia, raised ESR and prolonged PT

Serology: Anti-HAV IgM = acute infection; IgG antibodies common over 50yrs

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6
Q

What are the management for Hep A infection?

A

Good hygiene, killed by boiling water for 10 mins.

Active vaccination

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7
Q

How is Hep B transmitted?

A

Vertical transmission: mother to child during parturition. Mosts common way.

Horizontal transmission: mainly children through abrasions and close contact. HBV can survive on household items.

HBV transmitted via intravenous route (blood transfusion, drug users, tattooists). Sexual intercourse esp MSM. Virus found semen and saliva.

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8
Q

Which HBV antigens are present in blood?

A

Antigens: HBsAg appears in blood 6 weeks to 3 months after acute infection and then disappears.

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9
Q

Which antibodies are produced against HBV and when?

A

Antibody: Anti-HBs (surface protein) appears late and indicates immunity.

Anti-HBc (core protein) first antibody to appear. High titres of IgM anti-HBc suggests acute & continuing viral replication. IgM anti-HBc may be the only serological indicator of recent infection before rise in anti-HBs and after HBsAg decrease.

Anti-HBe appears after anti-HBc = related to decreased infectivity.

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10
Q

What are the clinical features of Hep B infections in adults?

Hep B infection in children is likely to be acute or chronic?

A

If perinatally acquired, Hep B infection is chronic not acute.

In adults, acute infection more common - nausea, anorexia, jaundice, hepatosplenomegaly. Serum sickness-like immunological syndrome i.e. rashes and polyarthritis affecting small joints unto 25% of cases. Fever.

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11
Q

What is the investigation for Hep B?

What are the specific tests for Hep B?

A

Investigation same as Hep A ==> bilirubin, AST/ALT raised, ESR raised, leukopenia, prolonged PT.

HBsAg cleared rapidly in acute infection so anti-HBc IgM is diagnostic. Patients must be tested for both HBsAg and anti-HBc antibodies if HBV suspected.

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12
Q

What is the prevention of HBV?

A

Avoid risk factors

Vaccination - HBV vaccine added to UK childhood vaccination programme.

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13
Q

What is Hepatitis D mechanism of action?

How is HDV diagnosed?

A

Hep D is activated in presence of HBV.
HDV always occurs as co-infection with HBV.

Diagnosis: confirmed by serum IgM anti-HDV in the presence of IgM anti-HBc.

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14
Q

How is Hep C transmitted?

A

HCV transmitted via blood - v common in haemophilia before blood screening. Common in intravenous drug users.

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15
Q

What is the clinical features of Hep C?

A

Acute infections mostly asymptomatic. Flu-like symptoms with jaundice and raised serum aminotransferases noticeable in routine blood test. Most patients don’t present till years later with chronic liver disease.

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16
Q

What are the serology/ DNA tests for HCV?

A

HCV RNA can be detected from 1-8 weeks after the infection.

Anti-HCV antibodies present 8 weeks from infection.

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17
Q

Prognosis of HCV

A

~90% asymptomatic patients develop chronic liver disease.

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18
Q

What are the clinical features of chronic hepatitis C infection?

A

Malaise & fatigue

Extrahepatic manifestation ie arthritis, cryoglobulinaemia with or without glomerulonephritis

Higher incidence of diabetes and associated with Lichen Planus

Progressive fibrosis leading cirrhosis (risk factors for exacerbation = excess alcohol, HIV, obesity & diabetes)

Once cirrhosis is developed, some go on to decompensated cirrhosis and risk of HCC.

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19
Q

Acute hepatic failure is defined as…

A

Acute liver injury with encephalopathy and deranged coagulation (INR>1.5) in a patient with previously normal liver.

Jaundice ==> encephalopathy varies from:

  1. Hyperacute - 7 days
  2. Acute - 8-24 days
  3. Subacute - 21-26 weeks
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20
Q

Acute liver failure is rare but lift-threatening. What are some of the causes?

A

Most common worldwide = viral (Hep A-E, rarely Hep C, CMV, Herpes simples, EBV, yellow fever)
Paracetamol overdose common in the UK.

Other drugs: NSAIDs,
anti-epileptic (valproate),
immunosuppressant (methotrexate),
antidepressants (amitriptyline, nortriptyline),
antibiotics (doxycycline, erythromycin, nitrofurantoin).

Metabolic causes (alpha-1 antitrypsin deficiency, Wilson’s disease)

Alcohol (fatty liver disease)

Primary biliary cholangitis ; primary sclerosing cholangitis

Haemochromatosis

Auto-immune hepatitis

HCC

21
Q

What does acute hepatic failure look like histological?

A

Substantial multiacinar necrosis

22
Q

What are the clinical features of acute hepatic failure?

A

Jaundiced patients with a small liver and hepatic encephalopathy.

Decreased mental state.

Fetor hepaticas common (strong pear-drop breath smell due to liver failing to filter out toxic substances (sulphur) which ends up in the bloodstream.

Asterexis (liver flap)

Contructional apraxia (can’t connect numbers)

Signs of chronic liver disease i.e. leukonychia, clubbing, palmar erythema, duputren’s contracture, spider naevi, xanthelasma, gynaecomastia etc

Ascites and splenomegaly rare.

23
Q

What is autoimmune hepatitis?

A

Inflammatory liver disease of unknown cause; T-cell mediated and auto-antibodies directed against hepatocyte surface antibodies.

24
Q

Risk factors for autoimmune hepatitis?

A

Female (Bimodal 10-30yrs or >40yrs)

FHx of autoimmune diseases i.e. pernicious anaemia, UC, glomerulonephritis, diabetes mellitus, autoimmune thyroiditis

25
Q

What are signs of autoimmune hepatitis?

A

40% acute hepatitis: fever, malaise, urticarial rash, polyarthritis, pleurisy, glomerulonephritis.

60% chronic hepatitis: asymptomatic or present with gradual jaundice

26
Q

What are the investigations for autoimmune hepatitis?

A

Serum bilirubin, AST, ALT and ALP raised. Hypergammaglobinaemia (esp IgG), auto-antibodies present/.

Anaemia, decreased WBC and platelets suggests hypersplenism.

Biopsy: mononuclear infiltrate of portal and peri-portal areas, necrosis ± fibrosis. Cirrhosis = worse prognosis.

27
Q

How do you diagnose autoimmune hepatitis?

A

Diagnosis by exclusion. Diagnostic criteria based on IgG, autoantibodies & histology.

28
Q

Which autoimmune antibodies are seen in autoimmune hepatitis?

A

Anti-smooth muscle antibodies (ASMA) +ve in 80% ; anti-nuclear antibody (ANA) +ve in 10%. IgG +ve in almost all patients.

29
Q

What is the pathophysiology of alcoholic liver disease?

A

Ethanol is metabolised in the liver ==> increased NADH/NAD ratio.

This results in increased hepatic fatty acid synthesis with decreased fatty acid oxidation ==> leading to accumulation of fatty acid.

Changes in oxidation/reduction also impair carbohydrate & protein metabolism causing centri-lobular necrosis.

TNF-a from kuppfer cells ==> oxygen species ==> tissue injury & fibrosis

30
Q

What is seen in biopsy of fatty liver?

A

Mallory bodies (dense cytoplasmic inclusions)

Mallory bodies are suggestive of but not specific for alcoholic liver disease

31
Q

What are the signs & symptoms of alcoholic liver disease?

A

Signs: Malaise, anorexia, tender, hepatomegaly ± jaundice, bleeding, ascites

Symptoms: diarrhoea & vomiting

Severe if jaundice and hepatic encephalopathy (asterexis) or coagulopathy

32
Q

How do you manage acutely unwell patient with alcoholic liver disease?

A

Screen for infections + ascitic fluid tap (treat for spontaneous bacterial peritonitis)

Stop alcohol (give chlordiazepoxide orally or lorazepam IV) ; smoking cessation

Vitamins: Vit K, Thiamine (to prevent wernicke-korsakoff encephalopathy) or Pabrinex (high dose Vit B)

Nutrition (parenteral)

Steroids

33
Q

How do you investigate alcohol liver disease?

A

Fatty liver:

  1. Bloods: Elevated MCV (indicates heavy drinking), AST, ALT, y-GT
  2. Ultrasound/CT: fatty infiltrations
  3. Liver biopsy: fatty infiltration

Alcoholic hepatitis:

  1. Leukocytosis
  2. Elevated bilirubin, AST, ALT, ALP, PT (prolonged PT may require liver biopsy)
  3. Low albumin
34
Q

What are the causes of chronic liver disease?

A

Metabolic: non-alcoholic fatty liver disease

Alcoholic liver disease

Viral: Hep B ± Hep D ; Hep C ; Hep E (immunosuppressed)

Drugs: Methydopa; isoniazid; ketoconazole, nitrofurantoin

Autoimmune

Hereditary (Wilson’s disease, haemochromatosis)

35
Q

What is wilson’s disease?

A

Autosomal recessive disorder of a copper transporting ATPase ==> impaired copper incorporation into hepatocytes & impaired excretion leads to copper accumulation in liver.

Signs: tremor, kayser-fleischer rings (copper in iris)

36
Q

What is haemochromatosis?

A

Inherited disorder (autosomal recessive) of iron metabolism - increased intestinal iron absorption which leads to iron deposition in liver.

Iron causes fibrosis.

Affects middle aged men more than women (menstrual bleeding protective)

Signs of chronic liver disease, cirrhosis, hepatomegaly, slate-grey skin pigmentation

37
Q

What is cirrhosis?

A

Diffuse irreversible liver damage leading to portal hypertension & liver failure.

Loss of normal hepatic structure with bridging fibrosis & nodular regeneration

38
Q

What are the causes of cirrhosis?

A

Most common cause = alcohol then NAFLD (in the west)

Chronic HBV±HDV/HCV infection

Others:

  1. Genetic disorders: haemochromatosis, a1-antitrypsin deficiency, wilson’s disease
  2. Autoimmune: autoimmune hepatitis, primary biliary cholangitis; primary sclerosing cholangitis
  3. Drugs: amiodarone, methydopa, methotrexate
39
Q

What are the signs of cirrhosis?

A

Leuconychia, clubbing, palmar erythema, dupuytren’s contracture, spider naevi, xanthelasma, gynaecomastia, ascites, hepatomegaly or small liver in late disease, splenomegaly

40
Q

What are the pathological architecture of the liver in cirrhosis?

A

Regenerating nodules separated by fibrous septa & loss of lobular architecture within nodules.

  1. Micronodular cirrhosis: regenerating nodules with uniform involvement of liver (alcohol & biliary tract disease)
  2. Macronodular cirrhosis: variable size nodules within larger nodules (chronic viral hepatitis)
41
Q

When is a liver transplant applicable?

A
  1. Acute liver failure
  2. Chronic liver disease - complications of cirrhosis no longer responsive to therapy
  3. Primary biliary cholangitis
  4. Chronic viral infections (HBV/HCV)
  5. Autoimmune hepatitis
  6. Alcohol liver disease
  7. Primary metabolic disorders
  8. NASH cirrhosis
42
Q

What are the complications of cirrhosis?

A
  1. Portal hypertension & GI bleed
  2. Ascites
  3. Hepatic encephalopathy
  4. HCC
  5. Bacteraemia/sepsis (Spontaneous bacterial peritonitis)
  6. Renal failure
43
Q

What’s the only definitive treatment for liver cirrhosis?

A

Liver transplant is the only definitive treatment for cirrhosis.

44
Q

What are the 3 types of portal hypertension?

A

Pre-hepatic: portal vein thrombosis before the liver

Intrahepatic:
1. Pre-sinusoidal: schistosomiasis; sarcoidosis, primary biliary cholangitis

2.Sinusoidal:
Cirrhosis

Post-hepatic: right heart failure, constrictive pericarditis, inferior vena cava obstruction

45
Q

What happens in portal hypertension?

What are the main sites of collaterals formed?

A

Portal vein is formed by the union of superior mesenteric and splenic veins.

As portal pressure rises (>10-12mmHg), venous system dilates and forms collaterals.

Main collateral sites: gastro-oesophageal junction, rectum, anterior abdomen wall via the umbilical vein, left renal vein, retroperitoneum, diaphragm.

Gastro-oesophageal varies are superficial - high risk of rupture (GI bleed)

46
Q

How do you manage acute variceal bleed?

A
  1. Resus: restore blood volume, blood for group & cross-matching, Hb, PT/INR, creatinine, electrolytes, liver biochem, liver culture. Ascitic tap
  2. Urgent endoscopy
  3. Vasoconstrictor therapy (Terlipressin)
47
Q

Which investigations are carried out in a cirrhotic patient?
Are these values up or down?

A

Bloods:
LFT normal or bilirubin, AST, ALT, ALP, yGT raised.

Later with loss of synthetic function:
Low albumin ± raised PT/INR

Low WCC/platelets indicate hypersplenism.

Find the cause: ferritin/total iron binding capacity, hepatitis serology, immunoglobulins, autoantibodies (AMA, ANA, SMA), caeroplasmin ± copper in pts over 40yrs and a-1 antitrypsin.

Ascitic tap for urgent MC&S if spontaneous bacterial peritonitis suspected

Liver biopsy confirms clinical diagnosis

48
Q

3 main signs of decompensated cirrhosis/liver disease?

A
  1. Jaundice
  2. Ascites
  3. Encephalopathy
49
Q

Which factors result in a decompensated liver disease?

A
  1. Dehydration
  2. Constipation
  3. Covert alcohol use
  4. Infection (spontaneous peritonitis)
  5. Opiate over-use
  6. Occult GI bleed

GI core conditions (11 decks)

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