WEEK 5 - Hepatic Disorders

• Allows the liver to take out glucose for storage after meals • Allows toxic molecules to be partially detoxified before blood moves on to the heart

Inflammation of the liver characterised by: Hepatomegaly Poor appetite Abdominal discomfort Abnormal liver function Jaundice Clay coloured stool Tea coloured urine

Infection - viral, bacterial, parasitic Alcohol Drugs and toxins Transfusion of incompatible blood

• RNA virus • Transmitted via faecal-oral route (contaminated food/water) • Asymptomatic infection in children • High risk groups: travellers, men who have sex with men

• Transmitted parenterally, sexually and perinatally • DNA virus • Becomes chronic after six months • The earlier the age of infection the greater the likelihood of carrying it for life

• RNA virus • Effects intravenous drug users (spread parenterally) • Becomes chronic after 6 months • Can cause liver failure if left untreated • Only 1 in 4 will recover

• RNA virus • Can only occur in people with Hep B • Can be prevented with Hep B vaccine as they share molecules of their viral coats • Causes a more severe infection • Spread parenterally, sexually and perinatally (same as Hep B)

• No vaccine, has many strains • Linked to undercooked meat and seafood • Spread via faecal-oral route

• Structurally similar to Hep C • Little or no symptoms • Spread parenterally, sexually and perinatally

• Causes direct cellular injury: necrosis and scarring of hepatocytes, hyperplasia and infiltration by mononuclear phagocytes • Leads to an immune response that damages and obstructs the bile ducts

Necrosis Encephalopathy Liver failure Death

• Abnormal LFTs = raised AST (aspartate transaminase) and ALT (alanine transaminase) • ALP = biliary system obstruction (lines the biliary duct) • LFTs may be in normal range in chronic liver disease

• Incubation period - most infectious during this time • Prodromal phase - early, non specific syndrome: fatigue, GI disturbances, weight loss, anorexia, headache, rash, fever, jaundice (last step) • Icteric phase - jaundice, yellow skin, itching, tea coloured urine, clay coloured stool, fatigue, hepatomegaly • Recovery phase - jaundice and other S&S subside, liver function returns to normal, full recovery in most people

Not based on symptoms alone as they are nonspecific • Blood tests for virus-specific antibodies • HBsAg - Hep B specific antigen LFTs for liver function indication

• Restriction of physical activity • Low fat and high carb diet • Smaller, more frequent meals to spread out metabolism • Hand washing and avoid contact with bodily fluids (no real treatment)

• HepB: treatments to slow progression - HepC: curable with 95% success rate

• Neurological impairment secondary to hepatic dysfunction - Characterised by neural disturbances due to increased ammonia levels

• Ammonia is a byproduct of protein metabolism • Inability of the liver to detoxify ammonia = ammonia build up = reaches the brain via the BBB • Ammonia is metabolised into glutamine - interferes with neurotransmitters, astrocyte oedema = brain herniation, oedema, death

• Hx of liver disease in addition to: • Signs and symptoms • Blood tests (for high ammonia levels)

• Fluid and electrolyte correction • Restrict dietary protein • Neomycin (eliminates bacteria for protein metabolism) • Lactulose (promotes excretion of ammonia)

Occurs at the end of chronic liver disease Irreversible inflammatory condition where liver tissue is replaced by dysfunctional fibrotic tissue

• Alcoholic cirrhosis • Biliary cirrhosis • Post-necrotic cirrhosis • Metabolic cirrhosis

Poorly understood • Fibrosis due to inflammation and necrosis • Functional hepatocytes replaced by scarred nodules • Leads to a hard, dysfunctional liver • Obstruction to vascular network reduces the blood flow to the liver and may lead to portal hypertension • Biliary duct obstruction leads to bile stasis and leakage of bile = necrosis of hepatocytes, jaundice and pain

Metabolism of alcohol produces acetaldehyde = damages hepatocytes, causes inflammation