Liver Disorders

Question 1

Normal anatomy of liver

Answer 1

Dual blood supply- 25% from hepatic artery (O2), 75% from portal vein
Blood drains from the GI tract, spleen, gall bladder and pancreas into the portal vein which then passes through the liver. Blood from the GI tract drains through the liver (oedema formation causes liver cirrhosis).
Liver is responsible for carbohydrate metabolism and synthesises plasma proteins, albumin, clotting factors, anti clotting factors, protease inhibitors. Also got steroidal hormone metabolism.
Liver has first go at cleaning up blood, absorbing sugars, amino acids, drugs, microbes and toxins from the GI tract.
Storage of vitamin A
Bile synthesis: necessary for fat and fat soluble vitamin absorption
Removes bacteria and toxins in GI tract, attempts to convert non- water soluble sub units into water soluble subs which can then be removed via kidneys

Question 2

Effects of liver injury

Answer 2

Reserved capacity - approx 25% loss to still function
Regenerative capacity stable cells, regeneration and recovery depends on extent and persistence of injury

Cirrhosis: permanent injury

Question 3

Types of injury

Answer 3

Microbes- viral hepatitis 
Toxins- aflatoxins
Drugs- paracetamol
Alcohol
Heavy metals- iron, copper

Question 4

Responses to infectious or toxic injury

Answer 4

Fatty change (steatosis): liver cells becomes infiltrated with fat, forcing organelles out. Mainly reversible. Caused by chronic alcoholism, malnutrition, diabetes, Cushing's syndrome. 
Hepatitis: inflammation of the liver. Can be drug induced, alcoholic hepatitis, viral hepatitis, autoimmune. Acute- self limited, progress to chronic hepatitis. Fulminant- rapid course, can be fatal within 2-3 weeks. Chronic- slower course, mild to severe. 
Cirrhosis- follows chronic inflammation. Can contain regenerating nodules of heoatocytes, but many bands of fibrous tissue. Causes- alcohol consumption, viral hepatitis etc. can be caused by haemochromatosis, iron overload eg from blood transfusions

Question 5

Effects of cirrhosis

Answer 5

Loss of hepatocytes leads to:
Decreased bile synthesis, fat absorption, fat sol vitamins absorption
Decreased carbohydrate metabolism, lipid metabolism
Decreased production of clotting anti clotting proteins
Decreased removal of steroidal hormones estrogen, progesterone
Decreased metabolism and removal of drugs
Loss of heoatocytes- decreased removal of bilirubin.
Portal hypertension- high BP in portal vein
Number one cause of hepatocellular cancer, primary liver cancer.

Question 6

Portal hypertension

Answer 6

High blood pressure in portal vein.

1. Ascites - oedema in he peritoneal cavity
   - increased hydrostatic pressure in portal vein
   - decreased oncotic pressure in the capillaries
   - loss of albumin
   - lymphatic drainage around liver is blocked by scarring
2. Blocked vessels
   - Splenomegaly- if blood cells get trapped in the digested spleen, loss of RBCs, WBCs, platelets. If all three, pancytopaenia.
   - Gynecomastia- steroidal hormones are not metabolised, due to ascites or bacterial peritonitis.
   - hepatic encephalopathy: personality changes, confusion, lack of consciousness, coma. Decreased hepatic ability to clear toxins from blood. Nitrogenous waste products, ammonia from amino acid metabolism or toxins from GI tract.