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24 Cards in this Set
- Front
- Back
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List some causes of cirrhosis |
- Alcoholic liver disease, occurs in 10-20% of heavy drinkers - Fatty non-alcoholic liver disease. Fat builds up and causes scar tissue - Chronic hepatitis C or B - Primary biliary cirrhosis - Hereditary haemochromatosis. Iron deposition. - Wilson's disease. Chrome deposition. |
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Define cirrhosis |
Represents the end stage of chronic liver disease in which much of the functional liver tissue is replaced by fibrous tissue. |
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What changes characterise cirrhosis? |
Diffuse fibrosis and conversion of the liver architecture into nodules containing proliferating hepatocytes surrounded by fibrous tissue Formation of nodules forms a balance between regenerative activity and restrictive scarring Fibrous tissue that replaces normally functioning liver tissue forms constrictive bands that disrupt flow in the vascular channels and biliary duct systems of the liver |
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Describe blood flow round the liver |
The liver has a high blood flow and low vascular resistance. The pressure in the portal vein leading into the liver is ~9mmHg Pressure in the hepatic vein leading from the lvier and to the vena cava is ~0mmHg Cirrhosis of the liver greatly increases resistance to blood flow |
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What is portal hypertension? |
Increased resistance to flow in the portal venous system and sustained increase in portal venous pressure |
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What are the 3 types of portal hypertension and what causes them? |
1. Prehepatic. Obstructive thrombosis, narrowing of portal vein before it enters the liver, massive splenomegaly with increased blood flow. 2. Posthepatic. Right sided heart failure and hepatic vein outflow obstruction. 3. Intrahepatic. Main cause in cirrhosis |
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Why is portal hypertension important? |
Main clinical consequences arise from the increased pressure and dilation of venous channels behind obstruction In addition, collateral channels open that connect the portal circulation with the systemic venous circulation |
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What are ascites? |
An increase in fluid in the peritoneal cavity - Only becomes evident when >500mL have accumulated - Amount can be great enough to distend the abdomen and cause breathing difficulties Fluid is generally serous, containing <3g of protein and a concentration of solutes similar to blood. |
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What is thought to cause ascites?
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Increased hydrostatic pressure due to portal hypertension
Water and salt retention by the kidney Decreased colloidal osmotic pressure due to impaired synthesis of albumin by the liver |
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How can ascites be treated?? |
Main focus is dietary restrictions and diuretics. Some restriction of water intake. Distal tube diuretics e.g. amiloride inhibits aldosterone dependent sodium reabsorption Loop diuretics e.g. furosemide act on descending loop to inhibit sodium and chloride reabsorption. |
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Why does spenomegaly occur in portal hypertension? What are its systemic consequences? |
Blood is shunted into splenic vein. Spleen often accumulates a number of blood elements, developing hyperspleenism. Formed elements in blood decrease in life span and so in number. Leads to anaemia, thrombocytopoenia and leukopoenia. |
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Tell me about portosystemic shunts |
As venous blood flow through the liver becomes obstructed, pressure in the portal veins increases. Large collateral veins form between portal and systemic veins that supply the lower rectum and oesophagus, and the umbilical veins of the falciform ligament that attach to the anterior wall of the abdomen |
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How do haemorrhoids form? |
Collaterals between inferior and internal iliac veins may give rise to haemorrhoids |
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How do caput medusae form? |
Foetal umbilical vein is still present in many patients. Forms a channel on anterior abdominal wall. Dilated veins around the umbilicus make up the caput medusae |
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How do oesophageal varices form and why are they dangerous? |
Collateral channels connecting the portal and coronary veins Reversal of flow and thin walled varicosities form in the submucosa of the oesophagus These varices are prone to haemorrhage, producing massive and sometimes fatal haemorrhage Impaired hepatic synthesis of coagulation factors and decreased platelet levels may further complicate control of oesophageal bleeding |
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How can oesophageal varices be treated? |
Non selective beta adrenergic blocking drugs e.g. propanalol, nadalol Reduce portal venous pressure be decreasing splanchnic blood flow, thereby decreasing blood flow in collateral channels |
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What is hepatorenal syndrome? |
Functional renal failure sometimes seen during terminal stages of liver disease with ascites Characterised by increasingly high levels of nitrogen containing compounds in blood, increased serum creatinine levels and oliguria Thought to be due to decreased renal blood flow |
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What is hepatic encephalopathy? |
CNS manifestation of liver failure Characterised by neural disturbances ranging from lack of mental alertness to confusion, coma and convulsions. |
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What causes hepatic encephalopathy? |
Liver loses its detoxifying capabilites and there is an accumulation of neurotoxins in the blood. Ammonium is produced by bacterial degradation of proteins and amino acids in the gut. Ammonium normally diffuses into portal blood and converted to urea in the liver. When intestinal blood bypasses the liver, or the liver is unable to detoxify, ammonia moves into the general circulation and then the cerebral circulation. |
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How can hepatic encephalopathy be treated? |
A non-absorbable antibiotic such as neomycin may be given to eradicate bowel bacteria. Alcohol should be eliminated. Prevent infections. Provide sufficient calories and carbs to prevent protein breakdown. |
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What are the 3 stages of ALD? |
Steatosis Hepatitis Cirrhosis |
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What changes are seen in steatosis? |
Accumulation of fat in liver. Liver becomes yellow and enlarged, with fat globules seen in histology. Increased NADH:NAD ratio causes fatty changes and lactic acidosis Reversible changes if alcohol intake discontinued |
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What changes are seen in hepatitis? |
Characterised by inflammation and necrosis of liver cells, initiated by TNF-a, IL-6, IL-8 This is linked to increased intestinal permeability and TNF-a, which triggers apoptotic pathways Key signs include jaundice, fever, hepatic tenderness, anorexia, nausea, ascites and liver failure. |
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What changes are seen in cirrhosis? |
Cirrhosis is late stage, irreversible liver disease, marked by inflammation, fibrosis and damaged membranes, preventing detoxification in the body.
The early cirrhotic liver has fine, uniform nodules on its surface With further cirrhosis, regenerative processes cause the nodules to become larger and more irregular Mallory bodies are an inclusion found in the cytoplasm of the hepatocytes, from damaged intermediate filamentes in the hepatocytes - appear pink on H&E staining. |
