MET1 Flashcards
What is oral lactulose used to treat? [1]
Constipation
Explain what a Fibroscan measures and how this occurs [2]
Non invasive procedure to assess the health of the liver.
Probe is placed on the surface of the skin. Elastic wave & ultrasound: get a measure of stiffness of the liver – indicates scarring / fibrosis: leads to cirrhosis and liver cancer
What type of imaging is a fibroscan? [1]
Ultrasound
When is ALT released? [1]
ALT released when liver cells lyse – higher in liver failure than other types. ALT is released in other organs, so the ratio can be used to determine liver failure
What is pabrinex and explain which pathology it may prevent by providing it [2]
Pabrinex: provides additional vitamins B and C to correct deficiencies that may have occurred. Incudes Thiamine. Thiamine deficiency can lead to Wernicke Encephalopathy
Desribe the action (and site of action) of terlipressin
- Terlipressin: is a synthetic analogue of vasopressin, which is an endogenous neurohormone that acts as a vasoconstrictor – maintains pressure for the kidneys
When is terlipressin indicated? [1]
oesophageal varices.
How do you treat Hepatic Encephalopathy? [1]
Lactulose: clears toxins from your blood by leading to frequent bowel movements, with less time for ammonia absorption and increased fecal nitrogen excretion.
When perfoming an ascites tap, what structure do you need to avoid?
- Ascites tap: performed in the right or left lower quadrant of the abdomen. Need to avoid inferior epigastric artery which runs within the rectus sheath approximately 4-8cm from the midline. Drain the abdomen of fluid
INR testing measures the function of which clotting factors? [4]
What is normal INR? [1]
Does high or low INR cause longer blood clotting time? [1]
- INR testing: The INR measures the function of a limited number of clotting factors (fibrinogen, II, VII, IX, X).
Normal INR is 1.0
The higher your PT or INR, the longer your blood takes to clot
What are the main main effector cells of liver fibrosis? [1]
stellate cells
Explain the difference between compensated and decompensated cirrhosis
Compensated cirrhosis:
1. Liver function is preserved
2. May be asymptomatic but still have increased risk of e.g liver cancer
3. no evidence of complications related to portal hypertension, such as ascites, gastro-oesophageal varices and variceal bleeding, hepatic encephalopathy, and/or jaundice
Decompensated cirrhosis
1. Complications of liver dysfunction: umbrella term for a spectrum of disease
2. reduced hepatic synthetic function and portal hypertension including ascites, gastrooesophageal varices and variceal bleeding, hepatic encephalopathy, and/or jaundice.
Describe the pathophysiology of cirrhosis [3]
State 4 disease it can lead to [4]
Hepatic fibrosis leads to cirrhosis with nodule formation. Prevents regeneration
* Activation of hepatic stellate cells: cause accumulation of collagen type I and III in the hepatic parenchyma and space of Disse
* Stellate cells also become more contractile
* Accumulation of collagen causes altered exchange between hepatocytes and plasma
* Disrupts blood flow and causes increased pressure in the portal venous system: portal hypertension, causing:
i. Ascites
ii. Gastro-oesophageal varices
iii. Rectal varices
iv. Promotes the diversion of nutrient carrying blood away from the liver and cause hepatic encephalopathy
Explain the results
Low Hb, Low plts and High INR: liver disease causes coagulation disorder leading to bleeding and subsequent anaemia.
Low albumin: the liver makes less albumin leading to deviations of the equilibrium between osmotic pressure and hydrostatic pressure in the blood vessels. Low albumin along with portal hypertension, results in the patient suffering from ascites and oedema. Albumin is also a marker of nutritional status.
High bilirubin: bilirubin (waste product from the breakdown of RBC). The liver has reduced ability to conjugate bilirubin, so it can’t be excreted, leading to high levels being present in blood. This causes jaundice
.
High ALP, AST, ALT and GGT: these liver enzymes are present at higher levels in the blood when leaking out of dying hepatocytes. Not extremely as liver was previously damaged by HCV.
High urea: main nitrogenous breakdown product of protein metabolism. High urea due GI bleeding being digested as a “protein rich meal”.
Low end of normal glucose: liver is unable to maintain blood glucose level due to damage.
Why are elevated levels of ALT & AST used to detect liver disease? [2]
Aminotransferases are enzymes contained in hepatocytes and leak into the blood with liver cell damage. Two enzymes are measured:
Aspartate aminotransferase (AST) is primarily a mitochondrial enzyme (80%; 20% in cytoplasm) and is also present in heart, muscle, kidney and brain. High levels are seen in hepatic necrosis, MI, muscle injury and congestive cardiac failure.
Alanine aminotransferase (ALT) is a cytosolic enzyme, more specific to the liver, so that a rise only occurs with liver disease, when liver cells lyse and release this into the blood.
