Liver diseases Flashcards
why does alcohol cause depositions of fat in the liver
alcohol is oxidised by way of alcoholic dehydrogenase via NAD to NADH. this results in NAD depletion in the liver. this means fatty acids cannot be oxidised. hence the NAD deficiency results in accumulation of fats in the liver.
chronic depositions of this fat can cause chronic damage to the liver resulting in cirrhosis
what is bridging necrosis
when the necrosis in the liver extends from the central veins to the portal tracts or across adjacent portal tracts.
how does acute liver failure manifest
nausea, vomiting and jaundice, also ALT raise. encephalopathy can be present.
ALT going down may not be a sign of improvement, rather a sign that the liver is fucked and doesn’t actually have much tissue left
what is liver failure in chronic liver disease most often associated
advanced fibrosis and cirrhosis.
what is cirrhosis
presence of parenchymal nodules surrounded by dense bands of fibrosis throughout the liver. this results in the liver surface taking on a more bumpy appearance
what does cirrhosis present as
anorexia, weight loss, weakness and symptoms of acute liver failure.
death from this is most commonly due to hepatic encephalopathy or bleeding from the torn oesophageal varices.
what are the characteristic signs of alcoholic damage to the liver cells
ballooned hepatocytes, neutrophil infiltration into the hepatoctyes, and mallory bodies.
whats the normal pathway for bilirubin production and excretion
Bilirubin is an end product of haem degradation that is processed by the liver and excreted in the bile. Haem is converted to unconjugated bilirubin in the blood where it is then bound to albumin for transport to the liver. Then in the liver it is conjugated. The bilirubin is then excreted in bile. Most bilirubin is then deconjugated in the gut lumen by bacteria and degraded to urobilinogens. The urobilinogens and the rest of the bilirubin is then excreted in the faeces.
what are mallory bodies
clumped keratin filaments in the cytoplasm of the hepatocyte as opposed to ot being evenly distributed.
whats alcoholic steatofibrosis
hepatisis stimulating the stellate cells to intiitate fibrosis.
starts around the central vein and wraps around the centrilobular hepatocytes in a chicken wire fence pattern. eventually spreading to portal tracts resulting in cirrhosis
what most commonly causes a peptic ulcer
helicobacter pylori. gram negative bacillus
how does the helicobacter cause a peptic ulcer
its enterotoxin causes excess secrtion of acid and inflammation of the area, resulting in destruction of the membrane and then ulceration.
why can the helicobacter pylori survuve in the stomach
urease enzyme which makes ammonia to neutralise the acid secretions from the stomach
whats the trreatment of peptic ulcer
Triple therapy treatment of omeprazole, and two antibiotics.
what are the 4 histological markers of peptic ulcers
- The most superficial layer of necrotic debris or Slough (Sl) (usually digested by gastric acid) so the base of the ulcer appears clean
- A layer of acute inflammatory infiltrate rich in neutrophils
- A layer of chronic mononuclear infiltrate and vascular (V) granulation tissue (healing starts in a chronic ulcer)
- Granulation tissue matures into a Fibrous (F) Scar (Sc) in the depth of the ulcer
