Liver Flashcards
3 concepts to know about the liver
- oxygen gradient around the lobule so centrilobular hepatocytes are more susceptible to low o2
- metabolic heterogeneity-centrilobular have high concentration of metabolic enzymes
- bile goes from hepatocytes to portal triad and is an active process
What are effects of the liver being unable to detoxify
- endogenous toxins: ammonia from normal normal gut flora is not converted to urea and ammonia can cross bbb and cause neurological effects-hepatic encephalopathy
- exogenous toxins like chlorophyll for herbivores. Chlorophyll is normally transformed by gut flora to phylloerythrin and excreted into bile but if it’s not (CHOLESTASIS), it circulates in the blood and builds up in the skin, in areas without melanin, the pigment can cause radiation damage when exposed to uv light-photosensitizatiom
What plasma proteins does the liver make and what can a decrease in those proteins cause
Albumin: hypoalbuminemia can cause ascities
Coagulation factors: decreased can result in coagulopathy
What are bile acid tests useful for and what dysfunctions can arise
- useful for congenital PSS: should expect in rise after eating
- will also see it in acquired PSS but with acquired, you already have cirrhosis and is probably already icteric
- non iceteric patients because it will be high before you see icterus
- dysfunction: icterus, fat maldigestion, failure to eliminate toxins normally secreted in bile
Two categories of cholestasis and causes
- extrahepatic or obstructive: tumors, choleliths, pancreatic lesions, fibrosis, parasites
- intrahepatic: hepatocellular damage or swelling blocks canaliculi, fibrosis/cirrhosis, cholangitis
Feline cholangitis lesion
Non suppuration is more common which is lymphoplasmacytic, biliary hyperplasia and fibrosis
Feline hepatic libidos is alp and ggt
Important part of pathogenesis for icterus
Very high alp and normal or mildly elevated ggt
Hepatocellular swelling results in cholestasis and reduced liver conjugation function.
Consequence of low surveillance of hepatoportal blood
Kuoffer cells not removing microbes or antigens—>antigen emit—>hyperglobulinemia
Not removing fdp can leave to dic
How can liver dysfunction cause ascites
- cirrhosis causing portal hypertension and increasing resistance to sinusoidal blood flow
- hypoalbunemia
- secondary effect on renal
What does the lesion for infectious hepatitis look like. Examples of liver abscesses and what’s the clinical consequence
Random distribution, white spots (necrosis, hepatitis)
- omphalophlebitis: ascending infection via umbilical veins
- rumenitis: hematogenous, can go to liver causing necrobacillosis
- importance: condemnation of liver at slaughter, low production, abscess can rupture and bleed and spread bacteria systemically
Causes of cholangitis
Parasitic like liver flukes
Idiopathic or nonsuppurative-lymphoplasmacytic
Bacterial-uncommon, ascending bacteria from GI
Circulatory problems-cause, lesion, pathophy
- passive congestion, chf causing low co, anemia, shock
- blood backs up to central vein and centrilobular, if severe can lead to necrosis because of hypoxia, fibrosis
Congenital portosystemic shunts lesion, consequences
-one big vessel either extrahepatic (more common) and intrahepatic, can lead to high BA after eating, ammonia, small liver (lack of GF)
Acquired PSS causes, lesion, consequences
- causes: cirrhosis/portal hypertension where blood seeks path of least resistance
- many small vessels, extra or intrahepatic
- ammonia, BA
What is cirrhosis and consequences of cirrhosis. Is liver enzymes high? What are the liver lesions like?
- fibrosis and modular regeneration of liver which changes the normal lobular architecture, small liver because scarring, common end of chronic dz
- liver failure, portal hypertension
- liver enzymes can be normal or mildly increased
- macronodular
