HPB diseases Flashcards

1
Q

cells of the liver

A

hepatocytes - metabolism
Kuppfer cells - inflammatory response
Stellate cells - responsible for fibrosis

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2
Q

the liver ‘digestion’

A

carbs: storage and release of glucose, formation of glycogen
Lipids: fatty acid metabolism & synthesis of lipoproteins
Protein: synthesis of albumin, transport proteins, proteases, clotting factors, acute phase proteins

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3
Q

bilirubin

A

bilirubin comes from the breakdown of heamoglobin
unconjugated bilirubin is hydrophobic strongly albumin bound, and is not excreted in the urine
conjugation makes it water soluble so it can then be excreted in urine or bile (giving urine its brown colour)
conjugated bilirubin is metabolised by gut flora to urobilinogen and some is resorbed (EH circulation)

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4
Q

unconjugated hyperbilirubinaemia

A

increased delivery of hamoglobin - haemolysis e.g haemolytic anaemia
ineffective eryhtropoesis - deficiendy of B12, folate, iron, sideroblastic anaemia
heamatoma - trauma
failure to cinjugate bilirubin - Gilberts

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5
Q

Sideroblastic anaemia

A

bone marrow produces ringed sideroblast rather than erythrocytes

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6
Q

conjugated hyperbilirubinaemia

A

acute hepatocellular dysfunction - viral hep, drugs, alcoholic hep, hepatic ischamia/hypoxia
chronic hepatocellular dysfunction
biliary obstruction - stones, carcinoma pancreas, bile duct disease

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7
Q

model of liver disease

A

acute hepatitis–>chronic hep–>hepatic fibrosis–>cirrhosis

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8
Q

features of acute hepatitis

A
lethargy
jaundice
RUQ pain
disordered clotting
encephalopathy
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9
Q

features of chronic hepatitis

A

usually none
occasional fatigue and non-specific Sx
often a chance finding

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10
Q

Cirrhosis

A

fibrotic tissue disrupts hepatic architecture - venous inflow dammed back leading to portal hypertension. hepatocyte function is deregulated
disorganised hepatocyte regeneration - hepatocyte function deregulated, and constant stimulation to regenrate
this leads to nodules of hepatocytes surrounded by fibrosis - cirrhosis
increased risk of hepatoma

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11
Q

metabolic effects of cirrhosis

A

reduced synthetic capacity (albumin, clotting factors, protein)
reduced clearance of waste products (jaundice, encephelopathy)
portal HTN (ascites, varices, splenomegaly)

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12
Q

further effects of cirrhosis

A

risk of hepatoma
vascular dilatation in splanchnic bed (abdo viscera), leading to central hypovolaemia, increasing RAS, causing salt and watre retention
fluid retention and vulnerability to renal clampdown
failure of sex hormone metabolism

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13
Q

causes of cirrhosis

A

alcohol
NAFLD/NASH (non alcoholic steatohepatitis)
autoimmune (PBC, hep)
hereditary (wilson’s, heamachromatosis, alpha-1-antitrypsin deficiency)
chronic viral infection (HBV, HCV)
cryptogenic

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14
Q

alcoholic hepatitis

A

if Maddrey score >32, 50% mortality at 1 month

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15
Q

pancreatic disease

A
acute pancreatitis (alcohol, stones, familial, drugs)
chronic pancreatitis: pain, exocrine insufficuency, endocrine insufficiency
Cancer
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