week 2 Flashcards

1
Q

list liver functions

A

amino acid, carbohydrate and lipid metabolism
storage of proteins, glycogen, vitamins and metals
plasma protein and enzyme synthesis
detoxification
production of bile
immune functions

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2
Q

components of portal triad

A

hepatic artery
portal vein
bile duct

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3
Q

three features of cirrhosis

A

diffuse process with fibrosis and nodules

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4
Q

components of bile

A
bile pigments (bilirubin - haemoglobin breakdown product)
bile acids/salts - cholesterol-based 
mucin
bicarbonate
cholesterol, phospholipids
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5
Q

haem breakdown to bilibrubin

A

haem broken down to biliverdin by haem oxygenase
biliverdin converted to bilirubin by biliverdin reductase
unconjugated must be bound to albumin

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6
Q

conjugation of bilirubin

A

ligandin presents UB to glucuronic acid
occurs in liver
UB enters hepatocytes via sinusoidal bilirubin transporter
UDP glucuronyl transferase converts UB to CB

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7
Q

pathway of conjugated bilirubin out of body

A

bilirubin to urobilinogen in small intestine
some goes to large intestine and is converted to stercobilin - in faeces
some goes to liver via portal vein and is converted tp urobilin in kidney - in urine

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8
Q

pre-hepatic jaundice

A
elevated haemolysis
more haemoglobin 
more bilirubin produced - unconjugated  - hyperbilirubinarmia 
large increase in UB
CB is normal or slight increase
no bilirubin in urine
increase of urobilinogen and stercobilin
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9
Q

hepatic jaundice

A

could be:
impaired uptake of CB
impaired conjugation of bilirubin
impaired transport of CB into bile canaliculi
increase in CB and UB
increase in bilirubin and urobilin in urine
stercobilin normal

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10
Q

post-hepatic jaundice

A
obstruction of hepatic, cystic or common bile duct - cholestasis
gall stones 
pancreatitis - swelling can block
pancreatic tumours
UB normal 
large increase in CB 
large increase of bilrubin in blood
urobilin in urine is absent 
stercobilin in faeces is absent
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11
Q

carbohydrate metabolism in the liver

A

storage as glycogen and released in glycogenolysis
gluconeogenesis - synthesis of glucose from other sources eg lactate, pyruvate, glycerol, alanine
glucose as an energy substrate - glycolysis, citric acid cycle, synthesis of FA and TG
conversion of fructose and galactose to glucose phosphates

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12
Q

lipid metabolism in the liver

A

mitochondrial beta oxidation of short chain fatty acids
synthesis of FA, TG, CHOL, phospholipids and lipoproteins
cartnitine acyl transferase allows FAs to enter mitochondria

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13
Q

protein metabolism in the liver

A

most circulating proteins are synthesised wholly or largely by liver
albumin, glycoproteins
glycation of protein

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14
Q

breakdown of RBCs

A

hb broken down into
haeme - converted to bilirubin
globins - broken into amino acids and recycled
iron - bound by transferrin and returned to iron stores in the liver or bone marrow

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15
Q

inherited metabolism disease presenting with acute onset liver failure

A

neonatal to 3 years
episodic vomitting since neonatal period, possible failure to thrive, possible family history
abnormal stress such as infection, fasting, exercise
progressive encephalopathy and anicteric multisystem failure and acidosis

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16
Q

what can be measured in a LFT

A
bilirubin
albumin
alanine aminotransferase (ALT)
aspartate aminotransferase (AST)
alkaline phosphatase
gamma glutamyl transferase (y-GT)
total protein
17
Q

role of AST and ALT in gluconeogenesis

A

they catalyse the transfer of amino groups from aspartic acid or alanine to ketoglutaric acid to produce oxaloacetic acid and pyruvic acid respectively

18
Q

function of (y-GT)

A

responsible for the transfer of glutamyl groups from gamma-glutamyl peptides to other peptides or amino acids

19
Q

LFTs in hepatocellular disease v cholestatic disease

A

hepatocellular - AST >3x url, ALP<2x url

cholestatic disease - AST <3x url, ALP >2x url

20
Q

gilberts syndrome

A

genetic defect on chromosome 2 for the locus coding for the UGT-1A1 protein
this protein is involved in converting UB to CB

21
Q

5 Fs for gall stones

A
female 
fair
fertile
forty
fat
22
Q

3 main types of gallstones

A

cholesterol stone - usually solitary, oval and large
bile pigment stone - multiple, irregular, hard and associated with chronic haemolysis
mixed stones - most common, multiple, multi-faced, laminated structure with layers of cholesterol, bile pigment and calcium salts

23
Q

pathology of gallstones

A

cholesterol supersaturation
biliary stasis - occurs during periods of fasting or starvation
increased bilirubin secretion - can be due to increased RBC breakdown in disease or failure of hepatic conjugation

24
Q

acute cholecystitis

A

impacted stone in gallbladder leading to GB oedema/inflamation and bacterial infection
raised inflammatory markers, sometimes normal LFT, can have jaundice
murphy’s sign - extreme tenderness over GB fundus

25
Q

curvoisier’s law

A

in the presence of a palpable enlarged gallbladder which is non-tender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones

26
Q

LFTs in biliary obstruction

A

ALP increased early - often associated with rise in GGT
bilirubin rises steadily
AST/ALT can be elevated in obstructive jaundice bus is much less prominent