3 liver and gall bladder function Flashcards

1
Q

describe the hepatic portal blood supply

A
  • blood supply in series
  • all organs’ drainage (deoxygenated) will be screen by liver before entering vena cava via hepatic vein
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2
Q

describe the liver structure

A

organised into lobule that are delineated into vascular and bile channels

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3
Q

how much biles does the liver produce a day

A

150-250mls

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4
Q

what are secreted by hepatocytes? (consituents of bile)

A
  • Bile salts: same as bile acids
    • Emulsification of fat droplets
  • Phospholipids (lecithin)- maintain bile
  • Bile pigment (bilirubin)
  • Cholesterol (bile is major site of secretion)
  • Inorganic ions- secrete bicarbonate ions, maintain fluid nature of bile
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5
Q

What does bile salts undergo?

A

enterohepatic recycling

reabsorbed actively in ileum, reclaim 95%, goes to portal venous system then in liver the hepatocytes can reclaim bile salts

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6
Q

what are bile pigments are major breakdown product of?

what does it combine with in the liver and why?

A

heamoglobin

glucuronic acid- increases polarity and solubility in water

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7
Q

what happens to bile pigments when acted upon by bacteria?

what happens to the product

A

in the colon, produces urobilinogens

some taken up by blood, excreted in feces and kidneys (as urobilin- yellow)

some converted to stercobilin (brown pigment in feces)

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8
Q

discuss inorganic secretion in bile

A

osmotic effect of bile acid secretion

Some reabsorption/further secretion by duct cells (dependent on rate of flow).

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9
Q

what is the rate of bile production dependent on?

A

hepatocyte secretion

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10
Q

what happens to bile during resting conditions (fasting)?

A

flow to duodenum prevented by sphincter of oddi

so enters gall bladder for storage

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11
Q

what happens to bile in gall bladder

A

become concentrated due to reabsorption of salt and water in the gall bladder

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12
Q

what happens to bile after a meal

A

neural influences and CCK- released in response to the presence of fat in duodenum

relaxes sphincter of Oddi and contracts gall bladder allowing bile to pass into duodenum

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13
Q

how are gallstones produced

A

cholesterol crystallisation from bile salts

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14
Q

discuss metabolism in the liver

A
  1. fructose and galactose converted into glucose
  2. glucose in liver taken up as glycogen, some coverted to TAG
  3. fats combine with protein fraction and released as lipoproteins (VDL, HDL, LDL)
  4. remainder glucose taken up by adipose tissue and muscle
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15
Q

metabolism in the liver- what does it synthesise

A

albumin- plasma protein, clotting factors,

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16
Q

important nutrients that the liver stores

A

vitamin ADEK (fat soluble), iron and copper

17
Q

why is liver a site of detoxofication and of what

A

Multiple enzyme system (cytochrome P450) allows modification of chemical structures, aim is generally to increase water solubility

  • Endogenous* e.g. insulin, glucagon, aldosterone, female sex hormones
  • Exogenous* e.g. drugs (some converted to active compound, some lost to first pass metabolism- must decrease dosage in LF due to decreased first pass metabolism)
18
Q

mechanisms involved in detoxification

A

Phase 1: oxidation/ reduction (increase reactivity)

phase 2: conjugation with

Amino acid, sulphate, glucuronic acid, acetic acid

(increase water solubility and excretion through kidneys)

methylation

19
Q

Jaundice

A

biluribin accumulation in plasma (>50 mM) – produces yellowing of skin, sclera and mucous membranes. May produce kernicterus – deposits of pigment in brain leading to nerve degeneration.

20
Q

causes of jaundice

A
  1. haemolytic jaundice - excessive haemolysis of red blood cells (overwhelms liver capacity for excretion of biluribin). (Pre hepatic jaundice)
  2. intrahepatic jaundice – defect in uptake or conjugation or secretion of biluribin by hepatic cells (common in acute hepatitis).
  3. obstructive jaundice – blockage of bile ducts.
  4. Physiological (not pathological) jaundice of the new born – babies have a poor capacity for conjugating biluribin.

ESP pre mature as liver immature

21
Q

types of hepatitis

A

Acute hepatitis: viral infections – hepatitis A, B, C

Drugs (e.g. paracetamol)

Chronic hepatitis (>6 months duration): viral infections – hepatitis B, C

22
Q

cirrhosis

A

Necrosis of liver cells – replaced by fibroblasts

caused by alcohol, hep B and C

no reversible treatment- stop cause, transplant and treat main cause