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sem 2 Liver and GI > The liver: An introduction to its function > Flashcards

The liver: An introduction to its function Flashcards

1
Q

is the liver the largest organ in the body?

A

no, 2nd largest organ in the body

also the largest gland

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2
Q

biliary tree

A

system of ducts to transport bile out of the liver into small intestine

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3
Q

how is the liver traditionally divided?

A
  • into 2 primary lobes by the falciform ligament

- green sac is the gall bladder with common bile duct delivering bile into the duodenum

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4
Q

blood supply to the lobes

A

each lobe receives its own blood supply

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5
Q

where does the liver gets it’s blood supply?

A
  • 75% of blood supply from portal vein (venous blood coming from GI tract, full of digested products)
  • 25% from hepatic artery
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6
Q

what are the 2 primary cells of the liver?

A

– Hepatocytes (60%), perform most metabolic functions

– Kupffer cells (30%), type of tissue macrophage, phagocytic activity by removing aged/damaged RBC’s, bacteria, viruses and immune complexes

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7
Q

hepatic lobule

A

hexagonal plates of hepatocytes arranged around central hepatic vein – at each of the 6 corners is a triad of branches of the portal vein, hepatic artery and bile duct

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8
Q

flow through the hepatic lobule

A
  • blood enters the lobules through branches of the portal vein and hepatic artery, then flows through small channels called sinusoids that are lined with hepatocytes
  • hepatocytes remove toxic substances (alcohol) from the blood, which then exits the lobule through the central vein (i.e., the hepatic venule)
  • flow of blood is in the opposite direction to the flow of bile.
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9
Q

blood entering the lobule vs blood leaving the lobule

A

blood entering the lobule = oxygen rich

leaving = low levels of oxygen, because hepatocytes along the sinusoids have used up much of the available oxygen

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10
Q

list the biliary system

A 
Bile secreted by hepatocytes 
↓
series of channels between cells (canaliculi)	
 ↓
small ducts 
↓
large ducts 
↓
linked onto common bile duct
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11
Q

How does the liver’s microstructure support its roles?

A
  • Massive surface area for exchange of molecules
  • Sophisticated separation of blood from bile
  • Specific positioning of pumps to achieve specific localisation of materials
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12
Q

kupffer cells acting as a protective barrier

A

as blood flows through intestinal capillaries it picks up many bacteria from intestine.

portal blood filtered through sinusoid and there is the removal of gut bacteria (less than 1% of bacteria entering portal blood succeeds in passing through liver into systemic circulation)

when a bacterium comes in contact with Kupffer cell, in <0.01sec the bacterium passes inward through the wall of the Kupffer cells to become permanently lodged there till it is digested

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13
Q

what is bile?

A

complex greenish yellow fluid made of water, electrolytes and a mix of organic molecules
-organic molecules are bile acids, cholesterol, bilirubin and phospholipids

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14
Q

role of bile

A

– Essential for fat digestion & absorption via emulsification

– Bile + pancreatic juice neutralises gastric juice as it enters the small intestine –> aids digestive enzymes

– Elimination of waste products from blood - bilirubin & cholesterol

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15
Q

what do epithelial ductal cells do?

A

modify the bile through water and bicarbonate-rich secretion

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16
Q

once bile is in the common bile duct what are the 2 possible routes of transport?

A
  • from the common bile duct to duodenum
  • from the common bile duct then diverted via the cystic duct to the gall bladder, where it is concentrated 5-fold and stored
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17
Q

how is entry of bile into the duodenum controlled?

A

opening of the Sphincter of Odii

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18
Q

what is bilirubin?

A

– Yellow pigment formed from breakdown of haemoglobin

– Useless & toxic but made in large quantities and must be eliminated

– The yellow pigment bilirubin is what gives bile its colour

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19
Q

Destruction of Aged RBC

A
  • Dead/damaged RBC’s (life cycle approx 120 days) are digested by macrophages throughout body (predominantly in the spleen)
  • Fe3+ is recycled
  • Globin chains are proteins - these chains are catabolized to various amino acids and then reused
  • Haem cannot be recycled so it is eliminated, converted in a series of steps to bilirubin
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20
Q

Formation & Elimination of Bilirubin

A
  • Haem converted into free bilirubin in a series of steps
  • Released into plasma – carried around bound to albumin
  • Albumin-bound bilirubin is stripped of albumin
  • Free bilirubin absorbed by hepatocytes → conjugated with glucuronic acid
  • Conjugated bilirubin secreted into bile → metabolised by bacteria intestinal lumen & eliminated into faeces/urine
  • Part of the bilirubin is broken down to colourless substances, hepatocytes produce urobilinogen, and colonic bacteria convert this to stercobilinogen - both substances can be oxidised to yellow urinary urobilin and brown faecal stercobilin.
21
Q

when is renal excretion of urobilin and stercobilinogen increased?

A

in cases of hepatitis and other damage to hepatocytes

22
Q

what is jaundice and what can cause it?

A

• Excessive quantities of either free or conjugated bilirubin accumulate in ECF
– this causes a yellow discolouration of the skin, sclera (opaque white fibrous outer layer of the eye) and mucous membranes is observed

23
Q

explain the rare case of “green” jaundice

A

caused by a mutation of the biliverdin reductase gene

  • meant biliverdin was NOT converted to bilirubin
  • built up in the plasma, giving the green colour
24
Q

pathophysiology of Jaundice

A
  1. Pre-hepatic (haemolytic)
  2. Hepatic
  3. Post-hepatic (obstructive)
25
Q

pathophysiology

  1. Pre-hepatic (haemolytic)
A
  • Increased haemolysis (destruction of RBC’s) can cause excess bilirubin and the liver has no capacity to process/conjugate it
  • Unconjugated bilirubin cannot be excreted in urine and remains in circulation
  • At birth and first few days of life there is an increased rate of RBC destruction as fetal Hb is replaced with adult Hb, which results in normal physiological jaundice, and also the liver is bit immature so there’s a delay in processing
  • Light therapy is used to treat cases of neonatal jaundice through the isomerisation of the bilirubin and consequently transformation into water-soluble compounds that the newborn can excrete via urine and stools

All newborns have raised unconjugated bilirubin and in 50-60% of full-term healthy neonates levels rise sufficiently to cause jaundice.

26
Q

pathophysiology

  1. Hepatic
A
  • Problems with hepatocytes e.g. damage to hepatocytes and biliary tree from cirrhosis, drugs, viral infections (hepatitis A,B,C,E & EBV) result in increase in unconjugated & conjugated serum bilirubin
  • Gilbert’s syndrome – congenital disorder where patients have a decreased enzyme that conjugates bilirubin with glucuronic acid leads to increase in unconjugated bilirubin
27
Q

Pathophysiology

3. Post-hepatic (obstructive)

A
  • Passage of conjugated bilirubin into the duodenum is blocked and it leaks into the circulation and urine making it very dark.
    o Get itching & pruritus.
28
Q

role of the liver

A

-metabolizes and excretes many compounds & toxins into bile

-vital in the metabolism & excretion of various substances that can be toxic to body
– Bilirubin, Ammonia
– all steroid hormones, inactivated by conjugation & excretion
– Drugs & exogenous toxins e.g. asprin, paracetamol, ethanol

29
Q

what happens to steroid hormones in the liver

also, how are they excreted

A

– All steroid hormones (oestrogen, androgens, cortisol & aldosterone) & thyroxine are inactivated & catabolised in liver

– Most excreted as glucuronide/sulphate conjugates

30
Q

impairment in liver function can lead to what?

A

overactivity of hormonal system

eg. gonadal dysfunction in men

31
Q

2/3 phases of drug/hormone metabolism in liver:

A

Phase 1
oxidation via cytochrome P450 enzymes, occurs in smooth ER, makes the substrate (more) polar

Phase 2
conjugation to make the substrate (more) water soluble/ conjugated with different groups, eg. glucuronyl (more important), acetyl methyl, glycol, sulphate and glutamate

Phase 3
conjugate substance is eliminated into blood or bile using ATPase pumps

32
Q

do all drugs do phase 1 and 2?

A

no

33
Q

what do the majority of drugs do in terms of the metabolism phases?

A

undergo 1 and 2 sequentially

34
Q

diff pathways of paracetamol metabolism (look at notes for proper info)

A

3 different pathway:

  1. Glucoronidation (phase 2)
  2. Sulphate conjugation (phase 2)
  3. N-hydroxylation & dehydration, then a glutathione conjugation because the intermediate product NAPQI is toxic (phase 1 and 2)
35
Q

paracetamol o/d means what?

A

enzymes that mediate the glucoronidation and sulphate conjugation reactions are compromised, so it goes through the third pathway

however, the glutathione enzymes can become saturated and the toxic intermediate will accumulate - causing liver necrosis and damage to kidneys

36
Q

ethanol metabolism

A
  • alcohol cannot be stored so much be oxidised in the liver in order to get rid of it
  • first step is oxidation of ethanol to acetaldehyde, catalysed by alcohol dehydrogenase containing the coenzyme NAD+
  • excess NADH and acetaldehyde produced by oxidation of ethanol needs to be gotten rid of
37
Q

how is excess NADH gotten rid of?

A
  1. conversion of pyruvic acid to lactic acid requires NADH
  2. used as a reducing agent in two pathways involved in lipogenesis–one to synthesize glycerol and the other to synthesis fatty acids. As a result, heavy drinkers may initially be overweight.
  3. used directly in the electron transport chain to synthesize ATP as a source of energy
38
Q

why might heavy drinkers initially be overweight?

A

excess NADH from oxidation of ethanol involved in lipogenesis - used to synthesis FA and glycerol

39
Q

what is the consequence of using NADH from ethanol oxidation directly in the ETC?

A

This reaction has the direct effect of inhibiting the normal oxidation of fats in the fatty acid spiral and citric acid cycle.

Fats or acetyl CoA may accumulate with the resulting production of ketone bodies

Accumulation of fat in the liver can be alleviated by secreting lipids into the blood stream

The higher lipid levels in the blood may be responsible for heart attacks.

40
Q

what problems can excess acetaldehyde cause? how is this fixed?

A

hepatitis and cirrhosis

-converted to acetate via the enzyme acetaldehyde dehydrogenase (ALDH2) and released harmlessly into the circulation

41
Q

alcohol flush reaction

A

condition in which the face and/or body experiences flushes or blotches, due to an accumulation of acetaldehyde

42
Q

what causes acetaldehyde accumulation and therefore alcohol flush reaction?

A

missense polymorphism of gene that encodes the enzyme ALDH2 - responsible for breaking down acetaldehyde (product of the metabolism of alcohol)

o 50% of Asians have one normal copy of the ALDH2 gene and one mutant copy that encodes an inactive mitochondrial isoenzyme

o A remarkably higher frequency of acute alcohol intoxication among Asians than among Caucasians has been repeatedly shown to be related to reduced activity of the mutant ALDH2-2 isoenzyme.

43
Q

when does alcoholic liver disease occur?

A

after prolonged heavy drinking, typically for at least 10 years, particularly among those who are physically dependent on alcohol

44
Q

Liver problems caused by alcohol include:

A
  • Fatty liver
    o Alcohol abuse can lead to the accumulation of fat within the liver cells
  • Alcoholic hepatitis
    o Excessive use of alcohol can cause acute and chronic hepatitis (inflammation of the liver)
  • Alcoholic cirrhosis
    o Anything which results in severe liver injury can cause cirrhosis. Common causes include excessive alcohol intake, chronic hepatitis B and C infection, intake of certain chemicals and poisons, too much iron/copper, severe reaction to drugs and obstruction of the bile duct
45
Q

what is cirrhosis of the liver

A

a degenerative disease where liver cells are damaged and replaced by scar formation

46
Q

with severe liver disease why might excessive bleeding occur?

A

hepatocytes are important depots for storage of fat-soluble vitamins D, K, E and Vit A

so, liver dysfunction ⇒ fat malabsorption ⇒ vitamin deficiency

vitamin K is essential for the formation of prothrombin and blood clotting factors II, VII and IX

lack of these factors causes excessive bleeding

47
Q

what does liver store

A
  • fat soluble vitamins E, D, K, A
  • vitamin B12 (enough stored to last 2-3 years)
  • folate, required in early pregnancy
  • iron is stored as ferritin by combining reversibly with apoferritin protein, which can be released when needed
48
Q

vit b12 deficiency causes what?

A

pernicious anaemia

49
Q

how does ferritin act as a blood iron buffer as well as a storage system?

A

when Fe in circulating body fluids reaches low level, the ferritin releases Fe

sem 2 Liver and GI (11 decks)

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