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Phase 1 Med (Liv) > Liver & friends (summary sheets) > Flashcards

Liver & friends (summary sheets) Flashcards

1
Q

What is a xenobiotic?

A

A foreign chemical substance not normally found or produced in the body which cannot be used for energy requirements

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2
Q

How can xenobiotics be absorbed?

A

Across lungs, skin or ingested

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3
Q

How are xenobiotics excreted?

A

In bile, urine, sweat and breath

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4
Q

Define lipophilic

A

Able to pass through plasma membranes to reach metabolising enzymes

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5
Q

Name 3 features of pharmacologically active compounds?

A
  • Lipophilic
  • Non-ionised at pH 7.4
  • Bound to plasma proteins to be transported in blood
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6
Q

Define microsome

A

A small particle consisting of a piece of endoplasmic reticulum to which ribosomes are attached

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7
Q

What is a microsomal enzyme?

A

An enzyme which is found in a microsome

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8
Q

What is a phase I reaction?

A

Modification - where there may be oxidation, reduction, hydrolysis etc

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9
Q

What is a phase II reaction?

A

Conjugation - when charged species are added to the compounds

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10
Q

In what reactions are microsomal enzymes involved in?

A

Mainly phase I, but may also be phase II

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11
Q

Where are microsomal enzymes located in the cell?

A

On the smooth endoplasmic reticulum

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12
Q

Where are microsomal enzymes located in general?

A

Mainly in the liver hepatocytes, but may be found in the kidneys and lungs too

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13
Q

What is a phase I reaction which is done by microsomal enzymes?

A

Biotransform substances (transformed from one chemical to another)

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14
Q

What is a phase II reaction which is done by microsomal enzymes?

A

Glucuronidation (the addition of glucuronic acid to a substance)

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15
Q

Name 5 things which may induce or inhibit microsomal enzymes

A
  • Drugs
  • Food
  • Age
  • Bacteria
  • Alcohol
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16
Q

Name 3 types of reactions which microsomal enzymes are involved in

A
  • Oxidation
  • Reduction
  • Hydrolytic
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17
Q

In what reactions are non-microsomal enzymes featured in?

A

Mainly phase II reactions

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18
Q

Where are non-microsomal enzymes located?

A

Mainly in the cytoplasm & mitochondria of hepatocytes in the liver, but may be in other tissues

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19
Q

Name 2 features of non-microsomal enzymes

A
  • They are non-specific

- They are non-inducible

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20
Q

What reactions are non-microsomal enzymes involved in?

A

All conjugation reactions except glucuronidation

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21
Q

How are most drugs excreted?

A

By the kidneys

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22
Q

Why is the removal of lipophilic drugs less effective?

A
  • They are passively absorbed

- This is due to the fact they can diffuse through cell membranes with ease

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23
Q

What is the aim of drug metabolism?

A

To make drugs more polar so they can’t get across lipid membranes

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24
Q

Where is the main site of drug metabolism?

A

The liver via Phase I & II reactions, which is sequentially

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25
Q

What is the aim of a phase I reaction?

A

To make the drug more hydrophilic so it can be excreted by kidneys (adding OH group). This means it can be used for conjugation reactions

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26
Q

Define non-synthetic catabolic

A

Chemical decomposition of complex substances by the body to form simpler ones, accompanied by the release of energy

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27
Q

Why do hydrophilic molecules not tend to reach the metabolising enzymes?

A

Since hydrophilic molecules are excreted easily

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28
Q

Name 4 types of oxidation

A
  • Hydroxylation (add OH)
  • Dealkylation (remove CH side chains)
  • Deamination (remove NH)
  • Hydrogen removal
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29
Q

What is reduction?

A

Adding hydrogen (to saturate unsaturated bonds)

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30
Q

What is hydrolysis?

A

To split a molecule into two or more molecules

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31
Q

What is functionalisation?

A
  • Introducing a reactive group to a drug
  • Product tends to be more reactive
  • Small increase in hydrophilicity
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32
Q

What are some functions of cytochrome P450 enzymes?

A
  • Type of microsomal enzyme

- Involved in phase I reactions

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33
Q

How do cytochrome P450 enzymes work?

A

Uses the heme group to oxidise substances

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34
Q

What is significant bout products of P450 enzymes?

A

They are more water soluble

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35
Q

What is the overall reaction of cytochrome P450 reductase?

A

NADPH + H+ + O2 + RH –> NADP + H2O + R-OH

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36
Q

Name 4 things what phase I reactions can do

A
  • Inactivate drugs
  • Further activate drugs
  • Activate drug from pro-drug (inactive form of drug)
  • Make a drug into a reactive intermediate (could be carcinogenic or toxic)
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37
Q

Define synthetic anabolic

A

The synthesis of complex molecules such as proteins & fats, from simpler ones

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38
Q

What is a conjugation reaction?

A
  • Attachment of substituent groups (from molecules of the body)
  • Usually inactive products
  • Catalysed by transferases
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39
Q

What is the purpose of conjugation reactions

A

Significantly increases hydrophilicity for renal excretion

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40
Q

Where do conjugation reactions tend to occur?

A

Mainly in the liver but can occur in other tissues like the lungs and kidneys

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41
Q

What is a glucuronidation reaction?

A

Adding a glucuronic acid group to the drug to make it more hydrophilic

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42
Q

Why might a drug be excreted straight away?

A

Due to it being a polar drug and it usually being excreted unchanged

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43
Q

Define analgesic

A

Used for pain relief

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44
Q

Name 3 things in which iron is essential for

A
  • Haemoglobin
  • Myoglobin
  • Bone marrow
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45
Q

Name 3 sources of iron in the diet

A
  • Beans
  • Meat
  • Egg yolk
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46
Q

Where does the homeostatic control of iron occur?

A
  • In the intestinal epithelium, in the duodenum

- Actively absorbs iron from digested food

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47
Q

How can the fraction of iron absorbed in the duodenum be altered?

A

By a negative feedback mechanism depending on the state of the bodies iron balance

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48
Q

What percentage of ingested iron is absorbed into the blood each day?

A

10%

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49
Q

How are iron ions transported into the blood?

A
  • Actively transported

- Transported into the duodenal intestinal epithelial cells

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50
Q

What is the intracellular store of iron?

A

Ferritin, which is a protein-iron complex

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51
Q

What happens to iron once it has been absorbed into the intestinal epithelial cells of the duodenum?

A
  • Released back into the intestinal lumen
  • At the tips of the villi the ferritin disintegrates into iron
  • Iron is excreted in the faeces
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52
Q

What happens when the bodies store of iron is enough?

A
  • Increased conc. of free iron in plasma and intestinal epithelial cells lead to increased transcription of gene for ferritin
  • Gives an increased synthesis of ferritin
  • Increased binding of Fe
  • Reduction of normal iron in blood
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53
Q

What happens when the bodies store of iron are too little?

A
  • Production of intestinal ferritin decreases
  • Decrease in the amount of iron bound to ferritin
  • Increase in number of unbound iron in blood
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54
Q

What happens to absorbed iron that doesn’t bind to ferritin?

A

Released into blood, where it is able to circulate, bound to the plasma protein transferrin

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55
Q

What is the function of transferrin?

A

Transports iron into the blood plasma to the bone marrow to be incorporated into new erythrocytes

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56
Q

What happens to excess iron once it is in the blood

A
  • Accumulates in tissues

- Most is stored in the Kupffer cells of the liver, in the form of liver ferritin

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57
Q

How is the bodies store of iron divided?

A
  • 50% in haemoglobin
  • 25% in heme containing proteins
  • 25% in liver ferritin
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58
Q

Name 3 types of proteins the liver makes

A
  • Plasma proteins
  • Clotting factors
  • Complement factors
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59
Q

Name 2 plasma proteins

A

Albumin and globulins

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60
Q

What is the most abundant plasma protein?

A

Albumin

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61
Q

What is the function of albumin?

A

Binding and transport of large, hydrophobic compounds

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62
Q

What is colloid osmotic pressure?

A

The effective osmotic pressure across blood vessel walls which are permeable to electrolytes but NOT large molecules

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63
Q

What is colloid osmotic pressure due to?

A

Plasma proteins

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64
Q

How does albumin maintain osmotic pressure?

A
  • It’s presence in plasma means that water concentration of the blood plasma is slightly lower than that of the interstitial fluid
  • Means there is a net flow of water OUT OF the interstitial fluid into the blood plasma
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65
Q

What are Starling forces?

A

Opposing forces which act to move fluid across the capillary wall

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66
Q

Name the 4 Starling forces

A
  • Capillary hydrostatic pressure
  • Interstitial hydrostatic pressure
  • Osmotic force due to plasma protein concentration
  • Osmotic force due to interstitial fluid protein concentration
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67
Q

Name the 2 Starling forces which favour fluid movement OUT of the capillary

A
  • Capillary hydrostatic pressure

- Osmotic force due to the interstitial fluid protein

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68
Q

Name the 2 Starling forces which favour fluid movement INTO the capillary

A
  • Interstitial hydrostatic pressure

- Osmotic force due to plasma protein concentration

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69
Q

How does bulk filtration of fluid out of the capillary at the arterial end occur?

A
  • Hydrostatic pressure from capillary is greater than that from interstitial fluid
  • Interstitial fluid protein concentration is smaller than osmotic pressure due to plasma proteins
  • Outward pressure exceeds the net inward pressure
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70
Q

How does bulk filtration of fluid in the capillary at the venous end occur?

A
  • Capillary hydrostatic pressure has reduced due to resistance encountered as the blood flows through the capillary
  • Net inward pressure exceeds the net outward pressure
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71
Q

How does oedema occur with liver failure?

A
  • Reduction in albumin in blood
  • A decrease in capillary oncotic pressure
  • Less of a difference in water conc. between plasma and interstitial fluid
  • Accumulation of water in interstitial fluid –> oedema
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72
Q

Name 4 conditions which can cause albumin decrease

A
  • Nephrotic syndrome
  • Haemorrhage
  • Gut loss
  • Burns
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73
Q

What is the main function of globulins?

A

Antibody functions

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74
Q

Which globulins are made in the liver?

A

Some alpha/beta globulins

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75
Q

Where are all clotting factors except IV and VIII made?

A

The liver

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76
Q

Where are clotting factors IV & VIII made?

A

Liver sinusoidal endothelial cells. IV is calcium and VIII is von Willebrand factor

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77
Q

Name one function of absorption linked to liver function

A

The liver produces bile salts which are essential for vitamin K absorption (fat soluble)

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78
Q

What is one of vitamin K’s functions, linked to the blood?

A

It is essential to the synthesis of numerous clotting factors (2, 7, 9, 10)

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79
Q

What is a complement factor?

A

A plasma protein which sticks to pathogens and is recognised by neutrophils

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80
Q

What is the function of a complement factor?

A
  • Help mark pathogens to kill

- Plays an important role in the immune response to pathogens

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81
Q

What is protein turnover?

A

The continuous degradation and re-synthesis of all cellular proteins

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82
Q

Give examples of when the rate of protein turn over increases

A
  • When tissue is undergoing structural re-arrangement e.g. gluconeogenesis, severe burns
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83
Q

What are the 2 primary methods of protein breakdown?

A

Lysosomal and ubiquitin-proteasome pathway

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84
Q

Where does lysosomal protein breakdown occur?

A

In the reticulo-endothelial system of the liver

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85
Q

What does the reticule-endothelial system of the liver compromise of?

A

Sinusoidal endothelial cells, Kupffer cells and pit cells

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86
Q

What is the function of sinusoidal endothelial cells in lysosomal protein break down?

A

Remove soluble proteins and fragments from the blood through fenestrations known as sieve plates on their luminal surface

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87
Q

What are sinusoidal endothelial cells important for removing in lysosomal protein break down?

A

Fibrin, fibrin degradation products, collagen and IgG complexes

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88
Q

What happens to proteins once they are in the liver from the sinusoidal endothelial cells in lysosomal protein breakdown?

A
  • The proteins are fused into lysosomes containing lysozyme (hydrolytic enzymes)
  • Broke down into amino acids
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89
Q

What are the functions of Kupffer cells in lysosomal protein breakdown?

A
  • Resident macrophages
  • Phagocytose matter by packaging them into phagosomes in the cell, which contain hydrolytic enzymes
  • Protein broke down into amino acids
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90
Q

Where does the ubiquitin-proteasome pathway occur?

A

Cytoplasm of cells

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91
Q

What is significant about degradation in the ubiquitin-proteasome pathway?

A

It is a selective process

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92
Q

Which proteins are rapidly degraded in the ubiquitin-proteasome pathway?

A
  • Those that are defective because of incorrect AA sequences
  • Those which are damaged to normal function
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93
Q

How come different proteins are degraded at different rates in the ubiquitin-proteasome pathway?

A

Depends on the structure of the protein - if it is denatured it is more readily digested

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94
Q

How can proteins be targeted for degradation in the ubiquitin-proteasome pathway?

A
  • Attachment of a small peptide (ubiquitin)
  • This directs the protein to a protein complex (proteasome)
  • This unfolds the protein and breaks it down into small peptides
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95
Q

Where does amino acid degradation and catabolism occur?

A

Hepatocytes of the liver

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96
Q

What happens to amino acids which aren’t require as building blocks for proteins?

A

Must undergo degradation (degraded into specific proteins)

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97
Q

What is catabolism?

A

The breakdown of complex substances to simpler ones accompanied by the release of energy

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98
Q

What does amino acid catabolism require?

A

The alpha amino group (nitrogen containing) to be removed

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99
Q

What is produced from amino acid catabolism?

A
  • Nitrogen (incorporated into other compounds or excreted)

- Carbon skeleton (can then be metabolised and used in Kreb’s cycle)

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100
Q

What are the 2 main catabolism processes?

A

Oxidative deamination and transamination

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101
Q

What is the main goal of oxidative deamination?

A

Results in liberation of an amino group as free ammonia

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102
Q

What is the only amino acid which undergoes rapid oxidative deamination?

A

Glutamate

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103
Q

What is the mechanism of oxidative deamination?

A
  • AA gives rise to a molecule of ammonia and is replaced by an oxygen atom from water to form a alpha-keto acid
  • The alpha-keto acid can be used in Kreb’s cycle for gluconeogenesis
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104
Q

What are the co-enzymes used in oxidative deamination?

A
  • NAD+ (forward)

- NADPH (backwards)

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105
Q

What enzymes catalyses the reaction in oxidative deamination?

A

Glutamate dehydrogenase

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106
Q

What is the basic principle of transamination?

A

Transfer of an alpha-amino group from amino acid to a keto-acid to form a alpha-keto-acid

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107
Q

What enzyme is used in transamination?

A

Aminotransferase

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108
Q

Where is aminotransferase found?

A

In the cytosol of the mitochondria, mainly in the kidneys and liver

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109
Q

What is the measurement of nitrogen balance used for?

A

A measure of the equilibrium of protein turnover

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110
Q

What is anabolic in terms of nitrogen balance?

A
  • Positive balance (net gain of amino acids)

- Nitrogen intake > nitrogen loss

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111
Q

What is catabolic in terms of nitrogen balance?

A
  • Negative balance (net loss of amino acids)

- Nitrogen intake < nitrogen loss

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112
Q

What is a healthy nitrogen balance?

A

When it is equilibrium

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113
Q

How can a negative nitrogen balance occur?

A

If any of the essential amino acids are missing from the diet

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114
Q

What is the most common cause of positive nitrogen balance?

A

Pregnancy

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115
Q

Give two causes of negative nitrogen balance

A
  • Malnutrition (most common)

- Multiple trauma/extensive trauma

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116
Q

What is the purpose of the glucose alanine cycle?

A

To produce a source of carbons for gluconeogenesis

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117
Q

Where are the enzymes of the urea cycle found?

A

In the liver, in the mitochondria of cytosol of hepatocytes

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118
Q

What is the mechanism of the urea cycle?

A
  • Arginine (from the diet or protein breakdown) is cleaved by arginase generating urea & ornithine
  • Ammonia and carbon dioxide is added to ornithine to create citrulline
  • Another molecule of ammonia is then added to citrulline to regenerate arginine
  • Cycle starts again
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119
Q

What does one turn of the urea cycle consume?

A
  • 3 ATP equivalents

- 4 high energy nucleotides (PO4-)

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120
Q

What compound is generated by the urea cycle?

A

Only urea, all other components are recycled

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121
Q

What is an effect of a deficiency of an enzyme which is used in the urea cycle?

A

Higher levels of ammonia in the blood

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122
Q

Why is high levels of ammonia associated with neurotoxicity?

A
  • Crosses blood-brain barrier easily
  • Once inside, it is converted to glutamate by glutamate dehydrogenase
  • Depletion in alpha-ketoglutarate
  • Fall of alpha-ketoglutarate causes fall of oxaloacetate so halts Kreb’s
  • Irreplaceable cell damage & neural cell death
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123
Q

What happens during the absorptive state of glucose regulation?

A
  • Ingested nutrients are absorbed from the GI tract into the blood
  • A proportion of nutrients are catabolised and used
  • The remainder are converted and stored for future use
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124
Q

What happens to the macronutrients during the absorptive state of glucose regulation?

A
  • Glucose is used to generate ATP
  • Amino acids are converted to proteins
  • Glycerol and fatty acids are converted to lipids
  • Glucose is converted to glycogen
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125
Q

What happens during the post-absorptive state of glucose regulation?

A
  • Nutrients are no longer absorbed from the GI tract

- Nutrient stores must supply the energy requirements of the body

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126
Q

What is the glucose regulation in the post-absorptive state?

A
  • Glucose is no longer being absorbed from the GI tract
  • Essential to maintain the plasma glucose concentration due to the fact that the CNS is dependent
  • There is 3 sources at this point.
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127
Q

What are the three main sources of glucose in the post-absorptive state?

A
  • Glycogenlysis
  • Lipolysis
  • Protein
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128
Q

Where does the hydrolysis of glycogen to monomers of glucose-6-phospate occur?

A

In liver and skeletal muscle

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129
Q

What is the process of glycogenolysis in the liver?

A
  • Glycogen is hydrolysed to monomers of glucose-6-phosphate

- Glucose-6-phosphate is enzymatically converted to glucose which enters the blood

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130
Q

How quick does hepatic glycogenolysis occur?

A
  • Within seconds of the right stimulus e.g. sympathetic nerves system stimulation
  • It is the first line of defence in maintaining plasma glucose conc.
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131
Q

How long does the hepatic supply of glucose last?

A

Only several hours before they are depleted

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132
Q

What is the process of glycogenolysis in skeletal muscle?

A
  • Glycogen is hydrolysed into glucose-6-phosphate
  • Glucose-6-phosphate undergoes glycolysis to yield ATP, pyruvate and lactate
  • ATP and pyruvate are used directly by muscle
  • Some of the lactate enters the blood, circulates to liver and is converted to glucose, which can reenter to blood
133
Q

What is the mechanism of lipolysis in the post-absorptive state?

A
  • Triglycerides are catabolised in adipose via hydrolysis to produce glycerol and fatty acids
  • Glycerol and fatty acids enter the blood by diffusion
  • Glycerol enter the liver which enzymatically converts it into glucose
134
Q

What is the mechanism of using protein for energy in the post-absorptive state?

A
  • Large quantities of protein are catabolised without significant cellular malfunction
  • Proteins supply AA’s, which enter the blood and are taken up by the liver
  • They are converted via the alpha-keto acid pathway to glucose, where they are revealed into blood
135
Q

What is gluconeogenesis?

A

The synthesis of glucose from precursors such as amino acids and glycerol

136
Q

How many molecules of ATP are consumed per molecule of glucose formed?

A

6

137
Q

How is most of the bodies fat stored?

A
  • In adipocytes which form tissues called adipose tissues

- Some is stored in hepatocytes

138
Q

What is the structure of a triglyceride?

A

3 fatty acids bound to a glycerol molecule

139
Q

What are lipids?

A

Esters of fatty acids and certain alcohol compounds

140
Q

Name 3 functions of lipids

A
  • Energy reserves
  • Structural part of cell membrane
  • Hormone metabolism
141
Q

What is the function of lipoproteins?

A

Used to transport cholesterol in the blood

142
Q

Where are HDL’s formed?

A

In the liver

143
Q

What are the two types of lipoproteins?

A

HDL and LDL

144
Q

What is the function of HDL?

A
  • Remove excess cholesterol from blood and tissue
  • Deliver cholesterol to the liver which secretes it into bile or converts it into bile salts
  • ‘Good’ cholesterol
145
Q

Where is LDL formed?

A

In the plasma

146
Q

What is the function of LDL?

A

Main cholesterol carriers and they deliver cholesterol to cells throughout the body

147
Q

What is the mechanism of LDL transport in the body?

A

LDLs bind to plasma membrane receptors specific for a protein component of the LDLs and are then taken up by the cells via endocytosis

148
Q

Why are LDLs considered ‘bad’ cholesterol?

A

Due to high plasma concentrations being associated with increased deposition of cholesterol in arterial walls and a higher incidence of heart attacks

149
Q

What is the function of cholesterol in the body?

A
  • Synthesis of cell membranes

- Steroid hormone production in the gonads and adrenal glands + aldosterone + cortisol

150
Q

Where is VLDL synthesised?

A

Hepatocytes

151
Q

What is the function of VLDL?

A

Carries triglycerides from glucose in liver to adipocytes

152
Q

Under resting conditions, what percent of the energy used in the body is derived from the catabolism of fatty acids?

A

50%

153
Q

What is the structure of an adipocyte in regards to fat?

A

Almost the entire cytoplasm of each adipocyte is filled with a single large fat droplet

154
Q

What is the larger structure of adipocytes?

A

Clusters of adipocytes form adipose tissue, most which is in deposits underlying the skin or surrounding internal organs

155
Q

What is the function of adipocytes?

A
  • Synthesise and store triglycerides

- To release fatty acids & glycerol into blood to provide energy required for ATP formation

156
Q

What is the process for ATP formation from fatty acids?

A
  • Coenzyme A linked to carbonyl end of a fatty acid
  • ATP –> AMP & 2Pi
  • The coenzyme A derivative of fatty acid then proceeds through beta-oxidation reactions
  • Acetyl coenzyme A split off from FA & 2 pairs of hydrogen atoms are transferred to coenzymes (1 to FAD & 1 to NAD+)
  • Hydrogen ions from coenzymes enter oxidative phosphorylation to form ATP
  • Cycle repeats
  • Each cycle shortens the chain by 2 carbons
157
Q

What is the hepatic metabolism of lipids?

A

Lipoprotein lipase hydrolyses triglycerides into lipoproteins (chylomicrons and VLDLs) into 2 free fatty acids and 1 glycerol molecule

158
Q

Where is hepatic lipase expressed?

A

Liver and adrenal glands

159
Q

What is the function of hepatic lipase?

A

Converts IDL (intermediate density lipoprotein) into LDL thereby packaging it with more triglycerides to be released in the body

160
Q

Where is bile secreted from?

A

The hepatocytes in the liver, pretty much continuous

161
Q

What is bile used for?

A
  • To emulsify fats

- As an excretory pathway for most steroid hormones, many drugs and some toxins

162
Q

Where is bile stored and concentrated?

A

In the gallbladder, as some NaCl and water are reabsorbed back into the blood

163
Q

Where does the gall bladder lie anatomically?

A

At the junction of the right-mid-clavicular line & costal margin

164
Q

What is the livers connection with the GI tract?

A

By the portal vein, which connects blood from the superior mesenteric vein (which in turn is effectively the venous drainage of both the small and large intestines)

165
Q

What is the functional unit of the liver?

A

Hepatic lobules (formed by hepatic plates stacked on top of each other)

166
Q

What is the structure of hepatic lobules?

A
  • Hexagonal in cross-section with a portal triad at each corner
  • Portal triad: hepatic portal vein, hepatic artery and bile duct
  • In the centre of each lobule is the central vein, which soon becomes the hepatic vein
167
Q

What is the structure of a hepatic sinusoid?

A

Blood vessel with fenestrated, discontinuous epithelium

168
Q

How are hepatocytes separated from the sinusoids?

A

The space of Disse

169
Q

What happens to substances which are absorbed from the small intestine?

A

Get into the hepatic sinusoid then go to the vena cava via the central vein or are took up by hepatocytes in which they can be modified

170
Q

What is significant about the blood in the hepatic artery?

A

It is oxygen rich

171
Q

What is significant about the blood in the portal vein?

A

It is nutrient rich

172
Q

What are the blood sources for the hepatic sinusoid?

A
  • Oxygen-rich from hepatic artery

- Nutrient-rich from the portal vein

173
Q

What is the larger structure of the hepatic lobules?

A
  • Wedge-like arrangements
  • Around 1-2 cells deep
  • Surrounded by sinusoids (containing mixed portal/hepatic artery blood)
174
Q

What is unique about the liver’s major blood supply?

A

It comes from a vein - the portal vein (80%). The rest comes from the hepatic artery

175
Q

How does the different types of blood get mixed in the hepatic sinusoids?

A
  • Branches of artery and vein leave the portal triad
  • They join and blood is mixed as it enter through the sinusoids
  • It flows through centre and exits via the central vein
  • Bile flows in the opposite direction to blood
176
Q

What cells are the sinusoids of the liver lined with?

A

A continuous layer of specialised endothelial cells interspersed with Kupffer cells

177
Q

What cells are on the undersurface of the sinusoids of the liver?

A

Stellate cells

178
Q

What is the function of stellate cells?

A

Producing the extracellular matrix in the Space of Disse in the liver

179
Q

What is present between adjacent hepatocytes?

A

Bile canaliculi

180
Q

Why are bile canaliculi’s not true vessels?

A

As they don’t have specialised walls

181
Q

What is the structure of bile canaliculi’s?

A
  • Groove running alongside the side of the hepatocytes
  • Bound together by tight junctions, gap junctions and desmosomes which cross both cell membranes
  • Actin filaments are found in the areas surrounding
182
Q

What is the function of bile canaliculi’s?

A

Serve to pump the formed bile towards the bile ducts

183
Q

What is the bile pathways to the GI tract?

A
  • Bile ducts in hepatic lobules lead to either left or right hepatic ducts
  • Left/right hepatic ducts join to form the common hepatic duct
  • Cystic duct joins the common hepatic duct to collect in gallbladder
  • Cystic duct + common hepatic duct = common bile duct
  • The pancreatic duct joins common bile duct at the point known as the Ampulla of Vater
  • These 2 ducts enter the duodenum at the major duodenal papilla (2nd part of duodenum)
  • Regulation of bile is done by the sphincter of Oddi (around both ducts)
184
Q

What are the 6 major components of bile?

A
  • Bile salts
  • Lectithin (phospholipid)
  • HCO3- and other salts
  • Cholesterol
  • Bile pigments
  • Trace metals
185
Q

What are bile salts manufactured by?

A

Hepatocytes

186
Q

What are present in the micelles in bile?

A

Bile salts, cholesterol and lecithin

187
Q

What is the purpose for micelles in bile?

A
  • Maintained even when concentrated
  • Due to bile salts being powerful detergents (needed for emulsification function)
  • Bile salts are also capable of damaging cells membrane, so kept in micelles to reduce damage until needed
188
Q

What is the function of HCO3- in bile?

A

Helps neutralise the acids in the duodenum

189
Q

What is the most important digestive component?

A

Bile salts

190
Q

What are the two different cell types which secrete the components of bile?

A

Hepatocytes and epithelial cells lining the bile ducts

191
Q

What do hepatocytes secrete in relation to bile?

A

Bile salts, cholesterol, lectithin and bile pigments

192
Q

What do epithelial cells lining the bile ducts secrete in relation to bile?

A

Most of the HCO3- rich solution

193
Q

What stimulates the secretion of HCO3- rich solution in the bile ducts?

A

By secretin in response to the presence of acid in the stomach

194
Q

What stimulates secretion by the pancreas?

A

Secretin in response to the presence of acid in the stomach

195
Q

Where does the gallbladder receive its bile from?

A

The common hepatic duct, which is formed by the left and right hepatic ducts

196
Q

How does hepatic bile enter the gallbladder?

A

By the cystic duct

197
Q

What happens to the bile in the gallbladder?

A
  • It is stored and concentrated

- Hepatic bile is relatively dilute

198
Q

What causes the contraction of the gallbladder?

A

The action of cholecystokinin

199
Q

What causes the release of cholecystokinin?

A

Due to fatty acid and amino acids in the duodenum

200
Q

What is significant about the vasculature of the gallbladder?

A
  • Cystic artery supplies oxygenated blood to gallbladder
  • Has no venous drainage
  • Gallbladder is stuck to the liver bed, so blood drains directly into the liver
201
Q

Summarise the enterohepatic circulation

A
  • Bile salts enter the intestinal tract via bile. They are absorbed by Na-coupled transporters in jejunum and terminal ileum (most here)
  • Absorbed bile salts are returned via portal vein to the liver
  • Uptake of bile salts into hepatocytes is driven by secondary active transport coupled to Na+
  • A small amount of bile salts escape this cycle
202
Q

What is bile synthesised from?

A

Cholesterol

203
Q

Where can the liver also secrete cholesterol from?

A

From when it is extracted from the blood, into the bile

204
Q

What is the mechanism for cholesterol homeostasis in the blood?

A

Bile secretion & excretion of cholesterol in the faeces

205
Q

Is cholesterol soluble in water?

A

No, as it is a lipid

206
Q

What is the differences between how cholesterol is stored in bile and the blood?

A
  • In bile, it is stored in micelles

- In blood, it is incorporated into lipoproteins

207
Q

What surrounds the common bile duct at the Ampulla of Vater?

A

The sphincter of Oddi

208
Q

What happens when the sphincter of Oddi is closed?

A

The dilute bile secreted by the liver is shunted into the gallbladder, where it is concentrated due to NaCl and water being absorbed into the blood

209
Q

What gets removed from bile in the gallbladder to concentrate it?

A

NaCl & water

210
Q

What is the pressure like the in the bile duct system?

A

It is low pressure

211
Q

What must the gallbladder do when it fills with bile?

A

Adaptive relaxation - when the size increases but the pressure doesn’t

212
Q

What is the function of choleosystokinin?

A
  • Causes the gallbladder to contract
  • Causes sphincter of Oddi to relax
  • Bile flows down cystic duct into common bile duct into duodenum, where it mixes with food & lipid digestion occurs
213
Q

What are bile pigments?

A

Substances formed from the harm portion of haemoglobin when old/damaged erythrocytes are broken down in the spleen and liver

214
Q

What is the predominant bile pigment and how is it extracted from blood?

A
  • Bilirubin
  • Extracted by hepatocytes
  • Actively secreted into bile
215
Q

What colour is bilirubin?

A

Yellow - it contributes to the colour of bile

216
Q

What happens to erythrocytes when they are old/damaged?

A

They are broke down by macrophages

217
Q

Where are erythrocytes broke down by macrophages?

A
  • In spleen/bone marrow

- Can also happen in the Kupffer cells of the liver

218
Q

Briefly outline the process of bilirubin metabolism

A
  • Erythrocytes are ingested into macrophages
  • Haemoglobin is broke down into haem & globin
  • Globin is broke down into amino acids which can be used for new erythrocytes in bone marrow
  • Haem is broke down into biliverdin, Fe2+ and CO by hemoxygenase
  • The Fe2+ is bound to transferrin, where it is shuttled to bone marrow to make new RBC’s
  • Biliverdin is reduced to unconjugated bilirubin by biliverdin reductase
  • Unconjugated bilirubin must be excreted. It is lipid soluble and insoluble in blood
  • Unconjugated bilirubin is bound to albumin and transported to liver
  • Glucuronic acid is added to unconjugated bilirubin by UDP glucuronyl transferase to make it conjugated, so it is soluble to be excreted
  • The conjugated bilirubin can then be stored in gallbladder, so it can enter the duodenum
  • Conjugated bilirubin travels to ileum/beginning of large intestine where it is reduced by hydrolysis by intestinal bacteria, forming urobilinogen
  • 10% of urobilinogen is transported back to the liver via albumin where it is oxidised to urobilin. Excreted in urine to give yellow colour
  • 90% is oxidised by intestinal bacteria to make stercobilin
  • Stercobilin is excreted into faeces (forms stercobilin)
219
Q

What is jaundice?

A

A yellow discolouration of the skin caused by high serum bilirubin level

220
Q

What are the 3 main types of jaundice?

A

Pre-hepatic, hepatic and post-hepatic/obstructive

221
Q

What is the physiology behind pre-hepatic jaundice?

A
  • Increased breakdown of erythrocytes resulting in increased levels of unconjugated bilirubin
  • Causes an increased serum unconjugated bilirubin without excess bilirubin in urine
  • Will have raised serum unconjugated bilirubin
222
Q

What are some signs/symptoms of pre-hepatic jaundice?

A
  • Yellow skin
  • Enlarged spleen (due to excess breakdown)
  • Stools brown and urine normal
223
Q

Give 4 causes of pre-hepatic jaundice

A
  • Malaria
  • Sickle cell anaemia
  • Thalassameia
  • Physiological jaundice of the newborn
224
Q

What is the physiology behind hepatic jaundice?

A
  • Result of hepatocellular swelling
  • Impaired cellular uptake, defect conjugation or abnormal secretion of bilirubin by the hepatocytes
  • Liver is damaged so is unable to metabolise unconjugated bilirubin resulting in a buildup ins serum uncojugtaed bilirubin
  • Increased conjugated and unconjugated bilirubin
  • Decreased urobilinogen
225
Q

What are some signs/symptoms of hepatic jaundice?

A
  • Urine will be dark
  • Stools can be pale or normal
  • Enlargement of the spleen
  • Yellow skin
226
Q

Give 5 causes of hepatic jaundice

A
  • Viral hepatitis
  • Drugs
  • Alcohol hepatitis
  • Cirrhosis
  • Jaundice of the newborn
227
Q

What is the physiology behind post-hepatic jaundice?

A
  • Occurs when the biliary system is damaged, inflamed or obstructed
  • Elevated serum conjugated bilirubin
  • Decreased urobilinogen
228
Q

What are some signs/symptoms of post-hepatic/obstructive jaundice?

A
  • Dark urine
  • Pale stools
  • No enlargement of the spleen
  • Yellow skin
229
Q

Give 5 causes of post-hepatic/obstructive jaundice

A
  • Gallstones
  • Pancreatic cancer
  • Gallbladder cancer
  • Bile duct cancer
  • Pancreatitis
230
Q

How can cancer/inflammation of the pancreas cause jaundice?

A

Due to the head of the pancreas being situated in the duodenal loop, near the common bile duct, so any inflammation will cause obstruction of the duct, therefore jaundice

231
Q

Where does acute pancreatitis pain radiate from?

A

The back

232
Q

What is Gilbert’s syndrome and what would it prevent with?

A
  • A shortage of UDP glycerol transferase

- Normal conjugated bilirubin but a raised unconjuagted bilirubin

233
Q

What is inside the micelles of the bile and why?

A

Cholesterol and phospholipids, as they are water-insoluble

234
Q

How do gallstones form?

A

When the concentration of cholesterol in bile becomes high in relation to phospholipids and bile salts, the cholesterol will crystallise out of solution to form gallstones

235
Q

What happens if a gallstone is small?

A

May be able to pass freely through the common bile duct into the intestine

236
Q

What happens to the movement of a larger gallstone?

A

It may become lodged in the opening of the gallbladder, causing painful contractile spasms of the smooth muscle

237
Q

What is the more serious problem of a larger gallstone?

A

May become lodged in the common bile duct, thereby preventing the bile from entering the intestines

238
Q

What can happen if there is a significant decrease in bile (physiologically)?

A
  • Can decrease fat digestion and absorption
  • This can result in an impaired absorption of fat-soluble vitamins, resulting in clotting problems and calcium malabsorption
239
Q

What can happen to stools if there is a significant decrease in bile?

A
  • The fat isn’t absorbed, so enters large intestine and appears in the faeces
  • Bacteria in the large intestine will convert some of the fat into FA derivatives, which alter salt and water movement so a net flow of water into large intestine - diarrhoea & fluid & nutrient loss
240
Q

What can happen if a gall stone becomes lodged at a point the prevents bile & pancreatic secretions?

A

Results in failure to both neutralise acid and adequately digest most organic nutrients - may result in severe nutritional deficiencies

241
Q

What is the positioning of the pancreas?

A

Completely retroperitoneal except from the tail

242
Q

Where is the tail of the pancreas located?

A

Attached to the spleen and is intraperitoneal

243
Q

What is the relevance of the head of the pancreas being closely related to the common bile duct?

A

A carcinoma or inflammation of the head of the pancreas can block the bile duct resulting in post-hepatic/obstructive jaundice

244
Q

Where does the uncinate process of the pancreas come from and what is the relevance?

A
  • Comes from the ventral bud (the rest of the pancreas comes from the dorsal bud)
  • The superior mesenteric vein and artery are enthralled between the head and the process
245
Q

How can disruption of the superior gasproduodenal artery eventually lead to haemorrhage and haematemesis?

A

A duodenal ulcer can eventually erode into the artery, causing the damage

246
Q

Describe how the pancreas develops as two separate outgrowths embryologically

A
  • The ventral and dorsal pancreas
  • During development of the embryo the ventral bud rotates around and fuses with the dorsal pancreas - in effect becoming the head of the pancreas
247
Q

Where does the pancreas receive its main blood supply from?

A

The coeliac trunk, which arises directly from the aorta and divides at the coeliac axis to form the gastric arteries, the hepatic artery and the splenic artery

248
Q

Why does the superior mesenteric artery run ‘through’ the head of the pancreas?

A

Due it being enveloped during the rotation of the dorsal and ventral pancreas when they fuse. It provides some supply to the head of the pancreas

249
Q

What is the venous drainage of the pancreas?

A

Mainly by the splenic vein, which then joins the superior mesenteric vein to form the portal vein

250
Q

Name two things what the exocrine pancreas secretes

A
  • Bicarbonate

- Digestive enzymes

251
Q

Where do exocrine secretions of the pancreas occur?

A

From the acinar tissue

252
Q

How are exocrine secretions secreted out of the pancreas?

A
  • Secreted into bile ducts which converge into the pancreatic duct
  • Joins the common bile duct just before it enters the duodenum at the ampulla of Vater
253
Q

What is the sphincter of Oddi?

A

A separates bundle of circular muscle which regulates flow into the duodenum and may serve also to prevent mixing of bile & pancreatic juice within the pancreatic duct

254
Q

What will reflux of bile down the pancreatic duct cause?

A

Acute inflammation due it the biles detergent properties

255
Q

Where does the accessory pancreatic duct usually emerge?

A

Above the ampulla of Vater

256
Q

Where is bicarbonate secreted from in the pancreas?

A

Epithelial cells lining the ducts (duct cells)

257
Q

What are the functions of pancreas bicarbonate?

A
  • In order to protect the duodenal mucosa from gastric acid

- Also buffers the material entering the duodenum to a pH suitable for enzyme action

258
Q

What mechanism does acid in the duodenum cause?

A
  • The release of the hormone secretin
  • This stimulates the secretion of bicarbonate from the pancreas and liver
  • Also potentiates the action of CCK which stimulates enzyme secretion
259
Q

Where is secretin produced?

A

The small intestine

260
Q

Name 3 things what secretin does

A
  • Stimulates the secretion of bicarbonate from pancreas and liver
  • Inhibits acid secretion
  • Inhibits gastric motility
261
Q

How do pancreatic duct cells secrete bicarbonate into the duct lumen?

A

By an apical membrane chloride/bicarbonate exchanger

262
Q

What is the mechanism of secretion of bicarbonate into the duct lumen of the pancreas?

A
  • Carbon dioxide and water form carbonic acid by the enzyme carbonic anhyrdrase
  • Carbonic acid dissociates
  • The H ion is pumped into the capillary by the Na/H exchanger
  • There is a Na/K ATPase pump to return Na to capillary
  • Also a potassium channel for the diffusion of K
  • The bicarbonate is pumped into the duct lumen by the Cl/HCO3- exchanger
  • Cl ions are recycled back into the lumen by the CFRT channel
263
Q

How can digestive enzymes be secreted?

A

Either in active form or as precursors e.g. pepsinogen

264
Q

Where are digestive enzymes secreted from?

A

By gland cells at the pancreatic end of the duct system

265
Q

What do the enzymes of the pancreas digest?

A
  • Triglycerides to fatty acids & monoglycerides
  • Polysaccharides to sugar
  • Proteins to amino acids
  • Nucleic acids to nucleotides
266
Q

Give 2 examples of active enzymes from the pancreas

A
  • Alpha-amylase (starch to maltose)

- Lipase (triglycerides to monoglyceride & fatty acids)

267
Q

Why are some enzymes from the pancreas released as precursors?

A

To protect pancreatic cells from autodigestion

268
Q

What is enterokinase?

A

A proteolytic enzyme that splits off a peptide from pancreatic trypsinogen froming the active enzyme trypsin

269
Q

Where is enterokinase found?

A

Embedded in the lumina plasma membranes of intestinal epithelial cells

270
Q

What is the function of trypsin and chymotrypsin?

A

Enzymes used to break peptide bonds in proteins to form peptide fragments

271
Q

Where is somatostatin produced?

A

By the D cells in the pancreatic islets.

272
Q

What is the function of somatostatin?

A

It is a powerful inhibitor of pancreatic exocrine secretion

273
Q

What are the 4 cell types of the Islets of Langerhans and what are their functions?

A
  • Alpha cells produce glucagon
  • Beta cells produce insulin & amylin
  • Delta/D cells produce somatostatin
  • PP cells produce pancreatic polypeptide
274
Q

What is the physiology of type I diabetes?

A

Pancreas failure to produce enough insulin

275
Q

What is the physiology of type II diabetes?

A

Cells fail to respond to insulin properly

276
Q

What controls most of the pancreatic exocrine secretions?

A

By stimuli arising from the intestinal phase of digestion

277
Q

Name two other phases which contribute to pancreatic exocrine secretions

A

Cephalic and gastric

278
Q

What happens in the cephalic phase of digestion related to pancreatic secretion?

A
  • Sensory experience of seeing & eating food

- Parasympathetic vagus nerve stimulation of acinar cells to produce digestive enzymes

279
Q

What happens in the gastric phase of digestion related to pancreatic secretion?

A

Initiated by presence of food in the stomach and parasympathetic vagus nerve stimulation of acinar cells to produce digestive enzymes

280
Q

What has happened by the end of the cephalic and gastric phases in relation to pancreatic secretion?

A
  • Pancreatic ducts are filled with inactive digestive zymogens, ready for release into the intestinal lumen with bicarbonate via sphincter of Oddi
  • Once FA & AA are present into the duodenum, CCK is release and the gallbladder contracts inducing enzyme secretion
281
Q

What are the two sources of blood for the liver and what are the proportions?

A
  • 25% from hepatic artery (oxygenated)

- 75% from hepatic portal vein (deoxygenated and nutrient rich)

282
Q

How is blood drained into the sinusoids in the liver?

A
  • The terminal branches of the portal vein and hepatic artery empty together in sinusoids surrounding hepatic cells
  • Blood leaves the liver via the hepatic vein which drains into the inferior vena cava.
283
Q

What is present in the blood which has just joined the inferior vena cava from the liver?

A
  • Deoxygenated
  • Detoxified
  • Contains the normal homeostatic nutrient levels
284
Q

Embryologically, what is the primitive gut made from and what structures does it provide?

A
  • Endoderm (epithelial lining, hepatocytes of liver & endocrine and exocrine cells of pancreas)
  • Visceral mesoderm (muscle & connective tissue)
285
Q

What are the components of the foregut?

A
  • Oral pharyngeal membrane (liver bud)
  • Coeliac artery
  • Oesophagus
  • Stomach
  • Liver
  • Biliary apparatus
  • 1/2 of duodenum
286
Q

What are the components of the midgut?

A
  • Liver bud (2/3rds transverse colon)
  • Superior mesenteric artery
  • Distal 1/2 of duodenum
  • Jejunum
  • Ileum
  • Appendix
  • Ascending colon
  • Right 2/3rds of transverse colon
287
Q

What are the components of the hindgut?

A
  • Inferior mesenteric artery
  • Left 1/3rd of transverse membrane
  • Sigmoid colon
  • Rectum
  • Anal canal
288
Q

What is the hepatic diverticulum?

A

A cellular expansion of the foregut which gives rise to the parenchyma (function part) of the liver

289
Q

Where does the hepatic diverticulum appear?

A

In the middle of the 3rd week as an outgrowth of the endodermal epithelium at the distal end of the foregut (duodenum)

290
Q

What does the liver bud contain (embryology)?

A

Rapidly proliferating cells that penetrate the septum transverse (thick mass formed in the embryo that gives rise to parts of the thoracic diaphragm and ventral mesentery)

291
Q

When does the bile duct form in embryology?

A

When the connection between the liver diverticulum and the foregut narrows

292
Q

How is the gallbladder and cystic duct formed embryologically?

A

From a small ventral outgrowth which develops from the bile duct

293
Q

How do the hepatic sinusoids form embryologically?

A

By further growth of the liver bud which allows epithelial liver cords to intermingle with umbilical and vitellien veins

294
Q

What do the liver cords of embryology develop into?

A

Hepatocytes (liver parenchyma) and form the lining of the biliary ducts

295
Q

What happens to the mesoderm of the ventral mesentery in the 6th week?

A

Gives rise to haematopoietic cells, Kupffer cells and connective tissue cells

296
Q

Where does haemotopoiesis happen in the embryo?

A

The liver

297
Q

At the 10th week, what percentage of the body weight is liver and why?

A
  • About 10%

- Due to the presence of large number of sinusoids and involvement of the liver in haemopoietic function

298
Q

At birth, what percentage of the body weight is liver and why?

A
  • About 5%

- Due to the existence of small number of haematopoietic islands in the liver and reduced haematopoietic function

299
Q

When does bile production start?

A

At the 12th week, by the hepatic cells

300
Q

When does the haematopoietic function of the liver subside?

A

During the last 2 months of intrauterine life

301
Q

Name two things which happen to the liver after birth

A
  • The left umbilical vein obliterates to form the ligamentum teres
  • The ductus venous undergoes fibrosis leaving a remnant called the ligamentum venosus
302
Q

What is a mesentery?

A

A fold of tissue that attaches the organs to the body wall

303
Q

What is intraperitoneal mesentery?

A

Double layer of the peritoneum that completely surrounds the organ

304
Q

What is retroperitoneal mesentery?

A

The organ is only covered by the peritoneum on its anterior side

305
Q

Where does ventral mesentery occur?

A

Only in the foregut

306
Q

What is the ventral mesentery derived from?

A

The septum transversum (also gives rise to the thoracic diaphragm)

307
Q

What mesenteries does the foregut have?

A

Dorsal and ventral

308
Q

What mesenteries does the midgut and hindgut have?

A

Dorsal

309
Q

What divides the ventral mesentery?

A

The liver

310
Q

How does the falciform ligament arise?

A

From the liver, attaches to anterior abdominal well (free edge contains the umbilical vein which becomes the ligament teres/round ligament after birth)

311
Q

How does the lesser omentum? arise?

A

From the liver, gives it to the ventral borders of the stomach and duodenum (free edge contains the hepatic artery, portal vein and bile duct)

312
Q

What is significant about the bare areas of the liver?

A

They aren’t covered by mesentery

313
Q

How come the abdominal organs are placed where they are?

A

Due to rotation of the stomach

314
Q

Briefly describe the formation of the lesser omentum

A
  • Stomach rotates 90 digress along a longitudinal axis (left now becomes anterior
  • The posterior wall grows quicker (now on right side) this gives the greater curvature
  • Stomach rotates around the anterior posterior axis, the pyloric region of the stomach moves right and up and the cardiac region of the stomach moves left and down
315
Q

Where is the pancreas located?

A

Retroperitoneally across the posterior abdominal wall, it sits behind the stomach across the back of the abdomen

316
Q

What does the exocrine part of the pancreas do?

A

Secretes digestive enzymes and bicarbonate into the duodenum

317
Q

What does the endocrine part of the pancreas do?

A
  • Secrete hormones into the bloodstream

- The cells are alpha, beta, delta and PP cells

318
Q

How does the pancreas develop embryologically?

A

From the endodermal lining of the duodenum as dorsal and ventral buds

319
Q

Where is the dorsal bud found?

A

The dorsal mesentery

320
Q

Where is the ventral bud found?

A

The ventral mesentery - close to the bile duct

321
Q

What happens when the duodenum rotates and becomes C-shaped?

A

The ventral bud and the entrance to the common bile duct in the duodenum are shifted dorsally

322
Q

Where does the ventral bud come to lie?

A

Immediately below and behind the dorsal bud, the parenchyma and duct systems of both buds fuse together

323
Q

What does the ventral pancreatic bud form?

A

The uncinate process and inferior part of the head of the pancreas

324
Q

What part of the pancreas does the dorsal bud form?

A

All except from the uncinate process and inferior part of the head of the pancreas

325
Q

How does the pancreatic duct develop?

A
  • Formed by the union of the ventral pancreatic duct with the distal part of the duct of dorsal bud
  • The main pancreatic duct & common bile duct enter the ampulla of Vater which enters the wall of the duodenum at the site of the major duodenal papilla
326
Q

How do the Islets of Langerhans develop?

A

From the parenchyma of the pancreas at the third month of fatal life

327
Q

When does insulin secretion begin?

A

At the fifth month

328
Q

How does pancreatic connective tissue develop?

A

From the visceral surround mesoderm

Phase 1 Med (Liv) (13 decks)

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