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EK Phase 2A > Introductory Clinical Sciences > Flashcards

Introductory Clinical Sciences Flashcards

1
Q

Define inflammation.

A

A local physiological response to tissue injury.

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2
Q

Give a benefit of inflammation.

A

Inflammation can destroy invading micro-organisms and can prevent the spread of infection.

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3
Q

Give a disadvantage of inflammation.

A

Inflammation can produce disease and can lead to distorted tissues with permanently altered function.

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4
Q

Define exudate.

A

A protein rich fluid that leaks out of vessel walls due to increased vascular permeability.

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5
Q

What are the 4 outcomes of inflammation?

A
  1. Resolution.
  2. Suppuration.
  3. Organisation (scar tissue formation).
  4. Progression onto chronic inflammation.
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6
Q

Give 6 causes of acute inflammation.

A
  1. Microbial infections (bacteria and viruses).
  2. Chemicals (corrosives, acids/alkalis).
  3. Physical agents (trauma, burns, frost bite).
  4. Hypersensitivity reactions (TB).
  5. Bacterial toxins.
  6. Tissue necrosis.
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7
Q

What does viral infection result in?

A

Cell death due to intracellular multiplication.

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8
Q

What does bacterial infection result in?

A

The release of exotoxins (involved in the initiation of inflammation) or endotoxins.

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9
Q

Give 5 cardinal signs of Acute inflammation.

A
  1. Redness (rubor).
  2. Swelling (tumor).
  3. Pain (dolor).
  4. Heat (calor).
  5. Loss of function.
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10
Q

How can acute inflammation be diagnosed histologically?

A

By looking for the presence of neutrophil polymorphs.

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11
Q

Give 3 endogenous chemical mediators of acute inflammation.

A
  1. Bradykinin.
  2. Histamine.
  3. Nitric Oxide.
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12
Q

What are 4 systemic effects of acute inflammation?

A
  1. Fever.
  2. Feeling unwell.
  3. Weight loss.
  4. Reactive hyperplasia of the reticuloendothelial system.
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13
Q

What cells are involved in chronic inflammation?

A

Macrophages and plasma cells (B and T lymphocytes).

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14
Q

What cell can form when several macrophages try to ingest the same particle?

A

Multinucleate giant cell.

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15
Q

Give 4 causes of chronic inflammation.

A
  1. Primary chronic inflammation.
  2. Transplant rejection.
  3. Recurrent acute inflammation.
  4. Progression from acute inflammation.
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16
Q

Give examples of primary chronic inflammation.

A
  1. Infective substances having resistance to phagocytosis e.g. TB, leprosy.
  2. Endogenous materials e.g. uric acid crystals.
  3. Exogenous materials e.g. asbestos.
  4. Autoimmune diseases e.g. chronic gastritis, rheumatoid arthritis etc.
  5. Other chronic inflammatory diseases e.g. chronic inflammatory bowel disease.
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17
Q

In which type of inflammation would you see neutrophil polymorphs?

A

Acute inflammation.

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18
Q

What are some macroscopic features of chronic inflammation?

A
  1. Chronic ulcer.
  2. Chronic abscess cavity.
  3. Granulomatous inflammation.
  4. Fibrosis.
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19
Q

What is granulation tissue?

A

Granulation tissue is composed of small blood vessels in a connective tissue matrix with myofibroblasts. It is important in healing and repair.

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20
Q

Define granuloma.

A

An aggregate of epithelioid histocytes.

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21
Q

Give an example of a granulomatous disease.

A

TB, leprosy, Crohn’s disease and sarcoidosis.

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22
Q

The activity of what enzyme in the blood can act as a marker for granulomatous disease?

A

Angiotensin converting enzyme.

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23
Q

What kind of disease is TB?

A

A granulomatous disease.

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24
Q

What is the difference between resolution and repair?

A

Resolution is when the initiating factor is removed and the tissue is able to regenerate. In repair, the initiating factor is still present and the tissue is unable to regenerate.

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25
Q

Name 5 types of cells capable of regeneration.

A
  1. Hepatocytes.
  2. Osteocytes.
  3. Pneumocytes.
  4. Blood cells.
  5. Gut and skin epithelial cells.
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26
Q

Name 2 types of cells that are incapable of regeneration.

A
  1. Myocardial cells.

2. Neuronal cells.

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27
Q

Define abscess.

A

Acute inflammation with a fibrotic wall.

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28
Q

Define thrombosis.

A

Formation of a solid mass from blood constituents in an intact vessel in the living.

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29
Q

Give 2 reasons why thrombosis formation is uncommon.

A
  1. Laminar flow.

2. Non sticky endothelial cells.

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30
Q

What are the 3 factors that can lead to thrombosis formation?

A
  1. Change in vessel wall. (endothelial injury)
  2. Change in blood constituents. (platelet aggregation, thrombus formation or fibrin deposition)
  3. Change in blood flow. (stasis of blood flow)
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31
Q

Define embolus.

A

A mass of material (often a thrombus) that is carried in the vascular system that is able to become lodged in a vessel and block it.

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32
Q

Define ischaemia.

A

Decreased blood flow to tissues w/o other complications

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33
Q

Define infarction.

A

Decreased blood flow with subsequent cell death.

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34
Q

Why are tissues with an end arterial supply more susceptible to infarction?

A

They only have a single arterial supply and so if this vessel is interrupted infarction is likely.

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35
Q

Give 3 examples of organs with a dual arterial supply.

A
  1. Lungs (bronchial arteries and pulmonary veins).
  2. Liver (hepatic arteries and portal veins).
  3. Some areas of the brain around the circle of willis.
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36
Q

What can happen if ischaemia is rectified?

A

Re-perfusion injury can occur due to the release of waste products.

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37
Q

What are the consequences of an arterial embolus?

A

An arterial embolus can go anywhere! The consequences could be stroke, MI, gangrene etc.

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38
Q

What are the consequences of a venous embolus?

A

An embolus in the venous system will go onto the vena cava and then through the pulmonary arteries and become lodged in the lungs causing a pulmonary embolism. This means there is decreased perfusion to the lungs.

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39
Q

Through which blood system would an embolus have travelled if it resulted in a pulmonary embolism?

A

Venous system.

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40
Q

What drug can be used to prevent Thrombosis?

A

Aspirin.

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41
Q

Define atherosclerosis.

A

Inflammatory process characterised by hardened fibrolipid plaques in the intima of a vessel wall.

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42
Q

Is atherosclerosis more common in the systemic or pulmonary circulation?

A

It is more common in the systemic circulation because this is a higher pressure system.

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43
Q

What are the 3 main constituents of an atheromatous plaque?

A
  1. Lipids.
  2. Fibrous tissue.
  3. Lymphocytes.
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44
Q

Give 5 risk factors for atherosclerosis.

A
  1. Cigarette smoking.
  2. Hypertension.
  3. Hyperlipidaemia.
  4. Uncontrolled diabetes mellitus.
  5. Lower socioeconomic status.
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45
Q

What can be done to prevent atherosclerosis?

A

Reduce risk factors and taking low dose aspirin regularly.

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46
Q

What is the primary cause of atherosclerosis?

A

Endothelial cell damage.

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47
Q

Why can cigarette smoking lead to atherosclerosis?

A

Cigarette smoking releases free radicals, nicotine and CO into the body. These all damage endothelial cells.

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48
Q

Why can hypertension lead to atherosclerosis?

A

A higher blood pressure means there is a greater force exerted onto the endothelial cells and this can lead to damage.

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49
Q

Define apoptosis.

A

Programmed cell death of a single cell.

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50
Q

What is the role of p53 protein?

A

p53 protein looks for DNA damage, if damage is present p53 switches on apoptosis.

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51
Q

What protein can switch on apoptosis if DNA damage is present?

A

p53 protein.

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52
Q

Activation of which family of protease enzymes can turn on apoptosis?

A

Caspases.

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53
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor.

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54
Q

Give an example of a disease where there is too much apoptosis.

A

HIV.

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55
Q

Define necrosis.

A

Unprogrammed death of a large number of cells due to an adverse event where cell death is not expected

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56
Q

Give 3 examples of events that can lead to necrosis.

A
  1. Frost bite.
  2. Avascular necrosis.
  3. Infarction.
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57
Q

Give 3 differences between apoptosis and necrosis.

A
  1. Apoptosis is programmed cell death whereas necrosis is unprogrammed.
  2. Apoptosis tends to effect only a single cell whereas necrosis effects a large number of cells.
  3. Apoptosis is often in response to DNA damage. Necrosis is triggered by an adverse event e.g. frost bite.
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58
Q

Define hypertrophy.

A

Increase in the size of a tissue due to an increase in the size of constituent cells.

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59
Q

Define hyperplasia.

A

Increase in the size of a tissue due to an increase in the number of constituent cells.

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60
Q

Define atrophy.

A

Decrease in the size of a tissue due to a decrease in the size of the constituent cells OR due to a decrease in the number of constituent cells.

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61
Q

Define metaplasia.

A

A change in the differentiation of a cell from one fully differentiated cell type to another fully differentiated cell type.

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62
Q

Give an example of a disease that demonstrates metaplasia.

A

Barrett’s oesophagus - the cells at the lower end of the oesophagus change from stratified squamous cells to columnar.

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63
Q

Define dysplasia.

A

Morphological changes seen in cells in the progression to becoming cancer. The cells become more ‘jumbled up’.

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64
Q

Define acute inflammation.

A

Initial and short lived tissue reactions to injury.

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65
Q

Define chronic inflammation.

A

Subsequent and prolonged tissue reactions to injury.

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66
Q

What happens to a cell when the telomere gets too short?

A

It can no longer divide.

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67
Q

Give an example of:

a) a dividing tissue.
b) a non dividing tissue.

A

a) Gut or skin tissue can divide.

b) Brain tissue is non dividing.

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68
Q

Why can excision be used as a cure for basal cell carcinoma?

A

Because BCC doesn’t metastasise.

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69
Q

Suggest a treatment that could be used for leukemia?

A

Chemotherapy. Leukemia is systemic, it circulates all around the body, therefore excision can’t be used.

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70
Q

Define carcinoma.

A

Malignant tumour of epithelial tissue.

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71
Q

Give an example of 5 carcinoma’s that can spread to bone.

A
  1. Breast.
  2. Kidney.
  3. Lung.
  4. Prostate.
  5. Thyroid.
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72
Q

Give an example of a carcinoma that can spread to the axillary lymph nodes.

A

Breast carcinomas.

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73
Q

Why is adjuvant therapy often used in the treatment of carcinomas?

A

Micrometastes are possible even if a tumour is excised and so adjuvant therapy is given to suppress secondary tumour formation.

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74
Q

Give an advantage and a disadvantage of conventional chemotherapy.

A
  • Advantage: works well for treatment against fast dividing tumours e.g. lymphomas.
  • Disadvantage: it is non selective for tumour cells, normal cells are hit too; this results in bad side effects such as diarrhoea and hair loss.
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75
Q

What kind of carcinomas would targeted chemotherapy be most effective against?

A

Slower dividing tumours e.g. lung, colon and breast.

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76
Q

What is the theory behind targeted chemotherapy?

A

It exploits the differences between cancer cells and normal cells; this means it is more effective and has less side effects.

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77
Q

What kind of drugs can be used in targeted chemotherapy?

A

Monoclonal antibodies (MAB) and small molecular inhibitors (SMI).

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78
Q

What is required for a tumour to invade through a basement membrane?

A
  1. Proteases.

2. Cell motility.

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79
Q

What is required for a tumour to enter the blood stream (intravasation)?

A
  1. Collagenases.

2. Cell motility.

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80
Q

What is required for a tumour to exit the blood stream (extravasation)?

A
  1. Adhesion receptors.
  2. Collagenases.
  3. Cell motility.
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81
Q

Give 2 promoters of tumour angiogenesis.

A
  1. Vascular endothelial growth factors.

2. Fibroblast growth factors.

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82
Q

Give 3 inhibitors of tumour angiogenesis.

A
  1. Angiostatin.
  2. Endostatin.
  3. Vasculostatin.
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83
Q

What 3 mechanisms do tumour cells use to evade host immune defence in the blood?

A
  1. Platelet aggregation.
  2. Adhesion to other tumour cells.
  3. They shed surface antigens so as to ‘distract’ lymphocytes.
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84
Q

Give an example of a malignant tumour that often spreads to the lung.

A

Sarcoma (via venae cavae -> heart -> pulmonary arteries).

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85
Q

Give an example of carcinomas that can spread to the liver.

A

Colon, stomach and pancreatic carcinomas can spread to the liver via the portal vein.

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86
Q

What causes the pain associated with acute inflammation?

A
  1. Stretching and distortion of tissues due to oedema and pus under high pressure in an abscess cavity.
  2. Chemical mediators e.g. bradykinin and prostaglandins, are also known to induce pain.
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87
Q

Describe the process of neutrophil polymorph migration into tissues as seen in acute inflammation.

A
  1. Margination of neutrophils.
  2. Pavementing of neutrophils.
  3. Neutrophils pass between endothelial cells.
  4. Neutrophils pass through basal lamina and migrate into adventitia.
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88
Q

What is the main source of histamine?

A

Mast cells; histamine is stored in granules in their cytoplasm.

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89
Q

What enzymatic cascade systems does plasma contain?

A
  1. The complement system.
  2. The kinin system.
  3. The coagulation system.
  4. The fibrinolytic system.
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90
Q

What is the role of tissue macrophages in acute inflammation?

A

They secrete chemical mediators that attract neutrophil polymorphs.

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91
Q

What is the role of the lymphatic system in acute inflammation?

A

Lymphatic channels dilate and drain away oedematous fluid therefore reducing swelling. Antigens are also carried to lymph nodes for recognition by lymphocytes.

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92
Q

What is the major role of neutrophil polymorphs in acute inflammation?

A

Phagocytosis!

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93
Q

Define carcinogenesis.

A

A multistep process in which a normal cell evolves into a cancerous cell via permanent genetic mutations

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94
Q

Give an example of a situation when transplacental exposure lead to an increase in cancer risk.

A

The daughters of mothers who had taken diethylstiboestrol for morning sickness had an increased risk of vaginal cancer.

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95
Q

What percentage of cancer risk is due to environmental factors?

A

85% environmental, 15% genetic.

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96
Q

Give 5 host factors that can affect cancer risk.

A
  1. Race.
  2. Diet.
  3. Constitutional factors (gender, age).
  4. Premalignant conditions.
  5. Transplacental exposure.
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97
Q

Name the 5 different categories of carcinogens.

A
  1. Viral.
  2. Chemical.
  3. Ionising and non-ionising radiation.
  4. Hormones, parasites and mycotoxins.
  5. Miscellaneous e.g. asbestos and metals.
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98
Q

What causes skin cancer?

A

Exposure to UV light.

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99
Q

Chemical carcinogens: what types of cancer do polycyclic aromatic hydrocarbons cause?

A

Lung cancer and skin cancer.

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100
Q

Chemical carcinogens: what can expose people to polycyclic aromatic hydrocarbons?

A

Smoking cigarettes and mineral oils.

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101
Q

Chemical carcinogens: what types of cancer do aromatic amines cause?

A

Bladder cancer.

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102
Q

Chemical carcinogens: what types of people are more susceptible to bladder cancer caused by aromatic amine exposure?

A

People who work in the rubber/dye industry.

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103
Q

Chemical carcinogens: what type of cancer do nitrosamines cause?

A

Gut cancer.

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104
Q

Chemical carcinogens: what type of cancer do alkylating agents cause?

A

Leukaemia; the risk is small in humans.

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105
Q

Define neoplasm.

A

An autonomous, abnormal, persistent new growth that continues to grow after the stimuli that caused the growth is removed

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106
Q

What is a neoplasm composed of?

A
  1. Neoplastic cells.

2. Stroma.

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107
Q

Describe neoplastic cells.

A

Neoplastic cells are derived from nucleated cells. They’re usually monoclonal and their growth and synthetic activity is related to the parent cell.

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108
Q

Describe the stroma of a neoplasm.

A

Connective tissue composed of fibroblasts and collagen; it is very dense. There is a lot of mechanical support and blood vessels provide nutrition for the neoplastic cells.

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109
Q

What is essential for neoplasm growth?

A

Angiogenesis.

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110
Q

What does a neoplasm release in order to initiate angiogenesis?

A

Vascular endothelial growth factors.

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111
Q

Why does necrosis often occur in the centre of a neoplasm?

A

The neoplasm grows quickly and outgrows its vascular supply.

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112
Q

What are the advantages of classifying neoplasms?

A

It helps to determine the appropriate treatment and prognosis.

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113
Q

What are the two ways in which neoplasms can be classified?

A
  1. Behavioural classification.

2. Histogenetic classification.

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114
Q

What is the behavioural classification of neoplasms?

A

Neoplasms can be classified as benign, malignant or borderline. Borderline tumours (e.g. some ovarian lesions) defy precise classification.

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115
Q

What is the histogenetic classification of neoplasms?

A

Histopathological tests specify tumour type by determining the cell of origin of a tumour. If the origin is unknown the tumour is said to be anaplastic.

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116
Q

What are the 7 main features of benign neoplasms.

A
  1. Localised.
  2. Non-invasive.
  3. Slow growth, low mitotic activity.
  4. Close resemblance to normal tissue.
  5. circumscribed or encapsulsted
  6. Necrosis and ulceration are rare due to slow growth.
  7. Exophytic growth.
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117
Q

What are the consequences of benign neoplasms?

A
  1. Pressure on adjacent structures.
  2. Obstruction to flow.
  3. Transformation into malignant neoplasms.
  4. Anxiety.
  5. Produce hormones
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118
Q

What are the 7 main features of malignant neoplasms.

A
  1. INVASIVE! Defining feature of a malignant tumour
  2. Metastases.
  3. Rapid growth, high mitotic activity.
  4. Little Resemblance to normal tissue.
  5. Poorly defined border due to invasive nature.
  6. Necrosis and ulceration are common.
  7. Endophytic growth.
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119
Q

What are the consequences of malignant neoplasms?

A

Destroy surrounding tissue, blood loss due to ulceration, pain, anxiety and all the benign effects

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120
Q

Define carcinoma.

A

MALIGNANT EPITHELIAL NEOPLASM!

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121
Q

Define sarcoma.

A

Malignant connective tissue neoplasm.

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122
Q

What is a rhabdomyoma?

A

Benign striated muscle neoplasm.

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123
Q

What is an adenoma?

A

Benign tumour of glandular epithelium.

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124
Q

What is a papilloma?

A

A non-glandular benign tumour.

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125
Q

What is a leiomyoma?

A

A benign smooth muscle neoplasm.

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126
Q

What is a neuroma?

A

A benign neoplasm of nerves.

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127
Q

What is a liposarcoma?

A

A malignant neoplasm of adipose tissue.

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128
Q

What is an Osteoma?

A

Benign neoplasm of bone tissue

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129
Q

What is an angioma?

A

Benign connective tissue neoplasm of the vasculature

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130
Q

What is a chondrosarcoma?

A

A malignant neoplasm of cartilage.

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131
Q

What is a melanoma?

A

A malignant neoplasm of melanocytes.

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132
Q

What type of tissue is affected in a Lipocarcinoma?

A

TRICK QUESTION
Lipo is adipose tissue which is a connective tissue. carcinoma is a malignant neoplasm of epithelial tissue.
Sarcoma is a malignant neoplasm of connective tissue

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133
Q

What is a lymphoma?

A

A malignant neoplasm of lymphoid cells.

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134
Q

Give examples of omas that are not neoplasms

A

Granuloma
Mycetoma
Tuberculoma

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135
Q

What kind of cancer is:
Burkitts Lymphoma
Ewings Sarcoma
Grawitz Tumour
Kaposi’s Sarcoma

A

Burkitts Lymphoma - Lymphoma
Ewings Sarcoma - Bone cancer
Grawitz Tumour - Renal cell carcinoma
Kaposi’s Sarcoma - Angiosarcoma

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136
Q

What is a teratoma?

A

A neoplasm that arises from all 3 germ cells of an embryo

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137
Q

What are blastomas?

A

These are embryonal tumours that resemble foetal tissue.

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138
Q

What are APUDomas?

A

Neuroendocrine tumours

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139
Q

What is a mesothelioma?

A

A malignant neoplasm of mesothelial cells.

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140
Q

Carcinomas and sarcomas are further classified according to the degree of differentiation. Is a carcinoma/sarcoma with a close resemblance to normal tissue classified as well differentiated or poorly differentiated?

A

A carcinoma/sarcoma with a close resemblance to normal tissue is classified as well differentiated. These types of neoplasms are low grade and have a better prognosis.

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141
Q

What must the immune system do in order to be effective?

A

The immune system has to discriminate self from non-self.

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142
Q

Describe innate immunity.

A

Non-specific, instinctive, present from birth, first line of defence. It is focused around physical and chemical barriers and phagocytosis. No lymphocyte involvement.

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143
Q

Give examples of physical and chemical barriers used in innate immunity?

A

Skin, mucociliary escalator, gastric acid, hairs, lysozymes etc.

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144
Q

What is the function of lysozyme?

A

It destroys bacterial cell walls.

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145
Q

Describe adaptive immunity.

A

Acquired, Specific, requires lymphocytes. immunological memory.

1st response is slow to build up the memory but the second responses are quicker and larger

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146
Q

Give examples of 3 polymorphonuclear leukocytes.

A
  1. Neutrophils.
  2. Basophils.
  3. Eosinophils.
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147
Q

Give examples of 3 mononuclear leukocytes.

A
  1. Monocytes.
  2. B lymphocytes.
  3. T lymphocytes.
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148
Q

In which primary lymphoid tissue do T cells mature?

A

Thymus.

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149
Q

In which primary lymphoid tissue do B cells mature?

A

Bone marrow.

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150
Q

How do T cells recognise antigens?

A

For T cells to recognise antigens they must be displayed by an antigen presenting cell and bound to MHC1/2. T cells can’t recognise soluble antigens.

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151
Q

What is the function of T helper 1 (CD4)?

A

It helps the immune response against intracellular pathogens. Secretes cytokines.

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152
Q

What is the function of T helper 2 (CD4)?

A

It helps produce antibodies against extracellular pathogens. Secretes cytokines.

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153
Q

What is the function of Cytotoxic T cell (CD8)?

A

It can kill cells directly by binding to antigens; they induce apoptosis.

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154
Q

What is the function of T reg (FoxP3)?

A

They regulate the immune response.

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155
Q

Which cells express MHC1?

A

Ubiquitously expressed by almost all mammalian cells and all nucleated cells express MHC1. e.g. a virus infected or cancer cell would express MHC1.

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156
Q

Which cells express MHC2?

A

Antigen presenting cells ONLY e.g. macrophages, B cells, dendritic cells.

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157
Q

Which MHC would an intracellular antigen (endogenous) lead to the expression of?

A

MHC1.

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158
Q

Which MHC would an extracellular antigen (exogenous) lead to the expression of?

A

MHC2.

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159
Q

What type of T cell binds to MCH1?

A

Cytotoxic T cells (CD8).

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160
Q

What type of T cells binds to MCH2?

A

Helper T cells (CD4).

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161
Q

What do B cells differentiate into?

A

Plasma cells. The plasma cells then produce antibodies.

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162
Q

What does a helper T cell bind to?

A

A T cell receptor which is bound to an antigen epitope which is bound to MHC2 on an APC.

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163
Q

Describe T cell Activation

A

Naive T cell with the TCR binds to the epitope of the antigen presented via MHC on the APC
Co stimulatory molecule CD28 binds to CD80/CD86 on the APC to allow for full activation of the T cell.
The T cell will release IL-2 which then rebinds to the T cell IL-2-R to initiate T cell differentiation via autocrine mechanism.
The T cell will divide into Th1 or TH2 depending on the IL-12 concentration present at the time of differentiation.

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164
Q

What determines if a CD4 T cell differentiates into a Th1 or Th2 subtype when activated?

A

The concentration of IL-12 present
High IL-12 = Th1
Low IL-12 = Th2

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165
Q

What cytokines are released from Th1 cells and Th2 cells

A

Th1 - IL2 and INFy
Th2 - IL-4, IL-5, IL-10

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166
Q

What is the function of a Th1 T cell

A

Th1 cells stimulate cellular immune response, activate NK cells and macrophages to increase the innate response

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167
Q

What is the function of a Th2 T cell

A

Stimulates the humoral immune response by promoting B cell proliferation and antibody production

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168
Q

Describe Th1 T cell activation

A

APC presents Ag with MHC II to a naive CD4 T cell
Stimulation with high levels of IL-12 activates CD4 T cells to Th1 cells
Th1 cells travel to secondary lymph tissues where they proliferate (clonal expansion and T memory cells)
Th1 recognises Ag on infected cells via TCR
Th1 secretes INFy to stop viral spread and activate macrophages

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169
Q

Which interleukin is secreted when a helper T cell is bound to a T cell receptor?

A

IL-2. This then binds to an IL-2 receptor on the T cell and produces a positive feedback mechanism leading to division and differentiation.

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170
Q

How many antibodies can each B cell make?

A

Each B cell can only make 1 type of antibody. This 1 antibody can only bind to 1 epitope.

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171
Q

What happens to B cells that recognise ‘self’?

A

They are killed in bone marrow.

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172
Q

Describe the process of a T helper cell binding to a B cell.

A

A B-cell antibody binds an antigen -> phagocytosis -> epitope is displayed on the surface of the B-cell bound to an MHC2 -> TH2 binds to B-cell epitope -> cytokine secretion of IL-4 and IL-5 induces B-cell clonal expansion and differentiation into plasma cells and memory B cells respectively

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173
Q

Give 3 functions of antibodies.

A
  1. Neutralise toxins.
  2. Opsonisation.
  3. Activate classical complement system.
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174
Q

Which immunoglobulin is found in breast milk and other secretions?

A

IgA.

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175
Q

What are the 2 most common immunoglobulins?

A

IgG and IgM.

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176
Q

Which region of an antibody binds antigens?

A

The fab region.

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177
Q

Which region of an antibody binds to B cells?

A

The Fc region.

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178
Q

Which interleukins stimulate class switching to IgA and IgE?

A

IgA = IL-4
IgE = IL-5

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179
Q

Name 5 types of cytokines.

A
  1. Interferons.
  2. Interleukins.
  3. Colony stimulating factors.
  4. Tumour necrosis factors.
  5. Chemokines
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180
Q

What is the function of interferons?

A

Interferons produce antiviral proteins.

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181
Q

What is the function of interleukins?

A

Interleukins cause cell division and differentiation.
can be pro-inflammatory or anti-inflammatory

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182
Q

What is the function of colony stimulating factor (CSF)?

A

CSF causes division and differentiation of bone marrow stem cells.

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183
Q

What is the function of tumour necrosis factor (TNF)?

A

TNF mediates inflammation and cytotoxic reactions.

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184
Q

What is the function of chemokines?

A

Chemokines attract leukocytes to sites of infection.

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185
Q

Define inflammation

A

A series of reactions that brings cells and molecules of the immune system to sites of infection or damage

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186
Q

Give an overview of the inflammatory response

A

Stop bleeding (coagulation)
Acute Inflammation (leukocyte recruitment)
Kill pathogens, neutralise toxins and limit pathogen spread
clear pathogens/dead cells (phagocytosis)
proliferation of cells to repair damage
remove blood clot - remodel extracellullar matrix
re-establish normal structure/function of tissue.

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187
Q

Give examples of secondary lymphoid tissue.

A

The spleen, lymph nodes, mucosa associated lymphoid tissue - MALT.

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188
Q

Describe the process of phagocytosis.

A
  1. Pathogen binds to neutrophil/macrophage.
  2. Engulfment of pathogen.
  3. Phagosome formation.
  4. Lysosome fusion - phagolysosome.
  5. Pathogen is destroyed.
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189
Q

Give 3 examples of O2 dependent mechanisms of killing.

A
  1. Killing using reactive oxygen intermediates.
  2. Superoxides can be converted to H2O2 and then to hydroxyl free radicals.
  3. NO leads to vasodilation and increased extravasation and so more neutrophils etc are in the tissues to destroy pathogens.
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190
Q

What is the role of NO in killing pathogens?

A

NO leads to vasodilation and increased extravasation. This means more neutrophils etc pass into the tissues to destroy pathogens.

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191
Q

Why can superoxides be used to destroy pathogens?

A

Superoxides can be converted to H2O2 and then to hydroxyl free radicals. Hydroxyl free radicals are highly reactive and can destroy pathogens.

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192
Q

What mechanisms or cells are involved in O2 independent killing?

A

Defensins, lysozyme, pH, TNF.

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193
Q

Where are complement system plasma proteins derived from?

A

The liver.

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194
Q

What are the 3 main modes of action of the complement system activation?

A
  1. Direct Pathogen lysis.
  2. Opsonitation - Increased phagocytosis.
  3. Inflammation - Activation of leukocytes such as macrophages via chemotaxis
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195
Q

What activates the classical complement pathway?

A

Antibodies.

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196
Q

Briefly describe the classical complement pathway.

A
  1. C1s cleaves C4 -> C4a and C4b.
  2. C4b binds C2b forming C4b2b. C4b2b is a C3 convertase and is responsible for C3 -> C3a and C3b.
  3. C4b2b binds C3b forming C4b2b3b.
  4. C5,6,7,8 and 9 also bind and eventually you get MAC formation. MAC is a pore like channel in a membrane.
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197
Q

What compound prevents excessive activation of the classical complement pathway?

A

C1 inhibitor.

- C1 inhibitor leads to a negative feedback loop.

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198
Q

What activates the lectin pathway?

A

Mannose binding protein.

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199
Q

What activates the alternative pathway?

A

Bacterial cell walls and endotoxin.

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200
Q

What are the 3 different pathways that make up the complement system?

A
  1. Classical.
  2. Lectin.
  3. Alternative.
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201
Q

Briefly describe the alternative pathway.

A
  1. C3 reacts slowly with H2O forming C3(H2O).
  2. C3(H2O) binds factor B. This becomes a substrate for cleavage by factor D.
  3. Factor B is split into Bb and Ba.
  4. Bb sticks to C3(H2O) forming C3(H2O)Bb.
  5. C3(H2O)Bb is a C3 convertase that cleaves C3 into C3b and C3a.
  6. C3b then binds to pathogens and causes opsonisation for improved phagocytosis. Also leads to MAC formation.
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202
Q

What is the function of these complement proteins:
MAC
C3a and C5a
C3b

A

MAC - Lyse microbes directly
C3a /C5a - Chemotaxis
C3b - Opsonisation

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203
Q

Which complement plasma proteins have opsonic properties when bound to a pathogen?

A

C3b and C4b.

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204
Q

What is the function of MAC in a pathogens’ membrane?

A

MAC is a leaky pore like channel. Ions and water pass through the channel and disrupt the intracellular microbe environment -> microbe lysis.

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205
Q

Which complement plasma proteins are pro-inflammatory and cause chemotaxis and activation of neutrophils and monocytes etc?

A

C3a and C5a.

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206
Q

What kind of immunity are PRR’s and PAMP’s associated with?

A

Innate immunity.

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207
Q

What are PRR’s a receptor for?

A

PAMP’s.

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208
Q

Name 3 receptors that make up the PRR family.

A
  1. Toll-like receptors (TLR).
  2. Nod-like receptors (NLR).
  3. Rig-like receptors (RLR).
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209
Q

What is the main function of TLR’s?

A

TLR’s send signals to the nucleus to secrete cytokines and interferons. These signals initiate tissue repair. Enhanced TLR signalling = improved immune response.

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210
Q

What is the main function of NLR’s?

A

NLR’s detect intracellular microbial pathogens. They release cytokines and can cause apoptosis if the cell is infected.

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211
Q

What disease could be caused by a non-functioning mutation in NOD2?

A

Crohn’s disease.

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212
Q

What is the main function of RLR’s?

A

RLR’s detect intracellular double stranded RNA. This triggers interferon production and so an antiviral response.

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213
Q

TLR’s are adapted to recognise damaged molecules. What characteristic do these damaged molecules often have in common?

A

They are often hydrophobic.

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214
Q

What kind of TLR’s can be used in vaccine adjuvants?

A

TLR4 agonists.

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215
Q

Give examples of diseases that can be causes by PRR’s failing to recognise pathogens.

A
  1. Atherosclerosis.
  2. COPD.
  3. Arthritis.
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216
Q

Give examples of 3 extracellular PRR.

A
  1. Mannose receptors.
  2. Scavenger receptors.
  3. TLR’s.
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217
Q

What is the function of mannose and scavenger extracellular receptors?

A

The induce pathogen engulfment.

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218
Q

Give an example of an intracellular PRR.

A

NLR.

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219
Q

Where are circulating PRR secreted from?

A

Epithelia, phagocytes and the liver. They can activate the complement cascade and induce phagocytosis.

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220
Q

What happens when a PAMP binds to a PRR?

A

The innate immune response and inflammatory response is triggered.

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221
Q

What is extravasation?

A

Leukocyte (WBC) migration across the endothelium.

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222
Q

What do macrophages at the tissues secrete to initiate extravasation?

A

TNF alpha.

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223
Q

Describe the process of extravasation.

A
  1. Macrophages at tissues release TNF alpha.
  2. The endothelium is stimulated to express adhesion molecules (eg. GAG) and to stimulate chemokines.
  3. Neutrophils bind to adhesion molecules (ICAM-1); they roll, slow down and become stuck to the endothelium.
  4. Neutrophils are activated by chemokines.
  5. Neutrophils pass through the endothelium to the tissue to help fight infection.
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224
Q

What 2 compounds can act as C3 convertase?

A
  1. C4b2b - produced in the classical and lectin pathways.

2. C3(H2O)Bb - produced in the alternative pathway.

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225
Q

What type of cancers results from transformations in the germ line?

A

Inheritable cancers (<10%).

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226
Q

What type of cancers results from transformations in somatic cells?

A

Non-inheritable cancers (>90%).

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227
Q

What factors can cause transformations in somatic cells?

A

Environmental factors e.g. UV, chemicals (smoking can cause lung cancer), pathogens (HPV can cause cervical cancer).

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228
Q

What are the 7 hallmarks for cancer?

A
  1. Evade apoptosis.
  2. Ignore anti-proliferative signals.
  3. Growth and self sufficiency.
  4. Limitless replication potential.
  5. Sustained angiogenesis.
  6. Invade surrounding tissues.
  7. Escape immuno-surveillance.
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229
Q

What are the two types of tumour antigens and where are they found?

A
  1. Tumour specific antigens; only found on tumour cells. Due to point mutations.
  2. Tumour associated antigens; found on normal cells and over expressed on tumour cells.
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230
Q

What is cancer immunosurveillance?

A

When the immune system recognises and destroys transformed cells, this is an important host protection process.

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231
Q

What is cancer immunoediting?

A

When the immune system kills tumour cells changes are induced in the tumour, the tumour cells are ‘edited’ by natural selection. The tumour cells are then disguised from the immune system, they escape destruction and recurrence is possible.

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232
Q

What are the 3 E’s of cancer immunoediting?

A
  1. Elimination.
  2. Equilibrium.
  3. Escape.
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233
Q

Give an example of active cancer immunotherapy.

A

Vaccination e.g. killed tumour vaccine, purified tumour antigens, APC-based vaccines etc.

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234
Q

Give an example of passive cancer immunotherapy.

A

T cell transfer, anti-tumour antibodies.

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235
Q

Why is hypoxia a prominent feature of a lot of malignant tumours?

A

Malignant tumours grow rapidly and so outgrow their blood supply.

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236
Q

Give 3 reasons why hypoxic tumours have a poor prognosis for the patient.

A
  1. Hypoxic tumours have growth factors for angiogenesis and so can receive nutrients for growth.
  2. They suppress the immune system.
  3. They are resistant to chemotherapy and radiotherapy.
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237
Q

Define Active immunity and give a natural and artificial example

A

The immunity which results from the production of antibodies by the immune system in response to the presence of an antigen.

Natural - body encounters a pathogen

Artificial - Vaccines, mimics,

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238
Q

Define passive immunity and give a natural and artificial example

A

the short-term immunity which results from the introduction of antibodies from another person or animal.

Natural - Maternal Igs passed onto baby through breast milk/ colostrum

Artificial - Antivenom / Ig injection from another organism

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239
Q

Give 3 advantages of active immunity.

A
  1. Induces immunological memory.
  2. Produces high affinity antibodies.
  3. It produces a persistent protective response against pathogens.
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240
Q

Give 2 advantages of passive immunity.

A
  1. Immediate effect.

2. Useful treatment for acute dangers e.g. snake venom.

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241
Q

Give 3 disadvantages of passive immunity.

A
  1. Short term.
  2. No immunological memory produced.
  3. Reaction is possible.
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242
Q

Describe the first immune response to initial exposure.

A
  1. Innate immune response.
  2. IgM predominates.
  3. Low affinity.
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243
Q

Describe the second immune response following exposure to a pathogen encountered before.

A
  1. Rapid and larger than the first.
  2. High affinity IgG.
  3. Adaptive immunity, T cell help.
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244
Q

What is the purpose of a vaccine and how do they work?

A

A form of artificial active immunity which usually requires 2 doses - a primer and then a booster.

They work by inducing an immune response to mimic a natural infection without being symptomatic.
This creates IgM and IgG Abs so that upon genuine exposure to the pathogen the body can fight it.

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245
Q

What are the different types of components used in vaccines?

A

Live attenuated - Genetically modified organism (eg. MMR)
Antigens
Toxins - Tetanus
CW constituents - Hep B
DNA/RNA - eg. COVID-19

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246
Q

Give 3 advantages of live vaccines.

A
  1. Very effective, prolonged and comprehensive.
  2. Immunological memory produced.
  3. Often only 1 vaccine is needed.
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247
Q

Give 2 disadvantages of live vaccines.

A
  1. Immunocompromised patients may become ill.

2. Vaccines often need to be refrigerated which can be a problem in remote areas.

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248
Q

Give 2 advantages of inactivated vaccines.

A
  1. There is no risk of infection.

2. Storage is less critical.

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249
Q

Give 3 disadvantages of inactivated vaccines.

A
  1. Inactivated vaccines tend to only activate the humoral response; there is a lack of T cell involvement.
  2. The response is often weak.
  3. Boosters are needed and so patient compliance may be poor.
250
Q

What is the role of an adjuvant?

A

An adjuvant is a substance added to a vaccination to stimulate an immune response. They convince your immune system that you’re infected.

251
Q

What can be used as an adjuvant?

A

Toxoids, proteins, chemicals (aluminium salts) etc.

252
Q

What are the 5 features of an ideal vaccine?

A
  1. Safe.
  2. Induces a suitable immune response.
  3. Shouldn’t require repeated boosters.
  4. Generates immunological memory.
  5. Stable and easy to transport.
253
Q

Give 3 advantages of transplantation.

A
  1. Improved quality of life.
  2. Improves survival rates.
  3. Cost effective.
254
Q

Why are immunosuppressive agents needed to prevent rejection?

A

Transplanted organs are recognised as non self and therefore are seen as a threat. Graft v host disease; T-cells destroy graft cells.

255
Q

On which chromosome are MHC proteins found?

A

Chromosome 6.

256
Q

Describe the transplant cascade.

A

Donor -> organ preservation -> implantation -> re-perfusion -> organ function.

257
Q

What are the main compounds involved in reperfusion injury?

A

Free radicals e.g. H2O2, O2-, OH-. They damage cell walls.

258
Q

Define allorecognition.

A

The ability of an organism to distinguish its own tissues from those of another. Recognition of non-self antigens.

259
Q

What are the consequences of transplant rejection?

A

Fibrosis and scarring.

260
Q

Describe the immune responses to detection of graft antigens.

A
  1. Innate immune response is activated.
  2. T cell mediated cytotoxicity.
  3. Ab mediated cytotoxicity.
  4. Hypersensitivity.
  5. Tolerance.
261
Q

Give 6 ways of preventing transplant rejection?

A
  1. Manage risk factors.
  2. Tissue typing.
  3. Cross match.
  4. Immunosuppressive agents.
  5. Sensitisation and desensitisation.
  6. Tolerance.
262
Q

Why is it important to get the balance right when using immunosuppressive agents?

A

Too much = infection.

Too little = rejection.

263
Q

What is involved in tissue typing?

A
  1. Blood group matching.

2. HLA typing.

264
Q

What is involved in cross matching?

A

Detecting anti HLA antibodies.

Cell based assays and solid phase assays can be used.

265
Q

Define tolerance with regards to transplant immunology.

A

Tolerance is the acquired modification to host immunity leading to drug free transplant survival with full immunocompetence.

266
Q

Define xenotransplantation.

A

Transplantation of tissues from one species to another.

267
Q

What is allergy?

A

An abnormal response to harmless foreign material.

268
Q

What is atopy?

A

The tendency to develop allergies.

269
Q

Which immunoglobulin is most commonly involved in allergic responses?

A

IgE.

270
Q

Which cells are most commonly involved in allergic responses?

A

Mast cells! Also eosinophils and basophils.

271
Q

What happens to IgE receptors when a ‘threat’ is identified?

A

The receptors cross-link.

272
Q

Which cells express high affinity IgE receptors?

A

Mast cells, basophils and eosinophils.

273
Q

What are the steps in an allergic response?

A

Allergen/threat is identified -> high affinity IgE receptors cross link -> IgE binds -> Mast cells are activated -> granules released -> histamine and cytokines. Cytokines induce a TH2 response.

274
Q

What is the main IgE receptor cell?

A

MAST CELLS!

275
Q

Which compound causes blood vessel dilation and vascular leakage in an allergic response?

A

Histamine.

276
Q

What is the role of cytokine release in an allergic response?

A

They induce a TH2 response.

277
Q

Which cells and which immunoglobulin is commonly involved in anaphylaxis?

A
  • Mast cells and basophils.

- IgE.

278
Q

Give examples of anaphylactic systemic effects.

A
  • CV: vasodilation, lowered BP.
  • Resp: bronchial SM contraction, mucus.
  • Skin: rash, swelling.
  • GI: pain, vomiting.
279
Q

Give 5 possible treatments for allergy and hypersensitivity.

A
  1. Avoid allergens.
  2. Desensitisation (immunotherapy, some risks).
  3. Prevent IgE production (interfere with TH2 pathway).
  4. Prevent mast cell activation.
  5. Inhibit mast cell products (e.g. histamine receptor antagonists).
280
Q

Define Immune Tolerance

A

Physiological destruction of T/B cells that recognise self antigens.
Central tolerance - Thymic tolerance of T cells
Peripheral Tolerance - If T/B cells evade central tolerance then they can be destroyed by Tregs in secondary lymphoid organs.

281
Q

Define Autoimmunity

A

Pathological response where the immune system recognises self antigens and attacks these tissues.

282
Q

Give some examples of organ-specific autoimmune diseases

A

T1DM - Endocrine pancreas - Beta cells
MS - oligodendrocytes of CNS
Pernicious anaemia - parietal cells of stomach
Hashimotos Thyroiditis - Anti-TPO Abs
Graves Disease - TSH-R
Myasthenia Gravis - Ach-R Abs

283
Q

Give some examples of non-specific organ autoimmune diseases

A

SLE - DNA:ANA
Autoimmune haemolytic anaemia - RBCs
immune thrombocytopenic purpura - Platelets

284
Q

Which infection is most often seen in patients with hypogammaglobulinemia?

A

Streptococcus penumonia sinusitis.

285
Q

Give 5 examples of PAMPs.

A
  1. Lipopolysaccharides.
  2. Endotoxins.
  3. Bacterial flagellin.
  4. Peptidoglycans.
  5. dsRNA.
286
Q

Which PRR responds to lipopolysaccharides?

A

TLR-4.
Responds to LPS on gram negative bacteria

287
Q

Is production of interferons (anti-viral proteins) part of the elimination phase of complement activation?

A

No

288
Q

Give 4 causes of acquired immunodeficiency.

A
  1. Cancer.
  2. HIV.
  3. Having chemotherapy.
  4. Taking immunosuppressants.
289
Q

What signs and symptoms might a person with HIV present with?

A

Fever, weight loss, recurrent infections, respiratory infections, TB.

290
Q

What immune system cells are affected in HIV?

A

There is CD4 deficiency and B cell defects too. The adaptive immunity is affected.

291
Q

What is the name of the disease that is characterised by B cell deficiency?

A

Hypogammaglobulinaemia.

292
Q

What infection is most commonly seen in patients with hypogammaglobulinaemia?

A

Streptococcus pneumonia.

293
Q

Describe hyper IgM syndrome.

A

High numbers of IgM. IgM is non specific and has a low affinity. IgM is unable to class switch to more ‘useful’ immunoglobulins and so IgA, IgE and IgG numbers are low.

294
Q

What are the consequences of complement deficiency?

A

Impaired opsonisation of encapsulated bacteria.

295
Q

What is terminal complement deficiency and what are its consequences?

A
  • Terminal complement deficiency is when there’s a problem with C5-8 and so MAC isn’t produced.
  • The consequences of this are chronic Neisserial infections and recurrent meningitis.
296
Q

What are the consequences of being deficient in C1 inhibitor?

A

Angioedema - facial swelling.

297
Q

What are the consequences of being deficient in C1, 2 or 4?

A

Increased likelihood of autoimmune disease especially systemic lupus erythematosus.

298
Q

What are the consequences of hyposplenism?

A

Reticuloendothelial function is decreased. This means the body has difficulty dealing with encapsulated bacteria e.g. streptococcus pneumonia.

299
Q

What is thymic aplasia?

A

A deficiency in mature T cells.

300
Q

How can immune function be assessed?

A
  1. Looking at neutrophil numbers, morphology and flow cytometry.
  2. Looking at B and T cell subsets, numbers and response to vaccines.
  3. Genetic studies.
301
Q

Give 3 examples of chronic inflammatory diseases.

A
  1. Rheumatoid arthritis.
  2. Crohn’s disease.
  3. TB.
302
Q

Name 3 conventional therapies used in managing CID.

A
  1. NSAIDs.
  2. DMARDs.
  3. Steroids.
303
Q

What disease are DMARDs most commonly used in the management of?

A

Rheumatoid arthritis.

DMARD - disease-modifying antirheumatic drug

304
Q

How do NSAIDs work in relieving inflammation.

A

NSAIDs inhibit COX 1 and 2. COX 2 is needed for prostaglandin synthesis. Prostaglandins are responsible for inflammation and pain. Therefore NSAIDs reduce symptoms of inflammation and pain.

305
Q

What is a disadvantage of long term NSAID use?

A

NSAIDs can cause gastric bleeding. They inhibit COX 1 which is needed for prostaglandin synthesis and prostaglandins are needed for gastric mucus production.

306
Q

Give 2 advantages of biological agents in treating chronic inflammatory disease?

A
  1. They’re extremely specific.

2. A low dose is very effective.

307
Q

Give 5 disadvantages of biological agents in treating chronic inflammatory disease?

A
  1. They’re very expensive.
  2. There is a risk of contamination.
  3. They’re always injected.
  4. They’re immunosuppressive.
  5. They need to be handled carefully to prevent denaturation.
308
Q

What class of biological agent is often used in the treatment of rheumatoid arthritis when DMARDs fail?

A

TNF blockers - they bind to TNF to prevent it interacting with its receptors.

309
Q

Name 3 TNF blockers.

A
  1. Etanercept (TNF alpha specific).
  2. Infliximab.
  3. Adalimumab.
310
Q

What compound is often combined with biological agents to make treatment cheaper?

A

Methotrexate.

311
Q

Give a side effect of using TNF blockers.

A

Increased susceptibility to TB.

312
Q

How do IL-6 blockers work?

A

IL-6 is an inflammatory cytokine. The biological agent binds to IL-6 so as to prevent it interacting with its receptor.

313
Q

Name an IL-6 blocker.

A

Tocilizumab.

314
Q

When are IL-6 blockers used?

A

They’re used in the treatment of rheumatoid arthritis when TNF blockers fail.

315
Q

What are the risks of using IL-6 blockers?

A

They dampen the immune response and so you have an increased risk of infection. There is also an incerased risk of shingles and chickenpox.

316
Q

Name 4 classes of biological agents and give an example of a drug for each.

A
  1. TNF blockers e.g. etanercept.
  2. IL-6 blockers e.g. Tocilizumab.
  3. Anti B lymphocytes e.g. rituximab.
  4. T cell activation blockers e.g. abatacept.
317
Q

In what region of the antibody is there reversible bonding between antibodies and antigens?

A

Complementarity determining region (CDR).

- Hydrogen bonds and VDW’s etc form cumulative weak interactions that together form a strong force.

318
Q

True or False. The heavy and light chains of an antibody are coded for by the same gene.

A

False. Distinct sets of genes code for the heavy and light chains.

319
Q

What region determines Ig class?

A

The constant region!

320
Q

What is the result of recombination in the Ig region?

A

Class switching.

321
Q

Describe complement fixation.

A

An antibody binds multiple antigens so as to bring the Fc regions together. The complement pathway is initiated in this process and you get MAC formation.

322
Q

Which compound is responsible for signalling when an antigen binds to an antibody?

A

Tyrosine kinase.

323
Q

What immunoglobulin do naive antibodies express?

A

IgM.

324
Q

Describe the process of class switching.

A

Antigen engagement and T cell help will result in class switching. A different FC region is used and there is affinity maturation.

325
Q

What do T cells recognise?

A

PEPTIDES

326
Q

Describe somatic hypermutation.

A
  1. Random mutations in CDR.
  2. Amino acid sequences are effected meaning Ab-Ag affinity is altered.
  3. High affinity B cell clones are selected via natural selection.
327
Q

Briefly describe the steps involved between T cell stimulation and plasma cell differentiation.

A
  1. T cells are stimulated.
  2. Cytokine release.
  3. B cell proliferation.
  4. Somatic hypermutation.
  5. High affinity B cell clones differentiate into plasma cells and memory cells.
328
Q

Give 4 uses of antibodies in medicine.

A
  1. Diagnostic tools.
  2. Immunoassays, Ab’s are used to measure the presence of a molecule.
  3. Flow cytometry, Ab’s label cells in suspension.
  4. Therapeutic uses, monoclonal Ab’s can act as specific antagonists for biological targets e.g. HERCEPTIN.
329
Q

Give an example of a proton pump inhibitor.

A

Omeprazole.

330
Q

Give an example of a statin.

A

Simvastatin.

331
Q

Give an example of an ACE inhibitor.

A

Enalapril.

332
Q

Give an example of a COX inhibitor.

A

Aspirin and ibuprofen.

333
Q

Give an example of a β2 adrenoceptor agonist.

A

Salbutamol.

334
Q

Give an example of a β1 adrenoceptor blocker.

A

Atenolol.

335
Q

Give an example of a Ca2+ channel blocker.

A

Amlodipine.

336
Q

Give an example of a broad spectrum antibiotic.

A

Amoxicillin.

337
Q

Give an example of an opiate analgesic.

A

Tramadol.

338
Q

What do most drugs target?

A

Proteins!

339
Q

Name 4 receptors that drugs target.

A
  1. Ligand gated ion channels.
  2. GPCR.
  3. Kinase linked.
  4. Cytosolic/nuclear.
340
Q

Give an example of a ligand gated ion channel.

A

Nicotinic Ach receptor.

341
Q

Give an example of a GPCR.

A

Muscarinic and β2 adrenoceptor.

GPCR’s usually interact with adenylate cyclase or phospholipase C

342
Q

Give an example of a kinase linked receptor.

A

Receptors for growth factors.

343
Q

Give an example of a cytosolic/nuclear receptor.

A

Steroid receptors; steroids affect transcription.

344
Q

What are agonists?

A

Agonists bind to a receptor and to activate it.

345
Q

What are antagonists?

A

Antagonists decrease the effect of an agonist. They show no response at a receptor.

346
Q

Describe the shape of a log dose-response curve.

A

Sigmoidal.

347
Q

What does EC50 tell us about a drug?

A

Its potency!

348
Q

What is EC50?

A

The concentration of a drug that gives half the maximal response.

349
Q

Would a drug with a lower EC50 have a lower or greater potency?

A

Greater potency.

350
Q

What does Emax tell us about a drug?

A

Efficacy - it is the maximum response achievable.

351
Q

What is the Intrinsic Activity of a drug?

A

The ability of a drug receptor complex to produce a maximum functional response

352
Q

How can you calculate the intrinsic activity?

A

Emax of partial agonist / Emax of full agonist

353
Q

Which is more efficacious, a full agonist or partial agonist?

A

A full agonist is more efficacious because a full agonist can give a 100% response.

354
Q

Would an antagonist shift a dose-response curve to the left or right?

A

The antagonist would shift the dose-response curve to the RHS. The drug therefore becomes less potent.

355
Q

Drug action: define affinity.

A

How well a ligand binds to a receptor.

356
Q

Drug action: define efficacy.

A

How well a ligand activates a receptor; how well it induces a conformational change and how much of a response is achieved

357
Q

What is the effect of fewer receptors on drug potency?

A

Fewer receptors will shift the dose-response curve to the RHS, this means drug potency will be reduced.

358
Q

What is the effect of fewer receptors on receptor response?

A

Receptor response is still 100% due to receptor reserve. (Partial agonists don’t have receptor reserve).

359
Q

What is the affect of less signal amplification on drug response?

A

Less signal amplification gives a reduced drug response.

360
Q

Describe allosteric modulation.

A

An allosteric modulator binds to a different site on a receptor and influences the role of an agonist.

361
Q

What factors govern drug action?

A

Receptor related:
Affinity
Efficacy

Tissue Related:
Receptor number
Signal amplification

362
Q

Define specificity and sensitivity in pharmacology

A

Specificity - The measure of a receptor’s ability to respond to a single ligand. (low specificity results in physiological responses not targeted or intended by the drug eg. side effects) the drug acts on a certain target (eg. adrenoceptors)

Sensitivity - the drug acts on a subtype of a specific target (eg. b1 adrenoceptors rather than all adrenoceptors)

363
Q

What is inverse agonism?

A

Where an agonist has a negative effect at a receptor and produces an opposite to expected response

364
Q

Does an antagonist show efficacy?

A

No. An antagonist has affinity but zero efficacy. An agonist however demonstrates affinity and efficacy.

365
Q

Pharmacology: define tolerance.

A

A reduction in the effect of a drug overtime. This can be due to continuous use of repeatedly high concentrations.

366
Q

What 3 ways can a receptor be desensitised?

A
  1. Uncoupled (an agonist would be unable to interact with a GPCR).
  2. Internalised (endocytosis, the receptor is taken into vesicles in the cell).
  3. Degraded.
367
Q

Can aspirin be described as a selective drug?

A

No. Aspirin is non-selective, it acts on COX1 and COX2.

368
Q

What is the function of COX1 and COX2?

A

They cyclise and oxygenate arachidonic acid and produce prostaglandin H2.

369
Q

What does prostaglandin H2 form when it interacts with synthases?

A

Prostanoids.

370
Q

Define pro-drugs and give an example of one.

A

Drugs that need to be activated enzymatically e.g. ACE inhibitors, enalapril.

371
Q

How do ACE inhibitors work?

A

Angiotensinogen is converted to angiotensin 1 via renin. Angiotensin 1 is then converted to angiotensin 2 via ACE. ACE inhibitors prevents angiotensin 1 binding and so you don’t get angiotensin 2 formation.

(Angiotensin 2 is a vasoconstrictor and so ACEi can be used in the treatment of hypertension).

372
Q

Give an example of a β lactam antibiotic.

A

Penicillin and amoxicillin.

373
Q

How do β lactam antibiotics work?

A

The inhibit transpeptidase and so prevent bacterial cell wall synthesis.

374
Q

How do diuretics work?

A

They inhibit ‘synporters’ in the loop of henle. This leads to increased H2O excretion and decreased salt reabsorption and so BP decreases.

375
Q

Give an example of loop of henle diuretics.

A
  • Furosemide, act on the ascending loop.

- Thiazides, act on the distal tubule.

376
Q

How can drugs be developed?

A
  1. Serendipity, by chance. e.g. penicillin.

2. Rational drug design. e.g. propranolol.

377
Q

Describe how rational drug design works.

A

Rational drug design is focused on developing an antagonist from an agonist. It looks at solubility, electrostatic charge and bulk.

378
Q

How do you determine whether insulin is long or short acting?

A

Small changes in amino acid sequence will determine whether insulin is long or short lasting - RECOMBINANT PROTEIN!

379
Q

Name 3 things that the chemical properties of a drug can influence?

A
  1. Administration.
  2. Distribution.
  3. Elimination.
380
Q

As the difference in concentration falls what happens to the rate of reaction?

A

The rate of reaction will slow down.

Rate is proportional to the concentration of drug

381
Q

What is the association between diffusion and concentration gradient?

A

Diffusion is proportional to concentration gradient; this is a first order process and represents an exponential function.

382
Q

How many litres of water are there in the following body compartments:

a) Plasma.
b) Interstitial space.
c) Intracellular space.

A

a) 3L.
b) 11L.
c) 28L.

383
Q

What are the 5 ways by which fluid can move between compartments?

A
  1. Simple diffusion.
  2. Facilitated diffusion.
  3. Active transport.
  4. Movement through extra-cellular spaces.
  5. Non-ionic diffusion.
384
Q

What can influence the degree of ionisation of weak acids and weak bases?

A

pH.

385
Q

What equation can be used to determine the degree of ionisation at a specific pH?

A

Henderson Hasselbach.

pH = log[A-]/[HA] + pKa.

386
Q

What can enhance non ionic diffusion?

A

Non ionic diffusion can be enhanced if adjacent compartments have pH difference.

387
Q

In terms of ionisation, what happens to Aspirin in the stomach?

A

Aspirin is a weak acid and so becomes less ionised in the stomach due to the low gastric pH.

388
Q

What is the advantage of aspirin becoming less ionised in the stomach?

A

This allows rapid non-ionic diffusion across the gut membrane into the plasma. Once in the plasma aspirin becomes more ionised again.

389
Q

What is the effect of an increase in pH on a weak acid?

A

The weak acid will become more ionised.

390
Q

What is the effect of an increase in pH on a weak base?

A

The weak base will become less ionised.

391
Q

What is the effect of a decrease in pH on a weak acid?

A

The weak acid will become less ionised.

392
Q

What is the effect of a decrease in pH on a weak base?

A

The weak base will become more ionised.

393
Q

Define bioavailability.

A

The amount of drug taken up as a proportion of the amount administered. It is a reflection of uptake.

394
Q

What route of drug administration has a bioavailability of 1?

A

IV infusion, all the drug administered will go into the plasma.

395
Q

Explain what would happen to the bioavailability of aspirin if gastric pH increased.

A

The bioavailability would decrease. Aspirin would be more ionised and so wouldn’t diffuse across the gut into the plasma as rapidly this would mean aspirin uptake would decrease.

396
Q

Give 2 factors that drug distribution in the plasma depends upon.

A
  1. Chemical properties.

2. Molecular size.

397
Q

Write an equation for the volume of distribution (Vd).

A

Vd = amount of drug administered/concentration of drug in plasma.

398
Q

If a drug had a high Vd what would that tell us about the drug?

A

This would indicate that the drug was highly lipid soluble and that most of the drug had moved into the intracellular space, less was in the plasma.

399
Q

What is the relationship between plasma concentration and Vd?

A

Plasma concentration is inversely proportional to Vd.

400
Q

Give 3 factors that can increase gastric pH.

A
  1. Ingesting alkaline foods.
  2. Antacids.
  3. Omeprazole (PPI).
401
Q

Give the two definitions for clearance.

A
  1. The volume of plasma from which a drug is completely removed per unit time.
  2. The rate at which plasma drug is eliminated per unit plasma concentration.
402
Q

Write an equation for renal clearance.

A

Renal clearance = Rate of appearance in urine / plasma concentration.

403
Q

What are the two ways by which drugs can be eliminated in the kidneys?

A
  1. Glomerular filtration.

2. Active secretion.

404
Q

What are the possible dangers of kidney damage with regards to renal clearance?

A

Kidney damage results in decreased renal clearance and so there is danger of accumulation, over dosage and toxicity.

405
Q

What compound do many lipid soluble drugs combine with to increase their hydrophilicity?

A

Glucuronic acid.

406
Q

Define hepatic extraction ratio (HER).

A

The proportion of a drug removed by one passage through the liver.

407
Q

What is the limiting factor when a drug has a high HER?

A

Hepatic blood flow, perfusion limited.

408
Q

What is the limiting factor when a drug has a low HER?

A

Diffusion limited. A low HER is slow and not efficient.

409
Q

What happens to high and low HER drugs when enzyme induction is increased?

A

The clearance of low HER drugs increases. There is minimal effect on high HER drugs.

410
Q

Where do phase 1 hepatic metabolism reactions occur?

A

In the smooth endoplasmic reticulum.

411
Q

What enzyme usually catalyses phase 1 reactions?

A

CYP450.

412
Q

What is a phase 2 hepatic metabolism reaction?

A

Phase 2 reactions involve conjugation and glucuronidation etc.
They usually inactivate products and increase hydrophilicity for renal excretion.

413
Q

Give 3 advantages of IV infusion.

A
  1. Steady state plasma levels are maintained.
  2. Highly accurate drug delivery.
  3. IV infusion can be used for drugs that would be ineffective when administered via an alternative route.
414
Q

Give 3 disadvantages of IV infusion.

A
  1. Expensive.
  2. Needs constant checking.
  3. Calculation error likely.
415
Q

Give an advantage of a drug having a low Vd.

A

It is easy to reach steady state and plasma concentration is ‘responsive’ to dose rate.

416
Q

Give 4 properties of the ‘ideal drug’.

A
  1. Small Vd (high bioavailability)
  2. Drug broken down effectively by enzymes.
  3. Predictable dose:response relationship.
  4. Low risk of toxicity.
417
Q

What are the advantages of pulsatile secretion as opposed to steady state?

A
  1. Enhanced responsiveness.

2. More information can be conveyed.

418
Q

What is the principal neurotransmitter in the body?

A

Acetylcholine.

419
Q

What receptor does Ach interact within the somatic nervous system and the Symp and P.symp divisions of the autonomic nervous system?

A

Pre-synaptic neurone all ahve nicotinic ACh-Rs
Post-synaptic nicotinic receptors at the neuromuscular junction. in Somatic and Sympathetic NS.
Post - synaptic muscarinic receptor in the parasympathetic NS.

420
Q

What type of receptor are nicotinic receptors?

A

Ligand gated ion channels.

421
Q

Briefly describe how Ach is synthesised.

A

Acetyl CoA, choline and choline acetyl trasnferase combine to form acetylcholine. Ach is taken up into a vesicle in the presynpatic cleft and will be released following Ca2+ influx.

422
Q

What enzyme is responsible for acetylcholine breakdown in the synaptic cleft?

A

Acetylcholinesterase.

423
Q

Describe the action of botulinum toxin at the NMJ,

A

Botulinum toxin inhibits Ach release at the NMJ. Protease degrade vesicle proteins.

424
Q

Describe the action of competitive antagonists at the NMJ.

A

They block Ach receptors. Competitive antagonists are muscle relaxants, adjuncts to general anaesthesia.

425
Q

Describe the action of depolarising agonists (blockers) at the NMJ.

A

Depolarising agonists cause receptor desensitisation.

426
Q

Describe the action of anticholinesterase inhibitors at the NMJ and give some examples of drugs.

A

There is increased Ach in the synaptic cleft. Ach can then compete with depolarising blockers.
neostigmine, rivastigmine

427
Q

What type of receptor are muscarinic receptors? give some examples and where they function.

A

GPCR.
M1 - Brain
M2 - heart
M3 - lungs

428
Q

Give examples of adverse muscarinic agonist effects.

A
  1. Diarrhoea.
  2. Urination.
  3. Miosis.
  4. Brachycardia.
  5. Emesis (vomiting).
  6. Lacrimation.
  7. Salivation.
429
Q

What happens in cholinergic crisis?

A

Overstimulation of Ach at NMJ results in SLUDGE
Salivation
Lactimation
Urination
Defaecation
GI distress
Emesis

430
Q

Give 2 examples of Ach action in the CNS.

A
  1. Motion sickness; Ach stimulates the vomiting centre in the brain.
  2. Ach leads to increase dopamine re-uptake and so can worsen the symptoms of Parkinson’s.
431
Q

Briefly describe catecholamine synthesis.

A

Tyrosine -> L-DOPA -> Dopamine -> Noradrenaline -> Adrenaline.

432
Q

Where does the conversion from Dopamine to Noradrenaline happen?

A

In a vesicle in the pre-synpatic neurone.

433
Q

Which enzymes inactivate catecholamines?

A

MAO and COMPT.

434
Q

Which protein does α1 interact with to activate phospholipase C?

A

Gq.

435
Q

What is the primary function of α1 adrenoceptors and where are they commonly found?

A

Found on vessels and sphincters
α1 leads to vasoconstriction and bladder contraction and pupil dilation.

436
Q

Which protein does α2 interact at the GPCR subunit ?

A

Gi.

437
Q

What is the primary function of α2 and where are they found?

A

Mainly found in the CNS
α2 is responsible for pre-synaptic inhibition; it inhibits NAd release and result in sedation, analgesia.

438
Q

What protein does β1,2,3 interact with in order to activate adenylate cyclase?

A

Gs.

439
Q

What is the role of adenylate cyclase?

A

It converts ATP to cyclic AMP, this then leads to PKA synthesis.

440
Q

What are the primary functions of β1 and where are they found?

A

Heart and kidneys
1. Increased cardiac effects e.g. force, rate and conduction. (ionotropic and chronotropic)
2. Increased renin secretion.

441
Q

What are the primary functions of β2 and where are they found?

A

Lungs
1. Bronchodilation.

2. Vasodilation.

442
Q

What are the primary functions of β3?

A
  1. Increase lipolysis.

2. Bladder relaxation.

443
Q

What would an α1 adrenergic antagonist do?

A
  1. Vasodilation.

2. Relaxation of bladder neck = reduced resistance to bladder outflow.

444
Q

What disease could an α1 adrenergic antagonist be used in the treatment of?

A

Hypertension
Symptomatic benign prostatic hypertrophy

445
Q

What would a β1 adrenergic antagonist do? (beta blockers)

A
  1. Reduce CO.
    used in hypertension, tachycardia

2. Reduce renin secretion.

446
Q

What diseases could an β1 adrenergic antagonist be used in the treatment of?

A

Hypertension, angina and arrhythmia, tachycardia.

447
Q

What would a b2 antagonist cause?

A

bronchoconstriction

448
Q

Give an example of a drug that is a b1 agonist and a disease that it could be used to treat.

A

Dobutamine
Cardiogenic shock

449
Q

Give an example of a cardio-selective beta blocker and a nonselective beta blocker.

A

Atenolol/metoprolol

Propanolol/labetalol.

450
Q

Define pain.

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

451
Q

Give 3 advantages of pain.

A
  1. Gives a warning for tissue damage.
  2. Immobilisation for healing.
  3. Memory establishment.
452
Q

Define acute pain.

A

Pain caused by nociceptor activation. It is of short duration,

453
Q

Define chronic pain.

A

Pain that is on-going or persistent, it lasts for >3-6 months.

454
Q

Define neuropathic pain.

A

Pain caused by a primary lesion or dysfunction of the nervous system.

455
Q

Define nociceptive pain.

A

Pain caused by actual or potential damage to non neural tissue, it is due to nociceptor activation.

456
Q

Are A delta fibres myelinated or unmyelinated?

A

Myelinated.

457
Q

Are C fibres myelinated or unmyelinated?

A

Unmyelinated.

458
Q

Describe the type of pain that A delta fibres conveys.

A

Quick, sharp, localised.

459
Q

Describe the type of pain that C fibres conveys.

A

Slow, dull, spread out.

460
Q

Describe pain wind up.

A

A perceived increase in pain intensity over time when a stimulus is repeatedly delivered. It is caused by C fibre stimulation.

461
Q

Describe the gate control theory.

A

Non-noxious stimuli trigger larger A beta fibres, these override smaller pain fibres and ‘close the gate’ to pain transmissions to the CNS.

462
Q

What is pain treatment focused on?

A
  1. Reducing excitatory neurotransmitters and nerve excitation.
  2. Enhancing inhibitory neurones.
463
Q

What are released in the presence of pain?

A

Endorphines.

464
Q

What is an adverse drug reaction?

A

A noxious and unintended response to a drug.
Remember ABCDEs

465
Q

Rawlins-Thompson system: Describe a type A adverse drug reaction.

A
  • Augmented.
  • Very common.
  • Predictable from physiological effects of the drug.
  • Often dose related.
466
Q

Rawlins-Thompson system: Describe a type B adverse drug reaction.

A
  • Bizarre.
  • Unpredictable.
  • Immunological mechanisms and hypersensitivity.
  • Often there is a history of allergy.
467
Q

Rawlins-Thompson system: Describe a type C adverse drug reaction.

A
  • Chronic.

- Occurs after long term therapy.

468
Q

Rawlins-Thompson system: Describe a type D adverse drug reaction.

A
  • Delayed.

- Occurs many years after treatment.

469
Q

Rawlins-Thompson system: Describe a type E adverse drug reaction.

A
  • End of use.

- Withdrawal reaction after long term use; complications of stopping medication.

470
Q

What is the treatment for a type A adverse drug reaction?

A

Reduce the dose.

471
Q

What is the treatment for a type B adverse drug reaction?

A

Withdraw drug immediately!

472
Q

Describe type 1 hypersensitivity and give an example of a condition that causes this reaction.

A

IgE mediated hypersensitivity. Acute anaphylaxis. IgE becomes attached to mast cells upon first exposure. Second Exposure you get IgE cross linking leads to mast cell degranulation -> histamine.
Atopy - athsma, pollen, fur

473
Q

Describe type 2 hypersensitivity and give an example of a condition that causes this reaction.

A

Antibody dependant cytotoxicity.
IgG/IgM mediated cytotoxicity by activating MAC complement when Ab binds to Ag. This incdes cell damage.
eg. Goodpastures syndrome, AIHA, Rheumatic Fever

474
Q

Describe type 3 hypersensitivity and give an example of a condition that causes this reaction.

A

Immune complex deposition;
IgG/IgA bind antigen. activate complement.
immune complexes have not been adequately cleared by innate immune cells, giving rise to an inflammatory response.
eg. SLE, Post strep glomerulonephritits

475
Q

Describe type 4 hypersensitivity and give an example of a condition that causes this reaction.

A

T cell-mediated.
Th1 activated by APC - initiates immune response
eg. DMT1, TB, MS, Guillian Barre

476
Q

Give 6 features of anaphylaxis.

A
  1. Rapid onset.
  2. Blotchy rash.
  3. Swelling of face and lips.
  4. Wheeze.
  5. Hypotension.
  6. Cardiac arrest if severe.
477
Q

What can cause a type 1 hypersensitivity reaction?

A

Pollen, cat hairs, peanuts etc. (allergies).

478
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection.

479
Q

What can cause a type 3 hypersensitivity reaction?

A

Fungal.

480
Q

What can cause a type 4 hypersensitivity reaction?

A

TB.

481
Q

What is the treatment for anaphylaxis?

A
  1. Commence basic life support (ABC).
  2. Stop infusion of drug.
  3. Give adrenaline Intramuscular 500mg and anti-histamines.
482
Q

Give 4 risk factors for hypersensitivity.

A
  1. Protein based macromolecules.
  2. Female > male.
  3. Immunosuppression.
  4. Genetic factors.
483
Q

Why are drug interactions such a big problem today?

A
  1. Ageing population.
  2. Polypharmacy.
  3. Increased use of over the counter drugs.
484
Q

Give 5 patient risk factors for drug interactions.

A
  1. Old age.
  2. Polypharmacy.
  3. Renal disease.
  4. Hepatic disease.
  5. Genetics.
485
Q

Give 3 drug related risk factors for drug interactions.

A
  1. Narrow therapeutic index.
  2. Steep dose/response curve.
  3. Saturable metabolism.
486
Q

Name 3 types of drug interaction.

A
  1. Synergy; interaction of 2 compounds leads to a greater combined effect.
  2. Antagonism; one drug blocks another.
  3. Other.
487
Q

How might drug interactions affect drug metabolism?

A

If a drug inhibits or induces CYP450 it might affect the metabolism of another drug.

488
Q

How does avocado affect CYP450? And what drug might this impact on?

A

Avocado is a CYP450 inductor. Warfarin is likely to be affected and the risk of blood clots will be increased.

489
Q

How does grapefruit juice affect CYP450? And what drugs might this impact on?

A

Grapefruit juice is a CYP450 inhibitor, it affects CYP3A4 specifically and increases the bioavailability of some drugs e.g. Ca2+ channel blockers and immunosuppressants.

490
Q

Are weak acids cleared quicker if urine is more acidic or more alkali?

A

Weak acids are cleared quicker if urine is more alkali.

491
Q

Are weak bases cleared quicker if urine is more acidic or more alkali?

A

Weak bases are cleared quicker if urine is more acidic.

492
Q

What drug acts as an antagonist at the μ receptor?

A

Naloxone.

493
Q

What enzyme is needed to metabolise codeine?

A

Codeine is a pro drug and needs to be metabolised by CYP2D6.

494
Q

What is the bioavailability of morphine taken orally?

A

50%.

495
Q

10mg of morphine is taken orally. What is the equivalent dose if given parenterally?

A

5mg.

496
Q

What is morphine metabolised to?

A

Morphine 6 glucuronide.

497
Q

Where might μ receptors be found?

A

In the epidural space and CSF.

498
Q

Give 5 side effects of opioid use.

A
  1. Respiratory depression.
  2. Sedation.
  3. Nausea.
  4. Vomiting.
  5. Constipation.
499
Q

Describe the dose-response curve for morphine.

A

As dose increases response increases. This association is initially rapidly and then the graph plateaus. It is not sigmoidal!

500
Q

Name a protein that can inhibit apoptosis.

A

BCL-2; it inhibits pro-apoptotic proteins e.g. caspase and therefore inhibits apoptosis.

501
Q

What disease might develop in someone with a non-functional BCL-2 protein?

A

Cancer.

502
Q

Where are mast cells found?

A

They are only found in tissues, not in the blood!

503
Q

What is dobutamine used in the treatment of and at what receptor is it an agonist?

A

Dobutamine is a beta 1 agonist. It is used in the treatment of heart failure.

504
Q

Define physiological antagonism.

A

A substance that produces effects that counteract the effects of another substance.

505
Q

What are the 3 actions of NSAIDS?

A
  1. Anti-inflammatory.
  2. Analgesic.
  3. Anti-pyrexic.
    (AAA).
506
Q

Name a local anaesthetic.

A

Lidocaine.

507
Q

How do local anaesthetics work?

A

They inhibit pain by stopping impulse conduction in sensory nerves.

508
Q

What drug inhibits ACh release at the NMJ?

A

Botulinum toxin.

It is used to treat urinary incontinence and also cosmetically as a muscle relaxant.

509
Q

Give 3 cytokines secreted by TH2.

A
  1. IL-4.
  2. IL-6.
  3. IL-13.
  4. IL-5.
  5. IL-10.
510
Q

What is the name of the variable region on an antibody?

A

Fab region.

511
Q

Name 3 cytokines secreted by TH1.

A
  1. IL-2.
  2. Gamma-interferon.
  3. TNF-beta.
512
Q

Name 2 cytokines secreted by TREG.

A
  1. IL-10.

2. TGF-beta.

513
Q

Define adenocarcinoma.

A

A malignant neoplasm of glandular epithelium.

514
Q

What is the initial reaction to tissue injury in inflammation?

A

Vessel lining becomes leaky (fluid exudate)
increased Permeability
mediator release (histamine and serotonin)
vessel dilation (plasma enters tissue w/clotting factors, nutrients, proteins and neutrophil polymorphs)
diagnostic presence

515
Q

What is the microscopic appearance of chronic inflammation?

A

cellular infiltrate (lymphocytes, plasma cells, macrophages)
Granulation tissue becomes fibrous tissue
tissue damage and necrosis

516
Q

What occurs during repair in chronic inflammation?

A 
Angiogenesis
Fibroblast proliferation
Production of collagen
macrophages migrate
formation of granulation tissue
517
Q

What is healing by 1st intention?

A 
Incision
no loss of tissue
fibrinogen release 
edges joined by fibrin (forms a clot)
replaced by collagen (little scar tissue)
structure and function restored
518
Q

What is healing by 2nd intention?

A 
Loss of tissue
Gap filled w/granulomatous tissue
adhesion of edges
organisation and fibrosis formation
leads to a big scar
519
Q

What is inadequate wound healing?

A 
Poor blood supply
poor nutrition
wound infection
immunosuppresion
diabetes
old age
520
Q

What is excessive wound healing?

A 
Hypertrophic scars
excessive collagen
stays within original wound site
keloid scars
Excessive granulation tissue that expands beyond wound edges
521
Q

How does ageing affect the skin?

A

Wrinkling of skin (dermal elastosis) is caused by UV-B light causing crosslinking of proteins such as collagen in the dermis.

522
Q

How does ageing affect the eyes

A

Cataracts are caused by UV-B cross linking of proteins in the lens causing opacity.

523
Q

How does ageing affect the bones?

A

Osteoporosis - loss of bone matrix predominantly in women after menopause.

524
Q

How does ageing affect the brain?

A

Dementia - Alzheimer’s or vascular dementia.

Can reduce likelihood of getting by reducing risk factors

525
Q

How does ageing affect the muscle?

A

Loss of muscle (sarcopenia).

Possible caused by reduced levels of GH and testosterone in later life.

526
Q

How does ageing affect the ears?

A

Deafness - The hair cells in the cochlear do not divide so when they are damaged by high volumes they will die.

527
Q

What is a basal cell carcinoma?

A

A skin cancer that is local and therefore will not metastasis

528
Q

Define Congenital

A

Present at birth

could be inherited or acquired

529
Q

What are homeobox genes

A

control anatomical development

when not expressed/mutated then defects occur

530
Q

Give some examples of congenital abnormalities

A

Spina bifida 🡪 failure of closure of neural tube

Cleft lip 🡪failure of closure of palate

Ventricular septal defect 🡪 hole in ventricles

Syndactyly 🡪 webbing of toes & fingers via apoptosis

GH deficiency 🡪 decreased GH thus don’t grow

Acromegaly 🡪 increased HG post puberty so get big hands, feet & jaw [epiphyseal plates have been sealed]

Achondroplasia 🡪 mutation in fibroblast GF receptor gene thus long bones grow slower than the rest of the body

Growth impairment 🡪 mutation in type II collagen gene

531
Q

Give some examples of inherited conditions

A

Chromosomal abnormality [3*Chr 21] 🡺 Downs syndrome
Autosomal dominant 🡺 Huntingtons disease
Autosomal recessive 🡺 Cystic fibrosis, Sickle cell
Sex linked 🡺 colour blindness
Co-dominant 🡺 blood groups

532
Q

Define polygenic inheritance

A

Where a characteristic is controlled by 2+ genes

533
Q

Define an inhertied condition

A

One that is caused by a genetic abnormalities inherited from parents

534
Q

Define an acquired condition and give an example

A

Caused by non genetic environmental factors

eg. foetal alcohol syndrome

535
Q

Define Tumour

A

Abnormal swelling

536
Q

Define carcinogenesis

A

The evolution of a cancer cell from a normal cell via permanent genetic mutations

537
Q

Define oncogenesis

A

Benign and malignant tumours

538
Q

Define oncogenic

A

Tumour Causing

539
Q

Define carcinogen

A

Cancer causing agents

540
Q

Define carcinogenic

A

cancer causing

541
Q

Define mutagenic

A

Acts of DNA

542
Q

What tumours commonly metastasise to the lung

A

Sarcomas and any common cancer

543
Q

What tumours commonly metastasise to the liver

A 
Colomic
stomach
pancreas
carcinoid (tumours of the small intestine)
these all have portal venous drainage
544
Q

What tumours commonly metastasise to the bone?

A 
Prostate
breast
thyroid
lung
kidney
545
Q 
Which of the following tumours never metastasises
malignant melanoma
small cell carcinoma of the lung
basal cell carcinoma of the skin
breast cancer
A

Basal cell carcinoma

546
Q 
Which of these does not commonly metastasise to bone?
lung cancer
breast cancer
prostate cancer
liposarcoma
A

Liposarcoma

547
Q

What term describes a cancer that has not invaded through the basement membrane?

A

Carcinoma in situ

548
Q

what in the name of a benign tumour of glandular epithelium?

A

adenoma

549
Q

What is the name of a malignant tumour of striated muscle?

A

Rhabdomyosarcoma

550
Q 
Which of these tumours does not have a screening programme in the UK?
Breast cancer
colorectal cancer
cervical cancer
lung cancer
A

Lung cancer

551
Q

What is the name of a benign tumour of fat cells?

A

lipoma

552
Q

What is the name of a malignant tumour of glandular epithelium?

A

Adenocarcinoma

553
Q

What is the name of a malignant tumour of glandular epithelium?

A

Adenocarcinoma

554
Q

What is the name of a malignant tumour of glandular epithelium?

A

Adenocarcinoma

555
Q

What is another name for fibroids?

A

Leomyoma of the uterus

556
Q

Give an example of a disease where there is a lack of apoptosis.

A

Cancer; mutations in p53 mean cell damage isn’t detected.

557
Q

Give examples of omas that are not neoplasms

A

Granuloma
Mycetoma
Tuberculoma

558
Q

Difference between a viral and bacterial infection on appearance?

A

Viral infections often look red. Bacterial infections often have white pus alongside the red inflammation

559
Q

How is inflammation classified?

A

Acute:
Sudden onset, short duration, usually resolves

Chronic:
Slow onset or sequel to acute
long duration
may never resolve

560
Q

What cells are involved in inflammation?

A

neutrophil polymores
macrophages
lymphocytes
endothelial cells
fibroblasts

561
Q

What is the function of neutrophil polymorphs?

A

Eat debris and bacteria
contain bags of enzymes (lysosomes) which are used to kill and digest phagocytosed bacterial
the first cells to arrive at the site of acute inflammation

562
Q

What is the function of a macrophage?

A

phagocytose debris and bacteria,
transport material to lymph nodes and present this to lymphocytes to initiate a secondary immune reaction.

563
Q

What are the functions of lymphocytes?

A

Produce chemicals involved in controlling inflammation and antibodies.
They are the immunological memory of the body.

564
Q

What is the sequence of an acute inflammation?

A

Injury or infection
neutrophils arrive and phagocytose and release enzymes
macrophages arrive and phagocytose
either resolution with clearance of inflammation or progression to chronic inflammation

565
Q

What is the sequence of Chronic Inflammation?

A

Progression from acute inflammation or starts as chronic inflammation
no or very few neutrophils
macrophages and lymphocytes and then fibroblasts
Can resolve if no tissue damage
often ends up with repair and formation of scars

566
Q

What are granulomas

A

Particular type of chronic inflammation with collections of macrophages or histiocytes surrounded by lymphocytes
May be due to myobacterial infection such as TB or leprosy, chrons disease, sarcoidosis

567
Q

What happens during repair?

A

replacement of damaged tissue by fibrous tissue
Collagen is produced by fibroblasts

568
Q

What factors prevent the blood from clotting under normal circumstances?

A

Laminar Flow - cells travel in the centre of arterial vessels and do not touch the sides

Endothelial cells which line the vessels are not sticky when health

569
Q

What is the time course of atherosclerosis throughout ages

A

Birth - no atherosclerosis
Late teenage/early 20s - fatty streaks in aorta which may not progress to established atherosclerosis
30s/40s/50s - development of established atherosclerotic plaques
40s to 80s - complications of atherosclerotic plaques including thrombosis, intraplaque haemorrhage

570
Q

What is the major overall complication of atherosclerosis?

A

blocks an artery (via a superadded thrombosis or plaque haemorrhage) that prevents blood flow to its tissues that it supplies. This will result in infarction of that tissue.

571
Q

Give examples of some specific atherosclerotic complications

A

Myocardial infarction
cerebral infarction
carotid atheroma
aortic aneurysms
peripheral vascular disease with intermittent claudication
gangrene

572
Q

What controls the caspases involved in apoptosis?

A

Fas receptor and Fas ligand
Bcl2 family such as Bax (promotor) and Bcl2 (inhibitor)

573
Q

Give some example of chemical carcinogens and the cacner they cause.

A

Polycyclic aromatic hydrocarbons - Lung and Skin
aromatic amines - Bladder
nitrosamines - Gut
alkylating agents - Leukaemia

574
Q

Give some examples of DNA viruses that can cause cancer and their associated cancers

A

Human Herpes virus 8 - Kaposi Sarcoma

EBV - burkitt lymphom, nasopharyngeal carcinoma

HBV - HCC

HPV - SCC of cervix, penis, anus, head and neck

Merkle cell polyomavirus - merkle cell carcinoma

575
Q

Give some examples of RNA viruses that can cause cancer

A

Human T lymphotrophic virus (HTLV-1) Adult T cell Leukaemia

HCV - HCC

576
Q

What proportion of viral infections will result in cancer?

A

10-15%

577
Q

Give some examples of biological agents that cause cancer

A

Hormones:
Oestrogen - increase mammary or endometrial cancer
Anabolic steroids - increase HCC risk

Mycotoxins:
Aflatoxin B1 - HCC

Parasites:
Chlonorchis sinesis - cholangiocarcinoma

Shistosoma - Bladder cancer

578
Q

Give some examples of other miscellaneous carcinogens

A

Asbestos
Metals

579
Q

Give some examples of premalignant conditions that can increase the risk of cancer

A

Colonic Polyps
Cervical Dysplasia
Ulcerative colitis
Undescended Testis

580
Q

Give an exogenous and Endogenous ligand that activates TLR 1/2/6

A

Exo:
Gram positive lipopeptides

581
Q

Give an exogenous and Endogenous ligand that activates TLR 3

A

Exo - dsDNA
Endo - mRNA

582
Q

Give an exogenous and Endogenous ligand that activates TLR 4

A

Exo - LPS, pneumolysin, Viral Proteins
Endo - Heatshock proteins

583
Q

Give an exogenous and Endogenous ligand that activates TLR 5

A

Exo - Flagellin

584
Q

Give an exogenous and Endogenous ligand that activates TLR 7/8

A

Exo - ssRNA

585
Q

Give an exogenous and Endogenous ligand that activates TLR 9

A

Exo - CpG DNA
Endo - DNA/mitochondrial DNA.

586
Q

Define Synergism in pharmacology

A

Where 2 drugs with the same pharmacodynamic effect work together to provide an even greater effect than expected if you used the 2 drugs simultaneously.
(1 + 1 > 2)

587
Q

Define summation in pharmacology

A

Where two drugs with the same pharmacodynamic effect work together to give an expected larger effect.
Eg. one drug reduces BP by 20mmHg and another reduces BP by 10mmHg. so together they reduce BP by 30mmHg
(1 + 1 = 2)

588
Q

Define antagnoism in pharmacology

A

where two drugs will have contradicting effects. one may block another from working and so the overall net effect is 0
(1 + 1 = 0)

589
Q

Define Potentiation in pharmacology

A

where one drug may increase the effect (potency) of another drug without affecting the effect of the first drug. (1 + 1 = 1 + 1.5)

590
Q

What are the physiochemical effects of a drug?

A

The interactions that 2 drugs would have outside of the body due to their sole chemical properties.

591
Q

Define Pharmacodynamics

A

The effects that a drug has on the body

592
Q

Define Pharmacokinetics

A

What happens to the drug in the body
How the drug is ADME
Absorbed
Distributed
Metabolised
Excreted

593
Q

Define Adsorption and give an example

A

Where a compound clings to the surface of another molecule
eg. In paracetamol overdose you could prescribe activated charcoal to stick to the paracetamol to prevent its absorption from the gut.

594
Q

What is enzyme induction during the metabolism of a drug?

A

Where a drug may induce the CYP450 enzymes which can result in increased metabolism of a drug/prodrug to a more potent state and therefore potentially induce overdose.

595
Q

WHat drugs may cause AKI?

A

NSAIDSs
ACEi
Furosemide
Gentimicin

596
Q

What properties of a drug can affect its absorption

A

Motility - how fast it passes through the GI-Tract
Acidity - The ionised to un-ionised ratio
Solubility
pH Gradient - Affects the ionisation of a drug

597
Q

What properties of a drug affect its distribution?

A

Whether it is soluble in plasma/tissues
Whether it is protein bound

598
Q

What can affect how a drug is metabolised?

A

Phase 1 and phase 2 reactions in the liver
Enzyme induction (decrease therapeutic effect) or Enzyme inhibition (increase therapeutic effect) via CYP450s

599
Q

What can affect how a drug is excreted?

A

Urine pH
Acids cleared faster if urine is weakly basic
Bases cleared faster if urine is weakly acidic

600
Q

What is a receptor?

A

A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects

601
Q

What are the effects of a competitive antagonist?

A

Decreases potency of a drug but does not affect the efficacy

602
Q

What are the effects of a non-competitive antagonist?

A

Decreases both the potency and efficacy.

603
Q

Give an example of a selective and non-selective b-adrenergic agonist

A

Non-selective - Isoprenaline: activates both b1 and b2 receptors to increase heart muscle contractility and cause bronchodilation.

Selective - SAB2A: Selective b2 agonist and so will only cause bronchodilation.

604
Q

Give an example of a cardio-selective beta blocker and a nonselective beta blocker.

A

Atenolol/metoprolol

Propanolol/labetalol.

605
Q

What are the 5 types of Muscarinic Receptors?

A

M1 -Brain
M2 -Heart
M3- All organs with a parasympathetic innervation
M4 - Mainly CNS
M5 - Mainly CNS

606
Q

What does activation of the M2 receptors on the SA and AV node do in the heart?

A

M2 at SA node - Decreases heart rate
M2 at AV node - decreases conduction velocity. Induces AV node block (increase PR interval)

607
Q

What happens when M3 receptors are activated?

A

Parasympathetic effects of GI, Urinary system, eye

608
Q

What is the only place in the body where the stimulation of M3 receptors causes a sympathetic response?

A

The skin - stimulation of M3 with ACh will cause sweating.

609
Q

What is the use of Atropine?

A

Atropine is a muscarinic antagonist
Used intravenously to increase heart rate and treat brady arrythmias and AV node block

610
Q

What is the used of inhaled antimuscarinics?

A

Used to result in airway bronchodilation by blocking the p.symp activation of bronchial smooth muscle.

611
Q

What can some side effects of using anti-muscarinics be?

A

Inhibiting other M receptors and therefore causing dry mouth, urinary retention, worse glaucoma.
(stop other parasympathetic actions from working)

612
Q

Give examples of drugs that will block the N1 receptor to inhibit ACh activity in the Somatic NS.

A

Rocuronium,
Suxamethonium
Pancuronium

all used as muscle relaxants in surgery.

613
Q

Give examples of alpha 1 blockers and what they can be used to treat

A

Doxazosin - Decrease BP
Phenoxybenzamine - Treats phaeochromocytoma

614
Q

What receptors are involved with the sympathetic and parasympathetic NS?

A

Sympathetic - Adrenergic receptors -alpha and beta

Parasympathetic - Cholinergic receptors - Nicotinic and Muscarinic

615
Q

Define an adverse drug reaction

A

An unwanted or harmful reaction following the administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug.

It has to be noxious and unintended

616
Q

What is the difference between a side effect and an adverse reaction?

A

Side effects are unintended effects but they can dome times be beneficial. An adverse reaction is never beneficial.

617
Q

Define Toxic , collateral and Hyper-susceptibility effects

A

When ADRs occur:
Toxic - Beyond the therapeutic range
Collateral - Within Therapeutic Range
Hyper-Susceptibility effects - Below therapeutic range

618
Q

Give examples of toxic effects of drugs

A

Nephrotoxicity
ototoxicity
dysarthria and ataxia
cerebellar signs and symptoms

619
Q

What are some causes for ADRs (Adverse Drug Reactions)?

A

Pharmaceutical variation
receptor abnormality
abnormal biological system unmasked by the drug
abnormal drug metabolism
immunological effects
drug-drug interactions
multifactorial.

620
Q

What is a Type F Drug reaction?

A

Failure of the drug to work.
Dose-related and is often caused by drug interactions either due to antagonism or enzyme induction/inhibition.

EK Phase 2A (15 decks)

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