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Phase 2a Medicine > 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

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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3
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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4
Q

What does viral infection result in?

A

Cell death due to intracellular multiplication.

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5
Q

What does bacterial infection result in?

A

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

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6
Q

Give 5 cardinal signs of inflammation.

A
  1. Redness (rubor).
  2. Swelling (tumor).
  3. Pain (dolor).
  4. Heat (calor).
  5. Loss of function.
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7
Q

How can acute inflammation be diagnosed histologically?

A

By looking for the presence of neutrophil polymorphs.

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8
Q

Give 3 endogenous chemical mediators of acute inflammation.

A
  1. Bradykinin.
  2. Histamine.
  3. Nitric Oxide.
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9
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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10
Q

What cells are involved in chronic inflammation?

A

Macrophages and plasma cells (B and T lymphocytes).

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11
Q

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

A

Multinucleate giant cell.

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12
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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13
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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14
Q

In which type of inflammation would you see neutrophil polymorphs?

A

Acute inflammation.

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15
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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16
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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17
Q

Define granuloma.

A

An aggregate of epithelioid histocytes.

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18
Q

Give an example of a granulomatous disease.

A

TB, leprosy, Crohn’s disease and sarcoidosis.

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19
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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20
Q

What kind of disease is TB?

A

A granulomatous disease.

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21
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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22
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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23
Q

Name 2 types of cells that are incapable of regeneration.

A
  1. Myocardial cells.

2. Neuronal cells.

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24
Q

Define abscess.

A

Acute inflammation with a fibrotic wall.

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25
Q

Define thrombosis.

A

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

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26
Q

Give 2 reasons why thrombosis formation is uncommon.

A
  1. Laminar flow.

2. Non sticky endothelial cells.

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27
Q

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

A
  1. Change in vessel wall.
  2. Change in blood constituents.
  3. Change in blood flow.
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28
Q

Define embolus.

A

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

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29
Q

Define ischaemia.

A

Decreased blood flow.

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30
Q

Define infarction.

A

Decreased blood flow with subsequent cell death.

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31
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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32
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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33
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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34
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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35
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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36
Q

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

A

Venous system.

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37
Q

What drug can be used to prevent Thrombosis?

A

Aspirin.

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38
Q

Define atherosclerosis.

A

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

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39
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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40
Q

What are the 3 main constituents of an atheromatous plaque?

A
  1. Lipids.
  2. Fibrous tissue.
  3. Lymphocytes.
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41
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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42
Q

What can be done to prevent atherosclerosis?

A

Reduce risk factors and taking low dose aspirin regularly.

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43
Q

What is the primary cause of atherosclerosis?

A

Endothelial cell damage.

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44
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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45
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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46
Q

Define apoptosis.

A

Programmed cell death of a single cell.

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47
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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48
Q

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

A

p53 protein.

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49
Q

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

A

Caspases.

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50
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor.

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51
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.

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52
Q

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

A

HIV.

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53
Q

Define necrosis.

A

Unprogrammed death of a large number of cells due to an adverse event.

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54
Q

Give 3 examples of events that can lead to necrosis.

A
  1. Frost bite.
  2. Avascular necrosis.
  3. Infarction.
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55
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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56
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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57
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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58
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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59
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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60
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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61
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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62
Q

Define acute inflammation.

A

Initial and short lived tissue reactions to injury.

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63
Q

Define chronic inflammation.

A

Subsequent and prolonged tissue reactions to injury.

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64
Q

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

A

It can no longer divide.

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65
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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66
Q

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

A

Because BCC doesn’t metastasise.

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67
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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68
Q

Define carcinoma.

A

Malignant tumour of epithelial tissue.

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69
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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70
Q

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

A

Breast carcinomas.

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71
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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72
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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73
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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74
Q

What kind of drugs can be used in targeted chemotherapy?

A

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

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75
Q

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

A
  1. Proteases.

2. Cell motility.

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76
Q

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

A
  1. Collagenases.

2. Cell motility.

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77
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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78
Q

Give 2 promoters of tumour angiogenesis.

A
  1. Vascular endothelial growth factors.

2. Fibroblast growth factors.

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79
Q

Give 3 inhibitors of tumour angiogenesis.

A
  1. Angiostatin.
  2. Endostatin.
  3. Vasculostatin.
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80
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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81
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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82
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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83
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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84
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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85
Q

What is the main source of histamine?

A

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

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86
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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87
Q

What is the role of tissue macrophages in acute inflammation?

A

They secrete chemical mediators that attract neutrophil polymorphs.

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88
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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89
Q

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

A

Phagocytosis!

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90
Q

Define carcinogenesis.

A

A multistep process in which normal cells become neoplastic cells due to mutations.

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91
Q

What percentage of cancer risk is due to environmental factors?

A

85% environmental, 15% genetic.

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92
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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93
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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94
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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95
Q

What causes skin cancer?

A

Exposure to UV light.

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96
Q

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

A

Lung cancer and skin cancer.

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97
Q

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

A

Smoking cigarettes and mineral oils.

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98
Q

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

A

Bladder cancer.

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99
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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100
Q

Chemical carcinogens: what type of cancer do nitrosamines cause?

A

Gut cancer.

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101
Q

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

A

Leukaemia; the risk is small in humans.

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102
Q

Define neoplasm.

A

An autonomous, abnormal, persistent new growth.

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103
Q

What is a neoplasm composed of?

A
  1. Neoplastic cells.

2. Stroma.

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104
Q

Describe neoplastic cells.

A

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

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105
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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106
Q

What is essential for neoplasm growth?

A

Angiogenesis.

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107
Q

What does a neoplasm release in order to initiate angiogenesis?

A

Vascular endothelial growth factors.

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108
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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109
Q

What are the advantages of classifying neoplasms?

A

It helps to determine the appropriate treatment and prognosis.

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110
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.
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111
Q

What are the consequences of malignant neoplasms?

A

Destroy surrounding tissue, blood loss due to ulceration, pain, anxiety.

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112
Q

Define carcinoma.

A

MALIGNANT EPITHELIAL NEOPLASM!

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113
Q

Define sarcoma.

A

Malignant connective tissue neoplasm.

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114
Q

What is a rhabdomyoma?

A

Benign striated muscle neoplasm.

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115
Q

What is an adenoma?

A

Benign tumour of glandular epithelium.

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116
Q

What is a papilloma?

A

A non-glandular benign tumour.

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117
Q

What is a leiomyoma?

A

A benign smooth muscle neoplasm.

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118
Q

What is a neuroma?

A

A benign neoplasm of nerves.

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119
Q

What is a chondrosarcoma?

A

A malignant neoplasm of cartilage.

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120
Q

What is a liposarcoma?

A

A malignant neoplasm of adipose tissue.

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121
Q

What is a melanoma?

A

A malignant neoplasm of melanocytes.

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122
Q

What is a lymphoma?

A

A malignant neoplasm of lymphoid cells.

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123
Q

What is a mesothelioma?

A

A malignant neoplasm of mesothelial cells.

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124
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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125
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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126
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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127
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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128
Q

What is the function of lysozyme?

A

It destroys bacterial cell walls.

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129
Q

Describe adaptive immunity.

A

Specific, requires lymphocytes. Memory and quicker response.

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130
Q

Give examples of 3 polymorphonuclear leukocytes.

A
  1. Neutrophils.
  2. Basophils.
  3. Eosinophils.
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131
Q

Give examples of 3 mononuclear leukocytes.

A
  1. Monocytes.
  2. B lymphocytes.
  3. T lymphocytes.
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132
Q

In which primary lymphoid tissue do T cells mature?

A

Thymus.

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133
Q

In which primary lymphoid tissue do B cells mature?

A

Bone marrow.

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134
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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135
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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136
Q

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

A

It helps produce antibodies against extracellular pathogens. Secretes cytokines.

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137
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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138
Q

What is the function of T reg (FoxP3)?

A

They regulate the immune response.

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139
Q

Which cells express MHC1?

A

All nucleated cells express MHC1. e.g. a virus infected or cancer cell would express MHC1.

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140
Q

Which cells express MHC2?

A

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

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141
Q

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

A

MHC1.

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142
Q

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

A

MHC2.

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143
Q

What type of T cell binds to MCH1?

A

Cytotoxic T cells (CD8).

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144
Q

What type of T cells binds to MCH2?

A

Helper T cells (CD4).

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145
Q

What do B cells differentiate into?

A

Plasma cells. The plasma cells then produce antibodies.

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146
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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147
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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148
Q

How many antibodies can each B cell make?

A

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

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149
Q

What happens to B cells that recognise ‘self’?

A

They are killed in bone marrow.

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150
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-cells -> cytokine secretion induces B-cell clonal expansion -> differentiation into plasma cells and memory B cells.

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151
Q

Give 3 functions of antibodies.

A
  1. Neutralise toxins.
  2. Opsonisation.
  3. Activate classical complement system.
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152
Q

Which immunoglobulin is found in breast milk and other secretions?

A

IgA.

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153
Q

Name 4 types of cytokines.

A
  1. Interferons.
  2. Interleukins.
  3. Colony stimulating factors.
  4. Tumour necrosis factors.
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154
Q

What is the function of interferons?

A

Interferons produce antiviral proteins.

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155
Q

What is the function of interleukins?

A

Interleukins cause cell division and differentiation.

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156
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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157
Q

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

A

TNF mediates inflammation and cytotoxic reactions.

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158
Q

What is the function of chemokines?

A

Chemokines attract leukocytes to sites of infection.

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159
Q

Give examples of secondary lymphoid tissue.

A

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

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160
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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161
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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162
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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163
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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164
Q

What mechanisms or cells are involved in O2 independent killing?

A

Defensins, lysozyme, pH, TNF.

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165
Q

Where are complement system plasma proteins derived from?

A

The liver.

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166
Q

What are the 3 main outcomes of complement system activation?

A
  1. Pathogen lysis.
  2. Increased phagocytosis.
  3. Activation of leukocytes.
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167
Q

What activates the classical complement pathway?

A

Antibodies.

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168
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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169
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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170
Q

What activates the lectin pathway?

A

Mannose binding protein.

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171
Q

What activates the alternative pathway?

A

Bacterial cell walls and endotoxin.

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172
Q

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

A
  1. Classical.
  2. Lectin.
  3. Alternative.
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173
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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174
Q

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

A

C3b and C4b.

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175
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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176
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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177
Q

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

A

Innate immunity.

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178
Q

What are PRR’s a receptor for?

A

PAMP’s.

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179
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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180
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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181
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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182
Q

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

A

Crohn’s disease.

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183
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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184
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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185
Q

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

A

TLR4 agonists.

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186
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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187
Q

Give examples of 3 extracellular PRR.

A
  1. Mannose receptors.
  2. Scavenger receptors.
  3. TLR’s.
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188
Q

What is the function of mannose and scavenger extracellular receptors?

A

The induce pathogen engulfment.

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189
Q

Give an example of an intracellular PRR.

A

NLR.

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190
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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191
Q

What happens when a PAMP binds to a PRR?

A

The innate immune response and inflammatory response is triggered.

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192
Q

What is extravasation?

A

Leukocyte (WBC) migration across the endothelium.

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193
Q

What do macrophages at the tissues secrete to initiate extravasation?

A

TNF alpha.

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194
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.

195
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.
196
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.
197
Q

What is cancer immunosurveillance?

A

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

198
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.

199
Q

Give an example of active cancer immunotherapy.

A

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

200
Q

Give an example of passive cancer immunotherapy.

A

T cell transfer, anti-tumour antibodies.

201
Q

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

A

Malignant tumours grow rapidly and so outgrow their blood supply.

202
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.
203
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.
204
Q

Give 2 advantages of passive immunity.

A
  1. Immediate effect.

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

205
Q

Give 3 disadvantages of passive immunity.

A
  1. Short term.
  2. No immunological memory produced.
  3. Reaction is possible.
206
Q

Describe the first immune response to initial exposure.

A
  1. Innate immune response.
  2. IgM predominates.
  3. Low affinity.
207
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.
208
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.
209
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.

210
Q

Give 2 advantages of inactivated vaccines.

A
  1. There is no risk of infection.

2. Storage is less critical.

211
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.
212
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.

213
Q

What can be used as an adjuvant?

A

Toxoids, proteins, chemicals (aluminium salts) etc.

214
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.
215
Q

Give 3 advantages of transplantation.

A
  1. Improved quality of life.
  2. Improves survival rates.
  3. Cost effective.
216
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.

217
Q

On which chromosome are MHC proteins found?

A

Chromosome 6.

218
Q

Describe the transplant cascade.

A

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

219
Q

What are the main compounds involved in reperfusion injury?

A

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

220
Q

Define allorecognition.

A

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

221
Q

What are the consequences of transplant rejection?

A

Fibrosis and scarring.

222
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.
223
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.
224
Q

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

A

Too much = infection.

Too little = rejection.

225
Q

What is involved in tissue typing?

A
  1. Blood group matching.

2. HLA typing.

226
Q

What is involved in cross matching?

A

Detecting anti HLA antibodies.

Cell based assays and solid phase assays can be used.

227
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.

228
Q

What is allergy?

A

An abnormal response to harmless foreign material.

229
Q

What is atopy?

A

The tendency to develop allergies.

230
Q

Which immunoglobulin is most commonly involved in allergic responses?

A

IgE.

231
Q

Which cells are most commonly involved in allergic responses?

A

Mast cells! Also eosinophils and basophils.

232
Q

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

A

The receptors cross-link.

233
Q

Which cells express high affinity IgE receptors?

A

Mast cells, basophils and eosinophils.

234
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.

235
Q

What is the main IgE receptor cell?

A

MAST CELLS!

236
Q

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

A

Histamine.

237
Q

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

A

They induce a TH2 response.

238
Q

Which cells and which immunoglobulin is commonly involved in anaphylaxis?

A
  • Mast cells and basophils.

- IgE.

239
Q

Give examples of anaphylactic systemic effects.

A
  • CV: vasodilation, lowered BP.
  • Resp: bronchial SM contraction, mucus.
  • Skin: rash, swelling.
  • GI: pain, vomiting.
240
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).
241
Q

Which infection is most often seen in patients with hypogammaglobulinemia?

A

Streptococcus penumonia sinusitis.

242
Q

Give 5 examples of PAMPs.

A
  1. Lipopolysaccharides.
  2. Endotoxins.
  3. Bacterial flagellin.
  4. Peptidoglycans.
  5. dsRNA.
243
Q

Which PRR responds to lipopolysaccharides?

A

TLRs.

244
Q

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

A

No

245
Q

Give 4 causes of acquired immunodeficiency.

A
  1. Cancer.
  2. HIV.
  3. Having chemotherapy.
  4. Taking immunosuppressants.
246
Q

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

A

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

247
Q

What immune system cells are affected in HIV?

A

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

248
Q

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

A

Hypogammaglobulinaemia.

249
Q

What infection is most commonly seen in patients with hypogammaglobulinaemia?

A

Streptococcus pneumonia.

250
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.

251
Q

What are the consequences of complement deficiency?

A

Impaired opsonisation of encapsulated bacteria.

252
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.
253
Q

What are the consequences of being deficient in C1 inhibitor?

A

Angioedema - facial swelling.

254
Q

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

A

Increased likelihood of autoimmune disease especially systemic lupus erythematosus.

255
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.

256
Q

What is thymic aplasia?

A

A deficiency in mature T cells.

257
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.
258
Q

Give 3 examples of chronic inflammatory diseases.

A
  1. Rheumatoid arthritis.
  2. Crohn’s disease.
  3. TB.
259
Q

Name 3 conventional therapies used in managing CID.

A
  1. NSAIDs.
  2. DMARDs.
  3. Steroids.
260
Q

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

A

Rheumatoid arthritis.

DMARD - disease-modifying antirheumatic drug

261
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.

262
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.

263
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.

264
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.
265
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.

266
Q

Name 3 TNF blockers.

A
  1. Etanercept (TNF alpha specific).
  2. Infliximab.
  3. Adalimumab.
267
Q

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

A

Methotrexate.

268
Q

Give a side effect of using TNF blockers.

A

Increased susceptibility to TB.

269
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.

270
Q

Name an IL-6 blocker.

A

Tocilizumab.

271
Q

When are IL-6 blockers used?

A

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

272
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.

273
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.
274
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.

275
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.

276
Q

What region determines Ig class?

A

The constant region!

277
Q

What is the result of recombination in the Ig region?

A

Class switching.

278
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.

279
Q

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

A

Tyrosine kinase.

280
Q

What immunoglobulin do naive antibodies express?

A

IgM.

281
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.

282
Q

What do T cells recognise?

A

PEPTIDES

283
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.
284
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.
285
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.
286
Q

Give an example of a proton pump inhibitor.

A

Omeprazole.

287
Q

Give an example of a statin.

A

Simvastatin.

288
Q

Give an example of an ACE inhibitor.

A

Enalapril.

289
Q

Give an example of a COX inhibitor.

A

Aspirin and paracetamol.

290
Q

Give an example of a β2 adrenoceptor agonist.

A

Salbutamol.

291
Q

Give an example of a β1 adrenoceptor blocker.

A

Atenolol.

292
Q

Give an example of a Ca2+ channel blocker.

A

Amlodipine.

293
Q

Give an example of a broad spectrum antibiotic.

A

Amoxicillin.

294
Q

Give an example of an opiate analgesic.

A

Tramadol.

295
Q

What do most drugs target?

A

Proteins!

296
Q

Name 4 receptors that drugs target.

A
  1. Ligand gated ion channels.
  2. GPCR.
  3. Kinase linked.
  4. Cytosolic/nuclear.
297
Q

Give an example of a ligand gated ion channel.

A

Nicotinic Ach receptor.

298
Q

Give an example of a GPCR.

A

Muscarinic and β2 adrenoceptor.

GPCR’s usually interact with adenylate cyclase or phospholipase C

299
Q

Give an example of a kinase linked receptor.

A

Receptors for growth factors.

300
Q

Give an example of a cytosolic/nuclear receptor.

A

Steroid receptors; steroids affect transcription.

301
Q

What are agonists?

A

Agonists bind to a receptor and to activate it.

302
Q

What are antagonists?

A

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

303
Q

Describe the shape of a log dose-response curve.

A

Sigmoidal.

304
Q

What does EC50 tell us about a drug?

A

Its potency!

305
Q

What is EC50?

A

The concentration of drug that gives half the maximal response.

306
Q

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

A

Greater potency.

307
Q

What does Emax tell us about a drug?

A

Efficacy.

308
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.

309
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.

310
Q

Drug action: define affinity.

A

How well a ligand binds to a receptor.

311
Q

Drug action: define efficacy.

A

How well a ligand activates a receptor; how well it induces a conformational change.

312
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.

313
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).

314
Q

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

A

Less signal amplification gives a reduced drug response.

315
Q

Describe allosteric modulation.

A

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

316
Q

What is inverse agonism?

A

Where an agonist has a negative effect at a receptor.

317
Q

Does an antagonist show efficacy?

A

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

318
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.

319
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.
320
Q

Can aspirin be described as a selective drug?

A

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

321
Q

What is the function of COX1 and COX2?

A

They cyclise and oxygenate arachidonic acid and produce prostaglandin H2.

322
Q

What does prostaglandin H2 form when it interacts with synthases?

A

Prostanoids.

323
Q

Define pro-drugs and give an example of one.

A

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

324
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).

325
Q

Give an example of a β lactam antibiotic.

A

Penicillin and amoxicillin.

326
Q

How do β lactam antibiotics work?

A

The inhibit transpeptidase and so prevent bacterial cell wall synthesis.

327
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.

328
Q

Give an example of loop of henle diuretics.

A
  • Furosemide, act on the ascending loop.

- Thiazides, act on the distal tubule.

329
Q

How can drugs be developed?

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

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

330
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.

331
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!

332
Q

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

A
  1. Administration.
  2. Distribution.
  3. Elimination.
333
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

334
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.

335
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.

336
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.
337
Q

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

A

pH.

338
Q

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

A

Henderson Hasselbach.

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

339
Q

What can enhance non ionic diffusion?

A

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

340
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.

341
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.

342
Q

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

A

The weak acid will become more ionised.

343
Q

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

A

The weak base will become less ionised.

344
Q

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

A

The weak acid will become less ionised.

345
Q

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

A

The weak base will become more ionised.

346
Q

Define bioavailability.

A

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

347
Q

What route of drug administration has a bioavailability of 1?

A

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

348
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.

349
Q

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

A
  1. Chemical properties.

2. Molecular size.

350
Q

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

A

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

351
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.

352
Q

What is the relationship between plasma concentration and Vd?

A

Plasma concentration is inversely proportional to Vd.

353
Q

Give 3 factors that can increase gastric pH.

A
  1. Ingesting alkaline foods.
  2. Antacids.
  3. Omeprazole (PPI).
354
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.
355
Q

Write an equation for renal clearance.

A

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

356
Q

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

A
  1. Glomerular filtration.

2. Active secretion.

357
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.

358
Q

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

A

Glucuronic acid.

359
Q

Define hepatic extraction ratio (HER).

A

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

360
Q

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

A

Hepatic blood flow, perfusion limited.

361
Q

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

A

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

362
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.

363
Q

Where do phase 1 hepatic metabolism reactions occur?

A

In the smooth endoplasmic reticulum.

364
Q

What enzyme usually catalyses phase 1 reactions?

A

CYP450.

365
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.

366
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.
367
Q

Give 3 disadvantages of IV infusion.

A
  1. Expensive.
  2. Needs constant checking.
  3. Calculation error likely.
368
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.

369
Q

Give 4 properties of the ‘ideal drug’.

A
  1. Small Vd.
  2. Drug broken down effectively by enzymes.
  3. Predictable dose:response relationship.
  4. Low risk of toxicity.
370
Q

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

A
  1. Enhanced responsiveness.

2. More information can be conveyed.

371
Q

What is the principal neurotransmitter in the body?

A

Acetylcholine.

372
Q

What receptor does Ach interact with in the somatic nervous system?

A

Post-synaptic nicotinic receptors at the neuromuscular junction.

373
Q

What type of receptor are nicotinic receptors?

A

Ligand gated ion channels.

374
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.

375
Q

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

A

Acetylcholinesterase.

376
Q

Describe the action of botulinum toxin at the NMJ,

A

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

377
Q

Describe the action of competitive antagonists at the NMJ.

A

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

378
Q

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

A

Depolarising agonists cause receptor desensitisation.

379
Q

Describe the action of anticholinesterases at the NMJ.

A

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

380
Q

What type of receptor are muscarinic receptors?

A

GPCR.

381
Q

Give examples of adverse muscarinic agonist effects.

A
  1. Diarrhoea.
  2. Urination.
  3. Miosis.
  4. Brachycardia.
  5. Emesis (vomiting).
  6. Lacrimation.
  7. Salivation.
382
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.
383
Q

Briefly describe catecholamine synthesis.

A

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

384
Q

Where does the conversion from Dopamine to Noradrenaline happen?

A

In a vesicle in the pre-synpatic neurone.

385
Q

Which enzymes inactivate catecholamines?

A

MAO and COMPT.

386
Q

Which protein does α1 interact with to activate phospholipase C?

A

Gq.

387
Q

What is the primary function of α1?

A

α1 leads to vasoconstriction.

388
Q

Which protein does α2 interact with in order to inhibit adenylate cyclase synthesis?

A

Gi.

389
Q

What is the primary function of α2?

A

α2 is responsible for pre-synaptic inhibition; it inhibits NAd release.

390
Q

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

A

Gs.

391
Q

What is the role of adenylate cyclase?

A

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

392
Q

What are the primary functions of β1?

A
  1. Increased cardiac effects e.g. force, rate and conduction.
  2. Increased renin secretion.
393
Q

What are the primary functions of β2?

A
  1. Bronchodilation.

2. Vasodilation.

394
Q

What are the primary functions of β3?

A
  1. Increase lipolysis.

2. Bladder relaxation.

395
Q

What would an α1 adrenergic antagonist do?

A
  1. Vasodilation.

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

396
Q

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

A

Benign prostatic hyperplasia.

397
Q

What would a β1 adrenergic antagonist do?

A
  1. Reduce CO.

2. Reduce renin secretion.

398
Q

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

A

Hypertension, angina and arrhythmia.

399
Q

Define pain.

A

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

400
Q

Give 3 advantages of pain.

A
  1. Gives a warning for tissue damage.
  2. Immobilisation for healing.
  3. Memory establishment.
401
Q

Define acute pain.

A

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

402
Q

Define chronic pain.

A

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

403
Q

Define neuropathic pain.

A

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

404
Q

Define nociceptive pain.

A

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

405
Q

Are A delta fibres myelinated or unmyelinated?

A

Myelinated.

406
Q

Are C fibres myelinated or unmyelinated?

A

Unmyelinated.

407
Q

Describe the type of pain that A delta fibres conveys.

A

Quick, sharp, localised.

408
Q

Describe the type of pain that C fibres conveys.

A

Slow, dull, spread out.

409
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.

410
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.

411
Q

What is pain treatment focused on?

A
  1. Reducing excitatory neurotransmitters and nerve excitation.
  2. Enhancing inhibitory neurones.
412
Q

What are released in the presence of pain?

A

Endorphines.

413
Q

What is an adverse drug reaction?

A

A noxious and unintended response to a drug.

414
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.
415
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.
416
Q

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

A
  • Chronic.

- Occurs after long term therapy.

417
Q

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

A
  • Delayed.

- Occurs many years after treatment.

418
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.

419
Q

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

A

Reduce the dose.

420
Q

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

A

Withdraw drug immediately!

421
Q

Describe type 1 hypersensitivity.

A

IgE mediated hypersensitivity. Acute anaphylaxis. IgE becomes attached to mast cells, IgE cross linking leads to mast cell degranulation -> histamine.

422
Q

Describe type 2 hypersensitivity.

A

IgG mediated cytotoxicity.

423
Q

Describe type 3 hypersensitivity.

A

Immune complex deposition; immune complexes have not been adequately cleared by innate immune cells, giving rise to an inflammatory response.

424
Q

Describe type 4 hypersensitivity.

A

T cell mediated.

425
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.
426
Q

What can cause a type 1 hypersensitivity reaction?

A

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

427
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection.

428
Q

What can cause a type 3 hypersensitivity reaction?

A

Fungal.

429
Q

What can cause a type 4 hypersensitivity reaction?

A

TB.

430
Q

What is the treatment for anaphylaxis?

A
  1. Commence basic life support (ABC).
  2. Stop infusion of drug.
  3. Give adrenaline and anti-histamines.
431
Q

Give 4 risk factors for hypersensitivity.

A
  1. Protein based macromolecules.
  2. Female > male.
  3. Immunosuppression.
  4. Genetic factors.
432
Q

Why are drug interactions such a big problem today?

A
  1. Ageing population.
  2. Polypharmacy.
  3. Increased use of over the counter drugs.
433
Q

Give 5 patient risk factors for drug interactions.

A
  1. Old age.
  2. Polypharmacy.
  3. Renal disease.
  4. Hepatic disease.
  5. Genetics.
434
Q

Give 3 drug related risk factors for drug interactions.

A
  1. Narrow therapeutic index.
  2. Steep dose/response curve.
  3. Saturable metabolism.
435
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.
436
Q

How might drug interactions affect drug metabolism?

A

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

437
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.

438
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.

439
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.

440
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.

441
Q

What drug acts as an antagonist at the μ receptor?

A

Naloxone.

442
Q

What enzyme is needed to metabolise codeine?

A

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

443
Q

What is the bioavailability of morphine taken orally?

A

50%.

444
Q

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

A

5mg.

445
Q

What is morphine metabolised to?

A

Morphine 6 glucuronide.

446
Q

Where might μ receptors be found?

A

In the epidural space and CSF.

447
Q

Give 5 side effects of opioid use.

A
  1. Respiratory depression.
  2. Sedation.
  3. Nausea.
  4. Vomiting.
  5. Constipation.
448
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!

449
Q

Name a protein that can inhibit apoptosis.

A

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

450
Q

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

A

Cancer.

451
Q

Where are mast cells found?

A

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

452
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.

453
Q

Define physiological antagonism.

A

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

454
Q

What are the 3 actions of NSAIDS?

A
  1. Anti-inflammatory.
  2. Analgesic.
  3. Anti-pyrexic.
    (AAA).
455
Q

Name a local anaesthetic.

A

Lidocaine.

456
Q

How do local anaesthetics work?

A

They inhibit pain by stopping impulse conduction in sensory nerves.

457
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.

458
Q

Give 3 cytokines secreted by TH2.

A
  1. IL-4.
  2. IL-6.
  3. IL-13.
  4. IL-5.
  5. IL-10.
459
Q

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

A

Fab region.

460
Q

Name 3 cytokines secreted by TH1.

A
  1. IL-2.
  2. Gamma-interferon.
  3. TNF-beta.
461
Q

Name 2 cytokines secreted by TREG.

A
  1. IL-10.

2. TGF-beta.

462
Q

Define adenocarcinoma.

A

A malignant neoplasm of glandular epithelium.

463
Q

What blood marker is investigated in a patient with suspected sarcoidosis?

A

ACE - released by granulomas

464
Q
A
465
Q

Why may a second dose of epinephrine be needed?

A 
Rapidly metabolised (short half life)
Rapidly excreted
466
Q

What blood marker is used as an indicator for anaphylaxis?

A

Mast cell tryptase

Histamine is only raised for a short time

467
Q

Which serum protein is an indicator of sensitisation?

A

IgE levels

468
Q

What type of IG is produced in type 3 hypersensitivity?

A

IgM, IgG

469
Q

What type of IG is produced in type 2 hypersensitivity?

A

IgG, IgM

470
Q

What type of IG is produced in type 1 hypersensitivity?

A

IgE

471
Q

What is the name of the IgE receptors?

A

FCepsilonR1 (mast cell, basophils)

FCepsilonR2 (b-cell, dendritic, monocytes) → Mop up free IgE

472
Q

What is the management of anaphylaxis?

A
  1. Stop IV infusion
  2. BLS (ABC’s)
  3. IM 500mg Adrenaline
  4. IV fluids (increase CO)
  5. IV antihistamine
  6. IV hydrocortisone
    N.B. If shock -> IV adrenaline
    Can lie patient flat to increase venous return & BP
473
Q

What is the function of bradykinin?

A 
"Bradykinin is a plasma derived inflammatory mediator"
Bronchoconstriction
Increase vessel permeability
Increased pain
Increased vasodilation
474
Q

What is the difference between dysplastic and cancerous cells?

A

Dysplastic cells stay in the epithelium

Cancerous cells invade into the stroma

475
Q

What causes melanoma?

A

UVA (and UVb) from the sun

476
Q

What are the typical systemic effects of acute inflammation?

A 
Pyrexia (fever)
Increased heart rate
Increased respiratory rate
Leukocytosis - elevated blood leukocytes
Malaise (fatigue)
477
Q

What are the symptoms of anaphylaxis?

A

Urticaria
Bronchospasm (tryptase)
Angiooedema
Hypotension (shock)

478
Q

What are the signs of an arterial thrombus?

A

Tissue necrosis

No pulse distal to clot

479
Q

What are the signs of a venous thrombus?

A

Swelling/redness - arterial blood not drained

480
Q

Meaning of an elevated d-dimer?

A

Increased clotting

481
Q

Swelling/redness - arterial blood not drained

A

Prostatic, renal, lung & breast

Often spread by lymphatics

482
Q

What are the different types of histamine receptors?

A

H1 receptor; Vasodilation, hypotension, flushing. Coronary artery vasoconstriction -> tachycardia, vascular permeability, pruritus, bronchospasm & rhinorrhoea.
H2 receptor; Increase atrial and ventricular contractility, atrial chronotropy & coronary artery vasodilation

483
Q

What are the 4 outcomes of acute inflammation?

A

. Resolution - back normal

  1. Supparation - walled off abscess/pus formation
  2. Organisation (granulation) - necrotic cells cause granulation tissue formation -> fibrosis
  3. Chronic inflammation - progression

Phase 2a Medicine (11 decks)

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