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Phase 2a > Introduction to clinical sciences > Flashcards

Introduction to clinical sciences Flashcards

1
Q

What is inflammation?

A

A reaction to an injury or infection involving neutrophils or macrophages

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2
Q

When is inflammation good?

A

°Fighting infections

°Protection from injury

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3
Q

When is inflammation bad?

A

°Autoimmune conditions

°Over-reaction to stimulus

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4
Q

How is acute inflammation classified?

A

°Sudden onset
°Short duration
°Usually resolves itself

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5
Q

How is chronic inflammation classified?

A

°Slow onset
°Long duration
°May never resolve

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6
Q

What cells are involved in inflammation?

A 
°Neutrophil polymorphs
°Macrophages
°Lymphocytes
°Endothelial cells
°Fibroblasts
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7
Q

Properties of neutrophil polymorphs?

A

°Short lived (~5 days)
°First on the scene of inflammation
°Have cytoplasmic granules full of enzymes to kill bacteria
°Die at the scene
°Release cytokines to attract other cells

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8
Q

Properties of macrophages?

A

°Long lived
°Phagocytic
°Ingest bacteria and debris
°Can present antigens

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9
Q

Properties of lymphocytes?

A

°Live for years
°Can produce cytokines
°Are capable of producing memory cells

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10
Q

Properties of endothelial cells?

A

°Line capillaries
°Can become sticky to allow inflammatory cells to appear
°Can become porous to allow cells to pass through to tissue
°Grow into areas of damage to form new capillary vessels

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11
Q

Example of acute inflammation?

A 
Acute appendicitis-
    °Unknown factors for inflammation
    °Neutrophils are present
    °Blood vessels dilate
    °Inflammation of serosal surface
    °Pain
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12
Q

Example of chronic inflammation?

A

Tuberculosis-
°No initial acute inflammation
°Mycobacteria ingested by macrophages
°Macrophages fail to kill bacteria
°Lymphocytes and additional macrophages appear
°Fibrosis occurs

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13
Q

Properties of fibroblasts?

A

°Long lived cells

°Form collagen in area of chronic inflammation and repair

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14
Q

How do granulomas occur?

A

When two or more macrophages attempt to engulf the same material at once, the cells end up joining together

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15
Q

Causes of acute inflammation?

A 
°Microbial infections
°Hypersensitivity reactions
°Physical agents (trauma)
°Chemicals
°Bacterial toxins
°Tissue necrosis
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16
Q

3 processes of the inflammatory response?

A

°Changes in the vessel calibre and flow
°Increased vascular permeability and formation of fluid exudate
°Formation of cellular exudate - emigration of neutrophil polymorphs to extracellular space

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17
Q

Causes of increased vascular permeability?

A

°Immediate transient chemical mediators e.g -
°Histamine
°Bradykinin
°C5a
°NOx
°Leucotrine B4
°Platelet activating factor
°Immediate sustained severe vascular trauma
°Delayed prolonged endothelial injury e.g. x-ray

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18
Q

What can endogenous chemical mediators cause?

A 
°Vasodilation
°Emigration of neutrophils
°Chemotaxins
°Increased vascular permeability
°Itching and pain
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19
Q

What are the systemic effects of inflammation?

A 
°Pyrexia (fever)
°Weight loss
°Reactive hyperaemia of the reticuloendothelial system
°Haematological changes
°Amyloidosis
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20
Q

Appearances of chronic inflammation?

A 
Macroscopic - 
    °Ulcers
    °Abscess cavity
    °Thickening of hollow viscus wall
    °Granulomatous inflammation
    °Fibrosis
Microscopic - 
    °Lymphocytes and macrophages
    °A few eosinophils
    °Destruction of tissue and formation of fibrous tissue
    °Tissue necrosis
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21
Q

Special multinucleate giant cells?

A

°Langhans cells (tuberculosis) horseshoe arrangement of peripheral nuclei
°Touton giant cells (xanthomas/dermatofibromas of the skin) have a central ring of nuclei peripheral to lipids

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22
Q

What is the difference between repair and resolution?

A

Resolution -
°Initiating factor is removed
°Tissue is undamaged or can regenerate
Repair -
°Initiating factor is still present
°Tissue is damaged can cannot regenerate

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23
Q

What are the features of lobar pneumonia?

A

°Single lobe of the lung
°Caused by streptococcus pneumonia
°Anti-biotics to clear
°Pneumocytes in the lung can regenerate

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24
Q

Healing by 1st intention?

A

°Involves a wound where the skin can be pulled together
°Space is filled with fibrin
°Forms a weak join
°Filled with collagen by fibroblasts

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25
Q

Healing by 2nd intention?

A

°Wound cannot be pulled together
°Capillaries, fibroblasts and collagen all form to repair the wound
°Grows in from the edges

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26
Q

How does repair happen in the brain?

A

Gliosis, collagen is produced by glial cells

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27
Q

Which cell types can regenerate?

A 
°Hepatocytes
°Pneumocytes
°Blood cells (all)
°Gut epithelium
°Skin epithelium
°Osteocytes
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28
Q

Why don’t clots form all the time?

A

°Laminar flow in the centre of the artery

°Endothelial cells are not sticky when they are healthy

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29
Q

What can cause thrombosis?

A

°Change in the vessel wall
°Change in the flow of blood
°Change in the blood constituents

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30
Q

How does thrombosis occur?

A

°Platelet aggregation leads to the coagulation cascade
°Platelets stick to collagen which is exposed under damaged endothelial cells
°Disrupts laminar flow and red blood cells get trapped with platelets
°Fibrin is deposited into the clot
°Positive feedback loop

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31
Q

What is a thrombus?

A

A solid mass of blood constituents formed within an intact vascular system during life

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32
Q

How do you prevent thrombosis?

A

°Movement
°Compression stockings
°Aspirin

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33
Q

What is an embolus?

A

A mass of material in the vascular system able to become lodged within a vessel and block it

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34
Q

What is ischaemia?

A

Reduction in blood flow without any other complications

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35
Q

What is infarction?

A

Reduction in blood flow that is so reduced that it cannot support the maintenance in the cells of a tissue, so they begin to die

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36
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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37
Q

What are 3 organs with a dual arterial supply?

A

°Lungs
°Liver
°Brain

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38
Q

What happens after ischaemia is fixed?

A

Re-perfusion injury meaning that the waste products that have accumulated during the reduced blood flow period are released

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39
Q

What are the consequences of an arterial embolus?

A

An arterial embolus can travel around the body with the consequences being stroke, MI, gangrene

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40
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

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41
Q

What is the definition of atherosclerosis?

A

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

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42
Q

What forms an atherosclerotic plaque?

A

°Fibrous tissue
°Lipids (cholesterol)
°Crystals (these dissolve)
°Lymphocytes

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43
Q

Which system do you find atherosclerosis in?

A

Low pressure systems such as the pulmonary ateries

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44
Q

How does a plaque form?

A

°Endothelial dysfunction
°Formation of lipid layer or fatty streak within the intima °Migration of leukocytes and smooth muscle cells into the vessel wall
°Foam cell formation
°Degradation of extracellular matrix.

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45
Q

What complications can arise from atherosclerosis?

A 
°Cerebral infarction
°Carotid atheroma
°Myocardial infarction
°Aortic 
°Gangrene
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46
Q

What are the risk factors for atherosclerosis?

A 
°Cigarette smoking. 
°Hypertension. 
°Hyperlipidaemia. 
°Uncontrolled diabetes mellitus. 
°Lower socioeconomic status.
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47
Q

How does smoking impact atherosclerosis?

A

Free radicals, nicotine and CO damage the endothelial cells

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48
Q

How does hypertension impact atherosclerosis?

A

Sheering forces created by high blood pressure causes damage to the endothelial cells which is the first stage of plaque formation

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49
Q

What is the definition of apoptosis?

A

The programmed death of a single cell

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50
Q

How does a cell apoptose?

A 
°Enzymes are released to shrink the cell
°The nucleus condenses
°The nucleus and DNA fragments
°An apoptic body forms from the contents of the cell
°The body is then phagocytosed
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51
Q

DNA damage can lead to a cell being apoptosed. What can happen to DNA to cause this?

A

°A single strand breaks
°Both strands break
°One of the bases becomes altered
°There is cross linkage of the strands

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52
Q

Which protein detects DNA damage?

A

P53

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53
Q

Which family of proteins can turn on apoptosis?

A

Caspases

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54
Q

Which receptor turns the proteins which regulate apoptosis on?

A

FAS receptor

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55
Q

What is the purpose of apoptosis in development?

A

Can separate the digits of the foetus

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56
Q

What disease has a lack of apoptosis?

A

Cancer, with even less in breast and colorectal cancer

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57
Q

What disease has increased apoptosis?

A

HIV, the CD4 cells are apoptosed at an increased rate

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58
Q

What is the definition of necrosis?

A

The large scale, unplanned death of cells

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59
Q

What are some clinical examples of necrosis?

A 
°Spider venom
°Frostbite
°Cerebral infarction
°Avascular necrosis (head of femur, scaphoid)
°Pancreatitis
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60
Q

What is coagulative necrosis?

A

A type of necrosis caused by ischaemia or infarction. The tissues are preserved for a few days . It can also be induced by a high temperature

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61
Q

What is liquefactive necrosis?

A

A type of necrosis which results in the tissues becoming liquidised. It is usually caused by a bacterial or fungal infection but can also be caused by an internal chemical burn

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62
Q

What is unique about caseous necrosis?

A

The presence of multinucleate giant cells

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63
Q

Define hypertrophy

A

An increase in the size of tissues caused by an increase in the size of the constituent cells

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64
Q

What are two ways that the size of cells can increase?

A

°Increase in the number of myofibrils present

°Increase in the volume of sarcoplasm

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65
Q

Define hyperplasia

A

An increase in the size of tissues caused by an increase in the number of constituent cells

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66
Q

What can cause endometrial hyperplasia?

A

Having more oestrogen than progesterone present

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67
Q

Define atrophy

A

A decrease in the size of a tissue caused by either a decrease in the number of constituent cells or a decrease in the size of the cells

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68
Q

Define metaplasia

A

A change in differentiation of a cell from one which is fully differentiated to a different fully differentiated cell

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69
Q

Give an example of metaplasia

A

Ciliated columnar epithelium in the trachea changing to because squamous epithelium due to smoking

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70
Q

Define dysplasia

A

Morphological changes seen in cells in the progression to becoming cancerous

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71
Q

What happens when telomeres get too short?

A

They can no longer replicate or divide

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72
Q

Give two examples of tissues that can divide

A

°Gut epithelium

°Skin epithelium

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73
Q

What is an example of a non-dividing tissue?

A

Brain

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74
Q

What can cause a reduction in dividing tissue?

A

°Free radicals
°Cross-linking of DNA proteins
°DNA damage
°Mitochondrial DNA damage

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75
Q

What are the symptoms of ageing?

A 
°Balding
°Dementia
°Deafness
°Cataracts
°Osteoporosis
°Dermal elastosis
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76
Q

What causes dermal elastosis?

A

UV-B causes cross-linking of collagen proteins which makes them less elastic

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77
Q

What causes cataracts?

A

UV-B causes cross-linking of collagen proteins which makes the lens cloudy

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78
Q

What causes osteoporosis?

A

A lack of oestrogen causes an increase in bone resorption and a decrease in bone formation

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79
Q

What can cause dementia?

A

°Atrophy of brain tissue
°Plaques (Lewy bodies)
°Neurofibrillary tangles

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80
Q

What causes sarcopenia (and what is it)?

A

°Muscle loss
°Decreased growth hormone
°Decreased testosterone
°Increased catabolic cytokines

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81
Q

What is unique about basal cell carcinoma?

A

It only invades the dermis of the skin and does not metastasise to other areas of the body = excision of the tumour will cure it

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82
Q

What is the definition of carcinogenesis?

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

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83
Q

What is oncogenesis?

A

The same as carcinogenesis but only applies to malignant cells

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84
Q

What percentage of cancer risk is environmental?

A

85% environmental, 15% genetic

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85
Q

Where is hepatocellular carcinoma more common?

A

Rare in the UK/US but has a high incidence in areas with increased incidence of Hep B/C

86
Q

What is the definition of a carcinoma?

A

Malignant tumour of epithelial tissue

87
Q

Give examples of carcinomas that commonly metastasise to the bone?

A 
°Prostate
°Breast
°Thyroid 
°Kidney
°Lung
88
Q

Why are adjuvant therapies used in cancer treatments?

A

Micro-metastases are possible even if a tumour is excised and so adjuvant therapy is given to suppress secondary tumour formation

89
Q

What are the host factors that affect cancer risk?

A 
°Race
°Diet 
°Constitutional factors (gender, age)
°Premalignant conditions 
°Transplacental exposure
90
Q

What is one advantage of conventional chemotherapy and one disadvantage?

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.

91
Q

What are the categories of carcinogens?

A 
°Viral
°Chemical
°Radiation
°Hormones, mycotoxins, parasites
°Miscellaneous
92
Q

What type of cancer do polycyclic aromatic hydrocarbons cause?

A

Skin and lung cancer via smoking and inhalation of mineral oils

93
Q

What cancer do aromatic amines cause?

A

Bladder cancer (common in the rubber industry)

94
Q

What type of cancer do nitrosamines cause?

A

Gut cancer

95
Q

What cancer do alkylating agents cause?

A

Leukaemia

96
Q

How is skin cancer caused?

A

UV-B rays

97
Q

What cancer does the inhalation of radioactive uranium in mines cause?

A

Lung cancer

98
Q

What cancer does radioactive iodine cause?

A

Thyroid

99
Q

What cancer can increased oestrogen cause?

A

Mammary/endometrial cancer

100
Q

What cancer does anabolic steroids cause?

A

Hepatocellular carcinoma

101
Q

What cancer does Aflatoxin B1 cause?

A

Hepatocellular carcinoma

102
Q

What cancer does chlorochis sinensis cause?

A

Cholangiocarcinoma

103
Q

What cancer does shistosoma cause?

A

Bladder cancer

104
Q

Which cancers can be caused by asbestos?

A

Mesothelioma, asbestosis, lung cancer

105
Q

What is the definition of a neoplasm?

A

A lesion resulting from the 𝗮𝘂𝘁𝗼𝗻𝗼𝗺𝗼𝘂𝘀 or relatively autonomous 𝗮𝗯𝗻𝗼𝗿𝗺𝗮𝗹 growth of cells which 𝗽𝗲𝗿𝘀𝗶𝘀𝘁𝘀 after the initiating stimulus has been removed

106
Q

What is the structure of neoplasms?

A

Made from neoplastic cells and a stroma

107
Q

What are the characteristics of neoplastic cells?

A

°Derived from nucleated cells
°Usually monoclonal
°Growth pattern and synthetic activity are related to the parent cell

108
Q

What are the characteristics of neoplasm stroma?

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.

109
Q

What needs to occur for a neoplasm to grow?

A

Angiogenesis

110
Q

What does the neoplasm release in order to become vasculated?

A

Vascular endothelial growth factor

111
Q

Why does necrosis occur in the centre of a neoplasm?

A

The neoplasm outgrows its vasculation so the centre does not receive blood flow and so necroses

112
Q

Why do we classify neoplasms?

A

It helps to determine the appropriate treatment and prognosis

113
Q

What are the two classifications of neoplasms?

A

°Behavioural

°Histological

114
Q

What are the features of benign neoplasms?

A 
°Localised and non-invasive 
°Slow growth rate
°Low mitotic activity
°Close resemblance to normal tissue
°Circumscribed or encapsulated
°Nuclear morphology is often normal
°Necrosis and ulceration is rare
°Growth on mucosal surfaces is often exocytotic (grows up and out)
115
Q

What are the features of malignant neoplasms?

A 
°Invasive
°Metastases
°Rapid growth rate
°Variable resistance to normal tissue
°Poorly defined/ irregular border
°Hyperchromatic nuclei and pleomorphic nuclei
°Increased mitotic activity
°Necrosis and ulceration are common
°Growth on mucosal surfaces is often endocytotic (grows down and in)
116
Q

Why worry about benign neoplasms?

A 
°Pressure is put on adjacent systems
°Can obstruct blood flow
°Can produce hormones
°Sometimes can transform into malignant neoplasms
°Anxiety
117
Q

Why worry about malignant neoplasms?

A 
°Destruction of adjacent tissue
°Metastases
°Blood loss from ulcers
°Obstruction of blood flow
°Hormone production
°Paraneoplastic effects
°Anxiety and pain
118
Q

What is the meaning of histogenesis?

A

The specific cell of origin of a tumour

119
Q

What is a papilloma?

A

Benign tumour of non-glandular, non-secretory epithelium

120
Q

What is an adenoma?

A

Benign tissue of the glandular/secretory epithelium

121
Q

What is a carcinoma?

A

Malignant tumour of epithelial cells

122
Q

What would a benign neoplasm found in lipid tissue be called?

A

Lipoma

123
Q

What would a benign neoplasm found in cartilage be called?

A

Chondroma

124
Q

What would a benign neoplasm found in bone be called?

A

Osteoma

125
Q

What would a benign neoplasm found in the vascular system be called?

A

Angioma

126
Q

What would a benign neoplasm of neuronal cells be called?

A

Neuroma

127
Q

What is a rhabdomyoma?

A

Benign neoplasm of striated muscle

128
Q

What is a leiomyoma?

A

Benign neoplasm of smooth muscle

129
Q

Which cancers do not follow sarcoma/carcinoma naming rules?

A

°Melanoma
°Lymphoma
°Mesothelioma

130
Q

What is a cancer called when it is contained within a cell?

A

Carcinoma in situ

131
Q

What is one advantage and one disadvantage of non-targeted chemotherapy?

A 
°Advantage = works well for treatment against fast dividing tumours 
°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
132
Q

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

A

°Proteases

°Cell motility

133
Q

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

A

°Collagenases

°Cell motility

134
Q

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

A

°Adhesion receptors
°Collagenases
°Cell motility

135
Q

What is needed for a tumour to grow at a metastatic site?

A

Growth factors

136
Q

What are the promoters of angiogenesis?

A

°Vascular endothelial growth factor

°Basic fibroblast growth factor

137
Q

What are the inhibitors of angiogenesis?

A

°Angiostatin
°Endostatin
°Vasculostatin

138
Q

What are the defence mechanisms of tumours to evade the host defence system?

A

°Platelet aggregation.
°Adhesion to other tumour cells.
°They shed surface antigens so as to ‘distract’ lymphocytes

139
Q

Where do tumours which enter the right atrium typically metastasise to?

A

The lung, specifically in small capillaries

140
Q

Where do tumours which enter the left atrium metastasise to?

A

Brain, bone, the entire body

141
Q

Cancer metastasis in the liver could come from where?

A

Colon, stomach, pancreas, carcinoid tumours of the intestine

142
Q

What is innate immunity?

A

Instinctive, non-specific, does not depend on lymphocytes, present from birth

143
Q

What is adaptive immunity?

A

Specific ‘Acquired/ learned’ immunity, requires lymphocytes, antibodies

144
Q

Which white blood cells are polymorphonuclear leukocytes?

A

Neutrophil, eosinophil, basophil

145
Q

Which white blood cells are mononuclear leukocytes?

A

Monocytes, T-cells, B-cells

146
Q

What can T-cells differentiate into?

A

°T-regulators
°T-helper cells (CD4, Th1, Th2)
°Cytotoxic (CD8)

147
Q

What is complement?

A

Group of ~20 serum proteins secreted by the liver that

need to be activated to be functional.

148
Q

What are the three ways in which complement works?

A

°Direct lysis
°Attract more Leukocytes to site of infection
°Coat invading organisms

149
Q

What are the 5 Ig proteins that need to be memorised?

A

MAGED (see textbook/slides on 15/11/19 for images)

150
Q

What are cytokines?

A

Proteins secreted by immune and non-immune cells

151
Q

What are interferons and what do the different types do?

A

Induce a state of antiviral resistance in uninfected cells & limit the spread of viral infection
°IFNα & β - produced by virus infected cells
°IFNγ - released by activated Th1 cells

152
Q

What is the function of interleukins?

A

°Can be pro-inflammatory (IL1) or anti-inflammatory (IL-10) °Can cause cells to divide, to differentiate and to secrete factors

153
Q

What do colony stimulating factors do?

A

°Involved in directing the division and differentiation on bone marrow stem cells

154
Q

What are chemokines?

A

Proteins that direct movement of leukocytes from the bloodstream into the tissues or lymph organs by binding to specific receptors on cells

155
Q

What does the CXCL chemokine control?

A

Neutrophils

156
Q

What does the CCL chemokine control?

A

Monocytes, lymphocytes, eosinophils, basophils

157
Q

What does the CX3CL chemokine control?

A

T-lymphocytes and natural killer (NK) cells

158
Q

What does the XCL chemokine control?

A

T-lymphocytes

159
Q

What are the characteristics of innate immunity?

A 
°Primitive (spread across species)
°‘Un-learned/instinctive’ response
°Does not depend on immune recognition by lymphocytes
°Does not have long lasting memory 
°Integrates with Adaptive response
160
Q

What are the characteristics of adaptive immunity?

A

°Response specific to antigen
°Learnt behaviour
°Memory to specific antigen
°Quicker response

161
Q

What 3 things compromise the innate immune system?

A

°Physical and chemical barriers
°Phagocytic cells (neutrophils and macrophages)
°Blood proteins (complement, acute phase)

162
Q

What are the stages of immunisation?

A 
°Exposure
°Antigen presents to T-cells
°Production of IgM
°Establishment of IgG
°Large amounts of IgG produced
163
Q

What can be recognised by PRRs?

A

°Gram +ve/-ve
°dsRNA
°CpG motifs

164
Q

What do secreted and circulating PRRs do?

A

°They are antimicrobial peptides secreted in lining fluids from epithelia and phagocytes
°They disrupt pathogen motility and kill them
°They also assist in phagocytosis

165
Q

What are lectins and collectins?

A

°Peptides PRRs that also contain carbohydrates
°They bind carbohydrates and lipids
°Can also activate complements which improves phagocytosis

166
Q

What are pentaxins?

A

°They are PRRs which have some antimicrobial actions
°React with the C-polysaccharide of pneumococci
°Active complements which improves phagocytosis

167
Q

What can different TLRs detect?

A 
°Gram +ve/-ve
°Flagellin
°CpG motifs
°dsRNA
°ssRNA
°LTAs
168
Q

What does TLR 1/2 detect?

A

Gram +ve lipopeptide

169
Q

What does TLR 3 detect?

A

dsRNA (exogenous) and mRNA (endogenous)

170
Q

What does TLR 4 detect?

A

Exogenous:
°LPS, pneumolysin, viral proteins
Endogenous:
°Heat shock proteins, HMGB1, hyaluronan, fibrinogen

171
Q

What does TLR 5 detect?

A

Flagellin

172
Q

What does TLR 2/6 detect?

A

Gram +ve lipopeptide

173
Q

What does TLR 7 detect?

A

ssRNA

174
Q

What does TLR 8 detect?

A

ssRNA

175
Q

What does TLR 9 detect?

A

CpG (exogenous) and DNA/mitochondrial DNA (endogenous)

176
Q

What are the other membrane bound PRRs?

A

°Mannose receptors on macrophages (react to fungi)
°Dectin-1 which is widespread on phagocytes and recognise beta-glucans in fungus
°Scavenger receptors on macrophages

177
Q

What are NLRs?

A

°Nod-like receptors

°Detection of peptidoglycan muranyl 1 dipeptide

178
Q

What is NOD2?

A

°Recognises muranyl 1 dipeptide which comes from them breakdown of peptidoglycans
°Activates the inflammatory signalling pathway
°Non-function of NOD2 leads to Crohn’s
°Hyper function of NOD2 leads to Blau syndrome

179
Q

What are RLRs?

A

°Rig-like receptors
°RIG-1 and MDA5 detect dsRNA and DNA
°Activate interferon production

180
Q

What is the link between PRRs and homeostasis?

A

°Blood neutrophil numbers may depend on TLR 4 signalling, which is independent of LPS
°Induction of endotoxin tolerance in the newborn gut
°PRRs mature the newborn gut
°Maintains the balance with commensal organisms

181
Q

How do PRRs recognise damage?

A

°TLRs adapt to recognise endogenous damage molecules - they share hydrophobicity
°Appearance of host molecules in unfamiliar contexts activate TLRs
°TLR signalling activates immunity and initiates tissue repair

182
Q

What are the extracellular damage molecules?

A

°Fibrinogen
°Hyaluronic acid
°Tenascin C

183
Q

What are the intracellular damage molecules?

A 
°HMGB1 
°mRNA
°Heat shock proteins
°Uric acid
°Stathmin
184
Q

How do PRRs work in adaptive immunity?

A

°Activation of PRRs and TLRs drive cytokine production and increase the likelihood of T-cell activation
°TLR 4 agonists are used in vaccine adjuvants
°TLR 7/8/9 adjuvants are used in development

185
Q

What conditions are PRRs linked to?

A

°Atherosclerosis
°Arthritis
°COPD
°IBD

186
Q

Which major diseases have been contained since vaccines have been introduced?

A 
°Diptheria
°Mumps
°Tetanus
°Pertussis (whooping cough)
°Poliomyelitis
°Smallpox
187
Q

What diseases are anti-toxins (passive immunisation) used for?

A

°Botulism
°Tetanus
°Diptheria

188
Q

What diseases are prophylaxis (passive immunisation) used for?

A

°Hepatitis
°Measels
°Rubella

189
Q

What diseases are anti-veins (passive immunisation) used for?

A

°Snake bite
°Insect bites
°Jellyfish stings

190
Q

What are the stages of active immunisation?

A

°Engage the innate immune system
°Elicits ‘danger’ signals that activate the immune system and triggers the PAMPs etc
°PAMPs activate TLRs
°TLRs activate specialist APCs e.g. Langerhans cells
°Engage the active immune system

191
Q

What is the initial response to antigen exposure?

A

°IgM predominantly
°Low affinity for Ab
°Germline repertoire
•Memory cells are made

192
Q

What is the secondary response/what happens when a disease is re-introduced following vaccination?

A

°Rapid and large response
°High levels and affinity of IgG
°Uses somatic cell line
°Hypermutation can occur

193
Q

What are the advantages of using a whole organism vaccine?

A

°Allows transient infection
°Activates full immune response
°Prolonged contact with the immune system
°1 dose required

194
Q

What are the disadvantages of using a whole organism vaccine?

A

°Immunocompromised patients may become infected
°Complications can occur
°In areas of poor sanitation it can lead to an outbreak of disease

195
Q

What are the advantages of using a whole inactivated organism vaccine?

A

°No risk of infection
°Storage is less critical
°Wide range of antigenic components present

196
Q

What are the disadvantages of using a whole inactivated organism vaccine?

A

°Does not activate T-cells
°Response can be weak
°Boosters needed
°Compliance issue

197
Q

What are the advantages of using a subunit vaccine?

A

°Safe
°No infection risk
°Easy to store

198
Q

What are the disadvantages of using a subunit vaccine?

A

°Response can be weak
°Boosters needed
°Consider gene heterogeneity of population by choice of antigen

199
Q

What are the 3 types of subunit vaccine?

A

°Inactivated exotoxins
°Capsular polysaccharide
°Recombinant microbial agents

200
Q

What effect does diphtheria toxin have on the body?

A

Inactivated mammalian elongation factor EF2

201
Q

What effect does tetanus toxin have?

A

Muscle contraction

202
Q

What is the aim of synthetic peptide vaccines?

A

To produce peptides including immunodominant B cell epitopes and stimulate memory T-cells

203
Q

What are the difficulties of synthetic peptide vaccines?

A

HLA knowledge is needed

204
Q

What is the aim of DNA vaccines?

A

Express genes from pathogen in host leading to T and B cell memory response

205
Q

What are the advantages of DNA vaccines?

A

°Safe
°No requirement for storage and transport
°Delivery is simple and adaptable (use a DNA gun)

206
Q

What are the disadvantages of DNA vaccines?

A

°Produces a mild response
°Need boosters
°Limited to proteins
°Could induce tolerance

207
Q

What is the aim of recombinant vector vaccines?

A

Imitate effects of transient infection with non-pathogenic organism

208
Q

What is a pathogen?

A

An organism that causes or is capable of causing disease

209
Q

What is a commensal organism?

A

An organism that colonises the host but causes no disease under normal circumstances

210
Q

What is an opportunist pathogen?

A

A microbe that only causes disease if the host defence is immunocompromised

211
Q

What is virulence/pathogenicity?

A

The degree to which a given organism is pathogenic

212
Q

What is asymptomatic carriage?

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease

Phase 2a (2 decks)

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