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Basic Pathology Flashcards

1
Q

Define inflammation

A

The local physiological response to to tissue injury, it is not itself a disease but a manifestation of disease

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2
Q

What beneficial effects might inflammation have?

A

Destruction of invading organisms and the walling off of an abscess cavity to prevent spread of infection

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3
Q

What harmful effects might inflammation have?

A

May produce disease e.g. abscess in the brain would act as a space occupying lesion; compressing vital surrounding structures

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4
Q

Define acute inflammation

A

the initial and often transient series of tissue reactions to injury

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5
Q

Define chronic inflammation

A

the subsequent and often prolonged tissue reactions following the initial response

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6
Q

How else can inflammation be categorised?

A

By differences in cell type involved

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7
Q

Outline the steps of acute inflammation

A
  1. Initial reaction of tissue to injury
  2. Vascular component: dilation of vessels
  3. Exudative component: vascular leakage of protein rich fluid
  4. Neutrophil polymorph is the characteristic cell recruited to the tissue
  5. Outcome may be resolution, suppuration (abscess), organisation, or progression to chronic inflammation
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8
Q

List some causes of inflammation

A

Microbial infections, hypersensitivity reactions, physical agents, chemicals, bacterial toxins, tissue necrosis

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9
Q

How might a bacteria cause inflammation?

A

Release specific exotoxins- chemicals synthesised by them that specifically initiate inflammation- or endotoxins, which are associated with their cells walls

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10
Q

When do hypersensitivity reactions occur?

A

When an altered state of immunological responsiveness causes an inappropriate or excessive immune reaction that damages the tissues

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11
Q

What are the macroscopic appearances of inflammation?

A
  1. Redness (Rubor)
  2. Heat (Calor)
  3. Swelling (Tumor)
  4. Pain (Dolor)
  5. (loss of function)
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12
Q

Why does redness occur in inflammation?

A

dilation of small blood vessels within the damaged area

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13
Q

Why does heat occur in inflammation?

A

(only in skin) due to increased blood flow (hyperaemia) through the region, resulting in vascular dilation and delivery of warm blood to the area

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14
Q

Why does swelling occur in inflammation?

A
  1. Swelling results from oedema- the accumulation of fluid in the extravascular space as part of the fluid exudate
  2. to a much lesser extent, the physical mass of cells migrating to the area
  3. as the inflammation process progresses, formation of new connective tissue also contributes to swelling
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15
Q

Outline why pain occurs in inflammation

A
  1. Stretching and distortion of tissue due to inflammatory oedema and pus under pressure in an abscess cavity
  2. Some chemical mediators of acute inflammation e.g. bradykinin, prostaglandins and serotonin, are known to induce pain
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16
Q

Why does loss of function occur in inflammation?

A

Movement is consciously and reflexively inhibited by pain, while severe swelling may physically immobilise the tissue

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17
Q

What is essential for the histological diagnosis of acute inflammation?

A

presence of neutrophil polymorphs

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18
Q

Name the 3 processes involved in acute inflammation

A
  1. Change in vessel calibre and, consequently, flow
  2. Increased vascular permeability and formation of the fluid exudate
  3. Formation of the cellular exudate- emigration of the neutrophil polymorphs into the extravascular space
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19
Q

List the time course mechanisms of increased vascular permeability

A
  1. Immediate transient chemical mediators
  2. Immediate sustained severe direct vascular injury
  3. Delayed prolonged endothelial cell injury
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20
Q

Give some examples of immediate transient chemical mediators that increase vascular permeability

A

histamine, bradykinin, nitric oxide, C5a, leucotriene B4, platelet activating factor

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21
Q

Give an example of immediate sustained severe direct vascular injury

A

trauma

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22
Q

Give examples of delayed prolonged endothelial cell injury

A

X-rays, bacterial toxins

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23
Q

List the stages in neutrophil polymorph emigration

A
  1. Margination of neutrophils
  2. Pavementing of neutrophils
  3. Pass between endothelial cells
  4. Pass through basal lamina and migrate into adventitia
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24
Q

What do endogenous chemical mediators cause?

A
  1. Vasodilation
  2. Emigration of neutrophils
  3. Chemotaxis
  4. Increased vascular permeability
  5. Itching and pain
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25
Q

List some chemical mediators released from cells

A

Histamine (others include: lysosomal compounds, eicosanoids, serotonin and chemokines)

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26
Q

The plasma contains four enzymatic cascade systems (which are interrelated), what are they?

A
  1. Complement
  2. The kinins
  3. The coagulation factors
  4. Fibrinolytic system
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27
Q

Draw the effect of coagulation factor XII (Hageman factor)

A

Refer to notes

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28
Q

Draw the diagram for the kinin system

A

Refer to notes

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29
Q

List the descriptive terms used for the macroscopic appearance of acute inflammation

A
  1. Serous
  2. Suppurative (purulent)
  3. Membranous
  4. Pseudomembranous
  5. Necrotising (gangrenous)
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30
Q

What are the systemic effects of inflammation?

A 
Pyrexia (fever)
Constitutional symptoms
Weight loss
Reactive hyperplasia of the reticuloendothelial system
Haematological changes
Amyloidosis
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31
Q

What is granulomatous inflammation?

A

A specific type of chronic inflammation

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32
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes

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33
Q

List the cells involved in chronic inflammation

A

Plasma cells, capillary endothelium, lymphocytes, multinucleate giant cells, macrophage, fibroblasts

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34
Q

What are the causes of chronic inflammation?

A
  1. Primary chronic inflammation
  2. Transplant rejection
  3. Progression from acute inflammation
  4. Recurrent episodes of acute inflammation
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35
Q

What are the macroscopic appearances of chronic inflammation?

A
  1. Chronic ulcer
  2. Chronic abscess cavity
  3. Thickening of the wall of a hollow viscus
  4. Granulomatous inflammation
  5. Fibrosis
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36
Q

List some microscopic appearances of chronic inflammation

A
  1. Cellular infiltrate consists of lymphocytes, plasma cells and macrophages
  2. Few eosinophil polymorphs may be present, but neutrophil polymorphs are scarce
  3. Multinucleate giant cells
  4. Production of new fibrous tissue
  5. Tissue necrosis
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37
Q

What are the predominant features in repair? and what are these processes regulated by?

A

Angiogenesis followed by fibroblast proliferation and collagen synthesis resulting in granulation tissue. Regulated by growth factors which bind to specific receptors.

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38
Q

List some examples of granulomatous disease

A

tuberculosis, leprosy, Chron’s disease, sarcoidosis

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39
Q

Describe the appearance of an epithelioid histiocyte

A

vague histiological resemblance to epithelial cells, large vesicular nuclei, plentiful eosinophil cytoplasm and are often rather elongated

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40
Q

Name an excretory product of epithelioid histiocytes

A

angiotensin converting enzyme

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41
Q

What clinical use do epithelioid histiocytes have?

A

Measurement of its activity in the blood can act as a marker for systemic granulomatous disease

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42
Q

What might the presence of granulomas be augmented by?

A

The presence of caseous necrosis or by the conversion of some of the histiocytes into multinucleate giant cells

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43
Q

Small traces of what element can induce granuloma formation?

A

Beryllium

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44
Q

Draw the cellular cooperation that occurs in chronic inflammation

A

See notes

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45
Q

When do histiocytic giant cells tend to form?

A

Particularly when foreign particles are too large to be ingested by just one macrophage

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46
Q

How are multinucleate giant cells thought to be formed?

A

‘By accident’ when two or more macrophages attempt simultaneously to engulf the same particle; their cell membranes fuse and the cells unite

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47
Q

In which condition are Langhan’s giant cells characteristically seen?

A

Tuberculosis

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48
Q

When are ‘foreign body giant cells’ characteristically seen?

A

In relation to particulate foreign body material

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49
Q

When are touton giant cells often seen?

A

When macrophages attempt to ingest lipids, and in xanthomas/ dermatofibromas of the skin

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50
Q

Give an example of how acute inflammation is involved in the CV system

A

In the response to acute MI and the generation of some complications of MI such as cardiac rupture

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51
Q

Give two conditions which chronic inflammation is associated with

A

Initiation, propagation and progression of cancer, myocardial fibrosis post MI

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52
Q

Outline how inflammation makes an important contribution to development of atheroma

A

Macrophages adhere to endothelium, migrate into the arterial intima and with T-lymphocytes, express cell adhesion molecules which recruit other cells into the area. The macrophages are involved in processing the lipids that accumulate in atheromatous plaques.

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53
Q

Explain the difference between exudate and transudate

A

Exudates have a high protein content beacue they reulst from increased vascular permeability. Transudates have a low protein content because the vessels have normal permeability characteristics.

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54
Q

Define granulation tissue

A

An important component of healing that comprises small blood vessels in a connective tissue matrix with myofibroblasts.

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55
Q

Define fibrous

A

Fibrous describes the texture of a non-mineralised tissue of which the principle component is collagen (e.g. scar tissue)

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56
Q

Describe the process of repair after surgical incision

A

Incision, Exudation of fibrinogen, weak fibrin join, epidermal regrowth and collagen synthesis, strong collagen join

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57
Q

List some cells that regenerate

A

hepatocytes, pneumocytes, all blood cells, gut epithelium, skin epithelium, osteocytes

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58
Q

List some cells that do not regenerate

A

myocardial cells, neurones

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59
Q

Why don’t blood clots form all the time?

A
  1. Laminar flow- cells travel in the centre of arterial vessels and don’t touch the sides
  2. Endothelial cells which line vessels are not ‘sticky’ when healthy
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60
Q

Define thrombosis

A

The formation of a solid mass from blood constituents in an intact vessel in a living person

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61
Q

What is the first stage of thrombosis?

A

platelet aggregation

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62
Q

What happens when platelets aggregate?

A

The platelets release chemicals when they aggregate which cause other platelets to stick to them and also which start off the cascade of clotting proteins in the blood

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63
Q

What 3 factors are involved in the triad used for assessing a patients’ risk of thrombosis

A
  1. Change in vessel wall
  2. Change in blood flow
  3. Change in blood constituents
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64
Q

Define embolism

A

This is the process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks a vessel

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65
Q

List some less common causes of embolus

A

air, cholesterol crystals, tumour, amniotic fluid, fat

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66
Q

Define ischaemia

A

Simply a reduction in blood flow to a tissue without any other implications

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67
Q

Define infarction

A

The reduction in blood flow to a tissue that is so reduced that it cannot even support mere maintenance of the cells in that tissue so they die.

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68
Q

List the organs less susceptible to infarction

A

liver, lungs and brain (due to multiple blood supplies)

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69
Q

List the steps involved in atherosclerosis

A
  1. Irritant
  2. Damage to endothelium
  3. LDL- cholesterol deposits
  4. Monocytes -> macrophages -> ‘foam cells’
  5. Plaque grows
  6. Smooth muscle cells migrate out of the layer into fatty plaque, forming a fibrous cap which shields the thrombotic material from blood
  7. Macrophage death induces calcium secretion into the plaque
  8. Plaque occludes the artery, hardens artery and can rupture
  9. If ruptured, thrombosis occurs and can completely block artery or embolise
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70
Q

Define apoptosis

A

Programmed cell death

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71
Q

Define necrosis

A

Unprogrammed cell death as a result of cell damage

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72
Q

What can a lack of apoptosis cause?

A

cancer

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73
Q

What can an excess of apoptosis cause?

A

psoriasis

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74
Q

Define hypertrophy

A

An increase in size of a tissue caused by an increase in size of constituent cells

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75
Q

Define hyperplasia

A

An increase in size of a tissue caused by an increase in number of constituent cells

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76
Q

Define atrophy

A

Decrease in size of a tissue caused by a decrease in size or number of constituent cells

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77
Q

Define metaplasia

A

Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type

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78
Q

Define dysplasia

A

imprecise term for the morphological changes seen in cells in the progression to becoming cancer

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79
Q

What is paternally inherited and associated with parental lifespan?

A

Telomere length

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80
Q

Give some characteristics of ageing

A

Balding, senile dementia, cataracts, deafness, dermal elastosis, loss of teeth, hypertension and ischaemic heart disease, osteoporosis, prostatic hyperplasia (in men), diverticular disease of colon, degenerative joint disease, ankle oedema due to heart failure

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81
Q

How and why can basal cell carcinoma of the skin be cured easily?

A

It only invades locally- it never spreads to other parts of the body and can be cured with complete excision

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82
Q

List the 5 common cancers that spread to bone

A

breast, prostate, lung, kidney, thyroid

83
Q

Which cancers are good for conventional chemotherapy?

A

Fast dividing tumours; germ cell tumours of testis, acute leukaemias, lymphomas, embryonal paediatric tumours, choriocarcinoma

84
Q

What type of inheritance does familial adenomatous polyposis have?

A

autosomal dominant

85
Q

What is a malignant tumour of striated muscle?

A

rhabdomyosarcoma

86
Q

What is a benign tumour of glandular epithelium?

87
Q

Name a benign tumour of fat

88
Q

What is a malignant tumour of glandular epithelium?

A

adenocarcinoma

89
Q

What is a benign tumour of smooth muscle?

90
Q

Is asbestos a human carcinogen?

A

yes- causes mesothelioma in lungs

91
Q

Where does ovarian cancer commonly spread to?

A

peritoneum

92
Q

Is transitional cell carcinoma of the bladder malignant or benign?

93
Q

Is radon gas a cause of lung cancer?

94
Q

Define carcinogenesis

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations (applies to malignant neoplasms)

95
Q

What is the difference between oncogenesis and carcinogenesis?

A

Oncogenesis applies to both benign and malignant tumours

96
Q

What percentage of cancer risk is environmental?

97
Q

What are the classes of carcinogens?

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

The carcinogen ‘aromatic amines’ is associated with what type of cancer and who is most likely to be exposed?

A

Bladder cancer- rubber/dye workers

99
Q

Which hormones are carcinogenic and which cancers are they associated with?

A

Increased oestrogen leads to increased incidence of mammary/endometrial cancer
Anabolic steroids leads to increased incidence of hepatocellular carcinoma

100
Q

Name a mycotoxin associated with hepatocellular carcinoma

A

Aflatoxin B1

101
Q

Name two parasites considered to be carcinogenic and give the cancers they are associated with

A

Chlonorchis sinensis- cholangiocarcinoma

Shistosoma- bladder cancer

102
Q

Name some premalignant conditions

A

colonic polyps, cervical dysplasia, ulcerative colitis, undescended testes

103
Q

Define tumour

A

Any abnormal swelling (Neoplasm, inflammation, hypertrophy, hyperplasia)

104
Q

Define neoplasm

A

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

105
Q

Describe the basic structure of neoplasms

A

Neoplastic cells and stroma (connective tissue framework for support and nutrition)

106
Q

What are the two methods for classifying neoplasms?

A

Behavioural- benign/malignant

Histogenic- cell of origin

107
Q

List some features of benign neoplasms

A 
Localised, non-invasive
Slow growth rate
Low mitotic activity
Close resemblance to normal tissue
Circumscribed or encapsulated
Nuclear morphometry often normal
Necrosis rare
Ulceration rare
Growth on mucosal surfaces often exophytic
108
Q

How can benign neoplasms cause morbidity and mortality?

A 
Pressure on adjacent structures
Obstruct flow
Production of hormones
Transformation to malignant neoplasm
Anxiety
109
Q

List some features of malignant neoplasms

A 
Invasive
Metastases
Rapid growth rate
Variable resemblance to normal tissue
Poorly defined or irregular border
Hyperchromatic nuclei
Pleomorphic nuclei
Increased mitotic activity
Necrosis common
Ulceration common
Growth on mucosal surfaces and skin often endophytic
110
Q

How do malignant neoplasms cause morbidity and mortality?

A 
Destruction of adjacent tissue
Metastases
Blood loss from ulcers
Obstruction of flow
Hormone production
Paraneoplastic effects
Anxiety and pain (lack of pain doesn't mean lack of cancer)
111
Q

What are the three main catergories that neplasms can arise from?

A
  1. Epithelial cells
  2. Connective tissues
  3. Lymphoid/haemopoietic organs
112
Q

How are benign epithelial neoplasms classified?

A

Papilloma- non-glandular, non-secretory epithelium (prefix with cell type of origin e.g. squamous cell papilloma)
Adenoma- glandular or secretory epithelium
(prefix with cell type of origin e.g. colonic adenoma)

113
Q

How are malignant epithelial neoplasms named?

A

‘Carcinoma’ prefixed by name of epithelial cell type e.g. transitional cell carcinoma

114
Q

What are malignant glandular epithelium neoplasms called?

A

adenocarcinomas

115
Q

List some benign connective tissue neoplasms

A 
Lipoma- adipocytes
Chondroma- cartilage
Osteoma- bone
Angioma- vascular
Neuroma- nerves
116
Q

What is a Rhabdomyoma?

A

Benign connective tissue neoplasm of striated muscle

117
Q

What is a Leiomyoma?

A

Benign connective tissue neoplasm of smooth muscle

118
Q

How are malignant connective tissue neoplasms named?

A

‘Sarcoma’ with prefix of origin e.g. Liposarcoma, Rhabdomyosarcoma etc

119
Q

What is the name given to a tumour when the cell-type of origin is unknown?

A

Anaplastic

120
Q

Give examples of when an ‘-oma’ isn’t a neoplasm

A

granuloma, mycetoma, tuberculoma

121
Q

What is melanoma?

A

malignant neoplasm of melanocytes

122
Q

What is mesothelioma?

A

malignant tumour of mesothelial cells

123
Q

What is lymphoma?

A

Malignant neoplasm of lymphoid cells

124
Q

Give some examples of eponymously named tumours

A

Burkitt’s lymphoma, Ewing’s sarcoma, Grawitz tumour, Kaposi’s sarcoma

125
Q

What is the name given to a tumour made up of cells not normally present at the site?

126
Q

What is the name given to embryonal tumours?

127
Q

What is the name given to a tumour that arises from both epithelial cell and connective tissue?

A

Carcinosarcoma

128
Q

Define innate immunity

A

non-specific, instinctive, does not depend on lymphocytes

129
Q

Define adaptive immunity

A

specific ‘acquired’ immunity, require lymphocytes, antibodies

130
Q

What is the lifespan of a neutrophil?

131
Q

What are the two main intracellular granules of neutrophils?

A
  1. Primary lysosomes- contain myeloperoxidase, muramidase, acid hydrolases, proteins (defensins)
  2. Secondary granules containing lactoferrin and lysozyme
132
Q

What is the average lifespan of monocytes

133
Q

What two main roles do monocytes have?

A

phagocytosis and Ag presentation

134
Q

What do monocytes differentiate in to when they enter tissue?

A

Macrophages

135
Q

What is the average lifespan of an eosinophil?

136
Q

What types of disease are eosinophils mainly associated with?

A

parasitic infections and allergic reactions

137
Q

What is the average lifespan of a basophil?

138
Q

What does binding of IgE to basophils cause?

A

Degranulation and release of histamine- main cause of allergic reactions

139
Q

What other cell are basophils similar to?

A

Mast cells

140
Q

Where do T lymphocytes mature?

141
Q

What receptor do T lymphocytes express?

142
Q

What are the 4 main types of T lymphocyte?

A
  1. T Helper 1 (CD4)
  2. T Helper 2 (CD4)
  3. Cytotoxic T cell (CD8)
  4. T reg
143
Q

Where do B lymphocytes mature?

A

Bone marrow

144
Q

What receptor do B lymphocytes express?

A

CD19 and CD20 (depending on maturity)

145
Q

What is the main role of B lymphocytes?

A

Express membrane bound antibody on cell surface, recognise antigen displayed by APC’s, differentiate in to plasma cells that make antibodies

146
Q

What receptor do Natural Killer cells express?

147
Q

What do Natural Killer cells recognise and kill?

A

Virus infected cells and Tumour cells

148
Q

How do NK cells kill?

A

By apoptosis

149
Q

How do viruses cause cell death?

A

By intracellular multiplication

150
Q

What is complement?

A

A group of ~20 serum proteins that need to be ‘activated’ to be functional

151
Q

What are the 3 ways that complement can be activated?

A
  1. Classical pathway- Ab bound to microbe
  2. Alternative pathway- Complement binds to microbe
  3. Lectin pathway- activated by mannose binding lectin bound to a microbe
152
Q

What are the 5 distinct classes of Immunoglobulin?

A 
IgG (1-4)
IgA (1-2)
IgM
IgD
IgE
153
Q

Define antibody

A

A protein produced in response to an antigen. It can only bind with the antigen that induced its formation

154
Q

Define antigen

A

A molecule that reacts with preformed antibody and specific receptors on T and B cells

155
Q

Define epitope

A

The part of the antigen that binds to the antibody/receptor binding site

156
Q

Define affinity

A

measure of binding strength between and epitope and an antibody site. The higher the affinity the better.

157
Q

What percentage of Immunoglobulin does IgG make up in the serum?

A

70-75% of total Ig in serum

158
Q

What percentage of Ig in serum does IgM make up?

159
Q

What percentage of Ig in serum does IgA make up?

160
Q

Which Ig predominates in mucous secretions?

161
Q

What percentage of Ig in serum does IgD make up?

162
Q

What percentage of Ig in serum does IgE make up?

163
Q

What does binding of an antigen to IgE trigger the release of?

164
Q

Give two examples of a cytokine

A

Interferons (IFN) and Interleukins (IL)

165
Q

What is the function of interferon?

A

Induce a state of antiviral resistance in uninfected cells and limit the spread of viral infection

166
Q

What are the three types of interferon?

A

IFN alpha- produced by virus infected cells
IFN beta- produced by virus infected cells
IFN gamma- released by activated T Helper 1 cells

167
Q

What are the two general types of interleukin?

A

anti-inflammatory and pro-inflammatory

168
Q

What effect can interleukin have on cells?

A

Can cause them to divide, differentiate and to secrete factors

169
Q

What are chemokines?

A

A group of approximately 40 proteins that direct movement of leukocytes (and other cells) from the blood stream into the tissues or lymph organs by binding to specific receptors of cells

170
Q

Which aspects of the immune system does innate immunity include?

A
  1. Physical and chemical barriers
  2. Phagocytic cells (neutrophils and macrophages)
  3. Serum proteins (complement, acute phase)
171
Q

Which cells are responsible for sensing microbes in the blood?

A

Monocytes and neutrophils

172
Q

Which cells are responsible for sensing microbes in tissues?

A

Macrophages and dendritic cells

173
Q

What do toll-like receptors (TLR) do?

A

Recognise pathogen-associated molecular patterns expressed by microbes

174
Q

What functions do complement have?

A

Lyse microbes directly (membrane attack complex)
Increase chemotaxis (C3a and C5a)
Opsonisation (C3b)

175
Q

What is extravasation?

A

The leakage and spread of blood or fluid from vessels into the surrounding tissues, which follows injury, burns, inflammation or allergy

176
Q

What are the two killing pathways present in polymorphs and macrophages?

A

O2 dependent and O2 independent

177
Q

Give two examples of Reactive Oxygen Intermediates (ROI) involved in Oxygen dependent killing pathways?

A 
Superoxides- converted to H2O2 then .OH (free radical)
Nitric oxide (NO)- vasodilation increases extravasation but also directly anti-microbial
178
Q

Give some examples of oxygen independent mechanisms of killing?

A

defensins (insert in to membrane), lysozyme, pH, TNF

179
Q

What is the function of C-reactive protein (CRP)?

A

Serum protein produced by the liver, binds to some bacterial cell walls. Promotes opsonisation, binds to C1q and activates complement

180
Q

What is the function of Mannose Binding Lectin (MBL)?

A

Binds to lectin on microbes, promotes opsonisation and activates complement

181
Q

What is the function of Surfactant Protein-A (SP-A)?

A

Binds haemagglutinin in influenza- reduces ability of virus to infect cells

182
Q

Which test measures the activity of the classical complement pathway?

A

CH50: 50% haemolytic complement activity of serum

183
Q

Which test measures the activity of the alternative complement pathway?

A

AH50: 50% haemolytic (alternative) complement activity of serum

184
Q

What is the ultimate goal of tumour immunology?

A

To induce clinically effective anti-tumour immune responses that would discriminate between tumour cells and normal cells in cancer patients

185
Q

What are the two types of tumour antigen?

A

Tumour specific antigens (TSA)

Tumour associated antigens (TAA)

186
Q

What evidence is there for tumour immunity?

A
  1. Spontaneous regression
  2. Regression of metastases after removal of primary tumour
  3. Infiltration of tumours by lymphocytes and macrophages
  4. Higher incidence of cancer amongst immunosuppressed/immunodeficient
187
Q

Define natural passive immunity

A

Occurs naturally by the transfer of maternal antibodies across the placenta to the developing foetus

188
Q

Define artificial passive immunity, give examples

A

Transfer of preformed antibodies to the circulation e.g. vaccination against measles in an immune compromised patient

189
Q

What are the drawbacks of passive immunity?

A
  1. Does not activate immunological memory
  2. No long term protection
  3. Possibility of reaction to anti-sera
190
Q

Define active immunisation

A

Challenging the subjects immune system to induce a state of immunity involving the production of high affinity protective antibodies against the immunogen

191
Q

What are the aims of a ‘perfect’ vaccine?

A
  1. To achieve long term protection (ideally from a small number of vaccinations)
  2. To stimulate both B and T cells
  3. To induce memory B and T cells
  4. To stimulate protective high affinity IgG production (possibly IgA too)
192
Q

What are the different types of vaccine?

A
  1. Whole organism (live attenuated or killed/inactivated pathogen)
  2. Subunit
  3. Peptides
  4. DNA vaccines
  5. Engineered virus
193
Q

What are the advantages of a live attenuated vaccine?

A
  1. Sets up a transient infection
  2. Activation of full natural immune response
  3. Prolonged contact with the immune system
  4. Stimulation of a memory response in the T and B cell compartments resulting in prolonged and comprehensive protection
  5. Often only a single vaccination required- good for 3rd world
194
Q

What are the disadvantages of live attenuated vaccination?

A
  1. Immunocompromised patients may become infected as a result of immunisation
  2. Complications- Live measles vaccine- 1 per 1 million develop post-infectious encephalomyelitis
    • attenuated organism can revert to a virulent form
  3. Refrigeration and transport
  4. Correct vaccine preparation is critical
195
Q

What are the advantages of a whole inactivated pathogen vaccine?

A
  1. No risk of infection
  2. Storage less critical
  3. A wide range of different antigenic components are present so a good immune response is possible
196
Q

What are the disadvantages of a whole inactivated pathogen vaccine?

A
  1. Tend to just activate humoral responses
  2. Lack of T cell involvement
  3. With transient infection the immune response can be quite weak
  4. Repeated booster vaccinations required
  5. Patient compliance can be an issue
197
Q

What is the treatment for acute cellular rejection of a transplant?

A

Methyl predisolone, anti-thrombocyte globulin (ATG) and rescue therapies

198
Q

What is the treatment for acute antibody-mediated rejection?

A

Plasmapheresis, IVIG and retuximab

199
Q

What is chronic transplant rejection characterised by?

A

Progressive decline of renal function, proteinuria and hypertension

200
Q

What is the treatment for chronic allograft injury?

A 
There is no treatment once it is established
Immunemodulation:
1. Management of risk factors
2. Avoid toxic drugs
3. Avoid infections
201
Q

What are the two methods of crossmatch?

A

Cell based assays and solid phase assay

202
Q

What are the clinical indications related to allergy?

A
  1. Epithelial- eczema, itching, reddening
  2. Excessive mucous production
  3. Airway constriction
  4. Abdominal bloating, vomiting, diarrhoea
  5. Anaphylaxis
203
Q

Which are the major cell types that express high affinity IgE receptors?

A

Eosinophil, Mast Cell and Basophil

Phase 2A (2 decks)

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