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MY PHASE 2A MEDICINE > Pathology > Flashcards

Pathology Flashcards

1
Q

Describe the process of fibrosis

A

dead tissue and exudate are removed by macrophages

defect is filled by specialised vascular connective tissue (granulation tissue)

granulation tissue produces collagen

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2
Q

Describe the steps of acute inflammation

A

Initial reaction of tissue to injury -> vascular component = dilation of vessels -> exudative component = vascular leakage of protein rich fluid

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3
Q

Give 4 examples of granulomatous disease

A

TB
Leprosy
Crohn’s
sarcoidosis

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4
Q

Give 4 examples of primary chronic inflammation

A

glandular fever
IBD
sarcoidosis
RA

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5
Q

Give 5 causes of acute inflammation

A 
microbial infections
hypersensitivity rxns
physical agents
 chemicals
bacterial toxins
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6
Q

How does a scar form?

A

granulation tissue contracts and gradually accumulates collagen

this then undergoes remodelling

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7
Q

What are the essential macroscopic appearances of acute inflammation?

A 
erythema
heat
swelling
pain
loss of function
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8
Q

What are the outcomes of acute inflammation?

A 
1 resolution
2 suppuration (abscess)
3 organisation (fibrosis) 
4 progression (to chronic inflammation)
5 tissue necrosis
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9
Q

What are the systemic effects of inflammation?

A 
1 pyrexia
2 constitutional symptoms
3 weight loss
4 reactive hyperplasia of RES
5 AMYLOIDOSIS
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10
Q

What cells are predominant in chronic inflammation?

A

lymphocytes, plasma cells, macrophages

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11
Q

What cellular component is essential for a histological diagnosis of acute inflammation?

A

the accumulation of neutrophil polymorphs in the extra cellular space

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12
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes (may also contain lymphocytes)

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13
Q

What is acute inflammation?

A

the initial and often transient series of tissue reaction to injury. May last few hours to days

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14
Q

What is chronic inflammation?

A

The subsequent and often prolonged tissue reaction to injury following the initial response

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15
Q

What is granulation tissue?

A

combination of capillary loops and myofibroblasts appearing during repair of specialised/complex tissue

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16
Q

What is inflammation?

A

The local physiological response to injury

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17
Q

What is the main role of T lymphocytes?

A

On contact with antigen -> produce a range of cytokines which recruit and activate other cell types

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18
Q

What is the role of histamine in acute inflammation?

A

chemical mediator ->causes vasodilation and immediate increased vascular permeability

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19
Q

What is the role of tissue macrophages in acute inflammation?

A

secrete cytokines (TNF-alpha, IL 1) after histamine and thrombin have acted on endothelial cells

clear away tissue debris and damaged cells

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20
Q

What would the presence of granulomas and eosinophils indicate?

A

parasitic infection e.g. worms

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21
Q

When does ‘organisation’ happen as a result of acute inflammation?

A

when there is substantial damage to connective tissue/ tissue lacks ability to regenerate specialised cells (FIBROSIS)

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22
Q

Where is histamine found?

A

stored in preformed granules in mast cells/basophils/eosinophils/leukocytes/platelets

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23
Q

Which chemicals are released early in the response to acute inflammation and what is their function?

A

histmaine and thrombin - neutrophil adhesion to endothelial surface

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24
Q

What is a thrombosis?

A

The solidification of blood contents that forms within the vascular system during life

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25
Q

What are the three factors that can lead to Thrombosis?

A

Virchow’s triad

  • Change in vessel wall
  • change in blood flow
  • change in blood constituents
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26
Q

What are the 4 potential outcomes of having a thrombus?

A

1 resolution
2 organisation (into scar tissue and consequent lumen narrowing)
3 re-canalisation
4 embolism

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27
Q

Define atherosclerosis.

A

A hardened plaque in the intima of an artery. It is an inflammatory process.

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28
Q

What conditions can an atherosclerotic plaque cause?

A
  1. Heart attack.
  2. Stroke.
  3. Gangrene.
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29
Q

What are the constituents of an atheromatous plaque?

A
  1. Lipid core.
  2. Necrotic debris.
  3. Connective tissue.
  4. Fibrous cap.
  5. Lymphocytes.
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30
Q

Give 5 risk factors for atherosclerosis.

A
  1. Family history.
  2. Increasing age.
  3. Smoking.
  4. High levels of LDL’s.
  5. Obesity.
  6. Diabetes.
  7. Hypertension.
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31
Q

In which arteries would you be most likely to find atheromatous plaques?

A

In the peripheral and coronary arteries.

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32
Q

Which histological layer of the artery may be thinned by an atheromatous plaque?

A

The media.

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33
Q

What is the precursor for atherosclerosis.

A

Fatty streaks

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34
Q

Describe in 5 steps the progression of atherosclerosis.

A
  1. Fatty streaks.
  2. Intermediate lesions.
  3. Fibrous plaque.
  4. Plaque rupture.
  5. Plaque erosion.
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35
Q

Progression of atherosclerosis: what are the constituents of fatty streaks?

A

Foam cells and T-lymphocytes. Fatty streaks can develop in anyone from about 10 years old.

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36
Q

Progression of atherosclerosis: what are constituents of intermediate lesions?

A
  • Foam cells.
  • Smooth muscle cells.
  • T lymphocytes.
  • Platelet adhesion.
  • Extracellular lipid pools.
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37
Q

Progression of atherosclerosis: what are the constituents of fibrous plaques?

A
  • Fibrous cap overlies lipid core and necrotic debris.
  • Smooth muscle cells.
  • Macrophages.
  • Foam cells.
  • T lymphocytes.

Fibrous plaques can impede blood flow and are prone to rupture.

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38
Q

Progression of atherosclerosis: why might plaque rupture occur?

A

Fibrous plaques are constantly growing and receding. The fibrous cap has to be resorbed and redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions, the cap becomes weak and the plaque ruptures. Thrombus formation and vessel occlusion.

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39
Q

What is the treatment for atherosclerosis?

A

Percutaneous coronary intervention (PCI).

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40
Q

What is the major limitation of PCI?

A

Restenosis

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41
Q

How can restenosis be avoided following PCI?

A

Drug eluting stents: anti-proliferative and drugs that inhibit healing.

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42
Q

What is the key principle behind the pathogenesis of atherosclerosis?

A

It is an inflammatory process!

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43
Q

Define atherogenesis.

A

The development of an atherosclerotic plaque.

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44
Q

Give a benefit of inflammation.

A

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

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45
Q

Give a disadvantage of inflammation.

A

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

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46
Q

Define exudate.

A

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

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47
Q

What does viral infection result in?

A

Cell death due to intracellular multiplication.

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48
Q

What does bacterial infection result in?

A

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

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49
Q

Give 3 endogenous chemical mediators of acute inflammation.

A
  1. Bradykinin.
  2. Histamine.
  3. Nitric Oxide.
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50
Q

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

A

Multinucleate giant cell.

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51
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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52
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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53
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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54
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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55
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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56
Q

Name 2 types of cells that are incapable of regeneration.

A
  1. Myocardial cells.

2. Neuronal cells.

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57
Q

Define abscess.

A

Acute inflammation with a fibrotic wall.

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58
Q

Give 2 reasons why thrombosis formation is uncommon.

A
  1. Laminar flow.

2. Non sticky endothelial cells.

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59
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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60
Q

Define ischaemia.

A

Decreased blood flow

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61
Q

Define infarction

A

Decreased blood flow with consequent cell death

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62
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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63
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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64
Q

Define atherosclerosis.

A

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

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65
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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66
Q

What are the 3 main constituents of an atheromatous plaque?

A
  1. Lipids.
  2. Fibrous tissue.
  3. Lymphocytes.
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67
Q

Define aneurysm

A

A localised permanent dilation of part of the vascular tree

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68
Q

What is apoptosis?

A

Programmed cell death of a single cell without the release of products harmful to surrounding cells

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69
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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70
Q

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

A

p53 protein

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71
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.

72
Q

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

A

HIV

73
Q

Define necrosis.

A

Traumatic cell death which induces inflammation and repair

74
Q

Give 3 examples of events that can lead to necrosis.

A
  1. Frost bite.
  2. Avascular necrosis.
  3. Infarction.
75
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.
76
Q

Define hypertrophy.

A

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

77
Q

Define hyperplasia.

A

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

78
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.

79
Q

Define metaplasia.

A

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

80
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.

81
Q

Define dysplasia.

A

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

82
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.

83
Q

Give an example of hypertrophy

A

Muscular hypertrophy of the left ventricle of the heart (as a response to sustained outflow
resistance)

84
Q

Give an example of hyperplasia

A

Hyperplasia of prostate smooth muscle either benign or cancerous

85
Q

Give an example of atrophy

A

Loss of innervation of muscle causes muscle atrophy

86
Q

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

A

It can no longer divide.

87
Q

Define carcinoma.

A

MALIGNANT EPITHELIAL NEOPLASM

88
Q

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

A
  1. Breast.
  2. Kidney.
  3. Lung.
  4. Prostate.
  5. Thyroid.
89
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.

90
Q

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

A
  1. Proteases.

2. Cell motility.

91
Q

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

A
  1. Collagenases.

2. Cell motility.

92
Q

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

A
  1. Adhesion receptors.
  2. Collagenases.
  3. Cell motility.
93
Q

Give 4 characteristics of neoplastic cells

A
  • Derive from nucleated cells
  • Usually monoclonal
  • Growth pattern is related to the parent cell
  • They continue to synthesise or secrete cell products such as collagen, mucin or keratin; these often accumulate within the tumour
94
Q

How are tumours classified?

A

Behaviourally or Histiogentically

95
Q

Give 2 promoters of tumour angiogenesis.

A
  1. Vascular endothelial growth factors.

2. Fibroblast growth factors.

96
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.
97
Q

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

A

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

98
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.

99
Q

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

A

Phagocytosis!

100
Q

Define carcinogenesis.

A

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

101
Q

What percentage of cancer risk is due to environmental factors?

A

85% environmental, 15% genetic.

102
Q

Define neoplasm.

A

An autonomous, abnormal, persistent new growth.

103
Q

What is a neoplasm composed of?

A
  1. Neoplastic cells.

2. Stroma.

104
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.

105
Q

What is essential for neoplasm growth?

A

Angiogenesis.

106
Q

What is the behavioural classification of neoplasms?

A

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

107
Q

What is the histogenetic classification of neoplasms?

A

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

108
Q

What are the 7 main features of benign neoplasms.

A
  1. Localised.
  2. Non-invasive.
  3. Slow growth, low mitotic activity.
  4. Close resemblance to normal tissue.
  5. Normal nuclei.
  6. Necrosis and ulceration are rare due to slow growth.
  7. Exophytic growth.
109
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.
110
Q

What are the 7 main features of malignant neoplasms.

A
  1. INVASIVE!
  2. Metastases.
  3. Rapid growth, high mitotic activity.
  4. Resemblance to normal tissue.
  5. Poorly defined border due to invasive nature.
  6. Necrosis and ulceration are common.
  7. Endophytic growth.
111
Q

What are the consequences of malignant neoplasms?

A
  • Destroy surrounding tissue
  • Blood loss due to ulceration
  • Pain
  • Anxiety.
112
Q

Define sarcoma.

A

Malignant connective tissue neoplasm.

113
Q

What is an adenoma?

A

Benign tumour of glandular epithelium.

114
Q

What is a papilloma?

A

A non-glandular benign tumour.

115
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.

116
Q

Define adenocarcinoma.

A

A malignant neoplasm of glandular epithelium.

117
Q

Describe adaptive immunity

A

Immune response specific to antigen, therefore is quicker.

Requires the use of lymphocytes

118
Q

Describe innate immunity

A

Non-specific immune response
instinctive
present from birth
first line of defence.

It is focused around physical and chemical barriers and phagocytosis. No lymphocyte involvement.

119
Q

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

A

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

120
Q

Describe the first immune response to initial exposure.

A
  1. Innate immune response.
  2. IgM predominates.
  3. Low affinity.
121
Q

Define allergy. Give example

A

An abnormal response to harmless foreign material. e.g. allergic rhinitis (hay fever)

122
Q

Define hypersensitivity. Give example

A

Undesirable reaction produced by normal immune system. e.g. anaphylaxis

123
Q

Define immunodeficiency. Give example

A

Ability of immune system to fight infectious disease/cancer is compromised.
(AIDS - acquired immunodeficiency disorder)

124
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.
125
Q

Give examples of 3 polymorphonuclear leukocytes.

A
  1. Neutrophils.
  2. Basophils.
  3. Eosinophils.
126
Q

Give examples of 3 mononuclear leukocytes.

A
  1. Monocytes.
  2. B lymphocytes.
  3. T lymphocytes.
127
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.

128
Q

What is the function of T helper (CD4+) cell?

A

Release cytokines

Produces antibodies against pathogens

129
Q

What is the function of cytotoxic (CD8+) cell?

A

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

130
Q

Which cells express MHC2?

A

Antigen presenting cells ONLY e.g. macrophages, B cells, dendritic cells. (presented to CD4+ cells)

131
Q

What type of T cell binds to MCH1?

A

CD8+

132
Q

What do B cells differentiate into?

A

Plasma cells. The plasma cells then produce antibodies.

133
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.

134
Q

Give 3 functions of antibodies.

A
  1. Neutralise toxins.
  2. Opsonisation.
  3. Activate classical complement system.
135
Q

Name 4 types of cytokines.

A
  1. Interferons.
  2. Interleukins.
  3. Colony stimulating factors.
  4. Tumour necrosis factors.
136
Q

What is the function of interferons?

A

Interferons produce antiviral proteins.

137
Q

What is the function of interleukins?

A

Interleukins cause cell division and differentiation.

138
Q

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

A

CSF causes division and differentiation of bone marrow stem cells.

139
Q

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

A

TNF mediates inflammation and cytotoxic reactions.

140
Q

What is the function of chemokines?

A

Chemokines attract leukocytes to sites of infection.

141
Q

Give examples of secondary lymphoid tissue.

A

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

142
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.
143
Q

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

A

Innate immunity.

144
Q

What happens when a PAMP binds to a PRR?

A

The innate immune response and inflammatory response is triggered.

145
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.
146
Q

Give 3 advantages of transplantation.

A
  1. Improved quality of life.
  2. Improves survival rates.
  3. Cost effective.
147
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.
148
Q

What are the different types of autopsy?

A

Hospital (10%)

Medico-legal: coronial/forensic(90%)

149
Q

What is the role of the coronial autopsy?

A 
To answer
• Who was the deceased?
• When did they die?
• Where did they die?
• How did their death come about?
150
Q

Why are deaths referred to the coroner?

A
  • presumed natural (not seen Dr for 2 weeks prior, not previously unwell)
  • presumed iatrogenic ( peri/postoperative deaths etc)
  • presumed unnatural ( suicide, accident, neglect)
151
Q

Who refers deaths to the coroner?

A
  • Drs
  • police
  • registrar of Births, Deaths, Marriages
  • relatives
152
Q

Who carries out autopsies?

A
  • histopathologist

- forensic pathologist (homocide, 3rd party involvement, neglect etc)

153
Q

What is atopy?

A

The tendency to develop allergies.

154
Q

Which immunoglobulin is most commonly involved in allergic responses?

A

IgE

155
Q

Which cells are most commonly involved in allergic responses?

A

Mast cells! Also eosinophils and basophils.

156
Q

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

A

The receptors cross-link.

157
Q

Which cells express high affinity IgE receptors?

A

Mast cells, basophils and eosinophils.

158
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.

159
Q

What is the main IgE receptor cell?

A

MAST CELLS!

160
Q

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

A

Histamine.

161
Q

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

A

They induce a TH2 response.

162
Q

Which cells and which immunoglobulin is commonly involved in anaphylaxis?

A
  • Mast cells and basophils.

- IgE.

163
Q

Give examples of anaphylactic systemic effects.

A
  • CV: vasodilation, lowered BP.
  • Resp: bronchial SM contraction, mucus.
  • Skin: rash, swelling.
  • GI: pain, vomiting.
164
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).
165
Q

What is anaphylaxis?

A

an acute allergic reaction to an antigen to which the body has become hypersensitive

166
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.

167
Q

Describe type 2 hypersensitivity.

A

IgG mediated cytotoxicity.

168
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.

169
Q

Describe type 4 hypersensitivity.

A

T cell mediated.

170
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.
171
Q

What can cause a type 1 hypersensitivity reaction?

A

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

172
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection.

173
Q

What can cause a type 3 hypersensitivity reaction?

A

Fungal

174
Q

What can cause a type 4 hypersensitivity reaction?

A

TB

175
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.
176
Q

Give 4 risk factors for hypersensitivity.

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

MY PHASE 2A MEDICINE (14 decks)

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