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Phase 2A ICS, Microbiology, Public Health, GP and ILAs > ICS Immunology > Flashcards

ICS Immunology Flashcards

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1
Q

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

A

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

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2
Q

Describe innate immunity.

A

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

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3
Q

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

A

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

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4
Q

What is the function of lysozyme?

A

It destroys bacterial cell walls.

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5
Q

Describe adaptive immunity.

A

Specific, requires lymphocytes. Memory and quicker response.

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6
Q

Draw the haematopoesis flowchart

A
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7
Q

Give examples of 3 polymorphonuclear leukocytes.

A
  1. Neutrophils.
  2. Basophils.
  3. Eosinophils.
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8
Q

Give examples of 3 mononuclear leukocytes.

A
  1. Monocytes.
  2. B lymphocytes.
  3. T lymphocytes.
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9
Q

In which primary lymphoid tissue do T cells mature?

A

Thymus.

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10
Q

In which primary lymphoid tissue do B cells mature?

A

Bone marrow.

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11
Q

How do T cells recognise antigens?

A

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

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12
Q

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

A

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

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13
Q

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

A

It helps produce antibodies against extracellular pathogens. Secretes cytokines.

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14
Q

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

A

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

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15
Q

What is the function of T reg (FoxP3)?

A

They regulate the immune response.

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16
Q

Which cells express MHC1?

A

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

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17
Q

Which cells express MHC2?

A

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

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18
Q

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

A

MHC1.

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19
Q

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

A

MHC2.

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20
Q

What type of T cell binds to MCH1?

A

Cytotoxic T cells (CD8).

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21
Q

What type of T cells binds to MCH2?

A

Helper T cells (CD4).

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22
Q

What do B cells differentiate into?

A

Plasma cells. The plasma cells then produce antibodies.

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23
Q

What does a helper T cell bind to?

A

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

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24
Q

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

A

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

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25
Q

How many antibodies can each B cell make?

A

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

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26
Q

What happens to B cells that recognise ‘self’?

A

They are killed in bone marrow.

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27
Q

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

A

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

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28
Q

Give 3 functions of antibodies.

A
  1. Neutralise toxins.
  2. Opsonisation.
  3. Activate classical complement system.
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29
Q

Which immunoglobulin is found in breast milk and other secretions?

A

IgA.

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30
Q

What are the 2 most common immunoglobulins?

A

IgG and IgM.

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31
Q

Which region of an antibody binds antigens?

A

The fab region.

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32
Q

Which region of an antibody binds to B cells?

A

The Fc region.

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33
Q

Name 4 types of cytokines.

A
  1. Interferons.
  2. Interleukins.
  3. Colony stimulating factors.
  4. Tumour necrosis factors.
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34
Q

What is the function of interferons?

A

Interferons produce antiviral proteins.

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35
Q

What is the function of interleukins?

A

Interleukins cause cell division and differentiation.

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36
Q

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

A

CSF causes division and differentiation of bone marrow stem cells.

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37
Q

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

A

TNF mediates inflammation and cytotoxic reactions.

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38
Q

What is the function of chemokines?

A

Chemokines attract leukocytes to sites of infection.

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39
Q

Give examples of secondary lymphoid tissue.

A

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

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40
Q

Describe the process of phagocytosis.

A
  1. Pathogen binds to neutrophil/macrophage.
  2. Engulfment of pathogen.
  3. Phagosome formation.
  4. Lysosome fusion - phagolysosome.
  5. Pathogen is destroyed.
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41
Q

Give 3 examples of O2 dependent mechanisms of killing.

A
  1. Killing using reactive oxygen intermediates.
  2. Superoxides can be converted to H2O2 and then to hydroxyl free radicals.
  3. NO leads to vasodilation and increased extravasation and so more neutrophils etc are in the tissues to destroy pathogens.
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42
Q

What is the role of NO in killing pathogens?

A

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

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43
Q

Why can superoxides be used to destroy pathogens?

A

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

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44
Q

What mechanisms or cells are involved in O2 independent killing?

A

Defensins, lysozyme, pH, TNF.

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45
Q

Where are complement system plasma proteins derived from?

A

The liver.

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46
Q

What are the 3 main outcomes of complement system activation?

A
  1. Direct lysis- MAC formation.
  2. Opsonisation- increased phagocytosis (C3b)
  3. Inflammation- macrophage chemotaxis (C3a and C5a).
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47
Q

What activates the classical complement pathway?

A

Antibodies.

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48
Q

What compound prevents excessive activation of the classical complement pathway?

A

C1 inhibitor.

- C1 inhibitor leads to a negative feedback loop.

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49
Q

What activates the lectin pathway?

A

Mannose binding protein.

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50
Q

What activates the alternative pathway?

A

Bacterial cell walls and endotoxin.

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51
Q

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

A
  1. Classical.
  2. Lectin.
  3. Alternative.
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52
Q

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

A

C3b and C4b.

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53
Q

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

A

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

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54
Q

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

A

C3a and C5a.

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55
Q

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

A

Innate immunity.

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56
Q

What are PRR’s a receptor for?

A

PAMP’s.

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57
Q

Name 3 receptors that make up the PRR family.

A
  1. Toll-like receptors (TLR).
  2. Nod-like receptors (NLR).
  3. Rig-like receptors (RLR).
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58
Q

What is the main function of TLR’s?

A

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

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59
Q

What is the main function of NLR’s?

A

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

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60
Q

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

A

Crohn’s disease.

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61
Q

What is the main function of RLR’s?

A

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

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62
Q

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

A

They are often hydrophobic.

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63
Q

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

A

TLR4 agonists.

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64
Q

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

A
  1. Atherosclerosis.
  2. COPD.
  3. Arthritis.
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65
Q

Give examples of 3 extracellular PRR.

A
  1. Mannose receptors.
  2. Scavenger receptors.
  3. TLR’s.
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66
Q

What is the function of mannose and scavenger extracellular receptors?

A

The induce pathogen engulfment.

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67
Q

Give an example of an intracellular PRR.

A

NLR.

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68
Q

Where are circulating PRR secreted from?

A

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

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69
Q

What happens when a PAMP binds to a PRR?

A

The innate immune response and inflammatory response is triggered.

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70
Q

What is extravasation?

A

Leukocyte (WBC) migration across the endothelium.

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71
Q

What do macrophages at the tissues secrete to initiate extravasation?

A

TNF alpha.

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72
Q

Describe the process of extravasation.

A
  1. Macrophages at tissues release TNF alpha.
  2. The endothelium is stimulated to express adhesion molecules and to stimulate chemokines.
  3. Neutrophils bind to adhesion molecules; they roll, slow down and become stuck to the endothelium.
  4. Neutrophils are activated by chemokines.
  5. Neutrophils pass through the endothelium to the tissue to help fight infection.
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73
Q

What 2 compounds can act as C3 convertase?

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

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

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74
Q

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

A

Inheritable cancers (<10%).

75
Q

What type of cancers results from transformations in somatic cells?

A

Non-inheritable cancers (>90%).

76
Q

What factors can cause transformations in somatic cells?

A

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

77
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.
78
Q

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

A
  1. Tumour specific antigens; only found on tumour cells. Due to point mutations.
  2. Tumour associated antigens; found on normal cells and over expressed on tumour cells.
79
Q

What is cancer immunosurveillance?

A

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

80
Q

What is cancer immunoediting?

A

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

81
Q

What are the 3 E’s of cancer immunoediting?

A
  1. Elimination.
  2. Equilibrium.
  3. Escape.
82
Q

Give an example of active cancer immunotherapy.

A

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

83
Q

Give an example of passive cancer immunotherapy.

A

T cell transfer, anti-tumour antibodies.

84
Q

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

A

Malignant tumours grow rapidly and so outgrow their blood supply.

85
Q

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

A
  1. Hypoxic tumours have growth factors for angiogenesis and so can receive nutrients for growth.
  2. They suppress the immune system.
  3. They are resistant to chemotherapy and radiotherapy.
86
Q

Give 3 advantages of active immunity.

A
  1. Induces immunological memory.
  2. Produces high affinity antibodies.
  3. It produces a persistent protective response against pathogens.
87
Q

Give 2 advantages of passive immunity.

A
  1. Immediate effect.

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

88
Q

Give 3 disadvantages of passive immunity.

A
  1. Short term.
  2. No immunological memory produced.
  3. Reaction is possible.
89
Q

Describe the first immune response to initial exposure.

A
  1. Innate immune response.
  2. IgM predominates.
  3. Low affinity.
90
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.
91
Q

Give 3 advantages of live vaccines.

A
  1. Very effective, prolonged and comprehensive.
  2. Immunological memory produced.
  3. Often only 1 vaccine is needed.
92
Q

Give 2 disadvantages of live vaccines.

A
  1. Immunocompromised patients may become ill.

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

93
Q

Give 2 advantages of inactivated vaccines.

A
  1. There is no risk of infection.

2. Storage is less critical.

94
Q

Give 3 disadvantages of inactivated vaccines.

A
  1. Inactivated vaccines tend to only activate the humoral response; there is a lack of T cell involvement.
  2. The response is often weak.
  3. Boosters are needed and so patient compliance may be poor.
95
Q

What is the role of an adjuvant?

A

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

96
Q

What can be used as an adjuvant?

A

Toxoids, proteins, chemicals (aluminium salts) etc.

97
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.
98
Q

Give 3 advantages of transplantation.

A
  1. Improved quality of life.
  2. Improves survival rates.
  3. Cost effective.
99
Q

Why are immunosuppressive agents needed to prevent rejection?

A

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

100
Q

On which chromosome are MHC proteins found?

A

Chromosome 6.

101
Q

Describe the transplant cascade.

A

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

102
Q

What are the main compounds involved in reperfusion injury?

A

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

103
Q

Define allorecognition.

A

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

104
Q

What are the consequences of transplant rejection?

A

Fibrosis and scarring.

105
Q

Describe the immune responses to detection of graft antigens.

A
  1. Innate immune response is activated.
  2. T cell mediated cytotoxicity.
  3. Ab mediated cytotoxicity.
  4. Hypersensitivity.
  5. Tolerance.
106
Q

Give 6 ways of preventing transplant rejection?

A
  1. Manage risk factors.
  2. Tissue typing.
  3. Cross match.
  4. Immunosuppressive agents.
  5. Sensitisation and desensitisation.
  6. Tolerance.
107
Q

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

A

Too much = infection.

Too little = rejection.

108
Q

What is involved in tissue typing?

A
  1. Blood group matching.

2. HLA typing.

109
Q

What is involved in cross matching?

A

Detecting anti HLA antibodies.

Cell based assays and solid phase assays can be used.

110
Q

Define tolerance with regards to transplant immunology.

A

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

111
Q

Define xenotransplantation.

A

Transplantation of tissues from one species to another.

112
Q

What is allergy?

A

An abnormal response to harmless foreign material.

113
Q

What is atopy?

A

The tendency to develop allergies.

114
Q

Which immunoglobulin is most commonly involved in allergic responses?

A

IgE.

115
Q

Which cells are most commonly involved in allergic responses?

A

Mast cells! Also eosinophils and basophils.

116
Q

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

A

The receptors cross-link.

117
Q

Which cells express high affinity IgE receptors?

A

Mast cells, basophils and eosinophils.

118
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.

119
Q

What is the main IgE receptor cell?

A

MAST CELLS!

120
Q

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

A

Histamine.

121
Q

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

A

They induce a TH2 response.

122
Q

Which cells and which immunoglobulin is commonly involved in anaphylaxis?

A
  • Mast cells and basophils.

- IgE.

123
Q

Give examples of anaphylactic systemic effects.

A
  • CV: vasodilation, lowered BP.
  • Resp: bronchial SM contraction, mucus.
  • Skin: rash, swelling.
  • GI: pain, vomiting.
124
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).
125
Q

Which infection is most often seen in patients with hypogammaglobulinemia?

A

Streptococcus penumonia sinusitis.

126
Q

Give 5 examples of PAMPs.

A
  1. Lipopolysaccharides.
  2. Endotoxins.
  3. Bacterial flagellin.
  4. Peptidoglycans.
  5. dsRNA.
127
Q

Which PRR responds to lipopolysaccharides?

A

TLRs.

128
Q

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

A

No

129
Q

Give 4 causes of acquired immunodeficiency.

A
  1. Cancer.
  2. HIV.
  3. Having chemotherapy.
  4. Taking immunosuppressants.
130
Q

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

A

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

131
Q

What immune system cells are affected in HIV?

A

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

132
Q

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

A

Hypogammaglobulinaemia.

133
Q

What infection is most commonly seen in patients with hypogammaglobulinaemia?

A

Streptococcus pneumonia.

134
Q

Describe hyper IgM syndrome.

A

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

135
Q

What are the consequences of complement deficiency?

A

Impaired opsonisation of encapsulated bacteria.

136
Q

What is terminal complement deficiency and what are its consequences?

A
  • Terminal complement deficiency is when there’s a problem with C5-8 and so MAC isn’t produced.
  • The consequences of this are chronic Neisserial infections and recurrent meningitis.
137
Q

What are the consequences of being deficient in C1 inhibitor?

A

Angioedema - facial swelling.

138
Q

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

A

Increased likelihood of autoimmune disease especially systemic lupus erythematosus.

139
Q

What are the consequences of hyposplenism?

A

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

140
Q

What is thymic aplasia?

A

A deficiency in mature T cells.

141
Q

How can immune function be assessed?

A
  1. Looking at neutrophil numbers, morphology and flow cytometry.
  2. Looking at B and T cell subsets, numbers and response to vaccines.
  3. Genetic studies.
142
Q

Give 3 examples of chronic inflammatory diseases.

A
  1. Rheumatoid arthritis.
  2. Crohn’s disease.
  3. TB.
143
Q

Give 3 cytokines secreted by TH2.

A
  1. IL-4.
  2. IL-6.
  3. IL-13.
  4. IL-5.
  5. IL-10.
144
Q

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

A

Fab region.

145
Q

Name 3 cytokines secreted by TH1.

A
  1. IL-2.
  2. Gamma-interferon.
  3. TNF-beta.
146
Q

Name 2 cytokines secreted by TREG.

A
  1. IL-10.

2. TGF-beta.

147
Q

Name 3 conventional therapies used in managing CID.

A
  1. NSAIDs.
  2. DMARDs.
  3. Steroids.
148
Q

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

A

Rheumatoid arthritis.

DMARD - disease-modifying antirheumatic drug

149
Q

How do NSAIDs work in relieving inflammation.

A

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

150
Q

What is a disadvantage of long term NSAID use?

A

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

151
Q

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

A
  1. They’re extremely specific.

2. A low dose is very effective.

152
Q

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

A
  1. They’re very expensive.
  2. There is a risk of contamination.
  3. They’re always injected.
  4. They’re immunosuppressive.
  5. They need to be handled carefully to prevent denaturation.
153
Q

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

A

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

154
Q

Name 3 TNF blockers.

A
  1. Etanercept (TNF alpha specific).
  2. Infliximab.
  3. Adalimumab.
155
Q

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

A

Methotrexate.

156
Q

Give a side effect of using TNF blockers.

A

Increased susceptibility to TB.

157
Q

How do IL-6 blockers work?

A

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

158
Q

Name an IL-6 blocker.

A

Tocilizumab.

159
Q

When are IL-6 blockers used?

A

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

160
Q

What are the risks of using IL-6 blockers?

A

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

161
Q

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

A
  1. TNF blockers e.g. etanercept.
  2. IL-6 blockers e.g. Tocilizumab.
  3. Anti B lymphocytes e.g. rituximab.
  4. T cell activation blockers e.g. abatacept.
162
Q

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

A

Complementarity determining region (CDR).

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

163
Q

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

A

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

164
Q

What region determines Ig class?

A

The constant region!

165
Q

What is the result of recombination in the Ig region?

A

Class switching.

166
Q

Describe complement fixation.

A

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

167
Q

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

A

Tyrosine kinase.

168
Q

What immunoglobulin do naive antibodies express?

A

IgM.

169
Q

Describe the process of class switching.

A

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

170
Q

What do T cells recognise?

A

PEPTIDES

171
Q

Describe somatic hypermutation.

A
  1. Random mutations in CDR.
  2. Amino acid sequences are effected meaning Ab-Ag affinity is altered.
  3. High affinity B cell clones are selected via natural selection.
172
Q

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

A
  1. T cells are stimulated.
  2. Cytokine release.
  3. B cell proliferation.
  4. Somatic hypermutation.
  5. High affinity B cell clones differentiate into plasma cells and memory cells.
173
Q

Give 4 uses of antibodies in medicine.

A
  1. Diagnostic tools.
  2. Immunoassays, Ab’s are used to measure the presence of a molecule.
  3. Flow cytometry, Ab’s label cells in suspension.
  4. Therapeutic uses, monoclonal Ab’s can act as specific antagonists for biological targets e.g. HERCEPTIN.
174
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.

175
Q

Describe type 2 hypersensitivity.

A

IgG mediated cytotoxicity.

176
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.

177
Q

Describe type 4 hypersensitivity.

A

T cell mediated.

178
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.
179
Q

What can cause a type 1 hypersensitivity reaction?

A

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

180
Q

What can cause a type 2 hypersensitivity reaction?

A

Transplant rejection.

181
Q

What can cause a type 3 hypersensitivity reaction?

A

Fungal.

182
Q

What can cause a type 4 hypersensitivity reaction?

A

TB.

183
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.
184
Q

Give 4 risk factors for hypersensitivity.

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

Phase 2A ICS, Microbiology, Public Health, GP and ILAs (5 decks)

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