Immunology Flashcards

1
Q

1 Define hypersensitivity

A

“the antigen-specific immune responses that are either inappropriate or excessive AND result in harm to host”

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2
Q
  1. List and describe the 4 types of hypersensitivity reactions
A

Type I -immediate (Allergy)
Type II - antiBody mediated
Type III - immune Complex mediated
Type Iv - cell mediated Delayed

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3
Q
  1. What are the 2 typical phases of a hypersensitivity reaction?
A
Sensitisation phase (activation of APCs and memory effector cells 
Effector phase (reexposure -> activation of memory cells)
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4
Q
  1. Over what time frame would a type II hypersensitivity reaction present over?
A

5-12 hours

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5
Q
  1. Which types of antibodies are usually involved in a type II hypersensitivity reaction?
A

IgG or IgM

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6
Q
  1. What causes tissue/cell damage in type II hypersensitivity?
A

Complement system (MAC,
C3a and b, C5a)
Antibody dependant cell cytotoxicity

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7
Q
  1. Give 2 examples of hypersensitivity reactions where the affected antigen is a receptor
A
Grave's disease (TSH receptor)
Myasthenia gravis (Acetylcholine receptor)
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8
Q
  1. What 4 approaches are used to combat cell/tissue damage in type II hypersensitivity?
A
Immune suppression (reverse complement activation)
Plasmapheresis (remove circ. antibodies and inflamm mediators)
Splenectomy (reduce opsonisation/phagocytosis)
IV immunoglobulin (replaced degraded IgG)
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9
Q
  1. What type of immune reaction is haemolytic disease of the newborn?
A

Type II hypersensitivity reaction (of a Rhesus negative mother against Rhesus antigen on foetal blood cells )

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10
Q
  1. How does type III hypersensitivity cause tissue damage?
A

Intermediate size immune complex deposition -> complement activation -> neutrophil chemotaxis, adherence and degranulation

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11
Q
  1. What is the most prevalent disease caused by type III hypersensitivity?
A

Systemic Lupus Erythematosus

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12
Q
  1. How does lupus typically present?
A
Women (9:1 F:M)
Every presentation unique but ..
may have repeated miscarriages, many have cardiac, resp, renal, joint and neuro features; most commonly:
low grade fever
photosensitivity
mouth ulcers
arthritis
pericarditis
pleuritis
fatigue
anorexia
butterfly malar rash
poor peripheral circulati
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13
Q
  1. Which inflammatory cells are typically involved in type IV hypersensitivity?
A

Lymphocytes

Macrophages

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14
Q
  1. What are the three main subtypes of type IV hypersensitivity?
A

Contact hypersensitivity,
Tuberculin hypersensitivity
Granulomatous hypersensitivity

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15
Q
  1. Over what time frame does type IV hypersensitivity typically present?
A

Usually develops within 24 to 72 hours

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16
Q
  1. In tuberculin hypersensitivity, in which tissue does the reaction take place?
A

In the dermis of the skin

17
Q
  1. In type IV hypersensitivity, how are resting macrophages activated?
A

By interferon gamma and tumour necrosis factor beta produced by TH1 lymphocyte

18
Q
  1. List four diseases which are associated with granuloma formation
A

Tuberculosis
Tuberculoid leprosy
Schistosomiasis
Sarcoidosis

19
Q
  1. Name 2 tests that utilise the tuberculin hypersensitivity
A
Mantoux test (TB)
Lepromin test (leprosy)
20
Q
  1. Which three common autoimmune diseases are caused by type IV hypersensitivity?
A

Insulin-dependent diabetes mellitus
Hashimoto’s thyroiditis CD8 + T cells and antibodies)
Rheumatoid arthritis (IgG)

21
Q
  1. What 4 specific treatments are currently available for type III and IV hypersensitivity?
A

Monoclonal antibodies:
B and T cells
cytokine network
antigen-presenting cells

Anti-TNF (for rheumatoid arthritis)

22
Q
  1. Name three drugs are used as steroid sparing agents.
A

azathioprine
mycophenolate mofetil
cyclophosphamide

23
Q
  1. Over what time frame do type I hypersensitivity reactions typically present?
A

Immediately - less than 30 minutes

24
Q
  1. What are two main mechanisms underlying the pathology of allergy?
A

Abnormal adaptive immune response (Th2 response and IgE production)
Mast cell activation

25
1. Explain the biodiversity hypothesis of the pathogenesis of allergy
Compositional and functional alterations of micro-biome (dysbiosis) due to Western lifestyle (medicalised birth, antibiotics, processed food, sanitised environments) is thought to target immune system towards Th2 response
26
1. What does evidence supporting the hygiene hypothesis suggested about the pathogenesis of allergy?
Children exposed animals, pets and microbes in the early postnatal period appear to be protected against certain allergic diseases (hayfever, eczema, asthma)
27
Year one: in what tissues would you find mast cells?
Most mucosal and epithelial tissues i.e. GI tract, skin, respiratory epithelium mIn connective tissue surrounding blood cells
28
1. What are the six main mast cell mediators implicated in allergy?
tryptase histamine platelet activating factor leukotrienes C4, D4 and D4
29
1. What is the cellular mechanism behind the formation of allergic urticaria?
Mast cell activation within epidermis, leading to release of histamine and leukotrienes / cytokines (mediators) resulting in increased vascular permeability and vasodilation thus redness and swelling.
30
1. What are the 6 main possible signs of anaphalaxis?
``` Difficulty breathing (due to bronchial constriction) Hypotension Cardiovascular collapse Generalised urticaria Angioedema Abdo pain, nausea and vomiting ```
31
1. What treatment options are available for severe allergies?
Allergen desensitisation / oral immunotherapy Anti-IgE monoclonal antibodies Anti-histamines Corticosteroids Leukotriene receptor antagonists (eg Montelukast)