Immunology Flashcards

from Sem 4

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
Q
  1. Explain the biodiversity hypothesis of the pathogenesis of allergy
A

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
Q
  1. What does evidence supporting the hygiene hypothesis suggested about the pathogenesis of allergy?
A

Children exposed animals, pets and microbes in the early postnatal period appear to be protected against certain allergic diseases (hayfever, eczema, asthma)

27
Q

Year one: in what tissues would you find mast cells?

A

Most mucosal and epithelial tissues i.e. GI tract, skin, respiratory epithelium
mIn connective tissue surrounding blood cells

28
Q
  1. What are the six main mast cell mediators implicated in allergy?
A

tryptase
histamine
platelet activating factor
leukotrienes C4, D4 and D4

29
Q
  1. What is the cellular mechanism behind the formation of allergic urticaria?
A

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
Q
  1. What are the 6 main possible signs of anaphalaxis?
A
Difficulty breathing (due to bronchial constriction)
Hypotension
Cardiovascular collapse
Generalised urticaria
Angioedema
Abdo pain, nausea and vomiting
31
Q
  1. What treatment options are available for severe allergies?
A

Allergen desensitisation / oral immunotherapy
Anti-IgE monoclonal antibodies
Anti-histamines
Corticosteroids
Leukotriene receptor antagonists (eg Montelukast)