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Immunology > Hypersensitivity reactions: from basics to clinic > Flashcards

Hypersensitivity reactions: from basics to clinic Flashcards

1
Q

What does the term hypersensitivity describe?

A
  • The antigen-specific immune responses that are either inappropriate or excessive and result in harm to hist
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2
Q

What are the mechanisms underlying hypersensitivity reactions?

A
  • The same as the mechanisms employed by the host to fight infections
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3
Q

What are some triggers of hypersensitivity reactions?

A
  • Exogenous antigens
  • Intrinsic antigens
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4
Q

Give some examples of exogenous antigens that trigger hypersensitivity

A
  • Non-infectious substances (innocuous)
  • Infectious microbes
  • Drugs (penicillin)
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5
Q

Give some examples of intrinsic antigens that trigger hypersensitivity

A
  • Infectious microbes ((mimicry)
  • Self0antigens (auto-immunity)
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6
Q

What are the different types of hypersensitivity reaction?

A
  • Type I or immediate (Allergy)
  • Type II or antiBody mediated
  • Type III or immune Complex mediated
  • Type IV or cell mediated (Delayed)
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7
Q

What are the different phases of a hypersensitivity reaction?

A
  • Sensitization phase
  • Effector phase
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8
Q

Outline the sensitization phase

A
  • First encounter with the antigen
  • Activation of antigen presenting cells and memory effector cells
  • A previously exposed individual to the antigen is said to be sensitized
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9
Q

Outline the effector phase

A
  • Pathologic reaction upon re-exposure
  • To same antigen and activation of the memory cells of the adaptive immunity
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10
Q

Outline a type II hypersensitivity reaction

A
  • Usually develops within 5-12 hours
  • Involves IgG or IgM antibodies
  • Targets cell bound antigens
  • Induces different outcomes such as tissue/cell damage and physiological change
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11
Q

What are the cell bound antigens targeted by type II hypersensitivity reactions?

A
  • Exogenous: blood group antigens, rhesus D antigens
  • Endogenous: self antigens
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12
Q

What are the immune mechanisms of type II hypersensitivity reactions associated with tissue/cell damage?

A
  • Complement activation - cell lysis, neutrophil recruitment (C3a/C5a), opsonisation (C3b)
  • Antibody-dependent cell cytotoxicity (NK cells)
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13
Q

Give some clinical examples of complement activation in type II hypersensitivity reactions

A
  • Haemolytic disease of the newborn
  • Transfusion reactions
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14
Q

Give some clinical examples of antibody-dependent cell cytotoxicity in type II hypersensitivity reactions

A
  • Autoimmune haemolytic anaemia
  • Immune thrombocytopenic purpura
  • Goodpasture’s syndrome
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15
Q

What causes haemolytic transfusion reactions?

A
  • Errors in patient identification
  • Improper labelling of blood specimen
  • Testing errors
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16
Q

What is the immune mechanism behind haemolytic transfusion reaction?

A
  • Incompatibility in the ABO antigens on RBCs
  • Donor RBC lysis induced by type II hypersensitivity
  • Involves recipient’s IgM
17
Q

What is the clinical outcome of haemolytic transfusion reaction?

A
  • Shock
  • Respiratory distress
  • Kidney failure
  • Death
18
Q

Outline the immune mechanism behind haemolytic disease of the newborn

A
  • Father is rhesus +
  • Mother is rhesus -
  • Baby is rhesus +
  • Rh antigens from developing foetus enter mother’s blood during delivery
  • Mother is sensitized and produces anti-Rh antibodies
  • If woman becomes pregnant with another Rh+ foetus, her anti-Rh antibodies cross the placenta
  • Foetal RBCs are damaged
19
Q

What are the symptoms of haemolytic disease of the newborn?

A
  • Severe life-threatening condition
  • Hydrops fetalis (drop in albumin - fluid in tissues not in blood)
  • Hepato/splenomegaly
  • Severe hyperbilirubinemia
  • Kernicterus
20
Q

Outline the immune mechanisms behind type II hypersensitivity reactions associated with physiological changes

A
  • Receptor stimulation
  • Receptor blockade
  • Protein blockade
21
Q

Give some clinical examples of type II hypersensitivity reactions associated with physiological changes

A
  • Grave’s disease - increased thyroid activity
  • Myasthenia gravis - impaired neuromuscular signalling
  • Pernicious anaemia
22
Q

What are the therapeutic approaches of type II hypersensitivity reactions that cause tissue/cell damage?

A
  • Corticosteroids - anti-inflammatory
  • Plasmapheresis - circulating antibodies and inflammatory mediators
  • Splenectomy - opsonisation/phagocytosis
  • Intravenous immunoglobulin - blockage of Fc receptor
23
Q

What are the therapeutic approaches of type II hypersensitivity reactions that cause physiological change?

A
  • Correct metabolism e.g. anti-thyroid drugs/ thyroidectomy in Grave’s disease
  • Replacement therapy e.g. vit B12 in pernicious anaemia
24
Q

Which diseases can be treated by plasmapheresis?

A
  • Myasthenia gravis
  • Goodpasture’s syndrome
  • Grave’s disease
  • Short term relief and allows healing of damaged tissue
25
Q

Outline type III hypersensitivity reactions

A
  • Usually develops within 3-8 hours
  • Involves immune complexes between IgG or IgM and antigens
  • Targets soluble antigens (foreign and endogenous)
  • Tissue damage caused by deposition of immune complexes in blood vessels
26
Q

What are the key factors affecting immune complex pathogenesis?

A
  • Complex size
  • Persistence of antigen
  • Host response
  • Local tissue factors
27
Q

Where do immune complexes congregate in the body following a type III hypersensitivity reaction?

A
  • Joint
  • Kidney
  • Skin
  • Heart
  • Results in multisystem disease
28
Q

What are the immune mechanisms behind type III hypersensitivity?

A
  1. Intermediate-sized immune complexes deposited in the tissue
  2. Complement activated
  3. Neutrophil chemotaxis
  4. Neutrophil adherence and degranulation
29
Q

Give some clinical examples of type III hypersensitivity reactions

A
  • Rheumatoid arthritis
  • Glomerulonephritis (infectious)
  • Systemic lupus erythematosus
30
Q

Outline type IV hypersensitivity reactions

A
  • Usually develops within 24-72 hours
  • Involves lymphocytes and macrophages
  • Triggered by environmental factors, infectious microbes and drugs
  • Different subtypes (contact hypersensitivity, tuberculin hypersensitivity, granulomatous hypersensitivity)
31
Q

What is contact hypersensitivity?

A
  • Type IV hypersensitivity reaction to exogenous antigens
  • Occurs 48-72 hours post-exposure
  • Epidermal reaction
  • Requires endogenous proteins
32
Q

What are some causes of contact hypersensitivity?

A
  • Nickel
  • Poison ivy
  • Latex
  • Organic chemicals
33
Q

How do we diagnose contact hypersensitivity?

A
  • Patch testing
34
Q

What is granulomatous hypersensitivity?

A
  • Occurs 21-48 days post exposure
  • Tissue damage
  • Examples: tuberculosis, leprosy, schistosomiasis
  • Type IV hypersensitivity reaction to exogenous antigens
35
Q

Which other diseases are caused by type IV hypersensitivity reactions to endogenous antigens?

A
  • Insulin-dependent diabetes mellitus
  • Hashimoto’s thyroiditis
36
Q

What are the therapeutic approaches to type III and IV hypersensitivity?

A
  • Anti-inflammatory and immunosuppressive drugs
  • E.g. NSAIDs, corticosteroids, steroid-sparing agents
  • Monoclonal antibodies

Immunology (3 decks)

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