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Immunology > Hypersensitivity Intro > Flashcards

Hypersensitivity Intro Flashcards

1
Q

Define hypersensitivity

A

The antigen specific immune responses that are either inappropriate or excesssive + result in harm to host

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2
Q

Types of triggers (antigens)

A
  • exogenous: non infectious substances, infectious microbes, drugs
  • intrinsic: infectious microbes, self antigens (autoimmunity)
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3
Q

Types of hypersensitivity reactions

A
  • Type I or immediate (Allergy)
  • Type II or antiBody-dependent cytotoxicity
  • Type III or immune Complexes mediated
  • Type IV or cell mediated (Delayed)
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4
Q

What is the sensitisation phase?

A
  • first encounter with antigen
  • activation of APCs + memory effector cells
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5
Q

What does it mean is a person is ‘sensitised’?

A

A previously exposed individual to the antigen is said to be ‘sensitised’

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6
Q

What is the effector phase of hypersensitivity reactions?

A

Pathologic reaction upon re-exposure to the same antigen + activation of memory cells of adaptive immunity

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7
Q

Describe type II hypersensitivity

A
  • antibody dependent cytotoxicity
  • usually develops within 5-12hrs re encounter
  • IgG + IgM involved
  • targets cell bound antigens:
    -exogenous: blood group antigens, Rhesus D antigens
    -endogenous: self antigens (autoimmune)
  • induces tissue/cell damage or physiological change
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8
Q

Outline Type II hypersensitivity associated with tissue/cell damage

A
  • IgG + IgM antibodies raised against cell bound antigens
  • complement activation: cell lysis, neutrophil recruitment, opsonisation
  • antibody dependent cell cytotoxicity: natural killer cells
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9
Q

What immunoglobulins are related to hypersensitivity reactions

A

Type I - IgE
Type II + III - IgG + IgM

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10
Q

Clinical examples of Type II hypersensitivity assocaited with tissue/cell damage - complement activation
What is the antigen?

A
  • haemolytic disease of newborn - Rhesus D
  • transfusion reactions - ABO system
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11
Q

When does Type II hypersensitivity occur?

A

Within 5-12 hours re-encounter

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12
Q

Clinical examples of Type II hypersensitivity assocaited with tissue/cell damage - antibody-dependent cell cytoxicity
What is the antigen?

A
  • autoimmune haemolytic anaemia - RBCs
  • immune thrombocytopenic purpua - platelets
  • goodpasture’s syndrome - collagen in glomerular basement memebrnae
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13
Q

Outline haemolytic transfusion reaction

A
  • incorrect blood is given
  • incompatibility of ABO antigens on RBCs
  • donor RBC lysis induced induced by type II hypersensitivity reaction IgM
  • causing shock, respiratory distress, kidney failure + death
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14
Q

Outline Type II hypersensitivity associated with physiological changes

A

immune response against receptor
(Type V)
- IgG reaction against cell bound antigens
- receptor stimation
- receptor blockade
- protein blockage

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15
Q

Clinical examples of Type II hypersensitivity assocaited with physiological changes
What is the antigen?

A
  • receptor stimulation: Grave’s disease - TSH receptor
  • receptor blockade: myasthenia gravis - acetylcholine receptor
  • protein blockade: pernicious anaemia - intrinsic factor
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16
Q

Treatment of type II hypersensitivity due to tissue/cell damage

A
  • corticosteroids
  • plasmapheresis
  • splenectomy
  • intravenous immunoglobulin > blocks Fc receptor
17
Q

Treatment of type II hypersensitivity due to physiological change

A
  • correct metabolism e.g. anti-thyroid drugs in Grave’s disease
  • replacement therapy e.g. pyridostigmine in Myasthenia gravis or B12 in pernicious anaemia
18
Q

Describe Type III hypersensitivity reactions

A
  • develops within 3-8 hours
  • involves immune complexes between IgG or IgM
  • targets soluble antigens
  • tissue damage caused by deposition of immune complexes in blood vessels
19
Q

What are the key factors affecting immune complexes pathogenesis in Type III hypersensitivity?
What does this cause?

A
  • Complex size
  • Persistent of antigen
  • Host response
  • Local tissue factor
    .
  • Persistence of ICs + deposition in blood vessels
20
Q

Clinical examples of Type III hypersensitivity reactions
What antigen is involved?

A
  • rheumatoid arthritis - Fc portion of IgG
  • glomerulonephritis - infectious microbes
  • systemic lupus erythematosus - double stranded DNA
21
Q

When does Type III hypersensitivity occur?

A

3-8 hours

22
Q

Describe Type IV hypersensitivity

A
  • develops within 24-72 hours
  • involves lymphocytes + macrophages
  • triggered by environmental factors, infectious microbes + drugs
23
Q

What are the subtypes of Type IV hypersensitivity

A
  • contact hypersensitivity
  • tuberculin hypersensitivity
  • granulomatous hypersensitivity
24
Q

Describe contact hypersensitivity

A

Subtype of Type IV hypersensitivity
- occurs 48-72 hours post exposure
- epidermal reaction
- e.g. nickel, poison ivy, latex, organic chemicals

25
Q

Diagnosis of contact hypersensitivity

A

Patch testing

26
Q

Outline granulomatous hypersensitivity

A

Subtype of Type IV hypersensitivity
- occurs 21-48 days post exposure
- tissue damage
e.g. TB, leprosy, schistosomiasis, sarcoidosis

27
Q

Outline tuberculin hypersensitivity

A

Subtype of Type IV hypersensitivity
- occurs 48-72 hours post exposure
- dermal reaction

28
Q

Therapeutic approaches to type III + IV hypersensitivity

A
  • NSAIDs
  • corticosteroids
  • steroid sparing agents
  • monoclonal antibodies
29
Q

4 examples of organ specific harmful effects of immune system

A
  • goodpasture’s syndrome
  • myasthenia gravis
  • haemolytic anaemia
  • grave’s disease
30
Q

2 examples of non-organ specific harmful effects of immune system

A

Systemic lupus erythematous
Rheumatoid arthritis

31
Q

What are the main blood groups defined by ABO system + their associated antigens

A

A - A antigen
B - B antigen
AB - A+B antigen
O - none

32
Q

Signs + symptoms of haemolytic disease of the newborn

A
  • jaundice
  • dark urine + pale faeces
  • hepatosplenomegaly
  • oedema
  • kernicterus
33
Q

Pathophysiology of haemolytic disease of the newborn

A
  • Rhesus + father and Rhesus - mother > R+ fetus
  • during 1st pregnancy, mother hasn’t been sensitised
  • Rhesus antigens from fetus enters mother’s blood
  • in response to fetal Rh antigen, mother produces anti-Rh antibodies
  • if there is a second pregnancy with R+ fetus, her anti-Rh fetus damages fetal RBCs
34
Q

Prevention of haemolytic disease of newborn

A

RhoGAM
Binds to fetal blood in mum’s circulation
Prevents mum from developing anti-Rh antibodies

35
Q

Describe the direct Coombs test

A
  • test baby’s blood
  • does it have anti-D antibodies bound to baby’s blood?
36
Q

Describe indirect Coomb’s test?

A
  • Test mum’s blood
  • Is mum producing anti-D antibodies?
37
Q

When is RhoGam administered?

A
  • if baby is Rb+: 30 weeks + at birth
  • if unkown: 8 weeks
38
Q

What is kernicterus?

A

Bilirubin induced neurological damage

39
Q

Examples of type IV hypersensitivity reactions

A
  • Hashimoto’s disease
  • type I DM
  • MS
  • Sjogern syndrome

Immunology (9 decks)

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