Hypersensitivity Flashcards

1
Q

What are different types of acquired immunity?

A
  1. Antibody response - humoral

2. Cell-mediated response

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2
Q

Describe ab response?

A

Occur quickly - systemic and widespread (ab soluble protein)

  1. Ag uptake
  2. APC process - present Ag B cells
  3. T cell - release cytokines
  4. B cell clonal expansion - diff plasma cells
  5. Ab production
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3
Q

Describe cell mediated response?

A

1st exposure

  • Ag processed - presented to naive T cell via MHC
  • T cell prolif - Ag specific memory cell

2nd exposure

  • T cell recognise Ag - release cytokines
  • Targeted apoptosis
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4
Q

What is hypersensitivity?

A

When immune system respond in exaggerated/ inappropriate way
Usually 2nd response
Type 1-3 - ab mediated
Type 4 - cell mediated

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5
Q

Type I Hypersensitivity?

A

Immediate/ anaphylaxis

Acute hypersensitivity w/ rapid onset - IgE mediated

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6
Q

What cells are involved type I hyper?

A

1st exposure - IgE made

2nd exposure - Ag bind Fc receptor on mast cell - cause histamine release and IL5

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7
Q

What does IL5 and histamine release cause?

A

IL5 -esoinophil release

Histamine; vascular dilation, increased vascular permeability, oedema, bronchospasm, urticarial rash

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8
Q

Diagnosis of type I?

A

Wheel and flare
Wheel - caused extravasation of serum = angio-oedema
Flare - redness caused by axon response

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9
Q

Management Type I?

A

Adrenaline
Antihistamine
Corticosteroid
Avoidance

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10
Q

What is type II hypersensitivity?

A

Cytotoxic reaction

Ab target cell surface self-ag = autoantibody

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11
Q

Mechanism type II?

A

Ab target autoantibody

Important

  • Acute transplant rejection/ blood transfusion
  • Haemolytic disease of new born
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12
Q

Type II - pregnancy and foetal blood?

A
  • 1st preg - baby RhD+ - foetal blood enter circulation - baby born but raised ab to RhD+
  • 2nd preg - if baby Rhd+ - IgG cross placenta and destroy foetal erythrocytes
  • Preformed ant-RhD given Rhd - mother after birth
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13
Q

Difference between pemphigus and phemigoid?

A

Type II

Pemphigus - autoab against desmoglein 1+3 - prevent formation of gap junction = epithelial shed (Esp mucosa)

Pemphigoid - autoab against hemidesmosomes - prevent binding epithelium w/ dermis at basement membrane - epithelial shed at skin and mucosa

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14
Q

Type III hypersensitivity?

A

Immune complex between Ab/Ag in serum
Complex deposits in lining blood vessel, glomeruli and lungs
Cause: complement activation, leukocyte binding and inflammation

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15
Q

Mechanism type III?

A
  1. Immune complex usually bind cā€™ - bind to erythrocyte and remodelled in liver
  2. Inflammation - complex bind in lining
  3. Become activated = histamine release
  4. Increase vascular permeability - further deposition
  5. Cause platelet aggregation
  6. Lysomal enzyme - further tissue damage
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16
Q

What is type III important in?

A

SLE, eryhtema multi-frome

17
Q

What is type IV hypersensitivity?

A

Delayed reaction which is cell mediated - slow to develop and slow to resolve

  1. T cell recognise Ag expressed
  2. Cytokine release
18
Q

What is type IV hypersensitivity important in?

A
  1. Lichenoid reaction

2. Contact dermatitis

19
Q

Mechanism type IV?

A

Ag in skin internalised by langerhan cells
Travel lymph node - present Ag to T cell
Form memory CD4 cells

Elicitation Phase

  • Langerhans cell move from epidermis - dermis
  • Present Ag to memory cell
  • Cause secretion and pro-inflame cytokines
  • Increased leukocyte attraction and neutrophil
  • Tissue damage due cytokines