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2.3.6. Immune System > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Define hypersensitivity

A

The Ag-specific immune responses that are either inappropriate or excessive and result in harm to host

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2
Q

Outline the diff types of hypersensitivity reactions

A

(A) Type 1 = Allergy, Ab mediated, IgE, membrane bound Ag

(B) Type 2 = Ab mediated, IgG/M, soluble Ab

(C) Type 3 = immune complex mediated, IgG/M

(D) Type 4 = cell mediated, delayed

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3
Q

What are the phases of hypersensitivity reaction?

A

Sensitisation phase = first encounter with Ag, activation of APCs and memory effector cells

Effector phase = pathologic reaction on re-exposure

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4
Q

Define type 1 hypersensitivity

A

immediate <30mins

Allergy

IgE = MAST CELL ACTIVATION

Abnormal TH2 response

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5
Q

Give examples of allergens that will set off an type 1 hypersensitivity reaction

A

Pollens

Dust mites, cats, dogs

Fungal spores

Insect venom

Medicines

Latex

Food: milk, nuts

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6
Q

What is the mechanism for type 1 hypersensitivity?

A

Abnormal adaptive immune response = TH2, IgE prod

Mast cell activation = sensitised pts, location determines disorder

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7
Q

What is the hygiene hypothesis?

A

Children exposed to animals, pets, microbes in the early postnatal period appear to be protected against certain allergic diseases

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8
Q

What is the biodiversity hypothesis?

A

Western lifestyle induces alternation of the symbiotic relationships with parasites and bacteria leading to dysbiosis (compositional and functional alterations of microbiome) of the microbiome at mucosal surfaces

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9
Q

What is a mast cell?

A

Activated by IgE cross linked BY ALLERGEN

MEDIATORS =

  • histamine = vasodilation, increased V permeability
  • heparin = increased V permeability
  • leukotrienes = increased V permeability, mucus prod
  • tryptase = remodel CT matrix
  • platelet-activating factor = attract leukocytes
  • TNF alpha = promotes inflam

Location = GI, skin, resp, CT surrounding blood cells

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10
Q

Outline the immune mechanism of an allergic reaction

A

Allergen 1st exposure - TH2 response

Allergen 2nd response = IgE cross-linking BY ALLERGEN

= mast cell degranulation

= increased vascular permeability, vasodilation, bronchial constriction

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11
Q

When is urtucaria seen?

A

Activation of mast cell in the EPIDERMIS

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12
Q

When in angioedema seen in allergic reactions?

A

Activation of mast cells in the DEEP DERMIS

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13
Q

Describe the manifestations of anaphylaxis

A

systemic activation of mast cells =

  • Hypotension, cardiovascular collapse
  • Generalised urticaria
  • Angioedema
  • Breathing problems
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14
Q

What therapy is available for type 1 hypersensitivity?

A

Allergen desensitisation

Anti-IgE monoclonal Ab

Against mast cell activation

  • Anti-histamine
  • Leukotriene receptor antagonist
  • Corticosteroids

ADVICE = avoid allergen, carry anti-histamines, consider desensitisation, regular cleaning, do not smoke

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15
Q

Define allergen desensitisation

A

Increasing doses of allergen extracts over a period of years

given to pts by injection or drops/tablets under the tongue (sublingual)

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16
Q

Outline type 2 hypersensitivity reactions

A

5-12 hrs

IgG/M Ab

Targets cell bound Ag (exogenous: blood group Ag, rhesus A Ag) (endogenous: self Ag)

Induced diff outcomes = tissue/cell damage, physiological change

17
Q

Outline the type 2 hypersensitivity mechanism

A

Compliment activation = MAC, neutrophil activation, opsonisation

Ab-dependent cell cytotoxicity = IgG

18
Q

Give an example of tissue/cell damage caused by type 2 hypersensitivity

A

Haemolytic transfusion reaction = incompatibility in ABO group or rhesus D

Haemolytic disease of the newborn = rhesus D incompatibility

19
Q

How can haemolytic disease of the newborn be prevented?

A

Give IgG anti-RhD after 1st preg

20
Q

Outline therapeutic approaches for tissue/cell damage caused by T2 hypersensitivity

A

Immune suppression

Plasmapheresis

Splenectomy

Intravenous immunoglobulin

21
Q

Outline type 3 hypersensitivity reactions

A

3-8hrs

Immune complexes between IgG/M and Ag

Targets soluble Ag

Tissue damage caused by immune complex deposition

22
Q

In T3 hypersensitivity where can IC be deposited?

A

Joints

Kidney

Small vessels

Skin

23
Q

What key actors affect immune-complex pathogenesis?

A

Complex size = small and large cleared, intermediate persist

Host response

Local tissue factors

24
Q

Give an examples of diseases caused by type 3 hypersensitivity

A

RA

Glomerulonephritis

SLE

25
Q

Outline type 4 hypersensitivity

A

Delayed = 24-72 hrs

Involves lymphocytes, macrophages

Subtypes: contact (epidermal reaction), tuberculin (dermal reaction), granulomatous (persistent Ag, wall of the infected cell)

26
Q

Outline the mechanism of tissue destruction in type 4 hypersensitivity

A

Sensitisation phase = APCs activating TH1

Effector phase = TH1 activating macrophages

27
Q

What diseases are caused by type 4 hypersensitivity to exogenous Ags?

A

Granulomatous = Tb, leprosy

Contact = nickel, poison ivy

28
Q

What disease are caused by type 4 hypersensitivity to endogenous Ags?

A

Autoimmune = DM, hashimotos

29
Q

Outline the therapy available for type 3 and type 4

A

Anti-inflam drugs

Monoclonal Abs

30
Q

How is anaphylaxis managed?

A

epipen = adrenaline = vasoconstriction

oxygen

IV anti-histamines

2.3.6. Immune System (3 decks)

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