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Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Type 1 Hypersensitivity Reaction

A

Allergic response within 5-10 mins of exposure to a specific allergen
IgE causing mast cell degranulation

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2
Q

T1HR Mechanism

A
  • Antigen (exogenous substance -pollen) stimulates B cell to produce specific IgE w help of t helper cells.
  • IgE binds and coats mast and basophils via Fc receptors and sensitises them
  • Later exposure to the same antigen cross links the bound IgE on sensitised mast cells
  • Triggers degranulation

Leads to
- Increased vasc perm
- broncho constriction
- chemotaxis of eosinophils, neuts and lymphocutes
- Hypotension
- oedema
- rashes
- anaphylaxis

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3
Q

Examples of T1HR

A

Asthma, Hayfever - antigen enters via resp mucus membrane

Urticaria

Anaphylaxis - antigen parentally administered

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4
Q

T2HR

A

Antibody mediated cytotoxic reaction involving IgG or IgM antibodies binding to cell surface antigen

Resulting in:
- Complement activation through classical pathway
- leads to lysis, mast cell activation and nut recruitment
- Mobilisation and activation of nuts, eosins, monos and NKs

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5
Q

T2HR example

A

Transfusion reactions
Autoimmune Haemolysis
Haemolytic disease of the newborn

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6
Q

T3HR example

A

Autoimmune eg SLE, RA

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7
Q

T4HR example

A

Pulmonary TB
Contact dermatitis
GVH disease

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8
Q

Pathophysiology of Anaphylaxis

A

T1 HR
Triggers: Drugs, food, environment

Phase 1: Initial exposure
- APC + Antigen -> T-Cell -> B cell
- B Cell produces specific IgE
- IgE binds to and coats basophils and mast cells, via the Fc receptors.
- Mast cells and basophils (Blood and tissue) are sensitised

Phase 2: Second exposure
- Antigen binds IgE on surface of mast and basophils.
- Causes mast cell degranulation systemically.

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9
Q

Early Phase Anaphylaxis

A

Early Phase:
- first 15-30 mins
- mast and baso degranulation
- early mediators: histamine, serotonin and triptase
- effects: bronchocons, VD, cap leakage, decreased pre load etc, nausea.

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10
Q

Late Phase Anaphylaxis

A

Late Phase
- 4-6 hours later
- Chemotaxis of eosinophils, neutrophils, lymphocytes
- leading to inflammation
- Mediators: PGs, LKs, BKs, platelet activating factor.
- Effects: Same as early phase.

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11
Q

Clinical Features of Anaphylaxis

A

Mucocutaneous
- VD + CL = Angioedema, urticaria

CV
- VD + CL = <BV = <Preload = <CO = < MAP = Collapse

Resp
- BC

GIT
- Nausea/vomiting, Diarrhoea

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12
Q

Histamine Role in Allergy

A

Basic amine derived from histidine
- H1 and H2.

MOA:
- H1: GqPCR
- H2: GsPCR

CVS:
- H1 = >AV delay, coronary VC. VD + CL due to >NO production.
- H2 = > ionotropy, coronary VD

RESP:
- H1: BC
- H2: BD

GIT: H2 = > Gastric acid secretion

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13
Q

Tryptase

A

Sereine protease located in mast cells.
Major component of mast cell degranulation.

Activates complement cascade, coagulation cascade and chemotaxis CVS: VD, CL
Resp: BC

Levels are measured to confirm anaphylaxis, however a negative level doesn’t exclude anaphylaxis

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14
Q

When is tryptase measured

A

Immediately, I hr, 4 hrs and >24hrs post onset of symptoms

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15
Q

Type 2 HR

A

Antibody mediated cytotoxic reaction
- Antigen is cell surface or tissue bound.
- IgG or IgM antibodies bind surface antigen
- Results in complement activation via classical pathway.
- Mobilisation and activations of immune response resulted cytotoxicity.

Results in antibody mediated damage to target cells

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16
Q

Clinical Picture of T2HR

A

Depends on target tissue.

  1. Organ specific diseases
    - Myasthenia Gravis
    - Glomerulonephritis
  2. Autoimmune Blood cell destruction
    - Haemolytic anaemia
    - thrombocytopenia
  3. Transfusion reactions
    - ABO incompatibility
  4. Haemolytic disease of the new born
    - Rh Isoimmunisation
  5. Hyperacute allograft rejection
17
Q

T3HR

A

Immune Complex Deposition

Immune complex mediated reaction
results in deposition of AG-AB complexes in host tissues.
This leads to complement activation - nut infiltration and tissue damage.

AG AB complexes are usually cleared by phagocytes
- In T3HR, three is either too many or the complexes are too small to be cleared effectively.
- AGAB excess leads to formation of immune complexes (complement activation)
- These immune complexes are deposited in the tissue, causing a reaction from the activated complements.
- The tissue depends on the reaction: Localised: complexes formed in the tissues resulting in localised effects
Systemic: Complexes formed in the circulation and then deposited in the tissues causing systemic effects.

Localised: Arthus Reaction
Systemic: serum sickness - vasculitis

18
Q

T4HR

A

Delayed Cell mediated HR

1) Antigen presentation to T cell = release of cytokines (IL2, IL4, IFNy)
2) Cytokines activate Macs = cell damage.
3) T cells become sensitised for future exposure

Inflammatory response and activation of macrophages is localised

19
Q

Mantoux test

A

Example of T4HR

1) Infection w m.tuberculosis
- Infection - T helper cells recognise antigen.
- T-Cells proliferate, forming a population of helper T cells that are sensitised.

2) Mantoux test
- T cells presented w antigen by APC.
- Recognised antigen
- Release cytokines + activate MACS
- localised reaction.C

20
Q

contact dermatitis

A

Haptens deposited in skin
Too small to to be antigenic
Combine w intradermal protein carriers to become antigenic

21
Q

Transplant Immunology

A
22
Q

Allograft

A

Graft from a genetically different donor of the same species
- Most organ transplants

23
Q

Autograft

A

Graft from a genetically identical donor
- Self self

24
Q

Xenograft

A

From different species
- Porcine valve

25
Q

Graft Vs Host
Transplant rejection

A

Transplant rejection
- Host vs Graft
- Blood transfusion is a blood transplant
- Your immune system recognises foreign tissue and destroys the graft
- Hyperacute, Acute and delayed.

  • Hyperacute: Mins - Hours. Antibody mediated. Immediate reaction to foreign antigen. Leads to destruction, immune response, graft wont take. EG ABO incompatability
  • Acute: Days to weeks
    Cell mediated or antibody mediated
  • Chronic Rejection: Weeks to years
    Common in cardiac transplant. Thrombosis and macrosclerosis, proliferation of SM cells due to repeated inflammation.
  • Due to poor HLA matching

GVH:
- Must involve cells that are able to form an immune response
eg BM transplant, stem cells
- these cells recognise the self cells as foreign and form an immune response to that.

Immunology (4 decks)

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