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Life Protection > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Hypersensitivity

A

Inappropriate stimulation of the adaptive immune system, resulting in tissue damage from inflammatory reactions, and even death.

Types I-V mechanisms:
types I, II, III, V – antibody mediated
type IV – T-cell mediated

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2
Q

Immediate hypersensitivity

A
  • initiated in a sensitised recipient (from previous contact with Ag) within minutes of further exposure to Ag
  • Ab-mediated eg Type
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3
Q

Delayed hypersensitivity

A

appears only after some days (48-72hr)

T-cell mediated – Type IV

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4
Q

Types of hypersensitivity

A
  1. immediate hypersensitivity IgE
  2. antibody mediated IgM, IgG
  3. immune complex mediated
  4. T cell mediated
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5
Q

Genetic susceptibility to immediate hypersensitivity

A

Polymorphs in genes (chr.5q31) IL-4, IL-5, IL-13

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6
Q

Hygiene hypothesis

A

Related to decrease in infections in early life

pre-natal/childhood infections train immune system => less likely to respond to environmental allergens
(Fewer allergies in children brought up on farms than city children)

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7
Q

Allergic response- sensitisation phase

A
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8
Q

Allergic response- effector phase

A

Mast cell degranulation
Mast cells release inflammatory mediators

Trigger mechanisms

  • allergen cross-linking
  • IgE on surface
  • FceRI receptors
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9
Q

Mast cell activation causes…

A
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10
Q

Late reaction (immediate hypersensitivity)

A
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11
Q

Eosinophils

A
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12
Q

Immediate hypersensitivity stages

A
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13
Q

Mast cells and non-atopic allergy

A

triggered by temperature extremes & exercise
IgE and Th2 not involved
mast cells hypersensitive to activation
~20%-30% of immediate hypersensitivity

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14
Q

Direct triggers of mast cell degranulation

A

Opiates, contrast media, vancomycin

C5a, C3a anaphylatoxins

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15
Q

Anaphylaxis

A

Systemic exposure to allergen (even small doses)

  • injections (drugs eg, penicillin)
  • insect bites (eg bee venom)
  • absorption across epithelia
    - - mucosa gut (peanut, shellfish; skin

Clinical manifestations

  • drop in blood pressure (vascular shock)
  • difficulty in breathing (airway constriction)
  • widespread oedema
  • Vomiting, abdominal cramps, diarrhoea
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16
Q

Allergy treatment

A

Antihistamines
Mast cell stabilisers (stop histamine release)
Decongestants (shrink swollen membrane sin nose)

Corticosteroids
Epipen (adrenaline)
Anti IL-4 Omalizumab

17
Q

type 2: cytotoxic

A

Antibody formed against antigen on cell surfaces → cell lysis by:
1) activation of the classical complement pathway IgG, IgM Abs

2) ADCC – antibody-dependent cell-mediated cytotoxicity by NK cells binding IgG Ab via their Fc receptors

3) phagocytosis of RBCs, platelets – mediated by
Fc receptors on macrophages and C3b
(from complement activation)

18
Q

Type 2: Haemolytic disease of newborn

A

Ab response to RhD on foetal rbc, when mother RhD-ve

Sensitisation -> no sensitisation (anti-D) -> haemolytic disease (rhesus prophylaxis introduced)

19
Q

What type of hypersensitivity is Grave’s?

A

Type 2/V

hyperthyroidism

20
Q

Type 3 immune complex mediated hypersensitivity

A

Ag/Ab (IgG, IgM) complexes form in excess and deposit on (or near) blood vessel walls in tissues causing local inflammation and tissue damage (immune complex disease)

Streptococcus      			 
Staphylococcus 			 
Malaria
Leprosy
Viruses

Inhaled antigens – Pigeon fancier’s lung (pigeon antigens
Farmer’s lung (fungi in mouldy hay)
Hep B

autoimmune- RA, SLE

21
Q

Goodpasture’s syndrome vs systemic lupus

A

Goodpastures- type 2

Lupus- 3

22
Q

Mechanism of inflammation

A 
complement activation →
      C5a, C3a 
   → release of mediators from
        mast cells,macrophages
   → attract neutrophils etc
       (C5a)
  neutrophils → FcRs, C3bR
   → enzymes, ROI, NO

basophil, platelet binding by FcgR
→ further release of vasoactive amines
platelets → microthrombi

23
Q

Type 4 cell mediated , delayed

A

T cell mediated eg TB, Listeria, herpes, measles

24
Q

Mechanism of type IV hypersensitivity

A
25
Q

What type of cells mediate type IV?

A

CD4+ Th1 cells

26
Q

Granuloma formation

A
  1. Mycobacterial, TH1-type granulomas
    Mycobacterium tuberculosis, M leprae infections
    eg TB – bacteria persist in alveolar macrophages
Ag presented on MHCII to CD4+ TH1 cells
macrophages activated (IFNg)

influx of monocytes to infection site
differentiate to macrophages, activated, retained
form granuloma (healed tubercule) to ‘seal off’ infected macrophage

The process is cytokine driven:
Th1 cell -> RANTES (chemokine for monocytes)
-> MIF (retention of macrophages)

macrophage -> MCP-1 (chemokine for monocytes)
-> TNF-alpha, IL1 (= ↑ adhesions for extravasation)

27
Q

Granuloma structure

A

persistent Ag in centre macrophages – necrosis
macrophages (from blood monocytes) form concentric rings of ‘epithelioid’ cells
other cell types – eosinophils, T-cells
giant cells – multinucleate
fibrous connective tissue (fibrosis)
calcification

CD8+ T cells:
possible source of cytokines
lyse bacterial-infected macrophages
produce granulysin – bactericidal

gamma-d-T cells: cytokine producing; cytotoxic

28
Q

Tuberculin reaction

A

skin test for memory TH1 cells against mycobacterial Ag
purified protein derivative (PPD) from culture filtrate
→ skin
presented on dendritic cells
→ firm red swelling at 48-72hr; T cells, macrophages

29
Q

Type V - stimulatory

A

modification of type 2

Persistent activation of target cell membrane receptor by autoAb, normally responding to hormone

-> TSH (thyroid stimulating hormone) receptor by auto Ab in thyrotoxicosis (Graves’ Disease) → continuous thyroxine release

Life Protection (10 decks)

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