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Supporting life block > Hypersensitivity &asthma > Flashcards

Hypersensitivity &asthma Flashcards

1
Q

Define hypersensitivity

A
  • Immunologically driven host-tissue damaging process’

- Immunologically driven tissue-irritating process

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2
Q

Outline the innate immune system

A
  • First lines of defence, general, rapid response
  • Complement system
  • neutrophils, basophils, eosinophils, mast cells, NKs
  • Macrophages, dendritic cells
  • APCs: macrophages, dendritic cells, follicular DCs & B cells
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3
Q

Outline the adaptive immune system

A
  • Directed by the innate immune cells, antigen specific
  • memory, late response
  • T& B cells
  • Antibodies: immunoglobulins(Ig) IgA, IgG, IgM,IgE,IgD
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4
Q

Outline the different types of hypersensitivity:

A

1.) Type I : immediate hypersensitivity (Allergy-Anaphylaxis& Atopy)
-Non-microbial environmental antigens that are innocuous. Response within minutes mediated by IgE-mast cells
2.) Type II: antiBody mediated
-IgM, IgG antibodies against cell surface/extracellular matrix complement-mediated
3.) Type III: Immune Complex mediated
-soluble immune complexes antigen-IgM or antigen-IgG
-complement mediated
4.) Type IV: cell mediated( Delayed)
-CD4& CD8 cells. cell killing & cytokine-mediated inflammation. 24-48h
-Takes longer to develop
ABCD pneumonic

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5
Q

What are the characteristics of the main allergens in type I hypersensitivity?

A
  • Individuals are rapidly exposed to them

- They do not induce macrophages/ dendritic cells typical responses driving Th1/Th17 (like microbes do)

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6
Q

Explain type I hypersensitivity

A
  • Immediate hallmarks= IgE production & activation of Th2 cells; mediated by IgE- mast cells
    1. ) Mast cells:
  • Cross-linking of 2 adjacent IgE molecules triggers mast cell activation
    2. ) may be triggered by inhaled allergens
    3. ) may be triggered by dust mites, pets, pollen, fungi, food allergies e.g peanuts; drugs such as antibiotics or chemotherapeutics
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7
Q

What are the 2 main mediators of mast cells

A

1.) Storage granules:
-Histamine: increased vascular permeability; smooth muscle contraction
-Tryptase: Tissue remodelling; increased mucus secretion
2.) De novo synthesis:
-Prostaglandins: increased vascular permeability
-Leukotrienes: smooth muscle contraction
-Cytokines: vasodilation
Systemic anaphylaxis eventually results. This is lethal

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8
Q

What actions make up ‘wheal and flare’ responses

A

-Vasodilation
-Vascular leak
These are caused by histamine

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9
Q

What interleukin activates Eosinophils

A

IL-5.

This then causes a release of granules, leading to tissue damage

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10
Q

What is systemic anaphylaxis

A
  • Type I hypersensitivity of the whole body

- can be lethal

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11
Q

What are the symptoms of type I hypersensitvity in the following organs:

  1. ) Lung
  2. )Nose
  3. ) Eye
  4. ) Skin
  5. ) Gut
A
  1. ) asthma, wheezing
  2. ) rhinitis, sneezing, runny nose
  3. ) Conjunctivitis
  4. ) Atopic dermatitis
  5. ) Food allergy
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12
Q

What lab tests can we use to help diagnose type I hypersensitivity

A
  • Total IgE (.100IU/mL)
  • specific IgE raised (e.g RAST)
  • Tryptase levels-transient (24-48h)
  • Can also use the skin prick test( >3mm wheal- swelling)
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13
Q

What is RAST?

A

Radio-allergosorbent test

  • done on a sample of blood
  • Detection of label is proportionate to the amount of IgE specific for the antigen
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14
Q

Give examples of type I hypersensitivity.

A
  • Pruritus( itch)
  • Urticaria(hives)
  • Allergic rhinitis (hay fever)
  • Asthma- immediate asthma
  • Systemic anaphylaxis- whole body
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15
Q

What do you expect to see in a positive skin prick test

A

-When exposed to the allergen a wheal & flare should result
Wheal & flare:
-leakage of plasma& protein (edema)
-vasodilation& congestion

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16
Q

What issues may be associated with/ the cause of asthma?

A
  • Bronchial hyperresponsiveness
  • Mucous cell metaplasia
  • Thickening of the bronchial wall
  • Bronchoconstriction
  • Inflammation
17
Q

What are the main characteristic features of asthma?

A
  • Variable airways narrowing–> leading to airflow obstruction that is reversible spontaneously or with treatment
  • Non-specific airways hyperresponsiveness to innocuous stimuli ( cold air, irritants, pollutants) —> leading to bronchoconstriction. Always present
  • Mucosal inflammation and airways remodelling
18
Q

What are the different phenotypes of asthma

A
  1. ) Allergic asthma: most easily recognised. Usually commences in child hood. Associated witth past/family history of allergic disease. Usually presents eosinophilic airway inflammation. Good response to ICS
  2. ) Non-allergic asthma: sputum may be neutrophilic, eosinophilic, or with few inflammatory cells. Less response to ICS
  3. ) Late-onset asthma: more common in women. Tendency to non-allergic; high doses of ICS required
  4. ) Asthma with fixed airflow limitation: long-standing asthma, airflow limitation thought to be due to airway wall remodelling
  5. ) Asthma with obesity: prominent respiratory symptoms; little eosinophilia
19
Q

Give e.g’s of type II hypersensivity

A
  • Grave’s disease
  • Insulin-resistant diabetes
  • Myasthenia gravis (Ab-ach)
  • Immune hemolytic anemia
  • Immune thrombocytopeic purpura
  • Glomerulonephritis
20
Q

Give e.g’s of Type IV hypersensitivity

A
  • Inflammatory bowel disease
  • Crohn’s
  • Contact sensitivity (Ni+2)
  • Asthma
  • Autoimmune myocarditis: myosin heavy chain protein
  • Type I diabetes mellitus: destruction of islet cells
21
Q

Give e.g’s of type III hypersensitivity

A 
Seum sickness:
-complexes in small arteries
-Vasdculitis
-renal glomeruli
-nephritis 
-joints synovia
-arthiritis 
Systemic immunologic diseases: 
-SLE
-nephritis
-arthiritis
-polyarteritis nodosa 
-Poststreptococcal glomerulonephritis
22
Q

Explain the role of inflammation in the pathology of asthma

A
  1. ) Inflammatory infiltrate: inflammatory cell recruitment, Th2 cells, mast cells & eosinophils
  2. ) Mucosal oedema: bronchial microvascular leak
  3. ) Mucus hypersecretion: blockage of airways by mucus plugs
  4. ) Bronchial smooth muscle contraction: action of inflammatory mediators
23
Q

Explain the role of remodelling in the pathology of asthma

A

Persistent alterations in airways structure

  1. ) Epithelial cell damage: leaky epithelium
  2. ) Reticular basement membrane thickening
  3. ) Airway smooth muscle thickening
  4. ) Submucosal mucus gland hypertrophy
24
Q

What is the early and late response in asthma

A

Early response: Hypersensitivity I

Late response: Hypersensitivity IV

25
Q

What are the associated risks of asthma ?

A 
Host factors(predisposition)
-genetic
-atopy(+ve skin prick tests-type I)
Environmental factors ( precipitate asthma exacerbations) 
-allergens
-occupational sensitizers( vehicle spray painting, baking) 
-air pollutants 
-respiratory viruses( common cold)
-exercise
-drugs (aspirin, NSAIDs)
26
Q

What are Curschmann spirals?

A

-Mucus plugs
-Casts from small bronchi
-Dangerous as it blocks air exchange &medication
(neutrophilic asthma?)

27
Q

What are charcot-leyden crystals ?

A
  • Needle-shaped

- from breakdown of eosinophils

Supporting life block (28 decks)

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