Asthma Flashcards

1
Q

What is FEV_1?

A

Forced Expiratory Volume in a second - used in the diagnosis of restrictive and obstructive respiratory diseases.
*This should be around 3/4 of the FVC (Forced vital capacity)

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2
Q

What is PEFR?

A

Peak Expiratory Flow Rate - how much the patient can blow out in one breath.

*At the same time - explain how you would take a peak flow - clinical skills

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3
Q

What is the definition of Asthma? (5)

A

intermittent attacks of bronchoconstriction due to a pathological change to the bronchioles that results from long standing inflammation.

  1. Increased mass of smooth muscle (hyperplasia and hypertrophy)
  2. accumulation of interstitial fluid (oedema)
  3. increase in secretion of mucus
  4. epithelial damage- exposes the nerve endings
  5. sub-epithelial fibrosis.
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4
Q

What happens to the airways in asthma (general)

A

Narrowing of the airways caused by inflammation and bronchoconstriction increases the airway resistance and decreases the FEV_1 and PEFR.

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5
Q

What type of nerve fibres are exposed (due to epithelial damage) and contribute to bronchial hyper-responsiveness?

A

Sensory fibres - C fibres, irritant receptors

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6
Q

What are the 2 components to bronchial hyper-responsiveness in asthma?

A
  1. Hypersensitivity

2. Hyper-reactivity

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7
Q

inhaled bronchoconstrictors are also known as…

A

Spasmogen

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8
Q

Give examples of spasmogens (2) and which receptors they act upon.

A

Histamine - activate the ASM H1 Receptors

Methacholine - activiate the ASM M3 Receptors

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9
Q

During an asthma attack bronchospasms are ______ action

A

an immediate

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10
Q

During an asthma attack an inflammatory reactions are ______ action

A

a delayed

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11
Q

A type 1 Hypersensitivity reaction is _____

A

early phase - bronchospasm and acute inflammation

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12
Q

A type 4 Hypersensitivity reaction is ______

A

Late phase - bronchospasm and delayed inflammation

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13
Q

Hyper-reactivity: Asthma as an immune imbalance - what two pathways does this involved on presentation of an allergen?

A

Non-atopic: low level TH1 response cell mediated immune response involving IgG and macrophages

Atopic: Strong TH2 response antibody mediated immune response involving IgE

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14
Q

What is TH1 response?

A

TH1 cell mediated response

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15
Q

MHC II cells are ____________

5

A

present on antigen presenting cells only
bind exogenous antigens
present the antigen to helper T-Cells
binds the CD4 adhesion molecules on helper T-Cells
presence of foreign bodies induces antibody production and attracts immune cells (EOINSPHILS) to the area of infection

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16
Q

TH2 response causes….

A

(Induction phase) maturation of TH0 cells into TH2 cells which under the influence of IL-4 and binding to B-cells causes them to mature to IgE secreting P cells

17
Q

The effector phase in development of allergic asthma is…..

A

Eosinophil differentiation and activation in response to IL-5 released from TH2 cells.

18
Q

Mast cells in airway smooth tissue express IgE receptors in response to…

A

IL-4 and IL-13 released from TH2 Cells.

19
Q

Phase 3 in allergic asthma development involves:

A

Activation of mast cells in the airway smooth muscle Subesquent presentation of the antigen and cross -links in IgE receptors stimulates calcium entry into mast cells and also the release of calcium from intracellular cells

20
Q

The release of Calcium from intracellular stores in phase 3 causes _______________

A

the release of secretory granules containing preformed histamine and production and release of other agents - Leukotrienes LTC4 and LTD4 - ASM contraction

21
Q

What are LTC4 and LTD 4 and their effects?

A

Leukotrienes - primary cause in bronchoconstriction in the airways (asthma)
in more severe cases - eosinophils cause bronchoconstriction (are attracted to the area by the leukotrienes)

22
Q

Leukotrienes can both

A

trigger asthma attacks and are also an important part in causing long term hypersensitivity in chronic asthma.

23
Q

True or False? Drugs are now produced to interfere in the action of Leukotrienes

A

True but they only provide protection not as effective once an asthma attack is in place.

Prevent the Leukotriene release from mast cells and eosinophil production - in turn prevents bronchoconstriction, mucous secretion and oedema.