RESP 210 Asthma Flashcards

1
Q

How do you define asthma?

A

Chronic inflammatory disorder of the airways characterised by airway hyper-responsiveness that is reversible either spontaneously or with treatment

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2
Q

What are the two types of asthma?

A

Extrinsic and Intrinsic

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3
Q

Describe extrinsic asthma

A

Atopic or occupational

IgE mediated with a definite extrinsic cause

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4
Q

Describe intrinsic asthma

A

No definite cause

Usually develops later in life and is more progressive

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5
Q

What is the general overview of the pathophysiology of asthma?

A

Bronchial hyper-sensitivity to an antigen and bronchial inflammation which can cause an inflammatory plug

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6
Q

Describe the process of a Type 1 - hypersensitivity reaction

A

1st exposure to the allergen: detected by dendritic cells which display it to T helper cells
Th2 cells release cytokines that stimulate B-cells to produce IgE
IgE attaches to mast cells
2nd exposure the antigen on the allergen cross links with IgE on the mast cells
= mast cell degranulation

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7
Q

What the fuck is released on mast cell degranulation? What is the result of this?

A

histamine, prostaglandins and leukotrienes

Bronchoconstriction, increased mucous production and microvascular leakage

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8
Q

Which cytokine stimulates eosinophillic differentiation and what does this result in? (Asthma week)

A

IL5 = epithelial damage, loss of tight junctions and smooth muscle contraction

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9
Q

What happens to the sub-mucosa in asthmatics with airway remodelling?

A

It becomes expanded with deposition of matrix proteins and cells making it easier for airways to close with even the slightest smooth muscle contraction

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10
Q

What happens to the epithelium in asthmatics with airway remodelling?

A

Loss of cilliated columnar cells
Increased mucus secreting goblet cells
Increased NO synthase
Increased susceptibility to infection therefore

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11
Q

What happens to the epithelial basement membrane in asthmatics with airway remodelling?

A

Deposition of repair collagens and proteoglycans here

Thickened due to activation of fibroblasts

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12
Q

What are the clinical features of asthma?

A
Recurrent wheeze
Breathless ness
Cough
Chest tightness
diurnal variation
Reversibilty
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13
Q

How might a severe attack of asthma present?

A

tachycardia
hyper expanded chest
silent chest +bradycardia = ominous

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14
Q

what investigations would you perform in an asthmatic?

A

Peak flow

Spirometry and skin prick test for allergens

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15
Q

What would you see on Spirometry in asthma?

A

Obstructive pattern flow loop
<70% FEV1/FVC ratio
Low FEV1
Low peak expiratory flow rate

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16
Q

What is the 1st line treatment for asthma and how does it work?

A

SABA - beta 2 agonists
Salbutamol terbutaline
bind to b2 receptors, increase cAMP production = bronchorelaxation

17
Q

What is step 2 in asthma management?

A

Inhaled corticosteroid e.g. beclometasone, fluticasone and budesonide

18
Q

What is the third line treatment in asthma management?

A

LABA - longer acting as it anchors into membrane = longer receptor stimulation
Should always be used in conjunction with an inhaled corticosteroid
Keep increasing steroid until control is achieved

19
Q

What is symbicort SMART?

A

combined inhaler for asthma that is used for prevention and relief

20
Q

In step 4 what additional treatments can be added in if others are ineffective?

A

Leukotriene receptor antagonist e.g. montelukast
Blocks these receptors = less bronchoconstriction and inflammation

Xanthines e.g. theophylline
decreased synthesis and secretion of inflammatory mediators
increased cAMP by inhibiting phosphodiesterase

21
Q

What drug can be used in severe persistent allergic asthma?

A

Omalizumab - anti IgE monoclonal Ab