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Respiratory > Asthma > Flashcards

Asthma Flashcards

1
Q

Definition

A

Chronic inflammatory condition of the lung airways

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2
Q

3 characteristics of asthma

A

Airflow limitation
Airway hyperreponsiveness
Inflammation of the bronchi

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3
Q

Is airflow limitation reversible?

A

yes, usually spontaneously/with treatment

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4
Q

What cell types are involved in inflammation of the bronchi?

A 
T lymphocytes
Mast cells
Eosinophils
Oedema
SM hypertrophy
Matrix deposition
Mucus plugging 
epithelial damage
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5
Q

What is extrinsic asthma

A

Atopic - implying a definite external cause

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6
Q

What is intrinsic asthma

A

when no causative agent can be identified - often ‘late onset’

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7
Q

Atopy

A

tendency to develop IgE antibody mediated reactions against environmental antigens

genetic and environmental factors affect serum IgE levels

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8
Q

What are bronchial provocation tests?

A

Patients inhale gradually increasing concentrations of either histamine or methacholine.

Patients with clinical Sx of asthma respond to very low doses

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9
Q

What is the eosinophilic asthma phenotype?

A

allergic, Th2

  • early onset, atopy associated
  • later onset, non-atopic
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10
Q

Which cells are jam packed with granules and have high affinity IgE receptors?

A

mast cells

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11
Q

What’s mast cell sensitisation?

A

when mast cells get IgE associated with its IgE receptors, and its then primed to be activated

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12
Q

What happens when a mast cell is activated?

A

it releases mediators and degranulates

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13
Q

3 mast cell mediators and what time frame are they released in?

A

Histamine seconds
Eicosanoids minutes
Cytokines hours

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14
Q

what is a very potent bronchoconstrictor?

A

histamine

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15
Q

What are cys-LT1 and cys-LT2?

A

cysteinyl-leukostrienes (a type of eicosanoid)

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16
Q

Precipitating factors for asthma

A 
major allergens
viral infections
cold air
exercise
irritant dusts
vapours and fumes
emotion & drugs
17
Q

Pathophysiology: what happens to the SM, epithelial cells and the basement membrane?

A

SM - inappropriate + excessive contraction of SM. hypertrophy + proliferation of SMCs

Epithelial cells - may be abnormal, altered expression of matrix regulating proteins. neoplasia: increase in number of goblet cells

BM - increased thickening

18
Q

What makes the airway narrow?

A

SM contraction
thickening of the airway by cellular infiltration
secretions within the airway lumen

19
Q

Presentation

A

cough + chest tightness
diurnal variation
worse at nights and early morning
provoked by triggers

20
Q

Presentation during an attack

A

reduced chest expansion, prolonged expiratory time and bilateral polyphonic wheezing

21
Q

Diagnostic tests

A

Skin prick test
CXR- hyperinflation?

PaO2 and PaCO2 down –> hyperventilation

Variable airflow limitation
Diurnal variation of PEFR - increased after inhalation of bronchodilator (reversibility testing)

22
Q

How would you rule out bronchopulmonary aspergillosis ?

A

CXR

23
Q

which out of bronchodilators and steroids alleviate symptoms and which target inflammation?

A

BDs- alleviate Sx

steroids- target inflammation

24
Q

What’s step 1 for BTS stepwise treatment for asthma?

A

occasional SABA for symptom relief e.g. salbutamol

short acting beta-2 agonist

25
Q

if SABA isn’t sufficient, what Tx would you add?

A

standard-dose inhaled steroid e.g. beclometasone

26
Q

when would you add salmeterol to Tx and review Dx?

A

its a LABA.

would add to inhaled steroid and SABA

(step 3)

27
Q

What’s step 4 for BTS stepwise treatment for asthma?

A

consider trials of high beclometasone (inhaled steroid)

28
Q

If all else fails, whats the final step in Tx?

A

regular oral prednisolone

29
Q

What’s the molecular difference between SABAs and LABAs?

A

a LABA is a SABA with an added long lopophilic chain

30
Q

how to B2-adrenoceptor agonists work?r

A

they relax bronchial smooth muscles (increasing cAMP), acting within minutes

31
Q

Mx for a really severe asthma attack?

A

02 40-60%, salbutamol nebuliser, prednisolone

Respiratory (16 decks)

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