Asthma Flashcards

1
Q

What is the definition of Asthma?

A

a Common REVERSIBLE chronic disorder of airways that is complex and characterized by variable and recurring symptoms of airflow obstruction: bronchial hyperresponsiveness and inflammaiton

*reversibility distinguishes it from COPD

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2
Q

what are the symptoms of Asthma?

A

dyspnoea, cough and wheeze

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3
Q

How do we diagnose Asthma?

A

History, Examination, Investigations

  • history of resp. symptoms
  • physical examination
  • demonstration of variable expiratory airflow obstruciton
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4
Q

what is the hygiene hypothesis?

A

Normally: child in womb has Th2 CD4 lymphocytic response (Type 1 hypersensitivity) to antigens that converts to a Th1 CD4 T lymphocytic response upon repeated exposure to antigens in neonatal life.

Hygiene Hypothesis: lack of stimulation by antigenic exposure results in a maintenance of Th2 hypersensitivity response to antigens throughout life = never converts to Th1 response.

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5
Q

What are the chronic effects of asthma?

A

poorly controlled asthma leads to a chronic thickening of the basement membrane and the destruction of the epithelial layer

destruction of the epithelial layer leads to a chronic inflammatory infiltrate

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6
Q

why are asthmatic symptoms more common at night?

A

because of the diurnal pattern of airway caliber = more bronchial narrowing at nightime

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7
Q

What result would we see on spirometry in someone with Asthma?

A

due to airway blocking, we see a reduced FEV1, decreased FEV1/FVC ratio, reduced Peak expiratory flow rate, and lower overall FVC

*key difference is that it’s reversible - try the methacholine challenge

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8
Q

describe the immunopathology of asthma

A
  1. allergen exposure
  2. mast cells in lumen/epithelium activated by allergen - release mediators
  3. mediators initiate acute reaction including bronchospasm = airflow obstruction
  4. quiescent CD4 Th2 lymph. become activated by cytokines secreted by allergen-stimulated cells = initiate more chronic inflammatory process
  5. Th2 cells secrete IL4 and IL5
  6. IL4 initiates B lymphocyte IgE release
  7. IgE amplifies mast cell event
  8. negative regulation of Th2 cells by Th1 and regulatory T cells is impaired in asthma
  9. IL5 activates eosinophils which induce acute inflammation
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9
Q

what auscultatory finding do we find in an asthmatic emergency?

A

Silent Chest

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10
Q

what is atopic triad?

A

a family history/personal history of

atopic dermatitis

seasonal allergic rhinitis (hay fever)

and conjunctivitis

This atopic triad favors a diagnosis of asthma in patients with suggestive symptoms

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11
Q

what type of wheeze do we hear in asthma?

A

polyphonic - multiple tone wheeze

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12
Q

what tests do we do to confirm an asthma diagnosis?

A

Bronchodilator response (positive selection) - with salbutamol

Bronchial provocation tests (negative selection) - with histamine or metacholine challenge

Allergen Challenge -

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13
Q

what is the first line drug in an asthma attack?

A

SABA

short acting beta 2 agonists

like salbutamol or terbutaline

these are beta 2 selective and adrenergic agonists

They are recommended for use AS NEEDED

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14
Q

what is a LABA and why do we never put patients exclusively on a LABA?

A

LABA= long acting beta 2 agonist ex) Salmeterol or formoterol

  • similar specific bronchodilatory effect of SABAs but sustained fo more than 12 hours
  • never give a LABA without corticosteroids b/c shown increased risk of death in patients who only use LABAs - this is due to muscle hypertrophy of the basement membrane over time - eventually the LABA won’t do anything for you it’s just chronic inflammation
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15
Q

Why do we use inhaled corticosteroids in Asthma?

A

b/c of anti-inflammatory activities

and

decreased cumulative inflammatory effects on airway: fewer mast cells, eosinophils, reduced hyperplasia and epithelial cell injury

Also, nonspeicific bronchial hyperresponsiveness decreases

*they suppress inflammation- not curative

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16
Q

What Inhaled Corticosteroid do we perscribe?

A

Fluticasone or Budesonide

17
Q

What is an LRA and why do we use it?

A

Leukotriene Receptor antagonist ex) montelukast, zafirlukast

  • they block the action of leukotriene C4, D4 and E4 at the leukotriene recpetor
  • the bronchodilation occurs within hours of hte first dose and is maximal within the first few days after administration
  • reduce the levels of circulating blood eosinophils

*used primarily in those who cannot tolerate ICS

18
Q

what is Anti-IgE therapy and why do we use it?

A

Anti-IgE monoclonal antibody- omalizumab

binds Fc ‘constant’ section of IgE that recognizes the high -affinity receptor on the surface of mast cells /basophils

Therefore, when given subcutaneous, omalizumab reduces circulating IgE levels by 95% and leads to down-regulation of the high affinity receptor on mast cells

19
Q

how is complete control of asthma defined?

A
  1. no daytime symptoms
  2. no night time awakening due to astham
  3. no need for rescue medication
  4. no exacerbations
  5. no limitations on activityincluding exercise
  6. normal lung function
  7. minimal side effects from medications
20
Q

Describe treatment steps in asthma classes

A

least severe asthma (step 1) = SABA as needed

Most severe asthma (Step 5)

= SABA + anti IgE treatment