L7 18 Mar 2019 Flashcards

Asthma

1
Q

What are the three types of chronic obstructive pulmonary disease?

A
  • emphysema: alveolar wall destruction, over inflation
  • chronic bronchitis: productive cough, airway inflammation
  • asthma: reversible obstruction
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2
Q

emphysema

A
  • irreversible enlargement of airspaces, distal to terminal bronchiole
  • most smokers suffer from this
  • too much coughing –> elasticity is lost, also tar deposit
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3
Q

chronic bronchitis

A
  • persistent cough with sputum production for at least 3 mths in two consecutive years; may progress to COPD and may overlap with emphysema –> hypersecretion of mucus and if persistene marked increase in goblet cells in small airways
  • therapy: mucolytics
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4
Q

asthma

A
  • chronic disorder of airways, usually caused by immunological reaction, marked by bronchoconstriction
  • increased airway sensitivity to various stimuli
  • inflammation of bronchial walls
  • increased mucus secretion
  • bronchial hyperresponsiveness
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5
Q

symptoms of asthma

A
  • recurrent episodes of wheezing
  • breathlessness
  • chest tightness
  • dry cough
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6
Q

four types of asthma

A
  • atopic asthma
  • non-atopic asthma
  • drug-induced asthma
  • occupational asthma
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7
Q

atopic asthma

A
  • triggered by environmental allergens (dusts, pollens, roach or animal dander, foods)
  • type I IgEmediated hypersensitivity reaction
  • hereditary, and also common type of asthma
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8
Q

non-atopic asthma

A

typically virus-induced inflammation lowers threshold to irritants

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9
Q

drug-induced asthma

A

salicylate (aspirin)-induced is a typical example

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10
Q

occupational asthma

A

exposure to fumes (plastics, organic solvents, chemical dusts)

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11
Q

common precipitating factors in aetiology of asthma

A
  • common cold/other viral infections, sinusitis, bronchitis/bronchiolitis
  • pollens (weeds, grasses, trees), dusts, feathers, animal fur, furniture stuffing, fungal spores
  • fumes (petrol, paint, tobacco, industrial chemicals), cold air, air pollutants
  • laughter, physical exertion, psychological stress, drugs
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12
Q

how is asthma diagnosed?

A
  • perisistent cough
  • wheezing (via stethoscope)
  • shortness of breath - stethoscope
  • spirometry - most common lung function test
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13
Q

complication of diagnosis(/misdiagnosis) with asthma

A
  • anaphylaxis: need epinephrine
  • pulmonary embolism: need blood thinning - warfarin
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14
Q

spirometry

A

measures FEV (forced expiratory volume)

  • not safe to do spirometry with methacoline and exercise challenges
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15
Q

pathologenesis of atopic asthma

A

Type I IgE-mediated hypersensitivity immediate reaction

  • alleren stimulates TH2 response
  • class switching from IgG (B cells) to IgE
  • IgE binds to Fc receptors on mast cells
  • subsequent exposure to allergen = mast cell activation
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16
Q

atopic asthma pathologenesis

mast cell mediators

A
  • ECF: eosinophil chemotactic factor
  • NCF: neutrophil chemotactic factor
  • PAF: platelet activating factor

late phase reaction = chemotactic factors + leukotrines

17
Q

pathology of atopic asthma

A
  • thickened basement membrane
  • increase mucous in bronchial lumen
  • goblet cell hyperplasia
  • hypertrophyof submucosal glands
  • hypertrophy/hyperplasia of smooth muscle
18
Q

clinical features of allergic asthma

A
  • family history usually positive
  • attacks related to specific antigens
  • history of eczema in childhood
  • IgE associated
  • skin test results usually positive
19
Q

clinical features of nonallergic asthma

A
  • family history usually negative
  • attacks related to infections, exercise and other stimuli
  • skin test usually negative
  • no history of eczema in childhood
  • not IgE associated
  • consider occupational asthma as a cause
20
Q

management of asthma

A
  • majority of cases:
    • short acting β2-agonist: bronchodilation
    • low-dose inhaled corticosteroid: broad spectrum anti-inflammatory response
  • therapy adapted with severity of disease