Asthma Flashcards

1
Q

clinical presentation of asthma

A

cough, wheeze, shortness of breath, sputum, chest tightness

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2
Q

signs of asthma

A
  • hypoxia

- wheezing

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3
Q

risk factors of asthma

A
  • family history
  • associated with other allergic conditions eg allergic rhinitis
  • allergens in the air
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4
Q

when are asthma symptoms worse?

A

early in the morning and late at night

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5
Q

investigations for asthma

A
  • peak flow
  • spirometry (also with the use of a nebulised SABA to determine reversibility)
  • blood gases
  • chest radiography (exclude underlying disease)
  • bronchoprovocation test (done when the patient has word-induced asthma)
  • skin prick (check for allergens)
  • pulse oxymetry
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6
Q

asthma vs COPD

A

asthma has an element of reversibility (cut off at 12% on PFTs)

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7
Q

treatment of asthma

A
  1. SABA prn
  2. low dose ICS + SABA prn
  3. medium dose ICS and SABA prn
  4. high-dose ICS, SABA/formoterol prn
  5. Anti-IgE/Anti-IL5/Macrolides, SABA/formoterol prn
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8
Q

if the patient’s asthma approves, what can you do?

A

you can step down on treatment i.e. decrease the dose or remove drugs altogether

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9
Q

where can leukotriene receptor antagonists be used?

A

From step 2 asthma onwards

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10
Q

management of an asthma exacerbation

A
  • investigations: peak flow,
  • treatment using salbutamol 5mg in nebulised form and IV steroids and bronchodilator eg ipratropium bromide i.e. SAMA
  • give oxygen if the spo2 is lower than 94%
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11
Q

if the drug does not work and the patient has chest tightness, what do you do?

A

swap the bronchodilator to magnesium sulfate because this has bronchodilator properties

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12
Q

if the patient’s asthma is as bad as needing ITU, how do you manage?

A

give IV salbutamol rather than rebulised salbutamol

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13
Q

what can cause or worsen asthma?

A
  • gestational asthma (can remain the same, be better or worsen)
  • occupational (work-exacerbated or work-induced)
  • reflux disease worsens asthma control
  • can be exacerbated due to respiratory tract infections
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14
Q

type 1 vs type 2 pneumocytes

A

type 1: gaseous exchange

type 2: produces surfactant; synthesises substances such as fibronectin and alpha-1-antitrypsin

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15
Q

asthma increases which value in PFTs?

A

residual volume

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16
Q

how would you diagnose asthma?

A

pulmonary function tests

17
Q

examples of obstructive lung disease

A
  • chronic bronchitis
  • emphysema
  • asthma
  • bronchiectasis
  • small-airway disease
  • bronchiolitis
18
Q

characteristics of asthma

A
  • episodic bronchoconstriction due to increased airway sensitivity to a variety of stimuli
  • inflammation of the bronchial walls
  • increased mucus secretion
19
Q

histopathology of asthma

A
  • increased mucosal goblet cells and submucosal glands
  • thickened basement membrane
  • bronchial smooth muscle hypertrophy
  • airway wall oedema
  • curschmann spirals
  • eosinophils
  • extracellular charcot-leyden crystals
20
Q

characteristics of acute severe asthma

A
  • state of unremitting attacks
  • long history of asthma
  • may prove fatal
21
Q

types of asthma

A

atopic: evidence of allergen sensitisation and immune activation (have allergic rhinitis and eczema)
- childhood-onset; type I hypersensitivity reaction
non-atopic: no evidence of allergen sensitisation

22
Q

triggers for bronchospasmic episodes

A
  • respiratory infections
  • exposure to irritants
  • cold air
  • stress
  • exercise
  • drugs eg aspirin
23
Q

what about non-atopic asthma?

A
  • no evidence of allergic sensitisation
  • less likely to have a positive family history
  • skin pricks are negative, usually
  • commonly triggers by RTIs or air pollutants
24
Q

drug-induced asthma?

A
  • aspirin-sensitive asthma
  • sensitive to small doses of it
    also experience urticaria
    presnt with recurrent rhinits and nasal polyps
25
Q

what to do after you use an inhaler?

A

rinse your mouth to prevent from developing candidiasis at the back of the mouth