Asthma 2010

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pahophysiology

Transcript of Asthma 2010

  • 1. Asthma Definition
    • Reactive airway disease
  • Chronic inflammatory lung disease
    • Inflammation causes varying degrees of obstruction in the airways
  • Asthma is reversible in early stages

2. Asthma

  • Affects approx 15% of New Zealanders which equates to 1 in 6 of the population
  • Incidence in New Zealand is increasing
  • Asthma hospitalization rates have markedly increased
  • Prevalence is higher in Maori & Pacific Island adults with hospital admissions twice as likely for Maori than non-Maori adults

3. Asthma

  • High morbidity due to:
    • Underdiagnosis and inappropriate therapy
    • Limited access to healthcare
    • Inaccurate assessment of severity
    • Delay in seeking help
    • Inadequate medical treatment
    • Nonadherence to prescribed therapy
    • Increase in allergens in the environment

4. Triggers

  • Pollens
  • Dust
  • Dust mites
  • Food colouring
  • Moulds/fungi
  • Animals
  • Feathers
  • Job-related factors
  • Cold/flu viruses
  • Stress, emotions
  • Change of weather
  • Change of season
  • Smoke
  • Cold air
  • Medicines
  • Fumes
  • Exercise

5. Asthma Pathophysiology

  • Early-Phase Response
    • Triggered when IgE receptors on mast cells beneath the bronchial wall are activated
    • Release inflammatory mediators (histamine, bradykinin, leukotriene, prostaglandins, chemotactic factors, and cytokines)
    • Mediators cause
      • bronchial smooth muscle constriction
      • increased vasodilation and permeability
      • epithelial damage

6. Asthma Pathophysiology

    • Early-Phase Response
    • Bronchospasm,increased mucous secretion, oedema formation, and increased amounts of tenacious sputum
    • Patient experiences wheezing, cough, chest tightness, and dyspnoea
    • Peaks within 30-60mins of exposure to trigger & subsides in another 30-90mins

7. Factors Causing Expiratory Obstruction in Asthma

  • Reduction in airway diameter
  • in airway resistance related to mucosal inflammation
  • Constriction of bronchial smooth muscle
  • Excess production of mucous

Fig. 28 - 3 8. Late-Phase Response

  • Peaks in 5 6 hrs
  • Infiltration with eosinophils & neutrophils
  • Inflammation as more inflammatory mediators produced
  • Bronchial reactivity
  • More severe than early-phase response & can last 24 hrs or more

9. Early and Late Phases of Responses of Asthma Fig. 28 - 1 10. Asthma Clinical Manifestations

  • Unpredictable and variable
  • Recurrent episodes of:
  • wheezing
  • breathlessness
  • cough
  • tight chest
  • Expiration may be prolonged from aninspiration-expiration ratio of 1:2 to 1:3 or 1:4
  • Between attacks may be asymptomatic with normal or near-normal lung function

11. Asthma Clinical Manifestations

  • Wheezing is an unreliable sign to gauge severity of attack
  • Severe attacks can have no audible wheezing due to reduction in airflow
  • Silent chest is ominous sign of impending respiratory failure

12. Asthma Clinical Manifestations

  • Difficulty with air movement can create a feeling of suffocation
    • Patient may feel increasingly anxious
    • Mobilizing secretions may become difficult

13. Asthma Clinical Manifestations

  • Examination of the patient during an acute attack usually reveals signs of hypoxaemia
    • Restlessness
    • Increased anxiety
    • Inappropriate behavior
    • Increased pulse and blood pressure

14. Features of Acute Severe Asthma

  • Unable to complete a sentence in 1 breath
  • RR> 25 breaths per min
  • Pulse rate > 110 beats per min
  • PERF (peak expiratory flow rate)