1. Respiratory Medicine 27/10/2016 Dr.Majeed Mohan Alhamammi 4th lecture
بسم الله الرحمن الرحيم
Respiratory Medicine
27/10/2016
Dr.Majeed Mohan Alhamammi
4th lecture

2. Objectives Defintion Epidemiology Clinical presentation Diagnosis
Complication
prognosis

3. Asthma
Asthma is a common chronic inflammatory condition of the lung airways whose cause is still incompletely understood.

4. Asthma has three characteristics:
Airflow limitation which is usually reversible spontaneously or with treatment .
Airway hyperresponsiveness to a wide range of stimuli .
Inflammation of the bronchi with eosinophils, T lymphocytes and mast cells with associated plasma exudation, oedema, marked smooth muscle hypertrophy, mucus plugging and epithelial damage.

5. Typical symptoms include
wheeze,
cough,
chest tightness
dyspnoea

6. Epidemiology The prevalence of asthma increased steadily.
The prevalence of asthma increased steadily.
that asthma affects 300 million people world-wide
an additional 100 million persons will be diagnosed by 2025.

7. World map showing the prevalence of clinical asthma (proportion of population (%)). Data drawn from the European Community Respiratory Health Study (ECRHS) and the International Study of Asthma and Allergies in Childhood (ISAAC).

8. Classification Asthma can be divided into:
extrinsic - implying a definite external cause
intrinsic or cryptogenic - when no causative agent can be identified.

9. Extrinsic asthma
occurs most frequently in atopic individuals who show positive skin-prick reactions to common inhalant allergens.
Positive skin-prick tests to inhalant allergens are shown in 90% of children and 50% of adults with persistent asthma.
Childhood asthma is often accompanied by eczema .

10. Intrinsic asthma
often starts in middle age ('late onset').
Non-atopic individuals may develop asthma in middle age
from extrinsic causes such as sensitization to occupational agents
aspirin intolerance
β-adrenoceptor-blocking agents.

11. Extrinsic causes must be considered in all cases of asthma and, where possible, avoided.

12. Factors implicated in the development of, or protection from, asthma.

14. The mast cell and its mediators
The mast cell and its mediators. GM-CSF, granulocytemonocyte colony stimulating factor; FGF-2, fibroblast growth factor 2; VEGF, vascular endothelial growth factor; TNF-α, tumor necrosis factor alpha.

15. Normal bronchial tube

16. Bronchi in asthma

17. Airway hyper-reactivity in asthma
Airway hyper-reactivity in asthma. This is demonstrated by bronchial challenge tests by the administration of sequentially increasing concentrations of either histamine, methacholine or mannitol. The reactivity of the airways is expressed as the concentration or dose of either chemical required to produce a certain decrease (usually 20%) in the FEV1 (PC20 or PD20 respectively).

18. Airway hyper-reactivity in asthma.

19. Changes in peak flow following allergen challenge
Changes in peak flow following allergen challenge. A similar biphasic response is observed following a variety of different challenges. Occasionally an individual will develop an isolated late response with no early reaction

20. Reversibility test. Forced expiratory man[oelig ]uvres before and 20 minutes after inhalation of a β2-adrenoceptor agonist. Note the increase in FEV1 from 1.0 to 2.5 L.

22. Serial recordings of peak expiratory flow (PEF) in a patient with asthma. Note the sharp overnight fall (morning dip) and subsequent rise during the day. In this example corticosteroids have been commenced, followed by a subsequent improvement in PEF rate and loss of morning dipping.

23. Exercise-induced asthma
Exercise-induced asthma. Serial recordings of FEV1 in a patient with bronchial asthma before and after 6 minutes of strenuous exercise. Note initial slight rise on completion of exercise, followed by sudden fall and gradual recovery. Adequate warm-up exercise or pre-treatment with a β2-adrenoceptor agonist, nedocromil sodium or a leukotriene antagonist (e.g. montelukast sodium) can protect against time in minute)exercise-induced symptoms.

24. Making a diagnosis of asthma
Compatible clinical history plus either/or: FEV1 ≥ 15%* (and 200 mL) increase following administration of a bronchodilator/trial of corticosteroids
> 20% diurnal variation on ≥ 3 days in a week for 2 weeks on PEF diary
FEV1 ≥ 15% decrease after 6 mins of exercise

25. Prolonged expiration exp,inspiratory rhonchi
Signs
Depend on severity
Conscious level normal-………. coma
Respiratory rate normal-tachypnoea-…….apnoea
Blood pressure hypertension(vasculitis) paradox
Pulse rate
Position
Chest examination normal in mild type
hyperinflation in chronic one
Prolonged expiration exp,inspiratory rhonchi

26. Level of asthma control

27. Management approach based on asthma control
Management approach based on asthma control. For children older than 5 years, adolescents and adults. (ICS = inhaled corticosteroid) *Receptor antagonist or synthesis inhibitors

28. Management approach based on asthma control
Management approach based on asthma control. For children older than 5 years, adolescents and adults. (ICS = inhaled corticosteroid) *Receptor antagonist or synthesis inhibitors

29. How to use a metered-dose inhaler.

30. Classification of severity of asthma exacerbations.
Symptoms  Speech
Mild Breathlessness With activity Sentences
Moderate With talking Phrases
Severe At rest Words
Impending Respiratory Failure At rest Mute
    

31. Mild Moderate Severe Impending Respiratory Failure
Signs
  Body position
Able to recline Prefers sitting Unable to recline Unable to recline
  Respiratory rate
Increased Increased Often > 30/min > 30/min  
 Use of accessory respiratory muscles
Usually not Commonly Usually Paradoxical thoracoabdominal movement

32. Moderate Severe Impending Respiratory Failure
 Pulsus paradoxus (mm Hg) Mental status
Mild < May beagitated
Moderate –25 Usually agitated Sever often > Usually agitate
Impending Often absent   Confused or drowsy

33. Mild Moderate Severe Impending Respiratory Failure
 Breath sounds Heart rate (beats/min)
Moderate wheezing at mid- to end-expiration < 100
Loud wheezes throughout expiration
Loud inspiratory and expiratory wheezes > 120
Little air movement without wheezes Relativebradycardia  
   

34. Mild Moderate Severe Impending Respiratory Failure
Functional assessment   
 PEF (% predicted or personal best)
> – < 50 or response to therapy lasts < 2 hours < 50   
SaO2 (%, room air)
> – < < 91  
 PaO2 (mm Hg, room air)
  Normal > < < 60   
PacO2 (mm Hg)
< <

35. Immediate treatment of patients with acute severe asthma.

36. Indications for assisted ventilation in acute severe asthma
Coma
Respiratory arrest
Deterioration of arterial blood gas tensions despite optimal therapy
PaO2 < 8 kPa (60 mmHg) and falling
PaCO2 > 6 kPa (45 mmHg) and rising
pH low and falling (H+ high and rising)
Exhaustion, confusion, drowsiness

38. Symbicort® efficacy enhanced by Turbuhaler Device
Device Comparison for lung deposition
Symbicort® efficacy enhanced by Turbuhaler Device
36%
Diskus 12%
Fine particles lead to higher lung deposition that leads to higher improvement in lung function1-5
Tubuhaler offers 3 times lung deposition than the diskus
1. Borgstrom L et al., Int J Clin Pract, 2005, 59, 12, Thorsson L et al., Int Journal of Pharmaceutics 168 (1998)
3. Usmani O, AM J Resp and Critical Care Medicine, vol ; Selroos et al., Treat Resp Med 2006; 5 (suppl 48): 584S.
5. Selroos et al., Treat Resp Med 2006; 5 (5):

39. Symbicort®… The only combination treatment offering flexibility in prescription1
1 inhalation
every morning
Extra doses
when needed
1 inhalation
every evening
1. Symbicort Turbuhaler 160/4.5 mg/dose SX Leaflet text

40. Many thanks

41. Q
QUIZ