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

Objectives Defintion Epidemiology Clinical presentation Diagnosis Complication prognosis

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

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.

Typical symptoms include wheeze, cough, chest tightness dyspnoea

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.

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).

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

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 .

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.

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

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

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.

Normal bronchial tube

Bronchi in asthma

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).

Airway hyper-reactivity in asthma.

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

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.

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.

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.

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

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

Level of asthma control

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

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

How to use a metered-dose inhaler.

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       

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

Moderate Severe Impending Respiratory Failure  Pulsus paradoxus (mm Hg) Mental status Mild < 10 May beagitated Moderate 10–25 Usually agitated Sever often > 25 Usually agitate Impending Often absent   Confused or drowsy  

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

Mild Moderate Severe Impending Respiratory Failure Functional assessment     PEF (% predicted or personal best) > 80 50–80 < 50 or response to therapy lasts < 2 hours < 50    SaO2 (%, room air) > 95 91–95 < 91 < 91    PaO2 (mm Hg, room air)   Normal > 60 < 60 < 60    PacO2 (mm Hg) < 42 < 42 42 42

Immediate treatment of patients with acute severe asthma.

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

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, 1488-1495 2. Thorsson L et al., Int Journal of Pharmaceutics 168 (1998) 119-127 3. Usmani O, AM J Resp and Critical Care Medicine, vol 172 2005; 1497-1504 4. Selroos et al., Treat Resp Med 2006; 5 (suppl 48): 584S. 5. Selroos et al., Treat Resp Med 2006; 5 (5): 305-315

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

Many thanks

Q QUIZ