bronchial asthma dr. shaikh mujeeb ahmed assistant professor almaarefa college ims 423 block

Bronchial Asthma

Dr. Shaikh Mujeeb AhmedAssistant ProfessorAlMaarefa College

IMS 423 BLOCK

Intended Learning Outcomes

• Describe pathophysiology of Bronchial asthma• Enumerate the predisposing factors for

asthma• Describe the clinical features of asthma• Interpret the spirometry results lab results and

correlate with severity of the disease.

EpidemiologyAccording to epidemiological studies

asthma affects 1-18% of population of different countries.

What is Asthma?

• Asthma is a chronic inflammatory disease of

the airways characterized by variable recurring

symptoms,

• air flow obstruction, and

• bronchial hyper responsiveness.

Airway obstruction

• Episodic wheezing• Difficulty breathing, • Chest tightness, and • Cough that often is worse at night and in the

early morning.

Types of Asthma

• Extrinsic – initiated by type I hypersensitivity– Atopic

• Intrinsic – Non immune mechanisms– Respiratory tract infections– Exercise, – Ingestion of aspirin,– Emotional upset, and – Exposure to bronchial irritants such as cigarette

smoke.

Some allergens which may cause asthma

House-dust mites which live in carpets, mattresses and upholstered furniture

Spittle, excrements, hair and fur of domestic animals

Plant pollen

Pharmacological agents (enzymes, antibiotics, vaccines, serums)

Food components

(stabilizers, genetically modified products)

Dust of book depo-sitories

Etiology & Pathogenesis

Early phase response

Late phase response

Etiology & Pathogenesis

Extrinsic (Atopic) Asthma

Allergen

Mast cells release inflammatory

mediators

WBCs enter region and release more

inflammatory mediators

• Type I hypersensitivity

• Mast cells’ inflammatory mediators cause acute response within 10–20 minutes

• Airway inflammation causes late phase response in 4–8 hours

Role of T lymphocytes

T - Lymphocytes

TH 1 - Lymphocytes TH 2 - Lymphocytes

B - Lymphocytes B - Lymphocytes

Plasma Cells Plasma Cells

Ig G & Ig M Ig E

Intrinsic (Nonatopic) Asthma

• Respiratory infections – Epithelial damage, IgE production

• Exercise, hyperventilation, cold air– Loss of heat and water may cause

bronchospasm• Inhaled irritants

– Inflammation, vagal reflex• Aspirin and other NSAIDs

– Abnormal arachidonic acid metabolism

Aspirin and other NSAIDs

Airway Obstruction in Asthma

inflammatory

mediatorsairway

inflammation

bronchospasm

edema

impaired

mucociliary

function

epithelial

injury

increased

airway

responsiveness

airflow limitation

Pathologic anatomyMacroscopic changes:

• viscous mucous/ mucopurulent phlegm

• airway dyskinesia with zones of spastic contraction and paralytic expansion of bronchi

• obstruction of airway lumen

• lung emphysema, pneumosclerosis• RV and RA hypertrophy and dilation

Microscopic changes:

• Bronchial wall infiltration with mast cells, eosinophils, basophils and T-lymphocytes

• Edema of mucous and submucous tunics • Destruction of bronchial epithelium• Hypertrophy of bronchial smooth muscles,• Hyperplasy of submucous glands • Microvessels dilation

Muscles

Cartilage

Gobletcells

Bronchial glands

cells Ciliated

Bronchioles (section)

Muscle contraction

Mucosal edema

Mucus secretion increase

Asthma

Risk Factors for Developing Asthma

• Genetic characteristics• Occupational exposures • Environmental exposures

Diagnosing Asthma: Medical History

• Symptoms– Coughing– Wheezing– Shortness of breath– Chest tightness

• Symptom Patterns • Severity• Family History

Diagnosing Asthma

• Troublesome cough, particularly at night• Awakened by coughing• Coughing or wheezing after physical

activity• Breathing problems during particular

seasons• Coughing, wheezing, or chest tightness

after allergen exposure • Colds that last more than 10 days• Relief when medication is used

Diagnosing Asthma

• Wheezing sounds during normal breathing

• Hyperexpansion of the thorax

• Increased nasal secretions or nasal polyps

• Atopic dermatitis, eczema, or other allergic skin conditions

Diagnosing Asthma:Spirometry

Test lung function when diagnosing asthma

Spirometry

• Measurement of • Forced expiratory volume (FEV1 )• forced vital capacity (FVC)• FEV1/VC• Peak Expiratory Flow rate (PEFR)

Pulmonary Function Tests

Reversibility Test

Inhalational challenge test

• Administration of sequential increasing conc. of either histamine , methacholine or mannitol.

Diurnal variation in PEFR

Exercise induced Asthma

• Allergic skin testing• X-ray chest• Induced sputum

differential eosinophil count - >2%

• FENO

Management

Asthma is extremely common and causes considerable morbidity. The aims of treatment are to:

Abolish symptoms Restore normal or best possible lung function Reduce the risk of severe attacks Enable normal growth to occur in children Minimize absence from school or employment.

This involves:

• patient and family education about asthma • patient and family participation in treatment • avoidance of identified causes where possible • use of the lowest effective doses of

convenient medications to minimize short-term and long-term side-effects.

Control of extrinsic factors• Measures must be taken to avoid causative

allergens such as the house-dust mite, moulds and certain food stuffs (e.g eggs ,checolate), particularly in childhood.

• Active and passive smoking should be avoided, as should beta-blockers in either tablet or eye drop form.

• Individuals intolerant to aspirin may benefit by avoiding salicylates and should avoid NSAIDs.

• 50% of individuals sensitized to occupational agents may be cured if they are kept permanently away from exposure. The remaining 50% continue to have symptoms that may be as severe as when exposed to materials at work, especially if they were symptomatic for a long time before the diagnosis was made.

This emphasises: • the importance of the rapid identification of

extrinsic causes of asthma and their removal wherever possible (e.g. occupational agents, family pets)

• once extrinsic asthma is initiated, it may become self-perpetuating possibly by non-immune mechanisms.

Drug treatment • The mainstay of asthma therapy is the use of

therapeutic agents delivered as aerosols or powders directly into the lungs The advantages of this method of administration are that drugs are delivered direct to the lung and the first-pass metabolism in the liver is avoided; thus lower doses are necessary and systemic unwanted effects are minimized.

• Both national and international guidelines have been published on the stepwise treatment of asthma based on three principles:

1. Asthma self-management with regular asthma monitoring using peak flow meters and individual treatment plans discussed with each patient and written down.

2. The appreciation that asthma is an inflammatory disease and that anti-inflammatory (controller) therapy should be started even in mild cases.

3. Use of short-acting inhaled bronchodilators (e.g. salbutamol and terbutaline) only to relieve breakthrough symptoms. Increased use of bronchodilator treatment to relieve increasing symptoms is an indication of deteriorating disease.

Drugs used in asthma• Quick relief medication

– short acting β2 agonist (salbutamol, terbutaline) – oral steroids– Anticholinergic agents

• Long-acting relief/disease controllers - Long-acting β2 agonists - salmeterol,

formoterol - Sodium cromoglicate (mast cell stabilizer)- Leukotriene modifiers• Other agents with bronchodilator activity

– Theophylline preparations

• Steroid-sparing agents - Methotrexate - Ciclosporin - Gold - Intravenous immunoglobulin - Anti-IgE monoclonal antibody - Omalizumab

Asthma severity classification

Clinical course, severity

Daytime asthma symptoms

Nighttime awakenings

FEV1, PEF

Intermittent< 1 /week 2 and < /month >80%

predicted. Daily variability < 20%

Mild

persistent

1 /week but not daily > 2 /month

>80% predicted. Daily variability – 20-30%

Moderate persistent

Daily > 1 /week> 60 but < 80% predicted. Variability>30%.

Severe persistent

Persistent, which limit normal activity

Daily<60% predicted. Variability > 30%.

Level of Asthma control

Managing Asthma: Peak Expiratory Flow (PEF) Meters

• Allows patient to assess status of his/her asthma

• Persons who use peak flow meters should do so frequently

• Many physicians require for all severe patients

Managing Asthma: Peak Flow Chart

People with moderate or severe asthma should take readings:– Every morning– Every evening– After an

exacerbation– Before inhaling

certain medications

Source: “What You and Your Family Can Do About Asthma” by the Global Initiative For Asthma Created and funded by NIH/NHLBI

A stepwise approach to the management of asthma

• Step 1: Occasional use of inhaled short-acting β2-adrenoreceptor agonist bronchodilators

• Step 2: Introduction of regular ‘preventer’ therapy• Step 3: Add-on therapy• Step 4: Poor control on moderate dose of inhaled

steroid and add-on therapy: addition of a fourth drug

• Step 5: Continuous or frequent use of oral steroids

Acute severe asthma

Patients with acute severe asthma typically have:

• inability to complete a sentence in one breath • respiratory rate ≥ 25 breaths per minute • tachycardia ≥ 110 beats/min (pulsus

paradoxus, is not useful as it is only present in 45% of cases)

• PEF < 50% of predicted normal or best.

Features of life-threatening attacks are: • a silent chest, cyanosis or feeble respiratory

effort • exhaustion, confusion or coma • bradycardia or hypotension • PEF < 30% of predicted normal or best

(approximately 150 L/min in adults).

Treatment of severe asthmaAt home • The patient is assessed. Tachycardia, a high respiratory rate

and inability to speak in sentences indicate a severe attack. • If the PEFR is less than 150 L/min (in adults), an ambulance

should be called. (All doctors should carry peak flow meters.) • Nebulized salbutamol 5 mg or terbutaline 10 mg is

administered. • Hydrocortisone sodium succinate 200 mg i.v. is given. • Oxygen 40-60% is given if available. • Prednisolone 60 mg is given orally.

At hospital The patient is reassessed. Oxygen 40-60% is given. The PEFR is measured using a low-reading peak flow meter,

as an ordinary meter measures only from 60 L/min upwards.Measure O2 saturation with a pulse oximeter.

Nebulized salbutamol 5 mg or terbutaline 10 mg is repeated and administered 4-hourly.

Add nebulized ipratropium bromide 0.5 mg to nebulized salbutamol/terbutaline.

Hydrocortisone 200 mg i.v. is given 4-hourly for 24 hours.

• Prednisolone is continued at 60 mg orally daily for 2 weeks. • Arterial blood gases are measured; if the Paco2 is greater than

7 kPa, ventilation should be considered. • A chest X-ray is performed to exclude pneumothorax. • One of the following intravenous infusions is given if no

improvement is seen:

– salbutamol 3-20 μg/min, or – terbutaline 1.5-5.0 μg/min, or – magnesium sulphate 1.2-2 g over 20 min.

• Arterial blood gases should always be measured in asthmatic patients requiring admission to hospital. Pulse oximetry is useful in monitoring oxygen saturation during the admission and reduces the need for repeated arterial puncture. Features suggesting very severe life-threatening attacks are:

• a high Paco2 > 45 • severe hypoxaemia Pao2 < 60 despite treatment with

oxygen • a low and falling arterial pH.

A Public Health Response to Asthma: Interventions

• Medical management• Education• Environment • Schools