By

Prof. M.ABDELAZIZ

Disorders of Respiratory Function

Main disorders of the respiratory system are :

1. Bronchial asthma

2. Cough

3. Allergic rhinitis

4. Chronic obstructive pulmonary disease

(COPD, also called emphysema)

Asthma

Asthma is a chronic inflammatory disorder of

bronchial airways that result in airway

obstruction in response to external stimuli

(as pollen grains, cold air and tobacco smoke).

Characters of airways in asthmatic patients :Characters of airways in asthmatic patients :

Airway hyper-reactivity: Airway hyper-reactivity: abnormal sensitivity ofabnormal sensitivity of

the airways to wide range of external stimuli. the airways to wide range of external stimuli.

InflammationInflammation• SwellingSwelling• Thick mucus production.Thick mucus production.

Bronchospasm Bronchospasm (constriction of the bronchial (constriction of the bronchial

muscles)muscles)..

http://link.brightcove.com/services/player/bcpid236059233?bctid=347806802

Symptoms of asthmaAsthma produces recurrent episodic attack of Acute bronchoconstriction Shortness of breath Chest tightness Wheezing Rapid respiration CoughSymptoms can happen each time the airways are irritated by inhaled irritants or allergens.

Causes Infection Emotional conditions Stress Exercise Pets Seasonal changes Some drugs as aspirin, β bockers

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

Asthma pathophysiology is quite difficult and insufficiently studied. Undoubtedly, in most cases the disease is based on 1 type hypersensitivity reaction. The genesis of any allergic reaction may be divided into immune, pathochemical and pathophysio-logic phases.

After involving into the airways allergens activate immunocompetent cells. As a result B-lymphocytes produce antibodies of Ig E class. In case of asthma T-lymphocytes are inhibited, so the activation of B-lympocytes and Ig E production are excessive, exceeding normal needs.

B-cell

Allergens

T-cell

Allergen-specificIgE

Further these antibodies bind to the surface of mast cells, basophils and eosinophils of bronchial mucous. When a new portion of allergen involves the respiratory system, it interacts with IgE-antibodies.

This is a first,

immune phase of

allergic reaction.

As a result of antigen-antibody reaction the peculiar “explosion” occurs. The membranes of mast cells, basophils and eosinophils of bronchial mucous wreck with output of biologically active substances (histamine, serotonin, chemotaxis factors, heparin, proteases, thromboxane, leukotrienes, prostaglandins),

which induce hyperergic inflammation, mucous

edema, spasm of smooth myocytes, glands

hypersecretion, viscous exudate formation in

bronchial lumen.

Airway fill with mucus

Muscles

contr

act

Airways swell

Asthma exacerbation, occurring as a result, is a clinical manifestation of the 3rd, pathophysiolo-gical, phase of allergic reaction.

The indicated mechanism is specific for atopic (exogenous) asthma genesis. In addition to this, autosensibilization of damaged pulmonary tissue, neuropsychic disturbances, corticoid insufficiency, adrenergic imbalance, impairment of arachidonic acid metabolism, genetic and some other factors probably play a certain role in genesis of nonatopic (endogenous) asthma.

Depending on etiology asthma is divided into:

1- exogenous (atopic) 2- and endogenous (non-atopic). By clinical course asthma is divided into1- intermittent (beginning, early) 2-and persistent (chronic, late). Depending on frequency of exacerbations,

limitations of patient’s physical activity and lung function persistent asthma is divided into:

mild, moderate and severe (lung function is assessed by forced expiratory volume in 1 second (FEV1) and peak expiratory flow (PEF) and daily variability of these parameters). There are also remission phase and exacerbations.

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%.

In recommendations of Global Initiative for Asthma (GINA) asthma is classified on the base of control assessment and is divided into well-controlled, partially controlled and uncontrolled.

Asthma control is considered as: daytime symptoms 2 /week; ability to engage in normal daily activity; the absence of nighttime awakenings as a result

of asthma symptoms; need in bronchodilators administration 2 /week; the absence of asthma exacerbations; normal or near normal lung function parameters.

Classic signs and symptoms of asthma are:

attacks of expiratory dyspnea shortness of breath cough chest tightness wheezing (high-pitched whistling

sounds when breathing out) sibilant rales

In typical cases in development of asthma exacerbation there are 3 periods – prodromal period, the height period and the period of reverse changes.At the prodromal period:

vasomotoric nasal reaction with profuse watery discharge,

sneezing, dryness in nasopharynx, paroxysmal cough with viscous sputum, emotional lability, excessive sweating, skin itch and other symptoms may occur.

At the peack of exacerbation there are:

expiratory dyspnea forced position with supporting on arms poorly productive cough

cyanotic skin and mucous tunics hyperexpansion of thorax with use of all

accessory muscles during breathing at lung percussion: tympanitis, shifted downward

lung borders at auscultation: diminished breath sounds,

sibilant rales, prolonged breathing-out, tachycardia.

in severe exacerbations: the signs of right-sided heart failure (swollen neck veins, hepatomegalia), overload of right heart chambers on ECG.

At the period of the reverse changes,

which comes spontaneously or under

pharmacologic therapy, dyspnea and breathlessness relieve

or disappear, sputum becomes not so viscous, cough turns to be productive, patient breathes easier.

The severe and prolonged asthma exacerbation with intensive progressive respiratory failure, hypoxemia, hypercapnia, respiratory acidosis,

increased blood viscosity and the most important sign is blockade of bronchial 2-receptors.

Stages: 1st - refractory response to 2-agonists (may be paradoxical reaction with bronchospasm aggravation)

2nd - “silent” lung because of severe bronchial obstruction and collapse of small and intermediate bronchi; 3rd stage – the hypercapnic coma.

In many cases asthma, particularly intermittent, manifests with few and atypical signs:

episodic appearance of wheezing; cough, heavy breathing occurring at night; cough, hoarseness after physical activity; “seasonal” cough, wheezing, chest tightness

(e.g., during pollen period of ambrosia); the same symptoms occurring during contact

with allergens, irritants; lingering course of acute respiratory

infections.

The complications of asthma exacerbations are:

pneumothorax lung atelectasis pneumonia acute or subacute cor

pulmonale asthmatic status.

Persistent asthma causes:

fibrosing bronchitis small bronchi

deformation and obliteration

emphysema pneumosclerosis, chronic respiratory

failure chronic cor pulmonale.

Asthma in childhood leads to growth inhibition and thoracic deformation.

Eosinophilia, moderate leukocytosis in blood count as well as increased serum level of Ig E can be found in patients with asthma, especially at asthma exacerbations.

Inflammatory cells, Curschmann's spirals (viscous mucus which copies small bronchi) and Charcot-Leyden crystals (crystallized enzymes of eosinophils and mast cells) can be observed in sputum.

Lab Data

hyperlucency of lung fields

low standing and limited mobility of diaphragm

expanded intercostal spaces

horizontal rib position.

especially in case of severe, persistent asthma, shows hypertrophy of right heart chambers.

Right axis deviation,Rs type complex in V1 lead,

low amplitude R in V5-V6 leads

Mild Intermittent Asthma Mild Persistent Asthma Moderate Persistent Asthma Severe Persistent Asthma

forced expiratory volume in 1 second (FEV1) and peak expiratory flow (PEF), which

The diagnosis and severity assessment of asthma is based mainly on parameters of

lung function. The most important of them are:

are measured during

spirometry at forced

breathing-out.

FEV1 and PEF directly depend on bronchial lumen size and elastic properties of surrounding lung tissue.

Expiration

Inspiration

PEF

Volume

FEF

FEF

PIF

Flow

Increase in FEV1 and PEF after inhalation of bronchodilators (2-agonists) of 15% and more is specific for asthma.

PEF also can be measured with the help of individual devices – peak flow meters

Typical clinical manifestations and lung function assessment are sufficient for diagnosis of asthma.

Airways Innervations Afferent nerves (sensory) Irritant receptors in upper airways. C-fiber receptors in lower airways.

Stimulated by :

Exogenous chemicals

Physical stimuli (cold air)

Endogenous inflammatory mediators

Efferent nerves (motor)

Parasympathetic supply

M3 receptors in smooth muscles and glands.

No sympathetic supply but B2 receptors in smooth muscles and glands

Aims of anti asthmatic drugs:

• To relieve acute episodic attacks of asthma (bronchodilators, quick relief medications).

• To reduce the frequency of attacks, and nocturnal awakenings (anti-inflammatory

drugs, prophylactic or control therapy ).

Anti asthmatic drugsBronchodilators

(Quick relief medications)

treat acute episodic attack of asthma

• Short acting 2-agonists• Antimuscarinics• Xanthine preparations

Anti-inflammatory Agents )control medications or

prophylactic therapy(

reduce the frequency of attacks

• Corticosteroids• Mast cell stabilizers• Leukotrienes antagonists• Anti-IgE monoclonal antibody• Long acting ß2-agonists

Anti asthmatic drugs

Bronchodilators : (Quick relief medications)are used to relieve acute attack of bronchoconstriction

1. 2 - adrenoreceptor agonists 2. Antimuscarinics3. Xanthine preparations

Sympathomimetics - adrenoceptor agonists

Mechanism of Action direct 2 stimulation stimulate adenyl

cyclase Increase cAMP bronchodilation

Inhibit mediators release from mast cells. Increase mucus clearance by (increasing

ciliary activity).

Classification of agonists Non selective agonists:

epinephrine - isoprenaline

Selective 2 – agonists (Preferable). Salbutamol (albuterol)

TerbutalineSalmeterolFormeterol

Non selective -agonists.Epinephrine Potent bronchodilator rapid action (maximum effect within 15 min). S.C. or by inhalation (aerosol or nebulizer). Has short duration of action (60-90 min) Drug of choice for acute anaphylaxis

(hypersensitivity reactions).

Nebulizer Inhaler

Disadvantages Not effective orally. Hyperglycemia CVS side effects:

tachycardia, arrhythmia, hypertension Skeletal muscle tremor Not suitable for asthmatic patients with

hypertension or heart failure.

Contraindication:

CVS patients, diabetic patients

Selective 2 –agonists drugs of choice for acute attack of asthma Are mainly given by inhalation (metered dose

inhaler or nebulizer). Can be given orally, parenterally. Short acting ß2 agonists

e.g. salbutamol, terbutaline Long acting ß2 agonists

e.g. salmeterol, formeterol

Short acting ß2 agonistsSalbutamol, inhalation, orally, i.v.

Terbutaline, inhalation, orally, s.c. Have rapid onset of action (15-30 min). short duration of action (4-6 hr) used for symptomatic treatment of acute

episodic attack of asthma.

Long acting selective ß2 agonists Salmeterol & formoterol: Long acting bronchodilators (12 hours) have high lipid solubility (creates depot effect) are given by inhalation are not used to relieve acute episodes of asthma used for nocturnal asthma (long acting

relievers). combined with inhaled corticosteroids to

control asthma (decreases the number and severity of asthma attacks).

Advantages of ß2 agonists Minimal CVS side effects suitable for asthmatic patients with hypertension or heart failure.

Disadvantages of ß2 agonists Skeletal muscle tremors. Nervousness Tolerance (B-receptors down regulation). Tachycardia over dose (B1-stimulation).

Muscarinic antagonists

Ipratropium – Tiotropium Act by blocking muscarinic receptors. Given by aerosol inhalation Quaternary derivatives of atropine Does not diffuse into the blood Do not enter CNS, minimal systemic side effects. Delayed onset of action Ipratropium has short duration of action 3-5 hr Tiotropium has longer duration of action (24 h).

Pharmacodynamics are short-acting bronchodilator. Inhibit bronchoconstriction and mucus secretion Less effective than β2-agonists. No anti-inflammatory action

Uses Main choice in chronic obstructive pulmonary

diseases (COPD). In acute severe asthma combined with β2-

agonists & steroids.

Methylxanthines Theophylline - aminophylline

Mechanism of Action are phosphodiestrase inhibitors cAMP bronchodilation Adenosine receptors antagonists (A1) Increase diaphragmatic contraction Stabilization of mast cell membrane

Bronchodilation

Bronchial tree

Bronchoconstriction

Adenyl cyclase

Phosphodiesterase

ATP

cAMP

3,5,AMP

B-agonists

TheophyllineAdenosine

Pharmacological effects :Bronchial muscle relaxationcontraction of diaphragm improve ventilationCVS: ↑ heart rate, ↑ force of contractionGIT: ↑ gastric acid secretionsKidney: ↑renal blood flow, weak diuretic actionCNS stimulation * stimulant effect on respiratory center. * decrease fatigue & elevate mood. * overdose (tremors, nervousness, insomnia,

convulsion)

Pharmacokinetics metabolized by Cyt P450 enzymes in liver T ½= 8 hourshas many drug interactions

Enzyme inducers: as phenobarbitone-rifampicin → ↑metabolism of theophylline → ↓ T ½.

Enzyme inhibitors: as erythromycin→ ↓ metabolism of theophylline → ↑T ½.

Uses Second line drug in asthma (theophylline) For status asthmatics (aminophylline, is

given as slow infusion).

Side Effects Low therapeutic index narrow safety margin

monitoring of theophylline blood level is necessary.

CVS effects: hypotension, arrhythmia. GIT effects: nausea & vomiting CNS side effects: tremors, nervousness,

insomnia, convulsion

Anti - inflammatory agents include:

Glucocorticoids Leukotrienes antagonists Mast cell stabilizers Anti-IgE monoclonal antibody (omalizumab)

Anti - inflammatory Agents:(control medications / prophylactic therapy)

reduce the number of inflammatory cells in the

airways and prevent blood vessels from leaking

fluid into the airway tissues. By reducing

inflammation, they reduce the spasm of airways

& bronchial hyper-reactivity.

GlucocorticoidsMechanism of action

Inhibition of phospholipase A2 ↓ prostaglandin and leukotrienes ↓ Number of inflammatory cells in airways. Mast cell stabilization →↓ histamine release. ↓ capillary permeability and mucosal edema. Inhibition of antigen-antibody reaction. Upregulate β2 receptors (have additive effect to

B2 agonists).

Pharmacological actions of glucocorticoids Anti-inflammatory actions Immunosuppressant effects Metabolic effects

– Hyperglycemia – ↑ protein catabolism, ↓ protein anabolism– Stimulation of lipolysis - fat redistribution

Mineralocorticoid effects: – sodium/fluid retention – Increase potassium excretion (hypokalemia) – Increase blood volume (hypertension)

Behavioral changes: depression Bone loss (osteoporosis) due to

Inhibit bone formation ↓ calcium absorption.

Routes of administration Inhalation:

e.g. Budesonide & Fluticasone, beclometasone Given by inhalation, given by metered-dose

inhaler Have first pass metabolism Best choice in asthma, less side effects

Orally: Prednisone, methyl prednisolone Injection: Hydrocortisone, dexamethasone

Glucocorticoids in asthma Are not bronchodilators Reduce bronchial inflammation Reduce bronchial hyper-reactivity to stimuli Have delayed onset of action (effect usually

attained after 2-4 weeks). Maximum action at 9-12 months. Given as prophylactic medications, used alone or

combined with beta-agonists. Effective in allergic, exercise, antigen and

irritant-induced asthma,

Systemic corticosteroids are reserved for: Status asthmaticus (i.v.).

Inhaled steroids should be considered for adults,

children with any of the following features using inhaled β2 agonists three times/week symptomatic three times/ week or more; or waking one night/week.

Clinical Uses of glucocorticoidsClinical Uses of glucocorticoids

1. Treatment of inflammatory disorders (asthma,

rheumatoid arthritis).

2. Treatment of autoimmune disorders (ulcerative

colitis, psoriasis) and after organ or bone marrow

transplantation.

3. Antiemetics in cancer chemotherapy

Side effects due to systemic corticosteroids Adrenal suppression Growth retardation in children Osteoporosis Fluid retention, weight gain, hypertension Hyperglycemia Susceptibility to infections Glaucoma Cataract Fat distribution, wasting of the muscles Psychosis

Inhalation has very less side effects: Oropharyngeal candidiasis (thrush). Dysphonia (voice hoarseness).

Withdrawal Abrupt stop of corticosteroids should be

avoided and dose should be tapered (adrenal insufficiency syndrome).

Mast cell stabilizerse.g. Cromolyn (cromoglycate) - Nedocromil act by stabilization of mast cell membrane. given by inhalation (aerosol, microfine powder,

nebulizer).Have poor oral absorption (10%)

Pharmacodynamics are Not bronchodilators Not effective in acute attack of asthma. Prophylactic anti-inflammatory drug Reduce bronchial hyper-reactivity. Effective in exercise, antigen and irritant-induced

asthma. Children respond better than adults

Uses Prophylactic therapy in asthma especially in

children. Allergic rhinitis. Conjunctivitis.

Side effects Bitter taste minor upper respiratory tract irritation (burning

sensation, nasal congestion)

Leukotrienes antagonistsLeukotrienes produced by the action of 5-lipoxygenase on

arachidonic acid. Synthesized by inflammatory cells found in the

airways (eosinophils, macrophages, mast cells). Leukotriene B4: chemotaxis of neutrophils Cysteinyl leukotrienes C4, D4 & E4:

bronchoconstriction  increase bronchial hyper-reactivity mucosal edema, mucus hyper-secretion

Leukotriene receptor antagonistse.g. zafirlukast, montelukast, pranlukast are selective, reversible antagonists of cysteinyl

leukotriene receptors (CysLT1receptors).

Taken orally. Are bronchodilators Have anti-inflammatory action Less effective than inhaled corticosteroids Have glucocorticoids sparing effect (potentiate

corticosteroid actions).

Uses of leukotriene receptor antagonists Are not effective to relieve acute attack of

asthma. Prophylaxis of mild to moderate asthma. Aspirin-induced asthma Antigen and exercise-induced asthma Can be combined with glucocorticoids (additive

effects, low dose of glucocorticoids can be used).

Side effects: Elevation of liver enzymes, headache, dyspepsia

Omalizumab is a monoclonal antibody directed against

human IgE. prevents IgE binding with its receptors on

mast cells & basophiles. ↓ release of allergic mediators. used for treatment of allergic asthma. Expensive-not first line therapy.

ASTHMA - definitionASTHMA - definition

Chronic inflammatory disorder of the airwaysChronic inflammatory disorder of the airways

Mast cells, eosinophils, T-lymphocytes

Recurrent episodes of wheezing, dyspnoea, and Recurrent episodes of wheezing, dyspnoea, and cough particularly at night and early morningcough particularly at night and early morning

Symptoms are associated with airflow limitation that Symptoms are associated with airflow limitation that is partly reversible either spontaneously or with is partly reversible either spontaneously or with therapytherapy

Bronchial hyperresponsiveness is present very often

COPD - definitionCOPD - definition

Chronic airflow limitation Chronic airflow limitation ( ( maximum expiratory flow, slow forced maximum expiratory flow, slow forcedemptying of the lungs) emptying of the lungs)

Airflow limitation is slowly progressiveand irreversible

Due to varying combinations of:• airway disease• emphysema

COPDCOPD

Chronic bronchitisChronic bronchitis

defined in clinical terms

chronic cough with sputum production

- (3 months a year, 2 successive years)

- excluded cardiac or other pulmonary causes

EmphysemaEmphysema

defined anatomically permanent,

destructive enlagrement of airspaces distal to the terminal bronchioles without obvious fibrosis

Chronic obstructive pulmonary disease

Interrelationship of chronic bronchitis and emphysema

Normal

Chronicbronchitis

Mixed(in variable

degree)

Emphysema

© Novartis

COPD - risk factorsCOPD - risk factors

Cigarette smokingCigarette smoking

11 - antitrypsin deficiency - antitrypsin deficiency

Solid fuel used for indoor heating or cooking without adequate ventilation

Heavily polluted environments

100

75

50

25

0

25

50 75

Age yrs

FEV

1%

Disability

Death

Never smokedNever smoked

Stopped Stopped atat

age 45 age 45 yrsyrs

Stopped Stopped atat

age 65 age 65 yrsyrs

Smoked regularlySmoked regularly

COPD - cellular and biochemical mechanismsCOPD - cellular and biochemical mechanisms

Inflammation: alveolar macrophages, neutrophilsInflammation: alveolar macrophages, neutrophils

Neutrophil and macrophage enzymes and oxidants

destroy components of extracellular matrix (collagen, elastin, fibronectine, proteoglycans)

Loss of cellular components of lung parenchyma: -elastase can induce apoptosis -cells exposed to oxidants may undergo apoptosis or necrosis

oxidative stress in smokers and in COPD patients

production of elastase, cathepsine G, collagenase

COPD - cellular and biochemical mechanismsCOPD - cellular and biochemical mechanisms

Destruction of lung parenchyma

ImbalanceImbalance

proteases antiproteases system

oxidants antioxidants

Small airwaysdisorder

Components of chronic obstructive pulmonary disease

Airflow limitationby spirometry

Chronic bronchitisEmphysema

Asthma

Simple bronchitis

Asthma with no airflow limitation

Emphysema

but no COPD

Asthma

Emphysema

Bronchitis

Bronchitis

trachea

bronchi

alveoli

Reversible airflow obstruction + ++ +

Airway inflammation + + + + +

Mucus hypersecretion + + + +

Goblet cell metaplasia + + +

Impaired mucus clearance + + + +

Epithelial damage ++ —

Alveolar destruction — ++

Smooth muscle hypertrophy + + —

Basement membrane thickening +++ —

Inflammation is an important component in the pathogenesis of asthma and COPD

The inflammatory response in asthma and COPD is markedly different, although some cell types are present in both diseases

The predominant inflammatory cells in asthma include Eosinophils Mast cells CD4+ T lymphocytes

The predominant inflammatory cells in COPD include Neutrophils CD8+ T lymphocytes Macrophages

The role of these cells in COPD is not fully understood

AsthmaSensitizing agent

COPDNoxious agent

Asthmatic airway inflammationCD4+ T-lymphocytesEosinophils

COPD airway inflammationCD8+ T-lymphocytesMacrophagesNeutrophils

Airflow limitation

Completelyreversible

Completelyirreversible

Asthma Normal DLCO Normal lung volume Normal elastic recoil Flow dominant BD

response

COPD Abnormal DLCO Hyperinflation Decreased elastic recoil Volume dominant BD

response

Sciurba FC, CHEST 2004;117S-124S

COPD is a chronic irreversible airflow obstruction, lung damage and inflammation of the air sacs (alveoli).

Smoking is a high risk factor Treatment:

Inhaled bronchodilators Inhaled glucocorticoids Oxygen therapy

Antibiotics specifically macrolides such as azithromycin to reduce the number of exacerbations.

Lung transplantation

Smoking CessationNicotinic receptor partial agonists such as varenicline Nicotine vaccine ,when nicotine is coupled to a carrier protein, it is possible to induce antibody formation to nicotineThe antibodies in the circulation then bind nicotine reversiblyThe binding, however, greatly slows delivery of nicotine to the brain, reducing its addiction potential. Clinical trials with nicotine vaccine are currently underway, and early studies show promise

Rennard, 2011

RimonabantIt is a canabinoid receptor antagonist that alters release of gamma amino butyric acid release which, in turn, modulates the release of dopamine that is the main downstream mediator of nicotine effectsFDA declined to approve rimonabant because of concerns for potential suicide risk Rennard, 2011

Inhaled bronchodilators Inhaled antimuscarinics (are superior to

β2 agonists in COPD) β2 agonists these drugs can be used either alone orcombined

salbutamol + ipratropium salmeterol + Tiotropium (long acting-less

dose frequency).

Summary

Drugs

B2 agonists

Salbutamol, terbutaline

– Short acting– main choice in acute attack of asthma– Inhalation

Adenyl cyclase

cAMPSalmeterol, formoterolLong acting, Prophylaxis

Nocturnal asthma

Antimuscarinics

Ipratropium (Short)

Tiotropium (long)

Main drugs For COPD

Inhalation

Inhalation

Blocks M receprtors

Xanthine derivatives

Theophylline

Aminophylline

(orally)

(parenterally)

•Inhibits phosphodiesterase cAMP

Bronchodilators (relievers for bronchospasm)

Corticosteroids

(Inhibits phospholipase A2)

Dexamethasone, Fluticasone, budesonide

Inhalation

prednisoloneOrally

Hydrocortisoneparenterally

Mast stabilizers

Cromoglycate (Cromolyn), Nedocromil

Inhalation, prophylaxis in children

Cysteinyl antagonists (CyLT1 antagoist)

Zafirlukastorally

Omalizumab (Anti IgE antibody)Injection, SC

Anti-inflammatory drugs (prophylactic)

What is the treatment of bronchial asthma?1.SABA2.LABA3.ICS4.Anticholinergics5.Antileukotriens6.IGE antagonists7.PDEI8.Anti-mediators9.Anti-inflammatory10.Interleukin antagonists11.Others

What is the treatment of COPD?1.SABA2.LABA3.ICS4.Anticholinergics5.Antileukotriens!!!!!!!6.IGE antagonists!!!!!!!7.PDEI8.Anti-mediators9.Anti-inflammatory10.Interleukin antagonists!!!!!!!!11.Others

Hansel and Barnes Lancet 2009; 374: 744–55

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