by prof. m.abdelaziz disorders of respiratory function main disorders of the respiratory system are...
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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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