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Bronchial AsthmaBronchial Asthma
A disease of the airways A disease of the airways
characterized by hyper-responsiveness characterized by hyper-responsiveness of the tracheo-bronchial tree to a of the tracheo-bronchial tree to a multiplicity of stimulimultiplicity of stimuli
Manifested: physiologically by Manifested: physiologically by widespread reversible narrowing of the widespread reversible narrowing of the air passages air passages
: clinically by paroxysm of : clinically by paroxysm of coughing, dyspnea, and wheezescoughing, dyspnea, and wheezes
Pathogenesis of AsthmaPathogenesis of AsthmaExposure to allergen synthesis of IgE: binds to mast cells in the Exposure to allergen synthesis of IgE: binds to mast cells in the
airway mucosaairway mucosa
Re-exposure to allergen/antigen Ag-Ab interaction on the surfaces of Re-exposure to allergen/antigen Ag-Ab interaction on the surfaces of the the mast cell triggers:mast cell triggers:
mediators of anaphylaxis:mediators of anaphylaxis: other mediators or a variety of other mediators or a variety of histamine, tryptase, PGDhistamine, tryptase, PGD22,, cytokines: cytokines:
leukotriene Cleukotriene C44, PAF, PAF interleukines 4 & 5, GMCSF, interleukines 4 & 5, GMCSF, TNF, TGFTNF, TGF
contraction of the airway contraction of the airway smooth smooth muscle muscle eosinophils & neutrophilseosinophils & neutrophils
ECP, MBP, Protease, PAFECP, MBP, Protease, PAF
edema, mucus hypersecretionedema, mucus hypersecretion increase in bronchial reactivity increase in bronchial reactivity
smooth muscle contractionsmooth muscle contraction
B. B. Inhaled irritants afferent Inhaled irritants afferent
pathways in the vagus nerves travel to pathways in the vagus nerves travel to the CNS efferent pathways from the CNS efferent pathways from the CNS travel to efferent ganglia the CNS travel to efferent ganglia postganglionic fibers release postganglionic fibers release acetylcholine binds to muscarinic acetylcholine binds to muscarinic receptors on airway smooth muscle receptors on airway smooth muscle bronchoconstriction bronchoconstriction
C. C. inhaled materials stimulate inhaled materials stimulate afferent receptors to initiate reflex afferent receptors to initiate reflex bronchoconstriction or release of bronchoconstriction or release of tachynins (substance P) directly tachynins (substance P) directly stimulate smooth muscle contractionstimulate smooth muscle contraction
Treatment of AsthmaTreatment of Asthma Aerosol delivery of drugsAerosol delivery of drugs
Should produce a high local Should produce a high local concentration in the lungs with a low concentration in the lungs with a low systemic delivery systemic delivery →→ minimizing side minimizing side effectseffects
Size of the particles: critical determinantSize of the particles: critical determinant >10 um – deposited in the mouth & >10 um – deposited in the mouth &
oropharynxoropharynx 0.5 um – inhaled, subsequently exhaled 0.5 um – inhaled, subsequently exhaled 1-5 um – allow deposition & most effective1-5 um – allow deposition & most effective
Treatment of AsthmaTreatment of Asthma
Aerosol delivery of drugsAerosol delivery of drugs Recommendation: slow, deep breath & Recommendation: slow, deep breath &
held for 5-10 secondsheld for 5-10 seconds
2-10%: deposited in the lung2-10%: deposited in the lung
To minimize systemic effects: To minimize systemic effects: poorly absorbed from the GIT poorly absorbed from the GIT Rapidly inactivated via first-pass hepatic Rapidly inactivated via first-pass hepatic
metabolismmetabolism Use of a large-volume “spacer”Use of a large-volume “spacer”
Treatment of AsthmaTreatment of Asthma
Aerosol delivery of drugsAerosol delivery of drugs 2 types of devices:2 types of devices:
Metered dose inhalers Metered dose inhalers Advantage: cheaper & portableAdvantage: cheaper & portable Disadvantage: most contain hydroflourocarbonsDisadvantage: most contain hydroflourocarbons
Nebulizers Nebulizers preferred for severe asthma exacerbations with preferred for severe asthma exacerbations with
poor inspiratory abilitypoor inspiratory ability Advantage: not requiring hand-breathing Advantage: not requiring hand-breathing
coordinationcoordination Can be delivered by face-mask to young children Can be delivered by face-mask to young children
& elderly& elderly
Treatment of AsthmaTreatment of Asthma Oral administration: Beta Adrenergic Receptor Oral administration: Beta Adrenergic Receptor
Agonists Agonists Has not gained wide acceptance Has not gained wide acceptance
Side Effects: tremulousness, muscle cramps, cardiac Side Effects: tremulousness, muscle cramps, cardiac tachyarrhythmias, metabolic disturbancestachyarrhythmias, metabolic disturbances
2 primary situations in which oral B adrenergic agonists 2 primary situations in which oral B adrenergic agonists are used:are used:
Brief courses of oral therapy are well tolerated & Brief courses of oral therapy are well tolerated & effective in young children who cannot manipulate effective in young children who cannot manipulate metered-dose inhalersmetered-dose inhalers
Local irritation with the use of aerosol preparationsLocal irritation with the use of aerosol preparations
Treatment of AsthmaTreatment of Asthma
Parenteral administrationParenteral administration
Indication:Indication:
Severe asthma requiring emergency Severe asthma requiring emergency treatment (when aerosolized therapy is not treatment (when aerosolized therapy is not available or has been ineffective)available or has been ineffective)
I. BronchodilatorsI. BronchodilatorsSympathomimetic AgentsSympathomimetic Agents
Directly relax airway smooth muscle by Directly relax airway smooth muscle by activating Gactivating Gss adenylyl cyclase-cAMP in the adenylyl cyclase-cAMP in the airway tissues that results in airway tissues that results in bronchodilatationbronchodilatation
Increase the conductance of large Ca+2-Increase the conductance of large Ca+2-sensitive K+ channels in airway smooth sensitive K+ channels in airway smooth muscle muscle → → hyperpolarization & relaxationhyperpolarization & relaxation
Inhibit release of inflammatory mediators & Inhibit release of inflammatory mediators & cytokines from the mast cells, basophils, cytokines from the mast cells, basophils, eosinophils, neutrophils, & lymphocytes eosinophils, neutrophils, & lymphocytes
Increase mucociliary transportIncrease mucociliary transport
a. Beta-2 Selective Agonistsa. Beta-2 Selective Agonists
Short-acting: Short-acting: Used only for symptomatic relief of asthmaUsed only for symptomatic relief of asthma
Terbutaline, albuterol, levalbuterol, Terbutaline, albuterol, levalbuterol, metaproterenol, pirbuterolmetaproterenol, pirbuterol
inhaled drugs: inhaled drugs: onset of action: 1-5 min., onset of action: 1-5 min., Peak effects: 15-30 min., Peak effects: 15-30 min., Duration of action: 2 – 6 hoursDuration of action: 2 – 6 hours
Terbutaline, albuterol, metaproterenolTerbutaline, albuterol, metaproterenol oral form: oral form:
DOA: 4-8 hrs.DOA: 4-8 hrs.
Terbutaline Terbutaline parenteral form (0.25mg SC)parenteral form (0.25mg SC)
a. Beta-2 Selective Agonistsa. Beta-2 Selective Agonists
Long acting: Long acting: Salmeterol, formoterolSalmeterol, formoterol
Given by inhalationGiven by inhalation
DOA: 12 hours or more DOA: 12 hours or more
Interact with corticosteroids to improve asthma Interact with corticosteroids to improve asthma controlcontrol
Salmeterol-fluticasoneSalmeterol-fluticasone Formoterol-budesonideFormoterol-budesonide
Not recommended as the sole therapy for asthmaNot recommended as the sole therapy for asthma
Used prophylactically in the treatment of asthmaUsed prophylactically in the treatment of asthma
b. Non-selective Beta-Agonists:b. Non-selective Beta-Agonists:
- EpinephrineEpinephrine- Rapid actingRapid acting- Injected SC or inhalationInjected SC or inhalation- Onset: 15 minutesOnset: 15 minutes- DOA: 60-90 minutesDOA: 60-90 minutes- SE: tachycardia, arrhythmias, worsening of the angina SE: tachycardia, arrhythmias, worsening of the angina
pectorispectoris
- EphedrineEphedrine- Longer duration of action Longer duration of action - Orally/parenterally administeredOrally/parenterally administered- Lower potencyLower potency- More pronounced central effects More pronounced central effects
- IsoproterenolIsoproterenol- Onset: 5 minutesOnset: 5 minutes- DOA: 60-90 minutesDOA: 60-90 minutes- SE: cardiac arrhythmiasSE: cardiac arrhythmias
I. BronchodilatorsI. BronchodilatorsMethylxanthine drugsMethylxanthine drugs
Caffeine (1,3,7-trimethyxanthine)Caffeine (1,3,7-trimethyxanthine) Theobromide (3,7-dimethylxanthene)Theobromide (3,7-dimethylxanthene) Theophylline (1,3-dimethylxanthine)Theophylline (1,3-dimethylxanthine)
Most commonly usedMost commonly used
Derivatives: Derivatives: AminophyllineAminophylline DyphyllineDyphylline oxtriptyllineoxtriptylline
I. BronchodilatorsI. BronchodilatorsMethylxanthine drugsMethylxanthine drugs
Mechanisms of action:Mechanisms of action:
inhibit cyclic nucleotide phosphodiesterases inhibit cyclic nucleotide phosphodiesterases →→ high high concentration of IC cAMP & cGMP concentration of IC cAMP & cGMP →→ smooth muscle smooth muscle
relaxationrelaxation = Cilomilast, Roflumilast, Tofimilast: Selective PDE4 = Cilomilast, Roflumilast, Tofimilast: Selective PDE4
inhibitorsinhibitors
inhibition of cell surface receptors for adenosineinhibition of cell surface receptors for adenosine = Enprofylline: xanthine derivative devoid of adenosine = Enprofylline: xanthine derivative devoid of adenosine antagonismantagonism
anti-inflammatory effect : inhibit synthesis & secretion of anti-inflammatory effect : inhibit synthesis & secretion of inflammatory mediators from mast cells & basophilsinflammatory mediators from mast cells & basophils
I. BronchodilatorsI. BronchodilatorsMethylxanthine drugsMethylxanthine drugs
Pharmacodynamics:Pharmacodynamics: CNS CNS : :
mild cortical arousal w/ increased alertness & deferral mild cortical arousal w/ increased alertness & deferral of fatigueof fatigue
nervousness; insomnianervousness; insomnia in high doses: medullary stimulation and convulsionsin high doses: medullary stimulation and convulsions primary SE: nervousness and tremorprimary SE: nervousness and tremor
CVSCVS: : have positive inotropic and chronotropic effectshave positive inotropic and chronotropic effects ArrhythmiaArrhythmia sinus tachycardia and increased cardiac outputsinus tachycardia and increased cardiac output rises the PVR and BP slightlyrises the PVR and BP slightly decrease blood viscosity and may improve blood flow decrease blood viscosity and may improve blood flow
(pentoxifylline)(pentoxifylline)
I. BronchodilatorsI. BronchodilatorsMethylxanthine drugsMethylxanthine drugs
Pharmacodymanics:Pharmacodymanics: GITGIT: :
stimulate secretion of gastric acid and digestive stimulate secretion of gastric acid and digestive enzymesenzymes
KidneysKidneys: : weak diureticsweak diuretics
Skeletal musclesSkeletal muscles: : have potent effects in improving contractility and in have potent effects in improving contractility and in
reversing fatigue of diaphragm in patient with COPDreversing fatigue of diaphragm in patient with COPD
Smooth muscleSmooth muscle: : inhibit antigen-induced release of histamine from inhibit antigen-induced release of histamine from
lung tissuelung tissue
I. BronchodilatorsI. BronchodilatorsMethylxanthine drugsMethylxanthine drugs
Pharmacokinetics:Pharmacokinetics: Absorbed readily & completely Absorbed readily & completely
Food slows the absorption of theophyllineFood slows the absorption of theophylline
40% protein bound40% protein bound
Distributed into all body compartmentsDistributed into all body compartments
Cross the placenta & pass into breast milkCross the placenta & pass into breast milk
Metabolism: liver by CYP 1A2 enzymeMetabolism: liver by CYP 1A2 enzyme
10% excreted unchanged10% excreted unchanged
Half-life: 3.5 hrs – children; 8 or 9 hrs – adultHalf-life: 3.5 hrs – children; 8 or 9 hrs – adult
Usual dose: 3-4 mg/kg every 6 hoursUsual dose: 3-4 mg/kg every 6 hours
I. BronchodilatorsI. BronchodilatorsMethylxanthine drugsMethylxanthine drugs
Drug Interactions:Drug Interactions: Erythromycin, cimetidine, cirrhosis, Erythromycin, cimetidine, cirrhosis,
CHF, acute pulmonary edemaCHF, acute pulmonary edema - - half-life half-life
Phenytoin, barbiturates, cigarette Phenytoin, barbiturates, cigarette smoking, rifampicin, oral smoking, rifampicin, oral contraceptivescontraceptives - - clearance clearance
I. BronchodilatorsI. BronchodilatorsMethylxanthine drugsMethylxanthine drugs
Toxicities:Toxicities: Sudden deathSudden death
Headache, palpitation, dizziness, nausea, Headache, palpitation, dizziness, nausea, hypotension, precordial painhypotension, precordial pain
Tachycardia, severe restlessness, agitation, Tachycardia, severe restlessness, agitation, emesis – plasma concentration of > 20 ug/mlemesis – plasma concentration of > 20 ug/ml
Focal & generalized seizures – 40 ug/mlFocal & generalized seizures – 40 ug/ml
I.I. BronchodilatorsBronchodilatorsAnti-Muscarinic AgentsAnti-Muscarinic Agents
Competitively inhibits the effect of acetylcholine Competitively inhibits the effect of acetylcholine at muscarinic receptors at muscarinic receptors →→ effectively block effectively block the contraction of the airway smooth muscle the contraction of the airway smooth muscle and increase in secretion of mucusand increase in secretion of mucus
Ipratropium bromideIpratropium bromide – a quarternary ammonium – a quarternary ammonium derivative of atropinederivative of atropine
TiotropiumTiotropium – structural analog of ipratropium, – structural analog of ipratropium, approved for COPD, permits once daily dosingapproved for COPD, permits once daily dosing
Delivered by aerosol (metered dose Delivered by aerosol (metered dose inhaler/nebulizer)inhaler/nebulizer)
Slightly less effective than beta agonistSlightly less effective than beta agonist
Effective in COPDEffective in COPD
II. Anti-inflammatoryII. Anti-inflammatory AgentsAgentsCorticosteroidsCorticosteroids
- Improving all indices of asthma: Improving all indices of asthma: severity of symptoms, tests of airway severity of symptoms, tests of airway caliber, bronchial reactivity, caliber, bronchial reactivity, frequency of exacerbation and quality frequency of exacerbation and quality of lifeof life
- Inhibiting airway inflammation: Inhibiting airway inflammation: - modulation of cytokine & chemokine modulation of cytokine & chemokine
production, production, - (-) of eicosanoid synthesis, (-) of eicosanoid synthesis, - (-) of accumulation of basophils, (-) of accumulation of basophils,
eosinophils & other leukocytes in lung eosinophils & other leukocytes in lung tissue, tissue,
- decrease vascular permeabilitydecrease vascular permeability
II. Anti-inflammatoryII. Anti-inflammatory AgentsAgentsCorticosteroidsCorticosteroids
- Preparations:Preparations: a. oral: a. oral: prednisoneprednisone b. IV: b. IV: methylprednisolonemethylprednisolone c. aerosol: c. aerosol: beclomethasone, flunisolide, beclomethasone, flunisolide,
budesonide, triamcinolone, fluticasone, budesonide, triamcinolone, fluticasone, mometasonemometasone
SESE: oral candidiasis, hoarseness, slow the rate : oral candidiasis, hoarseness, slow the rate of growth in children, decrease bone of growth in children, decrease bone mineral density, cataract, mood mineral density, cataract, mood disturbances, disturbances, appetite, & impaired appetite, & impaired glucose control in diabeticsglucose control in diabetics
- - CiclesonideCiclesonide
II. Anti-inflammatoryII. Anti-inflammatory AgentsAgentsCromolyn Sodium & NedocromilCromolyn Sodium & Nedocromil
- MOA: alteration in the function of delayed chloride MOA: alteration in the function of delayed chloride channels in the cell membrane, inhibiting cell channels in the cell membrane, inhibiting cell activationactivation- Inhibiting parasympathetic and cough reflexesInhibiting parasympathetic and cough reflexes
- Inhibition of the early response to Ag challengeInhibition of the early response to Ag challenge
- Inhibition of the inflammatory responseInhibition of the inflammatory response
- inhibiting mediator release from bronchial mast inhibiting mediator release from bronchial mast cellscells
- Suppressing the activating effects of chemotactic Suppressing the activating effects of chemotactic peptides on neutrophils, basophils & monocytespeptides on neutrophils, basophils & monocytes
- Taken prophylacticallyTaken prophylactically
- Used as aerosolUsed as aerosol
II. Anti-inflammatoryII. Anti-inflammatory AgentsAgentsCromolyn Sodium & NedocromilCromolyn Sodium & Nedocromil
- Effectively inhibit both antigen-and Effectively inhibit both antigen-and exercise-induced asthma & reducing exercise-induced asthma & reducing symptoms of allergic symptoms of allergic rhinoconjunctivitisrhinoconjunctivitis
- SESE: : - throat irritation, cough, mouth dryness, throat irritation, cough, mouth dryness, - chest tightness and wheezing, chest tightness and wheezing, - reversible dermatitis, reversible dermatitis, - myositis, myositis, - gastroenteritis, gastroenteritis, - pulmonary infiltration with eosinophils pulmonary infiltration with eosinophils
and anaphylaxisand anaphylaxis
II. Anti-inflammatory Agents II. Anti-inflammatory Agents Leukotriene-Synthesis InhibitorsLeukotriene-Synthesis Inhibitors
Leukotriene-Receptor AntagonistsLeukotriene-Receptor Antagonists Block the action of leukotrienes by : Block the action of leukotrienes by :
- inhibition of 5-lipoxygenase, thereby preventing - inhibition of 5-lipoxygenase, thereby preventing leukotriene synthesisleukotriene synthesis
- inhibition of the binding of leukotriene C4, D4, E4 - inhibition of the binding of leukotriene C4, D4, E4 to its cys-LT1 receptor on target tissues, thereby to its cys-LT1 receptor on target tissues, thereby preventing its action preventing its action
Drug categories Drug categories a. Zileuton a. Zileuton – a 5-lipoxygenase inhibitor– a 5-lipoxygenase inhibitor
- 600 mg QID- 600 mg QID - may cause hepatotoxicity- may cause hepatotoxicity - inhibits the formation of LTB4- inhibits the formation of LTB4
b. Zafirlukastb. Zafirlukast – 20mg BID – 20mg BID MontelukastMontelukast – 10mg OD – 10mg OD
- are Leukotriene D4-receptor - are Leukotriene D4-receptor antagonistsantagonists
II. Anti-inflammatoryII. Anti-inflammatory Agents Agents Leukotriene-Synthesis InhibitorsLeukotriene-Synthesis Inhibitors
Leukotriene-Receptor AntagonistsLeukotriene-Receptor Antagonists
ZileutonZileuton: absorbed rapidly: absorbed rapidly
metabolized extensively by metabolized extensively by CYPs & by UDP- glucuronosyltransferasesCYPs & by UDP- glucuronosyltransferases
short-acting drugshort-acting drug
half-life: 2.5 hrshalf-life: 2.5 hrs
93% protein-bound93% protein-bound
II. Anti-inflammatoryII. Anti-inflammatory Agents Agents Leukotriene-Synthesis InhibitorsLeukotriene-Synthesis Inhibitors
Leukotriene-Receptor AntagonistsLeukotriene-Receptor Antagonists
ZafirlukastZafirlukast: absorbed rapidly: absorbed rapidly
90% bioavailability90% bioavailability
99% protein-bound99% protein-bound
metabolized extensively by metabolized extensively by hepatic CYP2C9hepatic CYP2C9
half-life: 10 hrshalf-life: 10 hrs
II. Anti-inflammatoryII. Anti-inflammatory Agents Agents Leukotriene-Synthesis InhibitorsLeukotriene-Synthesis Inhibitors
Leukotriene-Receptor AntagonistsLeukotriene-Receptor Antagonists
MontelukastMontelukast: absorbed rapidly: absorbed rapidly
60 - 70% bioavailability60 - 70% bioavailability
99% protein-bound99% protein-bound
metabolized extensively by metabolized extensively by CYP3A4 & CYP2C9CYP3A4 & CYP2C9
half-life: 3 – 6 hrshalf-life: 3 – 6 hrs
II. Anti-inflammatoryII. Anti-inflammatory Agents Agents Leukotriene-Synthesis InhibitorsLeukotriene-Synthesis Inhibitors
Leukotriene-Receptor AntagonistsLeukotriene-Receptor Antagonists
Other Effects:Other Effects:
Have demonstrated an important role for Have demonstrated an important role for leukotrienes in aspirin-induced asthmaleukotrienes in aspirin-induced asthma
Their effect on symptoms, airway caliber, Their effect on symptoms, airway caliber, bronchial reactivity and airway bronchial reactivity and airway inflammation are less marked than the inflammation are less marked than the effects of inhaled corticosteroids, but they effects of inhaled corticosteroids, but they are almost equally effective in reducing the are almost equally effective in reducing the frequency of exacerbationsfrequency of exacerbations
Other Drugs in the Treatment of Other Drugs in the Treatment of AsthmaAsthma
1. Anti-IgE Antibodies1. Anti-IgE Antibodies- drugs that reduce the amount of IgE-bound - drugs that reduce the amount of IgE-bound to mast cellsto mast cells- inhibits synthesis of IgE by B-lymphocytes- inhibits synthesis of IgE by B-lymphocytes- - OmalizumabOmalizumab (anti-IgE MAb) (anti-IgE MAb)
= most important effect : reduction of the = most important effect : reduction of the frequency & severity of asthma exacerbationsfrequency & severity of asthma exacerbations
= delivered as a single SC injection q 2 – = delivered as a single SC injection q 2 – 4 weeks4 weeks
= 60% bioavailability= 60% bioavailability= peak serum levels: 7 – 8 days= peak serum levels: 7 – 8 days= half-life: 26 days= half-life: 26 days= elimination: liver reticuloendothelial = elimination: liver reticuloendothelial
system, bilesystem, bile
Other Drugs in the Treatment of Other Drugs in the Treatment of AsthmaAsthma
2. Calcium channel Blockers2. Calcium channel Blockers
- inhibit airway narrowing induced by - inhibit airway narrowing induced by variety of stimulivariety of stimuli
3. Nitric Oxide Donors3. Nitric Oxide Donors
- relaxation of smooth muscle and - relaxation of smooth muscle and vasculaturevasculature
- very lipophilic drug, can be inhaled as a - very lipophilic drug, can be inhaled as a gasgas
- more useful in pulmonary hypertension- more useful in pulmonary hypertension
Possible Future Possible Future TherapiesTherapies
Monoclonal antibodies directed Monoclonal antibodies directed against cytokinesagainst cytokines
Antagonist of cell adhesion Antagonist of cell adhesion moleculesmolecules
Protease inhibitorsProtease inhibitors ImmunomodulatorsImmunomodulators
Other Respiratory AgentsOther Respiratory Agents
Mucolytic AgentsMucolytic Agents1. Acetylcysteine (mucomyst)1. Acetylcysteine (mucomyst)
- reduce the thickness and stickiness of - reduce the thickness and stickiness of purulent and non-purulent pulmonary secretionspurulent and non-purulent pulmonary secretions
- antidote for paracetamol poisoning- antidote for paracetamol poisoning
2. Carbocysteine (SCMC)2. Carbocysteine (SCMC)- act by regulating and normalizing the - act by regulating and normalizing the
viscosity of secretion from the mucus cell of viscosity of secretion from the mucus cell of respiratory tractrespiratory tract
- decrease the size and number of mucus - decrease the size and number of mucus producing cellsproducing cells
3. Bromhexine3. Bromhexine- depolymerization of mucopolysaccharides, - depolymerization of mucopolysaccharides,
direct effect on bronchial glandsdirect effect on bronchial glands- liberation of lysosomal enzymes producing - liberation of lysosomal enzymes producing
cells which digest mucopolysaccharide fiberscells which digest mucopolysaccharide fibers
Mucokinetic & SecretolyticMucokinetic & Secretolytic 1. Ambroxol1. Ambroxol- increase respiratory tract secretions- increase respiratory tract secretions- enhance pulmonary surfactant production- enhance pulmonary surfactant production- stimulates cilia activity- stimulates cilia activity
ExpectorantExpectorant1. Vagal stimulants: glyceryl guiacolate, salt 1. Vagal stimulants: glyceryl guiacolate, salt solutionsolution2. Direct stimulants: KISS, bromhexine, SCMC, 2. Direct stimulants: KISS, bromhexine, SCMC, ambroxolambroxol
AntitussivesAntitussives1. Narcotic antitussives: heroin, codeine, 1. Narcotic antitussives: heroin, codeine, morphinemorphine2. Non-narcotic antitussive: 2. Non-narcotic antitussive: DextromethorphanDextromethorphan