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Bronchodilators sympathomimetics
- Bronchodilators like epinephrine, salbutamol, and terbutaline work by binding to beta-2 receptors in the lungs, relaxing smooth muscle and dilating airways. They have been used for thousands of years to treat respiratory conditions. - Sympathomimetic bronchodilators are classified as non-selective or beta-2 selective. Non-selective drugs like epinephrine activate both alpha and beta receptors and are more likely to cause side effects, while beta-2 selective drugs primarily target the lungs. - Inhalation is the preferred route of administration as it delivers drugs directly to the lungs, but oral and intravenous routes can also be used. Common side effects include
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Bronchodilators sympathomimetics
- 1. DR. FIROZ AHAKKIM MD RESPIRATORY MEDICINE BRONCHODILATORS
- 2. SYMPATHOMIMETICS NON- SELECTIVE EPINEPHRINE (ADRENALINE) EPHEDRINE ISOPRENALINE ORCIPRENALINE SYMPATHOMIMETICS β2- SELECTIVE SALBUTAMOL TERBUTALINE BAMBUTEROL FENOTEROL REPROTEROL PIRBUTEROL SALMETEROL EFORMOTEROL METHYLXANTHINES THEOPHYLLINE AMINOPHYLLINE CHOLINE THEOPHYLLINATE HYDROXYETHYL THEOPHYLLINE THEOPHYLLINE ETHANOLATE OF PIPERAZINE ANTICHOLINERGICS ATROPINE METHONITRATE IPRATROPIUM BROMIDE TIOTROPIUM BROMIDE BRONCHODILATORS
- 3. • In usefor thousand of years • Ephedra equisetina- used in ancient china • Modern sympathomimetics Are derivatives or analogues Based on structure of Epinephrine (adrenaline) SYMPATHOMIMETICS
- 4. They are bothalpha and beta adrenergic agonist that acts as a neurotransmitter in the sympathetic nervous system, Alpha receptor being predominantly stimulatory (vasoconstriction) and beta receptor predominantly inhibitory ( relaxation of smooth muscle in the respiratory tract, vasculature and uterus) SYMPATHOMIMETICS
- 5. β adrenergic receptors β2receptors produce bronchodilatation As well as vasodilatation β1 receptor stimulate heart muscle
- 7. • Are nonselective or poorly selective and are more likely to produce unwanted effects ( tachycardia, cardiac stimulation) • Adrenaline – alpha + beta 1 + beta 2 agonist • Ephedrine – alpha + beta 1 + beta 2 action • Isoprenaline – beta 1 + beta 2 agonist Non selective sympathomimetics
- 8. • The betaagonist produce bronchodilatation by stimulating beta 2 receptors situated in the smooth muscle of the bronchial tree, from the trachea down to the terminal bronchioles. This activates the enzyme adenyl cyclase , facilitating the conversion of ATP to cyclic AMP and resulting in the relaxation of smooth muscles in the bronchial wall. It also involves the activation of protein kinase with a reduction in ionic calcium concentration in bronchial smooth muscle Mechanism of action
- 10. • Other beneficialnon bronchodilator effects include enhanced mucociliary transport, diminished release of histamine and other chemical mediators of asthma from mast cells, inhibition of cholinergic neurotransmission and a possible increased ventilatory response to hypercapnia and hypoxia
- 11.
- 12. • Preferred routeis inhalation from MDI • 10 % of fraction leaving device reaches lungs, remaining impacting in oropharynx and being swallowed • Systemic side effects are generally insignificant in comparison to oral administration • Rapid onset of action compared with same drug taken orally • Onset of 3-6 min, 80% bronchodilatation in 5 min. Reaching peak in 30- 60 min, effect wearing off over 3-6 hr. Inhalation
- 13. • If unableto manage inhaled therapy • Slow onset of action , produce bronchodilatation after about 30 min and reaching a peak at 1-2 hr Oral medication
- 14. • In severeexacerbations • Onset of action is rapid, occuring within a few minutes and peak effect reached sooner than inhalation , duration of action being 4 hrs Parenteral medication
- 15. • When swallowedmay undergo conjugation in gut wall as well as in liver • Relatively small quantities of these drugs are excreted unchanged by the kidneys and dosage modification is unnecessary in renal insufficiency • Slightly penetrate the blood brain barrier and also cross placenta so that oral medication is perhaps better avoided in pregnancy. Metabolism and excretion
- 16. • Principal doselimiting adverse effect of beta agonist is Skeletal muscle tremors, particularly affecting hands. • Muscle cramps, tachycardia ( reduced peripheral vascular resistance, vasodilatation occuring as a result of stimulation of receptors in vascular smooth muscle) • Metabolic effects like hypokalemia, brought about by stimulation of pancreatic beta 2 receptors , resulting in increased insulin release and an intracellular potassium shift • Non specific effects – dryness of mouth, nausea , vomiting Adverse effects
- 17. • Paradoxical bronchoconstrictionoccuring after patients have taken beta 2 agonist by pressurized MDI or nebulization, are unusual and may be by drug or the constituent of propellant or physical charecteristics like temperature , ph , osmolality. • May worsen ventilation – perfusion mismatch in short term.may arise if pulmonary vessels that were previously reflexly constricted in response to local hypoxia are dilated by beta 2 receptor stimulation so that blood is shunted into areas of lung still relatively poorly ventilated. This can be overcome by administration of oxygen as a routine.
- 18. Drug oral doseIv bolus Iv infusion MDI Neb solution salbutamol 4mg tds 250µg 5µg /min initialy then 3 – 20µg/ min 100-200 µg 2.5- 5 mg terbutaline 5mg bd 250- 500 µg 1.5- 5 µg/ min 250- 500 µg 5-10 mg salmeterol 25-50µg formoterol 12- 24µg Dosage
- 19. • To relievewheeze • To prevent or reduce wheeze in patients with exercise induced asthma • Long acting bronchodilators may also be useful as a single dose before bedtime for patients who continue to experience nocturnal wheeze despite otherwise optimal treatment • Adrenaline ( epinephrine ) given to patients developing bronchospasm, serious upper airway narrowing, hypotension with collapse ( bee or wasp sting) (dose 3-5 ml of 1 : 10000 iv) Use in respiratory medicine