Dental Pharmacology - Ans
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This document discusses the autonomic nervous system and pharmacology of adrenergic and cholinergic drugs. It describes the types and functions of adrenergic receptors and lists direct-acting, indirect-acting and mixed adrenergic agonists. It also discusses adrenergic receptor blockers and their uses for conditions like hypertension. The document outlines the actions of cholinergic receptors and lists cholinergic agonists and their clinical uses. It concludes by discussing anticholinergic agents and ganglionic blockers.
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Dental Pharmacology - Ans
- 6. ADRENERGIC AGONISTS (SYMPATHOMIMETIC AGENTS) • Adrenergic agonists mimic the actions of sympathetic. • Adrenergic neurons release norepinephrine as the primary neurotransmitter. • NA from the synaptic cleft diffuses into circulation and gets inactivated by catechol-O- methyltransferase (COMT) and monoamine oxidase ( MAO)
- 8. Types, Distribution and Functions of Adrenergic Receptors
- 10. 1. Direct-acting Sympathomimetics Adrenergic Agonists Receptor Action Therapeutic Uses 1. Directly acting Adrenaline a1-, a2-, B1-, B2- and Anaphylactic shock, Bronchial asthma (acute), Cardiac arrest, to prolong the Duration of local anaesthesia, to control Epistaxis (ABCDE) • Noradrenaline a1-, a2- and B1-agonist Hypotensivestates Isoprenaline B1- andB2-agonist Heart block, cardiac arrest • Dobutamine Relatively selective Cardiogenic shock due to acute B1-agonist myocardial infarction (MI), congestive cardiac failure (CCF) or cardiac surgery Salbutamol (Albuterol) SelectiveB2-agonists Bronchial asthma Phenylephrine Selective a1-agonists Vasopressor agents, nasal decongestants, as mydriatic (phenylephrine), allergic rhinitis • Naphazoline a1 + a2-agonists Nasal decongestants (a1-stimulation), • Clonidine, a-Methyldopa a2-agonists Hypertension
- 11. Adverse effects and contraindications direct-acting Adverse effects – They are tachycardia, palpitation, headache, restlessness, tremor and rise in BP. – The serious side effects are cerebral haemorrhage and cardiac arrhythmias. contraindicated in most of the cardiovascular diseases such as hypertension, angina, cardiac arrhythmias, CCF, etc
- 12. 2. Indirect-acting Sympathomimetics Adrenergic Agonists Receptor Action Therapeutic Uses 2. Indirectly acting Amphetamine They act by releasing NA Narcolepsy, attention-deficit hyperkinetic Methamphetamine disorder (ADHD) Methylphenidate 3. Mixed acting Ephedrine a1, a2, B1 and B2 (direct action) Intravenous ephedrine is used for the + releases NA (indirect action) treatment of hypotension due to spinal anaesthesia Dopamine a1, a2, B1 and D1 + releases NA Cardiogenic shock, CCF with oliguria
- 13. Adverse effects and contraindications Indirect-acting • The side effects are restlessness, insomnia, confusion, fatigue, tremor, hallucinations and suicidal tendencies. • The cardiac side effects are tachycardia, palpitation, hypertension, angina and cardiac arrhythmias
- 14. ADRENERGIC RECEPTOR BLOCKERS (SYMPATHOLYTIC AGENTS) • Adrenergic-receptor antagonists block the effects of sympathetic pathway.
- 16. Irreversible Nonselective a-Blocker Phenoxybenzamine • Peripheral vascular resistance is reduced due to the blockade of vascular α1-receptors. • Used in the treatment of pheochromocytoma. • The side effects are hypotension, tachycardia, palpitation, diarrhea, and impotence.
- 17. Reversible Nonselective a-Blocker Phentolamine • Has rapid onset but short duration of action. It is used intra-operatively during surgery of pheochromocytoma, in hypertensive emergencies • Adverse effects – They include tachycardia, palpitation, arrhythmias; angina and Myocardial Infraction may be precipitated.
- 18. Selective α1-Blockers Prazosin, Doxazosin, Tamsulosin, Terazosin • Prazosin is a potent and selective a1-adrenergic receptor blocker. • Doxazosin is the longest-acting, selective a1- blocker. • Tamsulosin – an uroselective a1-blocker (a1A). At low doses, it reduces the resistance to flow of urine with little effect on BP. – It is the preferred a1-blocker for the treatment of benign prostatic hyperplasia (BPH)
- 19. Selective α1-Blockers • Therapeutic Uses – Essential hypertension – Benign prostatic hyperplasia – Pheochromocytoma • Adverse effects – First-dose phenomenon: Within 30–90 min of oral administration of prazosin, severe hypotension and syncopal attacks may be seen with first dose. • Therefore, the initial dose should be small . It is usually given at bed time so that the patient remains in bed for several hours and the risk of syncopal attack is reduced
- 21. BETA-ADRENERGIC BLOCKERS Mechanism of action – competitively block β-receptors. Pharmacological actions – Cardiovascular system: • Decrease heart rate (negative chronotropic effect). • Decrease the force of myocardial contractility (negative inotropic effect). – Respiratory system: • Blockade of B2-receptors in bronchial smooth muscle can produce severe bronchospasm in patients with COPD and asthma. • Selective B1-blockers such as atenolol, metoprolol, etc. are less likely to cause bronchospasm. – Skeletal muscle: • On chronic use, B-blockers may cause skeletal muscle weakness and tiredness due to blockade of B2-receptors of the skeletal muscle and blood vessels supplying it. They also reduce stress-induced tremors. – Metabolic effects: • B-Blockers inhibit glycogenolysis and delay recovery from hypoglycaemia. • They also mask the warning signs and symptoms of hypoglycaemia – Eye: B-Blockers on topical administration decrease IOP
- 22. BETA-ADRENERGIC BLOCKERS • Therapeutic uses – Hypertension – Angina pectoris and MI: B-Blockers reduce myocardial O2 demand – Congestive cardiac failure , carvedilol, metoprolol and bisoprolol – Pheochromocytoma – Glaucoma ,Timolol – Prophylaxis of migraine: Propranolol, atenolol and metoprolol – Hyperthyroidism: The signs and symptoms of hyperthyroidism such as tachycardia, palpitation, tremor, anxiety, etc – Acute anxiety states
- 23. BETA-ADRENERGIC BLOCKERS • Adverse effects – CNS: Sleep disturbances, fatigue and mental depression. – CVS: Bradycardia, heart block – Muscular weakness and tiredness – Withdrawal symptoms – Mask the warning signs and symptoms of hypoglycaemia
- 24. CHOLINERGIC AGENTS (CHOLINOMIMETICS, PARASYMPATHOMIMETICS) • Acetylcholine is rapidly hydrolyzed by cholin- esterases it has no therapeutic application. Cholinergic receptors • Muscarinic: M1, M2, M3 Activated by muscarine, Ach. • Nicotinic: NM (Skeletal muscle), NN (neuronal ) Activated by nicotine, Ach.
- 25. Muscarinic Receptor Stimulation • Eye (M3) - miosis • Heart (M2) - bradycardia and a decrease in blood pressure • Lungs (M3) – bronchospasm, increase secretion • Gastrointestinal - increase in motility (M3) , and secretion (M1) . • Glands (M3) - increase Secretion-sweat, salivation, and lacrimation • Blood vessels (M3) – vasodilatation
- 26. Cholinergic agonists Directly acting (on the receptors) Pilocarpine Acetylcholine Carbachol Bethanechol Indirectly acting (anti-cholinesterase) Reversible Physostigmine Edrophonium Neostigmine Irreversible Organophosphorus compounds Parathion Malathion Sarin (nerve gases)
- 27. Clinical Uses Directly acting • Postoperative urinary retention, paralytic ileus and dry mouth Bethanechol • Glaucoma Carbachol, Pilocarpine • Xerostomia Pilocarpine
- 28. Clinical Uses Indirectly acting Reversible Anticholinesterases • Glaucoma Physostigmine • Atropine poisoning Physostigmine • Myasthenia gravis Neostigmine , Edrophonium • Curare poisoning and reversal of non-depolarising neuromuscular blockade Neostigmine • Postoperative urinary retention and paralytic ileus Neostigmine
- 29. Clinical Uses Indirectly acting • Irreversible Anti-cholinesterases Organophosphorus compounds insecticides Acute toxicity • Excessive muscarinic and nicotinic stimulations Muscarinic effects: - Diarrhea - Urination - Miosis - Bradycardia - Bronchoconstriction - Lacrimation - Salivation - Sweating Nicotinic effects: - Skeletal muscle excitation followed by paralysis - CNS stimulation :confusion, convulsions, coma, and death occurs usually due to respiratory failure.
- 30. Irreversible Anti-cholinesterases Management of Organophosphorus compounds toxicity : • Muscarinic effects: atropine ( antimuscarinic) • Regeneration of AChE: pralidoxime
- 31. ANTICHOLINERGIC AGENTS (CHOLINERGIC RECEPTOR BLOCKERS) SKELETAL MUSCLE RELAXENT
- 32. ANTIMUSCARINIC AGENTS • These drugs block muscarinic-receptor- mediated actions of acetylcholine on heart, CNS, smooth muscles and exocrine glands. • Leading to opposite action of parasympathommetics.
- 33. Pharmacological Actions • Central Nervous System – Inhibit vomiting centre – excitation , hallucinations, Sedation, coma (high dose) • Exocrine Glands – Decreased secretions (salivary, bronchiolar, sweat) • Smooth Muscle – Relax smooth muscles in gastrointestinal tracts and Delay gastric emptying constipation – Relax smooth muscles in the respiratory Bronchial dilation. – Urinary retention • Eye – Mydriasis , decrease Lacrimation • Cardiovascular – Tachycardia
- 34. Clinical Uses • Preoperative Medication : (Atropine ) – They inhibit salivary and bronchial secretions. – To prevent bradycardia during anaesthesia. • Sialorrhoea (hypersalivation):(glycopyrrolate, propantheline) – Used to decrease salivary secretion, e.g. during dental procedures. • COPD and bronchial asthma: (Ipratropium ,Tiotropium) – They produce bronchodilatation
- 35. Clinical Uses • Antispasmodics in intestinal, renal colic and dysmenorrhoea. (hyoscine N- butyl bromide) • Ophthalmologic Examinations (Tropicamide) • Parkinsonism —Benzhexol • Motion Sickness —Scopolamine (hyoscine).
- 36. ANTIMUSCARINIC Adverse Effects • Decreased secretions (salivary, bronchiolar, sweat) ……. Dryness of the mouth • Mydriasis • Hyperthermia • Tachycardia • Sedation • Urinary retention and constipation • Behavioral: excitation and hallucinations
- 37. GANGLIONIC BLOCKERS • Blockade of sympathetic ganglia results in marked hypotension. • Blockade of parasympathetic ganglia results in ‘atropine-like’ actions. • Nicotine is obtained from tobacco leaves. It has a prolonged blocking effect on the autonomic ganglia.
- 38. THE END
Editor's Notes
- Drugs Acting on Autonomic Nervous System Adrenergic Transmission The transmitter in the sympathetic system is noradrenaline (NA; norepinephrine). Nerves that synthesize, store and release NA are called adrenergic (sympathetic) nerves. Synthesis of catecholamines begins with the amino acid tyrosine, which is transported into the adrenergic neuron by active transport. In the neuronal cytosol, tyrosine is converted to DOPA by tyrosine hydroxylase and DOPA to dopamine (DA) by DOPA decarboxylase. Dopamine enters the storage vesicles of the nerve terminal by active transport, where it is converted to NA by the enzyme dopamine B-hydroxylase (this enzyme is present only in the storage vesicles); the NA formed gets stored in the vesicles. In the adrenal medulla, NA is further converted to adrenaline by N-methyltransferase. Small quantities of NA are released continuously into the synaptic cleft and large quantities during nerve stimulation (Fig. 3.18). Three processes are involved in the termination of action of released NA in the synaptic cleft (fate of released NA in the synaptic cleft): Most of the released NA is taken back into the adrenergic nerve terminals (neuronal reuptake), which is either stored in the vesicles or inactivated by mitochondrial monoamine oxidase (MAO) in the cytosol. Neuronal reuptake is the most important mechanism through which the termination of action of NA takes place in the synaptic cleft. Small amount of NA from the synaptic cleft diffuses into circulation and gets inactivated in liver by catechol-O-methyltransferase (COMT) and MAO. Small quantity of NA is transported into other tissues (extraneuronal uptake).
- Effect of activation of a1-receptors Blood vessels: Constriction. GI sphincter (anal): Increase in tone. Urinary sphincter: Increase in tone. Radial muscle (iris): Contraction (mydriasis). Effect of activation of presynaptic a2 -receptors Mediate negative-feedback control on NA secretion (i.e. stimulation of a2-receptors decreases the release of NA from sympathetic nerve endings). Drugs Acting on Autonomic Nervous System Effect of activation of postsynaptic vascular a2 -receptors Mediate stimulatory effects: Vasoconstriction and venoconstriction. Effect of activation of a2 –receptors on various secretions Beta cells of islets of Langerhans in pancreas: Decrease in insulin secretion. Ciliary epithelium: Reduction of aqueous humor secretion. Sympathetic nerve endings: Decrease in NA release. Effect of activation of 1-receptors Heart: Cardiac stimulation. Kidney: Promote renin release. Stimulatory effects due to activation of 2-receptors Liver: Stimulation of glycogenolysis. Skeletal muscle: Contraction. Ciliary epithelium: Increase in secretion of aqueous humor. Uptake of K+ into cells. Inhibitory effects due to activation of 2-receptors Bronchial, uterine (pregnant), vascular, bladder smooth muscles: Relaxation. In GI smooth muscle, activation of both a and B receptors cause relaxation. Effect of activation of 3-receptors Adipose tissue: Lipolysis.
- CCF = congestive cardiac failure Narcolepsy is a chronic sleep disorder characterized by overwhelming daytime drowsiness and sudden attacks of sleep
- (1) Pheochromocytoma A tumor consisting of cells that release amounts of norepinephrine and epinephrine into the circulation. Symptoms include hypertension, tachycardia, and arrhythmias.
- Withdrawal symptoms: Abrupt withdrawal of B-blockers after chronic use is dangerous because they can precipitate angina or frank myocardial infarction and even sudden death. This is due to the upregulation (supersensitivity) of B-receptors in response to prolonged blockade
- Glaucoma is a group of eye conditions that damage the optic nerve, which is vital to good vision. This damage is often caused by an abnormally high pressure in the eyes.
- Myasthenia Gravis It is an autoimmune disorder where antibodies are produced against NM receptors of NMJ, resulting in a decrease in the number of NM receptors.