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Dental Pharmacology - Ans

this course to give dental students the basic of pharmacology

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Dental Pharmacology - Ans

  1. 1. AUTONMOIC NEURVOUS SYSTEM DENTAL PHARMACOLOGY
  2. 2. 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)
  3. 3. Types, Distribution and Functions of Adrenergic Receptors
  4. 4. 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
  5. 5. 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
  6. 6. 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
  7. 7. 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
  8. 8. ADRENERGIC RECEPTOR BLOCKERS (SYMPATHOLYTIC AGENTS) • Adrenergic-receptor antagonists block the effects of sympathetic pathway.
  9. 9. ALPHA-ADRENERGIC BLOCKERS
  10. 10. 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.
  11. 11. 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.
  12. 12. 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)
  13. 13. 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
  14. 14. BETA-ADRENERGIC BLOCKERS
  15. 15. 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
  16. 16. 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
  17. 17. 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
  18. 18. 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.
  19. 19. 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
  20. 20. 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)
  21. 21. Clinical Uses Directly acting • Postoperative urinary retention, paralytic ileus and dry mouth Bethanechol • Glaucoma Carbachol, Pilocarpine • Xerostomia Pilocarpine
  22. 22. 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
  23. 23. 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.
  24. 24. Irreversible Anti-cholinesterases Management of Organophosphorus compounds toxicity : • Muscarinic effects: atropine ( antimuscarinic) • Regeneration of AChE: pralidoxime
  25. 25. ANTICHOLINERGIC AGENTS (CHOLINERGIC RECEPTOR BLOCKERS) SKELETAL MUSCLE RELAXENT
  26. 26. 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.
  27. 27. 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
  28. 28. 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
  29. 29. Clinical Uses • Antispasmodics in intestinal, renal colic and dysmenorrhoea. (hyoscine N- butyl bromide) • Ophthalmologic Examinations (Tropicamide) • Parkinsonism —Benzhexol • Motion Sickness —Scopolamine (hyoscine).
  30. 30. ANTIMUSCARINIC Adverse Effects • Decreased secretions (salivary, bronchiolar, sweat) ……. Dryness of the mouth • Mydriasis • Hyperthermia • Tachycardia • Sedation • Urinary retention and constipation • Behavioral: excitation and hallucinations
  31. 31. 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.
  32. 32. THE END

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