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Parasympathlytic (Cholinergic antagonists) (Anticholinergic ) (Cholinergic Blockers) A- antimuscarinic agents (Muscarinic Antagonists): " Agents with high binding affinity for muscarinic receptors but no intrinsic activity. Pharmacologic effects opposite of the muscarinic agonists. " Competitive (reversible) antagonists of ACh " Antagonistic responses include: decreased contraction of GI and urinary tract smooth muscles, dilation of pupils, reduced gastric secretion, decreased saliva secretion. A- antimuscarinic agents (Muscarinic Antagonists): 1-Atropine (belladonna alkaloid) " (Competitive inhibitors) . -bind to muscarinic receptors and prevent Ach binding. " reversible blockade of ACh at muscarinic receptors by competitive binding! -reversal effect of atropine by increasing ACh or agonist ----> decreased blockade -atropine is central & peripheral muscarinic blocker. Muscarinic receptor blockade does not interfere with transmission at autonomic ganglionic sites, the adrenal medulla, or skeletal muscle fibers. Sympathetic adrenergic functions are not affected. X X MUSCARINIC RECEPTOR BLOCKADE ALLOWS SYMPATHETIC DOMINANCE IN DUAL INNERVATED ORGANS X Atropine actions "Eye: *mydriasis *unresponsiveness to light *cycloplegia *increase IOP " GIT: reduce activity of GIT. " Urinary system: reduce hyper motility. " Cardiovascular system: at low dose bradycardia at high dose tachycardia " Secretions: reduce secretions Therapeutic uses of atropine 1-Ophthalmic: Ophthalmologic examinations. mydriatic & cycloplegic effects. 2-antispasmotic agent : relax GIT & bladder (Treatment of smooth muscle spasms). 3-antidot for cholinergic agonists: Rx of over dose of organophosphate 4-antisecretory agent: reduce secretions of respiratory tract and salivary gland . (Reduction of nasal and upper respiratory tract secretions in cold and flu) Pharmacokinetics of atropine " Absorbed & metabolized by liver. " Eliminated by urine. " Half life/4hr. " Parenteral preparations (derivatives) are more potent than the parent compounds. Adverse effects of atropine " Dryness of mouth " Blurred vision " Increase in IOP " Attack of glaucoma " Tachycardia " Constipation " CNS effects " Collapse of circulatory & respiratory systems " Urine retention Treatment of atropine poisoning " Ventilation " Cold spongy " Diazepam " physostigmin Antimuscarinic agents 2-scopolamine: " greater actions on CNS (than atropine) Low doses of scopolamine produce CNS effects that are not seen with equivalent doses of atropine. " (longer duration of action than atropine) *actions & uses: prophylaxis of motion sickness drug side effects : sedation , amnesic action Antimuscarinic agents 3-ipratropium useful in Rx of asthma & chronic obstructive pulmonary disease " Administration: by inhalation as aerosol (to provide maximal concentration at the site of action) Synthetic amtimuscarinic agent 1- Probanthine 2- Methanthelin bromide " uses : treatment of peptic ulcer "C/I "Glaucoma "Stomach obstruction "Old patient "Cardiac disturbance B- anti nicotinic agent " Nicotinic Antagonists: Agents that bind to cholinergic nicotinic receptors but do not have efficacy.(Competitive antagonists). Antinicotinic include : 1- Ganglion blockers 2- Neuromuscular blockers 1-ganglionic blockers 1-Hexamthonim 2-Pentamethanium 3-Trimethaphan. Pharmacological effects of ganglionic blockers: " Eye: mydriasis , paralysis of accommodation " Respiratory tract: reduce secretions " Salivary glands: xerstomia " GIT: reduce secretions & motility " Cardiovascular: decrease blood pressure " Urinary tract : urinary retention " Sweat glands: decrease sweating " CNS: no direct effects Uses " Operation of neurosurgery " Hypertension with phochromocytoma 2- Neuromuscular blocking drugs which block Ach at N-M-J(neuromuscular junction), classified as: A- Non-Depolarizing Agent:- Tubocurarine Gallamine Pancuronium B- Depolarizing Agent:- Suxamethonium Decamethonium succinylcholine Neuromuscular blockers: " Neuromuscular blockers: Drugs used during surgical procedures and in intensive care units to cause paralysis. " Since skeletal muscle contraction is elicited by nicotinic (NM) cholinergic mechanisms. " Neuromuscular blockers interfere with transmission at the neuromuscular end plate and lack CNS activity. Neuromuscular Blockers Na+ Na + Ca 2+ α Action Potential ACH β α ACH ACH ACH ACH ACH ACH α ACH β ACH ACH α Motor neuron ACH ACH ACH α β α ACHEsterase Skeletal Muscle A-non depolarizing: First drug is curarine(d- tubocurarine)(Plant alkaloid). " They act as competitive antagonists at the ACh receptors of the endplate(act by blocking nAChR). " Blockade by these agents (such as tubocurarine and pancuronium) can be reversed by increasing the amount of ACh in the synaptic cleft, for example, by the administration of a cholinesterase inhibitor. Tubocurarine " Causes muscle paralysis . " Rapid onset of action. " Therapeutic Use: " As a muscle relaxant in various surgical procedures. Mechanism of action 1- at low dose : combine with nicotinic receptors & prevent the binding of Ach(competitive blockers) 2-at high dose: block the ion channels of the end plate. Actions " Paralysis of :muscle of face & eye, fingers, limbs , neck, trunk & diaphragm muscles. Theraputic uses! " With anesthesia to relax skeletal muscles " In tetanus " Fractures. "Side effect 1-hypotention . 2- bronchospasm Drugs interactions 1- cholinestrase inhibitors e.g neostigmine, physostigmine & edrophonium. (produce antagonist effect) 2-halogenated hydrocarbon anesthetics e.g halothane (increased muscle relaxant ) 3-aminoglycoside antibiotics e.g gentamicin (increased muscle relaxant ) "Botulinum Toxin (Botox): " Toxin produced by the bacterium Clostridium Botulinum. " purified & highly diluted for therapeutic use " Prevents Acetylcholine release from the nerve terminal. " Produces flaccid paralysis of skeletal muscle , Inhibition lasts from several weeks to 3 to 4 months. " Immuno resistance may develop with continued use. Botulinum toxin • The acetylcholine vesicle release process is blocked by botulinum toxin Therapeutic use botulinum toxin • Dermatological / Cosmetic Uses: • Local facial injections of botulinum toxin are widely used for the short-term treatment (1–3 months per treatment) of wrinkles associated with aging around the eyes; neck and mouth to control muscle spasms and to facilitate muscle relaxation . • Local injection of botulinum toxin has also become a useful treatment for generalized spastic disorders (eg, cerebral palsy). • Most studies have used type A botulinum toxin, but type B is also available. • Prevent excessive sweating (palm). .
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