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Cholinergic Pharmacology (Clinical Use (M3 inhibitor is given to asthma…
Cholinergic Pharmacology
Parasympathetic System
There is dual control (para and sympa) with opposing roles in the gut, bladder and heart
Roles of the parasympathetic system include stimulating digestive juice secretion, slowing heart rate, constricting pupils and contracting bladder
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ACh first binds to nicotinic receptors (ion channel) and then it binds to muscarinic receptors (G-protein coupled)
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Muscarinic Receptors
M2: Heart. Activation slows the heart rate. Atropine is a drug used to block the M2 receptor to treat bradycardia
M3: Glandular + smooth muscle. Activation causes bronchoconstriction, sweating, salivary gland secretion
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Short acting drug to block M3 to treat bronchoconstriction = ipratropium bromide
Long acting drug: Tiotropium
Clinical Use
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Side effects of anticholinergics include worse memory, drying of mouth and constipation
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Nicotinic blockers are used to inhibit ACh to inhibit muscle activity and induce relaxation in surgery
Acetylcholinesterase inhibitors are used to treat myasthenia gravis to increase the amount of ACh available for signalling
ACh stimulates reuptake of dopamine. Dopamine is low in Parkinsons. Benzatropine blocks the reputake and increases the amount of dopamine at the cleft
Neuromuscular Junction
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Botulinum toxin degrades ACh vesciles in the neuromuscular junction, causing paralysis
Pathology
Nerve gas and insecticides irreversibly inhibit acetylcholinesterase so there is a huge accumulation of ACh
Accumulation at neuromuscular junction causes twitching, weakness, paralysis
Accumulation in the CNS causes confusion, convulsions and coma
Accumulation at muscarinic junctions causes defecation, salivation, urination and bradycardia