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46 Cards in this Set

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Botulinum toxin (botox)
Mechanism: Prevents Ach release into symaptic cleft by block exocytosis
Effect: Weakening of the muscle and eventual paralysis, treats focal distonias, torticollis, wrinkles, hyperhydrosis (sweating), strabismus (double vision), Blepharospasms (eye twitch)
Edrophonium
Mechanism: Reversible Anti-cholinesterase, short-term inhibition of AchE at the synaptic junction thus prolonging the effects of Ach
Can diagnose MG and Eaton Lambert, too short-acting to be used as treatment
Neostigmine
Mechanism: Reversible Anti-cholinesterase, prevents degradation of Ach in the synaptic cleft by AchE
Treats MG, Eaton Lambert
Physostigmine
Mechanism: Reversible Anti-cholinesterase, prevents AchE from breaking down synaptic Ach - can also cross BBB (so treats atropine poisoning)
Treats Glaucoma (topical).
Reversal of anticholinergic toxicity or induced paralysis in surgery.
Reversible Anti-cholinesterases
Edrophonium, Neostigmine, Pheostigmine
prolong receptor exposure to Ach by preventing it's degradation in the synaptic cleft by AchE
Irreversible Anti-Cholinesterase
Parathion
Used in nerve gas and pesticide to induce respiratory paralysis
Neuromuscular nicotinic agonists
Succinylcholine - depolarization blockade at neuromuscular jcn
Ach induced desensitization due to over-stimulation causes temporary muscle paralysis, useful during short procedures
Succinylcholine
Mechanism: neuromuscular nicotinic agonist:
Binds nicotinic receptor but is less susceptible to AchE degradation and thus over-stimulates the receptor causing brief paralysis due to desensitization - used pre-surgery
Neuromuscular nicotinic antagonists
Pancuronium - non-depolarizing competetive inhibitor
No depolarization means no contractions so flaccid paralysis - useful during surgery, long-acting
Pancuronium
Neuromuscular nicotinic antagonist - non-depolarizing competetive inhibitor, competes for Ach binding spots and prevents action potential
Flaccid paralysis for surgery
Muscarinic agonists
Ach, Pilocarpine, Methacholine, bethanacol
Pilocarpine (2x) and Methacholine (3x) are much more resistant to AchE and thus increase parasympathetic effects of Ach binding to Muscarinic receptors. Bethanacol is selective for muscarinic (won't effect nicotinic) so most useful systemically
Pilocarpine
muscarinic agonist - resists degradation by AchE thus prolonging parasympathetic responses
Glaucoma (applied topically to avoid side effects) and Sjrogens (dry mouth) by decreasing intra-ocular pressure and increasing salivation/ secretions
Methacholine
resistant to AchE degradation thus serves as a strong muscarinic agonist
Bronchoconstriction - Diagnose but not treat asthma (actually exacerbates symptoms)
Bethanacoll
Exclusive affinity for muscarinic receptors, won't bind nicotinic so useful as agonist post-surgery
Post-surgery clearing of bladder, stimulation of GI motility
Uses of Atropine
decreases SLUDGE - salivation, lacrimation, urination, diaphoresis (sweating), GI tract motility, emisis (vomiting)

Increases: pupil dilation, blood pressure
Can be used as treatment against parasympathetics OR can be poison (kids eating shiny red berries) - side effects include: cardiac arrhythmias, raised intraocular pressure, tachycardia,
constipation, xerostomia and blurred vision
Muscarinic antagonist
Atropine - causes sympathetic symptoms
increased HR (tachycardia), decreased urination, pupil dilation
Indirect adrenergeci agonist - Inhibitors of Catecholamine storage
Amphetamine, PseudoEphedrine
Amphetamine
Release NorE, block re-uptake of NorE, weak MAO inhibitor
treats ADHD and narcolepsy, commonly abused as recreational drug - ecstacy/ MDMA
Pseudoephedrine
Indirect Alpha & Beta agonist - Releases all stored catecholamines (Mainly NorE) from vesicles to synaptic termina
CNS stimulation and nasal/sinus decongestant
Inhibitor of Catecholamine metabolism
Iproniazid - MAO inhibitor, prevents re-uptake of NorE
treats depression but must NOT be used with tyramine containing foods (wine, cheese) because this also releases NorE thus there would be massive wave of sympathetics and emergency hypertensive crisis
Iproniazid
MAO inhibitor - increases effects of sympathetics (agonist) by preventing breakdown and recycling of NorE
treats depression - must avoid Tyramine containing foods because these release NorE too (too much norE=hypertension)
tricyclic antidepressants
imipramine - very non-specific but increases NorE in CNS
block 5HT re-uptake (as well as several receptors)
catecholamine re-uptake blockers
Cocaine, imipramine
Cocaine blocks NET and stops re-uptake of Dopamine and Serotonin (thus the fun effects) - highly addictive drug - cravings caused by depletion of DA from dopaminergic nerve terminals
Imipramine
Blocks NorE Transport (NET) to increase it in the CNS
antidepressant, can also cause cardiac arrythmias
Non-selective Alpha and Beta agonists
Oxymetazoline - vasoconstrictor - increases peripheral resistance and blood pressure but no direct effect on heart due to carotid sinus baroreceptor reflex
nasal decongestion and opthalmic hyperemia - can cause hypertension
Oxymetazoline
Non-selective alpha and beta agonist - vasoconstrictor
Used to treat nasal congestion and high eye pressure
Alpha 1 agonist
Phenylephrine - increases vasoconstriction of vascular smooth muscle
emergency treatment of shock and nasal decongestion
Alpha 2 agonist
Clonidine - decreases sympathetic outflow (Gi-inhibitory)
treats hypertension and drug withdrawal
Phenylephrine
Alpha 1 agonist - vasoconstriction
treats shock and nasal congestion
Clonidine
Alpha 2 agonist - decreases sympathetic output, lowers vasoconstriction
treats hypertension and drug withdrawal
Non-specific Alpha 1 and Alpha 2 antagonists
Phenoxybenzamine (irreversible) and phentolamine (reversible) - inhibits sympathetics
treat pheochromocytoma
Phenoxybenzamine
irreversible due to covalent binding - inhibits sympathetics
treat pheochromocytoma
phentolamine
reversible non-specific alpha1/alpha2 antagonist, inhibits sympathetics
treat pheochromocytoma
Tamsulosin
alpha 1 antagonist - selective for smooth muscle of genitourinary tract (alpha 1a)
treats BPH specifically
Prazulosin
alpha 1 antagonist - non-selective
used to treat BPH
Beta 1 agonist
Dobutamine - increases contractility to increase total cardiac output
acute heart failure
Dobutamine
Beta 1 agonist - increases contractility and total cardiac output
acute heart failure
Alpha 1 antagonists
Prazulosin & Tamsulosin
treat BPH
Beta 2 agonist
Albuterol - bronchodilator
treats acute asthma - short acting
Albuterol
Beta 2 agonist - bronchodilation
treat acute asthma - short acting
Non-selective beta blocker (B1 antagonist)
Propanalol
was used to treat hypertension but replaced now by more selective beta blockers due to side effects including severe bronchoconstriction
Propanolol
non-selective beta 1 antagonist (blocker)
was used to treat hypertension but replaced now by more selective beta blockers due to side effects including severe bronchoconstriction
Atenolol
Selective Beta 1 antagonist (blocker)
treats hypertension with fewer side effects for people with COPD and diabetes
Selective beta 1 antagonist (blocker)
Atenolol
safer treatment for hypertension
Partial Beta 1 and Beta 2 antagonism
Pindolol - dulls sympathetic response by competitively binding receptor (prevents NorE from binding)
hypertension
Pindolol
Partial blockage of Beta 1 and Beta 2 - through partial stimulation but prevention of NorE binding and causing full effect it dulls the sympathetic response
hypertension