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cholinergic and adrenergic drugs from objectives list

acetylcholine (ACh)

-nicotinic and muscarinic agonist
-released @ first synapse outside spinal cord
-nt of PNS (acts on muscarinc receptors @ effector site)
-nt of SNS (ONLY on muscarinic receptors on sweat glands)
-short half-life, broken down by AChE (basement membrane of synaptic cleft) or BChE (plasma)

arecoline (Betel nuts)

-partial agonist of M1, M2 and M3 receptors
-PNS effects (pupillary constriction, bronchoconstriction)


-competitive antagonist of muscarinic receptors
-effects entirely dependent on normal (tonic) activity of PNS (may stimulate or inhibit depending on whether PNS is inhibiting or stimulating. Unmasks SNS effects)
-potent, highly specific
-crosses BBB (tertiary amine)
- decreases bronchial resistance to airflow, GI motility and secretions, bladder tone, secretions (including sweating) and HR (@ low doses); therapeutic doses increase HR; dilates pupils; usu no effect on BP
-primary tx for AChE inhibitors

botulinum toxin (Botox)

-inhibits ACh release from pre-synaptic neurons (different toxins interfere with different proteins required for vessicle fusion) leading to muscle paralysis
-used cosmetically to paralyze facial muscles and decrease wrinkles
-nerve recovery can occur by proximal axonal sprouting and muscle re-innervation by formation of a new neuromuscular junction


-non-depolarizing neuromuscular blocking agent (paralysis)
-competitive antagonist of nAChR at NMJ (does not cross BBB)
-used for people with liver dysfunction who cannot metabolize rocuronium
-can reverse effects w/ AChE inhibitors (allows more ACh to compete for receptors)


-very short acting AChE inhibitor (@ anionic site)
-used to dx MG (frees up more ACh to interact with receptors)
-does not cross BBB (charged quaternary ammonium group)


-muscarinic antagonist
-does not cross BBB (charged quaternary ammonium group)
-tx for GI disorders (decreases stomach acid secretion)
-used pre-anesthesia to block secretions
-used with AChE inhibitors (ie, NM block reversal agents like neostigmine) to prevent muscarinic side effects (ie bradycardia)


-neuronal and neuromuscular nicotinic receptor antagonist
-cause sympatholytic and parasympatholytic side effects (blocking ganglia)
-does not cross BBB (charged quaternary ammonium group)
-used as an experimental tool, not so much clinically


-inhibits AChE (carbamylates esteratic site, + quaternary ammonium binds anionic site)
-intermediate duration of action (usu 2-4 hours)
-does not cross BBB
-tx for MG
-used to reverse non-depolarizing NM blockers


-activates muscarinic receptors (for which they are named)
-toxicity leads to PNS symptoms (secretions everywhere, decreased heart rate)
-charged quaternary ammonium group but DOES cross BBB


-agonist of nicotinic receptors in muscle and CNS (higher affinity for CNS receptors)
-increase HR and BP (stimulation of ganglia and adrenal medulla, which lead to stimulation of CV reflex), CNS arousal
-used to aid in smoking cessation


-OP insecticide, AChE inhibitor
-absorbed via skin, mucous membranes, orally
-metabolized to paraoxon, which leads to headaches, convulsions, poor vision, vomiting, abdominal pain, diarrhea, tremor, dyspnea (with possible pulmonary edema and respiratory arrest), loss of consciousness
-toxicity treated w/ atropine


-AChE inhibitor (carbamlyates esteratic site)
-tx for MG
-tx for anticholinergic toxicity (ie, overdose of atropine, scopalamine, etc)
-can cross BBB


-muscarinic agonist
-tx for glaucoma (causes pupillary constriction and increased tension in ciliary body which decrease intraocular pressure)
-tx for dry mouth secondary to radiation therapy
-stimulate sweat glands for CF dx
-occasionally used to tread muscarinic antagonist toxicity


-binds OP-inactivated AChE
-oxime group removes P, + amine group binds anionic site
-can reverse OP poisoning if given early enough (high affinity for P group, removes from esteratic site of AChE)
-aka "2-PAM"


-AChE inhibitor (carbamylates esteratic site)
-does not cross BBB
-used a prophylaxis for nerve agents (ie Soman) in Gulf War
-used to treat MG and othostatic hypotension


-non-depolarizing neuromuscular blocking agent (paralysis)
-competitive antagonist of nAChR at NMJ (does not cross BBB)
-can reverse effects w/ AChE inhibitors (allows more ACh to compete for receptors)


-AChE inhibitor (phosphorylates esteratic active site, essentially irreversible)
-used as a biological weapon, can be absorbed thru skin or inhaled
-initial symptoms are increased secretions, followed by n/v/d and urination, muscle twitches that may lead to spasms
-treated with atropine and pralodixime


-muscarinic competitive antagonist, relative of atropine (but more CNS effects)
-used pre-anesthesia for sedation, amnesia, and to block secretions
-prevents motion sickness


-depolarizing neuromuscular blocking agent (paralysis)
-agonist of nicotinic receptors at NM junction (not ganglionic N receptors)
-creates a "deadzone" around end plate via prolonged depolarization; fiber can't be re-activated
-slowly hydrolyzed by BChE
-onset w/i 30 sec, lasts 5-10 min


-partial agonist of neuronal nicotinic receptor (primary effects are in CNS)
-aids in smoking cessation
-brand name "Chantix"


-beta-2 agonist
-fast-acting bronchodilator
-AEs may include tachycardia, htn, dry mouth, muscle cramps, h/a. nervousness, and other sympathomimetic responses


-increases NE release from pre-synaptic neurons (indirect)
-stimulates CNS
-treats narcolepsy and hyperkinetic syndrome
-AEs include tolerance, dependence, CV stimulation, mydriasis, dry mouth, psychosis


-selective beta-1 antagonist
-tx for htn and angina w/o neg AEs for those w/ compromised pulm function
-special considerations for diabetics (will block insulin release and GNG)
-does not cross BBB
-half-life ~6 hours


-alpha-2 agonist (inhibits NE release)
-specificity towards the presynaptic alpha-2 receptors in vasomotor center in the brainstem.
-tx for htn, off-label use as analgesic, tx for ADHD, reverse the effects of stimulants.....
-AEs include dry mouth, constipation, sedation, rebound htn


-SNS stimulant (inhibits uptake of NE, and DA)
-general sympathymimetic
-bad things happen when abused


-beta-1 agonist
-increases strength of cardiac contraction w/o increasing rate (greater inotropic than chronotropic effect)
-increase CO in heart failure pts
-AEs include tachycardia, htn, arrhythmias


-alpha-1 and beta-1 agonist (and dopamine receptor)
-increases NE release
-low doses --> reduced renal arterial resistance, inotropic effect (via beta-1 receptors)
-high doses --> vasopressor (alpha-1)
-tx for cardiogenic or septic shock, heart failure
-given as a drug cannot cross BBB, but endogenously an essential nt


-alpha-1 antagonist
-tx for htn (relaxes vascular sm musc,)
-tx for BPH (relaxes bladder)
-AEs include h/a, fatigue, tachycardia, chest pn, dyspnea,


-increases NE release from pre-synaptic neurons (indirect) but can also stimulate beta-2 and alpha-1
-response similar to epi, but slower and more persistant
-not broken down by MAO and COMT
-crosses BBB
-vasopressor, relaxes bronch sm musc (beta-2), stimulates CNS (insomnia, agitation, nausea), treats nasal congestion
-can cause dydriasis

epinephrine- CV

-endogenous agonist of adrenergic receptors
-low doses decrease BP (prefer beta-2 receptors --> vasodilation)
-high doses increase BP (alpha-1 effects stronger)
-increased ventricular contraction (beta-1), SV, CO
-initially increase HR, then slow due to vagal reflex
-decreased blood flow to skin and sk musc (@ high concentrations); increased flow to sk musc (@ low concentrations), hepatic flow, renal vascular resistance, pulm pressure, coronary blood flow

epinephrine- sm musc & metabolism

-relaxes bronch sm musc (beta-2)
-relaxes GI sm musc (alpha-2, beta-2)
-increases GI sphincter contraction (alpha-1)
-non-pregnant uterine relaxation (beta-2), pregnant uterine contraction (alpha-1)
-increased glucose and lactate from musc and liver glycogenolysis (beta-2)
-increased free fa (beta-3)
-increased insulin release (alpha-2)
-increased O2 consumption (via increased metabolism)

epinephrine- uses, AEs

-prolongs anasthesia
-cardiac arrest/heart block
-AEs include anxiety, h/a, cerebral hemorrhage


-blocks adrenergic neurons (disrupts AP --> nt release process, displaces NE from storage granues, blocks reuptake of NE)
-decreases vascular tone in aa and vv
-tx for htn
-orally effective, but slow and variable
-does not cross BBB
-may cause postural hypotension


-beta-1&2 agonist (bronchodilator and cardiac stimulant)
-increased CO due to positive inotropic and chronotropic effects
-reduced peripheral vasc resistance (decreased diastolic BP, systolic may increase but mean is decreased)
-relaxation of bronch and GI sm musc
-increased fa release
-insulin release
-erratic oral absorption, metabolized by COMT
-AEs include anxiety, h/a, cerebral hemorrhage, tolerance, fatal arrhythmias at large doses


-beta (and alpha-1) antagonist
-reduces peripheral vascular resistance, tx for htn
-doesn't significantly alter HR or CO
-may cause dizziness, drowsiness, weakness


-selective alpha-1 agonist
-not a catecholamine --> orally acitve, long availability


-selective beta-1 antagonist
-tx for htn and angina w/o neg AEs for those w/ compromised pulm function
-special considerations for diabetics (will block insulin release and GNG)
-overdose can cause hypotension, bradycardia, metabolic acidosis, seizures, cardiorespiratory arrest.


-endogenous alpha-1&2 and beta-1 receptor agonist
-vasoconstriction due mostly to alpha-1, some alpha-2 (arterial and venous, increases systolic and diastolic BP)
-decreases HR due to vagal reflex
-tx for hypotension
-AEs include anxiety, h/a, cerebran hemorrhage, arrhythmias, pulm edema


-non-selective, competitive alpha antagonist
-manages catacholamine excess (ie, pheochromocytoma)
-long duration (1-5 days)
-AEs include postural hypotension and reflex tachycardia


-non-selective, competitive alpha antagonist
-manages catacholamine excess (ie, pheochromocytoma)
-AEs include postural hypotension and reflex tachycardia


-selective alpha-1 agonist
-metabolized by MAO
-decreases secretions in nasal mucosa, dilates pupil, increases BP


-beta antagonist
-ISA (Intrinsic Sympathomimetic Activity- in high doses exerts effects like epi)
-tx for htn, angina
-half-life 3-4 hours


-alpha-1 competitive antagonist
-tx for primary htn
-vv less sensitive than aa, therefore postural hypotension not as much of a problem
-reflex tachycardia can occur, but not enhanced by increase release of NE (feedback on alpha-2 receptors still happens)


-non-selective beta antagonist
-also suppresses renin/angiotensin system @ kidney, effects take a while to develop
-tx for htn, arrhythmias, angina
-decreases HR, CO, conduction velocity, blood flow (to all areas but brain) and O2 consumption
-increases airway resistance (caution for asthma/COPD)
-inhibits glycogenolysis (caution for DM)
-AEs include heart failure (in compromised pts), cold extremeties, fatigue
-90% bound to plasma proteins, 1/2 life ~ 3 hrs
-crosses BBB


-blocks adrenergic neurons (inhibits uptake of NE into vesicles so it's broken down by MAO)
-tx for htn
-AEs include sedation and psychic depression


-beta-2 agonist
-relax sm musc (delay premature labor)
-AEs include increased HR, BP, arrhythmia


-beta-2 agonist (long-acting)
-bronchodilator (tx- inhaled for asthma and COPD)


-selective alpha-1 antagonist
-tx for htn and BPH
-may lead to reflex tachycardia
-AEs may include orthostatic or postural hypotension, syncope, nasal congestion


-beta-2 agonist
-fast-acting bronchodilator (when inhaled)
-delay premature labor (off label use)
-AEs include cardiac and CNS stimulation


-alpha antagonist, higher affinity for alpha-2
-tx for sexual dysfunction
-AEs include tachycardia, htn, dizziness, hallucinations, h/a, and panic attacks

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