ANS Drugs (Exam 1) Flashcards
Neostigmine
inj, cattle horses pigs sheep
rumen atony, intestinal motility in horses, reversal of neuromuscular blockers. sometimes used to tx myasthenia gravis (immediate acting)
Pyridostigmine
same MoA as neostigmine but longer duration. Used to tx myasthenia gravis in small animals
Oral
Edrophonium
anticholinesterase
used in dx of myasthenia gravis
Carbamate Insecticides
Muscarinic signs/DUMBBELS then nictonic excitment and eventually nicotinic blockade.
Likely to cross the blood brain barrier leading to CNS excitement/seizures.
Organophosphate insectacides
clinical signs similar to carbamate toxicity but metabolize slower and bond irreversably. Can be tx w/ atropine.
Atropine
nonspecific muscarinic antagonist (dry secretions, slow Gi, increase HR, dilate airways, dilate pupils)
Used most to tx bradycardias and OP/Carbamite toxicity
Bethanechol
Oral med for contraction of detrusor m.
Muscarinic agonist w/ some selectivity for M3
Direct parasympathomimetic
Glycopyrolate
like atropine but doesn’t cross BBB
Slower onset and longer duration
Preferred in rabbits
Oxybutynin and Propantheline
Urinary antispasmodic
Direct antimuscarinic and spasmolytic effects on smooth muscle (bladder and large intestine)
Used for detrusor hyperreflexia
Epinerphrine
activates all adrenergic receptors
used for cardiac arrest, anaphylaxis/anaphylactiodd rxns
Norepinephrine
alpha agonist, b-1 at higher doses, minimal b-2
increases mean blood pressure can cause a baroreceptor reflex (reflex vagal bradycardia)
Dopamine
acts directly/indirectly on alpha and beta-1 receptors and dopamine receptors.
Low doses of dopamine act on _____ causing ______
peripheral dopamine receptors
dilation of vascular beds
Moderate levels of dopamine activate ________ causing _________
b-1 receptors
+ inotropic and chronotropic effects
High doses of Dopamine activate ________ and cause ______
a-1 receptors
release of NE leading to vasoconstriction
Dobutamine
selective beta-1 agonist
+ inotrope
Isoproterenol
nonselective b1&2 agonist
used to tx bradyarrhythmias or acute bronchoconstriction
Phenyephrine
selective a-1 agonist
sytemic- vasopressor
local- vasoconstriction
local eye- mydriatic
Ractopamine
agonist at b-3 (most) and b1&2
reduces fat deposition and increase muscle deposition food animals
Albuterol/Salbutamol
Selective b-2 agonist
aerosol bronchodilator
Salmeterol
b-2 agonist inhaler bronchodilator
Clenbuterol
selective b-2 agonist
syrup for horses w/ COPD and mucokinetic agent
Tetrabutaline
selective b-2 agonist bronchodilator
oral bioavail. in horse is terrible
Isoxsuprine
b-2 agonist that acts as a peripherial vasodilator (skeletal muscle, distal limb) and causes uterine relaxation
Sometimes used as a tocolytic in cattle
PPA
indirectly increases release of NE in bladder neck/urethra
direct a-1 agonist
used to tx small animals (dogs mostly) for urethral sphincter hypotonus
Can be used synergistically w/ estrogens
Ephedrine/Pseudoephedrine
indirect release of NE and some direct a-1 and beta activation
vasocontriction, cardiac stimulation, bronchodilation, urinary sphincter contraction, mydriasis)
Can be in some chinese herbal therapies and OTC
Phenoxybenzamine
nonspecific alpha antagonist the irreversibly binds used to tx urinary retension by relaxing the internal urethral sphincter (smooth muscle) manage pheochromocytoma (tumor of adrenal medulla) - manage hypertension and blood pressure spikes caused by catecholamine release
Prazosin
alpha-1 antagonist
tx urinary retention by relaxing smooth muscle sphincter
greater effect and faster onset than phenooxybenzamine but potentially greater cardiovascular effects
Propanolol
non-selective beta antagonist
causes bradycardia through decreased firing of SA node, decreased AV node conduction, decreased cardiac output and myocardial oxygen demand
used to tx supraventricular tachyarrhythmias
Metoprolol
beta-1 selective antagonist
tx of methylxanthine (chocholate toxicity)
Atenolol
b-1 selective antagonist
doesn’t cross the BBB as much as propanolol
Esmolol
selective beta-1 antagonist
inj, doesn’t cross BBB, 20 min duration of action
lacks membrane-stabalizing effects of propanolol
Reserpine
indirect acting sympatholytic
blocks vesicular monamine transporters thus reducing norepinephrine uptake into vesicles and leading to reduced storage of NE and mediator depletion.
Calming agents for equines in long stall rest
Succinylcholine Phase I
activation of nicotinic Ach receptors similar to what Ach would do. Depolarizing NMB prolongs depolariztion of the motor end plate and prevents complete repolarization and thus stimulation by acetylcholine.
During this phase muscle fasciculation (transient) followed by flaccid paralysis.
Succinylcholine Phase II
In phase II the nicotinic receptors stay in an inactivated state and cannot respond to acetylcholine
If phase II block is reached paralysis duration will be longer
used for ET tube placement, prevention of laryngeal spasm
Competitive neuromuscular blockers
competative antagonists w/ Ach for nicotinic receptors at the motor end plate that will result in more generalized flaccid muscle paralysis. Derived from curarie.
Pancuronium
Competative aganoist w/ Ach for Nic. receptors- result in flaccid muscle paralysis
significant amount excreted in urine, some metabolized by liver and a small amount excreted into bile
Atracurium
undergoes spontaneous degradation in plasma (doesn’t rely on hepatic or renal function for clearance)
Vecuronium and Rocuronium
primarily metabolized by the liver and excreted in bile and urine
How do you reverse competative neuromuscular blockers (curarie derived drugs)
cholinesterase inhibitors which may be combined w/ an antimuscarinic like atropine of glycopyrrolate to block muscarinic effects.
How is Rocuronium’s action terminated?
sugmmadex
