Pharm Exan 2 Flashcards
acts to indirectly increase release of NE in the bladder neck and urethra to treat urinary incontinence. also has direct alpha 1 agonist activity
Phenylpropanolamine
nonspecific alpha antagonist that binds irreversibly to the receptor; used to treat urinary incontinence by relaxing the internal urethral sphincter; also to manage pheochromocytoma
Phenocybenzamine
alpha 1 antagonist used to treat urinary retention by relaxing the smooth muscle sphincter.
Prozasin
nonspecific beta antagonist; causes bradycardia, decreased AV node conduction, decreased cardiac output, ; used to treat tachyarrhythmias, feline hyperthyroidism and chocolate toxicity
propanalol
Beta 1 selective antagonist; long half life; better to be used to treat tachyarrhythmias in patients with asthma
Atenolol
Shortest duration of the “lols”
esmolol
Blocks NE uptake into the VEeesicles which reduces storage of NE and leads to mediator depletion; used to calm equines
Reserpine
The main inhibitory neurotransmitter in the CNS
Gamma-aminobutyric acid (GABA)
Part of the neuromuscular junction that interferes with synthesis, transport or release of acetylcholine.
Pre-synaptic
Part of the neuromuscular junction that interferes via stimulation of the nicotinic or alteration of the nicotinic acetylcholine receptor or acting on the muscle itself.
Post-synaptic
Depolarizing and noncompetitive neuromuscular blocker?
Succinylcholine
NMB: Activates nicotinic acetylcholine receptors but causes prolonged depolarization
Succinylcholine
NMB: not metabolized by acetylcholinesterase; just diffuses away
Succinylcholine
Clinical indications for this NMB include: endotracheal intubation, muscle relaxation during surgery, but should not be used during euthanasia
Succinylcholine
Duration of this NMB is around 2-3 mins but can be longer in ruminants and dogs
Succinylcholine
Pharmacological effects of this NMB is twitching followed by flaccid paralysis, transient bradycardia, increased IOP, Hyperkalemia due to twitching that releases K+.
Succinylcholine
Competitive NMB are non depolarizing or depolarizing?
non depolarizing
Nondepolarizing blocker that is mostly excreted unchanged by the kidney
pancuronium
nondepolarizing blocker that is mostly metabolized in the liver
Vecuronium and recuronium
nondepolarizing blocker that spontaneously degrades in plasma
Atracurium
Competitive blockers are reversed by:
cholinesterase inhibitors aka neostigmine or edrophonium
Sugammadex can terminate by chelation which competitive NMB?
Rocuronium
Most effective diuretic
Loop; 25 % Na Reabsorption
2nd most effective diuretic
Thiazide; 5% Na Reabsorption