EXAM 2 Flashcards
Epinephrine
Endogenous catecholamine, direct acting, sympathomimetics, adrenergic agonist. alpha and beta agonist, released by adrenal chromaffin cells, complex action: alpha and beta summation. cardiac (beta 1 positive inotrope and chronotrope resulting in increased cardiac output) vascular(alpha 1 vasoconstriction in renal, cutaneous, and visceral blood flow but in beta 2 skeletal muscle blood flow dilation) and lung(beta 2 bronchodilator) effects. Remember that epi is crazy potent at beta 2 receptors, more than ne
albuterol
selective beta 2 adrenergic agonist. for asthma and bronchospasm.
phenylephrine
selective alpha 1 adrenergic agonist. vascular smooth muscle constriction(increased blood pressure). Topical oral, or parental. Decongestant and vasopressor
clonodine
adrenergic agonist. selective alpha 2. cns and presynaptic inhibition of sympathetic neurons. so sedation, analgesia, decreased sympathetic outflow from cns, decreased ne release. increased parasympathetic outflow from cns. hypotension and bradycardia.
phenoxybenzamine
-non selective alpha adrenergic antagonist.
-non competitive.
-irreversibly blocks a1 and a2. -decreases blood pressure and tpr
prazosin
-adrenergic antagonist
- selective alpha 1
- vasodilation at arterial and venous
-decrease tpr (afterload)
-decrease venous return (preload)
- antihypertensive used in congestive heart failure (because of its effects on preload and afterload)
- produces less reflex tachycardia than other vasodilators
propanolol
-adrenergic antagonist
-non selective beta
-decreased heart rate and contractility at b1
- bronchoconstriction at b2 (we want to avoid this this sucks and is a limitation on non selective betas)
bethanechol
-cholinergic agonist
- direct acting muscarinic
-synthetic choline ester
-muscarinic stimulation
-gi and bladder selectivity (m3)
-promotes voiding by contracting detrusor and relaxing trigone and sphincter
-treats urinary retention when obstruction is absent
cholinergic agonism
parasympathomimetics, decreased co, vasodilation, bronchoconstriction, increased gi motility, more pee, lacrimation in pupils.
-endogenous form is acetylcholine which is rapidly degraded by ache and plasma butrylcholinesterase
cholinergic antagonists
-parasympatholytics,
- blocks endogenous acetylcholine,
-most are competetive and direct so are reversible.
atropine
-muscarinic cholinergic antagonist
-natural anticholinergic alkaloid
-enters cns (non quaternary, toxic, excitation followed by depression)
-concerns are tachyarrythmia, gi stasis, and urine retention
-adjunct during general anesthesia
ipratropium
-muscarinic cholinergic antagonist
- semisynthetic alkaloid derivative
- decreased bronchoconstriction and airway secretions
-quaternary so restricted distribution, has to be done via inhalation
- asthma and copd
nmj blockers
-used adjunct during anesthesia
-relax skeletal muscle no sedative effects
-especially in abdominal wall
given iv
-used any time we need skeletal paralysis
- spare receptors are big deal here, they can cause bad things
-can cause respiratory paralysis(but can be prevented with antihistamine pretreatment)
-can cause vagal(parasympathetic) reflex which can be minimized with anticholinergics
-can cause ganglionic blockade ie hypotension which can manage with sympathetic adrenergic agonists
-malignant hyperthermia
pancuronium
-nmj blocker
-competitive
-nondepolarizing at motor plate end
- initial weakness followed by paralysis
- long acting (2-3 hours)
- can be outcompeted by ache inhibitor
-renal elimination (half life increased with renal disease
- no histamine release
-little ganglionic blockade
-tachycardia due to muscarinic block
mivacurium
-nmj blocker
-competitive
-non depolarizing
-short duration(15 min)
-rapid hydrolysis by plasma eneterases, so half life not increased with renal disease
- little ganglionic blockade
-promotes histamine release
succinylcholine
-nmj blocker
- non competetive
-depolarizing
-2 ach molecules linked together
- resistant to acetylcholinesterase
- not pharmacologically reversible
-depolarizes causing inhibition of nicotinic receptor impulse, then repolarizes to cause paralysis
-ultra short acting, 1 min onset, 4 min action
- hydrolyzed by butrylcholinesterases
- some histamine
-hyperkalemia from intracellular potassium release
neostigmine
ace inhibitor that can reverse competetive nmj blockers
atenolol
-antihypertensive
-beta 1 selective antagonist
-decreased sv by ventricular b1
-decreased hr by sa node b1
-temporary increase in tpr (baroreceptor reflex)