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)
propranolol
-antihypertensive
-beta non selective antagonist
- same as atenolol except not selective
prazosin
-antihypertensive
-alpha a1 selective antagonist
-block a1=vasodilation
- temporarily increase cardiac output (baroreceptor reflex)
-no real positive considerations
–causes hypotension (first dose phenomena)
–reflex tachycardia
–fluid retention
carvedilol
-antihypertensive
-beta(decreased co) and alpha 1 antagonist(decreased tpr)
-competitive
clonidine
-antihypertensive
-alpha 2 selective agonist
-sympatholytic
- reduce cns sympathetic activity
- baroreceptor reflexes maintained
- rebound hypertension if discontinued
aliskiren
-antihypertensive
-renin inhibitor
prevents angioteninogen to ang 1
- efficacious and well tolerated
benazepril
-antihypertenisve
-ace inhibitor
-prevents ang1 to ang 2
-decreased sympathetic ns activity
- decrease vasoconstriction
-decrease tubular sodium and water retention
- decrease collecting duct water absorption
- efficacious and well tolerated
vasodilators
-disrupt excitation contraction coupling in vascular smooth muscle
- ec coupling
—depolarization activated calcium chennels from sarcoplasmic reticulum. increase myosin light chain kinase which makes contraction
prazosin
-vasodilation
-alpha 1 selective antagonist
nifedipine
-vasodilator
-vascular specific calcium channel antagonist (no effect on sa or av nodes
- calcium channel blocker (allosterically decrease ca channel activity)
-temp increase co due to baroreceptor reflex
nitroglycerine
-vasodilator
-exogenous no donor
-pure is explosive
- iv sublingual, oral, transdermal
- predominantly venous dilation
-decreases myocardial o2 demand
- manage chest pain, coronary artery disease, congestive heart failure,
,tolerance develops over time
sildenafil
- vasodilator
- pde5 inhibitor
-pde5 converts cGMP to 5’GMP
-so increases cGMP
-more cGMP=more PKG= less calcium= vasodilation
-pde5 is predominantly on pulmonary arteries
overall diuretics
-increase sodium and water excretion
- decrease blood volume
- decrease preload and co
- decrease bp
acetazolamide
-carbonic anhydrase inhibitor
-carbonic anhydrase catalyzes the conversion of co2 and water to carbonic acid
-ca inhibition (caiv) in the tubule lumen accumulation of hco3
-ca inhibition (caII) in tubule cells decreased hco3 formation and reabsorption
-increase in bicarbonate and sodium in pct
-promotes excretion of hco3
-mild diuresis and net loss of hco3
-metabolic acidosis
mannitol
-diuretics
- osmotic diuretic
- do not bind to receptors
-small non toxic molecules which are freely filtered into the tubular lumen but not reabsorbed
-keeps water in tubule via osmosis
-oppose osmotic pull of reabsorbed sodium
- more h2o excreted/ less reabsorbed
-used in emergency situations like cerebral edema, glaucoma, and renal failure
not used for peripheral edema because it can cause an initial rise in extracellular fluids and does not promote sodium elimination
furosemide
-diuretic
-loop diuretic
-block reabsorption of na cl and k
-increased exccretion of na cl ca k and water
- ihibit na k 2 cl symporter in the thick ascending limb
-high cieling diuretic. very effective
-used in edema heart failure renal dysfunction liver dysfunction and hyperkalemia
-side effects are hypokalemia, ototoxicity and water depletion
hydrochlorothiazide
-thiazide diuretic
-block reabsorption of na and cl
-increased excretion of na cl and k
-blocks nacl symporter in dct
-moderate diuresis
-blocks 5% na reabsorption
-useful in long term treatment of hypertension and heart failure
-decrease ca2 excretion to help with oesteoperosis and kidney stones
- side effects are k depletion, hyperlipidemia, glucose intolerance, water depletion
amiloride
- k sparing diuretic
-collecting tubule
-na channel inhibitor
-weak diuretic
-used in mild to moderate hypertension - promote k reabsorption
-treat hypokalemia
-useful in combination with thiazide or loop
side effects hyperkalemia
procainamide
-antiarrythmic
-class 1A sodium channel blocker
-moderate conduction slowing
- moderate sodium channel blockade
-increases effective refractory period
- used in supraventricular tachycardia
- blocks open na channels leading to an increased threshold of excitability
lidocaine
-class 1b sodium channel blocker
-antiarrythmic
-little change in conduction velocity
-shortens refractory period
-binds to inactivated sodium channels
—keeps them in inactivated state
—depolarization =inactivation
-effect is more in depolarized tissue
- less automaticity in deplarized cells
- rapid kinetics at normal resting membrane potentials
-slower kinetics at depolarized resting membrane potentials (damaged cells)
-used in ventricular tachycardia
flecainide
-class 1c sodium channel blocker
-antiarrythmic
-little change in refractory period
-profound decrease in conduction velocity
-used in life threatening ventricular tachycardia or fibrillation and for the treatment of refractory supraventricular tachycardia
amiodarone
-class III AP prolonging antiarrhythmic
-block k channels prolonging action potential
- dont affect na channels so velocity is not affected
-side effects include arrythmias, pulmonary fibrosis, thyroid issue, rash, grayness
diltiazem
-class IV non vascular specific calcium channel blocker antiarrhythmic
-primary effect slows av nodal conduction
- decrease ventricular response to atrial fibrillation
- well tolerated
-av nodal block with high doses
digoxin
- na pump inhibitor antiarrhythmic
- decrease av nodal conduction
dobutamine
-beta 1 stimulation
-cardiac contraction modulator
-ceiling effect(can onlystimulate heart so much)
- short term use (keep patient alive)
-increase sympathetic tone during heart failure
milrinone
-cardiac contraction modulator pde3 inhibitor
-increased camp levels= more pka=more ca= increase contraction
-mimics b1 stimulation
-ceiling effect
digoxin
cardic contraction modulator indirect na/ca exchanger inhibition
-decreases calcium efflux
-limits na ca exchanger indirectly
- cardiac glycoside
-na k atpase blocker (low intracellk, hi intracell na)
-more na in cell decreases ca effluc through exchanger
- can cause av block
pimobednan
cardiac contraction modulator calcium sensitizer
-sensitizes contractile machinery to calcium-
-related to an increased affinity of troponin c for calcium
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