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43 Cards in this Set

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Cpo
Xo x F
------
Vd
k
0.7
----
t1/2

k is elimination rate constant
Cl
rate out
---------
Cp

rate out is rate of drug elimination (mg/h)
rate out
(for calculation of renal clearance)
Cu x Uvol
----
t
Cl
(when Vd and t1/2 are known)
k x Vd
rate in (for i.v. dosing)
Xo
--
tau
(Xo is dose)
(tau is dosing interval)
rate in
(for p.o. dosing)
Xo x F
-------
tau
(tau is dosing interval)
(Xo is dose)
mcg/ml
= mg/L
slow acetylators are more likely to develop drug toxicity with which drugs?
SHIP

sulfapyridine
hydralazine
isoniazid
procainamide
alpha-methyldopa
(sympatholytic drugs)
alpha-methyl-NE (alpha2-adrenoceptor agonist that suppresses neuronal activity of RVLM and thus decreases efferent sympathetic nerve activity) formed from the central metabolism of this.

lowers bp via passive dilation of resistance arterioles and suppression of cardiac output (decreased venous return and cardiac contractility).

usually accompanied by slight bradycardia.
isoproterenol
(adrenergic agonists)

beta-adrenoceptor agonist that increases heart rate by direct stimulation of the SA node.
yohimbine
(alpha-adrenoceptor antagonists)

blocks the alpha2-adrenoceptors in the RVLM, causing an increase in efferent sympathetic nerve activity resulting in hypertension and tachycardia.

lipid-soluble compound.
pilocarpine
(cholinergic agonists)

can decrease heart rate by direct action at the SA node.
phenylephrine
(adrenergic agonists)

decreases heart rate via the arterial baroreflexes (increase in blood pressure resulting from constriction of resistance arterioles indirectly decreases heart rate via increased signal frequency from the carotid sinus).
alpha1 receptors
radial muscle, iris: contraction = mydriasis (pupil bigger).
canal of schlemm: enhanced normal outflow.
arterioles & venules (along with alpha2): constriction.
bronchial glands: decreased secretion.
proximal tubules: increased Na+/water reabsorption.
trigone (internal sphincter)(alpha 1a): contraction.
urethra: contraction.
emission and ejaculation (alpha 1a).
pilomotor muscles: contraction.
salivary glands: water and K+ secretion (thick).
alpha2 receptors
canal of schlemm: decreased production of aqueous humor.
arterioles and venules (along with alpha1): constriction.
stomach and intestines: decreased motility and tone, decreased secretion.
platelets: aggregation.
islet cells of pancreas (insulin): decreased secretion.
beta1 receptors
HEART:
atria & ventricles: increased contractility.
SA node: increased HR.
atrial conduction tissue: increased conduction velocity, decreased duration of AP, decreased refractory period.
A-V node: increased automaticity, increased conduction velocity, decreased conduction time, decreased refractory period, decreased duration of AP.
His-Purkinje system: (+)automaticity and conduction velocity, (-)conduction time, refractory period, and duration of AP.
ventricles: (+)automaticity and conduction velocity, (-)conduction time, refractory period, duration of AP.

JG cells: (+)renin secretion.

adipocytes: (+)lypolysis.
beta2 receptors
arterioles & venules: dilation (via circulating EPI).
bronchial muscle: relaxation.
uterus: relaxation.
skeletal muscle: (+)glycogenolysis, K+ uptake, tremor, increased contractility.
liver: (+)glycogenolysis and gluconeogenesis.
gallbladder & ducts: relaxation.
methacholine
(cholinergic agonists)

addition of a methyl group to the beta-carbon of acetycholine causes it to freeze in the trans conformation, making it specific for muscarinic receptors.

metabolized more slowly than ACh by AChase.

THERAPEUTIC USES: used as a provocative agent in the diagnosis of bronchial asthma.
carbachol (carbamoylcholine)
(cholinergic agonists)

replacement of acetyl group of ACh with carbamoyl.

both nicotinic and muscarinic effects (free rotation).

metabolized more slowly than ACh by AChase.

THERAPEUTIC USES: used to cause miosis (slow onset, long lasting) after surgery in the anterior chamber of the eye.
bethanechol
(cholinergic agonists)

methyl group added to the beta-carbon and replacement of acetyl group with carbamoyl group.

muscarinic agonist that acts primarily at smooth muscle of the GI and GU tracts.

metabolized more slowly than ACh by AChase.

THERAPEUTIC USES: used to treat bowel stasis, postoperative paralytic ileus, and urinary retention, either postop or neurogenic.

contraindications: asthma and COPD, peptic ulcer, congestive heart failure and hyperthyroidism)
succinylcholine
(cholinergic agonists)

two molecules of ACh yields this.

specificity for N2-cholinergic receptors found at nmj of skeletal muscle.

depolarizes the motor endplate, causing flaccid paralysis of skeletal muscle because the motor end-plate must repolarize completely before another full contraction can be elicited.

metabolized more slowly than ACh by AChase.

THERAPEUTIC USES: i.v. injection causes initial, single contraction of skeletal muscle followed by flaccid paralysis of 3-5 minutes. (depolarization blockade = non-competitive blockade)

major portion is degraded by plasma cholinesterase before it reaches junction.
acetylcholine
(cholinergic agonists)

THERAPEUTIC USES: causes a rapid and transient decrease in bp (via NO from vascular endothelial cells) and elicits baroreflexly-mediated tachycardia.

no direct cardiac suppression.

AFTER treatment with atropine: larger i.v. dose increases bp and heart rate by stimulating N1-cholinergic receptor at sympathetic ganglia.

(miochol) used to produce rapid and complete miosis before or after surgery involving anterior portion of the eye.
pilocarpine
(cholinergic agonists)

tertiary amine (goes wherever)

selective muscarinic agonist used primarily in treatment of glaucoma.

MOA: contraction of the meridional fibers of the ciliary muscle increases the iridiocorneal angle and/or the tone and alignment of the trabeculae allowing aqueous humor to flow more easily into canal of Schlemm.

IOP decreased by 20%.

contraction of ciliary muscle causes fixation of lens for near vision, impairing far vision. persistent miosis causes poor night vision.

also used to treat dry mouth assoc. with Sjogren's syndrome.

degraded by HEPATIC enzymes, not AChase or pseudocholinesterase.
cevimeline
(cholinergic agonists)

synthetic muscarinic agonist.

used to treat dry mouth and eyes assoc. with Sjogren's syndrome.

S/E's: GI cramping, sweating, UTI, rhinitis.
betaxolol
(beta-adrenoceptor antagonists)

decreases the production of aqueous humor by an unknown mechanism. (for glaucoma)

lower iop by 20-30%.

little effect on bronchiolar smooth muscle b/c it's relatively selective for beta1-adrenoceptors.

systemic absorption can cause bradycardia.
timolol
(beta-adrenoceptor antagonists)

decreases the production of acqueous humor by unknown mechanism. (for glaucoma)

lower iop by 20-30%.

systemic absorption can cause bronchoconstriction and bradycardia.
latanoprost
(treatment of glaucoma)

stable analog of PGF2alpha.

increase uveoscleral outflow.

lowers iop by 20-25%.
alpha-adrenoceptor agonists (for glaucoma treatment)
MOA: alpha1-receptor stimulation enhances the outflow of aqueous humor via normal, pressure-dependent pathway. alpha2-receptor stimulation decreases production of aqueous humor.

epinephrine
dipivefrin
apraclonidine
epinephrine
(adrenergic agonists)
(treatment of glaucoma)

alpha1-receptor: (+) normal outflow.

causes mydriasis via stimulation of alpha1-receptors in radial muscle of iris.
dipivefrin
(treatment of glaucoma)

lipid-soluble compound that penetrates into the anterior chamber before being hydrolyzed to epinephrine.

alpha1-receptor: (+) normal outflow.

causes mydriasis via stimulation of alpha1-receptors in radial muscle of iris.
apraclonidine
(treatment of glaucoma)

selective alpha2-adrenoceptor agonist that is used to prevent postsurgical ocular hypertension after trabeculoplasty. acts by decreasing the rate of production of aqueous humor.
acetazolamide
(treatment of glaucoma)

carbonic anhydrase inhibitor. (p.o.)

decreases production of aqueous humor.

avoid because of S/E's: headache, decreased libido, metallic taste, kidney stones and urinary frequency.
dorzolamide
(treatment of glaucoma)

carbonic anhydrase inhibitor. (topical)

decreases iop by 10-20%.
isofluophate (DFP)
(organophosphate AChase inhibitors)
(treatment of glaucoma)

MOA: lower iop by increasing amount of ACh available to contract meridional fibers of the ciliary muscle.

produces cataracts and is generally toxic: reserved for use in patients who prove refractory to all other types of therapy.
echothiophate
(organophosphate AChase inhibitors)
(treatment of glaucoma)

MOA: lower iop by increasing amount of ACh available to contract meridional fibers of the ciliary muscle.

produces cataracts and is generally toxic: reserved for use in patients who prove refractory to all other types of therapy.
mannitol
(treatment of glaucoma)

for the treatment of an acute attack of angle-closure glaucoma.

osmotic diuretic agent: given i.v. and does not leave the extracellular fluid volume. hyperosmolar ecf causes cellular dehydration and thus a fall in iop.
physostigmine
(carbamate AChase inhibitors)

reversible inhibitor of cholinesterase.

tertiary amine: enters CNS.

MOA: non-competitive, slowly-reversible inhibition of AChase. causes carbamoylation (rather than acetylation) of the active site of AChase. hydrolysis occurs spontaneously with a t1/2 of 15-30 minutes. no direct effect at ACh receptors.

THERAPEUTIC USES: Alzheimer's disease - superceded by newer drugs.
overdose/poisoning with anticholinergic agents.

not used b/c of numerous adverse S/E's?
donepezil
(carbamate AChase inhibitors)

reversible inhibitor of cholinesterase.

DOC for treatment of alzheimer's b/c more selective for CNS. decreases apathy, hallucinations, anxiety and behavioral problems.

S/E's: n/v, diarrhea, muscle cramps, fatigue, insomnia and anorexia.
neostigmine
(carbamate AChase inhibitors)

reversible inhibitor.

quaternary.

MOA: a direct agonist at cholinergic N2-receptor.
also inhibits AChase by carbamoylation at all peripheral sites (increases the conc. of ACh at the N2-receptor of the NMJ and at muscarinic sites: heart, salivary glands, etc). given with atropine, muscarinic stimulation will be blocked in the periphery, getting rid of side effects.

THERAPEUTIC USES: postoperative paralytic ileus;
atony of the GI and GU tracts;
myasthenia gravis;
reversal of muscle paralysis caused by competitive neuromuscular blocking agents.
pyridostigmine
(carbamate AChase inhibitors)

reversible inhibitor.

quaternary.

MOA: same as neostigmine.

long term p.o. dosing used to treat myasthenia gravis.
mild occular symptoms: give with corticosteroids.
mild/moderate general symptoms: give with thymectomy.
moderate/severe general symptoms: give with azathioprine (immunosuppresant).
edrophonium
(carbamate AChase inhibitors)

reversible.

quaternary.

MOA: does inhibit AChase at all peripheral cholinergic nerve junctions (carbamoylation of active site), but MAJORITY of its action at the nmj results from direct stimulation of cholinergic N2-receptors.

must be given i.v. or i.m. due to extremely short half-life.

THERAPEUTIC USES: diagnosis of myasthenia gravis;
titrate adequacy of treatment of myasthenia gravis;
distinguish between "myasthenic" (improves: undertreated, so you increase the dose) and "cholinergic" (weakness is worse: overtreated, so decrease dose) crisis in patients treated p.o. with pyridostigmine;
reversal of muscle paralysis caused by competitive neuromuscular blocking agents like d-tubocurarine.
carbaryl
(carbamate AChase inhibitors)

reversible.

lipid-soluble: goes into cns.

an insecticide used around the house.

often grouped with the irreversible organophosphate inhibitors of AChase b/c poisoning produces effects similar to those caused by the organophosphates.

treat poisoning with atropine alone.