Cytochrome P450 inducers
Phenobarbitol, Phenytoin, Rifampin, Carbamazepine
Cytochrome P450 inhibitors
Ketoconazole, Erythromycin (macrolide antibiotics), Chloramphenicol, Cimetidine
Acetaminophen
95% of the drug is glucuronylated or sulfated and excreted by kidney (phase II reactions), about 5% is metabolized by CYP2E1 to give NAPQI (highly toxic and conjugated with glutathione to be excreted by the kidney) -> at high doses of the drug more is con
N-acetylcysteine
precursor for glutathione production that is an antidote for acetaminophen poisoning because it reacts directly with NAPQI
Acetyl Choline
MOA: Cholinergic agonist (muscarinic and nicotinic)
1: vasodilation of endothelial cells, contraction/miosis of the eye, accommodation of the lens, secretion of salivary and lacrimal glands, constriction and increase in bronchi secretions, increase tone a
Bethanechol
MOA: ACh ester -> muscarinic agonist) -> not hydrolyzed by acetylcholinesterase
1: post-ganglionic PSNS effects + sweat
AE: sweating, salivation, flushing, low BP, nausea, abdominal pain, diarrhea, bronchospasm!
USE: lazy bladder/GI postop, xerostomia (dr
Carbachol
MOA: ACh ester -> muscarinic and nicotinic agonist -> poor substrate for AchE
1: post-ganglionic PSNS effects + sweat
AE: sweating, salivation, flushing, low BP, nausea, abdominal pain, diarrhea, bronchospasm!
USE: intraocular miosis during surgery, reduc
Methacholine
MOA: ACh ester -> muscarinic agonist -> hydrolyzed by AchE
1: post-ganglionic PSNS effects + sweat
AE: sweating, salivation, flushing, low BP, nausea, abdominal pain, diarrhea, bronchospasm!
USE: intraocular miosis during surgery, reduces intraocular pres
Muscarine
MOA: Natural alkaloid (can't be broken down by AChE) -> muscarinic agonist
1: post-ganglionic PSNS effects + sweat
AE: sweating, salivation, flushing, low BP, nausea, abdominal pain, diarrhea, bronchospasm!
Arecoline
MOA: Natural alkaloid (can't be broken down by AChE) -> muscarinic and nicotinic agonist
1: post-ganglionic PSNS effects + sweat
AE: sweating, salivation, flushing, low BP, nausea, abdominal pain, diarrhea, bronchospasm!
Pilocarpine
MOA: Natural alkaloid (can't be broken down by AChE) -> muscarinic agonist
1: post-ganglionic PSNS effects + sweat
AE: sweating, salivation, flushing, low BP, nausea, abdominal pain, diarrhea, bronchospasm!
USE: 2nd line agent for open angle glaucoma, man
Nicotine
MOA: nicotinic agonist (Nn), ganglion stimulation
1: low doses = PS and symp. stimulation -> symp in CVS, PS in GI, increase in secretions
High doses = ganglionic and NMJ blockade
AE: nausea, salivation, abdominal pain, vomiting, diarrhea, cold sweat, men
Edrophonium
MOA: Indirect acting cholinergic agent -> binds reversibly to the active site of AChE -> no covalent bond, short lived -> 4 ammonium
1: post-ganglionic parasympathetic effects, decreases HR (less effect on BP since there is no innervation to the vasculatu
Physostigmine
MOA: Carbamate anticholinesterase (covalent bond) 3 amine (not charged) -> can enter and stimulate CNS
1: post-ganglionic parasympathetic effects, decreases HR (less effect on BP since there is no innervation to the vasculature)
AE: sweating, salivation,
Neostigmine
MOA: Carbamate anticholinesterase (covalent bond) 4 ammonium (charged -> can't enter CNS)
1: post-ganglionic parasympathetic effects, decreases HR (less effect on BP since there is no innervation to the vasculature)
AE: sweating, salivation, diarrhea, bro
Pyridostigmine
MOA: Carbamate anticholinesterase (covalent bond) 4 ammonium (charged -> can't enter CNS)
1: post-ganglionic parasympathetic effects, decreases HR (less effect on BP since there is no innervation to the vasculature)
AE: sweating, salivation, diarrhea, bro
Echothiophate
MOA: organophosphate anticholinesterase (extremely stable covalent bond)
USE: glaucoma
Malathion (safe), Parathion (not safe)
MOA: organophosphate anticholinesterase (extremely stable covalent bond)
USE: thiophosphates insecticides -> prodrugs that must be converted to oxygen analogs
Tabun, Sarin, Soman
MOA: organophosphate anticholinesterases(extremely stable covalent bond)
USE: nerve agents
Galantamine, Tacrine, Rivastigmine, Donepezil (GTR-D)
MOA: Oral AChE inhibitor
USE: Treat symptoms of Alzheimer's
Pralidoxime
MOA: reverse the effects of anticholinesterases on the CNS (+ charged)
USE: treat organophosphate insecticide poisoning
Atropine
MOA: competitive muscarinic receptor antagonist -> 3 amine (CNS and PNS); HL = 4 hrs
1: Anti-PS effects + inhibit sweat glands
Eye -> increases intraocular pressure (mydriasis, cycloplegia),
GI -> reduced motility (doesn't decrease HCl production and can'
Scopolamine
MOA: alkaloid -> competitive muscarinic receptor antagonist -> 3 amine (PNS and even greater CNS!) low dose =sedation, high dose = excitement,
1: Anti-PS effects + inhibit sweat glands
Eye -> increases intraocular pressure (mydriasis, cycloplegia),
GI ->
Ipratropium
MOA: muscarinic antagonist -> 4 ammonium (no CNS)
1: bronchodilates
AE: dry mouth, blurred vision, sandy eyes, tachycardia, constipation and CNS effects; can exacerbate glaucoma in old ppl, caution with prostatic hypertrophy
USE: bronchodilator for asthma
Tiotropium
MOA: muscarinic antagonist -> 4 ammonium (no CNS)
1: Bronchodilates
AE: dry eyes/mouth, tachycardia, exacerbate glaucoma, may cause acute encephalopathy, falls, urinary retention, constipation and exacerbation and decompensation of underlying cognitive, f
Homatropine, Cyclopentolate, Tropicamide
MOA: tertiary amine muscarinic antagonists have a shorter duration of action than atropine
AE: dry eyes/mouth, tachycardia, exacerbate glaucoma, may cause acute encephalopathy, falls, urinary retention, constipation and exacerbation and decompensation of
Benzotropine, Trihexyphenidyl
MOA: tertiary amine muscarinic antagonists (gain access to CNS)
AE: dry eyes/mouth, tachycardia, exacerbate glaucoma, may cause acute encephalopathy, falls, urinary retention, constipation and exacerbation and decompensation of underlying cognitive, funct
Glycopyrrolate
MOA: QAC antimuscarinic agent
AE: dry eyes/mouth, tachycardia, exacerbate glaucoma, may cause acute encephalopathy, falls, urinary retention, constipation and exacerbation and decompensation of underlying cognitive, functional and behavioral deficits
USE:
Tolterodine
MOA: 3 amine antimuscarinic agent
AE: dry eyes/mouth, tachycardia, exacerbate glaucoma, may cause acute encephalopathy, falls, urinary retention, constipation and exacerbation and decompensation of underlying cognitive, functional and behavioral deficits
Hexamethonium, Mecamylamine, Trimethaphan
MOA: Ganglion blockers (Nicotinic Antagonists) -
1: blocks dominant ANS control for each organ: arterioles/veins/sweat glands are primarily sympathetic so the effect is parasympathomimetic; heart/iris/ciliary muscle/GI tract/urinary bladder/salivary gland
Tubocurarine
MOA: non-depolarizing NMJ blocker -> competitive antagonist
1: flaccid paralysis
AE: may block muscarinic receptors and cause histamine release
USE: adjuvant in anesthesia to relax skeletal muscle
Succinylcholine
MOA: depolarizing NMJ blocker persists in
1: flaccid paralysis
AE: malignant hyperthermia due to excessive release of Ca from the SR
prolonged paralysis in pts with AR butyrylcholinesterase polymorphism (decreased metabolism)
USE: rapid endotracheal intub
Hemicholinium
MOA: inhibits acetylcholine synthesis
1: blocks the CHT1 (choline/Na transporter), prevents uptake of choline required for ACh synthesis
USE: research tool
Vesamicol
MOA: inhibits acetylcholine storage
1: blocks the ACh/H+ antiporter that is used to transport ACh into vesicles thereby preventing storage
USE: research tool
Botulinum Toxin
MOA: inhibits acetylcholine release by degrading synaptobrevin
USE: injected to treat several diseases involving muscle spasms, also approved for cosmetic treatment of facial wrinkles
Epinephrine
MOA: nonselective alpha and beta agonist (enhanced with hyperthyroid and cocaine), physiological histamine antagonist (opposite effects on smooth muscle via different receptors)
1: Low doses = beta effects -> vasodilation (b2), increase HR (b1), decrease
Norepinephrine
MOA: alpha and beta1 agonist, little action on b2 receptors
1: CVS: vasoconstriction (a1) increases BP but CO is unchanged or decreased, which induces the BRR to cause bradycardia; if atropine is given before this it will cause tachycardia instead
AE: dec
Dopamine
MOA: activates dopamine receptors and alpha and beta receptors -> substrate for MAO and COMT, ineffective when given orally
1: Low doses = increases BP (b1), increases perfusion to the kidneys (D1);
High doses = stimulate alpha (vasoconstriction),
No effe
Fenoldopam
MOA: weak partial D1 agonist/antagonist, HL = 30 min
1: evokes arteriolar dilation (maintains renal perfusion, promotes natriuresis
AE: Very safe, contraindicated in glaucoma
USE: continuous IV for HTN emergency (especially pts with renal insufficiency)
Isoproterenol
MOA: b1 and b2 agonist
1: increases HR and contractility (B1), dilates arterioles of skeletal muscle and decreases TPR (b2); causes bronchodilation (b2)
USE: stimulate heart in emergencies (treat bradycardia or heart block), rarely as a bronchodilator
Dobutamine
MOA: selective b1 agonist (- isomer is a1 agonist/weak b1 agonist; + isomer is a1 antagonist/potent b1 agonist)
1: + inotrope -> increases CO (B1 -> increases cAMP) with little change in HR (doesn't significantly increase demand for O2)
USE: acute cardiac
Terbutaline
MOA: short acting b2 selective agonist (lasts 6 hrs)
1: bronchodilation (b2 -> Gs activates AC -> increase cAMP), decreases uterine contractions
AE: high doses can cause tachycardia, arrhythmias, tolerance (loss of response), tremors -> use nebulizer to d
Metaproterenol, Albuterol, Pirbuterol,
MOA: short acting b2 selective agonist (lasts 6 hrs)
1: bronchodilation (b2 -> Gs activates AC -> increase cAMP)
AE: high doses can cause tachycardia, arrhythmias, tolerance (loss of response), tremors -> use nebulizer to decrease systemic side effects),
Salmeterol, Formoterol
MOA: long acting b2 agonist (12 hours), slow onset of action (not suitable for prompt relief of bronchospasm)
1: bronchodilation (b2 -> Gs activates AC -> increase cAMP)
USE: prevent asthma attacks, treat COPD
Oxymethazoline
MOA: Adrenergic receptor agonist (alpha-1 and alpha-2)
1: cause vasocontriction (but systemically causes vasodilation)
USE: nasal spray decongestant
Phenylephrine
MOA: a1 selective agonist
1: vasoconstricts (a1), induces reflex bradycardia when given IV
USE: nasal decongestant, mydriatic (dilate pupil), treat supraventricular tachycardia
Xylometazoline
MOA: selective alpha-1 adrenergic agonist
1: vasoconstriction
USE: Nasal decongestant
Clonidine
MOA: partial a2 agonist
1: reduces sympathetic flow by acting on central presynaptic receptors -> decrease in PVR/CO/BP, does NOT decrease renal blood flow or GFR
AE: drowsiness, dry mouth, dizziness, headache and sexual dysfunction occur commonly -> rebo
Methyldopa
MOA: central a2 agonist (taken up by noradrenergic neurons and converted to alpha-methyl-norepinephrine -> also converted to a-methyldopamine)
1: diminishes adrenergic outflow from CNS leading to decreased PVR/BP (CO NOT decreased, does not decrease renal
Brimonidine
MOA: alpha 2 agonist
1: decreases the synthesis of aqueous humor
USE: treat glaucoma
Amphetamine
MOA: Indirect acting non-selective adrenergic agonist (releases NE from presynaptic terminals)
1: central stimulatory action -> increase BP by alpha agonist action on vasculature as well as b-stimulatory effects on the heart, increase alertness
AE: Depres
Methylphenidate
MOA:indirect acting adrenergic agonist (releases NE from presynaptic terminals); structural analog of amphetamine
1: increase alertness, BP, HR
USE: widely used to treat ADHD in children
Tyramine
MOA: in cheese and chianti wine -> indirect acting adrenergic agonist -> releases NE from presynaptic terminals
AE: normally oxidized by MAO, if the patient is taking MAO inhibitors it can precipitate serious vasopressor episodes
Ephedrine
MOA: alpha and beta agonist AND releases NE from nerve endings -> poor substrate for COMT or MAO -> long duration ->excellent absorption orally and penetrates the CNS
1: increases systolic and diastolic BPs, bronchodilation, increase alertness, decrease f
Pseudoephedrine
MOA: one of four ephedrine enantiomers
USE: over the counter decongestant (usually with H1-antagonists)
Phenoxybenzamine
MOA: irreversible nonselective antagonist of alpha-adrenergic receptors
1: decreases peripheral resistance (eliminate sympathetic tone on vasculature) -> reflex tachycardia; block inhibitory A2 (increase CO)
AE: reflex tachycardia (give b-blocker AFTER to
Phentolamine
MOA: reversible nonselective antagonist of alpha adrenergic receptors
1: decreases peripheral resistance (eliminate sympathetic tone on vasculature) -> reflex tachycardia; block inhibitory A2 (increase CO)
*Epinephrine Reversal
USE: short term control of
Prazosin
MOA:competitive selective a1 adrenergic antagonist
1: decrease PVR (relax arterial and venous smooth muscle) -> decreases BP, can improve urinary flow, no long term tachycardia (reflex tachycardia ONLY on first dose)
minimal changes in CO, renal blood flo
Terazosin, Doxazosin
MOA: a1 selective adrenergic blockers with longer half life
1: decrease PVR (relax arterial and venous smooth muscle) -> decreases BP
AE: first dose hypotensive response (give 1/3 normal dose), orthostatic hypotension, may need another drug to control ref
Tamulosin
MOA: a1 selective adrenergic antagonist
1: relax urinary smooth muscle (a-1a) -> weak effect on BP
USE: treat BPH
Yohimbine
MOA: a2 selective adrenergic antagonist
1: increased release of norepinephrine (blocks autoreceptors) -> leads to stimulation of cardiac b1 receptors and vascular a1 receptors
USE: used in past to treat erectile dysfunction
Propranolol
MOA: non-selective b-blocker and class II antiarrhythmic with extensive first pass metabolism (effects may take weeks, need to taper off) -> oral
1: slows heart rate and decreases contractility (B1), decreases glycogenolysis and glucagon secretion (carefu
Nadolol
MOA: non-selective b-blocker with a long duration of action -> oral
1: reduce BP by decreasing CO, contractility and HR (B1), decrease glycogenolysis and glucagon secretion (careful w/ diabetics)
AE: bronchoconstriction (lethal in asthmatics), can worsen
Timolol
MOA: non-selective b-blocker
1: decreases secretion of aqueous humor (decreases intraocular pressure)
AE: bronchoconstriction (lethal in asthmatics), can worsen angina or HTN(upregulation of receptors), CNS effects (sedation, sleep, sleep disturbances, de
Atenolol, Metoprolol
MOA: b1 selective adrenergic antagonist, class II antiarrhythmic
1: decreases BP by decreasing contractility and HR (b1)
inhibit renin release (b1), decrease sympathetic outflow, decrease cardiac remodeling (no norepi)
Inhibits phase 4
AE: bradycardia, hy
Esmolol
MOA: b1 selective adrenergic antagonist, class II antiarrhythmic -> ultra short acting
1: decreases BP by decreasing contractility and HR (b1)
Inhibits phase 4
USE: critically ill pts, HTN pts with impaired pulmonary fxn, diabetic HTN pts who are on insul
Labetalol
MOA: a1 and b-blocker -> IV, HL = 3-6 hrs
1: does not cause reflex tachycardia
AE: othostatic hypotension on first dose, contraindicated in pts with asthma, COPD, 2nd/3rd degree AV block or bradycardia
*contraindicated in pheochromocytoma and cocaine (blo
Carvedilol
MOA: a1 and b-blocker
1: negative inotrop, decreases remodeling (no norepi), decrease HR, inhibit renin release
USE: treat HTN and CHF (not acute or high risk w/o symptoms)
Pindolol
MOA: partial b-agonist(b-antagonist)
1:has intrinsic sympathomimetic activity (ISA) -> may produce smaller reductions in resting HR and BP
USE: preferred to treat HTN pts with diminished cardiac reserve or a propensity to bradycardia -> Preferred antihype
a-methyltyrosine (metyrosine)
MOA: competitive inhibitor of tyrosine hydroxylase,
1: inhibits of NE synthesis
USE: management of malignant pheochromocytoma, pre-op pts for resection of pheochromocytoma
Reserpine
MOA: irreversibly damages VMAT -> vesicles can't store NE and DA
1: inhibitor of NE storage/release -> causes depletion of NE since MAO degrades it in the cytoplasm -> gradual decrease in BP and slowing of cardiac rate
USE: treat HTN (not anymore)
Guanethidine
MOA: displaces NE from transmitter vesicles leading to depletion of NE -> also inhibits release of NE
1: inhibits NE storage/release -> causes a gradual decrease in BP and HR
USE: severely hypertensive patients (in the 70's)
Cocaine
MOA: blocks monoamine (NE) reuptake
1: Dopamine, NE and serotonin accumulate in synaptic space and results in potentiation and prolongation of their central and peripheral actions -> euphoria, HTN, tachycardia
USE: local anesthetic, recreational drug
Histamine
MOA: H1 agonist (PLC on endo, smooth muscle, nerve), H2 agonist (AC on gastric and cardiac)
1: H1 = vasodilation (via NO), increased capillary permeability, GI contraction, bronchoconstriction, pain/itching
H2 = gastric acid secretion, vasodilation in CVS
Cromolyn, Nedocromil
MOA: Histamine release inhibitors (histamine antagonists)
1: reduce immunologic mast cell degranulation (b2 agonists have a similar effect to reduce histamine release)
USE: treat asthma
Chlorpheniramine, Hydroxyzine, Meclizine, Promethazine, Dimenhydrinate, Diphenhydramine, Doxylamine
MOA: First generation H1 receptor antagonists, also block cholinergic, a-adrenergic, serotonin and local anesthetic receptor sites -> inverse agonists
AE: sedation, dry mouth
USE: #1 for allergic rhinitis and urticaria, treat motion sickness/nausea (not b
Fexofenadine, Loratadine, Acrivastine, Cetirizine
MOA: Second generation H1 receptor antagonists (liposoluble -> less sedating)
1: substrates of the P-glycoprotein transporter (prevent transport to CNS)
AE: dry mouth, LESS sedation,
USE: #1 for rhinitis and urticaria, treat motion sickness/nausea, not ef
Terfenadine, Astemizole,
MOA: 2nd gen H1 blockers, also block cardiac K+ channels
AE: when combined with CYP3A4 inhibitors may cause ventricular arrhythmias (taken off US market)
Ranitidine, Famotidine, Nizatidine (TIDINE)
MOA: H2 receptor antagonists
1: inhibits gastric acid secretion
AE: safe
USE: treat peptic ulcers, acute stress ulcers, GERD
Cimetidine,
MOA: H2 receptor antagonist
1: inhibits gastric acid secretion
AE: inhibits P450, anti-androgen (binds androgen receptors -> gynecomastia, reduced sperm count in men and galactorrhea in women)
USE: treat ulcers and GERD
Serotonin
MOA: 5-HT receptor agonist
Uses: none
Sumatriptan
MOA: 5HT-1D/1B receptor agonist (prototype)
USE: #1 acute severe migraine attacks
Metoclopramide
MOA: 5-HT4 receptor agonist
USE: prokinetic (enhance GI transit)
Cisapride
MOA: 5-HT4 receptor agonist
AE: severe cardiac effects (no longer available in US
USE: prokinetic (enhance GI transit)
Cyproheptadine
MOA: 5HT2 receptor antagonist -> also has potent H1 blocking actions
USE: allergic rhinitis, vasomotor rhinitis, cold urticaria, dematographism, treatment of smooth muscle manifestations of carcinoid tumor (serotonin syndrome)
Ondansetron, Granisetron
MOA: 5HT3 receptor antagonist
1: block ligand gated ion channel
USE: anti-emetics for severe nausea/vomiting associated with chemo
Ergotamine, Dihydroergotamine
MOA: Ergot alkaloids produced by claviceps purpurea (grain fungus) 5-HT antagonist, alpha antagonist, CNS dopamine antagonist
USE: specific for migraines (triptans preferred)
Bromocriptine, Cabergoline
MOA: Ergot alkaloids produced by claviceps purpurea (grain fungus) 5-HT antagonist, alpha antagonist, CNS dopamine antagonist
USE: treat hyperprolactinemia
Ergonovine
MOA: Ergot alkaloids produced by claviceps purpurea (grain fungus) 5-HT antagonist, alpha antagonist, CNS dopamine antagonist -> specific to the uterus
1: Vascular and uterine smooth muscle contraction
sensitivity increases in pregnancy -> small doses inv
Methylergonovine
MOA: Ergot alkaloids produced by claviceps purpurea (grain fungus) 5-HT antagonist, alpha antagonist, CNS dopamine antagonist -> specific to the uterus
1: Vascular and uterine smooth muscle contraction
sensitivity increases in pregnancy -> small doses inv
Dinoprostone
MOA: PGE2 analog -> vaginal insert, suppository or cervical gel
1: stimulate uterine contraction (oxytotic)
USE: ripen cervix at term before induction of labor with oxytocin, abortion in 2nd trimester, evacuation of uterine contents to manage missed abort
Carboprost Tromethamine
MOA: 15-Methyl-PGF-2 analog - IM injection
1: stimulate uterine contraction (oxytotic)
USE: induce abortion in second trimester, control postpartum hemorrhage due to uterine atony that has not responded to oxytocin or ergonovine, abortifacient
Misoprostol
MOA: PGE1 analog
1: Prevents damage in stomach from NSAIDs, also induce uterine contractions (oxytotic)
USE: reduce risk of NSAID induced gastric ulcers in pts at high risk
*cervical ripening and labor induction, treat postpartum hemorrhage, abortifacient
Alprostadil
MOA: PGE1 derivative
USE: maintain patency of the ductus arteriosus, impotence in urology
Prostacyclin
MOA: PGI2 derivative
USE: treat severe pulmonary HTN, prevent platelet aggregation in dialysis machines
Latanoprost
MOA: PGF2-alpha derivative
USE: #1 chronic glaucoma
Bimatoprost, Unoprostone, Travoprost
MOA: PGF2-alpha derivative -> newer related eicosanoids
USE: used in opthalmology
Zileuton
MOA: inhibition of 5-lipoxygenase
1: inhibits production of LT and PG from arachidonic acid
AE: elevation of liver enzymes
USE: treat moderate to severe asthma, especially in exercise/antigen and aspirin induced asthma (high LT from blockage of COX)
Zafirlukast, Montelukast
MOA: inhibition of the binding of LTC4/D4/E4 to its receptor in target tissues -> oral
AE: Churg Strauss (rarely), allergic granulomatous angiitis
USE: treat moderate to severe asthma (not acutely), treat asthma induced by aspirin/antigen/exercise
Hydrochlorothiazide
MOA: thiazide -> blocks Na+/Cl- cotransporter (NCC) in DCT (HL = 40hrs) -> most commonly used
1: increase excretion of Na+, K+, H2O
decrease excretion of Ca
Decreases PVR (decreased BV) which helps to lower BP by decreasing CO
AE: hypokalemia, hyponatremi
Chlorthalidone
MOA: thiazide -> blocks Na+/Cl- cotransporter (NCC) in DCT (HL = 40-60hrs) -> longest duration of action
1: increase excretion of Na+, K+, H2O
decrease excretion of Ca
Decreases PVR (decreased BV) which helps to lower BP
AE: hypokalemia, hyponatremia, hyp
Indapamide
MOA: thiazide -> blocks Na+/Cl- cotransporter (NCC) in DCT (HL = 14hrs)
1: increase excretion of Na+, K+, H2O
decrease excretion of Ca
Decreases PVR (decreased BV) which helps to lower BP
AE: hypokalemia, hyponatremia, hyperuricemia, hypercalcemia, hyperg
Metolazone
MOA: most potent thiazide -> blocks Na+/Cl- cotransporter (NCC) in DCT
1: increase excretion of Na+, K+, H2O
decrease excretion of Ca
Decreases PVR (decreased BV) which helps to lower BP
AE: hypokalemia, hyponatremia, hyperuricemia, hypercalcemia, hypergl
Furosemide (most common), Bumetanide, Torsemide, Ethacrynic acid
MOA: loop diuretics -> blocks Na+/Cl-/K+ cotransporter (NKCC2) in ascending LOH -> oral and parenteral, HL = 2-4 hours
1: decreases reabsorption -> increase Ca2+, Na+, K+ in tubular fluid -> increase H2O excretion, Ca2+ excretion
decreases renal vascular
Amiloride, Triamterene
MOA: K+ sparing diuretics -> block Na+ channels (ENaC in the collecting duct)
1: Decreases sodium reabsorption (ENaC) which increases Na+ and H2O excretion
Decreases K+ excretion
AE: hyperkalemia, hyponatremia, leg cramps, GI upset, dizziness, pruritis, h
Spironolactone, Eplerenone
MOA: K+ sparing aldosterone antagonists (act in collecting duct -> prevents translocation of receptor complex to nucleus) -> oral and strongly protein bound (t1/2 = 2-3 days)
1: decreases sodium reabsorption (ENaC) which increases Na+ and H2O excretion an
Acetazolamide
MOA: carbonic anhydrase inhibitor (acts in proximal tubular epithelial cells) -> less efficacious than other diuretics -> oral and well absorbed (HL = 3-6 hours), excreted unchanged in urine
1: decreases ability to exchange Na for K+ via diuresis, HCO3 is
Mannitol
MOA: Osmotic diuretic -> used IV only
1: raises osmotic pressure of plasma and draws H2O out of body tissues producing osmotic diuresis -> increases H2O excretion (does not affect Na excretion)
AE: extracellular water expansion (hyponatremia), tissue dehy
Conivaptan
MOA: ADH antagonist -> IV only (T1/2 = 5 hours) -> metabolized by and potent inhibitor of CYP 3A4
1: ADH controls permeability of collecting tubule to H2O -> V1 and V2 antagonist makes tubule H2O impermeable (dilute urine) -> increases H2O excretion, decr
Captopril, Enalapril (oral prodrug), Lisinopril
MOA: ACE inhibitors -> prevent action of Ag II (potent vasoconstrictor) -> oral (HL = 2-12 hrs)
1: vasodilates -> decreases PVR (lowers BP w/o reflexively increase CO, rate or contractility) -> decreased afterload
Decreases Na and H2O retention (decreases
Aliskiren
MOA: inhibits enzyme activity of renin -> prevents conversion of Ag to Ag I
1: decreases Ag II (vasodilation and decreased PVR/BP) and aldosterone (decreases Na/H2O retention)
AE: GI disturbances, hypotension, hyperkalemia*, renal impairment, risk of angi
Losartan, Valsartan, candesartan
MOA: Angiotensin Receptor blockers -> competitively block Ag II type I receptors -> once daily oral
1: arteriolar and venous dilation -> decreases PVR/BP, blocks aldosterone secretion and decreases Na/H2O retention -> DO NOT increase bradykinin
AE:: simil
Verapamil
MOA: Calcium channel blocker (only when open -> use dependent = works better when heart beats faster) -> Diphenylalkylamine -> least selective (cardiac and vascular smooth muscle) -> class IV antiarrhythmic -> oral (HL = 3-8hrs)
1: vasodilation, has intri
Dilitiazem
MOA: Calcium channel blocker (open depolarized channels only -> blocks better when heart is beating rapidly = use dependent) -> Benzothiazepine affects cardiac and vascular smooth muscle (less pronounced negative inotropic effect on the heart than verapam
Nifedipine
MOA: Calcium channel blocker -> 1st gen. dihydropyridine (shorter HL), greater affinity for Ca channels in vascular smooth muscle than cardiac
1: vasodilation (decrease PVR/BP), has intrinsic natriuretic effects (decreases H2O retention), reflex tachycard
Amlodipine, Felodipine
MOA: Calcium channel blocker -> 2nd gen. dihydropyridine (longer HL), greater affinity for vascular Ca channels than cardiac
1: vasodilation (decrease PVR/BP), has intrinsic natriuretic effects (decreases H2O retention), reflex tachycardia
AE: avoid in pa
Hydralazine
MOA: Direct vasodilator (mainly arterioles) -> oral or IV
1: vasodilation, reflex tachycardia, increase plasma renin (Na and H2O retention) -> decreases afterload
AE: Fluid retention and reflex tachycardia common, headache, nausea, sweating, flushing, per
Minoxidil
MOA: Direct vasodilator (mainly arterioles)
1: Vasodilation, reflex tachycardia, increase plasma renin (Na and H2O retention)
AE: severe fluid retention and reflex tachycardia (use with loop diuretic and b-blocker to prevent)
USE: treat HTN (last line ora
Nitroglycerine
MOA: converts to NO (activates GC -> increases cGMP) -> HL = 2-5 min (sublingual)
1: dilates coronary arteries (increases blood supply to heart), dilates large veins (decreases preload), reflex tachycardia and inotropic effect
AE: not used for managing HT
Nicardipine
MOA: calcium channel blocker -> IV infusion (HL = 30 min)
AE: reflex tachycardia
USE: HTN emergency
Sodium Nitroprusside
MOA: direct NO donor -> IV (HL = 1-2min)
1: prompt vasodilation of arteries and veins, reflex tachycardia
AE: oral is poison, hypotension (overdose), goose bumps, abdominal cramping, nausea, vomiting, headache, cyanide toxicity (rare product of metabolism
Bosentan
MOA: non-selective receptor blocker -> blocks initial transient depressor (ETA) and prolonged pressor (ETB) responses to IV endothelin
1: endothelins cause dose dependent vasoconstriction in vascular beds leading to pulmonary HTN -> prevents this
USE: tre
Digoxin
MOA: inhibits Na/K+ATPase -> leads to increased intracellular calcium -> HL = 36-40hrs, accumulates in muscle (high VD -> need loading dose), low TI
1: + inotrope, - chronotrope (
increase vagal tone
-> slows AV conduction), BR sensitization (increases af
Glucagon
MOA: stimulates adenylyl cyclase to produce increased cAMP (binds to GPCR)
1: + inotropic and chronotropic effects -> similar to b-agonists without requiring functioning b-receptors
USE: treat b-blocker OD
Milrinone, Inamrinone
MOA: PDE III inhibitor (increase cAMP levels)
1: + inotrope, increases CO, systemic and pulmonary vasodilator (reduces preload and afterload), shown to increase AV conduction slightly
USE: potentiate effects of dobutamine -> treat HF
Procainamide
MOA: class IA Na channel blockers -> intermediate speed of association/dissociation with Na channels (slower = more side effects) -> % is acetylated to NAPA which prolongs duration of action potential (class III), eliminated by kidney and metabolized by C
Disopyramide,
MOA: class IA Na channel blockers -> intermediate speed of association/dissociation with Na channels (slower = more side effects) -> oral -> 50% excreted unchanged by kidney, 30% converted in liver (CYP 3A4)
1: slows phase 0 depolarization (prolong AP and
Quinidine
MOA: class IA Na channel blocker-> intermediate speed of association/dissociation with Na channels (slower = more side effects) -> rapid oral absorption, forms metabolites (CYP 3A4) -> inhibits CYP2D6, 3A4 and P-glycoprotein (drug removal pump)
1: slows p
Lidocaine
MOA: class IB Na channel blockers -> fast association/dissociation (won't affect healthy tissue, only affects frequently depolarizing tissue) -> IV
1: shortens phase 3 repolarization (little effect on phase 0, depolarization in normal cells), no - inotrop
Mexiletine
MOA: class IB Na channel blockers -> fast association/dissociation (won't affect healthy tissue, only affects frequently depolarizing tissue) -> oral or IV
1: shortens phase 3 repolarization (little effect on phase 0, depolarization in normal cells)
AE: C
Tocainide
MOA: class IB Na channel blockers -> fast association/dissociation (won't affect healthy tissue, only affects frequently depolarizing tissue) -> oral and IV
1: shortens phase 3 repolarization (little effect on phase 0, depolarization in normal cells)
AE:
Flecainide
MOA: class IC Na channel blockers -> slow association/dissociation (effects normal tissue) -> oral (HL = 16-20hrs)
1: markedly slows phase 0 depolarization with no change in repolarization (no binding to K+ channels) -> slight prolongation of refractory p
Propafenone
MOA: class IC Na channel blockers -> slow association/dissociation (bad) -> oral, metabolized by CYP 2D6
1: markedly slows phase 0 depolarization with no change in repolarization (no binding to K+ channels)
AE: most likely to cause arrhythmias in normal t
Amiodarone
MOA: class III antiarrhythmic, blocks K+ channels and diminish outward K+ current during repolarization -> structurally related to thyroxine (contains iodine) -> oral (HL = weeks), high VD (need large LD)
1: prolong phase 3 (prolongs AP and QT interval),
Dofetilide
MOA: class III antiarrhythmic -> blocks K+ channels (ventricles) -> oral (HL = 10hrs), excreted in urine 80% unchanged
1: prolong phase 3 (mild class I and II effects)
AE: headache, chest pain, dizziness, v-tach, TDP (prolongs QT interval)
USE: #1 convert
Sotalol
MOA: class III antiarrhythmic -> potent non-selective b-blocker blocks K+ channels (delayed rectifiers)
1: prolong phase 3 (mild class I and II effects) -> prolongs duration of AP (lengthens refractory period)
AE: do not use for asymptomatic arrhythmias,
Adenosine
MOA: naturally occuring nucleoside, P1 receptor agonist -> HL = 15s (IV)
1: high doses decrease conduction velocity and prolongs refractory period and reduces automaticity of AV node
enhances K+ conductance, inhibits cAMP mediated Ca influx (hyperpolariza
Magnesium
MOA: functional Ca antagonist
USE: treat TDP, digitalis induced arrhythmias, prophylaxis of arrhythmia in acute MI
Isosorbide dinitrate
MOA: converted to NO in tissues (activate GC -> increases cGMP) -> Oral, quick onset
1: NO vasodilates (veins and venules), is antithrombotic and anti-inflammatory -> rapidly reduces myocardial O2 demand (systemic vasodilation = decreased preload), increa
Isosorbide mononitrate
MOA: converted to NO in tissues (activate GC -> increases cGMP) -> oral (sustained release available), 1 hr onset, nearly 100% bioavailability
1: NO vasodilates, is antithrombotic and anti-inflammatory -> rapidly reduces myocardial O2 demand (systemic vas
B-blockers (Acebutolol, atenolol, metoprolol, propranolol)
MOA: b-antagonists
1: - inotrope (decrease O2 demand for treatment of angina), increased EDV, ejection time
AE: bronchoconstriction (don't give in asthma/COPD), bradycardia, impotence, don't give in diabetes/chronic renal failure
contraindicated in varian
Ranolazine
MOA: Na channel blocker (facilitates Ca entry via Na/Ca exchanger) -> metabolized by CYP 3A4
1: reduces ventricular tension and myocardial demand (thought to produce relaxation, may modify FA oxidation)
AE: QT interval prolongation (main concern), nausea,
Aspirin
MOA: irreversible COX inhibitor -> antagonizes TXA2 synthesis (decreases GP IIb/IIIa -> prevents platelet aggregation)
1: prolongs bleeding time
USE: treat transient cerebral ischemia, reduce incidence of recurrent MI, decrease mortality in post MI pts
Clopidogrel
MOA: ADP receptor blocker -> irreversible inhibitor of P2Y12 -> prodrug converted by CYP2C19
AE: fewer side effects (preferred), thrombocytopenic purpura, some ppl are poor metabolizers and have lower plasma levels of active metabolite (at risk of cardiov
Ticlopidine
MOA: ADP receptor blocker -> irreversible inhibitor of P2Y12
AE: thrombocytopenic purpura, neutropenia
USE: prevent thrombosis in coronary stent
Dipyridamole
MOA: PDE inhibitors
1: increase cAMP, block uptake of adenosine (normally activates platelet AC via A2 receptors) -> coronary vasodilation
USE: combo with warfarin for prophylaxis of thromboemboli in pts with prosthetic valves, combo with aspirin for seco
Cilostazol
MOA: PDE inhibitors
1: increase cAMP, block uptake of adenosine (normally activates platelet AC via A2 receptors) -> coronary vasodilation
USE: treat intermittent claudication
Abciximab
MOA: irreversible monoclonal Ab -> blocks GP IIb/IIIa
USE: anticoagulation for acute coronary syndromes
Eptifibatide
MOA: reversible cyclic peptide antagonist of GP IIb/IIIa
USE: anticoagulation for acute coronary syndromes
Tirofiban
MOA: reversible nonapeptide antagonist of GP IIb/IIIa
USE: anticoagulation for acute coronary syndromes
Heparin (unfractionated - UFH)
MOA: binds and enhances anti-thrombin III effect -> injectible, rapid -> monitor with aPTT
1: inhibits thrombin IIa, factors IXa and Xa -> inhibits non fibrin-bound thrombin
AE: bleeding, hypersensitivity, heparin induced thrombocytopenia (HIT -> antibody
Enoxaparin, Dalteparin, Tinzaparin (LMW Heparin)
MOA: binds and enhances anti-thrombin III effect -> don't need to monitor -> superior bioavailability, longer half life, equal efficacy
1: inhibits Xa (less effect on thrombin)
AE: bleeding, hypersensitivity, heparin induced thrombocytopenia (HIT -> antib
Fondiparinux
MOA: Synthetic pentasaccharide -> bind antithrombin III and inhibit binding to Xa -> once daily SC injection
USE: prevention and treatment of DVT, initial treatment of VTE
Lepirudin, Bivalirudin, Argatroban
MOA: direct thrombin inhibitors -> parenteral, monitor with aPTT
1: inactivate fibrin-bound and unbound thrombin (independent from antithrombin III)
AE: no antidotes
USE: heparin induced thrombocytopenia (HIT)
Warfarin
MOA: inhibit vitamin K epoxide reductase -> monitor by PT (extrinsic, 7) -> small TI, highly bound to albumin (small fraction is free) -> oral
1: produce inactive clotting factor (no gamma-carboxyglutamyl side chains) -> inactivates factor 2, 7, 9, 10
AE:
Streptokinase
MOA: Thrombolytic protein produced by b-hemolytic strep -> catalyzes conversion of plasminogen to plasmin, also catalyzes the degradation of fibrinogen as well as clotting factors V and VII (rarely used) -> non-fibrin selective
1: lyse already-formed clot
Urokinase
MOA: human thrombolytic enzyme synthesized by kidney -> directly converts plasminogen to plasmin (non-fibrin selective)
1: lyse already-formed clots
AE: bleeding (especially when there are physiologically appropriate fibrin clots
USE: treat acute MI when
Alteplase, Reteplase, Tenecteplase
MOA: thrombolytic agent -> recombinant tissue plasminogen activator (t-Pa -> serine protease produced by human endothelial cells to activate plasminogen bound to fibrin in a thrombus) -> fibrin selective
1: lyse already-formed clots
AE: bleeding (especial
Anistreplase
MOA: plasminogen + streptokinase
1: activates plasmin, lyse already-formed clots
AE: bleeding (especially when there are physiologically appropriate fibrin clots
USE: treat acute MI when angioplasty (PCI) is not readily available
*Discontinued in US
Aminocaproic acid
MOA: inhibits plasminogen activation
USE: stops bleeding
Protamine sulfate
MOA: chemical antagonist of heparin, high in arginine -> cationic protein interacts with anionic heparin to form complex with no anticoagulant activity
USE: stop bleeding in pts with heparin OD
Vitamin K
MOA: cofactor for epoxide reductase
1: activates factor 2, 7, 9, 10
USE: treat deficiency or antagonist OD (warfarin), treat hypoprothrombinemia of the newborn (IM administration at birth is law in US), treat mothers receiving anticonvulsants prior to del
Plasma fractions
MOA: Clotting factors 8 and 9 for when factor activity is < 5-10% of normal
USE: factor 8 for Hemophilia A (classic), factor 9 for Hemophilia B (Christmas)
Simvastatin, Fluvastatin, Lovastatin, Pravastatin
MOA: competitive inhibitors of HMG CoA reductase (block first step in cholesterol synthesis)
1: deplete intracellular cholesterol supply, up-regulate LDL receptors, increase clearance of LDL from blood, modest decrease of TAGs and small increase in HDL
im
Rosuvastatin, Atorvastatin
MOA: competitive inhibitors of HMG CoA reductase (block first step in cholesterol synthesis) -> Most potent (don't start with these first)
1: deplete intracellular cholesterol supply, up-regulate LDL receptors, increase clearance of LDL from blood, ALSO s
Niacin (nicotinic acid)
MOA: inhibits AC (Gi) -> inhibits FA and TAG synthesis (inactivates TAG lipase), decrease HDL catabolism
1: favorably affects all lipid parameters and increases HDL significantly,
AE: intense cutaneous flush (prevent with aspirin - PG mediated), pruritis,
Gemfibril, Fenofibrate (Fibrates)
MOA: activate peroxisome proliferator activated receptor-a (PPAR-a -> expressed in liver and brown adipose)
1: decrease in plasma TAG levels and modest increase of HDL, modest reductions of LDL
AE: mild GI disturbances, myositis (renal insufficiency pts m
Cholestyramine, Colestipol
MOA: bile aciid binding resins -> bind anionic bile acids in intestinal lumen and prevent reabsorption (excreted in feces)
1: hepatocytes increase conversion of cholesterol into bile acids -> intracellular cholesterol decreases (up-regulates LDL receptors
Colesevelam
MOA: bile aciid binding resins -> bind anionic bile acids in intestinal lumen and prevent reabsorption (excreted in feces)
1: hepatocytes increase conversion of cholesterol into bile acids -> intracellular cholesterol decreases (up-regulates LDL receptors
Ezetimibe
MOA: inhibit NPC1L1 cholesterol transport protein (also inhibits absorption of phytosterols)
1: lowers LDL, small increase in HDL, mild decrease in TAGs
increases cholesterol synthesis and decreases incorporation into chylomicrons -> upregulation of LDL r
EPA, DHA
MOA: omega 3 fatty acids
1: reduce TAG biosynthesis and increase FA oxidation in the liver, increase HDL (long term), may increase total LDL as they lower TAG
Lovaza
MOA: ethyl ester of omega 3 FA
1: reduce TAG biosynthesis and increase FA oxidation in the liver, increase HDL (long term), may increase total LDL as they lower TAG
USE: FDA approved, adjunct to diet to reduce TAG levels in adult pt with very high (>500mg
Isoniazid
AE: when given to slow acetylators (NAT2 mutation) may cause neuropathy and hepatotoxicity
high acetylators have low blood drug levels
Codeine
AE: poor metabolizors (CYP2D6 mutations) have decreased metabolite levels (drug innefective)
Ultra-rapid metabolizers can have OD (respiratory depression)
6-mercaptopurine, azathioprine
AE: thiopurine S-methyl transferase (TPMT) polymorphism -> pts homozygous are at increased risk for myelosuppression (give 1/10th the dose) -> more common in caucaisians
Gefitinib
AE: EGFR mutation (inhibits tyrosine kinase) -> enhances drug effect -> 26% of Japanese have this
USE: non-small cell lung cancer
Primaquine (sulfas, antimalarials, chloramphenicol
AE: can cause hemolytic anemia in pts with G6PD deficiency (A- polymorphism is most common -> normally prevents from oxidative injury) -> Common in Africans
Ferrous Sulfate, ferrous gluconate, ferrous fumarate
MOA: oral iron derivatives
AE: nausea, GI discomfort, constipation, diarrhea, black stools
OD in children can cause necrotizing gastroenteritis w/ bloody diarrhea, shock, metabolic acidosis, coma, death
USE: treat iron deficiency anemias -> continue for 3
Iron dextran
MOA: parenteral iron
AE: hyperensitivity rxn (anaphylaxis), headache, arthralgias, fever, nausea, vomiting, flushing, pruritis
give small test dose first
USE: pts who can't tolerate or absorb oral iron, severe cases of iron deficiency anemia
Sodium ferric gluconate complex, iron sucrose complex
MOA: parenteral iron
AE: less likely to cause hypersensitivity (anaphylaxis)
USE: pts who can't tolerate or absorb oral iron, severe cases of iron deficiency anemia
Deferoxamine, deferasirox
MOA: iron chelators -> binds iron that has already been absorbed -> promotes excretion
USE: pts with oral iron OD, thalassemia major (chronic iron toxicity)
Vitamin B12 (cyanocobalamine or hydroxycobalamine)
USE: treat megaloblastic anemia -> parenteral injections required
Folic acid
USE: treat megaloblastic anemia -> parenteral or oral, treat deficiency caused by methotrexate
Erythropoietin
MOA: interacts with JAK/STAT receptors on RBC progenitors
1: stimulates erythroid proliferation and differentiation, induces release of reticulocytes from bone marrow
AE: HTN and thrombotic complications (especially in pts with renal failure or pts with a
Darbepoetin
MOA: interacts with JAK/STAT receptors on RBC progenitors -> long acting version (HL = 3x longer)
1: stimulates erythroid proliferation and differentiation, induces release of reticulocytes from bone marrow
AE: HTN and thrombotic complications (especially
Filgrastim
MOA: G-CSF -> interact with JAK/STAT
1: stimulate proliferation and differentiation of myeloid progenitor cells
AE: may cause bone pain,
USE: accelerate recovery of neutrophils after chemo, treat primary/secondary neutropenia
Sargramostim
MOA: GM-CSF -> interact with JAK/STAT
1: stimulate proliferation and differentiation of myeloid progenitor cells
AE: may cause fever, arthralgias and capillary damage -> rarely allergic rxns
USE: accelerate recovery of myeloid cells after chemo
IL-11
MOA: megakaryocytic growth factor
1: increases # of peripheral platelets
USE: treat pts with prior episodes of thrombocytopenia after cancer chemo (reduces need for platelet infusions)
Hydroxyurea
1: increases HbF
AE: bone marrow suppression, cutaneous vasculitis
USE: sickle cell, CML, polycythemia vera
Theophylline, aminophylline
MOA: Methylxanthines inhibit PDE3 (normally degrades cAMP to AMP) -> oral/injectible
1: increases cAMP, blocks adenosine receptors -> bronchodiilates
AE: narrow TI -> CNS (tremors, insomnia, convulsions), arrhythmias, increased GI motility,
erythromycin,
Beclomethasone, Dexamethasone, Flucitasone, Budesonide, Flunisolide
MOA: surface active corticosteroids -> inhibit phospholipase A2 (decrease synthesis of arachidonic acid and expression of COX) -> bind GREs in the nucleus (snythesizes substances to inhibit expression of inflammation and allergy
1: decrease LTs and PGs, i
Prednisolone, hydrocortisone
MOA: IV corticosteroids -> inhibit phospholipase A2 (decrease synthesis of arachidonic acid and expression of COX) -> bind GREs in the nucleus (snythesizes substances to inhibit expression of inflammation and allergy
1: decrease LTs and PGs, increase b-re
Omalizumab
MOA: monoclonal anti-IgE antibodies -> parenteral -> expensive*
1: binds IgE on sensitized mast cells and prevents release of mediators
USE: prophylactic in asthmatic pts
Ethinyl Estradiol
MOA: estrogen analog -> increase production of factor 7 and 10 and fibrinogen
1: prevent ovulation
AE: CV disease (thrombi -> especially smokers 35+), headache (stop if migraines), melasma (estrogen), amenorrhea, depression, insulin resistence and dyslipi
Mestranol
MOA: prodrug converted to Ethinyl Estradiol -> increase production of factor 7 and 10 and fibrinogen
1: prevent ovulation
AE: CV disease (thrombi -> especially smokers 35+), headache (stop if migraines), melasma (estrogen), amenorrhea, depression, insulin
Etonorgestrel (implants every 3 years, ring), Norelgestromin (Patch w/ EE), Medroxyprogesterone acetate (depot provera)
MOA: progestin analogs -> suppress LH and FSH
1: prevent ovulation, thicken cervical mucus plug, prevents sperm penetration, impairs implantation
AE: CV disease (thrombi -> especially smokers 35+), headache (stop if migraines), melasma (estrogen), amenorr
Norgestrel (can be used alone -> no thrombotic effect), Levonorgestrel (intrauterine systems every 5 years, used in plan B)
MOA: progestin analogs -> suppress LH and FSH
1: prevent ovulation, thicken cervical mucus plug, prevents sperm penetration, impairs implantation
AE: CV disease (thrombi -> especially smokers 35+), headache (stop if migraines), melasma (estrogen), amenorr
Norethindrone (can be used alone, no thrombotic effect), Norethindrone acetate
MOA: progestin analogs -> suppress LH and FSH
1: prevent ovulation, thicken cervical mucus plug, prevents sperm penetration, impairs implantation
AE: CV disease (thrombi -> especially smokers 35+), headache (stop if migraines), melasma (estrogen), amenorr
Desorgestrel, Norgestimate
MOA: progestin analogs -> suppress LH and FSH
1: prevent ovulation, thicken cervical mucus plug, prevents sperm penetration, impairs implantation
AE: CV disease (thrombi -> especially smokers 35+), headache (stop if migraines), melasma (estrogen), amenorr
Drospirenone
MOA: progestin analogs -> suppress LH and FSH
1: prevent ovulation, thicken cervical mucus plug, prevents sperm penetration, impairs implantation
*Anti-androgenic activity
AE: CV disease (thrombi -> especially smokers 35+), headache (stop if migraines), m
Contraceptive patch
Contains both ethinyl estradiol and norelgestromin
Ring
transvaginal delivery of ethinyl estradiol and etonorgestrel -> every cycle
Depo-provera
MOA: injection containing depot medroxyprogesterone acetate (DMPA)
AE: bone density loss with long term use
USE: IM every 3 months for contraception
Nonoxynol-9
1: surfactant destroys sperm cell membrane
USE: non-hormonal contraception
Oxytocin
MOA: peptide hormone secreted by posterior pituitary -> Gq protein in myometrium activates PLC -> activates voltage gated Ca channels and contraction of smooth muscle
1: oxytotic -> enhance uterine contractions
AE: fetal distress, placental abortion, uter
Magnesium Sulfate
MOA: uncouples excitation contraction in myometrial cells through inhibition of cellular action potentials
1: tocolytic -> decreases uterine contractions
AE: Mother -> respiratory depression, cardiac arrest
Neonate -> crosses placenta and may lead to resp
Indomethacin
MOA: NSAID, decreases PG
1: tocolytic -> decreases uterine contractions
AE: crosses placenta to cause oligohydramnios (decrease in fetal renal blood flow if used for more than 48 hours), premature closure of PDA (more common after 32 weeks)
USE: prolong i
Atosiban
MOA: competitive antagonist at oxytocin receptors
1: tocolytic -> decreases uterine contractions
USE: prolongs intrauterine life -> not available in the US