Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
84 Cards in this Set
- Front
- Back
Acetylcholine
|
Class: Muscarinic Agonist (Direct Acting)
Use: Glaucoma (limited use) Side Effects: potential toxicity if given IV or IM unwanted or excessive muscarinic stimulation Contraindications:asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction |
|
Carbachol
|
Class: Muscarinic Agonist (Direct Acting)
Use: Glaucoma (topically) Side Effects: potential toxicity if given IV or IM unwanted or excessive muscarinic stimulation Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction Other: muscarinic & nicotinic effects |
|
Bethanechol
|
Class: Muscarinic Agonist (Direct Acting)
Use: stimulate GI motility treat urinary retention Side Effects: potential toxicity if given IV or IM unwanted or excessive muscarinic stimulation Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction Other: little effect on nicotinic receptors |
|
Pilocarpine
|
Class: Muscarinic Agonist (Direct Acting)
Use: Glaucoma xerostomia Side Effects: potential toxicity if given IV or IM unwanted or excessive muscarinic stimulation Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction |
|
Edrophonium
|
Class: Acetylcholinesterase Inhibitor - Reversible (indirect acting)
Use: Diagnosing Myashenia Gravis (Tensilon test)...b/c it's short-acting Side Effects: - SLUDGE - skeletal m. fasciculations followed by paralysis - bradycardia, hypotension, shock - severe miosis - seizures, coma Treat poisoning with: - high dose atropine every 10 min. - pralidoxime - Diazepam for seizures Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction Other: quatern. ammonium compounds-don't enter CNS. |
|
physostigmine
|
Class: Acetylcholinesterase Inhibitor - Reversible (indirect acting)
Use: treating poisoning w/ atropine or other antimuscarinic agents Side Effects: - SLUDGE - skeletal m. fasciculations followed by paralysis - bradycardia, hypotension, shock - severe miosis - seizures, coma Treat poisoning with: - high dose atropine every 10 min. - pralidoxime - Diazepam for seizures Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction Other: nonquaternary...can get into CNS |
|
neostigmine
|
Class: Acetylcholinesterase Inhibitor - Reversible (indirect acting)
Use: Treatment of Myasthenia Gravis ...(longer acting) (like pyridostigmine) Side Effects: - SLUDGE - skeletal m. fasciculations followed by paralysis - bradycardia, hypotension, shock - severe miosis - seizures, coma Treat poisoning with: - high dose atropine every 10 min. - pralidoxime - Diazepam for seizures Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction Other:quatern. ammonium compounds-don't enter CNS |
|
pyridostigmine
|
Class: Acetylcholinesterase Inhibitor - Reversible (indirect acting)
Use: Treatment of Myasthenia Gravis ...(longer acting) (same as neostigmine) Side Effects: - SLUDGE - skeletal m. fasciculations followed by paralysis - bradycardia, hypotension, shock - severe miosis - seizures, coma Treat poisoning with: - high dose atropine every 10 min. - pralidoxime - Diazepam for seizures Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction Other: used by military to protect against nerve agents in chemical warfare |
|
rivastigmine
|
Class: Acetylcholinesterase Inhibitor - Reversible (indirect acting)
Use: Side Effects: - SLUDGE - skeletal m. fasciculations followed by paralysis - bradycardia, hypotension, shock - severe miosis - seizures, coma Treat poisoning with: - high dose atropine every 10 min. - pralidoxime - Diazepam for seizures Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction |
|
donepezil
|
Class: Acetylcholinesterase Inhibitor - Reversible (indirect acting)
Use: Side Effects: - SLUDGE - skeletal m. fasciculations followed by paralysis - bradycardia, hypotension, shock - severe miosis - seizures, coma Treat poisoning with: - high dose atropine every 10 min. - pralidoxime - Diazepam for seizures Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction |
|
Carbamate insecticides
|
Class: Acetylcholinesterase Inhibitors - Reversible
Use: Selectively toxic to insects...agricultural use Side Effects: Toxic effects may be severe - SLUDGE - skeletal m. fasciculations followed by paralysis - bradycardia, hypotension, shock - severe miosis - seizures, coma Treat poisoning with: - high dose atropine every 10 min. - pralidoxime - Diazepam for seizures Contraindications: asthma, bradycardia, hypotension, vasomotor instability, coronary a. disease, peptic ulcer disease, hyperthyroidism, weakened smooth m. of bladder/G.I. tract, urinary/intestinal obstruction Other: pralidoxime not useful for treating poisoning...just atropine |
|
Organophosphate insecticides
|
Class: Acetylcholinesterase Inhibitors (Irreversible)
Use: Selectively toxic to insects...agricultural use (may be absorbed through skin ) Side Effects: Same as other cholinesterase inhibitors Contraindications: same as other cholinesterase inhibitors Other: must be oxidized to active metabolites |
|
Nerve agents for chemical warfare & terrorism (Sarin, Soman, Tabun, VX)
|
Class: Acetylcholinesterase Inhibitors (Irreversible)
Use: nerve gases in chemical warfare Side Effects: Same as other cholinesterase inhibitors Contraindications: Same as other cholinesterase inhibitors Other: few drops can kill adult treat w/ atropine, physostigmine |
|
Sildenafil
|
Class: Inhibitor of cGMP phosphodiesterase type 5 (PDE-5)
Use:inhibit PDE-5 = less breakdown of cGMP = pronounced vasodilation = erection Side Effects:-some general vasodilation ...may result in hypotension w/ reflex increase in HR -blue-green color blindness Contraindications: -men w/ cardiovascular dx -men taking vasodilators (nitrates) or sympathomimetics Other: -Metabolism by CYP3A4 |
|
Vardenafil
|
Class: Inhibitor of cGMP phosphodiesterase type 5 (PDE-5)
Use: inhibit PDE-5 = less breakdown of cGMP = pronounced vasodilation = erection Side Effects: -some general vasodilation ...may result in hypotension w/ reflex increase in HR -blue-green color blindness Contraindications: -men w/ cardiovascular dx -men taking vasodilators (nitrates) or sympathomimetics Other: -Metabolism by CYP3A4 |
|
Tadalafil
|
Class: Inhibitor of cGMP phosphodiesterase type 5 (PDE-5)
Use: inhibit PDE-5 = less breakdown of cGMP = pronounced vasodilation = erection Side Effects: -some general vasodilation ...may result in hypotension w/ reflex increase in HR -blue-green color blindness Contraindications: -men w/ cardiovascular dx -men taking vasodilators (nitrates) or sympathomimetics Other: -Tadalafil - lasts 36 hours -Metabolism by CYP3A4 |
|
Pralidoxime/2-PAM
|
Class: Cholinesterase Reactivator
Use: binds to phosphate group that inhibits the enzyme, thereby reactivating it antidote for organophosphate poisoning Side Effects: Contraindications: doesn't work w/ carbamate insecticides Other: must be used w/in 2 hrs following exposure |
|
Atropine
|
Class: Muscarinic/Cholinergic Antagonists
Use: - preop. med to reduce secretions & block vagal reflexes of the heart - cardiac stimulant following some types of MI (when there's an increase in vagal tone) - antidote for poisoning w/ cholinesterase inhibitors or muscarinic agonists - pulmonary med to dry respiratory secretions - mydriatic & cycloplegic agent in opthalm. - antispasmodic for treatment of GI disorders (i.e. irritable bowel syndrome & biliary colic. Side Effects: General: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis Other: found in nightshade & jimsonweed |
|
Scopolamine
|
Class: Muscarinic/Cholinergic Antagonists
Use: - similar to atropine, but more of aCNS depressant effect(sedation & amnesia) than atropine - orally & in patch form for prevention of motion sickness and vertigo Side Effects: General: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis Other: found in nightshade & jimsonweed |
|
Dicyclomine
|
Class: Muscarinic/Cholinergic Antagonists
Use: - intestinal antispasmodic - treatment of irritable bowel syndrome (IBS) Side Effects: General: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis Other: - nonquaternary |
|
prophantheline
|
Class: Muscarinic/Cholinergic Antagonists
Use: - gastroenterology for antispasmodic effects (for IBS) Side Effects: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis Other: - quaternary compound w/ few CNS effects |
|
glycopyrrolate
|
Class: Muscarinic/Cholinergic Antagonists
Use: Side Effects: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis Other: quaternary (no CNS effects) |
|
ipratropium
tiatropium |
Class: Muscarinic/Cholinergic Antagonists
Use: Side Effects: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis Other: -tiatropium is a newer drug w/ longer duration of action (compared to ipratropium) - quaternary salts - few systemic effects |
|
benztropine
trihexyphenidyl |
Class: Muscarinic/Cholinergic Antagonists
Use: Side Effects: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis |
|
tolterodine
|
Class: Muscarinic/Cholinergic Antagonists
Use: Side Effects: • dry mouth • dry, hot skin • constipation, urine retention, etc... • visual disturbances, blurred vision, photophobia • CNS effects - sedation, confusion, amnesia (esp. in elderly pts) Treat acute poisoning w/: • physostigmine • benzodiaz. (for seizures) Contraindications: • glaucoma • prostatic hypertrophy (b/c of compression of urethra) • cardiovascular instability • severe ulcerative colitis |
|
Epinephrine
|
Class: Adrenergic receptor agonist (Mixed or Nonselective)
Use: • Used in circulatory shock - treat bronchospasm & vessel collapse due to anaphylactic shock (req's high dose) • asthma - treat bronchoconstriction • A-V block & cardiac arrest (high doses) • non A-V block bradycardias (low dose) • mixed w/ local anesthetics to prolong action at local sites of injection & minimize bleeding Mechanism: - stimulates all α & β receptors nearly equally Side Fx: Other: - must be given parenterally - actions last only a few minutes • low IV rates of epineph. infusion (reach mainly extrasynaptic α2 & β2 receptors) = decrease diastolic, increase systolic, pulse pressure & HR • high rates (reach α1 & β1 receptors) = increase diastolic & mean pressure, decrease HR (reflexly) |
|
Norepinephrine
|
Class: Adrenergic receptor agonist (Mixed or Nonselective)
Use: • used in neurogenic & septic shock (especially if shock persists after adequate fluid replacement) • support of BP during spinal anesthesia Mechanism: stimulates α1, α2 & β1 receptors equally (not β2)) Side Fx: Other: - must be given parenterally - actions last only a few minutes - increases all pressure measures & reflexly decreases HR at both high & low infusion rates |
|
Isoproterenol
|
Class: Adrenergic receptor agonist (Mixed or Nonselective)
Use: • asthma - bronchodilator • bradyarrhythmias • 3rd degree A-V block (until pacemaker can be inserted) • assist tilt table tests - diagnosis of unexplained syncopes Mechanism: stimulates all β but not α receptors Side Fx: Other: - must be given parenterally - actions last only a few minutes - both low & high rates decrease diastolic & mean pressures, while increasing pulse pressure & HR |
|
Dopamine
|
Class: Adrenergic receptor agonist (Mixed or Nonselective)
Use: • cardiogenic, neurogenic & septic shock • CHF pts • bradycardia in pts. not in cardiac arrest (if unresponsive to other treatments) Mechanism: stimulates D receptors (w/ low level stimulation of β1 & α1) - found mainly iin GI & renal arterial smooth muscle Side Fx: chance of actually decreasing rather than increasing renal blood flow Other: - must be given parenterally - actions last only a few minutes - low dose - D receptors - selectively increases blood flow to GI & kidney - intermediate dose - β1 receptors - stimulate cardiac contractility & rate - high dose - α1 receptors - mean arterial BP rises substantially (b/c of increase in TPR |
|
Dobutamine
|
Class: adrenergic receptor agonists (Selective β1-agonists)
Use: • CHF pts • certain forms of shock • stimulate heart during emergence from surgery Mechanism: selectively stimulates β1 receptors - increase CO & pulse pressure w/o increasing diastolic & mean BP Side Fx:administration after acute MI may lead to more O2 deficit, tachycardia &/or arrhythmia Other: must be given parenterally - actions last only a few minutes - mix of 2 stereoisomers • α1 agonist • potent β1 agonist w/ α1 antagonist |
|
Metaproterenol
|
Class: adrenergic receptor agonists (Selective β2-agonists)
Use: • bronchodilators (most often by inhalation)... COPD & asthma pts, and prevent exercise- bronchospams • terbutailine - also used to manage preterm labor - β2 -mediated uterine relaxation Mechanism: fairly selectively stimulate β2 receptors Side Fx: Other: - readily absorbed after oral administration - may last for hours |
|
Albuterol
|
Class: adrenergic receptor agonists (Selective β2-agonists)
Use: • bronchodilators (most often by inhalation)... COPD & asthma pts, and prevent exercise- bronchospams • terbutailine - also used to manage preterm labor - β2 -mediated uterine relaxation Mechanism: fairly selectively stimulate β2 receptors Side Fx: marked tachyarrhythmias Other: - readily absorbed after oral administration - may last for hours |
|
Terbutaline
|
Class: adrenergic receptor agonists (Selective β2-agonists)
Use: • bronchodilators (most often by inhalation)... COPD & asthma pts, and prevent exercise- bronchospams • terbutailine - also used to manage preterm labor - β2 -mediated uterine relaxation Mechanism: fairly selectively stimulate β2 receptors Side Fx: marked tachycardia in mother & fetus Other:- readily absorbed after oral administration - may last for hours |
|
Salmeterol
|
Class: adrenergic receptor agonists (Selective β2-agonists)
Use: • bronchodilators (most often by inhalation)... COPD & asthma pts, and prevent exercise- bronchospams • terbutailine - also used to manage preterm labor - β2 -mediated uterine relaxation Mechanism: fairly selectively stimulate β2 receptors Side Fx: Other: - readily absorbed after oral administration - may last for hours |
|
Pirbuterol
|
Class: adrenergic receptor agonists (Selective β2-agonists)
Use: • bronchodilators (most often by inhalation)... COPD & asthma pts, and prevent exercise- bronchospams • terbutailine - also used to manage preterm labor - β2 -mediated uterine relaxation Mechanism: fairly selectively stimulate β2 receptors Side Fx: Other: - readily absorbed after oral administration - may last for hours |
|
Phenylephrine
|
Class: adrenergic receptor agonists (Selective α1 agonists)
Use: • spinal & other anesthesia - maintain diastolic & mean BP • hemorrhoids • nasal congestion • mydriatic agent • given IV to treat paroxysmal supraventricular tachycardia (only rarely) Mechanism: α1 agonist Side Fx: local dermal tissue necrosis (due to massive local skin vasoconstriction) - b/c of injection of large amt. of α-agonist for systemic therapy misses vein & ends up in surrounding tissue - possibility of HTN Other: when given IV, raises diastolic & mean BP like NE, but w/ more reflex bradycardia than NE |
|
Midodrine
|
Class: adrenergic receptor agonists (Selective α1 agonists)
Use: • orthostatic HTN sypmtoms Mechanism: α1 agonist Side Fx: local dermal tissue necrosis (due to massive local skin vasoconstriction) - b/c of injection of large amt. of α-agonist for systemic therapy misses vein & ends up in surrounding tissue - possibility of HTN Other: - a prodrug - better absorbed w/ oral administration than phenyleph. |
|
Cocaine
|
Class: Indirect acting Sympathomimetics
Use: • good local anesthetic agent (exerts its own local vasoconstrictor action at site of local injection = retards its own loss from site) • pain relief & reducing epistaxis during intubation (rarely) Mechanism: - inhibits reuptake of NE at sympathetic nerve terminals Side Fx: CNS effects Other: must be given parenterally - actions last only a few minutes |
|
Pseudoephedrine
|
Class: Indirect acting Sympathomimetics
Use: nasal & bronchial congestion (promotes nasal & sinus drainage) Mechanism: stimulate release of NE from sympathetic nerve endings (independent of nerve APs) - also stimulate adrenergic receptors directly Side Fx: Other: |
|
Phentolamine
|
Class: Non-selective (α1 & α2) adrenergic blockers
Use: • Diagnosis of pheochromocytoma ("Phentolamine Test") - marked short-term fall in BP = presence of pheochromocytoma • used during surgery to remove pheocr. • reverse excess acute systemic vasoconstriction & related HTN produced by i.v. overdose w/ non-specific α-agonists (like NE) • prevent local dermal tissue necrosis (from accidental injection of non-specific α-agonists • New form (Ora Verse) - reverses oral soft-tissue anesthesia & related deficits from intraoral submucosal injection of local anesthetic containing a vasoconstrictor (like Epin.) Mechanism: short-acting (blocks both α1 & α2 receptors) - but not irreversibly Side Fx: nausea, vomiting, diarrhea increased GI motility Other: contraindicated in pts. w/ ulcers |
|
Prazosin
|
Class: Selective α1 adrenergic blockers
Use: • long-term treatment of mild to moderate primary HTN (esp. when given w/ diuretic to offset fluid retention) • relax smooth m. of the bladder neck & prostatic urethra = relief of obstructive urinary symptoms of BPH • Raynaud's Mechanism: α1 blocker Side Fx: 1st dose phenomenon - orthostatic hypotension w/ syncope...only severe on 1st day of administration - some salt & water retention - some tachycardia - but not as much as nonselective drugs, b/c no inhibition of α2-mediated neg. feedback control of NE release from symp. nerve endings in SA node |
|
Doxazosin
|
Class: Selective α1 adrenergic blockers
Use: - same as Prazosin, but longer acting...better for long-term control of chronic HTN (fewer doses pt. has to remember) Mechanism: α1 blocker Side Fx: Other: - newer than prazosin |
|
Tamsulosin
|
Class: Selective α1 adrenergic blockers
Use: drug of choice for BPH Mechanism: selective for blocking subtype A of α1 (α1A) receptor...main subtype in smooth m. of bladder neck & prostate Side Fx: more specific for BPH symptoms, less systemic side effects |
|
Alfuzosin
|
Class: Selective α1 adrenergic blockers
Use: treatment of BPH, but not receptor subtype selective - still demonstrates "uroselectivity" w/ unknown mechanism Mechanism: α1 blocker Side Fx: Other: available in extended release formulation for oral administration once daily |
|
Propranolol
|
Class:
Use: Mechanism: Side Fx: Other: |
|
Reserpine
|
Class: Adrenergic Neuron Blocker (Peripheral)
Use: A) one of 1st antihypertensives, but now rarely used MOA: A) depletes storage of peripheral NE in vesicles of sympathetic nerve endings (reduces BP by lowering cardiac output & TPR) SFx: A) sedation, mental depression C) migraines (via fx on serotonin) D) postural hypotension, bradycardia E) fluid retention F) nasal congestion Other: depleting action is irreversible...BP lowering persists even after stopping drug |
|
Methyldopa
|
Class: Adrenergic Neuron Blocker (Central)
Use: A) HTN during pregnancy B) rarely used now for Other forms of HTN MOA: A) prodrug, converted to methylnorepinephrine, accumulates in NE vesicles B) α2-receptor agonist on vasomotor centers in brain (decrease sympathetic outflow from CNS...less renal renin released... fall in TPR, CO may decrease) SFx: A) some postural hypotension, but less than most B) sedation C) dry mouth D) autoimmune disorders E) parkinsonian signs |
|
Clonidine (Catapres)
|
Class: Adrenergic Neuron Blocker (Central)
Use: A) HTN (very commonly prescribed) MOA: A) α2-receptor agonist on vasomotor centers in brain (decrease sympathetic outflow from CNS...less renal renin released... fall in TPR, CO may decrease) SFx: A) some postural hypotension, but less than most B) sedation C) dry mouth D) local skin rxns Other: availabe in patch form...smoOther BP control, less rebound HTN vs. oral drug |
|
Prazosin (Minipress)
|
Class: α1-Adrenergic Receptor Blocker
Use: A) HTN B) improves glucose tolerance (for diabetics) C) may lower cholesterol & triglycerides, raise HDLs MOA: A) block arterial α1-receptors...competitively inhibits binding of sympathetically released NE (less vasoconstriction = decreased BP by lowering TPR) B) same effect seen in veins (initial decrease in CO = decreased BP) SFx: A) severe "first dose" postural hypotension (esp. if taking diuretic)...less if: 1) start w/ low dose 2) pt. lays down 1st day 3) stop diuretic for few days before taking this (then restart diuretic) B) continued postural hypotension C) worsens stress-induced urinary incontinence (esp. elderly women) D) reflex tachycardia, fluid retention E) shouldn't be given concurrently w/ drugs for erectile dysfunction (dangerous drop in BP) Other: A) slowly increase dose B) shorter acting (taken 3x/day) |
|
Doxazosin (Cardura)
|
Class: α1-Adrenergic Receptor Blocker
Use: A) HTN B) improves glucose tolerance (for diabetics) C) may lower cholesterol & triglycerides, raise HDLs MOA: A) block arterial α1-receptors...competitively inhibits binding of sympathetically released NE (less vasoconstriction = decreased BP by lowering TPR) B) same effect seen in veins (initial decrease in CO = decreased BP) SFx: A) less severe "first dose" postural hypotension (esp. if taking diuretic)...less if: 1) start w/ low dose 2) pt. lays down 1st day 3) stop diuretic for few days before taking this (then restart diuretic) B) continued postural hypotension C) worsens stress-induced urinary incontinence (esp. elderly women) D) reflex tachycardia, fluid retention E) shouldn't be given concurrently w/ drugs for erectile dysfunction (dangerous drop in BP) Other: longer-acting...taken 1x/day |
|
Terazosin (Hytrin)
|
Class: α1-Adrenergic Receptor Blocker
Use: A) HTN B) improves glucose tolerance (for diabetics) C) may lower cholesterol & triglycerides, raise HDLs MOA: A) block arterial α1-receptors...competitively inhibits binding of sympathetically released NE (less vasoconstriction = decreased BP by lowering TPR) B) same effect seen in veins (initial decrease in CO = decreased BP) SFx: A) less severe "first dose" postural hypotension (esp. if taking diuretic)...less if: 1) start w/ low dose 2) pt. lays down 1st day 3) stop diuretic for few days before taking this (then restart diuretic) B) continued postural hypotension C) worsens stress-induced urinary incontinence (esp. elderly women) D) reflex tachycardia, fluid retention E) shouldn't be given concurrently w/ drugs for erectile dysfunction (dangerous drop in BP) Other: longer-acting...taken 1x/day |
|
Propranolol (Inderal)
|
Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonist at β1 & β2-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) however, inhibition of physiologic B2-mediated vasodilation limits antihypertensive effectiveness E) high lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) all non-cardiac symptoms are less severe w/ cardioselective β-blockers |
|
Nadolol (Corgard)
|
Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A competitive antagonist at β1 & β2-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) however, inhibition of physiologic B2-mediated vasodilation limits antihypertensive effectiveness E) low lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) all non-cardiac symptoms are less severe w/ cardioselective β -blockers |
|
Timolol (Blocadren)
|
Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina, arrhythmia, migraine or Other dx responsive to β-blockers C) treat "silent" ischemia MOA: A competitive antagonists at β1 & β2-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) however, inhibition of physiologic B2-mediated vasodilation limits antihypertensive effectiveness E) moderate lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) less severe non-cardiac side fx (b/c of ISA) |
|
Pindolol (Visken)
|
Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonists at β1 & β2-receptors B) has ISA, so lowers BP mainly by decrease in TPR C) less decrease in contractility & renin compared to Other non-selective blockers (partially stimulates vascular β receptors) D) moderate lipid solubility SFx: A) cardiac arrest (in pts. susceptible to A-V block) B) rebound HTN (w/ sudden withdrawal) C) bronchoconstriction (pts. may require inhalable bronchodilator) D) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) E) hypertriglyceridemia, fall in HDLs Other: often combined w/ nitrate (inhibit adverse reflex fx of nitrates) |
|
Atenolol (Tenormin)
|
Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonists at β1-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) low lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) less severe non-cardiac side fx |
|
Metoprolol (Lopressor/Toprol-XL)
|
Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonists at β1-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) moderate lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) E) hypertriglyceridemia, fall in HDLs |
|
Acebutolol (Sectral)
|
Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonists at β1-receptors B) has ISA C) low lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) E) hypertriglyceridemia, fall in HDLs F) less severe non-cardiac side fx |
|
Labetalol (Normodyne)
|
Class: α1/β Blocker
Use: A) severe forms of 1° HTN B) hypertensive emergencies (given i.v.) MOA: A) competitive inhibitor at α1 & β1,2-adrenergic receptors B) BP falls by decrease in mainly TPR (also some decrease in CO) SFx: A) postural hypotension (from α-blockade) B) bradycardia & A-V block (high dose of β-blockers) C) don't see reflex tachycardia seen w/ Other α1-blockers |
|
Nebivolol (Bystolic)
|
Class: NO-releasing β1 Blocker
Use: A) hypertensive pts. w/ impaired endothelial function MOA: A) competitive β1-antagonist B) increases production (vascular endothelium) & release, decreases degradation of NO = dilation of vascular smooth m. C) decreased renin release, HR, contractility (β1-blocking) D) so drop in BP due to both decreased TPR & CO SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) E) hypertriglyceridemia, fall in HDLs F) fatigue, headache |
|
Hydralazine
|
Class: Direct Arteriolar Dilators
Use: A) HTN B) not commonly used today MOA: A) decrease BP by decreasing TPR through directly dilating arterioles (not veins) B) unknown mechanism SFx: A) alone cause massive dilation of arterioles...increased capillary hyd. pressure = edema B) renal retention of Na+ & water C) drop in BP activates SNS = increased renin, NE, E = greater retention of Na+ & water (tachycardia, edema, loss of efficacy) D) Lupus-like rxn PK: A) "rapid" acetylators show smaller drug fx than "slow" acetylators B) combined w/ β-blocker & diuretic (to inhibit compensatory mechanisms) |
|
Minoxidil
|
Class: Direct Arteriolar Dilators
Use: A) most severe forms of HTN (w/ signs of renal insufficiency) B) not commonly used today for normal HTN MOA: A) decrease BP by decreasing TPR through directly dilating arterioles (not veins) B) active sulfate metabolite...opens ATP-sensitive K+ channels in arteriolar smooth m. = relaxation SFx: A) alone cause massive dilation of arterioles...increased capillary hyd. pressure = edema B) renal retention of Na+ & water C) drop in BP activates SNS = increased renin, NE, E = greater retention of Na+ & water (tachycardia, edema, loss of efficacy) D) hair growth PK: combined w/ β-blocker & diuretic (to inhibit compensatory mechanisms) |
|
Verapamil (Calan)
|
Class: Calcium Channel Blockers
Use: A) HTN B) angina (preventative) MOA: A) decreases Ca2+ entry through L-type Ca2+ channels in heart ...lowers ventricular contractility = lowers CO SFx: A) suppresses HR & A-V conduction (excessive bradycardia) B) nausea, headache C) constipation PK: available in slow-release formulations |
|
Diltiazem (Cardizem)
|
Class: Calcium Channel Blockers
Use: A) HTN B) angina (preventative) MOA: A) decreases Ca2+ entry through L-type Ca2+ channels in heart ...lowers ventricular contractility = lowers CO SFx: A) suppresses HR & A-V conduction (weaker effect than w/ verapamil) B) nausea, headache PK: available in slow-release formulations |
|
Nifedipine (Procardia)
|
Class: Calcium Channel Blockers
Use: A) effective in all types of HTN, esp. elderly & African Americans B) work well in pts. w/ high Na+ intake (irrespective of degree of Na+ sensitivity) C) primary pulmonary HTN (unique) D) angina (preventative & treatment of acute attacks) MOA: A) decreases Ca2+ entry through arterial L-type Ca2+ channels into vascular smooth m. cells = reduction in arterial vascular tone = drop in TPR B) inherent natriuretic capability SFx: A) reflex tachycardia (due to peripheral vasodilation) B) nausea, headache C) postural hypotension D) ankle edema PK: A) dihydropyridine B) long-acting, slow onset (avoid rapid, short-acting preparations) |
|
Felodipine (Plendil)
|
Class: Calcium Channel Blockers
Use: A) effective in all types of HTN, esp. elderly & African Americans B) work well in pts. w/ high Na+ intake (irrespective of degree of Na+ sensitivity) MOA: A) decreases Ca2+ entry through arterial L-type Ca2+ channels into vascular smooth m. cells = reduction in arterial vascular tone = drop in TPR B) inherent natriuretic capability SFx: A) reflex tachycardia (due to peripheral vasodilation) B) nausea, headache C) postural hypotension D) ankle edema PK: A) dihydropyridine B) long-acting, slow onset (avoid rapid, short-acting preparations) |
|
Furosemide (Lasix)
|
Class: Loop Diuretic
Use: A) CHF B) pulmonary edema C) HTN (thiazides better) D) hypercalcemia E) edema of nephrotic syndrome or liver cirrhosis F) used w/ hypertonic saline to treat hyponatremia MOA: A) act in the thick ascending limb - block Na+-K+-2Cl- symporter in apical membrane (called high ceiling diuretics b/c of high reabsorptive capacity of thick ascending limb - strongest effect) B) blocking Na+ reabsorption inhibits kidney's ability to produce dilute urine and C) prevents generation of hyperosmotic medullary interstitium around collecting duct...so also inhibit kidneys ability to produce concentrated urine D) via prostaglandins - increase renal blood flow & systemic venous capacitance = decreases left ventricular filling pressure E) enhances excretion of Na+, Cl-, K+, H+, Ca++, Mg++, NH4, bicarb, phosphate F) drug overdose (rapidly increase renal excretion) SFx: A) hypotension, hypovolemia, hyponatremia B) hypochloremic metabolic alkalosis & hypokalemia...may lead to cardiac arrhythmias C) Gout D) ototoxicity (more likely in pts. taking ototoxic aminoglycoside antibiotics...gentamycin) E) sulfonamide hypersensitivity rxns (use ethacrynic acid if pt. has allergy) F) (hyperglycemia, increased LDLs & triglycerides, hypomagnesemia...loss of lumen + potential, NSAIDS can decrease diuretic response, can increase plasma lithium...toxic) PK: A) sulfonamide derivative B) bound to plasma proteins C) secreted by proximal tubule via organic acid secretion D) excreted unchanged in urine or metabolized by kidney |
|
Hydrochlorothiazide
|
Class: Thiazide diuretic
Use: A) edema of heart failure B) HTN (less effective w/ low GFR) C) prevent calcium nephrolithiasis & osteoporosis (by decreasing excretion of CA2+) D) nephrogenic diabetes insipidus (paradoxical effect) E) ascites associated w/ liver cirrhosis (give spironolactone 1st to avoid hypokalemic alkalosis) MOA: A) inhibits Na+-Cl- symporter in distal convoluted tubule = NaCl excretion, water diuresis B) action independent of pt's acid-base balance C) ^ excretion of Na+, Cl- K+, H+; decreased excretion of Ca++ SFx: A) hypokalemia & metabolic alkalosis (increased excretion of K+ & H+ in late distal tubule & collecting duct) B) Gout C) sulfonamide allergy D) Stevens-Johnson syndrome E) hyperglycemia F) increase plasma LDL & total cholesterol, triglycerides G) fatal hyponatremia H) lithium toxicity PK: A) secreted by organic acid secretory system in proximal tubule |
|
Triamterene (Dyrenium)
|
Class: K+ sparing Diuretics (inhibitors of renal Na+ channels)
Use: A) limited diuretic capacity B) combined w/ other diuretics to treat edema, HTN (counterbalance hypokalemia) C) Liddle's Syndrome (pseudohypoaldosteronism...excess Na+ reabsorption, K+ & H+ secretion) MOA: A) block luminal Na+ channels in principal cells of late distal tubule & collecting duct - prevent K+ secretion B) decreased H+ secretion by intercalated cell (cortical collecting duct) SFx: A) life-threatening hyperkalemia B) not used w/ spironolactone (risk of A above) C) nausea, vomiting, leg cramps, dizziness D) cautionary use w/ ACE inhibitors (hyperkalemia) & agents that block renin E) kidney stones (poorly soluble) PK: A) secreted in proximal tubule by organic base secretory system B) orally administered C) metabolized in liver |
|
Chlorthalidone (Hygroton)
|
Class: Thiazide & thiazide-like diuretics
Use: A) edema of heart failure B) HTN (less effective w/ low GFR) C) prevent calcium nephrolithiasis & osteoporosis (by decreasing excretion of CA2+) D) nephrogenic diabetes insipidus (paradoxical effect) E) ascites associated w/ liver cirrhosis (give spironolactone 1st to avoid hypokalemic alkalosis) MOA: A) inhibits Na+-Cl- symporter in distal convoluted tubule = NaCl excretion, water diuresis B) action independent of pt's acid-base balance C) ^ excretion of Na+, Cl- K+, H+; decreased excretion of Ca++ SFx: A) hypokalemia & metabolic alkalosis (increased excretion of K+ & H+ in late distal tubule & collecting duct) B) Gout C) sulfonamide allergy D) Stevens-Johnson syndrome E) hyperglycemia F) increase plasma LDL & total cholesterol, triglycerides G) fatal hyponatremia H) lithium PK: A) secreted by organic acid secretory system in proximal tubule |
|
Indapamide (Lozol)
|
Class: Thiazide & thiazide-like diuretics
Use: A) edema of heart failure B) HTN (still effective w/ low GFR) C) prevent calcium nephrolithiasis & osteoporosis (by decreasing excretion of CA2+) D) nephrogenic diabetes insipidus (paradoxical effect) E) ascites associated w/ liver cirrhosis (give spironolactone 1st to avoid hypokalemic alkalosis) MOA: A) inhibits Na+-Cl- symporter in distal convoluted tubule = NaCl excretion, water diuresis B) action independent of pt's acid-base balance C) ^ excretion of Na+, Cl- K+, H+; decreased excretion of Ca++ SFx: A) hypokalemia & metabolic alkalosis (increased excretion of K+ & H+ in late distal tubule & collecting duct) B) Gout C) sulfonamide allergy D) Stevens-Johnson syndrome E) hyperglycemia F) unlike other thiazides, doesn't increase LDL, total cholesterol or triglycerides G) fatal hyponatremia H) lithium toxicity PK: A) most potent thiazide diuretic, with greatest oral absorption B) secreted by organic acid secretory system in proximal tubule |
|
Spironolactone (Aldactone)
|
Class: K+ sparing Diuretics (Aldosterone antagonists)
Use: A) edema & HTN (given w/ loop/thiazide diuretic)...prevents hypokalemia B) hyperaldosteronism MOA: A) antagonist at mineralocorticoid (aldosterone) receptors (prevents aldosterone-induced gene transcription) B) blocks effects of aldosterone in cortical collecting duct (aldo. ^ luminal Na+ conductance, ^ basolateral Na+/K+ ATPase activity, ^ secretion of K+ & H+) SFx: A) life threatening hyperkalemia B) never combined w/ other K+ sparing diuretics C) antiandrogen fx (by interactions w/ androgen, progesterone & other receptors) D) not combined w/ ACE inhibitors PK: A) synthetic steroid, metabolized in liver to canrenone B) efficacy depends on endogenous aldosterone levels C) intracellular site of action (not lumen) |
|
Eplerenone (Inspra)
|
Class: K+ sparing Diuretics (Aldosterone antagonists)
Use: A) edema & HTN (given w/ loop/thiazide diuretic)...prevents hypokalemia B) hyperaldosteronism MOA: A) antagonist at mineralocorticoid (aldosterone) receptors (prevents aldosterone-induced gene transcription) B) blocks effects of aldosterone in cortical collecting duct (aldo. ^ luminal Na+ conductance, ^ basolateral Na+/K+ ATPase activity, ^ secretion of K+ & H+) SFx: A) life threatening hyperkalemia B) never combined w/ other K+ sparing diuretics C) antiandrogen fx (by interactions w/ androgen, progesterone & other receptors) D) not combined w/ ACE inhibitors PK: A) synthetic steroid |
|
Captopril
|
Class: Angiotensin Converting Enzyme (ACE) Inhibitors
Use: A) 1° HTN pts (w/ low or high renin) B) HTN 2° to diabetic nephropathy MOA: A) inhibit conversion of angiotensin I to angiotensin II...reverses A-II mediated vasoconstriction = decrease in TPR & BP (also decreased aldosterone = Na+ & water retention reduced) B) blocks inactivation of bradykinin by ACE = increased bradykinin (& related PG vasodilators) = decreased BP & TPR C) blocks A-II stimulated NE release (so NE-mediated vasoconstriction is inhibited) SFx: A) 1st dose hypotension (decreased w/ smaller initial doses) B) not used in pts. w/ bilateral renovascular HTN (would cause more loss of GFR) C) chronic use may = hyperkalemia & excessive hypotension D) rash, loss of taste, renal problems (due to sulfhydryl group - only captopril) E) buildup of Bradykinin (= nonproductive cough) F) angioedema G) NSAIDS block antihypertensive fx of it (block bradykinin-mediated vasodilation H) harm fetal development PK: A) eliminated by kidneys |
|
Enalapril
|
Class: Angiotensin Converting Enzyme (ACE) Inhibitors
Use: A) HTN MOA: A) inhibit conversion of angiotensin I to angiotensin II...reverses A-II mediated vasoconstriction = decrease in TPR & BP (also decreased aldosterone = Na+ & water retention reduced) B) blocks inactivation of bradykinin by ACE = increased bradykinin (& related PG vasodilators) = decreased BP & TPR C) blocks A-II stimulated NE release (so NE-mediated vasoconstriction is inhibited) SFx: A) 1st dose hypotension (decreased w/ smaller initial doses) B) not used in pts. w/ bilateral renovascular HTN (would cause more loss of GFR) C) chronic use may = hyperkalemia & excessive hypotension D) buildup of Bradykinin (= nonproductive cough) E) angioedema F) NSAIDS block antihypertensive fx of it (block bradykinin-mediated vasodilation G) harm fetal development PK: A) prodrug B) eliminated by kidneys |
|
Lisinopril
|
Class: Angiotensin Converting Enzyme (ACE) Inhibitors
Use: A) HTN MOA: A) inhibit conversion of angiotensin I to angiotensin II...reverses A-II mediated vasoconstriction = decrease in TPR & BP (also decreased aldosterone = Na+ & water retention reduced) B) blocks inactivation of bradykinin by ACE = increased bradykinin (& related PG vasodilators) = decreased BP & TPR C) blocks A-II stimulated NE release (so NE-mediated vasoconstriction is inhibited) SFx: A) 1st dose hypotension (decreased w/ smaller initial doses) B) not used in pts. w/ bilateral renovascular HTN (would cause more loss of GFR) C) chronic use may = hyperkalemia & excessive hypotension D) buildup of Bradykinin (= nonproductive cough) E) angioedema F) NSAIDS block antihypertensive fx of it (block bradykinin-mediated vasodilation G) harm fetal development PK: A) eliminated by kidneys |
|
Fosinopril
|
Class: Angiotensin Converting Enzyme (ACE) Inhibitors
Use: A) HTN MOA: A) inhibit conversion of angiotensin I to angiotensin II...reverses A-II mediated vasoconstriction = decrease in TPR & BP (also decreased aldosterone = Na+ & water retention reduced) B) blocks inactivation of bradykinin by ACE = increased bradykinin (& related PG vasodilators) = decreased BP & TPR C) blocks A-II stimulated NE release (so NE-mediated vasoconstriction is inhibited) SFx: A) 1st dose hypotension (decreased w/ smaller initial doses) B) not used in pts. w/ bilateral renovascular HTN (would cause more loss of GFR) C) chronic use may = hyperkalemia & excessive hypotension D) buildup of Bradykinin (= nonproductive cough) E) angioedema F) NSAIDS block antihypertensive fx of it (block bradykinin-mediated vasodilation G) harm fetal development PK: A) prodrug B) long-acting C) eliminated by kidneys, but can be eliminated by liver (used in pts. w/ renal insufficiency) |
|
Losartan
|
Class: Angiotensin II Receptor Blockers (ARBs)
Use: A) HTN MOA: A) competitive antagonist of angiotensin II at its main receptor B) reverses A-II mediated vasoconstriction = decrease in TPR & BP (also decreased aldosterone = Na+ & water retention reduced) C) blocks A-II stimulated NE release (so NE-mediated vasoconstriction is inhibited) SFx: A) 1st dose hypotension (decreased w/ smaller initial doses) B) not used in pts. w/ bilateral renovascular HTN (would cause more loss of GFR) C) chronic use may = hyperkalemia & excessive hypotension D) harm fetal development PK: A) 1/2 is short acting, but active metabolite is longer acting (1 dose = 24 BP control) |
|
Valsartan
|
Class: Angiotensin II Receptor Blockers (ARBs)
Use: A) HTN MOA: A) competitive antagonist of angiotensin II at its main receptor B) reverses A-II mediated vasoconstriction = decrease in TPR & BP (also decreased aldosterone = Na+ & water retention reduced) C) blocks A-II stimulated NE release (so NE-mediated vasoconstriction is inhibited) SFx: A) 1st dose hypotension (decreased w/ smaller initial doses) B) not used in pts. w/ bilateral renovascular HTN (would cause more loss of GFR) C) chronic use may = hyperkalemia & excessive hypotension D) harm fetal development |
|
Aliskiren
|
Class: Renin Inhibitors
Use: A) HTN MOA: A) inhibits action of renin...so angiotensinogen not converted to angiotensin I...reverses A-II mediated vasoconstriction = decrease in TPR & BP (also decreased aldosterone = Na+ & water retention reduced) SFx: A) 1st dose hypotension (decreased w/ smaller initial doses) B) not used in pts. w/ bilateral renovascular HTN (would cause more loss of GFR) C) chronic use may = hyperkalemia & excessive hypotension D) harm fetal development PK: oral, taken 1x/day |
|
Reserpine
|
Class: Adrenergic Neuron Blocker (Peripheral)
Use: A) one of 1st antihypertensives, but now rarely used MOA: A) depletes storage of peripheral NE in vesicles of sympathetic nerve endings (reduces BP by lowering cardiac output & TPR) SFx: A) sedation, mental depression C) migraines (via fx on serotonin) D) postural hypotension, bradycardia E) fluid retention F) nasal congestion PK: depleting action is irreversible...BP lowering persists even after stopping drug |
|
Methyldopa
|
Class: Adrenergic Neuron Blocker (Central)
Use: A) HTN during pregnancy B) rarely used now for other forms of HTN MOA: A) prodrug, converted to methylnorepinephrine, accumulates in NE vesicles B) α2-receptor agonist on vasomotor centers in brain (decrease sympathetic outflow from CNS...less renal renin released... fall in TPR, CO may decrease) SFx: A) some postural hypotension, but less than most B) sedation C) dry mouth D) autoimmune disorders E) parkinsonian signs |
|
Clonidine
|
Class: Adrenergic Neuron Blocker (Central)
Use: A) HTN (very commonly prescribed) MOA: A) α2-receptor agonist on vasomotor centers in brain (decrease sympathetic outflow from CNS...less renal renin released... fall in TPR, CO may decrease) SFx: A) some postural hypotension, but less than most B) sedation C) dry mouth D) local skin rxns PK: availabe in patch form...smoother BP control, less rebound HTN vs. oral drug |
|
Nicotine
|
Class: Ganglionic Stimulant
Use: • CNS - wean pts. from nicotine addiction (gradually decrease dose) • CVS (via neuronal subtype) - low doses = adrenergic predominance (ie. increased peripheral vasoconstriction...HTN) - high doses = fall in BP (due to reversal of its ganglionic stimulating action to a ganglionic blocking action) • GI (via neuronal subtype) - increases motility at low doses, opposite at high doses • Skeletal m. - via muscular subtype in neuromuscular junctions Mechanism: acts on all subtypes of nicotinic receptors Side Fx: - CNS - can cause vomiting ...interactions w/ chemoreceptor trigger zone Toxicity: - treatment is symptom-directed - has short half life...inactivated rapidly - if ingest insecticide, induce vomiting w/ activated charcoal - Green tobacco sickness Other: passes placental barrier and bbb low doses - stimulant high doses - depressant |