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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