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69 Cards in this Set

  • Front
  • Back
Methyldopa
Centrally acting Sympathoplegic
-A2>A1
-replaces NE in adrenergic vesicles
-agonist at CNS adrenergic receptors
-used for HTN
Ephedrine
Direct/Indirect Adrenergic Agonist
- mimic actions of Epi
-mild stimulant,cross blood-brain, not effected by COMT (can take PO), racemic, decongestant
Metaraminol
Direct-indirect adrenergic agonist
- mimic actions of Epi, treatment for hypotension
Cocaine
Indirect adrenergic agonist
-Alpha receptors, displaces NE at receptors (elevated NE), decreases dopamine reuptake (elevated dopa),topical anesthetic, vasoconstrict
Tyramine
Indirect Adrenergic Agonist
found in fermented foods, inactivated by digestion, sympathomimetic if not digested
Amphetamine
indirect Adrenergic Agonist
elevates (NE, Serotonin, Dopa), enters CNS (no -OH group), elevated mood, decreased appetite
Diltiazem
non-Dihydropyradine Ca++ Blocker(don't give B-Blockers). acts in vessels&heart,decreased PVR/HR/contractility/o2 Demand,used with angina&HTN. Toxicity:AV block,additive with cardiac depressents&anti-HTN
Verapamil
non-Dihydropyradine Ca-blocker (don't give B-blockers). Act on vessels&heart, decrease PVR/HR/contractility. Use with angina, HTN.Toxicity:AV block, additive with cardiac depressants and anti-HTN
Nifedipine
Dihydropyradine Ca-blocker, acts on vessels, decrease PVR. Toxicity: hypotension, additive with vasodilators
Amlodipine
Dihydropyradine Ca-blocker. acts on vessels, decrease PVR. Toxicity: hypotension, additive with vasodilators. HIGH AFFINITY FOR CEREBRAL VESSLELS
Nicardipine
IV-Dihydropyradine Ca-blocker, acts on vessels, decrease PVR. Toxicity: hypotension, additive with vasodilators
Bepridil
Dihydropyradine Ca-blocker, also blocks Na channels. Decreases PVR, may cause torsades, don't use with hx of severe arrythmias
Clevidipine
IV-Dihydropyradine Ca-Blocker, decrease PVR, short onset/duration (acts like esmolol), fat emulsion, use for 24 hours only
Guanethidine
Ganglion Blocking (sympathetic nerve terminal blocker) replaces NE is vessicles (decreased NR at receptors), decreases BP, diarrhea, blocks nicotinic receptors. Toxic: orthostatic, sexual dysfunction
Resperine
Ganglion blocker (sympathetic nerve terminal blocker). Blocks re-uptake and storage of NE, decreased NE, Dopa, serotonin. Toxic: sedation, Gi disturbances
Clonodine
Central Acting Sympathoplegic, Alpha 2
decreases catecholamines, use for HTN, sleep, migrains, neuropathic pain. Causes initial increase BP
Metolprolol
Beta-antagonist, B1>B2, decrease HR & BP, decrease renin, safer with asthma. Use in angina,HTN, arrythmias. Causes decrease HR, fatigue. Membrane stabilizing
Atenolol
Beta-antagonist, B1>B2, decrease HR & BP, decrease renin, safer with asthma. Use in angina, HTN, arrythmias. Causes decreased HR, fatigue
Betaxolol
Beta-antagonist, B1>B2, decrease HR & BP, decrease renin, safer with asthma. Use in angina, HTN, arrythmias. Causes decreased HR, fatigue
Nebivolol
Beta-antagonist, B1>B2, decreased HR & BP, decreased renin, safer with asthma, use in angina, HTN, arrythmias. Cause decreased HR, fatigue
Butoxamine
Beta-antagonist, B2>B1, elevates PVR, used topically in eye
Timolol
Beta-antagonist, B1 and B2. Decreases HR and renin. Used with HTN, angina, arrythmias, migains, hyperthyroidism. Causes decreased HR, worse asthma, fatigue
Nadolol
Beta-antagonist, B1 and B2. Decreases HR and renin, used with HTN, angina, arrythmias, migrains, hyperthyroidism. Causes decreased HR, worse asthma, fatigue
Propranolol
Beta-antagonist, B1 and B2. Decreases HR and renin, used with HTN, angina, arrythmias, migrains, hyperthyroidism. Causes decreased HR, worse asthma, fatigue. Membrane stabilizing
Terazosin
Alpha-antagonist, A1
Relaxes arteries and veins, no increase in catecholamines. Used with BPH, HTN (1st dose effect)
Doxazosin
Alpha-antagonist, A1
Relaxes arteries and veins, no increase in catecholamines. Used with BPH, HTN (1st dose effect). Decreases insulin release
Prazosin
Alpha-antagonist, A1>>>>A2
relaxes arteries and veins, no increase in catecholamines, used for BPH, HTN (1st dose effect)
Phentolamine
Alpha-antagonist, A1=A2
Vasodilation, increase in catecholamines (A2 blocked). Used for pheochromocytoma, nasal congestion
Phenoxybenzamine
Alpha-antagonist, A1>A2
Covalent bonds, lowers BP (HR increased due to baroreceptors), inhibit NE reuptake. Use with pheochromocytome, nasal congestion. Toxicity:increased HR, hypotension
Tamsulosin
Alpha-antagonist, A1 competative (slight A1a).
Blocks prostate smooth muscle more than vascular, less effect on BP. Used with BPH
Pindolol
partial Beta-antagonist, B1,B2 sympathomimetic
Decrease BP, slight decrease HR. Use with HTN, arrythmias, migrains. May avoid worsening of bradycardia, fatigue
Acebutolol
Partial Beta-antagonist, B1, B2. Decreased BP, slight decrease in HR. Use with HTN, arrythmias, migrains. May avoid worsening of bradycardia, fatigue
Carteolol
Partial Beta-antagonist, B1, B2
Decrease BP, slight decrease HR, used with HTN, arrythmias, migrains. May avoid worsening bradycardia, fatigue
Celipiolol
Partial Beta-antagonist, B1, B2
Decreased BP, slight decrease HR. Use with HTN, arrythmias, migrains. May avoid worsening bradycardia, fatigue
Penbutolol
Partial Beta-antagonist, B1, B2
Decrease BP, slight decrease HR. Use with HTN, arrythmias, migrains. May avoid worsening bradycardia, fatigue
Carvedilol
Partial Beta-antagonist B>A1
Long 1/2 life, used for heart failure, causes fatigue
Esmolol
IV Beta-antagonist, B1>B2
Decreases BP & HR. Use for arrythmias, HTN, MI-intra-op. Short 1/2 life, easy to titrate
Nitroprusside
Vasodilator, release of NO (looks like NO), Toxicity: cyanide poisoning (from metabolism)-->use sodium thiosulfate, Thyocyonate also toxic. Renal excretion
Fenoldopam
Vasodilator, activates D1 receptors
Powerful vasodilation, causes hypotension, possible shock
Diazoxide
Vasodilator, opens K+ channels
Powerful vasodilation, hypotension, possible shock. renal excretion
Minoxidil
Vasodilator, metabolite opens K+ channels is vascular smooth muscle. Toxicity: hypertrichosis, stronger than hydralazine
Hydralazine
Vasodilator, causes NO release. Vasodilation arteries>veins, reflex tachycardia. Toxicity: tachycardia, increased side effects with doses >400mg (slow acytylators)
Nitroglycerine
Nitrate, release NO in smooth muscle. Increased cGMP, decrease PVR, vasodilation, increase coronary flow, synergistic hypotension with phosphodiesterase inhibitors, volitile, SL-avoids 1st pass, 4 byproducts, can build tolerance
Amyl Nitrite
Nitrate, release NO in smooth muscle. Sympathetic discharge (increase HR/contractility due to vasodilation), more potent than NTG, most volitile of nitrates, can be inhaled, tolerance
Isosorbide
Nitrate, release of NO. Metabolite of NTG
Losartin
Angiotensin receptor blocker (ARB)
reduces angiotensin II, decrease vasoconstriction, No bradykinin effect--> no cough, teratogenic
Valsartin
Angiotensin receptor blocker (ARB)
reduces angiotensin II, decrease vasoconstriction, No bradykinin effect--> no cough, teratogenic
Captopril
ACE-inhibitor
reduces angiotensin II, decrease vasoconstriction and proteinuria, increase bradykinin, used with HTN&DM, short 1/2 life, causes cough, teratogenic
Enalapril
ACE-inhibitor
reduces angiotensin II, decrease vasoconstriction & proteinuria, increase bradykinin, used with HTN, DM. can cause cough, teratogenic
Lisinopril
ACE-inhibitor
reduces angiotensin II, decrease vasoconstriction & proteinuria, increase bradykinin, used with HTN, DM. can cause cough, teratogenic
Benzepril
ACE-inhibitor
reduces angiotensin II, decrease vasoconstriction & proteinuria, increase bradykinin, used with HTN, DM. can cause cough, teratogenic
Fosinopril
ACE-inhibitor
reduces angiotensin II, decrease vasoconstriction & proteinuria, increase bradykinin, used with HTN, DM. can cause cough, teratogenic
Quinapril
ACE-inhibitor
reduces angiotensin II, decrease vasoconstriction & proteinuria, increase bradykinin, used with HTN, DM. can cause cough, teratogenic
Ramipril
ACE-inhibitor
reduces angiotensin II, decrease vasoconstriction & proteinuria, increase bradykinin, used with HTN, DM. can cause cough, teratogenic
Terbutaline
Beta-agonist, B2
Smooth muscle vasodilation, relax uterus
Ritodrine
Beta-agonist, B2
Smooth muscle vasodilation
Metaproterenal
Beta-agonist, B2
Bronchodilator
Isoproteranol
Beta-agonist, B2
Vasodilator, increase CO, decrease DBP/MAP, increase/decrease SBP
0.5-5mcg/min
Catecholamine
Dopamine
Adrenergic-agonist, D, B1, A1 (high doses)
dilate renal arteries, increase urine output, B1 inotrope/chronotrope
Low: 1-3mcg/kg/min
Med: 2-10mcg/kg/min
High: >10mcg/kg/min
Catecholamine
Dobutamine
Adrenergic-agonist, B1, A1 (high doses)
positive inotrope, used for heart failure/cardiogenic shock.
2.5-15mcg/kg/min (45mcg max)
catecholamine
Albuterol
Adrenergic agonist, B2
Broncholar smooth muscle relaxation
Phenylephrine
Adrenergic agonist, A1
Vasoconstriction, 100x less potent then Epi, not inactivated by COMT
Norepinephrine
Adrenergic agonist, A, B1
Alpha vasoconstriction, increases SBP/DBP, vagal reflex decreases HR.
8-12 mcg/min
Catecholamine
Methoxamine
Adrenergic Agonist, A1
alpha vasoconstriction
Epinephrine
Adrenergic Agonist, A1=A2, B1=B2
alpha vasoconstriction, B1 inotrope, B2 chronotrope/dilate skeletal muscle
1-10mcg/min
Catecholamine
Clonodine
Adrenergic Agonist, A2
central sympatholytic effects: decrease catecholamines, use to treat HTN, sleep, migrains, neropathic pain, initial increase in BP
Oxymetazoline
Alpha agonist
used in nasal spray, high doses cross blood-brain barrier, ADHD drug
Xylometazoline
Alpha agonist
used in nasal spray, high doses cross blood-brain barrier, ADHD drug
Labetalol
Beta-antagonist, B, A1. Use with HTN and angina. Lesslikely to cause bradycardia and cholesterol abnormalities. Metabolized by CYP2D6