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52 Cards in this Set
- Front
- Back
Major classes of antihypertensive drugs
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Diuretics
Sympathoplegics Vasodilators ACE inhibitors Angiotensin II receptor inhibitors |
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Major examples of antihypertensive diuretics
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Hydrachlorothiazide
Loop diuretics |
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Major examples of antihypertensive sympathoplegics (mech)
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Clonidine (alpha 2 agonist)
Methyldopa (alpha 2 agonist) Reserpine (prevent transport into vesicles leading to MAO metabolism) Guanethidine (reduces release of catecholamines by inhibiting Na/ATPase dependent pump) Prazosin (alpha 1 blocker veins and arteries) Beta blockers |
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Major examples of antiHTN vasodilators (mech)
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Hydralazine (incr influx of K, leading to membrane hyperpolarization of smooth muscle cells)
Minoxidil (open K+ATPase, hyperpolarization of SM cells) Nifedipine (CCB selective for SM) Verapamil (non selective CCB) Nitroprusside (cause release of NO from RBC's-direct vasodilator) Diazoxide (open K+ channels in SM and beta islet cells-decr insulin secretion) |
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Major examples of antiHTN ACEI's
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Captopril
Enalapril Fosinopril |
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Major examples of angiotensin II receptor inhibitors
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Losartan
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Antihypertensive drug side effects: HCTZ
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Hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude (weariness), hypercalcemia, hyperglycemia
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Antihypertensive drug side effects: loop diuretics
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Potassium wasting, metabolic alkalosis, hypotension, ototoxicity
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Antihypertensive drug side effects: clonidine
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Dry mouth, sedation, severe rebound hypertension
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Antihypertensive drug side effects: methyldopa
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Sedation, positive Coomb's
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Antihypertensive drug side effects: reserpine
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Sedation, depression, nasal stuffiness, diarrhea
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Antihypertensive drug side effects: guanethidine
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Orthostatic hypotension, dizziness, headache
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Antihypertensive drug side effects: prazosin
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1st dose orthostatic hypotension, sexual dysfct, diarrhea
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Antihypertensive drug side effects: beta blockers
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Impotence, asthma, CV effects (bradycardia, CHF, AV block) CNS effects (sedation, sleep alterations)
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Antihypertensive drug side effects: hydralazine
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Nausea, HA, lupus like syndrome, reflex tachy, angina, salt retention
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Antihypertensive drug side effects: minoxidil
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Hypertrichosis, percardial effusion, reflex tacycardia, angina, salt retention
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Antihypertensive drug side effects: nifedipine, verapamil
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Dizziness, flushing constipation (verapamil), AV block (verapamil), nausea, edema
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Antihypertensive drug side effects: nitroprusside
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Cyanide toxicity (release CN)
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Antihypertensive drug side effects: diazoxide
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Hyperglycemia (reduce insulin release, hypotension)
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Antihypertensive drug side effects: ACEI
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Hyperkalemia, cough, angioedema, taste change, hypotension, pregnancy problems (fetal renal damage), rash, incr renin
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Antihypertensive drug side effects: ARBs
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Fetal renal toxicity, hyperkalemia
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Hydralazine
(a) mechanism (b) clinical use (c) toxicity |
(a) increase cAMP which causes SM relaxation. Vasodilates arterioles>veins; afterload reduction
(b) severe HTN; CHF. First line therapy for HTN in pregnancy w/methyldopa (c) compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, HA, angina. Lupus like syndrome |
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Minoxidil
(a) mechanism (b) clinical use (c) toxicity |
(a) K+ chanel opener-hyperpolarizes and relaxes smooth muscle
(b) severe HTN (c) hypertrichosis; pericardial effusion; reflex tachycardia; angina; salt retention |
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CCB's
(a) major examples (b) mechanism (c) clinical use (d) toxicity |
(a) nifedipine, cerapamil, dilitiazem
(b) block voltage dependent L type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility. (c) HTN, angina, arrhythmias (not nif), Pirnzmetal's angina, Raynaud's (d) cardiac depression, peripheral edema, flushing, dizziness, and constipation |
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Nitroglycerin, isosorbide dinitrate
(a) mechanism (b) clinical use (c) toxicity |
(a) vasodilate by releasing NO in smooth muscle causing incr cGMP and smooth muscle relaxation. Dilate veins>>arteries. Decr preload.
(b) angina, pulmonary edema. Also used as aphrodisiac and erection enhancer (c) tachycardia, hypotension, flushing, HA, "Monday disease" in industrial exposure; tolerance during work week and loss of tolerance over weekend resulting in tachycardia, dizziness, and HA on reexposure |
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Malignant HTN treatment (and mechs)
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Nitroprusside (short acting; increase cGMP via direct release of NO)
Fenoldopam (dopamine D1 receptor antagonist-relax renal vascular smooth muscle) Diazoxide (K+ channel opener-hyperpolarizes and relaxes vascular smooth muscle) |
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Antianginal therapy: Nitrates
Affect on: (a) preload or afterload (b) end diastolic volume (c) contractility (d) HR (e) ejection time (f) mycoardial O2 consumption (g) BP |
(a) preload (b) decrease EDV (c) increase contractility (reflex resp) (d) increase HR (reflex resp) (e) decr ejection time (f) decrease MVO2 (g) decr |
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Antianginal therapy: beta blockers
(a) preload or afterload (b) end diastolic volume (c) contractility (d) HR (e) ejection time (f) mycoardial O2 consumption (g) BP |
(a) afterload
(b) EDV incr (c) contractility decr (d) HR decr (e) Ejection time incr (f) MVO2 decr (g) BP |
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Antianginal therapy: beta blockers + nitrates
(a) end diastolic volume (b) BP (c) contractility (d) HR (e) ejection time (f) MVO2 |
(a) no effect or decr EDV
(b) decr BP (c) little/no effect on contractility (d) decr HR (e) ejection time little or no effect (f) MVO2 drastically decreased |
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Calcium channel blockers in angina: nifedpine vs verapamil
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Nifedipine has similar effects to nitrates
Verapamil has similar effects to beta blockers |
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Major types of lipid lowering agents
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HMG CoA reductase inhibitors
Niacin Bile acid resins Cholesterol absorption blockers "fibrates" |
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HMGCoA Reductase inhibitors
(a) effect on LDL (b) effect on HDL (c) effect on TG's (d) mechanism (e) side effects/problems |
(a) effect on LDL:
(b) effect on HDL: + (c) effect on TG's: decr (d) mechanism: inhibit cholesterol precursor mevalonate (e) side effects/problems: reversible incr in LFT's |
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Niacin
(a) effect on LDL (b) effect on HDL (c) effect on TG's (d) mechanism (e) side effects/problems |
(a) effect on LDL: decrease
(b) effect on HDL: ++ (c) effect on TG's: decrease (d) mechanism: inhibit lipolysis in adipose tissue; reduce hepatic VLDL secretion into circulation (e) side effects/problems: red, flushed face which is decr by aspirin or LT use |
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Bile acid resins
(a) major examples (b) effect on LDL (c) effect on HDL (d) effect on TG"s (e) mechanism (f) side effects/problems |
(a) major examples: cholestyramine, colestipol, colesevelam
(b) effect on LDL: decrease (c) effect on HDL: slightly incr (d) effect on TG's: slightly incr (e) mechanism: prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more (f) side effects/problems: Tastes bad and causes GI discomfort; decr absorption of fat soluble vits; contraindicated in pts w/gallstones |
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Cholesterol absorption blockers
(a) major examples (b) effect on LDL (c) effect on HDL (d) effect on TG"s (e) mechanism (f) side effects/problems |
(a) major examples: ezetimibe
(b) effect on LDL: decrease (c) effect on HDL: none (d) effect on TG"s: none (e) mechanism: prevent cholesterol reabsorption at small intestine brush border (f) side effects/problems: rare incr LFT's |
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"Fibrates"
(a) major examples (b) effect on LDL (c) effect on HDL (d) effect on TG"s (e) mechanism (f) side effects/problems |
(a) major examples: gemfibrozil, clofibrate, bezafibrate, fenofibrate
(b) effect on LDL: decr (c) effect on HDL:+ (d) effect on TG"s: majorly decr (e) mechanism: upregulate LPL which increases TG clearance (f) side effects/problems: myositis; incr LFTs |
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Cardiac glycosides
(a) major example (b) mechanism (c) clinical use |
(a) digoxin (protein bound; urinary secretion)
(b) direct inhibition of NaK pump leads to indirect inhibition of Na/Ca antiporter. Increase intracellular Ca2+ positive inotropy. Also stimulates vagus. (c) CHF to incr contractility; afib (decr conduction to AV node and depress SA node) inhibition of Na/Ca antiporter. Increase intracellular Ca2+ positive inotropy. Also stimulates vagus. |
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(a) ECG changes seen in digoxin toxicity
(b) side effects of digoxin toxicity (c) enhancers for digoxin toxicity (c) antidote |
(a) may cause incr PR, decr QT, scooping of ST, T wave inversion
(b) Incr parasymp; n/v/d. blurry yellow vision; arrhythmia (c) renal failure (decr exretion), hypokalemia (digoxing competes with K+ binding at Na/K pump) and quinidine (decr dig clearance; displaces dig from tissue binding sites) (d) slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab frags, Mg2+ |
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Class I antiarrhythmics
General effects |
Slow or block conduction esp in depolarized cells. Decr slope of phase 4 depol, incr threshold for firing in abnormal pacemaker. Are state dependent (selectively depress tissue that is frequently depolarized).
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Class IA
(a) examples (b) effect (c) clinical use (d) toxicity |
(a) Quinidine, Procainamide, Disopyramide
(b) incr AP duration, incr effective refractory period, incr QT interval (c) atrial and ventricular arrhythmias esp reentrant and ectopic supraventricular and ventricular tachycardia (d) quinidine (HA, tinnitus, thombocytopenia, torsades de pointes due to prolonged QT); procainamide (reversible SLE like syndrome) |
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Class IB
(a) examples (b) effect (c) clinical use (d) toxicity |
(a) Lidocaine, Mexiletine, Tocainide
(b) decr AP duration; affect depolarized Purkinje and ventricular tissue (c) useful in acute ventricular arrhythmias (d) toxicities: local anesthetic. CNS stimulation/depression, cardiovascular depression |
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Class I C
(a) examples (b) effect (c) clinical use (d) toxicity |
(a) Flecainide, envainide, propafenone
(b) NO effect on AP duration (c) useful in V tachs that progress to VF and intractable SVT; usually used as last resort in tachyarrhythmias; for patients without structural abn (d) proarrhythmic esp post MI (CI); significantly prolongs refractory period in AV node |
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Class II antiarrhythmics
(a) examples (b) mechanism (c) clinical use (d) toxicity |
(a) beta blockers (-alolols)
(b) decr cAMP, decr Ca2+ currents, suppress abnormal pacemakers by decr slope of phase 4; AV node part sensitive (incr PR) (c) Vtach, SVT, slow ventr rate during afib and aflut (d) impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS (sedation, sleep alterations). May mask hypoglycemia signs. Metoprolol can cause dyslipidemia. |
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Class III antiarryhthmics
(a) examples (b) mechanism (c) clinical use |
(a) Sotalol, ibutilide, amiodarone
(b) increase AP duration, incr ERP (c) used when other antiarrythmics fail; incr QT |
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Side effect: ibutilide
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Torsades
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Side effect sotalol
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Torsades, excessive beta block
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Side effect: bretylium
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New arrythmias hypotension
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Side effect amiodarone
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Pulmonary fibrosis
Corneal and skin deposits Neuro effects Constipation CV effects (bradycardia, heart block, CHF) Hypothyroidism, hyperthyroidism |
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Class IV antiarrythmics
(a) examples (b) mechanism (c) toxicity |
(a) verapamil, diltiazem
(b) CCB' s that primarily affect AV node cells. Decr conduction velocity, incr ERP and PR interval. Used in prevention of nodal arrythmias (SVT) (c) constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression) |
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Adenosine
(a) mechanism of antiarrhythmic action (b) clinical use (c) toxicity |
(a) incr K+ out of cells hyperpolarizing cell and decreasing incracellular Ca+.
(b) drug of choice indiagnosing/abolishing AV nodal arrythmias (c) flushing, hypotension, chest pain |
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K+ use as an arrhythmias
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Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)
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Mg2+ use in arrhythmias
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Effective in torsades de pointes and digoxin toxicity
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