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52 Cards in this Set

  • Front
  • Back
Major classes of antihypertensive drugs
Diuretics
Sympathoplegics
Vasodilators
ACE inhibitors
Angiotensin II receptor inhibitors
Major examples of antihypertensive diuretics
Hydrachlorothiazide
Loop diuretics
Major examples of antihypertensive sympathoplegics (mech)
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
Major examples of antiHTN vasodilators (mech)
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)
Major examples of antiHTN ACEI's
Captopril
Enalapril
Fosinopril
Major examples of angiotensin II receptor inhibitors
Losartan
Antihypertensive drug side effects: HCTZ
Hypokalemia, mild hyperlipidemia, hyperuricemia, lassitude (weariness), hypercalcemia, hyperglycemia
Antihypertensive drug side effects: loop diuretics
Potassium wasting, metabolic alkalosis, hypotension, ototoxicity
Antihypertensive drug side effects: clonidine
Dry mouth, sedation, severe rebound hypertension
Antihypertensive drug side effects: methyldopa
Sedation, positive Coomb's
Antihypertensive drug side effects: reserpine
Sedation, depression, nasal stuffiness, diarrhea
Antihypertensive drug side effects: guanethidine
Orthostatic hypotension, dizziness, headache
Antihypertensive drug side effects: prazosin
1st dose orthostatic hypotension, sexual dysfct, diarrhea
Antihypertensive drug side effects: beta blockers
Impotence, asthma, CV effects (bradycardia, CHF, AV block) CNS effects (sedation, sleep alterations)
Antihypertensive drug side effects: hydralazine
Nausea, HA, lupus like syndrome, reflex tachy, angina, salt retention
Antihypertensive drug side effects: minoxidil
Hypertrichosis, percardial effusion, reflex tacycardia, angina, salt retention
Antihypertensive drug side effects: nifedipine, verapamil
Dizziness, flushing constipation (verapamil), AV block (verapamil), nausea, edema
Antihypertensive drug side effects: nitroprusside
Cyanide toxicity (release CN)
Antihypertensive drug side effects: diazoxide
Hyperglycemia (reduce insulin release, hypotension)
Antihypertensive drug side effects: ACEI
Hyperkalemia, cough, angioedema, taste change, hypotension, pregnancy problems (fetal renal damage), rash, incr renin
Antihypertensive drug side effects: ARBs
Fetal renal toxicity, hyperkalemia
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
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
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
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
Malignant HTN treatment (and mechs)
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)
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
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
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
Calcium channel blockers in angina: nifedpine vs verapamil
Nifedipine has similar effects to nitrates
Verapamil has similar effects to beta blockers
Major types of lipid lowering agents
HMG CoA reductase inhibitors
Niacin
Bile acid resins
Cholesterol absorption blockers
"fibrates"
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
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
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
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
"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
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.
(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+
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).
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)
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
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
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.
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
Side effect: ibutilide
Torsades
Side effect sotalol
Torsades, excessive beta block
Side effect: bretylium
New arrythmias hypotension
Side effect amiodarone
Pulmonary fibrosis
Corneal and skin deposits
Neuro effects
Constipation
CV effects (bradycardia, heart block, CHF)
Hypothyroidism, hyperthyroidism
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)
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
K+ use as an arrhythmias
Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)
Mg2+ use in arrhythmias
Effective in torsades de pointes and digoxin toxicity