Pharmacology Cardiology Q&a

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Q: ACE inhibitors- clinical use?
A: hypertension, CHF, diabetic renal disease

Q: ACE inhibitors- mechanism?
A: reduce levels of Angiotensin II, thereby preventing the inactivation of bradykinin (a potent vasodilator); renin level is increased

Q: ACE inhibitors- toxicity?
A: fetal renal damage, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)

Q: Acetazolamide- clinical uses?
A: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness

Q: Acetazolamide- mechanism?
A: acts at the proximal convoluted tubule to inhibit carbonic anhydrase. Causes self-limited sodium bicarb diuresis and reduction of total body bicarb stores.

Q: acetazolamide- site of action?
A: proximal convoluted tubule

Q: Acetazolamide- toxicity?
A: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy

Q: Acetazolamide causesÉ?
A: ACIDazolamide' causes acidosis

Q: Adenosine- clinical use?
A: DOC in diagnosing and abolishing AV nodal arrhythmias

Q: ADH antagonists- site of action?
A: collecting ducts

Q: adverse effect of Nitroprusside?
A: cyanide toxicity (releases CN)

Q: adverse effects of beta-blockers?
A: impotence, asthma, CV effects (bradycardia, CHF, AV block), CNS effects (sedation, sleep alterations)

Q: adverse effects of Captopril?
A: fetal renal toxicity, hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems, Rash, Increased renin, Lower Angiotensin II (CAPTOPRIL)

Q: adverse effects of Clonidine?
A: dry mouth, sedation, severe rebound hypertension

Q: adverse effects of ganglionic blockers?
A: severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction

Q: adverse effects of Guanethidine?
A: orthostatic and exercise hypotension, sexual dysfunction, diarrhea

Q: adverse effects of Hydralazine?
A: nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retention

Q: adverse effects of Hydrochlorothiazide?
A: hypokalemia, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia

Q: adverse effects of Loop Diuretics?
A: K+ wasting, metabolic alkalosis, hypotension, ototoxicity

Q: adverse effects of Losartan?
A: fetal renal toxicity, hyperkalemia

Q: adverse effects of Methyldopa?
A: sedation, positive Coombs' test

Q: adverse effects of Minoxidil?
A: hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retention

Q: adverse effects of Nifedipine, verapamil?
A: dizziness, flushing, constipation (verapamil), nausea

Q: adverse effects of Prazosin?
A: first dose orthostatic hypotension, dizziness, headache

Q: adverse effects of Reserpine?
A: sedation, depression, nasal stuffiness, diarrhea

Q: Amiodarone- toxicity?
A: pulmonary fibrosis, corneal deposits, hepatotoxicity, skin deposits resulting in photodermatitis, neurologic effects, consitpation, CV (bradycardia, heart block, CHF), and hypo- or hyperthyroidism.

Q: antidote?
A: slowly normalize K+, lidocaine,
A: cardiac pacer, and anti-Dig Fab fragments

Q: Beta Blockers- CNS toxicity?
A: sedation, sleep alterations

Q: Beta Blockers- CV toxicity?
A: bradycardia, AV block, CHF

Q: Beta Blockers- site of action?
A: Beta adrenergic receptors and
A: Ca2+ channels (stimulatory)

Q: BP?
A: decrease

Q: BP?
A: decrease

Q: Bretyllium- toxicity?
A: new arrhythmias, hypotension

Q: Ca2+ channel blockers- clinical use?
A: hypertension, angina, arrhythmias

Q: Ca2+ channel blockers- mechanism?
A: block voltage dependent L-type Ca2+ channels of cardiac and smooth muscle- decreasing contractility

Q: Ca2+ channel blockers- site of action?
A: Cell membrane Ca2+ channels of cardiac sarcomere

Q: Ca2+ channel blockers- toxicity?
A: cardiac depression, peripheral edema, flushing, dizziness, constipation

Q: Ca2+ sensitizers'- site of action?
A: troponin-tropomyosin system

Q: Cautions when using Amiodarone?
A: check PFTs, LFTs, and TFTs

Q: class IA effects?
A: increased AP duration, increased ERP increased QT interval. Atrial and ventricular.

Q: class IB- clinical uses?
A: post MI and digitalis induced arrhythmias

Q: class IB- effects?
A: decrease AP duration, affects ischemic or depolarized Purkinje and ventricular system

Q: class IB- toxicity?
A: local anesthetic.
A: CNS stimulation or depression.
A: CV depression.

Q: class IC- effects?
A: NO AP duration effect.
A: useful in V-tach that progresses to V-fib
A: and in intractable SVT
A: LAST RESORT

Q: class IC- toxicity?
A: proarrhythmic

Q: class II- effects?
A: decrease the slope of phase 4, increase PR interval (the AV node is particularly sensitive)

Q: class II- mechanism?
A: blocking the beta adrenergic receptor leads to decreased cAMP, and decreased Ca2+ flux

Q: class II- toxicity?
A: impotence, exacerbation of asthma, CV effects, CNS effects, may mask hypoclycemia

Q: Class III- effects?
A: increase AP duration,
A: increase ERP,
A: increase QT interval,
A: for use when other arrhythmics fail

Q: class IV- clinical use?
A: prevention of nodal arrhythmias (SVT)

Q: class IV- effects?
A: decrease conduction velocity, increase ERP, increase PR interval

Q: class IV- primary site of action?
A: AV nodal cells

Q: class IV- toxicity?
A: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression), and torsade de pointes (Bepridil)

Q: classes of antihypertensive drugs?
A: diuretics, sympathoplegics, vasodilators, ACE inhibitors, Angiotensin II receptor inhibitors

Q: clinical use?
A: angina, pulmonary edema (also, erection enhancer)
A: (Nitroglycerine, Isosorbide Dinitrate)

Q: clinical use?
A: CHF, atrial fibrillation

Q: contractility?
A: increase (reflex response)

Q: contractility?
A: decrease

Q: contraindications?
A: renal failure, hypokalemia, pt on quinidine

Q: decrease Digitoxin dose in renal failure?
A: NO

Q: decrease Digoxin dose in renal failure?
A: YES

Q: Digitalis- site of action?
A: Na/K ATPase

Q: Digoxin v. Digitoxin: bioavailability?
A: Digitoxin>95%
A: Digoxin 75%

Q: Digoxin v. Digitoxin: excretion?
A: Digoxin=urinary
A: Digitoxin=biliary

Q: Digoxin v. Digitoxin: half life?
A: Digitoxin 168hrs
A: Digoxin 40 hrs

Q: Digoxin v. Digitoxin: protein binding?
A: Digitoxin 70%
A: Digoxin 20-40%

Q: ejection time?
A: decrease

Q: ejection time?
A: increase

Q: EKG results?
A: inc PR, dec QT, scooping of ST, and T wave inversion

Q: end diastolic volume?
A: decrease

Q: end diastolic volume?
A: increase

Q: Esmolol- short or long acting?
A: very short acting

Q: Ethacrynic Acid- clinical use?
A: Diuresis in pateints with sulfa allergy

Q: Ethacrynic Acid- mechanism?
A: not a sulfonamide, but action is the same as furosemide

Q: Ethacrynic Acid- toxicity?
A: NO HYPERURICEMIA, NO SULFA ALLERGY; same as furosemide otherwise

Q: Furosemide- class and mechanism?
A: Sulfonamide Loop Diuretic. Inhibits ion co-transport system of thick ascending loop. Abolishes hypertonicity of the medulla, thereby preventing concentration of the urine.

Q: Furosemide- clinical use?
A: edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema), HTN, hypercalcemia

Q: Furosemide- toxicity? (OH DANG)
A: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

Q: Furosemide increases the excretion of what ion?
A: Ca2+ (Loops Lose calcium)

Q: HDL effect?
A: no effect

Q: HDL effect?
A: increase

Q: HDL effect?
A: moderate increase

Q: HDL effect?
A: increase

Q: HDL effect?
A: DECREASE

Q: how do we stop angina?
A: decrease myocardial O2 consumption by:
A: 1-decreasing end diastolic volume
A: 2- decreasing BP
A: 3- decreasing HR
A: 4-decreasing contractility
A: 5-decreasing ejection time

Q: HR?
A: increase (reflex response)

Q: HR?
A: decrease

Q: Hydralazine- class and mechanism?
A: vasodilator- increases cGMP to induce smooth muscle relaxation (arterioles>veins; afterload reduction)

Q: Hydralazine- clinical use?
A: severe hypertension, CHF

Q: Hydralazine- toxicity?
A: compensatory tachycardia, fluid retention, lupus-like syndrome

Q: Hydrochlorothiazide- clinical use?
A: HTN, CHF, calcium stone formation, nephrogenic DI.

Q: Hydrochlorothiazide- mechanism?
A: Inhibits NaCl reabsorption in the early distal tubule. Decreases Ca2+ excretion.

Q: Hydrochlorothiazide- toxicity? (hyperGLUC, plus others)
A: Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia, sulfa allergy.

Q: Ibutilide- toxicity?
A: torsade de pointes

Q: K+- clinical use?
A: depresses ectopic pacemakers, especially in digoxin toxicity

Q: K+ sparing diuretics- clinical use?
A: hyperaldosteronism, K+ depletion, CHF

Q: K+ sparing diuretics- site of action?
A: cortical collecting tubule

Q: K+ sparing diuretics- toxicity?
A: hyperkalemia, endocrine effects (gynecomastia, anti-androgen)

Q: LDL effect?
A: moderate decrease

Q: LDL effect?
A: large decrease

Q: LDL effect?
A: moderate decrease

Q: LDL effect?
A: decrease

Q: LDL effect?
A: decrease

Q: loop diuretics (furosemide)- site of action?
A: thick ascending limb

Q: Mannitol- clinical use?
A: ARF, shock, drug overdose, decrease intracranial/intraocular pressure

Q: Mannitol- contraindications?
A: anuria, CHF

Q: Mannitol- mechanism?
A: osmotic diuretic- increase tubular fluid osmolarity, thereby increasing urine flow

Q: mannitol- site of action?
A: proximal convoluted tubule, thin descending limb, and collecting duct

Q: Mannitol- toxicity?
A: pulmonary edema, dehydration

Q: mechanism?
A: vasodilate by releasing NO in smooth muscle, causing and increase in cGMP and smooth muscle relaxation (veins>>arteries)
A: (Nitroglycerine, Isosorbide Dinitrate)

Q: mechanism?
A: inhibits the Na/K ATPase,
A: increasing intracellular Na+
A: decreasing the function of the Na/Ca antiport
A: causing an increase in intracellular Ca2+

Q: mechanism?
A: Na+ channel blockers. Slow or block conduction. Decreased slope in phase 4 and increased threshold for firing in abnormal pacemaker cells.

Q: Mg+- clinical use?
A: effective in torsade de pointes and digoxin toxicity

Q: MVO2?
A: decrease

Q: MVO2?
A: decrease

Q: name five in class II?
A: propanolol, esmolol, metoprolol, atenolol, timolol

Q: name four HMG-CoA reductase inhibitors.
A: Lovastatin, Pravastatin, Simvastatin, Atorvastatin

Q: name four in class IA.
A: Quinidine, Amiodarone, Procainamide, Disopyramide

Q: name four in class III.
A: Sotalol, Ibutilide, Bretylium, Amiodarone

Q: name three ACE inhibitors?
A: Captopril, Enalapril, Lisinopril

Q: name three calcium channel blockers?
A: Nifedipine, Verapamil, Diltiazem

Q: name three in class IB.
A: Lidocaine, Mexiletine, Tocainide

Q: name three in class IC.
A: Flecainide, Encainide, Propafenone

Q: name three in class IV.
A: Verapamil, Diltiazem, Bepridil

Q: name three K+ sparing diuretics?
A: Spironolactone, Triamterene, Amiloride (the K+ STAys)

Q: name two bile acid resins.
A: cholestyramine, colestipol

Q: name two LPL stimulators.
A: Gemfibrozil, Clofibrate

Q: Nifedipine has similar action to?
A: Nitrates

Q: preferential action of the Ca2+ channel blockers at cardiac muscle?
A: cardiac muscle: Verapamil>Diltiazem>Nifedipine

Q: preferential action of the Ca2+ channel blockers at vascular smooth muscle?
A: vascular sm. Mus.: Nifedipine>Diltiazem>Verapamil

Q: Procainamide- toxicity?
A: reversible SLE-like syndrome

Q: Quinidine- toxicity?
A: cinchonism: HA, tinnitus, thrombocytopenia, torsade de pointes due to increased QT interval

Q: Ryanodine- stie of action?
A: blocks SR Ca2+ channels

Q: selectivity?
A: slectively depress tissue that is frequently depolarized (fast tachycardia)

Q: side effects/problems?
A: tastes bad and causes GI discomfort

Q: side effects/problems?
A: expensive, reversible increase in LFTs, and myositis

Q: side effects/problems?
A: red, flushed face which is decreased by ASA or long term use

Q: side effects/problems?
A: myositis, increased LFTs

Q: side effects/problems?
A: DECREASED HDL

Q: Sotalol- toxicity?
A: torsade de pointes, excessive Beta block

Q: Spironolactone- mechanism?
A: competitive inhibirot of aldosterone in the cortical collecting tubule

Q: TG effect?
A: slight increase

Q: TG effect?
A: decrease

Q: TG effect?
A: decrease

Q: TG effect?
A: large decrease

Q: TG effect?
A: no effect

Q: thiazides- site of action?
A: distal convoluted tubule (early)

Q: toxicity?
A: tachycardia, hypotension, headache - 'Monday disease'
A: (Nitroglycerine, Isosorbide Dinitrate)

Q: toxicity?
A: nausea, vomiting, diarrhea, blurred vision, arrhythmia

Q: Triamterene and amiloride- mechanism?
A: block Na+ channels in the cortical collecting tubule

Q: Verapamil has similar action to?
A: Beta Blockers

Q: what two vasodilators require simultaneous treatment with beta blockers to prevent reflex tachycardia and diuretics to prevent salt retention?
A: Hydralazine and Minoxidil

Q: which diuretics cause acidosis?
A: carbonic anhydrase inhibitors, K+ sparing diuretics

Q: which diuretics cause alkalosis?
A: loop diuretics, thiazides

Q: which diuretics decrease urine Ca2+?
A: thiazides, amiloride

Q: which diuretics increase urine Ca2+?
A: loop diuretics, spironolactone

Q: which diuretics increase urine K+?
A: all except the K+ sparing diuretics Spironolactone, Triamterene, Amiloride

Q: which diuretics increase urine NaCl?
A: all of them