Q: What are two toxicities associated with Cyclosporine?
A: 1. Predisposes to viral infections and lymphoma
A: 2. Nephrotoxic (preventable with mannitol diuresis)
Q: What are two toxicities of the Glitazones?
A: 1. Weight gain
A: 2. Hepatotoxicity (troglitazone)
Q: What are two toxicities of the Sulfonylureas?
A: 1. Hypoglycemia (more common with 2nd-generation drugs: glyburide, glipizide)
A: 2. Disulfiram-like effects (not seen with 2nd-generation drugs).
Q: What are two types of drugs that interfere with the action of Sucralfate and why?
A: Sucralfate cannot work in the presence of antacids or H2 blockers because it requires an acidic environment to polymerize.
Q: What can result due to antacid overuse?
A: Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
Q: What enzyme does Zileuton inhibit?
A: Lipoxygenase
Q: What enzymes are inhibited by NSAIDs, acetaminophen and COX II inhibitors?
A: Cyclooxygenases (COX I, COX II).
Q: What is a common side effect of Colchicine used to treat acute gout, especially when given orally?
A: GI side effects. (Note: Indomethacin is less toxic, more commonly used.)
Q: What is a common side effect of Misoprostol?
A: Diarrhea
Q: What is a possible result of overdose of Acetaminophen?
A: Overdose produces hepatic necrosis; acetaminophen metablolite depletes glutathione and forms toxic tissue adducts in liver.
Q: What is a possible toxicity of Alpha-glucosidase inhibitors used in type-2 diabetes?
A: GI disturbances.
Q: What is a possible toxicity of Ticlopidine, Clopidogrel usage?
A: Neutropenia (ticlopidine); reserved for those who cannot tolerate aspirin.
Q: What is a sign of toxicity with the use of thrombolytics?
A: Bleeding.
Q: What is action of insulin in the liver, in muscle, and in adipose tissue?
A: 1. In liver, increases storage of glucose as glycogen.
A: 2. In muscle, stimulates glycogen and protein synthesis, and K+ uptake.
A: 3. In adipose tissue, facilitates triglyceride storage.
Q: What is are two clinical uses of Cyclosporine?
A: 1. Suppresses organ rejection after transplantation
A: 2. Selected autoimmune disorders.
Q: What is the category and mechanism of action of Zafirlukast in Asthma treatment?
A: Antileukotriene; blocks leukotriene receptors.
Q: What is the category and mechanism of action of Zileuton in Asthma treatment?
A: Antileukotriene; blocks synthesis by lipoxygenase.
Q: What is the category of drug names ending in -ane (e.g. Halothane)
A: Inhalational general anesthetic.
Q: What is the category of drug names ending in -azepam (e.g. Diazepam)
A: Benzodiazepine.
Q: What is the category of drug names ending in -azine (e.g. Chlorpromazine)
A: Phenothiazine (neuroleptic, antiemetic).
Q: What is the category of drug names ending in -azol (e.g. Ketoconazole)
A: Antifungal.
Q: What is the category of drug names ending in -barbital (e.g. Phenobarbital)
A: Babiturate.
Q: What is the category of drug names ending in -caine (e.g. Lidocaine)
A: Local anesthetic.
Q: What is the category of drug names ending in -cillin (e.g. Methicillin)
A: Penicillin.
Q: What is the category of drug names ending in -cycline (e.g. Tetracycline)
A: Antibiotic, protein synthesis inhibitor.
Q: What is the category of drug names ending in -ipramine (e.g. Imipramine)
A: Tricyclic antidepressant.
Q: What is the category of drug names ending in -navir (e.g. Saquinavir)
A: Protease inhibitor.
Q: What is the category of drug names ending in -olol (e.g. Propranolol)
A: Beta antagonist.
Q: What is the category of drug names ending in -operidol (e.g. Haloperidol)
A: Butyrophenone (neuroleptic).
Q: What is the category of drug names ending in -oxin (e.g. Digoxin)
A: Cardiac glycoside (inotropic agent).
Q: What is the category of drug names ending in -phylline (e.g. Theophylline)
A: Methylxanthine.
Q: What is the category of drug names ending in -pril (e.g. Captopril)
A: ACE inhibitor.
Q: What is the category of drug names ending in -terol (e.g. Albuterol)
A: Beta-2 agonist.
Q: What is the category of drug names ending in -tidine (e.g. Cimetidine)
A: H2 antagonist
Q: What is the category of drug names ending in -triptyline (e.g. Amitriptyline)
A: Tricyclic antidepressant.
Q: What is the category of drug names ending in -tropin (e.g. Somatotropin)
A: Pituitary hormone.
Q: What is the category of drug names ending in -zosin (e.g. Prazosin)
A: Alpha-1 antagonist
Q: What is the category, desired effect, and adverse effect of Isoproterenol in the treatment of Asthma?
A: Nonspecific beta-agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Adverse effect is tachycardia (Beta 1).
Q: What is the category, desired effect, and period of use of albuterol in the treatment of Asthma?
A: Beta 2 agonist; desired effect is the relaxation of bronchial smooth muscle (Beta 2). Use during acute exacerbation.
Q: What is the category, desired effect, and possible mechanism of Theophylline in treating Asthma?
A: Methylzanthine; desired effect is bronchodilation, may cause bronchodilation by inhibiting phosphodiesterase, enzyme involved in degrading cAMP (controversial).
Q: What is the category, mechanism of action, and effect of Ipratroprium in Asthma treatment?
A: Muscarinic antagonist; competatively blocks muscarinic receptors, preventing bronchoconstriction.
Q: What is the category, mechanism of action, and particular use of beclomethasone and prednisone in Asthma treatment?
A: Corticosteroids; prevent production of leukotrienes from arachodonic acid by blocking phospholipase A2. Drugs of choice in a patient with status asthmaticus (in combination with albuterol.)
Q: What is the category, method of use, and adverse effects of Salmeterol in Asthma treatment?
A: Beta 2 agonist; used as a long-acting agent for prophylaxis. Adverse effects are tremor and arrhythmia.
Q: What is the clincial use for Misoprostol?
A: Prevention of NSAID-induced peptic ulcers, maintains a PDA.
Q: What is the clinical use for Clomiphene?
A: Treatment of infertility.
Q: What is the clinical use for Heparin?
A: Immediate anticoagulation for PE, stroke, angina, MI, DVT.
Q: What is the clinical use for Sildenafil (Viagra)?
A: Erectile dysfunction.
Q: What is the clinical use for Sucralfate?
A: Peptic ulcer disease.
Q: What is the clinical use for Warfarin?
A: Chronic anticoagulation.
Q: What is the clinical use of Mifepristone (RU486)?
A: Abortifacient.
Q: What is the clinical use of Tacrolimus (FK506)?
A: Potent immunosuppressive used in organ transplant recipients.
Q: What is the effect of the Glitazones in diabetes treatment?
A: Increase target cell response to insulin.
Q: What is the enzyme inhibited, the effect of this inhibition, and the clinical use of the antiandrogren Finasteride?
A: Finasteride inhibits 5 Alpha-reductase, this decreases the conversion of testosterone to dihydrotestosterone, useful in BPH
Q: What is the lab value used to monitor the effectiveness of Heparin therapy?
A: The PTT.
Q: What is the lab value used to monitor the effectiveness of Warfarin therapy?
A: The PT.
Q: What is the main clinical use for the thrombolytics?
A: Early myocardial infarction.
Q: What is the mecanism of action of Sucralfate?
A: Aluminum sucrose sulfate polymerizes in the acid environment of the stomach and selectively binds necrotic peptic ulcer tissue. Acts as a barrier to acid, pepsin, and bile.
Q: What is the mecanism of action of the COX-2 inhibitors (celecoxib, rofecoxib)?
A: Selectively inhibit cyclooxygenase (COX) isoform 2, which is found in inflammatory cells nad mediates inflammation and pain; spares COX-1 which helps maintain the gastric mucosa.
Q: What is the mecanism of action, effective period, and ineffective period of use for Cromolyn in treating Asthma?
A: Prevents release of mediators from mast cells. Effective only for the prophylaxis of asthma. Not effective during an acute attack.
Q: What is the mechanism of action and clinical use of the antiandrogen Flutamide?
A: Flutamide is a nonsteroidal competitive inhibitor of androgens at the testosterone receptor, used in prostate carcinoma.
Q: What is the mechanism of action and clinical use of the antiandrogens Ketoconazole and Spironolactone?
A: Inhibit steroid synthesis, used in the treatment of polycystic ovarian syndrome to prevent hirsutism.
Q: What is the mechanism of action of Acetaminophen?
A: Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.
Q: What is the mechanism of action of Allopurinol used to treat chronic gout?
A: Inhibits xanthine oxidase, decresing conversion of xanthine to uric acid.
Q: What is the mechanism of action of Aspirin?
A: Acetylates and irreversibly inhibits cyclooxygenase (COX I and COX II) to prevent the conversion of arachidonic acid to prostaglandins.
Q: What is the mechanism of action of Clomiphene?
A: Clomiphene is a partial agonist at estrogen receptors in the pituitary gland. Prevents normal feedback inhibition and increses release of LH and FSHfrom the pituitary, which stimulates ovulation.
Q: What is the mechanism of action of Colchicine used to treat acute gout?
A: Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.
Q: What is the mechanism of action of Cyclosporine?
A: Binds to cyclophilins (peptidyl proline cis-trans isomerase), blocking the differentiation and activation of T cells mainly by inhibiting the production of IL-2 and its receptor.
Q: What is the mechanism of action of Heparin?
A: Heparin catalyzes the activation of antithrombin III.
Q: What is the mechanism of action of Mifepristone (RU486)?
A: Competitive inibitor of progestins at progesterone receptors.
Q: What is the mechanism of action of Misoprostol?
A: Misoprostol is a PGE1 analog that increases the production and secretion of the gastic mucous barrier.
Q: What is the mechanism of action of NSAIDs other than Aspirin?
A: Reversibly inhibit cyclooxygenase (COX I and COX II). Block prostaglandin synthesis.
Q: What is the mechanism of action of Omeprazole, Lansoprazole?
A: Irreversibly inhibits H+/K+ ATPase in stomach parietal cells.
Q: What is the mechanism of action of Probenacid used to treat chronic gout?
A: Inhibits reabsorption of uric acid.
Q: What is the mechanism of action of Sildenafil (Viagra)?
A: Inhibits cGMP phosphodiesterase, casuing increased cGMP, smooth muscle relaxation in the corpus cavernosum, increased blood flow, and penile erection.
Q: What is the mechanism of action of the Alpha-glucosidase inhibitors?
A: Inhibit intestinal bursh border Alpha-glucosidases; delayed hydrolysis of sugars and absorption of sugars leading to decresed postprandial hyperglycemia.
Q: What is the mechanism of action of the glucocorticoids?
A: Decrease the production of leukotrienes and protaglandins by inhibiting phospholipase A2 and expression of COX-2.
Q: What is the mechanism of action of the H2 Blockers?
A: Reversible block of histamine H2 receptors
Q: What is the mechanism of action of the Sulfonylureas?
A: Close K+ channels in Beta-cell membrane leading to cell depolarization causing insulin release triggered by increase in Calcium ion influx.
Q: What is the mechanism of action of the thrombolytics?
A: Directly of indirectly aid conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots. (It is claimed that tPA specifically converts fibrin-bound plasminogen to plasmin.)
Q: What is the mechanism of action of Ticlopidine, Clopidogrel
A: Inhibits platelet aggregation by irreversibly inhibiting the ADP pathway involved in the binding of fibrinogen.
Q: What is the mechanism of action of Warfarin (Coumadin)?
A: Warfarin interferes with the normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, Protein C and S via vitamin K antagonism.
Q: What is the mechanism of Azathioprine?
A: Antimetabolite derivative of 6-mercaptopurine that interferes with the metablolism and synthesis of nucleic acid.
Q: What is the mechanism of Leuprolide?
A: GnRH analog with agonist properties when used in pulsatile fashion and antagonist properties when used in continuous fashion, causing a transient initial burst of LH and FSH
Q: What is the mechanism of Tacrolimus (FK506)?
A: Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.
Q: What is the memory key for the action of Sildenafil (Viagra)?
A: Sildenafil fills the penis
Q: What is the memory key for the effect of aluminum hydroxide overuse?
A: AluMINIMUM amount of feces.
Q: What is the memory key for the effect of magnesium hydroxide overuse?
A: Mg = Must go to the bathroom.
Q: What is the memory key to remember which pathway (extrinsic vs. intrinsic) and which lab value Warfarin affects?
A: WEPT: Warfarin affects the Extrinsic pathway and prolongs the PT.
Q: What is the possible mechanism and effect of Metformin in treating diabetes?
A: Mechanism unknown; possibly inhibits gluconeogenesis and increases glycolysis; effect is to decrease serum glucose levels
Q: What is the specific clinical use of Indomethacin in neonates?
A: Indomethacin is used to close a patent ductus arteriosus.
Q: What is used to reverse the action of Heparin?
A: Protamine Sulfate is used for rapid reversal of heparinization (positively charged molecule that binds to negatively charged heparin).
Q: What patients are at risk for life threatening hypotension when taking Sildenafil (Viagra)?
A: Those patients who are taking nitrates.
Q: What process does Zafirlukast interfere with?
A: Leukotrienes increasing bronchial tone.
Q: What type of gout is treated with Allopurinol?
A: Chronic gout.
Q: What type of gout is treated with Colchicine?
A: Acute gout.
Q: What type of gout is treated with Probenacid?
A: Chronic gout.
Q: What type of patient should not take Misoprostol and why?
A: Misoprostol is contraindicated in women of childbearing potential because it is an abortifacient.
Q: Which H2 Blocker has the most toxic effects and what are they?
A: Cimetidine is a potent inhibitor of P450; it also has an antiandrogenic effect and decreases renal excretion of creatinine. Other H2 blockers are relatively free of these effects.
Q: Why are the Sulfonylureas inactive in IDDM (type-1)?
A: Because they require some residual islet function.
Pharmacology Cardiology Q&a
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
المواضيع المتشابهه
pharmacology Q & A
تجميعاتي لمواقع على النت هامة
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