Cvs: Pharmacology

Front 1

What parameters increase the release of renin from the kidney?

Back 1

Reduced arterial pressure, decreased sodium delivery to the cortex, increased sodium at the distal tubule, and stimulation of sympathetic activity.

Front 2

Describe the steps from the release of renin to angiotensin III.

Back 2

Juxtaglomerular cells secrete renin. Renin cleaves angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II or III by ACE in the lung.

Front 3

Where, besides the kidney, can angiotensin II be produced?

Back 3

Angiotensin II can be produced locally (myocardium, adrenals, and vessel walls by the action of non-ACE pathways) by the action of chymases and cathepsins.

Front 4

What affect does ACE inhibitors have on CO, afterload, and preload?

Back 4

Increase CO and induce systemic arteriolar dilation (reduced afterload). Also cause venodilation and induce natriuresis (reducing preload).

Front 5

Enalapril and Captopril are examples of what?

Back 5

ACE inhibitors

Front 6

Diuretics ____ ACE inhibitors activity.

Back 6

Enhance.

Front 7

Theraputic uses of Enalapril?

Back 7

CHF, hypertension, slow the progression of renal disease in diabetics.

Front 8

What is valsartan?

Back 8

ARBs (angiotensin II receptor blocker). High affinity for AT1 receptors which normal cause vasoconstriction, aldosterone biosynthesis, proliferation/fibrosis of tissue in response to bound angiotensin II.

Front 9

Why do ACE inhibitors cause dry cough and angioedema?

Back 9

Increase bradykinin (vasodilation). Bradykinin is broken down by ACE.

Front 10

Whats the MOA of digitalis?

Back 10

Inhibit Na/K ATPase. Increases intracellular Na. Decreases exchange of intracellular Ca for Na. Intracellular Ca increases. This results in a positive inotropic effect.

Front 11

What are the adverse effects of digoxin?

Back 11

Arrhythmia. Increase parasympathetic activity: nausea, vomiting, diarrhea, blurry yellow vision.

Front 12

What neural effects does cardiac glycosides have?

Back 12

Cardiac glycosides = digitalis. Increase vagal activity, which inhibits SA node and conduction through AV node.

Front 13

What are cardiac glycosides used for?

Back 13

Atrial fib/flutter (decreases conduction at AV node and depression of SA node)
CHF (increases contractility)

Front 14

The half life of which of these drugs is prolonged in renal impairment: digoxin or digitoxin

Back 14

Digoxin is eliminated by the renal route, so its impaired. Digitoxin is excreted via the biliary route.

Front 15

What affects does quinidine have on digoxin?

Back 15

Quinidine decreases clearance

Front 16

What affect does hypokalemia have on digoxin?

Back 16

Digoxin competes with K at its binding site in Na/K ATPase. Decreasing K, increases digoxin binding and digoxin effects.

Front 17

How do class I antiarrhythmic drugs work?

Back 17

Block fast Na channels, thereby reducing the rate of phase 0 depolarization, prolonging the effective refractory period, increasing the threshold, and reducing phase 4 depolarization.

Front 18

Name the Class IA antiarrhythmics. What are they used for?

Back 18

Quinidine, procainamide, disopyramide.
Prolong the refractory period, slow conduction (phase 0), and increase action potential duration.
Suppress atrial and ventricular arrhythmias (broad spectrum).

Front 19

Name the Class IB antiarrhythmics. What are they used for?

Back 19

Lidocaine, mexiletine, tocainide.
Act on damaged tissue, b/c they act on Na channels that are firing rapidly (near -50 mV). They shorten phase 3 repolarization and decrease action potential duration. Tx: acute ventricular arrhythmia (post-MI) and in digitalis-induced arrhythmia.

Front 20

Name the Class IC antiarrhythmics. What are they used for?

Back 20

Flecainide, encainide, propafenone.
Markedly slow phase 0 depolarization.
No effect on AP duration. Used in VT that progress to VF. Particularly useful against PVC's.

Front 21

What are the Class II antiarrhythmics? Mechanism of action?

Back 21

Beta blockers.
Propranolol, esmolol, metoprolol, atenolol, timolol.
Reduce sympathetic stimulation. Decrease cAMP, decreases Ca current, which inhibit phase 4 depolarization. Increases PR interval (AV node is sensitive).

Front 22

What are beta-blockers used to treat?

Back 22

Treat tachyarrhythmias caused by increase in sympathetic activity. Also can be used for atrial flutter, fibrillation and for AV-nodal reentrant tachycardia.

Front 23

What are the Class III antiarrhythmics? Mechanism of action?

Back 23

Sotalol, ibutilide, amiodarone.
K channel blockers.
Increases AP duration, increases ERP.

Front 24

What are the adverse effects of amiodarone?

Back 24

Pulmonary fibrosis, corneal deposits, hepatotoxicity, photosensitivity (gray man syndrome), thyroid disorders.

Front 25

What are the Class IV antiarrhythmics? Mechanism of action?

Back 25

Ca channel blockers.
Verapamil, diltiazem.
primarily affect AV nodal cells, decrease conduction, increase ERP, increases PR.

Front 26

Class V antiarrhythmics include adenosine. What is its MOA?

Back 26

Adenosine causes an increase in K efflux and decreases Ca influx. Used to Tx WPW.

Front 27

What is atropine? What is it used to treat?

Back 27

Atropine blocks the effects of ACh. Increases sinus rate, nodal conduction, and decreases refractory period.
Used to treat bradyarrhythmias.

Front 28

What drugs reduce the half life of quinidine?

Back 28

Phenobarbital, phenytoin

Front 29

What antiarrhythmic drug causes torsade de point? How do you treat?

Back 29

Quinidine and Class III. Torsades de pointes has a characteristic twist of the QRS complex around the isoelectric point. It's associated with prolonged QT.
Magnesium sulfate.

Front 30

What drug is the best for treating ventricular tachycardia following an acute MI? Digitalis, quinidine, lidocaine, or obutamine.

Back 30

Lidocaine. It does not slow conduction.

Front 31

What class of antiarrhythmics do you use to treat atrial fibrillation caused by hyperthyroidism?

Back 31

Hyperthyroidism increases B-adrenoreceptors. Use beta blockers (Class II).

Front 32

What drug which you use as an adjunct to quinidine in the treatment of atrial flutter?

Back 32

Digitalis, because of its negative inotropic effects.

Front 33

What metabolite of nitroprusside is toxic?

Back 33

Nitroprusside liberates NO. It also releases cyanide ions which are converted in the liver (with thiosulfate) to thiocyanate by the enzyme rhodanase. Thiocyanate is excreted by the kidney.

Front 34

What does dipyridamole do?

Back 34

Coronary vasodilator. Interferes with uptake of the vasodilator adenosine. Potentiates the effect of PGI (prostacyclin) and dilates vessels and inhibits platelet aggregation.

Front 35

Loop diuretics can be used to treat hypertension, especially in individuals with diminished renal function. How do they work?

Back 35

Inhibits Na/K/2 Cl triporter.

Front 36

Side effects of loop diuretics.

Back 36

Potassium wasting, metabolic alkalosis, hypotension, ototoxicity

Front 37

What drug class should be used to treat hypertension in a patient with normal renal funciton?
MOA?
Adverse effects?

Back 37

Thiazides (hydrochlorothiazide). Inhibits Na/Cl cotransporter.
Side effects: hypokalemia, hyperlipidemia, hyperuricemia, hypercalcemia, hyperglycemia

Front 38

Prazosin (and terazosin, doxazosin) lowers total peripheral resistance by _____.

Back 38

Acting as an alpha-1 selective antagonists. Alpha 1 receptors are located in the skin, mucosa, intestine, and kidney.

Front 39

Prazosin may produce 1st dose _____.

Back 39

Orthostatic and exercise hypotension.

Front 40

Blocking B1-adrenoreceptors does what?
Blocking B2-adrenoreceptors does what?

Back 40

It reduces the heart rate and contractility.
It increases airway resistance, decreases glycogenolysis and peripheral vasodilation.

Front 41

How do metoprolol and propranolol differ?

Back 41

Metoprolol is B1-selective. Propranolol is nonselective.

Front 42

Name two centrally acting sympathomimetic agents that are used to treat hypertension.

Back 42

Methyl-dopa, clonidine. Both decrease total peripheral resistance.

Front 43

Methyl-dopa is used to treat? And how?

Back 43

Hypertension (when diuretics alone are not enough). They activate inhibitory presynaptic alpha adrenorceptors and postsynaptic alpha 2 receptors in the CNS to reduce sympathetic outflow.

Front 44

Why is reserpine useful in treating hypertension?

Back 44

Reserpine eliminates norepinephrine release in response to nerve impulse by preventing vesicular uptake.

Front 45

How does guanethidine reduce CO and TPR?

Back 45

Depletes norepinephrine concentrations.

Front 46

What two drugs are coadministered to patients who are put on hydralazine?

Back 46

Diuretic (because hydralazine elicits the baroreceptor reflex).
Beta blocker to prevent tachycardia.

Front 47

Which vasodilator drug can cause lupuslike syndrome?

Back 47

Hydralazine.

Front 48

Minoxidil increases K efflux and reduces L-type (voltage-sensitive) Ca channels, much like hyralazine. What strange side effect (beneficial for some) does it have?

Back 48

Hypertrichosis (hirsutism). Treat hair loss.

Front 49

What is furosemide and why is it coadministered with diazoxide or nitroprusside?

Back 49

Loop diuretic used to prevent fluid overload. Diazoxide and nitroprusside reduce blood pressure rapidly.

Front 50

What is first-line therapy for hypertension in pregnancy?

Back 50

Hydralazine and methyldopa.

Front 51

The -statins inhibit the cholesterol precursor, _______.

Back 51

Mevalonate. HMG-CoA reductase inhibitors: lovastatin, pravastatin, simvastatin, rosuvastatin. They slightly increase HDL

Front 52

What are the adverse effects of statins?

Back 52

Rhabdomyolysis, anxiety, irritability, hepatotoxicity and elevated LFT's.

Front 53

What does nicotinic acid?

Back 53

Reduces plasma VLDL by inhibiting the synthesis and esterification of FA in the liver and reducing lipolysis in adipose tissue. HDL also increases significantly.

Front 54

Gemfibrozil is a "fibrate" that is used to lower plasma lipids. What is its mode of action?

Back 54

It decreases triglyceride levels significantly by upregulating lipoproteinlipase.

Front 55

What drug acts within the intestine to reduce cholesterol absorption?

Back 55

Ezetimibe

Front 56

Cholestyramine, colestipol, and colesevelam do what to bile acid?

Back 56

They prevent intestinal reabsorption of bile acids. Liver must use cholesterol to make more.

Front 57

Besides its inotropic actions, what else do cardiac glycosides do?

Back 57

Increases vagal activity and decreases sympathetic tone.

Front 58

What is the order of potency do these Ca channel blockers have on vascular smooth muscle? On the heart?

nifedipine, diltiazem, verapamil

Back 58

Heart - verapamil > diltiazem > nifedipine

VSM - nifedipine > diltiazem > verapamil

Front 59

Which medication, if given to a patient who is on digoxin, may cause a dangerous arrhythmia?
Valsartan, hydrocholothiazide, hydralazine, lovastatin, tadalafil

Back 59

Hydrocholothiazide, which cause hypokalemia.

Front 60

Dobutamine is a synthetic catecholamine derivative that increases contractility. It acts on myocardial beta-1 adrenoceptors, increases cAMP, and Ca channels. When is it commonly used?

Back 60

Short-term therapy in individuals with severe chronic cardiac failure.

Front 61

If a patient with angina pectoris is allergic to asprin, clopidogrel can be used instead. What is the action of clopidogrel?

Back 61

Irreversiby blocks ADP receptors on platelets. Its used for arterial thromboembolism prophylaxis in high risk patients.

Front 62

What is the drug of choice for abolishing AV nodal arrhythmias such as paroxysmal supraventricular tachycardia?

Back 62

Adenosine. Toxicitiy: flushing, hypotension, chest pain.

Front 63

Nitrates venodilate which the most:
cardiac veins, large veins, small veins

Back 63

Large veins

Front 64

Amrinone lactate and milrinone reduce ___________ and vascular resistance and enhance cardiac output.

Back 64

Left ventricular filling pressure.

Front 65

What increases cardiac contractility, vasodilator, and acts by inhibiting phosphodiesterase (PDE III) in cardiac muscle thereby increasing cAMP and intracellular Ca?

Back 65

Amrinone and milrinone

Front 66

What is sotalol?

Back 66

Class III antiarrhythmic agent and a potent beta-blocker.

Front 67

What is the preferred antiarrhythmic in patients with severe heart failure?

Back 67

Amiodarone.

Front 68

Why should one avoid using flecainide in a patient with congestive heart failure?

Back 68

It has a negative inotropic effect.

Front 69

Which drug would be appropriate prophylactic antiarrhythmic therapy for someone who just had a MI?
Lidocaine
Metoprolol
Procainamide
Quinidine
Verapamil

Back 69

Metoprolol

Front 70

How do you suppress arrhythmias resulting from a reentry focus?

Back 70

Reentry is caused by tissue that slows conduction in only one direction. Use a drug that prevents conduction in either direction through the damaged area. Lidocaine (Class IC).

Front 71

Headache, dizziness, and tinnitus (characteristic of cinchoism) are caused by what drug?

Back 71

Quinidine.

Front 72

Why can amiodarone cause symptoms of hypothyroidism?

Back 72

Its structure is related to thyroid hormones.

Front 73

What drug should you use to treat a hypertensive diabetic? What drug is contraindicated?

Back 73

ACEi.

Beta-blockers because they mask the symptoms of hypoglycemia.

Front 74

What drug should you administer to a hypertensive, tachycardic patient with glaucoma.

Back 74

Beta-blocker