Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
74 Cards in this Set
- Front
- Back
What parameters increase the release of renin from the kidney?
|
Reduced arterial pressure, decreased sodium delivery to the cortex, increased sodium at the distal tubule, and stimulation of sympathetic activity.
|
|
Describe the steps from the release of renin to angiotensin III.
|
Juxtaglomerular cells secrete renin. Renin cleaves angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II or III by ACE in the lung.
|
|
Where, besides the kidney, can angiotensin II be produced?
|
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.
|
|
What affect does ACE inhibitors have on CO, afterload, and preload?
|
Increase CO and induce systemic arteriolar dilation (reduced afterload). Also cause venodilation and induce natriuresis (reducing preload).
|
|
Enalapril and Captopril are examples of what?
|
ACE inhibitors
|
|
Diuretics ____ ACE inhibitors activity.
|
Enhance.
|
|
Theraputic uses of Enalapril?
|
CHF, hypertension, slow the progression of renal disease in diabetics.
|
|
What is valsartan?
|
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.
|
|
Why do ACE inhibitors cause dry cough and angioedema?
|
Increase bradykinin (vasodilation). Bradykinin is broken down by ACE.
|
|
Whats the MOA of digitalis?
|
Inhibit Na/K ATPase. Increases intracellular Na. Decreases exchange of intracellular Ca for Na. Intracellular Ca increases. This results in a positive inotropic effect.
|
|
What are the adverse effects of digoxin?
|
Arrhythmia. Increase parasympathetic activity: nausea, vomiting, diarrhea, blurry yellow vision.
|
|
What neural effects does cardiac glycosides have?
|
Cardiac glycosides = digitalis. Increase vagal activity, which inhibits SA node and conduction through AV node.
|
|
What are cardiac glycosides used for?
|
Atrial fib/flutter (decreases conduction at AV node and depression of SA node)
CHF (increases contractility) |
|
The half life of which of these drugs is prolonged in renal impairment: digoxin or digitoxin
|
Digoxin is eliminated by the renal route, so its impaired. Digitoxin is excreted via the biliary route.
|
|
What affects does quinidine have on digoxin?
|
Quinidine decreases clearance
|
|
What affect does hypokalemia have on digoxin?
|
Digoxin competes with K at its binding site in Na/K ATPase. Decreasing K, increases digoxin binding and digoxin effects.
|
|
How do class I antiarrhythmic drugs work?
|
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.
|
|
Name the Class IA antiarrhythmics. What are they used for?
|
Quinidine, procainamide, disopyramide.
Prolong the refractory period, slow conduction (phase 0), and increase action potential duration. Suppress atrial and ventricular arrhythmias (broad spectrum). |
|
Name the Class IB antiarrhythmics. What are they used for?
|
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. |
|
Name the Class IC antiarrhythmics. What are they used for?
|
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. |
|
What are the Class II antiarrhythmics? Mechanism of action?
|
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). |
|
What are beta-blockers used to treat?
|
Treat tachyarrhythmias caused by increase in sympathetic activity. Also can be used for atrial flutter, fibrillation and for AV-nodal reentrant tachycardia.
|
|
What are the Class III antiarrhythmics? Mechanism of action?
|
Sotalol, ibutilide, amiodarone.
K channel blockers. Increases AP duration, increases ERP. |
|
What are the adverse effects of amiodarone?
|
Pulmonary fibrosis, corneal deposits, hepatotoxicity, photosensitivity (gray man syndrome), thyroid disorders.
|
|
What are the Class IV antiarrhythmics? Mechanism of action?
|
Ca channel blockers.
Verapamil, diltiazem. primarily affect AV nodal cells, decrease conduction, increase ERP, increases PR. |
|
Class V antiarrhythmics include adenosine. What is its MOA?
|
Adenosine causes an increase in K efflux and decreases Ca influx. Used to Tx WPW.
|
|
What is atropine? What is it used to treat?
|
Atropine blocks the effects of ACh. Increases sinus rate, nodal conduction, and decreases refractory period.
Used to treat bradyarrhythmias. |
|
What drugs reduce the half life of quinidine?
|
Phenobarbital, phenytoin
|
|
What antiarrhythmic drug causes torsade de point? How do you treat?
|
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. |
|
What drug is the best for treating ventricular tachycardia following an acute MI? Digitalis, quinidine, lidocaine, or obutamine.
|
Lidocaine. It does not slow conduction.
|
|
What class of antiarrhythmics do you use to treat atrial fibrillation caused by hyperthyroidism?
|
Hyperthyroidism increases B-adrenoreceptors. Use beta blockers (Class II).
|
|
What drug which you use as an adjunct to quinidine in the treatment of atrial flutter?
|
Digitalis, because of its negative inotropic effects.
|
|
What metabolite of nitroprusside is toxic?
|
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.
|
|
What does dipyridamole do?
|
Coronary vasodilator. Interferes with uptake of the vasodilator adenosine. Potentiates the effect of PGI (prostacyclin) and dilates vessels and inhibits platelet aggregation.
|
|
Loop diuretics can be used to treat hypertension, especially in individuals with diminished renal function. How do they work?
|
Inhibits Na/K/2 Cl triporter.
|
|
Side effects of loop diuretics.
|
Potassium wasting, metabolic alkalosis, hypotension, ototoxicity
|
|
What drug class should be used to treat hypertension in a patient with normal renal funciton?
MOA? Adverse effects? |
Thiazides (hydrochlorothiazide). Inhibits Na/Cl cotransporter.
Side effects: hypokalemia, hyperlipidemia, hyperuricemia, hypercalcemia, hyperglycemia |
|
Prazosin (and terazosin, doxazosin) lowers total peripheral resistance by _____.
|
Acting as an alpha-1 selective antagonists. Alpha 1 receptors are located in the skin, mucosa, intestine, and kidney.
|
|
Prazosin may produce 1st dose _____.
|
Orthostatic and exercise hypotension.
|
|
Blocking B1-adrenoreceptors does what?
Blocking B2-adrenoreceptors does what? |
It reduces the heart rate and contractility.
It increases airway resistance, decreases glycogenolysis and peripheral vasodilation. |
|
How do metoprolol and propranolol differ?
|
Metoprolol is B1-selective. Propranolol is nonselective.
|
|
Name two centrally acting sympathomimetic agents that are used to treat hypertension.
|
Methyl-dopa, clonidine. Both decrease total peripheral resistance.
|
|
Methyl-dopa is used to treat? And how?
|
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.
|
|
Why is reserpine useful in treating hypertension?
|
Reserpine eliminates norepinephrine release in response to nerve impulse by preventing vesicular uptake.
|
|
How does guanethidine reduce CO and TPR?
|
Depletes norepinephrine concentrations.
|
|
What two drugs are coadministered to patients who are put on hydralazine?
|
Diuretic (because hydralazine elicits the baroreceptor reflex).
Beta blocker to prevent tachycardia. |
|
Which vasodilator drug can cause lupuslike syndrome?
|
Hydralazine.
|
|
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?
|
Hypertrichosis (hirsutism). Treat hair loss.
|
|
What is furosemide and why is it coadministered with diazoxide or nitroprusside?
|
Loop diuretic used to prevent fluid overload. Diazoxide and nitroprusside reduce blood pressure rapidly.
|
|
What is first-line therapy for hypertension in pregnancy?
|
Hydralazine and methyldopa.
|
|
The -statins inhibit the cholesterol precursor, _______.
|
Mevalonate. HMG-CoA reductase inhibitors: lovastatin, pravastatin, simvastatin, rosuvastatin. They slightly increase HDL
|
|
What are the adverse effects of statins?
|
Rhabdomyolysis, anxiety, irritability, hepatotoxicity and elevated LFT's.
|
|
What does nicotinic acid?
|
Reduces plasma VLDL by inhibiting the synthesis and esterification of FA in the liver and reducing lipolysis in adipose tissue. HDL also increases significantly.
|
|
Gemfibrozil is a "fibrate" that is used to lower plasma lipids. What is its mode of action?
|
It decreases triglyceride levels significantly by upregulating lipoproteinlipase.
|
|
What drug acts within the intestine to reduce cholesterol absorption?
|
Ezetimibe
|
|
Cholestyramine, colestipol, and colesevelam do what to bile acid?
|
They prevent intestinal reabsorption of bile acids. Liver must use cholesterol to make more.
|
|
Besides its inotropic actions, what else do cardiac glycosides do?
|
Increases vagal activity and decreases sympathetic tone.
|
|
What is the order of potency do these Ca channel blockers have on vascular smooth muscle? On the heart?
nifedipine, diltiazem, verapamil |
Heart - verapamil > diltiazem > nifedipine
VSM - nifedipine > diltiazem > verapamil |
|
Which medication, if given to a patient who is on digoxin, may cause a dangerous arrhythmia?
Valsartan, hydrocholothiazide, hydralazine, lovastatin, tadalafil |
Hydrocholothiazide, which cause hypokalemia.
|
|
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?
|
Short-term therapy in individuals with severe chronic cardiac failure.
|
|
If a patient with angina pectoris is allergic to asprin, clopidogrel can be used instead. What is the action of clopidogrel?
|
Irreversiby blocks ADP receptors on platelets. Its used for arterial thromboembolism prophylaxis in high risk patients.
|
|
What is the drug of choice for abolishing AV nodal arrhythmias such as paroxysmal supraventricular tachycardia?
|
Adenosine. Toxicitiy: flushing, hypotension, chest pain.
|
|
Nitrates venodilate which the most:
cardiac veins, large veins, small veins |
Large veins
|
|
Amrinone lactate and milrinone reduce ___________ and vascular resistance and enhance cardiac output.
|
Left ventricular filling pressure.
|
|
What increases cardiac contractility, vasodilator, and acts by inhibiting phosphodiesterase (PDE III) in cardiac muscle thereby increasing cAMP and intracellular Ca?
|
Amrinone and milrinone
|
|
What is sotalol?
|
Class III antiarrhythmic agent and a potent beta-blocker.
|
|
What is the preferred antiarrhythmic in patients with severe heart failure?
|
Amiodarone.
|
|
Why should one avoid using flecainide in a patient with congestive heart failure?
|
It has a negative inotropic effect.
|
|
Which drug would be appropriate prophylactic antiarrhythmic therapy for someone who just had a MI?
Lidocaine Metoprolol Procainamide Quinidine Verapamil |
Metoprolol
|
|
How do you suppress arrhythmias resulting from a reentry focus?
|
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).
|
|
Headache, dizziness, and tinnitus (characteristic of cinchoism) are caused by what drug?
|
Quinidine.
|
|
Why can amiodarone cause symptoms of hypothyroidism?
|
Its structure is related to thyroid hormones.
|
|
What drug should you use to treat a hypertensive diabetic? What drug is contraindicated?
|
ACEi.
Beta-blockers because they mask the symptoms of hypoglycemia. |
|
What drug should you administer to a hypertensive, tachycardic patient with glaucoma.
|
Beta-blocker
|