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248 Cards in this Set
- Front
- Back
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What general class of drug is Furosemide?
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Loop diuretic
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What is furosemide’s mechanism of action and where does it act?
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Inhibits reabsorption of Na+ (and Cl-) in ascending loop of Henle
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What diuretic drug can be used in cases of low GFR? Why?
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Furosemide
Actively secreted by proximal tubules (has COOH group) |
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What is the most widely used diuretic in veterinary practice?
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Furosemide
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What part of the Furosemide molecule makes it potentially carcinogenic?
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Furan group
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Loop diuretics should never be used in conjunction with _________________ because of the increase in nephrotoxicity and ototoxicity seen in this combination.
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Aminoglycosides
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What are some common indications for use of furosemide?
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CHF, pulmonary edema, hypercalcuric nephropathy, uremia, adjunct therapy for hyperkalemia, and occasionally as antihypertensive agent.
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What general class of drug is acetazolamide?
MOA? |
Diuretic - Carbonic anhydrase inhibitor
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How and where do carbonic anhydrase inhibitors work?
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Decrease bicarbonate reabsorption, hydrogen ion secretion, and Na+ reabsorption, causing an increase in urine pH
Proximal Tubule |
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Carbonic anhydrase inhibitors are not widely used as general diuretics, but are occasionally used in the treatment of _____________.
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Glaucoma
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What are two problems with carbonic anhydrase inhibitors?
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1. K+ loss
2. Low efficacy which declines further after several days of treatment |
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List 3 carbonic anhydrase inhibitors
(Hint: all end in -amide) |
Acetazolamide
Dichlorphenamide Methazolamide |
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In order to be effective, what percentage of carbonic anhydrase activity must be inhibited?
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>99%
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What kind of diuretic is mannitol?
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Osmotic diuretic
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How and where do osmotic diuretics work?
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Freely filtered in glomerulus, increases osmolar concentration of filtrate, draws water into filtrate
Primarily in proximal tubule |
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Which of the following is FALSE about osmotic diuretics?
a. Freely filtered in glomerulus b. Undergoes limited reabsorption in renal tubules c. Pharmacologically inert d. Not metabolized e. Can be used in cases of low GFR |
E - Need adequate GFR for osmotic diuretics
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Place the following drugs in order of greatest to least effect on urine output:
Acetazolamide, Aminophylline, Furosemide, Mannitol, Triamterene |
Mannitol (10)
Furosemide (8) Acetazolamide (3)/ Aminophylline (3) Triamterene (2) |
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Mannitol is an excellent diuretic. Why don’t we send clients home with mannitol for their pets?
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It needs to be given IV. Will be broken down and digested in the gut.
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What kind of diuretic is isosorbide?
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Osmotic diuretic
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What are some indications for mannitol use?
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Reduce intraocular and intracerebral pressures, enhance excretion of some toxins (aspirin and ethylene glycol), promotion of diuresis in acute oliguric renal failure, rapidly reduce ascites/ edema with other diuretics where appropriate
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What are contraindications for mannitol?
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Low GFR, anuric renal failure -> can cause dehydration
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What class of diuretic is triamterene?
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Potassium sparing diuretic (non-aldosterone antagonist)
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How and where do potassium sparing diuretics work?
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Inhibit uptake of Na+ in distal portions of distal tubule
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What will an overdose of triamterene cause?
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Hyperkalemia
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What is the mechanism of action of thiazides?
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Prevent reabsorption of Na+/Cl- in distal tubule. Collecting tubular cells are confronted with extra Na+ and exchanges it for K+, so K+ is lost
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When are thiazides indicated?
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For moderate diuretic effect.
First line agents in treatment of edema from CHF and in high blood pressure. |
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What will thiazide toxicity cause?
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Hypokalemia
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Potassium supplements are commonly used with _______________.
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Thiazides
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What class of diuretic is ethacrynic acid?
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Loop diuretic
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What class of diuretic is bumetanide (Bumex)?
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Loop diuretic
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What class of diuretic is ameloride?
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Potassium sparing diuretic (non-aldosterone antagonist)
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How are potassium sparing diuretics (non-aldosterone antagonists) administered?
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Orally only.
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Of the thiazides, _____________ is poorly absorbed orally.
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Chlorothiazide
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When is chlorothiazide indicated?
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Nephrogenic diabetes insipidus
Hypertension Udder edema in dairy cattle |
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____________-induced hypokalemia may increase the likelihood of digitalis toxicity.
(Hint: diuretic) |
Thiazide
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What class of diuretic is spironolactone?
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Aldosterone antagonist
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What is the mechanism of action of spironolactone?
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Competetively binds to the aldosterone receptor
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______________, because of its K+ sparing effects, is often used in combination with thiazides.
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Spironolactone
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What are the toxic effects of spironolactone?
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Potassium retention
Some androgenic side effects Tumorigenic agent in animals at high doses |
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What class of diuretics do caffeine, theophylline, and theobromine belong to?
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Xanthines
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What are xanthines primarily used for?
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Bronchodilators
Secondarily act as diuretics |
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What can caffeine and theobromine cause in an overdose?
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Seizures
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What does aldosterone normally do and where does it do it?
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Na+ retention in the distal convoluted tubules and collecting ducts. Upregulates Na+/K+ ATPase on basal surface of principle cells of the collecting ducts.
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What class of drug is Digoxin?
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Digitalis glycoside
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What is the MOA of Digoxin?
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Poisons Na+/ K+ ATPase pumps on cardiac myocytes (competes with K+ for binding site)
Na+ is pumped out in exchange for Ca++ instead, causing increased contractility, prolonged refractory period of AV nodal cells (increased vagal tone). |
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What effects does digoxin have?
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Increased myocardial contractility (positive inotrope)
Slow heart rate in patients with atrial fibrillation Suppress supraventricular premature beats and tachycardia |
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What is the major condition digoxin is used to treat?
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Atrial fibrillation
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What is the major problem with digoxin?
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Narrow therapeutic range
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What are the signs of digoxin toxicity?
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Nausea - vomiting/ anorexia in mild toxicities, tachyarrhythmias and bradyarrhythmias in more severe ones. Increased sympathetic tone.
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What are some factors that may predispose to digoxin toxicity?
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Obesity
Ascites Hypokalemia Loading dose administration Quinidine Cachexia |
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What can you give for a digoxin-induced bradyarrhythmia?
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Atropine
IV potassium |
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What can you give for a digoxin-induced tachyarrhythmia?
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Lidocaine
Phenytoin |
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Late (delayed) afterdepolarizations are due to _____________.
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Cellular calcium overload
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What are the components of a digitalis glycoside?
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Sugars
An aglycone or genin, which consists of: - A steroid nucleus - A lactone ring |
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What does RAAS stand for?
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Renin-Angiotensin-Aldosterone System
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What is the half-life of digoxin?
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23-39 hours
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How is digoxin administered?
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Orally
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How is digoxin excreted?
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85% glomerular filtration
15% hepatic metabolism |
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What is the MOA of Pimobendan?
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Phosphodiesterase III inhibitor – reduces degradation of cAMP, which increases Ca++ influx via L-type Ca++ channels
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What is the major difference in action between pimobendan and beta-agonists?
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Pimobendan bypasses the beta receptor, so does not cause a downregulation of the receptor and its effects do not diminish over time.
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Pimobendan is a calcium sensitizer. What does this mean?
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It increases the troponin C affinity for calcium.
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Which of the following is FALSE about pimobendan?
a. It should be given before a meal b. It reduces inflammatory cytokines c. It causes moderate reduction in systemic and pulmonary vascular resistance through vasodilation d. It improves myocardial blood flow without increasing myocardial oxygen consumption e. It is excreted predominantly in the urine |
E – 90% excreted in feces after metabolism in the liver
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Which of the following is FALSE about pimobendan?
a. It is a positive inotropic agent b. It generally produces an increase in heart rate of around 25% c. It sensitizes myocardial proteins to the effects of calcium d. It is a phosphodiesterase inhibitor e. All of the above are true |
B – Pimobendan causes a mild slowing of the HR
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____________ is an “inodilator” – it has both properties of a positive inotrope and a vasodilator.
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Pimobendan
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When is pimobendan indicated?
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Heart Failure (not heart disease)
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Pimobendan produces the following cardiovascular effects EXCEPT:
a. Systemic arteriolar vasoconstriction due to increased cAMP in the smooth muscle cells b. Positive inotropic effects c. Increases myocardial efficiency d. Reduces left ventricular end diastolic pressure and reduced left atrial pressure e. Improves diastolic function (i.e. the ability of the heart to relax and fill) |
A – Pimobendan causes systemic arteriolar vasodilation
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What kind of drug is hydralazine?
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Systemic arteriolar dilator
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What is the MOA of hydralazine?
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Increases local concentration of prostacyclin
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How effective is hydralazine?
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Very effective, very potent.
Drops blood pressure by 10-15 mmHg. |
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How soon does hydralazine take effect?
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Within 30 minutes
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How long do the effects of hydralazine last?
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11-13 hours
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What are the potential adverse effects of hydralazine?
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Systemic hypotension
Tachycardia GI disturbances |
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What kind of drug is amlodipine? MOA?
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Systemic arteriolar dilator
Calcium channel blocker |
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Where does amlodipine work?
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Vascular smooth muscle only (unlike diltiazem and verapamil, which also affect conduction tissue and contractility)
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What is an indication for use of amlodipine?
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Hypertension, especially in cats
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What is the half life of amlodipine?
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30 hours
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Amlodipine produces many of the same effects as hydralazine as a systemic arteriolar dilator. What 2 benefits does it have over hydralazine?
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Does not produce reflex tachycardia seen with hydralazine
Better tolerated by GI tract |
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What does ACE (angiotensin converting enzyme) do? (Hint: it does 2 things!)
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Converts angiotensin I into angiotensin II
Degrades bradykinin. Bradykinin causes vasodilation. |
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Where is ACE active?
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Lungs
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What does renin do?
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Splits angiotensinogen into angiotensin I.
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Where is renin produced?
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Juxtaglomerular apparatus
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When are ACE inhibitors indicated?
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Long term management of chronic heart failure. Not for stabilizing acutely ill patients.
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List 5 ACE inhibitors.
(Hint: all end in -pril) |
Captopril
Enalapril Lisinopril Benazepril Ramipril |
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What happens to aldosterone with ACE inhibitors?
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Decreases – less angiotensin II, which stimulates aldosterone
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What happens to blood pressure on ACE inhibitors?
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Decreases – less angiotensin II, less vasoconstriction
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What happens to renin on ACE inhibitors?
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Increases – less aldosterone -> more Na+ wasting (more Na+ being seen by JGA, which secrete renin)
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ACE inhibitors compete for the binding site of ______________ on angiotensin converting enzyme.
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Angiotensin I
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Arrange the following ACE inhibitors in order of greatest to least affinity for the ACE binding site:
Captopril, Enalapril, Lisinopril |
Lisinopril> Enalapril> Captopril
This is also in order of decreasing half-lives. |
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What are some adverse effects of ACE inhibitors?
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They are uncommon. There can be GI Disturbance (captopril), cost (there is a generic form of enalapril now available), azotemia (nephrotoxicity at high doses). Hyperkalemia is rare.
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ACE inhibitors can cause arteriolar dilation resulting in decreased SVR and blood pressure. How does this compare to hydralazine?
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Ace inhibitors cause a 25-30% reduction in SVR compared to 50% in hydralazine.
ACE inhibitors cause a 3-5mmHg drop in blood pressure compared to a 10-15mmHg drop with hydralazine. ACE inhibitors kinda suck compared to hydralazine. |
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What is one explanation for why you see tachyphylaxis (attenuation of a response) with ACE inhibitors over time (months)?
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Other enzymes convert Angiotensin I to Angiotensin II in the absence of functional ACE. These include chymase, cathepsin G, and kallikrien
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Which ACE inhibitors are pro-drugs?
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Enalapril and Benazepril
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Which diuretics are highly protein bound?
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Loop diuretics, Spironolactone, Triamterene (60%)
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Which ACE inhibitor is excreted in approximately equal amounts in the bile and in the urine?
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Benazepril
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Why is enalapril often the ACE inhibitor of choice?
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It has gone generic, so it is now cheapest.
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What causes the functional azotemia sometimes seen with ACE inhibitors?
Is this reversible? |
Preferential dilation of efferent arterioles of glomerulus reducing glomerular hydrostatic pressure.
This is reversible – if you see this, then stop the ACE inhibitor. |
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Does enalapril prevent dogs with mitral regurgitation from going into heart failure?
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No.
SVEP trial said so. |
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What percent of ACE activity needs to be inhibited to see a noticeable effect?
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>90%
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What compound is also known as “endothelium-derived relaxing factor?”
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Nitric Oxide
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What do nitrates do?
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Relax vascular smooth muscle
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Nitrates are denitrated by a thiol-containing enzyme in vascular smooth muscle cells to form NO, which causes an increase in __________. This activates a serine/threonine kinase that phosphorylates myosin light chains, which inhibits contraction, resulting in smooth muscle relaxation.
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cGMP
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How are nitrates administered?
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Orally, sublingual spray/tablet, intravenously, or transcutaneously
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If you wanted acute effects of nitrates, how would you administer them?
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IV
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How are Isosorbide mononitrate and dinitrate administered?
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Orally
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What is the oral bioavailability of nitrates?
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Less than 10%
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How is nitroglycerin typically administered?
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Transdermally
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At low plasma concentrations, nitrates dilate ____________(arterioles/ veins). At higher concentrations, they may also dilate __________ (arterioles/ veins).
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Low = venodilator
High = venodilator + arteriolar dilator |
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How is nitroprusside different from other nitrates?
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It does not have an ester bond and forms NO directly.
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What is the efficacy of nitroglycerine and isosorbide in dogs and cats?
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Questionable efficacy
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What is the probable cause of nitrate tolerance (decrease in effect)?
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Thought to be sufhydryl group depletion due to RAAS activation
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What are 2 ways you might get around nitrate tolerance?
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Intermittent administration of nitrates
Concurrent administration of hydralazine |
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Why might you want special IV lines for administration of nitroglycerine?
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40-80% of the total nitroglycerine in a diluted IV solution is absorbed by the PVC tubing of normal IV lines.
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What is the half life of nitroglycerine?
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Short: 1-4 minutes
(hence the transdermal continuous infusion administration) |
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To which nitrate compound does tolerance not develop?
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Nitroprusside
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What does nitroprusside do?
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Potent vendilator and arteriolar dilator
May increase left ventricular compliance |
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What is the half-life of nitroprusside?
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A few minutes
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How is nitroprusside administered?
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IV
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When is nitroprusside indicated?
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Short term treatment of dogs with severe or fulminant heart failure
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How long do the effects of nitroprusside last once you discontinue it?
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5 minutes or less (in humans)
Need other long-acting drugs to wean patients off nitroprusside. |
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What are 2 adverse effects of nitroprusside?
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Hypotension
Cyanide toxicity |
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What is the generic name for aminophylline?
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Theophylline
(also contains ethylenediamine) |
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Which of the following drugs are highly protein bound? Choose all that apply.
a. Pimobendan b. Quinidine c. Diltiazem d. Phenobarbital e. NSAIDs |
All of these are highly protein bound, except for Phenobarbital (40-50%)
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What drugs can be used to treat inappropriate sinus tachycardia? (2)
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β-adrenergic blockers
Digitalis |
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What drugs can be used to treat ectopic atrial tachycardia? (3)
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Digitalis
Class I antiarrhythmatics (not Lidocaine) Class IV antiarrhythmatics |
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What drugs can be used to treat ventricular tachycardia in german shepherds? (2)
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β agonists
atropine (increase sinus rate) |
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What drugs can be used to treat digitalis-induced arrhythmias due to delayed afterdepolarizations? (2-3)
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Lidocaine
Phenytoin Possibly class IV (verapamil) |
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What drugs can be used to treat supraventricular tachycardia resulting from pre-excitation? (4)
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Class I (except Ib)
Class III Class IV Digitalis |
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What drugs can be used to treat primary (slow) atrial fibrillation? (2)
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Quinidine
Class III |
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What drugs can be used to treat secondary (fast) atrial fibrillation? (3)
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Digitalis
β-adrenergic blockers diltiazem |
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What drugs can be used to treat sustained monomorphic ventricular tachycardia? (3)
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Mexiletine
Class III Lidocaine for short-term suppression |
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What drugs can be used to treat nonsustained polymorphic ventricular tachycardia? (3)
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Class III
Possibly Mexiletine Lidocaine for short-term suppression |
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What drugs can be used to treat ventricular fibrillation? (1)
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Class III
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What drugs can be used to treat AV nodal reentrant (most supraventricular tachycardias)? (3)
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Class IV
Class II Digitalis |
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Class I drugs are so-called _________________.
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Membrane stabilizers
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What is the MOA of class I drugs?
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Sodium channel blockers
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What phase of the cardiac action potential do class I drugs act on?
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Phase 0 – the upstroke
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What effect do class I drugs have on conduction velocity?
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Slow conduction velocity in normal and/or abnormal cardiac tissue
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Name 3 class Ia agents.
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Quinidine
Procainamide Disopyramide |
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What do class Ia agents do?
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Depress conduction in normal and abnormal cardiac tissue
Prolong repolarization |
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Name 4 class Ib agents.
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Lidocaine
Tocainide Mexiletine Phenytoin |
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How do class Ib agents work on conduction velocity in normal vs. abnormal cardiac tissue?
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Normal cardiac tissue: not nearly as good as class Ia drugs on slowing conduction velocity
Abnormal cardiac tissue: profound prolongation of conduction velocity |
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What effect do class Ib drugs have on repolarization of Purkinje fibers?
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Accelerate repolarization, shorten action potential
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What effect do class Ib drugs have on refractory period of normal and abnormal myocardium?
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Normal: little to no effect
Damaged: may prolong refractory period |
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Are class Ic drugs used in veterinary medicine?
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No.
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_____________, a class Ia drug, depresses conduction velocity, breaks up reentrant ventricular arrhythmias, and prolongs refractory period of abnormal tissue to produce bidirectional block.
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Procainamide
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How is procainamide administered?
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IV and orally (tablets, capsules, and sustained release tablets)
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What is the half-life of procainamide in the dog?
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3 hours
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When is procainamide indicated?
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Ventricular tachyarrhythmias
Maybe for some supraventricular tachyarrythmias |
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When is procainamide usually used?
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When lidocaine fails.
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What is the bioavailability of procainamide?
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High
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How is procainamide metabolized?
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Liver primarily
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Why might humans have beneficial effects from procainamide at lower doses than in dogs?
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Humans metabolize it into an active derivative, NAPA, whereas dogs do not
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Which drug is commonly used to treat atrial fibrillations in the horse?
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Quinidine
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What class of drug is quinidine?
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Class 1a antiarrhythmatic
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What is the MOA of quinidine?
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Na channel blocker
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What does quinidine do to atrial, ventricular, and Purkinje cells?
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Prolongs refractory period, which interrupts reentrant pathways
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Quinidine has a vagolytic effect. What does this mean?
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It decreases vagal tone to the heart.
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When is quinidine indicated?
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Long-term suppression of ventricular premature depolarizations and ventricular tachyarrhythmias.
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Both _____________ and _______________, 2 class 1a drugs, tend to be proarrhythmatic (cause arrhythmias) and are not used extensively in dogs.
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Procainamide and Quinidine
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What is the half-life of quinidine in horses?
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4-5 hours
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What is the bioavailability of quinidine in dogs?
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80%
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What is the bioavailability of quinidine in horses?
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Much less than in dogs (40%?)
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How is quinidine typically administered?
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Orally
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Quinidine can predispose a patient to toxicity of what other cardiac drug?
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Digoxin
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Quinidine is a negative inotrope.
|
Just thought you’d like to know that.
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What are signs of quinidine toxicity?
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GI disturbances most commonly (anorexia, diarrhea, colic) - horses
Seizures/ ataxia at high toxic concentrations - dogs |
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____________ is a class 1b antiarrhythmatic agent that is also used for local anesthesia.
|
Lidocaine
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MOA of Lidocaine?
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Na+ channel blocker
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List 3-4 things lidocaine does.
|
1) Breaks up reentrant ventricular arrhythmias
- Depresses conduction velocity - Prolongs refractory period of abnormal tissue 2) Suppresses abnormal automaticity 3) Suppress delayed afterdepolarizations |
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When is lidocaine indicated?
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Suppress ventricular tachyarrhythmias
ONLY for acute arrhythmia management! |
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How is lidocaine administered?
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IV
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What is the half life of lidocaine?
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60-90 minutes. Needs loading dose to get to therapeutic concentrations quickly.
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Lidocaine is primarily metabolized by the liver. What happens to its half-life with reduced hepatic blood flow (as in shock and heart failure)?
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It is prolonged.
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How does the lidocaine dose in horses and cats compare to that in dogs?
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1/4 to 1/3 that in dogs
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What are some signs of lidocaine toxicity?
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CNS signs
- Drowsiness - Emesis - Nystagmus - Seizures |
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_______________ is a class 1b analog of lidocaine that is not extensively metabolized on its first pass through the liver.
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Mexiletine
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What does mexiletine do?
(Hint: lidocaine analog) |
1) Interrupts reentrant currents
- Slows conduction - depresses membrane responsiveness 2) Suppresses abnormal automaticity 3) Suppress delayed afterdepolarizations (Notice how it’s mostly similar to lidocaine…) |
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When is mexilietine indicated?
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EXCLUSIVELY ventricular tachyarrhythmias
i.e. dobies and boxers with DCM to prevent sudden death |
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What is the half-life of mexiletine?
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3-4 hours
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How is mexiletine administered?
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Orally
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What is the bioavailability of mexiletine?
|
Great - 85%
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How is mexiletine excreted?
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80% in the urine
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Mexiletine – toxicity?
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Rare, but vomiting and ataxia.
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What class of antiarrhythmatic is phenytoin?
|
Class 1b
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Phenytoin can be used to treat __________ toxicity.
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Digoxin
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Where are β1 receptors found?
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Cardiac muscle
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Where are β2 receptors found?
|
Primarily in bronchial and vascular smooth muscle
Kidney, pancreas Sinus node and AV node myocardium |
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What will activation of β1 receptors result in?
|
Increased HR
Increased myocardial contractility Increased AV conduction velocity Increased automaticity of subsidiary pacemakers |
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What will activation of β2 receptors result in?
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Smooth muscle relaxation
Renin, insulin release Some increase in cardiac contractility |
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What will β2 agonists do to blood vessels?
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Dilate them
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What will β2 agonists do to bronchioles?
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Dilate them
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What will a β1 blocker do?
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Decrease HR
Decrease myocardial contractility Decrease AV conduction velocity Decrease automaticity of subsidiary pacemakers |
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What will a β2 blocker do?
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Contract smooth muscle, which constricts bronchioles and blood vessels.
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What is the MOA of Class II antiarrhythmatic drugs?
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β-adrenergic blockers
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Why might you want a beta blocker specific for beta 1, especially in cats?
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Beta 2 blockers can cause bronchoconstriction, and since cats can get asthma, this may compromise their breathing ability.
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Why might beta 2 blockers be contraindicated in dogs?
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If they have diabetes, beta blockers can inhibit insulin release
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What are the 2 primary beta blockers used today in vet med?
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Propanolol and atenolol
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What is the half-life of benazepril?
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12 hours
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What is the half-life of enalapril?
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12 hours
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What is the half life of captopril?
|
3 hours
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What is the duration of effect of captopril?
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4 hours
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What is the duration of effect of enalapril?
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14 hours
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What is the duration of effect of benazepril?
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At least 24 hours with repeated administration
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Which ACE inhibitor has the longest half life?
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Lisinopril
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What receptors does propanolol block?
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Beta-1 and beta-2
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Name 4 beta-blockers.
(Hint: all end in –lol) |
Atenolol
Propanolol Metoproplol Sotalol |
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How is propanolol administered?
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Orally or IV
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What is the half life of propanolol in the dog?
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1.5 to 2 hours
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Is propanolol water or lipid soluble?
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Lipid-soluble
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Propanolol _____________(increases/ decreases) myocardial contractility.
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Decreases
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Propanolol is largely metabolized by the ________.
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Liver
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When is propanolol indicated?
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Canine and feline ventricular and supraventricular tachyarrhythmias
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Propanolol toxicity – go!
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Decreases contractility (not reversed by catecholamines!) -> can precipitate heart failure
Bronchoconstriction Systemic arteriolar constriction |
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Propanolol should not be used in patients with ________.
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Asthma
Diabetes |
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What kind of drug is atenolol?
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Beta blocker
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What receptors does atenolol block?
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Beta-1 receptor specific
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Sotalol is a nonselective beta blocker, but it is used primarily for its effects as a _______________.
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Potassium channel blocker
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What receptors does metoprolol block?
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Beta-1 receptor selective
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In dogs, beta-blockers are most commonly used to decrease ventricular rate in _________________.
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Atrial fibrillation
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You have a patient with atrial fibrillation and the atrial rate is 600 - 700 beats per minute. The ventricular rate is 200-240 beats per minute. What is your goal with whatever drug treatment you use?
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Decrease ventricular rate to below 160 bpm
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You have a patient with atrial fibrillation. What is the first drug you reach for? What are the common second-line drugs for this condition?
|
Commonly digoxin first, then
Add in a beta blocker or diltiazem |
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What does digoxin do to the AV node?
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Increases vagal tone to AV node
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What does a beta blocker do to the AV node?
|
Reduces sympathetic input to AV node
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What is the mechanism of action of class III antiarrhythmatics?
|
Potassium channel blockers
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What phase of the cardiac myocyte action potential do potassium blockers affect?
|
Phase 3
(the downward slope) |
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What affect does prolonging phase 3 of the action potential have on the refractory period?
|
Prolongs refractory period
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What will prolonging the refractory period do?
|
Makes it harder to fibrillate – prevents sudden death
Ventricular tachycardia can degenerate into ventricular fibrillation. |
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There are 2 isomers of sotalol. Both the d- and the l-isomers block ______________, but only the l-isomer blocks_________________.
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Both isomers: potassium channels
Only l-isomer: beta receptors |
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What is the half-life of sotalol?
|
2 hours
|
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What is the bioavailability of sotalol?
|
90%
|
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How is sotalol excreted?
|
Renal clearance
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Despite the short half life, sotalol can be administered __ time(s) a day.
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2
(BID or q12h) |
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Sotalol is a miracle drug for _________ (dog breed) with arrhythmogenic right ventricular cardiomyopathy.
|
Boxers
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_____________ is a class III antiarrhythmatic agent that has a half life of 3 days, is lipophilic, and concentrates in the myocardium.
|
Amiodarone
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Which of the following does Amiodarone do?
a. Prolongs action potential duration b. Blocks sodium channels c. Beta blocker d. Calcium channel blocker e. All of the above |
E – all of the above
(calcium channel blocker?) – from the notes |
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Amiodarone is limited to dogs (primarily Doberman pinschers) with _________________.
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DCM – Dilated cardiomyopathy
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Amiodarone is a “dirty drug.” Name 4 different toxicities that it has.
|
1. Hepatotoxicity
2. Pulmonary fibrosis 3. Neurotoxicity 4. Hypo- and hyperthyroidism |
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Class IV antiarrhythmatics are _________ channel blockers.
|
Calcium
|
|
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Where are calcium L-type channels found?
|
Vascular smooth muscle cells
Cardiac muscle cells |
|
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What is the significance of L-type calcium channels?
|
They are extremely sensitive to the effects of calcium channel blockers. Other types are not as sensitive.
|
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What is the effect of calcium channel blockage on cardiac contractility, sinoatrial depolarization, and AV conduction?
|
Decrease contractility
Slow SA depolarization Slow AV conduction |
|
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What is the effect of calcium channel blockage on systemic arterioles and systemic vascular resistance?
|
Relax arterioles
Decrease SVR |
|
|
Name 2 calcium channel blockers.
|
Diltiazem
Verapamil |
|
|
Name 3 conditions you might prescribe diltiazem for.
|
Atrial fibrillation
Supraventricular tachycardia Hypertrophic cardiomyopathy in cats |
|
|
How is diltiazem administered?
|
IV for acute situations
Oral low dose for chronic |
|
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What is the half-life of diltiazem?
|
2-4 hours
|
|
|
What is the bioavailability of diltiazem?
|
25%
|
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Name 5 effects associated with diltiazem toxicity.
|
Bradycardia
AV blocks Decreased contractility Systemic vasodilation Circulatory collapse |
