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54 Cards in this Set

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What drug is used to close a PDA?
indomethacin
What drug is used to keep PDA open? Why is that useful?
Patency is maintained by PGE synthesis
May be necessary to sustain life in conditions such as transposition of the great vessels
Antihypertensive therapy
1. Essential HTN
2. CHF
3. Diabetes mellitus
1. diuretics, ACE-I, ARBs, CCBs
2. diuretics, ACE-I, ARBs, B-blockers (compensated CHF), K+ sparing diuretics
3. ACE-I, ARBs, CCBs, diuretics, B-blockers, a-blockers
What HTN drugs are protective against diabetic nephropathy?
ACE inhibitors
What drug is first-line therapy for HTN in pregnancy (in addition to methyldopa)?
hydralazine
What three drugs block voltage-dependent L-type Ca channels of cardiac and SM --> reducing muscle contractility
Nifedipine, verapamil, diltiazem
What drug vasodilates by releasing NO in SM, causing an increase in cGMP and SM relaxation?
Nitroglycerin
1. Which drug vasodilates aterioles > veins?
2. Which drug vasodilates veings >> arteries?
1. hydralazine
2. nitroglycerin
Which CCB has the largest effect on cardiac muscle?
verapamil
(Verapamil = Ventricle)
Which drug is frequently co-administered with a B-blocker to prevent reflex tachycardia?
hydralazine
Name the toxicities for each of these drugs:
1. Hydralazine
2. CCBs
3. Nitroglycerin/isosorbide dinitrate
1. Compensatory tachycardia, fluid retention, nausea, headache, angina; Lupus-like syndrome
2. Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
3. Reflex tachy, hypotension, flushing, headache
1. Compensatory tachycardia, fluid retention, nausea, headache, angina; Lupus-like syndrome
2. Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
3. Reflex tachy, hypotension, flushing, headache
Name the toxicities for each of these drugs:
1. Hydralazine
2. CCBs
3. Nitroglycerin/isosorbide dinitrate
What is "Monday disease?"
From industrial exposure to nitroglycerin (e.g. munitions workers)
--developed tolerance for vasodilating action during the work week, but lost tolerance over the weekend
--resulted in tachycardia, dizziness, headache on re-exposure on Monday
What drug is used for angina and pulmonary edema, but can also be used as an aphrodisiac and erection enhancer?
Nitroglycerin
What three drugs can be used to treat malignant HTN?
What is the mechanism for each one?
1. Nitroprusside = short-acting, increases cGMP via direct release of NO
2. Fenoldopam = D1 receptor agonist (relaxes renal vascular SM)
3. Diazoxide = K+ channel opener, hyperpolarizes and relaxes vascular SM
Name the drug that can cause these side effects:
1. Cyanide toxicity from CN release
2. Compensatory tachycardia, fluid retention
3. Hyperglycemia from reduction in insulin release
4. AV block
1. Nitroprusside
2. Hydralazine
3. Diazoxide
4. CCBs
What is the goal/method of antianginal therapy? What 5 things are targeted?
Reduce myocardial O2 consumption by decreasing...
1. End diastolic volume
2. Blood pressure
3. HR
4. Contractility
5. Ejection time
What two partial B-agonists are contraindicated in angina?
Pindolol, acebutolol
What agent is best at lowering LDL? How does that agent work? How does it affect HDL, TGs?
Statins work by inhibiting mevalonate, a cholesterol precursor
HDL = slight increase
TG = slight decrease
What agent is best for increasing HDL? How does it work? What are its effects on LDL, TGs?
Niacin works by inhibiting lipolysis in adipose tissue, reducing hepatic VLDL secretion into circulation
LDL = moderate decrease
TGs = slight decrease
What lipid-lowering agent tastes bad and causes GI discomfort? Why is it used? How does it work?
Bile acid resins prevent intestinal absorption of bile acids, so the liver must use cholesterol to make more
LDL = moderate decrease
HDL = slight increase
TGs = slight increase
How does ezetimibe work? What is it used for?
Prevents cholesterol reabsorption at SI brush border
LDL = moderate decrease
HDL, TGs = no effect
What agent has the most potent effect on lowering TGs? How does it work? How does it affect LDL, HDL?
"Fibrates" upregulate LPL --> increasing TG clearance
LDL = slight decrease
HDL = slight increase
Side effects for each of these are...
1. Statins
2. Niacin
3. Bile acid resins
4. Ezetimibe
5. Fibrates
Side effects of lipid-lowering drugs...
1. hepatotoxicity (increased LFTs), rhabdomyolysis
2. red, flushed face (which is decreased by aspirin or long-term use); hyperglycemia, hyperuricemia
3. Tastes bad, GI discomfort, less absorption of fat-soluble vitamins, cholesterol gallstones
4. Rare increase in LFTs
5. Myositis, hepatotoxicity, cholesterol gallstones
Side effects of lipid-lowering drugs...
1. hepatotoxicity (increased LFTs), rhabdomyolysis
2. red, flushed face (which is decreased by aspirin or long-term use); hyperglycemia, hyperuricemia
3. Tastes bad, GI discomfort, less absorption of fat-soluble vitamins, cholesterol gallstones
4. Rare increase in LFTs
5. Myositis, hepatotoxicity, cholesterol gallstones
Side effects for each of these are...
1. Statins
2. Niacin
3. Bile acid resins
4. Ezetimibe
5. Fibrates
Which lipid-lowering agent exacerbates gout?
Niacin
Which two lipid-lowering agents can cause cholesterol gallstones?
Niacin, Fibrates
How does digoxin work?
Directly inhibits Na/K ATPase
Leads to indirect inhibition of Na/Ca exchanger
Increases intracellular Ca --> positive inotropy (increased contractility)
What is the clinical use of digoxin?
CHF (increases contractility), a-fib (decreases conduction at AV node and depression at SA node)
What is digoxin toxicity?
Cholinergic = nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh)
ECG = increased PR, decreased QT, scooping, T-wave inversion, arrhythmia, hyperkalemia
What worsenes digoxin toxicity?
1. Renal failure (decreased excretion)
2. Hypokalemia (permissive for digoxin binding at K-binding site on Na/K ATPase
3. Quinidine (decreases clearance; displaces digoxin from tissue-binding sites)
What is the antidote for digoxin toxicity?
Slowly normalize K+
lidocaine
cardiac pacer
anti-dig Fab fragments
Mg++
List the class I anti-arrhythmics. What is there general mechanism?
Na+ channel blockers = slow or block conduction, decrease the slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells
Class IA = "The Queen Proclaims Diso's pyramid" = Quinidine, Procainamide, Disopyramide
Class IB = "I'd Buy Lidy's Mexican Tacos" = Lidocaine, Mexiletine, Tocainide
Class IC = "Chipotle's Food has Excellent Produce" = Flecainide, Encainide, Propafenone
What effect to each of the sub-classes of class I antiarrhythmics have on AP duration?
Class IA = increased AP duration
Class IB = decreased AP duration
Class IC = no effect on AP duration
Which class is useful for both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia?
Class IA
Which class is useful for acute ventricular arrhythmias (esp. post-MI) and in digitalis-induced arrhythmias?
Class IB
What class is useful in V-tachs that progress to VF and in intractable SVT?
Class IC
Which class is best post-MI and which is contraindicated post-MI?
IB is Best post-MI
IC is Contraindicated post-MI
Which ion abnormality causes increased toxicity for all class I drugs?
hyperkalemia
What are the toxicities of IA, IB, and IC antiarrhythmics?
IA = quinidine (cinchonism--headache, tinnitus); thrombocytopenia; TdP due to increased QT interval; procainamide (reversible SLE-like syndrome)
IB = local anesthetic; CNS stimulation/depression, CV depression
IC = proarrhythmic, esp post-MI (contraindicated). Significantly prolongs refractory period in AV node

How do class II antiarrhythmics work?
B-blockers: decrease cAMP and Ca++ currents. Suppress abnormal pacemaker cells by decreasing the slope of phase 4
What is particularly sensitive to class IIs?
AV node
Which B-blocker is very short acting?
Esmolol
When are class IIs used?
V-tach, SVT, slowing V rate during a-fib/a-flutter
What are the toxicities of class IIs?
Impotence, exacerbation of asthma
CV (bradycardia, AV block, CHF)
CNS (sedation, sleep alterations)
May mask the signs of hypoglycemia
Which class II drug can cause dyslipidemia? How do you treat an overdose?
Metoprolol

Treat overdoes with glucagon
How do class III antiarrhythmics work?
K+ channel blockers = increase AP duration, increase ERP
What are side effects for the major class IIIs?
Sotalol = TdP, excessive B-block
Ibutilide = TdP
Bretylium = new arrhythmias, hypotension
Amiodarone = pulmonary fibrosis, hepatotoxicity, hypo/hyper-thyroidism (also corneal/skin deposits leading to polydermatitis, neurologic effects, constipation, bradycardia, heart block, CHF)
What should you remember to check when using amiodarone?
PFTs (pulmonary)
LFTs (liver)
TFTs (thyroid)
How do class IVs work? Name 2.
Verapamil, diltiazem decrease conduction velocity and increase both ERP and PR interval
When are class IVs used?
Prevention of nodal arrhythmias (e.g. SVT)
What are the major toxicities of class IVs?
Constipation, flushing, edema
CV (CHF, AV block, sinus node depression)
Other antiarrhythmics are...
1. adenosine
2. K+
3. Mg++
...what do they do?
1. increase K+ flow out of cells --> hyperpolarization; decreases Ica (drug of choice for diagnosing/abolishing SVT). Very short acting (15sec). Toxicity includes flushing, hypotension, chest pain.
2. Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)
3. Effect in TdP and digoxin toxicity
What blocks the effects of adenosine?
theophylline