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ZPharmacology > Cardiovascular/Renal Drugs EC > Flashcards

Cardiovascular/Renal Drugs EC Flashcards

1
Q

Drugs to treat Essential Hypertension

A

Diuretics
ACE inhibitors
ARBs
Ca channel blockers

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2
Q

Drugs to treat CHF

A 
Diuretics
ACE inhibitors 
ARBs
Beta-blockers (compensated CHF only)
K-sparing diuretics
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3
Q

DM hypertension treatment

A 
ACE inhibitors
ARBs 
Ca channel blockers
Diuretics
Beta-blockers
Alpha blockers
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4
Q

Nifedipine, Amlodipine, Verapamil, Diltiazem (MOA, Use, Tox)

A

Block voltage gated L-type Ca channels (reduce contractility in cardiac and smooth muscle)

Amlodipine and Nifedipine esp in Smooth Muscle
Verapamil and Diltiazem esp in Heart

Cardiac depression
AV block
Peripheral edema

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5
Q

Hydralazine (MOA, Use, Tox)

A

Increase cGMP = vasodilates arterioles

Severe hypertension
CHF
First line for HTN in pregnancy (w/ methyldopa)

Compensatory tachycardia (given w/ beta blocker to prevent - contra. in CAD)
Fluid retention
Lupus-like syndrome

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6
Q

Malignant hypertension treatment (Drugs, Use, Tox)

A

Nitroprusside (increase cGMP via NO release)
~can cause cyanide toxicity

Fenoldopam (D1 agonist - Lower BP and increased natriuresis)

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7
Q

Nitroglycerin, Isosorbide, Dinitrate (MOA, Use, Tox)

A

Increase cGMP via NO release
Dilates VEINS

Angina
Pulmonary edema

Reflex tachycardia
Hypotension
“Monday disease” (tolerance during week, loss of tolerance over weekend results in tachycardia, dizziness, and headache in new week)

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8
Q

Lovastatin, Pravastatin, Simvastatin, Atorvastatin, Rosuvastatin (MOA, Effects, Tox)

A

Block formation of mevalonate by inhibiting HMG-CoA reductase (results in UPREGULATION OF LDLR)

LDL=big decrease, HLD=mild increase, TG=mild decrease

Hepatotoxicity
Rhabdomyolysis

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9
Q

Niacin (vit. B3) (MOA, Use, Tox)

A

Inhibits lipolysis in adipose; reduces hepatic VLDL secretion into circulation

LDL=decrease, HDL=Increased, TG=mild decrease

Flushed face (decreased by aspirin or long term use)
Hyperglycemia
Hyperuricemia

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10
Q

Cholestyramine, Colestipol, Colesevelam (MOA, Use, Tox)

A

Prevent intestinal reabsorption of bile (results in UPREGULATION OF LDLR)

LDL=decrease, HDL=slight increase, TG=slight increase

Terrible taste
GI discomfort
Decrease fat soluble vitamin absorption
Cholesterol gallstones

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11
Q

Ezetimibe (MOA, Use, Tox)

A

Prevents cholesterol reabsorption at brush border

LDL=decrease

Hepatotoxicity
Diarrhea

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12
Q

Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate (MOA, Use, Tox)

A

Upregulate LPL (INCREASED TG CLEARANCE)

LDL=minor decrease, HDL=minor increase, TG=BIG decrease

Myositis
Hepatotoxicity
Cholesterol gallstones

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13
Q

Digoxin (MOA, Use, Tox, Contraindications/Antidote)

A

Na/K pump inhibition leads to inhibition of Na/Ca exchange and INCREASED INTRACELLULAR Ca (inotropy)

CHF
A-fib (decreased conduction at AV node and depression of SA node)

Cholinergic
ECG - Increase PR, decrease QT, ST scooping, T-wave inversion, Arrhythmia, AV block
Hyperkalemia

Contraindications:
Renal failure (renally excreted)
Hypokalemia (too much digoxin binding)
Quinidine (displaces from binding sites and and decrease clearance)

Antidotes: Slowly normalize K, Lidocaine, Cardiac pacer,
ANTI-DIGOXIN FAB FRAGMENTS, Mg

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14
Q

Antiarrhythmic Drug Classes

A

“No Bad-Boy Keeps Clean”

Na channel blockers
Beta-Blocker
K channel blockers
Ca channel blockers

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15
Q

Class I Antiarrhythmic Drugs and Class

A

“Double Quarter Pounder
Lettuce Tomatoes Mayo
Fries Please”

Disopyramide, Quinidine, Procainamide (IA)
Lidocaine, Tocainide, Mexiletine (IB)
Flecainide, Propafenone (IC)

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16
Q

Class IA Antiarrhythmics (Drugs, MOA, Use, Tox)

A

Quinidine, Procainamide, Disopyramide

Na blocker- Increase AP duration, Increase ERP, Increase QT.

Reentrant and Ectopic tachycardia

Quinidine causes cinchonism (headache & tinnitus)
Procainamide causes SLE-like syndrome
Disopyramide causes thrombocytopenia, TdP

17
Q

Class IB Antiarrhythmics (Drugs MOA, Use, Tox)

A

Lidocaine, Mexiletine, Tocainide

Na blocker- Decrease AP duration, Preferentially affect ischemic tissue.

Ventricular arrhythmias, and digitalis-induced arrhythmia

Local anesthetic, CNS, Cardiovascular depression

18
Q

Class IC Antiarrhythmics (Drugs, MOA, Use, Tox)

A

Flecainide, Propafenone

Na blocker- Ventricular tachycardias (last resort)

Proarrhythmic (esp post MI), Prolongs refractory period in AV node

19
Q

Class II Antiarrhythmics (Drugs, MOA, Use, Tox)

A

Metoprolol, Propranolol, Esmolol, Atenolol, Timolol

Beta-Blockers=Decrease SA and AV nodal activity by decreasing cAMP and Ca currents

Ventricular tachycardia, SVT, Slowing ventricular rate in A-fib

Impotence, Exacerbation of asthma, Sedation/sleep alteration, May mask signs of hypoglycemia

20
Q

Class III Antiarrhythmics (Drugs, MOA, Use, Tox)

A

Amiodarone, Sotalol

K blockers= Increase AP duration, Increase ERP, Increase QT (used as last resort)

Amiodarone= Class I, II, III and IV effects (alters lipid membrane), Pulmonary fibrosis, Hepatotoxicity, Hypo/Hyperthyroidism, Photodermatitis, Neuro

Sotalol= TdP, Excessive beta block

21
Q

Class IV Antiarrhythmics (Drugs, MOA, Use, Tox)

A

Verapamil, Diltiazem

Ca blockers=Decrease conduction velocity, Increase ERP, Increase PR,

Prevention of nodal arrhythmias (SVT)

Constipation, Edema, CHF, AV block, Sinus node depression)

22
Q

Adenosine

A

Hyperpolarize cell

Choice for supraventricular tachycardia (15 sec DOA)

Flushing, Hypotension, Chest pain
Effect blocked by caffeine and theophylline

23
Q

Mg

A

Effective in TdP and Digoxin toxicity

24
Q

Mannitol (Site of action, MOA, Use, Tox)

A

Proximal tubule

Osmotic diuretic (increase tubular fluid osmolarity, Decreases intracranial pressure)

Drug overdose and Elevated intracranial pressure

Pulmonary edema, Dehydration
CONTRAINDICATED IN ANURIA AND CHF

25
Q

Acetazolamide (Site of action, MOA, Use, Tox)

A

Proximal tubule

Carbonic anhydrase inhibitor (NaHCO3 diuresis)

Glaucoma, Urinary alkalinization, Metabolic alkalosis, Altitude sickness, Pseudotumor cerebri
“ACID-azolamide causes ACIDosis”

Hyperchloremic metabolic acidosis, Paresthesia, NH3 toxicity, Sulfa allergy

26
Q

Furosemide (Site of action, MOA, Use, Tox)

A

Loop diuretic (thick ascending limb)

Inhibits Na, K, Cl transport (abolishes gradient in medulla, preventing concentration of urine)
Stimulates PGE release (afferent arteriole vasodilation)
INCREASE Ca excretion

Edema (CHF, cirrhosis, nephrotic syndrome)
Hypertension
Hypercalcemia

“OH DANG”
Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout

27
Q

Ethacrynic acid (Site of action, MOA, Use, Tox)

A

Loop diuretic (thick ascending limb)

Inhibits Na, K, Cl transport (abolishes gradient in medulla, preventing concentration of urine)
Stimulates PGE release (afferent arteriole vasodilation)
Increase Ca excretion

Diuresis in patients ALLERGIC TO SULFA DRUGS

Causes hyperuricemia (NEVER USE WITH GOUT)

28
Q

Hydrochlorothiazide (Site of action, MOA, Use, Tox)

A

Early distal tubule

Inhibit NaCl reabsorption (reduces diluting capacity)
DECREASE Ca excretion

Hypertension, CHF, Idiopathic hypercalciuria, Nephrogenic diabetes insipidus

"hyperGLUC-HypoK-MAN"
HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia

HypoKalemic Metabolic Alkalosis
HypoNatremia

29
Q

Spironolactone, Eplerenone (Category, Site of action, MOA, Use, Tox)

A

K-Sparing diuretics

Collecting duct
Aldosterone receptor antagonists

Hyperaldosteronism, K depletion, CHF

Hyperkalemia (arrhythmias), Gynecomastia (spironolactone)

30
Q

Triamterene, Amiloride (Category, Site of action, MOA, Use, Tox)

A

K-Sparing diuretics

Collecting duct
Block Na channels

Hyperaldosteronism, K depletion, CHF

Hyperkalemia (arrhythmias)

31
Q

Changes in urine NaCl with diuretics

A

Increased with all diuretics (serum NaCl decreases)

32
Q

Changes in urine K with diuretics

A

Increase in all except K sparing (serum K decreases)

33
Q

What diuretics cause acidemia and by what mechanism?

A

Carbonic anhydrase inhibitors (decrease HCO3)

```
K sparing (aldosterone blockade prevents K & H secretion
Hyperkalemia also leads to increased K/H exchange)
~~~

34
Q

What diuretics cause alkalemia and by what mechanism?

A

Loop diuretics and Thiazides
~Volume contraction, Increased AT II, Increased Na/H exchange in prox. tubule, Increased HCO3 reabsorption (CONTRACTION ALKALOSIS)
~K loss leads to K exiting all cells in exchange for H entering
~In low K state, H is exchanged for Na leading to “paradoxical aciduria” and alkalosis

35
Q

Charges in urine Ca with diuretics

A

Increased with Loop diuretics (decrease paracellular reabsorption)

Decreased with Thiazides (enhanced paracellular reabsorption)

36
Q

Captopril, Enalapril, Lisinopril (MOA, Use, Tox)

A

ACE inhibitors
Decrease GFR (prevent constriction of efferent arterioles)
Prevents activation of bradykinin - potent vasodilator

Hypertension, CHF, Proteinuria, Diabetic renal disease, prevent unfavorable heart remodeling

“Captopril’s CATCHH”
Cough, Angioedema, Teratogen, Creatinine increase, Hyperkalemia, Hypotension

AVOID IN BILATERAL RENAL ARTERY STENOSIS (decrease GFR–> RENAL FAILURE)

37
Q

What diuretics cause hypocalcemia? Which cause hypercalcemia?

A

LOOPS LOSE CALCIUM!!!! (cause HYPOcalcemia)

Thiazides opposite (cause HYPERcalcemia)

ZPharmacology (23 decks)

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