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NURS 3550 > CVS Drugs Week 2 and 3 > Flashcards

CVS Drugs Week 2 and 3 Flashcards

1
Q

what are the 2 major forms of heart failure?

A

a) HF with left ventricular systolic dysfunction

b) Diastolic HF

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2
Q

What is heart failure?

A

Progressive disease, characterized by ventricular dysfunction, reduced CO, insufficient tissue perfusion, fluid retention.

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3
Q

What are the causes of HF?

A

Chronic hypertension and myocardial infraction.

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4
Q

What is cardiac remodeling?

A

In the inital phase, heart tries to compensate by remodeling itself. This puts more stress on the heart, and decreases the CO progressively.

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5
Q

what is cardiac dilation?

A

Result of increased venous pressure and reduced contractile force. Basically, the heart is dilating because of the fluid.

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6
Q

What is digoxin?

A

A cardiac glycoside. Effects the mechanical and electrical properties of the heart.

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7
Q

How does digoxin affect the heart?

A

Exerts a positive inotropic action on the heart. Increases the ventricular contraction, increasing CO.

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8
Q

What is the MA for digoxin?

A

Inhibits sodium potassium-ATPase. Increases Ca, which augments contractile force by facilitating the interaction of myocardial contractile proteins (actin and myosin).

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9
Q

Why is the relationship b/w potassium and inotropic action important for digoxin?

A

K+ competes with digoxin to bind to the enzyme. When K+ levels are low, digoxin binding increases. When K+ levels are high, thereapeutic effect is decreased.

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10
Q

What are the consequences of an increased CO (digoxin)?

A

a) sympathetic tone declines
b) urine production increases
c) renin release declines

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11
Q

What are the hemodynamic benefits to digoxin?

A

CO improves, HR decreases, heart size declines, constriction of arterioles and veins, water retention reverses, decreased blood volume, peripheral and pulmonary edema decreases, water weight is lost.

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12
Q

What are the neurohormonal benefits of digoxin in HF?

A

Inhibit renin release by decreasing Na absorption. Can decrease sympathetic outflow to CNS.

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13
Q

What electrical effects on the heart does digoxin have?

A

Digoxin can alter electrical activity in noncontractile tissue, and ventricular muscle. Can alter automaticity, refractionriness, and impulse conduction.

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14
Q

What are the cardiac adverse effects of digoxin?

A

Dysrythmias!!

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15
Q

What are some predisposing factors to dysrhythmias happening when taking digoxin?

A

Hypokalemia, elevate digoxin levels, heart disease.

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16
Q

What are some noncardiac adverse effects?

A

Anorexia, nausea vomiting- causes by simulation of the chemoreceptor trigger zone of medulla. Fatigue, visual disturbances also common.

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17
Q

What are some important drug interactions for digoxin?

A

Diuretics- loss of K
ACE inhibitors and ARBs- increase K levels
Sympathomimetics- increase hr and force
Quinidine- causes plasma levels of digoxin to rise
Verapamil- Ca channel blocker.

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18
Q

What are statins?

A

HMG-CoA inhibitors. Most effective drug for lowering LDL and total cholesterol. Lower risk of HF, MI, sudden death.

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19
Q

What are the beneficial actions of statins?

A
  • Lower LDL cholesterol
  • Elevate HDL cholesterol
  • Reduce triglyceride levels.
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20
Q

What is the MA of statins?

A

Depends on increasing the number of LDL receptors on hepatocytes. -
Inhibits hepatic HMG-CoA reductase. This decreases cholesterol production.

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21
Q

what are the therapeutic uses for statins?

A
  • hypercholesterolemia
  • Primary/secondary prevention of CV events
  • Primary prevention in peeps with normal LDL levels
  • Post MI therapy
  • Diabetes
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22
Q

When do you administer a statin?

A

AT NIGHT.

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23
Q

What statins are excreted in the urine?

A

Lovastatin, pitavastatin, pravastatin, simvastatin.

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24
Q

What statins are metabolized by CYP3A4?

A

Atorvastatin, lovastatin, simvastatin.

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25
Q

What are adverse effects of statins?

A

AE are uncommon, but some pts experience headache, rash, cramps, memory loss, GI problems. Usually transient.

26
Q

What is myopathy/rhabdomyolysis and statins?

A

Statins can injure muscle tissue. AE include muscle aches, tenderness, weakness. Rhabdomyolysis is muscle disintegration or dissolution.

27
Q

What are some important drug interactions for statins?

A

W/ other lipid lowering drugs, drugs that inhibit CYP3A4.

28
Q

What is angina pectoris?

A

Chest pain.

29
Q

What are the 3 forms of angina?

A

a) Chronic stable angina
b) Variant angina
c) Unstable angina

30
Q

What is the treatment strategy for angina?

A

a) Increase cardiac oxygen supply.

b) Decrease O2 demand

31
Q

What do nitrates do for stable angina?

A

Decrease O2 demand by dilating veins, which decreases preload.

32
Q

What do nitrates do for variant angina?

A

increase O2 supply by relaxing coronary vasospasm. Does not reduce O2 supply.

33
Q

What is nitroglycerin?

A

Acts on vascular smooth muscle to promote vasodilation. Acts on veins.

34
Q

What are the AE of nitro?

A

Headache, orthostatic hypotension,

reflex tachycardia.

35
Q

What are some important drug interactions for nitro?

A

Hypotensive drugs, BB, Verapamil, Diltiazem.

36
Q

How can you administer nitro?

A

PO, IV, sublingual, translingual, transdermal, topical,

37
Q

What is important to know about discontinuing nitro?

A

Stop slowly, abrupt discontinuation may cause vasospasm.

38
Q

What are the therapeutic uses of nitro?

A

Acute therapy of angina, sustained therapy of angina, intravenous therapy.

39
Q

What does the RAAS system do?

A

Regulates BP, blood volume, fluid and electrolyte balances.

40
Q

How does the RAAS system exert its effects?

A

Angiotensin 2 and aldosterone.

41
Q

What are the actions of angiotensin 2?

A

Vasoconstriction, release of aldosterone, alteration of cardiac and vascular structure.

42
Q

How does angiotensin 2 cause vasoconstriction?

A

Acts on sympathetic neurons to promote NE, acts on adrenal medulla to promote epi, acts on CNS to increase sympathetic outflow to blood vessels.

43
Q

How does angiotensin release aldosterone?

A

Acts on adrenal cortex to promote synthesis and secretion of aldosterone.

44
Q

How does angiotensin 2 alter cardiac and vascular structure?

A

Can cause hypertrophy and remodeling in the heart.

45
Q

What are the actions of aldosterone?

A

Regulating blood volume and blood pressure, pathologic cardiovascular effects.

46
Q

Explain the formation of angiotensin 2.

A

Renin catalyzes the formation of angiotensin 1.

47
Q

What causes renin release?

A

Decreased BP, blood volume, plasma Na content, reduced renal perfusion pressure.

48
Q

Why may reduced renal perfusion occur?

A

a) Stenosis of renal arteries
b) Reduced systemic BP
c) reduced plasma volume.

49
Q

What is renin secretion inhibited by?

A

Elevated BP, blood volume, and plasma sodium content.

50
Q

What is ACE?

A

Angiotensin Converting Enzyme (Kinase II).

Converts angiotensin 1 to angiotensin 2.

51
Q

How do ACE inhibitors produce their effects?

A

a) Reducing levels of angiotensin

b) Increase levels of bradykinin.

52
Q

What does reducing levels of angiotensin 2 by ACE inhibitors do?

A

a) Dilate blood vessels
b) reduce blood volume
c) Prevent/reverse pathologic changes in heart and blood vessels mediated by angiotensin 2 and aldosterone.

53
Q

How are ACE inhibitors administered?

A

Orally, except enalaprilat.

54
Q

What are prodrugs?

A

Drugs that have to undergo conversion to their active form. Except for lisinopril.

55
Q

How are ACE inhibitors excreted?

A

Kidneys.

56
Q

What are the therapeutic indications for ACE inhibitors?

A
  • Hypertension
  • Heart Failure
  • Myocardial Infraction
  • Diabetic and -Nondiabetic Nephropathy
  • Prevention of MI, Stroke, and Death in pts at high cardiovascular risk
  • Diabetic Retinopathy
57
Q

What are the adverse effects of ACE inhibitors?

A

First-Dose Hypotension, Cough, Hyperkalemia, Renal Failure, Fetal Injury, Angioedema.

58
Q

What is angioedema?

A

Fatal reaction that develops in 1% of patients. Symptoms- increased giant wheals, edema of tongue, glottis, lips, eyes, and phayrnx.

59
Q

What are important drug interactions with ACE inhibitors?

A
  • Diuretics
  • Antihypertensive Agents
  • Drugs that raise potassium levels
  • Lithium
  • NSAIDs
60
Q

CAPTOPRIL (side effects of ACE inhibitors)

A 
Cough/C1 esterase deficiency
Angioedema/Agranulocytosis
Proteinuria/Potassium Excess
Taste change
Orthostatic hypotension
Pregnancy
Renal Artery stenosis
Increase renin
Leukopenia/Liver toxicity
61
Q

What is cardiac dilation the result of?

A

Combo of increased venous pressure and reduced contractile force.

62
Q

What are the consequences of increased sympathetic tone?

A
  • Increased HR
  • Increased contractility
  • Increased venous tone
  • Increased arteriolar tone

NURS 3550 (11 decks)

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