Unit 3 Review

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A set of practice flashcards for nursing pharmacology students focusing on cardiovascular and respiratory medications.

Last updated 3:03 PM on 8/1/26
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389 Terms

1
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What is the classification of Captopril, and is it a prototype?

It is the prototypical Angiotensin-Converting Enzyme (ACE) inhibitor and was the first available drug in its class.

2
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How does Captopril's mechanism of action (MOA) affect Angiotensin?

It inhibits the enzyme that converts Angiotensin I to Angiotensin II (a potent vasoconstrictor).

3
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What effect does Captopril have on bradykinin and aldosterone?

It prevents the breakdown of bradykinin (a vasodilator) and inhibits aldosterone secretion, promoting diuresis of sodium and water.

4
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What are the primary clinical indications for Captopril?

It is indicated for hypertension, heart failure, and improving survival after an acute myocardial infarction (MI).

5
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What specific heart-wall benefit does Captopril provide following a heart attack?

It prevents ventricular remodeling (the thickening of heart walls).

6
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How does Captopril protect the kidneys in diabetic patients?

It provides nephroprotection by reducing proteinuria.

7
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What are the most common adverse effects of Captopril?

Common effects include a characteristic dry, nonproductive cough, fatigue, dizziness, and headache.

8
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What are two serious and potentially fatal adverse effects of Captopril?

Hyperkalemia (high potassium) and angioedema (swelling of the face or throat).

9
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What is the Black Box Warning for Captopril?

It is strictly contraindicated in pregnancy due to a Black Box Warning for fetal toxicity.

10
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When is Captopril contraindicated based on lab values and anatomy?

Contraindicated if baseline potassium is above 5mEq/L5\,mEq/L or if the patient has bilateral renal artery stenosis.

11
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What is the classification of Clonidine, and is it a prototype?

It is a centrally acting alpha2-adrenergic receptor agonist and is the prototypical drug for its class.

12
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How does Clonidine lower blood pressure via the Central Nervous System (CNS)?

It stimulates alpha2 receptors in the brain, which reduces sympathetic outflow and lack of norepinephrine production.

13
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What are the primary clinical reasons Clonidine is prescribed?

It is primarily used to treat hypertension and is also highly effective in managing opioid withdrawal symptoms.

14
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What are common adverse effects of Clonidine?

Common effects include orthostatic hypotension, fatigue, drowsiness, dry mouth, and constipation.

15
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What is the most critical safety instruction regarding the discontinuation of Clonidine?

It must NEVER be discontinued abruptly, as this can lead to severe, dangerous rebound hypertension.

16
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How is the Clonidine transdermal patch administered?

It is applied weekly, and the nurse must ensure the old patch is removed before applying a new one.

17
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Why does blood pressure 'Climb' if Clonidine is stopped fast?

Stopping it fast causes rebound hypertension (mnemonic: blood pressure will 'Climb').

18
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How does Clonidine affect the kidneys indirectly?

It reduces renin activity in the kidneys as a result of its central action.

19
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When is Clonidine use specifically contraindicated?

In patients with a known hypersensitivity; it should be used cautiously in those with severe liver or kidney disease.

20
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What should a nurse teach a patient regarding position changes when taking Clonidine?

Change positions slowly to avoid fainting due to orthostatic hypotension.

21
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What is the classification of Hydralazine?

It is a direct-acting vasodilator used to illustrate this class of antihypertensives.

22
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What is the mechanism of action (MOA) of Hydralazine?

It acts directly on arteriolar smooth muscle to cause relaxation, resulting in reduced Systemic Vascular Resistance (SVR).

23
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What are the primary uses for Hydralazine across different administration routes?

Oral form is for routine essential hypertension; injectable (IV) form is for hypertensive emergencies or hospitalized patients.

24
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What adjunct use does Hydralazine have in combination for heart failure?

Used with isosorbide dinitrate (BiDil) for heart failure, particularly in Black patients.

25
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What are common adverse effects of Hydralazine related to rapid vasodilation?

Dizziness, headache, anxiety, tachycardia (reflex tachycardia), and nausea.

26
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What unique and serious systemic adverse effect can Hydralazine cause?

The development of a systemic lupus erythematosus (SLE)-like syndrome.

27
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Which conditions contraindicate the use of Hydralazine?

Coronary artery disease and mitral valve dysfunction.

28
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What signs of SLE should a nurse teach a patient on Hydralazine to report?

Fever, joint pain, or skin rashes.

29
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Why might a provider order a beta blocker along with IV Hydralazine?

To control reflex tachycardia caused by rapid vasodilation.

30
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What mnemonic helps remember how Hydralazine works on the arterioles?

'Hydra for Hydrant'—like a fire hydrant opening up pipes (arterioles) to let blood flow easily.

31
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What is the classification of Losartan?

It is an Angiotensin II Receptor Blocker (ARB) and is the class representative.

32
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How does Losartan's mechanism of action (MOA) differ from ACE inhibitors?

It blocks the binding of Angiotensin II to its receptors in smooth muscle/adrenal glands, rather than blocking the production of Angiotensin II.

33
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Why is Losartan often prescribed for patients previously on ACE inhibitors?

It is used for patients with hypertension or heart failure who cannot tolerate ACE inhibitors (often due to cough).

34
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What are common adverse effects and safety warnings for Losartan?

Common effects include chest pain, fatigue, and diarrhea; it carries a Black Box Warning for fetal toxicity.

35
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When is Losartan strictly contraindicated?

In pregnancy (especially second and third trimesters) and lactation.

36
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What is the most important teaching point for a woman of childbearing age on Losartan?

She must avoid becoming pregnant while taking the drug due to the risk of fetal injury or death.

37
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Why is Losartan less likely to cause a dry cough than ACE inhibitors?

It does not allow bradykinin to accumulate in the lungs.

38
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What is a fun way to remember how Losartan interacts with receptors?

The '-sartan' drugs are 'Satan to the Receptors' because they block them so Angiotensin II cannot bind.

39
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What assessment should be done cautiously for patients on Losartan with organ dysfunction?

It should be used cautiously in patients with renal or hepatic dysfunction.

40
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What is the standard route for Losartan administration?

It is administered orally.

41
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What are the classifications of Atenolol (Tenormin)?

It is a cardioselective beta1-adrenergic receptor blocker and a Class II antidysrhythmic.

42
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How does Atenolol work in the heart (pharmacodynamics)?

It preferentially blocks beta1 receptors, resulting in negative chronotropic (rate), negative dromotropic (conduction), and negative inotropic (contractility) effects.

43
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What does Atenolol suppress in the kidneys?

It suppresses the activity of renin.

44
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What are the primary reasons Atenolol is prescribed?

Hypertension, angina pectoris, and after an acute MI to decrease mortality by protecting the heart from catecholamines.

45
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What are common cardiovascular and general adverse effects of Atenolol?

Bradycardia, hypotension, fatigue, and weakness.

46
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How does Atenolol affect glucose management in diabetic patients?

It can cause hypo- or hyperglycemia and masks the tachycardia typically signaling low blood sugar.

47
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When is the use of Atenolol strictly contraindicated?

Severe bradycardia, second- or third-degree heart block, heart failure, and cardiogenic shock.

48
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Why should Atenolol be used with caution in patients with asthma or COPD?

Any level of beta blockade can potentially promote bronchoconstriction.

49
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What is the critical teaching point for Atenolol regarding cessation?

Never stop taking it abruptly; it must be tapered to avoid rebound hypertension or MI.

50
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What is the most reliable indicator of hypoglycemia for a diabetic patient on Atenolol?

Sweating, because the drug masks the typical fast heart rate (tachycardia).

51
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What is the classification of Diltiazem (Cardizem), and what is its chemical class?

It is a Calcium Channel Blocker (CCB) and the only member of the benzothiazepine class.

52
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How does Diltiazem affect the heart's conduction system?

It inhibits calcium influx, slowing conduction through the SA and AV nodes to reduce heart rate.

53
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What are the primary indications for Diltiazem?

Hypertension, angina pectoris, and temporary control of rapid ventricular response in atrial fibrillation/flutter or PSVT.

54
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What are common adverse effects of Diltiazem?

Hypotension, bradycardia, peripheral edema, headache, dizziness, and constipation.

55
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When is Diltiazem contraindicated?

Acute MI, severe hypotension, shock, sick sinus syndrome, and second- or third-degree AV block (without a pacemaker).

56
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What mnemonic helps remember how Diltiazem and Verapamil relax the heart?

'V & D for Very-relaxing-Ducts'—they relax the conduction system and blood vessels.

57
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What juice should a patient avoid while taking Diltiazem?

Grapefruit juice, as it reduces metabolism and leads to toxicity.

58
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What are the requirements for parenteral (IV) administration of Diltiazem?

Continuous ECG monitoring is required.

59
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What patient monitoring is needed for Diltiazem regarding GI health?

Increase fluid and fiber intake to manage potential constipation.

60
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At what heart rate or blood pressure should a nurse withhold Diltiazem?

Pulse less than 60bpm60\,bpm or systolic blood pressure of 90mmHg90\,mmHg or lower.

61
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What are the two classifications of metoprolol?

Cardioselective beta1-adrenergic receptor blocker and Class II antidysrhythmic.

62
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How does metoprolol work in the myocardium?

It leads to a reduced heart rate, slowed AV node conduction, and decreased contractility by blocking beta1 receptors.

63
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What is the 'M' mnemonic for metoprolol's clinical use post-heart attack?

'M' for 'MI protection' (reduces risk of sudden cardiac death after MI).

64
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What are the primary uses for metoprolol?

Hypertension, angina pectoris, and heart failure.

65
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What signal of hypoglycemia does metoprolol mask in diabetic patients?

It masks tachycardia (fast heart rate).

66
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What are the contraindications for metoprolol regarding heart rhythm and failure?

Severe bradycardia, second- or third-degree heart block, cardiogenic shock, and uncompensated heart failure.

67
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How should a nurse teach a patient to discontinue metoprolol?

It must be tapered over 1 to 2 weeks to avoid rebound hypertension or MI.

68
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What are the available administration forms for metoprolol?

Oral (immediate-release tartrate and long-acting succinate) and parenteral (IV).

69
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Which assessment finding should the nurse prioritize before giving metoprolol?

The patient's pulse (withhold if less than 60bpm60\,bpm).

70
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What does the suffix '-olol' stand for in mnemonics for beta blockers?

It means it makes the heart rate go 'Lo-lo-lo'.

71
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What is the classification of nitroglycerin?

It is the prototypical organic nitrate and a potent antianginal.

72
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How does nitroglycerin predominantly affect the heart's workload?

It predominantly dilates veins, which decreases venous return (preload) and reduces myocardial oxygen demand.

73
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What are the clinical indications for the treatment and prevention of angina?

Used for stable, unstable, and vasospastic angina pectoris.

74
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What are the most common adverse effects of nitroglycerin?

Headache (usually transient), reflex tachycardia, and postural/orthostatic hypotension.

75
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Nitroglycerin is strictly contraindicated with which drug class?

Erectile dysfunction drugs (e.g., sildenafil, tadalafil) due to the risk of fatal hypotension.

76
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What is the mnemonic for nitroglycerin's effect on preload?

'Nitro for No preload' because it dilates veins and keeps blood in the 'pipes'.

77
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What are the storage requirements for sublingual nitroglycerin tablets?

Keep in original dark glass container; protect from air and moisture to keep them active.

78
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What is the protocol for acute chest pain when using nitroglycerin?

Stop activity, sit down, take one tablet; if no relief in 5 minutes, call 911 (then may take second and third doses).

79
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How can a patient prevent nitrate tolerance when using transdermal patches?

Remove the patch at night for a nitrate-free period of at least 8 hours.

80
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What are the diverse routes for nitroglycerin administration?

Sublingual, oral, topical (ointments/patches), and intravenous.

81
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What is the classification of Digoxin (Lanoxin)?

It is a cardiac glycoside.

82
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How does Digoxin produce a positive inotropic effect?

It inhibits the sodium-potassium ATPase pump, leading to increased intracellular calcium and stronger contraction.

83
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What are the negative chronotropic and dromotropic effects of Digoxin?

It increases vagal tone, causing a slower heart rate and slowed conduction.

84
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What are the primary clinical indications for Digoxin?

Systolic heart failure and heart rate control in atrial fibrillation or flutter.

85
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What are hallmark visual signs of Digoxin toxicity?

Visual disturbances such as blurred vision or yellow/green/purple halos.

86
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What electrolyte imbalance most significantly increases the risk of Digoxin toxicity?

Hypokalemia (low potassium).

87
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What is a fun way to remember the deep, slow heart beat of Digoxin?

'Digs for a deep beat' (heart beats deeper—stronger—and slower).

88
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What dietary instruction is given to patients regarding fiber and Digoxin?

Avoid eating large amounts of bran or high-fiber foods near the time of dosing as they decrease absorption.

89
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What is the term for a loading dose in Digoxin administration?

Digitalization.

90
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When should a patient notify their provider based on pulse check for Digoxin?

If pulse is below 60 or above 100bpm100\,bpm.

91
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What is the classification of Milrinone (Primacor)?

It is a phosphodiesterase inhibitor (PDI).

92
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Why is Milrinone called an 'inodilator'?

Because it is a positive Inotrope (stronger beat) and a potent Dilator (vasodilation).

93
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What is the mechanism of action (MOA) of Milrinone?

It increases intracellular cAMP.

94
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For what clinical purpose is Milrinone used short-term?

Short-term management of acute heart failure or support while awaiting heart transplant.

95
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What is the primary and most serious adverse effect of Milrinone?

Cardiac dysrhythmias, specifically ventricular dysrhythmias (occurring in 12%12\% of patients).

96
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What other adverse effects are common with Milrinone?

Hypotension, headache, and hypokalemia.

97
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What administration rule exists between intravenous Milrinone and Furosemide?

They must NOT be given in the same IV line; furosemide will precipitate immediately.

98
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Which medical conditions contraindicate the use of Milrinone?

Known drug allergy; may be avoided in severe aortic or pulmonary valvular disease.

99
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What should an ICU patient report immediately while receiving Milrinone?

Any chest pain (angina) or feeling faint (hypotension).

100
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What assessment finding is most critical to report during a Milrinone infusion?

New ventricular dysrhythmias on the ECG monitor.