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NURS 572 Advanced Pharmacotherapeutics UofA Nursing > Cardiac Meds > Flashcards

Cardiac Meds Flashcards

1
Q

What category of medication is clonidine part of?

A

alpha-2 agonist

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1
Q

What is the mechanism of action of clonidine, used in the treatment of hypertension?

A. Activation of peripheral alpha-2 receptors
B. Inhibition of peripheral alpha-2 receptors
C. Activation of central alpha-2 receptors
D. Inhibition of central alpha-2 receptors

A

C. Central Alpha-2 Agonist.
Clonidine is a central alpha-2 agonist that activates alpha-2 receptors at the level of the brain stem. This reduces sympathetic outflow, leading to decreased blood pressure.

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2
Q

Alpha-methyldopa, an alpha-2 agonist, has a major use in a specific subgroup of hypertensive patients. Which group benefits from this medication?

A. Hypertensive patients with renal dysfunction
B. Hypertensive patients with pulmonary hypertension
C. Hypertensive patients in pregnancy
D. Hypertensive patients with diabetes

A

C. Pregnancy. Alpha-methyldopa today is mainly used to treat hypertension in pregnant patients due to its safety profile.

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3
Q

How does activation of beta-1 adrenergic receptors affect the heart?

A. It decreases heart rate and contractility
B. It increases heart rate and reduces contractility
C. It decreases heart rate and increases contractility
D. It increases heart rate and contractility

A

D. Beta-1 adrenergic receptors are found on cardiac myocytes and their activation leads to an increase in the heart rate and contractility. This is primarily due to increased cyclic AMP levels leading to an influx of calcium.

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4
Q

Activation of a2 receptors has what effect on intracellular cAMP and neurotransmitter release?

A. cAMP levels increase, promoting presynaptic neurotransmitter release
B. cAMP levels decrease, promoting presynaptic neurotransmitter release
C. cAMP levels increase, inhibiting presynaptic neurotransmitter release
D. cAMP levels decrease, inhibiting presynaptic neurotransmitter release

A

D. Alpha-2 adrenergic receptors are coupled to the inhibitory regulatory protein Gi, which, when activated, decreases intracellular cyclic AMP levels. This modulation reduces the release of neurotransmitters at presynaptic sites, producing an inhibitory effect on autonomic activity.

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4
Q

What is a mechanism by which beta blockers can lower blood pressure?

A. Increase cardiac output
B. Decrease renin production in the kidney
C. Increase heart rate
D. Increase sympathetic nervous system stimulation

A

B. Beta blockers can lower blood pressure by decreasing renin production at the kidney.

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5
Q

What is a common suffix for Beta Blockers?

A. -pril
B. -sartan
C. -lol
D. -statin

A

C. -lol

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6
Q

How do beta blockers aid in the treatment of angina?

A. They increase heart rate
B. They decrease diastolic perfusion time
C. They increase cardiac contractility
D. They decrease cardiac contractility

A

D. Beta blockers work to slow the heart rate and decrease contractility, reducing the oxygen needed for the heart to function.

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7
Q

Which condition can be exacerbated by the use of non-selective beta-blockers?

A. Hypertension
B. Angina
C. Asthma
D. Tachycardia

A

C. Asthma can be exacerbated by non-selective beta blockers. These drugs may result in the constriction of airways and worsening of existing obstructive airway disease, such as asthma.

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8
Q

Why is a Hx of medication noncompliance a concern for patients taking clonidine (Catapres)?

A

Rebound hypertension when missed dose. Clonidine is administered 2-3 times a day because of the short half-life, causing non-compliance. Can use TTS (transdermal therapeutic system) applied every 7 days.

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9
Q

How do alpha-2 agonists worsen depression and erectile dysfunction?

A

Penetrates BBB and decreases sympathetic tone, causing fatigue. Worsens depression. Erection and ejaculation are controlled by PNS and SNS.

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10
Q

Which abnormal lab tests has been associated with the use of one of the alpha-2 agonists (specifically methyldopa)?

A

Pos. Coombs Test. Hemolytic anemia. When drug is present it may bind to RBCs stimulates autoimmune activation, causing a rxn, induces hyperbilirubinemia and anemia.

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11
Q

Which antidepressant works opposite of alpha-2 agonists?

A

Mirtazapine (Remeron) = alpha-2 antagoinst.

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12
Q

What class of medications has a “first dose phenomenon” of orthostasis?

A

Alpha-1 Receptor Blockers. Especially if on diuretics, beta-blockers, or CCBs

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13
Q

Do beta blockers have a diuretic effect?

A

slightly because it blocks the RAAS system and decreases resorption of NA/H2O having a slight diuretic effect and lower blood pressure.

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14
Q

Which 2 beta-blockers are known to reduce mortality in HF?

A

Carvedilol (Coreg) and Metoprolol succinate (Toprol XL)

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15
Q

Which beta blocker needs to be started low dose and titrated slowly?

A

Carvedilol (Coreg) - every 2 weeks. If too fast, causes HF exacerbation, low BP, SOB.

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16
Q

Why is IV Metoprolol no longer used in NSTEMI but is still used in STEMI?

A

Can cause cardiogenic shock in >70

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17
Q

How can beta-blockers reduce the risk of sudden cardiac death or V-fib in HF?

A

Reduces remodeling.

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18
Q

Which beta-blocker is useful in migraine treatment?

A

Propranolol. It is lipophilic and penetrates the BBB blocking beta-2 vasodilation.

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19
Q

Which medication should you not combine with propranolol in migraine tx?

A

DHE (dihydroergotamine) Additive vasoconstrictive effect.

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20
Q

Which long-acting beta blocker can you break the pill in half?

A

Metoprolol “succinate” (Toprol XL) Cannot crush

21
Q

Can beta-1 selective agents worsen asthma?

A

Yes. Bronchodilation is mediated by beta-2 receptors, if those are blocked, it will cause bronchoconstriction and bronchospasm.

22
Q

Which beta-blocker should be dose adjusted in pts with renal impairment?

A

Atenolol and nadolol.

23
Q

How do beta blockers worsen depression and erectile dysfunction?

A

Penetrates the BBB reducing sympathetic tone. Carvedilol, labetalol, metoprolol, nebivolol, and propranolol.

24
Q

Which of the following is NOT a common adverse effect of ACE inhibitors?

A. Cough
B. Hypotension
C. Bradyarrhythmia
D. Angioedema

A

C. Bradyarrhythmia.
ACE inhibitors can cause a persistent, dry cough (due to increased bradykinin levels); hypotension, especially in patients with elevated renin levels, and angioedema. Bradyarrhythmias are not commonly reported.

25
Q

Why do ACE inhibitors have the potential to increase serum creatinine levels?

A. They increase sodium and water retention
B. They decrease systemic vascular resistance
C. They decrease GFR due to efferent arteriole dilation
D. They decrease GFR due to afferent arteriole dilation

A

C. Angiotensin II promotes constriction of the efferent arteriole, which helps maintain GFR. Blocking angiotensin II production leads to dilation of the efferent arteriole, decreasing GFR if compensatory mechanisms cannot respond (e.g. in heart failure or CKD). This decrease in GFR is reflected by an increase in serum creatinine levels.

26
Q

Patients being treated with an ACE inhibitor who develop a persistent cough should:

A. Decrease ACE inhibitor dose
B. Increase ACE inhibitor dose
C. Switch to a beta blocker
D. Switch to an ARB

A

D. Switch to ARB.
Angiotensin receptor blockers block angiotensin II at the receptor level and thereby can achieve the same effects as ACE inhibitors without increasing bradykinin levels, which are responsible for the persistent cough side effect of ACE inhibitors.

27
Q

ACE inhibitors and ARBs have what potential effect on potassium levels?

A. Decreased serum potassium due to reduced aldosterone levels
B. Increased serum potassium due to reduced aldosterone levels
C. Decreased serum potassium due to increased aldosterone levels
D. Increased serum potassium due to increased aldosterone levels

A

B. By inhibiting ACE or angiotensin II receptor activity, these drugs decrease plasma aldosterone levels. Since aldosterone promotes renal potassium secretion, inhibiting its effect can result in hyperkalemia.

28
Q

Why are ACE inhibitors contraindicated in patients with bilateral renal artery stenosis?

A. They can precipitate acute renal failure
B. They can cause vasoconstriction of renal arteries
C. They can increase systemic blood pressure
D. They can lead to decreased sympathetic activity

A

A. ACE inhibitors prevent angiotensin II activity which normally constricts efferent arterioles, maintaining GFR. In patients with bilateral renal artery stenosis, efferent arteriole dilation can decrease GFR, causing acute renal failure.

29
Q

Which effect is NOT associated with ACEs and ARBs?

A. reduced afterload
B. reduced preload
C. vasodilator
D. reduced contractility

A

D. reduced contractility. That is associated with beta blockers.

30
Q

Ace Inhibitors (as a monotherapy) may be less effective for what racial group due to lower renin release?

A

African Americans

31
Q

How do ACEs and ARBs confer renal protective benefits for diabetics?

A

Decreases GFR

32
Q

ACEs and ARBs are safe in pregnancy. True or False?

A

False. They are considered a teratogen in pregnancy. Category D.

33
Q

Do NSAIDs reduce or increase effects of ACE-inhibitors?

A

Reduce. Inhibit prostaglandin production = vasoconstriction, reducing flow of afferent, causing a release of renin, activating RAAS that decreases effect of ACE-inhibitors (negates the action of ACEi)

34
Q

What effect do ACEi and ARBs have on serum potassium?

A

Increase. Can cause hyperkalemia.

35
Q

What 2 conditions are contraindicated for use of ARBs and ACEi?

A
  1. Bilateral renal artery stenosis
  2. Pregnany
36
Q

A 35-year-old woman has been recently diagnosed with hypertension. She is discussing medical options with her physician, and notes that she and her partner are trying to conceive. What side effect is she least likely to experience after starting nifedipine?

A. Constipation
B. Flushing
C. Peripheral edema
D. Tachycardia

A

A. Constipation. Dihydropyridine calcium channel blockers such as nifedipine are not associated with constipation. A common side effect of the non-dihydropyridine verapamil is constipation, occurring in 25% of patients.

37
Q

A patient is started on verapamil while in the hospital and develops bradycardia and faints. His cardiologist suspects that the drug has disrupted the patient’s cardiac conducting system. What is the most likely finding on the patient’s ECG?

A. Normal-appearing QRS complex independent of P waves; heart rate 45
B. Normal-appearing, irregularly spaced QRS complexes without P waves; heart rate 145
C. Sharp downward spike at the beginning of each P wave followed by normal-appearing QRS; heart rate 65
D. Wide and bizarre QRS, no P waves; heart rate 110

A

A. This ECG finding is suggestive of complete heart block, a complication of non-dihydropyridine calcium channel blockers such as verapamil. These drugs disrupt the L-type calcium channels which dive depolarization at the SA and AV nodes.

38
Q

A 50-year-old woman is discussing starting verapamil for stable angina with her physician. Which of the following would be a contraindication to verapamil therapy?

A. Atrial fibrillation
B. Heart block
C. Hypertension
D. Migraine

A

B. Heart block. Verapamil is a non-dihydropyridine calcium channel blocker that is contraindicated in patients with heart block and other conduction abnormalities. This class of drugs targets voltage gated L-type calcium channels, which are responsible for depolarization at the AV node. Blockade of these channels can cause or worsen heart block.

39
Q

A 65-year-old man with past medical history of hypertension and Mobitz type 1 2nd degree heart block presents to the emergency room with a headache. His vitals are significant for blood pressure of 190/120 and heart rate of 50 bpm. His neurological exam is normal and CT of the head is negative for abnormalities. Which of the following medications is most appropriate in his management?

A. Diltiazem
B. Nicardipine
C. Nimodipine
D. Verapamil

A

B. Nicardipine. Nicardipine is a dihydropyridine calcium channel blocker with a short acting IV formulation useful in the treatment of hypertensive emergency. A dihydropyridine is appropriate in this circumstance because of vascular smooth muscle specificity; this will avoid exacerbating his heart block while lowering his blood pressure through peripheral vasodilation.

40
Q

A 46-year-old woman comes into her primary care provider complaining of crushing chest pain that occasionally wakes her from sleep in the early morning. The pain is not related to exercise and resolves on its own. She is prescribed nifedipine. What is the PRIMARY mechanism of action of this drug that will improve her symptoms?

A. By Increasing ventricular wall tension
B. By decreasing SA and AV node conductance
C. By decreasing cardiac contractility
D. By directly vasodilating coronary vessels

A

D. Dihydropyridine calcium channel blockers like nifedipine, along with nitrates, are the prefered treatment for Prinzmetal (vasospastic) angina, as described by this patient; these medications directly dilate the spasming coronary vessels. Because of its rapid onset of action, nifedipine can be used for either prophylaxis or abortive therapy.

41
Q

Patient teaching related to amlodipine should include all of the following EXCEPT:

a) Rise slowly from a supine position to reduce orthostatic hypotension.
b) Increase calcium intake to prevent osteoporosis from a calcium blockade.
c) Avoid grapefruit juice as it affects the metabolism of this drug.
d) Monitor for swelling in the feet and ankles.

A

B.

42
Q

A common side effect and reason for discontinuing an angiotensin-converting enzyme inhibitor (ACEI) is:

a) Hypokalemia
b) Diarrhea
c) Cough
d) Hyperhidrosis

A

C.

43
Q

Which of the following adverse effects may occur due to a dihydropyridine-type calcium channel blocker?
Question 6 options:

a) Increased contractility

b) Bradycardia

c) Edema of the hands and feet

d) Hepatic impairment

A

C

44
Q

Abrupt withdrawal of beta blockers can be life threatening. Patients at highest risk for serious consequences of rapid withdrawal are those with:
Question 7 options:

a) Angina
b) Coronary artery disease
c) Both A and B
d) None of the above

A

C

45
Q

J.T. has hypertension, for which a calcium channel blocker has been prescribed. This drug helps control blood pressure because it:

a) Decreases heart rate
b) Reduces stroke volume
c) Increases the activity of the Na+/K+/ATPase pump indirectly
d) Decreases the amount of calcium inside the cell

A

D

46
Q

Patients with diabetes should use caution when taking a beta blocker as it can mask symptoms of hypoglycemia.

True or False

A

True

47
Q

An elderly patient being treated for chronic heart failure (CHF) has been placed on a multidrug combination treatment plan, furosemide and lisinopril. Which test should the APN monitor?

A. Serum sodium and chloride levels
B. Serum creatinine level
C. Urinalysis
D. Fasting blood sugar

A

B. Monitor serum potassium, BUN, and creatinine levels.

48
Q

The patient is an older adult who has a diagnosis of type 2 diabetes mellitus and hypertension. The APN is prescribing her a beta blocker today. The APN should teach her that which symptom is an indication of hypoglycemia that is not masked by beta blockers?

A. Dizziness
B. Diaphoresis
C. Fatigue
D. Syncope

A

B. For patients with diabetes who must take a beta blocker, these drugs do not mask the diaphoresis associated with hypoglycemia. Patients with diabetes should be taught to recognize this indication of hypoglycemia.

49
Q

Which medication sometimes induces a lupus-like syndrome that appears to be dose-related with an incidence highest in white women?

A. Hydralazine
B. Digoxin
C. Propranolol
D. Furosemide

A

A. Hydralazine sometimes induces a lupus-like syndrome. It appears to be dose-related in that it occurs almost exclusively with doses above 50 mg. The incidence is highest in white women. A positive antinuclear antibody (ANA) test is found in these patients, but no renal impairment is seen. Discontinuing the drug reverses the syndrome, but the ANA does not return to normal until 6 to 8 months after the drug is stopped.

50
Q

Which medication regimen should the APN consider for a patient who has had a myocardial infarction (MI)?

A. Verapamil, clopidogrel, and baby aspirin
B. Atenolol, furosemide, and fibric acid derivative
C. Lisinopril, metoprolol, clopidogrel, and atorvastatin calcium
D. Propranolol, nifedipine, warfarin sodium, and baby aspirin

A

C. A combination of an ACEI, a beta blocker (BB), antiplatelet therapy, and lipid-lowering therapy after MI is appropriate.

51
Q

Which instruction does the APN provide to an adult male patient who has been prescribed nitrate therapy for treatment of angina?

A. Take up to 3 doses every 5 minutes; if unrelieved, activate EMS.
B. Take 1 dose and wait 10 minutes before taking a second dose.
C. Activate EMS and take up to 3 doses every 5 minutes.
D. Depending on the severity of symptoms, titrate the dose up to 2 pills every 2 minutes.

A

A. For an angina episode, sublingual dosing is 0.4 to 0.6 mg every 5 minutes for up to three doses. If the angina is not relieved by the second dose, the recommendation is to take the third dose and call 911.

NURS 572 Advanced Pharmacotherapeutics UofA Nursing (19 decks)

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