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Nursing - Bloomberg > 💊370: Cardiac Drugs > Flashcards

💊370: Cardiac Drugs Flashcards

1
Q

What are HMG-CoA Reductase Inhibitors?

A

Statins

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2
Q

What is the mechanism of action of statins?

A

Inhibit rate limiting enzyme in cholesterol synthesis (HMG-CoA reductase)

  1. Lower LDL
  2. Increase HDL
  3. Decrease Triglycerides
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3
Q

What is the onset and max efficacy of statins?

A

Onset: 2 weeks

Max efficacy: 4-6 weeks

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4
Q

What are the side effects of statins?

A
  1. Hepatotoxicity
  2. Myopathy (muscle ache, weakness)
    (Rarely rhabdomyolysis) —> monitor creatine kinase (CK)
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5
Q

What are some drug interactions for statins?

A
  1. CYP450 inhibitors (statin accumulation and inc myopathy)
  2. Grapefruit juice
  3. Vibrates, niacin (myopathy)
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6
Q

What is the dosing and administration of statins?

A

Dose once daily at bedtime
PO only
(HMG-CoA reductase highest at night)

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7
Q

What is a HMG-CoA Reductase Inhibitor prototype?

A

Atrovastatin (Lipitor)

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8
Q

What is a Fibric Acid Derivative prototype?

A

Febofibrate (LipidilMicro, LipidilSupra)

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9
Q

What is another name for Fibric Acid Derivatives?

A

Fibrates

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10
Q

What are Fibrates used for?

A

CAD: Most effective agents to decrease Triglycerides

Also inc HDL, small effect on LDL

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11
Q

What is the mechanism of action for Fibrates?

A
  1. Breakdown Triglycerides and facilitate HDL formation

2. Enhances cholesterol elimination in bile

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12
Q

What is the onset of Fibrates?

A

3-4 weeks

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13
Q

What are the side effects of Fibrates?

A
  1. Gallstones (cholesterol inc in bike)
  2. GI effects (nausea, dyspepsia, diarrhea)
  3. Myopathy
  4. Rash
  5. Hepatotoxicity (monitor LFTs)
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14
Q

What are some drug interactions with Fibrates?

A
  1. Statin (myopathy)

2. Warfarin (bleeding, monitor INR)

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15
Q

What is the dosing and administration of Fibrates?

A

Once daily with meal

PO only

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16
Q

What is another name for Bile Acid Sequestrants?

A

Resins

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17
Q

What is a prototype of Resins?

A

Cholestyramine (Questran)

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18
Q

What are Resins used for?

A

CAD
Modest decrease LDL
Small inc HDL and Triglycerides

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19
Q

What is the mechanism of action of Resins?

A
  1. Cholesterol required to make bile acids
  2. Resins bind bile acids in gut to increase excretion
  3. Increased bile acid production in liver
  4. Removes cholesterol from blood
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20
Q

What is the onset and max effect of Resins?

A

Onset: 1 week

Max effect: 4 weeks

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21
Q

What are side effects of Resins?

A

Not absorbed by body, eliminated in feces
- only agent safe in pregnancy

  1. GI side effects (nausea, constipation, bloating, abdo pain, flatulence)
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22
Q

What are some drug interactions with Resins?

A

Reduce absorption of:

  1. Fat soluble vitamins (ADEK)
  2. Anionic drugs (digoxin, warfarin, levothyroxine, thiazides, fibrates)
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23
Q

What are anti-adrenergic drugs?

A
  1. B-Blockers

2. alpha1-adrenergic blockers

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24
Q

Which drugs work on the RAAS system?

A
  1. ACE inhibitors
  2. Angiotensin receptor blockers (ARBs)
  3. Aldosterone antagonists
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25
Q

What is the goal of drug therapy for angina?

A

Reducing oxygen demand

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26
Q

What are 5 clinical uses for Beta-Blockers?

A
  1. Prevent angina attacks
  2. Acute MI
  3. Heart failure
  4. Hypertension
  5. Dysrhythmias
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27
Q

What is the suffix for Beta-Blockers?

A

-olol

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28
Q

What is a non-selective Beta-Blocker?

A

Propranolol

Blocks both B1 and B2 receptors

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29
Q

What is a cardioselective B-Blocker?

A

Metoprolol

Blocks B1 receptors only

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30
Q

What is a vasodilating B-Blocker?

A

Carvedilol

Blocks alpha-1-adrenergic receptors and B-receptors

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31
Q

What is the mechanism of action for Beta-Blockers?

A
  1. Block B1 receptors in heart
  2. Dec HR, contractility, and AV conduction
  3. Dec renin release from kidneys
  4. Dec peripheral vascular resistance
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32
Q

What are side effects of B-Blockers?

A
  1. Bradycardia
  2. Decreased Cardiac Output (CO)
  3. CNS effects (sleep, fatigue, depression)

Non-selective agents:

  1. Bronchoconstriction
  2. Hypoglycaemia
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33
Q

What are some drug interactions with B-Blockers?

A

CCBs (excessive cardio suppression)

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34
Q

What is the dosing and administration of B-Blockers?

A

Orally once-twice daily
IV forms available

—> Rebound cardiac excitation if stopped abruptly
(Tachycardia, dysrhythmia, angina, MI)

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35
Q

What is the suffix for alpha1-adrenergic blockers?

A

-osin

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37
Q

What is the main clinical use for alpha1-adrenergic blockers?

A
  1. Hypertension

2. Benign Prostatic Hyperplasia (BPH)

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38
Q

What is the mechanism of action of alpha1-adrenergic blockers?

A

Block alpha1 receptors on arterioles and veins, preventing vasoconstriction

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39
Q

What are side effects of A1ABs?

A
  1. Orthostatic hypotension
  2. Reflex increased HR (May be managed with B-Blockers)
  3. Nasal congestion
  4. Sexual dysfunction (inhibition of ejaculation)
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40
Q

What is the dosing and administration of alpha1-adrenergic blockers?

A

Once daily at bedtime (to reduce orthostatic hypotension)

Start low dose and slowly titrate up

41
Q

What are the main cardiovascular disorders that use ACE inhibitors and ARBs?

A
  1. Hypertension
  2. Heart failure
  3. Acute MI
  4. Prevention of CV events
42
Q

What is the suffix for ACE inhibitors?

43
Q

What is a prototype of alpha1-adrenergic blockers?

A

Terazosin (Hytrin)

44
Q

What is the suffix for ARBs?

45
Q

What is a prototype of ARBs?

A

Losartan (Cozaar)

46
Q

What is the mechanism of action for ACE inhibitors?

A
  1. Blocking ACE inhibits angiotensin 2 production
  2. Vasodilation (dec afterload and CO, inc preload)
  3. Decreased aldosterone = salt and water excretion
  4. Decreased blood volume
  5. Decreased renal blood flow
  6. Prevents cardiac and vascular remodeling
  7. SNS - decreases O2 demand
  8. Blockade of bradykinin breakdown - side effect
47
Q

What is the mechanism of action for ARBs?

A
  1. Blocked angiotensin 2 receptors
  2. Prevents vasoconstriction in arterioles
  3. Inc preload in veins
  4. Inc salt and water excretion
  5. Decreased blood volume
  6. Prevents cardiac remodeling
  7. Decreased SNS transmission = dec O2 demand
48
Q

What are side effects of ARBs?

A
  1. First-dose hypotension
  2. Decreased GFR (serum creatinine)
  3. Hyperkalemia
  4. Fetal harm
  5. Angioedema
49
Q

What are side effects of ACE inhibitors?

A
  1. Increased production of bradykinin (histamine-like compound)
  2. Cough (persistent, dry, nonproductive)
  3. Angioedema
50
Q

What are drug interactions of ARBs and ACE inhibitors?

A
  1. Diuretics - intensify first-dose hypotension
  2. Anti-hypertensives (additive effects)
  3. Drugs that inc K+
  4. NSAIDs (Na+ retention, vasoconstriction, reduce anti-hypertensive effects)
51
Q

What is the dosing and administration of ARBs and ACE inhibitors?

A 
Once-twice daily (starting at low dose)
PO only (enalaprilat IV exception)

May be prescribed together

52
Q

What is a non-selective Aldosterone Receptor Blocker prototype?

A

Spironolactone

53
Q

What is a selective Aldosterone blocker prototype?

A

Eplereone (Inspra)

54
Q

What are the clinical uses of Aldosterone Receptor Blockers?

A
  1. Hypertension

2. Heart failure

55
Q

What is the mechanism of action of Aldosterone Receptor Blockers?

A
  1. Na+ and water excretion
  2. K+ retention
  3. Decreased blood volume and BP
56
Q

What are side effects of Aldosterone Receptor Blockers?

A
  1. Hyperkalemia

2. Endocrine effects (gynecomastia, menstrual irregularities, impotence, hirsutism)

57
Q

What are some drug interactions with Aldossteron Receptor Blockers?

A
  1. Drugs that increase K+ (ACE inhibitors, ARBs, potassium supplements)
  2. CYP450 inhibitors
58
Q

What is the dosing and administration of Aldosterone Receptor Blockers?

A

Once daily

PO only

59
Q

What are the 3 types of diuretics?

A
  1. Thiazide
  2. Loop
  3. Potassium-sparing
    - Non-aldosterone antagonists
    - Aldosterone antagonists
60
Q

What are the clinical uses of diuretics?

A
  1. Hypertension

2. Heart failure

61
Q

What is the mechanism of action for diuretics?

A
  1. Blocks reabsorption of Na+ and Cl in renal tubules
  2. Increased osmotic pressure in nephron prevents passive reabsorption of water
  3. Water and salt excretion
  4. Increased urine flow
  5. Decreased blood volume and BP
62
Q

Which diuretic works on the proximal convoluted tubule of the kidneys?

A

Mannitol

Osmotic Diuretics

63
Q

Which diuretic works on the ascending limb of Henle’s Loop of the kidneys?

A

Furosemide

Loop Diuretics

64
Q

Which diuretic works on the early distal convoluted tubule of the kidneys?

65
Q

Which diuretic works on the late distal convoluted tubule and Collecting Duct of the kidneys?

A
  1. Spironolactone (Aldosterone antagonists)

2. Triamterene (Non-Aldosterone Antagonists)

66
Q

What is a prototype of thiazide diuretics?

A

Hydrochlorothiazide (HCTZ)

67
Q

What is the onset of thiazide diuretics?

68
Q

What is a side effect of thiazide diuretics?

A

Decreased arterial resistance

69
Q

What is a prototype of Loop Diuretics?

A

Furosemide (lasix)

70
Q

Which diuretic class is most powerful?

A

Loop Diuretics

71
Q

What is the onset of Loop Diuretics?

A 
1 hour (PO)
5 min (IV)
72
Q

What are the 2 types of Potassium Sparing Agents?

A
  1. Non-Aldosterone Antagonists

2. Aldosterone antagonists

73
Q

What is a prototype for ACE inhibitors?

A

Ramipril (Altace)

74
Q

What is a prototype of Non-aldosterone antagonists?

A

Triameterene

Amiloride

75
Q

What is a prototype for Aldosterone antagonists?

A

Spironolactone

76
Q

What is the mechanism of action for Potassium Sparing Agents?

A

Inhibits Na+/K+ exchange in distal tubule
Na+ excreted
K+ retained

Used in combo with thiazide or Loop Diuretics tincounteract K+ loss

77
Q

What are side effects of diuretics?

A
  1. Nocturia
  2. Hypokalemia (thiazide and Loop)

Loop diuretics:

  1. Dehydration
  2. Ototoxicity
  3. Dec Na+ and Mg2+

PSAs:

  1. Hyperkalemia
  2. N/v, leg cramps, dizziness, blue urine
78
Q

What are some drug interactions with Diuretics?

A
  1. NSAIDs (cause salt and water retention)
  2. Digoxin toxicity (loop and thiazides)
  3. ARBs and ACE inhibitors (hyperkalemia with PSAs)
  4. Potassium supplements (PSAs)
79
Q

What is the main clinical uses of Calcium Channel Blockers (CCBs)?

A
  1. Angina
  2. Hypertension
  3. Arrhythmias
80
Q

What are the 2 subgroups of Calcium Channel Blockers (CCBs)?

A
  1. Dihydropyridines (affect blood vessels)

2. Non-dihydropyridines (affect heart and blood vessels)

81
Q

What is a prototype of a Dihydropyridine CCB?

A

Amlodapine (Norvasc)

82
Q

What is a prototype of a non-dihydropyridine CCB?

A

Dimtiazem (Cardizen CD)

Verapamil

83
Q

What is the mechanism of action for Calcium Channel Blockers?

A
  1. Blockade of contraction if arterioles
  2. Arteriolar dilation
  3. Decreased afterload
    - Dihydropyridines biggest effect
  4. Decreased conduction of heart
  5. Decreased contractility and HR
  6. Suppressed conduction of AV node
    - Non-Dihydropyridines biggest effect
84
Q

What are side effects of CCBs?

A
  1. Reflex inc HR
  2. Edema, flushing, headache
  3. Bradycardia
  4. Constipation
85
Q

What are some drug interactions with CCBs?

A
  1. B-Blockers (blunt reflex tachycardia with dihydropyridines)
  2. Diltiazem and digoxin
  3. Grapefruit juice
86
Q

What are the main clinical uses for Digoxin?

A
  1. Heart failure

2. Dysrhythmias

87
Q

What are the effects of Digoxin on the heart?

A
  1. Positive ionotrope (inc contractility and CO)

2. Negative chronotrope (dec HR)

88
Q

What is the mechanism of action for Digoxin?

A
  1. Blocks Na+/K+ exchange pump on myocytes
  2. Increased Ca2+ in myocytes
  3. Increased contractility and CO
89
Q

What are side effects of Digoxin?

A
  1. GI: anorexia, n/v
  2. Fatigue, visual disturbances
  3. Arrhythmias
90
Q

What are drug interactions with Digoxin?

A
  1. Diuretics (Loop and thiazide) inc K+
  2. ARBs, ACE inhibitors, PSAs (inc K+)
  3. Verapamil (counteracts inotropic actions)
  4. Sympathomimetics (eg. dopamine) potential for arrhythmias
91
Q

What is the clinical use for Nitrates?

92
Q

What is a prototype of nitrates?

A

Nitroglycerin (NTG)

93
Q

What is the mechanism of action for nitrates?

A
  1. Taken up by vascular smooth muscle (VSM)
  2. Conversation to nitric oxide (NO) in presence of sulfhydryl groups
  3. NO has direct vasodilators action on VSM

Greater effect on veins vs arteries

94
Q

What are the pharmacokinetics of nitrates?

A
  1. Highly lipid soluble (sublingual, transdermal)
  2. Large first pass effect (t1/2 = 5-7 min)
  3. NTG not given orally but other nitrates are
95
Q

What are side effects of nitrates?

A
  1. Headache
  2. Orthostatic hypotension (die to relaxed VSM, blood pools in veins)
  3. Reflex tachycardia
96
Q

What are drug interactions with nitroglycerin?

A
  1. B-Blockers, CCBs (tachycardia)
  2. Sildenafil (Viagra) intensify vasodilation
  3. Alcohol (additive vasodilation)
97
Q

What is the onset of Potassium-Sparing Agents?

Nursing - Bloomberg (52 decks)

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