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Nursing - Bloomberg > 💊370: Cardiac Drugs > Flashcards

💊370: Cardiac Drugs Flashcards

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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
What is the goal of drug therapy for angina?
Reducing oxygen demand
26
What are 5 clinical uses for Beta-Blockers?
1. Prevent angina attacks 2. Acute MI 3. Heart failure 4. Hypertension 5. Dysrhythmias
27
What is the suffix for Beta-Blockers?
-olol
28
What is a non-selective Beta-Blocker?
Propranolol | Blocks both B1 and B2 receptors
29
What is a cardioselective B-Blocker?
Metoprolol | Blocks B1 receptors only
30
What is a vasodilating B-Blocker?
Carvedilol | Blocks alpha-1-adrenergic receptors and B-receptors
31
What is the mechanism of action for Beta-Blockers?
1. Block B1 receptors in heart 2. Dec HR, contractility, and AV conduction 3. Dec renin release from kidneys 4. Dec peripheral vascular resistance
32
What are side effects of B-Blockers?
1. Bradycardia 2. Decreased Cardiac Output (CO) 3. CNS effects (sleep, fatigue, depression) Non-selective agents: 4. Bronchoconstriction 5. Hypoglycaemia
33
What are some drug interactions with B-Blockers?
CCBs (excessive cardio suppression)
34
What is the dosing and administration of B-Blockers?
Orally once-twice daily IV forms available —> Rebound cardiac excitation if stopped abruptly (Tachycardia, dysrhythmia, angina, MI)
35
What is the suffix for alpha1-adrenergic blockers?
-osin
37
What is the main clinical use for alpha1-adrenergic blockers?
1. Hypertension | 2. Benign Prostatic Hyperplasia (BPH)
38
What is the mechanism of action of alpha1-adrenergic blockers?
Block alpha1 receptors on arterioles and veins, preventing vasoconstriction
39
What are side effects of A1ABs?
1. Orthostatic hypotension 2. Reflex increased HR (May be managed with B-Blockers) 3. Nasal congestion 4. Sexual dysfunction (inhibition of ejaculation)
40
What is the dosing and administration of alpha1-adrenergic blockers?
Once daily at bedtime (to reduce orthostatic hypotension) Start low dose and slowly titrate up
41
What are the main cardiovascular disorders that use ACE inhibitors and ARBs?
1. Hypertension 2. Heart failure 3. Acute MI 4. Prevention of CV events
42
What is the suffix for ACE inhibitors?
-pril
43
What is a prototype of alpha1-adrenergic blockers?
Terazosin (Hytrin)
44
What is the suffix for ARBs?
-spartan
45
What is a prototype of ARBs?
Losartan (Cozaar)
46
What is the mechanism of action for ACE inhibitors?
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
What is the mechanism of action for ARBs?
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
What are side effects of ARBs?
1. First-dose hypotension 2. Decreased GFR (serum creatinine) 3. Hyperkalemia 4. Fetal harm 5. Angioedema
49
What are side effects of ACE inhibitors?
1. Increased production of bradykinin (histamine-like compound) 2. Cough (persistent, dry, nonproductive) 3. Angioedema
50
What are drug interactions of ARBs and ACE inhibitors?
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
What is the dosing and administration of ARBs and ACE inhibitors?
``` Once-twice daily (starting at low dose) PO only (enalaprilat IV exception) ``` May be prescribed together
52
What is a non-selective Aldosterone Receptor Blocker prototype?
Spironolactone
53
What is a selective Aldosterone blocker prototype?
Eplereone (Inspra)
54
What are the clinical uses of Aldosterone Receptor Blockers?
1. Hypertension | 2. Heart failure
55
What is the mechanism of action of Aldosterone Receptor Blockers?
1. Na+ and water excretion 2. K+ retention 3. Decreased blood volume and BP
56
What are side effects of Aldosterone Receptor Blockers?
1. Hyperkalemia | 2. Endocrine effects (gynecomastia, menstrual irregularities, impotence, hirsutism)
57
What are some drug interactions with Aldossteron Receptor Blockers?
1. Drugs that increase K+ (ACE inhibitors, ARBs, potassium supplements) 2. CYP450 inhibitors
58
What is the dosing and administration of Aldosterone Receptor Blockers?
Once daily | PO only
59
What are the 3 types of diuretics?
1. Thiazide 2. Loop 3. Potassium-sparing - Non-aldosterone antagonists - Aldosterone antagonists
60
What are the clinical uses of diuretics?
1. Hypertension | 2. Heart failure
61
What is the mechanism of action for diuretics?
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
Which diuretic works on the proximal convoluted tubule of the kidneys?
Mannitol | Osmotic Diuretics
63
Which diuretic works on the ascending limb of Henle’s Loop of the kidneys?
Furosemide | Loop Diuretics
64
Which diuretic works on the early distal convoluted tubule of the kidneys?
Thiazides
65
Which diuretic works on the late distal convoluted tubule and Collecting Duct of the kidneys?
1. Spironolactone (Aldosterone antagonists) | 2. Triamterene (Non-Aldosterone Antagonists)
66
What is a prototype of thiazide diuretics?
Hydrochlorothiazide (HCTZ)
67
What is the onset of thiazide diuretics?
2 hours
68
What is a side effect of thiazide diuretics?
Decreased arterial resistance
69
What is a prototype of Loop Diuretics?
Furosemide (lasix)
70
Which diuretic class is most powerful?
Loop Diuretics
71
What is the onset of Loop Diuretics?
``` 1 hour (PO) 5 min (IV) ```
72
What are the 2 types of Potassium Sparing Agents?
1. Non-Aldosterone Antagonists | 2. Aldosterone antagonists
73
What is a prototype for ACE inhibitors?
Ramipril (Altace)
74
What is a prototype of Non-aldosterone antagonists?
Triameterene | Amiloride
75
What is a prototype for Aldosterone antagonists?
Spironolactone
76
What is the mechanism of action for Potassium Sparing Agents?
Inhibits Na+/K+ exchange in distal tubule Na+ excreted K+ retained Used in combo with thiazide or Loop Diuretics tincounteract K+ loss
77
What are side effects of diuretics?
1. Nocturia 2. Hypokalemia (thiazide and Loop) Loop diuretics: 3. Dehydration 4. Ototoxicity 5. Dec Na+ and Mg2+ PSAs: 6. Hyperkalemia 7. N/v, leg cramps, dizziness, blue urine
78
What are some drug interactions with Diuretics?
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
What is the main clinical uses of Calcium Channel Blockers (CCBs)?
1. Angina 2. Hypertension 3. Arrhythmias
80
What are the 2 subgroups of Calcium Channel Blockers (CCBs)?
1. Dihydropyridines (affect blood vessels) | 2. Non-dihydropyridines (affect heart and blood vessels)
81
What is a prototype of a Dihydropyridine CCB?
Amlodapine (Norvasc)
82
What is a prototype of a non-dihydropyridine CCB?
Dimtiazem (Cardizen CD) | Verapamil
83
What is the mechanism of action for Calcium Channel Blockers?
1. Blockade of contraction if arterioles 2. Arteriolar dilation 3. Decreased afterload - Dihydropyridines biggest effect 1. Decreased conduction of heart 2. Decreased contractility and HR 3. Suppressed conduction of AV node - Non-Dihydropyridines biggest effect
84
What are side effects of CCBs?
1. Reflex inc HR 2. Edema, flushing, headache 3. Bradycardia 4. Constipation
85
What are some drug interactions with CCBs?
1. B-Blockers (blunt reflex tachycardia with dihydropyridines) 2. Diltiazem and digoxin 3. Grapefruit juice
86
What are the main clinical uses for Digoxin?
1. Heart failure | 2. Dysrhythmias
87
What are the effects of Digoxin on the heart?
1. Positive ionotrope (inc contractility and CO) | 2. Negative chronotrope (dec HR)
88
What is the mechanism of action for Digoxin?
1. Blocks Na+/K+ exchange pump on myocytes 2. Increased Ca2+ in myocytes 3. Increased contractility and CO
89
What are side effects of Digoxin?
1. GI: anorexia, n/v 2. Fatigue, visual disturbances 3. Arrhythmias
90
What are drug interactions with Digoxin?
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
What is the clinical use for Nitrates?
Angina
92
What is a prototype of nitrates?
Nitroglycerin (NTG)
93
What is the mechanism of action for nitrates?
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
What are the pharmacokinetics of nitrates?
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
What are side effects of nitrates?
1. Headache 2. Orthostatic hypotension (die to relaxed VSM, blood pools in veins) 3. Reflex tachycardia
96
What are drug interactions with nitroglycerin?
1. B-Blockers, CCBs (tachycardia) 2. Sildenafil (Viagra) intensify vasodilation 3. Alcohol (additive vasodilation)
97
What is the onset of Potassium-Sparing Agents?
2-3 hours

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