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Cardiovascular System > Cardiovascular Pharmacology Questions-Henkin > Flashcards

Cardiovascular Pharmacology Questions-Henkin Flashcards

1
Q

What is the most important consideration in choosing a blood pressure medication?

A

Heart rate

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2
Q

When are diuretics given to control BP?

A

To decrease preload or if volume overload.

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3
Q

What is a satisfactory time in which the target heart rate should be reached in a stress test?

A

7-13mins (better if more)

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4
Q

What is the main action of diuretics?

A

Increase urinary sodium and decrease blood volume

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5
Q

What is the main action of beta adrenergic blockers?

A

Decreased HR and renin, increased peripheral resistance

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6
Q

What is the main action of calcium antagonists?

A

Vasodilation, decreased AV conduction, decreased heart rate. Block L-type voltage gated calcium channels. Reduces the calcium entering cells, reducing contraction. Reduces afterload.

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7
Q

What is the main action of ACE inhibitors?

A

Vasodilators

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8
Q

What is the main action of alpha blockers?

A

Vasodilators

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9
Q

What is the main action of ARBs?

A

Vasodilators

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10
Q

What groups respond best to diuretics?

A

African-Americans and older people, with volume overload and sodium retention.

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11
Q

When are beta blockers used for HTN?

A

In patients with tachycardia, heart failure, coronary artery disease, and ischemia. Otherwise not first line because of side effects.

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12
Q

What drugs are considered first line for HTN (barring side effects)?

A

Calcium antagonists and ACE inhibitors

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13
Q

When are ARBs used in HTN?

A

Usually only as a replacement for ACE inhibitors for those that can’t tolerate them or occasionally in combinatino.

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14
Q

When are central acting drugs used for HTN?

A

Generally not used except for those resisting all other drugs and very difficult cases. Lots of side effects.

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15
Q

Effects of the sympathetic system on the heart

A
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16
Q

Mechanism of action of beta blockers

A

↓ myocardial contractility (negative inotropism, increased in long term use), ↓ heart rate (negative chronotropism), membrane stabilizing activity (quinidine-like), ↓ renin levels (↓ angiotensin II ↓ aldosterone), reduces arrhythmias of all types (atrial and ventricular).

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17
Q

What is the caveat to selective beta agonists?

A

At high doses, no longer selective.

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18
Q

What kind of selectivity is ideal for CV problems?

A

Want beta 1 blocked but not beta 2 because of bronchoconstriction and other effects.

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19
Q

What are the 3 classifications of considerations of Beta Blockers?

A
  1. Selectivity, 2. Water/fat solubility and halflife, 3. intrinsic sympathomimetic activity (ISA)
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20
Q

How are Beta blockers with Intrinsic sympathetic activity (ISA) different?

A

Some beta blockers also have partial antagonist and partial agonist activity. Under basal resting conditions stimulate center (weak stimulation of beta-adrenergic receptors) but once pt secretes more adrenaline, acts as antagonist-blocks catecholamine effects. Gives advantage of not causing bradycardia at rest, preventing tachycardia during exercise. Unlike other beta blockers, not show n to decrease mortality during MI (may slightly increase it) or after HF.

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21
Q

How does negative chronotropism affect the heart rate?

A
  1. Reduces sinus rhythm, 2. Can cause AV blocks
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22
Q

What are the adverse effects of beta blockers?

A

Negative choronotropism (bradycardia, AV blocks), Negative ionotropism, Bronchospasm, Insulin resistance, Peripheral vasoconstriction, Unopposed alpha stimulation.

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23
Q

How do beta blockers adversely affect diabetic patients?

A

Can mask hypoglycemia because patients know they are hypoglycemia due to sympathetic response.

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24
Q

Why are peripheral artery disease patients excluded from beta blocker therapy?

A

Because of vasoconstriction from unopposed alpha receptors.

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25
Q

What are the 3 classes of calcium channel blockers?

A

Verapamil, Diltiazem, Dihydropyridines

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26
Q

What is the major difference between beta blockers and calcium channel blockers?

A

Beta blockers reduce sinus activity at rest and during exercise. Ca channel blockers reduce at rest but don’t counteract effect of adrenergic stimulation. Don’t reduce tachycardia during exercise so not as good at preventing exercise induced angina.

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27
Q

How do dihydropyridines differ from other calcium channel antagonists?

A

Potent arterial dilation reduces blood pressure and causes reflex tachycardia but counteracted by effect on SAN and AVN so slight tachycardia remains.

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28
Q

Adverse effects of dihydropyridines

A

Vasodilation (flushing, headache, palpitations), ankle edema in about 5%

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29
Q

What was the effect of now discontinued fast acting dihydropyridines?

A

Caused reflex sympathetic response which caused increased mortality.

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30
Q

Adverse effects of verapamil

A

Bradycardia, AV block, constipation (especially with beta blockers)

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31
Q

Which calcium channel blocker has the highest effect of decreased contractility and AV conduction?

A

Verapamil

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32
Q

Which has a shorter half life, fat or water soluble drugs?

A

Fat soluble because it must first go through the liver. Dosing is variable.

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33
Q

Which kinds of drugs can pass the BBB and what are the adverse effects?

A

Penetrate the brain more easily and cause depression, sleep defects, etc.

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34
Q

What drug should be given to a patient with angina, tachycardia, HTN and 1st degree AV block?

A

Nitroglycerine. AV blocks are contraindication for beta blockers.

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35
Q

What is the difference in effects between IV and oral nitrates?

A

Orally is mostly venous and IV or subcutaneous is both artery and veins because of first pass.

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36
Q

What are the vascular effects of low concentrations of nitrates (orally)?

A

venous dilatation Increase venous capacitance ↓ ventricular preload (Starling low) ↓ pulmonary vascular pressure ↓ heart size increase in total coronary blood flow Redistribution of coronary flow from normal to ischemic region.

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37
Q

What are the vascular effects of high concentrations of nitrates (IV)?

A

arterial dilatation ↓ afterload, ↓ blood pressure.

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38
Q

Michanism of tolerance of nitrates

A

In order for NO to be activated, need SH groups prduced in the liver. Liver can’t keep up with constant production. Need to give the body a few hours for thiol (SH) replenishing. Should never give TID, usually if need to give BID tell patients to take in morning and noon and give night a rest.

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39
Q

When should a patient take nitrates if they have nocturnal angina?

A

Take in afternoon and night, morning rest.

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40
Q

What is the effect of nitrates combined with calcium channel blockers?

A

Reflex tachycardia

41
Q

What therapy should be used if nitrates are insufficient to get rid of angina?

A

Combination of nitrates and beta blockers. Cancel out adverse effects (tachycardia and LVEDV increase no longer problems)

42
Q

What drug is strongly counterindicated with nitrates?

A

Viagra. Need to be careful or can cause lethal hypotension.

43
Q

What is the upper limit of LDL?

A

For no risk factors: 160mg/dl

for 1 or 2 risk factors: 130

For atherosclerosis and diabetes and renal failure, coronary disease equivalent: 100 mg/dL

If atheroscleroris (post MI) +diabetes +smoking=70

44
Q

What is the lower limit of HDL?

A

40 for males, 50 for females

45
Q

What is the upper limit of triglycerides?

A

150 (200 worse)

46
Q

How much does 10mg of Simvastatin decrease cholesterol on average?

A

25%

47
Q

How much does each doubling of Simvastatin dose decrease cholesterol on average?

A

6%

48
Q

What is the highest acceptable dosage of simvastatin?

A

40mg

49
Q

What options are there to decrease cholesterol when indicators are still high?

A
  1. Increase Simvastatin dose, 2. Change to a stronger statin, 3. Add Ezetimibe, 4. Add fibrate
50
Q

What is the adverse affect of high doses of Simvastatin?

A

Increased rhabdomyolysis (muscle disorders), but not with other statins.

51
Q

What is the mechanism of resins?

A

Sequester bile acids and don’t allow resorption back into the liver and they are excreted into stool.

52
Q

What is the mechanism of Ezetimibe (phytosterols)?

A

Reduces absorption of cholesterol in intestines.

53
Q

What is the effect of Ezetimibe on the liver?

A

Increased cholesterol synthesis

54
Q

What is the net reduction of cholesterol due to Ezetimibe alone?

A

10-12%

55
Q

What is the best therapy to decrease cholesterol?

A

Ezetimibe and statin. Decrease absorption and synthesis. Rule of thumb: give up to max statin dose and then add Ezetimibe.

56
Q

When should Ezetimibe be taken during the day?

A

Doesn’t matter. Enterohepatic system is functional all day.

57
Q

What is average dietary cholesterol input per day?

A

300mg

58
Q

What is average cholesterol production by the body per day?

A

1000mg

59
Q

When should statins be taken during the day?

A

Before bed because cholesterol is synthesized in early morning. Except rosuvastatin which can be taken anytime since it has a long halflife.

60
Q

What is the maximum amount that statins can elevate HDL?

A

5%

61
Q

What is the maximum amount that statins can lower triglycerides?

A

10%

62
Q

What therapy should be initiated if statins and Ezetimibe aren’t enough?

A

Fibrates and Niacin

63
Q

What do fibrates act on?

A

PPAR-Alpha receptors: related to glucose metabolism and thiazolidinediones, stimulate synthesis of HDL via apoA and breakdown of VLDL/TG via lipoprotein lipase.

64
Q

How do fibrates affect HDL, VLDL and LDL?

A

Increase HDL, decrease TG and VLDL but go to LDL so may raise LDL in some patients. Give statins as well.

65
Q

What are the pros and cons of niacin?

A

Reduces LDL, TG and VLDL but has bad side effects.

66
Q

What are the beta 1 selective blockers that are used?

A

Metoprolol, atenolol, esmolol, acebutolol somewhat.

67
Q

Indications for beta blockers

A

HTN, angina, mitral valve prolapse, cardiac arrhythmias (supraventricular), congestive HF, Post MI, glaucoma, migraine prophylaxis, hyperthyroidism (decreased tachycardia), essential tremor, pheochromocytoma (with alpha blocker), anxiety and performance enhancement.

68
Q

What is the beta-blocker protocol post MI?

A

Routine, give highest dose tolerable to prevent arrhythmic effects. Limit of tolerance is bradycardia, hypotension or impotence. Can’t convert VFib to sinus but can turn SVTs.

69
Q

Propanolol Pharmacokinetics.

A

Fat soluble, rapid and complete absorption (1-3 hours), large first pass effect, preparations like sustained release increase halflife. Enters CNS, dosage is different depending on individual metabolism. In severe tachycardia given IV.

70
Q

Metoprolol pharmacokinetics

A

Beta1 selective. Fat soluble, better than propanolol. Extensive first-pass effect. Halflife 3-4h.

71
Q

Atenolol pharmacokinetics

A

Water soluble, low psychological side effects, beta-1 selective, longest halflife (5-8h), can’t be used in renal failure. Low data supporting increased survival post MI. Higher dose limit, 25-50 recommended but 100mg max.

72
Q

What drugs are affected by grapefruit juice?

A

Simvastatin, calcium channel blockers (Felodipine, Verapamil), Cyclosporin A

73
Q

What is the strongest statin?

A

Rosuvastatin

74
Q

What is the absolute contraindication for fibrates?

A

Renal failure. Accumulation causes rhabdomyelysis.

75
Q

What are the side effects of fibrates

A

Muscle pain (usually if CK>5x but not always), hepatitis (rarely, only worry if liver enzyme >3x)

76
Q

What are the adverse effects of niacin?

A

Flushing almost universal at least initially, many find it intolerable and compliance is

77
Q

What is the adverse effect of combining calcium channel blockers and statins?

A

Rhabdomyelysis. Major danger: kidney damage from breakdown products.

78
Q

What will blood tests show in rhabdomyelysis?

A

Normal Hb and Hct, high creatinine and urea (acute), high CPK, myoglobin in urine, no RBC.

79
Q

Drugs that induce CYP 450

A

Rifampin, Rifabutin, Carbamazepine, Phenobarbital, Phentoin

80
Q

Drugs that inhibit CYP 450

A

Cimetidine, Erythromycin, Ketoconazole, Ritonavir, Fluoxetine, paroxetine, Fefazodone, Quinidine, Venlafaxine.

81
Q

What is the therapeutic window of digoxin?

A

1-2ng/mL. 2 is toxic.

82
Q

What action does digoxin have?

A

Increases contractility (positive inotrope, decreases conduction time in AV node (AV delay). Used after Beta blockers or Calcium channel blockers. Recently increases morbidity in congestive HF so more used for AFib. Reduces sinus rhythm by increasing CO by baroreceptor response.

83
Q

What is the most common adverse effect of digoxin?

A

Arrhythmias, especially in hypokalemia (from diuretics)

84
Q

Drug interactions decreasing absorption of digoxin (lowers by 25%)

A

Cholestyramine, kaolin-pectin, neomycin, sulfasalazine. Bran.

85
Q

Drug interactions decreasing renal digoxin clearance and/or volume of distribution of digoxin (increasing by 70-100%)

A

Propafenone, quinidine, verapamil, amiodarone, thyroxine

86
Q

Drug interactions increasing absorption of digoxin (increase by 40-100%)

A

Erythromycin, omeprazole, tetracycline

87
Q

Drug interactions with variable effect of digoxin

A

Antacids (25%), captopril, diltiazem, nifedipine, nitrendipine

88
Q

What is the drug with the most interaction with digoxin?

A

Warfarin

89
Q

What are the psychiatric effects of digoxin toxicity?

A

Fatigue, delirium, confusion, dizziness, abnormal dreams

90
Q

What are the visual effects of digoxin toxicity?

A

Blurred or yellow vision

91
Q

What are the gastrointestinal effects of digoxin toxicity?

A

Anorexia, nausea, vomiting, abdominal pain

92
Q

What are the respiratory effects of digoxin toxicity?

A

Enhance ventilatory response to hypoxia

93
Q

What are the cardiac effects of digoxin toxicity?

A

Atrial and ventricular ectopic arrhythmias, sinoatrial and atrioventricular node conduction disturbances.

94
Q

How to avoid digoxin toxicity when adding another drug?

A

Decrease dose by about 50% and monitor levels.

95
Q

What is the ideal blood pressure to control to?

A

140/90 in otherwise healthy patients. 130/80 in diabetes.

96
Q

What is the consequence of decreased diastolic blood pressure?

A

Increased mortality because of decreased filling of coronary arteries during diastole.

97
Q

What are the indicators of ACE inhibitors?

A

HTN (to decrease SVR and vasodilate), LV systolic dysfunction (even if asymptomatic), renal impairment (often d/t diabetes+HTN)

98
Q

Adverse effects of ACE inhibitors

A

Hypotension, cough (in 5-20% d/t bradykinins, substance P or prostaglandins), angioedema (sudden and disappears at withdrawal), Hyperkalemia (major in ACEI/ARB combo, usually in pts with renal artery stenosis), fetopathy

99
Q

How are ARB side effects different from ACE inhibitors’?

A

Same except cough and angioneurotic edema.

Cardiovascular System (28 decks)

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