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CARDIOVASCULAR > CARDIOVASCULAR- Pharmacology > Flashcards

CARDIOVASCULAR- Pharmacology Flashcards

1
Q

Drugs used for Primary (essential) hypertension

A

Diuretics, ACE inhibitors, angiotensin II recetor blockers (ARBs), calcium channel blockers

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2
Q

For Hypertension with Cardiac Heart failure, which drugs are recommended?

A

Diuretics, ACE inhibitors/ ARBs, β blockers (compensated CHF), aldosterone antagonists

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3
Q

Which drugs must be used cautiously in decompensated CHF?

A

β blockers

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4
Q

When are β blockers contraindicated?

A

Cardiogenic shock

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5
Q

For patients with hypertension with Diabetes, which antihypertensive drugs are recommended?

A

ACE inhibitors/ ARBs. Calcium channel blockers, diuretics, β blockers, α blockers

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6
Q

Which antihypertensive drugs work as protective against diabetic nephropathy?

A

ACE inhibitors/ ARBs

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7
Q

Dihydropyridine Calcium channel blockers

A

Amlodipine, nimodipine, nifedipine

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8
Q

Non Dihydropyridine Calcium channel blockers

A

Diltiazem, Verapamil

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9
Q

Mechanism of action of Calcium channel blockers

A

Block voltage dependent L type calcium channels of cardiac and smooth muscle, thereby reduce muscle contractility

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10
Q

Which Calcium channel blockers have more effect in vascular smooth muscle?

A

Amlodipine= nifedipine> diltiazem> verapamil

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11
Q

Which Calcium channel blockers have more effect in heart?

A

Verapamil> diltiazem> amlodipine= nifedipine

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12
Q

Clinical use for Dihydropyridine Calcium channel blockers

A

(Except nimodipine)

Hypertension, angina (including prinzmetal), Raynaud phenomenom

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13
Q

Clinical use for Non Dihydropyridine Calcium channel blockers

A

Hypertension, angina, atrial fibrilation/ flutter

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14
Q

Clinical use for Nimodipine

A

Subarachnoid hemorrhage (prevents cerebral vasospasm)

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15
Q

These are Toxic effects of Calcium channel blockers

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation

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16
Q

Mechanism of Action of Hydralazine

A

↑ cGMP→ smooth muscle relaxation

Vasodilates arterioles> vein

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17
Q

Which effect does Hydralazine has?

A

Afterload reduction

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18
Q

Clinical use for Hydralazine

A

Severe hypertension, CHF

First line therapy for hypertension in pregnancy

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19
Q

First line therapy for hypertension in pregnancy

A

Metildopa

Hydralazine

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20
Q

Which drug is coadministered with hydralazine to prevent reflex tachycardia?

A

β blockers

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21
Q

Why are β blockers coadministered with hydralazine?

A

To prevent reflex tachycardia

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22
Q

Toxic effects of Hydralazine?

A

Compensatory tachycardia, fluid retention, nausea, headache, angina
Lupus like syndrome

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23
Q

When is Hydralazine contraindicated?

A

In angina/ Coronary artery disease

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24
Q

In hypertensive emergency which are the common used drugs?

A

Nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

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25
Q

How long does it takes for Nitroprusside to act?

A

Short acting

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26
Q

Which is the mechanism of action of Nitroprusside

A

↑ cGMP via direct release NO

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27
Q

Possible secondary effect of Nitroprusside

A

Can cause cyanide toxicity (releases cyanide)

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28
Q

Mechanism of Action of Fenoldopam

A

Dopamine D1 receptor agonist

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29
Q

Effect of Fenoldopam

A

Coronary, peripheral, renal, and splanchic vasodilation

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30
Q

Clinical effect of Fenoldopam

A

↓ BP

↑ natriuresis

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31
Q

Which is the mechanism of action of Nitroglycerin, isosorbide dinitrate?

A

Vasodilate by ↑ NO in vascular smooth muscle→ ↑ in cGMP and smooth muscle relaxation.

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32
Q

Which vessels are more dilated with Nitroglycerin, isosorbide dinitrate?

A

Dilates veins&raquo_space; arteries

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33
Q

What is the effect of Nitroglycerin, isosorbide dinitrate?

A

↓ preload

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34
Q

Clinical use for Nitroglycerin, isosorbide dinitrate

A

Angina, acute coronary syndrome, pulmonary edema

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35
Q

Toxic effect of Nitroglycerin, isosorbide dinitrate

A

Reflex tachycardia, hypotension, flushing, headache, “Monday disease” in industrial exposure

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36
Q

Which drug helps with the reflex tachycardia caused by Nitroglycerin, isosorbide dinitrate?

A

β blockers

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37
Q

What is the “Monday disease” ?

A

Development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure

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38
Q

Which is the goal in antianginal therapy?

A

Reduction of myocardial O2 consumption (MVO2) by ↓ 1 or more of the determinants of MVO2

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39
Q

Which are determinants of myocardial O2 consumption?

A

End diastolic volume
Blood pressure
Heart rate
Contractility

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40
Q

Which are the main medications in Antianginal therapy?

A

Nitrates
β Blockers
Nitrates + β blockers

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41
Q

What is affected with nitrates?

A

Preload

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42
Q

Which effects do Nitrates have as Antianginal therapy?

A 
↓ End diastolic volume
↓ Blood pressure
↑  Contractility (reflex response)
↑ Heart rate (reflex response)
↓ Ejection time
↓ MVO2
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43
Q

Effects of β Blockers as Antianginal Therapy

A 
↑ End diastolic volume
↓ Blood pressure
↓ Contractility 
↓ Heart rate 
↑ Ejection time
↓ MVO2
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44
Q

What effect do Nitrates + β blockers have as Antianginal Therapy?

A 
No effect or ↓ End diastolic volume
↓ Blood pressure
Little/ no effect in Contractility 
↓ Heart rate 
Little/ no effect on Ejection time
↓↓ MVO2
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45
Q

Which calcium channel blocker has similar effects to nitrates in Antianginal therapy?

A

Nifedipine

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46
Q

Which drugs are contraindicated in Angina?

A

partial β agonists

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47
Q

Which partial β agonists are contraindicated in Angina?

A

Pindolol and Acetabutol

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48
Q

Lipid lowering agents

A 
HMG- CoA reductase inhibitors
Niacin (vitamin B3)
Bile acid resins
Cholestherol absorption blockers
Fibrates
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49
Q

HMG-CoA reductase inhibitors

A 
Lovastatin
Pravastatin
Simvastatin
Atorvastatin
Rosuvastatin
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50
Q

Which effects do HMG-CoA reductase inhibitors have?

A

↓↓↓ LDL
↑ HDL
↓ Tiglycerides

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51
Q

What is the mechanism of action of Pravastatin?

A

Inhibit conversion of HMG- CoA to mevalonate, a cholesterol precursor

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52
Q

Side effect of HMG-CoA reductase inhibitors

A

Hepatotoxicity (↑ LFTs), rhabdomyolisis

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53
Q

When do HMG-CoA reductase inhibitors have increased risk for rhabdomyolisis?

A

When used with fibrates and niacin

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54
Q

Effect of Niacin

A

↓↓ LDL
↑↑ HDL
↓ Tiglycerides

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55
Q

What vitamin is Niacin?

A

Vitamin B3

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56
Q

Which mechanism of action does Niacin has?

A

Inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis

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57
Q

Possible side effects of Niacin

A

Red, flushed face
Hyperglycemia
Hyperuricemia

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58
Q

How do you decreased the probability of flushed face as a side effect of Niacin?

A

With aspirin or long term use

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59
Q

How is hyperglycemia manifested in Niacin administration?

A

Acanthosis nigricans

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60
Q

Which vitamin can exacerbate Gout?

A

Vitamin B3 (Niacin) because increases Hyperuricemia

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61
Q

Bile Acid Resins

A

Cholestyramine
Colestipol
Colesevelam

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62
Q

Effect of Bile Acid Resins

A

↓↓ LDL
Slightly ↑ HDL
Slightly ↑ Tiglycerides

63
Q

Which is the mechanism of action of Bile acid resins?

A

Prevent intestinal reabsorption of bile acids; liver mistuse cholesterol to make more

64
Q

What needs to be in mind before administering Bile acid resins?

A

Patients hate it- tastes bad and causes GI discomfort, ↓ absorption of fat soluble vitamins

65
Q

Another side effect of Bile acid resins

A

Cholesterol gallstones

66
Q

Cholesterol absorption blockers

A

Ezetimibe

67
Q

What is the effect of Ezetimibe?

A

↓↓ LDL

68
Q

Mechanism of action of Ezetimibe

A

Prevent cholesterol absorption at small intestine brush border

69
Q

Side effect of Cholesterol absorption blockers

A

Rare ↑ LFTs, diarrhea

70
Q

Name Fibrates

A

Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate

71
Q

Effect of Fibrates

A

↓ LDL
↑ HDL
↓↓↓ Tiglycerides

72
Q

Mechanism of action of Fibrates

A

Upregulate LPL → ↑ TG clearance

Activates PPAR α to induce HDL synthesis

73
Q

Side effects of Fibrates

A

Myositis (↑ risk with concurretn statins)
Hepatotoxicity (↑ LFTs)
Cholesterol gallstones

74
Q

When is increased the risk for Cholesterol gallstones when using fibrates?

A

With concurrent bile acid resins

75
Q

Cardiac glycoside

A

Digoxin

76
Q

How are the pharmacologic properties of Digoxin

A

75% bioaviailability
20-40 % protein bound
t1/2= 40 hours, urinary excretion

77
Q

Mechanism of action of digoxin

A

Direct inhibition of Na+/ K+ ATPase leads to indirects inhibition of Na+/ Ca2+ exchanger/ antiport.
↑ Ca2+ intracellular →positive inotropy. Stimulates vagus nerve → ↓ Heart rate

78
Q

Clinical use for Digoxin

A

CHF (↑ contractility)

Atrial Fibrilation

79
Q

What effect does Digoxin has in Atrial Fibrilation?

A

↓ conduction at AV node and depression of SA node

80
Q

Cholinergic side effects of Cardiac glycosides

A

Nausea, vomiting, diarhea, blurry yellow vision

81
Q

ECG changes due to use of Digoxin

A

↑ PR, ↓ QT, ST scooping, T wave inversion, arrhytmia, AV block

82
Q

Which electrolyte changes can Digoxin produce?

A

Hyperkalemia

83
Q

What does Hyperkalemia caused by Cardiac glycosides indicate?

A

Poor prognosis

84
Q

Which factros predispose to Digoxin toxicity?

A

Renal failure, hypokalemia, verapamil, amiodarone, quinidine

85
Q

Why verapamil, amiodarone, quinidine increase the possibility of Digoxin toxicity?

A

↓ Digoxin clearance; displaces digoxin from tissue binding sites

86
Q

Why does hypokalemia can increase the risk of toxic effects of Digoxin?

A

Permissive for digoxin binding at K+ binding site on Na+/ K+ ATPase

87
Q

Antidote for Digoxin toxicity

A

Slowly normalize K+, cardiac pacer, anti digoxin Fab fragments, Mg2+

88
Q

Class I Antiarrhytmics mechanism of Action

A

Na+ channel blockers

89
Q

What effect do Class I Antiarrhytmics have?

A

Slow or Block (↓) conduction (especially in depolarized cells)
↓ slope of phase 0 depolarization and ↑ threshold for firing in abnormal pacemaker cells

90
Q

Which is the dependant to use Class I Antiarrhytmics?

A

Are state dependent (selectively depress tissue that is frequently depolarized (eg. tachycardia))

91
Q

Which state ↑ toxicity for all class I drug?

A

Hyperkalemia

92
Q

How many classes of Antiarrythmics class I exist?

A

Class IA
Class IB
Class IC

93
Q

Class IA Antiarrythmics

A

Quinidine
Procainamide
Disopyramide

94
Q

Mechanism of Action of Class IA Antiarrythmics

A

↑ Action Potential duration, ↑ effective refractory period (ERP), ↑ QT interval

95
Q

Clinical use for Class IA Antiarrythmics

A

Both atrial and ventricular arrythmias, especially re-entrant and ectopic Supraventricular tachycardia and VT

96
Q

Toxic effect of Class IA Antiarrythmics

A

Thrombocytopenia

Torsades de pointes

97
Q

What is cinchonism?

A

Headache

Tinnitus

98
Q

Which Class IA Antiarrythmic causes cinchonism?

A

Quinidine

99
Q

Class IA Antiarrythmics that can cause reversible SLE like syndrome

A

Procainamide

100
Q

Class IA Antiarrythmic related to cause heart failure

A

Disopyramide

101
Q

How Class IA Antiarrythmics can cause torsades de pointes?

A

Due to ↑ QT interval

102
Q

Class IB Antiarrythmics

A

Lidocaine, Mexiletine

103
Q

Class IB Antiarrythmics mechanism of Action

A

↓ Action Potential

104
Q

Which tissue is preferentially affected with Class IB Antiarrythmics?

A

Ischemic or depolarized Purkinje and ventricular tissue

105
Q

Another drug that can also fall into the Class IB Antiarrythmics

A

Phenytoin

106
Q

Clinical use for Class IB Antiarrythmics

A

Acute ventricular arrhytmias (especially post MI)

Digitalis induced arrhytmias

107
Q

Which Antiarrythmics are better for post MI?

A

Class IB Antiarrythmics

108
Q

Toxic effects of Class IB Antiarrythmics

A

CNS stimulation/depression

Cardiovascular depression

109
Q

Class IC Antiarrythmics

A

Flecainide

Propafenone

110
Q

Which is the mechanism of action of Class IC Antiarrythmics?

A

Significantly prolongs refractory period in AV node

Minimal effect in Action potential duration

111
Q

Clinical use for Class IC Antiarrythmics

A

Supraventricular Tachycardia, including atrial fibrilation

112
Q

Antiarrythmics used as last resort in refractory Ventricular Tachycardia

A

Class IC Antiarrythmics

113
Q

When are Class IC Antiarrythmics contraindicated?

A

post MI

Structural and ischemic heart disease

114
Q

Toxic effect of Class IC Antiarrythmics

A

Proarrhytmic

115
Q

Who are Antiarrhytmics class II?

A

β blockers

Metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol

116
Q

Mechanism of action Antiarrhytmics class II

A

Decrease SA and AV nodal activity by ↓ cAMP, ↓ Ca2+ currents

Suppress abnormal pacemakers by ↓ slope of phase 4

117
Q

What effet do Antiarrhytmics class II have in AV node?

A

AV node particularly sensitive- ↑ PR interval

118
Q

Which characteristic does Esmolol has as Antiarrhytmic?

A

Very short acting

119
Q

Clinical use for Antiarrhytmics class II

A

Supraventricular Tachycardia

lowing ventricular rate during atrial fibrillation and atrial flutter

120
Q

Toxic effects of β blockers

A

Incompetence, exacerbation of COPD and asthma
Cardiovascular effects (bradycardia, aV block, CHF)
CNS effects (sedation, sleep alterations)
May mask the signs of hipoglycemia

121
Q

Which Antiarrhytmic class II can cause dyslipidemia?

A

Metoprolol

122
Q

Side effect of Propanolol

A

Can excacerbate vasospasm in Prinzmetal angina

123
Q

When are Antiarrhytmics class II contraindicated?

A

In cocaine users

124
Q

Why are β blockers contraindicated for cocaine users?

A

Risk of unopposed α adrenergic receptor agonist activity

125
Q

How is β blocker overdose treated?

A

With Glucagon

126
Q

Antiarrhytmics class III

A 
AIDS:
Amiodarone
Ibutilide
Dofelitide
Sotalol
127
Q

How do Antiarrhytmics class III work

A

K+ channel blockers

128
Q

Mechanism of action of Antiarrhytmics class III

A

↑ Action Potential duration, ↑ Effective refractory Potential

129
Q

When are Antiarrhytmics class III used?

A

When other antiarrhytmics fail

130
Q

Which ECG change do Antiarrhytmics class III cause?

A

↑ QT interval

131
Q

Clinical use of Antiarrhytmics class III

A

Atrial fibrillation, atrial flutter

132
Q

Antiarrhytmics class III used for Ventricular Tachycardia

A

Amiodarone

Sotalol

133
Q

Toxic effects caused by Sotalol

A

Torsades de pointes

Excessive β blockade

134
Q

Side effect of Ibutilide

A

Torsades de pointes

135
Q

You need to be careful when using amiodarone because it can cause…

A 
Pulmonary fibrosis
Hepatotoxicity
Hypothyroidism/Hyperthyroidism
Corneal deposits
Skin deposits (gray/blue) resulting in photodermatitis
Neurologic effects
Constipation 
Cardivascular effects
136
Q

Which is the reason amiodarone can cause Hypothyroidism/Hyperthyroidism?

A

Is 40% iodine by weight

137
Q

Cardiac side effect of Amiodarone

A

Bradycardia
Heart block
CHF

138
Q

When using amiodarone what do you need to check?

A

PFTs (pulmonary function tests)
LFTs (liver function tests)
TFTs (Tyroid function tests)

139
Q

Which antiarrhytmic effects does amiodarone has?

A

Class I, II, III, IV effects and altered the lipid membrane

140
Q

Class IV Antiarrhytmics

A

Verapamil

Diltiazem

141
Q

Effect of Class IV Antiarrhytmics

A

Ca2+ channel blockers

142
Q

Mechanism of Action of Class IV Antiarrhytmics

A

↓ Conduction velocity

↑ Effective refractory period

143
Q

ECG changes with Ca2+ channel blockers

A

↑ PR interval

144
Q

Clinical use for Class IV Antiarrhytmics

A

Prevention of nodal arrhytmias (eg. SPT)

Rate control on Atrial Fibrilation

145
Q

Toxic effect of Class IV Antiarrhytmics

A

Constipation, flushing, edema, Cardiovascular effects

146
Q

Which cardiovascular side effects do Class IV Antiarrhytmics have?

A

CHF
AV block
Sinus node depression

147
Q

Which are other antiarrhythmics that aren’t classified with other families?

A

Adenosine

Mg2+

148
Q

Mechanism of action of Adenosine

A

↑ K+ out of cells → hyperpolarizing the cell and ↓ Ica

149
Q

Drug of choice in diagnosing/ abolishing supraventricular tachycardia

A

Adenosine

150
Q

How long does it takes for Adenosine to act?

A

Very short acting (15 seg)

151
Q

Adverse effects of Adenosine

A

Flushing
Hypotension
Chest pain

152
Q

Who block the effects of Adenosine?

A

Effects blocked by Theophylline and caffeine

153
Q

When is Mg2+ used as Antiarrhythmic?

A

Effective in torsades de pointes and digoxin toxicity

CARDIOVASCULAR (6 decks)

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