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Flashcards in Cardiovascular Deck (102):
1

Amlodipine

Mechanism

  • L-type calcium channel blocker
  • Reduces cardiac and smooth muscle contractility

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine

 

2

Clevedipine

Mechanism

  • L-type calcium channel blocker
  • Reduces cardiac and smooth muscle contractility

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine

 

3

Nicardipine

Mechanism

  • L-type calcium channel blocker
  • Reduces cardiac and smooth muscle contractility

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine

 

4

Nifedipine

Mechanism

  • L-type calcium channel blocker
  • Reduces cardiac and smooth muscle contractility

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine

 

5

Nimodipine

Mechanism

  • L-type calcium channel blocker
  • Reduces cardiac and smooth muscle contractility

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine

 

6

Dihydropyridines

Site of action

Drug list

  • Act on vascular smooth muscle
  • Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

7

Non-dihydropyridines

Site of action

Drug list

  • Act on cardiac muscle
  • Diltiazem, verapamil

8

  • Act on vascular smooth muscle
  • Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

Dihydropyridines

Calcium channel blockers

9

  • Act on cardiac muscle
  • Diltiazem, verapamil

Non-dihydropyridines

Calcium Channel Blockers

10

Amlodipine

Clinical Use

  • Hypertension
  • Angina (including Prinzmetal)
  • Raynaud phenominon

11

Clevidipine

Clinical Use

  • Hypertensive urgency/emergency
  • Angina (including Prinzmetal)
  • Raynaud phenominon

12

Nicardipine

Clinical Use

  • Hypertension
  • Angina (including Prinzmetal)
  • Raynaud Phenomenon

13

Nifedipine

Clinical Use

  • Hypertension
  • Angina (including Prinzmetal)
  • Raynaud's Phenomenon

14

Nimodipine

Clinical Use

  • Subarachnoid hemorrhage
  • Prevents cerebral vasospasm

15

Diltiazem

Clinical Use

  • Hypertension
  • Angina
  • A. Fib/Flutter

16

Verapamil

Clinical Use

  • Hypertension
  • Angina
  • A.Fib/flutter

17

Amlodipine

Toxicity

  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia

18

Clevidipine

Toxicity

  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia

19

Nicardipine

Toxicity

  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia

20

Nifedipine

Toxicity

  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia

21

Nimodipine

Toxicity

  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia

22

Diltazem

Toxicity

  • Cardiac Depression
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia

23

Verapamil

Toxicity

  • Cardiac Depression
  • Peripheral edema
  • Hyperprolactinemia
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia

24

Hydralazine

Mechanism of action

  • î cGMP ⇒ smooth vessel relaxation
  • vasodilates arterioles > veins
  • Reduces Afterload

25

Hydralazine

Clinical Use

  • Severe Hypertension (especially acute)
  • HF (w/ organic nitrate)
  • Safe for Pregnancy
  • co-admin w/ beta-blocker to prevent reflex tachycardia

26

Hydralazine

Toxicity

  • Compensatory tachycardia 
  • Fluid retention
  • Headache
  • Angina
  • Lupus-like symptoms

 

  • Contraindicated in angina/CAD

27

Nitroprusside

Mechanism

  • Î cGMP via direct release of NO

28

Nitroprusside

Clinical Use

  • Hypertensive Emergency

29

Nitrprusside

Toxicity

  • Cyanide Toxicity

30

Fenoldopam

Mechanism

  • Dopamine D1 receptor agonist
  •  
  • Increased naturesis
  • reduced BP

31

Fenoldapam

Clinical Use

  • Hypertensive Emergency
  • coronary, peripheral, renal, splanchnic vasodilation

32

Fenoldapam

Toxicity

  • Reflex tachycardia
  • hypotension

33

Nitroglycerine

Mechanism

  • Vasodilation by increased NO of in vasc smooth muscle
  • ⇒ ^^ cGMP and smooth muscle relaxation
  • Dilate veins >> arteries
  • reduces preload

34

Isosorbide dinitrate

Mechanism

  • Vasodilation by increased NO of in vasc smooth muscle
  • ⇒ ^^ cGMP and smooth muscle relaxation
  • Dilate veins >> arteries
  • reduces preload

35

36

Isosorbide mononitrate

Mechanism

  • Vasodilation by increased NO of in vasc smooth muscle
  • ⇒ ^^ cGMP and smooth muscle relaxation
  • Dilate veins >> arteries
  • reduces preload

37

Nitroglycerine 

Clinical Use

  • Angina
  • Acute Coronary Syndrome
  • Pulmonary Edema

38

Isosorbide dinitrate

Clinical Use

  • Angina
  • Acute Coronary Syndrome
  • Pulmonary Edema

39

Isosorbide mononitrate

Clinical Use

  • Angina
  • Acute Coronary Syndrome
  • Pulmonary Edema

40

Nitroglycerine

Toxicity

  • Reflex Tacycardia (tx w/ Beta-blockers)
  • Hypotension
  • flushing
  • Headache
  • "Monday disease"
    • in industrial exposure; tolerance for vasodilation of actionduring work week
    • loss of tolerance over the weekend
    • ⇒ tachycardia, dizziness, headache on re-exposure

41

Isosorbide Dinitrate

Toxicity

  • Reflex Tacycardia (tx w/ Beta-blockers)
  • Hypotension
  • flushing
  • Headache
  • "Monday disease"
    • in industrial exposure; tolerance for vasodilation of actionduring work week
    • loss of tolerance over the weekend
    • ⇒ tachycardia, dizziness, headache on re-exposure

42

Isosorbide Mononitrate

Toxicity

  • Reflex Tacycardia (tx w/ Beta-blockers)
  • Hypotension
  • flushing
  • Headache
  • "Monday disease"
    • in industrial exposure; tolerance for vasodilation of actionduring work week
    • loss of tolerance over the weekend
    • ⇒ tachycardia, dizziness, headache on re-exposure

43

Digoxin

Mechanism

  • Direct inhibition of Na+/K+ ATPase ⇒
  • indirect inhibition of Na+/Ca2+ exchanger
  • ^^ [Ca2+]i ⇒ positive inotropy
  • Stimulates Vagus Nerve ⇒ reduced HR

44

Digoxin

Clinical Use

  • HF
    • increased Contractility
  • A.Fib
    • reduced conduction at AV node and SA node depression

45

Digoxin

Toxicity

  • Cholinergic
    • N/V/D
    • Blurry yellow vision
    • Arrhythmias
    • AV block
  • Hyperkalemia (poor prognostic)
  • Toxic factors
    • Renal Failure (reduced excretion)
    • hypokalemia (binds Na+/K+ ATPase
    • Verapamil/amidarone/quinidine (reduced clearance, displaces dig binding

46

Digoxin

Antidote

  • Slowly normalize K+
  • Cardiac Pacer
  • Anti-Digoxin Fab fragments
  • Mg2+

47

Lovastatin

Mechanism

  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients

48

Pravastatin

Mechanism

  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients

49

Simvastatin

Mechanism

  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients

50

Atorvastatin

Mechanism

  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients

51

Rosuvastatin

Mechanism

  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients

52

Lovastatin

Clinical Use

  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides 

53

Pravastatin

Clinical Use

  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides 

54

Simvastatin

Clinical Use

  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides 

55

Atorvastatin

Clinical Use

  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides 

56

Rosuvastatin

Clinical Use

  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides 

57

Lovastatin

Toxicity

  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)

58

59

Pravastatin

Toxicity

  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)

60

Simvastatin

Toxicity

  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)

61

Atorvastatin

Toxicity

  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)

62

Rosuvastatin

Toxicity

  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)

63

Cholestyramine

Mechanism

Bile Acid Resin

  • Prevents intestinal reabsorption of bile acids
  • Liver must use cholesterol to make more

64

Colestipol

Mechanism

Bile Acid Resin

  • Prevents intestinal reabsorption of bile acids
  • Liver must use cholesterol to make more

65

Colesevelam

Mechanism

Bile Acid Resin

  • Prevents intestinal reabsorption of bile acids
  • Liver must use cholesterol to make more

66

Cholestryramine

Clinical Use

  • vv - LDL
  • slightly ^ - HDL
  • slightly ^ - Triglycerides

67

Cholestipol

Clinical Use

  • vv - LDL
  • slightly ^ - HDL
  • slightly ^ - Triglycerides

68

Cholesevelam

Clinical Use

  • vv - LDL
  • slightly ^ - HDL
  • slightly ^ - Triglycerides

69

Cholestyramine

Toxicity

  • GI Upset
  • Reduced absorption of other drugs & fat soluble vitamins

70

71

Cholestipol

Toxicity

  • GI Upset
  • Reduced absorption of other drugs & fat soluble vitamins

72

Colesevelam

Toxicity

  • GI Upset
  • Reduced absorption of other drugs & fat soluble vitamins

73

Ezetimibe

Mechanism

  • Prevents Cholesterol absorption at small intestine brush border

74

Ezetimibe

Clinical Use

  • vv - LDL
  • minimal HDL/Triglyceride change

75

Ezetimibe

Toxicity

  • Rare
  • elevated LFTs
  • Diarrhea

76

Gemfibrozil

Mechanism

  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis

77

Clofibrate

Mechanism

 

  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis

78

Bezafibrate

Mechanism

 

  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis

79

Fenofibrate

Mechanism

 

  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis

80

Fenofibrate

Mechanism

 

  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis

81

Class that:

  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis

Drugs in that Class

Fibrates

 

Gemfibrozil

Clofibrate

Bezafibrate

Fenofibrate

82

Gemfibrozil

Toxicity

  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones

83

Clofibrate

Toxicity

  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones

84

Bezafibrate

Toxicity

  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones

85

Fenofibrate

Toxicity

  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones

86

Niacin

Mechanism

Vitamin B3

  • Inhibits Lipolysis (hormonse sensitive lipase) in adipose
  • Reduces hepatice VLDL synthesis

87

Niacin

Clinical Use

  • vv - LDL
  • ^^ - HDL
  • v - Triglycerides

88

Niacin

Toxicity

  • Red, flushed face (reduced by NSAID/ long term use)
  • Hyperglycemia
  • Hyperuricemia

89

Primary (Essential) Hypertension

Treatment 

  • Thiazide diuretics
  • ACE inhibitors
  • Angiotensis II receptor blockers
  • dihydropyridine Ca2+ channel blockers

90

Hypertension with Heart Failure

Treatment

  • Diuretics
  • ACE inhibitors
  • ARBs
  • Beta-blockers (compensated HF)
  • Aldosterone antagonists

91

Hypertension w/ Diabetes Mellitus

Treatment

  • ACE inhibitors
  • ARBs
  • Ca2+ channel blockers
  • Thiazide diuretics
  • Beta-blockers

92

Hypertension in Pregnancy

Treatment

  • Hydralazine
  • Labetalol
  • Methyldopa
  • Nifedipine

93

Anti-Arrhythmics

Class I

Mechanism

 

Sodium Channel Blocker

  • slows or blocks conduction 
  • reduced slopw of phase 0 depolerization
  • State dependent ( selectivly depress tissue that is frequently depolarized, ie. tachycardic)

94

Quinidine

Mechanism

  • Class Ia anti-arrhythmic

 

  • Increases AP duration
  • Increases ERP in ventricular AP
  • Prolongs QT interval

95

Procainamide

Mechanism

  • Class Ia anti-arrhythmic

 

  • Increases AP duration
  • Increases ERP in ventricular AP
  • Prolongs QT interval

96

Disopyramide

Mechanism

  • Class Ia anti-arrhythmic

 

  • Increases AP duration
  • Increases ERP in ventricular AP
  • Prolongs QT interval

97

Quinidine 

Clinical Use

  • Class Ia anti-arrhythmic

 

  • Both Atrial and Ventricular arrhythmias
  • especially re-entrant and ectopic SVT and VT

98

Procainamide

Clinical Use

  • Class Ia anti-arrhythmic

 

  • Both Atrial and Ventricular arrhythmias
  • especially re-entrant and ectopic SVT and VT

99

Disopyramide

Clinical Use

  • Class Ia anti-arrhythmic

 

  • Both Atrial and Ventricular arrhythmias
  • especially re-entrant and ectopic SVT and VT

100

Quinidine

Toxicity

 

  • Class Ia anti-arrhythmic

 

  • Cinchonism (quinine toxicity)
  • Headache, tinnitus
  • thrombocytopenia
  • TdP due to QT prolongation

101

Procainamide

Toxicity

 

  • Class Ia anti-arrhythmic

 

  • Reversible SLE -like symptoms
  • thrombocytopenia
  • TdP due to QT prolongation

102

Disopyramide

Toxicity

 

  • Class Ia anti-arrhythmia

 

  • Heart failure
  • thrombocytopenia
  • TdP due to QT prolongation