Cardiovascular Flashcards

1
Q

Amlodipine

Mechanism

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

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine
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2
Q

Clevedipine

Mechanism

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

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine
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3
Q

Nicardipine

Mechanism

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

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine
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4
Q

Nifedipine

Mechanism

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

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine
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5
Q

Nimodipine

Mechanism

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

Vascular smooth muscle

  • amlodipine = nifedipine > diltiazem > verapamil

Cardiac muscle

  • verapamil > diltiazem > amlodipine = nifedipine
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6
Q

Dihydropyridines

Site of action

Drug list

A
  • Act on vascular smooth muscle
  • Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine
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7
Q

Non-dihydropyridines

Site of action

Drug list

A
  • Act on cardiac muscle
  • Diltiazem, verapamil
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8
Q

Drug class

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

Dihydropyridines

Calcium channel blockers

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9
Q

Drug class

  • Act on cardiac muscle
  • Diltiazem, verapamil
A

Non-dihydropyridines

Calcium Channel Blockers

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10
Q

Amlodipine

Clinical Use

A
  • Hypertension
  • Angina (including Prinzmetal)
  • Raynaud phenominon
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11
Q

Clevidipine

Clinical Use

A
  • Hypertensive urgency/emergency
  • Angina (including Prinzmetal)
  • Raynaud phenominon
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12
Q

Nicardipine

Clinical Use

A
  • Hypertension
  • Angina (including Prinzmetal)
  • Raynaud Phenomenon
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13
Q

Nifedipine

Clinical Use

A
  • Hypertension
  • Angina (including Prinzmetal)
  • Raynaud’s Phenomenon
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14
Q

Nimodipine

Clinical Use

A
  • Subarachnoid hemorrhage
  • Prevents cerebral vasospasm
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15
Q

Diltiazem

Clinical Use

A
  • Hypertension
  • Angina
  • A. Fib/Flutter
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16
Q

Verapamil

Clinical Use

A
  • Hypertension
  • Angina
  • A.Fib/flutter
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17
Q

Amlodipine

Toxicity

A
  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia
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18
Q

Clevidipine

Toxicity

A
  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia
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19
Q

Nicardipine

Toxicity

A
  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia
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20
Q

Nifedipine

Toxicity

A
  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia
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21
Q

Nimodipine

Toxicity

A
  • Cardiac Depression
  • AV Block
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia
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22
Q

Diltazem

Toxicity

A
  • Cardiac Depression
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia
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23
Q

Verapamil

Toxicity

A
  • Cardiac Depression
  • Peripheral edema
  • Hyperprolactinemia
  • Flushing
  • Dizziness
  • Constipation
  • Gingival hyperplasia
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24
Q

Hydralazine

Mechanism of action

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