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Step 1 Pharm > Cardiovascular > Flashcards

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
Q

Hydralazine

Clinical Use

A
  • Severe Hypertension (especially acute)
  • HF (w/ organic nitrate)
  • Safe for Pregnancy
  • co-admin w/ beta-blocker to prevent reflex tachycardia
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26
Q

Hydralazine

Toxicity

A
  • Compensatory tachycardia
  • Fluid retention
  • Headache
  • Angina
  • Lupus-like symptoms
  • Contraindicated in angina/CAD
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27
Q

Nitroprusside

Mechanism

A
  • Î cGMP via direct release of NO
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28
Q

Nitroprusside

Clinical Use

A
  • Hypertensive Emergency
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29
Q

Nitrprusside

Toxicity

A
  • Cyanide Toxicity
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30
Q

Fenoldopam

Mechanism

A
  • Dopamine D1 receptor agonist
    • Increased naturesis
  • reduced BP
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31
Q

Fenoldapam

Clinical Use

A
  • Hypertensive Emergency
  • coronary, peripheral, renal, splanchnic vasodilation
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32
Q

Fenoldapam

Toxicity

A
  • Reflex tachycardia
  • hypotension
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33
Q

Nitroglycerine

Mechanism

A
  • Vasodilation by increased NO of in vasc smooth muscle
  • ⇒ ^^ cGMP and smooth muscle relaxation
  • Dilate veins >> arteries
  • reduces preload
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34
Q

Isosorbide dinitrate

Mechanism

A
  • Vasodilation by increased NO of in vasc smooth muscle
  • ⇒ ^^ cGMP and smooth muscle relaxation
  • Dilate veins >> arteries
  • reduces preload
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35
Q
A
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36
Q

Isosorbide mononitrate

Mechanism

A
  • Vasodilation by increased NO of in vasc smooth muscle
  • ⇒ ^^ cGMP and smooth muscle relaxation
  • Dilate veins >> arteries
  • reduces preload
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37
Q

Nitroglycerine

Clinical Use

A
  • Angina
  • Acute Coronary Syndrome
  • Pulmonary Edema
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38
Q

Isosorbide dinitrate

Clinical Use

A
  • Angina
  • Acute Coronary Syndrome
  • Pulmonary Edema
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39
Q

Isosorbide mononitrate

Clinical Use

A
  • Angina
  • Acute Coronary Syndrome
  • Pulmonary Edema
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40
Q

Nitroglycerine

Toxicity

A
  • 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
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41
Q

Isosorbide Dinitrate

Toxicity

A
  • 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
Q

Isosorbide Mononitrate

Toxicity

A
  • 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
Q

Digoxin

Mechanism

A
  • Direct inhibition of Na+/K+ ATPase ⇒
  • indirect inhibition of Na+/Ca2+ exchanger
  • ^^ [Ca2+]i ⇒ positive inotropy
  • Stimulates Vagus Nerve ⇒ reduced HR
44
Q

Digoxin

Clinical Use

A
  • HF
    • increased Contractility
  • A.Fib
    • reduced conduction at AV node and SA node depression
45
Q

Digoxin

Toxicity

A
  • 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
Q

Digoxin

Antidote

A
  • Slowly normalize K+
  • Cardiac Pacer
  • Anti-Digoxin Fab fragments
  • Mg2+
47
Q

Lovastatin

Mechanism

A
  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients
48
Q

Pravastatin

Mechanism

A
  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients
49
Q

Simvastatin

Mechanism

A
  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients
50
Q

Atorvastatin

Mechanism

A
  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients
51
Q

Rosuvastatin

Mechanism

A
  • Inhibits conversion of HMG-CoA to mevalonate
  • a cholesterol precurso
  • Reduced mortality in CAD patients
52
Q

Lovastatin

Clinical Use

A
  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides
53
Q

Pravastatin

Clinical Use

A
  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides
54
Q

Simvastatin

Clinical Use

A
  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides
55
Q

Atorvastatin

Clinical Use

A
  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides
56
Q

Rosuvastatin

Clinical Use

A
  • vvv - LDL
  • ^ - HDL
  • v - Triglycerides
57
Q

Lovastatin

Toxicity

A
  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)
59
Q

Pravastatin

Toxicity

A
  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)
60
Q

Simvastatin

Toxicity

A
  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)
61
Q

Atorvastatin

Toxicity

A
  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)
62
Q

Rosuvastatin

Toxicity

A
  • Hepatotoxicity (more with Low LFTs)
  • Myopathy (esp w/ fibrates or Niacin)
63
Q

Cholestyramine

Mechanism

A

Bile Acid Resin

  • Prevents intestinal reabsorption of bile acids
  • Liver must use cholesterol to make more
64
Q

Colestipol

Mechanism

A

Bile Acid Resin

  • Prevents intestinal reabsorption of bile acids
  • Liver must use cholesterol to make more
65
Q

Colesevelam

Mechanism

A

Bile Acid Resin

  • Prevents intestinal reabsorption of bile acids
  • Liver must use cholesterol to make more
66
Q

Cholestryramine

Clinical Use

A
  • vv - LDL
  • slightly ^ - HDL
  • slightly ^ - Triglycerides
67
Q

Cholestipol

Clinical Use

A
  • vv - LDL
  • slightly ^ - HDL
  • slightly ^ - Triglycerides
68
Q

Cholesevelam

Clinical Use

A
  • vv - LDL
  • slightly ^ - HDL
  • slightly ^ - Triglycerides
69
Q

Cholestyramine

Toxicity

A
  • GI Upset
  • Reduced absorption of other drugs & fat soluble vitamins
71
Q

Cholestipol

Toxicity

A
  • GI Upset
  • Reduced absorption of other drugs & fat soluble vitamins
72
Q

Colesevelam

Toxicity

A
  • GI Upset
  • Reduced absorption of other drugs & fat soluble vitamins
73
Q

Ezetimibe

Mechanism

A
  • Prevents Cholesterol absorption at small intestine brush border
74
Q

Ezetimibe

Clinical Use

A
  • vv - LDL
  • minimal HDL/Triglyceride change
75
Q

Ezetimibe

Toxicity

A
  • Rare
  • elevated LFTs
  • Diarrhea
76
Q

Gemfibrozil

Mechanism

A
  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis
77
Q

Clofibrate

Mechanism

A
  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis
78
Q

Bezafibrate

Mechanism

A
  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis
79
Q

Fenofibrate

Mechanism

A
  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis
80
Q

Fenofibrate

Mechanism

A
  • Upregulate LPL →^^ TG clearance
  • Activates PPAR-a to induce HDL synthesis
81
Q

Class that:

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

Drugs in that Class

A

Fibrates

Gemfibrozil

Clofibrate

Bezafibrate

Fenofibrate

82
Q

Gemfibrozil

Toxicity

A
  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones
83
Q

Clofibrate

Toxicity

A
  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones
84
Q

Bezafibrate

Toxicity

A
  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones
85
Q

Fenofibrate

Toxicity

A
  • Myopathy (increased w/ statins)
  • Cholesterol Gallstones
86
Q

Niacin

Mechanism

A

Vitamin B3

  • Inhibits Lipolysis (hormonse sensitive lipase) in adipose
  • Reduces hepatice VLDL synthesis
87
Q

Niacin

Clinical Use

A
  • vv - LDL
  • ^^ - HDL
  • v - Triglycerides
88
Q

Niacin

Toxicity

A
  • Red, flushed face (reduced by NSAID/ long term use)
  • Hyperglycemia
  • Hyperuricemia
89
Q

Primary (Essential) Hypertension

Treatment

A
  • Thiazide diuretics
  • ACE inhibitors
  • Angiotensis II receptor blockers
  • dihydropyridine Ca2+ channel blockers
90
Q

Hypertension with Heart Failure

Treatment

A
  • Diuretics
  • ACE inhibitors
  • ARBs
  • Beta-blockers (compensated HF)
  • Aldosterone antagonists
91
Q

Hypertension w/ Diabetes Mellitus

Treatment

A
  • ACE inhibitors
  • ARBs
  • Ca2+ channel blockers
  • Thiazide diuretics
  • Beta-blockers
92
Q

Hypertension in Pregnancy

Treatment

A
  • Hydralazine
  • Labetalol
  • Methyldopa
  • Nifedipine
93
Q

Anti-Arrhythmics

Class I

Mechanism

A

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
Q

Quinidine

Mechanism

A
  • Class Ia anti-arrhythmic
  • Increases AP duration
  • Increases ERP in ventricular AP
  • Prolongs QT interval
95
Q

Procainamide

Mechanism

A
  • Class Ia anti-arrhythmic
  • Increases AP duration
  • Increases ERP in ventricular AP
  • Prolongs QT interval
96
Q

Disopyramide

Mechanism

A
  • Class Ia anti-arrhythmic
  • Increases AP duration
  • Increases ERP in ventricular AP
  • Prolongs QT interval
97
Q

Quinidine

Clinical Use

A
  • Class Ia anti-arrhythmic
  • Both Atrial and Ventricular arrhythmias
  • especially re-entrant and ectopic SVT and VT
98
Q

Procainamide

Clinical Use

A
  • Class Ia anti-arrhythmic
  • Both Atrial and Ventricular arrhythmias
  • especially re-entrant and ectopic SVT and VT
99
Q

Disopyramide

Clinical Use

A
  • Class Ia anti-arrhythmic
  • Both Atrial and Ventricular arrhythmias
  • especially re-entrant and ectopic SVT and VT
100
Q

Quinidine

Toxicity

A
  • Class Ia anti-arrhythmic
  • Cinchonism (quinine toxicity)
  • Headache, tinnitus
  • thrombocytopenia
  • TdP due to QT prolongation
101
Q

Procainamide

Toxicity

A
  • Class Ia anti-arrhythmic
  • Reversible SLE -like symptoms
  • thrombocytopenia
  • TdP due to QT prolongation
102
Q

Disopyramide

Toxicity

A
  • Class Ia anti-arrhythmia
  • Heart failure
  • thrombocytopenia
  • TdP due to QT prolongation

Step 1 Pharm (10 decks)

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