Spring FPMQ MOAs Flashcards

1
Q

Doxazosin

A

Block alpha 1 or 2 in the periphery causing vasodilation

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2
Q

Cholestyramine

A

Positively charged resins bind negatively charged bile acids – the resins & bound bile acids are excreted in the stool

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3
Q

Fenofibrate

A

Activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha) to suppress genes associated with lipid metabolism
• Reduces triglyceride-rich lipoproteins
• Increases HDLs

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4
Q

Rosuvastatin

A

Inhibit the activity of HMG CoA (3-hydroxy-3-methylglutary coenzyme A) reductase – catalyzes the early rate limiting step of cholesterol biosynthesis

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5
Q

Levalbuterol

A

Beta-2 receptor activation leading to stimulation of adenylyl cyclase to increase cAMP, which leads to bronchodilation

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6
Q

Ipratropium

A

Blocks vagally-mediated airway tone, including vagally-mediated bronchoconstriction

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7
Q

Ramipril

A
  • Counter the activation of the renin-angiotensin-aldosterone system by blocking the conversion of ANG-1 to ANG-II and aldosterone secretion
  • Reduce peripheral resistance and reduce afterload, reduce sodium and water retention and reduce preload, reduce long-term remodeling of cardiac tissue
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8
Q

Oxymetazoline

A

Alpha stimulation vasoconstricts the nasal mucosa vessels, shrink swollen mucosa and improve breathin

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9
Q

Nitroprusside

A

Relax vascular smooth muscle by stimulating intracellular cGMP production. They cause predominantly venous dilation with some dose dependent arterial effects

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10
Q

Benazepril

A
  • Counter the activation of the renin-angiotensin-aldosterone system by blocking the conversion of ANG-1 to ANG-II and aldosterone secretion
  • Reduce peripheral resistance and reduce afterload, reduce sodium and water retention and reduce preload, reduce long-term remodeling of cardiac tissue
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11
Q

Losartan

A

Block the actions of ANG-II by blocking binding to ANG-II receptors leading to vasodilation and decrease in BP

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12
Q

Hydrochlorothiazide

A

Inhibit reabsorption of sodium and chloride in the distal tubules, resulting in increased urinary excretion of sodium and chloride

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13
Q

Montelukast

A

Antagonist at the leukotriene LTD4 and LTE4 receptor

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14
Q

Labetalol

A

Alpha-1 antagonists causes vasodilation decreasing peripheral resistance

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15
Q

Nitroglycerin

A

Relax vascular smooth muscle by stimulating intracellular cGMP production. They cause predominantly venous dilation with some dose dependent arterial effects

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16
Q

Niacin

A

Inhibits triglyceride synthesis
• Inhibits lipase to reduce free fatty acids
• Inhibits synthesis and esterification of fatty acids
– reduces LDL levels

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17
Q

Omega-3-fatty acids

A

Lower triglycerides – mechanism may be similar to fibrates

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18
Q

Tamsulosin

A

Select alpha-1a, primarily in prostate – good for BPH not HTN - can have BP changes

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19
Q

Irbesartan

A

Block the actions of ANG-II by blocking binding to ANG-II receptors leading to vasodilation and decrease in BP

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20
Q

Ranolazine

A

Believed inhibition of the inward sodium channel in ischemic myocardium, resulting in decreased calcium influx and decreased ventricular tension and oxygen consumption

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21
Q

Omalizumab

A

IgE binder - Recombinant DNA-derived monoclonal antibody directed to IgE, important in releasing mediator of the allergic response

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22
Q

Triamcinolone

A

Anti-inflammatory action by suppression of inflammatory gene expression (cytokines & chemokines)
-Reduce expression of the inflammatory cyclooxygenase II (COX II)

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23
Q

Nifedipine

A

Prevents release of internal calcium stored into the cell cytosol → heart muscle cell does not respond to calcium ion signal - Leading to relaxation of vessels in the periphery & decreased contractility in the heart

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24
Q

Isosorbide mononitrate

A

Relax vascular smooth muscle by stimulating intracellular cGMP production. They cause predominantly venous dilation with some dose dependent arterial effects

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25
Q

Carvedilol

A

Alpha-1 antagonists causes vasodilation decreasing peripheral resistance

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26
Q

Amlodipine

A

Prevents release of internal calcium stored into the cell cytosol → heart muscle cell does not respond to calcium ion signal - Leading to relaxation of vessels in the periphery & decreased contractility in the heart

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27
Q

Diphenhydramine

A

Histamine – 1 blocker

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28
Q

Lisinopril

A
  • Counter the activation of the renin-angiotensin-aldosterone system by blocking the conversion of ANG-1 to ANG-II and aldosterone secretion
  • Reduce peripheral resistance and reduce afterload, reduce sodium and water retention and reduce preload, reduce long-term remodeling of cardiac tissue
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29
Q

Theophylline

A

Phosphodiesterase inhibition (3,4,5) increases cAMP & cGMP in bronchial smooth muscle leading to bronchodilation

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30
Q

Felodipine

A

Prevents release of internal calcium stored into the cell cytosol → heart muscle cell does not respond to calcium ion signal - Leading to relaxation of vessels in the periphery & decreased contractility in the heart

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31
Q

Milrinone

A

Increase in cAMP activates cAMP-depended protein kinase activity that promotes phosphorylation of voltage-dependent calcium channels – increase in calcium influx during action potential increases force of contraction

32
Q

Nicotine

A

Stimulates acetylcholine (nicotinic) receptors in the CNS, producing psychoactive effects as mood elevation, decreased anxiety, decreased appetite, improved attentiveness, cognitive enhancement, etc.

33
Q

Atenolol

A

Beta-1 antagonists slow down HR by decreasing cardiac output – decreased HR & force of contraction

34
Q

Dobutamine

A
  • Short-term Tx of cardiac decompensation
    • Beta effect predominates – increase HR & force of contraction
    • Alpha effects may contribute to increased force of contraction
35
Q

Norepinephrine

A
  • Heart – rate may decrease by vagal reflex
    • Arteries – vasoconstriction
    • Veins – Venoconstriction
36
Q

Beclomethasone

A

Anti-inflammatory action by suppression of inflammatory gene expression (cytokines & chemokines)
-Reduce expression of the inflammatory cyclooxygenase II (COX II)

37
Q

Nebivolol

A

Beta-1 antagonists slow down HR by decreasing cardiac output

38
Q

Diltiazem

A
  • Block movement of calcium ions across cell membranes. Leading to relaxation of coronary vascular smooth muscle and coronary vasodilation. Also increase myocardial oxygen delivery and depress both impulse formation and conduction velocity in the AV node
    • Negative inotrope, negative chronotrope
39
Q

Sotalol

A
  • Potassium channel blocker – increases action potential duration and refractory period
  • Beta blocker activity – inhibits phase 4 depolarization (K channels)
40
Q

Bumetanide

A

Inhibit the reabsorption of sodium and chloride at the thick ascending limb of the loop of henle, increasing the excretion of sodium, water, chloride, calcium, and magnesium

41
Q

Atorvastatin

A

Inhibit the activity of HMG CoA (3-hydroxy-3-methylglutary coenzyme A) reductase – catalyzes the early rate limiting step of cholesterol biosynthesis

42
Q

Hydralazine

A

Cause vasodilation through release of NO

43
Q

Promethazine

A

H1-Receptor Antagonist

-Dopamine antagonism as well as H1 and muscarinic receptor antagonism

44
Q

Torsemide

A

Inhibit the reabsorption of sodium and chloride at the thick ascending limb of the loop of henle, increasing the excretion of sodium, water, chloride, calcium, and magnesium

45
Q

Epinephrine

A
  • Emergency Tx of anaphylactic shock & cardiac stimulation during arrest
    • Heart – Increased force of contraction (+ inotropic action), increase in rate (+ chronotropic action)
    • Arteries – Vasoconstriction in most arterial beds
    • Lungs – Bronchodilation, decongestion
46
Q

Hydroxyzine

A

H1-Receptor Antagonist on vestibular afferents in the CTZ and STN, Anti-cholinergic properties on M1 receptors in the CTZ and STN

47
Q

Mometasone

A

Anti-inflammatory action by suppression of inflammatory gene expression (cytokines & chemokines)
-Reduce expression of the inflammatory cyclooxygenase II (COX II)

48
Q

Fexofenadine

A

Anti-histamine effects

49
Q

Albuterol

A

Beta-2 receptor activation leading to stimulation of adenylyl cyclase to increase cAMP, which leads to bronchodilation

50
Q

Guaifenesin

A

Increases respiratory tract fluid secretions which helps loosen phlegm and bronchial secretions

51
Q

Terazosin

A

Block alpha 1 or 2 in the periphery causing vasodilation

52
Q

Valsartan

A

Block the actions of ANG-II by blocking binding to ANG-II receptors leading to vasodilation and decrease in BP

53
Q

Verapamil

A

Block movement of calcium ions across cell membranes. Leading to relaxation of coronary vascular smooth muscle and coronary vasodilation. Also increase myocardial oxygen delivery and depress both impulse formation and conduction velocity in the AV node
-Negative inotrope, negative chronotrope

54
Q

Cetirizine

A

Anti-histamine effects

55
Q

Salmeterol

A

Beta-2 receptor activation leading to stimulation of adenylyl cyclase to increase cAMP, which leads to bronchodilation

56
Q

Spironolactone

A

Blocks up regulation of Na+ & Na+/K+ ATPase leading to decreased Na+ resorption and increased K+ resorption

57
Q

Dopamine

A
  • Short-term cardiovascular support – effects highly dependent on dose
    • Increased cardiac output
    • Increased BP
    • Improved renal and intestinal perfusion
58
Q

Propranolol

A
  • non-selective block beta 1 & 2
    • Beta-1 decreased HR and force of contraction
    • Beta-2 predominates in bronchial tissue get bronchoconstriction
59
Q

Fluticasone

A

Anti-inflammatory action by suppression of inflammatory gene expression (cytokines & chemokines)
-Reduce expression of the inflammatory cyclooxygenase II (COX II)

60
Q

Pravastatin

A

Inhibit the activity of HMG CoA (3-hydroxy-3-methylglutary coenzyme A) reductase – catalyzes the early rate limiting step of cholesterol biosynthesis

61
Q

Varenicline

A

Partial agonist-antagonist and is highly selective for the alpha-4-beta-2 nicotinic acetylcholine receptor

62
Q

Enalapril

A
  • Counter the activation of the renin-angiotensin-aldosterone system by blocking the conversion of ANG-1 to ANG-II and aldosterone secretion
  • Reduce peripheral resistance and reduce afterload, reduce sodium and water retention and reduce preload, reduce long-term remodeling of cardiac tissue
63
Q

Digoxin

A
  • Blocks the Na+/K+ ATPase, which leads to increased intracellular sodium, which stimulates sodium calcium exchange. Which leads to increased intracellular calcium increasing contractility. Increases vagal tone which suppressed the AV node increasing refractory period and decreasing conduction velocity
64
Q

Clonidine

A

Bind the alpha-2 autoreceptor leading to decreased release of catecholamines (NE, Epi) form presynaptic cleft → leads to vasodilation since less catecholamines are present to bind other receptors such as alpha-1

65
Q

Loratadine

A

Anti-histamine effects

66
Q

Levocetirizine

A

Anti-histamine effects

67
Q

Simvastatin

A

Inhibit the activity of HMG CoA (3-hydroxy-3-methylglutary coenzyme A) reductase – catalyzes the early rate limiting step of cholesterol biosynthesis

68
Q

Tiotropium

A

Blocks vagally-mediated airway tone, including vagally-mediated bronchoconstriction

69
Q

Olmesartan medoxomil

A

Block the actions of ANG-II by blocking binding to ANG-II receptors leading to vasodilation and decrease in BP

70
Q

Phenylephrine

A

Alpha-1 selective leading to vasoconstriction

71
Q

Benzonatate

A

Acts as a local anesthetic on stretch receptors that trigger cough located in respiratory passages, lungs, and pleura

72
Q

Gemfibrozil

A

Activates peroxisome proliferator-activated receptor-alpha (PPAR-alpha) to suppress genes associated with lipid metabolism
• Reduces triglyceride-rich lipoproteins
• Increases HDLs

73
Q

Amiodarone

A
  • Has class I, II, II, and IV activity
    • Blocks NA channels slowing HR, impedes AV node conduction through beta blockade and calcium channels, prolongs atrial ventricular repolarization by inhibiting potassium channels
74
Q

Metoprolol tartrate

A

Beta-1 antagonists slow down HR by decreasing cardiac output – decreased HR & force of contraction

75
Q

Ezetimibe

A

Inhibits the intestinal absorption of cholesterol and related phytosterols by interacting with specific intestinal transporters – does NOT effect absorption of fat soluble vitamins

76
Q

Captopril

A
  • Counter the activation of the renin-angiotensin-aldosterone system by blocking the conversion of ANG-1 to ANG-II and aldosterone secretion
  • Reduce peripheral resistance and reduce afterload, reduce sodium and water retention and reduce preload, reduce long-term remodeling of cardiac tissue
77
Q

Furosemide

A

Inhibit the reabsorption of sodium and chloride at the thick ascending limb of the loop of henle, increasing the excretion of sodium, water, chloride, calcium, and magnesium