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PHARMA I > CARDIOMEDS MOA > Flashcards

CARDIOMEDS MOA Flashcards

1
Q

Antagonizes both β1 and β2 receptors this inhibiting effects of catecholamines on these receptors

• CV effects
Decrease contractility and heart rate

• Non-CV effects
May increase peripheral resistance

Bronchospasm

A

Non-selective agents

Nadolol, Pindolol, and Propranolol a

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2
Q

Antagonize β1 receptors to a greater extent than β2 receptors in typical doses
• CV effects

Decrease contractility and heart rate

A

Selective

Acebutolol, bisoprolol, esmolol, atenolol, and metoprolol a

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3
Q 
They possess non-selective beta blocking activity like propranolol and alpha blocking activity like prazosin
Effects seen:
▪ Decrease heart rate
▪ Decrease contractility
▪ Vasodilation
A

Alpha/beta adrenergic receptor antagonists

Labetalol, carvedilol (3rd gen. beta blockers)

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4
Q

o Block peripheral alpha 1 receptors → cause vasodilation secondary to inhibiting catecholamines mediated
vasoconstriction
▪ They block both arterial and venous alpha receptors

Decrease afterload of heart

Decrease peripheral vascular resistance

A

Selective alpha 1 adrenergic blockers

Doxazosin, prazosin, terazosin, tamsulosin (prostate selective)

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5
Q

Alpha 1A and 1D antagonistic effect increases selectivity for prostate

A

Tamsulosin

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6
Q

alpha 1 selective antagonist approved for BPH

A

Alfuzosin

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7
Q

Alpha 2 receptors are located in CNS→ presynaptic receptors so stimulation will decrease sympathetic outflow

A

Central acting alpha 2 adrenergic receptor agonist

Clonidine, guanabenz, guanfacine, methyldopa

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8
Q

inhibit conversion of angiotensin I to angiotensin II

A

Angiotensin inhibitors

ACEIs

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9
Q

Blocks angiotensin II from binding to the angiotensin type 1 receptor (AT1)→ blocking vasoconstriction and aldosterone
secreting effects of angiotensin II

Blocks the effect of ATII regardless of whether its generated by ACE, or some other enzymatic route

Does not interfere with metabolism of kinins and neuropeptides

A

Angiotensin Receptor Blockers

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10
Q

Metabolically converted to nitric oxide in vascular smooth muscle

vasodilating effects and reduces platelet adhesion and aggregation

A

Nitrates

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11
Q

Arteriolar vasodilator

Vasodilation causes SNS stimulation with increased heart rate and contractility, increased plasma renin activity and fluid
retention

A

Miscellaneous Vasodilators

Hydralazine

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12
Q

Venous and arteriolar vasodilator

Metabolized by smooth muscle cells to active metabolite NO → activates guanylate cyclase to form cGMP→ vasodilation

Unlike minoxidil, hydralazine, and other arteriolar vasodilators, SNP usually produces only a modest increase in HR and an overall decrease in myocardial O2 demand

A

Miscellaneous Vasodilators

Sodium Nitroprusside

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13
Q

Arteriolar vasodilator

Relaxation of smooth muscle with little effect on veins

Decrease SVR and BP by triggering SNS, inhibiting vagal tone, and renal homeostatic mechanisms leading to increase HR
CO and sodium/ fluid retention

A

Miscellaneous Vasodilators

Minoxidil (Rogaine)

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14
Q

Dopamine 1 agonist

Binds D1-like DA receptors and has moderate affinity for alpha 2 receptors (minimal adrenergic effects)

Binding D1 produces peripheral vasodilation with increase renal blood flow, diuresis and natriuresis

6x more potent than DA for renal vasodilation

A

Miscellaneous Vasodilators

Fenoldopam

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15
Q

Anti-anginal agent that doesn’t affect HR or BP

Inhibits late phase of inward sodium channel in ischemic cardiac myocytes during cardiac repolarization

Used as an additive agent after beta-blocker, nitrate and amlodipine

A

Miscellaneous Vasodilators

Ranolazine

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16
Q

Prevent breakdown of naturetic peptides

Naturetic peptides produce vasodilation and increase sodium excretion in kidneys

A

Neprilysin Inhibitor

17
Q

Angiotensin II receptor blocker and neprlysin inhibitor

Produces vasodilation and increases sodium excretion

A

Enteresto

18
Q

Calcium channels are located throughout the body

Calcium is needed for cardiac and smooth muscle contraction, and pacemaker activity in heart (SA node depolarization, AV node
conductance)

A

calcium channel blockers

19
Q

these diuretics are freely filtered into the lumen of the
nephron and not reabsorbed

This causes an increase in solutes in the nephron and
water follows the high solute concentration

A

diuretics

Osmotic Diuretics: Mannitol

20
Q

this diuretic Inhibits NaCl reabsorption into the distal convoluted tubule (DCT)

increase calcium reabsorption in the DCT

A

diuretics

Thiazide and Thiazide-Like Diuretics

21
Q

this diuretic binds to the Na+/K+/2Cltransport
system blocking the reabsoprtion of Clthus
sodium and water will follow

A

Loop Diuretics

Bumetanide, Ethacrynic acid, Furosemide, Torsemide

22
Q

this diuretic Inhibits aldosterone effects in the cortical collecting tubule and late distal tubule

A

Potassium Sparing Diuretics

Spironolactone/Eplerenone

23
Q

this diuretic Inhibits sodium transport through ion channels in the cortical collecting tubule and late distal tubule

A

Potassium Sparing Diuretics

Amiloride and Triamterene

24
Q

this diuretic is found in the brush border cells in the lumen of the nephron

Inhibition of this enzyme decreases sodium bicarb reabsorption in the PCT → water follows

May cause metabolic acidosis which decreases the effectiveness for diuresis

A

diuretics

Carbonic anhydrase inhibitors

25
Q

this diuretic Inhibits ADH in the collecting ducts of the nephron to promote free water excretion

A

diuretics

Antidiuretic hormone (ADH) antagonists (vasopressin antagonists)

Conivaptan, Tolvaptan

26
Q

Irreversible inhibitor of platelet CO

Therefore duration of effect is the time-span of the platelet (6-10 days)

what is this antiplatelet

A

aspirin

27
Q

Reversible inhibitor of platelet CO

Not useful clinically due to short duration

what is this antiplatelet

A

NSAIDs

28
Q

these selective adenosine diphosphate inhibitor inhibits the ADP receptor on the
surface of the platelet which prevents the expression of the
GP IIB/IIIa receptor, the final common result of platelet
activation

By inhibiting this receptor, these agents prevent ADP
induced platelet aggregation

There are multiple pathways to activate platelets → reason
for combining antiplatelets

A

Clopidogrel and prasugrel

29
Q

name the anticoagulant

Stimulates antithrombin III
• Inactivates thrombin and factors 9-12

A

Heparin

30
Q

name the anticoagulant

Interferes with hepatic synthesis of vit. K dependent coagulation factors II, VII, IX, and X

Impairs the function of protein C and S which are natural anticoagulants

A

Warfarin

31
Q

name the anticoagulant

used in patients with heparin induced thrombocytopenia (HIT)

Adjunctive therapy in patients undergoing percutaneous coronary intervention

A

Thrombin Inhibitors

Bivalirudin
Argatroban

32
Q

name the anticoagulant

Oral factor IIa (thrombin) inhibitor
▪ Free and clot bound thrombin activity

A

Dabigatran Etexilate

33
Q

name the anticoagulant, a Factor Xa Inhibitor

prophylaxis of DVT, treatment of DVT and PE

A

Fondaparinux (not very important, more concerned with oral drugs)

34
Q

name the anticoagulant, a Factor Xa Inhibitor

Synthetic oral direct factor Xa inhibitor

Inhibits free and clot-bound factor Xa activity

A

Rivaroxaban

35
Q

name the anticoagulant, a Factor Xa Inhibitor

Inhibits free Xa and prothrombinase activity

A

Apixaban

36
Q

name the thrombolytic

recombinant tissue plasminogen activator

Supposedly preferentially activates plasminogen that is bound to fibrin

A

Alteplase

37
Q

name the thrombolytic

synthesized by streptococci

Combines with proactivator plasminogen

A

Streptokinase

38
Q

name this hemostatic agent

completely inhibits plasminogen activity; may reverse the effects of thrombolytics

A

Aminocaproic acid and aprotinin

PHARMA I (138 decks)

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