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Pharmacology Block 2 > end > Flashcards

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1
Q
A
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2
Q

Phenylalkylamine

A

Verapamil

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3
Q

Benzothiazepine

A

Diltiazem

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4
Q

1,4-Dihydropyridines

A

Nifedipine (prototype) Amlodipine (longest acting)

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5
Q

Use-dependent CCBs

A

Verapamil Diltiazem

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6
Q

Voltage-dependent CCBs

A

Nifedipine Amlodipine

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7
Q

What CCB do you use for Angina?

A

Diltiazem Because decreases SA node firing rate, reduces cardiac after load by vasodilation, also increases blood flow to myocardium to prevent ischemia Nifednipine and Amlodipine can also be used because they reduce myocardial oxygen demand and arterial pressure

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8
Q

What CCBs are used for Supraventricular arrhythmias?

A

Diltiazem or Verapamil Because they reduce the firing rate of the SA node and reduce conduction through AV node

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9
Q

Which CCBs are used to treat hypertension?

A

Usually Dihydropyridines Because of potent vasodilator effects BUT may trigger reflex tachycardia particularly with short acting Dihydropyridines

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10
Q

Diuretics, Vasodilators

A

Fenoldopam, Dopamine, Atriopeptins

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11
Q

What is the mechanism of action of the vasodilatory diuretics??

A

Increase RBF without decreasing GFR FF decreases (reduces protein conc and hydroosmotic forces in peritubular capillaries)– allow Na and H20 to leak back into the tubule This reduces net reabsorption so Na excretion increases Weak as diuretics due to compensatory Na reabsorption in more distal nephron segment

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12
Q

Osmotic diuretic Freely filterable at glomerulus Not reabsorbed Metabolically inert

A

Mannitol

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13
Q

What is the mechanism of action of osmotic diuretics??

A

Given intravenously Act in tubular lumen as non-reabsorbable solute Urine volume and sodium excretion are proportional to the osmotic load Increases the urinary excretion of sodium, potassium, chloride, water and mannitol

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14
Q

What are osmotic diuretics used for?

A

Edema Glaucoma-reduces intraocular pressure Acute renal failure

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15
Q

Carbonic Anhydrase Inhibitor Orally active Weak diuretics Inhibited by acidosis-limits clinical use

A

Acetazolamide

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16
Q

What is the mechanism of carbonic anhydrase inhibitors?

A

Filtered and secreted by the organic acid transporter (OAT) - acts from tubular lumen Inhibit carbonic anhydrase in the proximal and distal tubule Carbonic anhydrase provides hydrogen ions for bicarbonate reabsorption Increase the excretion of sodium, potassium, bicarbonate and water Alkalinize the urine

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17
Q

What are Carbonic Anhydrase inhibitors used for?

A

Glaucoma - reduced aqueous humor formation and intraocular pressure Alkalinize the urine – decrease drug toxicity Mountain or altitude sickness Anticonvulsant SE= Metabolic acidosis, hypokalemia

18
Q

Loop Diuretics Rapid onset, short duration of action

A

Furosemide, Bumetanide, Ethacrynic Acid

19
Q

What is the mechanism of Loop Diuretics??

A

Filtered and secreted by the OAT Inhibits Na-K-2Cl symporter Acts on cortical and medullary segments of the ascending limb of the loop of Henle Increase excretion of Na, K, Cl and H20

20
Q

What are the Loop Diuretics used for?

A

Edema of cardiac, hepatic or renal origin Acute pulmonary edema HTN

21
Q

Thiazide and Thiazide-Like Diuretics Moderate onset of activity Long duration of action

A

Hydrochlorothiazide Metolazone

22
Q

What is the mechanism of action of Thiazide diuretics?

A

Filtered and secreted by the OAT Inhibits Na-Cl symporter Acts on cortical segment of distal tubule Increases excretion of Na, K, Cl and H20 Urine is hypertonic - unable to dilute

23
Q

What are the Thiazide Diuretics used for?

A

Edema due to CHF HTN Hypercalemia/Ca salt-renal caliculi

24
Q

K+ Sparring Diuretics, Aldosterone Antagonists

A

Spironolactone, Eplerenone

25
Q

K+ Sparring Diuretics, Na+ channel inhibitors

A

Amiloride, Triamterene

26
Q

What is the mechanism of action of the Potassium Sparring Diuretics?

A

Increase sodium excretion, reduce potassium excretion, Increase the urinary excretion of Na, Cl and H20

27
Q

What are the Potassium Sparring Diuretics used for?

A

Edema HTN Usually used in combo with thiazide loop diuretic to enhance natriuresis without potassium loss

28
Q

Catlyzes antithrombin inhibition of Xa and IIa (also IXa, XIa and XIIa)

A

Heparin

29
Q

LMWH’s - catalyze antithrombin inhibition of Xa

Subcutaneous

A

Enoxaparin

Dalteparin

30
Q

Direct Thrombin inhibitors

IV

A

Lepirudin

Bivalirudin

31
Q

Prodrug, Oral

Direct thrombin inhibitor that inhibits fibrin-bound and free thrombin

A

Dabigatran

32
Q

Reversible Xa inhibitor

Oral

A

Rivaroxaban

33
Q

Direct factor Xa Inhibitor

IV

A

Fondaparinux

34
Q

Heparin antagonist

A

Protamine sulfate

35
Q

Inhibits VKORC

Competitive inhibitor of vitamin K –> inactivation of II, VII, IX, X

A

Warfarin

36
Q

Binds fibrin

Activates fibrin-bound plasminogen –> plasmin = clot resolution

A

Tissue plasminogen activate (t-PA)

Alteplase

37
Q

Procoagulant - potent inhibitor of fibrinolysis

Blocks binding of plasmin to fibrin

A

Aminocaproic Acid

38
Q

Used as antiplatelet at low doses

Irreversible inhibitor of COX-1 in platelets

Inhibits platelet production of TXA2

A

Aspirin

39
Q

Phosphodiesterase inhibition,

Increase cAMP, decrease platelet aggregation

A

Dipyridamole

40
Q

Prodrugs

Act through P2Ya/P2Y12 receptors to inhibit G receptor activation

Increase cAMP

A

Ticlopidine

Clopidogrel

Prasugrel

Ticagrelor

41
Q

Glycoprotein IIb/IIIa receptor blocker

Fab fragment monoclonal antibody

Prevents binding of fibrinogen, vWF and other adhesive molecules

IV

A

Abciximab

42
Q

Glycoprotein IIb/IIIa receptor blocker

Cyclic heptapeptide

Block binding of fibrinogen activated platelets

IV

A

Eptifibatide

Pharmacology Block 2 (4 decks)

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