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PDA Block 2 > PDA Block 2 Week 3 > Flashcards

PDA Block 2 Week 3 Flashcards

1
Q

Fenoldopam

A

Glomerulus Vasodilator: increases renal blood flow without reducing glomerular filtration–> decreases FF–> reduces protein concentration and osmotic force–>reduces net reabsorption–> sodium excretion increases increases Na/K pump in distal tubule–> hypokalemia Weak diuretic–> Limited use

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2
Q

Dopamine

A

Glomerulus Vasodilator: increases renal blood flow without reducing glomerular filtration–> decreases FF–> reduces protein concentration and osmotic force–>reduces net reabsorption–> sodium excretion increases increases Na/K pump in distal tubule–> hypokalemia Weak diuretic. Dopamine agonists may be used to increases RBF in shock

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3
Q

Atriopeptin

A

Glomerulus Vasodilator: increases renal blood flow without reducing glomerular filtration–> decreases FF–> reduces protein concentration and osmotic force–>reduces net reabsorption–> sodium excretion increases increases Na/K pump in distal tubule–> hypokalemia Weak diuretic–> Limited use

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4
Q

Mannitol

A

Proximal/ ascending limb/distal tubule Non-reabsorbed solute limits the reabsorption of water from tubule. Sodium reabsorbed without water increases Na/K pump in distal tubule–> hypokalemia IV administration. Prophylaxis of acute renal failure. Edema. Glaucoma Related to volume overload and expansion of intravascular fluid volume

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5
Q

Acetazolamide

A

carbonic anhydrase inhibitor Blocks bicarbonate reabsorption–> blocks sodium reabsorption in proximal tubule. Increases urine pH. Lumenal: Na/ H+ and basolateral Na+/HCO3- increases Na/K pump in distal tubule–> hypokalemia. Excretion of Na, K, HC03 increases. Excretion of Cl- falls Glaucoma. Alkalinize urine to decrease drug toxicity.Treat symptoms of acute altitude sickness Metabolic acidosis–> reduces renal response to drug

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6
Q

Furosemide

A

Ascending LOH inhibits NaK2Cl : inhibit active Cl- reabsorption. 20-30% of filtered load of sodium is excreted increases Na/K pump in distal tubule–> hypokalemia Potent Diuretic ( rapid onset and short in duration). Management of edema due to cardiac, hepatic, or renal disease. Acute pulmonary edema. Hypertension Hyperglycemia.Hypokalemia. Hyperuricemia. Ototoxicity. Volume depletetion

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7
Q

Bumetanide

A

Ascending LOH inhibits NaK2Cl : inhibit active Cl- reabsorption. 20-30% of filtered load of sodium is excreted increases Na/K pump in distal tubule–> hypokalemia Potent Diuretic ( rapid onset and short in duration). Management of edema due to cardiac, hepatic, or renal disease. Acute pulmonary edema. Hypertension Hypokalemia. Hyperuricemia. Ototoxicity. Volume depletetion

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8
Q

Ethacrynic Acid

A

Ascending LOH inhibits NaK2Cl : inhibit active Cl- reabsorption. 20-30% of filtered load of sodium is excreted increases Na/K pump in distal tubule–> hypokalemia Potent Diuretic ( rapid onset and short in duration). Management of edema due to cardiac, hepatic, or renal disease. Acute pulmonary edema. Hypertension Hypokalemia. Hyperuricemia. Ototoxicity. Volume depletetion

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9
Q

Chlorothiazide

A

Cortical segment of ascending LOH inhibits Na/Cl co-transporter. Reduces GFR increases Na/K pump in distal tubule–> hypokalemia. Increases urate reabsorption in proximal tubule. Decreases exceretion of ca. Increase excretion of Na, Cl, K Diuresis is rapid (1hr) and long in duration. Management of edema in congestive heart failure. Hypertension. Manage hypercalciuria Hypokalemia, Hyperuricemia, Hyperglycemia

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10
Q

Hydrochlorothiazide

A

Cortical segment of ascending LOH inhibits Na/Cl co-transporter. Reduces GFR increases Na/K pump in distal tubule–> hypokalemia. Increases urate reabsorption in proximal tubule. Decreases exceretion of ca. Increase excretion of Na, Cl, K Diuresis is rapid (1hr) and long in duration. Management of edema in congestive heart failure. Hypertension. Manage hypercalciuria Hypokalemia, Hyperuricemia, Hyperglycemia

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11
Q

Metolazone

A

Cortical segment of ascending LOH inhibits Na/Cl co-transporter. Reduces GFR increases Na/K pump in distal tubule–> hypokalemia. Increases urate reabsorption in proximal tubule. Decreases exceretion of ca. Increase excretion of Na, Cl, K Diuresis is rapid (1hr) and long in duration. Management of edema in congestive heart failure. Hypertension. Manage hypercalciuria Hypokalemia, Hyperuricemia, Hyperglycemia

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12
Q

Spironolactone

A

distal tubule competitive antagonist of aldosterone= K+ sparing. Na+ excretion increases. K+ excretion decreases Weak diuretic. Hypertension. Refractory edema. Primary aldosteronism. Use with thiazide/Loop diuretic to reduce K+ lost Hyperkalemia. Gynecomastia ( Spironolactone>Eplerenon)

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13
Q

Eplerenone

A

distal tubule competitive antagonist of aldosterone= K+ sparing. Na+ excretion increases. K+ excretion decreases Weak diuretic. Hypertension. Refractory edema. Primary aldosteronism. Use with thiazide/Loop diuretic to reduce K+ lost Hyperkalemia. Gynecomastia ( Spironolactone>Eplerenon)

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14
Q

Triamterene

A

Principal cells of CD Inhibits ENaC–> decreases Na entry–> decrease Na/K exchange. At high dose:Triamterene reduces GFR Na+ excretion increases. K+ excretion decreases Weak diuretic. Used with thiazide or loop diuretic to reduce K+ loss. Treat edema or HTN Hyperkalemia ( don’t give with K+ supplements); Azotemia- mild

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15
Q

Amiloride

A

Principal cells of CD Inhibits ENaC–> decreases Na entry–> decrease Na/K exchange. At high dose: amiloride blocks Na/H and Na+ excretion increases. K+ excretion decreases Weak diuretic. Used with thiazide or loop diuretic to reduce K+ loss. Treat edema or HTN Hyperkalemia ( don’t give with K+ supplements); Azotemia- mild

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16
Q

Heparin (UFH)

A

Anti-thrombin Bind directly to AT. Catalyzes the inhibition of coagulation factors by AT. Binding induces a conformation change in AT that makes reactive site more accessible to protease. Catalyzes the inhibition of Xa IV administration (large size); Does not cross placenta; immediate onset; Monitor via aPTT Venous Thromboembolism: bolus injection followed by continuous IV infusion (aPTT of 1.8 to 2.5x normal = therapeutic. Cardiopulmonary bypass: Very high dose/aPTT prolonged indefinitely. Treat unstable angina/acute MI. Prophylactic use of heparin to prevent venous thrombosis (subQ) Bleeding. Heparin-induced thrombocytopenia (IgG mediated 1. Active bleeding; 2. recent surgery-intracranial, sp. Cord, eye 3. Severe uncontrolled HTN

17
Q

Enoxaparin

A

Low molecular weight heparins (LMWH) Catalyzes the inhibition of Xa Not absorbed in GI mucosa, given parenterally, longer half life than heparin (4-6 hrs), clearence by kidneys Treatment of acute DVT; prophylaxis of DVT; acute unstable angina and MI; hip replaecement surgery Incidence of bleeding is less in patients; incidence of thrombocytopenia is also lower compared to heparin 1. Active bleeding; 2. recent surgery-intracranial, sp. Cord, eye 3. Severe uncontrolled HTN 4. renal impairement

18
Q

Dalteparin

A

LMWH Catalyzes the inhibition of Xa Not absorbed in GI mucosa, given parenterally, longer half life than heparin (4-6 hrs), clearence by kidneys Treatment of acute DVT; prophylaxis of DVT; acute unstable angina and MI; hip replaecement surgery Incidence of bleeding is less in patients; incidence of thrombocytopenia is also lower compared to heparin 1. Active bleeding; 2. recent surgery-intracranial, sp. Cord, eye 3. Severe uncontrolled HTN 4. renal impairement

19
Q

Lepirudin

A

Binds to catalytic site and extended recognition site of thrombin Direct thrombin inhibitor administered intravenously; excreted by kidneys (T1/2= 1.3 hours) use as an alternative to heparin I patients undergoing coronary angioplasty or cardiopulmonary bypass surgery Bleeding, use cautiously in patients with renal failsure 1. Active bleeding; 2. recent surgery-intracranial, sp. Cord, eye 3. Severe uncontrolled HTN 4. renal impairement

20
Q

Bivalirudin

A

occupies catalytic site of thrombin with seqeuence that binds to exosite (Thrombin can regain function by cleavage) Direct thrombin inhibitor adminsitered intravenously. Excreted by kidneys. T1/2=25 minutes use as an alternative to heparin I patients undergoing coronary angioplasty or cardiopulmonary bypass surgery Bleeding, use cautiously in patients with renal failure 1. Active bleeding; 2. recent surgery-intracranial, sp. Cord, eye 3. Severe uncontrolled HTN 4. renal impairement

21
Q

Fondaparinux

A

Direct Factor Xa inhibitor Direct Factor Xa inhibitor: causes AT-mediated selective inhibition of factor Xa SubQ, reaches peak plasma levels in 2 hours and excreted in urine (1/2=17 hr) Prophylaxis of DVT in hip/ knee replacement, treat acute MI. Prophylaxis in patients with history of heparin-induced cytopenia Bleeding, Hemorrhage 1. Active bleeding; 2. recent surgery-intracranial, sp. Cord, eye 3. Severe uncontrolled HTN 4. renal impairement

22
Q

Protamin sulfate

A

Heparin antagonist low MW positively charged molecule that has high affinity for negatively charged molecules. Binding with Heparin–> formation of inactive complex. Used to reverse heparin following cardiopulmonary bypass. Weak anti-coagulant properies, can cause anaphlyactic reactions (fish). Can cause severe pulmonary hypertension

23
Q

Warfarin

A

Vitamin K antagonist Vit K–> required to cause conversion of inactive precursors of II, VII IX and X into active forms. Carboxylation reaction that results in Ca2+ binding sites for coagulation. Oral administration. Monitored by Prothrombin time (PT). Therapeutic effect is delayed (circulating factors are not affected). Rapidly absorbed extensively bound, . CYP2C9 metabolism Long term treatment of thromboembolic diasease, prophylaxias against thromboembolism in pt with prosthetic heart valves, atrial fibrillation Risk of bleeding( treat by discontinuing drug). Immediate reversal of warfarin requires fresh frozen plasma with active clotting factors CYP2C9, vitamin K deficiency, kindey disease. Genetic variations in CYP2C9 and VKORC1

24
Q

Dabigatran

A

reversible, direct thrombin inhibitor prodrug that is converted to active form that inhbits free and fibrin bound thrombin. In hibits coagulation by preventing thrombin-mediated effects ( including fibrinogen–> fibrin, activation of factors, inhibit thrombin induced platelet aggregation) oral administration. Half life is 14-17 hours. Eliminated via kidneys. Post-op thromboprophylaxis in pts with hip/knee replacement. Prevent stroke and systemic embolism in pt with novaular atrial fibrillation comparable to warfarin. risk of bleeding when used with pts with renal impairment Is a substrate for Pgp- do not co-administer with Pgp inducers

25
Q

Rivaroxaban

A

reversible, direct thrombin inhibitor binds directly to factor Xa (inhibit catalyzation of converstion from prothrombin–> thrombin) Oral administration. Half life of 5-9 hours. Dual mode of elimination ( eliminated in kidneys and metabolized by liver CYP. reduce risk of stroke and systemic embolism in pt with nonvalvular atrial fibrillation. NOAC (novel oral Anti-coagulant): achieves therpeutic anticoagulation withint hours and holds it longer than warfarin Risk of beeding substrate for PgP

26
Q

Tissue plasminogen activator (tPA)

A

endogenous activator breaks down clots by binding to fibrin and activates plasminogen–> plasmin (digests clots)

27
Q

Alteplase

A

binds fibrin binds fibrin with high affinity via lysine binding sites in amino terminus. Activates fibrin-bound plasminogen–> efficient degradation of clot fibrin Hemorrhage (lysis of fibrin at sites of injury, destroys clotting factors), incidence of bleeding is similar when pts receive streptokinase or alteplase; incidence of hemorrhage higher when therapy is combined with aspirin or heparin STEMI, acute ischemic stroke, pulmonary embolism active bleeding, recent surgery, GI bleeding, recent CVA, hermorrhage disorder, pregnancy

28
Q

Aminocaproic Acid

A

inhibitor of fibrinolysis binds to lysine binding sites of plasminogen and plasmin. Blocks binding of plasmin–> fibrin; competitive inhibitor of plasinogen to fibrin useful for treating Urinary tract bleeding

29
Q

Aspirin

A

Irreversible Cox 1/2 inhibitor Blocks thromboxane formation rapidly absorbed by Upper GI. Half life= 20 min. platelet cannot synthesize new COX enzyme–>single dose will inhibit enzyme for up to 10 days Induce bleeding and GI irritation MI Prophylaxis, acute phase of ischemic stroke

30
Q

Dipyridamole

A

Phosphodiesterase inhibition/ blockage of adenosine uptake ( increase cAMP) inhibits platelet aggregation (cAMP) oral administration Headache, GI upset, dizziness Prevention of thromboemboli (with warfarin) in patients with prosthetic heart valves

31
Q

Ticlopidine

A

inhibit ADP binding to P2Y12 Receptor inhibit ADP binding to P2Y12 receptor. (ADP released from activated platelets binds to P2Y1 and P2Y12 on platelet surface to induce aggregation) Irreversible Prodrug ( metabolized by CYP 2C19) Risk of bleeding, can cause neutropenia

32
Q

Clopidogrel

A

inhibit ADP binding to P2Y12 Receptor inhibit ADP binding to P2Y12 receptor. (ADP released from activated platelets binds to P2Y1 and P2Y12 on platelet surface to induce aggregation) Irreversible Prodrug ( metabolized by CYP 2C19) Risk of bleeding; activation of clopidogrel (CYP2c19) in potentially inhibited by H+ pump inhibitors unstble angina,STEMI, stroke, recent MI

33
Q

Prasugrel

A

inhibit ADP binding to P2Y12 Receptor inhibit ADP binding to P2Y12 receptor. (ADP released from activated platelets binds to P2Y1 and P2Y12 on platelet surface to induce aggregation) Irreversible prodrug that undergoes esterase mediated hydrolysis. Higher potency and more rapid onset, more consistent level of inhibition than clopidogrel Risk of bleeding reduce rate of thrombolytic events

34
Q

Ticagrelor

A

inhibit ADP binding to P2Y12 Receptor inhibit ADP binding to P2Y12 receptor. (ADP released from activated platelets binds to P2Y1 and P2Y12 on platelet surface to induce aggregation) Reverrsible not a prodrug Risk of bleeding, dyspnea use with aspirin for preventing thrombotic events in pts with UA, NSTEMI, STEMI

35
Q

Abciximab

A

Glycoprotein Iib/IIIa receptor blocker Fab fragment against platelet BP Iib/IIIa receptors to prevent fibrinogen binding and cross-linking. IV adminstration; function half life of 12-24 minutes risk of bleeding prevent plaletet aggregation and thrombosis in pts undergoing percutaneous cornoary interventions (coronary angioplasty and stent placement) Use with heparin or LMWH

36
Q

Eptifibatide

A

Glycoprotein Iib/IIIa receptor blocker competitive reveresible inhibitor of fibrinogen binding to GP Iib/IIIa IV administration; renal clearance. Platelet response returns to normal after 4-8 hours after discontinuing drug risk of bleeding; use with caution in pts with renal impairement unstable angina, MI (incombination with LMWH). 1. prevent coronary thrombosis in unstable angina or NSTEMI 2. prevent thrombosis in pt for cornary angioplasty or stent placement for STEMI

PDA Block 2 (3 decks)

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