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Pharma: Cardiovascular System > Chapter 20: Blood Drugs > Flashcards

Chapter 20: Blood Drugs Flashcards

1
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor aspirin?

A

MOA: decrease the formation of a clot; inhibits thromboxane A2 synthesis from arachidonic acid in platelets by irreversible acetylation of serine; this prevents archidonic acid from binding and inhibits COX1 which occurs in the portal circulation

indications: prophylactic treatment of transient cerebral ischemia, reduce incidents of MI, decrease mortality in pre/post MI patients
pharmokinetics: repeated infusion with aspirin has a cumulative effect on the function of platelets; used in combo with heparin or clopidogrel

adverse effects: higher doses inhibit prostacyclin formation, hemmorhagic strokes, GI bleeds

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2
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Triclopidine?

A

MOA: irreversibly inhibit binding of ADP to platelet receptors which inactivates GP IIb/IIIa receptors which are required for the platelets to bind to fibrinogen and to each other

indications: prevention of transient ischemia ttack and strokes; used with aspirin after coronary stent implantation

pharmokinetics:

adverse effects: neutropenia/agranulocytosis, TTP, aplastic anemia

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3
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Clopidogrel?

A

MOA: irreversibly inhibit binding of ADP to platelet receptors which inactivates GP IIb/IIIa receptors which are required for the platelets to bind to fibrinogen and to each other

indications: prevention of atheroscleotic events; prophylaxis in acute coronary syndrome (ex unstable angina); prophylaxis in percutaneous coronary intervention; preferred in ischemic heart diseases
pharmokinetics: oral ingestion and undergo hepatic metabolism; eliminated fecally and through urine

adverse effects: black box warning for patients that are poor metabolizers

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4
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Prasugrel?

A

MOA: irreversibly inhibit binding of ADP to platelet receptors which inactivates GP IIb/IIIa receptors which are required for the platelets to bind to fibrinogen and to each other; newest ADP receptor antagonist

indications: decrease thrombotic cardiovascular events in patients with acute coronary syndrome; more effective than Clopidogrel in reducing cardiovascular death, nonfatal heart attack and nonfatal stroke
pharmokinetics: oral ingestion and undergo hepatic metabolism; eliminated fecally and through urine

adverse effects: black box warning for bleeding, strokes, abrupt discontinuation in patients undergoing percutaneous coronary interventions

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5
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Prasugrel?

A

MOA: irreversibly inhibit binding of ADP to platelet receptors which inactivates GP IIb/IIIa receptors which are required for the platelets to bind to fibrinogen and to each other; newest ADP receptor antagonist

indications: decrease thrombotic cardiovascular events in patients with acute coronary syndrome; more effective than Clopidogrel in reducing cardiovascular death, nonfatal heart attack and nonfatal stroke
pharmokinetics: oral ingestion and undergo hepatic metabolism; eliminated fecally and through urine

adverse effects: black box warning for bleeding, strokes, abrupt discontinuation in patients undergoing percutaneous coronary interventions

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6
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Abciximab?

A

MOA: block GP IIb/IIIa receptor that which inhibits platelet aggregation by preventing binding of fibrinogen and vWF so that aggregation doesn’t occur

indications: percutaneous coronary intervention to prevent cardiac ischemic complications; unresponsive unstable angina; prophylaxis in MI
pharmokinetics: given IV along with heparin or aspirin

adverse effects: potential for bleeding

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7
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Eptifibatide and Tirofiban?

A

MOA: block GP IIb/IIIa receptor

indications: can decrease the incidence of thombotic complciations associated with acute coronary syndrome
pharmokinetics: rapidly cleared in plasma; Eptifibatide is excreted by the kidney; Tirofiban unchanged by kidney and feces

adverse effects: bleeding

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8
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Eptifibatide and Tirofiban?

A

MOA: block GP IIb/IIIa receptor

indications: can decrease the incidence of thombotic complciations associated with acute coronary syndrome
pharmokinetics: rapidly cleared in plasma; Eptifibatide is excreted by the kidney; Tirofiban unchanged by kidney and feces

adverse effects: bleeding

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9
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Dipyridamole?

A

MOA: coronary vasodilator; decreases platelet adhesion to thrombogenic surfaces

indications: prophylactic treatment of angina pectoris; given in combo with aspirin or warfarin; inhibits embolization from prosthetic heart valves
pharmokinetics: inhibits cyclic nucleotide phosphodiesterase which increases intracellular levels of cAMP which results in decreased thromboxane A2 synthesis

adverse effects: inappropriate use in elderly as a sole agent due to GI and orthostatic problems

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10
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Cilostazol?

A

MOA: vasodilator

indications: reduce symptoms of intermittent cla

pharmokinetics:

adverse effects:

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11
Q

What is the MOA, indications, pharmokinetics and adverse effects of the platelet aggregation inhibitor Cilostazol?

A

MOA: vasodilator

indications: reduce symptoms of intermittent claudication, treatment of Buerger disease, vascular sclerosis complicating diabetes, chronic cerebral ischemia
pharmokinetics: inhibits phosphodiesterase type III which increases cAMP levels in platelets preventing platelet aggregation and promotes vasodilation of blood vessels

adverse effects: decreases levels of plasma triglyceridesl increases HDL; headaches and GI problems ; contraindicated in patients with CHF

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12
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thrombin inhibitors (anticoagulants)?

A

MOA: binds to antithrombin III and inactivates coagulation factors thrombin (factor IIa) and Factor Xa

  • LMWHs complex with antithrombin III and inactivate Factor Xa but do not bind to thrombin
  • LMWHs are less likely to activate resting platelets

indications: prevent/treat acute DVT; treatment of PE and acute MI;
- prevent fibrin formation; coagulant of choice in pregnant women with prosthetic heart valves or venous thrombosis since these agents don’t cross the placenta

pharmokinetics: heparin inject IV acts within minutes; LMWH subcutaneous injection acts within hours
- heparin must be given parenterally since it doesn’t readily cross membranes and it is administered as a bolus to achieve immediate anticoagulation

adverse effects: bleeding complications(managed with protamine sulfate), HS, thombosis, thombocytopenia, abnormal liver function tests

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13
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thrombin inhibitor dabigatran etexilate?

A

MOA: direct thrombin inhibitor

indications: prevention of stroke and systemic embolus in patients with atrial fibrillation
pharmokinetics: oral anticoagulant

adverse effects: bleeding

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14
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the anticoagulant Lepirudin?

A

MOA: highly specific thombin antagonist with little effect on platelet aggregation

indications: treatment of HIT and other thomboembolic disorders and prevent further thombotic complications
pharmokinetics: administered IV; eliminated in urine

adverse effects: bleeding and about half of patients develop antibodies to this drug

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15
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the anticoagulant of Argatroban?

A

MOA: directly inhibits thombin

indications: prophetically for the treatment of thrombosis in patients with HIT, approved for percutaneous coronary interventions in patients at risk for having HIT
pharmokinetics: parenteral anticoagulant; metabolized by liver

adverse effects: bleeding

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16
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the anticoagulant Fondaparinux?

A

MOA: selectively inhibits antithrombin III which neutralizes the actions of Factor Xa

indications: prophylaxis of DVT; used in combo with warfarin for treatment of acute pulmonary embolism and acute DVT
pharmokinetics: subcutanous; eliminated in the urine

adverse effects: bleeding episodes but thombocytopenia is not a problem and this agent may be used in patients with HIT

17
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the anticoagulant Fondaparinux?

A

MOA: selectively inhibits antithrombin III which neutralizes the actions of Factor Xa

indications: prophylaxis of DVT; used in combo with warfarin for treatment of acute pulmonary embolism and acute DVT
pharmokinetics: subcutaneous; eliminated in the urine

adverse effects: bleeding episodes but thombocytopenia is not a problem and this agent may be used in patients with HIT

18
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Vitamin K antagonists? ex: Warfarin

A

MOA: warfarin treatment causes production of clotting factors with low activity due to lack of sufficient gamma-carboxyglutamyl side chains

indications: used to prevent acute DVT or PE after initial heparin treatment; prophylactically used in patients with acute MI, prosthetic heart valves and chronic atrial fibrillation
pharmokinetics: oral administration; 100% bioavailability; 99% plasma protein bound so it does not diffuse into CSF, urine, or breast milk; readily crosses placental barrier

adverse effects: bleeding disorders, drug interactions (sulfonamides), contraindicated in pregnancy since it is teratogenic and can cause abortion

19
Q

What is the MOA, indications, pharmokinetics, and adverse effects of thombolytic drugs in general?

A

MOA: all act to cleave plasminogen to plasmin which cleaves fibrin causing lysis of thrombi; clots are more resistant to lysis the more they age so initiate therapy earlier

indications: not really used anymore in DVT and PE because there is too high of a risk of serious bleeding; but they are still used in catheter and shunt function to prevent occlusion; also used to resolve clots in strokes
pharmokinetics: intracoronary delivery however they are usually administered IV since this route is more rapid, inexpensive and doesn’t have the risk of catheterization

adverse effects: hemmorhage; contraindicated in patients with healing wounds, pregnancy, history of cerebrovascular events, head trauma, intracranial bleeding, and metastatic cancer

20
Q

What is the MOA, indications, pharmokinetics, and adverse effects of thombolytic drugs in general?

A

MOA: all act to cleave plasminogen to plasmin which cleaves fibrin causing lysis of thrombi; clots are more resistant to lysis the more they age so initiate therapy earlier

indications: not really used anymore in DVT and PE because there is too high of a risk of serious bleeding; but they are still used in catheter and shunt function to prevent occlusion; also used to resolve clots in strokes
pharmokinetics: intracoronary delivery however they are usually administered IV since this route is more rapid, inexpensive and doesn’t have the risk of catheterization

adverse effects: hemmorhage; contraindicated in patients with healing wounds, pregnancy, history of cerebrovascular events, head trauma, intracranial bleeding, and metastatic cancer

21
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thombolytic drug Alteplase?

A
  1. 9MOA: low affinity for free plasminogen but rapidly activates plasminogen that is bound to fibrin in a thrombus; at low doses it has the advantage of lysing only fibrin
    indications: treatment of MI, massive PE, acute ischemic stroke; superior to streptokinase in dissolving older clots
    pharmokinetics: administered in a total dose of 0.9mg/kg

adverse effects: bleeding complications, GI, cerebral hemorrhage

22
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thombolytic drug Streptokinase?

A

MOA:

indications:

pharmokinetics:

adverse effects:

23
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thombolytic drug Urokinase?

A

MOA:

indications:

pharmokinetics:

adverse effects:

24
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thombolytic drug Streptokinase?

A

MOA: unspecific and systemic hydrolysis of fibrin plugs

indications: acute PE, DVT, acute MI, arterial thombosis, occluded shunts
pharmokinetics: administered within 4 hours of acute MI for 1hr

adverse effects: bleeding disorders; HS since streptokinase is a foreign protein that is antigenic

25
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thombolytic drug Urokinase?

A

MOA: cleaves arginine-valine bond of plasminogen to yield active plasmin

indications: only approved for lysis of PE, treatment of acute MI, arterial thromboembolism, coronary artery thrombosis and DVT
pharmokinetics: rapidly cleared by the liver

adverse effects: bleeding

26
Q

What is the MOA, indications, pharmokinetics, and adverse effects of the thombolytic drug Urokinase?

A

MOA: cleaves arginine-valine bond of plasminogen to yield active plasmin

indications: only approved for lysis of PE, treatment of acute MI, arterial thromboembolism, coronary artery thrombosis and DVT
pharmokinetics: rapidly cleared by the liver

adverse effects: bleeding

27
Q

What is the MOA, indications, pharmokinetics, and adverse effects of drugs used to treat bleeding?
ex: Aminocaproic acid and tranexamic acid
Protamine sulfate
Vitamin K
Aprotinin

A

Aminocaproic acid and tranexamic acid: inhibit plasminogen activation; potential side effect is intravascular thrombosis

Protamine sulfate: antagonize heparin; side effect is HS

Vitamin K: slow effects; therefore if immediate action is required, fresh frozen plasma should be administered

Aprotinin: stops bleeding by blocking plasmin; it can inhibit streptokinase; may cause renal dysfunction and HS

28
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Iron used to treat anemia?

A

restore the iron balance and correct iron deficiency seen in microcytic anemia
-adverse effects are GI disturbances

29
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Folic Acid used to treat anemia?

A

treatment of megaloblastic anemia

30
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Cyanocobalamin used to treat anemia?

A

in patients with bariatic surgery, vitamin B12 is needed in large doses

31
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Erythroporetin and darbepoetin used to treat anemia?

A

regulates blood proliferation and differentiation in bone marrow

  • effective in treating anemia caused be end stage renal disease, anemia caused in immunodeficient patients, and anemia caused by cancer
  • delay onset of action: not used in acute treatment of anemia
  • side effects include elevation in BP and arthralgia
  • in patients treated with erythropoetin, the dose should not exceed a hemoglobin level of 12g/dL since serious cardiovascular events, increased risk of death, and shortened time to tumor progression have been observed
32
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Hydroxyurea used to treat sickle cell disease?

A

increases fetal Hgb levels which dilutes the abnormal hemoglobin
-important side effect is bone marrow suppression and cutaneous vasculitis

33
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Pentoxifylline used to treat sickle cell disease?

A

-improves erythrocyte flexibility

34
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Pentoxifylline used to treat sickle cell disease?

A
  • improves erythrocyte flexibility and reduces viscosity of blood
  • decreases total peripheral vascular resistance, improves blood flow, enhances tissue oxygenation in patients with peripheral vascular disease

Pharma: Cardiovascular System (7 decks)

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