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Pharmacology II > Blood Drugs > Flashcards

Blood Drugs Flashcards

1
Q

what are the 4 dysfunctions of blood

A

thrombosis, bleeding, circulation problems, and anemia

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2
Q

this is formation of a clot; causes MI, DVT, pulmonary embolism, acute ischemic stroke

A

thrombosis

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3
Q

this causes hemophilia and Vitamin K def

A

excessive bleeding

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4
Q

this is a stroke due to blockage

A

ischemic

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5
Q

this is a stroke due to bleeding

A

hemorrhagic

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6
Q

this is a clot the adheres to the vessel wall ; can be arterial or venous

A

thrombus

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7
Q

this thrombus clot is most often in medium sized vessels caused by atherosclerosis ; causes lesions on surface of endothelial cells

A

arterial thrombus

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8
Q

this thrombus clot is triggered by blood stasis or inappropriate activation of the coagulation cascade ; clot rich in fibrin

A

venous thrombus

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9
Q

what is an intravascular clot that floats in the blood

A

embolus

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10
Q

what are central to the process of hemostasis

A

platelets

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11
Q

this is cessation of blood loss from a damaged bv

A

hemostasis

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12
Q

what is the triggering stimulus for formation of a thrombus

A

pathologic condition

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13
Q

these monitor the integrity of the vascular endothelium ; circulate freely in the absence of injury; chemical mediators

A

resting platelets

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14
Q

which two chemical mediators are synthesized and act as inhibitors of platelet aggregration

A

prostacyclin and nitric oxide

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15
Q

this molecule binds to platelet membrane receptors ; receptors coupled to the synthesis of cAMP

A

prostacyclin

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16
Q

increased cAMP=

A

reduced ic Ca

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17
Q

T or F: damaged endothelial cells synthesize more prostacyclin

A

F; synthesize less ( decreased binding to receptors and lowers levels of cAMP)

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18
Q

platelet membrane has receptors for which molecules

A

thrombin, thromboxanes, and exposed collagen;

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19
Q

what is the platelet response to vascular injury

A

prostacyclin gears up- thrombin, thromboxanes, collagen activation- platelet adhesion- platelet activation- platelet aggregration - clot formation - fibrinolysis

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20
Q

what happens during the thrombin, thromboxane and exposed collagen response to vasulcar injury

A

circulating levels of thrombin and thromboxane are usually low > intact endothelium covers collagen in inner vascular layers > when occupied, the platelet receptors trigger a series of reactions that lead to platelet aggregation

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21
Q

in this part of platelet formation; there is an endothelial injury and platelets adhere to and cover the exposed collagen of the subendothelium

A

platelet adhesion

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22
Q

in this part of platelet formation; receptors on the surface of platelets are activated by the collagen ; caused morphologic changes in the platelets and the release of chemical mediators

A

platelet activation

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23
Q

what are some chemical mediators of platelet activation

A

ADP, Thromboxane A2, serotonin, platelet activation factor, thrombin

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24
Q

what do the chemical mediators of platelet activation do

A

they bind to circulating platelets and active the platelets -> aggregation begins

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25
Q

in this part of platelet formation , Ca increase inside platelets results in activation of glycoprotein receptors that bind fibrinogen; fibrinogen ( protein in plasma) binds to GP receptors on 2 separate platelets

A

platelet aggregation

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26
Q

in this part of platelet formation, thrombin Is formed as part of the activation and aggregation cascade; thrombin helps convert fibrinogen to fibrin; cross linking of the fibrin strands stabilize the clot and forms a hemostatic platelet fibrin plug

A

clot formation

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27
Q

in this part of platelet formation, plasminogen is processed to plasmin ( fibrinolysin ) ;

A

fibrinolysis

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28
Q

what limits the growth of the clot and dissolves the fibrin network as wounds heal

A

plasmin

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29
Q

with this drug, platelet activation results in release of arachidonic acid from membrane phospholipids ; arachidonic acid is converted to prostaglandin H2 by Cox 1; prostaglandin H2 is converted to Thromboxane A2

A

aspirin

30
Q

this drug has a rapid effect; complete inactivation of platelets occurs with 160 mg daily use ; used mainly for prophylactic tx of stroke, reduced incidence of heart attack, and decreased mortality in heart attack pts

A

aspirin

31
Q

complications of this drug include increased incidence of hemorrhagic stroke and GI bleeding

A

aspirin

32
Q

what other drugs block COX-1

A

NSAIDS; can obstruct access of aspirin

33
Q

which drug is the only NSAID that irreversibly exhibits antithrombotic efficacy

A

Aspirin

34
Q

Are circulating platelets active or inactive

A

inactive

35
Q

fibrinogen is converted to fibrin by which molecule

A

thrombin

36
Q

this platelet aggregration inhibitor is used in the prevention of TIA and strokes in pts with previous event ; adjunct with aspiring following coronary stent implantation

A

ticlopidine

37
Q

this platelet aggregration inhibitor is used in the prevention of atherosclerotic events following recent heart attack or stroke

A

clopidogrel

38
Q

this platelet aggregation inhibitor is used to decrease thrombotic events in pts with acute coronary syndrome

A

prasugrel

39
Q

what are some adverse effects of Ticlopidine, clopidigrel, prasugrel, and ticagrelor ( platelet aggregation inhibitors)

A

prolonged bleeding, aplastic anemia, life threatening TTP

40
Q

term for when the body forms Ab against a gene coding for an important blood enzyme

A

TTP aka thrombotic thrombocytopenic purpura

41
Q

clopidogrel, prasugrel, and ticlopidine are all what types of drugs

A

pro drugs; they are also poor metabolizers which have higher rates of cardiovascular events ; can all three inhibit P450 system

42
Q

what type of toxicity is assoc with Ticlopidine

A

Phenytoin toxicity

43
Q

which of the platelet aggregation inhibitors does NOT require activation

A

Ticagrelor; this is the only one of the platelet aggr. inhibitors that is reversible thereby not inhibiting platelet function indefinitely

44
Q

with blood coagulation , how is fibrin formed

A

enzyme reactions produce factor Xa that converts prothrombin to thrombin

45
Q

what is the role of cell surfaces in blood coagulation

A

each rxn takes place at a localized active cell surface; complex made of membrane surface/ an enzyme/ a substrate/ and a cofactor

46
Q

T or F; coagulation should be restricted to the local site of vascular injury

A

T

47
Q

what are some endogenous inhibitors

A

Protein C, protein S, Antithrombin III, tissue factor pathway inhibitor

48
Q

this thrombin inhibitor is injectable and rapidly acting; high molecular weight protein ; used in the prevention of venous thrombosis , and in the tx of various thrombotic diseases

A

heparin

49
Q

this thrombin inhibitor is used in the tx of acute DVT and pulmonary embolism; decreases incidence of recurrent thromboembolic episodes; used during and after Sx to prevent postoperative thrombosis ; does not cross placenta

A

heparin

50
Q

adverse effects of this thrombin inhibitor include bleeding complications; hypersensitivity reactions; thrombosis ( causes reduction in antithrombin III activity); thrombocytopenia; CI in pts who have had Sx of the brain, eye, or spinal cord

A

heparin

51
Q

which direct thrombin inhibitor is a prodrug; used for prevention of stroke in pts with atrial fibrillation; oral anticoagulant ; side effect of bleeding

A

dabigatran ( pradaxa)

52
Q

this drug is a direct thrombin inhibitor; produced by recombinant DNA tech; pt can develop Ab which will slow renal elimination

A

Lepirudin

53
Q

this drug is a direct thrombin inhibitor; it is metabolized in the liver

A

argatroban

54
Q

these thrombin inhibitors selectively inhibit Factor Xa; does not have variable activity ; used in hip and knee Sx

A

Fondaparinux and Rivaroxaban

55
Q

this vit K antagonist was originaly developed as a rodenticide; now used as oral anticoagulant; high incidence of bleeding complications and large number of drug interactions

A

warfarins

56
Q

protein coagulation factors require Vitamin ____ as a cofactor for synthesis

A

Vitamin K

57
Q

which drug has a narrow Therapeutic index; 99 % bound to plasma albumin; and SHOULD NEVER be used in pregnancy

A

warfarin

58
Q

these drugs dissolve clots that have already been formed; they are used in acute thromboembolic disease; they activate the conversion of plasminogen to plasmin

A

thrombolytic drugs

59
Q

what can occur as a result of hemophilia or during complications in Sx; Tx is natural proteins Vit K or synthetic antagonists

A

bleeding

60
Q

what are some antibleeding meds

A

aminocaproic acid, protamine, and vitamin K

61
Q

condition caused by below normal plasma Hb concentration; caused by toxic effects of drugs; caused by nutritional def.

A

anemia

62
Q

this agent is used to treat anemia; its stored in intestinal mucosal cells; supplementation with ferrous sulfate is required; def. caused by blood loss, menstruation, and insuff intake during growth

A

iron

63
Q

this agent is used to treat anemia; def. caused by pregnancy, small intestine pathology, alcoholism; def. leads to megaloblastic anemia

A

folate ( folic acid)

64
Q

which tx of anemia is non toxic; rare hypersensitivity injections have been reported

A

folic acid

65
Q

agent used to treat anemia ; def result from low dietary levels, poor absorption ( pernicious anemia); results in megaloblastic anemia; side effects of nausea, HA, vomiting, and rhinitis

A

vitamin B12

66
Q

these are agents used to treat anemia caused by end stage renal disease, HIV , or Cx; HTN can result; Hb levels must be monitored

A

erythropoietin and darbepoetin

67
Q

this is a protein that regulates rbc proliferation and differentiation into the kidney

A

erythropoeitin

68
Q

what are some agents used to treat sickle cell

A

hydroxyurea and pentoxifylline

69
Q

this agent increases fetal Hb levels; prevents painful crises; bone marrow suppression can result

A

hydroxyurea

70
Q

this agent improves erythrocyte flexibility and reduces blood viscosity

A

pentoxyfylline

Pharmacology II (31 decks)

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