Blood Drugs Flashcards by Jessica Ward

what are the 4 dysfunctions of blood

thrombosis, bleeding, circulation problems, and anemia

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

thrombosis

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this causes hemophilia and Vitamin K def

excessive bleeding

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this is a stroke due to blockage

ischemic

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this is a stroke due to bleeding

hemorrhagic

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

thrombus

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

arterial thrombus

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

venous thrombus

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what is an intravascular clot that floats in the blood

embolus

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what are central to the process of hemostasis

platelets

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this is cessation of blood loss from a damaged bv

hemostasis

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what is the triggering stimulus for formation of a thrombus

pathologic condition

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

resting platelets

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

prostacyclin and nitric oxide

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

prostacyclin

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increased cAMP=

reduced ic Ca

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T or F: damaged endothelial cells synthesize more prostacyclin

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

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platelet membrane has receptors for which molecules

thrombin, thromboxanes, and exposed collagen;

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what is the platelet response to vascular injury

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

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

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

platelet adhesion

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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

platelet activation

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what are some chemical mediators of platelet activation

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

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what do the chemical mediators of platelet activation do

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

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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

platelet aggregation

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

clot formation

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

fibrinolysis

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

plasmin

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

aspirin

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

aspirin

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

aspirin

what other drugs block COX-1

NSAIDS; can obstruct access of aspirin

which drug is the only NSAID that irreversibly exhibits antithrombotic efficacy

Aspirin

Are circulating platelets active or inactive

inactive

fibrinogen is converted to fibrin by which molecule

thrombin

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

ticlopidine

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

clopidogrel

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

prasugrel

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

prolonged bleeding, aplastic anemia, life threatening TTP

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

TTP aka thrombotic thrombocytopenic purpura

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

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

what type of toxicity is assoc with Ticlopidine

Phenytoin toxicity

which of the platelet aggregation inhibitors does NOT require activation

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

with blood coagulation , how is fibrin formed

enzyme reactions produce factor Xa that converts prothrombin to thrombin

what is the role of cell surfaces in blood coagulation

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

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

what are some endogenous inhibitors

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

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

heparin

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

heparin

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

heparin

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

dabigatran ( pradaxa)

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

Lepirudin

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

argatroban

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

Fondaparinux and Rivaroxaban

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

warfarins

protein coagulation factors require Vitamin ____ as a cofactor for synthesis

Vitamin K

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

warfarin

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

thrombolytic drugs

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

bleeding

what are some antibleeding meds

aminocaproic acid, protamine, and vitamin K

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

anemia

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

iron

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

folate ( folic acid)

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

folic acid

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

vitamin B12

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

erythropoietin and darbepoetin

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

erythropoeitin

what are some agents used to treat sickle cell

hydroxyurea and pentoxifylline

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

hydroxyurea

this agent improves erythrocyte flexibility and reduces blood viscosity

pentoxyfylline