Anti Coagulants Flashcards by Iseoluwa Ojo

When there is an injury, Blood begins to ______ to prevent excessive blood loss and to prevent ________ from entering the bloodstream.

solidify

invasive substances

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Coagulation will occur instantaneously once a blood vessel has been severed.

T/F

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Coagulation

The mechanism of coagulation involves ______,_______, and ________ of platelets, as well as deposition and maturation of ________.

activation, adhesion and aggregation

fibrin

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Coagulation begins almost instantly after an injury to the endothelium lining a blood vessel.
T/F

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Coagulation is a complicated subject.
T/F

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To stop bleeding, the body relies on the interaction of ____ processes in which the _________ involves the first ____ of the _____ processes

three

Primary hemostasis

Two

Three

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To stop bleeding, the body relies on the interaction of three processes

1._________
2.__________
3.____________

Vasoconstriction

Platelet plug

Secondary hemostasis

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___________ is the body’s first response to injury in the vascular wall.

Vasoconstriction

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Vasoconstriction

When injury occurs, vessel walls _______, causing ________________

constrict

reduced blood flow to the site of injury.

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Platelet plug are activated when _____________________.

They stick together acting as a “_____ .”

They in turn activate the process which causes a _________ to form, known as ________

platelets aggregate to the site of the injury

plug

fibrin clot

secondary hemostasis.

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Platelets alone are enough to secure the damage in the vessel wall.

Platelets alone are not enough to secure the damage in the vessel wall.

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Secondary hemostasis is the activation of the _________ in a series of cascade complex to bring about ____________

blood clotting factors

the formation of fibrin.

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Coagulation factors

These factors activate each other in what is known as the __________. Whose end result m is that ________, a soluble plasma protein, is cleaved into ______, a nonsoluble plasma protein.

clotting cascade

fibrinogen; fibrin

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The fibrin proteins stick together forming a ______.

clot

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The clotting cascade occurs through two separate pathways that do not interact

T/F

The clotting cascade occurs through two separate pathways that interact, the intrinsic and the extrinsic pathway.

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Extrinsic pathway

extrinsic pathway is activated by _________ that causes blood to escape from the vascular system and get in contact with the damaged vessel.

external trauma

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Which pathway is faster

Intrinsic or extrinsic

Extrinsic

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____________ pathways involves factor VII.

Extrinsic

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Intrinsic pathway

The intrinsic pathway is activated by ______________.

The blood get in contact with ________ and is activated by _________,_________, chemicals, or ______.

trauma inside the vascular system

platelets, exposed endothelium

Collagen

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Intrinsic pathway

This pathway is (faster or slower?) than the extrinsic pathway

Slower

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Which pathway is more important

Extrinsic or intrinsic

Intrinsic

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Intrinsic pathways

It involves factors ______,_____,______,______

XII, XI, IX, VIII.

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FACTORS NAME
I ___________
II ___________
III ___________________
IV ______________
V _____________
VII _____________
VIII ________________
IX _____________
X _____________
XI _____________
XII ___________
XIII_____________

Fibrinogen
Prothrombin
Tissue factor or thromboplastin
Calcium
Proaccelerin (Labile factor)
Proconvertin (Stable factor)
Antihaemophilic factor A
Antihaemophilic factor B
Stuart-Prower factor
Hageman factor
Fibrin stabilising factor

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Thrombin System

_______ ions must be present for the thrombin system to begin

Calcium

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Thrombin System The activated clotting proteins/factors engage in a cascade of chemical reactions that finally produce a substance called ____

fibrin

Thrombin System Fibrin strands stick to the exposed vessel wall, _________ and forming a ______-like complex of strands

clumping together web

Thrombin System ___________ cells become caught up in the web, causing a _____

Red blood clot

Thrombin and Thrombolytics Thrombin is a proteolytic enzyme formed from _____ that facilitates the clotting of blood by __________

prothrombin catalyzing conversion of fibrinogen to fibrin.

Thrombin and Thrombolytics Thrombolysis, also called _______ therapy, is the _________ of blood clots formed in blood vessels, using ________.

fibrinolytic breakdown (lysis) medication

Thrombolytic therapy is the use of drugs to ________ or _________, which are the main cause of both heart attacks and stroke.

break up or dissolve blood clots

An immediate blood clot can lead to ________

Thrombosis

clot-busting drugs -- also known as ________ agents

thrombolytic

The most commonly used clot-busting drugs : include: •______________ •________________ •__________________ •_____________ •____________ • ——————

TNKase (tenecteplase) Abbokinase, Kinlytic (rokinase) Streptase (streptokinase, kabikinase) t-PA (class of drugs that includes ) Eminase (anistreplase) Retavase (reteplase)

Haemophilia is a medical condition in which _____________ is severely reduced, causing the sufferer to _______ from even a slight injury.

the ability of the blood to clot bleed severely

Haemophilia The condition is typically caused by a ______ lack of __________, most often factor ______ for haemophilia A and factor ____ for haemophilia B.

hereditary a coagulation factors VIII; IX

Platelets When bleeding occurs, chemical reactions change the _____ of the platelet to make it activated and become “ _______”

surface sticky

Vitamin K is an essential factor T/F

Vitamin K adds ________ group (functional group) to ________ residues on factors (____,____,____,____ )

carboxyl glutamic acid 2,7,9, &10

Vitamin K adds funtional group to protein ___,____,_____

S, C, & Z.

Consequences of Blood Clotting Problems Blood clotting could be dangerous and can lead to: 1._______ 2._________

Strokes Heart attacks.

Consequences of Blood Clotting Problems Conversely, the opposite which is bleeding can lead to: 1.________

Haemorrhage

Functions of Anticoagulants Stop _______ or sudden ______ Prevent ______ thrombosis Prevent pulmonary _________ Prevent Myocardial Infarctions Prevent ______ especially in those that are predisposed. Treat _______ in order to prevent stroke.

thrombosis; blood clot deep vein embolism; strokes artrial fibrillation

Classifications of Anticoagulants Parenteral Anticoagulants _________ _____________

Indirect thrombin inhibitors Direct thrombin inhibitors

Classifications of Anticoagulants; Parenteral Anticoagulants Indirect thrombin inhibitors which are: -_________ -_____________ Direct thrombin inhibitors -_________ (Inhibitor of thrombin)

Heparins; Low molecular weight heparins Lepirudin

Classifications of Anticoagulants: Oral Anticoagulants ________ derivatives _________ thrombin inhibitors __________ derivative _______________ inhibitors

Coumarin Oral direct Indandione Direct factor Xa

Classifications of Anticoagulants: Oral Anticoagulants Coumarin derivatives : ________,________ Oral direct thrombin inhibitors (_____________) Indandione derivative (_____________) Direct factor Xa inhibitors (______________)

dicumarol, warfarin dabigatran etexilate phenindione Rivaroxaban

Heparin Heparin is a (naturally or artificially?) -occurring anticoagulant produced by ________ and _______ to prevent formation and extension of blood clots

naturally basophils and mast cells

Heparin Heparin disintegrates clots that have already formed. T/F

F Heparin does not disintegrate clots that have already formed.

Heparin It permits the body's natural _________________________ , i.e. _________, to work normally to break down __________ clots

clot lysis mechanisms fibrinolysis previously formed

Heparin As the __________ is released, it neutralizes the action of heparin to allow clotting to occur

thrombokinase

Heparin is given _______ or _______ for treatment and prevention

intravenously or subcutaneously

Heparin works by inhibiting the three major clotting factors (________,_________,___________ )

thrombinp, thromboplastin, and prothrombin

Heparin It slows the process of ________ synthesis, decelerates the conversion of _______ to ________ , and inhibits the effects of ______ on ______, blocking its conversion to ______.

thromboplastin prothrombin to thrombin thrombin on fibrinogen fibrin

Low-molecular weight heparin is gradually replacing heparin for treatment of most patients with venous thromboembolism and acute coronary syndromes T/F With reason

T because it is cost-effective.

Low molecular weight heparin has different results to heparin administered by subcutaneous injection. T/F

F similar

Low molecular weight heparin ________® is an example (It lowers the activity of clotting proteins (__________) in the blood.

LOVENOX Xa and IIa

Warfarin is a (natural or synthetic?) derivative of ________, a chemical found naturally in —————- it _____eases blood coagulation by interfering with _________

synthetic coumarin many plants decr; vitamin K metabolism

Warfarin is an oral medication T/F

Warfarin stops the blood from clotting within the blood vessels and is used to stop existing clots from getting bigger (as in ________) and to stop parts of clots breaking off and forming emboli (as in _____)

DVT PE

The most common side effects of warfarin are ________ and ______

bleeding and bruising

Warfarin side effect The bleeding can be in the form of __________ from ___________

prolonged bleeding from cuts

Treatment with warfarin is monitored by ————— using the _______________, which is a measure of __________________

regular blood testing International Normalized Ratio (INR) how much longer it takes the blood to clot when oral anticoagulant drug is used

Warfarin inhibits the effective synthesis of biologically active forms of the vitamin ___-dependent clotting factors: ____,_____,_____,______ , as well as the regulatory factors ____,______, and _____

K II, VII, IX and X protein C, protein S and protein Z

Rivaroxaban Rivaroxaban is ______ available, (small or large?) -molecule, active site- directed _________ inhibitor

an orally Large factor Xa

Rivaroxaban There are no significant interactions between food, antacids, digoxin, aspirin, naproxen , etc T/F

rivaroxaban have been noted suggesting that dose adjustment of rivaroxaban would not be required when these agents are concurrently administered T/F

Dicumarol It is a potent (oral or IV?) anticoagulant that acts by _____________________ in the ______

oral inhibiting the synthesis of vitamin K-dependent clotting factors (prothrombin and factors VII, IX and X) liver

Dicumarol Dicumarol is produced _______ by conversion of (toxic or nontoxic?) _____ in moldy sweet clover hay, lespepeza hay or sweet vernal hay

naturally nontoxic; coumarin

Dicoumarol is starting to largely replace warfarin T/F

Dicoumarol is used especially in preventing and treating _________ disease Formerly called ______________

thromboembolic bishydroxycoumarin

Antiplatelets Also known as _________ They decrease ________ and inhibit ______ are effective in (arterial or venous?) circulation.

anti-aggregants. platelet aggregation thrombus formation. arterial

Mechanism of Action of antiplatelets They suppress the production of ________ and _______ due to their(reversible or irreversible?) inactivation of __________ enzymes.

prostaglandins and thromboxane Irreversible cyclooxygenase (COX)

Mechanism of Action of anti platelets ______ enzyme is required for synthesis of prostaglandins and thromboxane. They interfere with ________ process in primary hemostatis. They inhibit the process involved in _________ resulting in decreased _________ to one another.

COX platelet activation platelet activation adherence of platelets

Classes/Classifications of Antiplatets ____________ inhibitors (irreversible) ________________________ inhibitors _____________________ (PAR-1) —————- inhibitors (2B/3A) ______________ inhibitors. ____________ inhibitors

Cyclooxygenase (COX) Adenosine Diphosphate (ADP) receptors Protease Activated Receptor 1 Glycoprotein Adenosine Reuptake (ARU) Thromboxane

Common Examples Of Drug Classifications Cyclooxygenase (COX) inhibitors (irreversible) e.g - ______ Adenosine Diphosphate (ADP) receptors inhibitors e.g - _________,_______

Aspirin Clopidogrel -Ticlopidine

Ticlopidine (Oral or IV?) , ___________ inhibitor structurally (related or unrelate?) to any other agent in its class.

Oral; platelet-aggregation platelet-aggregation

Which is more efficacious? Which has less serious and less frequent adverse effect Aspirin or ticlopidine

Ticlopidine Aspirin

ticlopidine May be used for patients who are intolerant or to aspirin. T/F

Clopidogrel Selectively inhibits ___________________ Clopidogrel also inhibits ____________ induced by agonists other than ADP by ———————- by released ADP.

the binding of adenosine diphosphate (ADP) to its platelet receptor. platelet aggregation blocking the amplification of platelet activation

Clopidogrel Dose dependent inhibition of platelet aggregation can be seen ______ after single oral doses. Repeated doses of ____ mg per day inhibit ADP-induced platelet aggregation on the ____ day, and inhibition reaches steady state between Day ___ and Day ____

2 hours 75 first 3; 7

For patients with acute coronary syndrome (unstable angina), clopidogrel should be initiated with a ______ ——- mg loading dose and then continued at ____ mg once daily.

single 300 75

Aspirin (75 mg-325 mg once daily) should not be initiated or continued in combination with clopidogrel. T/F

F Aspirin (75 mg-325 mg once daily) should be initiated and continued in combination with clopidogrel.

Antifibrinolytic agents Examples ______ acid ________ acid

Tranexamic Aminocarproic

Aminocarproic acid It is an effective inhibitor for proteolytic enzymes like ______

plasmin

Tranexamic acid Often prescribed for __________ It competitively inhibits ________________ It degrades ______

excessive bleeding. the activation of PLASMINOGEN TO PLASMIN. FIBRIN

Prostacyclin (PGI2) Analogue –___________________ Glycoprotein IIB/IIIA receptors antagonists –________ –_______ –_______

Epoprostenol Abciximab; Eptifibatide; Tirofiban

Adenosine Diphosphate Antagonists – Reversible ______,______ – Irreversible ______,_______,_______

Ticagrelor Cangrelor Ticlopidine Clopidogrel Prasugrel

Thromboxane inhibitors – Thromboxane synthase inhibitors ___________ Thromboxane receptor antagonists ____,______,_____

Dazoxiben Terutroban Daltroban Sultroban

Protease-activated receptor-1 (PAR-1) antagonists –_________

Vorapaxar

Phosphodiesterase inhibitor (PDEI)/ Adenosine Reuptake Inhibitor –______ ___________ ____________

Dipyridamole – Pentoxifylline – Cilostazol

HEPARIN WARFARIN ROA Site of action Onset of action Duration of action Monitoring Pregnancy contradiction Antidote

Parenteral (IV & SC); oral Blood; liver Rapid; Slow Hours; days PTT (intrinsic pathway); PT/INR extrinsic NO; YES Protamine sulphate; vitamin K

ANTI-FIBRINOLYTIC CLASSIFICATION & EXAMPLES Aminocaproic acid Tranexamic acid _________

Aprotinin