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House Pharmacology > Anti Coagulants > Flashcards

Anti Coagulants Flashcards

1
Q

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

A

solidify

invasive substances

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2
Q

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

T/F

A

T

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3
Q

Coagulation

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

A

activation, adhesion and aggregation

fibrin

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4
Q

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

A

T

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5
Q

Coagulation is a complicated subject.
T/F

A

T

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6
Q

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

A

three

Primary hemostasis

Two

Three

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7
Q

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

1._________
2.__________
3.____________

A

Vasoconstriction

Platelet plug

Secondary hemostasis

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8
Q

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

A

Vasoconstriction

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9
Q

Vasoconstriction

When injury occurs, vessel walls _______, causing ________________

A

constrict

reduced blood flow to the site of injury.

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10
Q

Platelet plug are activated when _____________________.

They stick together acting as a “_____ .”

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

A

platelets aggregate to the site of the injury

plug

fibrin clot

secondary hemostasis.

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11
Q

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

A

F

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

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12
Q

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

A

blood clotting factors

the formation of fibrin.

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13
Q

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.

A

clotting cascade

fibrinogen; fibrin

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14
Q

The fibrin proteins stick together forming a ______.

A

clot

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15
Q

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

T/F

A

F

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

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16
Q

Extrinsic pathway

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

A

external trauma

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17
Q

Which pathway is faster

Intrinsic or extrinsic

A

Extrinsic

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18
Q

____________ pathways involves factor VII.

A

Extrinsic

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19
Q

Intrinsic pathway

The intrinsic pathway is activated by ______________.

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

A

trauma inside the vascular system

platelets, exposed endothelium

Collagen

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20
Q

Intrinsic pathway

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

A

Slower

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21
Q

Which pathway is more important

Extrinsic or intrinsic

A

Intrinsic

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22
Q

Intrinsic pathways

It involves factors ______,_____,______,______

A

XII, XI, IX, VIII.

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23
Q

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

A

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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24
Q

Thrombin System

_______ ions must be present for the thrombin system to begin

A

Calcium

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25
Q

Thrombin System

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

A

fibrin

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26
Q

Thrombin System

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

A

clumping together

web

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27
Q

Thrombin System

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

A

Red blood

clot

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28
Q

Thrombin and Thrombolytics

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

A

prothrombin

catalyzing conversion of fibrinogen to fibrin.

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29
Q

Thrombin and Thrombolytics

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

A

fibrinolytic

breakdown (lysis)

medication

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30
Q

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

A

break up or dissolve blood clots

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31
Q

An immediate blood clot can lead to ________

A

Thrombosis

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32
Q

clot-busting drugs – also known as ________ agents

A

thrombolytic

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33
Q

The most commonly used clot-busting drugs : include:

•______________
•________________
•__________________
•_____________
•____________
• ——————

A

TNKase (tenecteplase)

Abbokinase, Kinlytic (rokinase)

Streptase (streptokinase, kabikinase)

t-PA (class of drugs that includes )

Eminase (anistreplase)

Retavase (reteplase)

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34
Q

Haemophilia

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

A

the ability of the blood to clot

bleed severely

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35
Q

Haemophilia

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

A

hereditary

a coagulation factors

VIII; IX

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36
Q

Platelets

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

A

surface

sticky

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37
Q

Vitamin K

is an essential factor

T/F

A

T

38
Q

Vitamin K

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

A

carboxyl

glutamic acid

2,7,9, &10

39
Q

Vitamin K

adds funtional group to protein ___,____,_____

A

S, C, & Z.

40
Q

Consequences of Blood Clotting Problems

Blood clotting could be dangerous and can lead to:

1._______
2._________

A

Strokes

Heart attacks.

41
Q

Consequences of Blood Clotting Problems

Conversely, the opposite which is bleeding can lead to:

1.________

A

Haemorrhage

42
Q

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.

A

thrombosis; blood clot

deep vein

embolism; strokes

artrial fibrillation

43
Q

Classifications of Anticoagulants
Parenteral Anticoagulants

_________
_____________

A

Indirect thrombin inhibitors
Direct thrombin inhibitors

44
Q

Classifications of Anticoagulants; Parenteral Anticoagulants

Indirect thrombin inhibitors which are:

-_________
-_____________

Direct thrombin inhibitors
-_________ (Inhibitor of thrombin)

A

Heparins; Low molecular weight heparins

Lepirudin

45
Q

Classifications of Anticoagulants: Oral Anticoagulants

________ derivatives

_________ thrombin inhibitors

__________ derivative

_______________ inhibitors

A

Coumarin

Oral direct

Indandione

Direct factor Xa

46
Q

Classifications of Anticoagulants: Oral Anticoagulants

Coumarin derivatives : ________,________

Oral direct thrombin inhibitors (_____________)

Indandione derivative (_____________)

Direct factor Xa inhibitors (______________)

A

dicumarol, warfarin

dabigatran etexilate

phenindione

Rivaroxaban

47
Q

Heparin

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

A

naturally

basophils and mast cells

48
Q

Heparin

Heparin disintegrates clots that have already formed.

T/F

A

F

Heparin does not disintegrate clots that have already formed.

49
Q

Heparin

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

A

clot lysis mechanisms

fibrinolysis

previously formed

50
Q

Heparin

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

A

thrombokinase

51
Q

Heparin is given _______ or _______ for treatment and prevention

A

intravenously or subcutaneously

52
Q

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

A

thrombinp, thromboplastin, and prothrombin

53
Q

Heparin

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

A

thromboplastin

prothrombin to thrombin

thrombin on fibrinogen

fibrin

54
Q

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

T/F

With reason

A

T

because it is cost-effective.

55
Q

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

T/F

A

F

similar

56
Q

Low molecular weight heparin

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

A

LOVENOX

Xa and IIa

57
Q

Warfarin

is a (natural or synthetic?) derivative of ________, a chemical found naturally in —————-

it _____eases blood coagulation by interfering with _________

A

synthetic

coumarin

many plants

decr; vitamin K metabolism

58
Q

Warfarin is an oral medication
T/F

A

T

59
Q

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 _____)

A

DVT

PE

60
Q

The most common side effects of warfarin are ________ and ______

A

bleeding and bruising

61
Q

Warfarin side effect

The bleeding can be in the form of __________ from ___________

A

prolonged bleeding from cuts

62
Q

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

A

regular blood testing

International Normalized Ratio (INR)

how much longer it takes the blood to clot when oral anticoagulant drug is used

63
Q

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

A

K

II, VII, IX and X

protein C, protein S and protein Z

64
Q

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

A

an orally

Large

factor Xa

65
Q

Rivaroxaban

There are no significant interactions between food, antacids, digoxin, aspirin, naproxen , etc

T/F

A

T

66
Q

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

T/F

A

T

67
Q

Dicumarol

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

A

oral

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

liver

68
Q

Dicumarol

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

A

naturally

nontoxic; coumarin

69
Q

Dicoumarol is starting to largely replace warfarin

T/F

A

T

70
Q

Dicoumarol is used especially in preventing and treating _________ disease

Formerly called ______________

A

thromboembolic

bishydroxycoumarin

71
Q

Antiplatelets

Also known as _________

They decrease ________ and inhibit ______

are effective in (arterial or venous?) circulation.

A

anti-aggregants.

platelet aggregation

thrombus formation.

arterial

72
Q

Mechanism of Action of antiplatelets

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

A

prostaglandins and thromboxane

Irreversible

cyclooxygenase (COX)

73
Q

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.

A

COX

platelet activation

platelet activation

adherence of platelets

74
Q

Classes/Classifications of Antiplatets

____________ inhibitors (irreversible)

________________________ inhibitors

_____________________ (PAR-1)

—————- inhibitors (2B/3A)

______________ inhibitors.

____________ inhibitors

A

Cyclooxygenase (COX)

Adenosine Diphosphate (ADP) receptors

Protease Activated Receptor 1

Glycoprotein

Adenosine Reuptake (ARU)

Thromboxane

75
Q

Common Examples Of Drug Classifications
Cyclooxygenase (COX) inhibitors (irreversible) e.g - ______

Adenosine Diphosphate (ADP) receptors inhibitors e.g - _________,_______

A

Aspirin

Clopidogrel
-Ticlopidine

76
Q

Ticlopidine

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

A

Oral; platelet-aggregation

platelet-aggregation

77
Q

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

Aspirin or ticlopidine

A

Ticlopidine

Aspirin

78
Q

ticlopidine

May be used for patients who are intolerant or to aspirin.

T/F

A

T

79
Q

Clopidogrel

Selectively inhibits ___________________

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

A

the binding of adenosine diphosphate (ADP) to its platelet receptor.

platelet aggregation

blocking the amplification of
platelet activation

80
Q

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 ____

A

2 hours

75

first

3; 7

81
Q

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

A

single 300

75

82
Q

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

T/F

A

F

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

83
Q

Antifibrinolytic agents

Examples

______ acid

________ acid

A

Tranexamic

Aminocarproic

84
Q

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

A

plasmin

85
Q

Tranexamic acid

Often prescribed for __________

It competitively inhibits ________________

It degrades ______

A

excessive bleeding.

the activation of PLASMINOGEN TO PLASMIN.

FIBRIN

86
Q

Prostacyclin (PGI2) Analogue
–___________________

Glycoprotein IIB/IIIA receptors antagonists
–________ –_______ –_______

A

Epoprostenol

Abciximab; Eptifibatide; Tirofiban

87
Q

Adenosine Diphosphate Antagonists

– Reversible
______,______

– Irreversible
______,_______,_______

A

Ticagrelor Cangrelor

Ticlopidine Clopidogrel Prasugrel

88
Q

Thromboxane inhibitors

– Thromboxane synthase inhibitors
___________

Thromboxane receptor antagonists
____,______,_____

A

Dazoxiben

Terutroban Daltroban Sultroban

89
Q

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

A

Vorapaxar

90
Q

Phosphodiesterase inhibitor (PDEI)/ Adenosine Reuptake Inhibitor

–______

___________

____________

A

Dipyridamole – Pentoxifylline – Cilostazol

91
Q

HEPARIN WARFARIN

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

A

Parenteral (IV & SC); oral
Blood; liver

Rapid; Slow

Hours; days

PTT (intrinsic pathway); PT/INR extrinsic

NO; YES

Protamine sulphate; vitamin K

92
Q

ANTI-FIBRINOLYTIC
CLASSIFICATION & EXAMPLES Aminocaproic acid
Tranexamic acid
_________

A

Aprotinin

House Pharmacology (50 decks)

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