Anti Coagulants Flashcards
When there is an injury, Blood begins to ______ to prevent excessive blood loss and to prevent ________ from entering the bloodstream.
solidify
invasive substances
Coagulation will occur instantaneously once a blood vessel has been severed.
T/F
T
Coagulation
The mechanism of coagulation involves ______,_______, and ________ of platelets, as well as deposition and maturation of ________.
activation, adhesion and aggregation
fibrin
Coagulation begins almost instantly after an injury to the endothelium lining a blood vessel.
T/F
T
Coagulation is a complicated subject.
T/F
T
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
To stop bleeding, the body relies on the interaction of three processes
1._________
2.__________
3.____________
Vasoconstriction
Platelet plug
Secondary hemostasis
___________ is the body’s first response to injury in the vascular wall.
Vasoconstriction
Vasoconstriction
When injury occurs, vessel walls _______, causing ________________
constrict
reduced blood flow to the site of injury.
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.
Platelets alone are enough to secure the damage in the vessel wall.
F
Platelets alone are not enough to secure the damage in the vessel wall.
Secondary hemostasis is the activation of the _________ in a series of cascade complex to bring about ____________
blood clotting factors
the formation of fibrin.
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
The fibrin proteins stick together forming a ______.
clot
The clotting cascade occurs through two separate pathways that do not interact
T/F
F
The clotting cascade occurs through two separate pathways that interact, the intrinsic and the extrinsic pathway.
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
Which pathway is faster
Intrinsic or extrinsic
Extrinsic
____________ pathways involves factor VII.
Extrinsic
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
Intrinsic pathway
This pathway is (faster or slower?) than the extrinsic pathway
Slower
Which pathway is more important
Extrinsic or intrinsic
Intrinsic
Intrinsic pathways
It involves factors ______,_____,______,______
XII, XI, IX, VIII.
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
Thrombin System
_______ ions must be present for the thrombin system to begin
Calcium
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
T
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
T
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
T
rivaroxaban have been noted suggesting that dose adjustment of rivaroxaban would not be required when these agents are concurrently administered
T/F
T
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
T
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
T
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
