Exam 3 - Coagulation Flashcards
1
Q
prostacyclin
A
- PGI2
- type of prostaglandin
- secreted by endothelial cells
- acts as a vasodilator
- inhibits platelet aggregation
2
Q
nitric oxide
A
- NO
- secreted by endothelial cells
- acts as a vasodilator
- inhibits platelet aggregation
3
Q
CD39
A
- enzyme in the plasma membrane of endothelial cells
- active site faces the blood
- breaks down ADP
- inhibits platelet aggregation
4
Q
von Willebrand’s factor
A
- protein produced by endothelial cells
- binds to both collagen and platelets
- binding of glycoprotein receptors on the platelet’s membrane to VWF anchors the platelets to site of injury against force of blood flow
5
Q
platelet release reaction
and products released
A
- platelets contain secretory granules; when platelets stick to collagen, they degrandulate and release their products
- products released:
- adenosine diphosphate (ADP)
- serotonin
- thromboxane A2 (a prostaglandin)
6
Q
platelet plug
A
- ADP and thromboxane A2 released during platelet release reaction cause additional platelets to aggregate at the site of injury, forming a platelet plug
- this plug must be reinforced with fibrin strands
7
Q
fibrinogen and fibrin
A
- fibrinogen: soluble, liquid plasma protein
- fibrin: insoluble, solid fibrous protein
- activated platelets activate plasma clotting factors, converting fibrinogen into fibrin
- the plasma membrane of platelets has receptors for fibrinogen and fibrin, which promotes platelet aggregation and stabilizes the platelet plug
8
Q
clot retraction
A
contraction of the platelet mass that forms a more compact and effective plug
9
Q
serum
A
- fluid that is squeezed from the clot during clot retraction
- plasma without fibrinogen
10
Q
vitamin K-dependent clotting factors
A
- factor II
- factor VII
- factor IX
- factor X
- these clotting factors cannot be synthesized by the liver unless vitamin K is present
11
Q
factor XII
A
- protease
- first factor activated in the intrinsic pathway
12
Q
factor II
A
- prothrombrin
- vitamin K-dependent clotting factor
13
Q
intrinsic pathway
A
- the pathway that produces a clot of blood left in a test tube without the addition of any external chemicals
- initiated by exposure of plasma to hydrophilic surfaces in vitro (i.e. glass of a test tube) or to negatively charged structures such as collagen, polyphosphates, and neutrophil extracellular traps (NETs) in the exposed structures of a wound in vivo
- contact pathway
- plays an amplification role, increasing the clotting cascade initiated by the extrinsic pathway
14
Q
extrinsic pathway
A
- damaged tissues release a chemical that initiates a “shortcut” to the formation of fibrin
- clot formation is initiated by tissue factor that becomes exposed to factor VII and VIIa in the blood and forms a complex with factor VIIa
- the tissue factor greatly increased the ability of factor VIIa to activate factor X and factor IX
- clot formation is initiated by tissue factor that becomes exposed to factor VII and VIIa in the blood and forms a complex with factor VIIa
- initiates clot formation in vivo
15
Q
prothrombin
A
inactive glycoprotein that is converted into thrombin
16
Q
thrombin
A
active enzyme that converts fibrinogen into fibrin monomers
17
Q
common pathway
the presence of what two things are required?
A
- where the intrinsic and extrinsic pathways meet from factor X on
- requires the presence of Ca2+ (acts as an essential cofactor for the enzymatic activity of the clotting factors) and phospholipids (provided by platelets)
18
Q
organ that makes clotting factors
A
- liver
- this means that patients with liver disease will have diminished clotting proteins and if the liver disease is severe enough, hemorrhaging will occur due to impaired blood clotting
19
Q
tissue factor
A
- tissue thromboplastin or factor III
- a membrane glycoprotein found inside the walls of blood vessels (in the tunica media and tunica externa) and the cells of the surrounding tissues
- initiated extrinsic pathway
- also is released during the massive hemolysis of incompatible red blood cells that occurs during a transfusion reaction
- can lead to a severe clotting abnormality (DIC)
20
Q
phosphatidylserine
A
- becomes exposed at surfaces of platelets as they become activated and form a platelet plug
- anchors factor VIII and factor V complexes to the platelet surface, which greatly increased the formation of thrombin
21
Q
when a damaged blood vessel is repaired, activated factor promotes the conversion of an inactive molecule in plasma into the active form called
A
activated factor XII converts inactive molecule in plasma into the active form called kallikrein
22
Q
agents that convert plasminogen into active plasmin
A
- kallikrein
- tissue plasminogen activator (TPA)
- urokinase
- streptokinase (bacterial enzyme)
23
Q
plasmin
A
enzyme that digests fibrin into “split products” to promote dissolution of the blood clot
24
Q
thrombus
A
blood clot that obstructs a blood vessel
25
theories to explain why thrombi occur
* birth control pills
* smoking
* abnormal tendency to form clots (hypercoagulable state)
* inherited genetic defect
* i.e. *factor V Leiden* (present in 5% of Caucasian women)
* being bedridden
* abnormal vessel lining that serves to stimulate clot formation
* Atherosclerosis
* Varicose veins
* Phlebitis
* Infection
26
embolus
a thrombus that is moved by the blood away from its site of formation
27
pulmonary embolism
an embolus that lodges in the lungs
28
infarct
an _area of tissue necrosis_ that results from a sudden insufficiency of blood flow
29
list of anticoagulants
* Aspirin (acetylsalicylic acid)
* Sodium citrate
* *ethylenediaminetetraacetic acid* (EDTA)
* Heparin
* Warfarin (Coumadin)
30
Aspirin
* acetylsalicylic acid
* anticoagulant that works by permanently damaging the ability of platelets to clump
31
sodium citrate
* anticoagulant
* can prevent the clotting of blood in test tubes by binding to calcium
32
*ethylenediaminetetraacetic acid* (EDTA)
* anticoagulant
* prevents clotting of blood in test tubes by binding to calcium
33
Heparin
* anticoagulant
* mucoprotein
* can be added to a test tube to prevent clotting
* activated *antithrombin III* (a plasma protein that combines with and inactivates thrombin)
* given _intravenously_ during medical procedures
* acts immediately
34
Warfarin
* Coumadin
* most commonly used oral anticoagulant
* blocks the cellular activation of vitamin K
* creates a deficiency of reduced vitamin K by blocking vitamin K epoxide reductase, thereby inhibiting maturation of clotting factors
* must be given for several days before it becomes effective
* takes a few days for existing vitamin K-dependent clotting factors to be used up
* important for preventing blood clot formation in people with atrial fibrillation and to treat venous thromboembolism
35
*gamma-glutamyl carboxylase*
* hepatic enzyme
* adds a carboxyl group to glutamic acid residues on factors II (prothrombin), VII, IX, and X
* Vitamin K is oxidized
36
*vitamin K epoxide reductase*
* hepatic enzyme that reduces vitamin K back to its active form
37
vitamin K deficiency causes
* Warfarin blocking vitamin K epoxide reductase
* malabsorption
* prolonged antibiotic therapy
* impaired vitamin K metabolism in disease (i.e. hepatic failure)
* these lead to PIVKAs
38
PIVKAs
* proteins induced in by vitamin K absence
* partially or totally non-gamma carboxylated, which affects the coagulation factor's ability to bind to phospholipid
39
ribaroxaban
* Xarelto
* oral anticoagulant that directly inhibits activated factor X
40
DIC
* Disseminated intravascular coagulation
* when a potent stimulant of coagulation enters the blood and stimulates widespread diffuse blood clotting which can be so severe as to use up available platelets and clotting proteins (resulting in *consumptive coagulopathy*) so that hemorrhaging may ensue
41
Triggers of disseminated intravascular coagulation
* obstetrical complications
* infection
* cancer
* transfusion reaction
42
treatment for DIC
* low dose of heparin
* fresh frozen plasma to replace depleted clotting factors
