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
Q
theories to explain why thrombi occur
A
- 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
Q
embolus
A
a thrombus that is moved by the blood away from its site of formation
27
Q
pulmonary embolism
A
an embolus that lodges in the lungs
28
Q
infarct
A
an area of tissue necrosis that results from a sudden insufficiency of blood flow
29
Q
list of anticoagulants
A
- Aspirin (acetylsalicylic acid)
- Sodium citrate
- ethylenediaminetetraacetic acid (EDTA)
- Heparin
- Warfarin (Coumadin)
30
Q
Aspirin
A
- acetylsalicylic acid
- anticoagulant that works by permanently damaging the ability of platelets to clump
31
Q
sodium citrate
A
- anticoagulant
- can prevent the clotting of blood in test tubes by binding to calcium
32
Q
ethylenediaminetetraacetic acid (EDTA)
A
- anticoagulant
- prevents clotting of blood in test tubes by binding to calcium
33
Q
Heparin
A
- 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
Q
Warfarin
A
- 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
Q
gamma-glutamyl carboxylase
A
- hepatic enzyme
- adds a carboxyl group to glutamic acid residues on factors II (prothrombin), VII, IX, and X
- Vitamin K is oxidized
36
Q
vitamin K epoxide reductase
A
- hepatic enzyme that reduces vitamin K back to its active form
37
Q
vitamin K deficiency causes
A
- 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
Q
PIVKAs
A
- 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
Q
ribaroxaban
A
- Xarelto
- oral anticoagulant that directly inhibits activated factor X
40
Q
DIC
A
- 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
Q
Triggers of disseminated intravascular coagulation
A
- obstetrical complications
- infection
- cancer
- transfusion reaction
42
Q
treatment for DIC
A
- low dose of heparin
- fresh frozen plasma to replace depleted clotting factors
