Hematology Week 1: Hemostasis Flashcards
(89 cards)
1
Q
Hemostasis Definition
A
The stopping of a flow of blood
2
Q
3 things that can kill the patient in seconds that are hemostatic disorders
A
Massive Stroke
Massive MI
Massive pulmonary embolism
3
Q
Disseminated Intravascular Coagulation
A
4
Q
The importance of balance in hemostasis
A
5
Q
Vasoconstriction
A
6
Q
Primary hemostasis
A
Platelet adhesion to injury sites
7
Q
Secondary Hemostasis
A
formation of a fibrin clot
8
Q
Fibrinolysis
A
enzymatic breakdown of fibrin clot
9
Q
The stages of hemostasis
4 listed
A
- Vasoconstriction
- Primary hemostasis
- secondary hemostasis
- Fibrinolysis
10
Q
Platelets
made in?
A
11
Q
Platelets
Lifespan?
A
12
Q
Platelets
The amount in circulation?
A
13
Q
Platelets
where are they?
A
14
Q
Functions of Platelets
4 Listed
A
- Stick to damaged epithelium
- Store ADP, Ca2+, proteins for coagulation
- Stack aggregate
- Surface phospholipids for coagulation reactions
15
Q
Anatomy of a platelet
Membrane Receptors
3 listed
A
- glycoprotein 1b
- Glycoprotein 2b-3a
- Platelet agonist receptors
16
Q
Anatomy of a platelet
Granules
A
- Alpha Granules
- Dense Granules
17
Q
Glycoprotein 1b
A
Surface receptor on platelets that binds Von Willebrand Factor (vWF)
18
Q
Glycoprotein 2b-3a
A
Surface receptors on platelet that bind fibrinogen
19
Q
Glycoprotein 6
A
Surface receptor on platelet that binds collagen
20
Q
Thromboxane A2
A
Surface receptor on platelet that binds
21
Q
ADP Receptor on platelets
A
22
Q
Platelet Alpha Granules Proteins
3 listed
A
Von Willebrand Factor
Fibrinogen
Factors 5, 8, 13
23
Q
Platelet Dense Granule chemicals
3 listed
A
- ADP/ATP
- Calcium
- Serotonin
24
Q
How are platelet granules released?
A
released upon platelet activation aiding hemostasis
25
Platelet adhesion and aggregation inhibition
endothelium secretes
NO
PGI2
ADPase
to inhibit platelet adhesion and aggregation
26
Endothelium secretes what to inhibit platelet activation
3 listed
NO
PGI2
ADPase
27
Platelet receptor that binds to von Willebrand Factor
Glycoprotein 1b
28
Platelet receptor that binds to collagen
Glycoprotein VI
29
Platelet receptor that binds fibrinogen and vWF
Glycoprotein IIb-IIIa
mainly binds Fibrinogen but binds some to vWF
30
Coagulation cascade
a series on enzymatic reactions that amplifies until there is a thrombin burst that overcomes the natural anticoagulants present and polymerizes fibrinogen into an insoluble fibrin clot sealing injured vessels
31
The receptor that allows platelets to:
initial attachment and activation
GPIb
32
The receptor that allows platelets to:
Activation and spreading
GPVI
33
The receptor that allows platelets to:
Aggregation
GPIIb-IIIa
34
35
Formation of a fibrin clot steps
Platelet surface
fibrinogen interacts with thrombin to form a fibrin clot
36
Fibrinogen is cleaved by?
the enzyme thrombin
releases fibrinopeptides and forms fibrin monomer
37
What crosslinks fibrin monomers to form fibrin polymers?
Factor 13
38
Fibrinogen polymerization to fibrin
39
What clotting factors need to work?
4 listed
* Clotting factor (FI-XIII)
* Phospholipids
* Calcium
* Co-factors (if necessary)
40
Thrombin generation common pathway
* the intrinsic and extrinsic thrombin generation pathways converge on the common pathway
* Factor X is where the extrinsic and intrinsic pathways converge
* Factor X and cofactor Factor V activate prothrombin to thrombin which cleaves fibrinogen to fibrin
41
Thrombin actions
42
Factor IIa
Thrombin
43
Factor II
Prothrombin
44
Factor VIIa Cofactor
Tissue Factor
45
The extrinsic pathway
Factor VII
46
Tissue factor is a?
Transmembrane receptor on cells outside of the circulation that binds Factor VIIa to activate the extrinsic pathway of coagulation
47
Are platelets needed for the extrinsic pathway?
No only need Factor VII to come in contact with Tissue Factor
48
The Intrinsic Pathway of Coagulation
49
Procoagulant proteins
50
Anti-coagulant Proteins
Also Anti-thrombin!!!
51
Anti-thrombin function
inactivate thrombin
52
Fibrinolysis
dissolution of fibrin clot
53
tPA function
Endothelial cells release tissue plasminogen activator after stimulation by thrombin
tPA binds tightly to fibrin
54
tPA AKA
Tissue plasminogen activator (tPA)
55
tPA & Factor XII activates
Plasminogen into plasmin
56
Plasminogen is cleaved into
Plasmin
57
Plasminogen is cleaved by?
tPA and Factor XII
58
Production of plasmin
59
Plasmin Function
cleaves fibrin into breakdown products
* fibrin degradation products
* D-dimers
60
D-dimers are formed by?
Plasmins cleavage of a fibrin clot
61
tPA is inactivated by?
Plasminogen activator inhibitor (PAI-1)
62
PAI-1 AKA
Plasminogen activator inhibitor
63
PAI-1 is released from?
The endothelium
64
65
The primary site of synthesis for most proteins involved with hemostasis?
Liver
66
67
Hemostatic proteins synthesized by the live
Procoagulants 2, 5. 7, 9, 10. 13
Anticoagulants: Protein C, Protein S, Anti-thrombin
Fibrinogen
Plasminogen
68
Chronic liver disease hemostatic consideration
can result in both bleeding and thrombosis
69
Vitamin K dependent facotrs and proteins for hemostasis
SNoTT Factors: Factor 7, 9, 10, 2
Protein C and S
70
GLA domain requires
* Vitamin K for carboxylation of the enzyme GLA domain
* GLA domains on factors bind Ca2+ which allows enzyme to bind phospholipid
71
What is a GLA domain
on clotting factors bind calcium and phospholipids
72
Intrinisic pathway relates to what test?
Partial Thromboplastin Time (PTT)
73
Extrinsic Pathway relates to what test?
Prothrombin Time
74
Prothrombin Time (PT)
evaluates the extrinsic pathway and common pathway
time it takes to take prothrombin to thrombin
75
Warfarin is monitored by this test
PT
76
PT reagent
Thromboplastin
77
Thromboplastin
Reagent for PT made of tissue factor and phospholipid
78
INR
79
INR is not designed for?
Patients with liver disease
80
PTT AKA
PArtial Thromboplastin Time
81
PTT
evaluates intrinsic pathway and common pathway
82
hypercoagulable state considerations
4 listed
* increased procoagulant factors
* decreased anticoagulant factors
* reduced fibrinolysis
* increased fibrin degradation products
83
Neonates hemostatic considerations
3 listed
* lower levels of procoagulant factors compared to adults
* lower amount of intrinsic pathway factors
* Vitamin K factors also lower (prophylactic Vitamin K is given at birth)
84
Why is vitamin K given to neonates?
Vitamin K factors are lower at birth
85
Coagulation in different life stages
86
Three parts of the circulatory system
3 listed
87
Arterial hemostatic considerations
Platelets are more active here
antiplatelet agents for preventing arterial thrombosis (Myocardial infarctions)
88
Venous hemostatic considerations
2 listed
Clotting factors are more active here
anticoagulants targeting clotting factors for preventing venous thrombosis
89
Microcirculation hemostatic considerations
2 listed
* Large endothelial surface
* Platelet dysfunction is observable here
