Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > Coag > Flashcards

Coag Flashcards

1
Q

What is hemostasis?

A

The cessation of bleeding from a cut or severed vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the five hemostasis systems?

A 
Vascular
platelet
Coagulation
Anticoagulation
Fibrinolytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Deficiencies in any of the clotting systems can lead to what?

A

Hemorrhaging

Thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is vasoconstriction controlled by?

A

Local factors by the tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the first response to a cut?

A

Local factors released to vasoconstrict

Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Activated platelets at the side of injury release what? What do these do?

A

Thromboxane (A2)
Serotonin

Stimulate vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does the coagulation system produce that induces blood vessel endothelial cells to produce endothelin 1?

A

Thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the function of endothelin 1?

A

Potent vasoconstrictor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Platelets adhere to the side of a vessel through what? What does this cause?

A

Surface glycoproteins receptors

Causes change in shape of platelets, and activates further platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is in the ECM that is exposed during an injury, and causes initial platelet binding? What is the receptor on the platelet?

A

von Willebrand factor (vWf)

Receptor = GP1-b-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Willebrand factor disease?

A

loss of vWf, leading to increased bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

After initial platelet tethering, what protein binds collagen in the ECM, that begins to activate platlets?

A

Platelet glycoprotein VI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of fibrinogen?

A

A moleculer glue between activated GPIIa/IIIb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the three granules that platelets release?

A
  1. Dense granules
  2. Alpha granules
  3. chemokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the function of GPIb-alpha on platelets?

A

Initial tethering of platelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the function of GPVI on platelets? What does it bind to?

A

Binds collagen to initially activate platelet and release ADP, 5HT, and TXA2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the fuction of GPIIb/IIa on platelets?

A

Facilitates platelet-platelet interactions whn joined with fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the active drug in plavex?

A

Clopidogrel (P2Y12)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is it important that clotting be reversible?

A

So that clots can be destroyed in places not needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is thrombosis?

A

Inappropriate clot formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

True or false: the coagulation and anticoagulation systems act in isolation of each other

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does vasoconstriction aid in the process of a clot formation?

A

Allows blood to flow more slowly, and allow platelets to have a better chance of adhering to an injury site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do platelets adhere to the site of vessel injury?

A

Through cell surface glycoproteins activation, forming finger-like extensions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do platelets recruit more of themselves to the site of injury?

A

Release factors (ADP and Ca)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the function of the initial platelet response? How strong is this?

A

Form a platelet plug–not very strong initially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where is von Willebrand factor found? What does it do?

A

Found in the plasma and ECM, until it encounters exposed collage in the ECM. It binds to this, and recruits platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens to the platelet after it binds to vWF?

A

The GPVI binds to collagen in the ECM injury site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does the platelet produce to recruit more of itself?

A

ADP, serotonin, and thromboxane A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the function of the factors that platelets produce (ADP, serotonin, and thromboxane A2) when bound to the ECM?

A

bind to G-protein coupled receptors on platelets already adhering to the injury site, to further activate them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the function of GPVI on platelets?

A

Binds to the collagen in the ECM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the protein that is on platelets that, when activated, allows for binding of fibrinogen?

A

GPIII/IIb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the function of the GPII/IIb protein found on platelets?

A

Binds fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is fibrinogen? Where is it produced and found?

A

Molecular glue for platelets

Produced by liver
Found in circulation in high amounts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the function of GpIIb/IIIa inhibitors in treating MIs?

A

Inhibit platelet aggregation that occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the function of the purinergic P2Y12 receptors on platelets? What is it activated by?

A

Activated by ADP, and facilitates the aggregation of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the MOA of Plavex?

A

Antagonist to P2Y12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the three G-coupled protein receptors on platelets?

A

Purinergic P2Y12
Protease activated receptors
Thromboxane A2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the two chemicals released by endothelial cells to inhibit platelet aggregation?

A

NO

PGI2 (prostacycline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do NO and PGI2 do after release from endothelial cells?

A

Vasodilate

Prevent platelet adhesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the charge on platelets? Endothelial cells? Why is this significant?

A

Both negative, meaning they repel each other when there is no damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the end result of the platelet system?

A

Loose platelet clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the function of the coagulation system? How does this compare to the platelet system?

A

Form insoluble fibrin clots that are much more secure than platelet plugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the protein from the coag system that cross links and forms a meshwork to trap blood and serum in a clot?

A

Fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the precursor form of fibrin? How is it turned into fibrin?

A

Fibrinogen, cleaved by a protease-Thrombin

45
Q

What is the function of thrombin? (2)

A

Cleaves fibrinogen to form fibrin monomers

Activates Factor XIII

46
Q

What activates factor XIII? What does it do?

A

Induces fibrin fibers to cross-link, forming a stable blood clot

47
Q

What is the precursor form of thrombin? How does it become activated?

A

Prothrombin

Formed by a complex cascade of coag factors

48
Q

What are the descriptive names for factors I, II, III, and IV?

A 
I = Fibrinogen
II = Prothrombin
III = Tissue factors
IV = Ca
49
Q

Where is prothrombin found? What produces it?

A

Plasma

Liver

50
Q

What are the two pathways that activate Prothrombin?

A

Extrinsic pathway

Intrinsic pathway

51
Q

What starts the extrinsic pathway?

A

Tissue damage

52
Q

What happens in the extrinsic pathway after the initial tissue damage (and factor III release)?

A

Factor VII activated

53
Q

What does factor VII do in the extrinsic pathway?

A

Activates factor X

54
Q

What does factor X do in the extrinsic pathway?

A

Activates factor 5, then thrombin

55
Q

What is the composition of tissue factor complex in the extrinsic pathway?

A

Factor VIIa
Ca

Activates factor X

56
Q

How can thrombin increase the rate of the extrinsic pathway activation?

A

Increases factor V

57
Q

What are the four components of the prothrombin activator complex? What does it do?

A

Factors X and V, Ca, and phospholipids

Increases thrombin activation

58
Q

How does the small amount of thrombin that is induced from the extrinsic pathway lead to an autocrine-like action to increase its activity?

A

Form the prothrombin activator complex

59
Q

How is the intrinsic pathway begun? What is the first factor to be activated?

A

Exposure of collagen leads to the activation of factor 12

60
Q

What is the order of activation of the factors in the intrinsic pathway?

A

12, 11, 9, 10

61
Q

What happens after factor 9 activation in the intrinsic coag pathway? How fast is this?

A

Factor 10 is activated slowly

62
Q

What does factor 10 activated in the extrinsic and intrinsic pathway?

A

Activates prothrombin into thrombin

63
Q

What are the components of the tenase complex in the intrinsic pathway?

A

factors 9 and 8
Ca
Phospholipids

64
Q

Hemophilia A is caused by a deficiency in what factor? What does this inhibit the assembly of?

A

VIII (8)

Thus there is no tenase complex

65
Q

Where do the extrinsic and intrinsic pathway converge?

A

at factor X

66
Q

Which factors require vitamin K for the activity?

A

2, 7, 9, and 10 (vit K was born in 1972, iff 1=10) also, S and C proteins

67
Q

What is the purpose of vit K in the production of coag factors?

A

Used as a cofactor in the carboxylation of key glutamate residues in the factors (allows Ca to bind)

68
Q

What is the MOA of Warfarin?

A

Blocks the reduction of Vit K after Vit K has been oxidized in the production of coag factors

69
Q

Why are newborns and liver pts given Vit K?

A

Vit K comes from gut flora and is fat soluble. If there is no flora (babes) or if there is no bile to take up fatty soluble vit K, then vit K deficiency results

70
Q

What does the activated partial thromboplastin time (aPTT or PTT) measure?

A

The speed of the intrinsic pathway

71
Q

How is the PTT done?

A

Pt’s anticoagulated plasma is placed in tube and mixed with phospholipids and a negatively charged bead. Ca is added later to initiate clotting

72
Q

What does the prothrombin time (PT) measure?

A

The speed of the intrinsic pathway

73
Q

How is the prothrombin time measurement performed?

A

Pt’s blood is collected into citrated anticoagulant. Then Ca is added in the presence of thromboplastin and time is measured

74
Q

What is the function of thrombomodulin?

A

Interacts with thrombin to inactivate it, by converting thromin into an anticoagulant enzyme

75
Q

Where is thrombomodulin found?

A

On endothelial cells

76
Q

What is the function of protein C? What activates it?

A

Activated by thrombomodulin/thrombin complex that degrades Factors Va and VIIIa

77
Q

What is factor V leiden thrombophilia?

A

Mutation in factor V prevents it from being inactivated by protein C complex

(=hypercoagulability)

78
Q

What would be the consequence of a deficiency in protein C?

A

hypercoagulability

79
Q

What would a deficiency in thrombomodulin cause?

A

Hypercoagulability

80
Q

What is the tissue factor that is secreted by endothelial cells, that reduces thrombin formation by inhibiting factor VIIa/tissue factor complex?

A

Tissue factor pathway inhibitor (TFPI)

81
Q

What is antithrombin (type of molecule, what produces it, where its found), and how does it work?

A

It is a circulating protease produced by the liver, that inhibits thrombin production, and destroys thrombin

82
Q

What does antithrombin need in order to become activated?

A

Heparin sulfate

83
Q

True or false: heparin and antithrombin both have anticoagulation effects alone, but work faster when bound together

A

False- antithrombin is slow, but works

Heparin has no intrinsic anticoagulation effect

84
Q

Where is heparin sulfate usually found?

A

Endothelial cells surface in low quantities

85
Q

What is the function of the fibrinolytic system? When and where does it work?

A

Degradation of fibrin clots (after an injury has healed or in inappropriate places)

86
Q

What is the main protease that cleaves fibrin is what?

A

Plasmin

87
Q

What is the inactivated state of plasmin? Where is it found, and what organ produces it?

A

Plasminogen, which is produced by the liver and is found circulating in the blood or in a clot

88
Q

What activates plasminogen to plasmin? Where is this substance produced?

A

tPA (tissue Plasminogen Activator)

Produced by vascular endothelial cells

89
Q

What are the two factors that inhibit tPA? Where are each of these found?

A

Plasminogen activator inhibitor (PAI)- endothelial cells

Alpha-2-plasmin inhibitor - circulation

90
Q

What happens to plasminogen when a clot form via platelets and fibrin? What happens when the clot produces tPA?

A

Become enmeshed in the clot.

When the clot slowly increases tPA production, allows plasminogen to become activated, and breaks up the clot

91
Q

Deficiency in which factor produces hemophilia A and which for B? What is the inheritance pattern of this?

A

8A
9B

This is an X-linked recessive trait

92
Q

Which are the factors involved in the extrinsic pathway (in order)?

A

3
7
10
5

93
Q

What are the factors that are in the intrinsic pathway (in order)?

A 
12
11
9
8
10
5
94
Q

Which clotting factor(s) is/are at the end of both the intrinsic and extrinsic pathway? What does this/ do these do?

A

factor 10 and 5

These combine to form the prothrombin activator

95
Q

What are the two factors that make up the prothrombin activator complex?

A

10 and 5

96
Q

Which clotting factor(s) is/are inhibited by thrombomodulin?

A

factor 5 and 8

97
Q

Describe the pathway that thrombomodulin takes to inhibit factor 5. (3ish steps)

A

Thrombomodulin bind thrombin
activation of protein C, then S

Inhibition

98
Q

Where is antithrombin found? Where is heparin found? What is the effect of them binding?

A

Antithrombin is circulating in the tissue
Heparin is on endothelial cell

Binding increases antithrombin activity

99
Q

What is the condition where there is not enough platelets to form a clot? What are the symptoms of severe cases of this?

A

Thrombocytopenia

Small purpurea d/t many tiny hemorrhages

100
Q

What is the effect of liver disease on clotting factors? How is this effected?

A

Reduces platelets and clotting factors through a lack of vit K uptake

101
Q

What is the enzyme that reduces Vit K back to its usable form?

A

VKOR

102
Q

What is the MOA of asprin’s anticoagulant ability?

A

Inhibits TXA2

103
Q

What are the pro-aggregation factors for platelets?

A
  1. TXA2

2. Lower Blood flow

104
Q

What are the anti-aggregation factors for platelets?

A
  1. PGI2 and NO

2. Higher blood flow

105
Q

What is bernard-Soulier syndrome?

A

A deficiency of GpIb, resulting in a lack of coagulation

106
Q

What is the drug that blocks GpIIb/IIIa?

A

abciximab

107
Q

What is Glanzmann thrombasthenia?

A

A deficiency of GpIIb/IIIa

108
Q

Which two factors comprise the Tenase factor?

A

8 and 9

Physiology (75 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions