Brainscape's Knowledge GenomeTM

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


See full index

BECOM II Exam 5 > Clotting & Blood flow I&II > Flashcards

Clotting & Blood flow I&II Flashcards

1
Q

can platelet activation alone stop a large bleed?

A

no - need help from activation of coagulation cascade

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

role of fibrinolysis

A

removes the blood clot to restore blood flow to the repaired blood vessel

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

collagen

A

plays a role in platelet aggregation and activation

-normally hidden under endothelial lining

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

hemostasis

A

prevents blood loss from broken blood vessel

  • primary –> vascular spasm, platelet plug
  • secondary –> blood coagulation (clotting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

platelets

A

formed from megakaryocytes in bone marrow

  • no nuclei, have mitochondria for ATP
  • removed by tissue macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

prostacyclin (PGI2) and NO

A

inhibit platelet activation and aggregation

  • inhibited by COX2
  • vasodilate to increase laminar blood flow or directly prevent platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

heparan sulfate

A

activate antithrombin preventing blood clot

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

thrombomodulin

A

inhibit thrombin activation preventing coagulation

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

tissue factor inhibitor

A

inhibit tissue factors preventing coagulation

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

2 ways to inhibit platelet aggregation?

A
  1. endothelial integrity - collagen hidden

2. laminar flow by PGI2 and NO

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

role of ADP in platelet aggregation

A

needed for aggregation

  • ectonucleotidases –> break nucleotides –> no ADP or platelet aggregation
  • adenosine –> compete w/ ADP binding spot –> inhibit aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

GP 1b-5-6

A

receptor on platelet - binds to vWF attached to collagen

-do not recognize free vWF

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

GP 1a/2a and GP 6

A

bind collagen directly

-target for therapy

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

GP 2b/3a

A

most important - cannot be active all the time

-bind FREE vWF and fibrinogen to begin platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

thromboxane A2

A

secreted from activated platelets but also activates platelets (+ feedback)
-made from COX –> NSAIDs inhibit synthesis and coagulation

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

alpha vs. dense granules

A

release contents when platelets are activated

  • alpha = release fibrinogen, vWF, coagulation factor 5
  • dense = release ADP, Ca++
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

von willebrand factor

A

made in multimers

  • deficient in ADAMTS13 –> outoaggregation of platelets leading to thrombosis and thrombotic thrombocytopenia purpura (TTP)
  • binds collagen for GP 1a-5-9
  • increase half life of factor 8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ca++ during platelet activation

A

activation increases Ca++ levels –> myosin/actin interaction –> filopodial shape to clot easier and increase SA for binding
-do not coagulate without Ca++

19
Q

what results in the binding of ADP (to P2Y receptor) or thromboxane A2?

A

activate GP 2b/3a –> bind fibrinogen and vWF –> meshwork for platelet aggregation (platelet plug)
-GP 2b/3a inactive form until needed

20
Q

role of fibrinogen

A

connects the platelets together forming a weak plug

-GP 2b/3a binds the free fibrinogen and vWF to aggregate the platelets - does not need collagen

21
Q

what is the goal of coagulation cascade?

A

convert fibrinogen to fibrin and cross-link to make stronger

  • classical (intrinsic and extrinsic)
  • contemporary
22
Q

which factor combines with 11a to break 10 to 10a?

A

factor 8a

-8a + 11a forms intrinsic X-ase

23
Q

which factor combines with 10a converting prothrombin to thrombin?

A

5a

5a + 10a forms prothrombin complex

24
Q

what combines with tissue factor in extrinsic pathway?

A

7a

TF + 7a forms extrinsic X-ase which breaks 10 to 10a

25
Q

hemophilia

A

occurs with tissue factor mutation

-cannot do intrinsic or extrinsic pathways –> no coagulation

26
Q

what is required for platelet aggregation interconnecting with coagulation cascade?

A
  • neg charge surface on platelets from phospholipids

- Ca2+ for linking together

27
Q

role of thrombin

A
  • covert fibrinogen to fibrin
  • activate tissue factor 13 to cross link fibrin (strong)
  • also activate tissue factor 5,8,11
  • activates intrinsic mechanism
28
Q

what forms intrinsic tenase (Xase)?

A

factor 9a and 8a

-activate 10a

29
Q

what forms extrinsic tenase (Xase)?

A

tissue factor and 7a (factor 3)

-activate 10a

30
Q

what forms prothrombinase?

A

factor 10a and 5a

-convert prothrombin to thrombin

31
Q

contemporary model

A

-extrinsic (initiation) activates intrinsic (amplification) after producing thrombin

32
Q

what does thrombin activate in the contemporary pathway?

A
  • 11 –> 11a
  • 8 –> 8a combining with 9a (intrinsic Xase)
  • 5 –> 5a
  • increase platelet activation, fibrinogen, vWF
33
Q

difference b/w contemporary and classical model

A
  • contemporary - form thrombin 1st through extrinsic model then activate intrinsic
  • classical - do not need thrombin to activate intrinsic (have factor 12)
34
Q

protein C

A

thrombin inhibition

  • thrombomodulin (endothelium) binds with thrombin –> activate protein C –> inactivate 5a and 8a
  • requires protein S cofactor
35
Q

antithrombin

A

normal endothelium

-bind to heparan sulfate to inactivate thrombin, 9a, 10a, 11a –> stop coagulation

36
Q

tissue factor pathway inhibitor

A

normal endothelium

-inhibit 10a and 12a tissue factor complex –> stop coagulation

37
Q

role of Ca2+ in coagulation

A
  • platelet aggregation, change shape, and forming complexes

- hemophilia with hypocalcemia

38
Q

role of vitamin K in coagulation

A

coenzyme for synthesis for clotting factors

  • deficiency –> bleeding
  • warfarin can inhibit recycling
39
Q

role of plasmin

A

degrades the blood clot by chewing off fibrin –> forms D dimers (high levels in DVT)
-recombinant plasminogen activators to prevent blood clots

40
Q

petechiae

A

common platelet deficiency, not common coagulation deficiency
-platelet aggregation stops the bleeding for leaky capillary

41
Q

thrombocytopenia vs. thrombocytosis

A 
thrombocytopenia = bleeding tendency 
thrombocytosis = coagulation tendency
42
Q

prothrombin time

A

tissue factor + phospholipids + Ca2+

  • INR - standardization of plasma to see how good tissue factor is working
  • fast coagulation
  • use if on warfarin or suspected vit. K deficiency
43
Q

partial prothrombin time

A

phospholipids + Ca2+ + silica

  • no tissue factor or standardization –> rely on intrinsic pathway
  • slower coagulation

BECOM II Exam 5 (24 decks)

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