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Block 7; Week 4-Michelle > Fung-Coagulation > Flashcards

Fung-Coagulation Flashcards

1
Q

What is hemostasis?

A

balance between clotting and thrombosis
Precisely orchestrated process involving platelets, clotting factors and endothelium
Occurs at the site of vascular injury and culminates in the formation of a blood clot

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2
Q

What are the 2 types of disorders of hemostasis?

A

Hemorrhagic

Thrombotic

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3
Q

What are the normal steps of hemostasis?

A
  1. vasoconstriction
  2. platelet aggregation
  3. fibrin formation
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4
Q

What’s involved in vasoconstriction?

A

Purpose: reduces blood flow to the area
MOA: mediated by reflex neurogenic mechanisms, augmented by secretion of endothelin
Lasts how long? Transient!

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5
Q

What is primary hemostasis?

A

aggregation of platelets on endothelium

beginnings of a clot

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6
Q

What is secondary hemostasis?

A

cascade of reaction b/c of exposure of tissue factor @ site of vascular injury
thrombin formation

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7
Q

What are the 3 layers of blood vessels?

A

Intima: endothelium
Media: smooth muscle
Adventitia: CT

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8
Q

What is the role of vascular endothelium in hemostasis?

A

Inhibiting platelets
Suppressing coagulation
Promoting fibrinolysis
Modulating vascular tone and permeability

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9
Q

What are antithrombotic agents?

A 
heparin
Protein C & Protein S
Tissue Plasminogen Activator
Prostacyclin
Nitric Oxide
Thrombomodulin
Protein C receptor
Tissue Factory Pathway Inhibitor (TFPI)
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10
Q

What are prothrombotic agents?

A 
Factor V
Tissue Factor
Plastinogen Activator INhibitor-1 (PAI-1)
Thromboxane
Platelet Activating Factor
vWF
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11
Q

WHich substance is released after vascular injury?

Which layers of the blood vessel mediate vasoconstriction?

A

Tissue Factor

Media & Adventitia

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12
Q

The presence of which 2 things sets the stage for platelet adherence & activation?

A

collagen

vWF

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13
Q

What is the role of heparin in the body?

A

anti-thrombin

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14
Q

What is the role of prostacyclin & NO in the body?

A

vasodilators…that’s why they are anti-thrombotic

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15
Q

Where do platelets come from? What do they consist of?

A

come from megakaryocytic
consist of no nucleus, but have a cytoskeleton & cytoplasmic granules
alpha & dense granules

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16
Q

Which are more numerous in platelets–alpha or dense granules?

A

alpha are more numerous!

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17
Q

What does GP Ib/V/IX on the cytoskeleton of the platelet bind?

A

vwf

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18
Q

What does GpIIb/IIIa bind?

A

fibrinogen

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19
Q

What does GP1c/IIa bind?

A

fibronectin

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20
Q

WHat does CD62P (P selection) do?

A

these are adhesion molecules

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21
Q

What does the thrombin receptor on platelets do?

A

initiates platelet activation

along with ADP (found in dense granules)

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22
Q

What does the GP1a/2a bind?

A

collagen

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23
Q

What are the red cell antigens on platelets?

A

ABO, P, I, i Le (no Rh)

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24
Q

Which substances are found in the alpha granules (more numerous)?

A 
alpha: 
vwf
fibrinogen
Factor V
Promotes Angiogenesis: VEGF, EGF, PDGF
Inhibits Angiogenesis: angiostatin, thrombospondin, endostatin
INflammatory Factors: PF-4, IL-8, CCL5
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25
Q

Which substances are found in dense granules?

A

ATP
ADP
Calcium
Serotonin

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26
Q

Describe platelet adhesion & aggregation after vascular injury.

A

Collagen & vwf exposed after injury
Unactivated Platelets adhere to gp1b receptor on vwf
GP2b3a receptor on platelets active & bind fibrinogen that cross links & causes aggregation!

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27
Q

Describe all that is involved in the activation of platelets.

A

shape change
release of granules, including ADP in the dense ones
initiation of thromboxane A2 pathway (recruits more platelets)
GP2b/3a receptor active–fibrinogen welcome!

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28
Q

Describe how the coagulation pathways interact.

A

Extrinsic pathway activated by the presence of tissue factor. 7–7a
7a will activate factor 10 & apparently 9 (crossover to intrinsic)
Proximity of factors 11 & 12 activates 12–12a.
12a causes 11–11a
11a causes 9–9a.
9a activates 10–10a too.

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29
Q

Once 10a is active…what happens?

A

prothrombin w/ 10a–>thrombin (2a)
thrombin causes fibrinogen–fibrin.
13a causes fibrin to cross link.

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30
Q

What makes up the prothombinase complex?

A

Va & 10a

31
Q

What makes up the tenase complex?

A

8a, 10a, Ca++

32
Q

Which coagulation factor is fibrinogen?

A

Factor 1

33
Q

Which coagulation factor is prothrombin?

A

Factor 2

34
Q

Which coagulation factor is anti hemophilic factor? Where is it made?

A

Factor 8

made in the Kupffer cells of the liver

35
Q

Where are most coagulation factors made?

A

liver

36
Q

What is the coagulation factor for hagemann factor?

A

factor 12

37
Q

Which coagulation factor is fibrin stabilizing factor?

A

Factor 13

38
Q

Where does vwf come from?

A

endothelial cells

megakaryocytes

39
Q

Give a summary of primary hemostasis?

A 
Collagen & vwf exposed after injury
Circulating platelets adhere & become activated. Shape change. 
GpIIb (fibrinogen receptor) exposed.
Degranulate.
Thrombaxane A2 pathway
Release ADP
More platelets recruited
Activation of intrinisc pathway. 
Fibrinogen cleaved to fibrin. Clot formed.
40
Q

What are 4 important coagulation regulators?

A

Antithrombin
Activated protein C (APC)
Tissue Factor Pathway Inhibitor
Plasmin

41
Q

What does antithrombin regulate?

A 
thrombin
factor 9a
factor 10a
factor 11a
factor 12a
42
Q

What composes the activated protein C complex?

A

thrombin
thrombomodulin
Protein C
Protein S

43
Q

What does tissue factor pathway inhibitor regulate?

A

tissue factor
7a
10a

44
Q

What does plasmin do?

A

degrades fibrin

45
Q

What are the 4 thing that seem to activate 10–10a?

A

7a
9a
8a
5a

46
Q

With feedback inhibition, what does thrombin inhibit?

A

conversion of 8-8a & 5-5a

47
Q

What are the labs that can help you evaluate platelets?

A

Platelet count
Bleeding time
Platelet aggregometry (function tests)
Platelet flow cytometry

48
Q

What are the labs that can help you evaluate coagulation?

A

aPTT
PT
Thrombin time
Others

49
Q

When should you order a bleeding time test? What is a normal range?

A

only used when a patient has a hx of excessive bleeding

Normal range: 1.5-9.5 min

50
Q

When do you see prolongations in bleeding time?

A 
von Willebrand disease
Inherited platelet disorders
Uremia
Aspirin ingestion
Low platelet counts (<100,000)
51
Q

What is platelet aggregometry?

A

in vitro evaluation of platelet aggregation
stir plasma
subject to agonists
look for aggregation–if present you will have more light transmitted thru vial.

52
Q

Which agonists to aggregation are added to the plasma in the platelet aggregometry studies?

A 
ADP
Epinephrine
Arachidonate 
Collagen
Ristocetin aka vwf
53
Q

What’s the deal with platelet flow cytometry? What is it used to diagnose?

A

**looks at cell surface markers by using fluorescently labeled antibodies
Used to diagnose:
platelet surface glycoprotein deficiencies
disorders of platelet activation

54
Q

How do you measure platelets via platelet count? What is a normal range?

A

automated counter

140K-400K

55
Q

Which pathways does Prothrombin Time (PT) evaluate? How is this test done?

A

used to evaluate extrinsic & common pathways
Used to monitor warfarin therapy!
tissue factor & thromboplastin added w/ Ca++. Measure the time to clot.

56
Q

What is the reference range for normal PT times?

A

11-13.5 seconds

57
Q

Prolongation of PT can be caused by which factor deficiencies/inhibitors?

A 
Factor 7
Factor 10
Factor 5
Factor 2
Fibrinogen
58
Q

T/F INR is helpful in monitoring warfarin therapy along with PT.

A

True.

59
Q

Which pathways is activated partial thromboplastin time (aPTT) used to evaluate? How is it done?

A

intrinsic & common

phospholipid is added to plasma w/ Ca++

60
Q

What is normal value for aPTT?

A

27-35 seconds

61
Q

Which factor deficiencies/inhibitors could cause aPTT prolongation?
Which therapy is it used to monitor?

A 
Monitors heparin, hirudin, & argatroban therapy
Factor XII			
Factor XI
Factor IX			
Factor VIII
Factor X			
Factor V
Factor II			Fibrinogen
62
Q

What is thrombin time (TT) used to test? How is it done?

A

tests presence of functional fibrinogen

thrombin added to plasma & time to clot is measured

63
Q

What is a normal TT range? What might cause TT prolongation?

A

15-19 seconds
heparin, hirudin, argatroban
problems with fibrinogen

64
Q

What are mixing studies used to determine?

A

deficiency or inhibitor?

done when PT, PTT, or TT is off

65
Q

What is the process involved in a mixing study?

A

MIx patient’s plasma with normal plasma…
If better: deficiency
If not better: inhibitor present

66
Q

What forms D dimers? What is the significance of their lab presence?

A

plasmin mediated degradation of fibrin forms

fibrin is goin down!

67
Q

What is another name for the von willebrand factor assay? How is it done?

A

aka Ristocetin cofactor assay
patient plasma added to formalin fixed normal platelets in presence of ristocetin
if normal: platelet agglutination
If vwf deficient: decreased aggregation

68
Q

What is the anti-10a assay used to measure?

A

monitor heparin

69
Q

When do you do factor assays?

A

after mixing study shows that there is a factor deficiency

70
Q

What are the characteristics of platelet type bleeding?

A

petechiae common
mucosal bleeding common
more often in females

71
Q

What are the characteristics of coagulation type bleeding?

A

hemarthroses
deep hematomas
delayed bleeding
more often in males

72
Q

Excessive bleeding due to platelet defects is seen in which conditions?

A 
von willebrand disease
bernard soulier syndrome
glanzmann thrombastenia
platelet storage pool disorders
drugs
ITP
TTP
HUS
HIT
73
Q

What are some disorders that cause excessive bleeding due to coagulation defects?

A 
von willebrand disease
Hemophilia A
Hemophilia B
Liver Disease
Vit K Deficiency
DIC
74
Q

How is it that von willebrand disease is both a platelet defect & coagulation defect bleeding disorder?

A

vwf circulates bound to factor 8 to prevent its early degradation
in vwf deficiency–factor 8 gets destroyed earlier.

Block 7; Week 4-Michelle (5 decks)

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