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Hemostasis > Section 5: Coag Cascade > Flashcards

Section 5: Coag Cascade Flashcards

1
Q

Which two concentrations of sodium citrate are used? Which one is more common?

A
  • 3.2% and 3.8%
  • 3.2% used most of time
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2
Q

Erythrocetin

A

Substance with thromboplastic effect (initiates coag cascade)

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3
Q

If have low Hct and more plasma, do you need more or less anticoag?

A

More

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4
Q

If have high Hct and less plasma, do you need more or less anticoag?

A

Less

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5
Q

Specimen type in coag vs platelet studies

A
  • Coag studies = PPP
  • Platelet studies = PRP
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6
Q

What type of material can activate the coag cascade? What do we use instead?

A

Glass can activate the coag cascade, so use plastic

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7
Q

Coag sample storage

A
  • Refrigerator temp for 4 hr
  • Prothrombin Time (PT) held at RT
  • Freeze at <-20C (freeze/thaw fast or ice crystals denature proteins)
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8
Q

What is the Tenase complex in the intrinsic pathway?

A
  • FIXa
  • Calcium
  • PF3 phospholipid
  • FVIII:C
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9
Q

What is the Tenase complex in the extrinsic pathway?

A
  • FVIIa
  • Calcium
  • TF3
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10
Q

Purpose of Tenase complex

A

To activate Factor X

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11
Q

Components of the Prothrombinase Complex

A
  • FXa
  • FVa
  • PF3
  • Calcium
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12
Q

What are the Magic Four Factors? Describe them

A
  • FII, VII, IX, and X
  • All produced in liver
  • All vitamin K dependent
  • All depleted by Warfarin therapy
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13
Q

What does Vitamin K do to magic four factors?

A

Vit K participates in an oxidation reaction that adds a second carboxyl group to make a “complete” factor

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14
Q

How does Warfarin deplete the magic four factors?

A

Arrests Vit K in storage form and makes it unavailable to make complete factors

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15
Q

The only substance necessary to convert fibrinogen (FIa) to fibrin (FIIa)

A

Thrombin (FIIa)

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16
Q

Thrombin enhances the activity or modifies _______

A

Factors V, VIII, XI, and XIII

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17
Q

Describe Factors V and VIII

A
  • Labile factors that are short-lived in stored plasma bc not very stable
  • Only factors that are not enzymes
  • Referred to as cofactors that only function in complexes
  • Inactive forms can participate in cascade
  • Targets of Protein C (potent coag inhibitor)
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18
Q

How does Thrombin IIa act upon fibrinogen (I) molecule?

A

It splits fibrinopeptides A and B tips from the end of the two polypeptide chains, leaving the remainder as fibrin (Ia)

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19
Q

How is Factor XIII activated?

A

Thrombin + Calcium activate FVIII to stabilize the clot

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20
Q

Where is fibrinogen (FIa) made and what is its function?

A
  • Made in liver
  • Cross-links plts in aggregation
  • Absorbed in plt alpha granules
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21
Q

Acute phase reactant factor

A

FIa fibrinogen is APP

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22
Q

High fibrinogen associated with

A
  • Pregnancy/smoking
  • MI and stroke
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23
Q

Low and/or dysfunctional FIa associated with

A
  • bleeding
  • thrombosis
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24
Q

Describe FII (prothrombin)

A
  • made in liver
  • one of magic four
  • vit K dependent
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25
Q

FII activated by

A

Xa, Va, Calcium, PF3

26
Q

What does FIIa activate?

A

Activates FV, VIII, XI, XIII, Protein C, and Thrombin Activatable Fibrinolytic Inhibitor (TAFI)

27
Q

Describe TF3 (aka Factor III)

A
  • Found in all tissues esp. brain, liver, lung, and placenta
  • Released from injured tissues
  • Cofactor for activation of FVII
  • Part of Tenase complex
  • No known deficiency of TF3
28
Q

Factor IV is

A

Calcium

29
Q

What must you add to coag screening tests to overcome anticoagulant?

A

Calcium

30
Q

Calcium dependent steps in coag cascade

A
  1. extrinsic Tenase complex
  2. intrinsic Tenase complex
  3. Prothrombinase complex
31
Q

Factor V attaches to ____ and is inactivated by ____

A
  • Attaches to receptor on activated platelets
  • Inactivated by Protein C
32
Q

Describe Factor VI

A

It doesn’t exist

33
Q

What activates FVII?

A

TFIII and Calcium

34
Q

Describe Factor VIII

A
  • Coagulant or clottable portion (AHF or VIII:C)
  • Made in several tissues but mostly liver
  • Heat labile
35
Q

Factor VIII deficiency causes

A

Hemophilia A

36
Q

Factor VIII usually bound to ___

A

vWF
Unstable if not bound to vWF

37
Q

FVIII inactivated by

A

Protein C

38
Q

Describe vWF

A
  • Made by megakaryocytes and endothelial cells
  • ADAMTS13 cleaves vWF into smaller multimers
  • Aids plt adhesion to collagen
39
Q

vWF deficiency causes ___

A

vWF Disease

40
Q

What drug stimulates vWF release from ECs?

A

DDAVP

41
Q

Factor IX aka

A

Christmas factor

42
Q

Factor IX deficiency causes

A

Hemophilia B

43
Q

Factor X made where?

A

Liver

44
Q

Factor XI made where? Function?

A
  • Made in liver
  • Contact factor
  • Travels in blood complexed with High Molecular Weight Kininogen (HMWK) to amplify its function
45
Q

Glass may auto-activate which factor?

A

FXI

46
Q

FXI deficiency causes

A

Hemophilia C

47
Q

Describe Factor XII (Hagemon Factor)

A
  • Made in liver
  • Contact factor that is activated by contact with subendothelial tissue
  • FXIIa activates FXI with cofactor HMWK
48
Q

What is the only factor deficiency that does NOT cause bleeding?

A

Factor XII deficiency

49
Q

How is prekallikrein converted to Kallikrein?

A

XIIa activates Prekallikrein

50
Q

Role of Kallikrein + XIIa

A

To make more XII

51
Q

Kallikrein role

A
  • Activates kinin and fibrinolytic pathways
  • Kinins act as vasodilators and smooth muscle relaxants to reestablish blood flow
52
Q

Consequences of Factor XII deficiency

A
  • Alternate activation of IX by VIIa/TF3/Calcium
  • Thrombosis due to lack of fibrinolytic pathway activation (no clot breakdown)
53
Q

Describe where Factor XIII is made and its function

A
  • Made in liver
  • Functions to form covalent bonds btwn D domains in polymerized fibrin
54
Q

Which factor is not tested for in coag screening tests? What to do instead?

A
  • Factor XIII not tested
  • Urea clot lysis detects deficiency
55
Q

Describe where Prekallikrein is made and its function

A
  • Made in liver
  • Functions as contact factor
  • Activated by XIIa
  • Attached to HMWK
56
Q

Cofactor for PK activation

A

HMWK

57
Q

Kallikrein activate what?

A
  • More XII
  • Plasminogen to plasmin
  • Hydrolyzes bradykinins from HMWK to initiate kinin system
58
Q

Describe PK deficiency

A
  • does NOT cause bleeding
  • usually asymptomatic but may see abnormal clotting due to lack of fibrinolytic pathway activation
59
Q

Describe where HMWK (Fitzgerald factor) is made and its function

A
  • Made in liver
  • Contact factor that complexes with XI and PK
  • Cofactor with XIIa to activate XI
  • Substrate for Kallikrein in kinin production
60
Q

HMWK deficiency consequences

A
  • does NOT cause bleeding
  • usually asymptomatic but may see abnormal clotting due to lack of fibrinolytic pathway activation
61
Q

Bradykinins

A
  • Not really part of cascade, it just gets made
  • Functions to increase vascular permeability, contract smooth muscle, dilate small blood vessels, induce pain/inflammation, and release prostaglandins from tissues

Hemostasis (10 decks)

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