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Cardio/Pulm Final > Lecture 18: Clotting Cascade > Flashcards

Lecture 18: Clotting Cascade Flashcards

1
Q

Hemostasis occurs in how many steps?

A

3 steps

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2
Q

What is primary hemostasis?

A

Formation of a primary plug - clumping of blood platelets at site of injury

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3
Q

What is secondary hemostasis?

A

Formation of blood clot

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4
Q

Secondary hemostatic plug is formed by depositing of?

A

Insoluble strands of fibrin on the primary plug

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5
Q

What occurs during the 3rd sage of hemostasis?

A

Fibrinolysis - removal of clot

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6
Q

3 characteristics of hemostasis?

A

1) Must be fast
2) Localized
3) Carefully controlled

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7
Q

Goal of fibrin clot is altering which soluble protein into which insoluble one?

A

Fibrinogen (soluble)—–> Fibrin (insoluble)

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8
Q

What is the largest plasma protein and accounts for 4% of the total plasma proteins?

A

Fibrinogen

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9
Q

What is a zymogen and how is it activated?

A

Inactive form of an enzyme that can be activated by proteolysis.

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10
Q

What are the two sites on a zymogen and their function?

A

1) Pre- For secretion

2) Pro- Keeps it inactive

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11
Q

Zymogens are made where?

A

Liver

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12
Q

Zymogen are released into blood plasma and what makes them active?

A

Cleavage of the Pro- site by a protease in coagulating blood

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13
Q

Each zymogen serves first as a ________, then as a ______?

A

First as a substrate, then as an enzyme

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14
Q

The final substrate is?

A

Fibrinogen

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15
Q

Fibrinogen (factor I) is acted on by which enzyme and becomes?

A

Acted on by Thrombin (IIa), becomes fibrin

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16
Q

What is factor II and factor IIa?

A

Factor II = Prothrombin

Factor IIa = Thrombin

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17
Q

What does fibrin form at site of injury?

A

Polymerizes into clot - forms insoluble crosslink dam

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18
Q

What is factor III?

A

Tissue factor (TF)

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19
Q

What is factor IX?

A

Christmas Factor

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20
Q

What is factor XII?

A

Contact Factor

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21
Q

What is factor XIII?

A

Plasma transglutimase

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22
Q

Factor IX deficiency causes?

A

Hemophilia B: Christmas disease

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23
Q

Prothrombin is activated to thrombin by what kind of cleavage?

A

Proteolytic cleavage with a serine protease (prothrombinase)

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24
Q

Thrombin is itself a ________ and cuts at sites with which amino acids?

A

Serine protease and cuts at sites with ARG-GLY

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25
Q

Fibrinogen is made up of which subunits, that exist as?

A

3 subunits (α, β, and γ), exist as dimers

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26
Q

Thrombin cuts and releases what from fibrinogen?

A

A + B fibrinopeptides

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27
Q

Which domains of fibrinogen interact; type of bond?

A

E domain binds to D domain; H-bond

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28
Q

Why are A + B fibrinopeptides significant?

A

Prevent self-aggregation

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29
Q

Release of A fibrinopeptide allows for what interaction to occur; forms?

A

E domain (A sites) interacts with D domain (γ subunit) over + over; forms a “soft” clot

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30
Q

Cutting off ends of B sites allow for what interaction?

A

B chains interact to form 3D wall

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31
Q

Formation of a cross-linked fibrin (hard clot) requires what kind of bond, between which amino acids?

A

Covalent bond between NH2 of glutamine and NH3 of lysine.

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32
Q

What factor is responsible or the formation of the cross-linked fibrin?

A

Factor XIIIa - transglutaminase

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33
Q

What activates transglutaminase?

A

Thrombin

Factor XIII ——> Factor XIIIa

34
Q

Why must prothrombin be modified by post-translational modification?

A

Important for clot localization

35
Q

What occurs during the post-translational modification of prothrombin; new charge?

A

Carboxylation of several glutamic acid residues - adds another charge to side R-group on amino acid

“-2” negative charge

36
Q

What is the post-translational modified glutamate on prothrombin called?

A

γ-carboxyglutamate

37
Q

How does this -2 charge help localize prothrombin to damaged vessels?

A

Damage vessels release Ca2+ - so modified Prothrombin (-2 charge) has perfect binding site for Ca2+

38
Q

Ca2+ bound to prothrombin then binds where and unconvers?

A

To platelets which have exploded uncovering negatively charged phospholipids as they invert.

39
Q

Modification of Prothrombin (carboxylation) requires which vitamin?

A

Vitamin K

40
Q

Recycling of Vitamin K requires which enzyme?

A

Epoxide reductase

41
Q

How do Warfarin (coumadin) and Dicoumerol act on epoxide reductase; do what to prothrombin levels?

A

Competitive inhibition; decrease prothrombin levels

42
Q

Warfarin and Dicoumerol inhibit which step; classified as what kind of drugs?

A

Addition of carboxylic acid groups to prothrombin; anti-clotting drugs

43
Q

Safe and effective tx for Warfarin reversal?

A

IV Vitamin K

44
Q

Why must patients on Warfarin be watched carefully?

A

Warfarin is a rodenticide: rat poison

45
Q

Clotting cascase is an enzyme cascade of what type of proteases?

A

Serine

46
Q

What are the two pathways of the clotting cascade; lead to?

A

Intrinsic (workhorse) and extrinsic (starts process); common pathway

47
Q

Which pathway does not require a protein outside of blood to be activated?

A

Intrinsic pathway

48
Q

A broken vessel will release contact factors and activate?

A

Factor XII —-> XIIa

49
Q

What must be in the presence of XIIa to activate XI—->XIa?

A

Ca2+

50
Q

XIa activates IX in the presence of ?

A

PF3: platelet factor 3: phospholipids

51
Q

Where is PF3 located?

A

Interior platelets, become exposed when platelet disrupted

52
Q

Function of FVIII; activated by?

A

Helper protein (co-factor); activated by thrombin

53
Q

VIIIa complexes with and forms?

A

IXa to form IXa-VIIIa complex (tenase)

54
Q

Tenase in the presence of what activates?

A

In presence of PF3, Ca2+ will activate X—->Xa

55
Q

Xa complexes with to form?

A

Va to form Xa-Va complex (prothrombinase)

56
Q

V —-> Va requires?

A

Thrombin

57
Q

The Xa-Va complex activates; requires?

A

Prothrombin ——> Thrombin; PF3, Ca2+

58
Q

Hemophilia A and B are caused by issues with which factors?

A

A (Factor VIII)

B (Factor IX)

59
Q

How does a small signal get a large response in the cascade?

A

Amplification

i.e., activation of handful of Factor XII activates hundreds of Factor XI which activates thousands of IX

60
Q

What does the extrinsic pathway require than the intrinsic doesn’t and where is it found?

A

Tissue Factor (FIII) - found on surface of cells lining blood vessles

61
Q

Extrinsic pathway is activated by contact of; forms?

A

Factor VII with tissue factor (FIII); forms VIIa-TF complex

62
Q

What is the major pathway?

A

Extrinsic

63
Q

Where does the thrombin come from that is necessary for the earlier steps?

A
  • 1% of FVII circulates as FVIIa, which joins with TF when damage occurs, activates FX.
  • Platelets have some activated FVa, so FXa-FVa (prothrombinase) complex forms and you get thrombin burst
64
Q

The thrombin spark to get the intrinsic pathway (workhorse) going, comes from?

A

Extrinsic pathway (why it’s so important/major player)

65
Q

What other factors require addition of carboxyl and are vitamin K dependent?

A

X, IX, and VII

66
Q

Rate of clotting is greatly accelerated by?

A

Positive feedback

67
Q

Reference range from partial thromboplastin time (PTT)

A

20-35 seconds

68
Q

Partial thromboplastin time (PTT) measures the time between, which pathways involved?

A

Factor XII to Fibrin clot (intrinsic and common pathways)

69
Q

Prothrombin time (PT) is time between, which pathways involved?

A

Factor VII to Fibrin clot (extrinsic and common pathways)

70
Q

What is the normal range for prothrombin time (PT)?

A

12-14 seconds

71
Q

Initiating component for clotting in vivo?

A

TF

72
Q

Clotting in vivo does not include which factor?

A

Factor XII

73
Q

What is the phone number to remember steps for clotting in vivo?

A

379-8105

74
Q

Thrombin can bind what to regulate clotting cascade?

A

Binds fibrin - inactivates fibrin

75
Q

Thrombin can cut and inactivate which factors?

A

FVIIIA —> FVIIIi

Xa —> Xi

Va –> Vi

Prothrombin —> inactive form

76
Q

Thrombin complexes with thrombomodulin to create TTM complex, which cleaves and creates?

A

Protein C into active Protein Ca

77
Q

Activated Protein Ca plus other proteins inactivate which factors and cause a decrease in?

A

FVa and FVIIIa - decreases production of thrombin

78
Q

Why do activated Protein Ca’s localize to platelet areas with PF3?

A

Decorated with γ-carboxyglutamate

79
Q

Which common drug protects platelet integrity?

A

Aspirin

80
Q

What does Heparin do?

A

Activates antithrombin III - binds to Thrombin and Xa - inactivates

81
Q

What dissolves clot - fibrinolysis?

A

Tissue plasminogen factor (TPA)

82
Q

Calcium chelating agents have what affect on Ca2+ and what affect on clotting?

A

Decrease Ca2+ and this has an anti-clotting affect.

Cardio/Pulm Final (18 decks)

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