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Cardiopulmonary I > Clotting Cascade - White > Flashcards

Clotting Cascade - White Flashcards

1
Q

Barrier mass

A

Hemostatic plug, blood clot or thrombus

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2
Q

Primary hemostasis

A

Formation of a primary plug

Clumping of blood platelets at site of injury to create a physical plug

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3
Q

Secondary hemostasis

A

Formation of blood clot

Insoluble strands of fibrin become deposited on primary plug making it strong

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4
Q

Third stage of hemostasis

A

Fibrinolysis - removal of clot

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5
Q

Fibrin formed

A

By series of complex biochemical reactions from soluble plasma proteins called coagulation factors as they associate with injured blood vessels and the platelet plug

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6
Q

Fibrin clot

A

Goal is altering fibrinogen (soluble) into fibrin (insoluble)

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7
Q

Fibrinogen

A

4% plasma proteins
Largest of plasma proteins
Protein made of 3 subunits (a,B,y) that exist as dimers with domains D and E

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8
Q

Zymogens

A

Inactive enzyme that can be activated by proteolysis

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9
Q

Each zymogen in clotting cascade

A

First serves as a substrate then as an enzyme

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10
Q

Final substrate in clotting cascade is

A

Fibrinogen

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11
Q

Final enzyme in clotting cascade

A

Thrombin

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12
Q

Thrombin

A

Final enzyme in cascade
Converts fibrinogen to fibrin
Cuts at sites ARG-GLY
A serine protease

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13
Q

Fibrin

A

Insoluble crosslink dam

At site of wound only

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14
Q

Fibrinogen aka

A

Factor I

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15
Q

Prothrombin aka

A

Factor II

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16
Q

Tissue Factor aka

A

Factor III

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17
Q

Christmas Factor aka

A

Factor IX

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18
Q

Contact factor aka

A

Factor XII

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19
Q

Plasma transglutaminase aka

A

Factor XIII

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20
Q

Christmas disease

A

Factor IX deficiency

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21
Q

Fibrin aggregation

A

Forms soft clot

Alpha binds to gamma in a staggered arrangement (like bricks in a wall)

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22
Q

Hard clot formation

A

Covalent bonds formed between fibrin subunits (slower process)
Covalent bond formed between NH2 of glutamine and NH3 of lysine

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23
Q

Factor involved in hard clot formation

A

Factor XIIIa - transglutaminase

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24
Q

Thrombin activates

A

Transglutaminase

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25
Q

Prothrombin and clot localization

A

Glutamic acids must be modified by post-translational modifications (extra COO-)
-2 negative charge

26
Q

Why is glutamic acid residue getting carboxylated important?

A

Becomes a -2 charge
Helps localize prothrombin to damaged vessels
Damaged vessels release Ca2+ so modified prothrombin (with negative 2 charge) has perfect binding site for Ca2+

27
Q

What helps localize prothrombin to damaged vessels?

A

The negative 2 charge

So prothrombin binds to Ca2+ at wound

28
Q

Ca2+ and platelets

A

Ca2+ binds to platelets which have exploded uncovering negatively charged phospholipids at they invert

29
Q

Vitamin K

A

Modification of prothrombin requires vitamin K

30
Q

Drugs like vitamin K

A

Warfarin and Dicoumerol

31
Q

Warfarin

A

Competitive inhibitor of epoxide reductase
Enzyme binds them but they inhibit enzyme activity
Competitive inhibitor
Decrease prothrombin levels

32
Q

What decreases prothrombin levels?

A

Vit K
Warfarin
Dicoumerol

33
Q

2 types clotting cascades

A

In vivo

In the lab

34
Q

Tissue Factor

A

FIII
Found on surfaces of cells lining blood vessels, released when cut
An active component that is not part of the blood under normal conditions
Transmembrane protein

35
Q

Platelet Factor 3

A

On interior of platelets, exposed when platelet disrupted

Phospholipid surface of platelets and damaged vessels essential

36
Q

FVII

A

1% circulates as FVIIa, normally doesn’t come into contact with tissue factor until damage occurs.

37
Q

TF:FVIIa

A

This complex activates FX (factor 10)

38
Q

FVa released from

A

Platelets

39
Q

Thrombin spark

A

A microburst of thrombin gets created in association with platelets to get things going and amplifying

40
Q

Clotting cascade in the lab

A

Occurs in two pathways - intrinsic and extrinsic

41
Q

Intrinsic pathway

A

An accessory pathway, role unclear, deficiency can cause disease
The intro to the common pathway

42
Q

Extrinsic pathway

A

The SPARK to get the process started and is the major pathway
Requires an active component
Activated by contact of Factor VII with tissue factor

43
Q

Part of the intrinsic pathway that results in hemophilias

A

IXa <—— VIII

44
Q

Amplification of cascade

A

Small signal get large response

45
Q

What activates extrinsic pathway?

A

Contact of Factor VII with tissue factor (FIII)

46
Q

Common pathway

A

Extrinsic and intrinsic pathway converge

From FX to fibrin clot formation

47
Q

3 Factors that require Vitamin K

A

X, IX, VII

48
Q

Positive Feedback in clotting

A 
Accelerates the rate of clotting
Thrombin
FXIa
FXa
FVIIa
49
Q

Partial Thromboplastin Time

A

PTT think 12 and intrinsic

Clotting time from factor XII to fibrin clot —> intrinsic and common pathways: reference = 35 seconds

50
Q

Prothrombin time

A

PT think 7 and extrinsic

Clotting time from factor VII and fibrin clot —> extrinsic and common pathways: reference = 10-12 seconds

51
Q

Regulation and thrombin

A

Thrombin can complex with thrombomodulin to create a TTM complex
This cleaves Protein C into active protein C
Thrombin binds fibrin and inactivates same with FVIIIa, Xa and Va

52
Q

Protein C

A

Shuts shit down

53
Q

TTM

A

Thrombin complexed with thrombomodulin

54
Q

Anticlotters

A 
Warfarin and dicoumerol
Aspirin
Decrease Ca+
Heparin
TPA
55
Q

Aspirin

A

Protects platelet integrity

56
Q

Clotting end game

A

TPA - precursor to plasmin - dissolves clot - fibrinolysis

57
Q

TPA

A 
Tissue plasminogen factor
Precursor to plasmin
Dissolves clot
Fibrinolysis
1st genetically altered human protein approved - given to remove clot after stroke
58
Q

Pt comes in, infant son numerous bruises and lots of bleeding with circumcision. PT = 12 PTT = 55 seconds
Factor VIII is low. Diagnosis?

A

Hemophilia A

59
Q

Pt comes in….blah blah blah. Factor IX is low. Diagnosis

A

Hemophilia B

60
Q

Lab values for Vitamin K deficiency

A

PT = 35 s
PTT = 70 s
Low Factor IX, VII, X
Normal Factor VIII

Cardiopulmonary I (34 decks)

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