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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
Prothrombin and clot localization
Glutamic acids must be modified by post-translational modifications (extra COO-) -2 negative charge
26
Why is glutamic acid residue getting carboxylated important?
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
What helps localize prothrombin to damaged vessels?
The negative 2 charge | So prothrombin binds to Ca2+ at wound
28
Ca2+ and platelets
Ca2+ binds to platelets which have exploded uncovering negatively charged phospholipids at they invert
29
Vitamin K
Modification of prothrombin requires vitamin K
30
Drugs like vitamin K
Warfarin and Dicoumerol
31
Warfarin
Competitive inhibitor of epoxide reductase Enzyme binds them but they inhibit enzyme activity Competitive inhibitor Decrease prothrombin levels
32
What decreases prothrombin levels?
Vit K Warfarin Dicoumerol
33
2 types clotting cascades
In vivo | In the lab
34
Tissue Factor
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
Platelet Factor 3
On interior of platelets, exposed when platelet disrupted | Phospholipid surface of platelets and damaged vessels essential
36
FVII
1% circulates as FVIIa, normally doesn't come into contact with tissue factor until damage occurs.
37
TF:FVIIa
This complex activates FX (factor 10)
38
FVa released from
Platelets
39
Thrombin spark
A microburst of thrombin gets created in association with platelets to get things going and amplifying
40
Clotting cascade in the lab
Occurs in two pathways - intrinsic and extrinsic
41
Intrinsic pathway
An accessory pathway, role unclear, deficiency can cause disease The intro to the common pathway
42
Extrinsic pathway
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
Part of the intrinsic pathway that results in hemophilias
IXa <------ VIII
44
Amplification of cascade
Small signal get large response
45
What activates extrinsic pathway?
Contact of Factor VII with tissue factor (FIII)
46
Common pathway
Extrinsic and intrinsic pathway converge | From FX to fibrin clot formation
47
3 Factors that require Vitamin K
X, IX, VII
48
Positive Feedback in clotting
``` Accelerates the rate of clotting Thrombin FXIa FXa FVIIa ```
49
Partial Thromboplastin Time
PTT think 12 and intrinsic | Clotting time from factor XII to fibrin clot ---> intrinsic and common pathways: reference = 35 seconds
50
Prothrombin time
PT think 7 and extrinsic | Clotting time from factor VII and fibrin clot ---> extrinsic and common pathways: reference = 10-12 seconds
51
Regulation and thrombin
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
Protein C
Shuts shit down
53
TTM
Thrombin complexed with thrombomodulin
54
Anticlotters
``` Warfarin and dicoumerol Aspirin Decrease Ca+ Heparin TPA ```
55
Aspirin
Protects platelet integrity
56
Clotting end game
TPA - precursor to plasmin - dissolves clot - fibrinolysis
57
TPA
``` Tissue plasminogen factor Precursor to plasmin Dissolves clot Fibrinolysis 1st genetically altered human protein approved - given to remove clot after stroke ```
58
Pt comes in, infant son numerous bruises and lots of bleeding with circumcision. PT = 12 PTT = 55 seconds Factor VIII is low. Diagnosis?
Hemophilia A
59
Pt comes in....blah blah blah. Factor IX is low. Diagnosis
Hemophilia B
60
Lab values for Vitamin K deficiency
PT = 35 s PTT = 70 s Low Factor IX, VII, X Normal Factor VIII

Cardiopulmonary I (34 decks)

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