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Year 1 > Coagulation > Flashcards

Coagulation Flashcards

1
Q

Where are coagulation factors produced?

A

Liver, factor 8 also can be made in endothelial cells

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2
Q

Zymogens coagulation factors (5)

A

2, 7, 9, 10, 11

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3
Q

Vitamin K dependent

A

2, 7, 9, 10

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4
Q

Procofactors (3)

A

TF, 5, 8

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5
Q

When you have an injury to endothelial cells, you activate primary hemostasis and expose

A

Tissue factor (TF)

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6
Q

You have a very small amount of this factor in its activated cleaved form that binds to TF to form a complex with calcium

A

7a

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7
Q

TF-7a complex cleaves these two factors

A

9a, 10a

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8
Q

What cleaves prothrombin to thrombin

A

10a

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9
Q

F2a

A

thrombin

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10
Q

What cleaves fibrinogen to fibrin?

A

Thrombin

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11
Q

What restructures the platelet’s phospholipid membrane so that factors can bind and interact?

A

Thrombin

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12
Q

In the presence of calcium, 9a forms a complex with this factor

A

8a

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13
Q

9a-8a complex actives more of this factor, which subsequently forms a complex with what factor? (in presence of calcium)

A

10a, forms a complex with 5a. Cleaves prothrombin to thrombin much more aggressively

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14
Q

What factor is critical for crosslinking? What activates it?

A

13a, thrombin

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15
Q

List the 3 main functions of thrombin

A
  1. cleaves 5, 8, 11, 13
  2. Cleaves fibrinogen to fibrin
  3. Restructures platelet phospholipid membrane
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16
Q

Which two complexes bind to platelet?

A

5-10, 8-9

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17
Q

These residues are responsible for the high-affinity binding of calcium ions and interaction with platelet membrane

A

Gla residues (gamma-carboxyglutamate)

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18
Q

What is the role of the vitamin K dependent carboxylase?

A

carboxylates glutamic acid resides to gamma carboxy glutamic acid (gla)

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19
Q

Thrombin restructures platelet membrane to expose the net negative charge of this component

A

PS (phosphotidylserine)

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20
Q

In forming a carboxylated prozmogen, Vitamin K converts from what state?

A

Reduced to Oxidized

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21
Q

Epoxide reductase converts oxidized vitamin K to its reduced form. What are two blockers of this step? What are the consequences of this blockage

A

Coumadin and warfarin. If cant bring Vitamin K back to reduced form, it cant carboxylate and can’t function/clot as well. Have thinner blood

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22
Q

Prothombin time evaluates which pathway?

A

Extrinsic pathway

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23
Q

What is the only factor involved in the extrinsic pathway?

A

TF

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24
Q

In prothrombin time, the specimen is collected in this to remove calcium

A

citrate (can bind to calcium)

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25
Q

This was created to standardize the PT results across labs, since TF reagants are variably thrombogenic

A

International Normalized Ratio (INR)

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26
Q

What’s a normal INR? What’s a typical therapeutic INR?

A

normal=1, therapeutic=2-3

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27
Q

Partial thromboplastin time evaluates which pathway? What does it not include?

A

Intrinsic, no TF

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28
Q

PTT is used for monitoring

A

unfractured heparin

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29
Q

phospholipids - TF = ?

A

partial thromboplastin (PTT)

30
Q

What gets added first in PTT?

31
Q

What does silica activate

32
Q

Not a big deal if deficient in these factors

33
Q

Which two anticoagulants are Vitamin K dependent?

A

Protein C and S

34
Q

Serpin

A

serine protease inhibitor = antithrombin

35
Q

inactivates all serine protease coagulation factors by irreversible binding

A

antithrombin

36
Q

AT acts on all coagulation factors with the exception of these two

A

profactors 5 and 8

37
Q

antithrombin by itself is a very slow inhibitor. What does it need to work better?

38
Q

How much does heparin increase AT activity?

A

induces conformation change in AT resulting in a 10,000 fold increase in activity

39
Q

What are heparin sulfate molecules and where are they found?

A

Branches that come off on thriving endothelial cells nearby. AT comes by and binds, building a wall upstream and downstream that prevents extension of clot

40
Q

What is the key molecules that AT-heparin complex binds to?

41
Q

What are the two main systems for anticoagulation?

A

Heparin-AT system, Protein C and Protein S system

42
Q

What does activated Protein C cleave/deactivate?

A

F8 and F5 (note: it cleaves F8a to F8, thus deactivating it. just shorthanding the notes)

43
Q

TF complex is located on

A

tissue bearing cell

44
Q

F10-5 and F9-8 complex are located on

45
Q

Protein C receptor

A

EPCR (endothelial protein C receptor)

46
Q

EPCR is in close proximity to

A

Thrombomologin (TM)

47
Q

In anticoagulation, thrombin interacts with _____ allowing it to cleave ________

A

Thrombin interacts with TM, bringing it close to EPCR, allowing it to cleave and activate Protein C
(TM and EPCR are close to one another)

48
Q

Activated protein C interacts on membrane with this cofactor

49
Q

Protein C and S downregulate

A

F8 and F5.

50
Q

What are you deficient in potentially if hypercoagulant?

A

Protein C and S.

51
Q
  1. Primary hemostasis (platelet plug)
  2. Secondary hemostasis (fibrin clot)
  3. natural anticoagulant system
  4. ????
A
  1. fibrinolytic system
52
Q

when is the fibrinolytic system activated?

A

as soon as you activate primary hemostasis. as you start to form, you immediately start to break it down. not just cleaning up mess

53
Q

in the fibrinolytic system, an increase pressure from endothelial cells causes a release in what?

A

tPA= tissue plasminogen activator

54
Q

What does tPA do?

A

cleaves plasminogen to plasmin

55
Q

what activates plasminogen?

56
Q

What is function of plasmin?

A

Breaks up fibrin into fibrin degradation products

57
Q

what does tPA interact with DIRECTLY ON THE CLOT?

A

Plasminogen IN the clot. We want clot localized

58
Q

After plamin chews up fibrin, it releases fibrin degradation products and it will release itself. What binds to plasmin?

A

Alpha 2 antiplasms (a2

59
Q

What are inhibitors of fibrinolysis called?

A

Plasminogen Activator Inhibitors (PAIs)

60
Q

What activated PAIs?

61
Q

What is a D-dimer

A

specific fragments of fibrinogen. Plasmin snips off pieces of fibrin

62
Q

An increase in D-dimer indicates

A

clotting activity

63
Q

A normal DD would rule out the presence of

A

significant clots i.e. pulmonary embolus or deep vein thrombosis (blood clot in vein)

64
Q

In terms of laboratory test limitations, what does a D-dimer require?

A

A highly sensitive assay

65
Q

Explain “all D-dimer assays are not created equal”

A

different methods, machines, antibodies and FDA approval

66
Q

What factor has a major role in PTT?

67
Q

What is the common mutation in hemophilia A?

A

inversion of intron 22

68
Q

What is the common mutation in hemophilia A?

A

inversion of intron 22

68
Q

In terms of laboratory test limitations, what does a D-dimer require?

A

A highly sensitive assay

68
Q

Explain “all D-dimer assays are not created equal”

A

different methods, machines, antibodies and FDA approval

68
Q

What factor has a major role in PTT?

Year 1 (48 decks)

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