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Apex > Coagulation > Flashcards

Coagulation Flashcards

1
Q
A
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2
Q

What are the four steps of hemostasis?

A
  1. Vasospasm
  2. Primary hemostasis (platelet plug)
  3. Secondary hemostasis (creation of factors for fibrin mesh)
  4. Fibrinolysis
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3
Q

Where are platelets produced?

A

By megakaryocytes in the bone marrow

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4
Q

How many platelets can the spleen sequester?

A

Up to 1/3!

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5
Q

In the absence of vascular injury, the endothelium inhibits platelet function by secreting:

A

Prostaglandin I2 (inhibits vWF adherence)
AND
Nitric Oxide (inhibits TXA2 receptors)

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6
Q

When a platelet degranulates, what does it release?

A
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7
Q

What are the five receptors on platelet membranes?

A
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8
Q

Activated platelets express two glycoproteins on their surface:

A

GpIIb

GpIIIa

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9
Q

The primary purpose of the coagulation cascade is to produce:

A

Fibrin

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10
Q

The intrinsic pathway is measured by which lab??

A

“It’s longer, so it’s measured by the PTT”

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11
Q

The extrinsic pathway is measured by which lab?

A

“It’s shorter, so it’s measured by the PT”

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12
Q

What are the vitamin K dependent factors

A

2
7
9
10

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13
Q

What is the first factor activated in the extrinsic pathway?

A

Factor 3: Tissue factor

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14
Q

Which medication inhibits the extrinsic pathway?

A

Warfarin

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15
Q

What are the three steps of the extrinsic pathway?

A
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16
Q

which factor has the shortest half life?

A

factor 7 @ 4-6 hrs

In patients with liver disease, this will be the first one impacted

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17
Q

There are four intrinsic pathway factors:

A

8, 9, 11, 12

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18
Q

The intrinsic pathway is activated by:

A

blood trauma

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19
Q

Which medication inhibits the intrinsic pathway?

A

Heparin

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20
Q

What are the five steps of the intrinsic pathway?

A
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21
Q

A deficiency of what factor causes Hemophilia A?

A

Factor 8

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22
Q

How long does it take to form a clot via intrinsic action?

A

About 6 minutes

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23
Q

The primary goal of both the intrinsic and extrinsic pathways is to produce ________ in order to make fibrin

A

prothrombin activator

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24
Q

The final common pathway begins where:

A

prothrombin activator (created by Xa and Factor 5) converts prothrombin (2) into thrombin (2a)

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25
Q

What does thrombin do?

A

It changes fibrinogen into fibrin (a monomer)

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26
Q

What is plasminogen?

A

A pro-enzyme synthesized in the liver that, when activated to plasmin, breaks down fibrin into fibrin degradation products

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27
Q

Where is plasminogen found?

A

Its actually built into the clot! It remains dormant until it’s activated

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28
Q

How is a clot broken down naturally?

A

The injured tissue slowly releases tPA over several days

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29
Q

What does tPA stand for?

A

Tissue Plasminogen Activator

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30
Q

What are the stages of the contemporary theory of coagulation?

A
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31
Q

What is a normal aPTT?

A

25-35 seconds

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32
Q

What pathways does aPTT measure?

A

intrinsic and final common pathways

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33
Q

What medications does aPTT measure?

A

Heparin, but not LMWH

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34
Q

Factors must be reduced by ____% in order for the aPTT to be affected

A

30%

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35
Q

Which pathways does PT assess?

A

Extrinsic and final common pathways

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36
Q

What is a normal PT?

A

12-14 seconds

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37
Q

Why is a normal aPTT longer than a normal PT?

A

Because the intrinsic pathway takes longer than the extrinsic pathway

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38
Q

Factors must be reduced by ____% in order for the PT to be affected

A

30%

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39
Q

What is INR?

A

A ratio that standardized PT

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40
Q

What is a normal INR?

A

about 1x control

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41
Q

What is a therapeutic INR on Warfarin?

A

2-3x control

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42
Q

What is ACT?

A

The activated clotting time, which is more accurate than aPTT when large doses of heparin are administered

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43
Q

What platelet count signifies risk of spontaneous bleeding?

A

<20,000

44
Q

What platelet count signifies increased surgical bleeding risk?

A

< 50,000

45
Q

What does D Dimer measures?

A

Fibrin degradation products

46
Q

What is a normal D-Dimer?

A

<500

47
Q
A
48
Q

What is the MOA of heparin?

A

Binds to Antithrombin and increases its activity 1000x

49
Q

The heparin-AT complex neutralizes:

A

9a
10a
11a
12a
Inhibits platelet function

50
Q

What is the standard heparin dose for CPB?

A

300-400 units/kg

51
Q

The risk of protamine allergy is highest in which people?

A

Fish allergy
Using NPH insulin
Vasectomy

52
Q

Does heparin cross the placenta?

A

No

53
Q

Why does protamine cause pHTN?

A

Thromboxane A2 and serotonin release

54
Q

Why does protamine cause hypotension

A

increased histamine release

55
Q

Where is endogenous heparin produced?

A

Liver, basophils, mast cells

56
Q

Warfarin inhibits which factors?

A

All of the Vit K dependent ones:

2
7
9
10

57
Q

In order for Vit K supplementation to work, what pathology must be absent?

A

Liver disease. If their liver doesn’t work anyway Vit K won’t help

58
Q

Is warfarin protein bound?

A

Yes, highly

59
Q

What are the risk factors for Vit K deficiency?

A
60
Q

What is the drug name for exogenous Vit K?

A

Phytonadione

61
Q

How long does it take to restore clotting factors with Vit K administration?

A

4-8 hours

62
Q

How is Vitamin K administered?

A

Preferably oral. The IV form has a high risk of anaphylaxis and has to be given very slowly

63
Q

There are three classes of antiplatelet drugs:

A

ADP receptor antag.
GPIIb/IIIa antagonists
COX inhibitors

64
Q

Where do we obtain inactive Vit K?

A

Diet
Production by bacteria in the gut

65
Q

List the ADP receptor inhibitors

A

Clopidogrel
Ticlopidine
Ticagrelor

66
Q

List the GpIIb/IIIa antagonists

A

The “Ab Fibs”
Abciximab
Eptifibatide
Tirofiban

67
Q

List the non-specific COX inhibitors

A

Aspirin and NSAiDS

68
Q

List the COX-2 specific inhibitors

A

Celecoxib
Rofecoxib

69
Q

There are four classes of anticoagulants:

A

Heparins
Thrombin Inhibitors
Factor X inhibitors
Vit K antagonists

70
Q

List the thrombin inhibitors

A

Bivalirudin
Argatroban

71
Q

What is the MOA of Aminocaproic acid?

A

Plasminogen activator inhibitor

72
Q

What is the MOA of TXA?

A

Plasminogen activator inhibitor

73
Q

What is the MOA of desmopressin?

A

Stimulates Factor 8 and vWF release

74
Q

What is the most common inherited platelet disorder?

A

von Willebrand disease

75
Q

What lab abnormalities are seen with vWD?

A

Increased pTT and bleeding time

76
Q

Von Willebrand factor has two functions:

A

It serves as an anchoring point for platelets in exposed tissue AND it carries inactivated factor 8 in the blood stream

77
Q

Hemophilia A is factor ______ deficiency

A

8

78
Q

Hemophilia A is most common in males or females?

A

Males

79
Q

Which is more severe: hemophilia A or Hemophilia B

A

Hemophilia A

80
Q

What is the treatment for hemophilia A?

A

Factor 8 concentrate
FFP
Cryo
DDAVP

81
Q

Hemophilia B is factor _____ deficiency

A

9

82
Q

What is the treatment for Hemophilia B?

A

factor 9 concentrate has more side effects and is trickier to use than factor 8

83
Q

________ is a treatment option for both Hemophilia A & B

A

Recombinant Factor 7

84
Q

What are the risks of rFactor7?

A

A clot somewhere unfortunate:
MI
Embolic Stroke
PE
DVT

85
Q

Which conditions have the highest risk of causing DIC?

A

Sepsis
Obstetric Complications
Malignancy

86
Q

What considerations must be made for patients with antithrombin deficiency?

A

They won’t respond to heparin, because there’s no antithrombin to activate

87
Q

Protein C and S work as a team to inhibit:

A

Factor 5
Factor 8

88
Q

Factor V Leiden causes:

A

Resistance to the anticoagulant effects of protein c

89
Q

What are the triggers for sickle cell crisis?

A

Pain
Hypothermia
Dehydration
Acidosis

90
Q

What is the most common manifestation of sickle cell disease?

A

Vaso-Occlusive Crisis

Impaired tissue perfusion leads to ischemia

91
Q

________ reduces the frequency of vaso-occlusive crises

A

Hydroxyurea

92
Q

What is acute chest syndrome?

A

Dyspnea and pulmonary edema

93
Q

What perioperative factors precipitate acute chest syndrome in sickle cell patients?

A

Hypoventilation
Narcotics
Splinting
Pain

94
Q

What is a sequestration crisis?

A

The spleen removes sickled cells from the body faster than they can be produced in the marrow, leading to severe anemia

95
Q

What is an aplastic crisis?

A

Because the life span of HgbS is so short, even a mild reduction in bone marrow activity can cause severe anemia. Usually precipitated by a viral infection

96
Q

Factor 1 Name and Site of Synthesis

A

Fibrinogen

LIVER

97
Q

Factor 2 Name and Site of Synthesis

A

Prothrombin

LIVER

98
Q

Factor 3 Name and Site of Synthesis

A

Tissue Factor

VESSEL WALL

99
Q

Factor 4 Name and Site of Synthesis

A

CALCIUM

Dietary

100
Q

Factor 8 Name and Site of Synthesis

A

Antihemophilic

LIVER

101
Q

Factor 9 Name and Site of Synthesis

A

Christmas Factor

LIVER

102
Q

Factor 10 Name and Site of Synthesis

A

Stuart-Prower

LIVER

Xa combines with calcium and Factor 5 to form prothrombinase, which converts prothrombin into thrombin

103
Q

Factor 11 Name and Site of Synthesis

A

Plasma thromboplastin antecedent

104
Q

Factor 12 Name and Site of Synthesis

A

Hageman Factor

LIVER

105
Q

Factor 13 Name and Site of Synthesis

A

Fibrin stabilizing factor

LIVER

Apex (46 decks)

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