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ANAP 520 > TEST 3- HEMOSTASIS/COAG > Flashcards

TEST 3- HEMOSTASIS/COAG Flashcards

1
Q

Trapped plts, rbc and fibrin; forms clot.

A

Fibrin network

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2
Q

First cell belonging to the plt lineage

A

Megakaryoblast

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3
Q

Megakaryoblast formation into plt sequence..

A

Megakaryoblast

Megakaryocyte

Megakaryocyte breakup (into fragments)

Platelets

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4
Q

Platelets are anuclear. TRUE/FALSE

A

TRUE

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5
Q

Normal circulating conc of plts

A

150,000-450,000 plt/microliter

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6
Q

Halflife of plt

A

8-12 days

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7
Q

Contractile proteins found in the cytoplasm of plts

A

Actin
Myosin
Thrombosthenin

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8
Q

Purpose of ER and Golgi apparatus in cytoplasm of plt

A

ER: Ca++ storage

GA: enzyme synthesis

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9
Q

Plts contain mitochondria for ADP/ATP synthesis. TRUE/FALSE

A

TRUE

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10
Q

These two things are in the cytoplasm of plts and play a role in plt aggregation, plt antiaggregation and some vasoconstriction

A

PGs

TxA2 synthesis

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11
Q

Stabilizes fibrin threads and the clot; located in cytoplasm of plt.

A

Fibrin-stabilizing factor synthesis

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12
Q

Used to repair damaged tissue; promote healing; in cytoplasm of plt.

A

Growth factors

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13
Q

3 components of the cell membrane of plt

A

Glycoproteins coating
Phospholipids
Receptors

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14
Q

Part of the cell membrane that prevents plts from adhering to normal vascular endothelium

A

Glycoprotein coating

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15
Q

Part of cell membrane that plays a role in coagulation cascade

A

Phospholipids

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16
Q

Part of cell membrane that allows plts to become activated

A

Receptors

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17
Q

Prevention of blood loss

A

Hemostasis

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18
Q

How hemostasis is achieved (in order)

A 
Vascular constriction
Plt plug formation 
Blood coag/clot
Fibrin formation and repair of vessel
Clot lysis
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19
Q

4 Things that cause vascular constriction

A

Trauma

Vascular smooth muscle Spasm

Pain/SNS reflexes (NE/epi released when cut, etc.)

Plts–TxA2–vasoconstriction

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20
Q

The greater the trauma, the greater the amount of constriction, TRUE/FALSE

A

TRUE

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21
Q

Plts are activated when they contact _______ vascular endothelium and collagen in BV wall.

A

Damaged

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22
Q

When plts contact damaged vessel, they swell and exude _______, or “false feet” projections

A

Pseudopods

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23
Q

After exuding pseudopods, these contract and release clotting factors

A

Actin
Myosin
Thrombosthenin

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24
Q

After actin/myosin/thrombosthenin contract, plts get sticky and aggregate; adhere to _______ and ________ factor in BV wall

A

Collagen

Von willebrand factor

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25
Q

This activates other plts after plts start adhereing to BV wall

A

ADp and TxA2 secretion

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26
Q

Plts express ______ receptors to form platelet plug

A

Receptors

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27
Q

Fibrinogen receptors form fibrinogen _______, converted eventually to mesh/clot

A

Fibers

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28
Q

After fibrin threads form in plt plug, this may seal what type of injury?

A

Small BV injury

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29
Q

Larger injury requires what beyond plt plug formation?

A

Blood coagulation or blood clot

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30
Q

VWF deficiency can lead to major bleeding issues; how can we treat this?

A

Give VWF conc
DDAVP (desmopressin)
Cryoprecipitate

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31
Q

Blood coag/clot begins _____ min for minor injury; and ______ sec for major trauma

A

1-2 min minor

15-20 sec major trauma

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32
Q

In ______ min tear in vessel is filled with clot

A

3-6 min

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33
Q

Clot retracts in _______ min; closes tear more

A

20-60 min

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34
Q

Balance between procoagulants and anticoagulants

A

Normally anticoagulants predominate

After injury: procoagulants predominate

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35
Q

Procoagulants should only predominate ________, if not you can have coagulopathies.

A

Locally (to injury)

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36
Q

3 essential steps of coagulation

A

Activation of blood coag factors and formation of prothrombinase (prothrombin activator)

Prothrombinase converts prothrombin to thrombin

Thrombin converts fibrinogen to fibrin fibers = enmesh plts, blood cells, and plasma to form clot

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37
Q

2 pathways for prothrombinase formation

A

Extrinsic (tissue factor) pathway

Intrinsic (contact activation) pathway

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38
Q

Beginning with activation of Factor ____, both become a common pathway

A

X

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39
Q

If blood vessel ruptures, both pathways are activated simultaneously. TRUE/FALSE.

A

TRUE

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40
Q

Which pathway can become out of control or explosive?

A

Extrinsic pathway

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41
Q

What starts the extrinsic clotting pathway

A

Tissue damage

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42
Q

What starts the intrinsic clotting pathway

A

Contact with collagen of damaged blood vessel

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43
Q

Final outcome of both extrinsic/intrinsic pathway Stage 1.

A

Prothrombinase

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44
Q

______ pathway can feed into the ________ pathway; which part feeds in to the other?

A

Extrinsic can feed into intrinsic pathway

Thromboplastin/factor VII complex

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45
Q

This electrolyte plays major role in both clotting pathways; necessary

A

Ca++

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46
Q

Coagulation factors are synthesized where?

A

The liver

Abnormal liver fxn can lead to abnormal coag.

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47
Q

Prothrombinase converts prothrombin into ______; final outcome of stage ____.

A

Thrombin

Stage 2

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48
Q

Vitamin K dependent clotting factor

A

Prothrombin

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49
Q

Where do we get vitamin K?

A

Green leafy veggies

E.coli in bowel synthesizes vit K

50
Q

What are a couple of ways that we can cause deficits in vit K in our pts; possible causing decreased clotting ability?

A

Abx destroy normal flora of bowel

Enemas prior to sx, esp bowel sx

51
Q

Other vit K depending clotting factors besides prothrombin

A

Facet VII, IX, and X

52
Q

Vit K is fat soluble so have to have adequate _____ in GI tract to absorb it.

A

Bile

53
Q

Thrombin, along with _____ converts fibrinogen into _____, which forms final fibrin clot in stage 3.

A

Ca++

Fibrin

54
Q

2 ways production of thrombin enhances clotting

A

Feeds back into intrinsic pathway

Activates factor XIII which plays role in fibrin clot

55
Q

Prothrombin is an ______ globulin (plasma protein)

A

Alpha-2

56
Q

Thrombin converts fibrinogen to ______ mnomers, which polymerize to form fibrin and fibrin fibers.

A

Fibrin

57
Q

Thrombin further activates these factors, ending in more formation of prothrombinase.

A

Factor V, VIII, XI, XIII

58
Q

Thrombin activates _______; which strengthens bonds between fibrin fibers

A

Fibrin-stabilizing factor

59
Q

Meshwork of fibrin fibers entrapping plts, blood cells, plasma.

A

Clot

60
Q

Expresses most fluid (serum) from clot; type of drainage?

A

Clot retraction; Actin, myosin, thrombosthenin, and Ca++ in plts

Purulent drainage

61
Q

Pulls edges of blood vessel closer together; aids hemostasis and healing

A

Clot retraction

62
Q

Clot invaded by fibroblasts to form connective tissue in clot, lot changed to fibrous tissue and eventual repair, ________ enhance repair

A

Plt growth factors

63
Q

When is tissue restored to pretty much original form and fxn after injury?

A

If injury small

64
Q

What happens to repaired tissue after major injury?

A

Tissue not like former/original state = scar tissue. Will not fxn as before.

65
Q

Good example for tissue repair, but fxn not restored to original quality.

A

Heart tissue after MI; will not contract the same

66
Q

Inactive protein in clot until tPA released

A

Plasminogen

67
Q

What happens when tissue plasminogen activator (tPA) is released ?

A

Converts plasminogen to plasmin

68
Q

Proteolytic enzyme; digests fibrin fibers and procoagulants; lyses clot.

A

Plasmin

69
Q

4 things that prevent coagulation of normal BV

A

Vascular endothelium

Fibrin fibers absorb thrombin to prevent clot spread

Antithrombin III

Endogenous heparin

70
Q

4 Components to vascular endothelium that prevent coagulation.

A

Smooth

Mucopolysaccharide glycocalyx repels plts and clotting factors

Thrombomodulin binds thrombin (prevents clots)

Endothelial damage: activation of factor XII and plts

71
Q

Endogenous substance that combines and inactivates thrombin

A

Antithrombin III

72
Q

Endogenous heparin synthesized and secreted by what cells?

A

Mast cells

Basophils

73
Q

Synthesizes heparin in tissue spaces

A

Mast cells

74
Q

Synthesized heparin in the blood

A

Basophils

75
Q

Heparin combines with __________ III and increases effect by 100-1000 X’s

A

Antithrombin III

76
Q

Antithrombin III also combines with and removes what factors?

A

Factors VII, IX, X, XI, XII

77
Q

Clotting factors effected by heparin

A

Activated Factor VII, IX, X

Factor XI, XII

Thrombin

78
Q

Lovenox inhibits this as well as heparin

A

Activated factor X

79
Q

Clotting factors effected by warfarin

A

Factor VII, IX, X

Prothrombin

80
Q

How long it takes to convert prothrombin into thrombin; assesses extrinsic and common pathway.

A

Prothrombin time PT

81
Q

Normal PT level

A

11-16 sec

82
Q

Drug monitored when getting PT levels a lot of the time.

A

Coumadin

83
Q

This value standardizes the PT, so we can compare values.

A

INR

84
Q

Translate INR: 1

A

Prothrombin time is = international standard for normal

85
Q

Are there times you would be okay with a higher INR?

A

Yes. Ex: mechanical valve replacement

86
Q

Measures intrinsic and common pathway; monitors heparin therapy.

A

Activated partial thromboplastin time (aPTT)

87
Q

Normal PTT

A

26-42 sec

88
Q

Assesses the plasma level of the precursor of fibrin; need adequate amount to form fibers

A

Plasma fibrinogen

89
Q

Assesses for degradation products/breakdown of clots.

A

D-dimer test

90
Q

Condition where D-diner is extremely high.

A

DIC

91
Q

DIC is initially characterized by widespread __________, then _______ are used up faster than liver can produce them and _________ will predominate with extensive bleeding resulting.

A

Coagulation
Procoagulants
Anticoagulants

92
Q

Conditions that are at risk for developing DIC

A

Obstetric conditions

Burns

Infection, especially gram (-) septicemia

93
Q

Common to all pts with DIC

A

Hypotension
Hypoxemia
Acidosis
Stasis of capillary blood flow

94
Q

S/S of DIC

A

Hemorrhage everywhere !

95
Q

DIC will eventually lead to what?

A

Multisystem organ dysfunction and death

96
Q

Treatment/management of DIC

A

Blood product
Remove cause
Heparin or antithrombin III
Maintain organ viability

97
Q

What is the logic behind the controversial therapy of giving heparin etc during DIC?

A

If stop excessive procoagulation initially, then will stop the whole process

98
Q

How do we maintain organ viability when treating DIC ?

A

Mechanically ventilate
Vasopressors
Normal fluid balance

99
Q

Increased or decreased during DIC?

Bleeding time

A

Increased

100
Q

Increased or decreased during DIC?

Plt count

A

Decreased

101
Q

Increased or decreased during DIC?

Plasma fibrinogen

A

Decreased

102
Q

Increased or decreased during DIC?

Fibrin degradation products

A

Increased

103
Q

Increased or decreased during DIC?

D-dimer test

A

Increased

104
Q

Increased or decreased during DIC?

PT/INR

A

Increased

105
Q

Increased or decreased during DIC?

APTT

A

Increased

106
Q

Increased or decreased during DIC?

Clotting factors II, V, VII, X

A

Decreased

107
Q

Does not have to be ABO compatible, transfuse SLOW!!

A

PLATELETS

108
Q

Plt transfusion depends on both quantitative and qualitative measures, explain.

A

Some ppl may have dysfunctional plts, even if the level present is accurate

109
Q

When should you transfuse plts to stable pts w/o evidence of bleeding?

A

<10,000/uL

110
Q

Prophylaxis for invasive procedures such as LP, spinal/epidural, central line, liver biopsy or major sx

A

<50,000/ uL

111
Q

For massive transfusions (>1 or 2? Blood volume) of prbc’s, when should you transfuse plts?

A

<75,000/uL

112
Q

Plt transfusion level when pts having surgery on the eye or in the central nervous system

A

<100,000/uL

113
Q

Contains all the factor involved in coagulation; must be ABO compatible

A

FFP

114
Q

Why does FFP have to be ABO compatible

A

Contains antibodies that can respond to a recipients RBC antigens

115
Q

Indications for FFP

A

Correction of inherited factor deficiencies when there is not specific factor concentrate

PT or aPTT > 1.5 times normal

Correction of acquired factor deficiencies with clinical evidence of bleeding

Reversal of vit K antagonists (warfarin)

116
Q

Example of acquired factor deficiencies that may require FFP transfusion

A

Liver disease
DIC
Massive transfusion

117
Q

Used to reverse Coumadin

A

Vit K

118
Q

Used to reverse heparin

A

Protamine

119
Q

Contained in cryoprecipitate

A

Fibrinogen
VWF
Factor VIII
Factor XIII

120
Q

Indication for cryoprecipitate is DIC with fibrinogen

A

<80-100

121
Q

Indication for cryo during massive transfusion with fibrinogen

A

<100-150

122
Q

Cryo given for prophylaxis for what pts?

A

Hemophilia A

vWD

Congenital dysfibrinogenemias

ANAP 520 (6 decks)

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