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NURS 671 - Intro to Anesthesia > Hematology CH 38 > Flashcards

Hematology CH 38 Flashcards

1
Q

The intima (inner layer- Endothelial) has a role in modulating

A

Procoagulants (Hemostasis)
Anticoagulants
Fribrinolytics

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2
Q

What is an important function of the endothelial lining of blood vessels

A

They repel blood components away from the vessel was to prevent activation of clotting mechanism

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3
Q

What does the Media (2nd layer - Subendothelial) contain?

A

It is extremely thrombogenic and very active, contains collagen and fibronectin

Collagen - important in PLT attachment

Fibronectin - Aids with aching fibrin during plug formation

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4
Q

Where is NO and Prostacyclin made and what is their role?

A

Produced by Endothelial (inner layer) cells, and influence Adventitia (Outer layer - Externa)

They work by causing vasodilation and increasing the flow of blood, therefore interfere with PLT formation and aggregation; limit procoagulant mediations “wash them away”

NO –> Muscle relaxation
Prostacyclin –> Lipid molecule

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5
Q

NO specific affects PLT function, by inhibiting?

A

adhesion
aggregation
binding (btw fibrinogen + GPllb/llla)

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6
Q

What role does the adventitia (externa - outer layer) play?

A

Participates in control of blood flow by influencing vessel’s DEGREE OF CONTRACTION

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7
Q

Where are PLTs formed and stored?

A

Formed in bone marrow
1/3rd stored in Spleen

(megakaryoctes are precursors for PLTs)

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8
Q

PLTs contain a nucleus, T/F?

A

False! They do not contain a nucleus, DNA, nor RNA. So they do not reproduce.

THEY DO contain mitochondria in cytoplasm, so they participate in aerobic & anerobic metabolism

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9
Q

PLTs store a large amount of
A) Mg
B) Ca
C) K
D) Na

A

B) Calcium

AND… various enzymes like vWF, Fibrinogen, PLT Factor 4, PLT growth Factor

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10
Q

PLTs produce
A) ADP
B) Prostacyclin
C) Vit K
D) Thrombin

A

D) Thrombin. Role of thrombin is to activate some coagulation factors and influence recruitment of PLT to injury site

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11
Q

When vessel wall injury occurs, what happens next?

A

Immediately contracts to cause tamponade and decrease blood flow to decrease bleeding

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12
Q

What mediates contraction (vasoconstriction)?

A) ADP & Thromboxane A2
B) Gpllb/llla & Fibrinogen
C) vWF & Gplb
D) None of the above

A

A) ADP & Thromboxane A2

Contraction results from ANS reflexes and expression of f the aforementioned

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13
Q

What are the 3 steps to form a primary plug?

A

Adhesion
Activation
Aggregation

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14
Q

What happens during adhesion? (Select all that apply)

A) ADP & Thromboxane A2 vasoconstrict
B) TF influences PLT activation
C) GPlb & Fibrinogen bind to form a plug
D) Gpllb/llla & vWF attach to attract PLTs; make them “sticky”
E) none of the above

A

D) Gpllb/llla & vWF attach to attract PLTs; make them “sticky”

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15
Q

What happens during Activation? (select all that apply)

What happens during adhesion?

A) ADP & Thromboxane A2 vasoconstrict
B) TF influences PLT activation
C) GPlb & Fibrinogen bind to form a plug
D) Gpllb/llla & vWF attach to attract PLTs; make them “sticky”
E) none of the above

A

B & D

TF will influence PLTs to undergo transformation and become activated, GPllb/llla will project off these PLTs and attach to Fibrinogen to help form primary plug

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16
Q

What happens during aggregation?

A) ADP & Thromboxane A2 vasoconstrict
B) TF influences PLT activation
C) GPlb & Fibrinogen bind to form a plug
D) Gpllb/llla & vWF attach to attract PLTs; make them “sticky”
E) none of the above

A

E.
During this time PLT releases alpha & dense granules, contractile granules, thrombin, and other important procoagulant activators as mediators responsible for PLT aggregation. Here the primary plug is solidified.

Small injuries primary plug is sufficient
Large injuries require secondary plug

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17
Q

What pathway influences the start of extrinsic pathway?
A) contact activation pathway
B) common pathway
C) TF pathway
D) intrinsic pathway

A

C) TF pathway

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18
Q

what pathway influences the start of intrinsic pathway?
A) contact activation pathway
B) common pathway
C) TF pathway
D) extrinsic pathway

A

A) contact activation pathway

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19
Q

What factors are in the intrinsic pathway?
A) 3, 7
B) 2, 7, 9, 10
C) 10, 5, 2, 1
D) 11, 12, 9, 8

A

D) 11, 12, 9, 8

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20
Q

What factors are in the extrinsic pathway?
A) 3, 7
B) 2, 7, 9, 10
C) 10, 5, 2, 1
D) 11, 12, 9, 8

A

A) 3, 7

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21
Q

What factors are dependent on vitamin K?
A) 3, 7
B) 2, 7, 9, 10
C) 10, 5, 2, 1
D) 11, 12, 9, 8

A

B) 2, 7, 9, 10

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22
Q

What factors are in the common pathway?
A) 3, 7
B) 2, 7, 9, 10
C) 10, 5, 2, 1
D) 11, 12, 9, 8

A

C) 10, 5, 2, 1

Note: Factor 13 (stabilizing fibrin) is like the “step-sister” is it what helps create that cross-link fibrin mesh

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23
Q

What factor is involved throughout common pathway to help activate?
A) 3
B) 7
C) 10
D) 4

A

Factor 4 which is Calcium

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24
Q

What is the name of Factor 1? (describe action)
A) Antihempohiliac
B) Christmas
C) Calcium
D) Fibrinogen

A

D

Action - Form a clot

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25
Q

What is the name of Factor 2? (describe action)
A) Proaccelerin
B) Prothrombin
C) Stuart prower
D) Fibrinogen

A

B

Action - when IIa, activates I, V, VIII, IX, Xlll, PLTs, & Protein C

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26
Q

What is the name of Factor 3? (describe action)
A) Prothrombin
B) Christmas
C) Thromboplastin
D) Plasma thromboplastin antecedent

A

C

Action - Cofactor of VII

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27
Q

What is the name of Factor 4? (describe action)
A) Antihempohiliac
B) Christmas
C) Calcium
D) Fibrinogen

A

C

Action - Promotes clotting reactions

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28
Q

What is the name of Factor 5? (describe action)
A) Proaccelerin
B) Proconvertin
C) Christmas
D) Fibrin stabilizing

A

A

Action - Cofactor of X, forms prothrombinase complex

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29
Q

What is the name of Factor 6? (describe action)
A) Antihempohiliac
B) Christmas
C) Calcium
D) Unassigned

A

D

Action - NONE

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30
Q

What is the name of Factor 7? (describe action)
A) Antihempohiliac
B) Proconvertin
C) Calcium
D) Fibrinogen

A

B

Action - Activates IX & X

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31
Q

What is the name of Factor 8? (describe action)
A) Antihempohiliac
B) TF
C) Calcium
D) Fibrinogen

A

A

Action - Cofactor to IX

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32
Q

What is the name of Factor 9? (describe action)
A) Thromboplastin
B) Proconvertin
C) Christmas
D) Stuart Prower

A

C

Action - Activates X

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33
Q

What is the name of Factor 10? (describe action)
A) Antihempohiliac
B) Proconvertin
C) Stuart Prower
D) Fibrinogen

A

C

Action - Activates II, forms prothrombinase complex with V

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34
Q

What is the name of Factor 11? (describe action)
A) Prothrombin
B) Christmas
C) Thromboplastin
D) Plasma thromboplastin antecedent

A

D

Action - Activates IX

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35
Q

What is the name of Factor 12? (describe action)
A) Hageman
B) Christmas
C) Thromboplastin
D) Plasma thromboplastin antecedent

A

A

Action - Activates XI

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36
Q

What is the name of Factor 13? (describe action)
A) Prothrombin
B) Fibrin stabilizing
C) Thromboplastin
D) Plasma thromboplastin antecedent

A

B

Action - cross-links fibrin

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37
Q

What is the name of vWF Factor? (describe action)
A) Prothrombin
B) Christmas
C) Thromboplastin
D) Von Willebrand

A

D

Action - Mediates adhesion

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38
Q

Which 3 factors are NOT synthesized by liver?

A

III - synthesized by vascular wall and extravascular cell membranes; released from traumatized cells

IV - comes from out diet

vWF - Synthesized in Endothelial cells

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39
Q

What is the name of Prekallikrein Factor? (describe action)
A) Christmas
B) Stuart Prower
C) Fletcher
D) Von Willebrand

A

C

Action - Activates XII, cleaves HMWK

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40
Q

What is the name of High MW Kininogen (HMWK) Factor? (describe action)
A) Tissue Factor
B) Contact activation factor
C) Fletcher
D) Von Willebrand

A

B

Action - Supports activation of prekallikrein, XII, XI

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41
Q

Which mediators vasoconstriction? (select all that apply)
A) ADP
B) tPA
C) Serotonin
D) NO
E) Protein C & S
F) Thromboxane A2
G) Urokinase
H) AT III
I) Plasminogen
J) Prostacyclin

A

A, C, F

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42
Q

Which mediators vasodilate? (select all that apply)
A) ADP
B) tPA
C) Serotonin
D) NO
E) Protein C & S
F) Thromboxane A2
G) Urokinase
H) AT III
I) Plasminogen
J) Prostacyclin

A

D, J

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43
Q

Which mediators have fibrinolytic properties? (select all that apply)
A) ADP
B) tPA
C) Serotonin
D) NO
E) Protein C & S
F) Thromboxane A2
G) Urokinase
H) AT III
I) Plasminogen
J) Prostacyclin

A

B, G, I

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44
Q

Which mediators have anticoagulant properties? (select all that apply)
A) TF
B) vWF
C) Serotonin
D) Fibronectin
E) Protein C & S
F) Collagen
G) Urokinase
H) AT III
I) Plasminogen
J) Thrombomodulin

A

A, E, H

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45
Q

Which mediators have procoagulant properties? (select all that apply)
A) TF
B) vWF
C) Serotonin
D) Fibronectin
E) Protein C & S
F) Collagen
G) Urokinase
H) AT III
I) Plasminogen
J) Thrombomodulin

A

B, D, F, J

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46
Q

What are 2 antifibrinolytic drugs used to combat clot degradation?

A

Aminocaproic acid
Tranexamic acid

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47
Q

Is Vit K a procoagulant or anticoagulant?

A

Procoagulant

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48
Q

Which is the site where the intrinsic and extrinsic converge?
A) V
B) X
C) Va
D) II
E) Xa
F) lla

A

E) Xa

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49
Q

Which factor is first depleted (dt short half life) of all VIT K dependent factors?
A) 2
B) 7
C) 9
D) 10

A

B) 7

Tx: Vit K 10-20mg IM

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50
Q

Thrombin (Factor lla) assists in activating which factors?
A) 3, 7
B) 2, 7, 9, 10
C) 1, 5, 8, 13
D) 10, 5, 2, 1
E) 11, 12, 9, 8

A

C) 1, 5, 8, 13

And, it influences recruitment of PLTs to sire of injury.

Thrombin can also behave as an anticoagulant

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51
Q

In what 3 ways does thrombin behave as an anticoagulant? (select 3)
A) Activates l
B) Releases tPA
C) Binds with vWF
D) Simulates Gpllb/llla
E) Binds with AT3
F) Stimulates Protein C & S

A

B) Releases tPA to prevent clot formation
E) Binds with AT3 to interfere with coagulation
F) Stimulates Protein C & S to inhibit clot formation

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52
Q

If you have a low Vit K and low INR, what do you give?

A

FFP

53
Q

Protein C & S inhibit which coagulation factors?
A) 1, 5, 8, 13
B) 2, 7, 9, 10
C) 3, 5, 8
D) 10, 5, 2, 1
E) 11, 12, 9, 8

A

C) 3, 5, 8

54
Q

AT 3 corrals which clotting factors to influence factor ll?
A) 1, 5, 8, 13
B) 11, 12, 9, 8
C) 2, 7, 9, 10
D) 10, 5, 2, 1
E) 12, 11, 10, 9

A

E) 12, 11, 10, 9

55
Q

Fibrinolysis is highly regulated by?

A

plasma proteins

56
Q

A clot is primarily composed of?

A

plasminogen, plasmin, fibrin and fibrin degrading products

57
Q

How many days should aspirin be withheld prior to surgery?

A) 3-4 hours
B) 1-2 days
C) 24-48 hours
D) 7-10 days
E) 30 days

A

D) 7-10 days

58
Q

Aspirin inhibits?

A

Inhibits cyclooxyrgenase (irreversibly), therefore decreasing PLT function

59
Q

NSAIDS inhibit COX irreversibly. T/F

A

F

Inhibit Cox reversibly

60
Q

NSAIDs should be withheld how many days before surgery?
A) 3-4 hours
B) 1-2 days
C) 24-48 hours
D) 7-10 days
E) 30 days

A

C) 24-48 hours

61
Q

What is a normal bleeding time?

A

2-8 minutes

62
Q

Bleeding time evaluates what?

A

PLT function & count & microvascular contraction

63
Q

What is a normal PLT count?

A

150-300K/mm3

64
Q

How low can your PLT be and still be sufficient for hemostasis?

A

100K

65
Q

What PLT level would be mild thrombocytopenia?

A

50-100K

66
Q

What PLT level would be severe thrombocytopenia?

A

<50K

Spontaneous bleed is rare, but may be prolonged in sx.

PLT < 20K will have spontaneous bleeding

67
Q

What is the primary role of PLTs?

A

maintain vascular integrity
aggregate
initiate clotting cascade

68
Q

What is a normal PT time

A

10-15 sec

69
Q

Is PT affecting the intrinsic or extrinsic pathway?

A

Extrinsic

think PET - E for extrinsic

Extrinsic factors 3,7

70
Q

What is a normal PTT value?

A

25-40 sec

71
Q

Is PTT affecting the intrinsic or extrinsic pathway?

A

Intrinsic

think PITT - I for intrinsic

Intrinsic Factors 12,11,9,8

72
Q

T/F. Any factor deficiency (intrinsic, extrinsic, or common pathway) will lead to increased risk of bleed.

A

False

For sure only factor 8,9 will cause bleeding if deficient (seen with hemophilia)

73
Q

What is a normal INR?

A

less than or equal to 1.1 (normal healthy person)

2-3 (therapeutic range)

Book says overall (1.5-2.5)

74
Q

What is a normal ACT?

A

90-150 sec

monitors ability to clot

75
Q

What is a normal TT?

A

9-13 sec

it is a measure of fibrinolytic pathway

76
Q

TEG benefits ability to evaluate?

A

PLT reactions
Coagulation
Fibrinolysis

77
Q

TEG provides an indication of

A

Clot strength
PLT # & function
Intrinsic Pathway defect
Thrombin formation
Rate of fibinolysis

78
Q

What labs help evaluate fibrinolysis?

A

DDimer
Fibrin degradation products
TEG

79
Q

What are the 3 major reasons for transfusing in OR?

A

Replace volume
Replace coagulation factors
Improve oxygen carrying capacity

80
Q

What is the recommended dose for PLT infusion?

A

1 unit/10kg BW

This should improve PLT count by 5-10K

81
Q

What is the normal life span of PLT vs if it is donated?

A

Normal: 7-10 days
Donated: 4-5 days

82
Q

PLTs pose a high risk of bacterial transmission. T/F

A

True.

They are stored at room temperature for 4-5 days making it an excellent medium for bacterial growth

83
Q

How do we get FFP and what does it contain?

A

It is the fluid portion of whole blood, frozen to persevere it contents.

Contains: Coag factors and naturally occurring inhibitors

Doesn’t provide PLTs

84
Q

What are alternatives to replace 1 unit of FFP?

A

4-5 PLT concentrates
1 unit single donor apheresis PLT
1 unit fresh whole blood

85
Q

Cryo is rich in?

A

Fibrinogen
Factors 8, 13
Fibronectin

86
Q

When would you give cry?

A

test indicates fibrinolysis
concentration of fibrinogen < 80-100mg/dL + bleeding
adjunct in MTP
congenital fibrinogen deficiencies

If desmopressin and vWF/Vlll concentrate are ineffective in try vWD, then cryo can be given

87
Q

When do you use recombinant factor Vll?

A

Hemophilia A (Vlll) & B (lX)
Inhibitor disorders of Vlll & lX
Factor Vll deficiency
Universal hemostatic agent

*will reverse prolonged INR but not replace clotting factors

*caution in pts predisposed to thrombosis

Tx very expensive

suggested dose: 20-45 mcg/kg

88
Q

A pt with an abnormal PT/INR and normal PTT would have what deficiency (ies)?

What is the treatment?

A

Factor Vll Deficient

Tx: FFP

89
Q

A pt with an abnormal PTT and normal PT/INR would have what deficiency (ies)?

What is the treatment?

A

Factor Vlll, lX, Xl Deficient or on heparin tx

Tx: FFP, Protamine

90
Q

A pt with an abnormal PT/INR and abnormal PTT would have what deficiency (ies)?

What is the treatment?

A

Factor X, V, ll Deficient
Dysfrbrinogen
Heparin (high level)
Warfarin
Vit K deficient
Liver disease
DIC

Tx: FFP, Cryo, Protamine

91
Q

Abnormal BT and PLT count, what can you give to treat?

A

PLT concentrate

92
Q

Abnormal BT, what can you give to treat?

A

PLT concentrate

93
Q

Abnormal PT/PTT/INR, PLT count, & fibrinogen is low, what can you give to treat?

A

Pt is in DIC!

Tx: FFP, Cryo, PLT concentrate, whole blood

94
Q

Abnormal PT, what can you give to treat?

A

FFP

95
Q

Abnormal BT and PTT count, what can you give to treat?

A

vWD!

Tx: Desmopressin, vWF/Vlll, and if those don’t work then cryo

96
Q

In liver disease, you will see a decrease in which clotting factors?

A

ll, Vll, lX, X & Fibrinogen

you will also see,
Vit K deficiency
Dysfibrinogenemia
enhanced fibrinolysis
DIC
Thrombocytopenia dt hypersplenism

97
Q

What does this TEG indicate?

A

normal

98
Q

What does this TEG indicate?

A

Anticoagulants/hemophilia

99
Q

What does this TEG indicate?

A

PLT blockers

100
Q

What does this TEG indicate?

A

Fibrinolysis

101
Q

What does this TEG indicate?

A

Hypercoagulation

102
Q

What does this TEG indicate?

A

DIC stage 1

103
Q

What does this TEG indicate?

A

DIC stage 2

104
Q

What happen to RBCs when they are stored for >7days?

A

-Decreased 2,3-DPG —Oxyhemoglobin shift to the left (love = reduced O2 release)
-Decreased ATP
-Decreased pH (d/t increased lactic acid
-Impaired ability to change shape
-Hemolysis
-Increased Potassium (caution in neonates and renal failure pts)
-Increased production of proinflammatory mediators

105
Q

What are the functions of vWF?

A

1) facilitate platelet adhesion
2) plasma carrier for factor 8

**vWF synthesized by the endothelial cells and magakaryocytes

106
Q

What labs will be abnormal in vWF disease?

A

1) prolonged BT and PTT (Apex)
2) decreased vWF (Nagelhout)
3) decreased vWF activity (measured by ristocetin (an antibiotic) cofactor essay
4) decreased factor 8

107
Q

What are the treatment options for vWF disease?

A

1) Desmopressin
2) F8/vWF concentrate
3) IV immunoglobulins
4) cryo can be used only if ristocetin cofactor <50%
5) Tranexamic acid

108
Q

What are the treatment options for hemophiliac patients?

A

-Factor 8 concentrate
-Desmopression 0.3mcg/kg

109
Q

How does Warfarin work?

A

-Warfarin inhibit the enzyme vitamin K epoxide reductase complex 1, which is responsible for converting inactive Vit K to active (Apex)

110
Q

What lab tests indicate DIC?

A

Increased PT, PT, D-dimer
Decreased Platelet, Fibrinogen

111
Q

Who is at risk for DIC?

A

Sepsis (highest risk)
Postoperative
Obstetric
Blood transfusion reactions
Cancer

112
Q

Treatment options for DIC

A

Treat the underlying cause
For DIC due to sepsis, antithrombin administration

113
Q

what triggers sickle cell crisis?

A

hypoxemia
hypothermia
infection
dehydration
venous stasis
acidosis

114
Q

What is the most common surgery among sickle cell patients?

A

Cholecystectomy due to excess bilirubin from rapid breakdown of sickle erythrocytes

115
Q

What is the most common hemoglobin type in sickle cell disease (SCD)?

A

Hemoglobin S

116
Q

What are the appropriate anesthesia management for patients with SCD?

A

provide adequate hydration
promote adequate oxygen saturation
ensure normothermia
maintain acid-base balance
provide proper patient positioning
Adequate pain management
Caution with vaso-oclusive devices such as tourniquets
For high risk procedure, decrease hemoglobin S level <30%

*preop blood transfusion is a debate

117
Q

What are clinical signs of HIT?

A

-Decreased of >50% in platelet count from baseline or total platelet count <100,000 on heparin or LMWH
-S/Sx: thrombocytopenia, resistance to heparin, thrombosis, positive to assay tests

118
Q

What test gives a definite dx to HIT?

A

C-serotonin release assay is the gold standard

119
Q

Why does HIT type 2 have worse outcomes?

A

-Immunoglobulin G response
-Thrombocytopenia does not resolve spontaneously–> must d/c heparin
-associated with thrombosis

120
Q

Which of the following drugs belong to the ADP receptor inhibitors?

A

a) ASA
b) clopidogrel
c) ticlopidine
d) ticagrelor
e) cangrelor

121
Q

Platelet GP 2b/3a receptor blockers drugs

A

abciximab
tirofiban
eptifibatide

122
Q

Direct thrombin inhibitors drugs

A

bivalirudin
dabigatran

123
Q

Direct factor Xa inhibitors drugs

A

rivaroxaban, apixaban, edoxaban, betrixaban

124
Q

When should the patient stop taking unfractionated heparin or LMWH?

A

6 hours or 12-24 hours before procedure

125
Q

Pt had BMS (bare metal stent) implanted 15 days ago, pt is scheduled for an elective noncardiac surgery, you are the anesthesia provider, ok for surgery?

A

box 38.11
Elective non-cardiac surgery should be delayed 30 days after BMS implantation, 6 months after DES implantation

126
Q

Should patient stop taking ASA while on dual antiplatelet therapy?

A

with dual antiplatelet therapy (DAPT) after coronary stent who must undergo surgical procedure that mandate D/c of P2Y12 inhibitor therapy (clopidogrel or ticagrelor), recommended that ASA should be continued

127
Q

What component of blood product is appropriate for hemophilia A?

A

Preferred viral inactivated plasma derived or recombinant concentrates > Cryo > FFP

other treatments desmopressin (only works for Hemophilia A), tranexamic acid, and epsilon aminocaproic acid

128
Q

What treatment is appropriate for Hemophilia B?

A

FFP, tranexamic acid, aminocaproic acid

129
Q

What cause sickle cell disease?

A

autosomal recessive genetic abnormality of the beta-globin gene

NURS 671 - Intro to Anesthesia (8 decks)

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