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Board Review CRNA (Sweat Book) > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What are the 4 stages of hemostasis?

A

I: Primary
II: Secondary
III: Anticoagulation
IV: Fibrinolysis

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2
Q

What are the 4 main stages of primary hemostasis?

A

1) adhesion
2) activation
3) aggregation
4) fibrin

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3
Q

______ promotes platelet ADHESION.

A

von Willebrand factor (vIII)

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4
Q

Where is vWF manufactured and released from?

A

endothelial cells

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5
Q

vWF is the ligand for the _______ receptor found on the platelet.

A

GP1b

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6
Q

What is the life span of a PLT?

A

8-12 days

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7
Q

What is the normal value for PLT’s?

A

150,000-400,000 cells per mL

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8
Q

What percent of the PLT’s can be found sequestered in the spleen?

A

33%

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9
Q

What is the MOST common inherited coagulation defect?

A 
vWF disease (vIII)
*the more common form is characterized by insufficient production of vWF by endothelial cells
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10
Q

Why should you still suspect vWF disease in a pt with a normal PLT count and increased bleeding time?

A

they may have enough platelets, but it is the vWF that adheres the PLT to the injury site

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11
Q

What is the 1st line treatment for vWF disease? How does it work?

A

D-amino D-arginine vasopressin (DDAVP, desmopressin)–> a non pressor analogue of arginine vasopressin causes release of endogenous stores of vWF
effective in 80% of cases

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12
Q

What is the dosing for DDAVP for vWF?

A

0.3mcg/kg IV infusion for 10-20 minutes

PLT adhesion is increased within 30 minutes of injection and wears off at 4-6 hours

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13
Q

What is the concern with DDAVP administration in vWF disease type 2B?

A

thrombocytopenia

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14
Q

What is given to patients that do not respond to desmopressin for vWF disease?

A

cryoprecipitate or factor VIII concentrate (Humate-P)

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15
Q

What factors does cryoprecipitate have?

A

factor VIII, I (fibrinogen), XIII

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16
Q

What is needed to activate the PLT?

A

thrombin (activated factor II or IIa)

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17
Q

What is synthesized and released from the activated PLT?

A

thromboxane A2 and ADP

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18
Q

What is the role of thromboxane and ADP?

A

uncovers fibrinogen receptors on the platelet by conformational change—> it binds to the receptor activating signal transduction—> fibrinogen then attaches thereby linking other PLT’s to each other

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19
Q

What is formed during aggregation?

A

platelet plug

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20
Q

How strong is a PLT plug?

A

water soluble and friable

also called a white thrombus or white clot

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21
Q

_______ aggregates platelets.

A

fibrinogen (factor I)

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22
Q

What occurs in the PLT after the thrombin attaches?

A

it is activated–> phospholipase A2 liberates arachidonic acid–> cyclooxygenase converts arachidonic acid to prostaglandin G2–> PGG2 is metabolized to PGH2–> PGH2 is converted to a variety of prostaglandins and thromboxane A2

This is the arachidonic acid cascade.

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23
Q

Name the arachidonic acid cascade.

A

phospholipase A2 liberates arachidonic acid–> cyclooxygenase converts arachidonic acid to prostaglandin G2–> PGG2 is metabolized to PGH2–> PGH2 is converted to a variety of prostaglandins and thromboxane A2

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24
Q

What part of hemostasis does drugs like aspirin, NSAIDs, and Plavix effect?

A

platelet aggregation

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25
Q

What is the fibrinogen receptor?

A

GPIIb/IIIa

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26
Q

Name common anti-fibrinogen receptor drugs.

A

Eptifibatide (integrilin)
Abciximab (Reopro)
Tirofiban (Aggrastat)

Remember “EAT”

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27
Q

How many hours before surgery should the following drugs be discontinued?
Eptifibatide (integrilin)
Abciximab (Reopro)
Tirofiban (Aggrastat)

A

Eptifibatide (integrilin)–> 24 hours
Abciximab (Reopro)–> 72 hours
Tirofiban (Aggrastat)–> 24 hours

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28
Q

How many hours before surgery should the following drugs be discontinued?
Aspirin
NSAIDs

A

Aspirin: 7-10 days (life of PLT)
NSAID: 24-48 hours

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29
Q

How do the following drugs work?
Eptifibatide (integrilin)
Abciximab (Reopro)
Tirofiban (Aggrastat)

A

They cap the fibrinogen receptor to prevent attachment of fibrinogen–> so no aggregation

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30
Q

Name 2 anti ADP drugs.

A

Clopidogrel (Plavix)–> anti ADP agent (life of PLT)

Ticlopidine (Ticlid)–> inhibits ADP induced fibrinogen aggregation

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31
Q

How many hours before surgery should the following drugs be discontinued?
Clopidogrel (Plavix)
Ticlopidine (Ticlid)

A

Clopidogrel (Plavix)–> 7-10 days (life of PLT)

Ticlopidine (Ticlid)—> 14 days

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32
Q

How does the drug Dipyridamole (Persantine) work? What is it commonly used for?

A

increases cAMP in pt’s—> increased cAMP prevents aggregation of PLTs
commonly used in combination with warfarin to treat prosthetic heart valves

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33
Q

What is the MOST common ACQUIRED blood clotting defect?

A

inhibition of cyclooxygenase production by aspirin or NSAIDs

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34
Q

There is no factor ______.

A

VI

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35
Q

Where do platelets come from?

A

bone marrow–> thrombocytes

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36
Q

Secondary Hemostasis is all about the production of _____.

A

Fibrin

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37
Q

If it requires vitamin K it MUST be made in the ______.

A

liver

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38
Q

What are the vitamin K dependent factors?

A

II, VII, IX, X (procoagulants) and protein C & S (anticoagulants)

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39
Q

All procoagulant factors except _____, _______, and ______ are made in the liver.

A

vWF (VIII) made in endothelial cells, tissue factor (III) made in the tissues, and calcium (IV) from diet

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40
Q

______ is woven into platelets and crosslinked.

A

fibrin

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41
Q

How strong is a fibrin clot?

A

insoluble in water; stable

also called a red clot or red thrombus

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42
Q

Cross-linking of fibrin strands requires coagulation factor _______. The final steps in fibrin production involve the ________ pathway.

A

XIIIa (fibrin stabilizing factor)

extrinsic, intrinsic, and final common pathways

43
Q

________ gets converted into fibrin and creates a _____ bond after being stabilized by XIIIa.

A

fibrinogen
covalent

*cryo contains I, VIII, XIII–> helps stabilize fibrin

44
Q

What is the Leroy Brown story of the extrinsic, intrinsic, and final common pathways?

A

Look man, I picked up 0.37 cents outside (EXTRINSIC) and I really want those potato wedges… I can’t pay 12.00 but I can give you 11.98 (INTRINSIC)….. “No man”…. Look fool, It’s common on Friday the 13th to kill 1, 2, 5, 10 of you fools (COMMON)

45
Q

What is the textbook answer for appropriate heparinization for cardiac surgery?

A

400-450

46
Q

Warfarin (coumadin) interferes with the ______ pathway.

A

extrinsic

47
Q

Prothrombin time (PT) and the International Normalized Ratio (INR) assess the _________ pathway.

A

extrinsic

48
Q

Heparin interferes with the ________ pathway.

A

intrinsic

49
Q

Partial thromboplastin time (PTT) and activated coagulation time (ACT) assess the ______ pathway.

A

intrinsic

50
Q

What is the second MOST common INHERITED coagulation disorder?

A

hemophilia A

So both are factor VIII

1) vWF
2) VIII:C hemophilia factor

51
Q

What is the difference in hemophilia A and hemophilia B?

A

hemophilia A is from factor VIII:C, hemophilia B is from christmas factor IX deficiency

52
Q

What is the most important clue to clinically significant bleeding disorders in an otherwise healthy patient?

A

THE HISTORY

53
Q

What is the most common reason for coagulopathy in patients receiving massive blood transfusions?

A

Lack of platelets

*PLT’s in stored blood are non functional after 1-2 days…. there is also dilution of factors V and VIII

54
Q

What is the only acceptable clinical indication for transfusion of packed red blood cells?

A

to increase oxygen carrying capacity of blood

55
Q

ALL procoagulants except ______ are present in fresh frozen plasma.

A

platelets

56
Q

Cryoprecipitate contains factor _______, factor ______, and factor ______.

A

factor I (fibrinogen), factor VIII (both vWF and C), and factor XIII (fibrin stabilizing factor)

57
Q

How is cryoprecipitate harvested?

A

from FFP as it is thawing

58
Q

One unit of platelets will increase count by _______.

A

5,000-10,000/mm3

59
Q

One unit of RBCs will increase Hct by ______% or ____g/dl.

A

3-4% or 1g/dl

60
Q

1 cc/kg of RBCs will increase Hct by _____%.

A

1%

61
Q

Massive transfusion is defined as ___________.

A

one complete blood volume transfused within 24 hours

62
Q

What is the role of antithrombin?

A

it binds thrombin (factor IIa) and factor Xa GREATLY
it binds IX, XI, and XII to a LESSER extent
removes them from circulation–> anticoagulating the blood

63
Q

How does heparin work?

A

increases the effectiveness of antithrombin 1,000 fold or more

64
Q

Where is antithrombin made?

A

the liver

65
Q

Heparin binds to _______.

A

antithrombin III

66
Q

Heparin increases the rate of thrombin-antithrombin reaction by _______.

A

1000 fold or more

67
Q

Name 2 disease processes that can cause an acquired antithrombin deficiency state.

A

1) cirrhosis of liver

2) nephrotic syndrome

68
Q

What is the MOST common reason a patient can be unresponsive to heparin?

A

b\c they have an antithrombin deficiency

69
Q

What is the appropriate ACT result indicating that a patient has been adequately heparinized before a CABG?

A

> 400s
if the ACT is low you can give FFP because FFP contains all coagulation and anticoagulation factors made by the liver–> including antithrombin

70
Q

What pathway or pathways does heparin block?

A

classical intrinsic and final common pathway

71
Q

What is the reversal for heparin?

A

protamine

72
Q

How does protamine work to reverse heparin?

A

it is a positively charged substance that combines electrostatically with heparin, a negatively charged substance–> this is a neutralization reaction

73
Q

Protamine reverses the action of heparin by ______.

A

neutralization

74
Q

Warfarin (coumadin) binds to ______ receptors in the ______.

A

vitamin K receptors in the liver—> production of vit K dep factors (II, VII, IX, X) is depressed

75
Q

What pathway is blocked with warfarin?

A

classical extrinsic and final common pathways

76
Q

Recombinant hirudin, ximelagatran, and argatroban are direct _____ inhibitors.

A

thrombin

77
Q

What two tests assess heparin?

A

PTT and ACT

78
Q

Heparinization is adequate if the ACT is > _______ sec.

A

400-450 sec

79
Q

What is the normal value? bleeding time

A

3-10min

80
Q

What is the normal value? platelet

A

150-400,000 cells/ml

81
Q

What is the normal value? prothrombin time (PT)

A

12-14 sec

82
Q

What is the normal value? activated partial thromboplastin time (PTT)

A

25-35 sec

83
Q

What is the normal value? activate coagulation time (ACT)

A

80-150sec

84
Q

_______ is the body’s clot buster.

A

plasmin

85
Q

How does plasminogen (inactivated form of plasmin) get converted into plasmin? (2)

A

tpa and upa
tissue type plasminogen activator
urokinase type plasminogen activator

86
Q

When a clot is formed, what is there all along that will assist in the destruction of the clot at a later time?

A

plasminogen is incorporated into the clot as it is formed

87
Q

Plasminogen, the inactive form of plasmin, is synthesized in the ________ and circulates in the blood.

A

liver

88
Q

Where is TPA made and what is its role?

A

its made in endothelial cells—> released when needed to convert plasminogen into plasmin

89
Q

Aprotinin and Amicar (epsilon aminocaproic acid) work by _______.

A

inhibiting plasmin

90
Q

When plasmin is inhibited, fibrin that is formed breaks down _______, so bleeding is _______.

A

slowly; decreased

91
Q

What is the definitive test for DIC?

A

none

92
Q

Name some conditions that contribute to or cause DIC?

A

sepsis, hemolysis, transfusion reaction, ischemia, hypotension, obstetrical emergencies (abruptio placenta, amniotic fluid embolism), acute DIC in surgical patients

93
Q

What are some causes of acute DIC in surgical patients?

A

infection, shock, and ischemia are MOST common precipitating factors of acute DIC in surgical patients

94
Q

What lab abnormalities reflect consumption of clotting factors and enhanced fibrinolysis that can be seen with DIC?

A

decreased–> PLTs, fibrinogen, prothrombin, levels of factors V-VIII-XIII
increased–> fibrin degradation products

95
Q

What is the most common cause of isolated high “PT”?

A

liver disease

96
Q

What is the treatment for coagulation abnormalities associated with liver disease?

A

replace clotting factors with FFP, cryoprecipitate, and vit K as needed

97
Q

Coagulation abnormalities can be associated with massive blood transfusion. What is deficient in transfused blood?

A

platelets, and factors V and VIII

Treatment: platelet transfusion, FFP (supplies all coagulation factors), cryoprecipitate is a primary source of factor I (fibrinogen), VIII, and XIII

98
Q

What clotting factor is considered the physiologic initiator of the coagulation cascade?

A

III (tissue factor or thromboplastin)

99
Q

Antithrombin III inhibits what 5 clotting factors?

A

II, IX, X, XI, XII

II and X MOST profoundly inhibited

100
Q

How does protamine work to reverse heparin? What kind of reaction is this?

A

combines electrostatically; neutralization

101
Q

Name 3 substances that convert plasminogen to plasmin.

A

1) tpa
2) upa
3) streptokinase

102
Q

When is aprotinin generally used in anesthesia? How does it work?

A

for repeat sternotomies and works by inhibiting plasmin

103
Q

What is the BEST test for primary hemostasis, or platelet function?

A

standardized skin bleeding time

104
Q

What are the typical manifestations of DIC?

A

bleeding, with oozing from tubes, wounds, and vascular access sites

Board Review CRNA (Sweat Book) (38 decks)

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