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APEX > Unit 9 - Coagulation Pt 2 > Flashcards

Unit 9 - Coagulation Pt 2 Flashcards

1
Q

examples of ADP receptor inhibitors

A

Clopidogrel
Ticlodipine
Prasugrel
Ticagrelor

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2
Q

how long should ADP receptor inhibitors be stopped prior to surgery

A

Clopidogrel: 5-7 days
Ticlodipine: 14 days
Prasugrel: 7-10 days
Ticagrelor: 5-7 days

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3
Q

how long should GpIIb/IIIa receptor antagonists be stopped before surgery

A

Abciximab: 3 days
Eptifibatide: 1 day
Tirofiban: 1 day

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4
Q

how long should non-specific COX inhibitors be stopped before surgery

A

Aspirin: 7 days
NSAIDs: 1-2 days

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5
Q

how long should COX2 inhibitors be stopped prior to surgery

A

None
(rofecoxib, celecoxib)

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6
Q

when should unfractionated heparin be stopped prior to surgery

A

6 hours

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7
Q

when should LMWH be stopped prior to surgery

A

1-2 days
(enoxaparin, daltaparin, tinzaparin)

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8
Q

when should thrombin inhibitors be stopped prior to surgery

A

Argatroban: 4-6 hours
Bivalirudin: 2-3 hours

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9
Q

when should Fondaparinux be stopped prior to surgery

A

4 days

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10
Q

when should warfarin be stopped prior to surgery

A

2-4 days

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11
Q

MOA of Fondaparinux

A

factor 10 inhibitor

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12
Q

examples of plasminogen activators

A

tPA
streptokinase

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13
Q

when to stop tPA before surgery

A

1 hr

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14
Q

when to stop streptokinase before surgery

A

3 hrs

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15
Q

how do non-specific COX inhibitors prevent platelet aggregation

A

by blocking COX-1

stops conversion of arachidonic acid to prostaglandins and ultimately thromboxane A2

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16
Q

MOA of Amicar

A

plasminogen activator inhibitor

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17
Q

MOA of aprotinin

A

inhibits plasma, kallikrein, thrombin, and protein C

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18
Q

MOA of TXA

A

plasminogen activator inhibitor

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19
Q

MOA of DDAVP

A

Stimulates factor 8 and vWF factor release

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20
Q

purpose of antifibrinolytics in surgery

A

help preserve integrity of fibrin clot during surgery

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21
Q

synthetic derivative of the amino acid lysine

A

TXA

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22
Q

MOA of TXA

A

binds to lysine binding site on plasminogen & prevents conversion to plasmin

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23
Q

affinity of TXA at modest doses

A
  • strong affinity for 5 lysine binding sites on plasminogen
  • competitively prevents activation of plasminogen to plasmin
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24
Q

affinity of TXA at high doses

A

noncompetitive plasmin inhibitor

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25
Q

Most common inherited disorder of platelet function

A

von willebrand disease

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26
Q

plt count in von willebrand disease

A

normal - it’s a qualitative plt disorder

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27
Q

how is von willebrand factor synthesized

A

by vascular endothelium & megakaryocytes

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28
Q

2 key functions of von willebrand factor

A
  1. Anchors platelet to vessel wall at site of vascular injury (platelet adhesion)
  2. Carries inactivated factor 8 in the plasma
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29
Q

type 1 von willebrand disease

A

mild-moderate reduction in amount of vWF produced

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30
Q

type 2 von willebrand disease

A

the vWF that is produced doesn’t work well

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31
Q

type 3 von willebrand disease

A

severe reduction in the amount of vWF produced

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32
Q

lab findings with von willebrand disease

A
  • PTT and bleeding time ↑
  • No change in PT/INR, plt count, or fibrinogen
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33
Q

synthetic analogue of ADH

A

DDAVP

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34
Q

in what type of von willebrand disease can DDAVP be used

A

type 1, type 2

Patients with type 3 do not respond because they don’t produce cVW

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35
Q

MOA of DDAVP

A

stimulates endogenous vWF release and increases factor 8 activity

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36
Q

dose of DDAVP

A

0.3 mcg/kg IV

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37
Q

how long does a dose of DDAVP improve bleeding time

A

12-24 hours

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38
Q

contents of cryo

A

factors 8, 13, fibrinogen, and vWF

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39
Q

what can be used to treat any type of von willebrand factor disease

A

cryo
FFP

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40
Q

1st line for type 3 vWF disease

A

purified 8-vWF concentrate

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41
Q

treatment of vWF that reduces risk of transfusion-related infection

A

Purified 8-vWF concentrate:

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42
Q

disease of factor 8 deficiency

A

hemophilia A

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43
Q

pt population more likely to be affected by hemophilia A

A

males

X-linked

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43
Q

pt population more likely to be affected by hemophilia A

A

males

X-linked

44
Q

factor 8 activity assoc with spontaneous bleeding

A

< 1%
(severe disease)

44
Q

factor 8 activity assoc with spontaneous bleeding

A

< 1%
(severe disease)

45
Q

factor 8 activity assoc with increased surgical bleeding

A

activity 6-30% of normal

46
Q

lab values in hemophilia A

A
  • PTT ↑
  • No change in PT/INR, Plt count, bleeding time, or fibrinogen
47
Q

SE of giving DDAVP rapidly

A

hypotension

r/t vasodilation

48
Q

disease of factor 9 deficiency

A

hemophilia B

49
Q

severe vs mild hemophilia B disease

A
  • Severe disease (factor 8 activity < 1%) assoc. with spontaneous bleeding
  • Mild disease (factor 8 activity 6-30% normal) doesn’t cause spontaneous bleeding but is assoc with increased surgical bleeding
50
Q

half life of factor 8 concentrate

A

8-12 hours

51
Q

half life of factor 9 concentrate

A

18-24 hours

52
Q

risk of giving factor 9 concentrate

A

thromboembolic complications

53
Q

when might recombinant factor 7 be needed in a hemophilia patient

A

when they develop inhibitors that prevent exogenous factors from achieving therapeutic goals

54
Q

MOA of recombinant factor 7

A

Exact MOA unclear
both classic and contemporary cell-based theories of coagulation suggest that factor 7 contributes to thrombin generation by facilitating tissue factor at the site of vascular injury and on the surface of the platelet

55
Q

risks of recombinant factor 7

A

arterial & venous thrombosis

MI, embolic stroke, DVT, PE

56
Q

3 Conditions Assoc. with High Risk DIC

A
  1. Sepsis (highest risk = gram negative bacilli)
  2. OB complications (highest risk = preeclampsia, placental abruption, and AFE)
  3. Malignancy (highest risk = adenocarcinoma, leukemia, lymphoma)
57
Q

dose of recombinant factor 7 for hemophilia pts

A

90-120 mcg/kg

58
Q

MOA of recombinant factor 7

A

exact MOA unclear
classic and contemporary cell-based theories of coagulation suggest that factor 7 contributes to thrombin generation by facilitating tissue factor at the site of vascular injury and on the surface of the platelet

59
Q

adverse effects assoc with recombinant factor 7

A

Can increase the risk of arterial thrombosis (Ml and embolic stroke) as well as venous thrombosis (DVT or pulmonary embolism)

60
Q

what is DIC

A

disordered clotting & fibrinolysis that leads to simultaneous occurrence of hemorrhage and systemic thrombosis

61
Q

lab values assoc with DIC

A

↑ PT/PTT, D-dimer
↓ platelets, fibrinogen

62
Q

how are procoagulants kept at bay in normal physiology

A

antithrombin and tissue factor pathway inhibitor (TFPI)

63
Q

how does DIC lead to organ failure

A

systemic activation of coagulation = increased fibrin formation = microvascular thrombosis = organ failure

64
Q

what leads to hemorrhage in DIC

A

Widespread fibrin deposition consumes the body’s supply of fibrinogen, coagulation factors, and platelets = hemorrhage

65
Q

s/s DIC

A
  • ecchymosis
  • petechiae
  • mucosal bleeding
  • bleeding at IV puncture sites
  • prolonged PT and PTT
  • increased D-dimer and fibrin split products
  • decreased fibrinogen and antithrombin
66
Q

3 conditions assoc with high risk for DIC

A
  1. Sepsis
  2. OB complications
  3. Malignancy
67
Q

infections at highest risk for DIC

A

gram negative bacilli

68
Q

OB complications at highest risk for DIC

A

preeclampsia
placental abruption
AFE

69
Q

malignancies at highest risk for DIC

A

adenocarcinoma
leukemia
lymphoma

70
Q

treating DIC

A
  • Definitive treatment: reverse cause
  • Treat hypovolemia with IV fluids
  • Replace consumed blood components with FFP, platelets, and cryo
  • IV heparin or LMWH for severe microvascualr thrombosis
71
Q

factors inactivated by antithrombin

A

factors 9, 10, 11, & 12

ultimately leads to thrombin (factor 2a) inhibition

72
Q

factors inactivated by antithrombin

A

factors 9, 10, 11, & 12

ultimately leads to thrombin (factor 2a) inhibition

73
Q

causes of antithrombin deficiency

A
  • congenital
  • acquired from repeated heparin admin (consumes body’s supply of AT)
74
Q

treatment for antithrombin deficiency

A
  • AT concentrate
  • FFP

Patients with antithrombin deficiency are unresponsive to heparin

74
Q

treatment for antithrombin deficiency

A
  • AT concentrate
  • FFP

Patients with antithrombin deficiency are unresponsive to heparin

75
Q

treatment for antithrombin deficiency

A
  • AT concentrate
  • FFP

Patients with antithrombin deficiency are unresponsive to heparin

76
Q

what causes Heparin-Induced Thrombocytopenia

A
  • Occurs when the body mounts an immune response against heparin after it binds to PF4
  • IgG antibodies activate platelets
  • results in uncontrolled clot formation
77
Q

patho of HIT type 1

A
  • Heparin-induced platelet aggregation
  • Occurs after large heparin dose
78
Q

onset of HIT type 1

A

1-4 days after heparin admin

79
Q

plt count in HIT type 1 vs type 2

A

type 1 = < 100,000
type 2 = < 50,000

80
Q

treatment of HIT type 1

A

resolves spontaneously even if heparin is continued

81
Q

patho of HIT type 2

A
  • antiplatelet IgG antibodies attack factor 4 immune complex = plt aggregation
  • occurs after any heparin dose
82
Q

onset of HIT type 2

A

5-14 days after heparin admin

83
Q

morbidity of HIT type 1 vs type 2

A

type 1 = minimal morbidity
type 2 = high risk of amputation and death

84
Q

treatment of HIT type 2

A
  • d/c heparin
  • anticoagulate with direct thrombin inhibitor (Bivalirudin, Hirudin, Argatroban)
85
Q

risks of protein C or S deficiency

A

can produce hypercoagulable state and ↑ risk thrombus

Creates a feedback mechanism that prevents unnecessary clot formation

85
Q

risks of protein C or S deficiency

A

can produce hypercoagulable state and ↑ risk thrombus

Creates a feedback mechanism that prevents unnecessary clot formation

86
Q

treatment of protein C and S deficiency

A
  • Start thromboembolism treatment with heparin - pt will switch to Warfarin
  • May require life-long anticoagulation with warfarin
87
Q

factor 5 leiden mutation

A

Causes resistance to anticoagulant effect of protein C

88
Q

treatment of Factor 5 Leiden Mutation

A
  • anticoagulation only for pts with thromboembolism
  • Lifelong anticoagulation is unwarranted unless pt has recurrent thrombotic events
89
Q

Patho of sickle cell anemia

A
  • Inherited disorder that affects erythrocytes
  • Amino acid substitution (valine is substituted for glutamic acid) on the beta globulin chain alters BC geometry
  • alters RBC function
90
Q

how does sickle cell anemia alter RBC function

A
  • deoxygenation of HgbS leads to sickling
  • if severe, sickling causes RBCs to clump together and cause mechanical obstruction
  • sickled cells more prone to hemolysis and removal by spleen
91
Q

lifespan of sickled cells vs normal blood cells

A

sickled = 12-17 days
normal = 120 days

92
Q

anesthetic management of sickle cell anemia

A

focuses on avoiding triggers that promote sickling

avoid: pain, hypothermia, hypoxemia, acidosis, dehydration

93
Q

most common manifestation of sickle cell disease

A

Vaso-Occlusive Crisis

94
Q

med that reduces incidence and severity of sickle cell crisis

A

hydroxyurea

95
Q

causes of acute chest syndrome

A

thrombosis
embolism
infection

96
Q

diagnosis of acute chest syndrome

A

requires new lung infiltrates on CXR and at least one: chest pain, cough, dyspnea, wheezing

97
Q

potential causes of acute chest syndrome

A

hypoventilation, narcotics, splinting, pain

98
Q

what causes sequestration crisis in sickle cell

A

Occurs when spleen removes RBCs from circulation at a faster rate than the bone marrow produces them

99
Q

consequences of sequestration crisis in sickle cell

A

anemia
hemodynamic instability

100
Q

why are pts with sickle cell at risk for aplastic crisis

A

RBCs with HgbS have a short half life

even a small amount of bone marrow suppression can cause anemia

101
Q

common cause of aplastic crisis in sickle cell pts

A

parvovirus B19

102
Q

sickle cell patients at highest risk for pneumococcal disease

A

children

103
Q

pneumococcal disease prophylaxis in sickle cell pts

A

pneumococcal vaccination and daily penicillin up to 5 yrs of age

104
Q

diagnosis seen in 50% of sickle cell patients

A

asthma

105
Q

complication in 10% of sickle cell patients

A

pulmonary HTN

APEX (54 decks)

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