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PGY 4 > Medical therapy, bleed, clot > Flashcards

Medical therapy, bleed, clot Flashcards

1
Q

What is the maximum dose infusion of tPA?

A

2 mg/hr

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2
Q

What is the maximum total dose of tPa?

A

100 mg

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3
Q

What level of fibrinogen do you stop tPA?

A

100 mg/dL or < 1 g/L

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4
Q

What hematologic investigations are required for: Patients who have no bleeding history and will undergo minor procedures, such as lipoma excision.

A

None

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5
Q

What hematologic investigations are required for: Patients who have no previous bleeding history but will undergo a major operation.

A

aPTT and platelet count

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6
Q

What hematologic investigations are required for: Patients whose bleeding history raises concern for defective hemostasis and those whose procedure might impair hemo- stasis (e.g., cardiac or neurosurgical interventions).

A

1) How well will patient form platelet plug? platelet count
2) How effective is coags? PT and aPTT
3) Size and stability of fibrin clot? Factor 8 deficiency, fibrinolysis screening

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7
Q

What hematologic investigations are required for: A history or physical findings highly suggestive of abnormal hemostasis, and the surgical procedure is not a factor.

A

1) How well will patient form platelet plug? platelet count
2) How effective is coags? PT and aPTT
3) Size and stability of fibrin clot? Factor 13 deficiency, fibrinolysis screening
4) vWD or qualitiative platelet disorder? Bleeding time after 600 mg ASA
5) Factor 8 and 9 levels
6) Dysfibrogenemia? Thrombin time (TT)

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8
Q

Which factors does PT measure?

A

Extrinsic pathway of clotting: 2, 5, 7, 9, 10, protein c&s, tissue factor, fibrinogen

End point is time required in seconds for a fibrin clot to form

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9
Q

What would cause an abnormal PT?

A

consumptive coagulopathy, warfarin, vit k deficiency, liver disease

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10
Q

Which factors does activated partial thrombplastin time (aPTT) measure?

A

Intrinsic pathway and final common pathway -

All factors except factor 7

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11
Q

What blood test do you use to monitor warfarin therapy?

A

PT/INR

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12
Q

What blood test do you use to monitor heparin therapy?

A

aPTT

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13
Q

What would cause an abnormal aPTT?

A

Consumptive coagulopathy, heparin, lupus anticoagulants

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14
Q

What factor does thrombin time (TT) measure?

A

Fibrinogen (functional)

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15
Q

What test do you use to monitor fibrinolysis?

A

thrombin time (TT)

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16
Q

Which variables does activated clotting time measure?

A

Global clotting function

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17
Q

What blood test do you use to monitor intra-op heparin therapy

A

ACT

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18
Q

What factors/variables are measured by bleeding time (BT)?

A

Platelet number and function

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19
Q

What would cause abnormal bleeding time (BT)?

A

abnormal platelet function, antiplt drugs, thrombocytopenia, uremia, von willebrand disease

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20
Q

What variable does thromboelastography measure?

A

clotting kinetics

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21
Q

What blood test is used for monitoring during or after cardiopulmonary bypass?

A

thromboelastography

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22
Q

What variable does fibrin degradation products (FDPs) measure?

A

Fibrinolysis

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23
Q

What does euglobulin lysis time (ELT) measure?

A

Fibrinolysis - e.g. diagnosing DIC

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24
Q

What blood test would help with detecting hemophilia A and B?

A

aPTT

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25
Q

What does ROTEM measure?

A

like thromboelestography, a point of care testing which measures clotting kinetics. used for directing blood product administration in bleeding trauma, post-partum hemorrhage etc.

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26
Q

Which blood test can help you differentiate DIC from primary fibrinolytic state?

A

ELT Euglobulin lysis time (time it takes to lyse a clot). Diagnostic of primary fibronolyis if shortened ELT in patients without thrombcytopenia or schistocytosis

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27
Q

What is the most common inherited bleeding disorder?

A

von willebrand disease

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28
Q

What does von willebrand factor do?

A

Binds to both platelets and endothelial components to build an adhesive bridge for primary hemostasis. also acts as a carrier protein for factor 8

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29
Q

What are the 3 types of von willebrand disease?

A

1 - Autosomal dominant, minimal bleeding

2 - Autosomal but varied, variable bleeding

3 - Autosomal recessive, severe bleeding

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30
Q

What type of von willebrand disease have the most severe bleeding?

A

autosomal recessive

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31
Q

What are the 4 types of type 2 von willebrand disease?

A

2A - loss of high molecular weight multimers => decreased plt function

2B - increased affinity for GP Ib

2M - Reduced binding of GP Ib despite having large vWF multimers

2N - altered factor 8 binding site therefore rapid clearance of 8

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32
Q

What should type 1 vWD patients be treated with perioperatively if they have mild to moderate bleeding?

A

avoid NSAIDS. DDAVP.

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33
Q

What should patients with type 3 vWD be treated with?

A

For serious bleeding or major surgery - replacement therapy - vWF, factor 8-vWF concentrates or cryoprecipitate (goal to keep activity of factor 8/vWF between 50-100% for 3-10 days)

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34
Q

What are 4 types of giant platelet disorders?

A

1 - Structural defects e.g. Bernard Soulier syndrome

  1. With abnormal neurtrophils e.g. May-Hegglin
  2. With systemic manifestations - hereditary macrothrombocytopenia with hearing loss
  3. With no specific abnormalities e.g. Mediterranean macrothrombocytopenia
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35
Q

How do you treat patients with giant platelet disorders?

A

Education to avoid activities with minor trauma. Platelet transfusion os significant hemorrhage.

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36
Q

What is Glanzmann’s thrombasthenia?

A

An autosomal recessive disease which causes defect in GP 2b 3a which renders platelets unable to aggregate.

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37
Q

What does GP 2b 3a do?

A

Allows platelets aggregate and bind to soluble proteins and vWF

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38
Q

How do you treat patients with Glanzmann’s thrombasthenia who bleed significantly?

A

Platelet transfusion

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39
Q

What are the 2 types platelet granule deficiencies associated with storage pool disorders?

A

Alpha granules which contain: vWF, fibrinogen, platelet derived growth factor, thrombospondin)

Dense granules which release: ADP and serotonin

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40
Q

What is gray platelet syndrome?

A

Alpha granule storage disorder. Typically minimal mucosal bleeding. DDAVP given periprocedurally and platelet transfusions.

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41
Q

What factors are deficient in patients with hemophilia A?

A

Factor 8

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42
Q

What factors are deficient in patients with hemophilia B?

A

Factor 9

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43
Q

What factors are deficient in patients with hemophilia C?

A

Factor 11 (uncommon)

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44
Q

Which factor is protected from premature degradation by vWF?

A

Factor 8

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45
Q

How can you clinically distinguish the difference between hemophilia A and B?

A

Clinically indistinguishable

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46
Q

What stage of hemostasis is defective in hemophilia bleeding?

A

Secondary hemostasis - a normal platelet plug forms but stabilization of plug by fibrin is defective because inadequate thrombin

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47
Q

What is the hallmark of severe hemophilia?

A

Spontaneous bleeding into joints and muscles

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48
Q

How can you raise factor concentrations in patients with mild hemophilia A?

A

DDAVP

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49
Q

Prior to elective surgery, what level of factor 8 is required in hemophilia patients?

A

Over 80%. Factor 8 concentrations can be given.

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50
Q

What causes acquired platelet dysfunction (7):?

A

1- uremia

2 - liver disease

3 - cardiopulmonary bypass

4 - hematologic malignancy

5- thrombotic thrombocytopenia purpura

6 - immune thrombocytopenic purpura

7 - hypersplenism

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51
Q

How does liver disease result in thrombocytopenia?

A

Portal hypertension, splenic sequestration and decreased thrombopoietin production

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52
Q

How can you treat actively bleeding uremic patients or those undergoing major surgery?

A

1 - Correct anemia to hematocrit 25-30% to improve platelet aggregation and adheshion.

2- DDAVP to enhance release of vWF

3 - Conjugated estrogen - mechanism unknown.

4 - Dialysis for uremic complications

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53
Q

What are vitamin K dependent coagulation factors?

A

10, 9, 7, 2 (1972) protein C&S

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54
Q

How do you treat bleeding in patients with vitamin K deficiency/on warfarin?

A

Treat with vitamin K or FFP.

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55
Q

When reversing warfarin with vitamin K - how long does it take to take effect? How long does it last?

A

At least 6 h to take effect but more durable reversal than FFP which only lasts 6 h

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56
Q

When reversing warfarin with FFP - how long does it take to take effect? How long does it last?

A

Immediate, lasts 6 h

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57
Q

DIC is primarily due to the uncontrolled production of what?

A

Thrombin - leading to intravascular fibrin deposition and thrombosis of the microvasculature > end organ damage

58
Q

In DIC what causes the coagulopathy?

A

Thrombosis of the microvasculature leading to end organ damage, initiates systemic tPA release which induces thrombolysis and consumptive coagulopathy

59
Q

What are the most common precipitants of DIC?

A

Sepsis, malignancy, trauma, amniotic fluid embolism, placental abruption

60
Q

What are the clinical symptoms of the first stage of DIC?

A

Asymptomatic - compensated activation of hemostatic system

61
Q

What happens to the lab values in the 1st phase of DIC?

A

1 - PT normal

2 - aPTT normal

3 - TT normal

4 - Platelet count normal

5 - Thrombin antithrombin complex elevated

6 - Prothrombin fragmin elevated

7 - Fibrinogen normal

8 - FDP normal

62
Q

What happens to the lab values in the 2nd phase of DIC?

A

1 - PT elevated

2 - aPTT elevated

3 - TT elevated

4 - Platelet count decreased

5 - Thrombin antithrombin complex elevated

6 - Prothrombin fragmin elevated

7 - Fibrinogen decreased

8 - FDP elevated

63
Q

What are the clinical features of 2nd phase of DIC?

A

Bleeding from injuries/venipuncture, renal/hepatic/pulmonary function impaired

64
Q

What happens to the lab values in the 3rd phase of DIC?

A

1 - PT very elevated

2 - aPTT very elevated

3 - TT very elevated

4 - Platelet count very decreased

5 - Thrombin antithrombin complex elevated

6 - Prothrombin fragmin elevated

7 - Fibrinogen very decreased

8 - FDP very elevated

65
Q

What are the clinical features of 3rd phase of DIC?

A

Ecchymoses, multiorgan failure

66
Q

What is the overriding goal in treating DIC?

A

Correcting precipitating disease

67
Q

What is the goal target for resuscitating DIC?

A

Often have to give factors and platelets. Goal Fibrinogen > 100 mg/dL

68
Q

What can cause a primary hyperfibronolytic state?

A

Malignancy, liver failure, trauma, congenital deficiency of fibrinolysis inhibitors.

Very difficult to discern from secondary fibrinolysis (DIC) - requires Euglobulin lysis time (ELT)

69
Q

What is the treatment for primary fibrinolysis?

A

Transexamic acid (and aminocaproic acid). These are competitive inhibitors for the conversion of plasminogen to plasmin. Often factor 5 and 8 also given.

70
Q

How does heparin work?

A

Binds to and activates antithrombin preventing clot formation and propgation. Antithrombin accelerates ability to inactivate 2 (thrombin), 10a, and 9a

71
Q

What does a d-dimer measure?

A

Product of fibrin proteolysis by plasmin - indicates that fibrinolysis happening

72
Q

What other than DVT can cause elevated d-dimer?

A

Surgery, trauma, pregnancy, malignancy, thrombotic disorders

73
Q

What are 5 duplex findings of a DVT?

A

Incompressible vein, absense of flow in vein, absent flow augmentation with distal compression, vein diameter increased, increased echogenicity

74
Q

What is the sensitivity of utrasound to identify asymptomatic calf DVTs?

A

Only 40%, can’t rule out based on ultrasound alone. Wells criteria increases predictive value.

75
Q

What are 9 elements of the Wells score for DVT?

A

1 - previous DVT

2 - active cancer

3 - entire leg swollen

4 - tenderness along deep venous territory

5 - collateral veins (not varicose)

6 - pitting edema isolated to affected leg

7 - paralysis/paresis/immobilization

8 - major surgery/bed bound x 3 or more days

9 - calf swelling at least 3 cm larger than other side

76
Q

When do you use d-dimers in DVT workup?

A

Clinically likely but venous duplex shows no DVT

or clinically unlikely

77
Q

What age of thrombus is thrombolysis effective?

A

< 10 days, afterwards thrombus is adherent to walls and organized

78
Q

How frequently do DVTs recurr in 1st year?

A

15%

79
Q

Should you anticoagulate calf DVTs?

A

Controversial - 2016 chest guidelines state 3 months of anticoagulation

80
Q

How should you treat femoropopliteal DVT?

A

Usually anticoagulation alone. Sometimes thrombus removal required if clot in the popliteal trifurcation because blocks outflow from entire calf and can have more morbidity.

81
Q

How should you treat iliofemoral DVT?

A

Endo/open recanalization. Anticoagulation rarely works alone and 30% will have venous claudication/ulceration

82
Q

Why does unfractionated heparin have to be monitored?

A

Nonspecific binding (plasma proteins, platelet factor 4, macrophages, endothelial cells) therefore unpredictible pharmacokinetics and narrow therapeutic window

83
Q

What are 5 drawbacks of unfractionated heparin?

A

1 - need for hospitalization

2 - frequent blood draws

3 - difficulty promptly reaching therapeutic range

4 - potential for HITT

5 - variable response

84
Q

What are 5 advantages of LMWH compared with UFH?

A

1 - longer half life (3-5h)

2 - more consistent response/no monitoring

3 - less major bleeding

4 - lower mortality

5 - better bioavailability

85
Q

How should you treate acute VTE in cancer patients?

A

2016 chest guidelines suggest LMWH or DOAC over vitamin K antagonists because studies shows higher failure rate of VKA

86
Q

Which 2 drugs have FDA approval to treat HIT?

A

Direct thrombin inhibitors - argatroban and bivalrudin

87
Q

Why are vitamin K antagonists procoagulant in first 3 days?

A

Inhibits coagulation factors 10, 9 ,7, 2 but also inhibits natural anticoagulants protein C & S. Protein C & S have much shorter half life so inhibition of these anticoagulants initially make patients prothrombotic.

88
Q

How long do you need to overlap heparin and warfarin?

A

5 days

89
Q

Name 4 direct acting oral anticoagulants (DOAC) and what they inhibit

A

1 - Rivaroxaban - Xa

2 - Apixaban - Xa

3 - Edoxaban - Xa

4 - Dabigatran - Thrombin

90
Q

What did the EINSTEIN trial show?

A

rivaroxaban noninferior to warfarin

91
Q

Which trial showed Apixaban non inferior to warfarin?

A

Amplify

92
Q

Do DOACs have less major bleeding compared with VKA?

A

Rivaroxaban - no difference EINSTEIN

Apixaban (amplify), edoxaban (hokusai), dabigatran (recover) has less bleeding

93
Q

What agent reverses dabigatran?

A

Idaricuzumab

94
Q

How long does idaricuzumab take to reverse dabigatran? How long does it last?

A

Immediate, 24 h

95
Q

Should you use compression stockings to prevent post thrombotic syndrome?

A

Chest guidelines 2016 no longer recommend compression stockings, no benefit in SOX trial. But still may be of some use for symptom releif.

96
Q

How do you know whether to continue anticoagulation for DVT after 3 months?

A

D-Dimer elevation (PROLONG study). Those with d-dimer elevation and no continuation of anticoagulation had higher VTE recurrence rate.

97
Q

Which trials showed the benefit of adding ASA to anticoagulation for decreasing long term VTE recurrence?

A

WARFASA, ASPIRE, INSPIRE

98
Q

What did AMPLIFY-EXT show?

A

Addition of low dose apixaban after 6 - 12 months of therapeutic anticoagualtion can reduce recurrence of VTE without significantly increasing bleeding risk (NNT 14 to prevent 1 recurrent VTE)

99
Q

*What is the half life of heparin IV and SC?

A

IV - 1.5 h, SC - 8h

100
Q

Why does warfarin induced skin necrosis occur?

A

Initial prothrombotic state (inhibition of natural anticoagulants protein C & S) cause small vessel thrombosis of the skin

101
Q

What are 2 disadvantages of DOACs compared with warfarin?

A

Not easily reversed, no easy access lab test to evaluate therapeutic efficacy

102
Q

How do you manage life threatening bleeding in patient on DOACs?

A

FFP/cryo wont work. Transfuse blood and PCC (prothrombin concentration complex e.g. octaplex) and recombinant factor 7a

103
Q

When can you hold plavix in patients who underwent bare metal coronary stenting? DES?

A

6 months for BMS, 1 year for DES

104
Q

How does apiximab work?

A

GP 2a 3b inhibition -> inhibits platelet aggregation

105
Q

What percentage of patients show inadequate platelet inhibition with clopidogrel?

A

30%

106
Q

How do thrombolytic agents work?

A

All activate plasminogen, which directly or indirectly convert plasminogen to plasmin then plasmin degrades a number of factors including fibrinogen, fibrin, prothrombin, 5 7

107
Q

Acidosis can result in coagulopathy. What is a strategy to prevent this effect in reperfusion injury?

A

Pre-emptive resp and metabolic alkalosis prior to clamp removal

108
Q

What are 6 classes of causes for coaulopathy?

A

1- inherited coagulopathies

2 - acquired coagulopathies

3 - drug induced

4 - hypothermia

5 - acidosis

6 - dilutional

109
Q

How do you prevent dilutional coagulopathies when resuscitating major bleeding?

A

Massive transfusions of pRBC need adequate FFP ratio

110
Q

Which infusion solution has recognized anticoagulation and antiplatelet properties?

A

Hypertonic saline

111
Q

What are 4 indications for transfusing pRBC?

A

American Society of Anesthesiologists - no longer based on Hgb alone.

1 - Symptomatic anemia,

2- hgb < 60 in healthy patients

3- massive hemorrhage

4-decreased oxygen carrying capacity

112
Q

How much should your platelets go up after transfusing a unit?

A

30 - 60k uL

113
Q

What are 2 indications to transfuse platelets?

A

< 10k, or bleeding patient < 50k

114
Q

What does FFP contain?

A

All clotting factors, esp 10 9 7 2 protein C/S and antithrombin 3

115
Q

What are 5 indications for transfusing FFP?

A

1 - warfarin related bleeding

2 - massive transfusion

3 - thrombotic thrombocyotepenic purpura

4 - coag factor deficiencies

5 - anti thrombin 3 deficiency

116
Q

What does cryoprecipitate contain?

A

Fibrinogen, factors 5, 8, 13, vWF

117
Q

What is are 2 indications to transfuse cryoprecipitate?

A

1 - Hypofibrinogenemia (consumptive coagulopathy, primary fibrinolysis, therapeutic thrombolysis)

2 - Massive hemorrhage

118
Q

What does DDAVP do?

A

Desmopressin is an arginine vasopressin analogue that stimulates the release of vwF from the vascular endothelium.

119
Q

What are 2 indications for DDAVP?

A

Uremic platelet dysfunction, some von Willebrand diseases

120
Q

What is protamine?

A

Derived from salmon sperm, protamine reverses heparin

121
Q

*What dose of protamine do you give to reverse heparin?

A

1 mg per 100 units of heparin given in the past 6h

122
Q

When do you transfuse factor 7a

A

Hemophelia. Off label use - massive hemorrhage, ICH, trauma, cardiac surgery

No evidence for these indications and increased thromboembolic events and cost

123
Q

When do you use transexamic acid/aminocaproic acid?

A

Primary fibrinolysis.

Surgical patients with high bleeding risk.

2011 cochrane review shows it decreases periop blood loss/allogenic transfusion.

124
Q

What are chitosans?

A

Deacetylated form of chitin - gauze bandage which promotes rapid hemostatic clot formation

125
Q

What is mineral zeolite?

A

Absorbs water, thus concentrating clotting factors and platelets. Also may activate factor 12. (Caution - exothermic!)

126
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130
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131
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132
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133
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134
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136
Q

How long do you hold ASA and plavix before a surgery?

A

Plavix - 5 days. Typically don’t need to hold ASA

137
Q

What is type 1 vs type 2 HITT?

A

Type 1 - innocuous benign drop in plt within 2 days of heparin initiation. 10-30% of pts. Plt counts generally normalize w continued heparin admin.

Type 2 - Antibody mediated disorder requiring cessation of heparin, avoid vit K antagonists and immediate treatment with alternative anticoagulant.

138
Q

Name 4 risk factors for HITT

A

1) Women (2x risk)
2) Orthopedic surgery
3) Malignancy (2x risk)

139
Q

What is the timeline for HIT?

A

Immunizing heparin exposure 1-12 weeks earlier

UFH dose - 5-10 days after get thrombocytopenia typically but can have “rapid onset HIT” immediately.

140
Q

The clinical diagnosis of DIC (5):

A
  1. An underlying disease state known to be associated with DIC
  2. Prolongation of the thrombin time and partial thromboplastin time
  3. Plt < 100,000
  4. Presence of fibrinogen (fibrin degradation products)
  5. Low levels of anti thrombin 3.
141
Q

What is purpura fulminans?

A

Symmetricl peripheral gangrene. Skin and soft tissue necrosis caused by infection or DIC leading to microvascular thrombosis.

PGY 4 (25 decks)

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