Chapter 95 Flashcards
Hemostasis, thrombosis, fibrinolysis
1
Q
What induces endothelial cells to express adhesion molecules in venous thrombosis?
A
Hypoxemia
This process helps tether tissue factor–bearing leukocytes and microparticles to the endothelial surface.
2
Q
What role do neutrophil extracellular traps (NETs) play in thrombosis?
A
They provide a scaffold that binds platelets, promotes activation and aggregation, and activates the contact system of coagulation
NETs are webs of chromatin released from activated neutrophils.
3
Q
What exacerbates local thrombus formation in venous thrombosis?
A
Impaired blood flow
This condition reduces the clearance of activated clotting factors.
4
Q
What can happen to thrombi that extend into the proximal veins of the leg?
A
They can dislodge and travel to the lungs, causing pulmonary embolism.
5
Q
What is the primary focus for treating arterial thrombosis?
A
Inhibition of platelet aggregation
Other treatments may include anticoagulants and fibrinolytic agents in acute settings.
6
Q
What effect does low-dose rivaroxaban have when combined with dual-antiplatelet therapy?
A
Reduces recurrent ischemic events and stent thrombosis in patients with acute coronary syndrome.
7
Q
What is the mainstay for prevention and treatment of venous thromboembolism (VTE)?
A
Anticoagulants
8
Q
Why are antiplatelet drugs less effective for preventing venous thrombosis?
A
Due to the limited platelet content of venous thrombi.
9
Q
What is the reduction in risk for recurrent VTE when aspirin is used for secondary prevention?
A
About 30%
(overlap of venous and arterial thrombosis)
10
Q
What benefit does fibrinolytic therapy provide for patients with massive pulmonary embolism?
A
Achieves more rapid restoration of pulmonary blood flow compared to anticoagulant therapy alone.
11
Q
How do arterial thrombi form on disrupted atherosclerotic plaques?
A
Plaque rupture exposes thrombogenic material, triggering platelet aggregation and fibrin formation.
12
Q
What characterizes arterial thrombi?
A
They are rich in platelets and appear white due to high shear in injured arteries.
13
Q
Where does venous thrombosis commonly occur?
A
In the deep veins of the leg.
14
Q
What are potential complications of venous thrombosis?
A
Postthrombotic syndrome and pulmonary embolism.
15
Q
What are the characteristics of venous thrombi?
A
They form under low-shear conditions, contain few platelets, and consist mostly of fibrin and trapped red cells (appear red)
16
Q
What substances do endothelial cells synthesize to inhibit platelets?
A
Prostacyclin and nitric oxide
17
Q
What is the function of ecto-ADPase CD39 on endothelial cells?
A
Attenuates platelet activation by degrading ADP
18
Q
How do endothelial cells regulate thrombin generation?
A
By expressing heparan sulfate proteoglycans on their surface
binds to antithrombin and enhances its activity
o also bind tissue factor pathway inhibitor (TFPI)
19
Q
What is the role of tissue factor pathway inhibitor (TFPI) in coagulation?
A
A naturally occurring inhibitor of coagulation that binds to endothelial cells
20
Q
What happens when heparin is administered?
A
Displaces glycosaminoglycan-bound TFPI from the vascular endothelium
21
Q
What initiates the protein C anticoagulant pathway?
A
Thrombin binding to thrombomodulin
22
Q
What does activated protein C do?
A
Degrades and inactivates activated factor Va and factor VIIIa
23
Q
What enhances the protein C pathway by about 20-fold?
A
EPCR on the endothelial cell surface
EPCR-endothelial cell protein C receptor
24
Q
What are the two types of plasminogen activators synthesized by the vascular endothelium?
A
- t-PA (tissue plasminogen activator)
- u-PA (urokinase plasminogen activator)
25
What is the major regulator of both t-PA and u-PA?
type 1 plasminogen activator inhibitor (PAI-1)
26
What role does annexin II play in fibrinolysis?
Acts as a coreceptor for plasminogen and t-PA that promotes their interaction
27
What is the lifespan of platelets once they enter circulation?
7 to 10 days
28
What regulates megakaryocytic proliferation and platelet production?
Thrombopoietin
29
What is the role of thrombin in platelet activation?
A potent platelet agonist that amplifies platelet recruitment and activation
30
What receptors do platelets use to adhere to collagen?
* α2β1
* GP VI
31
What receptors do platelets use to bind von Willebrand factor (vWF)?
* GP Ibα
* GP IIb/IIIa (αIIbβ3)
32
What effect does low shear conditions have on platelet activation?
Collagen can capture and activate platelets on its own
33
What is the role of vWF in high shear conditions?
Must act in concert with collagen to support optimal platelet adhesion and activation
34
What is the significance of ADAMTS13 in relation to vWF?
Proteolytically processes vWF to prevent the accumulation of unusually large multimers
35
What is the consequence of ADAMTS13 deficiency?
Results in microvascular thrombosis due to large vWF multimers tethering platelets to the endothelium
## Footnote
thrombotic thrombocytopenic purpura (TTP)
36
How does circulating vWF differ from immobilized vWF?
Circulating vWF is in a coiled conformation; immobilized vWF is elongated and exposes the platelet-binding A1 domain
37
What initiates signaling pathways that result in platelet activation?
Adhesion to collagen and vWF
38
What is the role of thromboxane A2 in platelet activation?
It is a potent vasoconstrictor that activates ambient platelets and recruits them to the site of injury
39
Which receptor is the most important ADP receptor on platelets?
P2Y12
40
What is the effect of thromboxane A2 and ADP binding to their receptors?
Increases intracellular calcium concentration in platelets
41
What is the final product of the coagulation system?
Fibrin
42
What are the three enzyme complexes involved in thrombin generation?
* Extrinsic tenase
* Intrinsic tenase
* Prothrombinase
43
What complex is formed on exposure of tissue factor-expressing cells to blood?
Extrinsic tenase
44
What initiates the activation of the extrinsic tenase complex?
Tissue factor binding to factor VIIa.
45
What is the role of factor IXa in the intrinsic tenase complex?
It activates factor X.
46
What enhances the catalytic efficiency of the prothrombinase complex?
Incorporation of factor Xa into the complex.
47
What does thrombin convert soluble fibrinogen to?
Insoluble fibrin.
48
What are the components of fibrinogen?
* Aα chain
* Bβ chain
* γ chain.
49
What stabilizes the fibrin network?
Factor XIIIa.
50
What is the structure of fibrinogen described as?
Trinodular structure with a central E domain and two D domains.
51
True or False: Activated platelets release growth factors that promote wound healing.
True.
52
Aggregation serves as the final step in formation of the platelet plug by linking platelets to each other through _______.
[GP IIb/IIIa].
53
What is the current view on the contact system in coagulation?
The contact system is regarded as unimportant for hemostasis, as patients deficient in these factors do not have bleeding problems.
## Footnote
The contact system includes factor XII, prekallikrein, and high-molecular-weight kininogen.
54
How does the contact system contribute to thrombosis?
Emerging evidence suggests the contact system plays a role in thrombosis through several mechanisms.
## Footnote
These mechanisms include activation by medical devices, neutrophil extracellular traps, and polyphosphate release.
55
What triggers clotting through the contact system?
Blood-contacting medical devices, such as stents or mechanical heart valves, and extracorporeal circuits trigger clotting by **activating factor XII**.
## Footnote
This activation is essential for coagulation processes.
56
What is the role of factor XIIa in coagulation?
Factor XIIa converts prekallikrein to kallikrein and activates factor XI, propagating coagulation.
## Footnote
The reaction is accelerated by high-molecular-weight kininogen.
57
What are neutrophil extracellular traps (NETs)?
NETs are web-like structures extruded by activated neutrophils, composed of nuclear DNA, histones, and proteases.
## Footnote
NETs promote coagulation by binding and activating platelets, trapping red blood cells, and activating the contact pathway.
58
How do NETs promote coagulation?
NETs promote coagulation by:
* Binding and activating platelets
* Trapping red blood cells
* Activating the contact pathway
## Footnote
This shows the multifaceted role of immune responses in coagulation.
59
What role do polyphosphates play in coagulation?
Polyphosphates released from activated platelets can activate factor XII and promote the activation of factor XI by thrombin.
## Footnote
This indicates that surfaces and cells contribute to coagulation at multiple sites.
60
What has research shown about the contact system's role in thrombus growth?
Studies suggest the contact system contributes to the growth of arterial and venous thrombi.
## Footnote
This has been observed in both animal and human studies.
61
What effect does lowering factor XI levels have in knee arthroplasty patients?
Lowering factor XI levels or inhibiting factor XIa reduces the risk of postoperative VTE to a greater extent than enoxaparin.
## Footnote
This highlights factor XI as a potential target for new anticoagulants.
62
What initiates fibrinolysis?
Fibrinolysis begins when plasminogen activators convert plasminogen into plasmin, which then degrades fibrin into soluble fragments.
63
What are the two types of plasminogen activators in blood?
The two types of plasminogen activators are t-PA and u-PA.
64
What is the role of t-PA?
t-PA mediates intravascular fibrin degradation.
65
How does u-PA function?
u-PA binds to a specific u-PA receptor (u-PAR) on cell surfaces, where it activates cell-bound plasminogen.
66
What regulates fibrinolysis?
PAI-1 and PAI-2 inhibit plasminogen activators, and alpha2-antiplasmin, which inhibits plasmin.
## Footnote
PAI-1 and PAI-2 inhibit plasminogen activators, and alpha2-antiplasmin, which inhibits plasmin.
67
How does t-PA convert plasminogen?
t-PA cleaves a single peptide bond to convert single-chain Glu- or Lys-plasminogen into two-chain plasmin.
68
Why is Lys-plasminogen a better substrate for t-PA?
Lys-plasminogen has an open conformation that exposes the t-PA cleavage site, making it a better substrate than Glu-plasminogen.
69
What increases t-PA activity?
prescence of fibrin
70
How does alpha 2-antiplasmin inhibit plasmin?
Alpha 2-antiplasmin inhibits circulating plasmin by docking to its first kringle domain and then inhibiting the active site.
71
What role does factor XIIIa play in fibrinolysis?
Factor XIIIa cross-links small amounts of alpha 2-antiplasmin onto fibrin, preventing premature fibrinolysis.
72
How do annexin II and endothelial cells interact with t-PA?
Annexin II on endothelial cells binds t-PA and plasminogen, promoting their interaction.
73
What is the role of TAFI in fibrinolysis?
TAFI is synthesized in the liver and circulates in blood in a latent form, activated by thrombin bound to thrombomodulin
## Footnote
TAFI-
74
How does activated TAFI (TAFIa) affect fibrinolysis?
TAFIa attenuates fibrinolysis by cleaving Lys residues from degrading fibrin, removing binding sites for plasminogen, plasmin, and t-PA.
75
What is the relationship between TAFI and coagulation?
TAFI links fibrinolysis to coagulation by being activated by the thrombin-thrombomodulin complex, which also activates protein C.
76
What is the mechanism of action of u-PA?
u-PA is synthesized as a single-chain polypeptide with minimal enzymatic activity, converted into an active two-chain form by plasmin.
77
How does scu-PA activate plasminogen?
scu-PA does not activate plasminogen in the absence of fibrin but can activate fibrin-bound plasminogen
78
What is the effect of soluble u-PAR?
Soluble u-PAR can cause **acute kidney injury** by inducing the formation of reactive oxygen species in kidney tubules.
79
What is the association between lipoprotein(a) and atherosclerosis?
Lipoprotein(a) possesses kringle domains and **competes with plasminogen** for cell surface binding, which may explain its association with atherosclerosis.
80
Example of mixed (hereditary and acquired) hypercoagulable state
hyperhomocysteinemia
81
What is the primary role of hemostasis?
Preserves vascular integrity by balancing blood fluidity and preventing excessive bleeding after vascular injury
82
What can perturbation of hemostasis lead to?
Thrombosis
83
What are the common consequences of arterial thrombosis?
ACS, ischemic stroke, limb gangrene
84
What can thrombosis in the deep veins of the leg lead to?
Postthrombotic syndrome and pulmonary embolism
85
How does a healthy vascular endothelium regulate hemostasis?
By inhibiting platelets, promoting coagulation, and suppressing fibrinolysis
86
What is the composition of the vascular endothelium?
A monolayer of endothelial cells that separates blood from the prothrombotic subendothelial components
87
What do endothelial cells synthesize to inhibit platelet activation?
Prostacyclin and nitric oxide
88
What is the function of ecto-ADPase (CD39) on endothelial cells?
Attenuates platelet activation by degrading ADP
89
Which anticoagulant activity is regulated by intact endothelial cells?
Thrombin generation
90
What do endothelial cells express to enhance antithrombin activity?
Heparan sulfate proteoglycans
91
What initiates the protein C anticoagulant pathway?
Thrombin binding to Thrombomodulin
92
What do endothelial cells synthesize to modulate fibrinolysis?
Tissue and urokinase plasminogen activators (t-PA and u-PA)
93
What is the life span of platelets after entering circulation?
7 to 10 days
94
What regulates the fragmentation of bone marrow megakaryocytes to form platelets?
Thrombopoietin
95
What do platelets adhere to during the formation of a thrombus?
Exposed collagen and von Willebrand factor (vWF)
96
What is the role of thromboxane A2 in platelet activation?
Triggers the release of ADP and recruits ambient platelets
97
Which receptor is targeted by ADP to activate platelets?
P2Y12
98
What do arterial thrombi typically form on?
Disrupted atherosclerotic plaques
99
Which conditions increase the risk for venous thrombosis?
Pregnancy, presence of antiphospholipid antibodies, metastatic cancer, hormonal replacement therapy
100
What type of thrombus is characterized by low-shear conditions and consists mostly of fibrin and trapped RBC?
Venous Thrombus
101
What is the most common inherited thrombophilia?
Factor V Leiden
102
What is the role of aspirin in antiplatelet therapy?
Inhibits platelet COX-I
103
Which antiplatelet drug selectively inhibits ADP-induced platelet aggregation?
Thienopyridines (ticlopidine, clopidogrel, prasugrel)
104
What differentiates Ticagrelor from thienopyridines?
Does not require metabolic activation and produces reversible inhibition of the ADP receptor
105
What is the mechanism of action of Cangrelor?
Rapidly acting reversible inhibitor of P2Y12
106
What is the main effect of Dipyridamole as an antiplatelet agent?
Inhibits phosphodiesterase to block cAMP breakdown
107
What is Cangrelor?
A rapidly acting reversible inhibitor of P2Y12 that is administered intravenously
## Footnote
It has an immediate onset of action and a half-life of 3 to 5 minutes.
108
What is the main mechanism of action of Dipyridamole?
Inhibits phosphodiesterase, blocks cAMP breakdown, and increases intracellular cAMP
## Footnote
This results in reduced intracellular calcium and inhibition of platelet activation.
109
What is Vorapaxar and its effect?
Inhibits PAR-1, reducing the risk for cardiovascular death, myocardial infarction, or stroke by 13% but doubling the risk for intracranial bleeding.
110
What is the mechanism of action of Heparin?
Activates antithrombin and accelerates inhibition of thrombin and factor Xa.
111
What is Heparin-Induced Thrombocytopenia (HIT)?
A condition that occurs 5-14 days after initiation of heparin, characterized by a platelet count of ≤50,000/μL or a decrease of ≥40% from baseline.
112
What is the typical prophylaxis dose of Low-Molecular-Weight Heparin?
4000-5000 units SC once daily or 2500-3000 units SC twice daily.
113
What is Fondaparinux?
A synthetic analogue of antithrombin-binding pentasaccharide sequence that does not bind to endothelial cells or plasma proteins.
114
What is the recommended management for Warfarin induced bleeding?
Withhold warfarin if INR is between 3.5 and 9; administer vitamin K if at high risk for bleeding; prefer prothrombin complex concentrate over fresh frozen plasma.
115
What are the vitamin K-dependent clotting proteins affected by Warfarin?
Factor II (prothrombin), VII, IX, X; it also impairs anticoagulant proteins C and S.
116
What is the dosing for Direct Oral Anticoagulants (DOACs)?
Dabigatran and Edoxaban are started after a 5-day course of parenteral anticoagulant; Rivaroxaban and Apixaban can be given orally.
117
What is the primary action of Fibrinolytic Drugs like Streptokinase?
Induces a conformational change in plasminogen that activates both free and fibrin-bound plasminogen.
118
What is the dose for Tenecteplase?
Weight-based IV bolus of 30-50 mg over 5 seconds.
119
True or False: Heparin binds to endothelial cells, affecting its clearance.
True
120
Fill in the blank: The APTT or _______ level is used to monitor heparin.
anti-factor Xa
121
What is the duration of action for Low-Molecular-Weight Heparin?
Longer plasma half-life, approximately 4 hours.
122
What is the mechanism of action of Direct Oral Anticoagulants?
They bind reversibly to the active site of their target enzyme, factor Xa (thrombin).
123
What is the dose of Alteplase?
90-100 mg over 60-90 minutes.
124
True regarding Platelets:
A. Platelets enter the circulation after the fragmentation of bone marrow megakaryocytes regulated by Thrombopoietin
B. Once they enter the circulation, platelets have a life span of 7 to 10 days.
C. Platelets adhere to exposed collagen and von Willebrand factor (vWF) and form a monolayer that supports and promotes thrombin generation and subsequent fibrin formation
D. All of the Above
D
125
Which serves as the final effector in platelet aggregation, and a logical target for potent antiplatelet drugs?
A. Thromboxane A2
B. GP IIb/IIIa
C. PAR-1
D. ADP
B
126
In the coagulation system, which enzyme complex involved in thrombin generation, is formed from the binding of factor VIIA and tissue factor after Vascular injury?
A. Prothrombinase
B. Intrinsic Tenase
C. Extrinsic Tenase
D. Both B and C
C
127
Which of the following acquired or triggering factors entail a higher risk for Venous Thombosis?
A. Pregnancy
B. Presence of antiphospholipid antibodies
C. Metastatic cancer
D. Use of hormonal replacement therapy
E. All of the above
C
128
Causes of Acquired Protein C deficiency
decreased synthesis of normal protein as seen in severe liver disease, or in those given warfarin; Protein C consumption can occur with severe sepsis, DIC, and after surgery
129
True of VTE risk in obesity
A. VTE increases ~ 1.2x for every 10- kg/m 2 increase in BMI
B. visceral fat, expresses
proinflammatory cytokines and adipokines, which may promote coagulation
C. Obesity leads to immobility
D. A mild risk for VTE
A, B, C, D
130
The following has the highest risk for VTE:
A. major orthopedic surgery
B. prolonged bed rest
C. presence of antiphospholipid
antibodies
D. obesity
A
## Footnote
**Highest risk**
* major orthopedic surgery,
* neurosurgery,
* polytrauma,
* metastatic cancer
**Intermediate risk**
* prolonged bed rest,
* presence of antiphospholipid
antibodies,
* the puerperium
**Mild risk**
* pregnancy,
* obesity,
* long-distance travel,
* the use of oral contraceptives or
hormonal replacement therapy
131
Match the following antiplatelet drugs with their mode of action
1. Aspirin
2. Tirofiban
3. Cangrelor
4. Ticlodipine
A. inhibits platelet COX-I
B. inhibit ADP-induced platelet aggregation by irreversibly blocking P2Y12
C. inhibits PAR-1, the major thrombin receptor on human platelets
D. target the GPIIb/ IIIa receptor.
1. A
2. D
3. B
4. B
132
133
What percentage of DVT in pregnancy occurs in the left leg?
More than 90%
## Footnote
This is likely due to the enlarged uterus compressing the left iliac vein.
134
When are the levels of procoagulant proteins increase in pregnancy?
3rd trimester of pregnancy
## Footnote
This includes factors such as factor VII, fibrinogen, and vWF, along with suppression of natural anticoagulant pathways.
135
Which deficiencies in pregnant women are associated with the highest VTE risk?
Deficiency in antithrombin, protein C, or protein S
## Footnote
These deficiencies significantly increase the risk of venous thromboembolism.
136
True or False:
Women with thrombophilia have a higher daily risk for VTE during pregnancy
False
## Footnote
This risk is higher during post-partum than during pregnancy.
women needing thromboprophylaxis require treatment throughout pregnancy and for AT LEAST 6 WEEKS POSTPARTUM
137
For how long do women needing thromboprophylaxis require treatment during pregnancy?
Throughout pregnancy and for at least 6 weeks postpartum
## Footnote
This is crucial for managing VTE risk.
138
Which of the following Glycoprotein IIb/IIIa Receptor Antagonists is the most specific?
A. abciximab
B. eptifibatide
C. tirofiban
D. vorapaxar
A
139
True regarding Heparin
A. Activates antithrombin and slows down inhibition of thrombin & factor Xa.
B. Binding of heparin to endothelial cells explains its dose-dependent clearance
C. Weight-adjusted heparin nomograms for patients with Acute Coronary Syndrome uses an initial bolus of 5000 units or 80 units/kg, followed by an infusion of 18 units/kg/hr
D. All of the above
B
140
True regarding Heparin-Induced Thrombocytopenia (HIT)
A. occurs 5-14 days from initiation of heparin but may be earlier if previously on heparin within past 3 months
B. Platelet count of ≤50,000/μL or a decrease in platelet count of ≥40% from baseline
C. More common with low molecular- weight heparin than with unfractionated heparin
D. More common in medical patients than in surgical patients
A
141
Which of the following can be given in the presence of HIT?
A. Platelet transfusion
B. Whole blood transfusion in the presence of active bleeding
C. Apixaban
D. Argatroban
C and D
142
143
What is the mean molecular weight of Low-Molecular-Weight Heparin (LMWH)?
Around 5000 Dalton
## Footnote
This is approximately 1/3 of Unfractionated Heparin (UFH).
144
How do the shorter heparin chains in LMWH affect their binding to endothelial cells and macrophages?
They bind less avidly, eliminating rapid dose-dependent and saturable clearance mechanisms.
145
What is the plasma half-life of Low-Molecular-Weight Heparin?
Approximately 4 hours.
146
What is the bioavailability of LMWH after subcutaneous injections?
About 90%.
147
What is the prophylaxis dose range for LMWH?
4000-5000 U SC once daily; 2500-3000 U SC twice daily.
148
What is the treatment dose for Venous Thromboembolism (VTE) using LMWH?
150-200 U/K once daily; 100 U/K twice daily.
149
What is the LMWH dosage for unstable angina?
100-120 U/K SC twice daily.
150
Which of the following is true of Fondaparinux?
A. Synthetic analogue of antithrombin-binding pentasaccharide sequence
B. Exhibits complete bioavailability after subcutaneous injection
C. Clearance does not depend on dosage
D. All of the above
D
## Footnote
Binds only to antithrombin
Catalyzes inhibition of factor Xa by antithrombin and does not enhance the rate of thrombin inhibition.
Exhibits complete bioavailability after subcutaneous injection.
No binding to endothelial cells or plasma proteins, clearance of fondaparinux does not depend on the dosage, and its plasma half-life is 17 hours
Contraindicated in patients with creatinine clearance lower than 30 mL/min, and it should be used with caution in those with a creatinine clearance lower than 50 mL/min.
Dosage: VTE prophylaxis & ACS: 2.5 mg SC OD
VTE treatment: 7.5 mg SC OD; <50Kg: 5 mg SV OD; >100kg: 10 mg SC OD
151
How does the major bleeding rate of Fondaparinux compare to enoxaparin?
50% lower rate of major bleeding than enoxaparin.
152
What is the dosage of Fondaparinux for VTE prophylaxis?
A. 2.5 mg SC OD
B. same with ACS
C. 5mg SC OD
D. A and B
D
## Footnote
VTE prophylaxis & ACS: 2.5 mg SC OD
VTE treatment:
7.5 mg SC OD
<50Kg: 5 mg SV OD
>100kg: 10 mg SC OD
153
True regarding management of Warfarin induced bleeding
A. In asymptomatic patients whose INR is between 3.5 and 9, warfarin should be withheld until the INR returns to the therapeutic range
B. If the patient is at high risk for bleeding, sublingual or oral vitamin K can be administered
C. Prothrombin complex concentrate is preferred over fresh frozen plasma
D. All of the Above
D
154
Which of the following can be given as an all oral regimen for VTE?
A. rivaroxaban
B. edoxaban
C. dabigatran
D. apixaban
E. A and D
E
## Footnote
Dabigatran, rivaroxaban, apixaban, and edoxaban are also licensed for treatment of patients with VTE
Dabigatran and edoxaban are started after patients have received at least a 5-day course of treatment with a parenteral anticoagulant such as LMWH
155
Which Direct Oral Anticoagulants are licensed for thromboprophylaxis after elective hip & knee replacement surgery?
A. Rivaroxaban
B. Dabigatran
C. Apixaban
D. all of the above
D
## Footnote
These medications help prevent blood clots post-surgery.
156
What can be used for qualitative assessment of anticoagulant activity for factor Xa inhibitors?
A. prothrombin time
B. APTT
C. both
D. either
A
## Footnote
dabigatran- APTT
157
How long should DOACs be withheld before surgical procedures if renal function is impaired?
1-2 days or longer
## Footnote
This is to reduce the risk of bleeding during surgery.
158
Which of the following is licensed for dabigatran reversal in patients with serious bleeding or in those requiring urgent surgery or intervention?
A. Idarucizumab
B. Andexanet-alfa
C. ciraparantag
D. all of the above
A
## Footnote
Idarucizumab is given intravenously as a 5-g bolus and is supplied in a box containing two 50-mL vials, each containing 2.5 g of idarucizumab. Idarucizumab rapidly reverses the anticoagulant effects of dabigatran and normalizes the aPTT, diluted thrombin time, or ecarin clot time.
159
The following statements are true regarding Estrogen therapy use except:
A. Oral contraceptives, estrogen replacement therapy and SERMS are all associated with an increased risk for VTE
B. Routine screening for thrombophilia in young women considering oral contraceptive is recommended
C. The risk for VTE is highest during the first year of oral contraceptive use and persists only for the duration of use
D. Aromatase inhibitors are used in place of tamoxifen for the treatment of estrogen receptor positive breast cancer
B
160
The following statements are true regarding acquired hypercoagulable state in pregnancy except:
A. 90% of the DVT in pregnancy occur in the right leg
B. Risk for VTE is similar in all three trimester
C. Pregnant women needing thromboprophylaxis require treatment through out pregnancy and for at least 6 weeks post partum
D. Pregnant women have five to sixfold higher risk for VTE
A
161
3. The following are alternative anticoagulant to HIT except:
A. Fondaparinux
B. Enoxaparin
C. Apixaban
D. Rivaroxaban
B
162
What is the most common form of thrombophilia?
A. Factor V Leiden Mutation
B. Prothrombin Gene Mutation
C. Antithrombin Deficiency
D. Protein C and Protein S deficiency
A
163
Which is more fibrin specific among the following fibrinolytics?
A. Tenecteplase
B. Alteplase
C. Reteplase
D. Streptokinase
A
