Drugs of hemostasis Flashcards

(121 cards)

1
Q

Heparin is released by these cells, and abundant in liver, lungs and intestines

A

Mast cells

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2
Q

Heparin promotes inactivation of these clotting factors

A

Factors Xa and IIa

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3
Q

Does heparin cross the placenta?

A

No; can be used during pregnancy

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4
Q

Can heparin be used during pregnancy?

A

Yes - does NOT cross placenta

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5
Q

This drug promotes inactivation of Factors Xa and IIa, and does not cross the placenta so it can be used during pregnancy

A

Heparin

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6
Q

Low molecular weight heparin has a greater capacity to potentiate inhibition of this molecule

A

Factor Xa

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7
Q

The pentasaccharide form of heparin (Fondaparinux) accelerates only inhibition of this by antithrombin

A

Factor Xa

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8
Q

Heparin accelerates the ability of this molecule to inactivate Xa and thrombin (factor IIa)

A

Antithrombin

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9
Q

LMWH and synthetic fondaparinux target this molecule selectively

A

Factor Xa

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10
Q

Do heparins dissolve formed clots?

A

NO
but inhibit existing or new clot expansion

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11
Q

Is heparin activity delayed or immediate?

A

Immediate

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12
Q

Are lower or higher doses of heparin used for thrombosis events?

A

Higher doses

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13
Q

Are lower or higher doses of heparin used for thrombosis prevention?

A

Lower doses

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14
Q

Can heparin be given with other anticoagulants?

A

No, is contraindicated

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15
Q

Can heparin be given to someone with malignant hypertension?

A

No, is contraindicated

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16
Q

Acute heparin-induced thrombocytopenia (HIT) is triggered by this response to heparin-PF4 complex

A

IgG

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17
Q

Acute heparin-induced thrombocytopenia (HIT) is triggered by IgG response to this

A

Heparin-PF4 complex

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18
Q

Clinical Acute heparin-induced thrombocytopenia (HIT) prediction rules are the 4 T’s:

A

Thrombocytopenia
Timing with respect to heparin exposure
New thrombosis or other sequelae of HIT post heparin
Likelihood of other causes of thrombocytopenia

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19
Q

Heparin is contraindicated in disease of these two organs

A

Liver and kidney

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20
Q

This form of heparin is cleared by the reticuloendothelial system and is preferred in cases of severe renal impairment

A

Unfractionated heparin

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21
Q

These are the two main adverse effects of heparin

A

Thromboembolisms (limb ischemia, MI, stroke)
Osteoporosis

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22
Q

What is Protamine sulfate?

A

Heparin antidote

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23
Q

This molecule forms inactive complex with heparin

A

Protamine sulfate

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24
Q

Protamine sulfate is less effective against this form of heparin

A

LMWH

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25
This form of heparin has poor Protamine sulfate binding, so does not have an antidote
Fondaparinux
26
This is the route of administration of LMWH and Fondaparinux
Subcutaneous
27
Anticoagulation response is predictable with these forms of heparin, so outpatient is possible
LMWH Fondaparinux
28
These forms of heparin have less frequent bleeding and low risk of HIT
LMWH Fondaparinux
29
These are heparin alternatives in patients with HIT due to absence of platelet interactions
Parenteral anticoagulants: direct thrombin (factor II) inhibitors Argatroban, Bivalirudin
30
These heparin alternatives lack antidote and have relatively short duration of actions
Argatroban, Bivalirudin Direct thrombin inhibitors
31
Argatroban and Bivalirudin are direct inhibitors of this
Thrombin (Factor II) Are heparin alternatives
32
Warfarin (Coumadin) inhibits this enzyme
Vitamin K epoxide reductase
33
Warfarin (Coumadin) depletes this molecules by preventing a key processing step
Factors II, VII, IX, X
34
Warfarin (Coumadin) blocks synthesis of these anticoagulant proteins, so may require bridge treatment (due to temporary hypercoagulability)
Proteins C and S
35
Warfarin (Coumadin) blocks synthesis of anticoagulant proteins C and S, so may require bridge treatment with this
Heparin
36
Does Warfarin (Coumadin) follow linear kinetics?
No - small dose adjustments can produce large response changes
37
Does Warfarin (Coumadin) cross the placenta?
YES - contraindicated in pregnancy
38
Can Warfarin (Coumadin) be used in pregnancy?
NO - crosses the placenta contrast to heparin, which does not cross the placenta
39
Warfarin (Coumadin) activity is monitored by this value
Prothrombin time (PT) normalized to international normalized ratio (INR)
40
Warfarin (Coumadin) is inactivated by biotransformation, mainly by this enzyme
CYP 2C9
41
Does vitamin K epoxide reductase directly alter clotting factors?
NO Gamma glutamyl carboxylase reaction makes functional zymogens, and reduced vit K is a cofactor
42
Warfarin resistance is typically related to this
High vitamin K intake in diet (kale, spinach, greens) Noncompliance and phlebotomy/lab errors are also factors Genetic factors are rarely mechanisms of resistance
43
These are the three main adverse effects of warfarin
Bleeding Skin necrosis (3-10 days after start) Teratogenicity
44
Skin necrosis can occur with warfarin due to abrupt loss of this
Anticoagulant effect of protein C/S
45
This treatment for blood clots is contraindicated in ulcer history, bleeding disorders, hepatic or renal disease, recent surgery, pregnancy
Wafarin
46
This is a 4-factor prothrombin complex concentrate (4F-PCC) containing factors II, VII, IX and X
Kcentra
47
Kcentra reverses the effects of this drug
Warfarin
48
This is the black box warning of Kcentra (warfarin reversal)
Venous and arterial thromboembolic events
49
Kcentra contains these molecules
Factors II, VII, IX, and X is a 4-factor prothrombin complex concentrate (4F-PCC)
50
This drug is for management of acute hemorrhages caused by excess fibrinolytic activity
Aminocaproic acid
51
This drug is for heavy menstrual bleeding and short-term bleeding prevention in hemophiliacs
Tranexamic acid
52
This drug induces release of von Willebrand’s factor, indicated for von Willebrand’s disease, hemophilia A
Desmopressin
53
Heparin activity is monitored by this value
activated partial thromboplastin time (aPTT) Target is 1.5-2.5 increase compared to aPTT without heparin
54
Wafarin activity is monitored by this value
Prothrombin time (PT) assess using INR
55
With warfarin, this should be patient PT/normal PT
1.7
56
Without warfarin, this is patient PT/normal PT
1.0
57
Does this describe heparin or wafarin: IV route
Heparin
58
Does this describe heparin or wafarin: Oral route
Warfarin
59
Does this describe heparin or wafarin: Rapid onset
Heparin
60
Does this describe heparin or wafarin: Slow onset
Warfarin
61
Does this describe heparin or wafarin: Acute duration
Heparin
62
Does this describe heparin or wafarin: Long duration
Warfarin
63
Does this describe heparin or wafarin: Protamine sulfate is fast antidote
Heparin
64
Does this describe heparin or wafarin: Vitamin K (slow) and fresh plasma (fast) are antidoes
Warfarin
65
Does this describe heparin or wafarin: Safer in pregnancy
Heparin
66
Does this describe heparin or wafarin: Teratogenic
Warfarin
67
This contains all coagulation factors, making it an effective option for rapid reversal of warfarin-induced anticoagulation in patients with life-threatening bleeding
Fresh frozen plasma (FFP)
68
This is a slow antidote for warfarin
Vitamin K takes hours to replenish the effective levels of active factors
69
Reduced vitamin K is required for this enzyme
Gamma glutamyl carboxylase which activates clotting factors Warfarin inhibits vitamin K epoxide reductase, which prevents the activation of Vitamin K
70
Does this describe heparin or wafarin: Enhances antithrombin activity
Heparin
71
Does this describe heparin or wafarin: Monitored by aPTT
Heparin
72
Does this describe heparin or wafarin: Monitored by PT
Warfarin
73
This is a direct, competitive inhibitor of thrombin Is considered more consistent than warfarin
Dabigatran
74
Dabigatran is a direct, competitive inhibitor of this
Thrombin
75
This is an oral prodrug converted to active dabigatran by carboxylesterases in intestine and liver
DOACs: Dabigatran Etexilate
76
Is Dabigatran more or less effective than warfarin in Afib therapy?
Equally effective
77
Does Dabigatran have a lower or higher incidence of stroke or embolism compared to warfarin?
Lower
78
Does Dabigatran have a lower or higher risk of major bleeding episodes compared to warfarin?
Similar risk
79
Does warfarin or Dabigatran require regular monitoring?
Warfain Dabigatran does NOT
80
Can Dabigatran be used during pregnancy?
Yes, with caution
81
Abrupt discontinuation of Dabigatran should be avoided because risk of this returns rapidly
Stroke
82
This is an antidote to Dabigatran
Idarucizumab
83
This is a monoclonal antibody that binds dabigatran and metabolites
Idarucizumab
84
Idarucizumab is an antidote to this
Dabigatran Does not reverse apixaban, edoxaban, or rivaroxaban response
85
Rivaroxaban is a direct inhibitor of this
Factor Xa
86
This is a direct inhibitor of Factor Xa
Rivaroxaban
87
This is a specific reversal agent for Rivaroxaban
Andexanet alfa
88
Andexanet alfa is a specific reversal agent of this
Rivaroxaban
89
This is a black box warning of Rivaroxaban
Avoid abrupt discontinuation as stroke risk returns quickly
90
Should warfarin or DOACs be used for most patients with nonvalvular AF requiring anticoagulant therapy?
DOACs
91
Should warfarin or DOACs be used for patients with AF and any of the following: mechanical prosthetic valve, rheumatic mitral stenosis, severe chronic kidney disease
Warfarin
92
ADP activates platelets, and initiates COX-1 dependent synthesis of this molecule, which leads to activation of GPIIb/IIIa that bind fibrinogen
Thromboxane A2
93
ADP activates platelets, and initiates COX-1 dependent synthesis of thromboxane A2, which leads to activation of this molecule that binds fibrinogen
Glycoprotein IIb/IIIa
94
Aspirin irreversibly blocks this enzyme
COX-1 Reduces synthesis of thromboxane A2, a platelet aggregation stimulator
95
Aspirin onset of action is very fast, and lasts this long
Lifetime of platelet (7-10 days)
96
Is bleeding time increased or decreased as an adverse effect of aspirin?
Increased
97
A common drug interaction of aspirin is with these, which results in loss of antiplatelet activity
Reversible NSAIDs (ibuprofen, naproxen)
98
Clopidogrel (Plavix) is an antagonist to this
ADP *is a prodrug
99
This drug blocks ADP binding to P2Y12 receptors to inhibit glycoprotein IIb/IIIa activation required for platelets to bind to fibrinogen and associated aggregation
Clopidogrel (Plavix)
100
Clopidogrel (Plavix) blocks ADP binding to these receptors
P2Y12 receptors
101
Clopidogrel (Plavix) inhibits activation of this, which is required for platelets to bind to fibrinogen and associated aggregation
Glycoprotein IIb/IIIa
102
Clopidogrel (Plavix) is converted to an active metabolite by this enzyme
CYP2C19
103
PPIs reduce transformation of clopidogrel to active form by inhibiting this enzyme Omeprazole > esomeprazole
CYP2C19
104
Hematological adverse events occur with this ADP antagonist Including TTP and neutropenia
Ticlopidine
105
Ticlopidine is this type of drug
ADP antagonist (blocks P2Y12 receptors)
106
All Glycoprotein IIb/IIIa inhibitors are this type of drug
Parenteral
107
Abciximab is this type of drug
Glycoprotein IIb/IIIa inhibitor
108
Tirofiban is this type of drug
Glycoprotein IIb/IIIa inhibitor
109
Eptifibatide is this type of drug
Glycoprotein IIb/IIIa inhibitor
110
Adverse effects of this Glycoprotein IIb/IIIa inhibitor include bleeding and hypersensitivity
Abciximab
111
Effects of this Glycoprotein IIb/IIIa inhibitor last only for duration of infusion
Tirofiban
112
Effects of this Glycoprotein IIb/IIIa inhibitor persist ~10 hours
Eptifibatide
113
Many herbals have increased risk of bleeding when used with anticoagulants or platelet aggregation inhibitors, including these 5
Ginger Garlic Fish oil Ginseng Feverfew
114
This DOAC does not have an antidote
Edoxaban
115
Dipyridamole increases this molecule to block Thromboxane A2
cAMP
116
Dipyridamole increases cAMP to block this molecule
Thromboxane A2
117
This drug increases cAMP to block Thromboxane A2
Dipyridamole
118
Warfarin is contraindicated in these 5 conditions
Gastric ulcers Liver disease Kidney disease Recent surgery Pregnancy
119
This drug binds to antithrombin and induces a conformational change that accelerates antithrombin interaction with thrombin and Factor Xa
Heparin
120
What is the MOA of ticlopidine, clopidogrel, cangrelor, and prasugrel?
Noncompetitive inhibitors of platelet ADP (P2Y12) receptors that reduce platelet aggregation capability
121
This is a small molecule competitive inhibitor of platelet GPIIb/IIIa receptors, and prevents interaction with fibrinogen to reduce platelet aggregation capability
Tirofiban