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AntiCoag Flashcards

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1
Q

Finely regulated dynamic process of maintaining fluidity of
the blood, repairing vascular injury, and limiting blood loss while avoiding vessel occlusion (thrombosis) and inadequate perfusion of vital organs

A

Hemostasis

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2
Q

inactived if there are no injuries and because
of the intrinsic presence of anticoagulants

A

Platelets

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3
Q

Common causes of dysregulated hemostasis

A

○Hereditary or acquired defects in the clotting
mechanism
○ Secondary effects of infection or cancer

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4
Q

designed to stop bleeding at the site of vascular injury
through complex interactions between the vascular endothelium, platelets, procoagulant proteins, anticoagulant proteins, and fibrinolytic proteins

A

Coagulation System

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5
Q

THREE LAYERS OF BLOOD VESSELS

A

Endothelin
Subendothelium
Smooth Muscle

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6
Q

Endothelin produces

A

Nitric Oxide and Prostacyclin

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7
Q

Layer of the bv that heparin sulfate and thrombomodulin

A

Endothelin

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8
Q

A Natural coagulant

A

Heparin sulfate

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9
Q

Once bound, clotting factors II, IX, X will be
inactivated

A

Heparin sulfate

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10
Q

Heparin sulfate attracts and binds _________

A

antithrombin III

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11
Q

Composed of fibroblasts with abundant elastic and collagen fibers

A

Subendothelium

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12
Q

Changes vessel diameter to regulate blood flow and blood pressure

A

Smooth Muscle

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13
Q

Primary Hemostasis

A

Vascular constriction
Primary platelet plug formation

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14
Q

Secondary hemostasis

A

○ Clot propagation through fibrin formation ○ Coagulation cascade
○ Clot retraction/ repair
○ Fibrinolysis

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15
Q

The initial phase of the blood coagulation process is ____________

A

vascular constriction

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16
Q

T/F: Activation of platelets is absolutely required for hemostasis to proceed.

A

True

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17
Q

Platelets become activated by ___________

A

thrombin

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18
Q

Platelets clump by binding to ___________ that becomes exposed following rupture of the endothelial lining of vessels.

A

collagen

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19
Q

To ensure the stability of the initially loose platelet plug, a _____________ mesh (also called the clot) forms and entraps the plug.

A

fibrin

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20
Q

_____________ will bind to the smooth muscle and will
cause contraction

A

Endothelin

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21
Q

Pain is felt because of the

A

nociceptors

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22
Q

T/F: Nitric oxide and prostacyclin will not be released because of the injury therefore, platelets will be activated

A

True

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23
Q

Damaged endothelium layer will secrete

A

Von Willebrand Factor (VWF)

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24
Q

This exposes platelets to collagen thus a change in the shape of collagen can be obserbed

A

Von Willebrand Factor

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25
activates phospholipase A2 (PLA2) which will be used in the synthesis of arachidonic acid (AA).
Calcium
26
Arachidonic acid requires ____________ in order to metabolize to form thromboxane.
cyclooxygenase (COX)
27
The end of the platelet plug will provide a __________ environment that will allow the coagulation cascade to proceed
negative
28
Intrinsic
12 -> 11 -> 9 -> 8 ->
29
Extrinsic
3 -> 7
30
Common Pathway junction
Intrinsic : 8 (with help of 3 and Ca) will activate X Extrinsic: after 7a, PF4 and Ca will complex and activate X
31
will attach to Factor X and will activate Prothrombin (II) and Thrombin (Ila)
Factor 5
32
T/F: Prothrombin III is not too strong so Fibrinogen is needed
True
33
Activated form of Fibrinogen
Fibrin
34
activates Fibrinogen (I) to Fibrin (Ia)
Thrombin
35
insoluble to blood and provides the “jelly” structure of the blood.
Fibrin
36
In Clot retraction/repair Platelets will release
myosin and actin
37
contractile proteins that allow contraction between spaces and connection of both ends of endothelial tissues
Myosin and Actin
38
to regenerate cells -> Stimulate the production of endothelial cells and signal mitosis
VEGF (Vascular Endothelial Growth Factor
39
to regenerate smooth muscle
PDGF (Platelet Derived Growth Factor)
40
T/F: only VEGF signlas mitosis
False
41
Irreversible inhibits of Cyclooxygenase
Aspirin
42
T/F: When taking Aspirin, platelets are permanently inhibited
True
43
In Aspirin, replacement platelets restore overall function in
3-7 days
44
T/F: Patient canundergo a surgical procedure within 7 days of aspirin intake
False
45
dose of aspirin as antiplatelet effect
80 - 160 mg
46
Aspirin should not be taken with
NSAIDS
47
T/F: Aspirin should be taken with food
True
48
Glycoprotein IIb/IIIa Inhibitors
EPTIFIBATIDE, TIROFIBAN
49
is Glycoprotein IIb/IIIa Inhibition reversible or nonreversible
reversible
50
Glycoprotein IIb/IIIa Inhibitors can cause
Reduced adhesion Reduced aggregation
51
Most commonly used in the Philippines
Abciximab
52
Inhibits platelet aggregation by reversibly binding to platelet IIb/IIIa receptors, which in turn results in steric hindrance.
Abciximab
53
ADP Inhibitors drugs
Clopidogrel (PlavixR), Prasugrel (EentR), Ticlopidine(TiclidR) Ticagrelor (BrilantaR, BriliqueR, PossiaR)
54
Blood thinner
ADP Inhibitors
55
Used for Ischemic Stroke only
ADP Inhibitors
56
No ADP → Calcium will be inhibited →
no Thromboxane
57
Given to Myocardial Infarction, Requires hepatic conversion to be active, Irreversible inhibition
Clopidogrel (PlavixR), Prasugrel (EentR), Ticlopidine(TiclidR)
58
● Does not require hepatic activation. ● Reversible inhibition of ADP receptor
Ticagrelor (BrilantaR, BriliqueR, PossiaR)
59
Inhibit phosphodiesterase to reduce cAMP degradation
PDE/Adenosine Uptake Inhibitors
60
cAMP is an inhibitor of
platelet aggregation and uptake of adenosine
61
PDE/Adenosine Uptake Inhibitors (drugs)
Dipyridamole, Cilostazol
62
Antiplatelets
Aspirin GLYCOPROTEIN IIb/IIIa INHIBITORS ADP Inhibitors PDE/Adenosine Uptake Inhibitors
63
ANTICOAGULANTS
Heparins and Fondaparinux Direct Thrombin Inhibitors WARFARIN NOAC’S FACTOR Xa INHIBITORS
64
● Prevents coagulation cascade
ANTICOAGULANTS
65
Highly acidic. Neutralized by a base
Unfractionated Heparin
66
Binds to antithrombin III to form a complex
Unfractionated Heparin
67
Unfractionated Heparin targets factors ________
Xa and IIa
68
Unfractionated Heparin is always given as
IV or SC
69
Unfractionated Heparin may cause a moderate, transient __________ and _____________
thrombocytopenia and thrombosis
70
● May be linked to osteoporosis in chronic use
Unfractionated Heparin
71
Do not bind to thrombin but inactivate Xa
Low Molecular Weight Heparins (LMWH)
72
test used to determine the effectiveness of a drugs, particularly UFHs
Activated partial thromboplastin time
73
can aPTT be used in LMWH
No, because LMWH only has a minimal effect on Factor II
74
LWMH is given as
once- or twice- daily SC injections
75
Synthetic drug, pentasaccharide found in LMWH
Fondaparinux (ArixtraR)
76
T/F: Fondaparinux does not inhibit thrombin
true; only factor X
77
Fondaparinux is given as
Daily subcutaneous dose
78
Direct Thrombin Inhibitors
Bivalirudin Argatroban Dabigatran (PradaxaR)
79
Direct Thrombin Inhibitors are derived from
the medicinal leech Hirudo medicinalis
80
Often used as an alternative for heparin in patients who had HITT
Direct Thrombin Inhibitors
81
Can DTI use aPTT?
Yes
82
DTI that binds to thrombin active site only
Argatroban, Dabigatran
83
Administer to patients who are in the cath lab and are expected to undergo angioplasty and angiogram
Argatroban
84
Short-acting (4 hours), Twice daily oral medication, Approved for stroke prevention in atrial fibrillation
Dabigatran (PradaxaR)
85
Also used in deep vein thrombosis (DVT) prevention in post op hip and knee surgery
Dabigatran (PradaxaR)
86
Antidote for toxicity of Dabigatran
Idarucizumab (PraxbindR)
87
Vitamin K reductase inhibitor
WARFARIN
88
why do we “bridge” a patient with heparin when we start or stop warfarin
because it can cause initial period of hypercoagulability, followed by hypo-coagulability
89
T/F: Antibiotics may kill off normal gut flora
True
90
Must not be taken with warfarin as it increase clearance and drop INR (thrombosis)
CYP450 inducers (carbamazepine, phenytoin, barbiturates, rifampin)
91
Must not be taken with warfarin as it reduce clearance and increase the INR (hemorrhage)
Inhibitors (amiodarone, SSRI’s, cimetidine)
92
When the INR is too high
there is increased risk of hemorrhage
93
When the iNR is too low
there is increase risk for thrombosis
94
The most specific antidote for warfarin toxicity is
vitamin K
95
In case of life-threatening hemorrhage, additional measures need to be taken like
administration of fresh frozen plasma or prothrombin complex concentrate
96
Novel oral anticoagulants
NOAC’S FACTOR Xa INHIBITORS
97
RIVAROXABAN, APIXABAN
NOAC’S FACTOR Xa INHIBITORS
98
Approved for use in stroke prevention in non-valvular atrial fibrillation
NOAC’S FACTOR Xa INHIBITORS
99
Also used in post op hip and knee surgeries for DVTP
NOAC’S FACTOR Xa INHIBITORS
100
a.k.a fibrinolytics, Catalyze conversion of plasminogen → plasmin causing a break down of fibrin
Thrombolytics
101
Used in acute stroke (after CT confirms no hemorrhage)
Thrombolytics
102
Can Cause Intracerebral hemorrhage
Thrombolytics
103
● Does not show affinity for fibrin-bound plasminogen ● Needs to forms complex first with plasminogen ○ The complex will forms plasmin
STREPTOKINASE
104
● Show affinity for fibrin bound plasminogen ● Will show affinity in the fibrinogen
tPA ANALOGUES
105
Alteplase Tenecteplase Reteplase
tPA ANALOGUES
106
● Normal human tPA ● will stimulate fibrinogen to plasmin
Alteplase
107
● Mutated human tPA ● Longer duration of action
Tenecteplase
108
● Mutated human tPA ● Faster onset, longer duration of action
Reteplase
109
T/F: Vitamin K oral dosing may be faster than IV dosing
true
110
for hemophilia A
Factor VIII concentrate
111
for hemophilia B
Factor IX concentrate
112
mixture of factors II, VII, IX, X, C, Used in mixed deficiencies, and NOAC overdoes
OctaplexR and BeriplexR
113
Will not replacement clotting factor but stimulate the deficient clotting factors
VASOPRESSIN AGONISTS
114
Desmopressin
Vasopressin agonist
115
V2 agonist ● Increases the concentration of vWF and factor VIII ● Used to prepare hemophilia A or vWD patients for surgery
Desmopressin
116
ANTIPLASMIN AGENT
Aminocaproic Acid (AmicarR) and Tranexamic Acid
117
● Prevents the formation of plasmin ● Inhibits the fibrinolysis
ANTIPLASMIN AGENT
118
Given in heavy bleeding
Tranexamic Acid
119
Oral agents ● Inhibit fibrinolysis by inhibiting plasminogen activation ● Increases the concentration of vWF and factor VIII
Aminocaproic Acid (AmicarR) and Tranexamic Acid
120
○ Treat hemophilia ○ Prophylaxis for high risk patients ○ Used in postoperative bleeding
Uses of Aminocaproic Acid (AmicarR) and Tranexamic Acid

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