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Pcol2 > AntiCoag > Flashcards

AntiCoag Flashcards

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
Q

activates phospholipase A2 (PLA2) which will be used in the synthesis of arachidonic acid (AA).

A

Calcium

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26
Q

Arachidonic acid requires ____________ in order to metabolize to form thromboxane.

A

cyclooxygenase (COX)

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27
Q

The end of the platelet plug will provide a __________ environment that will allow the coagulation cascade to proceed

A

negative

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28
Q

Intrinsic

A

12 -> 11 -> 9 -> 8 ->

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29
Q

Extrinsic

A

3 -> 7

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30
Q

Common Pathway junction

A

Intrinsic : 8 (with help of 3 and Ca) will activate X
Extrinsic: after 7a, PF4 and Ca will complex and activate X

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31
Q

will attach to Factor X and will activate Prothrombin (II) and Thrombin (Ila)

A

Factor 5

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32
Q

T/F: Prothrombin III is not too strong so Fibrinogen is needed

A

True

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33
Q

Activated form of Fibrinogen

A

Fibrin

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34
Q

activates Fibrinogen (I) to Fibrin (Ia)

A

Thrombin

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35
Q

insoluble to blood and provides the “jelly” structure of the blood.

A

Fibrin

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36
Q

In Clot retraction/repair Platelets will release

A

myosin and actin

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37
Q

contractile proteins that allow
contraction between spaces and connection of both
ends of endothelial tissues

A

Myosin and Actin

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38
Q

to regenerate cells -> Stimulate the production of endothelial cells and signal mitosis

A

VEGF (Vascular Endothelial Growth Factor

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39
Q

to regenerate smooth muscle

A

PDGF (Platelet Derived Growth Factor)

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40
Q

T/F: only VEGF signlas mitosis

A

False

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41
Q

Irreversible inhibits of Cyclooxygenase

A

Aspirin

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42
Q

T/F: When taking Aspirin, platelets are permanently inhibited

A

True

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43
Q

In Aspirin, replacement platelets restore overall function in

A

3-7 days

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44
Q

T/F: Patient canundergo a surgical procedure within 7 days of aspirin intake

A

False

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45
Q

dose of aspirin as antiplatelet effect

A

80 - 160 mg

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46
Q

Aspirin should not be taken with

A

NSAIDS

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47
Q

T/F: Aspirin should be taken with food

A

True

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48
Q

Glycoprotein IIb/IIIa Inhibitors

A

EPTIFIBATIDE, TIROFIBAN

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49
Q

is Glycoprotein IIb/IIIa Inhibition reversible or nonreversible

A

reversible

50
Q

Glycoprotein IIb/IIIa Inhibitors can cause

A

Reduced adhesion
Reduced aggregation

51
Q

Most commonly used in the Philippines

52
Q

Inhibits platelet aggregation by reversibly binding to platelet IIb/IIIa receptors, which in turn results in steric hindrance.

53
Q

ADP Inhibitors drugs

A

Clopidogrel (PlavixR), Prasugrel (E entR), Ticlopidine(TiclidR) Ticagrelor (BrilantaR, BriliqueR, PossiaR)

54
Q

Blood thinner

A

ADP Inhibitors

55
Q

Used for Ischemic Stroke only

A

ADP Inhibitors

56
Q

No ADP → Calcium will be inhibited →

A

no Thromboxane

57
Q

Given to Myocardial Infarction, Requires hepatic conversion to be active, Irreversible inhibition

A

Clopidogrel (PlavixR), Prasugrel (E entR), Ticlopidine(TiclidR)

58
Q

● Does not require hepatic activation.
● Reversible inhibition of ADP receptor

A

Ticagrelor (BrilantaR, BriliqueR, PossiaR)

59
Q

Inhibit phosphodiesterase to reduce cAMP degradation

A

PDE/Adenosine Uptake Inhibitors

60
Q

cAMP is an inhibitor of

A

platelet aggregation and uptake of adenosine

61
Q

PDE/Adenosine Uptake Inhibitors (drugs)

A

Dipyridamole, Cilostazol

62
Q

Antiplatelets

A

Aspirin
GLYCOPROTEIN IIb/IIIa INHIBITORS
ADP Inhibitors
PDE/Adenosine Uptake Inhibitors

63
Q

ANTICOAGULANTS

A

Heparins and Fondaparinux
Direct Thrombin Inhibitors
WARFARIN
NOAC’S FACTOR Xa INHIBITORS

64
Q

● Prevents coagulation cascade

A

ANTICOAGULANTS

65
Q

Highly acidic. Neutralized by a base

A

Unfractionated Heparin

66
Q

Binds to antithrombin III to form a complex

A

Unfractionated Heparin

67
Q

Unfractionated Heparin targets factors ________

A

Xa and IIa

68
Q

Unfractionated Heparin is always given as

69
Q

Unfractionated Heparin may cause a moderate, transient __________ and
_____________

A

thrombocytopenia and
thrombosis

70
Q

● May be linked to osteoporosis in chronic use

A

Unfractionated Heparin

71
Q

Do not bind to thrombin but inactivate Xa

A

Low Molecular Weight Heparins (LMWH)

72
Q

test used to determine the effectiveness of a drugs, particularly UFHs

A

Activated partial thromboplastin time

73
Q

can aPTT be used in LMWH

A

No, because LMWH only has a minimal effect on Factor II

74
Q

LWMH is given as

A

once- or twice- daily SC injections

75
Q

Synthetic drug, pentasaccharide found in LMWH

A

Fondaparinux (ArixtraR)

76
Q

T/F: Fondaparinux does not inhibit thrombin

A

true; only factor X

77
Q

Fondaparinux is given as

A

Daily subcutaneous dose

78
Q

Direct Thrombin Inhibitors

A

Bivalirudin
Argatroban
Dabigatran (PradaxaR)

79
Q

Direct Thrombin Inhibitors are derived from

A

the medicinal leech Hirudo medicinalis

80
Q

Often used as an alternative for heparin in patients who
had HITT

A

Direct Thrombin Inhibitors

81
Q

Can DTI use aPTT?

82
Q

DTI that binds to thrombin active site only

A

Argatroban, Dabigatran

83
Q

Administer to patients who are in the cath lab and are
expected to undergo angioplasty and angiogram

A

Argatroban

84
Q

Short-acting (4 hours), Twice daily oral medication, Approved for stroke prevention in atrial fibrillation

A

Dabigatran (PradaxaR)

85
Q

Also used in deep vein thrombosis (DVT) prevention in post
op hip and knee surgery

A

Dabigatran (PradaxaR)

86
Q

Antidote for toxicity of Dabigatran

A

Idarucizumab (PraxbindR)

87
Q

Vitamin K reductase inhibitor

88
Q

why do we “bridge” a patient with heparin when we start or stop warfarin

A

because it can cause initial period of hypercoagulability, followed by hypo-coagulability

89
Q

T/F: Antibiotics may kill off normal gut flora

90
Q

Must not be taken with warfarin as it increase clearance and drop
INR (thrombosis)

A

CYP450 inducers (carbamazepine, phenytoin,
barbiturates, rifampin)

91
Q

Must not be taken with warfarin as it reduce
clearance and increase the INR (hemorrhage)

A

Inhibitors (amiodarone, SSRI’s, cimetidine)

92
Q

When the INR is too high

A

there is increased risk of
hemorrhage

93
Q

When the iNR is too low

A

there is increase risk for
thrombosis

94
Q

The most specific antidote for warfarin toxicity is

95
Q

In case of life-threatening hemorrhage, additional measures need to be taken like

A

administration of fresh frozen plasma or prothrombin complex concentrate

96
Q

Novel oral anticoagulants

A

NOAC’S FACTOR Xa INHIBITORS

97
Q

RIVAROXABAN, APIXABAN

A

NOAC’S FACTOR Xa INHIBITORS

98
Q

Approved for use in stroke prevention in non-valvular atrial
fibrillation

A

NOAC’S FACTOR Xa INHIBITORS

99
Q

Also used in post op hip and knee surgeries for DVTP

A

NOAC’S FACTOR Xa INHIBITORS

100
Q

a.k.a fibrinolytics, Catalyze conversion of plasminogen → plasmin causing a break down of fibrin

A

Thrombolytics

101
Q

Used in acute stroke (after CT confirms no hemorrhage)

A

Thrombolytics

102
Q

Can Cause Intracerebral hemorrhage

A

Thrombolytics

103
Q

● Does not show affinity for fibrin-bound plasminogen
● Needs to forms complex first with plasminogen
○ The complex will forms plasmin

A

STREPTOKINASE

104
Q

● Show affinity for fibrin bound plasminogen
● Will show affinity in the fibrinogen

A

tPA ANALOGUES

105
Q

Alteplase
Tenecteplase
Reteplase

A

tPA ANALOGUES

106
Q

● Normal human tPA
● will stimulate fibrinogen to plasmin

107
Q

● Mutated human tPA
● Longer duration of action

A

Tenecteplase

108
Q

● Mutated human tPA
● Faster onset, longer duration of action

109
Q

T/F: Vitamin K oral dosing may be faster than IV dosing

110
Q

for hemophilia A

A

Factor VIII concentrate

111
Q

for hemophilia B

A

Factor IX concentrate

112
Q

mixture of factors II, VII, IX, X, C, Used in mixed deficiencies, and NOAC overdoes

A

OctaplexR and BeriplexR

113
Q

Will not replacement clotting factor but stimulate the deficient clotting factors

A

VASOPRESSIN AGONISTS

114
Q

Desmopressin

A

Vasopressin agonist

115
Q

V2 agonist
● Increases the concentration of vWF and factor VIII
● Used to prepare hemophilia A or vWD patients for surgery

A

Desmopressin

116
Q

ANTIPLASMIN AGENT

A

Aminocaproic Acid (AmicarR) and Tranexamic Acid

117
Q

● Prevents the formation of plasmin ● Inhibits the fibrinolysis

A

ANTIPLASMIN AGENT

118
Q

Given in heavy bleeding

A

Tranexamic Acid

119
Q

Oral agents
● Inhibit fibrinolysis by inhibiting plasminogen activation
● Increases the concentration of vWF and factor VIII

A

Aminocaproic Acid (AmicarR) and Tranexamic Acid

120
Q

○ Treat hemophilia
○ Prophylaxis for high risk patients
○ Used in postoperative bleeding

A

Uses of Aminocaproic Acid (AmicarR) and Tranexamic Acid

Pcol2 (20 decks)

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