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PHARMACOLOGY > Blood coagulation > Flashcards

Blood coagulation Flashcards

1
Q

INJURY
▪ Exposes reactive subendothelial matrix proteins
such as:

A
  • Collagen

- Von Willebrand Factor

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2
Q

Injury Result

A
  • Platelet adherence and activation
  • Secretion and synthesis vasoconstrictors
  • Platelet recruitment and activating proteins
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3
Q

▪ Synthesized from arachidonic acid within
platelets.
▪ A platelet activator and potent vasoconstrictor.

A

THROMBOXANE A2 (TXA)

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4
Q

PRODUCTS SECRETED FROM PLT GRANULES

A 
▪ Adenosine diphosphate 
▪ Serotonin
▪ Bind fibrinogen
▪ Cross link adjacent platelets.
▪ Aggregation and formation of platelet plug
▪ Thrombin generation and fibrin clot.
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5
Q

serotonin

A
  • Activation of platelet
  • Conformational change in alpha and beta
    integrin (IIb/IIIa) receptor.
    2b3a
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6
Q

DEFECTS IN FORMATION OF PLATELET PLUG

A

▪ Defects in primary hemostasis, platelet function defects, Von Willebrand Disease.
▪ Bleeding mucosal sites with injury.
- Gingiva, skin, heavy menses

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7
Q

DEFECTS IN THE CLOTTING MECHANISM

A

▪ Secondary hemostasis, Hemophilia A
▪ Tend to bleed into deep tissues
- Joints, muscle, retroperitoneum
▪ No inciting event, recur unpredictably

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8
Q

will do binding with fibronectin and
thrombin. This binding will produce more feedback
to produce more thrombin

A

vWF

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9
Q

Platelets will be activated and release substances

like

A

ADP,5-HT, TXA2 in circulation.

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10
Q

▪ Platelet rich

A

WHITE THROMBI

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11
Q

Fibrin rich

A

RED THROMBI

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12
Q

Form in the high
flow rate and high
shear force
environment of arteries

A

WHITE THROMBI

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13
Q

▪ With large number
of trapped RBC

Venous clots

A

▪ With large number

of trapped RBC

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14
Q

white thrombi is dominated by

A

platelet nidus

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15
Q

red thrombi is dominated by

A

firbin tail

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16
Q

white thrombi effects

A
  • Downstream ischemia (of
    extremities or vital organs)
  • Result: limb amputation
    and organ failure
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17
Q

Red thrombi effects

A 
- Severe swelling and 
pain (of affected extremity)
- Pulmonary Embolism –
part of the clot breaks off 
from its location in the 
deep venous system and 
travels as an embolus; 
most feared consequence
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18
Q

TF/VIIa

A

TFP inhibitor

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19
Q

VIIIa

A

Protein C/Protein S

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20
Q

IXa, XIa, Xa, Va, Thrombin

A

Antithrombin III/Heparin

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21
Q

NATURAL ANTICOAGULANT SYSTEMS

A

NATURAL ANTICOAGULANT SYSTEMS

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22
Q

THE IDEAL ANTI - CLOTTING DRUG

A

▪ Can preserve the tissue factor and VIIa initiation
phase
▪ Weakening the secondary pathway

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23
Q

ANTIPLATELET AGENTS

A 
Thromboxane A2 inhibitor
Phosphodiesterase inhibitor
Glycoprotein (GP) IIb/IIIa blockers
ADP - receptor 
antagonist
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24
Q

Thromboxane A2

inhibitor

A 
Acetylsalicylic acid (ASA) 
(aspirin)
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25
Q

Phosphodiesterase

inhibitor

A

Dipyridamole

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26
Q

Glycoprotein (GP)

IIb/IIIa blockers

A

Abciximab
Tirofiban
Eptifibatide (“ATE”)

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27
Q

ADP - receptor antagonist

A 
Clopidogrel
Prasugrel
Cangrelor
Ticlopidine
Ticagrelor
Vorapaxar (Thrombin receptor inhibitor)
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28
Q

Platelet function is regulated by 3 categories

A
  1. Agents generated outside the platelets that
    interact with platelet membrane receptor
  2. Agents generated within the platelet that interact
    with membrane receptors
  3. Agents generated within the platelet that act
    within the platelet
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29
Q

Agents generated outside the platelets that

interact with platelet membrane receptor

A

o Catecholamines
o Collagen
o Thrombin
o Prostaglandin

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30
Q

Agents generated within the platelet that interact

with membrane receptors

A

o ADP (clopidogrel)
o Prostaglandin D2
o Prostaglandin E2
o Serotonin

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31
Q

Agents generated within the platelet that act

within the platelet

A 
o Prostaglandin endopoxides
o Thromboxane A2 (aspirin)
o Cyclic nucleosides
o CAMP
o CGMP
o Calcium Ions
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32
Q

An arachidonate product that causes platelets to change shape, release their
granules and aggregate

A

▪ Prostaglandin thromboxane A2

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33
Q

Inhibit synthesis of TXA2 ▪ By irreversible acetylation of cyclooxygenase

A

Aspirin

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34
Q

Aspirin dose approved for primary prophylaxis of AMI

A

325 mg/d

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35
Q

As an adjunct to risk factor management by

smoking cessation

A

Aspirin

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36
Q

aspirin SE

A

bleeding, gastritis/ gastric ulcers,

allergic reaction and Reye syndrome

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37
Q

▪ Antiplatelet effects by irreversibly blocking ADP
receptors on platelets
▪ No effect on prostaglandin metabolism

A

CLOPIDOGREL AND TICLOPIDINE

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38
Q

Thienopyridine derivatives

A

CLOPIDOGREL AND TICLOPIDINE

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39
Q

Ticlopidine S/E

A

▪ Nausea, dyspepsia and diarrhea (20%)
▪ Hemorrhage (20%)
▪ Leukopenia (1%)

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40
Q

Ticlopidine dose

A

250 mg 2x/day

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41
Q

Approved for prevention of stroke in patients with
history of transient ischemic arrack (TIA) or
thrombotic stroke, and in combination with aspirin
for the prevention of coronary stent thrombosis.

A

Ticlopidine

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42
Q

clopidogrel is associated with

A

neutropenia, thrombotic

thrombocytopenic purpura

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43
Q

Clopidogrel loading dose

A

300 mg oral dose (80%of platelet

activity is inhibited)

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44
Q

Maintenance dose:

A

75 mg/d, achieve maximum

platelet inhibition

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45
Q

Antiplatelet effect:

A

7-10 days

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46
Q

Approved for patients with unstable angina or nonST-elevation acute myocardial infarction (NSTEMI) in combination with aspirin; for patients with STEMI; recent MI, stroke or established peripheral arterial disease

A

CLOPIDOGREL

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47
Q

Clopidogrel is Prodrug that requires activation via the

A

cytochrome P450 enzyme isoform CYP2C19.

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48
Q

example of Drug that impair CYP2C19 function

A

Omeprazole

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49
Q

T or F

▪ In contrast to clopidogrel, cytochrome P450 genotype status is not an important factor in prasugrel pharmacology

A

T

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50
Q

▪ Similar to clopidogrel
▪ Given orally
▪ Approved for patients with acute coronary
syndrome

A

PRASUGREL

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51
Q

▪ Newer type of ADP inhibitor (cyclopentyl
triazolopyrimidine)
▪ Approved for oral use in combination with aspirin
in patients with acute coronary syndrome

A

TICAGRELOR

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52
Q

▪ Parenteral P2Y12 inhibitor
▪ Approved for IV use of coronary interventions in
patients without previous ADP P2Y12 inhibitor
therapy.

A

CANGRELOR

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53
Q

▪ Used in patients with Acute Coronary Syndrome

▪ Target the platelet IIb/IIIa receptor complex

A

PLATELET GLYCOPROTEIN IIb/ IIIa BLOCKERS

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54
Q

▪ IIb/IIIa complex: function as receptor

A
  • Fibronectin and von Willebrand factor

- Glanzmann’s thrombasthenia

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55
Q

▪ Chimeric monoclonal antibody directed against
IIb/IIIa complex
▪ Include vibronectin receptor
▪ First agent approved in this class of drugs

A

ABCIXIMAB

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56
Q

Abciximab is used in

A
  • Percutaneous Coronary Intervention

- Acute Coronary Syndrome

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57
Q

T or F

EPTIFIBATIDE AND TIROFIBAN Do not block the vibronectin receptor

A

T

58
Q

▪ Inhibit ligand binding to IIb/IIIa receptor by

occupancy of receptor

A

EPTIFIBATIDE AND TIROFIBAN

59
Q 
cyclic peptide derived from rattlesnake venom that contains a variation of the 
RGD motif (KGD).
A

Eptifibatide

60
Q

peptidomimetic inhibitor with RGD sequence motif.

A

Tirofiban

61
Q

▪ Vasodilator that inhibits platelet function

▪ Inhibit adenosine uptake and cGMP phosphodiesterase activity

A

DIPYRIDAMOLE

62
Q

as combination therapy with

aspirin to prevent cerebrovascular ischemia

A

DIPYRIDAMOLE

63
Q

DIPYRIDAMOLE May also be used in combination with warfarin for

A

primary prophylaxis of thromboemboli in patients

with prosthetic heart valves.

64
Q

▪ Used to perform cardiac stress test.

A

DIPYRIDAMOLE

65
Q

▪ Newer phosphodiesterase inhibitor
▪ Promotes vasodilation
▪ Inhibit platelet aggregation

A

CILOSTAZOL

66
Q

cilostazol is used to treat

A

intermittent claudication

67
Q

ANTICOAGULANTS

A

▪ Unfractionated Heparin
▪ Fondaparinux
▪ LMWH (low molecular weight heparins)
▪ Direct Thrombin Inhibitors (Parenteral)

68
Q

LMWH (low molecular weight heparins)

A
  • Enoxaparin
  • Dalteparin
  • Tinzaparin
69
Q

▪ Direct Thrombin Inhibitors (Parenteral)

A
  • Argatroban
  • Bivalirudin
  • Hirudin (Desirudin/Lepirudin)
70
Q

▪ Fondaparinux is a specific factor

A

Xa inhibitor

71
Q

Fondaparinux will only involve factor Xa but

heparin will involve

A

Factor XIIa, XIa, IXa, Xa and IIa.

72
Q

key step in the coagulation pathway.

Inhibition of one molecule of ______ can inhibit
the generation of 50 molecules of thrombin (IIa).

A

Factor Xa

73
Q

factor Xa will be affected by

A

low molecular weight

heparins and unfractionated heparin.

74
Q

TOXICITY OF HEPARIN

A 
Bleeding
▪ Reversible alopecia
▪ Osteoporosis
▪ Spontaneous fractures
▪ Accelerated clearing of postprandial lipemia
▪ Mineralocorticoid deficiency
▪ Heparin-induced Thrombocytopenia
75
Q

HIT is High in UHF treatment of what source

A

bovine

76
Q

HIT clinical manifestations

A

o Venous thrombosis and occlusion of arteries
o Risk of thrombosis for indwelling catheters
o Skin necrosis

77
Q

Tx HIT

A

o Discontinue heparin

o Use fondaparinux

78
Q

CONTRAINDICATIONS OF HEPARIN

A 
▪ HIT
▪ Hypersensitivity
▪ Active bleeding
▪ Hemophilia
▪ Significant thrombocytopenia
▪ Purpura
▪ Severe hypertension
▪ Intracranial hemorrhage
▪ Infective endocarditis
▪ Active tuberculosis
▪ Ulcerative lesions of the GIT
▪ Threatened abortion
▪ Visceral carcinoma
▪ Advance renal disease
▪ Recent surgery of the brain, spinal cord and eye
▪ Lumbar puncture
▪ Regional anesthetic block
▪ Caution:
- In pregnancy used only when clinically  indicated
79
Q

PLASMA CONCENTRATION OF HEPARIN

A

▪ 0.2 to 0.4 unit/mL (protamine titration)

▪ 0.3 to 0.7 unit/mL (anti Xa unit)

80
Q

Heparin initial bolus injection

A

80-100 unit/kg/hr

81
Q

Heparin continuous infusion:

A

15 to 22 unit/kg/hr

82
Q

Heparin low dose prophylaxis

A

▪ Subcutaneous administration

▪ 5000 units every 8 to 12 hours

83
Q

T or F

***Heparin is not administered by IM because it causes
necrosis

A

T

84
Q

Enoxaparin frequency

A

30mg 2x daily or 40mg once daily subQ

85
Q

Correspond to therapeutic anti Xa level of 0.5 to 1 unit/mL

A

Enoxaparin Full dose: 1mg/kg subQ every 12 hours

86
Q

Target anti Xa level of 1.5 units/mL

A

1.5 mg/kg once a day

87
Q

Prophylactic dose: ________subQ once daily

A

5000 units

88
Q

Dalteparin Therapeutic dose for venous disease:

A

200 units/kg

once a day

89
Q

Dalteparin Therapeutic dose for acute coronary syndrome:

A

120 units/kg every 12 hours

90
Q

LMWH is used with caution in px with

A

renal insufficiency

91
Q

▪ For venous thromboembolism
▪ Bind antithrombin with high specific activity = less
bleeding
▪ Efficient inactivation of factor Xa

A

FONDAPARINUX

92
Q

▪ Long half-life of 15 hours

▪ Alternative anticoagulant for HIT

A

Fondaparinux

93
Q

o A highly basic peptide; antagonist

o Combines with heparin as an ion pair to form stable complex devoid of anticoagulant activity

A

Protamine s04

94
Q

__ mg of protamine sulfate IV for every 100 units of heparin

A

1

95
Q

Rate of infusion should not exceed

A

50mg in any 10-minute

period

96
Q
  • For excess Dalteparin, it is removed by
A

plasmapheresis

97
Q

T or F
Protamine does not reverse the
activity of fondaparinux

A

T

98
Q

Bind at both catalytic and active site of thrombin and substrate recognition site

A

▪ HIRUDIN and BIVALIRUDIN

99
Q

Bind only at thrombin site

A

ARGATROBAN and MELAGATRAN

100
Q

▪ Specific irreversible thrombin inhibitor from leech saliva

A

HIRUDIN

101
Q

Hirudin recombinant form

A

Lepirudin

102
Q

▪ Bivalent inhibitor of thrombin and platelet
activation
▪ Administered IV

A

BIVALIRUDIN

103
Q

▪ FDA approved for percutaneous coronary

angioplasty

A

BIVALIRUDIN

104
Q

▪ Reach and inactivate fibrin bound thrombin in
thrombi
▪ Has little effect on platelets or the bleeding time

A

LEPIRUDIN

105
Q

FDA approved for

thrombosis related to HIT

A

LEPIRUDIN

106
Q 
▪ Small molecule thrombin inhibitor
▪ FDA approved in patients with HIT
▪ Has a short half-life
▪ Needs aPTT monitoring 
▪ Clearance is dependent on liver function
A

ARGATROBAN

107
Q

▪ An oral prodrug metabolized to the DTI

melagatran

A

XIMELAGATRAN

108
Q

Vitamin K Antagonist

A

Warfarin

109
Q

WARFARIN

▪ A synthesized agent from

A

BISHYDROXYCOUMARIN

110
Q

99% of racemic warfarin is bound to

A

plasma albumin

111
Q

T or F

The levorotatory S-warfarin is four times more
potent than the dextrorotatory R-warfarin

A

T

112
Q

Warfarin ▪ Mechanism of Action

A
  • Block the gamma- carboxylation of
    several glutamate residues in prothrombin
    and factors VII, IX, and X
113
Q

Resistance to warfarin:

A

presence of Vitamin K

reductase

114
Q

Four Vitamin K dependent factors includes:

A

II, VII, IX, and X

115
Q

Half-life: VII (__), IX (__hours), X (__

hours), II (__ hours)

A

6, 24, 40, 60

116
Q

For you to completely coagulate a patient,
if a half-life of prothrombin is 60 hours and
there is a presence of protein C and S,
you need to overlap it with a short acting

A

anti-coagulant (heparin)
- There is a tendency to clot if you do not
overlap it with heparin

117
Q

warfain

▪ Crosses the placenta

A
  • Cause a hemorrhagic disorder in the fetus
  • Affect fetal proteins with gammacarboxyglutamate residues found in bone
    and blood
  • Cause a serious birth defect
118
Q

warfarin

▪ Cutaneous necrosis

A
  • First weeks of therapy
  • Frank infarction of the breast, fatty
    tissues, intestine, and extremities
119
Q

Defined as progression or recurrence of a
thrombotic event while in the therapeutic range
These individuals may have their INR target raised

A

WARFARIN RESISTANCE

120
Q

Most commonly seen in patients with advanced
cancers, typically of gastrointestinal origin
(Trousseau’s syndrome)

A

WARFARIN RESISTANCE

121
Q

Reversal of warfarin action

A
  • Discontinue the drug
  • Oral or parenteral vitamin K1
    (phytonadione)
  • Fresh-frozen plasma
  • Prothrombin complex concentration
    o BEBULIN and Proplex T
122
Q

▪ Direct thrombin inhibitors (Oral)

A

Dabigatran

123
Q

▪ Direct Oral Factor Xa inhibitors

A
  • Rivaroxaban
  • Apixaban
  • Edoxaban
124
Q

Reversal Agents for Direct Oral Anticoagulant

A
  • Idarucizumab (reversal agent for dabigatran alone)
  • Andexanet alfa (is a factor Xa “decoy” molecule without procoagulant activity that competes for binding to anti-Xa drugs)
  • Ciraparantag
125
Q

FIBRINOLYTIC AGENTS

A

▪ Streptokinase
▪ Recombinant tissue plasminogen activator
▪ Inhibitors of Fibrinolysis
▪ Fibrinolytic Drugs

126
Q

▪ Recombinant tissue plasminogen activator

A
  • Alteplase
  • Reteplase
  • Tenecteplase
127
Q

Inhibitors of Fibrinolysis

A
  • E-aminocaproic acid

- Tranexamic acid

128
Q

Rapidly lyses thrombi by catalyzing the

formation of serene protease PLASMIN

A

▪ Fibrinolytic Drugs

129
Q

FIBRINOLYTIC AGENTS

includes

A

Streptokinase, Urokinase,

Anistreplase, t-PA

130
Q

A protein (but not an enzyme in itself) synthesized
by streptococci that combines with the
proactivator plasminogen. This enzymatic
complex catalyzes the conversion of inactive
plasminogen to active plasmin.

A

STREPTOKINASE

131
Q

▪ A human enzyme synthesized by the kidney that directly converts plasminogen to active
plasmin. Plasmin itself cannot be used because
naturally occurring inhibitors (antiplasmins) in
plasma prevent its effects.
▪ The absence of inhibitors for Urokinase permits its
use.
▪ Lyse thrombin from within.

A

UROKINASE

132
Q

▪ Another recombinant human t-PA from which
several amino acid sequences have been
deleted.
▪ Less expensive recombinant human t-PA.
▪ Leads to major fibrin – binding domain, less fibrin
specific.

A

RETEPLASE

133
Q

▪ A mutant form of t-PA that has a longer half-life,
and it can be given as an intravenous bolus.
Reteplase and Tenecteplase are as effective as
alteplase and have simpler dosing schemes
because of their longer half-lives.
▪ More fibrin – specific than t-PA.

A

TENECTEPLASE

134
Q

▪ Plasminogen activated endogenously
▪ Activate plasminogen bound to fibrin
▪ Confines fibrinolysis to the formed thrombus and
avoids systemic activation

A

TISSUE PLASMINOGEN ACTIVATOR (t-PA)

135
Q

▪ Human t-PA, manufactured by recombinant DNA

technology

A

ALTEPLASE

136
Q

▪ An Isolated plasminogen streptokinase activator
complex
▪ Consist of complex of purified human
plasminogen and bacterial streptokinase
▪ Acylated to protect enzyme site
▪ Acyl group hydrolyzes, free the streptokinase pro
activator complex

A

ANISTREPLASE

137
Q

FIBRINOLYTIC INHIBITORS

A

AMINOCAPROIC ACID
TRANEXAMIC ACID
SERINE PROTEASE INHIBITORS

138
Q 
▪ Similar to amino acid Lysine
▪ A synthetic inhibitor of fibrinolysis
▪ Completely inhibits plasminogen activation
▪ Rapidly absorbed orally
▪ Cleared by kidney
A

AMINOCAPROIC ACID

139
Q

▪ Analog of aminocaproic acid with the same
chemical properties
▪ Orally administered
▪ Loading dose - 15mg/kg
▪ Following dose - 30 mg/kg every 6 hours

A

TRANEXAMIC ACID

140
Q

▪ Aprotinin is a serine protease inhibitor
▪ Inhibit fibrinolysis by free plasmin
▪ Inhibit plasmin- streptokinase complex in patient
who received thrombolytic agent
▪ Reduces bleeding by as much as 50%
▪ For open heart procedures
▪ Liver transplantation

A

SERINE PROTEASE INHIBITORS

PHARMACOLOGY (13 decks)

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