Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology II > Bleeding, Coagulopathy, and Anticoagulation > Flashcards

Bleeding, Coagulopathy, and Anticoagulation Flashcards

1
Q

What is the “Hemostasis Tripod”?

A

Primary hemostasis
Coagulation
Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define “Primary Hemostasis”

A

Mediated by platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define “Coagulation”

A

A chemical process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define “Vasoconstriction”

A

A mechanical process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Platelets adhere to disrupted vessel wall via?

A

Platelet surface membrane glycoprotein receptor Ib and vWF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Platelets also adhere to one another via?

A

Surface receptor glycoprotein IIb/IIIa and fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name three actions of platelets

A

Production of arachidonic acid vasoconstrictors, release of various proteins from platelet storage granules, and provide site for generation of thrombin and subsequent fibrin formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name two arachidonic acid vasoconstrictors

A

Thromboxane A2 and prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What types of proteins are released from platelet storage granules?

A

Platelet agonists ADP and serotonin, coagulation factors vWF and coagulation factor V, heparin-binding proteins, growth factor/chemokines PDGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Platelet surface provides site for?

A

Generation of thrombin and subsequent fibrin formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the “extrinsic system”?

A

Tissue Factor-Factor VII pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In the extrinsic system, complex forms between?

A

Tissue factor and factor VII after tissue factor is exposed to blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In the extrinsic system, after factor VII is activated, what happens?

A

Tissue factor-factor VIIa complex binds and activates factor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In the extrinsic system, factor Xa is responsible for what conversion?

A

Converts prothrombin (factor II) to thrombin (factor IIa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The conversion of prothrombin to thrombin requires what cofactor?

A

Factor V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The conversion of prothrombin to thrombin is most efficient in the presence of?

A

A phospholipid surface, e.g., activated platelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the alternate (“secondary”) pathway of coagulation?

A

Amplifies the effects of the first pathway, same initiating factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In the secondary pathway, what activates factor IX?

A

Tissue factor VIIa complex activates factor IX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Factor IX and cofactor VIII activate what?

A

Factor X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

The secondary pathway results in the formation of?

A

Thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the first step in the third coagulation pathway?

A

Thrombin itself activates factor XI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does factor XIa activate?

A

Factor IX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does the third pathway result in?

A

Pathway proceeds to additional thrombin formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is necessary for the conversion of fibrinogen into fibrin?

A

Thrombin and coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Thrombin and coagulation facilitates its own formation by?

A

Activating coagulation factors and cofactors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Thrombin and coagulation is a strong activator of?

A

Platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does thrombin and coagulation mediate fibrinogen cleavage?

A

Forms fibrin monomers and subsequent polymers; cross linking of fibrin takes place by thrombin-activated factor XIII (the ultimate step in the coagulation cascade)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does Tissue factor pathway inhibitor (TFPI) do?

A

Inhibits the impact of tissue factor, which stops the whole cascade from beginning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What activates circulating protein C?

A

Endothelial cell-bound enzyme thrombomodulin in association with thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Activated protein C degrades what?

A

Cofactors V and VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Activation of protein C requires what essential cofactor?

A

Protein S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What forms complexes and inactivates thrombin and factor Xa?

A

Antithrombin III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Antithrombin III is strongly enhanced by the presence of?

A

Heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Protein C inhibits which pathway of coagulation?

A

Secondary pathway and final pathway (breaks down activated factors V and VIII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Protein C initiates the breakdown of?

A

Fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does Protein C shut down the coagulation cascade?

A

By inactivating Factors V and VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are tPA and uPA and where are they found?

A

Plasminogen activator molecules found in endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What causes the release of tPa and uPA?

A

Several stimuli, including hypoxia, acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

At what two levels is fibrinolysis inhibited at?

A

Activator inhibitors (PAIs) and circulating protease inhibitors (e.g., alpha 2-antiplasmin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the most common congenital coagulation disease?

A

von Willebrand disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is Type I vWD?

A

Reduced concentration (10-45% normal levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is Type II vWD?

A

Dysfunctional vWF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is IIa subtype of vWD?

A

Variable qualitative defect in GP-1 binding and multimer formation (quality not good)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is IIb subtype of vWD?

A

“Gain of function” defect, excessive binding to platelet GP-1 (vWF works too well and you get MORE platelet aggregation) – makes you hyper-coaguble, the opposite problem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is IIm subtype of vWD?

A

Monomers have decreased GP-1 binding, multimers normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is IIn subtype of vWD?

A

Defect in binding to factor VIII, may be diagnosed as hemophilia A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is type III vWD?

A

Absent vWF (homozygous for gene defect); don’t make any vWF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

In which type of vWD do patients know they have it because they are symptomatic early on and likely experience severe disease?

A

Type III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Desmopressin (DDAVP) is used to treat which types of vWD?

A

Type I and IIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

DDAVP is an analogue of?

A

Vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

DDAVP promotes the release of vWF stored in?

A

Endothelial cell-associated Weibel-Palade bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

vWF links exposed collagen to?

A

Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How is DDAVP given?

A

Nasal spray (Stimate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

DDAVP is contraindicated in which type of vWD?

A

Type IIb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How do you treat more severe forms of vWD?

A

Replacement with transfused factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How long does treatment continue after surgery?

A

4-7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Initially, clotting is mostly dependent on?

A

Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Coagulation disease results in?

A

Late re-bleeding after fibrinolysis (clots don’t stabilize- these patients need to be treated with something that ensures clot stays long enough to prevent late re-bleeding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the most commonly inherited coagulation disorder?

A

Hemophilia A (classic hemophilia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is Hemophilia A inherited?

A

Sex-linked recessive, 1 of 10k male births

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Levels of which factor are variable in Hemophilia A?

A

Factor VIII; mild hemophilia up to 40% of normal, severe <1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Patients with factor VIII greater than what percentage rarely bleed spontaneously, but will have bleeding problems after surgery or trauma?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What develops in 10-15% of severely affected hemophiliacs?

A

Anti-factor VIII antibodies (factor VIII inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Factor VIII levels are also decreased in what disease? Why?

A

vWD because vWF acts as a carrier molecule for factor VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How do you treat mild-moderate Hemophilia A?

A

DDAVP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

DDAVP releases endogenous factor VIII from where?

A

Liver sinusoids and endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

DDAVP also releases what?

A

vWF resulting in a transient increase in factor VIII levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How do you treat severe Hemophilia A?

A

Factor VIII transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What does Hemophilia B is also known as?

A

Christmas disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Hemophilia B affects what?

A

Factor IX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Name 3 hypercoaguable coagulation diseases

A

Protein C deficiency, Protein S deficiency, Factor V Leiden

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Where are Proteins C and S synthesized?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Proteins C and S depend on?

A

Vitamin K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Mild forms of Protein C/S deficiency predispose individuals too?

A

Thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Severe forms of Protein C/S deficiency lead to?

A

Not compatible with life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is Factor V Leiden disease?

A

Polymorphic factor V which resists inactivation by activated protein C (protein C not able to bind normally to factor V)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Factor V Leiden is present in what % of people of what descent?

A

5% of North American Caucasians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Factor V Leiden is rare in people of what descent?

A

Asians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Factor V Leiden may predispose individuals to?

A

Deep venous thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the source of coagulation factors?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the source of Protein C, Protein S, and fibrinogen?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Thrombocytopenia, sometimes seen in liver disease patients, is the result of?

A

Portal hypertension and associated splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Function of what is impaired in cirrhotic patients?

A

Thrombocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is MELD score?

A

Model for end-stage liver disease score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the formula of MELD score based on?

A

Serum bilirubin, serum creatinine, INR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

MELD score predicts how many month mortality?

A

3 month (how likely are you to still live in 3 months if you don’t get a new liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Higher MELD score indicates?

A

Worse liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What disease also presents with coagulation abnormalities and risk for enhanced bleeding?

A

Renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

In patients with renal failure, low levels of what may contribute to the impaired function of primary hemostasis?

A

Hematocrit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Is low hematocrit frequently an important factor in renal disease patients?

A

Less frequently because most patients are regularly treated with erythropoietin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How can you test the extent of hematocrit defect?

A

Platelet Function Assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Why do renal failure patients have coagulation abnormalities?

A

Attributed to impaired platelet adhesion, aggregation, and release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What has been shown to correct prolonged bleeding time in patients with uremia?

A

DDAVP

94
Q

If insufficient correction of bleeding is achieved with DDAVP, what can be used?

A

Platelet concentrates

95
Q

What additional measures need to be corrected in patients with uremia?

A

Anemia and hemodialysis

96
Q

What is Aspirin’s mechanism of action?

A

Irreversible inhibitor of platelet membrane-associated cyclooxygenase

97
Q

Aspirin blocks the formation of what?

A

Thromboxane A2

98
Q

What is Thromboxane A2?

A

A potent platelet agonist and vasoconstrictor

99
Q

Do high or low doses of aspirin preferentially inhibit Thromboxane A2?

A

Low

100
Q

What does aspirin do to platelet aggregation?

A

Irreversible (and relatively weak) inhibition of platelet aggregation

101
Q

Aspirin may be associated with?

A

Significant impairment of primary hemostasis and mild enhancement of bleeding

102
Q

What is the life span of a platelet?

A

10 days

103
Q

How many days are usually required after termination of aspirin use to restore adequate platelet function and effective hemostasis?

A

5-7 days

104
Q

How long will the effect of aspirin last?

A

For the interval needed to produce a sufficient number of new platelets not affected

105
Q

What are the two more important adverse effects of aspirin?

A

Bleeding and the occurrence of hemorrhagic gastritis (or even gastric ulceration)

106
Q

For most dental procedures, we want to continue/discontinue aspirin?

A

Continue (risks > benefits)

107
Q

Clopidogrel is AKA?

A

Plavix

108
Q

Clopidogrel is an oral prodrug metabolized by?

A

Liver

109
Q

What % of the absorbed drug becomes active form?

A

15%

110
Q

Clopidogrel is subject to?

A

Cytochrome genetic polymorphisms

111
Q

What is the half life of Clopidogrel?

A

8 hours

112
Q

The effects of Clopidogrel last how long in relation to a platelet?

A

For the platelet’s lifetime

113
Q

Clopidogrel binds irreversibly to what receptor on the platelet surface?

A

P2Y12 ADP receptor (prevents ADP-mediated platelet aggregation)

114
Q

Clopidogrel is comparable to aspirin as secondary prophylaxis in patients with what three conditions?

A

MI, stroke, or peripheral arterial disease

115
Q

Is there any benefit to combining clopidogrel with aspirin vs aspirin alone?

A

Combination superior after acute coronary event, PCI, and coronary stent placement

116
Q

Is clopidogrel or aspirin more expensive?

A

Clopidogrel- much more expensive

117
Q

Does clopidogrel or aspirin result in more clinical bruising/bleeding?

A

Clopidogrel

118
Q

Is clopidogrel safe to continue through most oral surgery?

A

Yes, like aspirin

119
Q

Name three other P2Y12 blockers

A

Ticlopidine (Ticlid), Prasugrel (Efient), and direct-acting reversible inhibitors

120
Q

Name two direct-acting reversible inhibitors

A

Ticragelor (Brilinta), Cangrelor (Kengreal)

121
Q

Do Ticlopidine and Prasugrel have a more or less rapid onset compared to clopidogrel?

A

More rapid onset

122
Q

Which P2Y12 blocker is also a prodrug but with rapid conversion to active form?

A

Prasugrel (Efient)

123
Q

What is the benefit of direct-acting, reversible inhibitors?

A

Direct acting = more rapid onset

Reversible binding = shorter half-lie

124
Q

What is Dipyramidole’s mechanism of action?

A

Has anti platelet effect by inhibition of phosphodiesterase

125
Q

Inhibition of phosphodiesterase results in?

A

Intracellular accumulation of cyclic AMP

126
Q

Dipyramidole has shown what effects in clinical trails?

A

No significant efficacy on the prevention of thromboembolic disease

127
Q

Dipyramidole how shown what effects in vitro?

A

Potent inhibitor of platelet aggregation

128
Q

What are the most potent inhibitors of platelet aggregation?

A

Glycoprotein Receptor IIb/IIIa inhibitors

129
Q

What is the mechanism of action of Glycoprotein Receptor IIb/IIIa inhibitors?

A

Competitive inhibitors for fibrinogen binding to the platelet IIb/IIIa receptor

130
Q

Are IV or oral forms of Glycoprotein Receptor IIb/IIIa inhibitors most effective?

A

IV forms highly effective in interventional cardiology, oral forms not effective

131
Q

Coumadin is what class of drug?

A

Anti-coagulant

132
Q

Coumadin is an antagonist of?

A

Vitamin K

133
Q

What is Coumadin’s mechanism of action?

A

Blocks the essential vitamin K-dependent carboxylation of coagulation factors II, VII, IX, and X

134
Q

By blocking these coagulation factors, Coumadin results in?

A

Formation of biologically inactive proteins and decreases the coagulant activity of these factors in plasma

135
Q

Effect of Coumadin is a function of what?

A

The decay in the concentration of the coagulation factors, not the drug itself

136
Q

The half-life of vitamin K-dependent coagulation factors ranges from?

A

6 h to 60 h

137
Q

The full effect of Coumadin therapy is delayed for how long?

A

2 or 3 days

138
Q

Full restoration of normal coagulation after termination of Coumadin therapy requires how many days?

A

At least 3-5 days

139
Q

Dose-effect relationship of Coumadin varies considerably due to what three factors?

A

Binding to plasma albumin, variable vitamin K intake, variable clearance by the liver

140
Q

What is the most important side effect of Coumadin treatment?

A

Bleeding

141
Q

What may occur with an associated protein C deficiency in patients on Coumadin?

A

Rare Coumadin-induced skin necrosis

142
Q

In rare Coumadin-induced skin necrosis, are levels of coagulation factors still normal?

A

Yes; a net pro-coagulant state results

143
Q

The new oral anticoagulants are inhibitors of what factor?

A

Xa

144
Q

What new drug is a direct thrombin inhibitor?

A

Pradaxa

145
Q

What three new drugs are factor Xa inhibitors?

A

Xarelto, Eliquis, Savaysa

146
Q

Are the new oral anticoagulants affected by diet, liver function, etc. or require regular lab monitoring?

A

No

147
Q

What is the onset and half-life of new oral antiocoagulants?

A

Relatively rapid onset (2-3 hours) and short half-life (8-12 hours)

148
Q

Impaired renal function affects new oral anticoagulants how?

A

Increases and prolongs drug effect

149
Q

How do the new oral anticoagulants compare to Coumadin with stroke prevention?

A

Comparable

150
Q

How do the new oral anticoagulants compare to Coumadin with risk of extra cranial bleeding?

A

Same, oral anticoagulants possibly higher

151
Q

Is routine testing of effect available for new oral anticoagulants?

A

No

152
Q

Can you reverse new oral anticoagulants?

A

Very limited

153
Q

How much is known about the safety of new oral anticoagulants?

A

Little- once bleeding starts, there may be little to do but wait

154
Q

Discontinuing new oral anticoagulant for how many days before oral surgery is prudent?

A

1-2 days

155
Q

Discontinuing new oral anticoagulant before oral surgery is longer in which patients?

A

Renal patients

156
Q

What is Idarucizamab (Praxbind)?

A

Reversal of dabigatran (Pradaxa); is is an anti-dabigatran mAb fragment

157
Q

When is Praxbind indicated?

A

For emergency surgery or life-threatening bleeding

158
Q

Peak effect of Praxbind is?

A

Within 4 hours; reverses anticoagulation immediately

159
Q

Patients on Praxbind remain in normal coagulation state in how much time?

A

24 hours (Pradaxa may be resumed at that time)

160
Q

What risk is associated with Praxbind?

A

Exposure to underlying thrombotic disease consequence

161
Q

Serious risk of Praxbind in patients with?

A

Hereditary fructose intolerance because solution contains Sorbitol

162
Q

What is Andexanet Alfa?

A

Not yet approved; Factor Xa decoy protein given as infusion

163
Q

Andexanet Alfa reverses anticoagulation in?

A

Less than 5 minutes

164
Q

What is PER977 (ciraparantag, aripazine)?

A

Nonspecific agent for anti-Xa and anti-thrombin agents (heparin, dabigatran)

165
Q

How is Heparin given?

A

Parenterally

166
Q

What is Heparin a mixture of?

A

Glycosaminoglycans of various molecular sizes isolated from intestines or lungs of pig, cow or other cattle

167
Q

What does Heparin bind to?

A

Antithrombin III

168
Q

Binding to Antithrombin III causes?

A

Potentiates inhibition of factors IIa (thrombin) and Xa more than 1000-fold

169
Q

Effect of heparin after IV administration is?

A

Immediate

170
Q

What kind of half-life does Heparin have?

A

Dose-dependent half-life

171
Q

After IV administration of a 5000U bolus of Heparin, the mean half life is?

A

60-90 min

172
Q

Heparin is often given as?

A

Continuous IV infusion

173
Q

How is Heparin monitored?

A

Frequent laboratory monitoring, usually by aPTT (because anticoagulant effect of heparin may be highly variable)

174
Q

In special conditions like surgery, what can be used to monitor heparin?

A

Whole blood activated clotting time (ACT)

175
Q

When must heparin be given parenterally?

A

When used as prophylaxis against thrombosis, requires frequent subcutaneous injections

176
Q

How are LMWHs given?

A

Parenterally- usually subcutaneous

177
Q

What is the average MW of LMWHs?

A

4-6 kDa

178
Q

What type of effects can be seen with LMWHs?

A

In some situations have a more favorable antithrombotic effect and induce fewer bleeding complications than unfractionated heparin

179
Q

What two benefits are associated with LMWHs?

A

Predictable inter- and intraindividual bioavailability and clearance & much longer half-life compared to unfractionated heparin

180
Q

Predictable inter- and intraindividual bioavailability reduces the need for?

A

Frequent laboratory monitoring and frequent dose adjustments

181
Q

Much longer half-life compared to unfractionated heparin is advantageous when?

A

When stable anticoagulation is required over a long period of time

182
Q

much longer half-life compared to unfractionated heparin may complicate situations that require?

A

Easily adjustable anticoagulation, like patients at high risk for bleeding

183
Q

Large randomized controlled trials have demonstrated the efficacy and safety of LMWH in the postoperative prevention of?

A

Venous thromboembolism in surgical patients

184
Q

What are pentasaccharides?

A

Parenteral drugs

185
Q

What is the prototype of pentasaccharides?

A

Arixtra (fondaparinux)

186
Q

When are pentasaccharides indicated?

A

For DVT prophylaxis or DVT/PE treatment

187
Q

What is the mechanism of action of pentasaccharides?

A

Synthetic compounds that exert antithrombin-dependent exclusive inhibition of factor Xa

188
Q

Is Xa inhibition direct or indirect by pentasaccharides?

A

Indirect

189
Q

Some evidence that pentasaccharides are superior to LMWH for prophylaxis of?

A

Venous thromboembolism in patients undergoing hip or knee replacement

190
Q

What is the most frequent adverse effect of heparin or heparin derivative treatment?

A

Bleeding

191
Q

What is heparin-induced thrombocytopenia (HIT)?

A

An immunological response to heparin characterized by thrombocytopenia and thromboembolism

192
Q

When does HIT occur?

A

5-7 days after initial exposure to heparin, but may be an immediate complication if the patient has received heparin previously

193
Q

Alternative anticoagulant therapy may consist of treatment with hirudin or heparinoids but not with coumarin derivatives, which may cause?

A

Skin necrosis

194
Q

Long-term use of heparin has been associated with?

A

Osteopenia

195
Q

Is there a higher or lower incidence of osteopenia with LMWH?

A

Lower incidence

196
Q

What is a thrombolytic agent?

A

Plasminogen activators (recombinant endogenous plasminogen activators, tPA)

197
Q

How are plasminogen activators administered?

A

At a dose 1000x physiological concentration

198
Q

What is the most important side effect of thrombolytic treatment?

A

Bleeding

199
Q

What 3 signs on a physical exam might point to a defect in the coagulation system?

A

Abnormal bruising, petechiae, splenomegaly

200
Q

Preoperative screening in patients with signs or symptoms of a bleeding tendency includes what three tests?

A

A platelet count, a PTT, and PT/INR

201
Q

If an abnormality in primary hemostasis is suspected, what is tested and what is measured?

A

Platelet function is tested and vWF is measured

202
Q

Is platelet function testing widely clinically relevant?

A

No

203
Q

What is PT/INR?

A

Prothrombin time test; mixture of calcium and thromboplastin is added to citrated blood and the time to clot formation is measured

204
Q

What does the PT value reflect?

A

The coagulation ability of the TF-VIIa coagulation pathway

205
Q

Tissue thromboplastin is a mixture of?

A

TF and phospholipid membrane fragments

206
Q

What is normal PT?

A

Averages 12 +/- 2 seconds

207
Q

Define INR

A

Ratio of patient’s PT to the individual laboratory standard; provides a standardized way to report the PT time relative to control

208
Q

Are PT or INR values comparable between laboratories?

A

INR values are comparable between laboratories, but PT values are not

209
Q

PT is prolonged by deficiencies in what 5 things?

A

Factors VII, X, V, prothrombin, fibrinogen

210
Q

PTT measures?

A

Slower “intrinsic” pathway: normal is roughly 25-40 sec

211
Q

PTT is used commonly to monitor?

A

Anticoagulation with heparin

212
Q

Deficiencies in what two factors will not be detected with PTT test?

A

VII or XIII

213
Q

PTT is used commonly to monitor?

A

Anticoagulation with heparin

214
Q

In vitro, PTT requires all clotting factors except?

A

Factor VII

215
Q

Prolonged aPTT (activated partial thromboplastin time) may indicate?

A

Use of heparin, antiphospholipid antibody (esp lupus anticoagulant), coagulation factor deficiency, sepsis, or presence of antibodies against coagulation factors

216
Q

What was the standard method for assessing primary hemostasis for many years?

A

Bleeding time

217
Q

Bleeding time can be affected by ingestion of?

A

Aspirin

218
Q

Is bleeding time sensitive or specific?

A

Neither

219
Q

What is used in place of bleeding time?

A

Platelet function analyzer-100 (PFA-100)

220
Q

How does PFA-100 work?

A

Blood sample put into test cartridge, vacuum draws blood through thin glass coated with collagen and E/ADP, coating activates platelets in the moving sample and promotes platelet adherence and aggregation

221
Q

Closure time is measured by?

A

Time it takes for a clot to form inside the glass tube and prevent further blood flow

222
Q

An initial screen for PFA-100 is done with?

A

Collagen/EPI

223
Q

If CT is normal on initial screen, what does this indicate?

A

Unlikely that a platelet dysfunction exists

224
Q

What is used to confirm an abnormal collagen/EPI test?

A

A collagen/ADP test is run

225
Q

If the collagen/ADP test is normal, then the abnormal collagen/EPI test may be due to?

A

Aspirin ingestion

226
Q

If both collagen/ADP and collagen/EPI tests are abnormal, then what does this indicate?

A

Patient likely has a platelet dysfunction

227
Q

What is the gold standard for platelet function analysis?

A

Platelet aggregometry (PAA)

228
Q

What is studied in PAA?

A

The response of either whole blood or platelet-rich plasma to specific agents known to induce aggregation of platelets is studied

229
Q

How does PAA work?

A

A beam of light passes through a suspension of stirred platelets and the percent transmission is measured.
When an agonist such as thrombin is added, a small initial drop in light transmission typically occurs as platelets change shape from discs to spheres.
As platelet aggregation occurs, light transmission increases

230
Q

Platelet aggregation tests use a battery of agonists like?

A

ADP, collagen, ristocetin, and arachidonic acid

Pharmacology II (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions