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Pro & Anticoagulants Flashcards

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1
Q

4 locations that constitute “major” bleeding:

A

1) intracranial
2) intraspinal
3) intraocular
4) mediastinal

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2
Q

Risk factors for bleeding while on anticoagulation:

A
  • anti-coagulation effect (long half-life, no great tests)
  • increased age
  • female
  • hx of GI bleed
  • use of ASA with other anticoagulation
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3
Q

3 As of platelet plug formation:

A
  • adhesion
  • activation
  • aggregation
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4
Q

How is primary hemostasis defined?

A

any disruption in endothelium

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5
Q

Adhesion is dependent on what?

A

von Willebrand’s factor (vWF)/Factor III

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6
Q

How does vWF work and where is it synthesized?

A
  • acts as a bridge; one end attaches to the PLT and the other to the damaged tissue
  • synthesized and released from endothelial cells
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7
Q

Which clotting factor is not made in the liver?

A

vWF (localized in the endothelial cell)

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8
Q

MOA of Desmopressin/DDAVP:

A
  • stimulates large release of vWF from the endothelium (adhesion)
  • shortens bleeding time in patients with mild hemophilia A or VWD (quantitative issue)
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9
Q

Desmopressin is most effective in which types of VWD?

A

type I and III (quantitative issues)

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10
Q

Dose of desmopression:

A

0.3mg/kg over 15-30 min to avoid hypotension

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11
Q

Describe what happens during the activation stage of clot formation:

A
  • thrombin combines with a thrombin receptor on PLT surface
  • PLT changes shape and releases mediators that promote aggregation (adhesion)
  • these important mediators = ADP and Thromboxane A2
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12
Q

MOA of theinopyridine derivatives:

A

antiplatelet effect results from the inhibition of ADP-induced PLT aggregation

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13
Q

Most common theinopyridine derivative:

A

Clopidogrel (Plavix)
- irreversible - lasts the life of the PLTs

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14
Q

When should Plavix be d/c’ed prior to surgery? The other drugs of this class?

A

Plavix - 7 days
other drugs - 2-3 days

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15
Q

MOA of cyclooxygenase inhibitors:

A

inhibit PLT cyclooxygenase and prevent the synthesis of thromboxane A2 (activation)

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16
Q

What substance triggers the formation of thromboxane A2?

A

Thrombin A2

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17
Q

Which drugs are considered cyclooxygenase inhibitors?

A
  • ASA
  • NSAIDS
  • Celebrex (COX-2 inhibitor)
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18
Q

Pre-op recommendations for COX inhibitors?

A

ASA - 7-10 days
NSAIDs - 1-2 days
- COX-2 inhibitors take as scheduled

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19
Q

After the 3 steps of primary hemostasis, the clot remains (lipid/water) soluble until activated by ____.

A

water soluble until activated by fibrinWhat

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20
Q

What are the 2 major parts of the 3rd step in primary hemostasis?

A

1) ADP and thromboxane A2 uncover fibrin receptors (GPIIb/IIIa)
- fibrin links PLTs together
(this is all part of aggregation)

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21
Q

MOA of GPIIb/IIIa inhibitors:

A

inhibit PLT aggregation by interfering with the PLT-fibrin receptors (GPIIb/IIIa)

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22
Q

Most common GPIIa/IIIb inhibitor:

A

Reopro (abciximab)

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23
Q

Reopro should be stopped ___ days/hours before surgery

A

3 days
(others in this class need just 1 day)

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24
Q

What is the key player in secondary hemostasis?

A

fibrin

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25
Describe the events of secondary hemostasis:
- fibrin production incorporates all clotting factors - after PLT aggregation, fibrin is woven into the PLTs, they are crosslinked and insoluble in water
26
What is a major factor in secondary hemostasis?
thrombin activation
27
Which clotting factors are Vitamin K dependent?
2, 7, 9, 10 Prothrombin Stable Christmas Factor Stuart Prower Factor
28
Most clotting factors are produced in the _____ except:
liver except: Factor III (vWF) produced in the endothelium and Factor IV (Calcium) which is taken from the diet
29
MOA of coumadin:
- binds to the Vitamin K receptors in the liver and competitively inhibits Vitamin K - depresses production of Vitamin K dependent clotting factors
30
Lab tests to monitor coumadin levels:
PT & INR
31
When to stop coumadin prior to procedure:
5 days & may need bridging depending on reason for taking it and risk for clotting if they stopped
32
Main player in anticoagulation:
anti-thrombin (ATIII)
33
MOA of anti-thrombin:
- neutralizes factors Xa, IX, X, XI, and XII by forming complexes with them - removal of these factors from the blood leads to anticoagulation
34
Which patients tend to have anti-thrombin deficiency?
cirrhosis and nephrotic syndrome (both lead to decreased circulating levels)
35
MOA of heparin:
- increases the effectiveness of anti-thrombin x1000 - interferes with the intrinsic and final pathway - aPTT and ACT access the intrinsic pathway
36
#1 reason for unresponsiveness to heparin: Treatment:
- anti-thrombin deficiency - treatment = FFP (contains all coagulation and anti-coagulation factors made by the liver - including anti-thrombin)
37
What ACT level demonstrates adequate heparinization for cardiac pump cases?
>400
38
MOA of unfractionated heparin:
- larger MW will catalyze the inhibition of both factor IIa and Xa
39
Compare onset of IV and SQ unfractionated heparin:
IV = immediate anticoagulation activity SQ = 2-5 hour delay *small-dose SQ for DVT prophylaxis generally does not prolong APTT
40
When to stop heparin prior to procedure?
4-6 hours
41
Reversal agent for heparin:
protamine
42
How does LMWH differ from unfractionated?
- lack of monitoring the anticoagulation response - prolonged half-life - NOT reversible with protamine - ONLY catalyzes inhibition of Factor Xa - less protein bound
43
2 examples of LMWH:
Lovenox and Dalteparin
44
When to stop LMWH prior to procedure?
24-36 hours
45
MOA of direct thrombin inhibitors:
bind to thrombin in varying degrees
46
Example of a direct thrombin inhibitor:
Bivalrudin
47
When to stop Bival prior to procedure?
4-6 hours
48
What is a PCC?
Prothrombin Complex Concentrate concentrations of coagulation factors (II, VII, IX, and I) in varying degrees used for emergent reversal in the US
49
Which PCCs contain 4 factors?
- KCENTRA - Octaplex (used for warfarin reversal)
50
Which PCCs contain 3 factors?
- FEIBA - Profilnine - Bebulin
51
Use of Bebulin:
indicated for prevention and control of bleeding episodes in adult patients with hemophilia B
52
What factors does bebulin contain?
- Factor IX (Christmas factor) - Factor II (Prothrombin) - Factor X (Stuart-Prower factor) - low amounts of factor VII *combo of vitamin K dependent clotting factors
53
Another name for hemophilia B?
Factor IX deficiency Christmas disease
54
Uses for Apixaban (Eliquis) anti Xa:
- stroke prevention - DVT/PE treatment and prevention
55
Examples of direct-acting oral anticoagulants:
- Apixaban (Eliquis) - Rivaroxaban (Xarelto) - Edoxaban (Savaysa) - Dabigatran (Pradaxa)
56
Lab test to measure apixaban levels:
no reliable lab test
57
Uses for Xarelto:
- stroke prevention - DVT/PE treatment and prevention - atherosclerosis to reduce CV events (**main difference between Xarelto and Eliquis)
58
When to stop Xarelto prior to procedure?
need 2 day off time
59
Which direct-acting oral anticoagulants have a slightly longer half-life?
Edoxaban (Savaysa) - 10-14 hours compared to 7-11 hours with others Pradaxa - 12-14 hours with normal renal function
60
Most direct-acting oral anticoagulants work on Factor Xa. Which one does not and which factor does it affect?
Pradaxa works on IIa (thrombin)
61
When to d/c Pradaxa prior to procedure?
hold x 2 days with normal renal fxn hold x 3 days for renal insufficiency
62
Methods for reversal of Pradaxa?
- activated charcoal (if taken with 2-4 hours) - dialysis - Praxbind (monoclonal antibody, $$$$)
63
Main player in fibrinolysis:
plasmin (plasminogen --> plasmin, then plasmin breaks down the fibrin the clot)
64
Inactive form of plasmin = Where is it formed?
- plasminogen - formed in the liver and circulates in the blood
65
2 agents that convert plasminogen to plasmin:
- tissue-type plasminogen activator (tPA) - urokinase-type plasminogen activator (uPA)
66
3 anti-fibrinolytics:
- TXA - EACA (Amicar) - Aprotinin
67
MOA of TXA and EACA:
lysine analogs that competitively inhibit the activation of plasminogen to plasmin
68
MOA of Aprotinin:
polypeptide serin protease inhibitor; inhibits plasmin so fibrin breakdown is slow
69
Crash Trials demonstrated what in regards to TXA?
- reduced r/f death d/t bleeding - needs to be given early (within 3 hours of bleeding)
70
Which anti-fibrinolytic has an oral form? Why would it be prescribed?
TXA for heavy menstrual bleeding
71
SE of TXA?
- can inhibit plasmin at high levels - increased seizures in one study
72
Aprotinin is primarily used in which patient population?
cardiac bypass cases, esp repeat operations to decrease postop bleeding
73
Risks of Aprotinin:
- primary allergic rxn after first dose, severe anaphylaxis after second dose - worsen renal dysfxn
74
MOA of protamine:
inhibits PLTs and serine proteases involved with coagulation
75
Use of protamine:
reverses unfractionated heparin (NOT LMWH) through a neutralization rxn
76
Dose of protamine:
1mg protamine neutralizes 100 units of heparin
77
Adverse rxns of protamine:
- anaphylaxis - acute pulmonary vasoconstriction - RV heart failure - hypotension *give slowly over 20 mins)
78
Caution use of protamine in...
- patients who have received it before - vasectomies - NPH insulin (20-30% of patients develop antibodies)
79
Protamine is a (acid/base)
base

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