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Pro & Anticoagulants Flashcards

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
Q

Describe the events of secondary hemostasis:

A
  • fibrin production incorporates all clotting factors
  • after PLT aggregation, fibrin is woven into the PLTs, they are crosslinked and insoluble in water
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26
Q

What is a major factor in secondary hemostasis?

A

thrombin activation

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27
Q

Which clotting factors are Vitamin K dependent?

A

2, 7, 9, 10
Prothrombin
Stable
Christmas Factor
Stuart Prower Factor

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28
Q

Most clotting factors are produced in the _____ except:

A

liver

except: Factor III (vWF) produced in the endothelium and Factor IV (Calcium) which is taken from the diet

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29
Q

MOA of coumadin:

A
  • binds to the Vitamin K receptors in the liver and competitively inhibits Vitamin K
  • depresses production of Vitamin K dependent clotting factors
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30
Q

Lab tests to monitor coumadin levels:

A

PT & INR

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31
Q

When to stop coumadin prior to procedure:

A

5 days & may need bridging depending on reason for taking it and risk for clotting if they stopped

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32
Q

Main player in anticoagulation:

A

anti-thrombin
(ATIII)

33
Q

MOA of anti-thrombin:

A
  • neutralizes factors Xa, IX, X, XI, and XII by forming complexes with them
  • removal of these factors from the blood leads to anticoagulation
34
Q

Which patients tend to have anti-thrombin deficiency?

A

cirrhosis and nephrotic syndrome (both lead to decreased circulating levels)

35
Q

MOA of heparin:

A
  • increases the effectiveness of anti-thrombin x1000
  • interferes with the intrinsic and final pathway
  • aPTT and ACT access the intrinsic pathway
36
Q

1 reason for unresponsiveness to heparin:

Treatment:

A
  • anti-thrombin deficiency
  • treatment = FFP (contains all coagulation and anti-coagulation factors made by the liver - including anti-thrombin)
37
Q

What ACT level demonstrates adequate heparinization for cardiac pump cases?

38
Q

MOA of unfractionated heparin:

A
  • larger MW will catalyze the inhibition of both factor IIa and Xa
39
Q

Compare onset of IV and SQ unfractionated heparin:

A

IV = immediate anticoagulation activity
SQ = 2-5 hour delay
*small-dose SQ for DVT prophylaxis generally does not prolong APTT

40
Q

When to stop heparin prior to procedure?

41
Q

Reversal agent for heparin:

42
Q

How does LMWH differ from unfractionated?

A
  • lack of monitoring the anticoagulation response
  • prolonged half-life
  • NOT reversible with protamine
  • ONLY catalyzes inhibition of Factor Xa
  • less protein bound
43
Q

2 examples of LMWH:

A

Lovenox and Dalteparin

44
Q

When to stop LMWH prior to procedure?

A

24-36 hours

45
Q

MOA of direct thrombin inhibitors:

A

bind to thrombin in varying degrees

46
Q

Example of a direct thrombin inhibitor:

A

Bivalrudin

47
Q

When to stop Bival prior to procedure?

48
Q

What is a PCC?

A

Prothrombin Complex Concentrate

concentrations of coagulation factors (II, VII, IX, and I) in varying degrees

used for emergent reversal in the US

49
Q

Which PCCs contain 4 factors?

A
  • KCENTRA
  • Octaplex (used for warfarin reversal)
50
Q

Which PCCs contain 3 factors?

A
  • FEIBA
  • Profilnine
  • Bebulin
51
Q

Use of Bebulin:

A

indicated for prevention and control of bleeding episodes in adult patients with hemophilia B

52
Q

What factors does bebulin contain?

A
  • 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
Q

Another name for hemophilia B?

A

Factor IX deficiency
Christmas disease

54
Q

Uses for Apixaban (Eliquis) anti Xa:

A
  • stroke prevention
  • DVT/PE treatment and prevention
55
Q

Examples of direct-acting oral anticoagulants:

A
  • Apixaban (Eliquis)
  • Rivaroxaban (Xarelto)
  • Edoxaban (Savaysa)
  • Dabigatran (Pradaxa)
56
Q

Lab test to measure apixaban levels:

A

no reliable lab test

57
Q

Uses for Xarelto:

A
  • stroke prevention
  • DVT/PE treatment and prevention
  • atherosclerosis to reduce CV events (**main difference between Xarelto and Eliquis)
58
Q

When to stop Xarelto prior to procedure?

A

need 2 day off time

59
Q

Which direct-acting oral anticoagulants have a slightly longer half-life?

A

Edoxaban (Savaysa) - 10-14 hours compared to 7-11 hours with others
Pradaxa - 12-14 hours with normal renal function

60
Q

Most direct-acting oral anticoagulants work on Factor Xa. Which one does not and which factor does it affect?

A

Pradaxa works on IIa (thrombin)

61
Q

When to d/c Pradaxa prior to procedure?

A

hold x 2 days with normal renal fxn
hold x 3 days for renal insufficiency

62
Q

Methods for reversal of Pradaxa?

A
  • activated charcoal (if taken with 2-4 hours)
  • dialysis
  • Praxbind (monoclonal antibody, $$$$)
63
Q

Main player in fibrinolysis:

A

plasmin

(plasminogen –> plasmin, then plasmin breaks down the fibrin the clot)

64
Q

Inactive form of plasmin =
Where is it formed?

A
  • plasminogen
  • formed in the liver and circulates in the blood
65
Q

2 agents that convert plasminogen to plasmin:

A
  • tissue-type plasminogen activator (tPA)
  • urokinase-type plasminogen activator (uPA)
66
Q

3 anti-fibrinolytics:

A
  • TXA
  • EACA (Amicar)
  • Aprotinin
67
Q

MOA of TXA and EACA:

A

lysine analogs that competitively inhibit the activation of plasminogen to plasmin

68
Q

MOA of Aprotinin:

A

polypeptide serin protease inhibitor; inhibits plasmin so fibrin breakdown is slow

69
Q

Crash Trials demonstrated what in regards to TXA?

A
  • reduced r/f death d/t bleeding
  • needs to be given early (within 3 hours of bleeding)
70
Q

Which anti-fibrinolytic has an oral form? Why would it be prescribed?

A

TXA for heavy menstrual bleeding

71
Q

SE of TXA?

A
  • can inhibit plasmin at high levels
  • increased seizures in one study
72
Q

Aprotinin is primarily used in which patient population?

A

cardiac bypass cases, esp repeat operations to decrease postop bleeding

73
Q

Risks of Aprotinin:

A
  • primary allergic rxn after first dose, severe anaphylaxis after second dose
  • worsen renal dysfxn
74
Q

MOA of protamine:

A

inhibits PLTs and serine proteases involved with coagulation

75
Q

Use of protamine:

A

reverses unfractionated heparin (NOT LMWH) through a neutralization rxn

76
Q

Dose of protamine:

A

1mg protamine neutralizes 100 units of heparin

77
Q

Adverse rxns of protamine:

A
  • anaphylaxis
  • acute pulmonary vasoconstriction
  • RV heart failure
  • hypotension
    *give slowly over 20 mins)
78
Q

Caution use of protamine in…

A
  • patients who have received it before
  • vasectomies
  • NPH insulin

(20-30% of patients develop antibodies)

79
Q

Protamine is a (acid/base)

Pharm (19 decks)

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