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Pharm Exm 4 > Anticoagulants > Flashcards

Anticoagulants Flashcards

(50 cards)

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1
Q

Which factors are glycoproteins

A

8, 5, 3, Protein S

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2
Q

Which factors are serine proteases

A

7, 9, 10, 11, 12

2

Protein C (Anticoagulant)

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3
Q

Links factors to anionic lipids

A

Ca++

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4
Q

Factor 5 Leiden is resistant to ______

A

Activated protein C

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5
Q

All factors except ___ are made in the ____

A

vWF, liver

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6
Q

vWF is produced where?

A

Endoth., subendoth., Megakaryocytes

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7
Q

Tissue factor pathway aka

A

extrinsic pathway

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8
Q

Collagen exposure initiates this pathway

A

Intrinsic

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9
Q

TF is expressed where?

Factor 7 resides where?

A

TF = On surface of cells outside of (but near) blood vessels

Factor 7 = In blood

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10
Q

7 activates…

A

10

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11
Q

Calcium’s role in 7/10 interaction with tissue factor

A

Ca++ located near the site of binding, helps interaction with phospholipid membranes

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12
Q

___, ___, and ___ bind to collagen on the wall of damaged blood vessels

What are the next 4 steps?

A
  • Factor 7
  • HMWK
  • Prekallikrein
  1. Factor 7 cleaves: Prekallikrein –> kallikrein AND cleaves 11->11a
  2. Kallikrein activates more 7
  3. HMWK anchors kallikrein and 11a to damaged surface
  4. Factor 9 binds factor 8a on platelet surface —-> Activates factor 10
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13
Q

Thrombins two effects

A
  1. Converts fibrinogen –> fibrin (insoluble)
  2. Activates factor 13 (which in turn cross links fibrin)
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14
Q

Prothrombin time

A

recalcified blood and thromboplastin

  • Clots in 12-14 seconds
  • Monitor oral anticoag therapy
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15
Q

aPTT

A

Recalcified blood + phospholipid

  • Clots in 24-36s
  • Monitor heparin therapy
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16
Q

BT

A

2-9 minutes

Abnormal when defect is in platelet number or function

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17
Q

Prolonged PT

A

oral anticoag

defect in extrinsic or common

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18
Q

Prolonged aPTT

A

Intrinsic/common

(heparin)

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19
Q

INR =

A

(Patient PT / Control PT)C

C= international sensitivity index that corrects for different thromboplastin reagents

Therapeutic range should = 2-3

(except for recurrent PE or prosthetic valves, 3-4)

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20
Q

All coumarin derivatives are _____

A

water soluble lactones

Warfarin is most common (racemic mixture, S isomer is most potent)

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21
Q

inandione anticoagulant example and 2 properties

Study These Flashcards
A

Anisindione

Orally active with significant AE’s

22
Q

Warfarin MOA

Study These Flashcards
A

Inhibiton of vitamin K epoxide reductase

23
Q

Vitamin K actions

Study These Flashcards
A

Vitamin K is essential for post trans modification of factors 2, 7, 9, 10 C, S

Vitamin K carboxylase catalyzes the gamma-carboxylation of Glu in prothrombin (Vit K is oxidized in this process, needs epox. red. to be renewed)

24
Q

This must happen for onset of Warfarin action

Study These Flashcards
A

depletion of the pool of factors in circulation

(maximal anticoagulation takes 3-5 days to achieve)

25
Dosage of warfarin
Loading dose = 5mg/day Maintenance dose = 2.5-5 mg/day
26
Warfarin metabolism
CYP2C9 (half life = 36-48 hours) \*\*termination of action is NOT correlated with warfarin levels in circulation, but with the regeneration of normal clotting factors
27
Treatment for warfarin overdose
STOP WARFARIN administer Vit K1 (high levels can activate the reductase) \*\*plasma if severe hemorrhage to replace clotting factors
28
Warfarin CI'd in...
pregnancy (in those who are or may become) passes through placenta -- fetal hemorrhage and FWS (nasal hypoplasia
29
Drugs with Decreased PT | (DDI's with warfarin)
1. Barbiturates 2. Cholestyramine 3. Rifampin 1. Diuretics 2. Vit K
30
Heparin MOA
Binds to +charged region of AT3 (increases rate that it interacts with plasma protease factors) \* can dissociate and then interact with more AT3
31
Antithrombin inactivates which factors
Thrombin, 5a, 7a, 9a
32
Time to effect of heparin
immediate anticoagulation effect disappears within hours of stopping therapy (*cleared rapidly from blood, t1/2 is 30-180min*)
33
Dosing of heparin
adjust according to coagulation studies aPTT therapeutic range = 1.5-2x normal
34
Iatrogenic hemorrhage can be caused by
warfarin heparin
35
Heparin induced hemorrage treatment
protamine sulfate | (binds to heparin to neutralize)
36
Heparin-induced thrombocytopenia is due chiefly to \_\_\_\_
direct action on platelets Develops 7-12 days after starting therapy *\*\*AB's develop against platelet-heparin complex*
37
Heparin risks in treatment
HIT Osteoporosis (with extended therapy)
38
Heparin - Straight chain sulfated mucopolysaccharides produced by \_\_\_\_
mast cells and basophils
39
\_\_\_\_\_\_\_ are required for heparin binding to AT3
Sulfate groups (N or O sulfation)
40
1. LMWH obtianed from? 2. Vs. standard heparin? 3. MOA?
1. **depolymerization of unfractionated porcine heparin** 2. **(Vs Regular heparin)** 1. Equal efficacy, 2. increased BA from subQ site of administration, 3. NO MONITORING needed 4. More predictable PK profile 5. Lower risk for HIT and osteoporosis 6. Longer Half life 3. **Preferentially binds to factor 10a, only SLIGHTLY affects thrombin activity**
41
Fondaparinux Sodium MOA
**Synthetic sulfated pentasaccharide that inhibits Factor 10a** Indirectly inhibits 10a by binding to AT no monitoring required
42
Use for Fondaparinux advantage? disadvantage?
VTE and Hip/knee surgical prophylaxis Advantage = Low thrombocytopenia risk \*\*Activation NOT reversed by protamine sulfate!
43
Drugs for prevention of thrombosis in NV Afib
**Rivaroxaban, Apixaban** Both = dose reduction in patients with IMPAIRED renal function Increased risk of stroke after stopping
44
Edoxaban function, use, and risks
**orally available 10a inhibitor** **Tx of VTE and PE** after 5-10 days of IV anticoagulant, prevent thrombosis in NV Afib Risk = **ischemic events** after stopping, and **spinal hematoma** in LP or epidural *\*\*Dont use in patients with GOOD renal function (CrCL \>95)*
45
Non-heparinoid parenteral agents dont act through example?
AT3 (inhibit FREE thrombin and fibrin-bound thrombin) Desirudin
46
1. Desirudin MOA 2. no effect on... 3. Excretion? 4. May cause?
1. specific IRREVERSIBLE inhibitor of thrombin (bivalent binding at active site and exosite I) 2. \*\*no effect on AT, aPTT increases dose-dependent 3. Excreted renally 4. May cause HS rxns
47
Bivalirudin MPA
Binds to catalytic site and exosite I of thrombin Binding is REVERSIBLE (rapid onset and short duration) Given IV during PCI procedure does NOT induce antibody formation
48
Bivalirudin vs desirudin
B = reversible, no AB's D = irrev. HS rxn
49
Argatroban MOA? * Inhibits which thrombins? * Monitoring needed? * Metabolism?
_binds reversibly to active site of thrombin_ (doesnt interact with AT) * Can inhibit **free** and **clot-associated thrombin** * **aPTT** monitoring * **3A4** and **3A5** metabolism
50
Argatroban is derived from ____ and approved for... Dabigatran etexilate (prodrug) is an oral direct thrombin inhibitor that is indicated for...
Argatroban = _L-arg_, Prophylaxis and Tx for patients with HIT Dabigatran = indicated for Prevention of stroke/systemic embolus with NV afib

Pharm Exm 4 (7 decks)

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