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Pharm Exm 4 > Anticoagulants > Flashcards

Anticoagulants Flashcards

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

A

Anisindione

Orally active with significant AE’s

22
Q

Warfarin MOA

A

Inhibiton of vitamin K epoxide reductase

23
Q

Vitamin K actions

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

A

depletion of the pool of factors in circulation

(maximal anticoagulation takes 3-5 days to achieve)

25
Q

Dosage of warfarin

A

Loading dose = 5mg/day

Maintenance dose = 2.5-5 mg/day

26
Q

Warfarin metabolism

A

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
Q

Treatment for warfarin overdose

A

STOP WARFARIN

administer Vit K1 (high levels can activate the reductase)

**plasma if severe hemorrhage to replace clotting factors

28
Q

Warfarin CI’d in…

A

pregnancy

(in those who are or may become)

passes through placenta – fetal hemorrhage and FWS (nasal hypoplasia

29
Q

Drugs with Decreased PT

(DDI’s with warfarin)

A
  1. Barbiturates
  2. Cholestyramine
  3. Rifampin
  4. Diuretics
  5. Vit K
30
Q

Heparin MOA

A

Binds to +charged region of AT3

(increases rate that it interacts with plasma protease factors)

* can dissociate and then interact with more AT3

31
Q

Antithrombin inactivates which factors

A

Thrombin, 5a, 7a, 9a

32
Q

Time to effect of heparin

A

immediate

anticoagulation effect disappears within hours of stopping therapy (cleared rapidly from blood, t1/2 is 30-180min)

33
Q

Dosing of heparin

A

adjust according to coagulation studies

aPTT therapeutic range = 1.5-2x normal

34
Q

Iatrogenic hemorrhage can be caused by

A

warfarin

heparin

35
Q

Heparin induced hemorrage treatment

A

protamine sulfate

(binds to heparin to neutralize)

36
Q

Heparin-induced thrombocytopenia is due chiefly to ____

A

direct action on platelets

Develops 7-12 days after starting therapy

**AB’s develop against platelet-heparin complex

37
Q

Heparin risks in treatment

A

HIT

Osteoporosis (with extended therapy)

38
Q

Heparin - Straight chain sulfated mucopolysaccharides produced by ____

A

mast cells and basophils

39
Q

_______ are required for heparin binding to AT3

A

Sulfate groups

(N or O sulfation)

40
Q
  1. LMWH obtianed from?
  2. Vs. standard heparin?
  3. MOA?
A
  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
Q

Fondaparinux Sodium MOA

A

Synthetic sulfated pentasaccharide that inhibits Factor 10a

Indirectly inhibits 10a by binding to AT

no monitoring required

42
Q

Use for Fondaparinux

advantage?

disadvantage?

A

VTE and Hip/knee surgical prophylaxis

Advantage = Low thrombocytopenia risk

**Activation NOT reversed by protamine sulfate!

43
Q

Drugs for prevention of thrombosis in NV Afib

A

Rivaroxaban, Apixaban

Both = dose reduction in patients with IMPAIRED renal function

Increased risk of stroke after stopping

44
Q

Edoxaban function, use, and risks

A

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
Q

Non-heparinoid parenteral agents dont act through

example?

A

AT3

(inhibit FREE thrombin and fibrin-bound thrombin)

Desirudin

46
Q
  1. Desirudin MOA
  2. no effect on…
  3. Excretion?
  4. May cause?
A
  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
Q

Bivalirudin MPA

A

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
Q

Bivalirudin vs desirudin

A

B = reversible, no AB’s

D = irrev. HS rxn

49
Q

Argatroban MOA?

  • Inhibits which thrombins?
  • Monitoring needed?
  • Metabolism?
A

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
Q

Argatroban is derived from ____ and approved for…

Dabigatran etexilate (prodrug) is an oral direct thrombin inhibitor that is indicated for…

A

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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