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Pharm Test 2 > Antithrombolytics > Flashcards

Antithrombolytics Flashcards

1
Q

Anticoag Rxs

A
  • Heparin/enoxaparin/fondaparinux
  • Warfarin
  • RivaroXaban, apiXaban
  • DabigaTran/Argatroban/Desirudin/Bivalrudin
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2
Q

Antiplatelet Rx

A
  • Aspirin, clopidogrel, prasugrel

* Abciximab / tirofiban / eptifibatide

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3
Q

Thombolytic

A

Alteplase

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4
Q

DOWN Clot formation Rxs

PROPHYLAXIS

A

Anticoagulants

Antiplatelets

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5
Q

UP Clot dissolution Rxs

A

Thrombolytic

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6
Q

Antithrombin catalysts

A

Heparin
Enoxaparin
Fondaparinux

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7
Q

Block clotting factor synthesis

A

Warfarin

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8
Q

Direct Xa inhibitors

A

RivaroXaban

ApiXaban

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9
Q

Direct thromibn (IIa) inhibitors

A

DabigaTran
Argatroban
Desirudin
Bivalrudin

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10
Q

Block platelet activation (G2b/3a activation)

A

Aspirin
Clopidogrel
Prasurel

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11
Q

Block glycoprotein 2b/3a function

A

Abciximab
tirofiban
Eptifibatide

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12
Q

Plasminogen activator

A

Alteplase

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13
Q

Red clot Tx

A

Anticoags

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14
Q

White clot Tx

A

Anticoags + antiplatelets

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15
Q

Just anticoag needed - Red clots

Hypercoaguable states

A
  • stasis
  • Afib
  • immobility (DVT/PE)
  • Foreign objects
  • extracorporeal devices
  • vascular access devices (heparin lock/central venous line)
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16
Q

White clots from

A 
*Atherosclerosis
ACS -->UA, MI
CVD -->TIA, CVA
PVD
*Foreign objects (PCI, heart valve)
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17
Q

Treat ischemic CVA w/

A

Anticoag

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18
Q

Treat Hemorrhagic CVA w/

A

NO anticoag

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19
Q

Anticoags/antiplatelets

Physiology

A

Inhibit prevent clot growth

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20
Q

Anticoag/antiplatelet

Rx interaction

A

Many

Herbals

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21
Q

Anticoags/Antiplatelets

Contraindications

A
  • Bleeding
  • Impending surgery (ex. Spinal anesthesia/puncture–>hematoma–>paralysis)
  • Hypersensitivity
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22
Q

Anticoags

Indirectly affect clotting factors UNFINISHED

A

Antithrombin catalys

-Heparin

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23
Q

What starts extrinsic pathway?

A

Tissue factor

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24
Q

What starts intrinsic pathway?

A

Intravascular trigger

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25
Q

What starts common pathway?

A

Factor 10

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26
Q

Which factor is prothrombin/thrombin?

A

II/IIa

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27
Q

Goal of anticoagulation?

A

Diminish activity of Factors 10a +/- 2a (common pathway)

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28
Q

What type of enzymes are clotting factors?

A

Zymogens (proenzymes)

29
Q

Heparin

Bio characteristics

A
  • polysaccharide
  • glycosaminoglycan
  • VERY suflated, VERY acidic
30
Q

Unfractionated heparin

Chains?

A

Mixture of long chains

Some have pentasaccharide/some don’t

31
Q

LMW Heparin

A

Mixture of short chains

Some have pentasaccharide/some don’t

32
Q

Fondaparinux

A

Pure pentasaccharide

33
Q

Antithrombin (AT)

A

Most potent anticoag in body

Looks like xymogem - 10A attaches, irreversible, suicide anti-coag

34
Q

Heparins catalyze what?

A

Antithrombin (AT)

x1000

35
Q

Heparin pentasaccharide mechanism for 10a + 2a?

A

10a - pentasaccharide increases at affinity for this

2a - long chain bridges this and AT, easier to bump into each other

36
Q

Heparin antidote

A

Protamine = (+), binds with (-) heparin, inactive complax

NO w/ short heparin chains

37
Q

Heparin-induced Thrombocytopenia (HIT)

A
  • Hypersensitivity
  • Autoimmune (PF4-heparin complex activate platelet)
  • Get clot- gangrene
38
Q

HIT

Tx

A

NO treat with Heparin/LMW, warfarin

*USE fondaparinux/argatoban (off-label)

39
Q

LMW heparin/Fondaparinux

Future indications

A

Soon will include indications of unfractionated heparin

40
Q

Heparin dosing

A

Read label carefully, don’t overdose

41
Q

Heparin in pregnancy/neonate

A

USE W NO preservative (benzyl alcohol) fetal death

42
Q

Heparin bleeding time monitored with

A

aPPT

43
Q

Where does clotting occur?

A

On platelet surfaces

Not in solution

44
Q

Warfarin blocks

A

Gla formation

Factor can’t attach to membrane

45
Q

Vitamin K

A

Reduces Gla, then recycled by VKORC (nadh)

46
Q

Warfarin blocks

A

VKORC regeneration of Vitamin K,

Not enough Gla for factors (10a) to stick to surface

47
Q

INR 1

A

Normal clotting activity

48
Q

Warfarin effects delayed - why?

A

Waiting for clotting factors to be used up (10a/2a take forever), and to build up useless clotting factors

49
Q

Initiating warfarin

A

Heparin-bridge while waiting warfarin to get to steady state (slow onset)

50
Q

Warfarin

S.E.

A
  • Bleeding
  • Clotting ?!? = stopping Protein C + S early (BRIDGE!)
  • DEAD BABY
  • NO HIT
51
Q

Warfarin

Physiology

A

*S enantiomer - CYP2C9 metab
*t 1/2 = 20-60 h (human variation)
-CYP2C9 (elimination)
-VKORC (efficacy)
MONITOR INR

52
Q

Warfarin

Rx interactions

A

Many

*need low Vitamin K (competitive inhibitor)

53
Q

INR

A 
HIGH = less clotting
LOW = more clotting
54
Q

10a /2a inhibitors

A

NOT WITH Afib + heart valve

55
Q

If inhibit metabolism Rivaroxaban?

A

Up efficacy

56
Q

Argatroban

MOA

A

Direct 2a (thrombin
inhibitor - blocks catalytic site)
*tx HIT

57
Q

Hirudo medicinalis

A

Saliva - hirudin (anticoag) - surgery(reattaching fingers)

58
Q

Hirudin derivatives

A

Desiruden (t1/2= 2-3 hrs)
Bivalirudin (t/12 = shorter)
*Direct thrombin (2a) inhibitors

59
Q

COX 1 + ADP blocker

A

Synergistic effect

60
Q

Aspirin

A

Irreversible COX inhibitor

- if stop - takes awhile to regenerate platelets (1week)

61
Q

What if clopidogrel given to non metabolizer?

A

No effect, clopidogrel is pre-drug, need metabolism to activate

62
Q

W/ heart valves?

A

Now, only warfarin

63
Q

Thombolytics

A

Atleplase - plasminogen-like (fibrin), works best on fresh clots

64
Q

Thienopyridine Anti-platelet agents (“grels”)

A

PRODRUG = Cyp metab to activate

65
Q

Prasugrel

Thienopyridine Anti-platelet agents (“grels”)

A

More bleeding than clopidogrel

66
Q

Clopidogrel

Thienopyridine Anti-platelet agents (“grels”)

Special metablolism consideration

A

CYP2C19 poor metabolizers = UP risk (MI/Ischemic Stroke/Death)

67
Q

GP 2b/3a blocker Anti-platelet drugs

A

Block GP 2b/3a from binding fibrinogen, vWF+ others

68
Q

Alteplase

GP 2b/3a blocker Anti-platelet drugs

A

Works best on fresh clots (less fibrin linking)

FOR ER CLOT BUSTING = T1/2 = 10 mins (shorter than Streptokinase)

Pharm Test 2 (13 decks)

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