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Exam 4 Antiplatelets PHRM 844 > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

what is the extrinsic pathway?

A

1.requires a factor (TF) extrinsic to the blood
- important when vessel is damaged and blood leaks out
- rapid to start clot formation

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2
Q

what is the intrinsic pathway?

A

triggered when collagen is exposed on the wall of the blood vessel
- blood in test tube clots by this mechanism

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3
Q

how is the extrinsic pathway activated in the cascade?

A
  1. TF on cell surface by blood vessels
  2. factor 7 resides in blood
  3. TF binds to factor 7 and activates it
  4. factor 7a binds and cleaves to factor 10.
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4
Q

what is the activation of the intrinsic pathway?

A
  1. factor 9 converts to 9a and binds to factor 8a on the surface of platelets and activates factor 10.
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5
Q

what happens after both pathways converge when bound to factor 10?

A
  1. factor 10 converts to 10a
  2. cleaves to prothrombin that activates thrombin
  3. that activates fibrinogen to fibrin
  4. forms the clot with factor 13 cross-linking to make it stable
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6
Q

what feedback mechanisms increase coagulation?

A
  1. thrombin
  2. platelet activation
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7
Q

what feedback mechanisms decrease coagulation?

A
  1. antithrombin
    – reaction accelerated by heparin
  2. protein c system
    – activated by thrombin binding to thrombomodulin
  3. factor 10 a
    – activates tissue factor pathway inhibitor (TFPI)
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8
Q

what are common tests for hemostatic function? why?

A

All ordered for panel
1. platelet count
2. prothrombin time (PT/INR)
– how long it takes to clot (plasma, thromboplastin and Ca)
3. aPTT
– monitor heparin therapy
4. fibrinogen
– range 200-400
5. D-dimer
- range <500

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9
Q

what test is an intrinsic pathway?

A

aPTT

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10
Q

what test is a extrinsic pathway?

A

PT

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11
Q

what structure is this?

A

warfarin

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12
Q

what is the role of Ca2+ in coag and in blood samples?

A
  1. Links certain factors to phospholipid membranes
  2. Helps to prevent clots by removing calcium ions needed for the coagulation cascade to proceed
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13
Q

what is warfarin or derived from?

A
  1. found in spoiled clover that caused hemorrhage in cow
  2. water soluble and racemic mix
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14
Q

what is the MOA of warfarin?

A

vitamin k antagonist
- inhibit CKORC1 and block reduction of Vit K epoxide back to its active form

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15
Q

what factors does warfarin affect?

A

2, 7, 9, 10 & proteins s & c

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16
Q

what is the onset of action and d/c therapy for warfarin?

A

Onset:
– deplete pool of circulating factors
– 3-5 day onset
D/C:
– takes several days to return to normal PT (re-synthesized)

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17
Q

what is the metabolism of warfarin?

A

CYP2C9 (s-warfarin)

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18
Q

what is the termination of action of warfarin?

A

not correlated with plasma warfarin levels but reestablish normal clotting factors

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19
Q

what do you do in a warfarin overdose?

A
  1. latrogenic hemorrhage
    – d/c warfarin
    – admin K1
    – in serious
    – plasma replace clotting factors faster than vit K therapy
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20
Q

what happens in warfarin necrosis?

A
  1. deficient of protein C
    – warfarin decrease protein C faster than coag factors ; can increase coagulation of blood
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21
Q

what are some adverse effects of warfarin?

A
  1. hemorrhage
  2. drug interactions
  3. no to pregnancy as can cross placenta and cause hemorrhage
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22
Q

what are some drug interactions with warfarin?

A
  1. Vit K (bypass VCOR1 inhibition)
  2. antibiotics (reduce vit K in GI tract)
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23
Q

what are the reversal agents for warfarin?

A
  1. reversed immediately? exogenous Vit K (kcentra) admin IV
  2. oral vit K
    –> overdose in absence of acute major bleeding
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24
Q

what class of drugs inhibit factor 2a/10a?

A
  1. UFH
  2. LMWH
  3. non-heparinoids (fondaparinox)
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25
Q

what is this structure?

A

heparin

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26
Q

what is active in heparin in its structure?

A

pentasaccharides

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27
Q

what is the mechanism of heparin?

A
  1. binds to AT and changes conformation to form complex
  2. bound to AT inc. interaction with target factors
  3. accelerates AT rxns to inactivate thrombin and factor 10A
  4. LMWH bind to 10a more since too small to bind to thrombin
28
Q

how do you give heparin?

29
Q

how can you adjust heparin doses?

A

based on aPTT
- cleared rapid from blood

30
Q

when does the heparin disappear after d/c?

A

within hours

31
Q

how do you reverse heparin effects?

A

protamine sulfate
–> binds tightly to neutralize anticoag action
–> LMW polycationic protein

32
Q

what are major adverse reactions with heparin?

A
  1. HIT/HAT
  2. osteoporosis
33
Q

what are the types of HIT?

A

type 1: mild
type 2: 7-12 days after therapy to form complex

34
Q

what i the chemistry of heparin?

A
  1. produced by mast cells and basophils
  2. extracted from porcine small intestine or bovine lung
  3. sulfate groups (- charge) required for binding to antithrombin
35
Q

what is an indirect factor 10a inhibitor?

A

fondaparinux

35
Q

what are the advantages of LMWH?

A
  1. more predictable PK profile
  2. lower incidence in thrombocytopenia and osteoporosis
35
Q

what is the use for fondaparinux?

A
  1. VTE
  2. prophylaxis in patients
35
Q

what drugs are LMWH? what are their daltons?

A

enoxaparin –> 2000-8000
dalteparin –> 2000-9000

36
Q

what is fondaparinux?

A

synthetic sulfated pentasaccharide

37
Q

would protamine sulfate work on fondaparinux?

A

no, not reversed due to low potential for thrombocytopenia

38
Q

what structure is this?

A

findaparinux

39
Q

what are DOACs?

A
  1. apixaban
  2. edoxaban
  3. rivaroxaban
  4. betrixaban
40
Q

what are rivaroxaban and edoxaban used for?

A

tx/prevention of VT/PE
2. prevent thrombosis in NV afib

41
Q

what is edoxaban used for?

A
  1. tx of VTE/PE
  2. NV afib
42
Q

how long do you have to wait to use edoxaban for VTE/PE treatment?

A

5-10 days with parenteral

43
Q

when can you not use edoxaban?

A

when Crcl is >95

44
Q

what is betrixaban used for?

A

prevention of VTE in hospitalized patients at risk for VTE

45
Q

what structure is this?

A

rivaroxaban

46
Q

what structure is this?

47
Q

what structure is this?

48
Q

what structure is this?

A

betrixaban

49
Q

what i the antidote for DOACs

50
Q

what drugs is andexanet approved for use for?

A

apixaban and rivaroxaban

51
Q

what is the mechanism for DTIs (direct thrombin inhibitors)?

A
  1. DTI can bind to active site of thrombin, to exosite of thrombin or both
  2. can inhibit both soluble and fibrin bound thrombin
  3. can also reduce platelet aggregation
51
Q

what is a BBW for andexanet?

A

increased risk of thromboembolic events

52
Q

what are some DTIs?

A

Hirudin
lepirudin
bivalirudin

53
Q

what is hirudin?

54
Q

what is lepirudin? what is it used for?

A
  • given IV
  • reversible inhibition
  • tx for HIT
  • recomb form of hirudin grown in yeast
55
Q

what is there to know about bivalirudin and its structure?

A

4 aa are catalytic site binding
arg is cleaved by thrombin
last bit of structure binds to exosite 1 (asn-leu)

56
Q

what structure is this?

A

bivalirudin

57
Q

what is argatroban?

A

DIT
- derived from L-arginine
- reversible binding to thrombin
- monitor using aPTT
- used for HIT or prophylaxis in PCI procedures

58
Q

what is dabigatran? what is its use?

A
  • oral DTI
  • indicated for prevention of stroke and systemic embolism in patients with non-valv afib
59
Q

what is this stricture?

A

dabigatran

60
Q

what is the reversal agent for dabigatran?

A

idarucizumab

61
Q

what is idarucizumab? (praxbind)

A
  • humanized IgG1 FAB fragment against dabigatran
  • only binds to dabigatran

Exam 4 Antiplatelets PHRM 844 (3 decks)

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