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PMCOL 344 > Anti-Coagulants > Flashcards

Anti-Coagulants Flashcards

1
Q

what is clotting

A

coagulation, blood converting into solid gel called clot or thrombus

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2
Q

where/why does coagulation occur

A

around platelets to reinforce plug

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3
Q

what is the reason for blood coagulation

A

secondary hemostasis, vital hemostatic defense mechanism

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4
Q

are defects in coagulation or defects in platelets worse

A

defects in coagulation are worse

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5
Q

what are 5 classes/types/examples of anticoagulants

A 
warfarin
Heparins
rivaroxaban (and apixiban and edoxaban)
dabigatran etexilate
hirudins
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6
Q

what are 2 heparins

A

unfractionated heparin and low molecular weight heparin

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7
Q

what are 3 circulatory stasis needs for anticoagulation

A

atrial fibrillation(blood pool in atrium), immobilization, deep vein thrombosis

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8
Q

what is immobilization/ why do we need anticoagulations for that

A

Knee or hip replacement are immobilized for awhile, used anticoagulants to prevent clot

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9
Q

what are 3 hypercoagulable states needs for anticoagulation

A

malignancy, deficiencies in anti-clotting factors, pregnancy

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10
Q

what are 2 main states that make you need anticoagulation

A

circulatory stasis and hypercoagulable states

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11
Q

why do we need anticoagulations for atrial fibrillation

A

blood pool in atrium

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12
Q

which factor turns prothrombin into thrombin

A

factor 10a

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13
Q

which pathway step is where extrinsic and intrinsic meet

A

10

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14
Q

what is coagulation mechanically

A

a proteolytic cascade involving serine proteases

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15
Q

what is the role of calcium with platelets

A

site of injury, serine becomes exposed so it has a negative charge on the outside of platelet, and ca binds and is a bridge between -ve coagulation factors

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16
Q

what happens with phosphatidyl serine when the platelets are activated

A

they flip to the opposite to give the platelet a negative charge

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17
Q

how do you take warfarin

A

orally

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18
Q

what is the mechanism of action of warfarin

A

vitamin K reductase antagonist

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19
Q

what does warfarin interfere with

A

carboxylation of glutamid acit residues in clotting factors 2,7,9,10

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20
Q

what does warfarin lead to

A

accumulation of inactive clotting factors that cannot bind to negatively charged surfaces via Ca++

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21
Q

what is a main problem with warfarin in females

A

it is a teratogen

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22
Q

what is a teratogen

A

any agent that causes an abnormality following fetal exposure during pregnancy

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23
Q

when does peak warfarin concentration and effect occur

A

blood conc: 1hr

peak pharmacological effect: 48h

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24
Q

why may you be put on warfarin and heparin at the same time

A

for a few days because warfarin takes a few days to work

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25
Q

why does warfarin take a few days to work

A

because some coagulation factors may already be carboxylated with a negative charge, so warfarin cannot effect them

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26
Q

how do you monitor warfarin

A

using international normalized ratio (INR)

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27
Q

does warfarin have drug interactions

A

yes, even with foods

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28
Q

is there a large margin of safety for warfarin

A

no

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29
Q

what are 3 main unwanted effects from warfarin

A

bleeding liver damage necrosis of soft tissue

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30
Q

how are heparins administered

A

IV or SubQ

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31
Q

what is the structure of heparins

A

negatively sulfated glycosaminoglycan, very long sugars with unique pentasaccharide sequence (for its mechanism)

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32
Q

what part of heparins structure is important for its mechanism

A

pentasaccharide sequence

33
Q

what is the mechanism of heparin

A

binds antithrombin III (ATIII), induces confomational change, increase affinity for serine protease active site of coagulation cascade

34
Q

what is ATIII + what does it do

A

antithrombin III, endogenous anticoagulant via pentasaccharide sequence

35
Q

where does heparin make a conformation change

A

in antithrombin III

36
Q

what happens when heparin makes a conformation change in antithrombin III

A

increases its affinity for active site of serine proteases of coagulation cascade

37
Q

what is unfractionated heparin good for

A

inhibiting thrombin IIa

38
Q

what is low molecular weight heparin good for

A

inhibiting Xa

39
Q

how long does heparin take to kick in

A

quick

40
Q

antiplatelets vs anticoagulants

A

Anticoagulants slow down clotting, thereby reducing fibrin formation and preventing clots from forming and growing. Antiplatelet agents prevent platelets from clumping and also prevent clots from forming and growing.

41
Q

which heparin version is better and why

A

low molecular weight, more favorable pharmacokinetics: longer elimination half life, less frequent dosing, more predictable anticoagulation effects

42
Q

what are 3 unwanted effects of heparin

A

bleeding, heparin induced thrombocytopenia/thrombosis, osteoporosis

43
Q

what is thrombocytopenia

A

reduced platelet count

44
Q

how can heparin cause thrombocytopenia

A

some people get antibodies to an antigen on the platelet surface

45
Q

how do you take rivaroxaban + how often

A

orally active, once a day

46
Q

what is the mechanism of rivaroxaban

A

reversible, direct competitive inhibitor of Xa

47
Q

what is Factor xa role

A

enzyme in second to last step in cascade, convers prothrombin to thrombin

48
Q

why is rivaroxaban work well

A

10000 fold selectivity for Factor Xa than other serine proteases of coagulation pathway

49
Q

what are 2 unwanted effects of rivaroxaban

A

bleeding and people with renal failure (60% drug is excreted by kidneys, so with kidney issues they accumulate in blood)

50
Q

what are 2 drugs similar to rivaroxaban

A

apixiban and edoxaban

51
Q

how do you take dabigatran etexilate + how often

A

orally active, once/ twice a day

52
Q

what happens when you take dabigatran etexilate into your body

A

it is rapidly converted by plasma esterases to dabigatran

53
Q

what is the mechanism of action of dabigatran

A

reversible, direct competitive inhibitor of thrombin

54
Q

what are 2 unwanted effects of dabigatran

A

bleeding and people with renal failure (80% drug is excreted by kidneys, so with kidney issues they accumulate in blood)

55
Q

where was warfarin derived from

A

sweet clover

56
Q

where was heparin derived from

A

liver (extracted from)

57
Q

where was hirduin derived from

A

leech

58
Q

what is hirduin (simple)

A

anticoagulant from medicinal leech

59
Q

what is the mechanism of hirduin

A

specific inhibitor of thrombin

60
Q

what is the structure of hirduins

A

65 amino acid (7 kDa protein)

61
Q

what are 2 other types of hirduin and what is their deal

A

lepirudin (recombinant) and bivalirudin (20aa synthetic)

62
Q

what is the deal with hirduin and ATIII

A

hirduin doesnt need it

63
Q

what does hirduin not need to work

A

ATIII is not needed

64
Q

is hirduin reversible

A

slowly

65
Q

what is the deal with lepirudin

A

its a recombinant hirduin

66
Q

what is the deal with bivalirudin

A

20 amino acid hirduin-based synthetic peptide

67
Q

what is another name for thrombolytic drugs

A

fibrinolytic drugs

68
Q

what is another name for fibrinolytic drugs

A

thrombolytic drugs

69
Q

what do thrombolytic/fibrinolytic drugs do

A

break down clots that have already formed

70
Q

what is r-tPA stand for

A

recombinant tissue-plasminogen activator

71
Q

what does tPA do

A

turns plasminogen into plasmin

72
Q

how is r-tPA administered

A

IV

73
Q

what are 3 examples of r-tPAs

A

alteplase, duteplase, reteplase

74
Q

what does plasmin do

A

breaks down fibrin resulting in clot lysis

75
Q

what is streptokinase

A

non-enzymatic protein (47kDa) from hemolytic streptococci

76
Q

what is the mechanism of action of streptokinase

A

forms stable complex with plasminogen, inducing conformational change to gain enzymatic activity so there is more plasmin made

77
Q

what can inactivate streptokinase

A

anti-streptokinase antibodies

78
Q

what drug do you give a patient with ATIII deficiency and why

A

rivaroxaban because its a direct Xa inhibitor (lower in pathway, it converts prothrombin to thrombin)

PMCOL 344 (27 decks)

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