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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
why does warfarin take a few days to work
because some coagulation factors may already be carboxylated with a negative charge, so warfarin cannot effect them
26
how do you monitor warfarin
using international normalized ratio (INR)
27
does warfarin have drug interactions
yes, even with foods
28
is there a large margin of safety for warfarin
no
29
what are 3 main unwanted effects from warfarin
bleeding liver damage necrosis of soft tissue
30
how are heparins administered
IV or SubQ
31
what is the structure of heparins
negatively sulfated glycosaminoglycan, very long sugars with unique pentasaccharide sequence (for its mechanism)
32
what part of heparins structure is important for its mechanism
pentasaccharide sequence
33
what is the mechanism of heparin
binds antithrombin III (ATIII), induces confomational change, increase affinity for serine protease active site of coagulation cascade
34
what is ATIII + what does it do
antithrombin III, endogenous anticoagulant via pentasaccharide sequence
35
where does heparin make a conformation change
in antithrombin III
36
what happens when heparin makes a conformation change in antithrombin III
increases its affinity for active site of serine proteases of coagulation cascade
37
what is unfractionated heparin good for
inhibiting thrombin IIa
38
what is low molecular weight heparin good for
inhibiting Xa
39
how long does heparin take to kick in
quick
40
antiplatelets vs anticoagulants
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
which heparin version is better and why
low molecular weight, more favorable pharmacokinetics: longer elimination half life, less frequent dosing, more predictable anticoagulation effects
42
what are 3 unwanted effects of heparin
bleeding, heparin induced thrombocytopenia/thrombosis, osteoporosis
43
what is thrombocytopenia
reduced platelet count
44
how can heparin cause thrombocytopenia
some people get antibodies to an antigen on the platelet surface
45
how do you take rivaroxaban + how often
orally active, once a day
46
what is the mechanism of rivaroxaban
reversible, direct competitive inhibitor of Xa
47
what is Factor xa role
enzyme in second to last step in cascade, convers prothrombin to thrombin
48
why is rivaroxaban work well
10000 fold selectivity for Factor Xa than other serine proteases of coagulation pathway
49
what are 2 unwanted effects of rivaroxaban
bleeding and people with renal failure (60% drug is excreted by kidneys, so with kidney issues they accumulate in blood)
50
what are 2 drugs similar to rivaroxaban
apixiban and edoxaban
51
how do you take dabigatran etexilate + how often
orally active, once/ twice a day
52
what happens when you take dabigatran etexilate into your body
it is rapidly converted by plasma esterases to dabigatran
53
what is the mechanism of action of dabigatran
reversible, direct competitive inhibitor of thrombin
54
what are 2 unwanted effects of dabigatran
bleeding and people with renal failure (80% drug is excreted by kidneys, so with kidney issues they accumulate in blood)
55
where was warfarin derived from
sweet clover
56
where was heparin derived from
liver (extracted from)
57
where was hirduin derived from
leech
58
what is hirduin (simple)
anticoagulant from medicinal leech
59
what is the mechanism of hirduin
specific inhibitor of thrombin
60
what is the structure of hirduins
65 amino acid (7 kDa protein)
61
what are 2 other types of hirduin and what is their deal
lepirudin (recombinant) and bivalirudin (20aa synthetic)
62
what is the deal with hirduin and ATIII
hirduin doesnt need it
63
what does hirduin not need to work
ATIII is not needed
64
is hirduin reversible
slowly
65
what is the deal with lepirudin
its a recombinant hirduin
66
what is the deal with bivalirudin
20 amino acid hirduin-based synthetic peptide
67
what is another name for thrombolytic drugs
fibrinolytic drugs
68
what is another name for fibrinolytic drugs
thrombolytic drugs
69
what do thrombolytic/fibrinolytic drugs do
break down clots that have already formed
70
what is r-tPA stand for
recombinant tissue-plasminogen activator
71
what does tPA do
turns plasminogen into plasmin
72
how is r-tPA administered
IV
73
what are 3 examples of r-tPAs
alteplase, duteplase, reteplase
74
what does plasmin do
breaks down fibrin resulting in clot lysis
75
what is streptokinase
non-enzymatic protein (47kDa) from hemolytic streptococci
76
what is the mechanism of action of streptokinase
forms stable complex with plasminogen, inducing conformational change to gain enzymatic activity so there is more plasmin made
77
what can inactivate streptokinase
anti-streptokinase antibodies
78
what drug do you give a patient with ATIII deficiency and why
rivaroxaban because its a direct Xa inhibitor (lower in pathway, it converts prothrombin to thrombin)

PMCOL 344 (27 decks)

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