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I3 Exam 1 > Antithrombotics - Shworak > Flashcards

Antithrombotics - Shworak Flashcards

(69 cards)

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1
Q

What is the treatment for red clots?

A

anticoagulants

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2
Q

What is the treatment for white clots?

A

antiplatelets/anticoagulants

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3
Q

Where do red clots usually occur

A

usually venous, low velocity blood flow

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4
Q

Where do white clots occur

A

usually arterial, high velocity blood flow

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5
Q

What are red clots made of

A

RBC and fibrin

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6
Q

What are white clots made of

A

platelets and fibrin

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7
Q

When do you see red clots

A

stasis (blood pooling/low flow):

  • atrial fibrillation
  • hip/knee
  • travel

foreign objects:

  • extracorporeal devices
  • vascular access devices
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8
Q

When do you see white clots?

A

atherosclerosis - plaques forming on large arteries

  • acute coronary syndrome
  • cerebral vascular disease
  • peripheral vascular disease
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9
Q

PCI

A

when patient has a heart attack and you insert a catheter up the femoral artery to keep the coronary artery open
- anti platelet agents used

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10
Q

What is the physiological mechanism of anticoagulants and antiplatelets

A

inhibit/prevent clot growth

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11
Q

What is the adverse reaction for anticoagulants and antiplatelets

A

bleeding

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12
Q

What are contraindications for anticoagulants and antiplatelets

A

bleeding, impending surgery, hypersensitivity

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13
Q

What are drug interactions with anticoagulants and antiplatelets

A

herbals (garlic, fish oil, ginseng, ginko)

- numerous drug interactions

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14
Q

What is the black box warning for anticoagulants and antiplatelets

A

spinal anesthesia/puncture –> hematoma —> paralysis, monitor neuro status

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15
Q

What is the key target for anticoagulation

A

the common pathway to inhibit fibrin formation = reduce activity Xa, IIa

  • prevent further growth of the clot
  • clot is still there and you need your own fibrinolytic mechanism to resolve the clot
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16
Q

what is heparin

A

a natural polysaccharide with lots of sulfates

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17
Q

Heparin’s sulfates have a pka of 1.5, which properties should heparin have?

A
  1. 5 = very acidic
    - acids are ionized in base, unionized in acid
    - blood plasma is very basic relative to heparin
    - will be highly ionized
    - won’t be orally absorbed, won’t cross placental barrier, extremely low volume of distribution
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18
Q

What is unfractionated heparin

A

mixture of long chains

- some chains have a pentasaccharide with sulfates in a specific structure

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19
Q

What are LMW heparin

A

mixture of short chains, generated from unfractionated heparin that has its chains chewed up
- some chains have pentasaccharide and some don’t

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20
Q

What is fondaparinux

A
  • only the pentasaccharide
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21
Q

How does unfractionated heparin work?

A
  • catalyst that catalyzes anti thrombin
  • anti thrombin is the most potent anti coagulant molecule in the plasma
  • heparin enhances the ability of anti thrombin to neutralize coagulation proteases
  • 1000 fold faster
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22
Q

Xa and IIa mechanisms with AT

A

antithrombin binds to the pentassacharide

  • you get an activation by speeding up the interaction between anti thrombin and Xa
  • anti thrombin is a suicide protease inhibitor
  • factor IIa needs long chains
  • antithrombin binds to one portion of the chain and IIa will bind to another portion and they will diffuse along the chain until they run into eachother
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23
Q

What is Xa neutralization dependent on?

A

pentasaccharide dependent

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24
Q

What is IIa neutralization dependent on?

A

long chain dependent

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25
What is heparin dosing determined by?
monitoring aPTT to maintain 2x normal
26
What is LMW heprain and fondaparinux dosing determined by
by weight, no routine monitoring
27
Does heparin cross the placental barrier?
no! can be used in pregnancy unless it has preservative in it
28
What is a heparin antagonis
protamine sulfate - chain length dependent: works best with long chain - partially effective against LMW - can't use it to neutralize fondaparinux (not big enough)
29
A 65 yo woman is having hip replacement surgery. She has impaired renal function. What should you give for DVT prophylaxis after surgery?
DVT = red clot | - anticoagulant
30
What is the major adverse reaction for LMW heparin?
bleeding
31
Which drug doesn't cause heparin induced thrombocytopenia
Fondaparinux, can be used to treat HIT
32
What is the preferred treatment for HIT
fondaparinux or argatoban
33
What is contraindicated in HIT
warfarin, LMW heparin, heparin
34
Where does coagulation occur
on the platelets
35
Gla domains
- chelate Ca2+ - enable attachment to platelet membrane - required to have functional coagulation factors - occur on both pro and anti coagulation factors
36
What does warfarin do?
prevents the formation of Gla residues - won't localize to platelet surface - reduced clotting on platelet plug - inhibits VKORC - less vitamin K - less Gla residues
37
Are warfarin effects delayed or immediate?
warfarin effects are delayed until functional clotting factors turn over
38
Warfarin adverse affects
- bleeding - inhibition of protein C and S occurs rapidly can lead to initial procoagulant state = enhanced clotting early on - contraindicated in HIT
39
Which form of warfarin is the active form
S form, metabolized in the enzyme by Cyp2c9 | - variable half life
40
What is the half life of warfarin
20 h - 60 h
41
A patient on warfarin has a stable INR. he decides a low vitamin K diet isn't good and goes on a kale binge. What will happen?
INR will decrease slowly over day
42
What is the INR
if reducing efficacy of warfarin, clot faster = faster bleeding time = decreased INR
43
What is a direct Xa inhibitor
rivaroxaban
44
What is a direct thrombin inhibitor
dabigaTran | T for two and thrombin
45
What are approved indications for dabigaTran
- AF not due to mechanical heart valve
46
Do rivaroxaban and dabigtran require monitoring?
no, routine monitoring not necessary
47
What are the adverse effects for rivaroxaban and dabigtran
bleeding
48
P-gp and CYP3A4
many drugs bind to P-gp and CYP3A4 - P-gp and CYP3A4 synergize to reduce bioavaibility - inducing/inhibiting Pgp/CYP3C4 can produce large changes in plasma drug levels
49
What selectively inhibits thrombin
dabigaTram
50
What selectively inhibits FXa
rivaroxaban, LMW heparin
51
What is the mechanism of argatroban
blocks the catalytic site of thrombin | - anticoagulation in HIT
52
What is Hirudin
protein anticoagulant - found in leaches - highly specific for thrombin - directly bind to thrombin, suicide inhibitors - create 1:1 inactive complex
53
Antiplatelet agents
in primary hemostasis the platelet bind to subendothelium - upregulate COX1 - upregulate TXA2 - granules contain ADP - ADP binds to other platelets that leads to more activation signals - induce conformational change in the IIb/IIIa receptor
54
What targets COX 1?
aspirin | - irreversible inhibition
55
What blocks ADP receptors
clopidogrel and prasugrel = less IIb/IIIa = less platelet aggregation
56
What blocks IIb/IIIa receptors
abcimixab, tirofiban, eptifibatide | * HAVE a,b in their name
57
What activates clopidogrel
- CYP2C9 activates **genetic variability - reactive thiol that forms irreversible disulfide bond - irreversible agent
58
After PCI, patients are placed on chlopidogrel for several months to prevent stent thrombosis. What is the most likely consequences if standard dose is given to a patient with genetically low CYP2C9 activity?
- worried about stent thrombosis | - if you have stent thrombosis, you will block blood flow to the heart and have a heart attack
59
What activates clopidogrel
prodrug activated by CYP2C9
60
What activates prasugrel
prodrug with more predictable clinical effects
61
What are adverse reactions for clopidogrel and prasugrel
premature discontinuation events
62
When is prasugrel contra indiciated
previous history of stroke/TIA - if you don't know wether the events are due to an occlusion, don't give prasugrel because you're at risk of an additional stroke
63
Alteplase
tissue plasminogen activator (tPA) - binds to fibrin = clot specificity = fibrin degradation - works best on fresh clots - can cause a system lytic state
64
What does tPA do
- tPA binds to fibrin and takes a nibble out of fibrinogen and releases plasmin which is a protease that will degrade the fibrin strands into fibrin degradation products
65
Where is tPA synthesized
- tPA is produced by vascular endothelium
66
Which drug is a plasminogen activator
alteplase - clot buster - patient has heart attack and can't get to cath lab in 14 hours - or if stroke inject within the 4.5 hour window
67
warfarin
- inhibits VCORK to inhibit vitamin k reduction | - lots of variability
68
What are argatroban, desirudin, bivalrudin
IIa inhibitors
69
Which drugs block GP-11b/IIIa activity
aspirin, clopidogrel (genetic variation in the activation), prasugrel (no genetic variation, but stronger drug)

I3 Exam 1 (12 decks)

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