Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

I3 Exam 1 > Antithrombotics - Shworak > Flashcards

Antithrombotics - Shworak Flashcards

1
Q

What is the treatment for red clots?

A

anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the treatment for white clots?

A

antiplatelets/anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do red clots usually occur

A

usually venous, low velocity blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where do white clots occur

A

usually arterial, high velocity blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are red clots made of

A

RBC and fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are white clots made of

A

platelets and fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When do you see white clots?

A

atherosclerosis - plaques forming on large arteries

  • acute coronary syndrome
  • cerebral vascular disease
  • peripheral vascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the physiological mechanism of anticoagulants and antiplatelets

A

inhibit/prevent clot growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the adverse reaction for anticoagulants and antiplatelets

A

bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are contraindications for anticoagulants and antiplatelets

A

bleeding, impending surgery, hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are drug interactions with anticoagulants and antiplatelets

A

herbals (garlic, fish oil, ginseng, ginko)

- numerous drug interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the black box warning for anticoagulants and antiplatelets

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is heparin

A

a natural polysaccharide with lots of sulfates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is unfractionated heparin

A

mixture of long chains

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is fondaparinux

A
  • only the pentasaccharide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Xa neutralization dependent on?

A

pentasaccharide dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is IIa neutralization dependent on?

A

long chain dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is heparin dosing determined by?

A

monitoring aPTT to maintain 2x normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is LMW heprain and fondaparinux dosing determined by

A

by weight, no routine monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Does heparin cross the placental barrier?

A

no! can be used in pregnancy unless it has preservative in it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a heparin antagonis

A

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
Q

A 65 yo woman is having hip replacement surgery. She has impaired renal function. What should you give for DVT prophylaxis after surgery?

A

DVT = red clot

- anticoagulant

30
Q

What is the major adverse reaction for LMW heparin?

A

bleeding

31
Q

Which drug doesn’t cause heparin induced thrombocytopenia

A

Fondaparinux, can be used to treat HIT

32
Q

What is the preferred treatment for HIT

A

fondaparinux or argatoban

33
Q

What is contraindicated in HIT

A

warfarin, LMW heparin, heparin

34
Q

Where does coagulation occur

A

on the platelets

35
Q

Gla domains

A
  • chelate Ca2+
  • enable attachment to platelet membrane
  • required to have functional coagulation factors
  • occur on both pro and anti coagulation factors
36
Q

What does warfarin do?

A

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
Q

Are warfarin effects delayed or immediate?

A

warfarin effects are delayed until functional clotting factors turn over

38
Q

Warfarin adverse affects

A
  • bleeding
  • inhibition of protein C and S occurs rapidly can lead to initial procoagulant state = enhanced clotting early on
  • contraindicated in HIT
39
Q

Which form of warfarin is the active form

A

S form, metabolized in the enzyme by Cyp2c9

- variable half life

40
Q

What is the half life of warfarin

A

20 h - 60 h

41
Q

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?

A

INR will decrease slowly over day

42
Q

What is the INR

A

if reducing efficacy of warfarin, clot faster = faster bleeding time = decreased INR

43
Q

What is a direct Xa inhibitor

A

rivaroxaban

44
Q

What is a direct thrombin inhibitor

A

dabigaTran

T for two and thrombin

45
Q

What are approved indications for dabigaTran

A
  • AF not due to mechanical heart valve
46
Q

Do rivaroxaban and dabigtran require monitoring?

A

no, routine monitoring not necessary

47
Q

What are the adverse effects for rivaroxaban and dabigtran

A

bleeding

48
Q

P-gp and CYP3A4

A

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
Q

What selectively inhibits thrombin

A

dabigaTram

50
Q

What selectively inhibits FXa

A

rivaroxaban, LMW heparin

51
Q

What is the mechanism of argatroban

A

blocks the catalytic site of thrombin

- anticoagulation in HIT

52
Q

What is Hirudin

A

protein anticoagulant

  • found in leaches
  • highly specific for thrombin
  • directly bind to thrombin, suicide inhibitors
  • create 1:1 inactive complex
53
Q

Antiplatelet agents

A

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
Q

What targets COX 1?

A

aspirin

- irreversible inhibition

55
Q

What blocks ADP receptors

A

clopidogrel and prasugrel = less IIb/IIIa = less platelet aggregation

56
Q

What blocks IIb/IIIa receptors

A

abcimixab, tirofiban, eptifibatide

* HAVE a,b in their name

57
Q

What activates clopidogrel

A
  • CYP2C9 activates **genetic variability
  • reactive thiol that forms irreversible disulfide bond
  • irreversible agent
58
Q

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?

A
  • worried about stent thrombosis

- if you have stent thrombosis, you will block blood flow to the heart and have a heart attack

59
Q

What activates clopidogrel

A

prodrug activated by CYP2C9

60
Q

What activates prasugrel

A

prodrug with more predictable clinical effects

61
Q

What are adverse reactions for clopidogrel and prasugrel

A

premature discontinuation events

62
Q

When is prasugrel contra indiciated

A

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
Q

Alteplase

A

tissue plasminogen activator (tPA)

  • binds to fibrin = clot specificity = fibrin degradation
  • works best on fresh clots
  • can cause a system lytic state
64
Q

What does tPA do

A
  • 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
Q

Where is tPA synthesized

A
  • tPA is produced by vascular endothelium
66
Q

Which drug is a plasminogen activator

A

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
Q

warfarin

A
  • inhibits VCORK to inhibit vitamin k reduction

- lots of variability

68
Q

What are argatroban, desirudin, bivalrudin

A

IIa inhibitors

69
Q

Which drugs block GP-11b/IIIa activity

A

aspirin, clopidogrel (genetic variation in the activation), prasugrel (no genetic variation, but stronger drug)

I3 Exam 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions