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From Flashcardlet big > Hemostatis agent > Flashcards

Hemostatis agent Flashcards

1
Q

What is Tisseel

A

Topical sealant containing fibrinogen and thrombin (small amount of aprotinin)

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2
Q

What is FLOSEAL?

A

topical agent that consists of gelatin matrix hemotstatic sealant that is composed of human thrombin and a proprietary gelatin matrix.

Augment the coagulation cascade at multiple site. It has proven efficiacy in cardiac surgery.

Best to use with arterial bleeding

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3
Q

What is COSEAL?

A

Surgical sealant composed of polyethylene gycol (PEGS)

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4
Q

What is surgicel?

A

oxidized cellulose

provides a platform for hemostasis to occur

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5
Q

What is dose of protamine for reversal of heparin?

A

1 gram of protamine per 100 units of heprain

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6
Q

What is the range of dosing for factor VII

A

According to body weight

65ug/Kg to 100ug/k–NovoSeven is available in the hospital at 1.2, 2.4, and 5 mg Vials.

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7
Q

How does factor VII work

A

stimulates the coagulation cascade by activation of thrombin at the site of tissue injury by tissue factor-dependent and independent mechanisms.

Tissue-factor dependent mechanism results in production of FactorX which leads to the generation of thrombin.

The tissue factor independent mechanisms include activation, aggregation, recuitment and stablization of platelets that are resistant to fibrinolysis.

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8
Q

What is BioGlue

A

Has two components—purified bovine serum albumin (BSA) and glutaraldehyde.

polymerize reaction in 20 to 30 seconds and reaches full strength in 2 minutes

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9
Q

Name 2 new anitplatelet durgs

A

Prasugrel
ticagrelor
Cangrelor

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10
Q

What study and dosing is important regarding ASA and bypass grafts

A

Antiplatelet trialists Collaboration

restarting ASA before surgery or withing 24 hours after surgery had a similar benefit on vein graft patency.

75 to 325 mg.

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11
Q

Effect of ASA on mortality

A

Study from mayo clinic in 16 3 patients showed preoperative asa pts had a significantly lower post operative mortality (1.7% vs 4.4). No difference in bleeding.

NEJM study showed that preoperative ASA in isoalted CABG patients resulted in 27% reduction in-hospital mortality.

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12
Q

Name 3 thienopyridines

A

prodrugs that are biotransformed into molecules that bind irrecversible to P2Y12 receptor.

Ticlopidine
Clopodigrel
prasugrel

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13
Q

Why plavix in pts with ACS

A

CURE: clopidogrel in Unstable ANgina to precent recurrent events—ASA + plavix

This resulted in a reduced cardiovascular death, myocardial infarction, or stroke in patients with ACS

11% relative risk reduction.

benefit was mainly before surgery.

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14
Q

What is Prasugrel

A

Associated with increased bleeding risk

surgery should be delayed by 7 days.

similar active metabolite to plavix

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15
Q

What is Ticagrelor

A

Nonthienopyridine, pyrimidine derivative, direct-acting, and reversible antagonis of the ADP receptor P2Y12 with a plasma half-life of about 12 hours

More rapid, potent and consistent effect on platelet function compared with clopidogreal.

Currently indicated for the treatment of patients with ACS on the basis of the PLATO trial.

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16
Q

What is PLATO trial

A

Large, multicenter trial, with pts in ACS with/without ST MI.

Composite of death, MI, stroke, at 12 months was signficant reduced with ticagrelor compared to clopidogrel. 4.5% vs 5.9%

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17
Q

According to recent recommendations of the 2011 ESC guidelines for NSTEM with ACS

A

Ticagrelor is considered first line therapy.

Prasugrel is recommended only for P2Y12 inhibitor naive patients whom coronary antomy is known and are who are proceeding with PCI

Plavix is for pts who cannot receive ticagrelor or prasugrel.

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18
Q

How long should you stop ticagrelor

A

5 days before surgery

ticagrelor higher potency; platelet inhibition is the same as plavix in first 24 to 28 hour

only 3 to 5 days from discontinuation is there less platlete inhibiton compared to plavix.

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19
Q

What is the evidence for GPIIbIIIa

A

Abciximab
Eptifibatide
tirofiban

PURSUIT study in patients with NSTEMI and ACS

30 day mortality was 26.1% vs 30.8%

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20
Q

When do you stop Eptifibatide and tirofiban before cardiac surgery

A

2 to 4 hours

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21
Q

When you stop Abciximab?

A

It has a short plasma half-life of about 10 minutes but it dissociated slowly from the platelet receptors

12 hours before CABG, if not you have to give platelets..

22
Q

List the stages of hemostasis

A
  1. Vascular phase–immediate response (local and myogenic spasm)
  2. Platelet phase–goal to make a platelet plug
  3. Clotting phase (turns loose platelet plug into a stable fibrin clot)
23
Q

3 pathways that are involved in clotting cascade

A

intrinsic—(contact activation pathway)
extrinsic pathway–(tissue factor), activated by TG released by endothelium follow vessel damage
Final common pathway and results in fibrin formation

24
Q

List co-factors involved in coagulation cascade

A

Calcium—required to convert tenase to prothrombinase to covert prothrombin to thrombin
Vitamin K—required for the production of factors II, VII, IX and X

25
Q

What is fibrinolysis

A

process of clot break down and primarily controlled by plasmin
Plasminogen is inactive form
activated by tPA

inactivated by alpha 2 antiplasmin and serine protease inhibitors

26
Q

What happens with Anti-thrombin levels

A

ATIII levels are usually 100% active but with heparinization activity is reduced to 30%

If you have resistance of heparin in OR, then one of the key step is to give FFP to replenish your ATIII store and have your heparin effect.

27
Q

How is Argatroban cleared

A

Hepatic

28
Q

How are lepirudin and Bivalidudin cleared

A

Renal

29
Q

What is Thromboelasography and what does it measure

A 
TEG monitors hemostasis as a whole
The life of a clot
time to initial clot formation
Evaluation of clot in the acceleration 
Assess clot strengthening and retraction 
Detect clot lysis
30
Q

TEG parameters of interest

A

R value - time from initiation of the test to the initial fibrin formation

K value- time from the beginning of clot formation until the amplitude of the TEG reaches 20 mm

maximal amplitude (MA) repsents clot strength which is depentedn on the number of function of platelts and its intercation

alpha angle

31
Q

What is action and potential role for DDAVP?

A

increase factor VIII and VwF
Appropriate for pts with kidney disorders (Uremic bleeding)
May have a role in pts who were taking ASA pre-op
Meta analysis showed a 9% reduction in blood loss (not clinically signficant)

32
Q

What are 3 stages of hemostasis

A

Vascular phase
platelet phase
Clotting phase

33
Q

What two things should be corrected before giving factor VIIa

A

Hypothermia and acidosis reduced ability of Factor VII

34
Q

What percentage of patients do not respond to plavix

A

about 30%

35
Q

a. How is Bivalirudin and Lepirudin cleared from body?

b. How is Argatroban cleared?

A

a. Rena

b. Liver *So you can use if a pt has HIT and renal insufficiency

36
Q

List two Anti-Factor Xa oral medication

A

Rivaroxaban

Apixaban

37
Q

What is mechanism of action of Dabigitran

A

Oral, direct competitive thrombin, inhibitor

Re-Ly study showed in AF that 110 vs warfarin was equal and 150 vs warfarin resulted in less stroke 1.69 vs 1.11% with similar bleeding

Limitation was the time spent in therapeurtic range on warfarin was limited for pt. when pts were in therapeutic range greater >70%) of time there was no difference

38
Q

How does heparin work

A

Heparin potentiates the action of ATIII (which normally acts by inhibiting thrombin) by 1000 time so it inhibits thrombin and the subsequent anticoagulation effect.

39
Q

How is Ticragrelor different from plavix

A

Like the thienopyridines prasugrel, clopidogrel and ticlopidine, ticagrelor blocks adenosine diphosphate (ADP) receptors of subtype P2Y12.

In contrast to the other antiplatelet drugs, ticagrelor has a binding site different from ADP, making it an allosteric antagonist, and the blockage is reversible.

Moreover, the drug does not need hepatic activation, which might work better for patients with genetic variants regarding the enzyme CYP2C19 (although it is not certain whether clopidogrel is significantly influenced by such variants).

40
Q

What is abicimab

A

Abciximab is made from the Fab fragments of an immunoglobulin that targets the glycoprotein IIb/IIIa receptor on the platelet membrane.

Abciximab has a plasma half-life of about ten minutes, with a second phase half-life of about 30 minutes. However, its effects on platelet function can be seen for up to 48 hours after the infusion has been terminated

41
Q

What is factors help regulate the coagulation cascade

A

inactivates factors V and VIIIa in the presence of Protein S
Anti-thrombin III–inhibits thrombin and factors IX, A and XI
Prostayclin, inhibits platelet aggregation and causes vasodilation

42
Q

What is mechanism of action of Fondaparinux

A

Pentasaccharide Factor Xa inhibitor.

Within heparin and heparan sulfate this monomeric sequence is thought to form the high affinity binding site for the anti-coagulant factor antithrombin III (ATIII). Binding of heparin/HS to ATIII has been shown to increase the anti-coagulant activity of antithrombin III 1000 fold. In contrast to heparin, fondaparinux does not inhibit thrombin.

43
Q

What is mechanism of action of Bilvalirudin

A

reversible direct thrombin inhibitor

Chemically, it is a synthetic congener of the naturally occurring drug hirudin (found in the saliva of the medicinal leech Hirudo medicinalis).

Bivalirudin, overcomes many limitations seen with indirect thrombin inhibitors, (heparin)
is a short, synthetic peptide that is potent, highly specific, and a reversible inhibitor of thrombin, inhibits both circulating and clot-bound thrombin, while also inhibiting thrombin-mediated platelet activation and aggregation.

Bivalirudin has a quick onset of action and a short half-life. It does not bind to plasma proteins (other than thrombin) or to red blood cells.

No risk for Heparin Induced Thrombocytopenia/Heparin Induced Thrombosis-Thrombocytopenia Syndrome (HIT/HITTS).

Does not require a binding cofactor such as antithrombin and does not activate platelets.

44
Q

Name inibition of coagulation cascade

A 
Natural anticoagulants---ATIII, Protein C and Protein S
Fibrinoytic system (Plasmin--degrades fibrinogen)
45
Q

What degree is platlete aggregability reduced after CPB

A

by about 60%

and bleeding time is longer

these outcome persist for more then 24 hours

46
Q

What is normal weight of Heparin (UF) and LWMH (Enoxaprin)

half life of heparin

half life of Enoxaparin

A

UF = 750 - 1000 kDA
LMWH 1- 10 kDA

UF = 60 to 90 min 
LMWH = 4.5 hours * only partially reverses protamine
47
Q

What are complications of warfarin

A

Vit K antagonist
Half life is 36 to 42 hours
Vit K causes reversal in 8 to 24 hours

Complications: Bleeding/ Skin necrosis (Vit C and S deficiency), fetal abnormalities

48
Q

What is loading dose and time of action for plavix

A

Research showing 600 mg of Plavix is better (900 mg made no difference)
onset of action is within 2 hours
Inhibits ADP induced aggregation
Requires 5 days for platelet activity to return

49
Q

Prasugrel details

A

Inhibits ADP induced platelet aggregation
with 60 mg of oral loading dose
onset of action is < 30 minutes
peal effect in 4 hours
greater risk of bleeding: not in pts with previous stroke, age > 75; or pts with PUD

50
Q

Details of the GPIIb/IIIa inhibitors

A

Antiplatelet agents–inhibit aggregation by preventing fibrinogen, von Willebrand factor, and other adhesive ligands to bind to GP IIb/IIA

51
Q

What is Octaplex

A

Prothrombin Complex Concentrate (PCC) is a combination of blood clotting factors II, VII, IX and X, as well as protein C and S.

It reverses the effect of warfarin (a coumarin anti-coagulant) and is used in cases of significant bleeding in patients with a coagulopathy (INR > 8.0, prolonged prothrombin time, raised d-dimer).

lasts for 6 to 12 hours. only 25 to 50 ml, no risk of TRALI

52
Q

What is Gelfoam?

A

A compressed sponge, water insoluble, off-white, prepared from porcine skin.

Absorb 45 times its weight of blood, Absorbs in 4 to 6 weeks, minimal inflammatory response

aids clotting process by producing mechanical matrix for clotting and/or release of thromboplastin when platelets come in contact with it

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