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CPR Week 4 > 3.4.4. Hemostasis > Flashcards

3.4.4. Hemostasis Flashcards

1
Q

What are the three stages of hemostasis?

A

Primary

Secondary

Fibrinolysis

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2
Q

What is the primary stage of hemostasis?

A

(vasconstriction) activation, adhesion and aggregation (of platelets/ forms white thrombus, predominantly in the arteries - causes ischemia)

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3
Q

What is the secondary stage of hemostasis?

A

activation of the coagulation cascade - conversion of fibrinogen to fibrin (red thrombus - predominantly in the veins - causes embolism)

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4
Q

What is the fibrinolysis stage of hemostasis?

A

activation of plasmin to break down fibrin

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5
Q

***In order to prevent occlusion, drugs inhibit what?***

A

***In order to prevent occlusion, drugs inhibit primary and secondary and activate fibrinolysis***

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6
Q

Endothelium of vessels is inherently anti-thrombogenic, damage exposes the underlying extracellular matrix, which activates _____ and triggers the formation of a thrombus.

A

Endothelium of vessels is inherently anti-thrombogenic, damage exposes the underlying extracellular matrix, which activates platelets and triggers the formation of a thrombus.

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7
Q

How does the primary stage of hemostasis progress? (What is its mechanism of action)

A
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8
Q

How is Aspirin an anti-thrombogenic? Does this effect of Aspirin benefit from increased dosages?

A
  • COX-1 inhibitor (irreversible)
  • Decreases the production of Thromboxane A2 (potent stimulator of platelet aggregation and adhesion)
  • At high doses, may decrease anti-thrombotic action by decreasing the synthesis of PGI2 [no additional benefit to increased aspirin dosing]
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9
Q

What are the risks of Aspirin use?

A
  • Risks: GI bleed, allergic reaction (asthma), contraindicated in children (Reye’s Syndrome)
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10
Q

What are the Thienopyridines? What are some examples of these?

A

ADP Receptor Inhibitors: “Thienopyridines”

Clopidogrel, Ticlopidine, Prasugrel, (-grel)

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11
Q

How do the thienopyridines work?

A

irreversible inhibitors of ADP receptors [which inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen by preventing their expression on the platelet cell surface]

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12
Q

Are the thienopyridines pro-drugs? What is their speed of onset?

A

Are ***pro-drugs***, activated hepatically and of slow onset (prasugrel is slightly faster)

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13
Q

Thienopyridines may be used in conjunction with what to increase their anti-platelet activity?

A

May be used in conjunction with aspirin to provide additional anti-platelet activity

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14
Q

What are the side effects of Thienopyridine use?

A

Side effects:

neutropenia

thrombocytopenia

TTP/HUS may be seen

 Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)
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15
Q

What are some indications for use of thienopyridines?

A

Use for: acute coronary syndrome, coronary stenting, and decreasing the incidence or recurrence of thrombotic stroke

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16
Q

Are there any reversible ADP inhibitors?

A

***Ticagrelor is a reversible ADP inhibitor, that is not a pro-drug and better overall in efficacy but is MUCH more expensive***

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17
Q

What is the mechanism of action of Dipyridanole?

A

inhibits the cellular uptake of adenosine (which modulates vasodilation and aggregation activity) and increases cGMP/AMP levels through PDE inhibition [specifically PDE3]

  • ultimately inhibits platelet aggregation and causes vasodilation
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18
Q

What are the indicated uses for Dipyridanole?

A
  • limited use: usually prophylaxis of angina or thrombus with prosthetic heart valves [when combined with warfarin]
    • also indicated for: intermittent claudication, coronary vasodilation, prevention of stroke or other TIAs (when combined w/aspirin)
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19
Q

What are the risks associated with taking dipyridanole?

A

Risks: nausea, headaches, hypersensitivity, hypotension, facial flushing, abdominal pain

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20
Q

What does Cilostizol do?

A

inhibits platelet aggregation

antithrombotic and vasodilator

PDE3 inhibitor; increases cAMP

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21
Q

What is an indicated use of Cilostizol?

A

approved for use with claudication due to peripheral arterial disease

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22
Q

What are the risk of taking Cilostizol?

A

Risks: use of drugs that inhibit metabolism via CYP3A4 or CYP2C19

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23
Q

Once present what must happen to GPIIa/IIIb for a clot to form? What drugs interfere with this process?

A

GPIIa/IIIb must be activated by agonists (such as TxA2, collagen, chronic tissue damage) in order to bind fibrinogen and lead to aggregation of activated platelets

Fibrinogen Receptor Blockers interfere with this

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24
Q

How do you administer Fibrinogen Receptor Blockers (FRBs)

A

These drugs will be administered via IV (often with aspirin or warfarin)

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25
What are the indications for FRBs?
Indications: unstable angina, percutaneous transluminal coronary angioplasty
26
What is a major side effect of FRBs?
Major side effect is bleeding, as well as thrombocytopenia
27
What is Abciximab?
a Fab (fragment antigen binding) fragment of humanized monoclonal antibody (partially derived from mouse IgG) which binds GPIIb/IIIa and blocks ligand binding An FRB!
28
What does Abciximab prevent?
prevents platelet aggregation and formation of thrombus
29
What are the uses of abciximab?
Uses: during angioplasty (reduces the risk of ischemia, MI)
30
What is eptifibatide?
reversible (synthetic) heptapeptide inhibitor of the fibrinogen binding site, inhibits ligand binding
31
What is a contraindication of eptifibatide?
renally cleared contraindicated with renal insufficiency
32
What is a use of Eptifibatide?
use to treat unstable angina
33
What is Tirofiban?
similar, smaller synthetic molecule inhibitor of GPIIa/IIIb
34
What are the uses of Tirofiban?
Use: management of unstable angina, angioplasty
35
What is unfractionated heparin (UFH)?
highly sulfated glycosaminoglycan (negatively charged) Made by mast cells used to prevent venous thrombus
36
What does UFH do to prevent venous thrombus?
enhances the activity of endogenous antithrombin protein to inhibit thrombin and factor Xa \*\*\*binds antithrombin and acts as a catalytic surface and increase activity by 1,000 fold\*\*\* Thrombin can then detach and inhibit other thrombin/Xa molecules
37
When do we use UFH?
Use for embolism, MI/stroke
38
What should we see in the aPTT with UFH treatment?
Should observe 1.5-2 fold increase in aPTT
39
How do we give UFH? Why might we use it instead of Low Molecular Weight Heparin (LMWH)?
Immediate onset (IV use only) LMWHeparin is better, but UFH has antidote for overdose (protamine sulfate - but too much PS causes increased bleeding)
40
When administering anti-coagulants, what two lab values do we need to keep track of?
monitor aPTT vs INR
41
What is fondaparinux?
Synthetic version of LMWH
42
What are two bonuses of using LMWH or fondaparinux?
Don’t need to monitor aPTT because does not inhibit thrombin, only factor Xa better/more predictable pharmacokinetics
43
What do we use LMWH or fondaparinux for?
Used for DVTs
44
What are the risks and contraindications of LMWH and fondaparinux?
Risks: bleeding, heparin induced thrombocytopenia “HIT” (autoimmune reaction that destroys platelets (Ig-mediated) Contraindicated prior to major surgeries
45
What is a class of alternatives to heparin?
hirudin derived compounds (-irudin)
46
What are the hirudin derived compounds?
direct and irreversible thrombin inhibitors found in leech saliva
47
What is lepirudin and how does it work?
lepirudin: recombinant version of hirudin, works independently of antithrombin to inactivate fibrin-bound thrombin. Rapid onset, renal clearance
48
What is bivalirudin, does it work fast, how is it cleared?
bivalirudin: bivalent thrombin inhibitor, rapid onset, short half-life, renal clearance
49
What is argatroban?
argatroban: small synthetic molecule, short half-life, needs continuous IV
50
What are the risk associated with argatroban use?
risks: cleared by CYP450 system, dose reduction required with liver disease, elevated INR - difficult to transition to warfarin
51
What are the indications for use of the hirudin compounds?
Indications for use: HIT-induced thrombosis, coronary angioplasty - USED IN PLACE OF HEPARIN FOR ANTICOAGULATION
52
Whe monitoring the aPTT with hirudin compounds, what increases are we looking for?
MUST monitor aPTT, aim for 1.5-3 fold increase
53
What is warfarin?
THE oral coagulant, dicumarol based analogue Originally was rat poison, may have also been used in IEDs/bombs
54
Is warfarin a safe drug to use?
No, LOTS of issues (and drug interactions)
55
What is the MoA of Warfarin? | (Mech of Action)
* Blocks the formation of inactive forms of clotting factors * no effect on those previously synthesized * slow onset of action * inhibits the Vitamin K epoxide reductase and decreases available K+ (essential cofactor for factor generation) * prevents gamma-carboxyglutamate post-translational modification of “Gla domains” and activation of clotting factors
56
Warfarin is used for:
Use for: DVT, PE, a. fib, heart valve replacement, less effective for prevention of new thrombus
57
What kind of therapeutic index are we looking at with Warfarin?
Very narrow therapeutic index
58
What are we worried about with Warfarin?
May cause excessive bleeding, “catastrophic hemorrhage” low renal clearance
59
How can we fix Warfarin caused issues?
“Antidote” is vitamin K and fresh frozen plasma
60
What is a contraindication for Warfarin?
Contraindicated in pregnancy, crosses the placenta and is teratogenic
61
Compare Warfarin and Heparin
![](https://lh4.googleusercontent.com/ttQBc3bxWYzpKPlykavUZSbyycUHe_98-ji1AB2t9Df6dgK3N_e7KhfGdjP67kYnJB1zQ8SYE3E_7_Gf6mebG-FGw79_BQ6k4INAY-L_TODyAXM1UzRvzjlCm1Bi9F0tMw)
62
What is the bonus of using Warfarin alternatives?
No longer requires the blood monitoring
63
What is dabigatran?
orally active direct thrombin inhibitor prodrug
64
How is dabigatran cleared? What are some uses for it?
Use: a. fib, prevent DVT, in hip/knee replacements no CYP450 metabolism; renal clearance
65
What is Rivaroxaban? How is it metabolized and where is it cleared?
orally active, direct inhibitor of factor Xa CYP3A4 metabolism; mainly renal clearance
66
What is Apixaban?
orally active, direct inhibitor of factor Xa
67
What do we use Apixaban for? How is it metabolized and where is it cleared?
prevent DVT CYP3A4 metabolism; less renal clearance
68
What is the clinical use of Warfarin alternatives?
clinical use (both riva- & apixaban): Treatment and prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis in patients with atrial fibrillation. Oral agents do not usually require coagulation monitoring
69
What is the toxicity associated with riva- and apixaban?
toxicity (both riva- & apixaban): bleeding (no specific reversal agent available)
70
In an acute event, how do we administer thrombolytic drugs?
Thrombolytic Drugs: exclusively IV use in an acute event
71
What are some uses for thrombolytic drugs?
acute myocardial infarction acute ischemic stroke acute PE acute DVT
72
What are some contraindications of thrombolytic drugs?
bleeding, HTN, and surgery
73
What are some thrombolytic drugs?
Alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA)
74
What is the MoA of these thrombolytics? Their clinical use? What about their toxicities?
![](https://lh5.googleusercontent.com/upJZNk34znRxorXtizjl4RrfCntwLAzIvlEth_wahmDceeo5XRttNVqDzExbqPeCDS35pjCFaSt_o7A6BHepT4eUQ03g4bQBy6FLQjEgIYlqvEbmsHPqgkI-mtEJXtbLXw)
75
What are the Tissue Plasminogen activators?
"plase"s ## Footnote natural endothelium derived only cleaves fibrin-bound plasminogen increased bleeding risk
76
What is Streptokinase? How does it work?
bacterially derived complexes with plasminogen proactivator to catalyze conversion of plasminogen to plasmin active on circulating and fibrin-bound plasminogen
77
What is urokinase? What does it do?
found in the kidney directly converts plasminogen to plasmin active on bound circulating and fibrin-bound plasminogen
78
What are we interested in Factor VII use as a pro-coagulant?
In trauma, giving factor VII as a pro-coagulant has been promising in pre-clinical studies should only work at the site of injury Reduce # of blood transfusions No proof of increased survival (YET!!!!) Currently only used in hemophilliacs that don’t respond to factor 8

CPR Week 4 (19 decks)

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