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Pharmacology > EXAM #2: HEMATOLOGICAL AGENTS > Flashcards

EXAM #2: HEMATOLOGICAL AGENTS Flashcards

1
Q

Outline the roles of the the five major hemostasis systems: vascular, platelet, coagulation, anti-coagulation, and fibrinolytic.

A

1) Vascular= vasoconstriction
2) Platelet= platelet plug
3) Coagulation= insoluble clot with fibrin
4) Anti-coagulation= inhibits coagulation
5) Fibrinolytic system= degrades clot

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2
Q

What is the role of GP1b in platelet activation?

A

GP1b binds vWF, to bind to collagen and activate platelets

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3
Q

What factors are secreted by platelets when activated? What is their function?

A

ADP
TXA2
5-HT

Activate GP IIb/IIIa, which eventually allows for the platelet plug to form and function as vasoconstrictors*

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4
Q

What is the function of activated GP IIb/IIIa platelets?

A

Binding to fibrinogen; the glue that binds platelets together to form the platelet plug

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5
Q

What is the is the role of thrombin in hemostasis?

A

1) Cleaves fibrinogen into fibrin

2) Further activates platelets by binding and activating PAR

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6
Q

Draw the coagulation system: intrinsic; extrinsic: and common pathway.

A

N/A

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7
Q

What is the source of TF in the extrinsic pathway?

A

Tissue Factor is released from damaged tissue to cause the cessation of bleeding from external trauma

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8
Q

What are the two mechanisms of the anti-coagulation system?

A

1) Prevent thrombin mediated clot formation by inhibiting thrombin and Xa
2) Destruction of fibrin

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9
Q

Draw the anticoagulation system.

A

N/A

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10
Q

What are the roles of Protein S and C in the anticoagulation system

A

1) Destruction of: VIIIa and Va

2) Reduce thrombin

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11
Q

What is anti-thrombin?

A

Circulating plasma protease that inhibits thrombin and Factor Xa

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12
Q

What speeds up the activity of anti-thrombin?

A

Heparin-sulfate

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13
Q

What binds the active site of thrombin?

A

Fibrinogen; this is where fibrinogen is converted to fibrin

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14
Q

What binds the E1 site on thrombin?

A

Fibrin

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15
Q

What is the purpose of Fibrin binding to thrombin at the E1 site?

A

This limits the diffusion of thrombin away from the clot

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16
Q

What is important to remember about thrombin bound to fibrin?

A

Antithrombin/heparin CANNOT inhibit thrombin already bound to fibrin at E1

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17
Q

What are the characteristics of a venous thrombosis?

A

Red thrombi

  • High RBC i.e. red
  • Platelet poor
  • Occur where flow is slow

Can lead to venous and pulmonary embolism*

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18
Q

What is important to remember about venous thrombosis from a management standpoint?

A

Antiplatelet therapies are NOT as useful b/c the clot are PLATELET-POOR

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19
Q

What are the characteristics of an arterial thrombosis?

A

White thrombus

  • Rich in platelets
  • Often occur on top of ruptured atherosclerotic plaques
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20
Q

What is important to remember about arterial thrombosis from a management standpoint?

A

Platelet-RICH; therefore, good targets for antiplatelet therapy

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21
Q

What are the common causes of hereditary thrombophilias?

A
  • Factor V Liden Deficiency (cannot interact with proteins C and S)*
  • Protein C defieicny
  • Protein S deficiency
  • Antithrombin deficiency
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22
Q

What are the major acquired causes of thrombosis?

A

1) Cancer
2) A-fib
3) Mechanical heart valve
4) Major surgery
5) Stasis
6) Oral contraceptives

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23
Q

List the anti-platelet drugs.

A

Aspirin

Dipyridamole

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24
Q

What are the major uses of antiplatelet drugs?

A

1) Primary prevention of MI and CVA (white thrombus)

2) Secondary preventinon of recurrence

25
Q

What is the mechanism of action of aspirin?

A
  • Irreversible COX-1 antagonist

- Inhibits PG synthesis important in the production of Thromboxane A2

26
Q

What is the role of Thromboxane A2 in platelet activation?

A
  • Thromboxane A2 is a factor secreted by activated platelets causing them to aggregate
  • ASA prevents the synthesis of this secretory product
27
Q

What is the mechanism of action of Dipyridamole?

A
  • First, elevated intracellular Ca++ ACTIVATES platelets
  • cAMP reduces intracellular Ca++ in platelets

Dipyridamole increases cAMP to REDUCE intracellular Ca++ and REDUCE platelet activation

28
Q

List the P2Y12 antagonists.

A

Clopidrogrel
Prasugrel
Ticagrelor
Cangrelor

29
Q

What is the mechanism of action of the P2Y12 antagonists?

A
  • Platelets contain P2Y1 and P2Y12 GPCRs that bind ADP
  • ADP is secreted from activated platelets; it exposes GpIIb/IIIa binding sites for fibrinogen
  • P2Y12 antagonists BLOCK ADP from interacting with P2Y12 receptors
30
Q

What is the difference between Clopidrogrel/ Prasugrel, and Ticagrelor/Cangrelor?

A

Clopidrogrel and Prasugrel=

  • Pro-drugs that have be activated by the liver
  • irreversible

Ticagrelor and Cangrelor =

  • Do NOT need to be activated
  • Reversible
31
Q

What enzyme activates Clopidogrel? Why is this important?

A

CYP2C19

  • There is a high degree of polymorphism that may REDUCE the activity of Clopidogrel
  • OMPEPRAZOLE inhibits CYP2C19 and may POTENTIATE effects
32
Q

What are the important clinical considerations with the P2Y12 antagonists?

A

Preasugrel and Ticagrelor= superior results but more fatal bleeding

**CONTRAINDICATED in patients with hx of intracranial bleeding.

33
Q

List the GP IIb/IIIa antagonists.

A 
Abciximab 
Integrilin
Eptifibatide 
Tirofiban
Lamifiban
34
Q

How is Abciximab typically used in clinical practice?

A

1) Adjunct therapy in patients undergoing PTCA/ PCI, and in conjunction with ASA and heparin
2) ACS

35
Q

How are Tirofiban and Eptifibatide used clinically?

A

Unstable angina/ ACS

36
Q

What is the mechanism of action of Abciximab?

A

Fab segment of a monoclonal antibody directed at GPIIb/IIIa, which prevents fibrinogen binding

Note that Abciximab also binds receptors for GPIIIb/IIIa on leukocytes, which may account for its anti-inflammatory and antiproliferative effects

37
Q

What is the mechanism of action of Eptifibatide?

A

Peptide that binds and inhibits GPIIb/IIIa

38
Q

What is the mechanism of action of Tirofiban?

A

Non-peptide small molecule that binds and inhibits GPIIb/IIIa

39
Q

What are the adverse effects associated with GPIIb/IIIa antagonists?

A
  • Thrombocytopenia

- Bleeding

40
Q

What is the mechanism of action of Vorapaxar?

A
  • Inhibits the protease activated receptor (PAR) on the platelet surface; recall, Thrombin binds this receptor and further activated platelets
  • Vorapaxar is a PAR receptor antagonist
41
Q

What is the adverse effect of Vorapaxar? When is Vorapaxar contraindicated?

A

Life-threatening intracranial bleeding

Thus, it is CONTRAINDICATED in patients with a history of previous stroke of intracranial bleed

42
Q

What is DAPT?

A

Dual anti-platelet therapy:

  • ASA
  • P2Y12 antagonist/ ADP antagonist
43
Q

When is DAPT utilized clinically?

A

S/p PCI

44
Q

What is antiplatelet triple therapy?

A

ASA + Clopidigrel + Warfarin

45
Q

What are the four different types of anticoagulant drugs?

A

1) Indirect inhibitors of thrombin or Xa i.e. activators of antithrombin
2) Direct thrombin inhibitors
3) Direct Factor Xa inhibitors
4) Vitamin K antagonists

46
Q

List the indirect inhibitors of thrombin and/or Factor Xa.

A

Heparin
Enoxaparin
Fondaparinux

47
Q

List the direct thrombin inhibitors.

A

Lepirudin
Bivalrudin
Argatroban
Dabigatran

48
Q

List the direct Factor Xa inhibitors.

A

Rivaroxaban

Apixaban

49
Q

List the vitamin K antagonists.

A

Warfarin

50
Q

What are the indications for anticoagulants?

A
  • Treatment and prevention of venous thrombosis/ venous thromboembolism
  • Used in conjunction with antiplatelet drugs to treat MI
51
Q

What is the mechanism of action of heparin?

A
  • Recall heparin-sulfate endogenously binds and increases the activity of antithrombin
  • Specifically, a specific pentasaccharide sequnce binds and changes the conformation of antithrombin
  • Works are a molecular “bridge” to bring thrombin in close proximity to anti-thrombin (Factor Xa)

**Only longer Heparin molecules can work as a molecular bridge*

52
Q

Where does Heparin-sulfate come from?

A

Pig intestinal mast cells

53
Q

What is unfractionated heparin?

A

Heparin with pentasaccharide chains of 5-30 kDa

54
Q

Why is unfractionated heparin used in the hospital setting?

A
  • Must be given IV
  • Short 1/2 life
  • Binds numerous plasma and tissue proteins that can make dosing challenging
  • Clearance mechanisms make half-life dose dependent
55
Q

How is Heparin cleared from the body? What are the treatment implications?

A

1) Kidney/ liver
2) Rapid binding on endothelial cells*****

There is a dose dependent clearance i.e. higher doses extend the half-life

56
Q

How is Heparin monitored?

A

aPTT or PTT

Essentially a measure of the intrinsic pathway

57
Q

What are the adverse effects of Heparin?

A

1) Bleeding

2) Osteoproisis

58
Q

How do you manage severe bleeding in Heparin administration?

A

1) Discontinue use; heparin has a short-half life

2) Protamine in severe cases, a Heparin inhibitor

59
Q

What drug is the antidote to Heparin?

A

Protamine

Pharmacology (64 decks)

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