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Cardio - Pharmacology > Lecture 8 > Flashcards

Lecture 8 Flashcards

1
Q

What’s the difference between a thrombus and clot?

A

Thrombus - clot formed in vivo

Clot - formed in vitro

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2
Q

Name and characterize two different thrombus

A

1) Red = Venous end = RBC, platelets, fibrin -> due to stasis ->DVT->PE
2) White = Arterial end = WBC, platelets, fibrin -> due to turbulence (i.e. atherosclerosis) -> MI

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3
Q

What is thrombosis?

A

Formation of thrombus (clot) in the ABSENCE of BV injury (i.e. no bleeding occurred)

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4
Q

What is Hemostasis? and the Process?

A

Plugging of a blood vessel to prevent blood loss.

1) Vasoconstriction: collagen exposed -> platelets ->bind and release ADP and 5-HT (vasoconstrictor).
2) Platelet Activation/Adhesion: Upon activation of platelets - release 5-HT/ADP/Thromboxane, platelets adhere via GP2b/3a.
3) Fibrin Deposition: Fibrinogen is converted to Fibrin - blankets the platelets/cells/proteins (clot)

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5
Q

What is the function of 5-HT?

A

Powerful vasoconstrictor

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6
Q

What is the function of ADP?

A

Causes platelet activation and change in shape.

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7
Q

How is thromboxane formed in the platelet?

A

Phospholipase A2 cleaves the PM and liberates Arachadonic Acid. AA is converted to Thromboxane via COX.

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8
Q

What activates platelets?

A

Collagen, VWF, thrombin, thromboxane, ADP

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9
Q

What kind of pathway is the Coagulation Pathway?

A

Amplification…each step creates an active enzyme that amplifies the next product.

2 pathways - INTRINSIC and EXTRINSIC.

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10
Q

What is prothrombin? How is it activated?

A

Prothrombin is the precursor for thrombin. Activated via Factor 10a. Thrombin is also known as 2a.

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11
Q

What is the intrinsic pathway?

A

A part of the coagulation pathways that converges at the level of Factor 10. Initiated by the cleavage of Factor 12 - Factor 12a.

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12
Q

What is the extrinsic pathway?

A

Tissue factor is exposed upon injury -> TF = Thromboplastin -> Factor 7 is converted to 7a -> Factor 10 is converted to 10a -> Prothrombin - Thrombin 2a -> Fibrinogen converted to Fibrin

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13
Q

What are the Factor-a’s?

A

Proteolytic Enzymes

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14
Q

What pathway is faster and why?

A

The extrinsic pathway is faster because less steps.

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15
Q

How is the Coagulation Pathway SELF regulated?

A

1) The thrombin-thrombmodulin complex activate Pn C –> inactivates inhibitors of plasminogen -> plasminogen converted to plasmin. Plasmin promotes fibrolysis.
2) Activation of Anti-Thrombin 3.

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16
Q

What physiological/pathological factors promote thrombosis?

A

Virchow’s Triad

1) Endothelial Dysfunction
2) Blood flow - turbulence, stasis of the blood
3) (Hyper) Coagulability Factors - in the blood

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17
Q

Drugs may affect co-agulation by impacting…?

A

1) Coagulation
2) Platelet activation/adhesion
3) Fibrinolysis

18
Q

The following are Pro/Anti coagulants…(characteristics)

1) Vitamin K
2) Heparin
3) Warfarin

A

1) Vitamin K - pro-coagulant
2) Heparin - injected (not orally available), short term - ANTI
3) Warfarin - orally available, long term - ANTI

19
Q

What is the pathway for Heparin?

A

Heparin(-ve, heavy) promotes the activity of antithrombin 3 (AT3)

  • Form a complex with AT3 being the AS
  • AT3 disables the protease activity -> Factor 10a and Thrombin (2a)

LMW Heparin + AT3 -> Factor 10 inhibition
Heparin + AT3 -> Factor 10 and 2a inhibition

Functions in the Intrinsic Pathway

20
Q

What is LMW Heparin?

A

low molecular heparin - self administered, longer half life

21
Q

What pathway does Heparin function in?

A

Intrinsic

22
Q

What happens if you get a clot in the following:

1) Coronary Vessel
2) Carotid Vessel

A

1) MI

2) Stroke

23
Q

How do you monitor the activity of Heparin?

A

APTT - Activated Partial Thromboplastic time.
Time it takes to clot after the addition of the following:
Ca2+, contact activator, phospholipid (mimics platelet membrane)

Test of: Intrinsic Pathway

24
Q

The APTT tests which coagulation pathway?

A

Intrisinic

25
Q

What are the adverse effects (AE) of Heparin?

A

Haemorrhage, thrombocytopenia (decrease in thrombocytes aka platelets), osteoporosis

26
Q

What is the importance of Vitamin K?

A

Necessary in the formation of functional factors 2, 7, 9, 10
Reduced Vit K is a cofactor in the carboxylation of glutamate in factors.
Factor 2: Thrombin, 7: TF activates this, 10: Converts Thrombinogen to thrombin.

27
Q

What are the function of coumarin derivatives? (Mechanism)

A

Inhibit Reduction of Vitamin K -> thus inhibiting function of gamma carboxylation of the factors -> factors can’t be activated.

Competing for Vit K reductase.

28
Q

Warfarin Mechanism? Where does it work?

A

Competes for Vit K reductase. Only functions against factors not yet performed - slow onset.
Works IN-VIVO only

29
Q

What can cause changes in the activity of Warfarin?

A

Highly bound to plasma protein - therefore increase levels of protein/liver function can alter the function of warfarin.
Vitamin K levels - if low levels of vitamin K, Warfarin can illicit a stronger effect
p450 levels: if the pathway is busy metabolizing other drugs, Warfarin levels can increase
Impaired platelet functions: can’t initiate/produce clotting factors as effectively thus Warfarin doesn’t have to compete as much.

30
Q

Warfarin AE

A

Haemorrhage

31
Q

How can you reverse the effect of Warfarin?

A

Vit K, Frozen Plasma

32
Q

How do you monitor Warfarin?

A

PT; Prothrombin time
Functions through the Extrinsic System
Time it takes to clot after the addition of calcium, TF

INR: standardized values: PT of Patient/PT of standardized value

33
Q

What are the features of some new anti-coagulant agents?

A

Low MW, Orally available, Predictable Dose-Response

Direct Attack on Factor 10a, and Thrombin

34
Q

What does Aspirin do?

A

Aspirin is an anti-platelet drug.
Inhibits COX = no thromboxane

The portal vein sees a lot of platelets without COX - aspirin localized effect (first pass effect).
Spare PGI2: promotes dilation and decreases clotting

35
Q

What is thromboxane

A

A protein produced in the COX pathway.

Promotes vasoconstriction and clotting

36
Q

What is PGI2

A

Promotes dilation and decreases clotting

37
Q

What does Abciximab do?

A

Binds to Gp2b/GP3a - prevents platelet adhesion/aggregation

38
Q

What does clopidigrel do?

A

ADP antagonist - therefore no platelet activation

39
Q

What is the fibrinolysis pathway?

A

Thrombin/Thrombomodulin activates Protein C -> inactivates inhibitor of plasminogen -> plasminogen - plasmin->fibrinolysis

40
Q

What does Streptokinase do?

A

Activates plasminogen ->plasma -> clot buster
1 x use
antigenic

FIBRINOLYTIC DRUG

41
Q

What does Alteplase do?

A

rTPA (recombinant tissue plasminogen activator)
Use may times since its not antigenic
CLOT SELECTIVE

FIBRINOLYTIC DRUG

Cardio - Pharmacology (4 decks)

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