Brainscape's Knowledge GenomeTM

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


See full index

Cardiology > Anticoagulant, anti platlet and anti thrombotic drugs > Flashcards

Anticoagulant, anti platlet and anti thrombotic drugs Flashcards

1
Q

What is haemostasis?

A

arrest of blood loss from a damaged vessel

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

What are the sequence of events in haemostasis?

A
  • endothelial damage
  • platelet plug
  • fibrin clot formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What occurs in the production of the platelet plug?

A
  • Platelets aggregate at the site of injury.
  • Activated platelets release a number of factors that cause more platelets to come to scene.
  • Platelets stick together which stems the loss of blood.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does the fibrin clot form?

A
  • Through the blood clotting cascade, liquid blood is turned into a solid and stable clot.
  • The clot is caused by the transformation of fibrinogen to fibrin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the role of pseudopodia in primary haemostasis?

A

helps platelets stick together

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

What do activated platelets do?

A
  • extend pseudopodia

- synthesise and release thromboxane A2 (TXA2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does TXA2 bind to?

A

-TXA2 receptor which causes the release of 5-HT and ADP

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

What is 5-HT?

A

Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the effect of TXA2 on smooth muscle?

A
  • When TXA2 binds to the TXA2 receptorr it causes vasoconstriction.
  • serotonin released binds to 5-HT receptors and also causes vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the role of ADP in primary haemostasis?

A

ADP binds to platelet GPCR purine recetors (P2Y12)

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

What does the activation of P2Y12 do?

A
  • activates more platelet
  • aggregate platelets into a soft plug at site of injury
  • expose acidic phospholipids on the platelet surface that initiate coagulation of blood and solid clot formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does P2Y12 aggregate platelets into a soft plug at site of injury?

A

[via increased expression of platelet glycoprotein (GP) receptors that bind fibrinogen]. TXA2 acts similarly

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

What is the role of GPIIb/IIIa receptor?

A

Allows plasma fibrinogen to bind to receptors which causes a physical bridge between platelets. Augmented by TXA2

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

What are the sequence of events in the coagulation cascade?

A
  • inactive factor 10 is converted into active factor 10a by tenase
  • inactive factor 2 is converted to active factor 2 by prothrombinase
  • fibrinogen is converted to a fibrin by thrombin (factor 2)
  • a solid clot is formed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the other name for factor 2a?

A

thrombin

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

What is the name for the inactive factor 2?

A

prothrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is thrombosis?

A

pathological haemostasis

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

What predisposes you to thrombosis?

A

Virchow’s triad

  • endothelial damage
  • abnormal blood flow
  • increased coagubility of the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an arterial thrombus?

A

white thrombus: mainly platelets in a fibrin mesh

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

Where do emboli travel to in an arterial thrombus?

A

the brain or other organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What drug treats arterial thrombi?

A

antiplatelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a venous thrombus?

A

red thrombus: white head, jelly like red tail, fibrin rich

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where do emboli travel to in a venous thrombus?

A

lungs usually

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

What drug treats venous thrombi?

A

anticoagulants

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

What does warfarin do?

A

blocks a modification of factors X and II essential for their function

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

What does rivaroxiban do?

A

Directly inhibits factor Xa

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

What does heparin, LMWHs and fondaparinux do?

A

inactivate factor Xa via antithrombin III

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

What does dabigatran do?

A

directly inhibits factor IIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What else does heparin do?

A

Inactivates factor IIa via antithrombin III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How d pre cursers produce active factors?

A

They are post transationally modified for example by gamma carboxylation of glutamate residues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where deos Vit K come in?

A

The carboxylase enzyme that mediates carboxylation requires vitamin K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the oxidised form or Vit K called?

A

epoxide

33
Q

What is the reduced form of Vit K called?

A

hydroquinone

34
Q

Which form of Vit K is important in gamma carboxylation?

A

reduced Vit K

35
Q

How does warfarin act upon Vit K?

A

Warfarin inhibits Vit K thereby stopping the action of the clotting factors 2,7,9 and 10

36
Q

When are anticoagulants used?

A
  • deep vein thrombosis (DVT)
  • prevention of post-operative thrombosis
  • patients with artificial heart valves
  • atrial fibrillation
37
Q

Whats the major risk of anticoagulants?

A

haemorrhage

38
Q

How is warfarin administered?

A

orally

39
Q

What is the absorption of warfarin like?

A

very good

40
Q

What is the onset of action of warfarin?

A

slow (2-3) days. whilst inactive factors replace active gamma carboxylated factors that are slowly cleared from the plasma

41
Q

How does warfarin compete with Vit K?

A

It compeetess with it to prevent conversion of Vit K to reduced Vit K to stop gamma carboxylation

42
Q

How is the degradation of warfarin?

A

takes ages to leave body

43
Q

Why is heparin used over warfarin in life threatening situations?

A

Warfarin takes too long to become activated

44
Q

How long do you have to wait after stopping warfarin until an operation can be done?

A

4-5 days as it takes five half lives for an agent to be cleared from the body

45
Q

What are the warnings for warfarin?

A
  • low therapeutic index
  • warfarin must be monitored on a regular basis
  • overdose can be treated by Vit K administration
  • overdose can also be treated by plasma clotting factors
46
Q

What factors potentiate warfarin action and thereby increase the risk of haemorrhage?

A
  • liver disease – decreased clotting factors
  • high metabolic rate – increased clearance of clotting factors
  • drug interactions
47
Q

What factors lessen warfarin action and thereby increase risk of thrombosis?

A
  • psychological state (pregnancy)
  • vit K consumption
  • drug interactions
48
Q

What is antithrombin III?

A

an important inhibitor of coagulation

49
Q

What does antithrombin III do?

A

neutralises all serine protease factors in the coagulation cascade by binding to their active site in a 1 to 1 ratio

50
Q

How do heparin and antithrombin III work together?

A

When antithrombin bind to heparin, it increased the rate of deactivation of active factor 2 and 10. Reduced conversion of fibrinogen to fibrin so no clot.

51
Q

How is factor 2 inactivated?

A

heparin binds to antithrombin III and factor II simultaneously

52
Q

How is factor X inactivated?

A

Heparin needs to bind to antithrombin The acceleration of the inactivation is aided by LMWHs.

53
Q

Give two examples of LMWHs

A

enoxaparin and dalteparin

54
Q

When are LMWHs not used?

A

renal failure

55
Q

What is the admistration route of heparin and LMWHs?

A

heparin - IV or SC

LMWH- SC

56
Q

What is the elimination order of heparin and LMWHs?

A

heparin- zero order

LMWH - first order

57
Q

What are the adverse effects of heparin and LMWHs?

A
  • haemorrhage
  • osteoporosis
  • hypersensitivity reactions
58
Q

What are examples of newer olly active agents that inhibit thrombin or factor 10?

A

rivaroxiban and dabiatran

59
Q

Why are the newer drugs so good?

A
  • convenience of administration

- predictable degree of anticoagulation

60
Q

What does aspirin do?

A

irreversibly blocks cycloxygenase (COX) in platelets, preventing TXA2 synthesis, but also COX in endothelial cells inhibiting production of antithrombotic prostaglandin I2 (PGI2)

61
Q

when and how is aspirin used?

A

Used orally, mainly for thromboprophylaxis in patients at high cardiovascular risk

62
Q

What is the main adverse effect of aspirin?

A

gastrointestinal bleed and ulceration

63
Q

How dies clopidogrel work?

A

Links to P2Y12 receptor by a disulphide bond producing irreversible inhibition

64
Q

When is clopidogrel used?

A

when patients are intolerant to aspirin

65
Q

How is clopidogrel administered?

A

orally

66
Q

What re the effects of combining aspirin and clopidogrel?

A

synergistic effect - work well to enhance action

67
Q

When is tirofiban used?

A

Given IV in short term treatment to prevent myocardial infarction in high risk patients with unstable angina (with aspirin and heparin)

68
Q

When are fibrinolytics used?

A

Fibrinolytics are used principally to reopen occluded arteries in acute myocardial infarction (M.I.), or stroke – less frequently life-threatening venous thrombosis or pulmonary embolism

69
Q

How are fibrinolytics administered?

A

IV

70
Q

What is a better treatment than fibrinolytics?

A

percutaneous coronary intervention

71
Q

What drug do fibrinolytics work well with?

A

aspirin

72
Q

What is streptokinase?

A

Not an enzyme, but a protein extracted from cultures of streptococci

73
Q

What does streptokinase do?

A

Reduces mortality in acute M.I. (given IV, or intracoronary) but action blocked after 4 days by the generation of antibodies. Further doses not to be given after this time

74
Q

What are the disadvantages of streptokinases?

A

May cause allergic reactions (not be given to patients with recent streptococcal infections)

75
Q

What are Alteplase and duteplase

A

Are recombinant tissue plasminogen activator (rt-PA)

76
Q

What do Alteplase and duteplase do?

A

Are more effective on fibrin bound plasminogen than plasma plasminogen and show selectivity for clots

77
Q

Do Alteplase and duteplase cause allergic reactions?

A

no

78
Q

What is the major adverse effect of fibrinolytics?

A

The major adverse effect of fibrinolytics is haemorrhage that may be controlled by oral tranexamic acid which inhibits plasminogen activation

Cardiology (32 decks)

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