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Therapeutics > Session 1: CVD disease > Flashcards

Session 1: CVD disease Flashcards

1
Q

What is haemostasis and its main functions?

A

Stops haemorrhage from injured blood vessels.
1. maintains the fluidity of the blood.
2. stops bleeding in response to vessel trauma/ damage.
3. remove thrombus/ clot when vessel repair is complete.

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2
Q

What is the mechanism of haemostasis?

A
  1. Injured vessel
  2. Vascular spasm reduces blood flow to the injured vessel.
  3. Platelet plug formation.
  4. Platelet activation
  5. Coagulation catalyses the conversion of fluid blood to solid fibrin gel or clot.
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3
Q

What are the triggers of vascular smooth muscle/ vasoconstriction?

A
  • pain impulse
    -thromboxane and seratonin from platelets
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4
Q

How does platelet plug formation occur?

A

the platelets stick to the exposed sub-endothelial collagen and von Willebrand factor via receptors and are activated. Adjacent platelets aggregate through binding to fibrinogen.

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5
Q

What happens during platelet activation?

A

platelets adhere to the vessel wall which changes shape and secrete granule content. They synthesise mediators’ thromboxane and platelet-activation factor. Platelets aggregate due to agonist response. They expose acidic phospholipids to the surface to promote thrombin formation and release calcium.

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6
Q

What are coagulation factors?

A

Plasma proteins are made by the liver.

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7
Q

How are coagulation factors activated?

A

By proteolytic cleavage at the sites of the vessel injury to become proteases. Leads to the generation of protease thrombin

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8
Q

What does protease thrombin do?

A

Convert soluble fibrinogen to insoluble gel-like fibrin which gives the blood clot mechanical strength.

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9
Q

What are the two pathways in the coagulation cascade?

A
  1. contact activation pathway (intrinsic) XII to XIIa
  2. Tissue factor pathway (Extrinsic) VII to VIIa.
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10
Q

What is the common pathway?

A

Factor X to Xa.
Generates thrombin from prothrombin.

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11
Q

What is the intrinsic pathway activated by?

A

Exposed sub-endothelial collagen in vivo.

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12
Q

What is the extrinsic pathway activated by?

A

tissue factor after trauma to vascular wall and adjacent tissue.

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13
Q

What inhibits fibrinolysis?

A

Plasminogen activator-1

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14
Q

Name some diseases with enhanced coagulation

A

Venous thromboembolism (pulmonary arteries)
1. DVT
Arterial thromboembolism
2. MI (coronary artery)
3. ischaemic stroke (ceberal artery)

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15
Q

What is the treatment for venous thromboembolism (DVT)?

A

immediate fibrinolytic.
Prophylaxis = anti-coagulants

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16
Q

What is the treatment for arterial thromboembolism?

A

immediate fibrinolytics.
prophylaxis = anti-coag/ anti-platelet

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17
Q

Name examples of in vivo anticoagulants

A

LMW heparin, oral anticoagulants (vit k antagonist) DOACs (thrombin FXa inhibitors)

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18
Q

What does SCORE calculate?

A

risk of dying from CVD disease

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19
Q

What is used to calculate 10 year morbidity of CVD disease in england wales?

A

QRISK

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20
Q

What is ASSIGN and why is different from QRISK?

A

used in Scotland. uses FHx and social deprivation

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21
Q

When should risk calculators not be used for?

A

Patients that are already high risk such as those with diabetes.

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22
Q

What is INR?

A

International normalised ratio.
The exact maintenance dose of warfarin.

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23
Q

What does the INR test measure?

A

the time for blood to clot (prothrombin). Used to monitor blood-thinning medication.

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24
Q

Which parts of the coagulation pathway does it measure?

A

extrinsic and common pathway

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25
Q

What is PT time?

A

prothrombin time is the time necessary to generate fibrin after activation of FVII. Normal range is 10-15 secs. Required FVII, V, X, prothrombin and fibrinogen

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26
Q

Advantages of point of care coagulation tests

A
  • more convenient
  • better treatment adherence
  • measured easily
  • fewer complications
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27
Q

Disadvantages of point of care coagulation tests

A
  • overestimate low INR values
  • underestimate high INR values
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28
Q

What is the ideal INR range?

A

2-3

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29
Q

INR value above what is critical?

A

4.9 = increasing bleeding risk

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30
Q

Why is optimising the patient’s INR therapeutic range challenging?

A

VKAs have a narrow range and can be affected by patient characteristics, co-morbidities, diet and drug interactions.

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31
Q

What does COVID-19 patients have a risk of?

A

hypercoagulation.

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32
Q

Why does COVID-19 increase thrombosis risk?

A

SARS-COV-2 infection in the lung epithelial cells trigger an inflammatory response that promotes coagulation and thrombosis

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33
Q

What treatment is available for covid patients for thrombosis?

A

prophylactic dose of LMWH within 14 hrs of admission

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34
Q

What areas of uncertainty are there in CVD management?

A
  • hypertension in pregnancy - reluctance to do studies in pregnant women.
  • risk calculation/ assessment inaccurate - inaccurate BMI measurement
  • polypharmacy in the elderly
  • lack of compliance - urine sample, not taking meds regularly
  • drug resistance - clopidogrel no effect on 1/5 people (genetics?)
35
Q

What are the three phases of coagulation?

A
  1. Initiation
  2. Amplification
  3. Propagation
36
Q

What is the initiation phase of coagulation?

A

When vascular structure is compromised. FVII interacts with TF. Exposed subendothelial collagen with FXII

37
Q

What is the amplification phase of coagulation?

A

A cascade of proteolytic enzyme activity. e.g. one FXa/FVa generates thousands of thrombin molecules.

38
Q

What is the propagation phase of coagulation?

A

“thrombin burst” at the platelet surface is generated by FXa/FVa. Formation of a stable clot on the site of injury

39
Q

What word describes the dissolution of the clot, disolving small inappropriate clots at the site of completed repair?

A

Fibrinolysis

40
Q

What is the mechanism of fibrinolysis?

A

inactive zymogen plasminogen is incorporated into the clot. Activated by the tissue plasminogen activator from the endothelial cells. plasminogen becomes plasmin (active protease) = digests fibrin threads

41
Q

What is the drug class and indication of heparin?

A

Anti-coagulant. treatment and prophylaxis of venous thrombosis. Prevents embolism in AF and cardiac conditions.

42
Q

What is the MOA of heparin?

A

Binds reversibly to ATIII which inactivates factors IIa and Xa. Can also inactivate factors IX, XI and plasmin. LMWH only inhibits FXa.

43
Q

Contraindications and interactions of Heparin

A

haemophilia and other haemorrhagic disorders, use w apixaban increases bleeding risk

44
Q

Why is heparin the choice of anti-coagulants in pregnant women?

A

Does not cross the placenta and is not excreted in the milk.

45
Q

What is the drug class and indication of apixaban?

A

DOAC, FXa inhibitor. AF, reduces ischaemic stroke risk and prevention and treatment of VTEs

46
Q

What is the MOA of apixaban?

A

Reversibly and selectively inhibits FXa in its free and bound form without ATIII. Interferes with conversion of prothrombin to thrombin = prevents cross-linked fibrin clots

47
Q

Contraindications and interactions of apixaban

A

active, clinically significant bleeding, and increase bleeding risk when used with heparin. Avoid St johns wort as CYP450 induction will reduce levels of med.

48
Q

What are the side effects of apixaban?

A

haemorrhage, nausea, wound healing problems

49
Q

What is the drug class and indication of dabigatran?

A

Direct thrombin inhibitors. treat and prevent VTE, DVT, PE, stroke and AF-related embolism.

50
Q

What is the MOA of dabigatran?

A

Competitive, direct thrombin inhibitor. Thrombin is a serine protease which enables the conversion of fibrinogen to fibrin. the inhibition prevents the development of a thrombus

51
Q

Contraindications and interactions of dabigatran

A

active bleeding and prosthetic heart values. apixaban increases bleeding risk.

52
Q

What are the side effects of dabigatran?

A

haemorrhage, GI discomfort, nausea and diarrhoea.

53
Q

Why is dabigatran a safer alternative to warfarin?

A

lower risk of bleeding and less monitoring required

54
Q

What is the drug class and indication of warfarin?

A

Oral anticoagulant, Vit K antagonist. Prophylaxis for patients with prothrombic tendencies such as AF, DVT, PE, and heart valve recipients.

55
Q

What is the MOA of warfarin?

A

Vitamin K antagonist inhibits the reduction of Vit K by vit k epoxide reductase. binds to the vitamin K epoxide reductase complex subunit 1, irreversibly inhibiting the enzyme, prevents the conversion of vitamin K epoxide into Vitamin K1

56
Q

Contradindications of warfarin

A

First trimester of pregancy can cause congential malformations

57
Q

What are the interactions of warfarin?

A

Vit k2 as it is the same as vit k1 and antibiotics

58
Q

Side effects of warfarin?

A

haemorrhaging

59
Q

How is warfarin mainly eliminated?

A

metabolism. 80% in urine and 20% in hepatobiliary system

60
Q

What are antiplatelet drugs?

A

Decreases platelet aggregation and inhibit thrombus formation

61
Q

What drug class is aspirin and its indications?

A

NSAID. Used as a secondary prevention of CVD following an MI, angina pectoris, stroke and PVD. Anti-inflammatory and anti-pyretic

62
Q

What is the MOA of aspirin?

A

irreversible, non-selective Cox inhibitor, cox-1 enzyme preventing prostaglandin production which is responsible for sensitivity of pain receptors.

63
Q

How does aspirin inhibit platelet aggregation?

A

preventing the production of prostaglandins stops the conversion of arachidonic acid to thromboxane A2, which is a potent inducer of platelet aggregation, preventing thrombosis and CVD events.

64
Q

What are the contraindications of asiprin?

A

GI irritation, Peptic ulcers (cox-1 inhibition increases acid secretion)

65
Q

What does aspirin interact with?

A

bleeding risk when used with anti-coagulants such as warfarin

66
Q

Side effects of aspirin?

A

bleeding, ulceration, Gi irritation

67
Q

What is the drug class of clopidogrel?

A

Antiplatelet. Prevents blood clots in PVD, coronary artery disease, cerebrovascular disease.

68
Q

What is the MOA of clopidogrel?

A
  • prodrug of platelet inhibitor for MI and stroke. Active form carboxylesterase-1 irreversibly binds to P2Y12ADP prevents ADP from binding to P2Y12 = prevents activation of GPIIb/IIa complex and platelet aggregation
69
Q

What are the side effects of clopidogrel?

A

Diarrhoea, GI discomfort, haemorrhage

70
Q

What drug class does Vorapaxar belong to?

A

Antiplatelet - platelet aggregation inhibitor.

71
Q

What are the indications of vorapaxar?

A

reduces thrombotic CVD events in patients with MI or peripheral arterial disease

72
Q

What is the MOA of vorapaxar?

A

Inhibits platelet aggregation through reversible antagonism of PAR-1 (protease-activated receptor)/ thrombin receptor. Vorapaxar blocks PAR-1 and inhibits thrombin-induced platelet aggregation and TRAP, (thrombin receptor agonist protease).

73
Q

What are the contraindications of vorapaxar and interactions?

A

Hx of peptic ulcers, increased bleeding risk with other anticoagulants.

74
Q

Main side effect of vorapaxar?

A

haemorrhage

75
Q

Can vorapaxar be used in pregancy?

A

No

76
Q

What drug class is abciximab?

A

Antiplatelet. adhesion inhibitor

77
Q

What are the indications of abciximab?

A

prevention of thrombosis during PCI - should only be used once to decrease the chance of thrombocytopenia

78
Q

What is the MOA of abciximab?

A

It is a GPIIa/IIb receptor antagonist. inhibits platelet aggregation by preventing the binding of fibrinogen, vWF and other adhesive molecules. This causes a conformational change taht blocks access to receptors.

79
Q

What drug class is streptokinase?

A

CLOT BUSTER. purified fibrinolytic bacterial protein.

80
Q

What are the indications of streptokinase?

A

Administered 3 hour acute treatment for MI, PE and ischaemic stroke, breaks down thrombosis.

81
Q

What is the MOA of streptokinase?

A

Converts thrombus-bound plasminogen to plasmin for clot dissolution. HIghly specific complex with plasminogen molecules to form plasmin which degrades fibrin clots and fibrinogen.

82
Q

What are the contraindications of streptokinase?

A

acute pancreatitis, aneurysm, aortic dissection, AV malformation….

83
Q

What are the interactions of streptokinase?

A

use with anticoagulants/ antiplatelets = increase bleeding risk

84
Q

What are the side effects of streptokinase?

A

epigastric pain, malaise, diarrhoea, not to be used in pregnancy as it could lead to maternal haemorrhage

Therapeutics (7 decks)

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