Anti-coagulation Flashcards

1
Q

Define heamostasis

A

The body’s response to stop bleeding and loss of blood

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2
Q

What does haemostasis depend on?

A

Vessel wallPlateletsCoagulation systemFibrinolytic system

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3
Q

Define thrombosis

A

Formation of a solid mass of blood within the circulatory system during life

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4
Q

Give some of the characteristics of an arterial thrombi

A

PaleGranularLines of ZahnLower cell content- takes a while to build up

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5
Q

Give some of the characteristics of venous thrombi

A

Deep redSoftGelatinousHigher cell content

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6
Q

How do vitamin K antagonists work?

A

Prevent vitamin K epoxide from being converted to its active form. It is needed as a cofactor in synthesising certain clotting factors

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7
Q

Which clotting factors need vitamin K epoxide to be produced?

A

Factor 2Factor 7Factor 9Factor 10

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8
Q

Describe INR

A

International Normalised Ratio- ratio of prothrombin clotting times of test sample compared to control sample - measure extrinsic pathway of coagulation

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9
Q

What is the therapeutic INR range of warfarin?

A

2.0-3.0

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10
Q

How would you reverse the action of warfarin?

A

Stop warfarin treatmentIV vitamin KProthrombin complex concentrateFFP

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11
Q

What is prothrombin complex concentrate?

A

Clotting factors: 2, 7, 9, 10

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12
Q

What is FFP?

A

Fresh frozen plasma- donated from blood transfusions- replaces the active clotting factors

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13
Q

Describe aPTT

A

Activated Partial Thromboplastin Time- monitors intrinsic coagulation pathway- plasma sample mixed with intrinsic pathway activator- meausre time to form a thrombusnormal = 30-50 seconds

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14
Q

Describe heparin induced thrombpcytopaemia

A

Autoimmune response to heparin on the platelet surface, causing immune complex aggregationStop heparin Add hirudin (anticoag. peptide found naturally in saliva of leeches)

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15
Q

How would you reverse the actions of heparin?

A

Stop heparinGive protamine sulphate- dissociates heparin from AT3- irreversibly binds to heparin

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16
Q

How would you monitor heparin doses?

A

aPTT- activate partial thromboplastin time- only for unfractionated heparin - not needed for low molecular weight heparin

17
Q

Give the mechanism of aspirin

A

COX1 enzyme inhibitorPrevents thromboxane A2 production. TA2 stimulate phospholipase C which increase Ca2+ levels and leads to platelet aggregation

18
Q

ADRs of aspirin

A

GI bleedingBronchospasm

19
Q

Describe dypyridamole

A

Used with warfarin as prophylaxis against thrombosis in people with prosthetic heart valves

20
Q

Mechanism for dypiridamole

A

Inhibits phosphodiesterase enzyme- increase cAMP, increasing Ca2+ causing platelet aggregation

21
Q

ADRs of dypiridamole

A

HypotensionNauseaDiarrhoeaHeadache

22
Q

Describe clopidogrel

A

Secondary prevention of CVS or cerebrovascular events- used if Pt is allergic to aspirin

23
Q

Mechanism of clopidogrel

A

ADP antagonist- inhibits interaction of ADP-ADP receptor interaction- limits platelet aggregation

24
Q

ADRS of clopidogrel

A

HaemmorhageGI disturbances - nausea, vomiting, dicomfort

25
Q

Describe glycoprotein IIb/ IIIa inhibitors

A

Abciximab- prevents ischaemic cardiac complications in Pts having PCI- short term MI prevention in unstable angina patients

26
Q

Mechanism for glycoprotein IIb/ IIIa inhibitors

A

Is a monoclonal antibody to glycoprotein IIb and IIIa receptors- prevents platelet aggregation

27
Q

ADRs of glycoprotein IIb and IIIa inhibitors

A

HaemorrhageNausea Vomiting Hypotension

28
Q

What is the normal clearing mechanism for a thrombus?

A

Plasmin which cleaves fibrin

29
Q

How do fibrinolytic drugs bring about their action?

A

Generate plasminBind to and activate endogenous plaminogen

30
Q

When would you use streptokinase?

A

Venous thrombosis (life-threatening)Pulmonary embolismArterial thromboembolismAcute MI

31
Q

How does streptokinase work?

A

Forms a complex with plasminogen and activate plasmin which goes onto cleave fibrin

32
Q

Describe some characteristics of streptokinase

A

Derived from haemolytic streptococci so is antigenic- repeated use can result in anaphylaxisUse tissue plasminogen-activator instead

33
Q

Describe t-PAs

A

Tissue plasminogen activators- alteplase and reteplaseConvert plasminogen to plasmin

34
Q

When would you use t-PAs?

A

Acute MIPulmonary embolism

35
Q

What are some contraindications for thrombolytic therapy?

A

Peptic ulcerRecent trauma/surgeryHistory of cerebral haemorrhageUncontrolled hypertensionCoagulation deficitPrevious streptokinase therapy