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Pharmacology 1 > Haemostasis and drugs > Flashcards

Haemostasis and drugs Flashcards

1
Q

what is haemostasis?

A

balance between normal blood functioning and preventing blood loss

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2
Q

where is haemostasis most effective?

A

small blood vessels (arterioles), capillaries and venules

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3
Q

what is haemostasis a complex interaction between?

A

vasoconstriction
platelets
coagulation (clotting factors + inhibitors)
fibrinolysis

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4
Q

name the two types of blood clotting and the substances involved in each

A

venous - clotting factors activated (inherited/acquired)

arterial - involves platelets

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5
Q

what is a thrombosis?

A

formation of a thrombus within the vessel

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6
Q

what can cause a thrombus?

A

pooling of blood in veins - DVT

damaged vessels - atheromatous plaques

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7
Q

describe the formation of a thrombus

A

fibrin framework - platelets and other blood cells become trapped
attached to vessel wall - leads to impeded blood flow and reduced profusion of tissue

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8
Q

what is the difference between a venous and arterial thrombosis?

A

venous - coagulation major factor

arterial - platelet aggregation major factor - coagulation also involved

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9
Q

what is an embolus?

A

fragment or whole thrombus which detaches from wall of blood vessel

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10
Q

what happens when an embolus occurs?

A

fragment or whole thrombus travels through blood vessels- blocks small vessels in pulmonary, cardiac, CNS circulation

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11
Q

what results from a embolus?

A 
pulmonary embolism (PE)
myocardial infarction (MI)
stroke
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12
Q

what might be targeted to modify the thrombosis process?

A
  • coagulation (most useful in venous thrombosis)
  • platelet aggregation (important in arterial thrombosis)
  • clot, thrombus breakdown (if prophylaxis fails)
    (drugs aim to inhibit thrombus without preventing haemostasis)
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13
Q

what drugs are used to modify coagulation?

A

heparins (anticoagulants)

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14
Q

is heparin present in the body naturally?

A

yes - present in lungs, liver and mast cells

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15
Q

what impact does the molecular weight of the heparin have?

A

heparin - standard, unfractioned (natural form)
low MW heparin - more effective, less side effects
both activate anti-thrombin

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16
Q

name two low MW heparins

A

enoxaparin - clexane

dalteparin

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17
Q

describe the action of heparin

A
  • activates anti-thrombin (AT)
  • activated AT forms complexes with clotting factors: thrombin, factors Xa (+ FIXa/XIa) causing them to be inactivated
  • heparin increase rate of complex formation
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18
Q

what are some of the disadvantages to using heparin?

A

poorly absorbed orally - must be give IV or Sub-cut

risk of haemorrhage

19
Q

what would be done if haemorrhage occurred in a patient using heparin?

A

mild: cease admin
severe: give protamine sulphate (forms complex with heparin - inactivating)

20
Q

name a commonly used oral anticoagulant

A

warfarin

21
Q

how does warfarin work?

A
  • related to structure of vit. K
  • antagonises vit K role in formation of various clotting factors (II- prothrombin, VII and IX)
  • warfarin prevents conversion of these active factors
  • precursors to these factors are inactive in coagulation
22
Q

what are the problems associated with warfarin?

A

slow onset - fully anti-coagulated after 3 days
activity influenced by vit K - intake, absorption, gut flora
probs with antibiotics
many interactions - foods/drugs
risk of haemorrhage

23
Q

what is the INR target for recurrent DVT?

A

3.0 (2.5-3.5)

24
Q

when taking warfarin haemorrhage is at increased risk, what would you do to reverse the effect of warfarin?

A

mild: stop admin
severe: vit K, clotting factors, whole blood, fresh frozen plasma

25
Q

can warfarin be used during pregnancy?

A

no - teratogen (must be avoided in early pregnancy and ideally throughout)

26
Q

how can warfarin interact with other drugs?

A

enzyme induction - eg. carbamazepine

enzyme inhibition - eg. cimetidine

27
Q

name two of the new generation of anticoagulants

A

Rivaroxaban (Xarelto)

Dabigatran (Pradaxa)

28
Q

what is the target for Rivaroxaban?

A

inhibitor of Factor Xa

29
Q

what is the target for Dabigatran?

A

thrombin inhibitor

30
Q

what happens when platelets are activated?

A

the platelets form ‘legs’ which stick to other platelets

31
Q

explain the process of platelet aggregation

A 
vessel damaged
collagen exposed
platelets bind here and are activated
increased synthesis of TxA2
increased GPIIb/IIIa receptors expression on platelet
platelets aggregate
32
Q

which two substances are produced from an atheromatous plaque by the COX enzyme?

A 
thromboxane A2 (TxA2)- promotes aggregation of platelets by reducing cAMP
Prostacyclin (PGI2) - reduces platelet aggregation by increasing cAMP
* a balance of both is important
33
Q

name three targets for affecting platelet activation and aggregation

A

synthesis of thromboxane A2
cAMP levels in platelets
Glycoprotein IIb/IIIa receptors on platelets

34
Q

What is the action of Aspirin as an antiplatelet drug?

A

irreversibly blocks platelet COX enzyme - reducing TxA2 synthesis (platelets won’t clump together)
platelets have no nuclei so no new enzyme is synthesised (eg. aggregation reduced)

35
Q

why is only a low dose of aspirin given as a antiplatelet drug?

A 
low dose (75mg) used to avoid reducing enzyme in endothelium (PGI2)
* aspirin alters balance of platelet TxA2 and endothelial PGI2
36
Q

What is the action of Dipyridamole as an antiplatelet drug?

A 
inhibits phosphodiesterase (PDE) enzyme - prevents breakdown of cAMP in platelets (eg. reduces platelet aggregation)
blocks adenosine uptake into platelets, red cells and endothelial cells - inhibits TxA2 synthesis
37
Q

What is the action of Clopidogrel as an antiplatelet drug?

A

inhibits glycoprotein IIb/IIIa receptor expression on platelets
inhibits ADP recetors - blocking activation of the glycoprotein IIb/IIIa pathway (this is the final common pathway for platelet aggregation/ important in cross linking platelets and fibrin)

38
Q

what are fibrinolytic drugs used for?

A

dissolve pre-existing clot or thrombus - most effective in acute/emergency situation (within 6hrs of onset)

39
Q

name four fibrinolytic drugs

A

alteplase
reteplase
urokinase
streptokinase

40
Q

what are the dangers of using fibrinolytic drugs?

A

danger of haemorrhage - clotting factors used up

risk of emboli - fragment could split from thrombus

41
Q

how are fibrinolytic drugs usually administered and why?

A

IV or intracoronary admin as fast acting

42
Q

explain how alteplase works

A

inside thrombus fibrin strands bound to plasminogen
alteplase binds to this complex and converst inactive plasminogen to active plasmin
plasmin then digests fibrin - thrombus dissolves

43
Q

name an anti-fibrinolytic drug

A

tranexamic acid - reduces activation of plasminogen to plasmin

44
Q

when would anti-fibrinolytic drugs be used?

A

when high risk of bleeding - such as bleeding disorders

Pharmacology 1 (11 decks)

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