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pharmacology 2 > drugs and stroke > Flashcards

drugs and stroke 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 drugs are used to modify coagulation?

A

heparins (anticoagulants)

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13
Q

is heparin present in the body naturally?

A

yes - present in lungs, liver and mast cells

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14
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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15
Q

name three low MW heparins

A

enoxaparin
dalteparin
tinemaparin

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16
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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17
Q

what are some of the disadvantages to using heparin?

A

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

risk of haemorrhage

18
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)

19
Q

name a commonly used oral anticoagulant

A

warfarin

20
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

21
Q

what are the problems associated with warfarin?

A

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

22
Q

what is the INR target for recurrent DVT?

A

3.0 (2.5-3.5)

23
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

24
Q

can warfarin be used during pregnancy?

A

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

25
Q

how can warfarin interact with other drugs?

A

enzyme induction - eg. carbamazepine

enzyme inhibition - eg. cimetidine

26
Q

name four thrombin inhibitors

A

Rivaroxaban (Xarelto)
Dabigatran (Pradaxa)
bivalirudin
lepirudin

27
Q

what is the target for Rivaroxaban?

A

inhibitor of Factor Xa

28
Q

what is the target for Dabigatran?

A

thrombin inhibitor

29
Q

what happens when platelets are activated?

A

the platelets form ‘legs’ which stick to other platelets

30
Q

explain the process of platelet aggregation

A 
vessel damaged
collagen exposed
platelets bind here and are activated
increased synthesis of TxA2increased GPIIb/IIIa receptors expression on platelet
platelets aggregate
31
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
32
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

33
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)

34
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

35
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

36
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)

37
Q

what are thrombolytic agents used for?

A

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

38
Q

name four thrombolytic agents

A

alteplase
reteplase
urokinase
streptokinase

39
Q

what are the dangers of using thrombolytic agents?

A

danger of haemorrhage - clotting factors used uprisk of emboli - fragment could split from thrombus

40
Q

how are thrombolytic agents usually administered and why?

A

IV or intracoronary admin as fast acting

41
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

pharmacology 2 (11 decks)

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