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Cardiovascular > Pharmacology- clots > Flashcards

Pharmacology- clots Flashcards

1
Q

what is haemostasis

A

arrest of blood loss from a damaged vessel

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2
Q

what is exposed when a vascular wall is damaged

A

collagen and tissue factor (thromboplastin)

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3
Q

what happens in primary haemostasis

A

platelet adhesion, activation and aggregation (by fibrinogen)

local vasoconstriction

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4
Q

what is the final step of haemostasis

A

activation of blood clotting and the formation of a stable clot by fibrin enmeshing platelets

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5
Q

what do activated platelets release

A

thromboxane A2 which causes mediator release (serotonin (5-HT) and adenosine diphosphate (ADP)) and vasoconstriction

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6
Q

what does ADP do

A

binds to platelet GPCR purine receptors causing;

  • further platelet activation
  • formation of soft plug
  • initiate coagulation of blood and solid clot formation
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7
Q

what converts fibrinogen to fibrin in order to form a solid clot

A

thrombin

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8
Q

what is thrombosis

A

a haematological plug in the absence of bleeding

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9
Q

describe aterial thrombus

A

(white) mainly platelets in fibrin mesh

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10
Q

where do aterial embolis often lodge

A

in brain

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11
Q

what is the primary treatment of arterial thrombus

A

antiplatelet drugs (block aggregation and activation of platelets)

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12
Q

describe the components of a venous thrombus

A

(red) fibrin rich

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13
Q

where do venous embolis often lodge

A

in lung

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14
Q

what is the primary treatment of venous thrombus

A

anticoagulants

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15
Q

name six anticoagulants

A

warfarin, rivaroxiban, heparin, LMWH, dabigatran, fondaparinux

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16
Q

what is the role of vitamin K

A

mediates enzymes producing clotting factors II, VII, IX and X (precursors of active clotting factors e.g. thrombin= IIa)

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17
Q

what do all anticoagulants carry a risk of

A

haemorrhage

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18
Q

how does warfarin work

A

competes with vit k to bind, preventing production of active clotting factors and coagulation

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19
Q

how is warfarin administered

A

orally

20
Q

what is the half life of warfarin and why is that important

A

usually 40 hours (variable)- if patient needs op

21
Q

how is the overdosage of warfarin treated

A

with administration of Vit K

22
Q

why does warfarin have a low therapeutic index

A

as hard to balance anticoagulant effect and haemorrhage. use complicated by delay to maximal effects and several medical and environmental influences

23
Q

what can increase risk of haemorrhage with warfarin

A

liver disease (decreased clotting factors), high metabolic rate (increased clearance of clotting factors), drug interactions

24
Q

what factors can lessen warfarin action

A

physiological state (pregnancy, hypothyroidism), vitamin K consumption, drug interactions

25
Q

what is antithrombin III

A

an important inhibitor of coagulation which neutralise all clotting factors (a.k.a serine protease factors) in the coagulation cascade

26
Q

what binds to antithrombin III to increase its affinity for clotting factors

A

heparin- greatly increases rate if inactivation

27
Q

name two low molecular weight heparins

A

enoxaprin and dalteparin

28
Q

how do LMWH’s work

A

inhibit factor Xa (not thrombin)

29
Q

how is heparin administered

A

IV or SC

30
Q

how are LMWHs administered

A

SC

31
Q

why is heparin preferred in renal failure

A

as LMWH is eliminated via renal excretion

32
Q

what are the adverse effects of heparin and LMWH

A

haemorrhage (and rarely…), osteoporosis, hypersensitivity reactions

33
Q

how do orally active inhibitors work

A

inhibit thrombin or factor Xa

34
Q

what is TXA2

A

thromboxane A2, is released from activated platelets

35
Q

how does aspirin work

A

irreversibly blocks cycloxygenase in platelets, preventing TXA2 synthesis

36
Q

what is the main adverse effect of

A

gastrointestinal bleeding and ulceration

37
Q

what is clopidogrel and how/ when is it used

A

anti-platelet drug, orally, in patients with aspirin intolerance

38
Q

what happens when clopidogrel and aspirin are combined

A

have a synergistic effect

39
Q

what is tirofiban and how/ why is it administered

A

antiplatelet drug, IV, prevents MI in patients with high risk unstable angina

40
Q

what is the role of the fibrinolytic cascade

A

opposes the coagulation cascade

41
Q

when are fibrinolytics used

A

to reopen occluded arteries in acute MIs or stroke (less frequently venous thrombosis/ PE)

42
Q

how are fibrinolytics administered

A

IV, and have beneficial effect with aspirin

43
Q

what is streptokinase and why is it used

A

fibrinolytic drug, reduces mortality in MI

44
Q

what are alteplase and duteplase

A

recombinant tissue plasminogen activators, fibrinolytic drugs

45
Q

how are alteplase and duteplase administered and what is their main side effect

A

iv infusion, haemorrhage- controlled by tranexamic acid which inhibits plasminogen activation

Cardiovascular (34 decks)

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