16 drugs affecting blood coagulation, platelet aggrgation and thrombolysis Flashcards Preview

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Flashcards in 16 drugs affecting blood coagulation, platelet aggrgation and thrombolysis Deck (36)
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1

haemostasis

prevention of blood loss after an injury that results in vessel damage
coagulation platelet activation and vasoconstriction

2

thrombosis

when blood clots form inappropriately in the wrong places and pathlogical

3

structure of thrombus

fibrin protein framework with aggregated platelets and blood cells embedded within it

4

where does a thrombus begin

lodged to a vessel wall, it can impede blood flow to tissres and reduce their oxygen supply and cause heart attack

5

venous thrombosis

coagulation

6

arterial thrombosis

platelet aggregation

7

embolus

fragment or a whole thrombus detaches from vessel wall and travels through circulation to other tissues
pulmonary embolism, or if in brain a stroke or if in heart a heart attack

8

actue coronary syndrome

unstable angine nstemi and stemi
coronary artery thrombosis

9

how can we classif acs with an ecg

st elevation then this is stemi
if we get st inversion or depression and then blood markers this is nstemi but if no blood markers then its angina

10

treat acs

opioids, reduce cardiac workload (beta blocker and GTN), prevent further thrombosis with aspirin ticagrelor/ clopidogrel, heparins. statins

11

clotting cascade ( coagulation)

damage to vessel to activation of clotting cascade to fibrin to thrombus

12

role of thrombin

converts sluble fibrinogen to insoluble fibrin

13

intrinsic pathway of coagulation cascade

all of the components are rpesent in blood
contact activation - damaged surface

14

extrinsic pathway of coagulation cascade

requires the contribution of factors outside the blood
most important for thrombin formation
tissue factor- trauma

15

heparin - what is it

heparine is an anticoagulant used for venous thrombosis
it is from a family of sulphated mucopolysaccharides
negative charge and repeating groups essential for its activity
unfractionated (injected by IV ) or in low molecular weight (given subcutaneously, can iject self) which is faster and more longer lasting action than unfractionated
risk of haemorrhage if severe give a positively charged protamine which will form a complex with negatively charged heparin

16

action of heparin

inhibits action of thrombin, factors X abd IX
increases the rate by 1000 fold of the formation of the antithrombin III - thrombin complex
heparin binds to both ATIII and IIa
heparin binds to ATIII but not Xa but does sill help increase the strength of binding
LMW heparins only affect Xa (bind to ATIII)

17

warfarin

oral anticoagulant
used in venous thrombo embolisn
prevents stroke in patients with atrial fibrillation
antagonises vitamin K by competitively inhibiting vitamin k reductase which is involved in vitamin K recyclin

18

role fo vitamin K

Important in formation of factors II (prothrombin), VII IX and X
prevents carboxylation of precursors so precursors are inactive in prpomoting coagulation

19

problems of warfarin

slow onset as must reduc existing levels of vitamin k also activity influenced by vitamin k levels
if severe risk of haemorrhage give vitamin k or clotting factors
teratogenic - causes birth defects

20

drugs that increase the enzymes responsible for metabolising warfarin will increase or decrease its effects

decrease

21

drugs which compete with warfarin for the same protein binding sites will increase of decrease its effects

increase because higher conc of free warfarin in the blood

22

dabigatran

direct inhibitor of thrombin and does not require monitoring like warfarin

23

rivaroxaban

inhibitor of factor Xa

24

describe how platelets can form a thrombus

damage to vessel
platelet adhesion activation and aggregation

25

platelets

cell fragments in the blood

26

describe in detail the process of platelet aggrgation

triggered by tissue damage that exposes glycoproteins that arrent normally on the surface of blood vessels .
protein within the connective tissue eg collagen will bind to the glycoprotein receptors on the urface of platelets , platelet then undergoes shape change and becomes activated
releases TXA2 and ADP which will activat surrounding platelets and then express a different glycoprotein receptor on its surface that wilkl be abke to bind with fibrinogen

27

thromboxane A2

relased from platelets, activates other platelets by enhancing expression of glycoprotein IIb and IIIa receptors. other platelets activate, get chain reaction and platelets become cross linked by fibrinogen
increases platelet aggregation by decreasing levels of cAMP

28

prostacyclin

ihbiits activation stops chain reaction from preading
decreases platelet aggregation by increasing levels of cyclic AMP

29

how is TXA2 and \pgi2 formed`

membrane phospholipids cleaved by arachidonic acid and then cox enzyme comes into play with prostaglandin endoperoxides which then synthesis thromboxane and prostacyclin

30

aspirin

antiplatelet drug
irreversibly blocks the platelet COX enzyme so reduces thromboxane synthesis
we use low doeses to avoid reducing the cox enzyme in the endotheliumas this is also the source of prostacyclins