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Flashcards in Dixon coagulation disorders Deck (30):
1

what types of thromboembolic diseases are there

thrombosis
thrombus
embolus

2

definition of thrombosis

inappropriate in vivo clot

3

definition of thrombus
difference between arterial and venous thrombosis

fixed clot in unbroken blood vessel

arterial thrombosis: platelet plug
venous thrombosis: coagulation

4

definition of embolus,

solid mass that travels in blood stream

5

which is most dangerous? thrombus or embolus?

embolus as it can cause a pulmonary embolism (blood clot stuck in lung), brain aneurysm (clot to the brain)

6

what are the contributing processes to a thromboembolic disease

injury to blood vessel wall
altered blood flow
abnormal coagulation

7

what are predisposing factors for a thromboembolic disease

atherosclerosis
blood stasis
cardiovascular prosthetic device
oestrogen containing oral contraceptives

8

examples of thromboembolic disorders/diseases

myocardial infarction
stroke/transient stroke/ischaemic attack (mini stroke)
pulmonary embolism
DVT

9

what kind of drugs can manage thromboembolic diseases

anticoagulats drugs
antiplatelets drugs
fribrinolytic agents

10

indications of anti coagulants?

DVT, pulmonary embolism, prevention of stroke in patients with atrial fibrillation

11

discuss unfractionated heparin

rapidly effective anticoagulant drug
given via continuous IV infusion
it reduces thrombin induced platelet activation (high doses)
decreases fibrin formation (low dose)
inhibits in vivo and in vitro blood clotting
overdose of heparin treated with protamine
will be used along with warfarin until warfarin takes effect in body

12

what is the mechanism of action of unfractionated heparin

increases effectiveness of anti thrombin 3 on serine protease coagulation factors

heparin must bind to both the coagulation enzyme (thrombin) and AT3, whereas binding to the enzyme is not required for inhibition of factor Xa

inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin-induced activation of platelets and of factors V and VIII.

13

mechanism of low molecular weight heparins

doesn't effect thrombin activity
greater bioavailability than unfractionated heparin
longer half life too

binds to AT3, binding to the enzyme is not required for inhibition of factor Xa

14

discuss vitamin K antagonists

e.g. warfarin

it inhibits the reduction of vitamin K by inhibiting vitamin k reductase. (reduced vit K is needed to mature clotting factors in liver)
in vivo only
long onset of action
must be monitored
overdose can be treated with vitamin K and coagulation factors

warfarin may produce transient paradoxical pro coagulant effect due to reducing vit C before reduction of clotting factors

15

drawbacks of using warfarin

slow onset of action - heparin is used until it starts
many drug interactions
monitoring requirement
side effects: haemorrage in nose, pharynx, gi and urinary tracts

16

what are the newer direct acting oral coagulants?

dabigatrin - direct thrombin inhibitor

rivaroxaban - factor 10a inhibitor

17

indication for antiplatelet drugs

secondary prevention of myocardial infarction

18

discuss COX inhibition (as seen in aspirin)

irreversible inhibition of COX1

arachidonic acid is prevented by COX inhibitors into converting to cyclic endoperoxides

causes reduction in prostacyclin and TXA2 productioni

endothelial cells can synthesis new COX1 but platelets are unable to as they lack a nucleus

19

discuss prostacyclin analogues

examples: iloprost and epoprostenol

mimics action of prostacyclin

20

what drugs target GP2b/3a receptor system, examples and side effects

1) inhibitors of ADP-induced GP2b/3a receptor activation e.g. clopidogrel, ticagrelor
side effects: bleeding, nausea, neutropenia

2) GP2b/3a receptor antagonist e.g. tirofiban, abciximab
side effects: bleeding

21

discuss fibrinolytic drugs

example: streptokinase
treatment of acute life-treatening thromboembolic disorders e.g. myocardial infarction
promotes formation of plasmin = promotes clot lysis

synthetic versions of endogenous tissue plasminogen activator (tpa) e.g. alteplase, reteplase, tenecteplase
selective for plasminogen bound to fibrin within clots
requires intravenous infusion
tenecteplase and reteplase - Intravenous injection

22

types of coagulation deficiencies

haemophilia
von willebrands disease
vitamin k deficiency

23

discuss the different types of haemophilia

type A: factor 8 deficiency (most common)
type B: factor 9 deficiency
type C: factor 11 deficiency

24

what are symptoms of haemophilia

excessive bleeding, easily bruised, haematomas

25

treatment for haemophilia

administration of missing factor

26

discuss von willebrands disease

deficiency of von willibrands factor = decrease in platelet adhesion

increase tendancy to bleed - in many cases asymptomatic

27

how is von willebrands disease treated

vasopressin analogue, desmopressin, stimulates release of von willebrand's factor from endothelial cells

28

discuss vitamin k deficiency

present in green veg, synthesised by gut flora
needed for synthesis of factor 2, 7, 9, 10 and protein c

causes: lack of gut flora, malnutrition, reduced fat absorption, overdose of warfarin

29

how to treat vit k deficiency

vit k supplements

30

how to treat excessive haemorrhage

dental, menstruation, haemophilia, von willebrand's disease

drug treatment: various anti-fibrinolytics e.g. aprotinin: inhibits plasmin, used before open heart surgery
tranexamic acid: inhibits plasminogen activation