Haemostasis and coagulation

Question 1

Haemostasis

Answer 1

mechanism of forming a clot

thrombosis is pathological

Question 2

clotting mechanisms

Answer 2

intrinsic: exposed collagen from injured blood vessel wall (test tube has anti-coagulants for when taking bloods
extrinsic: damaged tissue release thromboplastin

Question 3

the amplification cascade

Answer 3

inactive X-> acitve X (thromboplastin, clotting factors (foreign surface))

prothrombin-> thrombin-> XIII (active X)

fibrinogen-> fibrin (thrombin) -> stable fibrin (XIII)

Question 4

Fibrinogen can be used as

Answer 4

CV risk factor
smokers have it raised
pregnancy raised to reduce blood loss during birth

Question 5

Platelets

Answer 5

non- nuclear cellular fragments

Question 6

platelet adhesion

Answer 6

adheres to subendothelial surface on damage/ disease due to binding to von willebrand’s factor (a protein)

Question 7

inactive factor X is a

Answer 7

serine protease

Question 8

factor X is a

Answer 8

serine

Question 9

adhesion causes a release of…

Answer 9

ADP signalling and thromboxane (signalling) promote aggregation
5-HT: vasoconstrictor NT

Question 10

what happens when ADP receptors are activated

Answer 10

glycoprotein IIb-IIa expressed by platelets- enables crosslinking by vWF and fibrinogen-> mesh

Question 11

clot consists of…

Answer 11

coagulated platelet factors and platelets

Question 12

platelet plug promotes

Answer 12

coagulation reaction: -ve phospholipids or activated platelets adhered localise fibrin formation

Question 13

Bleeding time

Answer 13

incisions to forearm with venous cuff

increased in platelet dysfunction and thrombocytopenia

Question 14

Prothrombin time

Answer 14

INR
ttime for coagulation following addition of thromboplastin
see how long to use up
prolonged in abnormality of factors, liver disease and warfarin
liver disease (produces coagulation)

Question 15

activated partial thromboplastin time (APTT)

Answer 15

examines intrinsic pathway, altered in changes of factors

Question 16

when do you use INR

Answer 16

when prescribing warfarin
(healthy is 1)
maybe goes to 2,3

Question 17

Thrombosis

Answer 17

unwanted blood clots

Question 18

atherosclerosis

Answer 18

• Atherosclerosis arteries lined with cholesterol deposits
• Foam cells form beneath endothelium (cholesterol, macrophage) forms fatty streak- gets calcified- atheroma (narrowing artery)- plaque- when ruptures stimulate anti-inflammatory response- platelets form (clot in coronary artery- heart attack, cardiac muscle dies- VF) long term- develop heart failure
• Risk factors accelerate (male- being a female oestrogen tends to protect CV system, smoking, age) high bp- damages endothelium

Question 19

AF

Answer 19

pacemakers around heart set up, random events to ventricles- irregular increase in hr

risk of clots in atria, if in LA-> thromboembolic stroke

risk of TIA- clot from heart to brain- resolves in 24hr

Rx: anticoagulant

Question 20

Haemophilia

Answer 20

genetic- X chromosome

low or lacking factor VIII of clotting cascade

haemorrhage and prolonged bleeding

treat with factor VIII blood donors
or analogue of vasopressin (ADH) sprayed up nose increases VIII release

Question 21

haemophilia B (Christmas disease)

Answer 21

deficiency factor IX- treated with prophylactic factor IX

Question 22

Von Williebrand’s disease

Answer 22

hereditary lack or defect of vWF
impaired platelet reaction
increased bruising, nose bleeds, mucosal bleeding
Rx: vasopressin analogue, factor VIII or vWF

Question 23

Liver disease

Answer 23

reduced synth of clotting time

Question 24

thrombocytopenia

causes

Answer 24

reduced platelet number
spontaneous skin bleeding- purpura
idiopathic
viral
drug induced bruising
toxins

Rx: drug induced- stop and treat with steroids to suppress IR
if unresponsive then splenectomy (spleen is site of platelet degradation)

Question 25

DIC: Disseminated intravascular coagulation

Answer 25

EMERGENCY

large amounts of fibrin generated by
depletes the body of coagulation factors
procoagulant material eg. amniotic fluid
vast consumption of clotting factors and platelets
widespread haemorrhage and thrombosis
give platelets and fresh frozen plasma

Question 26

factor V Leiden mutation

Answer 26

abnormal factor v
SNP
less susceptible to deactivate
increased risk of thrombosis esp with oral contraceptive and pregnancy