coagulation

Question 1

what is the intrinsic coagulation pathway activated by?

Answer 1

exposed endothelial collagen

Question 2

what is the extrinsic coagulation pathway activated by?

Answer 2

external factors damage the endothelial cells which then release factors such as thromboplastin to activate the extrinsic pathway.

Question 3

what are the main steps in the clotting cascade?

Answer 3

extrinsic and intrinsic going to activate factor 10.
factor 10 acts as the enzyme to turn prothrombin into thrombin.
thrombin acts as the enzyme that turns fibrinogen into fibrin.
fibrin turns into stable fibrin to form the clot with the help of factor 13.

Question 4

what are the 3 reactions that happen after the blood vessel wall is damaged?

Answer 4

the adhesion reaction,
the release reaction,
the coagulation reaction

Question 5

what happens during the adhesion reaction of the mechanical plug process?

Answer 5

the platelets sticks to the subendothelial layer due to binding of VMF.

Question 6

what happens during the release reaction of the mechanical plug process?

Answer 6

the endothelial cells release ADP and thrombin, to start platelet aggregation.

Question 7

what happens during the coagulation reaction of the mechanical plug process?

Answer 7

platelets are activated, they have negative charged phospholipids on their surface which bind to damaged site and they localise fibrin formation.

Question 8

what is thromboplastin?

Answer 8

released b extrinsic pathway.

Question 9

what does INR measure?

Answer 9

this measures the time between thromboplastin release (extrinsic pathway activated) and the coagulation reaction.

Question 10

what does a longer INR (prothrombin time) suggest?

Answer 10

a problem with the clotting cascade.

Question 11

what other problems does atrial fibrillation cause?

Answer 11

clots could form in the left atrium and break off and go to the Brian and cause a cardioembolic stroke.
if the clot is in the right atrium then it could break off into the lungs and cause a pulmonary embolism.

Question 12

what are the common atherosclerotic sites?

Answer 12

abdominal aorta, coronary arteries, carotid argues

Question 13

what is the difference between clotting and coagulation.

Answer 13

coagulation is the formation of fibrin.

clotting is both coagulation and platelet action.

Question 14

why does the dose of warfarin need to be individualised to the patient?

Answer 14

as the metabolism of each patient is different due to SNPs so if a patient has low clearance rates, the dose needs to be lower.
of the patient has a high clearance rate the dose of warfarin needs to be higher.

Question 15

what does the warfarin target?

Answer 15

if targets the vitamin K reductase.

Question 16

what is warfarin resistance in a person?

Answer 16

the target, vitamin K reductase, can have resistance to the binding warfarin so you will need a higher dose of warfarin to have the safe effect.

Question 17

what is a prodrug?

Answer 17

the drug is inactive and needs to be metabolised into its active form.

Question 18

what does the cytochrome p450 do?

Answer 18

it is a superfamily of enzymes in the liver, which metabolises different drugs using different pathway.

Question 19

what are drug inhibitors or drug inducers?

Answer 19

inhibitors are drugs that slow the metabolism of another drug.
inducers are drugs that speed up the metabolism of another drug.

Question 20

how does the drug interaction of inhibitors work?

Answer 20

the drug inhibits the cytochrome p450 which stops it from metabolising the other drug.

Question 21

how does the drug interaction of inducers work?

Answer 21

the drug can increase the number of cytochrome p450 present so the metabolism of another drug with increase .

Question 22

if drug1 is a cytochrome p450 inducer, how will the dose of drug2 need to be adjusted?

Answer 22

as the metabolism of the drug is increased, the clearance of the drug is increased.
so if the patient will need a higher dose to have the same effect.

Question 23

if drug1 is a cytochrome p450 inhibitor, how will the dose of drug2 need to be adjusted?

Answer 23

the metabolism of the other drug will be reduced so the clearance of drug2 is reduced so the patient will need a lower dose otherwise the concentration may be toxic.

Question 24

why shouldn’t you use both macrolides/quinolones and warfarin?

Answer 24

the macrolides/quinolones can increase the INR and inhibit the warfarin

Question 25

why should you not take NSAIDs and warfarin together?

Answer 25

NSAIDs (like aspirin) are anti platelets so increase bleeding, and warfarin stops clots forming so there is a big risk of uncontrollable bleeding.

Question 26

what does clopidogrel do?

Answer 26

it is a prodrug anti platelet.

Question 27

what does beta blockers do?

Answer 27

inhibits adrenaline ect to slow down heart and reduce blood pressure.

Question 28

why can’t you use a beta blocker and salbutamol?

Answer 28

salbutamol is a beta2 agonist, whereas beta blocker is a beta 2 antagonist. so the beta blocker will inhibit the action of salbutamol.

Question 29

what are the key drug interactions to avoid?

Answer 29

warfarin and macrolides/quinolones (antibiotics) as rick of uncontrollable bleeding
warfarin and NSAIDs (aspirin) as risk of increased bleeding
simvastatin (a statin) and macrolides.