dental management of haemostatic problems

Question 1

coagluation steps

Answer 1

• conversion of soluble proteins in blood into final polymer that is insoluble
• coagulation cascade
• positive feedback mechanisms
• one protein promotes production of another …
• final protein leads to polymerisation of a fibrinogen into fibrin (non soluble)

Question 2

pathways of coagluation

Answer 2

extrinsic

intrinsic

Question 3

extrinsic coagluation pathay

Answer 3

• set off by subendothelial tissue

Question 4

intrinsic coagulation pathway

Answer 4

• APTT
• inside a vessel
• triggered by rupture to the endothelial trauma, cells release phospholipid

Question 5

measring coagulation

Answer 5

Blood collected in citrate

• this chelates Ca2+
• Ca2+ is a clotting factor IV, required for both intrinsic and extrinsic pathways
• therefore if you take it away blood can no longer clot

Question 6

prothrombin time measures

Answer 6

extrinsic pathway

Question 7

warfarin does

Answer 7

• these are important as warfarin inhibits II, VII, IX and X

- stops coagulation

Question 8

INR

Answer 8

• Ratio of patients PT: normal PT

Question 9

APTT (activated partial thromboplastin time) and what does it measure

Answer 9

• phospholipid, silica and Ca2+ added to sample to trigger coagulation cascade
• time how long to clot formation
• measures intrinsic pathway and also final common pathway

Question 10

which factors related to haemophilia and what indicates it

Answer 10

8 and 9

- if APTT is raised and INR is normal may indicate haemophilia

Question 11

causes of haemostatic problems

Answer 11

1) congenital bleeding disorders

2) acquired bleeding disorders

Question 12

congenital disorers

Answer 12

haemophilia

Von willebrands

Question 13

von willebrands

Answer 13

• shortage of VWBF
• important in platelet adhesion, lack of the factor causes a deficiency in platelet function (increased bleeding time, marker of platlet function)
• aka factor 8 VWF bind to factor 8 to stop breakdown in the blood
• important as a factor for supporting and preventing the breakdown of factor 8 (increased APTT)

Question 14

liver involemtn

Answer 14

production of most coagulation factors

Question 15

what can the liver be comprimised by

Answer 15

jaundice
cancer
paracetamol overfose

Question 16

kidney disease influence

Answer 16

prolonged bleedimg tiem

Question 17

drugs affecting bleeding

Answer 17

1) Warfarin
2) Aspirin
3) Clopidogrel
4) Heparin

Question 18

asprin

Answer 18

causes irreversible inactivation of COX within platelets

effect within the hepatic portal vien

Question 19

arachidonic acid pathwat

Answer 19

part of inflam cascade

- acid turns into no of inflammatory mediators

Question 20

what does asprin do

Answer 20

kill pain

Question 21

how does asrpin work

Answer 21

inhibits prostaglandins production effect

• anticoagulant effect is through inbibition of thromboxane A2 production o
• platelets are like packets of thromboxane A2 and when they rupture it released thromboxin A2 and causes other platlets to come into the area and pop – positive feedback then forming a platlet clog

Question 22

which factros are driven to active factors for coagulation cascade

Answer 22

2 7 9 10

Question 23

which enzyme does warfarin block

Answer 23

vit K epoxide reductase

therefore cannot cyle back to vit K

Question 24

how to reverse warfain effect

Answer 24

create vit K excess

Question 25

what does vit k convert to to activate factors

Answer 25

vit K epoxide

Question 26

heparin binds to

Answer 26

antithrombin 3

Question 27

what does heparin do

Answer 27

Anticogulent
Binds to and activates antithrombin 3, therefore has a bigger effect
- this inhibits factors 10 and 2 of final common pathway
- inhibits coagulation cascade
- therefore less effect of friborgen to fibrin

Question 28

how to reverse heparin

Answer 28

protamine sulphate

Question 29

clopidogrel

Answer 29

P2Y12 inhibitor (involved in platelet aggregation and linking to the fibrin meshwork)

Question 30

avoiding a haemorrage for warfinised patient

Answer 30

chekc INR within 72 hhours
INF less than 4
avoid ID block where possiible

Question 31

avoiding a haemorrage for thosse on antiplatelets

Answer 31

• monotherapy – continue as planned (i.e. on one medication)
• multiple (eg asprin and clopidogrel)
• no evidence of increased bleeding risk but may consider hospital based treatment

Question 32

haemophilia avoiding a haemorrage

Answer 32

• liase with haematologist
• DDAVP (releases bodys stores of factor 8 into body)
• recombinant factor VIII/IX
• mild may need no preoperative management

Question 33

types of heamorrage

Answer 33

primary
reactonary
secondayr

Question 34

primary haemorrage

Answer 34

• as soon as tooth removed

- will be due to bleeding disorder or local cause

Question 35

secondary haemorrgae

Answer 35

• not immediate, but within 48 hours of extraction

- don’t ETOH, exercise, heat, anaesthetic wearing off (due to adrenaline wearing off)

Question 36

secondary haemrrahge

Answer 36

pproximately 1 week after surgery due to infection

Question 37

potentail sources of bleeding

Answer 37

bone

gingivae

Question 38

packing of woud

Answer 38

1) Surgicel
- resorbable oxidised cellulose
- helps clot form
2) Gelatin sponge
- absorbs up to 45 times own weight in blood
- pressure tamponades bleed

Question 39

what does sutring do

Answer 39

comprress gingival blood supply

Question 40

ongoing bleed

Answer 40

1) Tranexamic acid
2) may need reversal of anticoagulant (if possible)
- Warfarin (omit/vit K)
- Heparin (omit/protamine sulphate)

Question 41

4 measures to deal with haemorrhage from a dental socket

Answer 41

pressure/bite on gauze
stich
pack transexaminc acid

Question 42

how does DDAVP ac

Answer 42

induces relese of actor 8 from vascular endothelia into the cicualtion

Question 43

other names for DDAVP

Answer 43

desmopressin
synthetic vasopressin
synthetic ADH

Question 44

which part of coagualtion cascade inhibite by warfarin

Answer 44

all