Blood Disorders Flashcards
coagulation cascade
series of reactions catalysed by protein enzy,es known as coagulation factors
steps in response to bleeding, to clot the blood and stop bleeding
extrinsic coagulation cascade
response to tissue damage/factors
factor 7 - 7a
intrinsic coagulation cascade
response to triggers from the blood
collagen triggers this
1 - 1a, 8-8a for stable clot
antithrombotic medicine
injectable - herapin
oral anticoaugalnt - courmarin
antiplatelet - asprin
injectable drugs
usually temporary
unfractioned heparin, low molecular weight heparin
unfractioned heparin
injected, infusion, active for few mins
rapid control, rapid onset
inhibits antithrombin3
hospital based tx
low molecular weight heparin
given subcutaneous injection
stops clotting without increase bleeding risk
uncomfortable to administer
no dental issue
oral anticoagulants
interfere with coagulation cascade
warfarin, apixaban, edoxoban, rivaroxaban, dabigatran
oral antiplatelets
interfere with platelet numbers/function
low dose apsirinm clopidogrel, dipyramidole,abciximab
safe dental care with no drugs being a risk
hygiene therapy, RPD, restorative, endo, ortjo
caution dental care - big risks
extractions, minor oral surgery, implants, periodontal surgery
indications for anticoagulation
conditions wjere blood clots form
atrial fibrillation, deep vein thrombosis, heart valve disease, mechanical heart valves, thrombophilia
types of anticoagulants
coumarins - warfarin
indanediones - phenindione
direct thrombin inhibitor - dabigatran
factor 6a inhibitor - apixaban, rivaroxaban
warfarin is a
anticoagulant, vitamin K agonist, interferes with action of VitK and changes syntehsis of clotting factors
2, 7, 9 , 10
warfarin onset
slow, 2-3 days
initial hypercoagulability due to protein C + S inhibition [immediately]
increased coagulation risk initially, may be on heparin in hospital
if stopping, when starting again, pulmonary embolism risk
warfarin + INR
normal 2-3 if on anticoagulant
3-4 in prosthetic valve, higher risk of DVT
checked every 4-8 weeks,
INR
measurement of how long it takes for blood to clot
not always well controlled, foods and medicines can interact with warfarin and upset INR
warfarin + dental px
cause prolonged bleeding, haemorrhage
INR and bloof test 72hrs of tx
early in day, early in week
local haemostatic measures - sutures, cellular sponge, LA infiltration
post op instructions, contact number
drug interactions w warfarin
potentiating drugs = increase INR
- amiodarone, antibiotics, alcohol, NSAIDs [no ibu]
inhibiting drugs = decrease INR
- carbamazepine
avoid prescribing for px on warfarin
aspirin, NSAIDs, azole antifungals [fluconazole]
need to monitor INR, GP
hazards taking warfarin
haemorrhage, 1% risk of bleed, 25% fatal
due to trauma like fall, serious if older
soft tissue injury - bleeding into muscles
rapid reversal of vitK agonist possible in hospital
new oral anticogulants
to resolve issues of warfarin
- dont need to monitor aciton, predicatable bioavailability
- rapid onset of action, 1hr
- short duration of action, 1 day
- short tx
- reversable agents for severe bleeding/trauma
good for those rurally
how do new oral anticoagulants work and examples
prevent factor Xa
- rivaroxaban [1x daily]
- apixaban [2]
- edoxaban [1]
- diabigatran [1]
dental tx and NOACs
assess bleeding risk, early in day, limit initial tx
if high risk - miss/delay morning dose
restart immediately
haemostatic measures
keep 20 mins after to assess bleeding
NOAC drug interactions
safe with antibiotics except erythromycin
safe with antifungals, LA, antivirals
AVOID NSAIDS, CARBAMEZEPINE
antiplatelets
stop platelet aggregation
antiplatelet standard therapy
low dose aspirin 75mg
clopidogrel
dipyridamole
antiplatelets in clinical practice
inhibits platelet aggregattiom, inhibits thrombus formation in arterial medication
local haemostatic measures
dual therapy
non-aspirin single therapy, dual therapy with aspirin
do nto interrupt tx, expect prolonged bleeding, haemostasis
if 2 antip without aspirin
discuss w doctor
post op and contact no
antiplatelets + dental drug interactions
avoud NSAIDs if poss
clopidogrel = erythromycin/fluconazole reduce efficacy
ticagrelor = claeithromycin
carbamazepine / omperazole reduce efficacy
inherited bleeding disorders
an acquired defect which affects the coagulation of bloof
affects - coagulation cascade, platelets
haemophilia
too little clot formed
thrombophilia
too much clot formed
disorders reducing coagulation factors
factor VIII defiency
haemphilia A
factor IX deficiencu
haermphiia B
von willebrands
reduced factor VIII, redued platelet aggregation
haemophilia A + B
inheritance, sex linked recessive gene
defective X chrmosome, males affected, females carrier
severity depnds of amount of factor produced
haemophilia iu
international unit
1iu is normal
carrier 0.5iu
severe = <0.02
mod = 0.02-0.09
mild - 0.1-0.4
haemophilia A
deficiency in factor 8
haemophilia A management
severe/mod
- recombinant factor 8
mild/carriers
- DDAVP, oral tranexamic acid
DDAVP
desmopressin, releases factor 8 which has been bound to endothelial cells, temporary boost to f8 levels and clotting abiluty
doesnt itself have effects of coagulation cascade, cannot be used reguarly as only displaces those on wall, wont work
tranexamic acid
inhibitor of fibrinolysis, keeps any clot that is formed
same effect as increasing f8 in blood
haemophilia B
chrtistmas disease
deficiency of factor 9 IX
management of haemophilia B
severe/mod
mild/carriers
- recomvinant factor 9
- no alternative
coagulation factor inhibitors
antibodies which develop to f8 and 9
antibody response produced
give new drugs infrequently
each dose has to be higher to overcome inhibitors from previous dose
von willebrand disease
factor 8 problem associated w platelet issues
high incidence
poor clot activty
autosomal dominant, bothh sexes equally effected
type1/2 mild, tpye 3 severe
management of von willebrands
severe/mod
- DDAVP
mild/carriers
- oral tranexamic acid
haematologist advice, tailored tx
rare bleeding disorders
hard to characterise, defects of other factors in coagulation cascade
management of px w bleeding disorders
high degree factor activty, low rik
assess risks, location of tx may need to be done in hospital or sepcialist
haemophilia dental care managing
sev/mod - haemophilia centre
mild/carrier - dpenedent on procedure, review at haem centre every 2 years
which procedures require special care for haemphilia px
administration of LA, extractions, minor oral surgery, periodontal surgery, biopsies
LA safe or danger in haem px
safe - buccal infiltration, intraligamentary, intrapapillary
danger - inferior alveolar nerve block, lingual infiltration , posterior superior nerve block
most important aspect of care w those w bleeding disorders
PREVENTION
OHI, regular dental visits, fluoride, sealants, dietary advice, smoking cessation
thrombophilia
increased risk of clot development, greater than clot breakdown
acquired imposed on genetic tendency
can lead to blockage of major blood vessels in heart/lungs
thrombophilia inherited syndromes
inherited - protein C/S deificency, factor V leiden, antithrombin III deficiency
acquired - antiphospholipid syndrome lupus, oral contraceptive, trauma, cancer, pregnancy
thrombocytopenia
low number of normal platelets
drug related - alcohol, penicillin
thrombocythemia
high number of poor functioning platelets
qualitative platelet disorders
normal platelet number but abnormal function
inherited - hermanksy, bernaer soulier syndrome
acquired - cirrhpsis, drigs, alcohol
dental care + platelet disorders
no additonal precaution
greater than 100x109/L
platelet count and place of dental care
below 100x109/L = primary care
below 50x109/L = hospital
above 500x109/L = either
special care for - extractions, periodontla surgeyr, oral surgeyr
