bleeding tendency for dentist
TRANSCRIPT
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Bleeding tendency
Normal haemostasis
Factors involved in normal
haemostasis
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Bleeding: Clinical Features
Local - Vs - General, spontaneous . . Hematoma & Joint bleed -
Coagulation
Skin/Mucosal Petechiae & PurpuraPLT
wound / surgical bleeding
Immediate - (PLT) Delayed - (Coagulation)
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Hemostasis
BV Injury
Platelet
Aggregation
Platelet
Activation
Blood Vessel
Constriction
Coagulation
Cascade
Stable Hemostatic Plug
Fibrinformation
Reduced
Blood flow
Tissue
Factor
Primary hemostatic plug
Neural
Lab TestsCBC-PltBT,(CT)PTPTT
Plt StudyMorphologyFunction
Antibody
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Primary Hemostatic Disorders
Vascular defect - fragilityPetechiae, purpura, ecchymoses
senile purpura
vitamin C deficiency (scurvy)
connective tissue disorders Osler-Weber-Rendu syndrome -
hereditary malformations
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Senile Purpura
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Primary HemostaticDisorders
Vascular defect - cont.
Infectious and hypersensitivity
vasculitides- Rickettsial and
meningococcal
infections
- Henoch-Schonlein purpura
(immune)
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Primary HemostaticDisorders
Platelet disorders: platelets (thrombocytopenia)
petechiae
spontaneous bleeding after
trauma
CNS bleeding (severe
plt) Platelet dysfunction -
mucocutaneous bleeding
Prolonged bleeding time (BT)
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Bleeding Time Test
Timer is started uponincision
Bleeding time = time
to complete cessationof free blood flow fromincision
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Thrombocytopenia -Causes
Marrow injury/failure- aplastic or myelophthesic
anemia
- drugs, infections
- megaloblastic anemia, PNH
Decreased survival- immune (ITP, drugs,
infections)
- nonimmune (DIC, TTP)
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Idiopathic ThrombocytopenicPurpura (ITP)
Acute - children (post infection)
Chronic - adults ( females, 20-40yrs)- autoimmune disorder
- antiplatelet antibodies (IgG
against plateletglycoproteins)
- IgG coated platelets removed by
spleen ( platelet survival)
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Primary HemostaticDisorders
Platelet dysfunction:Inherited - autosomal recessive Bernard-Soulier disease
- large platelets
- lack of glycoproteins (1b-IXcomplex)
- failure of platelet adhesion
Glanzmanns thrombasthenia
- normal platelet morphology
- lack of glycoproteins (IIb-IIIa
complex)
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Primary HemostaticDisorders
Platelet dysfunction:Acquired - common
Aspirin and NSAID
- cyclo-oxygenase inhibitors
- lack of thromboxane A2 and
PGE- failure of platelet aggregation
Systemic disorders - i.e.
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Primary Hemostatic Disorders
Plasma proteins required foradhesion to subendothelium:
von Willebrand disease
- quantitative or qualitative
deficiency of vWF molecule
- binds to exposedsubendothelial collagen
- mediates initial platelet
adhesion
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Secondary Hemostasis
Consolidates initial plateletplug into stable clot
Disorders - deficiencies of
plasmaclotting factors
Clinical - bleeding from large
vessels into joints(hemarthroses), muscles, deepsoft tissues (hematomas, large
ecchymoses)
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Secondary HemostaticDisorders
Laboratory findings: Normal bleeding time, platelet
count
Prolonged prothrombin time(PT)
deficiencies of II, V, VII, X
Prolonged activated partialthromboplastin time (aPTT)
all factors except VII, XIII
Mixing studies - normal plasma
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Screening Tests of Blood Coagulation
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Factor VIII Deficiency
Classic hemophilia (hemophilia
A)
X-linked disorder (affects 1males)
Most common hereditary
disease with severe bleeding
30% new mutations (not
hereditar
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Factor VIII Deficiency
Classic hemophilia - cont. Clinically severe if
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Factor IX Deficiency
Christmas disease(hemophilia B)
X-linked recessive disorder
Indistinguishable fromclassic hemophilia
Requires evaluation of factor
VIII and IX activity levels todiagnose
Treatment - factor IX
concentrate
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Secondary HemostaticDisorders
Acquired coagulation disorder: Vitamin K deficiency
- neonates - decreased
intestinal
flora and dietary intake
- oral anticoagulants
(coumadin)
- fat malabsorption syndromes
Required for factors II, VII, IX, X
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Combined Primary andSecondary Hemostatic
Disordersvon Willebrands DiseaseAutosomal dominant (or
recessive) Primary defect - platelet
adhesion
(prolonged bleeding time) Secondary defect - deficiency
of factor VIII; normally
stabilizes factor VIII in
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Von Willebrands Disease
Clinical - often mild- excessive bleeding fromwounds- spontaneous bleeding from
mucous membranes Different types - quantity or
loss of selective multimers Diagnosis - ristocetin induced
plt aggregation or multimer
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von Willebrand Factor multimeric analysis
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Combined Primary andSecondary Hemostatic
DisordersDisseminated IntravascularCoagulation
Primary - platelet consumption( bleeding time, platelets)
Secondary - factor consumption
( PT, aPTT) Major pathologic processes -
obstetric complications,
neoplasms, infection (sepsis),
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Disseminated IntravascularCoagulation
Multiple initiating
factorsTissue factorThromboplastic substances
Widespreadendothelial injury
platelet
aggregationActivates extrinsic pathway Activates intrinsic pathwa
Microvascular thrombosis
Clotting factorconsumptionFibrinolysis
plasmin
Fibrin split products Bleeding
Tissue injury,Hemolyticanemia
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Disseminated Intravascular
Thrombosis (DIC)
Acute DIC - bleeding- i.e. major trauma
- give fresh frozen plasma Chronic DIC -
thrombosis
- i.e. cancer
- give heparin or
anticoagulant
C bi d P i d
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Combined Primary andSecondary Hemostatic
DisordersSevere Liver Disease
Primary - dysfunctional platelets
and/or thrombocytopenia ( BT) Secondary - decrease in all
coagulation factors except vWF (PT, aPTT)
Vitamin K will promote synthesis of
factors II, VII, IX, X
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Summary Hemostatic Disorders
BT Plt PTPTT
1
o
hemostasis
-
-
--
2o Factor VIII/IX
deficiency - - -2o Vitamin K
deficiency - -
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Approach to bleeding disordersPersonal history of bleeding
With surgery Tonsillectomy, circumcision
Epistaxis
a
Immediate bleeding after trauma or surgerysuggest platelet or severe protein deficiency.
Bleeding 2-5 days post trauma or surgery suggestplasma protein deficiency .
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Family history
X linked
Autosomal al
* Drug history Oral anticoagulant, Heparin,Aspirin
* Physical examination
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Initial lab works
CBC : Platelet count
PT (INR)APTT
Bleeding time
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Signs and Symptoms of
Coagulation Disorders Bleeding Ecchymoses
Petechiae Hemarthroses
Hematomas
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Petechiae
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Platelets versus Coags
Petechiaeplatelets low or dysfunctional
Ecchymoses, hematomas,
hemarthrosesseen more frequently with
low clotting factors or dysfunction
Bleeding can be seen with either
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Hematom
a
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Hemarthrosis
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Hematom
a
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Management :
Always be on the safe side
Dont do invasive procedures if you are in doubt.
Always check with haematology/ internal medicine.
Check the above tests if normal you can proceed
Remember some cases of bleeding tendency
might go first to you, like AML with gingival hypertrophy.
Always check Drugs
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HEPARIN THERAPY
Enhances activity of AT III
Parenteral administration required
Onset of action immediate
Monitor aPTT
Lower dose may work in patients withoutactive thrombosis
HEPARIN THERAPY
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HEPARIN THERAPYLow Molecular Weight Heparin-
Advantages
Less heterogeneous than heparin
Less inhibition of platelet function Longer half life - Can give 1-2x/day
Much less thrombocytopenia
? safer, equally effective
HEPARIN
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HEPARINLow Molecular Weight Heparin-
Disadvantages
Bleeding-? Less than with heparin
(probably not) Most cross react with heparin RE:
thrombocytopenia
Each preparation is different Less overall experience with the drug
COUMADIN (warfarin)
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COUMADIN (warfarin)Mechanism of Action
Inhibits Vitamin K dependent carboxylase activity
Prevents reduction of Vitamin K
Humans secrete des--carboxyglutamic acid, an
inactive protein DOES NOT AFFECT PROTEINS ALREADY
SYNTHESIZED
Monitor using prothrombin time
Multiple interactions with other drugs
Antidote-Vitamin K
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What do if no help
if INR< 1.5 safe to do procedures, so if
patient on Warfarin , stop Warfarin 2 days
before surgery.
Heparin stop if unfractionated 2 hours before
SX. If low MW Heparin 4-6 hours stop
surgery
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Systemic illnesses can predispose to
bleeding like liver diseases, Chronic renal
failure.
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Depending on the underlying cause
abnormalities of the platelet should be
corrected before any procedure .
How to correct depends on the underlying
cause either with platelets transfusion or
other modalities to increase the count ,like
steroids , IVIg in ITP.
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If on Aspirin please stop Aspirin at least
one week before SX. If urgent please
check bleeding time if prolonged please
give platelets. Which should be 1-2 hourbefore SX.
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For congenital causes of bleeding please
contact haemtology.
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leukaemias
Can predispose to bleeding due to
1- low platelets count
2- DIC
3-Hyerviscosity syndrome.
Oral manifestations of acute leukaemia
Includes : gingival hypertrophy, bleeding ,and ulcers.
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Oral manifestations of leukaemia
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