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Contents
Haemostasis
Vascular Phase
Platelet Phase
Clot formation
Clot retraction
Fibrinolysis
Bleeding Disorders
Diagnosis of bleeding disorders
Clinical implication in periodontology
Haemo
stasis
Haima + Stasis
Prevent blood
loss
Maintains blood flow
Prevents bleeding
• Stages of Hemostasis
Vascular Phase
PLATELET Phase
•1,50,000 to 400,000 per cu mm
Lifespan is 9 – 12 days
• Thrombocyte = “ thrombos” + “ Kytos”
Platelets
• Membrane
• Outer glycocalyx layer—
glycoproteins
• Inner lipoprotein layer—
phospholipid
Platelet PLUG
Blood coagulation
Role of thrombin
Fibrin formation
SEM of clot
• Release of fibrin stabilizing factor
• Contractile protein of platelets
• Activated and accelerated by thrombin
and Ca ions.
ROLE OF ENDOTHILIUM
Approach to the diagnosis of bleeding
disorder
Clinical Evaluation
History
Physical Examination
Family history
Laboratory Evaluation
Screening test
Specific test
Clinical Features of Bleeding Disorders
Platelet disorders Coagulation
disorders
Site of bleeding Skin Deep in soft
tissues
(epistaxis, gum, Mucous
vaginal, GI tract) membranes,
joints, muscles)
Petechiae Yes No
Ecchymoses (“bruises”) Small, superficial Large, deep
Hemarthrosis / muscle bleeding Extremely rare Common
Bleeding after cuts & scratches Yes No
Bleeding after surgery or trauma Immediate, Delayed (1-2
days),
usually mild often severe
Platelet Coagulation
Petechiae, Purpura Hematoma, Joint bl.
Tests for Primary Hemostasis
• Bleeding time platelet & vascular phases
• PFA – 100 system Platelet function
• Platelet count Quantification of platelets
• Blood smear Quantitative & morphological
abnormalities of platelets ,
Detection of underlying
haemotological disorder
Tests for Secondary hemostasis
• Clotting factor Crude test of coagulation phase
• Prothrombin factor Extrensic & common pathway
• Activated partial
thromboplastin time Intrensic & common pathway
PLATELET COUNT
 NORMAL 150,000 - 400,000 CELLS/MM3
< 100,000 Thrombocytopenia
50,000 - 100,000 Mild Thrombocytopenia
< 50,000 Sev Thrombocytopenia
BLEEDING TIME
 PROVIDES ASSESSMENT OF PLATELET COUNT
AND FUNCTION
NORMAL VALUE
2-8 MINUTES
PROTHROMBIN TIME
 Measures Effectiveness of the Extrinsic Pathway
 Measures the activity of V, VII, X, II , I
NORMAL VALUE
11-16 SECS
Prothrombin time prolongs..
Extrinsic pathway factor deficiencies
(FII, V, VII, X)
– Inherited or acquired
– Consumption (DIC)
– oral anticoagulant therapy
INR
INR: International normalized ratio
-was established by the WHO and the International Committee on Thrombosis
and Hemostasis for reporting the results of prothrombin tests
-All PT results are standardized by this calculation:
INR= ( Patient PT / Control PT)ISI
ISI= International sensitivity index
- Given by the manufacturer for each particular thromboplastin reagent and
instrument combination
ACTIVATED THROMBOPLASTIN TIME
 Measures Effectiveness of the Intrinsic
Pathway & common pathway
NORMAL VALUE
25-40 SECS
APTT prolongs..
1. Intrinsic pathway factor deficiencies (FXII, XI,VIII, IX, HMWK,
prekallikrein )
- Inherited or acquired
- Consumption (DIC)
- PIVKA factors in cumarin therapy
2. Specific inhibitors against FXII, XI, VIII, IX, HMWK, prekallikrein
3. Lupus anticoagulant
4. Non-fractionated heparin therapy
THROMBIN TIME
 Time for Thrombin To Convert
Fibrinogen Fibrin
 A Measure of Fibrinolytic Pathway
NORMAL VALUE
9-13 SECS
TT Prolongs..
1. Hypo- afibrinogenaemia
2. Dysfibrinogenaemia
3. Non fractionated heparin
4. Fibrinogen/ fibrin degradation product s
5. Chronic liver disease
SPECIFIC TESTS
Tests for specific Platelet Functions
1. Platelet aggregration test
2. Flow cytometry
3. Test for platelet secretion
4. Clot retraction test
5. Platelet procoagulant activity
Test for Coagulation Phase
1. Quantitative estimation of Fibrinogen
2. Coagulation factor assays
3. F XIII Qualitative assay
Latex agglutination test for Fibrinolysis
Bleeding
Disorders
Inherited
• Vascular
• Platelet
• coagulation
• Fibrinolytic
Acquired
• Vascular
• Platelet
• coagulation
HEMORRHAGIC DISORDERS
Hemorrhagic syndromes are characterized by a disorder
of one or more factors that participate in hemostasis.
The majority of hemorrhagic syndromes are blood vessel
disorders, platelet number and function disorders, or
coagulation factor disorders:
• vasculopathies
• thrombocytopenias
• thrombocytopathies
• coagulopathies.
Vasculopathies
• Vasculopathies may be inherited or acquired. Inherited
forms result from blood vessel structure disorders
(inherited telangiectasia,Rendu-Osler-Weber’s disease)
while acquired disorders can be a consequence of
inflammatory or immune processes that damage blood
vessel walls.
• In clinical practice, acquired disorders are found more
frequently (secondary purpuras, infections,
effects of some drugs, allergic purpura, effect of aspirin,
vitamin C deficiency, etc.).
Thrombocytopenias
• Thrombocytopenia, or reduced circulating platelet count,
can be inherited or acquired; the acquired form being
more frequent.
• Thrombocytopenia occurs as a result of:
– decreased platelet formation with normal platelet
survival time (effects of irradiation, drugs, malignant
tissue pressure on bone marrow, leukemias, aplastic
anemias) or
− increased platelet degradation or platelet deposit in
spleen with decreased platelet survival (DIC, effects
of drugs, bacterial or viral infections, inherited idiopathic
thrombocytopenic purpura, chronic leukemias, lupus
erythematosus,Hodgkin’s disease, massive transfusions
and liver cirrhosis).
Thrombocytopathies
• Inherited Qualitative Platelet Disorders may be due
to abnormalities of
1. platelet membrane glycoproteins,
- Glanzmann Thrombastenia, abnormal GPIIb/IIIa
– Bernard-Soulier Syndrome, abnormal GPIb, GPIX and
GPV
– platelet-type of vWD, abnormal GPIb
2. platelet granules,
• These may occur due to absence of granules in
platelets, storage pool disorder (characterized by
disturbed platelet aggregation to collagen, adrenaline
and thrombin), or disturbed release (absence of T A2).
3. platelet coagulant activity, or
4. signal transduction and secretion.
• defects in arachidonic acid metabolism,
• cyclooxigenase deficiency, platelets unable to produce
thromboxane; endothelium may not produce
prostacyclin,
• thromboxane synthesis deficiency, and
• defects in platelet secretion and the second wave of
platelet aggregation, found in response to epinephrine or
ATP.
Coagulopathies
ACQUIRED BLOOD CLOTTING
DISORDERS
They occur in:
– vitamin K deficiency,
– liver diseases,
– liver transplantation,
– disseminated intravascular coagulation,
– renal diseases,
– primary pathological fibrinolysis
– during the course of anticoagulant therapy.
• The extent and severity of periodontal disease
determines the necessity for a surgical or nonsurgical
treatment approach in its management.
• The nature and severity of an acquired bleeding
disorder, and the degree of invasive dental procedures,
determines the need to modify the treatment to be
provided.
• Various Illnesses, along with pharmacotherapy,may
contribute to the tendency for excessive bleeding.
Pre-operative management of patients starts with a medical
history focusing on the previous bleeding history of the
patient and medical conditions associated with bleeding.
Presence of following illness may need a modification in
treatment protocol to minimize the risk of intra-operative
and postoperative bleeding.
• Chronic renal failure
• Lack of vitamin K
• Liver failure
• Aspirin
• Antiplatelet medication
• Anticoagulant therpay
• Platelet count should be assessed
Surgeries
• Iv infusion 1 hr before
• Level should be 50% higher in plasma for
Regional anesthesia
Missing factors
• Antifibrinolytic mouthwash (Lee , Boyle)
Scaling and root
planing
• regional anesthesia should be avoided
LA
• Conservative design
• Mandibular molar
Flap
• Curettage of extraction socket
• Granulation tissue
Prevention of
infection
Intra-operative measures include a number of systemic and local
measures administered prior to, or during, the procedure to prevent
unlikely bleeding diathesis.
Hemostatic agent
• Absorbable
gelatin
• Absorbable
collagen
• Microfibrillar
collagen
• Oxidised
cellulose
• Thrombin
• Tranexamic acid
• Fibrin glue
• PRP
Other means
• Sponge
• Surgical splint
• Electrocautery
• Laser
• Moistened or
hemostatic
soaked gauze
Hard tissue
• Bone burnishing
• Bone wax
General recommendations is crucial for preventing
bleeding, postoperatively.
Prohibition of
Rinsing
Liquid , high
protein diet
Antifibrinolytic
mouthwash
Antibiotics
Pain
medication
References :-
• Textbook of Medical Physiology ,10th edition,Hall &
Guyton
• Essentials of hematology , Shirish M Kawthalkar
• Periodontal Medicine, Rose
• Bleeding disorders and periodontology, Philip
Vassilopoulos & Kent Palcanis , Periodontology 2000,
Vol. 44, 2007, 211–223.
• Coagulation Pathway and Physiology, Jerry B. Lefkowitz
• Hemostasis And Hemorrhagic Disorders, R. Baklaja, M.
C. Pešic´, J. Czarnecki
• Platelet function analysis,Paul Harisson, Blood Reviews
(2005) 19, 111–123
Thank You

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Blood Coagulation.pptx

  • 1.
  • 2. Contents Haemostasis Vascular Phase Platelet Phase Clot formation Clot retraction Fibrinolysis Bleeding Disorders Diagnosis of bleeding disorders Clinical implication in periodontology
  • 6.
  • 7. • Stages of Hemostasis
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  • 13. •1,50,000 to 400,000 per cu mm Lifespan is 9 – 12 days • Thrombocyte = “ thrombos” + “ Kytos” Platelets
  • 14. • Membrane • Outer glycocalyx layer— glycoproteins • Inner lipoprotein layer— phospholipid
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  • 28. • Release of fibrin stabilizing factor • Contractile protein of platelets • Activated and accelerated by thrombin and Ca ions.
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  • 37. Approach to the diagnosis of bleeding disorder Clinical Evaluation History Physical Examination Family history Laboratory Evaluation Screening test Specific test
  • 38.
  • 39. Clinical Features of Bleeding Disorders Platelet disorders Coagulation disorders Site of bleeding Skin Deep in soft tissues (epistaxis, gum, Mucous vaginal, GI tract) membranes, joints, muscles) Petechiae Yes No Ecchymoses (“bruises”) Small, superficial Large, deep Hemarthrosis / muscle bleeding Extremely rare Common Bleeding after cuts & scratches Yes No Bleeding after surgery or trauma Immediate, Delayed (1-2 days), usually mild often severe
  • 41.
  • 42. Tests for Primary Hemostasis • Bleeding time platelet & vascular phases • PFA – 100 system Platelet function • Platelet count Quantification of platelets • Blood smear Quantitative & morphological abnormalities of platelets , Detection of underlying haemotological disorder
  • 43. Tests for Secondary hemostasis • Clotting factor Crude test of coagulation phase • Prothrombin factor Extrensic & common pathway • Activated partial thromboplastin time Intrensic & common pathway
  • 44. PLATELET COUNT  NORMAL 150,000 - 400,000 CELLS/MM3 < 100,000 Thrombocytopenia 50,000 - 100,000 Mild Thrombocytopenia < 50,000 Sev Thrombocytopenia
  • 45. BLEEDING TIME  PROVIDES ASSESSMENT OF PLATELET COUNT AND FUNCTION NORMAL VALUE 2-8 MINUTES
  • 46.
  • 47. PROTHROMBIN TIME  Measures Effectiveness of the Extrinsic Pathway  Measures the activity of V, VII, X, II , I NORMAL VALUE 11-16 SECS
  • 48. Prothrombin time prolongs.. Extrinsic pathway factor deficiencies (FII, V, VII, X) – Inherited or acquired – Consumption (DIC) – oral anticoagulant therapy
  • 49. INR INR: International normalized ratio -was established by the WHO and the International Committee on Thrombosis and Hemostasis for reporting the results of prothrombin tests -All PT results are standardized by this calculation: INR= ( Patient PT / Control PT)ISI ISI= International sensitivity index - Given by the manufacturer for each particular thromboplastin reagent and instrument combination
  • 50.
  • 51. ACTIVATED THROMBOPLASTIN TIME  Measures Effectiveness of the Intrinsic Pathway & common pathway NORMAL VALUE 25-40 SECS
  • 52. APTT prolongs.. 1. Intrinsic pathway factor deficiencies (FXII, XI,VIII, IX, HMWK, prekallikrein ) - Inherited or acquired - Consumption (DIC) - PIVKA factors in cumarin therapy 2. Specific inhibitors against FXII, XI, VIII, IX, HMWK, prekallikrein 3. Lupus anticoagulant 4. Non-fractionated heparin therapy
  • 53. THROMBIN TIME  Time for Thrombin To Convert Fibrinogen Fibrin  A Measure of Fibrinolytic Pathway NORMAL VALUE 9-13 SECS
  • 54. TT Prolongs.. 1. Hypo- afibrinogenaemia 2. Dysfibrinogenaemia 3. Non fractionated heparin 4. Fibrinogen/ fibrin degradation product s 5. Chronic liver disease
  • 55. SPECIFIC TESTS Tests for specific Platelet Functions 1. Platelet aggregration test 2. Flow cytometry 3. Test for platelet secretion 4. Clot retraction test 5. Platelet procoagulant activity Test for Coagulation Phase 1. Quantitative estimation of Fibrinogen 2. Coagulation factor assays 3. F XIII Qualitative assay Latex agglutination test for Fibrinolysis
  • 56. Bleeding Disorders Inherited • Vascular • Platelet • coagulation • Fibrinolytic Acquired • Vascular • Platelet • coagulation
  • 57. HEMORRHAGIC DISORDERS Hemorrhagic syndromes are characterized by a disorder of one or more factors that participate in hemostasis. The majority of hemorrhagic syndromes are blood vessel disorders, platelet number and function disorders, or coagulation factor disorders: • vasculopathies • thrombocytopenias • thrombocytopathies • coagulopathies.
  • 58. Vasculopathies • Vasculopathies may be inherited or acquired. Inherited forms result from blood vessel structure disorders (inherited telangiectasia,Rendu-Osler-Weber’s disease) while acquired disorders can be a consequence of inflammatory or immune processes that damage blood vessel walls. • In clinical practice, acquired disorders are found more frequently (secondary purpuras, infections, effects of some drugs, allergic purpura, effect of aspirin, vitamin C deficiency, etc.).
  • 59. Thrombocytopenias • Thrombocytopenia, or reduced circulating platelet count, can be inherited or acquired; the acquired form being more frequent. • Thrombocytopenia occurs as a result of: – decreased platelet formation with normal platelet survival time (effects of irradiation, drugs, malignant tissue pressure on bone marrow, leukemias, aplastic anemias) or − increased platelet degradation or platelet deposit in spleen with decreased platelet survival (DIC, effects of drugs, bacterial or viral infections, inherited idiopathic thrombocytopenic purpura, chronic leukemias, lupus erythematosus,Hodgkin’s disease, massive transfusions and liver cirrhosis).
  • 60. Thrombocytopathies • Inherited Qualitative Platelet Disorders may be due to abnormalities of 1. platelet membrane glycoproteins, - Glanzmann Thrombastenia, abnormal GPIIb/IIIa – Bernard-Soulier Syndrome, abnormal GPIb, GPIX and GPV – platelet-type of vWD, abnormal GPIb 2. platelet granules, • These may occur due to absence of granules in platelets, storage pool disorder (characterized by disturbed platelet aggregation to collagen, adrenaline and thrombin), or disturbed release (absence of T A2).
  • 61. 3. platelet coagulant activity, or 4. signal transduction and secretion. • defects in arachidonic acid metabolism, • cyclooxigenase deficiency, platelets unable to produce thromboxane; endothelium may not produce prostacyclin, • thromboxane synthesis deficiency, and • defects in platelet secretion and the second wave of platelet aggregation, found in response to epinephrine or ATP.
  • 63. ACQUIRED BLOOD CLOTTING DISORDERS They occur in: – vitamin K deficiency, – liver diseases, – liver transplantation, – disseminated intravascular coagulation, – renal diseases, – primary pathological fibrinolysis – during the course of anticoagulant therapy.
  • 64. • The extent and severity of periodontal disease determines the necessity for a surgical or nonsurgical treatment approach in its management. • The nature and severity of an acquired bleeding disorder, and the degree of invasive dental procedures, determines the need to modify the treatment to be provided. • Various Illnesses, along with pharmacotherapy,may contribute to the tendency for excessive bleeding.
  • 65. Pre-operative management of patients starts with a medical history focusing on the previous bleeding history of the patient and medical conditions associated with bleeding. Presence of following illness may need a modification in treatment protocol to minimize the risk of intra-operative and postoperative bleeding. • Chronic renal failure • Lack of vitamin K • Liver failure • Aspirin • Antiplatelet medication • Anticoagulant therpay
  • 66. • Platelet count should be assessed Surgeries • Iv infusion 1 hr before • Level should be 50% higher in plasma for Regional anesthesia Missing factors • Antifibrinolytic mouthwash (Lee , Boyle) Scaling and root planing • regional anesthesia should be avoided LA • Conservative design • Mandibular molar Flap • Curettage of extraction socket • Granulation tissue Prevention of infection Intra-operative measures include a number of systemic and local measures administered prior to, or during, the procedure to prevent unlikely bleeding diathesis.
  • 67. Hemostatic agent • Absorbable gelatin • Absorbable collagen • Microfibrillar collagen • Oxidised cellulose • Thrombin • Tranexamic acid • Fibrin glue • PRP Other means • Sponge • Surgical splint • Electrocautery • Laser • Moistened or hemostatic soaked gauze Hard tissue • Bone burnishing • Bone wax
  • 68. General recommendations is crucial for preventing bleeding, postoperatively. Prohibition of Rinsing Liquid , high protein diet Antifibrinolytic mouthwash Antibiotics Pain medication
  • 69. References :- • Textbook of Medical Physiology ,10th edition,Hall & Guyton • Essentials of hematology , Shirish M Kawthalkar • Periodontal Medicine, Rose • Bleeding disorders and periodontology, Philip Vassilopoulos & Kent Palcanis , Periodontology 2000, Vol. 44, 2007, 211–223. • Coagulation Pathway and Physiology, Jerry B. Lefkowitz • Hemostasis And Hemorrhagic Disorders, R. Baklaja, M. C. Pešic´, J. Czarnecki • Platelet function analysis,Paul Harisson, Blood Reviews (2005) 19, 111–123