physiology of blood and its current concepts in coagulation

Blood and coagulation current concepts

Blood and its current concepts in coagulationDR. Akash ArdeshanaMDS-I ,Department of paedodontics and Preventive Dentistry,KMSDCH.

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contentIntroductionBlood: properties , composition , function.Plasma proteinsRBCBlood indexHemoglobinBlood groupWBC

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INTRODUCTIONBlood is a circulating tissue composed of fluid plasma and cells (red blood cells, white blood cells, platelets). Medical terms related to blood often begin with hemo- or hemato- ( haemo- and haemato-) from the Greek word "haima" for "blood".Blood is a connective tissue present in fluid form.

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Properties of bloodColour - RedForms 6-8 % of total body weight.Average adult volume:Males 5 LitresFemales 4.5LitresNew born 450 mlpH = 7.4Specific Gravity = 1.052 1.061Viscosity = 3 5 times more viscous than water.

4K Sembulingam Essentials of Medical Physiology-6rd edition.

Composition of blood

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Plasma:solids: 7-8%organic substancesinorganic substancesWater: 92-93% Gases:

OrganicInorganic Plasma proteinNaAmino acidsCaCarbohydrateKFatMgHormones Hco3Enzymes ClAntibodies Fe, cu


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8Functions

Respiratory

Excretory

Homeostasis

Defense

Maintenance of body temperature

Transport

Storage

Acid-base regulation

Nutritional

Plasma proteinNormal values of the plasma proteins are:Total proteins : 7.3 g/dL (6.4 to 8.3 g/dL)Serum albumin : 4.7 g/dLSerum globulin : 2.3 g/dLFibrinogen : 0.3 g/dL

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FunctionCoagulation of bloodDefense mechanism of bodyTransport mechanismMaintenance of osmotic pressure in bloodRegulation of acid-base balanceViscosity of bloodRole in erythrocyte sedimentation rateRole as reserve proteins

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Development of blood cells

11Guyton and Hall Text book of medical physiolog 12th edition 2011.

Red Blood CellsAlso known as erythrocytes.

Most abundant cells of the blood.

transport hemoglobin, which in turn carries oxygen from the lungs to the tissues.12

Morphology Shape: Biconcave discs

Size: 7.2 micrometers Thickness: 2.2 micrometers at the thickest point and 1 micrometer or less in the center.

The average volume: 85 to 90 cubic micrometers.

Normal value Male : 5-6 million/mm3Female : 4.5-5.5 million/mm3Infant : 6-7 million/mm3

13Ganong Review of Medical Physiology-23rd Edition.

Production of Red Blood CellsI. U Life:3rd week-3rd month -- yolk sac3rd month-5th month -- liver5th month onwards -- RBM

Post-natal : Red Bone Marrow


Relative rates of red blood cell production in the bone marrow of different bones at different ages

Genesis of Blood Cells

15Guyton and Hall Text book of medical physiolog 12th edition 2011.Ganong Review of Medical Physiology-23rd Edition.

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Factor necessary for erythropoises Regulation of Red Blood Cell Production Role of Erythropoietin


Thyroxine: Accelerates the process of erythropoiesis at many levels.

Hemopoietic growth factor: IL-3, IL-6, IL-11.

Vitamins:K Sembulingam Essentials of Medical Physiology-6rd edition.

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Maturation of Red Blood CellsRequirement for Vitamin B1 (Cyanocobalamin) and Folic Acid.Both of these are essential for the synthesis of DNA, because each in a different way is required for the formation of thymidine triphosphate, one of the essential building blocks of DNA. Therefore, lack of either vitamin B12 or folic acid causes abnormal and diminished DNA and, consequently, failure of nuclear maturation and cell division. 18Guyton and Hall Text book of medical physiolog 12th edition 2011.

Furthermore, the erythroblastic cells of the bone marrow, in addition to failing to proliferate rapidly, produce mainly larger than normal red cells called macrocytes.19

LIFE SPAN AND FATE OF RBCSAverage life span -- about 120 days. Spleen -- Graveyard of red blood cells. Daily 10% red blood cells, which are senile, get destroyed in normal young healthy adults.

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Function of RBC

Transport the oxygen from the lung to the tissue.Transport the carbon dioxide from the tissue to the lung.Buffering action in blood.In blood group determination.

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VARIATIONS OF RBC IN NUMBERIN SIZEIN SHAPE

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VARIATIONS IN RBC COUNTPHYSIOLOGICAL VARIATIONSIncrease in count--Physiological PolycythemiaAge Sex High altitudeMuscular exerciseAfter meal

Decrease in countHigh barometric pressuresleep

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PATHOLOGICAL VARIATIONS

Decrease in no. ANAEMIA

Increase in no. - POLYCYTHAEMIA

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VARIATIONS IN RBC SIZEMicrocytesIron deficiency anemia

MacrocytesMegaloblastic anemia

AnisocytesPernicious anemia

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Variation in shape1. Crenation: Shrinkage -- hypertonic condition.2. Spherocytosis: Globular hypotonic condition.4. Sickle cell: Crescentic -- sickle cell anemia.5. poikilocytosis: unusual shapes due to deformed cell membrane.

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AnemiaAnemia is defined as an abnormal reduction in the number of circulating red blood cells, the quantity of hemoglobin and the volume of packed cell in a given unit of blood.

Types:

Pernicious anemiaAplastic anemiaThalassemiaSickle cell anemiaErythroblastosis fetalisIron deficiency anemia 27

Effects of Anemia on Function of theCirculatory System:

one of the major effects of anemia is greatly increased cardiac output, as well as increased pumping workload on the heart.

acute cardiac failure.

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29TitleThe impact of sickle cell disease on oral health-related quality of life.

Author Ralstrom E, da Fonseca MA, Rhodes M, Amini H

JournalPediatr Dent. 2014 Jan-Feb;36(1):24-8.Level of evidenceIIIAimThe purpose of this study was to characterize the impact of sickle cell disease (SCD) on oral health and examine its impact on quality of lifeMethodFifty-four study subjects were recruited from the sickle cell clinic and 52 control subjects from the adolescent medicine clinic at Nationwide Children's Hospital, Columbus, Ohio. A dental exam was performed to determine each participant's caries burden. The Child Oral Health Impact Profile survey was used to assess their oral health-related quality of life ResultMost subjects in both the SCD and control groups rated their overall health and oral health as "good" or "excellent." There was no statistically significant difference in OHRQoL between these groups. Additionally, no significant relationship was found between white blood cell count, medication intake, or the number of sickle cell crises as related to the caries burden. Statistically significant differences were detected in caries burden between the control group and the sickle cell hemoglobin C disease (HbSC) group (P.001). Logistic regression analyses revealed that children with S-ECC were nearly twice as likely to have low ferritin levels and were over six times more likely to have iron deficiency anaemia than caries-free controls.ConclusionChildren with S-ECC appear to be at significantly greater odds of having low ferritin status compared with caries-free children and also appear to have significantly lower haemoglobin levels than the caries-free control group. Children with S-ECC also appear to be at significantly greater odds for iron deficiency anaemia than cavity-free children.

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Bibliography Guyton and Hall Text book of medical physiolog 12th edition 2011.Ganong Review of Medical Physiology-23rd Edition.K Sembulingam Essentials of Medical Physiology-6rd edition.Textbook of Physiology 4th Edition by ChaudaryText book of medical pathology 6th edition by Harsh Mohan.

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Ralstrom E, da Fonseca MA, Rhodes M, Amini H. The impact of sickle cell disease on oral health-related quality of life. Pediatr Dent. 2014 Jan-Feb;36(1):24-8Schroth RJ1, Levi J, Kliewer E, Friel J, Moffatt ME. Association between iron status, iron deficiency anaemia, and severe early childhood caries: a case-control study. BMC Pediatr. 2013 Feb 7;13:22.Hegde AM1, Joshi S, Rai K, Shetty S.Evaluation of oral hygiene status, salivary characteristics and dental caries experience in acute lymphoblastic leukemic (ALL) children. J Clin Pediatr Dent. 2011 Spring;35(3):319-23.

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ContentPlatelets: structure ,development ,function disorder

Hemostasis and blood coagulationEvent in HemostasisMechanismIntravascular anti coagulantBleeding conditionAnti coagulantLocal hemostasis measuredLaboratory evaluation

Blood transfusion

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Platelets or thrymbocytes STRUCTURE

(Platelets = small plate; thrombo = lump or clot; cytes = cells) GENERAL FEATURES:

Platelets are the smallest blood cells, colourless, spherical, oval or rounded granulated bodies

2.5 microns in diameter with an average volume 7.5 cubic microns.

Leishman staining shows a faint blue cytoplasm with distinct reddish purple granules; nucleus is not present99K Sembulingam Essentials of Medical Physiology-6rd edition.

Under Electron Microscope

Platelet membranes important features

it shows extensive invagination with a complicated canalicular system in contact with the ECF.

the main lipids in lipoprotein layer of cell membrane are: phospholipids, cholesterol and glycoprotein;

it contains various receptors meant for combining with specific substances like: collagenfibrinogen100K Sembulingam Essentials of Medical Physiology-6rd edition.

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Cytoplasm contains:

Golgi aparatus, endoplasmic reticulum, mitochondria, microtubule, microvessels, filaments and different types of granules.Protein Myosin and Actin (Resp for Contraction of platelet)Protein named Thrombosthenin for clot retractionVon Willebrand factor for adherence of plateletsFibrin stabilising FactorPlatelet derived growth factor repair of damaged blood vessels

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Platelet activating Factor Aggregation of platelets during injury of blood vessels.Enzymes like ATP and enzymes for synthesis of prostaglandins Hormonal substance like histamine and adrenalineOther chemical substances like glycogen, blood group antigens and in organic substances like calcium, copper, magnesium and iron.103Guyton and Hall Text book of medical physiolog 12th edition 2011

Platelet under electron microscope

Canalicular system Golgi complex Mitochondria Cell membrane Dense granules Lysosome Glycogen granule Microvesicles Microtubule a-granules 104

Count and variation COUNT AND VARIATIONS Normal count is 1.5 to 4 lacs/ cumm (average: 2.59 lacs/ cumm). Its count is very much constant.

The circulating platelets represent approx. 60-75% of the platelet pool of the body, the remaining are mostly in the spleen. Therefore, spleen acts as a reservoir of platelets.

Life span: 8-12 days.

Destruction: mainly in the spleen. In hypersplenism (overactivity of spleen), the platelets may almost disappear from circulation


Variations:

Thrombocytosis i.e. increase in platelet count.

Causes:after administration of epinephrine due to splenic contraction.after trauma e.g. surgery, injury, child birth etc.splenectomy (removal of spleen) stress - causes increased epinephrine release resulting in spleen contraction.HemorrhageAllergic Condition


Thrombocytopenia i.e. decrease in platelet count.

Causes:

Bone marrow depression.splenomegalyViral infection e.g. dengue fever (particularly attacks platelets).Aplastic and pernicious anemiaAcute infectionsTyphoidTuberculosis

Thrombocytopenia leads to purpura which is associated with bleeding disorders107

Development of platelets Development of Platelets

Site of origin : bone marrow

Steps Pluripotent stem cell

Committed stem cell (polyploid precursor cell)

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Megakaryoblast (Stage I)

Pro-megakaryocyte (Stage II)

Granular megakaryocyte (Stage III) Platelets 109

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Function of platelets 1. ROLE IN BLOOD CLOTTINGPlatelets are responsible for the formation of intrinsic prothrombin activator. This substance is responsible for the onset of blood clotting111

2. ROLE IN CLOT RETRACTIONIn the blood clot, blood cells including platelets are in between the fibrin threads. Cytoplasm of platelets contains the contractile proteins, namely actin, myosin and thrombosthenin, which are responsible for clot retraction.112

3. ROLE IN PREVENTION OF BLOOD LOSS (HEMOSTASIS)

secrete 5-HT constriction of blood vessels.Due to the adhesive property, the platelets seal the damage in blood vessels like capillaries. By formation of temporary plug.113

4. ROLE IN REPAIR OF RUPTURED BLOOD VESSEL

Platelet-derived growth factor (PDGF) formed in cytoplasm of platelets is useful for the repair of the endothelium and other structures of the ruptured blood vessels.114

The activated platelets:

change the shape i.e. put out pseudopodia discharge their granule contents, and stick to each other, called platelet aggregation115K Sembulingam Essentials of Medical Physiology-6rd edition.

Inactive platelets

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Active platelets

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Life Span and Fate of PlateletsLife span : 10 days

Destroyed by tissue macrophages system in spleen

spleenectomy increases platelet counts118

Disease involving blood plateletsPurpura: Purplish discoloration of the skin and mucous membranes due to the spontaneous extravasation of blood and it self as a symptoms rather then a disease entity.

Nonthrombocytopenic purpuraThrombocytopenic purpura1. primary2. secondary

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Thrombocytasthenia: Thrombocytasthenia is a variety of disease characterized by a qualitative defect in blood platelets.

Thrombocythemia: increase in the number of circulating blood platelets.

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121TitleGingival inflammation and platelet count in patients with leukemia:preliminary resultsAuthor Patrcia Daniela Melchiors Angst,Danilo Antnio Milbradt Dutra, Carlos Heitor Cunha Moreira, Karla Zanini Kantorski

JournalBraz Oral Res. 2011 Nov-Dec;25(6):544-9Level of evidenceIIIaim The aim of this cross-sectional study was to assess the correlation between the Gingival Index and Bleeding on Probing with the platelet count in patients with leukemia.MethodTwo trained and calibrated examiners evaluated the Plaque Index, Gingival Index (GI), Probing depth, Bleeding on Probing (BOP), and Clinical Attachment Loss. Hematologic data were collected from a blood test performed on the same day as the periodontal examination. Thirty-seven patients (26 males), aged between 15 and 80 years (mean age 41.7 18.31) wereevaluated.ResultCorrelation between platelet count and BOP (p > 0.05), or between platelet count and GI (p > 0.05), were both weak and not statistically significant.ConclusionIt can be concluded from the preliminary results that the low platelet count was not correlated with the higher prevalence of gingival and periodontal bleeding in patients with leukemia.

Hemostasis and Blood Coagulation122

Events in Hemostasis:Hemostasis prevention of blood loss

Mechanisms: (1) Vascular constriction (2) Formation of a platelet plug (3) Formation of a blood clot (4) Eventual growth of fibrous tissue

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Vascular Constriction:

The contraction results from: (1) local myogenic spasm(2) local autacoid factors from the traumatized tissues and blood platelets(3) nervous reflexes.124

Formation of the Platelet Plug:When platelets come in contact with a damaged vascular surface, change their shape. They begin to swell; they assume irregular forms with numerous irradiating pseudopods protruding from their surfaces. their contractile proteins contract forcefully and cause the release of granules that contain multiple active factors; they become sticky so that they adhere to collagen in the tissues and the protein called von Willebrand factor that leaks into the traumatized tissue from the plasma.125Guyton and Hall Text book of medical physiolog 12th edition 2011

they secrete large quantities of ADP; and their enzymes form thromboxane A2.

The ADP and thromboxane in turn act on nearby platelets to activate them as well, and the stickiness of these additional platelets causes them to adhere to the original activated platelets.

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Importance of the Platelet Mechanism for Closing Vascular Holes: The platelet-plugging mechanism is extremely important for closing minute ruptures in very small blood vessels that occur many thousands of times daily.127

Blood Coagulation in theRuptured Vessel The clot begins to develop in 15 to 20 seconds if the trauma to the vascular wall has been severe, and in 1 to 2 minutes if the trauma has been minor.

Activator substances from the traumatized vascular wall, from platelets, and from blood proteins adhering to the traumatized vascular wall initiate the clotting process128Guyton and Hall Text book of medical physiolog 12th edition 2011

PHYSICAL EVENTS:


Mechanism of BloodCoagulationBasic Theory. More than 50 important substances that cause or affect blood coagulation have been found in the blood and in the tissues.some that promote coagulation, called procoagulants, and others that inhibit coagulation, called anticoagulants130Guyton and Hall Text book of medical physiolog 12th edition 2011


Prothrombin activator is generally considered to be formed in two ways: (1) by the extrinsicpathway that begins with trauma to the vascular wall and surrounding tissues.

(2) by the intrinsicpathway that begins in the blood itself.132Guyton and Hall Text book of medical physiolog 12th edition 2011

Clotting factors

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Extrinsic pathway


Intrinsic pathway


ROLE OF CALCIUM IN BOTH THE PATHWAYS

Calcium ions are required for promotion or acceleration of all the blood clotting reactions. when blood is removed from a person,it can be prevented from clotting by reducing the calcium ion concentration By deionizing the calcium by causing it to react with substances such as citrate ion By precipitating the calcium with substances such as oxalate ion.


INTERACTION BETWEEN EXTRINSIC AND INTRINSIC PATHWAYAfter blood vessels rupture, clotting occurs by both pathways simultaneously.

Extrinsic pathway can be explosive ,once initiated clotting can occur in as little as 15 seconds.

The intrinsic pathway is much slower to proceed usually requiring 1 to 6 minutes to cause clotting.137Guyton and Hall Text book of medical physiolog 12th edition 2011

Clot RetractionSerumWithin a few minutes after a clot is formed, it begins to contract and usually expresses most of the fluid from the clot within 20 to 60 minutes.138

FIBRINOLYSISLysis of blood clot inside the blood vessel is called fibrinolysis.This occurs by a substance Fibrinolysin / plasmin

Significance allows reopening of the affected blood vessel and prevents the development of infarction.

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Tissue plasminogen activatorPlasminogenPlasmin dissolves the clot by digesting fibrin

(Action)

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Intravascular AnticoagulantsEndothelial Surface Factors:smoothness of the endothelial cell surface.layer of glycocalyx on the endothelium.thrombomodulin

Antithrombin action of fibrin and Antithrombin III

Heparin141Guyton and Hall Text book of medical physiolog 12th edition 2011 v

Conditions causing excessive bleeding in humans..

Vitamin K deficiency:

Vitamin K is necessary for liver to formation of five of the important clotting factors: prothrombin, Factor VII, Factor IX, Factor X, and protein C.

In the absence of vitamin K, subsequent insufficiency of these coagulation factors in the blood can lead to serious bleeding tendencies.142

Hemophilia:This is characterized by prolonged coagulation time and hemorrhagic tendency.Type: Hemophilia A Hemophilia B Hemophilia C

Von Willebrands Disease:Parahemophilia:Hypofibrinogenemia:Fibrin-stabilizing factor deficiencyThrombocytopenia

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Thromboembolic Conditions in the Human Being:1)Thrombus and emboli2)Disseminated Intravascular Coagulation3)Femoral Venous Thrombosis and Massive pulmonary embolism144

Anticoagulants forClinical UseIn some thromboembolic conditions, it is desirable to delay the coagulation process. Various anticoagulants have been developed for this purpose.

Heparin as an Intravenous Anticoagulant:

Injection of relatively small quantities, about 0.5 to 1 mg/kg of body weight, causes the blood-clotting time to increase from a normal of about 6 minutes to 30 or more minutes.The action of heparin lasts about 1.5 to 4 hours.The injected heparin is destroyed by an enzyme in the blood known as heparinase.


Coumarins as Anticoagulants:

When a coumarin, such as warfarin, is given to a patient, the plasma levels of prothrombin and Factors VII, IX, and X, all formed by the liver, begin to fall, indicating that warfarin has a potent depressant effect on liver formation of these compounds.

Warfarin causes this effect by competing with vitamin K .Guyton and Hall Text book of medical physiolog 12th edition 2011146

The coagulant activity of the blood decreases to about 50 per cent of normal by the end of 12 hours and to about 20 per cent of normal by the end of 24 hours.

Normal coagulation usually returns 1 to 3 days after discontinuing coumarin therapy.Guyton and Hall Text book of medical physiolog 12th edition 2011147

Prevention of Blood Coagulation Outside the BodySiliconized containersHeparinVarious substances that decrease the concentration of calcium ionsDeionizes the blood calcium sodium, ammonium, or potassium citrateGuyton and Hall Text book of medical physiolog 12th edition 2011148

Local hemostatic measureMechanical methodsPressureUse of hemostatsSuture and ligation

Thermal agents:cautery cryosurgeryElectrosurgeryArgon- beam coagulator

Textbook of oral and maxillofacial surgery by Nelima Anil Malik 2nr edition 149

Chemical method:Local agents:Monsels solution and tannic acidBone waxThombinGelfoamOxycelFibrin glueAdrenaline

Textbook of oral and maxillofacial surgery by Nelima Anil Malik 2nr edition

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Systemic agent:Whole bloodFresh frozen plasmaCryoprecipitateEthamsylateTextbook of oral and maxillofacial surgery by Nelima Anil Malik 2nr edition

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Topical Thrombin Agents152

Laboratory EvaluationBleeding Time (BT)Clotting Time (CT)Prothrombin Time (PT)Partial thromboplastin Time (PTT)Thrombin Time (TT)

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BLOOD COAGULATION TESTS

BLEEDING TIME :Provides assessment of platelet count & functionProlonged BT:-Congenital & acquired disorder of platelet function Von Willebrand diseaseThrombocytopeniaPurpura

Normal value:- 3-6 Minutes


Dukes Method: With the Duke method, the patient is pricked with a special needle or lancet, preferably on theearlobeorfingertip, after having been swabbed with alcohol. The prick is about 34mm deep. The patient then wipes the blood every 30 seconds with a filter paper. The test ceases when bleeding ceases.

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CLOTTING TIMEProlonged in Hemophilia.

MethodCapillary Glass Method

Normal Clotting Time: 4-9 Min.

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PROTHROMBIN TIMEMeasures Effectiveness of the Extrinsic Pathway Prolonged PT:-Deficiency of ProthrombinDisseminated Intravascular CoagulationVit. K deficiency

Normal value : 10-15 SECS


Method:The prothrombin time is most commonly measured usingblood plasma. Blood is drawn into atest tubecontaining liquidcitrate. The blood is mixed, then centrifuged to separate blood cells from plasma.Tissue factor (Tissue thrombopastin)is then added and the clotting time is checked

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PARTIAL THROMBOPLASTIN TIME

Measures Effectiveness of the Intrinsic PathwayMeasures coagulation disorders.Prolonged PTT-Factor III deficiencyIncreases in HemophiliaAnticoagulation with heparinNORMAL VALUE25-40 SECS


Method-Blood samples are collected in tubes withoxalateorcitrateto arrest coagulation by binding to calcium. In order to activate the intrinsic pathway, phospholipid, an activator(such assilica,celite,kaolin,ellagic acid), andcalcium(to reverse the anticoagulant effect of the oxalate) are mixed into theplasmasample. The time is measured until athrombus(clot) forms

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THROMBIN TIMEIs a measure of the rate of conversion of fibrinogen to fibrin Prolonged TTContamination with heparinAcquired (DIC, liver disease)

NORMAL VALUE 9-13 SECS


Method-After liberating the plasma from the whole blood bycentrifugation, bovineThrombinis added to the sample of plasma. The clot is formed and is detected optically or mechanically by a coagulation instrument. The time between the addition of the thrombin and the clot formation is recorded as the thrombin clotting time


164TitleAutologous plasma rich in growth factors in the prevention of severe bleeding after teeth extractions in patients with bleeding disorders: a controlled comparison with fibrin glue.Author Cocero N1, Pucci F1, Messina M2, Pollio B2, Mozzati M3, Bergamasco L1.

JournalBlood Transfus. 2014 Oct 29:1-8. doi: 10.2450/2014.0124-14Level of evidenceIIIBackground Dental extractions in haemophiliacs may cause secondary bleeding, requiring repeated surgical and haematological interventions. As a local haemostatic, fibrin glue has recognised efficacy but, as a plasma-derived product, it carries the risk of viral infections. We, therefore, compared fibrin glue with an autologous haemostatic, plasma rich in growth factors (PRGF), in a controlled trial.MethodOne hundred and twenty patients with different blood disorders were randomised into two cohorts to undergo dental extraction procedures without hospitalisation. Prior to the extractions, patients underwent systemic haematological treatment. Complications were defined as secondary bleeding after the 7-day follow-up period or protracting after the repair procedure.ResultThere were 106 extractions in the group managed with fibrin glue: secondary bleeding affected 3/60 patients (5%) on the third day after extraction and necessitated additional surgery and systemic treatment. In the PRGF arm there were 204 extractions secondary bleeding affected two patients (3.3%) on the first day after extraction and was arrested with surgery without systemic treatment. Four out of the five secondary bleeds occurred in patients with haemophilia A. ConclusionThe bleeding rates in the study and control arm prove that PRGF works as well as fibrin glue as a local haemostatic. Further assets are that PRGF has autologous origin, does not require additional systemic treatment in post-extraction repair surgery, is associated with an earlier onset of neo-angiogenesis and, overall, can reduce patients' distress and costs to the health system.

165TitlePlatelet Concentrate Versus Platelet TransfusionAuthor Nadia Cocero, Laura Bergamasco2, Marco Mozzati3Journal(Int Dent Res 2012;2(2):33-36Level of evidenceIIIaim Surgical treatment of patients with severe thrombocytopaenia (

physiology of blood and its current concepts in coagulation

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