This document summarizes various hemostatic disorders including those arising from vessel wall, platelet, and coagulation system abnormalities. It describes several inherited and acquired conditions that can cause bleeding disorders like hemophilia A, von Willebrand disease, and liver disease. Diagnostic tests for evaluating hemostasis are outlined including bleeding time, platelet count, prothrombin time, and activated partial thromboplastin time. Treatment approaches for different disorders are also mentioned.
This document provides information on bisphosphonate-related osteonecrosis of the jaws (BRONJ). It begins with background on bisphosphonates, including their uses, mechanisms of action, and side effects. It then discusses the history, estimated incidence, risk factors, clinical presentation, staging, and treatment of BRONJ. The document aims to educate on this condition caused by prolonged bisphosphonate use that results in exposed bone in the jaw.
This document provides information on disseminated intravascular coagulation (DIC), including its pathophysiology, causes, clinical manifestations, diagnosis, and treatment. DIC is characterized by excessive activation of coagulation leading to microvascular thrombosis. It is not a primary disease but can arise from various clinical conditions. Common causes in infants and children include sepsis, trauma, and malignancies. The pathophysiology involves tissue damage and inflammation that activates coagulation. Diagnosis is based on laboratory tests showing consumption of platelets and coagulation factors. Treatment focuses on treating the underlying condition, replacing coagulation factors if bleeding is present, and administering anticoagulants if thrombosis occurs.
This document summarizes a seminar presentation on approaches to bleeding disorders in pediatric patients. It provides an overview of homeostasis and the blood clotting process, as well as some common bleeding disorders seen in pediatrics. The diagnosis of bleeding disorders involves taking a medical history, performing a physical exam, and conducting laboratory investigations such as platelet count, bleeding time, prothrombin time, activated partial thromboplastin time, and thrombin time to evaluate the platelet count and function, as well as factors in the intrinsic and extrinsic coagulation pathways.
This document discusses hemostasis and various bleeding disorders. It defines hemostasis and describes the primary and secondary stages. The primary stage involves platelet plug formation from platelet adhesion, activation, and aggregation. The secondary stage activates the intrinsic and extrinsic coagulation pathways. The document outlines various signs and symptoms of bleeding disorders and provides examples. It discusses screening tests like complete blood count, prothrombin time, activated partial thromboplastin time, and bleeding time. Finally, it analyzes several case scenarios involving abnormal coagulation test results.
This document discusses the approach to evaluating and managing a child presenting with a bleeding tendency. Key points include obtaining a thorough history including details of the bleeding, family history of bleeding disorders, and reviewing systems. A full examination focusing on sites of bleeding and developmental milestones is important. Initial investigations would include a CBC, coagulation studies, and bone marrow examination if ITP is suspected. Common causes discussed are immune thrombocytopenia, hemophilia A/B, and von Willebrand disease. Treatment is aimed at the underlying cause and ranges from observation to IVIG, steroids, platelet transfusions, or specialized coagulation factor replacement.
Disseminated intravascular coagulation (DIC) is a pathological condition where widespread blood clot formation occurs throughout the small blood vessels of the body. It can be acute, subacute, or chronic. DIC results from the activation of coagulation pathways due to factors like sepsis, trauma, malignancy, or obstetric complications. This leads to fibrin deposition, thrombosis, multi-organ failure, and bleeding manifestations as clotting factors are depleted. Treatment involves controlling the underlying condition, replacing clotting factors, and using anticoagulants.
Upper GI bleeding (UGIB) is a common cause of emergency hospital admission. A 60-year-old woman presented with vomiting brown material, fatigue, and breathlessness. UGIB is defined as bleeding along the GI tract from the mouth to ligament of Trietz. The most common causes are duodenal ulcer, gastric ulcer, and esophageal varices. Treatment involves stabilizing the patient, administering proton pump inhibitors or vasoconstrictors, and potentially endoscopic therapies like ligation or embolization. Surgery may be indicated for severe bleeding or failure of other treatments. Prognosis depends on the cause and presence of comorbidities, with older age and shock being poor prognostic factors.
Surgeons are doing surgeries because of normal blood clotting and wound healing. Suppose if your patient’s blood doesn’t clot properly and you come to know this only on the table, it would be a nightmare to any surgeon irrespective of their subspecialty. In this PPT, I am discussing about how to handle a patient with bleeding diathesis during and after surgery. Indeed it is a challenging and fascinating problem. I hope you will enjoy the video. You can watch all my teaching videos in the following links: surgicaleducator.blogspot.com; youtube.com/c/surgicaleducator.
This document provides information on bisphosphonate-related osteonecrosis of the jaws (BRONJ). It begins with background on bisphosphonates, including their uses, mechanisms of action, and side effects. It then discusses the history, estimated incidence, risk factors, clinical presentation, staging, and treatment of BRONJ. The document aims to educate on this condition caused by prolonged bisphosphonate use that results in exposed bone in the jaw.
This document provides information on disseminated intravascular coagulation (DIC), including its pathophysiology, causes, clinical manifestations, diagnosis, and treatment. DIC is characterized by excessive activation of coagulation leading to microvascular thrombosis. It is not a primary disease but can arise from various clinical conditions. Common causes in infants and children include sepsis, trauma, and malignancies. The pathophysiology involves tissue damage and inflammation that activates coagulation. Diagnosis is based on laboratory tests showing consumption of platelets and coagulation factors. Treatment focuses on treating the underlying condition, replacing coagulation factors if bleeding is present, and administering anticoagulants if thrombosis occurs.
This document summarizes a seminar presentation on approaches to bleeding disorders in pediatric patients. It provides an overview of homeostasis and the blood clotting process, as well as some common bleeding disorders seen in pediatrics. The diagnosis of bleeding disorders involves taking a medical history, performing a physical exam, and conducting laboratory investigations such as platelet count, bleeding time, prothrombin time, activated partial thromboplastin time, and thrombin time to evaluate the platelet count and function, as well as factors in the intrinsic and extrinsic coagulation pathways.
This document discusses hemostasis and various bleeding disorders. It defines hemostasis and describes the primary and secondary stages. The primary stage involves platelet plug formation from platelet adhesion, activation, and aggregation. The secondary stage activates the intrinsic and extrinsic coagulation pathways. The document outlines various signs and symptoms of bleeding disorders and provides examples. It discusses screening tests like complete blood count, prothrombin time, activated partial thromboplastin time, and bleeding time. Finally, it analyzes several case scenarios involving abnormal coagulation test results.
This document discusses the approach to evaluating and managing a child presenting with a bleeding tendency. Key points include obtaining a thorough history including details of the bleeding, family history of bleeding disorders, and reviewing systems. A full examination focusing on sites of bleeding and developmental milestones is important. Initial investigations would include a CBC, coagulation studies, and bone marrow examination if ITP is suspected. Common causes discussed are immune thrombocytopenia, hemophilia A/B, and von Willebrand disease. Treatment is aimed at the underlying cause and ranges from observation to IVIG, steroids, platelet transfusions, or specialized coagulation factor replacement.
Disseminated intravascular coagulation (DIC) is a pathological condition where widespread blood clot formation occurs throughout the small blood vessels of the body. It can be acute, subacute, or chronic. DIC results from the activation of coagulation pathways due to factors like sepsis, trauma, malignancy, or obstetric complications. This leads to fibrin deposition, thrombosis, multi-organ failure, and bleeding manifestations as clotting factors are depleted. Treatment involves controlling the underlying condition, replacing clotting factors, and using anticoagulants.
Upper GI bleeding (UGIB) is a common cause of emergency hospital admission. A 60-year-old woman presented with vomiting brown material, fatigue, and breathlessness. UGIB is defined as bleeding along the GI tract from the mouth to ligament of Trietz. The most common causes are duodenal ulcer, gastric ulcer, and esophageal varices. Treatment involves stabilizing the patient, administering proton pump inhibitors or vasoconstrictors, and potentially endoscopic therapies like ligation or embolization. Surgery may be indicated for severe bleeding or failure of other treatments. Prognosis depends on the cause and presence of comorbidities, with older age and shock being poor prognostic factors.
Surgeons are doing surgeries because of normal blood clotting and wound healing. Suppose if your patient’s blood doesn’t clot properly and you come to know this only on the table, it would be a nightmare to any surgeon irrespective of their subspecialty. In this PPT, I am discussing about how to handle a patient with bleeding diathesis during and after surgery. Indeed it is a challenging and fascinating problem. I hope you will enjoy the video. You can watch all my teaching videos in the following links: surgicaleducator.blogspot.com; youtube.com/c/surgicaleducator.
This document discusses various disorders of coagulation and hemostasis. It describes the normal physiologic mechanisms of hemostasis, coagulation pathways, and fibrinolysis. It then discusses several specific bleeding disorders including von Willebrand disease, hemophilia, disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), immune thrombocytopenic purpura (ITP), and qualitative platelet defects. Laboratory tests used to evaluate coagulation and bleeding disorders are also outlined.
This document provides an overview of approaches to evaluating and treating bleeding disorders and acute anemia. It discusses evaluating the clinical history and laboratory tests to distinguish between local and systemic bleeding issues and primary versus secondary hemostatic defects. Common causes of bleeding like hemophilia, von Willebrand disease, liver disease, and medications are reviewed. Emergency treatment options and dosing calculations for replacing coagulation factors in hemophilia are also covered.
Bleeding and clotting disorders dr anoop k ranoop k r
This document discusses bleeding and clotting disorders, including the diagnosis and evaluation of bleeding problems. It describes the principal presentations of bleeding disorders such as easy bruising, bleeding from mucous membranes, and excessive bleeding after trauma. It then covers specific types of bleeding disorders like those affecting platelets or coagulation factors. The document outlines typical screening tests used to evaluate bleeding disorders and describes both inherited and acquired causes of platelet and coagulation abnormalities.
1) An 85-year-old woman was hospitalized for severe anemia with a hemoglobin of 3 g/dL.
2) A 76-year-old man seen for forgetfulness and difficulty walking was found to have peripheral neuropathy and anemia with hypersegmented neutrophils on blood smear.
3) A 16-year-old female with autoimmune hepatitis developed anemia with heavier menses and petechiae; bone marrow showed mild dyserythropoiesis and hypocellularity.
How to approach a child with bleeding disorderKamran Akbar
This document provides guidance on evaluating and treating children with bleeding disorders. It outlines the key steps in the clinical approach: obtaining a medical history, conducting a physical exam, and ordering laboratory tests. Common inherited disorders include hemophilia A/B and von Willebrand disease, while acquired disorders include DIC and vitamin K deficiency. Based on the history and exam findings, specific laboratory tests are interpreted to identify coagulation factor deficiencies or other causes of bleeding. Common treatments target the underlying disorder, such as intravenous immunoglobulins for ITP or DDAVP for von Willebrand disease.
This document discusses disorders of primary hemostasis, which involve problems with platelets and blood vessels. It describes how bleeding disorders are diagnosed by determining if a bleeding tendency is present, if it is inherited or acquired, and if it affects primary hemostasis. The principal presentations of bleeding disorders are then outlined, including easy bruising, bleeding from mucous membranes, menorrhagia, and excessive bleeding after trauma. Specific types of bleeding in different locations are also detailed. The document concludes by discussing typical screening tests used to evaluate bleeding disorders.
Dental Management of Patients with Bleeding DisordersDr Afsal S M
The document discusses the dental management of patients with bleeding disorders. It defines bleeding disorders and classifies them into vascular, platelet, and coagulation factor deficiencies. It describes specific disorders like hemophilia A/B, von Willebrand disease, and thrombocytopenic purpura. For dental procedures involving patients with bleeding disorders, the document recommends consulting hematologists, using local hemostatic agents, and in some cases replacing coagulation factors. It provides guidance for managing anticoagulated patients on medications like heparin, warfarin, and aspirin. The goal is to minimize bleeding risks during and after dental treatments through careful techniques and medical coordination.
approach to a bleeding child with blood disorders.pptxtsholanangmaoka
This document describes the approach to three cases of bleeding in children. Case 1 involves a 5-month-old male with intracranial bleeding and seizures who was found to have a subdural hematoma requiring surgery. Despite resuscitation efforts, the child did not survive the surgery. Case 2 is a 2-year-old male with bruising and a very low platelet count, consistent with thrombocytopenia. Case 3 involves a 1-year-old male with knee swelling and fever, who was found to have a low platelet count, consistent with disseminated intravascular coagulation. The document provides definitions of types of bleeding, the stages of hemostasis, differential diagnoses, and management strategies for bleeding
This document provides information on portal hypertension and its surgical management. It begins with the history of portal hypertension, describing early anatomists who studied the portal venous system. It then covers the anatomy of the portal system and pathophysiology of portal hypertension. Etiologies of portal hypertension including pre-hepatic, hepatic, and post-hepatic causes are discussed. Clinical presentation, diagnosis, evaluation, and general management approaches are summarized. The document concludes by focusing on surgical options for treating portal hypertension including devascularization procedures and liver transplantation.
This document provides an overview of bleeding and coagulation disorders. It discusses the components of hemostasis including primary hemostasis mediated by platelets and vessel walls and secondary hemostasis involving the coagulation factors. Common disorders are described such as platelet disorders, hemophilia, and von Willebrand disease. Clinical features and laboratory evaluation including screening coagulation tests are reviewed. Specific conditions like immune thrombocytopenic purpura and thrombotic thrombocytopenic purpura are then explained in more detail covering etiology, pathogenesis, clinical presentation, and diagnosis.
A 17-year-old male with hemophilia A presented with abdominal pain, vomiting, and hematemesis. He had a history of similar episodes and noncompliance with factor 8 replacement therapy. Evaluation found a duodenal hematoma with bleeding. He received blood transfusions and increased factor 8 replacement. His abdominal pain improved with morphine but he developed complications including acute pancreatitis. Management of hemophilia A focuses on preventing bleeding through factor replacement and treating complications of the condition and missed treatments.
Approach to patients with upper gi bleedingRajesh S
This document provides an overview of a seminar on gastrointestinal bleeding. It begins with an introduction and outline. It then covers topics like the anatomy of the GI tract and sources of bleeding. Diagnostic assessments including history, exams, and tests are reviewed. Approaches to resuscitation, classification of shock, and fluid management are outlined. Etiologies of upper and lower GI bleeding like ulcers, varices, and tumors are summarized. Endoscopic and surgical management strategies are also discussed. Risk factors for poor prognosis with GI bleeding are listed. The document concludes with a risk score to predict need for intervention in GI bleeding cases.
This document discusses vasculitis, which is an inflammatory destruction of blood vessels. It can affect all ages but some types are restricted to certain groups. It has both genetic and environmental components. Symptoms vary depending on the size of vessels involved and can include fatigue, rashes, nerve problems, and organ damage. Diagnosis involves clinical features, lab tests, and sometimes biopsies. Treatment is usually with steroids and other immunosuppressants to induce and maintain remission. Complications can be serious if not treated properly.
Basic approach to a case of anemia. Investigations to do and to arrive at the diagnosis. (Management not discussed). Peripheral smear findings with pictures are included.
This document summarizes several diseases involving platelets. It discusses thrombocytopenia, which is a low platelet count and can be primary or secondary. Primary thrombocytopenia is often autoimmune while secondary can result from bone marrow infiltration, infection, or medication. Purpura is bruising or bleeding into the skin and can be thrombocytopenic or non-thrombocytopenic. Other diseases discussed include thrombotic thrombocytopenic purpura (TTP), Wiskott-Aldrich syndrome, familial thrombocythemia, and thrombocytopathic purpura. The document provides details on causes, clinical features, oral manifestations, laboratory findings, and treatment for each condition.
The document discusses various types and causes of shock, including hypovolemic, cardiogenic, septic, neurogenic, hypoadrenal, and anaphylactic shock. It covers the pathophysiology, signs and symptoms, classification, management, and treatment of shock. Key points include that shock results from inadequate tissue perfusion due to various etiologies, management involves identifying the cause and restoring circulating volume through intravenous fluids, blood products, and surgical intervention if needed.
This document discusses bleeding disorders and provides details on specific disorders such as von Willebrand disease, hemophilia, and immune thrombocytopenia. It describes the pathophysiology of hemostasis and the coagulation cascade. Signs and symptoms of bleeding disorders are outlined depending on whether they affect the primary or secondary phase of hemostasis. The diagnostic approach and differential diagnosis for evaluating bleeding disorders is also summarized.
The document discusses various hemorrhagic and thrombotic disorders. It describes the normal hemostasis process and key tests used in evaluation. Several specific disorders are then covered in more detail, including immune thrombocytopenic purpura (ITP), hemophilia, von Willebrand disease, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), antiphospholipid syndrome (APS), and various thrombotic disorders. For each condition, it discusses causes, clinical presentation, diagnosis and management.
This document discusses hemostasis and blood transfusion. It begins with definitions of hemostasis and describes the five stages of hemostasis: vascular phase, platelet phase, coagulation phase, clot retraction, and fibrinolysis. It then discusses investigations for disorders of hemostasis, including clinical evaluation and laboratory tests. Major disorders of hemostasis are outlined, including inherited and acquired issues with blood vessels, platelets, and coagulation. The document also covers blood components, indications for component therapy, and potential complications of blood transfusion.
The thyroid gland is the largest endocrine gland located in the neck. It produces thyroid hormones such as T4 and T3 that regulate metabolism. The thyroid follicles contain colloid made of thyroglobulin, which iodine is attached to in order to produce the hormones. The hormones are then released into circulation and have widespread effects increasing the basal metabolic rate and promoting growth and development. Thyroid hormone production is regulated by TSH from the pituitary gland in a negative feedback loop. Disorders can result from too much or too little thyroid hormone production and affect many body systems.
The document provides an overview of the anatomy and physiology of the visual system. It discusses the major parts of the eye including the sclera, cornea, iris, retina, rods and cones. It describes how light is focused on the retina through the lens system and how visual signals are transmitted via the optic nerve and pathways to the visual cortex. It also covers topics like color vision, accommodation, dark adaptation and various eye movements.
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This document discusses various disorders of coagulation and hemostasis. It describes the normal physiologic mechanisms of hemostasis, coagulation pathways, and fibrinolysis. It then discusses several specific bleeding disorders including von Willebrand disease, hemophilia, disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), immune thrombocytopenic purpura (ITP), and qualitative platelet defects. Laboratory tests used to evaluate coagulation and bleeding disorders are also outlined.
This document provides an overview of approaches to evaluating and treating bleeding disorders and acute anemia. It discusses evaluating the clinical history and laboratory tests to distinguish between local and systemic bleeding issues and primary versus secondary hemostatic defects. Common causes of bleeding like hemophilia, von Willebrand disease, liver disease, and medications are reviewed. Emergency treatment options and dosing calculations for replacing coagulation factors in hemophilia are also covered.
Bleeding and clotting disorders dr anoop k ranoop k r
This document discusses bleeding and clotting disorders, including the diagnosis and evaluation of bleeding problems. It describes the principal presentations of bleeding disorders such as easy bruising, bleeding from mucous membranes, and excessive bleeding after trauma. It then covers specific types of bleeding disorders like those affecting platelets or coagulation factors. The document outlines typical screening tests used to evaluate bleeding disorders and describes both inherited and acquired causes of platelet and coagulation abnormalities.
1) An 85-year-old woman was hospitalized for severe anemia with a hemoglobin of 3 g/dL.
2) A 76-year-old man seen for forgetfulness and difficulty walking was found to have peripheral neuropathy and anemia with hypersegmented neutrophils on blood smear.
3) A 16-year-old female with autoimmune hepatitis developed anemia with heavier menses and petechiae; bone marrow showed mild dyserythropoiesis and hypocellularity.
How to approach a child with bleeding disorderKamran Akbar
This document provides guidance on evaluating and treating children with bleeding disorders. It outlines the key steps in the clinical approach: obtaining a medical history, conducting a physical exam, and ordering laboratory tests. Common inherited disorders include hemophilia A/B and von Willebrand disease, while acquired disorders include DIC and vitamin K deficiency. Based on the history and exam findings, specific laboratory tests are interpreted to identify coagulation factor deficiencies or other causes of bleeding. Common treatments target the underlying disorder, such as intravenous immunoglobulins for ITP or DDAVP for von Willebrand disease.
This document discusses disorders of primary hemostasis, which involve problems with platelets and blood vessels. It describes how bleeding disorders are diagnosed by determining if a bleeding tendency is present, if it is inherited or acquired, and if it affects primary hemostasis. The principal presentations of bleeding disorders are then outlined, including easy bruising, bleeding from mucous membranes, menorrhagia, and excessive bleeding after trauma. Specific types of bleeding in different locations are also detailed. The document concludes by discussing typical screening tests used to evaluate bleeding disorders.
Dental Management of Patients with Bleeding DisordersDr Afsal S M
The document discusses the dental management of patients with bleeding disorders. It defines bleeding disorders and classifies them into vascular, platelet, and coagulation factor deficiencies. It describes specific disorders like hemophilia A/B, von Willebrand disease, and thrombocytopenic purpura. For dental procedures involving patients with bleeding disorders, the document recommends consulting hematologists, using local hemostatic agents, and in some cases replacing coagulation factors. It provides guidance for managing anticoagulated patients on medications like heparin, warfarin, and aspirin. The goal is to minimize bleeding risks during and after dental treatments through careful techniques and medical coordination.
approach to a bleeding child with blood disorders.pptxtsholanangmaoka
This document describes the approach to three cases of bleeding in children. Case 1 involves a 5-month-old male with intracranial bleeding and seizures who was found to have a subdural hematoma requiring surgery. Despite resuscitation efforts, the child did not survive the surgery. Case 2 is a 2-year-old male with bruising and a very low platelet count, consistent with thrombocytopenia. Case 3 involves a 1-year-old male with knee swelling and fever, who was found to have a low platelet count, consistent with disseminated intravascular coagulation. The document provides definitions of types of bleeding, the stages of hemostasis, differential diagnoses, and management strategies for bleeding
This document provides information on portal hypertension and its surgical management. It begins with the history of portal hypertension, describing early anatomists who studied the portal venous system. It then covers the anatomy of the portal system and pathophysiology of portal hypertension. Etiologies of portal hypertension including pre-hepatic, hepatic, and post-hepatic causes are discussed. Clinical presentation, diagnosis, evaluation, and general management approaches are summarized. The document concludes by focusing on surgical options for treating portal hypertension including devascularization procedures and liver transplantation.
This document provides an overview of bleeding and coagulation disorders. It discusses the components of hemostasis including primary hemostasis mediated by platelets and vessel walls and secondary hemostasis involving the coagulation factors. Common disorders are described such as platelet disorders, hemophilia, and von Willebrand disease. Clinical features and laboratory evaluation including screening coagulation tests are reviewed. Specific conditions like immune thrombocytopenic purpura and thrombotic thrombocytopenic purpura are then explained in more detail covering etiology, pathogenesis, clinical presentation, and diagnosis.
A 17-year-old male with hemophilia A presented with abdominal pain, vomiting, and hematemesis. He had a history of similar episodes and noncompliance with factor 8 replacement therapy. Evaluation found a duodenal hematoma with bleeding. He received blood transfusions and increased factor 8 replacement. His abdominal pain improved with morphine but he developed complications including acute pancreatitis. Management of hemophilia A focuses on preventing bleeding through factor replacement and treating complications of the condition and missed treatments.
Approach to patients with upper gi bleedingRajesh S
This document provides an overview of a seminar on gastrointestinal bleeding. It begins with an introduction and outline. It then covers topics like the anatomy of the GI tract and sources of bleeding. Diagnostic assessments including history, exams, and tests are reviewed. Approaches to resuscitation, classification of shock, and fluid management are outlined. Etiologies of upper and lower GI bleeding like ulcers, varices, and tumors are summarized. Endoscopic and surgical management strategies are also discussed. Risk factors for poor prognosis with GI bleeding are listed. The document concludes with a risk score to predict need for intervention in GI bleeding cases.
This document discusses vasculitis, which is an inflammatory destruction of blood vessels. It can affect all ages but some types are restricted to certain groups. It has both genetic and environmental components. Symptoms vary depending on the size of vessels involved and can include fatigue, rashes, nerve problems, and organ damage. Diagnosis involves clinical features, lab tests, and sometimes biopsies. Treatment is usually with steroids and other immunosuppressants to induce and maintain remission. Complications can be serious if not treated properly.
Basic approach to a case of anemia. Investigations to do and to arrive at the diagnosis. (Management not discussed). Peripheral smear findings with pictures are included.
This document summarizes several diseases involving platelets. It discusses thrombocytopenia, which is a low platelet count and can be primary or secondary. Primary thrombocytopenia is often autoimmune while secondary can result from bone marrow infiltration, infection, or medication. Purpura is bruising or bleeding into the skin and can be thrombocytopenic or non-thrombocytopenic. Other diseases discussed include thrombotic thrombocytopenic purpura (TTP), Wiskott-Aldrich syndrome, familial thrombocythemia, and thrombocytopathic purpura. The document provides details on causes, clinical features, oral manifestations, laboratory findings, and treatment for each condition.
The document discusses various types and causes of shock, including hypovolemic, cardiogenic, septic, neurogenic, hypoadrenal, and anaphylactic shock. It covers the pathophysiology, signs and symptoms, classification, management, and treatment of shock. Key points include that shock results from inadequate tissue perfusion due to various etiologies, management involves identifying the cause and restoring circulating volume through intravenous fluids, blood products, and surgical intervention if needed.
This document discusses bleeding disorders and provides details on specific disorders such as von Willebrand disease, hemophilia, and immune thrombocytopenia. It describes the pathophysiology of hemostasis and the coagulation cascade. Signs and symptoms of bleeding disorders are outlined depending on whether they affect the primary or secondary phase of hemostasis. The diagnostic approach and differential diagnosis for evaluating bleeding disorders is also summarized.
The document discusses various hemorrhagic and thrombotic disorders. It describes the normal hemostasis process and key tests used in evaluation. Several specific disorders are then covered in more detail, including immune thrombocytopenic purpura (ITP), hemophilia, von Willebrand disease, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), antiphospholipid syndrome (APS), and various thrombotic disorders. For each condition, it discusses causes, clinical presentation, diagnosis and management.
This document discusses hemostasis and blood transfusion. It begins with definitions of hemostasis and describes the five stages of hemostasis: vascular phase, platelet phase, coagulation phase, clot retraction, and fibrinolysis. It then discusses investigations for disorders of hemostasis, including clinical evaluation and laboratory tests. Major disorders of hemostasis are outlined, including inherited and acquired issues with blood vessels, platelets, and coagulation. The document also covers blood components, indications for component therapy, and potential complications of blood transfusion.
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The thyroid gland is the largest endocrine gland located in the neck. It produces thyroid hormones such as T4 and T3 that regulate metabolism. The thyroid follicles contain colloid made of thyroglobulin, which iodine is attached to in order to produce the hormones. The hormones are then released into circulation and have widespread effects increasing the basal metabolic rate and promoting growth and development. Thyroid hormone production is regulated by TSH from the pituitary gland in a negative feedback loop. Disorders can result from too much or too little thyroid hormone production and affect many body systems.
The document provides an overview of the anatomy and physiology of the visual system. It discusses the major parts of the eye including the sclera, cornea, iris, retina, rods and cones. It describes how light is focused on the retina through the lens system and how visual signals are transmitted via the optic nerve and pathways to the visual cortex. It also covers topics like color vision, accommodation, dark adaptation and various eye movements.
This document summarizes the transport and exchange of respiratory gases in the body. It discusses the diffusion of oxygen and carbon dioxide across membranes, factors that affect diffusion, and the roles of hemoglobin and bicarbonate ions in transporting oxygen and carbon dioxide in the blood and tissues. The oxygen-hemoglobin dissociation curve and factors that can shift it are also described.
Spermatogenesis is the process by which male germ cells develop into mature sperm cells. It begins at puberty and continues throughout a man's life. The process occurs in the testes and epididymis. In the testes, spermatogonia undergo mitosis and meiosis to form haploid spermatids. Spermatids then undergo spermiogenesis to form mature sperm, acquiring motility and other structures. Hormones like FSH, LH and testosterone regulate spermatogenesis, which produces several hundred million sperm daily.
Alveolar bone forms the sockets that hold teeth in place and is a component of the periodontium. It develops during tooth formation and is resorbed when teeth are lost. Alveolar bone consists of alveolar bone proper that lines tooth sockets and supporting alveolar bone made of cortical plates and spongy bone. It undergoes remodeling to accommodate tooth movement and is sensitive to pressure and functional demands, making it important for orthodontics and adapting to tooth loss.
Dentin is the hard tissue that forms the bulk of the tooth beneath enamel. It consists of a bone-like matrix with dentinal tubules that contain odontoblast processes and nerves. Dentin is less mineralized than enamel but provides strength and protects the pulp. The three main theories of dentin hypersensitivity are direct neural stimulation, transduction, and the most accepted hydrodynamic theory, which proposes that fluid movement in the dentinal tubules causes mechanical stimulation of intratubular nerves when exposed dentin is subjected to stimuli.
This document summarizes the specialized mucosa and papillae found on the dorsal surface of the tongue. It describes the four main types of papillae - filliform, fungiform, circumvallate, and foliate papillae. It details their locations, histological features, and functions. The document also discusses taste buds and their role in gustation. Finally, it covers the clinical significance of some variations in tongue morphology and the differences seen in other species.
The document provides information on the structure and functions of the dental pulp. It begins with definitions and general anatomy, describing the pulp as a soft connective tissue enclosed within dentin. It then discusses the zones and structural features of the pulp in more detail. This includes the odontoblastic zone containing odontoblasts and nerve endings, the cell-free zone with capillaries and nerves, and the cell-rich zone with fibroblasts and blood vessels. Key cell types like odontoblasts, fibroblasts, and immune cells are also described. The functions of the pulp in dentin formation, nutrition, and defense are highlighted.
This document discusses the various sequelae that can result from pulpitis, including both acute and chronic forms of pulpitis, apical periodontitis, periapical abscess, osteomyelitis, and periapical cysts. It provides details on the etiology, clinical features, and treatment for each condition. Pulpitis can lead to further inflammation of the surrounding tissues like the apical periodontium and bone. Without proper treatment, pulpitis risks developing into more serious conditions such as apical abscesses or osteomyelitis that require surgical intervention.
This document provides an overview of forensic odontology and the role of dental evidence in various contexts. It discusses personal identification using dental records, identification in mass disasters, extracting dental DNA for identification, analyzing bite marks, and the duties of forensic odontologists, such as documenting evidence, comparing records, and testifying as expert witnesses. The key applications of forensic odontology include identifying unknown remains, assisting in mass disasters, and analyzing bite marks and other dental evidence in legal cases.
1. Amelogenesis involves the life cycle of ameloblasts from the pre-secretory to post-secretory phases as they form enamel.
2. In the secretory phase, ameloblasts deposit enamel matrix proteins and undergo partial mineralization, developing Tome's process which is responsible for enamel rod and interrod formation.
3. Enamel maturation then occurs, fully mineralizing the enamel from the dentin-enamel junction outward in a gradual process modulated by alternating ameloblast types.
The document discusses the periodontal ligament. It describes the periodontal ligament as the connective tissue that surrounds the root and connects it to the alveolar bone. It is made up of principal fibers, cells, ground substance, blood vessels and nerves. The principal fibers are organized into groups like the alveolar crest fibers, horizontal fibers, oblique fibers, and apical fibers that provide support and resist various forces on the teeth. The periodontal ligament also contains cells like fibroblasts, cementoblasts and osteoblasts that allow for remodeling of the tissues. It carries out functions like shock absorption and sensation in addition to attachment of teeth to bone.
Odontogenic tumors arise from tooth-forming tissues and can be divided into three categories: tumors of odontogenic epithelium without mesenchyme, tumors with both epithelium and mesenchyme, and tumors of mesenchyme alone. Ameloblastoma is the most common odontogenic tumor, representing 1% of jaw tumors. It typically presents as a multilocular radiolucency in the mandible and is classified as solid/multicystic, unicystic, or peripheral. Histologically it demonstrates islands of epithelial cells resembling dental lamina. Treatment involves wide local excision due to its persistence and recurrence.
Dental caries is caused by acids produced by bacteria in the mouth that metabolize sugars. It is a chemoparasitic process involving tooth demineralization in two stages. Key factors are the "cariogenic" bacteria Streptococcus mutans and Lactobacillus, along with frequent sugar consumption. Early theories attributed caries to worms, humoral imbalances, or chemical/parasitic causes. Current understanding involves the interplay of host tooth/plaque, carbohydrate substrates, and cariogenic microbes. Nursing bottle caries occurs when babies sleep with bottles containing sugars.
This document discusses ethics in research. It defines research ethics as applying ethical standards to all stages of research, from planning to evaluation. Key principles discussed include honesty, objectivity, integrity, care for participants, openness, respect for intellectual property, confidentiality, non-discrimination, and social responsibility. The document also covers issues like authorship, plagiarism, peer review, research with animals and humans, and addressing misconduct. Overall, it emphasizes that ethical research promotes values like trust, accountability and protecting participants.
This document discusses dental ethics and ethical principles that dental professionals should follow. It notes that dentistry, as a profession, is bound by an ethical code of conduct that seeks to determine what actions professionals should and should not take. The document outlines basic ethical principles like autonomy, justice, and confidentiality. It also provides examples of ethical and unethical behaviors. Additionally, it discusses professional codes of ethics, reasons for having codes, and how to resolve ethical dilemmas.
The document discusses stainless steel crowns, including their definition as prefabricated crown forms adapted to individual teeth and cemented. It covers the history, classifications, indications and contraindications for stainless steel crowns in both primary and permanent teeth. The clinical procedure section describes tooth preparation, crown selection and adaptation, and cementation."
This document defines and classifies oral habits such as thumb sucking and tongue thrusting. It discusses the etiology, diagnosis, and treatment of these habits. Specifically, it notes that oral habits can lead to dentofacial deformities if they persist for long periods. Diagnosis involves examining the patient's swallowing pattern and looking for signs like an open bite. Treatment may involve counseling, reminder appliances to interrupt the habit, or myofunctional exercises to train correct tongue and swallowing posture. The goal is to intercept oral habits before they cause dental or skeletal issues.
This document discusses space management and space maintainers. It begins by defining space management and explaining that premature loss of primary teeth is a common cause of malocclusion. It then discusses the objectives and indications of space maintenance, as well as causes of space loss. The document provides details on different types of space maintainers, including removable, fixed, band and loop, and lingual arch space maintainers. It discusses factors to consider for space maintenance such as the amount of space closure, eruption timing of permanent successors, and oral musculature. Overall, the document provides a comprehensive overview of space management and different approaches to space maintenance.
This document provides information on managing medically compromised patients in dentistry. It discusses various conditions including heart diseases, leukemia, diabetes mellitus, and cystic fibrosis. For each condition, it describes clinical manifestations, oral manifestations, and important considerations for dental treatment. Key points discussed include the need for medical consultations, antibiotic prophylaxis if needed, and modifying treatment for patients with low platelet counts or susceptibility to infections.
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7shruti jagirdar
Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
to be treated is characteristically a disease of aging ( e.g., Alzheimer's disease) or
because the population to be treated is known to include substantial numbers of
geriatric patients (e.g., hypertension).
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
This presentation gives information on the pharmacology of Prostaglandins, Thromboxanes and Leukotrienes i.e. Eicosanoids. Eicosanoids are signaling molecules derived from polyunsaturated fatty acids like arachidonic acid. They are involved in complex control over inflammation, immunity, and the central nervous system. Eicosanoids are synthesized through the enzymatic oxidation of fatty acids by cyclooxygenase and lipoxygenase enzymes. They have short half-lives and act locally through autocrine and paracrine signaling.
Congestive Heart failure is caused by low cardiac output and high sympathetic discharge. Diuretics reduce preload, ACE inhibitors lower afterload, beta blockers reduce sympathetic activity, and digitalis has inotropic effects. Newer medications target vasodilation and myosin activation to improve heart efficiency while lowering energy requirements. Combination therapy, following an assessment of cardiac function and volume status, is the most effective strategy to heart failure care.
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Giloy in Ayurveda - Classical Categorization and SynonymsPlanet Ayurveda
Giloy, also known as Guduchi or Amrita in classical Ayurvedic texts, is a revered herb renowned for its myriad health benefits. It is categorized as a Rasayana, meaning it has rejuvenating properties that enhance vitality and longevity. Giloy is celebrated for its ability to boost the immune system, detoxify the body, and promote overall wellness. Its anti-inflammatory, antipyretic, and antioxidant properties make it a staple in managing conditions like fever, diabetes, and stress. The versatility and efficacy of Giloy in supporting health naturally highlight its importance in Ayurveda. At Planet Ayurveda, we provide a comprehensive range of health services and 100% herbal supplements that harness the power of natural ingredients like Giloy. Our products are globally available and affordable, ensuring that everyone can benefit from the ancient wisdom of Ayurveda. If you or your loved ones are dealing with health issues, contact Planet Ayurveda at 01725214040 to book an online video consultation with our professional doctors. Let us help you achieve optimal health and wellness naturally.
Gene therapy can be broadly defined as the transfer of genetic material to cure a disease or at least to improve the clinical status of a patient.
One of the basic concepts of gene therapy is to transform viruses into genetic shuttles, which will deliver the gene of interest into the target cells.
Safe methods have been devised to do this, using several viral and non-viral vectors.
In the future, this technique may allow doctors to treat a disorder by inserting a gene into a patient's cells instead of using drugs or surgery.
The biggest hurdle faced by medical research in gene therapy is the availability of effective gene-carrying vectors that meet all of the following criteria:
Protection of transgene or genetic cargo from degradative action of systemic and endonucleases,
Delivery of genetic material to the target site, i.e., either cell cytoplasm or nucleus,
Low potential of triggering unwanted immune responses or genotoxicity,
Economical and feasible availability for patients .
Viruses are naturally evolved vehicles that efficiently transfer their genes into host cells.
Choice of viral vector is dependent on gene transfer efficiency, capacity to carry foreign genes, toxicity, stability, immune responses towards viral antigens and potential viral recombination.
There are a wide variety of vectors used to deliver DNA or oligo nucleotides into mammalian cells, either in vitro or in vivo.
The most common vector system based on retroviruses, adenoviruses, herpes simplex viruses, adeno associated viruses.
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
5. TOURNIQUET TEST
Evaluates vascular integrity
Place B.P. cuff and inflate to 90-100mm Hg over
forearm
Wait for 5 minutes
Check for number of Petechiae within a 2.5 cm circle
Normal-less than 10 Petechiae
Rumbell Leed phenomenon
6.
7.
8.
9.
10. BLEEDING TIME
Time interval taken from oozing of blood to the
arrest of bleeding from a standard cut.
Normal
1-6 minutes
Duke and Ivy methods
Prick on the finger tip and check for the time taken
for stoppage of blood oozing out
11. PLATELET COUNT
Determines increase or decrease of
platelets
Normal
1,50,000-4,00,000mm³
Blood smear examination
Hemocytometer analyzer
12. CLOTTING TIME
Time taken for the blood to clot after collecting
from the body
Intrinsic clotting factors
Capillary tube method
Normal
5-10 minutes
13. PROTHROMBIN TIME/I.N.R.
Indicates total prothrombin present in blood
Thromboplastin and calcium added to pt serum and is
expressed in ratio(International Normalized Ratio=I.N.R.)
Normal
11-13 seconds
I.N.R.
1.0-2.0
Evaluates extrinsic system and F I,II,V,VII,X
14. ACTIVATED PARTIAL THROMBOPLASTIN TIME
(a.P.T.T.)
Tests intrinsic and common pathway system
Activity of VIII,IX,XI,XII
Kaolin added to patient plasma
Normal value
15-35 seconds
15. THROMBIN TIME
Test the ability to form initial clot from
fibrinogen
Thrombin is added to plasma and time taken
to clot is noted
Normal
9-13 seconds
28. Ehlers Danlos Syndrome
Inherited connective tissue disorder
Joint Hypermobility
Cutaneous Fragility
Hyperextensibility of skin
11 subtypes –unique biochemical defects and
clinical features
29. Clinical features
Type 1-classic form
Varicose veins and prematurity
Type VIII
Early onset periodontal disease
Type VII
children
Microdontia
Dentinal structural defects in primary dentition
Bleeding after brushing
30.
31.
32. Oral Manifestation
Fragile gingiva and oral mucosa
Gingival hyperplasia and fibrous nodules
Hypermobilty of T.M.J.
Lack of normal scalloping of D.E.J.
Pulp stones
Periodontal destruction
Gorlin sign
33.
34.
35. SCURVY
Dietary deficiency of Vit C
Defect in collagen synthesis
Petechial hemorrhages at the hair follicles
Purpura on lower extremities
Hemorrhage to muscles, joints ,nail beds,
gingival tissues
36. Oral manifestations
Gingiva appears ulcerated and boggy
Foul breath
Loss of bone
Loosening of teeth
Implementation of Vit C
1 g/d of Vit C-rapid resolution
37.
38. Cushing's Syndrome
Corticosteroid intake or production
Protein wasting and atrophy of connective
tissue
Skin bleeding and easy bruising
39. Henoch-Schönlein Purpura
Immune complex mediated hypersensitivity
Children with acute infections
Vasculitis and purpuric lesions
Joint pain and abdominal pain
hematuria
40.
41. Glanzmann Thrombasthenia
Chronic hereditary hemorrhagic disease
Autosomal recessive trait
Deficiency of platelet glycoprotein II b & III a
Spontaneous bleeding after minor trauma
Purpuric hemorrhage of skin
Prolonged bleeding time
Microfibrillar collagen & C- Aminocaproic Acid
42.
43. Wiskott-Aldrich Syndrome
X-linked recessive genetic condition
Immunoglobulin M Deficiency
Defect in WAS p
Thrombocytopenic purpura
Eczema
Petechiae and purpuric rashes
Boils, Otitis Media, Bloody Diarrhea
Respiratory infection
44.
45. High potential for Malignant Lymphoma
Laboratory findings
Prolonged bleeding time
Anisocytosis
Reduced platelet
Reduced Adenosine Diphosphate Nucleotide
46. Bernard Soulier Syndrome
Autosomal dominant disease
Deficiency of surface membrane
glycoprotein of platelets –binding of Vwf
Prolonged bleeding time
Large platelets
Defective platelet aggregation
51. ACUTE
90% in children
Below 10 years
Viral or upper respiratory infections
Fall and winter seasons
Onset is sudden and severe
Recovers within 3-6 months
52. CHRONIC
Adults-women
20-40 years
Insidious -history of long standing bruises
S.L.E.,A.I.D.S.,lymphoproliferative disorders
and hemolytic anemia
53. Clinical features
Below 40,000 mm³
Pinpoint Petechial hemorrhages
Purpura and bruises
Arms,legs,thighs,chest,neck
Mucosal bleeding in G.I.T.
Risk of intracranial hemorrhage-<20,000mm³
54.
55. Oral manifestations
Spontaneous bleeding from gingiva
Blood filled bullae
Profuse oozing of blood from gingival margin
Purplish globs of clotted blood on teeth
Bleeding along occlusal line
Multifocal Petechial red spots that do not blanch
seen on soft palate
56.
57. DRUG INDUCED T.P.
Reversible within 7-10 days of discontinuation
Aspirin induces functional platelet defect
Single 100mg-rapid complete inhibition of platelet
cyclooxygenase activity and thrombaxone
production
Prolonged bleeding time
58. MOSCHOWITZ DISEASE
Also called as T.T.P.
Life threatening multisystem disorder
Presence of thrombotic microangiopathies
Micro vascular lesions with platelet
aggregation
63. Hemophilia A-factor VIII
Hemophilia B- factor IX
Hemophilia C-factor XI
Hemophilia A:
1 in 10,000
X-linked recessive bleeding disorder
Only Males are affected
1/3rd of patients-no family history
64. CLINICAL FEATURES
Hemorrhage to joints, subcutaneous tissues,
internal organs
Massive hematoma
30-50%-neonatal bleeding from umbilical cord
Petechiae is rare
Cyclic remissions and exacerbations
65.
66.
67. CLASSIFICATION
Clinical severity depends on extent of
clotting factor deficiency
<1%-severe with life threatening bleeding
1-5%-moderate with post traumatic bleeding
5-20%-mild disease
68. Oral Manifestations
Massive and prolonged gingival hemorrhage
Tooth eruption and exfoliation with bleeding
Mandibular pseudo tumor
Subperiosteal bleeding with reactive new bone
formation causing tumor like expansion of bone
Hematoma formation following nerve block
anesthesia
69.
70. Investigations
Prolonged a.P.P.T.(Activated Partial Thromboplastin Time)
Whole blood coagulation time is prolonged
Factor VIII is reduced
Normal bleeding time
Normal prothrombin time
Functional assay
71. Rₓ
Factor VIII & IX replacement
30% for mild
60% for major surgeries
FRESH FROZEN PLASMA
Desmopressin
0.3 µg/kg body weight-I.V. or S.C. before dental procedures
Increases F VIII,Vwf antigen,ristocetin co factor activity
72.
73.
74. Von willebrands disease
Autosomal dominant disorder
Abnormality of Vwf
Males and females
Acquired form
Wilms tumor
S.L.E.
75. TYPES
Type I
Partial quantitative decrease of Vwf and F VIII
Type II
Qualitative defect of Vwf
Type III
Severe form Less than 1%
Type IV
Platelet type mimicking platelet disorder
76.
77. Laboratory Findings
Prolonged bleeding time
Normal clotting time
Normal prothrombin time
Normal serum fibrinogen
Increased capillary fragility
Positive tourniquet test
79. Anticoagulant Coagulopathies
Heparin
Binds with antithrombin III
Inhibit activation of F IX,X,XI
Reduces thrombin generation & fibrin formation
Duration of action-3-4 hours
Antidote-Protamine Sulphate
80. COUMARIN
Warfarin and dicumarol
Slow thrombin production and clot formation
Blocks the action of Vit K
F II,VI,IX,X reduced
Anticoagulant effect reversed by F.F.P.
I.N.R. monitors the anticoagulation levels
Returns to normal within 2-4 days after discontinuation
81. Intramuscular injection cause bleeding and hematoma
Additive effect when used with aspirin
Drug potency increased with
Metronidazole
Penicillin
Erythromycin
Cephalosporin
Tetracycline
82. LIVER DISEASES
Depends on extent of liver damage
Impaired protein synthesis
Clotting and fibrinolytic systems reduced
Acute or chronic disease
Decreased Vit K dependent factors
F II,VII,IX,X
Rx is Vit K therapy for 3 days
F.F.P.
Desmopressin
83. VIT K DEFICIENCY
Production of poorly functioning Vit K dependant
factors
Severe hemorrhage in acutely ill patients of 7-10
days
Rapid fall in F VII elevates I.N.R. resulting
prolongation of a.P.T.T
Supplementation of Vit K restores the defect
84. DISSEMINATED INTRAVASCULAR
COAGULATION
Due to widespread IV activation of clotting cascade
Initially forms microthrombi and emboli throughout
vasculature
bleeding tendency due to consumption of clotting factors
bruising or purpura
Oozing from venepuncture and surgical wound sites
86. Investigations
↑P.P.T. &P.T.
↑Fibrin Degradation Products
↓serum fibrinogen levels(<1mg/ml)
↓ factor V and factor VIII activities
Thrombocytopenia
87. Rₓ
I.V. heparin to prevent thrombi initially
Fluid resuscitation
Treat underlying cause
Correct clotting abnormalities with
Fresh frozen plasma
Cryoprecipitate
Platelet transfusion
88. ORAL FINDINGS & GUIDLINES
Spontaneous gingival bleeding
Hemosiderin deposits on tooth surface
Poor oral hygiene
Higher caries rate
Severe periodontal diseases
Risk of hematoma formation
Hemarthrosis to T.M.J.
89. MEDICAL CONSULTATION
Bleeding
Alcohol abuse
Anticoagulation therapy
Corticosteroid therapy
Need for additional medications
Change in dosage or alternative medication
90. LABORATORY INVESTIGATIONS
BLEEDING TIME
PLATELET COUNT
PROTHROMBIN TIME
ACTIVATED PARTIAL THROMBOPLASTIN
I.N.R.
THROMBIN TIME
CLOTTING TIME
91. ORAL SURGICAL PROCEDURES
Replacement of coagulation factor 50-100%
Post operative maintenance therapy
Factor concentrates
D.D.A.V.P.
Cryoprecipitate
F.F.P.
Packing of extraction socket with Hemostatic
agents
92. Gingival bleeding not responding to
antifibrinolytics requires 20-30% F VIII,F IX
Local Hemostatic methods
Pressure packs
Vasoconstrictors
Suturing
Surgical stents
Topical thrombin
93.
94. ANTIFIBRINOLYTIC AGENTS
E.A.C.A.
Tranexamic acid
Block conversion of plasminogen to plasmin
Clot stabilization
50 mg/kg-topically
250mg/ml-systemically as oral rinse(6hrs,7-10 )
Fibrin glue
Forms an adhesive gel & attract platelets
95. PAIN CONTROL
Hypnosis
Intravenous sedation
Nitrous oxide analgesia
Intrapulpal anesthesia for pulp extirpation
Periodontal ligament and gingival papillary
injections
L.A. with epinephrine
96. Aspirin & N.S.A.I.Ds contraindicated
acetaminophen and codeine
Intramuscular injections should be avoided
due to risk of hematoma
Ice packs in area of hematoma during nerve
blocks
97. PERIODONTAL THERAPIES
Inflamed and swollen gingiva treated with
chlorhexidine mouth wash
Use of cavitron or hand instrument prior to deep
scaling
Deep scaling & root planning performed in
quadrants
Post treatment Antifibrinolytic oral rinses
Periodontal surgical procedures-↑50%
98. RESTORATIVE THERAPY
Rubber Dam Isolation
Avoid Trauma with high speed evacuators
Matrices,wedges,retraction cords use with caution
Avoid denture related trauma with careful insertion
99. ENDODONTIC THERAPY
Root canal treatment is the choice
Avoid filling beyond apex
Application of epinephrine to the apical
region provides Hemostasis
100. PEDIATRIC DENTAL THERAPY
Extraction of mobile teeth with periodontal space
anesthesia with proper oral hygiene measures
Bleeding control with gauze pressure
Crown preparation with minimal removal of
enamel at gingival region
Topical fluoride therapy
Pit and fissure sealants
101. ORTHODONTIC THERAPY
Avoid mucosal lacerations with brackets,
bands and wires
Use of extra oral force
Shorter treatment appointments
102. PATIENTS ON ANTICOAGULANTS
I.N.R.- >3.5-4.0
No treatment without coumarin modification
I.N.R.- <3.5-4.0
Minor procedures with local measures without drug modification
During significant bleeding
Drug modification
INR-<2.0-3.0
Local measures
Extensive surgeries-I.N.R.-<1.5
103. EMERGENCIES
Palliative Treatment
Infections treated with high dose antibiotics
Extractions should be avoided till bleeding
controlled
Aspirin & N.S.A.I.Ds not indicated
Consultation with physician