Von willebrands disease
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Von Willebrand disease (VWD) is the most common inherited bleeding disorder, caused by mutations resulting in decreased or impaired von Willebrand factor (VWF). VWF promotes clotting by forming bridges between platelets and injured endothelium, and between platelets. It also carries and protects factor VIII. VWD is classified into three main types - type I is most common due to VWF deficiency; type II involves functional defects; type III is most severe with very low VWF. Treatment involves desmopressin, VWF replacement, or factor VIII depending on type and severity of bleeding. Careful management is needed around surgery, delivery, and circumcision.
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Von Willebrand Disease
Von Willebrand Disease is the most common hereditary bleeding disorder; roughly 1 in every 100 people suffers from the disease. People who suffer from VWD have blood that does not clot properly.
Normally when a person is injured and starts to bleed, the von Willebrand factor in the blood attaches to small blood cells called platelets. This helps the platelets stick together to form a clot at the site of the injury and stop bleeding. When a person has VWD, the clot might take longer to form or not form the way it should and bleeding might take longer to stop. This can lead to heavy, hard-to-stop bleeding. Although rare, the bleeding can be severe enough to damage joints or internal organs, or even be life-threatening.
http://www.nlm.nih.gov/medlineplus/plateletdisorders.html#cat1
http://www.cdc.gov/ncbddd/vwd/facts.html
von Willebrand disease
Von Willebrand disease is caused by mutations in the von Willebrand factor gene and results in bleeding problems. There are several types of von Willebrand disease characterized by differences in von Willebrand factor amount and function. Treatment depends on disease severity and involves desmopressin, factor replacement therapy, or antifibrinolytics to prevent and control bleeding.
VWD
The document describes 3 cases of von Willebrand disease (VWD), with Case 1 having Type I VWD characterized by a partial deficiency of von Willebrand factor (vWF), Case 2 having Type 2N VWD or Normandy VWD characterized by a qualitative defect with normal levels of vWF, and Case 3 having the most severe Type III VWD characterized by a complete deficiency of vWF. VWD is an inherited bleeding disorder caused by defects in vWF that leads to reduced platelet adhesion and coagulation Factor VIII levels. The classification and treatment of the different VWD types is outlined based on the level and functional abnormalities of vWF
Von willebrand factor
von Willebrand factor (VWF)is a blood glycoprotein involved in hemostasis, specifically, platelet adhesion. It is deficient and/or defective in von Willebrand disease and is involved in many other diseases, including thrombotic thrombocytopenic purpura.
Von Willebrand Disease
Introduction of von Willebrand disease
Types of VWD
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Von willebrand's disease
This document summarizes von Willebrand disease, an inherited bleeding disorder caused by decreased levels or function of von Willebrand factor. The main types are type 1, the most common, with low von Willebrand factor levels; type 2 with abnormal von Willebrand factor function; and type 3 where it is absent. Symptoms range from mild to severe bleeding. Diagnosis involves tests of von Willebrand factor antigen, activity, and structure. Treatment focuses on replacing missing clotting factors or stabilizing clots. Complications can include anemia or death from bleeding if not managed.
Von willebrand disease
Von Willebrand disease is the most common inherited bleeding disorder. It is caused by deficiencies or defects in von Willebrand factor, which plays a key role in hemostasis. The document discusses the synthesis, structure, and function of VWF, as well as its clearance mechanisms. It then covers the classification of VWD into types 1, 2, and 3 based on the nature and severity of the VWF deficiency. Diagnostic testing and evaluation algorithms are presented. Management strategies for VWD include local hemostatic measures, antifibrinolytic agents, hormonal therapies, desmopressin to increase VWF levels, and VWF/FVIII concentrates for replacement therapy.
Von willebrand disease
Von Willebrand disease is a genetic bleeding disorder caused by missing or defective von Willebrand factor. It results in easy bruising, excessive bleeding, and heavy periods. There are several types classified by the von Willebrand factor defect. Treatment depends on severity but may include desmopressin, clotting factor concentrates, hormonal treatments, or antifibrinolytics. Pregnancy requires extra precautions due to risks of bleeding and transmission to offspring.
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Von Willebrand Disease
Von Willebrand Disease is the most common hereditary bleeding disorder; roughly 1 in every 100 people suffers from the disease. People who suffer from VWD have blood that does not clot properly.
Normally when a person is injured and starts to bleed, the von Willebrand factor in the blood attaches to small blood cells called platelets. This helps the platelets stick together to form a clot at the site of the injury and stop bleeding. When a person has VWD, the clot might take longer to form or not form the way it should and bleeding might take longer to stop. This can lead to heavy, hard-to-stop bleeding. Although rare, the bleeding can be severe enough to damage joints or internal organs, or even be life-threatening.
http://www.nlm.nih.gov/medlineplus/plateletdisorders.html#cat1
http://www.cdc.gov/ncbddd/vwd/facts.html
von Willebrand disease
Von Willebrand disease is caused by mutations in the von Willebrand factor gene and results in bleeding problems. There are several types of von Willebrand disease characterized by differences in von Willebrand factor amount and function. Treatment depends on disease severity and involves desmopressin, factor replacement therapy, or antifibrinolytics to prevent and control bleeding.
VWD
The document describes 3 cases of von Willebrand disease (VWD), with Case 1 having Type I VWD characterized by a partial deficiency of von Willebrand factor (vWF), Case 2 having Type 2N VWD or Normandy VWD characterized by a qualitative defect with normal levels of vWF, and Case 3 having the most severe Type III VWD characterized by a complete deficiency of vWF. VWD is an inherited bleeding disorder caused by defects in vWF that leads to reduced platelet adhesion and coagulation Factor VIII levels. The classification and treatment of the different VWD types is outlined based on the level and functional abnormalities of vWF
Von willebrand factor
von Willebrand factor (VWF)is a blood glycoprotein involved in hemostasis, specifically, platelet adhesion. It is deficient and/or defective in von Willebrand disease and is involved in many other diseases, including thrombotic thrombocytopenic purpura.
Von Willebrand Disease
Introduction of von Willebrand disease
Types of VWD
Symptoms of VWD
Diagnosis of VWD
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Von willebrand's disease
This document summarizes von Willebrand disease, an inherited bleeding disorder caused by decreased levels or function of von Willebrand factor. The main types are type 1, the most common, with low von Willebrand factor levels; type 2 with abnormal von Willebrand factor function; and type 3 where it is absent. Symptoms range from mild to severe bleeding. Diagnosis involves tests of von Willebrand factor antigen, activity, and structure. Treatment focuses on replacing missing clotting factors or stabilizing clots. Complications can include anemia or death from bleeding if not managed.
Von willebrand disease
Von Willebrand disease is the most common inherited bleeding disorder. It is caused by deficiencies or defects in von Willebrand factor, which plays a key role in hemostasis. The document discusses the synthesis, structure, and function of VWF, as well as its clearance mechanisms. It then covers the classification of VWD into types 1, 2, and 3 based on the nature and severity of the VWF deficiency. Diagnostic testing and evaluation algorithms are presented. Management strategies for VWD include local hemostatic measures, antifibrinolytic agents, hormonal therapies, desmopressin to increase VWF levels, and VWF/FVIII concentrates for replacement therapy.
Von willebrand disease
Von Willebrand disease is a genetic bleeding disorder caused by missing or defective von Willebrand factor. It results in easy bruising, excessive bleeding, and heavy periods. There are several types classified by the von Willebrand factor defect. Treatment depends on severity but may include desmopressin, clotting factor concentrates, hormonal treatments, or antifibrinolytics. Pregnancy requires extra precautions due to risks of bleeding and transmission to offspring.
Von wille brand disease
Von Willebrand disease is a bleeding disorder caused by low levels of the clotting protein von Willebrand factor. There are three main types of the disease - type 1 involves a small amount of von Willebrand factor present, type 2 involves normal levels but defects in function/structure, and type 3 involves no von Willebrand factor present. Symptoms include easy bruising, excessive bleeding, and heavy menstrual periods. The disease is usually inherited and testing involves bleeding time, factor VIII levels, and von Willebrand factor specific tests. Treatment focuses on avoiding aspirin/NSAIDs and using drugs like DDAVP or clotting factor replacements.
Coagulation Disorders
This document discusses coagulation disorders and bleeding disorders. It describes the normal hemostatic mechanisms including the vascular, platelet and coagulation systems. Bleeding disorders can cause spontaneous or excessive bleeding and can be due to increased vascular fragility, platelet deficiencies or dysfunctions, or derangements of clotting factors. Specific disorders discussed include hemophilia A/B, von Willebrand's disease, and disseminated intravascular coagulation. Laboratory tests that can identify coagulation disorders include the tourniquet test, bleeding time, clotting time, platelet count, clot retraction time, prothrombin time, activated partial thromboplastin time, and thrombin time. Further specific tests may
Von willebrand disease
By Srivardhan Vanka, Intern - Batch of 2014, J.I.P.M.E.R.
References from UpToDate and Wintrobe's Hematology 13th Edition and various studies done till December 2019. Quoted when appropriate.
Hemophilia a
This document provides information about hemophilia, including its causes, types, clinical manifestations, diagnosis, treatment, and management. Key points include:
- Hemophilia is an inherited bleeding disorder caused by deficiencies in coagulation factors VIII or IX. It is passed down in an X-linked recessive pattern.
- There are two main types: hemophilia A caused by factor VIII deficiency, and hemophilia B caused by factor IX deficiency.
- Bleeding can occur spontaneously or after injury in joints, muscles or other tissues. Diagnosis is made through family history and coagulation factor assays.
- Treatment involves replacement of the missing clotting factor, usually through intravenous infusions of
Bleeding Disorders: Causes, Types, and Diagnosis
1) Bleeding disorders can involve vascular, platelet, or coagulation disorders and cause symptoms like bruising, bleeding, and prolonged bleeding from minor cuts.
2) Important bleeding disorders discussed include hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency), von Willebrand disease (a disorder of the von Willebrand clotting factor), and fibrinogen deficiency.
3) These disorders are diagnosed through tests of bleeding time and clotting factor levels and activity. Treatment involves replacing the missing clotting factor through products like cryoprecipitate, desmopressin, or clotting factor concentrates.
Vwd
This document discusses three cases of von Willebrand disease (VWD) and provides details on evaluating and diagnosing the condition.
Case 1 is an 18-year-old woman with easy bruising and heavy menses, who has type 1 VWD. Case 2 is a 32-year-old pregnant woman with a family history of bleeding, who has type IIN (VWD Normandy). Case 3 is a 55-year-old woman with life-long severe bleeding who has type 3 VWD.
The document then provides in-depth information on VWD classification, laboratory evaluation, clinical presentation, treatment options including DDAVP and Humate-P, and modifiers like blood type and comor
Von willebrands disease
Von Willebrand disease is the most common inherited bleeding disorder, caused by mutations that impair the function or production of von Willebrand factor. There are three main types - type 1 is characterized by a quantitative deficiency, type 2 involves qualitative defects, and type 3 is the rarest form with extremely low von Willebrand factor levels. Patients typically present with mucocutaneous bleeding or bleeding after trauma or surgery. Diagnosis involves testing von Willebrand factor antigen levels, activity, and multimers. Treatment options include desmopressin, von Willebrand factor replacement, antifibrinolytics, and adjuvant therapies depending on severity and bleeding history.
OVERVIEW Disorders of platelets
The document provides an overview of platelet disorders, describing how platelets function in hemostasis and how genetic and acquired factors can influence this process, leading to bleeding or clotting symptoms. It discusses various qualitative and quantitative platelet disorders, outlining approaches to diagnosing and differentiating disorders based on platelet production, distribution, or destruction. Evaluation of thrombocytopenia and diagnostic tools for platelet functional disorders are also reviewed.
Hemophilia
a powerpoint on hemophilia i needed to make.
**if you want to join an online class if you are interested in history, science, math, english, and other things, join my class!!**
Hemostasis Disorders
Hemostasis is the process of blood clotting and subsequent dissolution of the clot following tissue repair. It involves 3 main events: 1) vascular constriction, 2) platelet aggregation forming a temporary plug, and 3) fibrin formation creating a stable clot. The clot must later dissolve for normal blood flow to resume. Von Willebrand disease is a bleeding disorder caused by deficient or abnormal von Willebrand factor, which helps platelets bind to collagen. It ranges from mild to severe and is diagnosed based on bleeding history and lab tests of von Willebrand factor and coagulation factors. Treatment depends on severity but may include desmopressin or coagulation factor replacement.
vWD
This document discusses three cases of von Willebrand disease (VWD) and provides information about VWD.
Case 1 is described as type 1 VWD based on test results showing reduced but present von Willebrand factor (vWF) antigen and activity. Case 2 is diagnosed as vWD Normandy based on low factor VIII and normal vWF antigen and multimers. Case 3 has complete deficiency of vWF and is diagnosed as type 3 VWD.
The document then provides details on the classification, symptoms, diagnosis, and treatment of VWD, the most common inherited bleeding disorder. It is caused by mutations in vWF resulting in deficient or defective vWF.
Von willebrands disease
Von Willebrand disease is the most common inherited bleeding disorder caused by mutations that decrease or impair von Willebrand factor, which promotes platelet adhesion and clotting. It ranges from mild to severe. Type I is the most common form with a quantitative deficiency, while type II has qualitative defects affecting function. Treatment involves desmopressin, which releases stored VWF, or VWF replacement for refractory or severe cases. Careful management is needed around procedures and delivery to maintain adequate VWF and factor VIII levels through replacement to prevent bleeding.
5. bleeding disorder
This document discusses hemostasis, bleeding disorders, and platelet disorders. It begins by explaining normal hemostasis and the mechanisms involved in maintaining a fluid blood state and forming clots at sites of injury. It then defines bleeding disorders as problems with blood clotting that result in abnormal bleeding. Common causes discussed include defects in blood vessels or blood itself, clotting factor deficiencies, platelet abnormalities, and liver disease. Finally, it examines several specific platelet disorders like thrombocytopenia, immune thrombocytopenic purpura, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and those resulting from bone marrow infiltration or disseminated intravascular coagulation.
Coagulation disorders
This document discusses coagulation disorders and provides information on hemophilia A, hemophilia B, and disseminated intravascular coagulation (DIC). It notes that hemophilia A is an X-linked bleeding disorder caused by a deficiency in coagulation factor VIII, while hemophilia B is caused by a deficiency in factor IX. Von Willebrand disease is described as the most common inherited bleeding disorder involving a quantitative or qualitative abnormality of von Willebrand factor. DIC is defined as an acquired syndrome characterized by systemic intravascular coagulation that can lead to thrombosis and bleeding complications.
Inherited Bleeding Disorders
This document provides an overview of inherited bleeding disorders, focusing on von Willebrand disease, hemophilia A, and hemophilia B. It classifies inherited bleeding disorders and discusses their prevalence. For von Willebrand disease, it describes the classification, etiology, functions of von Willebrand factor, diagnosis of different types, and management. It also discusses the formation of the primary hemostatic plug. For hemophilia A and B, it covers clinical manifestations, diagnosis, and management, including use of factor replacement therapies.
Hemophilia
Hemophilia is a genetic disorder that impairs the body's ability to control blood clotting. It is caused by mutations in genes that code for proteins essential for blood clotting. The two main types are hemophilia A, caused by a factor VIII deficiency, and hemophilia B, caused by a factor IX deficiency. Hemophilia is diagnosed through family history, blood tests, and bleeding symptoms that can range from mild bruising to heavy internal bleeding. Treatment focuses on replacing the missing clotting factor through infusions or drugs like desmopressin. Hemophilia affects about 1 in 5,000 male births.
Coagulation disorders Pathology. Dr. Umme HAbiba
Key coagulation disorders covered in this document include hemophilia A caused by a factor VIII deficiency, hemophilia B from a factor IX deficiency, and von Willebrand disease where von Willebrand factor is defective
Bleeding and clotting disorders dr anoop 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.
Von willebrand factor
Von Willebrand factor (VWF) is a blood glycoprotein involved in hemostasis. It is synthesized in endothelium and megakaryocytes, where it forms large multimers and anchors platelets to sub-endothelium. VWF levels vary by blood group, and are decreased in conditions like Von Willebrand disease and increased in cardiovascular disease. Von Willebrand disease is the most common inherited bleeding disorder, classified into types 1, 2, and 3 based on quantitative or qualitative VWF deficiencies. Treatment involves cryoprecipitate, DDAVP, or factor VIII concentrate.
Approach to patients with bleeding disorders
This document provides an overview of haemostasis and bleeding disorders. It defines haemostasis and its normal mechanism, then discusses the haemostatic system components and their role in haemostasis and thrombosis prevention. It describes different types of haemorrhagic disorders including those due to vascular defects, platelet abnormalities, coagulation factor deficiencies, and disseminated intravascular coagulation. Specific bleeding disorders like thrombocytopenia, immune thrombocytopenic purpura, hemophilia, and thrombotic thrombocytopenic purpura are also summarized.
Coagulation disorders
Von Willebrand disease is the most common inherited bleeding disorder caused by quantitative or qualitative deficiencies in von Willebrand factor. It is classified into types 1, 2A, 2B, 2M, 2N, and 3 based on pathophysiology. Diagnosis involves testing VWF activity, ristocetin cofactor activity, and multimer analysis. Treatment depends on severity but may include desmopressin, VWF concentrates, or antifibrinolytics. Hemophilia is caused by factor VIII or IX deficiency and classified by severity. Treatment involves factor replacement or bypassing agents for bleeding episodes and immune tolerance induction for inhibitors. Complications include hemarthroses, target joints, and
Factor v deficiency
Factor v deficiency is rare
first described in a Norwegian patient in 1943, Identified by Dr. Paul Owren .
Fewer than 200 cases of congenital factor V deficiency have been reported worldwide since 1943.
inheritance of factor V deficiency is autosomal recessive.
usually only needed for severe bleeds or before surgery.
there is no concentrate containing only factor V.
fresh plasma or (FFP) infusions are used to correct the deficiency temporarily and should be given daily during a bleeding episode.
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Von wille brand disease
Von Willebrand disease is a bleeding disorder caused by low levels of the clotting protein von Willebrand factor. There are three main types of the disease - type 1 involves a small amount of von Willebrand factor present, type 2 involves normal levels but defects in function/structure, and type 3 involves no von Willebrand factor present. Symptoms include easy bruising, excessive bleeding, and heavy menstrual periods. The disease is usually inherited and testing involves bleeding time, factor VIII levels, and von Willebrand factor specific tests. Treatment focuses on avoiding aspirin/NSAIDs and using drugs like DDAVP or clotting factor replacements.
Coagulation Disorders
This document discusses coagulation disorders and bleeding disorders. It describes the normal hemostatic mechanisms including the vascular, platelet and coagulation systems. Bleeding disorders can cause spontaneous or excessive bleeding and can be due to increased vascular fragility, platelet deficiencies or dysfunctions, or derangements of clotting factors. Specific disorders discussed include hemophilia A/B, von Willebrand's disease, and disseminated intravascular coagulation. Laboratory tests that can identify coagulation disorders include the tourniquet test, bleeding time, clotting time, platelet count, clot retraction time, prothrombin time, activated partial thromboplastin time, and thrombin time. Further specific tests may
Von willebrand disease
By Srivardhan Vanka, Intern - Batch of 2014, J.I.P.M.E.R.
References from UpToDate and Wintrobe's Hematology 13th Edition and various studies done till December 2019. Quoted when appropriate.
Hemophilia a
This document provides information about hemophilia, including its causes, types, clinical manifestations, diagnosis, treatment, and management. Key points include:
- Hemophilia is an inherited bleeding disorder caused by deficiencies in coagulation factors VIII or IX. It is passed down in an X-linked recessive pattern.
- There are two main types: hemophilia A caused by factor VIII deficiency, and hemophilia B caused by factor IX deficiency.
- Bleeding can occur spontaneously or after injury in joints, muscles or other tissues. Diagnosis is made through family history and coagulation factor assays.
- Treatment involves replacement of the missing clotting factor, usually through intravenous infusions of
Bleeding Disorders: Causes, Types, and Diagnosis
1) Bleeding disorders can involve vascular, platelet, or coagulation disorders and cause symptoms like bruising, bleeding, and prolonged bleeding from minor cuts.
2) Important bleeding disorders discussed include hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency), von Willebrand disease (a disorder of the von Willebrand clotting factor), and fibrinogen deficiency.
3) These disorders are diagnosed through tests of bleeding time and clotting factor levels and activity. Treatment involves replacing the missing clotting factor through products like cryoprecipitate, desmopressin, or clotting factor concentrates.
Vwd
This document discusses three cases of von Willebrand disease (VWD) and provides details on evaluating and diagnosing the condition.
Case 1 is an 18-year-old woman with easy bruising and heavy menses, who has type 1 VWD. Case 2 is a 32-year-old pregnant woman with a family history of bleeding, who has type IIN (VWD Normandy). Case 3 is a 55-year-old woman with life-long severe bleeding who has type 3 VWD.
The document then provides in-depth information on VWD classification, laboratory evaluation, clinical presentation, treatment options including DDAVP and Humate-P, and modifiers like blood type and comor
Von willebrands disease
Von Willebrand disease is the most common inherited bleeding disorder, caused by mutations that impair the function or production of von Willebrand factor. There are three main types - type 1 is characterized by a quantitative deficiency, type 2 involves qualitative defects, and type 3 is the rarest form with extremely low von Willebrand factor levels. Patients typically present with mucocutaneous bleeding or bleeding after trauma or surgery. Diagnosis involves testing von Willebrand factor antigen levels, activity, and multimers. Treatment options include desmopressin, von Willebrand factor replacement, antifibrinolytics, and adjuvant therapies depending on severity and bleeding history.
OVERVIEW Disorders of platelets
The document provides an overview of platelet disorders, describing how platelets function in hemostasis and how genetic and acquired factors can influence this process, leading to bleeding or clotting symptoms. It discusses various qualitative and quantitative platelet disorders, outlining approaches to diagnosing and differentiating disorders based on platelet production, distribution, or destruction. Evaluation of thrombocytopenia and diagnostic tools for platelet functional disorders are also reviewed.
Hemophilia
a powerpoint on hemophilia i needed to make.
**if you want to join an online class if you are interested in history, science, math, english, and other things, join my class!!**
Hemostasis Disorders
Hemostasis is the process of blood clotting and subsequent dissolution of the clot following tissue repair. It involves 3 main events: 1) vascular constriction, 2) platelet aggregation forming a temporary plug, and 3) fibrin formation creating a stable clot. The clot must later dissolve for normal blood flow to resume. Von Willebrand disease is a bleeding disorder caused by deficient or abnormal von Willebrand factor, which helps platelets bind to collagen. It ranges from mild to severe and is diagnosed based on bleeding history and lab tests of von Willebrand factor and coagulation factors. Treatment depends on severity but may include desmopressin or coagulation factor replacement.
vWD
This document discusses three cases of von Willebrand disease (VWD) and provides information about VWD.
Case 1 is described as type 1 VWD based on test results showing reduced but present von Willebrand factor (vWF) antigen and activity. Case 2 is diagnosed as vWD Normandy based on low factor VIII and normal vWF antigen and multimers. Case 3 has complete deficiency of vWF and is diagnosed as type 3 VWD.
The document then provides details on the classification, symptoms, diagnosis, and treatment of VWD, the most common inherited bleeding disorder. It is caused by mutations in vWF resulting in deficient or defective vWF.
Von willebrands disease
Von Willebrand disease is the most common inherited bleeding disorder caused by mutations that decrease or impair von Willebrand factor, which promotes platelet adhesion and clotting. It ranges from mild to severe. Type I is the most common form with a quantitative deficiency, while type II has qualitative defects affecting function. Treatment involves desmopressin, which releases stored VWF, or VWF replacement for refractory or severe cases. Careful management is needed around procedures and delivery to maintain adequate VWF and factor VIII levels through replacement to prevent bleeding.
5. bleeding disorder
This document discusses hemostasis, bleeding disorders, and platelet disorders. It begins by explaining normal hemostasis and the mechanisms involved in maintaining a fluid blood state and forming clots at sites of injury. It then defines bleeding disorders as problems with blood clotting that result in abnormal bleeding. Common causes discussed include defects in blood vessels or blood itself, clotting factor deficiencies, platelet abnormalities, and liver disease. Finally, it examines several specific platelet disorders like thrombocytopenia, immune thrombocytopenic purpura, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and those resulting from bone marrow infiltration or disseminated intravascular coagulation.
Coagulation disorders
This document discusses coagulation disorders and provides information on hemophilia A, hemophilia B, and disseminated intravascular coagulation (DIC). It notes that hemophilia A is an X-linked bleeding disorder caused by a deficiency in coagulation factor VIII, while hemophilia B is caused by a deficiency in factor IX. Von Willebrand disease is described as the most common inherited bleeding disorder involving a quantitative or qualitative abnormality of von Willebrand factor. DIC is defined as an acquired syndrome characterized by systemic intravascular coagulation that can lead to thrombosis and bleeding complications.
Inherited Bleeding Disorders
This document provides an overview of inherited bleeding disorders, focusing on von Willebrand disease, hemophilia A, and hemophilia B. It classifies inherited bleeding disorders and discusses their prevalence. For von Willebrand disease, it describes the classification, etiology, functions of von Willebrand factor, diagnosis of different types, and management. It also discusses the formation of the primary hemostatic plug. For hemophilia A and B, it covers clinical manifestations, diagnosis, and management, including use of factor replacement therapies.
Hemophilia
Hemophilia is a genetic disorder that impairs the body's ability to control blood clotting. It is caused by mutations in genes that code for proteins essential for blood clotting. The two main types are hemophilia A, caused by a factor VIII deficiency, and hemophilia B, caused by a factor IX deficiency. Hemophilia is diagnosed through family history, blood tests, and bleeding symptoms that can range from mild bruising to heavy internal bleeding. Treatment focuses on replacing the missing clotting factor through infusions or drugs like desmopressin. Hemophilia affects about 1 in 5,000 male births.
Coagulation disorders Pathology. Dr. Umme HAbiba
Key coagulation disorders covered in this document include hemophilia A caused by a factor VIII deficiency, hemophilia B from a factor IX deficiency, and von Willebrand disease where von Willebrand factor is defective
Bleeding and clotting disorders dr anoop 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.
Von willebrand factor
Von Willebrand factor (VWF) is a blood glycoprotein involved in hemostasis. It is synthesized in endothelium and megakaryocytes, where it forms large multimers and anchors platelets to sub-endothelium. VWF levels vary by blood group, and are decreased in conditions like Von Willebrand disease and increased in cardiovascular disease. Von Willebrand disease is the most common inherited bleeding disorder, classified into types 1, 2, and 3 based on quantitative or qualitative VWF deficiencies. Treatment involves cryoprecipitate, DDAVP, or factor VIII concentrate.
Approach to patients with bleeding disorders
This document provides an overview of haemostasis and bleeding disorders. It defines haemostasis and its normal mechanism, then discusses the haemostatic system components and their role in haemostasis and thrombosis prevention. It describes different types of haemorrhagic disorders including those due to vascular defects, platelet abnormalities, coagulation factor deficiencies, and disseminated intravascular coagulation. Specific bleeding disorders like thrombocytopenia, immune thrombocytopenic purpura, hemophilia, and thrombotic thrombocytopenic purpura are also summarized.
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Coagulation disorders
Von Willebrand disease is the most common inherited bleeding disorder caused by quantitative or qualitative deficiencies in von Willebrand factor. It is classified into types 1, 2A, 2B, 2M, 2N, and 3 based on pathophysiology. Diagnosis involves testing VWF activity, ristocetin cofactor activity, and multimer analysis. Treatment depends on severity but may include desmopressin, VWF concentrates, or antifibrinolytics. Hemophilia is caused by factor VIII or IX deficiency and classified by severity. Treatment involves factor replacement or bypassing agents for bleeding episodes and immune tolerance induction for inhibitors. Complications include hemarthroses, target joints, and
Factor v deficiency
Factor v deficiency is rare
first described in a Norwegian patient in 1943, Identified by Dr. Paul Owren .
Fewer than 200 cases of congenital factor V deficiency have been reported worldwide since 1943.
inheritance of factor V deficiency is autosomal recessive.
usually only needed for severe bleeds or before surgery.
there is no concentrate containing only factor V.
fresh plasma or (FFP) infusions are used to correct the deficiency temporarily and should be given daily during a bleeding episode.
bleeding disorders 1 Dr.Nannika Pradhan
This document provides an overview of approaches to bleeding disorders, including classification, investigation, and treatment. It discusses disorders affecting the blood vessel wall, platelets, and coagulation factors. Specific disorders covered include hemophilia A/B, von Willebrand disease, idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation. Evaluation, laboratory testing, and management strategies are described for different bleeding disorders. The importance of specialized treatment planning for long-term management is emphasized.
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This document presents a case study of a 11-year old female patient with Von Willebrand Disease Type III who presented with epistaxis and bleeding from the scalp due to a head injury. Von Willebrand Disease is a genetic bleeding disorder caused by a deficiency of the Von Willebrand Factor, a clotting protein. The patient's lab work showed low levels of Von Willebrand Factor and Factor VIII. She was diagnosed with Von Willebrand Disease Type III and treated with tranexamic acid to reduce bleeding and Von Willebrand Factor replacement therapy.
Von willebrand disease
Von Willebrand disease is the most common inherited bleeding disorder in humans. It results from a deficiency or abnormality of von Willebrand factor, a protein required for normal clotting. There are several types of von Willebrand disease classified based on the genetic mutation and severity of symptoms. Type 1 is the most common and usually causes mild symptoms like nosebleeds, while Type 3 is the most severe form and can result in life-threatening bleeding. The condition is diagnosed through blood tests measuring von Willebrand factor levels and activity. Treatment depends on the type but may include the drug Desmopressin to increase von Willebrand factor levels for minor procedures.
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Hemophilia is a bleeding disorder caused by deficiencies in clotting factors VIII or IX. It can range from mild to severe depending on factor levels. The knees, elbows, and ankles are most prone to recurrent bleeding in joints (hemarthrosis) leading to hemophilic arthropathy. Treatment involves replacing the missing clotting factor, though some develop inhibitors requiring bypassing agents. For mild cases, desmopressin can stimulate factor release instead of replacement. Surgery and radiation synovectomy may help joints with persistent bleeding. Von Willebrand disease also involves a platelet dysfunction protein.
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Hemophilia is a genetic bleeding disorder caused by deficiencies in coagulation factors VIII or IX. It affects males primarily and can range from mild to severe. The main types are hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency). Treatment involves replacing the missing clotting factor through prophylactic or on-demand regimens to prevent or treat bleeding episodes. Complications can include hemarthrosis, joint damage, fractures, and pseudotumors, so treatment seeks to maintain adequate factor levels and address medical issues promptly. Proper diagnosis and laboratory testing are needed to determine severity and guide personalized management.
bleeding_disorders.ppt
This document discusses bleeding disorders and hemostasis. It begins by describing the four phases of hemostasis: vascular, platelet, coagulation, and fibrinolytic. It then discusses specific bleeding disorders including platelet disorders, coagulation factor deficiencies like hemophilia A/B and von Willebrand disease, and acquired disorders. Laboratory tests for evaluation of hemostasis are also outlined. Clinical manifestations of platelet versus coagulation factor disorders are compared. Specific treatment approaches for various bleeding disorders are then reviewed.
Hemorragics.pptx
This document discusses hemorrhagic diatheses in children, focusing on hemophilia. Hemophilia is a congenital coagulopathy caused by deficiencies in coagulation factors VIII or IX. It results in bleeding disorders of variable severity. Symptoms include easy bruising, hemarthrosis (bleeding into joints), and intramuscular bleeding. Treatment involves replacement of the deficient coagulation factor through concentrates or cryoprecipitate. Prophylactic treatment and lifestyle modifications can help prevent complications like chronic joint damage.
Homestasis Surgery
The document discusses various bleeding disorders including their causes, presentations, and treatments. It covers platelet disorders, coagulation factor deficiencies, von Willebrand disease, hemophilia A and B, disseminated intravascular coagulation (DIC), and liver disease. Treatment options discussed include cryoprecipitate, factor concentrates, DDAVP, vitamin K, fresh frozen plasma, and recombinant factor VIIa.
07 C.disorders.pptx
The document discusses various coagulation disorders including:
1. Congenital coagulation disorders such as hemophilia A and B which are caused by deficiencies in coagulation factors VIII and IX.
2. Acquired coagulation disorders including disseminated intravascular coagulation (DIC), vitamin K deficiency, liver disease, and antibodies against coagulation factors.
3. The pathogenesis, clinical features, laboratory findings, and treatment of various coagulation disorders are explained.
DVT Current Concept
1. Deep vein thrombosis (DVT) is caused by Virchow's triad of stasis, vessel damage, and hypercoagulability. Prolonged bed rest, major surgery, trauma, pregnancy, and cancer are common risk factors.
2. General anesthesia increases DVT risk compared to epidural anesthesia. Blood type A is also associated with higher risk.
3. DVT diagnosis involves tests like duplex ultrasound, MRI, and blood tests. Treatment includes anticoagulants like heparin and warfarin to prevent clots from worsening. Compression stockings and early mobilization are also used prophylactically.
Venous Thromboembolism
This document provides an overview of venous thrombo-embolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). It discusses the prevalence and impact of VTE, defining key terms like anticoagulants and thrombolytics. The presentation contents are outlined as covering the prevalence, diagnostic modalities and algorithm, and updates to the medical management of VTE. Diagnostic tests for VTE include ultrasound Doppler, D-dimer testing, and imaging studies like CT scans. Treatment involves anticoagulation or thrombolysis to prevent clots from growing or causing harm.
Hemophilia a
Hemophilia A is the most common form of hemophilia, caused by reduced levels or activity of coagulation factor VIII. This leads to prolonged and unstable clot formation when bleeding occurs. Symptoms can range from bleeding after circumcision or venipuncture in infants to spontaneous bleeding in joints in older patients. Diagnosis involves tests that show prolonged activated partial thromboplastin time and low factor VIII levels. Treatment replaces the missing clotting factor, with severity and location of bleeding determining dosage. Preventative treatment and education on self-administered factor replacement can help manage symptoms.
Bleeding and Thrombotic Disorders
This document discusses bleeding and thrombotic disorders. It provides information on hemostasis, mechanisms of bleeding, key aspects of diagnosis such as history and clinical characteristics. It covers laboratory testing including platelet count, bleeding time, platelet function assay, prothrombin time, activated partial thromboplastin time, thrombin time and tests for fibrinolysis. It also discusses hereditary and acquired causes of bleeding disorders and provides details on specific conditions like hemophilia, von Willebrand disease and treatments.
TMP_Public_Presentation
The Public Presentation does not include any confidential information or findings from this Team Masters Project with BioMarin Pharmaceutical.
BioMarin and KGI titled our project as:
"Recurrent bleeding in patients with mechanical flow devices: an environmental study."
Deep Vein Thrombosis
This research paper discusses deep vein thrombosis (DVT), which commonly affects the deep veins in the lower extremities. The paper outlines various risk factors for DVT, including immobility, venous hypertension, damage to veins, hyperviscosity of blood, genetic deficiencies, and obesity. Clinical features of DVT include pain, swelling, and tenderness in the affected extremity. Diagnosis is made using venous Doppler ultrasound and D-dimer testing. Treatment involves immediate anticoagulation to prevent pulmonary embolism and clot propagation. The duration and type of anticoagulation depends on individual patient factors. Inferior vena cava filters may be used in some cases where anticoagulation is contraindicated
DVT Presentation.ppt
This document discusses thromboembolic diseases, which include deep vein thrombosis (DVT) and pulmonary embolism (PE). It notes that DVT and PE incidence increases during pregnancy and the postpartum period. Pregnancy increases the risk of these conditions 5-10 times due to hormonal and physiological changes. The document then discusses various risk factors for DVT/PE and diagnostic methods. It also outlines treatments which include anticoagulants like heparin and warfarin, as well as compression stockings and exercise.
1578185 - McGraw-Hill Professional ©CHAPTER 172Approach
1578185 - McGraw-Hill Professional ©
CHAPTER 172
Approach to Patients with Bleeding
Disorders
Kathryn Webert, MD, MSc, FRCPC
Catherine P. M. Hayward, MD, PhD
Key Clinical Questions
When should a bleeding disorder be suspected?
How should patients suspected of bleeding disorders be evaluated?
How does one interpret the results of hemostasis testing?
What is the general approach to management of an individual with a bleeding
disorder?
INTRODUCTION
In general, severe bleeding disorders are uncommon, unlike mild bleeding problems, which
can be more challenging to diagnose. Most episodes of clinically significant bleeding
requiring medical attention result from local causes (eg, a duodenal ulcer), surgery, or
1578185 - McGraw-Hill Professional ©
trauma. However, it is important to recognize when bleeding problems are more serious or
more frequent due to an underlying hemostatic abnormality.
Abnormal bleeding represents an important health care problem. For example, in the
United States, it has been estimated that at least 5% to 10% of women of childbearing age
seek medical care for menorrhagia and have bleeding severe enough to require medical
intervention. Among the many defects that can cause abnormal bleeding, inherited and
acquired von Willebrand disease (VWD) and platelet function disorders are much more
common than defects in coagulation and fibrinolytic proteins.
PATHOPHYSIOLOGY
REVIEW OF NORMAL HEMOSTASIS
Hemostasis consists of the following steps: (1) initiation and formation of the platelet
plug, also known as primary hemostasis; (2) propagation and amplification of the clotting
“cascade” or secondary hemostasis, which involves activation of a series of coagulation
factors resulting in the generation of thrombin that cleaves fibrinogen to fibrin; (3) cross-
linking of fibrin; (4) termination of procoagulant response by antithrombotic control
mechanisms; (5) removal of the clot by fibrinolysis; and (6) tissue repair and regeneration.
When a vessel is injured, platelets adhere to exposed collagen and other components
of the subendothelium as the first defense against bleeding. This initial adhesion is
dependent on von Willebrand factor (VWF) as well as specific platelet receptors (eg,
glycoprotein IbIXV) for VWF and collagen. This adhesion leads to platelet activation and
shape change as well as platelet aggregation, which promotes recruitment of additional
platelets.
Coagulation is initiated in vivo when endothelial or vascular cells are damaged. This
results in exposure of blood to tissue factor (TF), which binds to factor VII (FVII) and its
activated form, factor VII (FVIIa). TF-FVIIa complexes (extrinsic tenase) then activates
factors IX and X directly. Activated factor IX can also form a complex with factor VIIIa as
well as phospholipids and calcium, called the intrinsic tenase complex, which promotes
further conversion of factor X to factor Xa. The generated factor Xa associates with
activated factor V, phospholi ...
1578185 - McGraw-Hill Professional ©CHAPTER 172Approach
1578185 - McGraw-Hill Professional ©
CHAPTER 172
Approach to Patients with Bleeding
Disorders
Kathryn Webert, MD, MSc, FRCPC
Catherine P. M. Hayward, MD, PhD
Key Clinical Questions
When should a bleeding disorder be suspected?
How should patients suspected of bleeding disorders be evaluated?
How does one interpret the results of hemostasis testing?
What is the general approach to management of an individual with a bleeding
disorder?
INTRODUCTION
In general, severe bleeding disorders are uncommon, unlike mild bleeding problems, which
can be more challenging to diagnose. Most episodes of clinically significant bleeding
requiring medical attention result from local causes (eg, a duodenal ulcer), surgery, or
1578185 - McGraw-Hill Professional ©
trauma. However, it is important to recognize when bleeding problems are more serious or
more frequent due to an underlying hemostatic abnormality.
Abnormal bleeding represents an important health care problem. For example, in the
United States, it has been estimated that at least 5% to 10% of women of childbearing age
seek medical care for menorrhagia and have bleeding severe enough to require medical
intervention. Among the many defects that can cause abnormal bleeding, inherited and
acquired von Willebrand disease (VWD) and platelet function disorders are much more
common than defects in coagulation and fibrinolytic proteins.
PATHOPHYSIOLOGY
REVIEW OF NORMAL HEMOSTASIS
Hemostasis consists of the following steps: (1) initiation and formation of the platelet
plug, also known as primary hemostasis; (2) propagation and amplification of the clotting
“cascade” or secondary hemostasis, which involves activation of a series of coagulation
factors resulting in the generation of thrombin that cleaves fibrinogen to fibrin; (3) cross-
linking of fibrin; (4) termination of procoagulant response by antithrombotic control
mechanisms; (5) removal of the clot by fibrinolysis; and (6) tissue repair and regeneration.
When a vessel is injured, platelets adhere to exposed collagen and other components
of the subendothelium as the first defense against bleeding. This initial adhesion is
dependent on von Willebrand factor (VWF) as well as specific platelet receptors (eg,
glycoprotein IbIXV) for VWF and collagen. This adhesion leads to platelet activation and
shape change as well as platelet aggregation, which promotes recruitment of additional
platelets.
Coagulation is initiated in vivo when endothelial or vascular cells are damaged. This
results in exposure of blood to tissue factor (TF), which binds to factor VII (FVII) and its
activated form, factor VII (FVIIa). TF-FVIIa complexes (extrinsic tenase) then activates
factors IX and X directly. Activated factor IX can also form a complex with factor VIIIa as
well as phospholipids and calcium, called the intrinsic tenase complex, which promotes
further conversion of factor X to factor Xa. The generated factor Xa associates with
activated factor V, phospholi ...
Similar to Von willebrands disease (20)
1578185 - McGraw-Hill Professional ©CHAPTER 172Approach
1578185 - McGraw-Hill Professional ©CHAPTER 172Approach
1578185 - McGraw-Hill Professional ©CHAPTER 172Approach
1578185 - McGraw-Hill Professional ©CHAPTER 172Approach
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Kpsc diabetes in pregnancy pathway 8.6.2012
The document outlines guidelines for managing diabetes in pregnancy across medical centers. It discusses:
1. Individual centers being graded on compliance with performing HbA1c tests on all prenatal patients and FBS tests for GDM patients at 6 weeks postpartum. Bonuses may be tied to these performance measures.
2. Risk stratification of patients into low, medium, and high risk groups based on diabetes history and control. This determines interventions like medication management and fetal monitoring.
3. Screening all prenatal patients for GDM risk and providing diabetes education. High risk patients receive early glucose testing while low risk patients are tested at 24-28 weeks.
4. Postpartum follow-up
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The document discusses issues with the current scheduling system including too many changes and vague requests. It proposes implementing scheduled cesarean sections on call days to improve efficiency by ensuring the primary surgeon performs the surgery and eliminating wasted time. This could add 30 hours of clinic access per month. Some providers argue they are too busy, but deliveries have decreased so scheduling cesareans this way could help protect staffing levels. No more than 2 cesareans would be scheduled per provider per call day.
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This document provides guidelines for managing twin pregnancies, including determining chorionicity and amnioticity. It recommends that all twins undergo an NT ultrasound before 14 weeks to validate chorionicity/amnionicity and detect early complications. Management of monochorionic twins requires more intensive surveillance due to increased risks of complications affecting fetal growth and well-being. Dichorionic twins generally require less frequent monitoring while monochorionic twins should be monitored more closely, with delivery planned before 37 weeks.
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This document summarizes recommendations for using progesterone to prevent preterm birth based on a woman's history and cervical length. It recommends 17-hydroxyprogesterone caproate injections weekly from 16-20 weeks until 36 weeks for women with a prior spontaneous preterm birth. For women without a prior preterm birth but an incidental short cervical length of 10-20mm before 24 weeks, it recommends daily vaginal progesterone until 36 weeks. Safety follow-up of children exposed to 17-hydroxyprogesterone caproate in clinical trials found no differences compared to placebo.
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The document discusses improving patient satisfaction scores related to communication about medications at Riverside Medical Center's maternity service. The goal is to increase the HCAHPS medication communication score from 66% to 75% by December 2012 and 85% by June 2013. This will be achieved through education of providers, patients, and staff. Providers will be educated on medications through meetings and flashcards. Patients will receive verbal and written information about new medications. Staff will track medication discussions on patient care boards. Progress will be measured through education documentation and eventual HCAHPS scores.
Hcahps score trends in the past 4 years
This document shows trends in patient experience scores over 4 years from 2008-2012 at KP Riverside Medical Center based on the HCAHPS survey. The line graphs depict scores for various measures related to nurse and doctor communication, responsiveness of staff, pain management, medication communication, discharge processes, cleanliness and quietness. Scores fluctuate over time but generally remain between 60-90% for most measures.
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Pph share drive
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Late preterm delivery
Late preterm infants born between 34 0/7 and 36 6/7 weeks have higher rates of morbidity than full term infants. During the initial birth hospitalization, late preterm infants are more likely to experience conditions like temperature instability, hypoglycemia, respiratory distress, and jaundice. The risks are even higher for late preterm infants whose mothers have complications like hypertension, diabetes, bleeding, or infections. Readmission rates within the first year are also higher, around 15%, for late preterm infants compared to full term infants. Late preterm infants also have higher mortality rates within the first year of life and are at greater risk for long-term neurodevelopmental issues.
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The document summarizes key findings from a review of literature on polycystic ovary syndrome (PCOS). It finds that the most consistent predictors of PCOS are hyperandrogenemia (high levels of "male" hormones) in 60-80% of cases, hirsutism (excess hair growth) in 60% of cases, and polycystic ovaries in 75% of cases. It also discusses debates around definitions of PCOS and relationships with insulin resistance.
Induction summary
This document provides guidelines for induction of labor, including:
1. Recommending inpatient and outpatient Cytotec inductions arrive at 7:00 PM to facilitate admission/discharge decisions and additional Cytotec doses if needed.
2. Inpatient Pitocin-only inductions should arrive at 6:00 AM to start Pitocin before 7:00 AM.
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Hyperemesis6 12
Hyperemesis Gravidarum is a condition characterized by persistent and severe nausea and vomiting during pregnancy. It can lead to weight loss of 5% or more of the woman's pre-pregnancy weight and the presence of ketones in the urine. Potential causes include multiple gestation, trophoblastic disease, or genetic conditions like trisomy 21. Treatment focuses on managing symptoms, avoiding triggers, dietary changes, medications like antihistamines, phenothiazines, and serotonin antagonists. Intravenous fluids and supplementation of vitamins and minerals may be needed to address nutritional deficiencies and prevent complications like Wernicke's encephalopathy. Enteral nutrition through nasojejunal feeding tubes is preferable to parent
Gbs 2010
The document summarizes changes to CDC guidelines for prevention of early-onset group B streptococcal (GBS) disease. Key changes include: expanded laboratory detection options for GBS; revised thresholds for reporting GBS in urine cultures; clarified definitions of adequate antibiotic prophylaxis and high risk for anaphylaxis; and adjustments to neonatal management algorithms to reduce unnecessary evaluations. Guidelines emphasize using cefazolin over clindamycin or vancomycin when possible for penicillin-allergic women.
Foley bulb
The document discusses the use of Foley bulbs for cervical ripening and labor induction. It finds that:
1) A Foley bulb induction is as effective as common prostaglandin methods like misoprostol for cervical ripening and inducing labor, with fewer risks of complications.
2) Inflating the Foley bulb to 60-80ml is more effective for cervical dilation and shorter delivery times than only inflating to 30ml.
3) Using a Foley bulb alone without additional prostaglandins or oxytocin is equally effective while avoiding increased need for pain management.
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Asymptomatic short cervix and vaginanal, progesterone
1. Vaginal progesterone reduces preterm birth in women with an asymptomatic sonographic short cervix in the midtrimester. The meta-analysis found vaginal progesterone once daily from identification of a short cervix <25mm until 37 weeks decreases preterm birth <33 weeks by 45% and decreases neonatal morbidity and mortality.
2. Treatment with vaginal progesterone was associated with significant reductions in preterm birth before 28 weeks, 33 weeks, and 35 weeks as well as composite neonatal morbidity and mortality.
3. There were no significant differences in adverse maternal events or congenital anomalies between the vaginal progesterone and placebo groups.
Prevention of pertussis
The document discusses pertussis (whooping cough) prevention, treatment, and epidemiology. It provides guidelines for vaccinating pregnant women and new mothers with Tdap to prevent transmission to infants. It describes the symptoms and phases of pertussis, recommends antibiotic treatment and prophylaxis, and defines close contacts for evaluation and post-exposure prophylaxis. Pertussis cases are increasing significantly in California and infants are most at risk for severe disease.
Magnesium sulfate
The document discusses evidence that magnesium sulfate administered to mothers at risk of preterm birth reduces the risk of cerebral palsy in infants. Several large randomized controlled trials and meta-analyses involving over 15,000 women found magnesium sulfate decreased the risk of cerebral palsy without increasing mortality. The number needed to treat to prevent one case of cerebral palsy is estimated at 63 women. The document also describes a modified magnesium sulfate neuroprotection protocol used at Riverside Hospital for imminent preterm deliveries between 23 and 33 weeks.
Labor down
1) Studies on delayed pushing, also called "laboring down", have shown mixed results, with the main consistent benefit being a reduced need for operative vaginal deliveries in nulliparous women with epidurals.
2) Delaying pushing can prolong the second stage of labor by about an hour and may increase risks like chorioamnionitis with delays over 1 hour.
3) Delayed pushing may be considered for nulliparous women with epidurals who do not have an urge to push and the fetal head is not yet at station +2, as long as the fetal heart rate is reassuring and no other risk factors exist. The delay should not exceed 90 minutes.
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Von willebrands disease
- 1. Von Willebrand Disease Douglas Montgomery MD 7/10/2008
- 12. Delayed, severe Immediate, mild Bleeding after surgery Common Rare Hemarthroses, muscle hematomas Large, palpable Small, superficial Ecchymoses Absent Present Petechiae Not usually Yes Bleeding after minor cuts Deep in soft tissues (joints, muscles) Skin, mucous membranes (gingivae, nares, GI and genitourinary tracts) Site of bleeding Clotting factor deficiency Platelet defect Clinical characteristic