hemolytic uremic syndrome
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This document provides an overview of hemolytic uremic syndrome (HUS). It begins with background information, noting that HUS is characterized by hemolytic anemia, thrombocytopenia, and acute kidney injury. It is most common in children under 5. HUS is then classified as typical (diarrhea-associated) or atypical. The etiopathogenesis of typical HUS involves shiga toxin-producing bacteria like E. coli damaging endothelial cells. Clinically, HUS presents with anemia, oliguria, hematuria, and hypertension. Investigations show anemia, thrombocytopenia, and schistocytes on blood smear. Management involves supportive care, antibiotics, and plasma therapy. The
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Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by thrombocytopenia, acute renal impairment, and microangiopathic hemolytic anemia. It has typical and atypical variants, with the typical variant caused by Shiga toxin-producing E. coli. HUS presents with varied symptoms depending on etiology and can progress to end-stage renal disease if left untreated. Treatment involves supportive care, dialysis if needed, and addressing the underlying cause. Outcomes depend on prompt diagnosis and intervention to prevent complications.
Hemolytic uremic Syndrome
Hemolytic-uremic syndrome (HUS) is a disease characterized by hemolytic anemia, low platelet count, and kidney failure. It is predominantly seen in children and can be caused by infections from E. coli or other bacteria. There are typical and atypical forms of HUS. The typical form is usually caused by Shiga toxin-producing bacteria and their toxins damaging the endothelial cells in the kidneys and other organs. Atypical HUS is linked to genetic complement factor abnormalities. Treatment involves supportive care, antibiotics if infection is present, and plasma therapy to replace deficient complement factors for atypical cases. Most patients survive the acute phase but some may have long-term kidney or other organ damage.
Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. It is most commonly caused by infections from Shiga toxin-producing bacteria like E. coli O157:H7. The Shiga toxin damages endothelial cells and causes blood clots to form in the kidneys. Treatment involves fluid replacement, dialysis, and plasma exchange to support kidney function and replace lost blood cells. While HUS prognosis is generally good, some children may have long term kidney damage or rarely die from severe complications.
Hemolytic uremic syndrome
Hemolytic-uremic syndrome (HUS) is a disease characterized by hemolytic anemia, low platelet count, and kidney failure. It is predominantly seen in children and can be typical (caused by E. coli or Shigella infection) or atypical (caused by complement abnormalities or other infections). Treatment involves supportive care, antibiotics for infections, and plasma therapy for complement abnormalities to replace deficient factors. With aggressive treatment, over 90% of patients survive the acute phase, though some may have long term kidney or other organ damage.
Haemolytic uremic syndrome
Hemolytic Uremic Syndrome (HUS) is a clinical syndrome characterized by microangiopathic hemolytic anemia, acute kidney injury, and thrombocytopenia. It is caused by Shiga toxin-producing bacteria like E. coli O157:H7 or by complement dysregulation. Treatment involves supportive care and addressing the underlying cause, such as antibiotics for bacterial infections or plasma therapy for complement abnormalities. With proper management, the prognosis is generally good, though permanent kidney damage can occur without timely treatment.
Hemolytic Uremic Syndrome: A Dangerous Complication of E. coli
In this presentation provided by the nation's foremost food poison law firm - Marler Clark, Hemolytic Uremic Syndrome (HUS) is explained. HUS is a rare and highly dangerous result of an E. coli infection and can result in acute kidney failure
Sideroblastic anemia - Etiopathogenesis, Clinical features, Advances in Manag...
Sideroblastic anemia - Etiopathogenesis, Clinical features, Advances in Manag...Chetan Ganteppanavar
This document discusses sideroblastic anemia, including:
- It is characterized by abnormal iron deposits in erythroblast mitochondria, producing ringed sideroblasts instead of healthy red blood cells.
- It can be hereditary or acquired. Hereditary types often have normocytic or microcytic anemia while acquired types are usually normocytic or macrocytic.
- Causes include genetic disorders affecting heme synthesis, alcohol use, vitamin deficiencies, and exposures like lead.
- Symptoms depend on severity of anemia but can include fatigue, weakness, and heart/organ damage from iron overload.
- Diagnosis involves blood tests showing elevated iron levels and ringed siderHUS
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. It is most commonly caused by infections from Shiga toxin-producing bacteria like E. coli O157:H7. The Shiga toxin damages endothelial cells and causes blood clots to form in the kidneys. Treatment involves fluid replacement, dialysis, and plasma exchange to support kidney function and replace lost blood cells. While the prognosis is generally good for typical HUS caused by infection, atypical non-infection related HUS has a worse prognosis.
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Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by thrombocytopenia, acute renal impairment, and microangiopathic hemolytic anemia. It has typical and atypical variants, with the typical variant caused by Shiga toxin-producing E. coli. HUS presents with varied symptoms depending on etiology and can progress to end-stage renal disease if left untreated. Treatment involves supportive care, dialysis if needed, and addressing the underlying cause. Outcomes depend on prompt diagnosis and intervention to prevent complications.
Hemolytic uremic Syndrome
Hemolytic-uremic syndrome (HUS) is a disease characterized by hemolytic anemia, low platelet count, and kidney failure. It is predominantly seen in children and can be caused by infections from E. coli or other bacteria. There are typical and atypical forms of HUS. The typical form is usually caused by Shiga toxin-producing bacteria and their toxins damaging the endothelial cells in the kidneys and other organs. Atypical HUS is linked to genetic complement factor abnormalities. Treatment involves supportive care, antibiotics if infection is present, and plasma therapy to replace deficient complement factors for atypical cases. Most patients survive the acute phase but some may have long-term kidney or other organ damage.
Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. It is most commonly caused by infections from Shiga toxin-producing bacteria like E. coli O157:H7. The Shiga toxin damages endothelial cells and causes blood clots to form in the kidneys. Treatment involves fluid replacement, dialysis, and plasma exchange to support kidney function and replace lost blood cells. While HUS prognosis is generally good, some children may have long term kidney damage or rarely die from severe complications.
Hemolytic uremic syndrome
Hemolytic-uremic syndrome (HUS) is a disease characterized by hemolytic anemia, low platelet count, and kidney failure. It is predominantly seen in children and can be typical (caused by E. coli or Shigella infection) or atypical (caused by complement abnormalities or other infections). Treatment involves supportive care, antibiotics for infections, and plasma therapy for complement abnormalities to replace deficient factors. With aggressive treatment, over 90% of patients survive the acute phase, though some may have long term kidney or other organ damage.
Haemolytic uremic syndrome
Hemolytic Uremic Syndrome (HUS) is a clinical syndrome characterized by microangiopathic hemolytic anemia, acute kidney injury, and thrombocytopenia. It is caused by Shiga toxin-producing bacteria like E. coli O157:H7 or by complement dysregulation. Treatment involves supportive care and addressing the underlying cause, such as antibiotics for bacterial infections or plasma therapy for complement abnormalities. With proper management, the prognosis is generally good, though permanent kidney damage can occur without timely treatment.
Hemolytic Uremic Syndrome: A Dangerous Complication of E. coli
In this presentation provided by the nation's foremost food poison law firm - Marler Clark, Hemolytic Uremic Syndrome (HUS) is explained. HUS is a rare and highly dangerous result of an E. coli infection and can result in acute kidney failure
Sideroblastic anemia - Etiopathogenesis, Clinical features, Advances in Manag...
Sideroblastic anemia - Etiopathogenesis, Clinical features, Advances in Manag...Chetan Ganteppanavar
This document discusses sideroblastic anemia, including:
- It is characterized by abnormal iron deposits in erythroblast mitochondria, producing ringed sideroblasts instead of healthy red blood cells.
- It can be hereditary or acquired. Hereditary types often have normocytic or microcytic anemia while acquired types are usually normocytic or macrocytic.
- Causes include genetic disorders affecting heme synthesis, alcohol use, vitamin deficiencies, and exposures like lead.
- Symptoms depend on severity of anemia but can include fatigue, weakness, and heart/organ damage from iron overload.
- Diagnosis involves blood tests showing elevated iron levels and ringed siderHUS
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. It is most commonly caused by infections from Shiga toxin-producing bacteria like E. coli O157:H7. The Shiga toxin damages endothelial cells and causes blood clots to form in the kidneys. Treatment involves fluid replacement, dialysis, and plasma exchange to support kidney function and replace lost blood cells. While the prognosis is generally good for typical HUS caused by infection, atypical non-infection related HUS has a worse prognosis.
Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal injury, most commonly caused by toxin-producing strains of E. coli. The toxins produced by these bacteria damage endothelial cells in the kidneys and other organs, leading to platelet aggregation and thrombosis. This causes fragmentation of red blood cells and kidney dysfunction. HUS diagnosis is based on laboratory findings of hemolytic anemia, low platelet count, and kidney involvement. Treatment is largely supportive through dialysis, blood transfusions, and controlling blood pressure and electrolyte abnormalities. Most patients recover renal function, but some are left with chronic kidney disease.
Haemolytic Uremic Syndrome
Haemolytic uremic syndrome (HUS) is a clinical syndrome characterized by renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. It is most commonly caused by Shiga toxin-producing bacteria like E. coli O157:H7 through damage to endothelial cells. There are two main categories of HUS - Shiga-toxin associated HUS and non-Shiga-toxin associated HUS. Treatment for HUS focuses on symptomatic relief through dialysis, blood transfusions, and managing complications. The prognosis is generally good, though outcomes can be worse in cases with very high white blood cell counts or persistent kidney damage and failure.
Myeloproliferative disorders
The document discusses myeloproliferative disorders (MPDs), which are clonal stem cell disorders characterized by increased blood cell counts and enlarged spleen and bone marrow. It focuses on chronic myeloid leukemia (CML), describing it as a MPD caused by a genetic mutation that results in uncontrolled white blood cell growth. CML progresses through chronic, accelerated, and blast phases, with symptoms ranging from fatigue to organ enlargement. Diagnosis involves blood and bone marrow tests detecting elevated white and platelet counts and the Philadelphia chromosome genetic abnormality associated with CML.
Sickle cell disease
This document provides an outline about sickle cell anemia. It defines sickle cell anemia as a blood disorder caused by inheritance of the sickle hemoglobin gene from both parents. The disorder is characterized by rigid, sickle shaped red blood cells that can block blood vessels. Clinical features include painful vaso-occlusive crises in the bones, joints and organs. Laboratory findings show anemia and the presence of sickle cells. Treatment focuses on prevention, pain management during crises, blood transfusions, and newer therapies like hydroxyurea. Prognosis has improved due to better care, though sickle cell anemia currently has no cure.
Approach to anemia
Approach to anemia - Iron, Megaloblastic, Hemolytic, Autoimmune, Cytopenia, Marrow and Management - Advances, Sideroblastic
An Overview of Hemolytic anemia
This document summarizes different types of hemolytic anemias. It describes the features shared by hemolytic anemias such as a shortened red blood cell lifespan and increased erythropoiesis. Two main types of hemolysis are discussed: extravascular hemolysis where red blood cells are destroyed within macrophages, and intravascular hemolysis where they lyse within blood vessels. Specific causes of hemolysis are then outlined, including inherited disorders like hereditary spherocytosis and enzyme deficiencies like glucose-6-phosphate dehydrogenase deficiency. Features of acquired conditions like paroxysmal nocturnal hemoglobinuria and immune-mediated hemolytic anemias are also summarized.
Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a disease characterized by hemolytic anemia, low platelet count, and kidney failure. It predominantly affects children and can be caused by infections from E. coli or pneumococcal bacteria or complement factor abnormalities. The typical pathophysiology involves Shiga toxin or other bacterial toxins damaging endothelial cells and platelets. Treatment involves supportive care, antibiotics for infections, plasma therapy for complement abnormalities, and long-term prognosis depends on severity and treatment.
Aplastic anemia
Usman Ghani, a 7-year-old boy, presented with pallor, easy fatigability, and bruising. Investigations revealed very low blood counts and a bone marrow biopsy showed hypoplastic/aplastic bone marrow. He was diagnosed with aplastic anemia. Aplastic anemia is a condition where the bone marrow fails to produce sufficient new blood cells, leading to pancytopenia. Treatment involves blood transfusions, antibiotics, growth factors, immunosuppressive drugs, and stem cell transplantation depending on the severity of the condition.
Guest Lecture: April 2014: Haematological manifestations of hiv
Guest Lecture: April 2014: Haematological manifestations of hivSri Lanka College of Sexual Health and HIV Medicine
Haematological manifestations of HIV by Dr Senani Williams (FRCPath, MD), Consultant Haematologist, Faculty of Medicine, University of Kelaniya, Sri LankaThalassemia
Thalassemia is an inherited blood disorder caused by variants or missing genes that affect hemoglobin production. This results in reduced red blood cells and mild to severe anemia. There are two main types - alpha and beta thalassemia. Symptoms range from none in minor cases to severe anemia requiring transfusions in major cases. Investigations include blood tests to check hemoglobin levels, red blood cell size and count, and hemoglobin electrophoresis to confirm the diagnosis. Management focuses on blood transfusions and iron chelation therapy to prevent organ damage from excess iron.
Haemolytic anemia
Hemolytic anemia is characterized by accelerated red blood cell destruction and vigorous blood regeneration. It can be classified as intrinsic or extrinsic, congenital or acquired. The site of red blood cell destruction can be intravascular or extravascular. Common causes of hemolytic anemia include hereditary spherocytosis, thalassemias, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, and immune-mediated hemolytic anemia. Evaluation of hemolytic anemia involves determining whether the anemia is hemolytic, the site of red blood cell destruction, the etiology, and severity through blood smears, reticulocyte counts, LDH and
Anemia of chronic disease
Anemia of chronic disease (ACD), also known as anemia of inflammation, is a common type of anemia associated with chronic infections, inflammatory disorders, and some cancers. It is characterized by inadequate red blood cell production, low serum iron levels, and low iron binding capacity. The anemia is usually mild to moderate in severity. Treatment involves addressing the underlying chronic condition causing the inflammation.
Thrombocytopenia
When your blood has too few platelets, mild
to serious bleeding can occur. Bleeding can occur inside your body (internal
bleeding) or underneath your skin or from the surface of your skin (external
bleeding).
A normal platelet count in adults ranges
from 150,000 to 450,000 platelets per microliter of blood. A platelet count of
less than 150,000 platelets per microliter is lower than normal. If your blood
platelet count falls below normal, you have thrombocytopenia.
However, the risk for serious bleeding
doesn't occur until the count becomes very low—less than 10,000 or 20,000
platelets per microliter. Mild bleeding sometimes occurs when the count is less
than 50,000 platelets per microliter.
Many factors can cause a low platelet
count, such as:
-- The body's bone marrow doesn't make enough
platelets.
-- The bone marrow makes enough platelets, but
the body destroys them or uses them up.
-- The spleen holds on to too many platelets.
The spleen is an organ that normally stores about one-third of the body's
platelets. It also helps your body fight infection and remove unwanted cell
material.
-- A combination of the above factors.
-- How long thrombocytopenia lasts depends on
its cause. It can last from days to years.
The treatment for this condition also
depends on its cause and severity. Mild thrombocytopenia often doesn't require
treatment. If the condition causes or puts you at risk for serious bleeding,
you may need medicines or blood or
platelet transfusions. Rarely, the spleen may need to be removed.
Microangiopathic hemolytic Anemia & Hemolytic Uremic Syndrome
Microangiopathic hemolytic anemia (MAHA) is caused by damage to red blood cells as they pass through abnormally narrowed small blood vessels. This leads to fragmentation of red blood cells seen on peripheral blood smears. MAHA is associated with thrombotic microangiopathy syndromes like thrombotic thrombocytopenic purpura and hemolytic uremic syndrome (HUS). HUS is primarily caused by endothelial injury from bacterial toxins like Shiga toxin from E. coli O157:H7, leading to platelet aggregation and blood clots in small vessels that obstruct blood flow and damage red cells. Classic HUS mostly affects children after intestinal infection and is clearly associated with Shiga-
Autoimmune Hemolytic Anemia (AIHA)
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
Auto immune hemolytic anemia
Autoimmune hemolytic anemia is caused by antibodies that bind to and prematurely destroy red blood cells. It is classified into warm and cold types based on antibody characteristics and mechanisms of hemolysis. Workup involves a Coombs test to detect antibodies coating red blood cells via direct or indirect agglutination. Treatment depends on type but may include steroids, splenectomy, cold protection, or rituximab.
Hemolytic anemia ppt presentation
Hemolytic anemias are caused by increased red blood cell destruction. They are characterized by normochromic, normocytic anemia with reticulocytosis, increased indirect bilirubin and LDH, and absent haptoglobin. Causes include membrane defects, metabolic abnormalities, hemoglobinopathies, and immune or non-immune mechanisms. Specific conditions discussed include hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, drug-induced hemolysis, alloimmune hemolytic anemia, and warm or cold autoimmune hemolytic anemia. Management depends on the underlying cause and may involve transfusions, medications, or splenectomy.
Aplastic anemia
This document discusses aplastic anemia, which is a failure of the bone marrow to produce sufficient new blood cells, leading to pancytopenia (low red blood cells, white blood cells, and platelets). It may be idiopathic or secondary to drugs, radiation, infections, or immune diseases. Symptoms include anemia, infections, and bleeding. Diagnosis involves a bone marrow biopsy showing hypoplastic marrow. Treatment options include supportive care with transfusions, immunosuppressive drugs like antithymocyte globulin, bone marrow transplantation, and growth factors.
Hemolytic anemia; Harrison 19th edition
Hereditary hemolytic anemias can be caused by defects in the red blood cell's hemoglobin, membrane, metabolic machinery or enzymes. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme defect causing hemolytic anemia. It results from a lack of the enzyme G6PD, which protects red blood cells from oxidative damage. Patients with G6PD deficiency typically present with neonatal jaundice or acute hemolytic anemia triggered by factors like fava beans, infections or drugs. An acute hemolytic episode is characterized by symptoms like jaundice and dark urine over hours to days, along with signs of intravascular and extravascular hemolysis on lab tests.
The KIDNEY - PATHOGENESIS OF GLOMERULAR DISEASES
The document discusses glomerular diseases, which involve the renal glomeruli. It describes the classification of glomerular diseases into primary and secondary types. The major clinical manifestations are proteinuria, hematuria, hypertension, and impaired renal function. Six major glomerular syndromes are discussed: acute nephritic syndrome, nephrotic syndrome, acute renal failure, chronic renal failure, asymptomatic proteinuria, and asymptomatic hematuria. The pathogenesis of glomerular injury is examined by exploring the roles of endothelial, mesangial, epithelial and parietal cells as well as the glomerular basement membrane. Immunological and non-immunological mechanisms are involved in glomerular disease pathogenesis.
hemolytic uremic syndrome
hemolytic uremic syndrome
introduction
epidemiology
etiology
pathophysiology
clinical fea
diagnosis
treatment
compilaction
prognosis
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Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal injury, most commonly caused by toxin-producing strains of E. coli. The toxins produced by these bacteria damage endothelial cells in the kidneys and other organs, leading to platelet aggregation and thrombosis. This causes fragmentation of red blood cells and kidney dysfunction. HUS diagnosis is based on laboratory findings of hemolytic anemia, low platelet count, and kidney involvement. Treatment is largely supportive through dialysis, blood transfusions, and controlling blood pressure and electrolyte abnormalities. Most patients recover renal function, but some are left with chronic kidney disease.
Haemolytic Uremic Syndrome
Haemolytic uremic syndrome (HUS) is a clinical syndrome characterized by renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. It is most commonly caused by Shiga toxin-producing bacteria like E. coli O157:H7 through damage to endothelial cells. There are two main categories of HUS - Shiga-toxin associated HUS and non-Shiga-toxin associated HUS. Treatment for HUS focuses on symptomatic relief through dialysis, blood transfusions, and managing complications. The prognosis is generally good, though outcomes can be worse in cases with very high white blood cell counts or persistent kidney damage and failure.
Myeloproliferative disorders
The document discusses myeloproliferative disorders (MPDs), which are clonal stem cell disorders characterized by increased blood cell counts and enlarged spleen and bone marrow. It focuses on chronic myeloid leukemia (CML), describing it as a MPD caused by a genetic mutation that results in uncontrolled white blood cell growth. CML progresses through chronic, accelerated, and blast phases, with symptoms ranging from fatigue to organ enlargement. Diagnosis involves blood and bone marrow tests detecting elevated white and platelet counts and the Philadelphia chromosome genetic abnormality associated with CML.
Sickle cell disease
This document provides an outline about sickle cell anemia. It defines sickle cell anemia as a blood disorder caused by inheritance of the sickle hemoglobin gene from both parents. The disorder is characterized by rigid, sickle shaped red blood cells that can block blood vessels. Clinical features include painful vaso-occlusive crises in the bones, joints and organs. Laboratory findings show anemia and the presence of sickle cells. Treatment focuses on prevention, pain management during crises, blood transfusions, and newer therapies like hydroxyurea. Prognosis has improved due to better care, though sickle cell anemia currently has no cure.
Approach to anemia
Approach to anemia - Iron, Megaloblastic, Hemolytic, Autoimmune, Cytopenia, Marrow and Management - Advances, Sideroblastic
An Overview of Hemolytic anemia
This document summarizes different types of hemolytic anemias. It describes the features shared by hemolytic anemias such as a shortened red blood cell lifespan and increased erythropoiesis. Two main types of hemolysis are discussed: extravascular hemolysis where red blood cells are destroyed within macrophages, and intravascular hemolysis where they lyse within blood vessels. Specific causes of hemolysis are then outlined, including inherited disorders like hereditary spherocytosis and enzyme deficiencies like glucose-6-phosphate dehydrogenase deficiency. Features of acquired conditions like paroxysmal nocturnal hemoglobinuria and immune-mediated hemolytic anemias are also summarized.
Hemolytic uremic syndrome
Hemolytic uremic syndrome (HUS) is a disease characterized by hemolytic anemia, low platelet count, and kidney failure. It predominantly affects children and can be caused by infections from E. coli or pneumococcal bacteria or complement factor abnormalities. The typical pathophysiology involves Shiga toxin or other bacterial toxins damaging endothelial cells and platelets. Treatment involves supportive care, antibiotics for infections, plasma therapy for complement abnormalities, and long-term prognosis depends on severity and treatment.
Aplastic anemia
Usman Ghani, a 7-year-old boy, presented with pallor, easy fatigability, and bruising. Investigations revealed very low blood counts and a bone marrow biopsy showed hypoplastic/aplastic bone marrow. He was diagnosed with aplastic anemia. Aplastic anemia is a condition where the bone marrow fails to produce sufficient new blood cells, leading to pancytopenia. Treatment involves blood transfusions, antibiotics, growth factors, immunosuppressive drugs, and stem cell transplantation depending on the severity of the condition.
Guest Lecture: April 2014: Haematological manifestations of hiv
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Haematological manifestations of HIV by Dr Senani Williams (FRCPath, MD), Consultant Haematologist, Faculty of Medicine, University of Kelaniya, Sri LankaThalassemia
Thalassemia is an inherited blood disorder caused by variants or missing genes that affect hemoglobin production. This results in reduced red blood cells and mild to severe anemia. There are two main types - alpha and beta thalassemia. Symptoms range from none in minor cases to severe anemia requiring transfusions in major cases. Investigations include blood tests to check hemoglobin levels, red blood cell size and count, and hemoglobin electrophoresis to confirm the diagnosis. Management focuses on blood transfusions and iron chelation therapy to prevent organ damage from excess iron.
Haemolytic anemia
Hemolytic anemia is characterized by accelerated red blood cell destruction and vigorous blood regeneration. It can be classified as intrinsic or extrinsic, congenital or acquired. The site of red blood cell destruction can be intravascular or extravascular. Common causes of hemolytic anemia include hereditary spherocytosis, thalassemias, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, and immune-mediated hemolytic anemia. Evaluation of hemolytic anemia involves determining whether the anemia is hemolytic, the site of red blood cell destruction, the etiology, and severity through blood smears, reticulocyte counts, LDH and
Anemia of chronic disease
Anemia of chronic disease (ACD), also known as anemia of inflammation, is a common type of anemia associated with chronic infections, inflammatory disorders, and some cancers. It is characterized by inadequate red blood cell production, low serum iron levels, and low iron binding capacity. The anemia is usually mild to moderate in severity. Treatment involves addressing the underlying chronic condition causing the inflammation.
Thrombocytopenia
When your blood has too few platelets, mild
to serious bleeding can occur. Bleeding can occur inside your body (internal
bleeding) or underneath your skin or from the surface of your skin (external
bleeding).
A normal platelet count in adults ranges
from 150,000 to 450,000 platelets per microliter of blood. A platelet count of
less than 150,000 platelets per microliter is lower than normal. If your blood
platelet count falls below normal, you have thrombocytopenia.
However, the risk for serious bleeding
doesn't occur until the count becomes very low—less than 10,000 or 20,000
platelets per microliter. Mild bleeding sometimes occurs when the count is less
than 50,000 platelets per microliter.
Many factors can cause a low platelet
count, such as:
-- The body's bone marrow doesn't make enough
platelets.
-- The bone marrow makes enough platelets, but
the body destroys them or uses them up.
-- The spleen holds on to too many platelets.
The spleen is an organ that normally stores about one-third of the body's
platelets. It also helps your body fight infection and remove unwanted cell
material.
-- A combination of the above factors.
-- How long thrombocytopenia lasts depends on
its cause. It can last from days to years.
The treatment for this condition also
depends on its cause and severity. Mild thrombocytopenia often doesn't require
treatment. If the condition causes or puts you at risk for serious bleeding,
you may need medicines or blood or
platelet transfusions. Rarely, the spleen may need to be removed.
Microangiopathic hemolytic Anemia & Hemolytic Uremic Syndrome
Microangiopathic hemolytic anemia (MAHA) is caused by damage to red blood cells as they pass through abnormally narrowed small blood vessels. This leads to fragmentation of red blood cells seen on peripheral blood smears. MAHA is associated with thrombotic microangiopathy syndromes like thrombotic thrombocytopenic purpura and hemolytic uremic syndrome (HUS). HUS is primarily caused by endothelial injury from bacterial toxins like Shiga toxin from E. coli O157:H7, leading to platelet aggregation and blood clots in small vessels that obstruct blood flow and damage red cells. Classic HUS mostly affects children after intestinal infection and is clearly associated with Shiga-
Autoimmune Hemolytic Anemia (AIHA)
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
Auto immune hemolytic anemia
Autoimmune hemolytic anemia is caused by antibodies that bind to and prematurely destroy red blood cells. It is classified into warm and cold types based on antibody characteristics and mechanisms of hemolysis. Workup involves a Coombs test to detect antibodies coating red blood cells via direct or indirect agglutination. Treatment depends on type but may include steroids, splenectomy, cold protection, or rituximab.
Hemolytic anemia ppt presentation
Hemolytic anemias are caused by increased red blood cell destruction. They are characterized by normochromic, normocytic anemia with reticulocytosis, increased indirect bilirubin and LDH, and absent haptoglobin. Causes include membrane defects, metabolic abnormalities, hemoglobinopathies, and immune or non-immune mechanisms. Specific conditions discussed include hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, drug-induced hemolysis, alloimmune hemolytic anemia, and warm or cold autoimmune hemolytic anemia. Management depends on the underlying cause and may involve transfusions, medications, or splenectomy.
Aplastic anemia
This document discusses aplastic anemia, which is a failure of the bone marrow to produce sufficient new blood cells, leading to pancytopenia (low red blood cells, white blood cells, and platelets). It may be idiopathic or secondary to drugs, radiation, infections, or immune diseases. Symptoms include anemia, infections, and bleeding. Diagnosis involves a bone marrow biopsy showing hypoplastic marrow. Treatment options include supportive care with transfusions, immunosuppressive drugs like antithymocyte globulin, bone marrow transplantation, and growth factors.
Hemolytic anemia; Harrison 19th edition
Hereditary hemolytic anemias can be caused by defects in the red blood cell's hemoglobin, membrane, metabolic machinery or enzymes. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme defect causing hemolytic anemia. It results from a lack of the enzyme G6PD, which protects red blood cells from oxidative damage. Patients with G6PD deficiency typically present with neonatal jaundice or acute hemolytic anemia triggered by factors like fava beans, infections or drugs. An acute hemolytic episode is characterized by symptoms like jaundice and dark urine over hours to days, along with signs of intravascular and extravascular hemolysis on lab tests.
The KIDNEY - PATHOGENESIS OF GLOMERULAR DISEASES
The document discusses glomerular diseases, which involve the renal glomeruli. It describes the classification of glomerular diseases into primary and secondary types. The major clinical manifestations are proteinuria, hematuria, hypertension, and impaired renal function. Six major glomerular syndromes are discussed: acute nephritic syndrome, nephrotic syndrome, acute renal failure, chronic renal failure, asymptomatic proteinuria, and asymptomatic hematuria. The pathogenesis of glomerular injury is examined by exploring the roles of endothelial, mesangial, epithelial and parietal cells as well as the glomerular basement membrane. Immunological and non-immunological mechanisms are involved in glomerular disease pathogenesis.
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Gi bleed hegazy
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Classification, Diagnosis, and Management of Thrombocytopenia; Heparin-Induced Thrombocytopenia; Idiopathic Thrombocytopenia; Thrombotic Thrombocytopenic Purpura
Nephortic syndrome
Nephrotic syndrome may be caused by primary (idiopathic) renal disease or by a variety of secondary causes. Patients present with marked edema, proteinuria, hypoalbuminemia, and often hyperlipidemia.
Nephrotic syndrome is a primary glomerular disease characterized by the following:
Marked increase in protein in the urine (proteinuria)
Decrease in albumin in the blood (hypoalbuminemia)
Edema (The swelling (edema), can be most noticeable on the face, around the eyes, around the feet and ankles, and in the belly area (or the abdomen).
High serum cholesterol and low-density lipoproteins (hyperlipidemia)
Nephrotic syndrome is a clinical disorder characterized by marked increase of protein in the urine ( proteinuria ), decrease in albumin in the blood (hypoalbuminemia ),edema, & excess lipids in the blood ( hyperlipidemia )
Pathophysiology
Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus.
Although generally considered a disorder of childhood, nephrotic syndrome does occur in adults, including the elderly. Causes include:
Chronic glomerulonephritis
Diabetes mellitus with intercapillary glomerulosclerosis
Amyloidosis of the kidney
Systemic lupus erythematosus
Multiple myeloma and renal vein thrombosis.
NSAIDs
Pre eclampsia
Approach to GI Bleeding in Children
This document discusses gastrointestinal bleeding in children. It notes that GI bleeding accounts for 10-20% of pediatric gastroenterology referrals and around 0.4% of PICU admissions are due to life-threatening GI bleeding. The presentation, classification, causes, diagnostic workup, and treatment of upper and lower GI bleeding in neonates, infants, and children are described in detail over multiple sections. Key points include distinguishing the source and severity of bleeding, identifying specific etiologies, and managing bleeding through supportive care, endoscopic procedures, medications, and surgery as needed.
Approach to anaemia
This document provides an overview of anemia, including its classification, causes, signs and symptoms, diagnostic approach, and management principles. It presents a clinical case of an 18-year-old female with weakness, lethargy and heavy menstrual bleeding, then reviews epidemiology of anemia, the red blood cell lifecycle, classification of anemia by severity, etiology and morphology, diagnostic workup, and general management strategies focusing on identifying and treating underlying causes. The take-home message emphasizes that anemia requires investigation to determine its cause, and prevention through supplementation is important for reducing prevalence.
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Nephrological assessment
The nephrological assessment is very important nursing procedure help to rule out the provisional diagnosis of patient and their general condition. it also help in certain type of investigation and treatment of patient.
Gi bleed peds awais
This document discusses gastrointestinal (GI) bleeding in infants and children. It covers:
1. Definitions of different types of GI bleeding like melena, hematochezia, and hematemesis.
2. Pathophysiology of GI bleeding including consequences of blood loss, higher risk in children, and compensatory mechanisms.
3. Causes of GI bleeding in different age groups ranging from neonates to adolescents. Common causes include esophagitis, gastritis, ulcers, varices, and infections.
4. Evaluation involves a thorough history, physical exam, lab tests like CBC and coagulation studies, and endoscopic procedures to identify the source of bleeding. Management is then
Hematuria
Hematuria can be caused by various upper and lower urinary tract diseases. Common causes of glomerular hematuria include IgA nephropathy, Alport syndrome, and thin basement membrane disease. Post-streptococcal glomerulonephritis is associated with a preceding streptococcal infection. Membranous nephropathy presents with nephrotic syndrome. Goodpasture disease involves anti-GBM antibodies attacking the lungs and kidneys. Diagnosis involves urinalysis, renal biopsy, and identifying underlying causes or associations. Treatment depends on the specific condition but may include antibiotics, steroids, immunosuppressants, blood pressure control, and addressing complications.
Jaundice and LFT interpretation
This document provides guidance on evaluating a patient presenting with jaundice. It outlines a systematic approach including focused history, examination, differential diagnosis, and appropriate lab tests and imaging. Liver function tests can indicate hepatitic or cholestatic patterns. Case examples demonstrate applying this approach, such as using imaging and endoscopy to diagnose an ampullary tumor, managing a variceal bleed in cirrhosis, and identifying acute hepatitis B. Key considerations include complications of liver disease and importance of screening high-risk populations.
Nephrotic syndrome By Sachin Dwivedi
Nephrotic syndrome is a kidney disorder characterized by protein in the urine, low blood albumin levels, high blood lipids, and swelling. It is caused by damage to the glomerular capillary membrane in the kidney. Clinically, it presents with edema, proteinuria, hyperlipidemia, and hypoalbuminemia. Treatment involves fluid restriction, diuretics, corticosteroids, and ACE inhibitors to control symptoms and manage complications like infection, atherosclerosis, and renal failure. Prognosis depends on the underlying cause, with minimal change disease having a good prognosis if it responds to steroids.
Portal Hypertension
A presentation on the pathology and current management (with Especial emphasis on surgical management) of Portal Hypertension; a common complication of liver cirrhosis among other liver diseases. Being a copy of seminar presentation I for the HepatoPancreaticoBiliary Unit of the Division of General Surgery, Ahmadu Belllo University Teaching Hospital, Zaria.
Bleeding git.ppt
This document discusses gastrointestinal bleeding, including:
- Gastrointestinal bleeding can arise from any location in the GI tract and represents the initial symptom of GI disease in 1/3 of patients.
- Clinical presentations of GI bleeding include hematemesis, melena, hematochezia, occult bleeding, and symptoms of blood loss/anemia.
- Common causes of upper GI bleeding are peptic ulcers and esophageal varices, while diverticulosis and colon polyps are common causes of lower GI bleeding.
- The approach to a patient with GI bleeding involves stabilizing their hemodynamic status, identifying the source of bleeding, stopping active bleeding, treating the underlying cause, and preventing recurrent
Similar to hemolytic uremic syndrome (20)
shock and blood trasfution problems and complications
shock and blood trasfution problems and complications
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3学分转移联合办学等情况复杂不知道怎么整理材料的。时间紧迫自己不清楚递交流程的。
如果你是以上情况之一请联系我们我们将在第一时间内给你免费咨询相关信息。我们将帮助你整理认证所需的各种材料.帮你解决国外学历认证难题。
国外旧金山大学旧金山大学硕士学位证成绩单办理方法：
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留信网认证的作用:
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2:同时对留学生所学专业登记给予评定
3:国家专业人才认证中心颁发入库证书
4:这个认证书并且可以归档倒地方
5:凡事获得留信网入网的信息将会逐步更新到个人身份内，将在公安局网内查询个人身份证信息后，同步读取人才网入库信息
6:个人职称评审加20分
7:个人信誉贷款加10分
8:在国家人才网主办的国家网络招聘大会中纳入资料，供国家高端企业选择人才
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对于老客户或者被老客户介绍过来的朋友，我们都会适当给一些优惠。
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hemolytic uremic syndrome
- 1. HEMOLYTIC UREMIC SYNDROME • Presenter- Hassani Bakari • Facilitator- Dr. Joshua( Pediatrician)
- 2. OUTLINE OF THE PRESENTATION • Background • Classification of the hemolytic uremic syndrome • Etiopathogenesis • Clinical features • Investigation • Management
- 3. • BACKGROUND • It is a clinical syndrome characterized by macroangiopathic hemolytic anemia. Thrombocytopenia Acute kidney failure • it is the most common cause of AKI in children. • Predominantly affect children( under 5)
- 4. TYPES OF HUS • Into two broad categories Typical HUS- diarrhea associated (commonest one Atypical HUS- non diarrhea associated( infrequent and most severe)
- 5. infection associated Systemic disease associated Drug induced Genetic • Verotoxin/shiga like toxin producing E.coli(0 157:H7), Shiga toxin producing shigella(STPSD 1) • Systemic Lupus Erythematosus • Quinine(most common) • Cytotoxic drugs such as Cisplatin, mitomycin C • Von Willebrand Factor-cleaving protease deficiency(ADAM TS 13) • Neuraminidase producing S.pneumonia • Anti phospholipid syndrome • Cyclosporine • Complement H and I deficiency • HIV CLASSIFICATION OF HUS BASED ON ETIOLOGY
- 6. E.coli
- 7. SOURCES OF INFECTION • Milk and animal products( poorly cooked beef ,pork, lamb) • Human feco-oral transmission • Vegetables ,salads drinking water contaminated with the bacteria
- 8. ETIOPATHOGENESIS –typical HUS • Typical / Diarrhea associated • Commonly due to shiga toxin producing shigella dysenteriae type 1(developing nations) • And Escherichia coli serotype 0157:H7 ( commonly ,In Developed nations) • Shiga toxin or shiga like toxin cause endothelia damage • Leading to platelets adhesion, aggregation, and activation • Leading to narrowing of small vessels in glomerular due to formed thrombi • This cause damage to passing RBC leading to hemolytic anemia
- 9. ETIOPATHOGENESIS –typical HUS…………. • Formed thrombi reduce GFR leading to AKI • Consumptive thrombocytopenia as platelets adhere to damaged endothelial
- 10. Pathogenesis of typical HUS
- 11. CLINICAL FEATURES • HUS develops 5-10 days after onset of diarrhea, abdominal pain and fever • Then acute anemia(pallor) • Oliguria • Hematuria and Hypertension
- 12. CLINICAL FEATURES…….. • Complications of fluid overload( Pulmonary edema, Hypertensive encephalopathy) • Neurological manifestation such as irritability Seizures Encephalopathy • Bleeding manifestation ( possible but rare)
- 13. INVESTIGATIONS • CBC-anemia, thrombocytopenia and reticulocytosis • Peripheral blood smear (schistocytes) • LDH • Bilirubin level-unconjugated • RFT-Cr and BUN • Urine analysis –hematuria, proteinuria, hemoglobinuria
- 15. INVESTIGATION……. • To check for EHEC or Shigella from stool culture • From urine culture(Rarely HUS can arise from UTI due to E.Coli
- 16. MANAGEMENT OF HUS • Supportive • Antibiotics • Plasma therapy
- 17. a) SUPPORTIVE • It is cornerstone of primary approach • If there is fluid deficit-fluid supplementation is of paramount importance • If the is fluid overload –fluid restriction • Correct electrolyte imbalance-hyponatremia, hyperkalemia
- 18. a) supportive care……. • Early initiation of dialysis if –(a ,e ,i, o ,u ) • If significant anemia is present –give PRBCs very carefully • Platelet transfusion- not generally required( to be considered only in uncontrolled severe bleeding)
- 19. (b) Use of antibiotics • Use of antimicrobial agent{contradicting)- no evidence of benefit • [c] Plasma infusion in severe cases • Complement replacements
- 20. PROGNOSIS OF HUS • Immediate outcome of classical HUS is relative better than aHUS • It has less than 5% mortality with good supportive care • 10-30% develop CKD • 5-10% develop ESRD in the next 10yrs
- 21. •THANK YOU
- 22. REFERENCES • Journal of nephrology and therapeutic-review of articles on HUS by Jagabandhu et al • Current diagnosis and treatment book 22 edition • Medscape