This document provides an overview of renovascular disorders. It begins by introducing how the kidneys rely on blood pressure and are vulnerable to vascular diseases. It then classifies renovascular disorders by anatomic location and describes several specific disorders in more detail, including thrombotic microangiopathies (like HUS and TTP), renal artery stenosis, ischemic renal disease, and others. It provides information on pathogenesis, clinical presentation, treatment, and prognosis for each.
Thrombotic microangiopathy and the kidney - Dr. Mohamed Mamdouh AbdAlBaryMNDU net
TTP is characterized by unusually large von Willebrand factor multimers and platelet-rich thrombi in capillaries and arterioles due to ADAMTS13 deficiency, while aHUS is typically caused by dysregulated complement activation on endothelial cells from genetic mutations or autoantibodies. TMA can be caused by a variety of conditions including infections, drugs, pregnancy, transplantation, and other diseases, with manifestations varying depending on the organs involved but commonly involving renal failure, neurological symptoms, and thrombocytopenia.
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
Thrombotic Microangiopathy associated with proteasome inhibitorsAhad Lodhi
This case report describes a 63-year-old man who developed acute kidney injury and thrombotic microangiopathy after receiving treatment with the proteasome inhibitor carfilzomib. A kidney biopsy showed features of thrombotic microangiopathy and arteriolar damage. The authors propose that proteasome inhibitors may cause kidney injury by decreasing VEGF production through inhibition of the NF-κB pathway, disrupting normal endothelial cell function and integrity. The patient's kidney function recovered after discontinuing carfilzomib with supportive management. This case adds to evidence that proteasome inhibitors can cause thrombotic microangiopathy through their effects on VEGF signaling.
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.
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.
This case presentation describes a 27-year-old female who presented with decreased urine output, swelling of the face and feet, anorexia, and vomiting two days after a cesarean section. Laboratory investigations revealed thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury. A renal biopsy showed features of thrombotic microangiopathy. She was diagnosed with postpartum atypical hemolytic uremic syndrome (aHUS). Treatment included plasma exchange, hemodialysis as needed, and supportive care. Her clinical parameters improved with treatment and she was discharged after three weeks.
Thrombotic microangiopathy and the kidney - Dr. Mohamed Mamdouh AbdAlBaryMNDU net
TTP is characterized by unusually large von Willebrand factor multimers and platelet-rich thrombi in capillaries and arterioles due to ADAMTS13 deficiency, while aHUS is typically caused by dysregulated complement activation on endothelial cells from genetic mutations or autoantibodies. TMA can be caused by a variety of conditions including infections, drugs, pregnancy, transplantation, and other diseases, with manifestations varying depending on the organs involved but commonly involving renal failure, neurological symptoms, and thrombocytopenia.
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
Thrombotic Microangiopathy associated with proteasome inhibitorsAhad Lodhi
This case report describes a 63-year-old man who developed acute kidney injury and thrombotic microangiopathy after receiving treatment with the proteasome inhibitor carfilzomib. A kidney biopsy showed features of thrombotic microangiopathy and arteriolar damage. The authors propose that proteasome inhibitors may cause kidney injury by decreasing VEGF production through inhibition of the NF-κB pathway, disrupting normal endothelial cell function and integrity. The patient's kidney function recovered after discontinuing carfilzomib with supportive management. This case adds to evidence that proteasome inhibitors can cause thrombotic microangiopathy through their effects on VEGF signaling.
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.
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.
This case presentation describes a 27-year-old female who presented with decreased urine output, swelling of the face and feet, anorexia, and vomiting two days after a cesarean section. Laboratory investigations revealed thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury. A renal biopsy showed features of thrombotic microangiopathy. She was diagnosed with postpartum atypical hemolytic uremic syndrome (aHUS). Treatment included plasma exchange, hemodialysis as needed, and supportive care. Her clinical parameters improved with treatment and she was discharged after three weeks.
This document discusses thrombotic thrombocytopenic purpura (TTP). It begins by presenting a case of a 32-year-old woman presenting with headaches, difficulty speaking and moving her tongue, and numbness. Her exam and labs show thrombocytopenia and schistocytes. The document then discusses the differential diagnosis, epidemiology, terminology, definitions, types, presentations, investigations, and treatment of TTP, with a focus on plasma exchange therapy to remove antibodies and replace deficient ADAMTS13 protease.
Thrombotic Microangiopathies and AntiPhospholipid SyndromeRichard McCrory
This document discusses various thrombotic microangiopathies (TMAs) including their causes, pathophysiology, clinical findings, and treatments. It covers hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, atypical hemolytic uremic syndrome, and antiphospholipid syndrome. The key pathological finding in all TMAs is endothelial injury and thrombus formation in small blood vessels. Recent research suggests dysregulation of the alternative complement pathway may be a unifying factor. Emerging treatments targeting complement, such as eculizumab, show promise in halting disease progression.
- A new version of this lecture is available at: https://www.slideshare.net/MohammedGawad/thrombotic-microangiopathy-tma-in-adults-and-acute-kidney-injury-dr-gawad
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
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UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
This document provides an overview of thrombocytopenia and its causes and classification. It discusses the normal physiology of platelet production and defines thrombocytopenia. The four main causes of thrombocytopenia are outlined as artifactual, deficient platelet production, accelerated platelet destruction, and abnormal platelet distribution. Specific causes under each category are then examined in more detail over several paragraphs.
This document discusses hypercoagulation states and thrombosis. It defines thrombosis and reviews the coagulation pathway and its relation to hypercoagulation. It describes arterial and venous thrombosis, their causes, and treatment approaches. The importance of obtaining a thorough medical history and family history is emphasized. Laboratory tests for diagnosing a hypercoagulation state are also reviewed.
Hemophilia is perhaps the most well-known inherited bleeding disorder, although it is relatively rare. It affects mostly males. Many more people are affected by von Willebrand disease, the most common inherited bleeding disorder in America caused by clotting proteins.
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.
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.
The document discusses several clonal disorders of hematopoietic stem cells including:
1) Myelodysplastic syndromes which affect myeloid cell lines and cause cytopenias. Treatment is limited and includes transfusions, growth factors, and stem cell transplant.
2) Myeloproliferative disorders like polycythemia vera, essential thrombocythemia, and myelofibrosis which involve stem cell proliferation. Treatment focuses on controlling symptoms and reducing risks of thrombosis.
3) Chronic myeloid leukemia is driven by the Philadelphia chromosome and progresses from chronic to blast phase without treatment. Imatinib targets the abnormal BCR-ABL gene.
This document summarizes the management of oral surgery patients with thrombocytopenia. It begins with an introduction on the challenges of treating patients with bleeding disorders. It then covers basic platelet physiology, describing their production in bone marrow and role in hemostasis. The main types of platelet disorders are outlined as quantitative (too few platelets) and qualitative (dysfunction). Specific causes, diagnoses, and treatment approaches for different platelet disorders are discussed. Three case studies are also referenced to illustrate management of thrombocytopenic patients undergoing oral surgery.
Platelets were first observed in 1841 and were termed "platelets" in 1882. Their role in hemostasis through adhesion, secretion, and aggregation was established over the late 19th century. Megakaryocytes were recognized as rare bone marrow cells that produce platelets, with this relationship established in 1906. Thrombocytopenia can result from impaired platelet production, increased platelet destruction, or platelet sequestration. It is classified based on etiology, with immune thrombocytopenia and drug-induced thrombocytopenia as common causes of accelerated platelet destruction.
The document discusses thrombocytopenia, defined as a platelet count below 150,000/mm3. Various causes of thrombocytopenia are covered, including decreased production, immune-mediated causes, and sequestration. A history and physical exam can help diagnose the cause, while tests like CBC, smear, and bone marrow exam provide further information. Treatment depends on the underlying condition but may involve steroids, IVIG, splenectomy, or platelet transfusions.
This document summarizes quantitative and qualitative platelet disorders. The most common causes of abnormal bleeding are decreased platelet production, survival, or increased destruction/consumption. Disorders can be congenital or acquired and involve decreased megakaryocyte production, BM infiltration, ineffective thrombopoiesis, or disorders of thrombopoiesis control. Increased platelet destruction can be immunologic due to ITP, drugs, transfusion, or non-immunologic consumption. Functional platelet disorders involve adhesion, aggregation, or secretion defects which may be hereditary or acquired.
This document summarizes a presentation on atypical hemolytic uremic syndrome (aHUS). The key points are:
1) Atypical HUS is caused by dysregulation of the alternative complement pathway leading to thrombotic microangiopathy. There is often an underlying genetic predisposition that is triggered by stressors like pregnancy.
2) Treatment with plasma therapy and transplantation previously had limited success due to recurrent disease.
3) The monoclonal antibody eculizumab, a C5 inhibitor, is highly effective at treating and preventing recurrence of aHUS. However, the high cost of the medication presents barriers to treatment.
Aplastic anemia is a bone marrow failure syndrome characterized by pancytopenia and a hypoplastic bone marrow. It can be acquired (80% of cases) due to infections, chemicals, radiation or drugs or inherited (20% of cases). Treatment involves supportive care like blood transfusions and treatment of infections as well as curative options like hematopoietic stem cell transplant or immunosuppressive therapy. Prognosis has improved with better supportive care but risks include infection, bleeding, graft failure, GVHD and treatment resistance.
This document describes a case of HIV-associated thrombocytopenia in a 38-year old male patient. He presented with frank hematuria and weakness. Laboratory tests showed thrombocytopenia with a platelet count of 6,000/μl. Further testing revealed the patient was HIV-positive. He was diagnosed with HIV-associated thrombocytopenia and started on oral steroids, antiretroviral therapy, and supplements. Within 4 days his symptoms resolved and his platelet count improved to 70,000, at which point he was discharged. The document then provides background information on HIV-associated thrombocytopenia, its pathophysiology and treatment.
Cases in INTERNAL MEDICINE part one PART FIFTH DR MAGDI SASIcardilogy
This document provides a summary of a case involving a 40-year-old male who was admitted with sudden onset headache and seizure. An MRI scan revealed sagittal sinus thrombosis. He had recently recovered from aplastic anemia. Laboratory results showed anemia with reticulocytosis. Paroxysmal Nocturnal Hemoglobinuria (PNH) is the most likely diagnosis, as PNH can involve thrombosis and is associated with aplastic anemia.
Thrombotic thrombocytopenic purpura in pregnancy as grave as it comes jiacm...Sachin Adukia
This case report describes an 18-year-old pregnant woman diagnosed with thrombotic thrombocytopenic purpura (TTP) at 26 weeks gestation. She presented with fever, headache, seizures, and was found to have microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. She underwent an emergency delivery of a stillborn infant due to severe preeclampsia. MRI revealed features of posterior reversible encephalopathy syndrome (PRES). Plasma exchange therapy was initiated and her symptoms improved. TTP is a rare but life-threatening condition in pregnancy that requires prompt diagnosis and treatment such as plasma exchange to improve outcomes.
The document discusses various drug-induced hematological disorders including thrombocytopenia, thromboembolic diseases, aplastic anemia, hemolytic anemia, neutropenia, and agranulocytosis. It provides information on the mechanisms, risk factors, signs and symptoms, diagnosis, morbidity and mortality, prevention, and management of each condition. Common causative agents are identified for each disorder.
Drug-induced blood disorders can affect red blood cells, white blood cells, and platelets. Common types include thrombocytopenia, hemolytic anemia, megaloblastic anemia, and aplastic anemia. Symptoms depend on the specific disorder but may include fatigue, bleeding, and infections. Causative agents include certain medications like sulfonamides, quinine, and chemotherapy drugs. Diagnosis involves blood tests and bone marrow biopsy. Treatment focuses on removing the offending drug, blood transfusions, and immunosuppressive therapy. Drug-induced hematological disorders are rare but potentially life-threatening, so monitoring patients on high-risk medications is important.
This document discusses thrombotic thrombocytopenic purpura (TTP). It begins by presenting a case of a 32-year-old woman presenting with headaches, difficulty speaking and moving her tongue, and numbness. Her exam and labs show thrombocytopenia and schistocytes. The document then discusses the differential diagnosis, epidemiology, terminology, definitions, types, presentations, investigations, and treatment of TTP, with a focus on plasma exchange therapy to remove antibodies and replace deficient ADAMTS13 protease.
Thrombotic Microangiopathies and AntiPhospholipid SyndromeRichard McCrory
This document discusses various thrombotic microangiopathies (TMAs) including their causes, pathophysiology, clinical findings, and treatments. It covers hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, atypical hemolytic uremic syndrome, and antiphospholipid syndrome. The key pathological finding in all TMAs is endothelial injury and thrombus formation in small blood vessels. Recent research suggests dysregulation of the alternative complement pathway may be a unifying factor. Emerging treatments targeting complement, such as eculizumab, show promise in halting disease progression.
- A new version of this lecture is available at: https://www.slideshare.net/MohammedGawad/thrombotic-microangiopathy-tma-in-adults-and-acute-kidney-injury-dr-gawad
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
This document provides an overview of thrombocytopenia and its causes and classification. It discusses the normal physiology of platelet production and defines thrombocytopenia. The four main causes of thrombocytopenia are outlined as artifactual, deficient platelet production, accelerated platelet destruction, and abnormal platelet distribution. Specific causes under each category are then examined in more detail over several paragraphs.
This document discusses hypercoagulation states and thrombosis. It defines thrombosis and reviews the coagulation pathway and its relation to hypercoagulation. It describes arterial and venous thrombosis, their causes, and treatment approaches. The importance of obtaining a thorough medical history and family history is emphasized. Laboratory tests for diagnosing a hypercoagulation state are also reviewed.
Hemophilia is perhaps the most well-known inherited bleeding disorder, although it is relatively rare. It affects mostly males. Many more people are affected by von Willebrand disease, the most common inherited bleeding disorder in America caused by clotting proteins.
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.
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.
The document discusses several clonal disorders of hematopoietic stem cells including:
1) Myelodysplastic syndromes which affect myeloid cell lines and cause cytopenias. Treatment is limited and includes transfusions, growth factors, and stem cell transplant.
2) Myeloproliferative disorders like polycythemia vera, essential thrombocythemia, and myelofibrosis which involve stem cell proliferation. Treatment focuses on controlling symptoms and reducing risks of thrombosis.
3) Chronic myeloid leukemia is driven by the Philadelphia chromosome and progresses from chronic to blast phase without treatment. Imatinib targets the abnormal BCR-ABL gene.
This document summarizes the management of oral surgery patients with thrombocytopenia. It begins with an introduction on the challenges of treating patients with bleeding disorders. It then covers basic platelet physiology, describing their production in bone marrow and role in hemostasis. The main types of platelet disorders are outlined as quantitative (too few platelets) and qualitative (dysfunction). Specific causes, diagnoses, and treatment approaches for different platelet disorders are discussed. Three case studies are also referenced to illustrate management of thrombocytopenic patients undergoing oral surgery.
Platelets were first observed in 1841 and were termed "platelets" in 1882. Their role in hemostasis through adhesion, secretion, and aggregation was established over the late 19th century. Megakaryocytes were recognized as rare bone marrow cells that produce platelets, with this relationship established in 1906. Thrombocytopenia can result from impaired platelet production, increased platelet destruction, or platelet sequestration. It is classified based on etiology, with immune thrombocytopenia and drug-induced thrombocytopenia as common causes of accelerated platelet destruction.
The document discusses thrombocytopenia, defined as a platelet count below 150,000/mm3. Various causes of thrombocytopenia are covered, including decreased production, immune-mediated causes, and sequestration. A history and physical exam can help diagnose the cause, while tests like CBC, smear, and bone marrow exam provide further information. Treatment depends on the underlying condition but may involve steroids, IVIG, splenectomy, or platelet transfusions.
This document summarizes quantitative and qualitative platelet disorders. The most common causes of abnormal bleeding are decreased platelet production, survival, or increased destruction/consumption. Disorders can be congenital or acquired and involve decreased megakaryocyte production, BM infiltration, ineffective thrombopoiesis, or disorders of thrombopoiesis control. Increased platelet destruction can be immunologic due to ITP, drugs, transfusion, or non-immunologic consumption. Functional platelet disorders involve adhesion, aggregation, or secretion defects which may be hereditary or acquired.
This document summarizes a presentation on atypical hemolytic uremic syndrome (aHUS). The key points are:
1) Atypical HUS is caused by dysregulation of the alternative complement pathway leading to thrombotic microangiopathy. There is often an underlying genetic predisposition that is triggered by stressors like pregnancy.
2) Treatment with plasma therapy and transplantation previously had limited success due to recurrent disease.
3) The monoclonal antibody eculizumab, a C5 inhibitor, is highly effective at treating and preventing recurrence of aHUS. However, the high cost of the medication presents barriers to treatment.
Aplastic anemia is a bone marrow failure syndrome characterized by pancytopenia and a hypoplastic bone marrow. It can be acquired (80% of cases) due to infections, chemicals, radiation or drugs or inherited (20% of cases). Treatment involves supportive care like blood transfusions and treatment of infections as well as curative options like hematopoietic stem cell transplant or immunosuppressive therapy. Prognosis has improved with better supportive care but risks include infection, bleeding, graft failure, GVHD and treatment resistance.
This document describes a case of HIV-associated thrombocytopenia in a 38-year old male patient. He presented with frank hematuria and weakness. Laboratory tests showed thrombocytopenia with a platelet count of 6,000/μl. Further testing revealed the patient was HIV-positive. He was diagnosed with HIV-associated thrombocytopenia and started on oral steroids, antiretroviral therapy, and supplements. Within 4 days his symptoms resolved and his platelet count improved to 70,000, at which point he was discharged. The document then provides background information on HIV-associated thrombocytopenia, its pathophysiology and treatment.
Cases in INTERNAL MEDICINE part one PART FIFTH DR MAGDI SASIcardilogy
This document provides a summary of a case involving a 40-year-old male who was admitted with sudden onset headache and seizure. An MRI scan revealed sagittal sinus thrombosis. He had recently recovered from aplastic anemia. Laboratory results showed anemia with reticulocytosis. Paroxysmal Nocturnal Hemoglobinuria (PNH) is the most likely diagnosis, as PNH can involve thrombosis and is associated with aplastic anemia.
Thrombotic thrombocytopenic purpura in pregnancy as grave as it comes jiacm...Sachin Adukia
This case report describes an 18-year-old pregnant woman diagnosed with thrombotic thrombocytopenic purpura (TTP) at 26 weeks gestation. She presented with fever, headache, seizures, and was found to have microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. She underwent an emergency delivery of a stillborn infant due to severe preeclampsia. MRI revealed features of posterior reversible encephalopathy syndrome (PRES). Plasma exchange therapy was initiated and her symptoms improved. TTP is a rare but life-threatening condition in pregnancy that requires prompt diagnosis and treatment such as plasma exchange to improve outcomes.
The document discusses various drug-induced hematological disorders including thrombocytopenia, thromboembolic diseases, aplastic anemia, hemolytic anemia, neutropenia, and agranulocytosis. It provides information on the mechanisms, risk factors, signs and symptoms, diagnosis, morbidity and mortality, prevention, and management of each condition. Common causative agents are identified for each disorder.
Drug-induced blood disorders can affect red blood cells, white blood cells, and platelets. Common types include thrombocytopenia, hemolytic anemia, megaloblastic anemia, and aplastic anemia. Symptoms depend on the specific disorder but may include fatigue, bleeding, and infections. Causative agents include certain medications like sulfonamides, quinine, and chemotherapy drugs. Diagnosis involves blood tests and bone marrow biopsy. Treatment focuses on removing the offending drug, blood transfusions, and immunosuppressive therapy. Drug-induced hematological disorders are rare but potentially life-threatening, so monitoring patients on high-risk medications is important.
Diseminated Intravascular Coagulopathy And OthersRHMBONCO
DIC is a pathologic process secondary to an underlying illness where widespread activation of coagulation leads to microvascular fibrin deposition and compromised blood supply. The main features are attributable to excessive thrombin generation. Clinical conditions associated with DIC include sepsis, trauma, organ destruction, malignancy, and vascular abnormalities. The pathogenesis involves tissue factor-dependent microvascular fibrin deposition via the extrinsic coagulation pathway. Treatment focuses on treating the underlying condition, and transfusions are only used if bleeding risk is present.
An approach to a patient with Thrombocytopeniaaminanurnova
This document discusses thrombocytopenia (low platelet count) and its causes and evaluation. It describes the normal physiology of platelets and hemostasis. Common causes of thrombocytopenia include decreased platelet production (bone marrow problems), increased platelet destruction (immune mechanisms like ITP), and increased consumption (DIC). Evaluation involves history, exam, blood smear review, and identifying potential causes like drugs, infections, malignancies or autoimmune disorders. Specific conditions discussed in detail include ITP, HIT, DIC, and thrombocytopenia in cardiac patients.
Abstract Transplant- associated Thrombotic Microangiopathy (TA- TMA) is a hematopoietic disorder that leads to inflammatory and thrombotic changes of microvasculature with associated hemolytic anemia, thrombocytopenia and organ failure i.e. acute renal failure. This syndrome is visualized more commonly in allogeneic hematopoietic stem cell transplants (HSCTs) compared to autologous transplant. TA- TMA offers a diagnostic challenge as it can’t be categorized in the two most recognized TMA’s i.e. Atypical Hemolytic Uremic Syndrome (aHUS) or Thrombotic Thrombocytopenic Purpura (TTP). Despite the fact, that the patient receiving the transplant might face complications associated with the transplant i.e. infection, graft-versus-host disease (GVHD) , and disseminated intravascular coagulation (DIC), as well as the side effects of immunosuppressive drugs, all of which can be misdiagnosed as TMA. Since, the pathophysiology of this syndrome is not understood; management of the syndrome is suboptimal with a high mortality rate. A recent study of TA-TMA patients has identified the patients diagnosed with TA-TMA lack suppression of ADAMTS13 which is a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 1 and do not have a complete response to plasma exchange, thus indicating characteristics a TTP-like disorder is not involved. Recent advances in the treatment of aHUS may offer a therapeutic option in the aHUS-like TMAs associated with HSCTs, which still faces the difficulties associated with the diagnosis and treatment of TA-TMA. Keywords: Transplant- associated Thrombotic Microangiopathy (TA- TMA), hematopoetic, hemolytic anemia, thrombocytopenia, acutre renal failure, Atypical Hemolytic Uremic Syndrome (aHUS), Thrombotic Thrombocytopenic Purpura (TTP), graft-versus-host disease (GVHD) , disseminated intravascular coagulation (DIC)
Thrombocytopenia is defined as a platelet count below 150,000/microL. The main causes are decreased platelet production, increased platelet destruction, and altered platelet distribution. Decreased production can result from bone marrow damage, infections, toxins, or drugs. Increased destruction is most common, and can be immune-mediated (as in ITP) or non-immune (as in DIC or TTP). Altered distribution occurs in splenomegaly. Drug-induced thrombocytopenia can occur via direct toxicity, bone marrow suppression, or immune mechanisms like those seen with heparin or abciximab. Pseudo-thrombocytopenia due to platelet clumping must be
Nephrotic syndrome is defined by heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is caused by damage to the glomerular basement membrane that increases pore size and protein leakage. Loss of protein like albumin leads to edema as serum oncotic pressure decreases. Steroids are first line treatment but some patients are steroid resistant. Kidney biopsy guides treatment, which may include immunosuppressants for steroid resistant forms. Complications include infection, hypercoagulability, and renal failure.
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.
This document provides detailed information on polycythemia vera (PV), including its pathophysiology, clinical features, diagnosis, differential diagnosis, and laboratory evaluation. PV is a myeloproliferative neoplasm characterized by excessive red blood cell production. Key points: PV results from abnormal stem cell clone producing increased red blood cells, white blood cells, and platelets. Symptoms include bleeding, thrombosis, pruritus, headache, and visual issues due to hyperviscosity. Diagnosis requires elevated red blood cell count/mass and meeting criteria set by the Polycythemia Vera Study Group or WHO guidelines, which may include genetic testing for JAK2 mutation. Differential diagnosis excludes secondary causes of polycy
Rheumatological diseases can affect any organ system and cause life-threatening complications requiring intensive care. The document discusses several key rheumatological conditions that intensivists should be aware of including:
1) Macrophage activation syndrome, a potentially lethal complication seen in rheumatological diseases characterized by uncontrolled inflammation.
2) Scleroderma renal crisis, a rheumatological emergency caused by thickening of renal arteries leading to hypertension and kidney failure.
3) Catastrophic antiphospholipid syndrome, a rare but severe form of antiphospholipid antibody syndrome involving rapid multi-organ failure.
Early recognition and management of these rheumatological conditions is important to prevent poor outcomes for patients in intensive care
Cardiorenal syndromes describe disorders where dysfunction in the heart and kidneys negatively impact one another. There are 5 subtypes based on etiology and chronicity. Type 1 involves acute kidney injury secondary to heart failure. Type 2 is chronic cardiac dysfunction causing chronic kidney disease. Type 3 is acute worsening of kidney function inducing heart issues. Type 4 is primary chronic kidney disease contributing to cardiac complications. Type 5 involves systemic conditions affecting both organs. Managing cardiorenal syndromes focuses on decongestion through diuresis while preventing worsening of renal function with neurohormonal blockade.
Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It can be caused by primary glomerular diseases like minimal change disease, membranous nephropathy, and focal segmental glomerulosclerosis or secondary to conditions like diabetes, infections, drugs, and amyloidosis. Treatment involves managing edema, lipids, and the underlying cause. Kidney biopsy is needed to identify the specific glomerular lesion causing nephrotic syndrome and guide treatment.
Disseminated intravascular coagulation (DIC) is a syndrome characterized by widespread activation of coagulation that can occur as a result of various underlying conditions. It results from an imbalance between coagulation and anticoagulation processes in the body. DIC can be acute, with bleeding and shock being dominant symptoms, or chronic, where thrombosis and clotting may predominate. The most common triggers of DIC are infectious diseases, cancer, obstetric complications, and severe tissue injury. Diagnosis involves identifying symptoms of bleeding and thrombosis, abnormal laboratory coagulation test results, and ruling out other conditions. Treatment focuses on treating the underlying cause, replacing coagulation factors, platelets, and fibrinogen, and
The document discusses several hemostasis problems commonly seen in critical illness, including critical illness coagulopathies, uncontrolled bleeding and massive transfusion, anticoagulation-associated problems, and case scenarios. It provides details on acquired hypocoagulable states, the coagulation cascade, disseminated intravascular coagulation, sepsis-associated coagulopathy, heparin-induced thrombocytopenia, immune thrombocytopenic purpura, and pregnancy-related thrombocytopenias. Treatment involves addressing the underlying cause, transfusing blood products, and considering anticoagulants or direct thrombin inhibitors depending on the clinical situation.
1. The document provides guidelines for the management of transfusion dependent thalassemia, including recommendations for who to transfuse, compatibility testing, target pre-transfusion and post-transfusion hemoglobin levels, use of vitamin C during chelation, cardiac and liver complications, indications for splenectomy, risks of infection, endocrine diseases, fertility and pregnancy considerations, and osteoporosis management.
2. Major topics covered include appropriate transfusion thresholds, testing to avoid alloimmunization, chelation therapy protocols, monitoring and treatment of iron overload complications in major organs, and preventing infections that are leading causes of death.
3. Guidelines aim to optimize transfusion regimens and chelation
This document discusses several causes of hematuria in pediatrics including IgA nephropathy, Alport syndrome, acute poststreptococcal glomerulonephritis (APSGN), and hemolytic-uremic syndrome (HUS). IgA nephropathy is the most common chronic glomerular disease in children characterized by IgA deposits in the glomeruli. Alport syndrome is a hereditary nephritis caused by mutations in type IV collagen genes. APSGN occurs 1-2 weeks after a streptococcal infection and presents with gross hematuria, edema, and renal impairment. HUS is characterized by microangiopathic hemolytic anemia, thrombocytopenia,
CARDIAC COMPLICATIONS & ITS MANAGEMENT OF CKDMohd Tariq Ali
Uremic cardiomyopathy is the primary manifestation of cardiac complications in patients with chronic kidney disease. It results from the combined effects of pressure and volume overload on the heart from conditions like hypertension as well as the uremic state itself. This leads to left ventricular hypertrophy initially as an adaptive response but later maladaptive changes like cardiomyocyte death, fibrosis, and dilated cardiomyopathy if left unmanaged. Early initiation of hemodialysis, preferably non-conventional daily or nocturnal dialysis, can help halt progression of uremic cardiomyopathy while kidney transplantation has been shown to reverse it.
Hemolytic uremic syndrome (HUS) is defined by the simultaneous occurrence of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. It can be classified as typical or atypical, with typical HUS caused by infections like E. coli or Shigella dysenteriae. Streptococcus pneumoniae is a common cause of atypical HUS in young children, often presenting as pneumonia or meningitis. Treatment involves supportive care, antibiotics, and potentially plasma exchange or eculizumab.
This document provides an overview of immune thrombocytopenic purpura (ITP), including its pathogenesis, diagnostic criteria, incidence, physical exam findings, diagnostic testing, differential diagnosis, treatment, and references. ITP is diagnosed based on isolated thrombocytopenia without an alternative cause. It results from increased platelet destruction and inhibited platelet production due to autoantibodies against platelet membrane glycoproteins. Treatment involves glucocorticoids such as prednisone to support platelet counts until remission or more definitive therapy is established.
Similar to Renovascular disorder final shivaom (20)
The 3-year final analysis of a trial of the M72/AS01E tuberculosis vaccine showed:
1) The vaccine provided 49.7% efficacy against bacteriologically confirmed pulmonary tuberculosis over 3 years in HIV-negative, M. tuberculosis infected adults.
2) Among vaccinated participants, M72-specific antibody and CD4+ T cell responses increased after vaccination and were sustained over 3 years.
3) Serious adverse events, potential immune-mediated diseases, and deaths occurred at similar rates between the vaccine and placebo groups, demonstrating an acceptable safety profile over 3 years.
This document discusses various diagnostic modalities for pulmonary and extrapulmonary tuberculosis. It describes the characteristics of Mycobacterium tuberculosis and provides global burden statistics. It also discusses extra-pulmonary TB locations. Molecular techniques for diagnosis include Xpert MTB/RIF, which can simultaneously detect TB and rifampin resistance in under two hours. Other techniques discussed are line probe assays, drug susceptibility testing, radiology, tests for latent TB, and examinations of body fluids and biopsies. The document provides details on sensitivities and specificities of different diagnostic tests.
This document provides an overview of thyroid gland physiology, hypothyroidism, and its management. It discusses the anatomy and development of the thyroid gland. It describes how thyroid hormones are synthesized through iodination and coupling of thyroglobulin. The regulation of the hypothalamic-pituitary-thyroid axis by TSH is also summarized. Factors that can affect thyroid function during pregnancy like hCG levels and iodine intake are highlighted. The document provides context on hypothyroidism screening and treatment in pregnancy.
This document discusses various rheumatologic emergencies that require prompt treatment to prevent serious complications or death. It defines emergencies as situations that immediately endanger life or organ function. True emergencies have mortality rates around 50% even with timely intervention. Examples of rheumatologic emergencies discussed include septic arthritis, Atlantoaxial dislocation, acute upper airway obstruction in RA, acute transverse myelitis and cerebrovascular accident in SLE, alveolar hemorrhage and pulmonary renal syndrome in vasculitis, scleroderma renal crisis, respiratory muscle weakness in inflammatory myopathies, and catastrophic antiphospholipid syndrome. The document provides details on symptoms, diagnostic evaluation, and treatment approaches for each of
A 46-year-old lady presented to the emergency room with a 2-month history of productive cough occasionally containing blood, 2 weeks of feverish feelings without chills or sweats, and 2 weeks of worsening shortness of breath. On examination, she had decreased breath sounds bilaterally with rhonchi, rales, and wheezes. Laboratory tests showed an elevated white blood cell count and CRP along with clubbing on physical exam. A CT scan was performed.
This document summarizes two patient cases presented at a radio clinical meeting. The first case is a 73-year-old woman with a 1-month history of difficulty swallowing food and shortness of breath, as well as cough and weight loss. Examination findings include decreased breath sounds and a soft, non-tender abdomen. The second case is a 55-year-old man with a 2-month history of cough, shortness of breath, and abdominal pain. Examination reveals decreased breath sounds on the left side and tenderness in the abdomen. Both patients underwent lab tests and imaging.
This document discusses several medical disorders that can occur during pregnancy including hypertension, preeclampsia, chronic essential hypertension, gestational hypertension, renal disease, and cardiac disease. It provides details on the pathophysiology, diagnosis, risk factors, treatment and management of these conditions. Medical care has advanced to allow more women with serious medical problems to become pregnant, but these disorders can increase risks for both mother and fetus. Careful monitoring and treatment are important to balance health risks.
Clinical approach to solitary pulmonary nodule finalShivaom Chaurasia
The document discusses the clinical approach to solitary pulmonary nodules (SPNs). It defines SPNs and outlines their classification. It discusses evaluating SPNs to determine if they are benign or malignant. Small, slow growing nodules under 3 cm have a lower likelihood of being cancerous. Diagnostic testing includes chest imaging like CT scans to monitor size and characteristics. Biopsies may be done if risk of cancer is high or unclear. For cancerous nodules or those likely cancerous, surgical resection is the treatment when possible. Close monitoring can be done for small, low risk nodules.
Myasthenia Gravis is a neuromuscular junction disorder characterized by skeletal muscle weakness and fatigability. It is caused by antibodies that interfere with acetylcholine receptor function, reducing the efficiency of nerve impulse transmission and causing muscle weakness. Symptoms include weakness of eye muscles, facial muscles, and limbs which worsens with repeated use and improves with rest. Diagnosis involves tests like repetitive nerve stimulation, blood tests for antibodies, and response to medication. Treatment options include anticholinesterase medications, immunosuppressants, plasmapheresis, IVIG, and sometimes thymectomy. With current treatments prognosis is generally good though exacerbations can occasionally cause life-threatening crises requiring respiratory support.
Multiple myeloma (MM) is a malignant proliferation of plasma cells that produce monoclonal immunoglobulins. The cause is unknown but risk factors include exposure to petroleum products and radiation. MM most commonly affects elderly individuals and presents with bone pain, pathological fractures, anemia, renal failure and infections. Diagnosis requires bone marrow plasmacytosis above 10%, radiologic evidence of lytic bone lesions, and demonstration of an M protein. Treatment involves induction therapy such as bortezomib/lenalidomide combinations, followed by stem cell transplantation if eligible and long-term maintenance to prolong remission.
Mixed connective tissue disease (MCTD) is characterized by features of systemic lupus erythematosus, systemic sclerosis, polymyositis, and rheumatoid arthritis. It is defined by very high levels of anti-U1RNP antibodies. Clinical features include Raynaud's phenomenon, joint and muscle involvement, lung and heart disease, gastrointestinal issues, and kidney disease. Diagnosis requires clinical and serological criteria including high titers of anti-U1RNP antibodies. Treatment depends on organ system involvement but may include analgesics, steroids, immunosuppressants, and calcium channel blockers. Prognosis is variable depending on degree of organ involvement.
This systematic review and network meta-analysis compared the efficacy of different drug treatments for type 1 hepatorenal syndrome. The analysis included 13 randomized controlled trials comparing terlipressin to placebo or other drugs like norepinephrine. The results showed moderate evidence that terlipressin may reduce short-term mortality compared to placebo. Terlipressin and norepinephrine were both found to be more effective at reversing hepatorenal syndrome compared to midodrine plus octreotide. However, the evidence was limited by the small sizes and short follow-ups of the included studies. Larger, higher quality trials are still needed to evaluate the real-world effectiveness and safety of terlipressin for treating type 1 hepatorenal
This document provides an overview of interstitial lung disease (ILD). ILD involves the lung parenchyma between the alveoli and small airways. There are over 200 known ILDs classified into groups based on predominant inflammation/fibrosis or granulomatous reaction. Idiopathic pulmonary fibrosis is the most common ILD and has a poor prognosis. Diagnosis involves clinical history, imaging like HRCT, pulmonary function tests showing restriction, and sometimes lung biopsy. Management focuses on identifying and removing causes, suppressing inflammation, and lung transplantation for severe cases.
This document summarizes the management of inflammatory bowel disease. The two major types of IBD are ulcerative colitis and Crohn's disease. For ulcerative colitis, treatment depends on severity and location, and may include mesalazine, corticosteroids, immunosuppressants, or colectomy for severe cases. Crohn's disease treatment focuses on inducing remission and maintaining remission without steroids using enteral nutrition, medications like budesonide, immunosuppressants, biologics, or surgery for complications. Surgical management depends on disease severity and location for both conditions.
The HOPE-3 trial evaluated the effects of combination therapy with rosuvastatin, candesartan, and hydrochlorothiazide versus placebo in over 12,000 individuals without cardiovascular disease but at intermediate risk. It found that the combination therapy lowered blood pressure and LDL cholesterol more than placebo and reduced the risk of cardiovascular events like heart attack and stroke by 29% over 5.6 years of follow up. However, the combination therapy also increased adverse effects like muscle pain compared to placebo.
This document provides an overview of Hodgkin lymphoma (HL), including:
- HL is a malignancy of mature B lymphocytes that represents 10% of lymphomas diagnosed annually.
- Classical HL has high cure rates of over 85% with radiation and chemotherapy. However, late therapy-related toxicities are a new challenge.
- Staging is important for selecting appropriate therapy intensity, with early stage patients having a better prognosis than advanced stage.
- Treatment depends on stage and risk factors, and may involve chemotherapy alone or with radiation for early stage disease. Advanced stage is treated with chemotherapy only.
- Late effects of therapy include secondary cancers and heart disease, so reducing radiation exposure is a focus of research.
Hepatitis A is an enterically transmitted viral infection that causes inflammation of the liver. It is typically self-limited and does not result in chronic infection. The virus is shed in the feces during the incubation period and patients are most infectious prior to the onset of symptoms. Diagnosis is made by detecting IgM antibodies to Hepatitis A virus. There is no specific treatment, so management focuses on supportive care and prevention of transmission through hand hygiene and vaccination.
This document provides an overview of approaches to headache by Dr. Shivaom Chaurasia. It begins by defining headache and discussing common causes, which include primary headaches that often result in disability without an underlying organic disease, and secondary headaches that have a specific underlying cause like head trauma, vascular disorders, or nonvascular intracranial disorders. The document then examines the pathophysiology of headache, important aspects to cover in a headache history, potential investigations, management strategies for different headache types including migraine, tension, and cluster headaches, and indicators for referral to a neurologist.
The document summarizes guidelines from the Global Initiative for Chronic Obstructive Lung Disease (GOLD) for the assessment, diagnosis, and treatment of chronic obstructive pulmonary disease (COPD). It outlines GOLD's objectives to provide an evidence-based review and treatment guidance for COPD. Key points covered include defining COPD, assessing severity and exacerbation risk, pharmacological and non-pharmacological treatment strategies for stable COPD and exacerbations, and monitoring disease progression. The guidelines provide algorithms for initiating and adjusting COPD medications based on symptoms, exacerbation history, and risk level.
This document provides information on acute encephalitis syndrome, including its definition, epidemiology, etiology, pathogenesis, clinical manifestations, laboratory diagnosis, differential diagnosis, and management. Acute encephalitis syndrome is defined as an acute onset fever with changes in mental status or seizures. It is commonly caused by viruses and can involve inflammation of the brain tissue. Diagnosis involves examination of CSF and imaging studies. Treatment focuses on supportive care and antiviral medications like acyclovir.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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2. INTRODUCTION:
The Kidneys depend on systemic blood pressure (SBP) to maintain
adequate renal blood flow , adequate GFR, tubular function and overall
salt and water balance.
This explains the vulnerability of kidneys to diseases involving the renal
vasculature.
Vascular injury to kidneys is usually a manifestation of generalized
vascular pathology.
4. Thrombotic Microangiopathies
1. Hemolytic Uremic Syndrome (HUS)
2.Thrombotic Thrombocytopenic Purpura (TTP)
In both conditions, there is:
Microangiopathic hemolytic Anemia (MAHA), with anemia, RBCs
fragmentation, schistocytes, intravascular PLT clumping and hence
thrombocytopenia
Typical renal histological lesions include intraglomerular platelet and fibrin
thrombi, with ischemia and arteriolar lesions
5. Hemolytic Uremic Syndrome (HUS)
Commonest cause of AKI in children
Children (< 4 years) ------> 90 % of cases
It is loosely defined as presence of microangiopathic hemolytic angiopathy
and renal impairment.
6. Forms of HUS
1. Typical, or Diarrhea-associated (D+ HUS):
Onset is explosive, with AKI
Most cases below 5 years
Diarrohea, often bloody preceeds MAHA within 1 week in 80% cases
Abdominal pain, cramping and vomiting frequent whereas fever is typically absent.
Neurologic symptoms including dysphagia, hyperreflexia, blurred vision, memory
deficit, encephalopathy, preservation and agraphia may often develop.
SEIZURE and cerebral infarction may develop in severe cases.
7. PATHOGENESIS
Shiga toxin(Stx1 and Stx2) are referred as verotoxin. They are produced by E.coli and
shigella dysenteriae
Verotoxin-producing E.Coli O157:H7 (VTEC), with damage to the vascular
endothelium(largely confined to kidneys)
After entry into circulation Shiga toxin binds to glycolipid surface receptor
globotriaosylceramide (gb3) which is richly expressed in renal vasculature.
Upon entering into cell it induces inflammatory cytokines (IL-8), monocyte chemotactic
protein 1 and stromal cell derived factor 1 and chemokines (cxcr4 and cxcr7) this action
results in platelet aggregation and microangiopathic process.
8. 2. Atypical, or (D-HUS) :
It results from complement deregulation, may be congenital or acquired
Patient may have low C3 and a normal C4 characteristics of alternating pathway activation.
Factor H deficiency most common defect. Factor H competes with Factor B to prevent formation
of Cb3
A familial varient of aHUS -DEAP HUS ( Deficiency of CFHR plasma proteins and CFH AutoAb
Positve) when autoantibody to factor H is formed.
Older children and adults, most of them have no diarrhea
Familial, associated with factor H deficiency which limit cleavage of unusual large von Willebrand;
leading to continuing platelet activation
Poorer prognosis, death in > 50 % of cases
9. Thrombotic Thrombocytopenic
Purpura (TTP)
Tradiationally, TTP is characterized by the pentad: MAHA, Thrombocytopenia,
neurologic symptoms, fever and renal failure.
Pathophysiology involves accumulation of ultra-large multimers of Von
willebard factor as a result of absence or markedly decreased activity of
plasma protease ADAMTS 13,
These ultra large multimers forms clots and shear erythrocytes resulting in
MAHA;TTP
TTP is now defined as large MAHA associated with ADAMTS13 activity (less
then 5-10%), however only absence of ADAMTS13 alone may not produce TTP; often
triggering factors (infection, surgery, pancreatitis or pregnancy) is required to induce
clinical TTP
If untreated TTP has mortality rate exceeding 90 %, even with modern therapy 20 % die
within 1st month from complication of microvascular thrombosis.
10. In idiopathic TTP, the formation of an autoantibody to ADAMTS13 (IgG or IgM) either increases
its clearance or inhibits its activity.
Upshaw-Schülman syndrome is a hereditary condition characterized by congenital deficiency
of ADAMTS13.
TTP in these patients can start within the first weeks of life but in some instances may not
present until adulthood, especially during pregnancy.
Both environmental and genetic factors are thought to influence the development of TTP.
Plasma transfusion is an effective strategy for prevention and treatment.
Drug-induced TMA is a recognized complication of treatment with some chemotherapeutic
agents, immunosuppressive agents, and quinine.
11. HUS/TTP TREATMENT
Treatment should be based on pathophysiology.
Autoantibody-mediated TTP and DEAP HUS respond to the
combination of plasma exchange and prednisone. In addition to
removing the autoantibodies, plasma exchange with fresh-frozen
plasma replaces ADAMTS13.
Plasma infusion is usually sufficient to replace the ADAMTS13 in
Upshaw-Schülman syndrome.
Drug-induced TMA secondary to endothelial damage typically does not
respond to plasma exchange and is treated primarily by discontinuing
use of the agent and providing supportive care.
Plasma infusion/exchange is effective in certain types of aHUS as it
replaces complement-regulatory proteins.
12. RADIATION NEPHROPATHY
Either local or total body irradiation can produce microangiopathic injury.
The kidney is one of the most radiosensitive organs, and injury can result with as
little as 4–5 Gy.
Such injury is characterized by renal insufficiency, proteinuria, and hypertension
usually developing ≥6 months after radiation exposure.
Renal biopsy reveals classic TMA with damage to glomerular, tubular, and
vascular cells, but systemic evidence of MAHA is uncommon.
No specific therapy is available.
13. HIV RELATED TMA
HIV-related TMA is a complication encountered mainly before widespread use of
highly active antiretroviral therapy. It is seen in patients with advanced AIDS and
low CD4+ T cell counts although it can be the first manifestation of HIV infection.
The presence of MAHA, thrombocytopenia, and renal failure are suggestive, but
renal biopsy is required for diagnosis since other renal diseases are also
associated with HIV infection.
The mechanism of injury is unclear, although HIV can induce apoptosis in
endothelial cells. ADAMTS13 activity is not reduced in these patients.
Cytomegalovirus co-infection may also be a risk factor. Effective antiviral therapy
is key, while plasma exchange should be limited to patients who have evidence of
TTP.
14. SCLERODERMA (PROGRESSIVE
SYSTEMIC SCLEROSIS)
Kidney involvement is common (up to 52%) in patients with widespread scleroderma,
with 20% of cases resulting directly from scleroderma renal crisis.
Other renal manifestations in scleroderma include transient (prerenal) or medication-
related forms of acute kidney injury (e.g., associated with D-penicillamine, nonsteroidal
anti-inflammatory drugs, or cyclosporine).
Salt and water retention with microvascular injury can lead to pulmonary edema.
Cardiac manifestations, including myocarditis, pericarditis, and arrhythmias, denote an
especially poor prognosis.
15. Glomerulonephritis and vasculitis associated with antineutrophil cytoplasmic antibodies and
systemic lupus erythematosus have been described in patients with scleroderma. Anti-U3-RNP
may identify young patients at risk for scleroderma renal crisis.
Anticentromere antibody, in contrast, is a negative predictor of this disorder. Because of the
overlap between scleroderma renal crisis and other autoimmune disorders, a renal biopsy is
recommended for patients with atypical renal involvement, especially if hypertension is absent.
Scleroderma renal crisis occurs in 12% of patients with diffuse systemic sclerosis but in only 2%
of those with limited systemic sclerosis Mild proteinuria is usually present ± HTN
Sclerodermal renal crisis is most severe form characterized by-
Accelerated HTN ( Ratinopathy and Encephalopathy may follow Htn)
Rapid decline in renal function
Nephrotic range proteinuria
Hematuria
16. Systemic Sclerosis
Pathology:
Intimal proliferation of interlobular arteries, with deposition of mucoplysaccharides: Onion-Skin
appearance
Fibrinoid necrosis of afferent arterioles
Treatment:
Treatment with ACE inhibition is the first-line therapy unless contraindicated.
The goal of therapy is to reduce systolic and diastolic blood pressure by 20 mmHg and 10
mmHg, respectively, every 24 h until blood pressure is normal. Additional antihypertensive
therapy may be given once the dose of drug for ACE inhibition is maximized.
Both ACE inhibitors and angiotensin II receptor antagonists are effective.
Poor prognosis; Before the availability of angiotensin-converting enzyme (ACE) inhibitors,
the mortality rate for scleroderma renal crisis was >90% at 1 month. Introduction of renin-
angiotensin system blockade has lowered the mortality rate to 30% at 3 years.
Nearly two-thirds of patients with scleroderma renal crisis may require dialysis support, with
recovery of renal function in 50% (median time, 1 year). because of other organ
involvement, especially restrictive cardiomyopathy
17. ANTIPHOSPHOLIPID SYNDROME
Antiphospholipid syndrome can be either primary or secondary to systemic
lupus erythematosus and is mediated by antiphospholipid antibodies—
mainly anticardiolipin antibodies , lupus anticoagulant, or anti-β-2
glycoprotein I antibodies (antiβ2GPI).
TMA is commonly present in renal biopsies, although signs of MAHA and
platelet consumption are usually absent.
Hypertension is common.
Treatment
lifelong anticoagulation.
Glucocorticoids may be beneficial in accelerated hypertension.
Immunosuppression and plasma exchange may be helpful for catastrophic
episodes of antiphospholipid syndrome but by themselves do not reduce
recurrent thrombosis.
18. HELLP SYNDROME
HELLP (hemolysis, elevated liver enzymes, low
platelets) syndrome is a dangerous complication of
pregnancy associated with microvascular injury.
Occurring in 0.2–0.9% of all pregnancies and in 10–20% of
women with severe preeclampsia, this syndrome carries a
mortality rate of 7.4–34%.
Most commonly developing in the third trimester, 10% of
cases occur before week 27 and 30% post-partum.
Renal failure occurs in half of patients with HELLP
syndrome,.
19. Although renal failure is common, the organ that defines this syndrome is the liver.
Subcapsular hepatic hematomas sometimes produce spontaneous rupture of the liver
and can be life-threatening.
Neurologic complications such as cerebral infarction, cerebral and brainstem
hemorrhage, and cerebral edema are other potentially life-threatening complications.
Nonfatal complications include placental abruption, permanent vision loss due to
Purtscher-like (hemorrhagic and vaso-occlusive vasculopathy) retinopathy, pulmonary
edema, bleeding, and fetal demise.
A history of MAHA before pregnancy is of diagnostic value.
Serum levels of ADAMTS13 activity are reduced (by 30–60%) in HELLP syndrome but not
to the levels seen in TTP (<5%).
HELLP syndrome usually resolves spontaneously after delivery, although a small
percentage of HELLP cases occur post-partum. Plasma exchange should be considered if
hemolysis is refractory to glucocortcoids and/or delivery, especially if TTP has not been
ruled out.
20. POEMS Syndrome
POEMS syndrome is a systemic disease characterized by polyneuropathy,
organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes.
Peripheral neuropathy with severe motor sensory deficit is the hallmark of the disease.
Another characteristic is that >95% of monoclonal light chain is of the lambda isotype.
IgA also makes up about 50% of the monoclonal protein.
Organomegaly can involve any organ and often presents as lymphadenopathy. In the
kidney, the hypertrophy frequently is unilateral.
Most patients present with mild to moderate renal impairment and low grade
proteinuria.
Progression to end stage renal ds may occur.
21. SICKLE CELL NEPHROPATHY
Renal complications in sickle cell disease result from occlusion of the vasa recta in the renal
medulla.
The low partial pressure of oxygen and high osmolarity predispose to hemoglobin S
polymerization and erythrocyte sickling.
Sequelae include hyposthenuria, hematuria, and papillary necrosis (which can also occur in
sickle trait).
The kidney responds by increases in blood flow and glomerular filtration rate mediated by
prostaglandins.
Proteinuria is present in 20–30%, and nephrotic-range proteinuria is associated with
progression to renal failure.
Chronic kidney disease is present in 12–20% of patients.
Despite the frequency of renal disease, hypertension is uncommon in patients with sickle cell
disease.
23. Renal Artery Stenosis (RAS) and
Ischemic Renal Disease:
RAS
Prevalence:
2-4 % in general population
30-40 % in accelerated HTN and
renal insufficiency
Causes:
Atherosclerosis:(ARV D)
90 %
Elderly
Fibromuscular Dysplasia:
5-10 %
Young
Ischemic Renal Disease
Atherosclerosis of 1 or both renal
Artery
Elderly male
± HTN
Often with atherosclerotic PVD (68%)
IHD (45%)
CHF (33%)
History of stroke (28%)
Progressive loss of renal function
24.
25.
26. Atherosclerotic Reno-vascular
disease:
It accounts for >90% of all RVD, in patients > 55, or < 30 Years of age
Lesions of RAS are 90% ostial (within the1st one cm of renal artery origin)
It can be demonstrated in:
>10% of patients undergoing coronary angiography
>40% with peripheral vascular disease (PVD), with > 5 vessels
involvement
30% with congestive cardiac failure (CCF), aged >70 years
15-20 % with ESRD
It is increased with aging and is associated with common atherogenic risk factors:
Hypertension
Hypercholesterolemia
Smoking
Diabetes
27. Clinical Presentations:
Hypertension (HTN), with Chronic Kidney Disease (CKD), a pro-atherogenic state
make the incidental finding of ARVD, rather than being the cause of it..
Epi-gastric bruit
Hypokalemia and metabolic alkalosis
Flash pulmonary edema(5%):
Sudden onset of acute heart failure in absence of myocardial ischemic event
Commonly at night(due to posture-related redistribution of fluid or may be due to diurnal
variations of vasoactive peptides)
Mechanism may be due to reduced natriuretic ability, coupled with LVH and severe HTN in
patients with severe bilateral RAS
Acute Kidney Injury (AKI), due to arterial occlusion
28. Prognosis of ARVD:
Renal outcome is determined by the presence of parenchymal disease
giving the picture of ischemic nephropathy (intrarenal atheroma, or
cholesterol embolization)
The correlation between the severity of proximal lesions(degree of
stenosis or occlusion) and renal function is poor.
Poor prognosis (5-year survival<20 %)
29.
30.
31. Treatment of RAS:
Conservative medical management:
Cessation of smoking/weight loss/exercise
Strict Control of HTN
Lipid lowering agents
Aspirin
Revascularization, especially successful in significant RAS associated
AKI, or with flash pulmonary edema:
Percutaneous Transluminal Renal Angioplasty (PTRA), with stenting (PTRAS), in
>95% of cases
Surgical reconstruction: celiac, or mesenteric –to- Renal Bypass, in remainder of
cases
Balloon angioplasty:
Uncontrolled HTN
Success rate: 82-100 %
Recurrence rate: 10 % (follow-up with duplex U/S)
32. Fibromuscular Dysplasia (FMD):
It accounts for 10% of all RVD
Most commonly in young women (20-35 Ys)
The stenotic lesions are distal and appear like “string of beads”, at angiography
Clinically, presented with severe HTN, but renal failure is unusual
It is usually associated with other arterial lesions (carotid stenosis in 10% of
cases)
Revascularization cure the HTN and restores the kidney function completely;
because the kidney beyond the FMD, is usually healthy
Fibromuscular dysplasia of the renal artery, medial type (elastic tissue stain)
The media shows marked fibrous thickening, and the lumen is stenotic
33. Atheroembolic RVD:
Cholesterol embolisation syndrome (CES) is occurring in:
Elderly patients with widespread atherosclerosis (almost exclusively)
As complication of abdominal aorta/renal artery manipulation or surgery
As a consequence of angiography
Clinically:
Renal insufficiency &/or HTN
Livideo reticularis
Evidence of embolisation in other organs: Cerebrovascular events, retinal artery
occlusion, acute pancreatitis, ischemic bowels, gangrene of extremities
Urine analysis:
Cholesterol crystals (not usually present)
Increased cellularity
Proteinuria (mild)
Eosinophiluria
34.
35. Treatment of CES
Control HTN (avoid hypotension)
Adequate hydration
Anticoagulants may delay healing of ulcerated atherosclerotic lesions
Dialysis may be needed
36. Thromboembolic Occlusion of
Renal Arteries
Causes:
Intrinsic pathology in renal vessels:{In situ thrombosis}
Post-traumatic.. Young patients (blunt trauma, deceleration injury,..)
Atherosclerotic.. Old patients
Dissection/Aneurysm/Arteriography
Inflammatory: Takayasau, syphilis, systemic vasculitis, thrombangitis obliterans
Embolization: {originating in distant vessels}; much more common
(90%) and usually unilateral
Tumor/Fat emboli
Emboli from left heart (most common), as left mural thrombus following MI or AF, or bacterial
endocarditis, septic/aseptic valvular vegetations..
Paradoxical emboli, passing through patent foramen ovale or ASD
37. Clinical Manifestations Of
Thromboembolism
Difficult to diagnose, require high index of suspicion
Variable, depend on: extent/time course of occlusion and state of pre-
existing renal circulation
Acute renal thrombosis/infarction
Sudden onset of flank pain/tenderness (absent in 55 %)
Fever/nausea/vomiting
Hematuria (microscopic)
Deteriorated renal function: transient (unilateral), or severe (bilateral)
Hypertension, usually transient (renin release in peri-infarction zone)
Elevated TLC, AST, LDH, ALP (renal enzymes in infarction)
38. Clinical Manifestations Of
Thromboembolism
Gradual unilateral occlusion --> may go undetected
Patients with RAS & established collateral circulation have no symptoms
(little/no infarction)
Thus, the spectrum of clinical manifestations lies between some extremes
in different occasions:
ARF
Unexplained Progressive Azotemia (old patient ± refractory HTN)
HTN + Azotemia (renal transplant)
40. Clinical Manifestations of RVT
Depend on extent and rapidity of occlusion:
1. Acute:
Nausea/vomiting
Flank Pain
Hematuria
Leucocytosis
Compromised renal functions
Increased renal size on U/S
2. Chronic:
Dramatic ↑ of proteinuria
Tubular Dysfunction: Glucosuria, aminoaciduria, phosphaturia and impaired
urinary acidification
41. Diagnosis of RVT
Investigations:
Doppler U/S: more sensitive then USG alone
CT Angiogram- 100% sensitive
Magnetic Resonance Angiography is another good option but is more expensive.
Treatment:
Anticoagulation Therapy and treatment of underlying cause
Endovascular Thrombolysis may be considered in severe cases
Occasionally, neprectomy may be undertaken for life-threatning complication
Vena caval filters may be used to prevent migration of thrombi