Thrombocytopenia
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Polycythemia Vera
Polycythemia vera is a rare acquired myeloproliferative disorder characterized by an overproduction of red blood cells. It results from a mutation in the JAK2 signaling molecule in 95% of cases. Symptoms include headache, dizziness, and fatigue due to expanded blood volume. Laboratory findings show elevated hematocrit and low erythropoietin levels. Treatment involves regular phlebotomy to reduce red blood cell counts and medications to control thrombocytosis and itching.
Thrombocytopenia
Thrombocytopaenia, or low platelet count, can be caused by decreased platelet production or increased platelet destruction. Causes of decreased production include bone marrow diseases and medications. Increased destruction can be due to immune-mediated causes like Idiopathic Thrombocytopenic Purpura (ITP) or non-immune causes like disseminated intravascular coagulation. ITP is caused by autoantibodies that bind to and destroy platelets, and presents with mild bleeding and a normal bone marrow with increased megakaryocytes. Thrombocytopaenia is diagnosed based on blood counts, smear, and ruling out other potential causes through testing and history. Treatment depends on severity but
Thrombocytopenia
This document provides definitions and information about thrombocytopenia (platelet count <150,000/ml). It discusses increased bleeding risk with very low platelet counts and common clinical presentations. Potential causes of thrombocytopenia include decreased platelet production, increased platelet destruction, dilutional effects, and pseudothrombocytopenia. Specific conditions covered in detail include immune thrombocytopenic purpura, heparin-induced thrombocytopenia, thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Evaluation, diagnosis, and treatment approaches are outlined for the different conditions.
Polycythemia vera
Polycythemia vera is a chronic myeloproliferative disorder characterized by an absolute increase in red blood cells, total blood volume, leukocytosis, thrombocytosis, and splenomegaly. It is caused by a clonal proliferation of a hematopoietic stem cell. Symptoms include headaches, visual disturbances, thrombosis, pruritus, and splenomegaly. Diagnosis involves meeting certain criteria including elevated hematocrit. Treatment involves phlebotomy to reduce red blood cell mass and hydroxyurea or interferon-alpha to reduce platelet and white blood cell counts and reduce risk of thrombosis.
Macrocytic Anemia
A 33-year-old male presents with symptoms of fatigue, shortness of breath, palpitations, and headaches for the past 2 weeks. Laboratory tests show macrocytic anemia. Macrocytic anemia is a type of anemia where red blood cells are abnormally large. It can be caused by vitamin B12 or folate deficiencies, such as pernicious anemia which is an autoimmune disorder causing B12 malabsorption. Treatment depends on the underlying cause but may include B12 injections or oral supplements.
Acute And Chronic Inflammation
Acute inflammation is the immediate response to tissue injury and involves vasodilation, increased vascular permeability leading to edema, and leukocyte emigration. The key events in acute inflammation are vascular changes, leukocyte migration into tissues, and the release of chemical mediators. Chronic inflammation is a prolonged inflammatory response involving lymphocytes, macrophages and plasma cells that can lead to tissue destruction and attempts at repair through fibrosis. [/SUMMARY]
Thrombocytopenia
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
Megaloblastic anemia
Megaloblastic anemia is a type of macrocytic anemia caused by a failure of DNA synthesis, resulting in asynchronous maturation of red blood cell nuclei and cytoplasm. The most common causes of megaloblastic anemia are vitamin B12 and folic acid deficiencies. Treatment involves treating the underlying deficiency, with vitamin B12 therapy for B12 deficiency and oral folic acid supplementation for folic acid deficiency. Response to treatment is monitored through improvement of hematological markers and symptoms over 1-8 weeks.
Recommended
Polycythemia Vera
Polycythemia vera is a rare acquired myeloproliferative disorder characterized by an overproduction of red blood cells. It results from a mutation in the JAK2 signaling molecule in 95% of cases. Symptoms include headache, dizziness, and fatigue due to expanded blood volume. Laboratory findings show elevated hematocrit and low erythropoietin levels. Treatment involves regular phlebotomy to reduce red blood cell counts and medications to control thrombocytosis and itching.
Thrombocytopenia
Thrombocytopaenia, or low platelet count, can be caused by decreased platelet production or increased platelet destruction. Causes of decreased production include bone marrow diseases and medications. Increased destruction can be due to immune-mediated causes like Idiopathic Thrombocytopenic Purpura (ITP) or non-immune causes like disseminated intravascular coagulation. ITP is caused by autoantibodies that bind to and destroy platelets, and presents with mild bleeding and a normal bone marrow with increased megakaryocytes. Thrombocytopaenia is diagnosed based on blood counts, smear, and ruling out other potential causes through testing and history. Treatment depends on severity but
Thrombocytopenia
This document provides definitions and information about thrombocytopenia (platelet count <150,000/ml). It discusses increased bleeding risk with very low platelet counts and common clinical presentations. Potential causes of thrombocytopenia include decreased platelet production, increased platelet destruction, dilutional effects, and pseudothrombocytopenia. Specific conditions covered in detail include immune thrombocytopenic purpura, heparin-induced thrombocytopenia, thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Evaluation, diagnosis, and treatment approaches are outlined for the different conditions.
Polycythemia vera
Polycythemia vera is a chronic myeloproliferative disorder characterized by an absolute increase in red blood cells, total blood volume, leukocytosis, thrombocytosis, and splenomegaly. It is caused by a clonal proliferation of a hematopoietic stem cell. Symptoms include headaches, visual disturbances, thrombosis, pruritus, and splenomegaly. Diagnosis involves meeting certain criteria including elevated hematocrit. Treatment involves phlebotomy to reduce red blood cell mass and hydroxyurea or interferon-alpha to reduce platelet and white blood cell counts and reduce risk of thrombosis.
Macrocytic Anemia
A 33-year-old male presents with symptoms of fatigue, shortness of breath, palpitations, and headaches for the past 2 weeks. Laboratory tests show macrocytic anemia. Macrocytic anemia is a type of anemia where red blood cells are abnormally large. It can be caused by vitamin B12 or folate deficiencies, such as pernicious anemia which is an autoimmune disorder causing B12 malabsorption. Treatment depends on the underlying cause but may include B12 injections or oral supplements.
Acute And Chronic Inflammation
Acute inflammation is the immediate response to tissue injury and involves vasodilation, increased vascular permeability leading to edema, and leukocyte emigration. The key events in acute inflammation are vascular changes, leukocyte migration into tissues, and the release of chemical mediators. Chronic inflammation is a prolonged inflammatory response involving lymphocytes, macrophages and plasma cells that can lead to tissue destruction and attempts at repair through fibrosis. [/SUMMARY]
Thrombocytopenia
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
Megaloblastic anemia
Megaloblastic anemia is a type of macrocytic anemia caused by a failure of DNA synthesis, resulting in asynchronous maturation of red blood cell nuclei and cytoplasm. The most common causes of megaloblastic anemia are vitamin B12 and folic acid deficiencies. Treatment involves treating the underlying deficiency, with vitamin B12 therapy for B12 deficiency and oral folic acid supplementation for folic acid deficiency. Response to treatment is monitored through improvement of hematological markers and symptoms over 1-8 weeks.
Common bleeding and clotting disorders
Bleeding disorders result from problems with blood clotting and can range from mild to life-threatening. The coagulation cascade describes the series of biochemical reactions involved in clotting. There are two pathways - intrinsic and extrinsic - that activate clotting factors and ultimately form a fibrin clot. Common symptoms include bruising, nosebleeds, and heavy periods. Investigations may include blood tests of clotting factors and bleeding time. Specific deficiencies are diagnosed through factor assays and gene analysis. Treatment depends on the underlying condition.
DIC
1. The man with multiple fractures shows signs of disseminated intravascular coagulation (DIC) including diffuse bleeding, prolonged prothrombin time and partial thromboplastin time, low platelet count, and positive D-dimer.
2. The postpartum woman experienced heavy bleeding after delivery of a stillborn fetus. Her symptoms progressed to include hypotension, tachycardia, ecchymosis, and laboratory findings consistent with DIC such as low platelet count and prolonged clotting times.
3. Both patients presented with clinical signs and laboratory abnormalities indicative of DIC, a coagulopathy that can develop as a complication of trauma, infection, cancer, or obstetric complications
Edema
This document discusses different types and causes of edema. It identifies four main pathophysiologic categories of edema: 1) increased hydrostatic pressure, 2) reduced plasma oncotic pressure, 3) inflammation, and 4) other causes like lymphatic obstruction or sodium/water retention. Increased hydrostatic pressure can result from conditions like congestive heart failure or venous thrombosis. Reduced oncotic pressure is often due to decreased albumin from issues like nephrotic syndrome or cirrhosis. Inflammation can cause edema through increased permeability. Lymphatic obstruction from infections, tumors, or other causes can also lead to edema formation.
Idiopathic thrombocytopenic purpura
Idiopathic thrombocytopenic purpura (ITP) is a bleeding disorder caused by the immune-mediated destruction of platelets. It most commonly presents in children between 1-7 years of age, usually after a viral infection. ITP results in low platelet counts and spontaneous bruising or bleeding. Diagnosis involves low platelet count, absence of other abnormalities, and normal bone marrow with increased or normal megakaryocytes. Treatment depends on if it is acute or chronic ITP, and may include corticosteroids, IVIG, anti-D immunoglobulin, thrombopoietin receptor agonists, or splenectomy in severe cases.
Polycythemia
Polycythemia is a condition characterized by an abnormal increase in the red blood cell count. There are two types: relative polycythemia, caused by a decrease in plasma volume leading to a higher concentration of red blood cells; and absolute polycythemia, caused by overproduction of red blood cells in the bone marrow. Polycythemia vera is a specific myeloproliferative disorder and type of absolute polycythemia caused by a mutation in the JAK2 gene, leading to uncontrolled red blood cell production. Symptoms include headaches, dizziness, and blood flow issues from hyperviscosity. Treatment involves phlebotomy to reduce red blood cell counts and medications to control bone marrow
systemic lupus erythematosus
Systemic Lupus Erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems. It typically affects young women and is characterized by periods of disease flares and remissions. While the exact cause is unknown, genetic and environmental factors likely contribute to abnormal immune system functioning and production of autoantibodies. Common clinical manifestations include malar rash, arthritis, kidney problems, and hematological abnormalities. Diagnosis involves identifying clinical features and detecting autoantibodies such as antinuclear antibodies and anti-dsDNA antibodies. With proper management, 10-year survival rates are over 90%.
Thrombocytopenia
This document defines thrombocytopenia as a platelet count below 150,000 per microlitre and discusses its causes, which include increased platelet destruction, decreased platelet production, and other rare conditions. It outlines the workup for thrombocytopenia, including a medical history focusing on medications, physical exam, and lab tests. Treatment depends on the underlying cause but may include treating infections, discontinuing offending drugs, corticosteroids, IVIG, splenectomy, or platelet transfusions in severe cases. The main goals are to identify the cause and treat any underlying condition driving the low platelet count.
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Approach to thrombocytopenia
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.
Dic syndrome
Disseminated intravascular coagulation (DIC) is an acquired syndrome where there is widespread activation of the coagulation system, leading to microvascular thrombosis and organ damage. It can occur acutely when large amounts of procoagulants are suddenly released, or chronically with small continuous releases over time. Left untreated, it can cause life-threatening hemorrhage. Diagnosis involves looking for signs of bleeding and thrombosis, as well as using scoring systems to assess coagulation markers. Treatment focuses on treating the underlying condition while providing supportive care and replacing clotting factors.
The inflammatory process
The document summarizes the inflammatory process in three phases:
Phase I is the acute phase lasting 1-2 weeks involving vascular responses, swelling, pain, heat, and loss of function due to chemical mediators. Phagocytosis occurs as leukocytes remove dead tissue.
Phase II is the tissue formation phase lasting 2-3 weeks involving regeneration, collagen synthesis, wound contraction, and vascularization.
Phase III is the remodeling phase lasting up to 1 year involving collagen remodeling and scar maturation to adapt to original tissue. Treatment planning focuses on controlling inflammation, encouraging repair, and functional rehabilitation.
Thrombocytopenia ppt Health Advice
This Thrombocytopenia ppt help you in understanding the what is platelet and why it get low count and its causes, signs and treatment, diagnosis, Prevention, Cure and Insurance Coverage, Myths and Facts, FAQs, Home Natural remedies, Medical Advice and everything you need to know.
Read more at: http://www.thebesthealth.org/thrombocytopenia
What is Thrombocytopenia?
Thrombocytopenia is a medical disorder in which a person suffers from a low level of blood platelets. Platelets (or thrombocytes) are colorless blood cells that help blood to clot and stop bleeding by clumping and forming plugs in the wounds of the blood vessels.
It often occurs as a result of various disorders such as leukemia or an immune system problem. It may be a side effect of taking certain medication and this condition affects both children and adults. It can be a mild and cause few signs or symptoms. In rare cases, the platelets count may occur dangerous internal bleeding.
How is thrombocytopenia treated?
If your doctor feels that there is no serious threat to your health, he or she may choose not to treat thrombocytopenia. Treatment for thrombocytopenia depends on the cause and the effect it has on your health. For example,
Your doctor may switch you to another medication, if you are taking a medication that causes thrombocytopenia
Your doctor may prescribe steroids, immunoglobulin, or other medications, if the cause for thrombocytopenia is problems with your immune system
He may suggest platelet transfusion if your platelet count is extremely low
In some cases, the doctor may remove the patient spleen in order to keep it from destroying platelets. Spleen helps the body fight against infections, removing it may place the person at higher risk for certain types of infections. However several vaccinations are given before the splenectomy to help prevent infection
When to Call the Doctor
Call your healthcare provider if you have:
Headache, confusion, or dizziness
Blood when you cough, or difficulty breathing
Bloody urine, vomit, or bowel movements
Vaginal bleeding after menopause OR unusually heavy vaginal bleeding.
Systemic lupus erythematosus (SLE)
Seminar presentation by 4th year medical student under supervision of a doctor. Reference is as in the slide presentation, Nelson's.
nephritic and nephrotic syndrome
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
Platelet disorders
Primary and Secondary Hemostasis is Discussed
This is a copy of a lecture provided as an overview of platelet disorders for board preparation to the MercyOne Des Moines Internal Medicine Residency
Systemic lupus erythematosus (sle)
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that causes inflammation and damage to tissues and organs. Deposits of connective tissue and fibrin collect in blood vessels and organs, leading to necrosis and inflammation. While there is no cure, remissions are possible with proper management. The cause is unknown but genetic and environmental factors play a role. Signs and symptoms include rashes, arthritis, fatigue, and organ involvement. Diagnosis involves tests for autoantibodies and organ function. Treatment focuses on managing symptoms, avoiding triggers, and monitoring for organ complications using medications, supplements, and lifestyle changes.
Systemic sclerosis
A 60-year-old woman presented with painful, sclerotic hands and fingers due to progressive cutaneous scleroderma. She was started on a compounded topical cream containing ketamine, baclofen, gabapentin, verapamil, and pentoxifylline, which provided significant pain relief and improved sensation within a month. At a 6-month follow up, she had been largely weaned off opioid pain medications. The customized treatment targeted the pathophysiology of the condition and helped manage her debilitating symptoms.
idiopathic thrombocytopinic purpura
This document provides information about Idiopathic Thrombocytopenic Purpura (ITP), including:
- ITP is a blood disorder characterized by a decreased number of platelets, which can cause easy bruising and bleeding.
- There are two main forms - acute (seen in children and resolves in <6 months) and chronic (onset at any age and lasts >6 months).
- The cause is unknown in most cases but involves antibodies destroying platelets. Diagnosis involves ruling out other causes through testing.
- Treatment options depend on severity but may include steroids, IVIg, splenectomy, thrombopoietin receptor agonists, and experimental agents.
systemic lupus erythematosus
This document provides information about systemic lupus erythematosus (SLE). It defines SLE as a multi-system autoimmune disease affecting various organs mediated by autoantibodies and immune complexes. The causes are unknown but may involve genetic, hormonal, and environmental factors. SLE can affect many organ systems like the kidneys, lungs, heart, and nervous system, causing a variety of clinical manifestations. Diagnosis involves evaluating symptoms, medical history, physical exam, and laboratory tests. Treatment depends on disease severity and organ involvement, and may include medications like NSAIDs, antimalarials, corticosteroids, and cytotoxic drugs. Special considerations are given to SLE in pregnancy and neonates.
OVERVIEW Disorders of platelets
The document provides an overview of platelet disorders, describing how platelets function in hemostasis and how genetic and acquired factors can influence this process, leading to bleeding or clotting symptoms. It discusses various qualitative and quantitative platelet disorders, outlining approaches to diagnosing and differentiating disorders based on platelet production, distribution, or destruction. Evaluation of thrombocytopenia and diagnostic tools for platelet functional disorders are also reviewed.
Thrombocytopenia
Thrombocytopenia refers to a decrease in platelets in the blood. It can be caused by vitamin deficiencies, medications, liver failure decreasing thrombopoietin production, or conditions like ITP or leukemia. Symptoms include bruising, petechiae, nosebleeds, and fatigue. Diagnosis involves blood tests to check counts, functions, and potential causes. Treatment focuses on addressing the underlying cause and sometimes administering platelet transfusions for newborns with thrombocytopenia.
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.
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Common bleeding and clotting disorders
Bleeding disorders result from problems with blood clotting and can range from mild to life-threatening. The coagulation cascade describes the series of biochemical reactions involved in clotting. There are two pathways - intrinsic and extrinsic - that activate clotting factors and ultimately form a fibrin clot. Common symptoms include bruising, nosebleeds, and heavy periods. Investigations may include blood tests of clotting factors and bleeding time. Specific deficiencies are diagnosed through factor assays and gene analysis. Treatment depends on the underlying condition.
DIC
1. The man with multiple fractures shows signs of disseminated intravascular coagulation (DIC) including diffuse bleeding, prolonged prothrombin time and partial thromboplastin time, low platelet count, and positive D-dimer.
2. The postpartum woman experienced heavy bleeding after delivery of a stillborn fetus. Her symptoms progressed to include hypotension, tachycardia, ecchymosis, and laboratory findings consistent with DIC such as low platelet count and prolonged clotting times.
3. Both patients presented with clinical signs and laboratory abnormalities indicative of DIC, a coagulopathy that can develop as a complication of trauma, infection, cancer, or obstetric complications
Edema
This document discusses different types and causes of edema. It identifies four main pathophysiologic categories of edema: 1) increased hydrostatic pressure, 2) reduced plasma oncotic pressure, 3) inflammation, and 4) other causes like lymphatic obstruction or sodium/water retention. Increased hydrostatic pressure can result from conditions like congestive heart failure or venous thrombosis. Reduced oncotic pressure is often due to decreased albumin from issues like nephrotic syndrome or cirrhosis. Inflammation can cause edema through increased permeability. Lymphatic obstruction from infections, tumors, or other causes can also lead to edema formation.
Idiopathic thrombocytopenic purpura
Idiopathic thrombocytopenic purpura (ITP) is a bleeding disorder caused by the immune-mediated destruction of platelets. It most commonly presents in children between 1-7 years of age, usually after a viral infection. ITP results in low platelet counts and spontaneous bruising or bleeding. Diagnosis involves low platelet count, absence of other abnormalities, and normal bone marrow with increased or normal megakaryocytes. Treatment depends on if it is acute or chronic ITP, and may include corticosteroids, IVIG, anti-D immunoglobulin, thrombopoietin receptor agonists, or splenectomy in severe cases.
Polycythemia
Polycythemia is a condition characterized by an abnormal increase in the red blood cell count. There are two types: relative polycythemia, caused by a decrease in plasma volume leading to a higher concentration of red blood cells; and absolute polycythemia, caused by overproduction of red blood cells in the bone marrow. Polycythemia vera is a specific myeloproliferative disorder and type of absolute polycythemia caused by a mutation in the JAK2 gene, leading to uncontrolled red blood cell production. Symptoms include headaches, dizziness, and blood flow issues from hyperviscosity. Treatment involves phlebotomy to reduce red blood cell counts and medications to control bone marrow
systemic lupus erythematosus
Systemic Lupus Erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems. It typically affects young women and is characterized by periods of disease flares and remissions. While the exact cause is unknown, genetic and environmental factors likely contribute to abnormal immune system functioning and production of autoantibodies. Common clinical manifestations include malar rash, arthritis, kidney problems, and hematological abnormalities. Diagnosis involves identifying clinical features and detecting autoantibodies such as antinuclear antibodies and anti-dsDNA antibodies. With proper management, 10-year survival rates are over 90%.
Thrombocytopenia
This document defines thrombocytopenia as a platelet count below 150,000 per microlitre and discusses its causes, which include increased platelet destruction, decreased platelet production, and other rare conditions. It outlines the workup for thrombocytopenia, including a medical history focusing on medications, physical exam, and lab tests. Treatment depends on the underlying cause but may include treating infections, discontinuing offending drugs, corticosteroids, IVIG, splenectomy, or platelet transfusions in severe cases. The main goals are to identify the cause and treat any underlying condition driving the low platelet count.
APLA SYNDROME SEMINAR PHARMACY PRESENTATION
This presentation on APLA SYNDROME will help you understand the definition, clinical features, risk factors involved, including etiology, physical examination, diagnosis and Management.
It also includes an overview on complications of APLA syndrome and prevention.
Approach to thrombocytopenia
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.
Dic syndrome
Disseminated intravascular coagulation (DIC) is an acquired syndrome where there is widespread activation of the coagulation system, leading to microvascular thrombosis and organ damage. It can occur acutely when large amounts of procoagulants are suddenly released, or chronically with small continuous releases over time. Left untreated, it can cause life-threatening hemorrhage. Diagnosis involves looking for signs of bleeding and thrombosis, as well as using scoring systems to assess coagulation markers. Treatment focuses on treating the underlying condition while providing supportive care and replacing clotting factors.
The inflammatory process
The document summarizes the inflammatory process in three phases:
Phase I is the acute phase lasting 1-2 weeks involving vascular responses, swelling, pain, heat, and loss of function due to chemical mediators. Phagocytosis occurs as leukocytes remove dead tissue.
Phase II is the tissue formation phase lasting 2-3 weeks involving regeneration, collagen synthesis, wound contraction, and vascularization.
Phase III is the remodeling phase lasting up to 1 year involving collagen remodeling and scar maturation to adapt to original tissue. Treatment planning focuses on controlling inflammation, encouraging repair, and functional rehabilitation.
Thrombocytopenia ppt Health Advice
This Thrombocytopenia ppt help you in understanding the what is platelet and why it get low count and its causes, signs and treatment, diagnosis, Prevention, Cure and Insurance Coverage, Myths and Facts, FAQs, Home Natural remedies, Medical Advice and everything you need to know.
Read more at: http://www.thebesthealth.org/thrombocytopenia
What is Thrombocytopenia?
Thrombocytopenia is a medical disorder in which a person suffers from a low level of blood platelets. Platelets (or thrombocytes) are colorless blood cells that help blood to clot and stop bleeding by clumping and forming plugs in the wounds of the blood vessels.
It often occurs as a result of various disorders such as leukemia or an immune system problem. It may be a side effect of taking certain medication and this condition affects both children and adults. It can be a mild and cause few signs or symptoms. In rare cases, the platelets count may occur dangerous internal bleeding.
How is thrombocytopenia treated?
If your doctor feels that there is no serious threat to your health, he or she may choose not to treat thrombocytopenia. Treatment for thrombocytopenia depends on the cause and the effect it has on your health. For example,
Your doctor may switch you to another medication, if you are taking a medication that causes thrombocytopenia
Your doctor may prescribe steroids, immunoglobulin, or other medications, if the cause for thrombocytopenia is problems with your immune system
He may suggest platelet transfusion if your platelet count is extremely low
In some cases, the doctor may remove the patient spleen in order to keep it from destroying platelets. Spleen helps the body fight against infections, removing it may place the person at higher risk for certain types of infections. However several vaccinations are given before the splenectomy to help prevent infection
When to Call the Doctor
Call your healthcare provider if you have:
Headache, confusion, or dizziness
Blood when you cough, or difficulty breathing
Bloody urine, vomit, or bowel movements
Vaginal bleeding after menopause OR unusually heavy vaginal bleeding.
Systemic lupus erythematosus (SLE)
Seminar presentation by 4th year medical student under supervision of a doctor. Reference is as in the slide presentation, Nelson's.
nephritic and nephrotic syndrome
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
Platelet disorders
Primary and Secondary Hemostasis is Discussed
This is a copy of a lecture provided as an overview of platelet disorders for board preparation to the MercyOne Des Moines Internal Medicine Residency
Systemic lupus erythematosus (sle)
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that causes inflammation and damage to tissues and organs. Deposits of connective tissue and fibrin collect in blood vessels and organs, leading to necrosis and inflammation. While there is no cure, remissions are possible with proper management. The cause is unknown but genetic and environmental factors play a role. Signs and symptoms include rashes, arthritis, fatigue, and organ involvement. Diagnosis involves tests for autoantibodies and organ function. Treatment focuses on managing symptoms, avoiding triggers, and monitoring for organ complications using medications, supplements, and lifestyle changes.
Systemic sclerosis
A 60-year-old woman presented with painful, sclerotic hands and fingers due to progressive cutaneous scleroderma. She was started on a compounded topical cream containing ketamine, baclofen, gabapentin, verapamil, and pentoxifylline, which provided significant pain relief and improved sensation within a month. At a 6-month follow up, she had been largely weaned off opioid pain medications. The customized treatment targeted the pathophysiology of the condition and helped manage her debilitating symptoms.
idiopathic thrombocytopinic purpura
This document provides information about Idiopathic Thrombocytopenic Purpura (ITP), including:
- ITP is a blood disorder characterized by a decreased number of platelets, which can cause easy bruising and bleeding.
- There are two main forms - acute (seen in children and resolves in <6 months) and chronic (onset at any age and lasts >6 months).
- The cause is unknown in most cases but involves antibodies destroying platelets. Diagnosis involves ruling out other causes through testing.
- Treatment options depend on severity but may include steroids, IVIg, splenectomy, thrombopoietin receptor agonists, and experimental agents.
systemic lupus erythematosus
This document provides information about systemic lupus erythematosus (SLE). It defines SLE as a multi-system autoimmune disease affecting various organs mediated by autoantibodies and immune complexes. The causes are unknown but may involve genetic, hormonal, and environmental factors. SLE can affect many organ systems like the kidneys, lungs, heart, and nervous system, causing a variety of clinical manifestations. Diagnosis involves evaluating symptoms, medical history, physical exam, and laboratory tests. Treatment depends on disease severity and organ involvement, and may include medications like NSAIDs, antimalarials, corticosteroids, and cytotoxic drugs. Special considerations are given to SLE in pregnancy and neonates.
OVERVIEW Disorders of platelets
The document provides an overview of platelet disorders, describing how platelets function in hemostasis and how genetic and acquired factors can influence this process, leading to bleeding or clotting symptoms. It discusses various qualitative and quantitative platelet disorders, outlining approaches to diagnosing and differentiating disorders based on platelet production, distribution, or destruction. Evaluation of thrombocytopenia and diagnostic tools for platelet functional disorders are also reviewed.
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Thrombocytopenia
Thrombocytopenia refers to a decrease in platelets in the blood. It can be caused by vitamin deficiencies, medications, liver failure decreasing thrombopoietin production, or conditions like ITP or leukemia. Symptoms include bruising, petechiae, nosebleeds, and fatigue. Diagnosis involves blood tests to check counts, functions, and potential causes. Treatment focuses on addressing the underlying cause and sometimes administering platelet transfusions for newborns with thrombocytopenia.
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.
Thrombocytopenia
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.
An approach to a patient with Thrombocytopenia
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.
CME thrombocytopenia
This document provides an overview of thrombocytopenia (low platelet count). It defines thrombocytopenia as a platelet count below 150,000/microL and describes the degrees of severity. The causes of thrombocytopenia include decreased platelet production in the bone marrow, increased platelet destruction, and dilution of platelets. Specific conditions that can cause thrombocytopenia like immune thrombocytopenia, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, and drug-induced thrombocytopenia are discussed in more detail. Evaluation and management of thrombocytopenia in pregnancy and neonates is also reviewed.
Thrombocytopenia
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.
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immundeficiencydiseases-160925065412.pdf
This document provides an overview of immunodeficiency diseases. It describes how immunodeficiencies can be primary, due to abnormalities in immune system development, or secondary, resulting from other diseases or conditions. The major types of primary immunodeficiencies are then classified and examples in each category are outlined, including humoral deficiencies affecting B cells, cellular deficiencies affecting T cells, combined deficiencies, and disorders of complement and phagocytosis. Clinical features, diagnostic tests, and treatment approaches are summarized for several specific immunodeficiency syndromes.
Immunodeficiency diseases
This document provides an overview of immunodeficiency diseases. It describes how immunodeficiencies can be primary, due to abnormalities in immune system development, or secondary, resulting from other diseases or conditions. The major classifications of primary immunodeficiencies are then outlined, including humoral deficiencies affecting B cells, cellular deficiencies affecting T cells, combined deficiencies, and disorders of complement and phagocytosis. Several specific primary immunodeficiency diseases are then described in more detail. Secondary immunodeficiencies resulting from external factors like malnutrition, infection, or drugs are also briefly discussed.
HIV Manifestations
Complications of HIV in:
- Central nervous system
- Respiratory system
- Gastrointestinal tract
*There are notes provided in some slides.
Amyloidosis 2
This document discusses amyloidosis, including its pathogenesis, classification, and specific entities. The basic mechanism involves the abnormal folding and accumulation of proteins into fibrils, which can damage tissues through pressure effects, vessel wall infiltration, and cytotoxicity. Amyloidosis is classified as either generalized/systemic, involving multiple organs, or localized, affecting a single tissue. Specific entities discussed include reactive systemic amyloidosis associated with chronic inflammation; hemodialysis-associated amyloidosis involving beta-2 microglobulin; and hereditary forms like familial Mediterranean fever and familial amyloidotic neuropathy.
Congenital and Acquired Immunodeficiency
This document summarizes a presentation on congenital and acquired immunodeficiencies. It discusses primary immunodeficiencies caused by genetic defects present at birth, such as X-linked agammaglobulinemia. It also discusses secondary immunodeficiencies that develop later in life due to infections, malnutrition or medical treatments, the most common being HIV/AIDS. The presentation covers defects that can occur in lymphocytes development and function, as well as innate immunity. Specific primary immunodeficiencies discussed include SCID, CGD, and leukocyte adhesion deficiency.
Immunodeficiency_DISORDERS.pptx.........
This document provides an overview of immunodeficiency diseases. It begins by defining immunodeficiency diseases as impairments of the body's defense mechanisms, including both specific immune functions like humoral and cell-mediated immunity as well as non-specific mechanisms. The document then distinguishes between primary immunodeficiencies, which are due to abnormalities in immune system development, and secondary immunodeficiencies caused by diseases, drugs, or other processes interfering with mature immune systems. It proceeds to describe several common primary immunodeficiency diseases categorized by deficiencies in humoral immunity, cellular immunity, or combined deficiencies. It concludes by outlining disorders of non-specific immunity including phagocyte and complement deficiencies.
Immunodeficiency - SCID & LAD
Contents- Introduction to Immunodeficiency | Types | SCID | LAD
Immunodeficiency is the inability to produce an adequate immune response because of insufficiency or absence of antibodies, immune cells or both.
SCID & LAD are the two immunodeficiencies from primary immunodeficiency.
Autoimmune
This document discusses several topics related to immunology and autoimmune diseases:
1. It describes the different types of hypersensitivity reactions and the stages of HIV/AIDS defined by CD4+ T-cell counts and common associated diseases.
2. It explains that autoimmune diseases result from an immune response against one's own cells and discusses genetic and environmental factors that can lead to this breakdown of self-tolerance.
3. Examples are given of organ-specific autoimmune diseases that affect the thyroid, stomach, blood, pancreas, adrenal glands, parathyroid, and muscles.
Immunodeficiency Disorder
This document discusses immunodeficiency disorders, including:
- Primary/congenital immunodeficiencies are inherited and cause susceptibility to infections starting in childhood. There are over 125 identified disorders.
- Secondary/acquired immunodeficiencies are caused by other diseases, environmental factors like infections, medications, malnutrition or aging. Examples include AIDS.
- Immunodeficiencies can affect B cells, T cells, or phagocytes. Common disorders discussed are agammaglobulinemia, SCID, and chronic granulomatous disease. Management involves immunoglobulin replacement, antibiotics, stem cell transplant or gene therapy.
Diseases of the Immune System
Primary immunodeficiencies are caused by genetic defects that impair the immune system's ability to fight infections. They can be classified as humoral, affecting antibody production; cellular, affecting T cells and cell-mediated immunity; or combined. Common primary immunodeficiencies include X-linked agammaglobulinemia, isolated IgA deficiency, common variable immunodeficiency, hyper IgM syndrome, and severe combined immunodeficiency. Secondary immunodeficiencies are acquired, having underlying causes like infections, malnutrition, aging, or drugs. Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV).
-immunopathology-2.ppt
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibodies against nuclear antigens. It predominantly affects women and can involve multiple organ systems. The disease is caused by a combination of genetic and environmental factors that lead to immune tolerance breakdown and production of autoantibodies like anti-dsDNA and anti-Sm. These autoantibodies form immune complexes that deposit in tissues, especially the kidney glomeruli, and cause inflammation and damage. Clinical manifestations include a butterfly rash, arthritis, serositis, and kidney involvement. Treatment involves immunosuppression with corticosteroids and other drugs.
Immunology xi immunodeficiency
This document discusses various topics related to immunodeficiency and HIV/AIDS, including:
1) It describes primary and secondary immunodeficiencies, noting that primary deficiencies are caused by genetic defects while secondary deficiencies result from other diseases or environmental factors.
2) It provides an overview of opportunistic infections associated with AIDS, including Pneumocystis pneumonia and infections caused by toxoplasma, cytomegalovirus, and mycobacteria.
3) It discusses treatment for HIV/AIDS, including highly active antiretroviral therapy (HAART) and prophylaxis for opportunistic infections like Pneumocystis pneumonia.
Autoimmunity.pptx
The document discusses autoimmunity and several autoimmune diseases. It explains that autoimmunity occurs when the immune system attacks the body's own tissues, as in diseases like Hashimoto's thyroiditis, pernicious anemia, Graves' disease, myasthenia gravis, systemic lupus erythematosus, multiple sclerosis, and rheumatoid arthritis. These diseases are caused by a combination of autoantibodies, T cells, cytokines and other immune responses that damage organs like the thyroid, red blood cells, muscles, joints and nervous system. Treatment involves replacing missing hormones or proteins, or suppressing the immune system.
106117.pptx
1. WBC pathology involves the study of white blood cell counts, differentials, and abnormalities.
2. Key abnormalities include leukopenia, leukocytosis, and leukemia. Leukopenia involves low white blood cell counts while leukocytosis means high white blood cell counts.
3. Leukemia is a cancer of the bone marrow characterized by the uncontrolled production of abnormal white blood cells. The main types are acute and chronic leukemias.
Immunodeficiency disorders,2010
Immunodeficiency disorders are associated with defects or impairments in immune function that can be congenital or acquired. Primary immunodeficiency diseases involve genetic defects affecting B cell, T cell, or phagocytic cell development. Common symptoms include recurrent infections, failure to thrive, and increased susceptibility to opportunistic infections. HIV/AIDS is an acquired immunodeficiency disorder that progressively weakens the immune system by attacking CD4 cells, leaving the body vulnerable to opportunistic infections.
shock.ppt3333333333333333333333333333333
Shock results from the failure of the cardiovascular system to provide sufficient blood circulation.
To maintain circulatory homeostasis the following mechanisms must be present –
1. a functioning of heart to circulate blood .
A sufficient amount of blood volume .
The capability of the vascular system , accommodating blood flow to the capillaries and returning to the right side of the heart.
HIV AIDS.pptx
WBC are the most important part of the immune system
N - Neutrophils attack bacteria
B - lymphocytes make antibodies
T- lymphocytes
Responsible for coordinating the immune system’s attack on viruses fungi and some bacteria
The CD4 cells coordinate a body’s immune response to an invader (bacteria, virus, etc.)
BUT, when HIV enters CD4 cells for reproduction, it damages the CD4 cell, eventually killing it.
The body’s immune system works hard making more CD4 cells
Overtime, HIV destroys the CD4 cells faster than the immune system can make new ones
So, HIV damages the immune system that usually protects the body from infection.
HIV infections cause a progressive depletion of CD4 cells which eventually leads to immunodeficiency, constitutional diseases(general effect of a disease and that may affect the general well-being/ status of an individual ), neurologic complication( confusion and forgetfulness, inability to concentrate ), opportunistic (are infections that occur more sever and neoplasm (a new abnormal growth of tissue).
HIV is retrovirus that attacks the immune
system.
Over time, the immune system and the body loses it
ability to fight the virus.
It is a period of 4-7 weeks
● Immune system produces antibodies
● This is when viral set point is established
● High viral set point tends to exhibit more rapid disease progression
● Can be asymptomatic or with persistent generalized
lymphadenopathy (swollen lymph nodes)
● 40-90% of newly infected show flu like symptoms like fever, rash,
oral ulcers, loss of appetite, weight loss, malaise, inflamed lymph
nodes.
This stage could last an average of 10 years
Decrease in lean body mass without apparent total body
weight changes
Vitamin B12 deficiency, increased susceptibility to food
borne and waterborne pathogens
In this stage, symptoms like fever, sweats, skin.
problems and fatigue can be seen
A decline in nutrients status or body composition
may occur.
A small proportion of persons infected with the virus develop
AIDS and within month following primary infection.
Some HIV infected individuals exhibit no signs of disease
progression.
A lowered viral load set point. Lesser virulence of the virus and
protective genetic mutations appear to contribute to this state.
Acquired:To come into control of something new
Immune Deficiency:Decrease or weakness in the body’s ability to fight off infections and illnesses
Syndrome:A group of signs and symptoms that occur together and characterize a particular abnormality
AIDS is the final stage of the disease caused by infection with a type of virus called HIV.
HIV is the virus that causes AIDS
Not everyone who is infected with HIV has AIDS
Everyone with AIDS is infected with HIV
AIDS is result of the progression of HIV Infection
Anyone infected with HIV, although healthy, can still
transmit the virus to another person
During HIV infection ,nutrient require
Cns infections biplave nams
Acute infections of the nervous system like bacterial meningitis can be life-threatening if not recognized and treated early. The document discusses various acute infections including bacterial meningitis, viral meningitis, encephalitis, and fungal infections. It provides details on the clinical presentation, diagnosis, and management of bacterial meningitis, which is often characterized by the classic triad of fever, headache, and neck stiffness, and requires prompt lumbar puncture and antibiotic treatment to identify the pathogen and prevent complications.
Immunodeficiency disease by Dr. Rakesh Prasad Sah
This document discusses immunodeficiency disorders, including primary and secondary immunodeficiencies. Primary immunodeficiencies are inherited defects in immunity and include disorders of specific immunity, phagocytosis, complement, and humoral or cellular immunity. Examples provided include agammaglobulinemia, common variable immunodeficiency, and combined immunodeficiencies like severe combined immunodeficiency. Secondary immunodeficiencies result from diseases that interfere with immune function, such as infections, malnutrition, or immunosuppressive therapies. The document also discusses infections associated with different immunodeficiencies and treatments for some conditions.
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Introduction and types of immunity I Pharmaceutical Microbiology
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Morphological and Selective Biochemical characterization of some specimen
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Thrombocytopenia
- 2. Decreased Production: Nutritional Deficiencies B12, Folate Bone marrow failure Aplastic anaemia Bone marrow infiltrations Leukaemia Metastasis Granulomatous disease
- 3. Ineffective haematopoiesis Myelodysplastic syndromes Selective Impairment Drud induced (alcohol, Thiazides, cytotoxic) Infections ( Measles, HIV) Sequestration Hypersplenism
- 4. Decreased Survival: Immunological destruction Primary autoimmune Acute ITP Chronic ITP Secondary Autoimmune SLE
- 5. Alloimmune Post transfusion Neonatal Drug associated Quinidine, heparin, Sulfa compounds Infections HIV, Dengue fever, Infectious mononucleosis
- 6. Nonimmunologic DIC TTP Giant haemangiomas Dilutional Massive transfussions
- 7. Autoimmune disorder in which platelet sensitization by autoantibodies takes place, leading to destruction of opsonized platelets primarily by the mononuclear phagocytic system.
- 8. Primary: Acute Chronic Secondary: Lymphoproliferative disorders SLE HIV Evan’s syndrome
- 9. Thrombocytopenia in ITP is mediated by anti- platelet antibodies directed against the platelet specific glycoproteins (GP) IIb- IIIa, Ib-IX or Ia-IIa. Antibodies against viral protein antigen that are cross reactive against platelet antigens.
- 10. Antibody coated platelets are susceptible to phagocytosis by the cells of the mononuclear phagocytic system. Spleen plays a crucial role for 2 reasons; Anti-platelet antibody production site Destruction of sensitized platelet IgG
- 11. Petechiae Easy bruising Epistaxis Bleeding gums Melena Hematuria
- 12. A diagnosis of ITP should be made only after other causes of platelet deficiences have been ruled out. CBC: Anaemia Thrombocytopenia BT Coagulation studies
- 13. Bone marrow examination: Megakaryocytic hyperplasia with both mature and maturing forms increased.