Homocysteine
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The document discusses homocysteine and its relationship to various diseases. It notes that elevated homocysteine levels are an independent risk factor for cardiovascular disease and that up to 40% of heart attacks occur in people with normal cholesterol. It also discusses links between higher homocysteine levels and increased risks of osteoporosis, pregnancy complications, Alzheimer's disease, cancer, and other conditions. The document provides details on genetic and lifestyle factors that can increase homocysteine levels.
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Homocysteine
Homocysteine is a sulfur-containing amino acid and intermediate product of methionine metabolism. It exists in three forms in plasma/serum and is involved in two metabolic pathways - remethylation and trans-sulfuration. Genetic or acquired deficiencies in enzymes and vitamins involved in homocysteine metabolism can lead to hyperhomocysteinemia, which is associated with various diseases like cardiovascular disorders. Laboratory tests are available to measure homocysteine levels to screen for deficiencies and diseases. Elevated homocysteine promotes oxidative damage and impaired vascular function.
Homocysteine And Cardiovascular Disease
This document discusses homocysteine and its relationship to cardiovascular disease. Homocysteine is an amino acid produced during metabolism that can accumulate in high levels due to genetic or nutritional factors. High homocysteine levels are associated with damage to blood vessels and an increased risk of cardiovascular problems like heart attacks and strokes. The document reviews research studies investigating the effects of homocysteine and whether vitamin supplements can help lower levels and reduce cardiovascular risk.
Homocysteine: An Overlooked Biomarker in Clinical Medicine
High levels of homocysteine (Hcy), or a high "H score," predicts risk for over 100 diseases like cardiovascular disease (CVD), cerebrovascular accident (CVA), diabetes, and renal disease. Elevated plasma Hcy is an important, strong, and modifiable risk factor that can predict higher long-term mortality when elevated at baseline. Hcy levels are affected by genetic mutations, nutritional deficiencies, diseases, and drugs, and testing is recommended for those with vascular diseases or risk factors. Elevated Hcy can damage arteries in several ways and is a stronger predictor of CVD risk than cholesterol.
Homocysteine
Homocysteine is an amino acid formed from the essential amino acid methionine. Elevated levels of homocysteine (hyperhomocysteinemia) increase the risk of cardiovascular diseases through several mechanisms. It damages blood vessel walls, promotes atherosclerosis and thrombosis. Vitamins B6, B12 and folic acid help regulate homocysteine levels and reduce cardiovascular risk by supporting homocysteine metabolism through remethylation and transsulfuration pathways. Maintaining normal homocysteine levels through diet and supplements may help prevent cardiovascular diseases.
homocisteine and heart disease
Homocysteine is a byproduct of methionine metabolism that can accumulate in the body if certain vitamins and minerals are deficient. Elevated homocysteine levels are associated with an increased risk of heart disease and blood clots. Normal homocysteine levels are between 5-15 micromoles per liter, while levels over 100 micromoles per liter indicate severe hyperhomocysteinemia. A study found that a diet high in fruits, vegetables, and berries effectively lowered homocysteine levels by increasing folate levels in the blood.
Hyperhomocysteinemia and its implications in atherosclerosis ppt copy (2) ...
This document discusses hyperhomocysteinemia and its implications for atherosclerosis in India. It begins by defining homocysteine and its metabolism. It then discusses the various causes of hyperhomocysteinemia, including genetic and nutritional factors. It notes the high prevalence of hyperhomocysteinemia in India compared to worldwide, due to common vegetarian diets, vitamin deficiencies, genetic factors like MTHFR deficiency, and environmental factors. It discusses the mechanisms by which hyperhomocysteinemia promotes atherosclerosis and cardiovascular disease. It concludes by summarizing various Indian studies finding associations between hyperhomocysteinemia and more severe, premature, and fatal coronary artery disease.
Homocysteine
Slide 1 : Homocysteine
Slide 2 : Outline.
Slide 3 : Homocysteine & Source of Homocysteine
Slide 4 : Levels of Homocysteine
Slide 5 : Metabolism of Homocysteine.
Slide 6 : Causes for excess Homocysteine levels.
Slide 7 : CVD Risk in INDIA.
Slide 8 -11 : EXCESS OF HOMOCYSTEINE LEVELS IN INDIANS
Slide 12 : Effect of Homocysteine in CVD.
Slide 13: AHA (American Heart Association)
Slide 14: Lowering Homocystiene levels
Platelet Aggregation
A patient has a history of recurrent gum bleeding since childhood. While platelet counts and coagulation tests are normal, an inherited platelet disorder is suspected. The doctor's diagnostic approach would include a detailed bleeding history, physical exam looking for bruises/petechiae, and first-line screening tests like a bleeding time and platelet function analyzer. Further specific tests may include light transmission aggregometry to assess platelet aggregation in response to various agonists and help identify potential defects in adhesion, activation, secretion or aggregation. Interpreting the different waveforms is important to determine abnormalities consistent with disorders like Glanzmann's thrombasthenia or storage pool disease.
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Homocysteine
Homocysteine is a sulfur-containing amino acid and intermediate product of methionine metabolism. It exists in three forms in plasma/serum and is involved in two metabolic pathways - remethylation and trans-sulfuration. Genetic or acquired deficiencies in enzymes and vitamins involved in homocysteine metabolism can lead to hyperhomocysteinemia, which is associated with various diseases like cardiovascular disorders. Laboratory tests are available to measure homocysteine levels to screen for deficiencies and diseases. Elevated homocysteine promotes oxidative damage and impaired vascular function.
Homocysteine And Cardiovascular Disease
This document discusses homocysteine and its relationship to cardiovascular disease. Homocysteine is an amino acid produced during metabolism that can accumulate in high levels due to genetic or nutritional factors. High homocysteine levels are associated with damage to blood vessels and an increased risk of cardiovascular problems like heart attacks and strokes. The document reviews research studies investigating the effects of homocysteine and whether vitamin supplements can help lower levels and reduce cardiovascular risk.
Homocysteine: An Overlooked Biomarker in Clinical Medicine
High levels of homocysteine (Hcy), or a high "H score," predicts risk for over 100 diseases like cardiovascular disease (CVD), cerebrovascular accident (CVA), diabetes, and renal disease. Elevated plasma Hcy is an important, strong, and modifiable risk factor that can predict higher long-term mortality when elevated at baseline. Hcy levels are affected by genetic mutations, nutritional deficiencies, diseases, and drugs, and testing is recommended for those with vascular diseases or risk factors. Elevated Hcy can damage arteries in several ways and is a stronger predictor of CVD risk than cholesterol.
Homocysteine
Homocysteine is an amino acid formed from the essential amino acid methionine. Elevated levels of homocysteine (hyperhomocysteinemia) increase the risk of cardiovascular diseases through several mechanisms. It damages blood vessel walls, promotes atherosclerosis and thrombosis. Vitamins B6, B12 and folic acid help regulate homocysteine levels and reduce cardiovascular risk by supporting homocysteine metabolism through remethylation and transsulfuration pathways. Maintaining normal homocysteine levels through diet and supplements may help prevent cardiovascular diseases.
homocisteine and heart disease
Homocysteine is a byproduct of methionine metabolism that can accumulate in the body if certain vitamins and minerals are deficient. Elevated homocysteine levels are associated with an increased risk of heart disease and blood clots. Normal homocysteine levels are between 5-15 micromoles per liter, while levels over 100 micromoles per liter indicate severe hyperhomocysteinemia. A study found that a diet high in fruits, vegetables, and berries effectively lowered homocysteine levels by increasing folate levels in the blood.
Hyperhomocysteinemia and its implications in atherosclerosis ppt copy (2) ...
This document discusses hyperhomocysteinemia and its implications for atherosclerosis in India. It begins by defining homocysteine and its metabolism. It then discusses the various causes of hyperhomocysteinemia, including genetic and nutritional factors. It notes the high prevalence of hyperhomocysteinemia in India compared to worldwide, due to common vegetarian diets, vitamin deficiencies, genetic factors like MTHFR deficiency, and environmental factors. It discusses the mechanisms by which hyperhomocysteinemia promotes atherosclerosis and cardiovascular disease. It concludes by summarizing various Indian studies finding associations between hyperhomocysteinemia and more severe, premature, and fatal coronary artery disease.
Homocysteine
Slide 1 : Homocysteine
Slide 2 : Outline.
Slide 3 : Homocysteine & Source of Homocysteine
Slide 4 : Levels of Homocysteine
Slide 5 : Metabolism of Homocysteine.
Slide 6 : Causes for excess Homocysteine levels.
Slide 7 : CVD Risk in INDIA.
Slide 8 -11 : EXCESS OF HOMOCYSTEINE LEVELS IN INDIANS
Slide 12 : Effect of Homocysteine in CVD.
Slide 13: AHA (American Heart Association)
Slide 14: Lowering Homocystiene levels
Platelet Aggregation
A patient has a history of recurrent gum bleeding since childhood. While platelet counts and coagulation tests are normal, an inherited platelet disorder is suspected. The doctor's diagnostic approach would include a detailed bleeding history, physical exam looking for bruises/petechiae, and first-line screening tests like a bleeding time and platelet function analyzer. Further specific tests may include light transmission aggregometry to assess platelet aggregation in response to various agonists and help identify potential defects in adhesion, activation, secretion or aggregation. Interpreting the different waveforms is important to determine abnormalities consistent with disorders like Glanzmann's thrombasthenia or storage pool disease.
Homocystinuria
Homocystinuria is a disorder of methionine metabolism caused by an inability to metabolize homocysteine. There are three main types: classic homocystinuria caused by cystathionine β-synthase deficiency; defects in methylcobalamin formation; and methylenetetrahydrofolate reductase deficiency. Symptoms vary but can include developmental delay, dislocated lenses, skeletal abnormalities, thromboembolism, and intellectual disability. Treatment depends on the type but may include vitamin B6, betaine, folic acid, vitamin B12, methionine supplementation, and dietary restrictions.
Folate
Folic acid is essential for one carbon metabolism and the synthesis of DNA, RNA, and proteins. Rich sources include green leafy vegetables and yeast. Deficiency can cause megaloblastic anemia and fetal neural tube defects. It is caused by inadequate intake, increased need during pregnancy, malabsorption, medications, and B12 deficiency trapping folate. Symptoms include fatigue, sore tongue, and neurological issues. Diagnosis involves blood tests of folate, B12, and homocysteine levels. Treatment is oral folic acid supplementation.
Homocystinuria
Homocystinuria is a disorder of methionine metabolism, leading to an abnormal accumulation of homocysteine and its metabolites (homocystine, homocysteine-cysteine complex, and others) in blood and urine. Normally, these metabolites are not found in appreciable quantities in blood or urine.
Hemoglobinopathies
1) Hemoglobinopathies are inherited disorders affecting hemoglobin structure or production, ranging from asymptomatic to fatal. The most common types are sickle cell disease and thalassemias.
2) Thalassemias are caused by deficient production of globin chains, leading to imbalanced globin synthesis and red blood cell damage. Beta thalassemias result from low beta chain production while alpha thalassemias involve alpha chains.
3) Clinical features vary by specific disorder from mild anemia to transfusion-dependent anemia and organ damage. Management involves treatment of complications, transfusions, chelation therapy, and in severe cases, stem cell transplant.
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1. HIV can cause a variety of hematological manifestations including anemia, leukopenia, thrombocytopenia, and coagulation disorders due to bone marrow infiltration and effects on hematopoietic progenitor cells.
2. The bone marrow in HIV/AIDS commonly shows hypercellularity, dysplasia of the erythroid and myeloid lineages, plasmacytosis, and lymphoid aggregates. Opportunistic infections also frequently involve the bone marrow.
3. HIV is associated with increased risk of aggressive B-cell lymphomas such as diffuse large B-cell lymphoma. Lymphomas in HIV often involve extranodal sites and the bone marrow.
Protein c and protein s
Protein C and protein S are proteins that help regulate blood clot formation. They work together to inactivate factors V and VIII, slowing down clot formation. Deficiencies in protein C or protein S can lead to excessive clotting. There are inherited and acquired causes of low levels or abnormal function of these proteins. Inherited causes include insufficient production or abnormal function, while acquired causes include liver disease, vitamin K deficiency, and certain medical conditions or treatments.
Hyperuricemia
This document summarizes information about hyperuricemia and uric acid. It discusses that uric acid is produced from the breakdown of purines and defines hyperuricemia. The document outlines the physiology of uric acid production and excretion by the kidneys. It describes some causes of high uric acid levels like Lesch-Nyhan syndrome and gout. The document also discusses hypouricemia and mentions several methods for measuring uric acid levels like chemical, enzymatic, IDMS and HPLC methods. It provides reference ranges and notes some physiological variations in uric acid levels.
G6PD Deficiency Anaemai
- Individuals with G6PD deficiency do not show symptoms until exposed to oxidative stress, such as certain foods or medicines.
- G6PD is responsible for producing NADPH, which generates glutathione to protect red blood cells from damage by free radicals. In G6PD deficiency, insufficient NADPH leads to hemolysis upon exposure to oxidative stress.
- Diagnosis involves testing for G6PD enzyme activity levels, which are reduced in deficiency. Exposure to oxidative triggers can cause a hemolytic crisis characterized by dark urine and jaundice.
Thrombophilia
This document discusses hypercoagulable states (thrombophilia). It presents two case studies of patients presenting with deep vein thrombosis (DVT). It then defines thrombophilia as a disorder associated with an increased tendency to form blood clots. The document reviews hemostasis and coagulation mechanisms, inherited and acquired risk factors for hypercoagulability, and recommends a stepwise approach to thrombophilia testing that considers the clinical scenario and implications of testing.
RBC Membrane Defects
This document discusses red blood cell membrane defects such as hereditary spherocytosis and hereditary elliptocytosis. Hereditary spherocytosis is caused by defects in membrane proteins like spectrin, ankyrin, band 3, and protein 4.2 which results in reduced cell surface area, impaired flexibility, and increased permeability. This makes the red blood cells spherical in shape and prone to destruction in the spleen. Hereditary elliptocytosis is caused by weakened linkages in the membrane skeleton that results in elliptical shaped red blood cells. Both conditions are inherited and can cause anemia.
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This document discusses microalbuminuria (MA) in a 50-year-old female patient with type 2 diabetes. It defines MA as urinary albumin excretion between 20-200 ug/min or 30-300 mg/24 hours. The document discusses screening, causes, prevalence, and significance of MA. MA is a marker of early kidney damage and predicts increased risk of cardiovascular disease. Tight control of blood pressure, glucose, and lipids is recommended for patients with MA.
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The document discusses kidney functions and urine formation. The kidney removes waste, regulates electrolytes and water, and maintains acid-base balance. Urine is formed in nephrons through glomerular filtration, tubular reabsorption, and tubular secretion. Tests like creatinine clearance and inulin clearance are used to measure glomerular filtration rate (GFR) as an indicator of kidney function. Proper collection and preservation of urine samples is important for accuracy in clearance and other renal function tests.
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This document discusses various peptides and hormones involved in insulin production and diabetes, including proinsulin, C-peptide, glucagon, GLP-1, TNFa, and adiponectin. It notes that proinsulin to insulin ratio above 20% predicts future type 2 diabetes. C-peptide measures endogenous insulin secretion and its presence reduces diabetes complications. TNFa causes insulin resistance while adiponectin increases insulin sensitivity, and their levels are useful markers. The conclusion emphasizes measuring proinsulin, C-peptide, adiponectin and TNFa to monitor insulin resistance and drug responses.
Disorders of platelets
Platelets play a key role in hemostasis. Disorders of platelets can be quantitative, involving too few or too many platelets, or qualitative, involving platelet function defects. Common causes of thrombocytopenia include decreased production, increased destruction, sequestration, or pseudothrombocytopenia. Immune thrombocytopenic purpura is an immune-mediated disorder treated with steroids, IVIG, or splenectomy. Thrombotic thrombocytopenic purpura involves a deficiency in ADAMTS13 treated with plasma exchange. Von Willebrand disease involves defects in von Willebrand factor.
Hemoglobinopathies
The document discusses abnormal hemoglobin metabolism and hemoglobinopathies. It provides information on hemoglobin structure, definitions of thalassemias and hemoglobinopathies, specifics on sickle cell anemia and thalassemia, Bart's hydrops fetalis, and diagnosis of hemoglobinopathies. Sickle cell anemia results from a single amino acid substitution causing hemoglobin S, which polymerizes and makes red blood cells rigid and sickle-shaped. Thalassemias involve absent or reduced alpha or beta globin chains. Diagnosis involves family history, symptoms, lab tests, and analyzing hemoglobin structure.
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Homocystinuria
Homocystinuria is a disorder of methionine metabolism caused by an inability to metabolize homocysteine. There are three main types: classic homocystinuria caused by cystathionine β-synthase deficiency; defects in methylcobalamin formation; and methylenetetrahydrofolate reductase deficiency. Symptoms vary but can include developmental delay, dislocated lenses, skeletal abnormalities, thromboembolism, and intellectual disability. Treatment depends on the type but may include vitamin B6, betaine, folic acid, vitamin B12, methionine supplementation, and dietary restrictions.
Folate
Folic acid is essential for one carbon metabolism and the synthesis of DNA, RNA, and proteins. Rich sources include green leafy vegetables and yeast. Deficiency can cause megaloblastic anemia and fetal neural tube defects. It is caused by inadequate intake, increased need during pregnancy, malabsorption, medications, and B12 deficiency trapping folate. Symptoms include fatigue, sore tongue, and neurological issues. Diagnosis involves blood tests of folate, B12, and homocysteine levels. Treatment is oral folic acid supplementation.
Homocystinuria
Homocystinuria is a disorder of methionine metabolism, leading to an abnormal accumulation of homocysteine and its metabolites (homocystine, homocysteine-cysteine complex, and others) in blood and urine. Normally, these metabolites are not found in appreciable quantities in blood or urine.
Hemoglobinopathies
1) Hemoglobinopathies are inherited disorders affecting hemoglobin structure or production, ranging from asymptomatic to fatal. The most common types are sickle cell disease and thalassemias.
2) Thalassemias are caused by deficient production of globin chains, leading to imbalanced globin synthesis and red blood cell damage. Beta thalassemias result from low beta chain production while alpha thalassemias involve alpha chains.
3) Clinical features vary by specific disorder from mild anemia to transfusion-dependent anemia and organ damage. Management involves treatment of complications, transfusions, chelation therapy, and in severe cases, stem cell transplant.
Hematological manifestations of hiv
1. HIV can cause a variety of hematological manifestations including anemia, leukopenia, thrombocytopenia, and coagulation disorders due to bone marrow infiltration and effects on hematopoietic progenitor cells.
2. The bone marrow in HIV/AIDS commonly shows hypercellularity, dysplasia of the erythroid and myeloid lineages, plasmacytosis, and lymphoid aggregates. Opportunistic infections also frequently involve the bone marrow.
3. HIV is associated with increased risk of aggressive B-cell lymphomas such as diffuse large B-cell lymphoma. Lymphomas in HIV often involve extranodal sites and the bone marrow.
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Protein C and protein S are proteins that help regulate blood clot formation. They work together to inactivate factors V and VIII, slowing down clot formation. Deficiencies in protein C or protein S can lead to excessive clotting. There are inherited and acquired causes of low levels or abnormal function of these proteins. Inherited causes include insufficient production or abnormal function, while acquired causes include liver disease, vitamin K deficiency, and certain medical conditions or treatments.
Hyperuricemia
This document summarizes information about hyperuricemia and uric acid. It discusses that uric acid is produced from the breakdown of purines and defines hyperuricemia. The document outlines the physiology of uric acid production and excretion by the kidneys. It describes some causes of high uric acid levels like Lesch-Nyhan syndrome and gout. The document also discusses hypouricemia and mentions several methods for measuring uric acid levels like chemical, enzymatic, IDMS and HPLC methods. It provides reference ranges and notes some physiological variations in uric acid levels.
G6PD Deficiency Anaemai
- Individuals with G6PD deficiency do not show symptoms until exposed to oxidative stress, such as certain foods or medicines.
- G6PD is responsible for producing NADPH, which generates glutathione to protect red blood cells from damage by free radicals. In G6PD deficiency, insufficient NADPH leads to hemolysis upon exposure to oxidative stress.
- Diagnosis involves testing for G6PD enzyme activity levels, which are reduced in deficiency. Exposure to oxidative triggers can cause a hemolytic crisis characterized by dark urine and jaundice.
Thrombophilia
This document discusses hypercoagulable states (thrombophilia). It presents two case studies of patients presenting with deep vein thrombosis (DVT). It then defines thrombophilia as a disorder associated with an increased tendency to form blood clots. The document reviews hemostasis and coagulation mechanisms, inherited and acquired risk factors for hypercoagulability, and recommends a stepwise approach to thrombophilia testing that considers the clinical scenario and implications of testing.
RBC Membrane Defects
This document discusses red blood cell membrane defects such as hereditary spherocytosis and hereditary elliptocytosis. Hereditary spherocytosis is caused by defects in membrane proteins like spectrin, ankyrin, band 3, and protein 4.2 which results in reduced cell surface area, impaired flexibility, and increased permeability. This makes the red blood cells spherical in shape and prone to destruction in the spleen. Hereditary elliptocytosis is caused by weakened linkages in the membrane skeleton that results in elliptical shaped red blood cells. Both conditions are inherited and can cause anemia.
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Microalbuminuria
This document discusses microalbuminuria (MA) in a 50-year-old female patient with type 2 diabetes. It defines MA as urinary albumin excretion between 20-200 ug/min or 30-300 mg/24 hours. The document discusses screening, causes, prevalence, and significance of MA. MA is a marker of early kidney damage and predicts increased risk of cardiovascular disease. Tight control of blood pressure, glucose, and lipids is recommended for patients with MA.
creatinine clearance test
The document discusses kidney functions and urine formation. The kidney removes waste, regulates electrolytes and water, and maintains acid-base balance. Urine is formed in nephrons through glomerular filtration, tubular reabsorption, and tubular secretion. Tests like creatinine clearance and inulin clearance are used to measure glomerular filtration rate (GFR) as an indicator of kidney function. Proper collection and preservation of urine samples is important for accuracy in clearance and other renal function tests.
Myeloproliferative Neoplasms
Myeloproliferative neoplasms (MPNs) are a group of disorders where the bone marrow produces too many red or white blood cells. The presentation outlines the history, classification, signs and symptoms, causes related to genetic mutations like JAK2, diagnosis through blood and bone marrow tests, and treatments including medications, radiation, surgery, and stem cell transplant. MPNs include chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, myelofibrosis, and rare disorders like chronic neutrophilic leukemia and mast cell disease.
Albumin and albumin & globin ratio
albumin role , synthesis, function, factor affect, increase in , decrease in use of a\g ratio how calculate a\g ratio. why need,
Disorders of Lipoprotein Metabolism
Comprehensive description of various primary dyslipidemias, cholesterol transport and molecular mechanisms involved.
View in slideshow after downloading for better experience.
Prepared in Dec 2013.
Determination of Blood Glucose Using Glusose Oxidase-Peroxidase Method
This document discusses blood glucose determination using the oxidase-peroxidase method. It begins by introducing diabetes and its prevalence worldwide. It then describes the materials and methodology used, which involves collecting a blood sample, separating the plasma, and adding an O-toluidine reagent before measuring absorbance. The results showed the patient's glucose level was within the normal range. It further discusses hyperglycemia and hypoglycemia, the different types of diabetes, diagnostic criteria, and gestational diabetes.
C peptide
This document discusses various peptides and hormones involved in insulin production and diabetes, including proinsulin, C-peptide, glucagon, GLP-1, TNFa, and adiponectin. It notes that proinsulin to insulin ratio above 20% predicts future type 2 diabetes. C-peptide measures endogenous insulin secretion and its presence reduces diabetes complications. TNFa causes insulin resistance while adiponectin increases insulin sensitivity, and their levels are useful markers. The conclusion emphasizes measuring proinsulin, C-peptide, adiponectin and TNFa to monitor insulin resistance and drug responses.
Disorders of platelets
Platelets play a key role in hemostasis. Disorders of platelets can be quantitative, involving too few or too many platelets, or qualitative, involving platelet function defects. Common causes of thrombocytopenia include decreased production, increased destruction, sequestration, or pseudothrombocytopenia. Immune thrombocytopenic purpura is an immune-mediated disorder treated with steroids, IVIG, or splenectomy. Thrombotic thrombocytopenic purpura involves a deficiency in ADAMTS13 treated with plasma exchange. Von Willebrand disease involves defects in von Willebrand factor.
Hemoglobinopathies
The document discusses abnormal hemoglobin metabolism and hemoglobinopathies. It provides information on hemoglobin structure, definitions of thalassemias and hemoglobinopathies, specifics on sickle cell anemia and thalassemia, Bart's hydrops fetalis, and diagnosis of hemoglobinopathies. Sickle cell anemia results from a single amino acid substitution causing hemoglobin S, which polymerizes and makes red blood cells rigid and sickle-shaped. Thalassemias involve absent or reduced alpha or beta globin chains. Diagnosis involves family history, symptoms, lab tests, and analyzing hemoglobin structure.
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This document discusses the potential linkages between periodontal disease and systemic diseases like coronary heart disease and stroke. It suggests that periodontal disease may influence these conditions through three main mechanisms: shared risk factors, the periodontium acting as a reservoir for bacteria and inflammatory mediators, and transient bacteremias from periodontal infections potentially causing endothelial dysfunction. The document reviews evidence on specific inflammatory markers and pathogens that may provide biological pathways for this periodontal-systemic connection. It proposes models to explain potential direct and indirect impacts of periodontal infection on atheroma formation and thrombus development that can lead to heart disease and stroke.
Preventing Spina Bifida
Spina Bifida can be reduced by 70% if all women who could possibly become pregnant would take a multivitamin.
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Pukhraj Aloe Vear Juice for Hypertension- Presentation
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1. The document discusses the relationship between migraine and thrombofilia, specifically looking at the MTHFR C677T polymorphism which is associated with higher homocysteine levels and cardiovascular disease risk.
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jhh2014122a
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Hypertension
This document discusses hypertension (high blood pressure), including:
1. Hypertension is one of the most common diseases worldwide, affecting around 20% of adults. It is a major risk factor for heart disease and stroke.
2. The definition of hypertension is a blood pressure of 140/90 mmHg or higher. Risk increases with severity. Factors like age, ethnicity, sex, obesity, diet and alcohol intake affect risk.
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- 4. Annual publication rates within the fields of homocysteine and folate http://www.ncbi.nlm.nih.gov/PubMed at present there is virtually a "new paper every day" on the subject
- 35. Who should have their Homocysteine level tested?
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