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Hemophilia is a genetic bleeding disorder in which body loses the ability to stop bleeding due to low levels or absence of proteins known as ‘’clotting factors’’ which are necessary for clotting of blood. Hemophilia leads to excessive bleeding.
Hemophilia : causes, symptoms, diagnosis and treatment
Hemophilia : causes, symptoms, diagnosis and treatment
Lazoi Lifecare Private Limited
Hemophilia
Hemophilia
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Hemophilia is a common hereditary coagulation disorder due to deficiency or reduce activity of clotting factor VIII or clotting factor IX. This disorder is a X- linked recessive disorder. Types: Hemophilia A- deficiency of clotting factors VIII Hemophilia B- deficiency of clotting factors IX Hemophilia C- deficiency of clotting factors XI Parahaemophilia- deficiency of clotting factor V Causes of hemophilia Hemophilia has a sex-linked recessive inheritance. In most cases Hemophilia caused by a mutation in a gene that encodes for one of the clotting factors . Since the hemophilia gene is located on the X chromosome, Hemophilia usually occurs in males, and Female is the carrier of hemophilia. Diagnosis Complete blood cell count Coagulation studies FVIII assay Normal values for FVIII assays are 50-150%. Values in hemophilia are as follows: Mild: >5% Moderate: 1-5% Severe: <1% Treatment of Hemophilia Other Types of Treatment Desmopressin (DDAVP) Antifibrinolytic Medicines Vaccinations- hepatitis A and B. Gene Therapy Gene Therapy New Drugs for Hemophilia treatment New Drugs for Hemophilia treatment Bangladesh perspectives Bangladesh would have 10800 hemophiliacs. But, initially the patients does not concern about hemophilia. Patients are usually diagnosed only after bleeding episode and sometimes the episode are causes serious consequences. Conclusion Primary diagnosis with the success of gene therapy and availability of the new bioengineered products the prospect of the hemophiliacs will be brighter in near future.
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Hemophilia is a bleeding disorder that slows down the blood clotting process. People who have hemophilia often have longer bleeding after an injury or surgery. People who have severe hemophilia have spontaneous bleeding into the joints and muscles. Hemophilia occurs more commonly in males than in females.The two most common types of hemophilia are hemophilia A (also known as classic hemophilia) and hemophilia B (also known as Christmas disease). People who have hemophilia A have low levels of a blood clotting factor called factor eight (FVIII). People who have hemophilia B have low levels of factor nine (FIX). The two types of hemophilia are caused by permanent gene changes (mutations) in different genes. Mutations in the FVIII gene cause hemophilia A. Mutations in the FIX gene cause hemophilia B. Proteins made by these genes have an important role in the blood clotting process. Mutations in either gene keep clots from forming when there is an injury, causing too much bleeding that can be difficult to stop Hemophilia A is the most common type of this condition. One in 5,000 to 10,000 males worldwide have hemophilia A. Hemophilia B is less common, and it affects 1 in 20,000 to 34,500 males worldwide.
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Hemophilia is a genetic bleeding disorder in which body loses the ability to stop bleeding due to low levels or absence of proteins known as ‘’clotting factors’’ which are necessary for clotting of blood. Hemophilia leads to excessive bleeding.
Hemophilia : causes, symptoms, diagnosis and treatment
Hemophilia : causes, symptoms, diagnosis and treatment
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Hemophilia
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Myzak
Hemophilia is a common hereditary coagulation disorder due to deficiency or reduce activity of clotting factor VIII or clotting factor IX. This disorder is a X- linked recessive disorder. Types: Hemophilia A- deficiency of clotting factors VIII Hemophilia B- deficiency of clotting factors IX Hemophilia C- deficiency of clotting factors XI Parahaemophilia- deficiency of clotting factor V Causes of hemophilia Hemophilia has a sex-linked recessive inheritance. In most cases Hemophilia caused by a mutation in a gene that encodes for one of the clotting factors . Since the hemophilia gene is located on the X chromosome, Hemophilia usually occurs in males, and Female is the carrier of hemophilia. Diagnosis Complete blood cell count Coagulation studies FVIII assay Normal values for FVIII assays are 50-150%. Values in hemophilia are as follows: Mild: >5% Moderate: 1-5% Severe: <1% Treatment of Hemophilia Other Types of Treatment Desmopressin (DDAVP) Antifibrinolytic Medicines Vaccinations- hepatitis A and B. Gene Therapy Gene Therapy New Drugs for Hemophilia treatment New Drugs for Hemophilia treatment Bangladesh perspectives Bangladesh would have 10800 hemophiliacs. But, initially the patients does not concern about hemophilia. Patients are usually diagnosed only after bleeding episode and sometimes the episode are causes serious consequences. Conclusion Primary diagnosis with the success of gene therapy and availability of the new bioengineered products the prospect of the hemophiliacs will be brighter in near future.
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Hemophilia is a bleeding disorder that slows down the blood clotting process. People who have hemophilia often have longer bleeding after an injury or surgery. People who have severe hemophilia have spontaneous bleeding into the joints and muscles. Hemophilia occurs more commonly in males than in females.The two most common types of hemophilia are hemophilia A (also known as classic hemophilia) and hemophilia B (also known as Christmas disease). People who have hemophilia A have low levels of a blood clotting factor called factor eight (FVIII). People who have hemophilia B have low levels of factor nine (FIX). The two types of hemophilia are caused by permanent gene changes (mutations) in different genes. Mutations in the FVIII gene cause hemophilia A. Mutations in the FIX gene cause hemophilia B. Proteins made by these genes have an important role in the blood clotting process. Mutations in either gene keep clots from forming when there is an injury, causing too much bleeding that can be difficult to stop Hemophilia A is the most common type of this condition. One in 5,000 to 10,000 males worldwide have hemophilia A. Hemophilia B is less common, and it affects 1 in 20,000 to 34,500 males worldwide.
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Hemophilia is a rare disorder in which your blood doesn't clot normally because it lacks sufficient blood-clotting proteins (clotting factors). If you have hemophilia, you may bleed for a longer time after an injury than you would if your blood clotted normally. Small cuts usually aren't much of a problem.
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Dr. Faiza delivers an insightful lecture on the distinguishing characteristics of skeletal, smooth, and cardiac muscles, offering a comprehensive understanding of their histology, physiological anatomy, electrophysiological properties, and contractile mechanisms. Through meticulous tabulation and comparison, she aims to equip learners with a detailed comprehension of the unique features and functionalities of each muscle type. Beginning with a detailed exploration of histological differences, Dr. Faiza outlines key distinctions such as multinucleation in skeletal muscle, mononucleation in smooth and cardiac muscles, and the presence of striations in skeletal and cardiac muscles. She meticulously elucidates the structural arrangement of each muscle type, highlighting their cellular morphology and organization within tissues. Transitioning to physiological anatomy, Dr. Faiza navigates through various aspects including innervation, level of control, initiation of contraction, and modification by hormones. By delineating the role of the somatic nervous system in skeletal muscle control, and contrasting it with the autonomic nervous system's influence on smooth and cardiac muscles, she offers a nuanced understanding of neural regulation in muscle physiology. Furthermore, Dr. Faiza delves into electrophysiological properties, elucidating the mechanisms underlying action potential generation, duration, and ionic basis in each muscle type. Through insightful analysis, she reveals how differences in action potential characteristics contribute to variations in muscle contraction speed, duration, and resistance to fatigue. Finally, Dr. Faiza meticulously examines the contractile mechanisms of skeletal, smooth, and cardiac muscles, shedding light on the sliding filament theory, mechanisms of calcium action, and speed of contraction. By comprehensively comparing these mechanisms, she provides learners with a deep understanding of the intricate processes governing muscle contraction and function. Through engaging presentation and meticulous analysis, Dr. Faiza's lecture serves as a valuable resource for students seeking a thorough understanding of the fundamental differences between skeletal, smooth, and cardiac muscles.
Difference Between Skeletal Smooth and Cardiac Muscles
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MedicoseAcademics
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These are simplified slides discussing the regulation of cardiac output and venous return. Learning objectives: 1. Comprehend the determinants of cardiac output and factors affecting cardiac output 2. Comprehend the factors affecting stroke volume and heart rate and total peripheral resistance 3. Identify the factors regulating venous return 4. Discuss the causes of high and low output cardiac failure 5. Enlist the functions of veins and recognise the significance of venous reservoirs Study Resources: 1. Chapter 20, Guyton and Hall Textbook of Medical Physiology, 14th edition 2. Chapter 30 and 32, Ganong’s Review of Medical Physiology, 26th edition 3. Chapter 10, Human Physiology by Lauralee Sherwood, 9th edition 4. Physiology, Cardiac Output - StatPearls https://www.ncbi.nlm.nih.gov/books/NBK470455/
Cardiac Output, Venous Return, and Their Regulation
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In this lecture on circulatory shock, Dr. Faiza, an Assistant Professor of Physiology, delves into the profound implications of inadequate blood flow throughout the body, leading to tissue damage. The session begins by defining circulatory shock and elucidating its physiological causes, including decreased cardiac output, diminished blood volume, decreased vascular tone, obstruction to blood flow, excess metabolic rate, and abnormal perfusion patterns. Dr. Faiza categorizes shock into various types, such as cardiogenic shock, hypovolemic shock, neurogenic shock, obstructive shock, anaphylactic shock, and septic shock, and explores the pathophysiological basis of each. Furthermore, the lecture examines the stages of shock, from the non-progressive phase where compensatory mechanisms aim for full recovery to the progressive phase where shock worsens steadily without intervention, potentially leading to irreversible damage. Dr. Faiza discusses therapeutic interventions for shock, including replacement therapy, blood and plasma transfusion, sympathomimetic drugs, and other adjunctive treatments like head-down positioning, oxygen therapy, and glucocorticoids.
Circulatory Shock, types and stages, compensatory mechanisms
Circulatory Shock, types and stages, compensatory mechanisms
MedicoseAcademics
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