Hereditary spherocytosis HY
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Hereditary spherocytosis is an autosomal dominant condition typically seen in those of Northern European descent that causes hemolytic anemia, jaundice, and splenomegaly. Laboratory findings include increased mean corpuscular hemoglobin concentration, spherocytes on peripheral smear, and abnormal tests for red blood cell membrane stability like the acidified glycerol lysis test and eosin-5-maleimide binding test. Treatment involves folic acid, blood transfusions, and splenectomy.
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Haemolytic anemia pratyasha paripurna
Hemolytic anemia occurs when the destruction of red blood cells outpaces their production. It can develop intrinsically due to abnormalities in red blood cells, such as in sickle cell anemia or thalassemia. Or it can occur extrinsically due to infection, autoimmune disorders, medications or splenic sequestration of normal red blood cells. Symptoms include pallor, fatigue, jaundice and dark urine. Treatment depends on the underlying cause but may include blood transfusions, medications to suppress the immune system, splenectomy or stem cell transplant.
Role of peripheral blood
In the work-up of a disease, the peripheral smear gives a very good information of what disease the patient may be suffering from. It also gives direction for further evaluation, all impacting the treatment and well being of the patient.
Laboratory testing of spherocytic anaemia
Here are the answers to the MCQs:
1. a
2. D
3. d
4. b
5. a
6. a
7. b
8. b
9. a
10. b
Hereditary spherocytosis asif new
Hereditary spherocytosis is a genetically determined hemolytic anemia characterized by spherical shaped red blood cells (RBCs) due to defects in RBC membrane proteins. It is mainly caused by deficiencies in ankyrin that result in loss of lipid bilayer from the RBC membrane. This leads to extravascular hemolysis and severity depends on the specific gene mutation. Diagnosis is made through osmotic fragility testing of RBCs, examination of spherocytes on peripheral blood smear, and detection of membrane protein deficiencies using SDS-PAGE.
Hereditary spherocytosis asif new
Hereditary spherocytosis is a genetically determined hemolytic anemia characterized by spherical shaped red blood cells (RBCs) due to defects in RBC membrane proteins. It results from deficiencies in proteins like ankyrin that maintain the biconcave discoid shape of normal RBCs. This leads to premature destruction of RBCs in the spleen resulting in anemia, jaundice, and splenomegaly. The diagnosis is based on findings of spherocytes on peripheral blood smear, increased osmotic fragility of RBCs, and identification of membrane protein deficiencies using techniques like SDS-PAGE.
Hemolytic anemia 3
Hemolytic anemias are a group of disorders characterized by premature destruction of red blood cells exceeding the bone marrow's ability to produce new cells. They can be classified as hereditary or acquired, and involve intracorpuscular or extracorpuscular hemolysis. Common causes include abnormalities of red blood cell enzymes or membrane, autoimmune reactions, infections, and extrinsic factors like hypersplenism. Clinical manifestations vary but often include anemia, jaundice, and splenomegaly. Laboratory findings provide evidence of increased red blood cell destruction and bone marrow compensation. Membrane disorders like hereditary spherocytosis and elliptocytosis are caused by genetic defects affecting membrane proteins.
Blood film
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/evaluation-of-peripheral-blood-smear.html
Evaluation of the Peripheral Blood Smear
Haemolytic anaemia
Haemolytic anaemia is a disorder where red blood cells are destroyed faster than they can be replaced. It can be inherited or acquired. Inherited causes include defects in the red blood cell membrane like hereditary spherocytosis, defects in haemoglobin like sickle cell anaemia and thalassaemia, or metabolic defects. Acquired causes include immune haemolytic anaemia due to autoantibodies or drug reactions, or non-immune causes like paroxysmal nocturnal haemoglobinuria. Common symptoms include anaemia, jaundice, and enlargement of the spleen and liver.
Recommended
Haemolytic anemia pratyasha paripurna
Hemolytic anemia occurs when the destruction of red blood cells outpaces their production. It can develop intrinsically due to abnormalities in red blood cells, such as in sickle cell anemia or thalassemia. Or it can occur extrinsically due to infection, autoimmune disorders, medications or splenic sequestration of normal red blood cells. Symptoms include pallor, fatigue, jaundice and dark urine. Treatment depends on the underlying cause but may include blood transfusions, medications to suppress the immune system, splenectomy or stem cell transplant.
Role of peripheral blood
In the work-up of a disease, the peripheral smear gives a very good information of what disease the patient may be suffering from. It also gives direction for further evaluation, all impacting the treatment and well being of the patient.
Laboratory testing of spherocytic anaemia
Here are the answers to the MCQs:
1. a
2. D
3. d
4. b
5. a
6. a
7. b
8. b
9. a
10. b
Hereditary spherocytosis asif new
Hereditary spherocytosis is a genetically determined hemolytic anemia characterized by spherical shaped red blood cells (RBCs) due to defects in RBC membrane proteins. It is mainly caused by deficiencies in ankyrin that result in loss of lipid bilayer from the RBC membrane. This leads to extravascular hemolysis and severity depends on the specific gene mutation. Diagnosis is made through osmotic fragility testing of RBCs, examination of spherocytes on peripheral blood smear, and detection of membrane protein deficiencies using SDS-PAGE.
Hereditary spherocytosis asif new
Hereditary spherocytosis is a genetically determined hemolytic anemia characterized by spherical shaped red blood cells (RBCs) due to defects in RBC membrane proteins. It results from deficiencies in proteins like ankyrin that maintain the biconcave discoid shape of normal RBCs. This leads to premature destruction of RBCs in the spleen resulting in anemia, jaundice, and splenomegaly. The diagnosis is based on findings of spherocytes on peripheral blood smear, increased osmotic fragility of RBCs, and identification of membrane protein deficiencies using techniques like SDS-PAGE.
Hemolytic anemia 3
Hemolytic anemias are a group of disorders characterized by premature destruction of red blood cells exceeding the bone marrow's ability to produce new cells. They can be classified as hereditary or acquired, and involve intracorpuscular or extracorpuscular hemolysis. Common causes include abnormalities of red blood cell enzymes or membrane, autoimmune reactions, infections, and extrinsic factors like hypersplenism. Clinical manifestations vary but often include anemia, jaundice, and splenomegaly. Laboratory findings provide evidence of increased red blood cell destruction and bone marrow compensation. Membrane disorders like hereditary spherocytosis and elliptocytosis are caused by genetic defects affecting membrane proteins.
Blood film
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/evaluation-of-peripheral-blood-smear.html
Evaluation of the Peripheral Blood Smear
Haemolytic anaemia
Haemolytic anaemia is a disorder where red blood cells are destroyed faster than they can be replaced. It can be inherited or acquired. Inherited causes include defects in the red blood cell membrane like hereditary spherocytosis, defects in haemoglobin like sickle cell anaemia and thalassaemia, or metabolic defects. Acquired causes include immune haemolytic anaemia due to autoantibodies or drug reactions, or non-immune causes like paroxysmal nocturnal haemoglobinuria. Common symptoms include anaemia, jaundice, and enlargement of the spleen and liver.
Haemolytic anaemias
Haemolytic anaemias are a group of anemias caused by the premature breakdown of red blood cells in the bloodstream or spleen. There are two main types - intrinsic defects that cause red blood cell damage from within, such as hereditary spherocytosis, and extrinsic defects that cause damage from outside factors like immune mediated hemolysis. Symptoms include anemia, jaundice, splenomegaly and gallstones. Laboratory tests show signs of increased red blood cell breakdown like elevated bilirubin and LDH, as well as signs of the bone marrow attempting to compensate with reticulocytosis and nucleated red blood cells. Intravascular hemolysis specifically causes hemoglobinemia,
Spherocytes significance and differential diagnosis
This document discusses spherocytes, which are red blood cells that have lost their biconcavity and appear as densely stained spheres. Spherocytes can be caused by membrane defects or immune-mediated lysis of the membrane. The most common membrane defect is hereditary spherocytosis, which is caused by a genetic defect in membrane proteins. Immune-mediated hemolytic anemias that can cause spherocytosis include warm autoimmune hemolytic anemia and cold agglutinin disease. Laboratory tests shown to identify spherocytes include a peripheral smear, osmotic fragility testing, and Coombs testing to distinguish immune from non-immune causes.
Wbc & platelets anomalies
This document summarizes various anomalies seen in white blood cells (WBCs) and platelets. It describes several types of toxic granulation, Dohle bodies, hypersegmented neutrophils, and other abnormalities seen in neutrophils. It also discusses Barr bodies, degenerated neutrophils, vacuolated neutrophils, and giant neutrophils. Further, it provides information on Pelger-Huet anomaly, Chediak-Higashi syndrome, Alder-Reilly anomaly, May-Hegglin anomaly, and Auer rods. The document concludes by mentioning smudge or basket cells and platelet satellitism.
An Overview of Hemolytic anemia
This document summarizes different types of hemolytic anemias. It describes the features shared by hemolytic anemias such as a shortened red blood cell lifespan and increased erythropoiesis. Two main types of hemolysis are discussed: extravascular hemolysis where red blood cells are destroyed within macrophages, and intravascular hemolysis where they lyse within blood vessels. Specific causes of hemolysis are then outlined, including inherited disorders like hereditary spherocytosis and enzyme deficiencies like glucose-6-phosphate dehydrogenase deficiency. Features of acquired conditions like paroxysmal nocturnal hemoglobinuria and immune-mediated hemolytic anemias are also summarized.
Thalassemia
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lab work up for hemolytic anemia
This document discusses the workup and evaluation of hemolytic anemia. Common tests include a complete blood count, peripheral smear, LDH, haptoglobin, and indirect bilirubin. Changes in LDH and low haptoglobin are sensitive indicators of hemolysis. Hemolytic anemias can be hereditary or acquired. The workup depends on the suspected cause and may include hemoglobin electrophoresis, Coombs testing, and flow cytometry to identify the specific type of hemolytic anemia.
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4a..hemolytic anemia
This document discusses hematological disorders including hemolytic anemias and congenital red blood cell disorders. It provides details on laboratory tests used to evaluate anemias, such as a complete blood count, blood smear, and hemoglobin electrophoresis. Specific disorders covered include thalassemias, sickle cell disease, glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis, and hereditary elliptocytosis. The roles of decreased red blood cell production and increased red blood cell destruction in causing anemia are explained.
Hereditary spherocytosis
Hereditary spherocytosis is a genetically transmitted form of anemia where red blood cells are sphere-shaped rather than disk-shaped, making them prone to hemolysis. Symptoms include fatigue, pallor, jaundice, and in acute cases hypoxemia and hyperbilirubinemia. Diagnosis involves observing the lack of central pallor in red blood cells and increased fragility in hypotonic solutions. The condition is caused by defects in genes coding for membrane proteins, preventing red blood cells from maintaining their disk shape and surviving passage through the spleen. Treatment options include blood transfusions, folic acid supplementation, and splenectomy.
Hemolytic anaemias
This document provides an overview of hemolytic anemias, including definitions, causes, clinical features, investigations, and management. It discusses hereditary spherocytosis, elliptocytosis, sickle cell disease, thalassemia, enzyme deficiencies affecting red blood cells, and other structural defects and extracellular factors that can cause hemolysis. For each condition, it outlines the genetic basis, clinical presentation, investigations such as blood films and bone marrow aspirates, and potential complications.
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www.indiandentalacademy.com
Abnormal red blood cell morphologies
- Red blood cell morphology can provide clues to underlying diseases. Abnormalities include variation in size (anisocytosis), shape (poikilocytosis), color, and presence of inclusion bodies.
- Microcytosis and macrocytosis indicate abnormally small or large red blood cells, seen in iron deficiency, thalassemia, and liver/bone marrow diseases. Hypochromic cells appear pale due to low hemoglobin.
- Poikilocytosis describes variations in shape like elliptical, tear-drop, sickle, and fragmented (schistocyte) cells, associated with hemolytic anemias, thalassemia, and coagulation disorders. Inclusion bodies include Howell-J
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Dr. Akshay Shetty's presentation discusses sickle-cell anemia and thalassemias. It introduces sickle-cell anemia as resulting from a genetic mutation causing abnormal hemoglobin S production. The presentation covers the epidemiology and pathogenesis of sickle-cell anemia and discusses the clinical features and investigations. It then introduces thalassemias as disorders involving impaired globin chain production, describing alpha-thalassemia which involves alpha chain deletion and beta-thalassemia involving defective beta chain production. The objectives are to discuss sickle-cell anemia, thalassemias, their epidemiology, pathogenesis, clinical features and investigations.
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2. blood cells morphology
This document summarizes the morphology of different blood cells as seen on a blood film. It describes the components of blood including red blood cells, white blood cells such as neutrophils, lymphocytes, monocytes, eosinophils and basophils, as well as platelets. Examples of each cell type are shown along with descriptions of their distinguishing characteristics. Potential artefacts that can occur on blood films due to issues like improper fixation, heating or prolonged storage are also outlined.
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Hereditary spherocytosis is a hereditary hemolytic anemia caused by a red blood cell membrane defect that results in spherocytosis. The misshapen red blood cells, called spherocytes, are destroyed by the spleen, leading to hemolysis and a shortage of red blood cells. Clinical features include jaundice, splenomegaly, and gallstones. Laboratory findings show microspherocytes on peripheral blood film and increased reticulocytes, with normal red blood cell size.
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This document summarizes information about hemolytic anemias. It discusses intrinsic hemolytic anemias, which are due to red blood cell defects, and extrinsic hemolytic anemias, which are due to factors outside the red blood cell. Radioactive chromium survival studies can be used to measure red blood cell lifespan if hemolytic processes are mild or obscure. The document then describes various types of hereditary hemolytic anemias like hereditary spherocytosis, elliptocytosis, pyropoikilocytosis, stomatocytosis, and paroxysmal nocturnal hemoglobinuria. Diagnostic tests for these conditions like osmotic fragility testing and autohemolysis are also summarized.
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Haemolytic anaemias
Haemolytic anaemias are a group of anemias caused by the premature breakdown of red blood cells in the bloodstream or spleen. There are two main types - intrinsic defects that cause red blood cell damage from within, such as hereditary spherocytosis, and extrinsic defects that cause damage from outside factors like immune mediated hemolysis. Symptoms include anemia, jaundice, splenomegaly and gallstones. Laboratory tests show signs of increased red blood cell breakdown like elevated bilirubin and LDH, as well as signs of the bone marrow attempting to compensate with reticulocytosis and nucleated red blood cells. Intravascular hemolysis specifically causes hemoglobinemia,
Spherocytes significance and differential diagnosis
This document discusses spherocytes, which are red blood cells that have lost their biconcavity and appear as densely stained spheres. Spherocytes can be caused by membrane defects or immune-mediated lysis of the membrane. The most common membrane defect is hereditary spherocytosis, which is caused by a genetic defect in membrane proteins. Immune-mediated hemolytic anemias that can cause spherocytosis include warm autoimmune hemolytic anemia and cold agglutinin disease. Laboratory tests shown to identify spherocytes include a peripheral smear, osmotic fragility testing, and Coombs testing to distinguish immune from non-immune causes.
Wbc & platelets anomalies
This document summarizes various anomalies seen in white blood cells (WBCs) and platelets. It describes several types of toxic granulation, Dohle bodies, hypersegmented neutrophils, and other abnormalities seen in neutrophils. It also discusses Barr bodies, degenerated neutrophils, vacuolated neutrophils, and giant neutrophils. Further, it provides information on Pelger-Huet anomaly, Chediak-Higashi syndrome, Alder-Reilly anomaly, May-Hegglin anomaly, and Auer rods. The document concludes by mentioning smudge or basket cells and platelet satellitism.
An Overview of Hemolytic anemia
This document summarizes different types of hemolytic anemias. It describes the features shared by hemolytic anemias such as a shortened red blood cell lifespan and increased erythropoiesis. Two main types of hemolysis are discussed: extravascular hemolysis where red blood cells are destroyed within macrophages, and intravascular hemolysis where they lyse within blood vessels. Specific causes of hemolysis are then outlined, including inherited disorders like hereditary spherocytosis and enzyme deficiencies like glucose-6-phosphate dehydrogenase deficiency. Features of acquired conditions like paroxysmal nocturnal hemoglobinuria and immune-mediated hemolytic anemias are also summarized.
Thalassemia
Thalassemia is an inherited blood disorder caused by variants or missing genes that affect hemoglobin production. This results in reduced red blood cells and mild to severe anemia. There are two main types - alpha and beta thalassemia. Symptoms range from none in minor cases to severe anemia requiring transfusions in major cases. Investigations include blood tests to check hemoglobin levels, red blood cell size and count, and hemoglobin electrophoresis to confirm the diagnosis. Management focuses on blood transfusions and iron chelation therapy to prevent organ damage from excess iron.
lab work up for hemolytic anemia
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Wbc's disorders
This document summarizes different types of disorders of white blood cells (WBCs), including increased WBCs (leukocytosis) and decreased WBCs (leukopenia). It describes five main types of leukocytosis - neutrophilia, eosinophilia, basophilia, monocytosis, and lymphocytosis - and provides their definitions and common causes. It also discusses types of leukopenia such as neutropenia, eosinopenia, and lymphopenia, and outlines their typical causes and clinical manifestations.
4a..hemolytic anemia
This document discusses hematological disorders including hemolytic anemias and congenital red blood cell disorders. It provides details on laboratory tests used to evaluate anemias, such as a complete blood count, blood smear, and hemoglobin electrophoresis. Specific disorders covered include thalassemias, sickle cell disease, glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis, and hereditary elliptocytosis. The roles of decreased red blood cell production and increased red blood cell destruction in causing anemia are explained.
Hereditary spherocytosis
Hereditary spherocytosis is a genetically transmitted form of anemia where red blood cells are sphere-shaped rather than disk-shaped, making them prone to hemolysis. Symptoms include fatigue, pallor, jaundice, and in acute cases hypoxemia and hyperbilirubinemia. Diagnosis involves observing the lack of central pallor in red blood cells and increased fragility in hypotonic solutions. The condition is caused by defects in genes coding for membrane proteins, preventing red blood cells from maintaining their disk shape and surviving passage through the spleen. Treatment options include blood transfusions, folic acid supplementation, and splenectomy.
Hemolytic anaemias
This document provides an overview of hemolytic anemias, including definitions, causes, clinical features, investigations, and management. It discusses hereditary spherocytosis, elliptocytosis, sickle cell disease, thalassemia, enzyme deficiencies affecting red blood cells, and other structural defects and extracellular factors that can cause hemolysis. For each condition, it outlines the genetic basis, clinical presentation, investigations such as blood films and bone marrow aspirates, and potential complications.
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Abnormal red blood cell morphologies
- Red blood cell morphology can provide clues to underlying diseases. Abnormalities include variation in size (anisocytosis), shape (poikilocytosis), color, and presence of inclusion bodies.
- Microcytosis and macrocytosis indicate abnormally small or large red blood cells, seen in iron deficiency, thalassemia, and liver/bone marrow diseases. Hypochromic cells appear pale due to low hemoglobin.
- Poikilocytosis describes variations in shape like elliptical, tear-drop, sickle, and fragmented (schistocyte) cells, associated with hemolytic anemias, thalassemia, and coagulation disorders. Inclusion bodies include Howell-J
Sickle cell Anemia & thalassemia
Dr. Akshay Shetty's presentation discusses sickle-cell anemia and thalassemias. It introduces sickle-cell anemia as resulting from a genetic mutation causing abnormal hemoglobin S production. The presentation covers the epidemiology and pathogenesis of sickle-cell anemia and discusses the clinical features and investigations. It then introduces thalassemias as disorders involving impaired globin chain production, describing alpha-thalassemia which involves alpha chain deletion and beta-thalassemia involving defective beta chain production. The objectives are to discuss sickle-cell anemia, thalassemias, their epidemiology, pathogenesis, clinical features and investigations.
Hematology basics pt 1 jpg
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2. blood cells morphology
This document summarizes the morphology of different blood cells as seen on a blood film. It describes the components of blood including red blood cells, white blood cells such as neutrophils, lymphocytes, monocytes, eosinophils and basophils, as well as platelets. Examples of each cell type are shown along with descriptions of their distinguishing characteristics. Potential artefacts that can occur on blood films due to issues like improper fixation, heating or prolonged storage are also outlined.
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This document summarizes several hematological disorders including anemia, sickle cell anemia, and thalassemia. It discusses the origins and functions of blood, classifications of anemia, causes and symptoms of iron deficiency anemia, and treatments including oral iron therapy and blood transfusions. For sickle cell anemia, it covers alleles, pathophysiology, clinical features like vaso-occlusive crises, and treatments including pain management, oxygenation, and antibiotics. For thalassemia, it discusses decreased synthesis of hemoglobin chains, classifications, clinical features such as prominent facial bones and enlarged organs, diagnosis, and treatments including blood transfusions and iron chelation therapy.
Hemolytic anemia
Hereditary spherocytosis is a hereditary hemolytic anemia caused by a red blood cell membrane defect that results in spherocytosis. The misshapen red blood cells, called spherocytes, are destroyed by the spleen, leading to hemolysis and a shortage of red blood cells. Clinical features include jaundice, splenomegaly, and gallstones. Laboratory findings show microspherocytes on peripheral blood film and increased reticulocytes, with normal red blood cell size.
Thalassemia
Thalassemia is a genetic blood disorder caused by an imbalance in the synthesis of the globin chains that make up hemoglobin. There are three main types: alpha thalassemia affects alpha chain synthesis; beta thalassemia affects beta chain synthesis; and delta-beta thalassemia affects delta and beta chain synthesis. Treatment involves regular blood transfusions to provide healthy red blood cells, iron chelation therapy to remove excess iron from the body, and folic acid supplements to support red blood cell production. Future treatments may involve gene therapy by inserting a normal hemoglobin gene into stem cells.
Hematology
This document summarizes information about hemolytic anemias. It discusses intrinsic hemolytic anemias, which are due to red blood cell defects, and extrinsic hemolytic anemias, which are due to factors outside the red blood cell. Radioactive chromium survival studies can be used to measure red blood cell lifespan if hemolytic processes are mild or obscure. The document then describes various types of hereditary hemolytic anemias like hereditary spherocytosis, elliptocytosis, pyropoikilocytosis, stomatocytosis, and paroxysmal nocturnal hemoglobinuria. Diagnostic tests for these conditions like osmotic fragility testing and autohemolysis are also summarized.
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Lochia rubra lasts from birth to 3-4 days postpartum and consists of dark or bright red blood and clots. Lochia serosa lasts from days 4-10 or 14 and is pink or brown blood that gradually decreases. Lochia alba lasts from days 11-6 weeks and is white or yellow and light in quantity. Lochia may increase with breastfeeding or sloughing of the placental site scab around days 7-14.
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Noninvasive positive pressure ventilation (NPPV) is recommended for patients with severe COPD exacerbation, cardiogenic pulmonary edema, acute respiratory failure, postoperative hypoxemic respiratory failure, and immunosuppressed patients to facilitate early extubation. Contraindications for NPPV include medical instability such as cardiac or respiratory arrest, severe acidosis, acute respiratory distress syndrome, nonrespiratory organ failure, unstable cardiac arrhythmias or hemodynamic instability, encephalopathy, or gastrointestinal bleeding. Inability to protect the airway due to being uncooperative, agitated, or unable to clear secretions with a high aspiration risk are also contraindications. Mechanical issues like a recent esophageal anastomosis or
Management of endometriosis HY
This document provides guidance on managing endometriosis. It lists symptoms that could indicate suspected endometriosis such as chronic pelvic pain, painful periods, painful sex, and painful bowel movements. For patients with suspected endometriosis, the document recommends considering over-the-counter pain relievers and birth control pills initially, and performing a laparoscopy if symptoms do not improve or if there are concerns about infertility, medical contraindications, need for diagnosis, or potential malignancy.
Lung cancer HY
This document discusses the four main types of lung cancer: adenocarcinoma, squamous cell carcinoma, small cell carcinoma, and large cell carcinoma. It provides information on the incidence, typical location in the lungs, and common clinical associations for each type of lung cancer. Adenocarcinoma makes up 40-50% of lung cancers and is usually located in the periphery of the lungs. Squamous cell carcinoma accounts for 20-25% of cases and is typically central. Small cell carcinoma comprises 10-15% of lung cancers and is also usually central. Large cell carcinoma represents 5-10% of lung cancers and tends to be peripheral.
Leukocyte adhesion deficiency HY
Leukocyte adhesion deficiency is caused by a defect in CD18-containing integrins, which impairs leukocyte adhesion and endothelial transmigration. This results in recurrent skin and mucosal infections without pus formation, impaired wound healing, and delayed umbilical cord separation beyond 3 weeks of age. Laboratory findings include leukocytosis and neutrophilia.
Intrauterine fetal demise HY
Intrauterine fetal demise is defined as fetal death at 20 weeks or later. It is diagnosed by the absence of fetal cardiac activity on ultrasound. Management depends on gestational age - between 20-23 weeks dilation and evacuation or vaginal delivery is recommended, while at 24 weeks or later vaginal delivery is recommended, though cesarean delivery is an option based on maternal history. A complication can be coagulopathy if the fetus is retained for several weeks.
Infectious mononucleosis HY
Infectious mononucleosis is characterized by fever, tonsillitis or pharyngitis that may have exudates, enlarged lymph nodes in the neck, fatigue, and possibly enlargement of the liver and spleen. Complications can include airway obstruction, autoimmune conditions affecting red blood cells or platelets, and rupture of the spleen.
Indications for urgent dialysis (aeiou) HY
Acidosis, electrolyte abnormalities, ingestion of toxic substances, overload states, and uremia are indications for urgent dialysis according to the AEIOU mnemonic. Specifically, metabolic acidosis with a pH below 7.1, hyperkalemia causing ECG changes or arrhythmias, ingestion of toxic alcohols, volume overload refractory to diuretics, and uremia causing encephalopathy, pericarditis or bleeding require immediate dialysis treatment.
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