This document discusses disorders of osmoregulation and provides guidance on evaluating and managing patients with abnormalities in sodium balance and water homeostasis. It reviews key concepts such as calculating plasma osmolality, distinguishing types of polyuric states like diabetes insipidus, and developing a systematic approach to hyponatremia. Clinical cases are presented to demonstrate how to identify the etiology and determine appropriate treatment for conditions that cause hypo- and hypernatremia.
A 22-year-old male presented with jaundice, fatigue, and muscle pain for 6 months. Liver tests showed elevated bilirubin, AST, and prolonged PT/INR, suggesting a chronic liver disease. A 19-year-old female with history of chicken pox 8 months ago developed jaundice. Liver tests showed direct hyperbilirubinemia, elevated AST and markedly elevated ALP, indicating a cholestatic picture with ongoing activity. A 32-year-old alcoholic male with known cirrhosis showed mild elevation of AST and direct hyperbilirubinemia, with AST/ALT ratio of 3:1, consistent with alcoholic liver disease with ongoing activity.
An overview about approach to diagnosis of anemia for new learners. It is not all about approach to anemia, approach to anemia really needs a lot of knowledge about each groups of anemia such as microcytic, normocytic and macrocytic anemia.
Thalassemia is an inherited blood disorder caused by reduced or absent production of hemoglobin subunits (globin chains). There are two main types: alpha thalassemia involves a deficiency of alpha globin chains, while beta thalassemia involves a deficiency of beta globin chains. The severity of symptoms depends on how many globin genes are affected. Alpha thalassemia ranges from silent carrier state with no symptoms to hydrops fetalis, which is fatal if untreated.
Evaluation of liver function tests pptDhiraj Kumar
The document discusses liver function tests used to evaluate liver disease. It provides details on various tests including:
- Serum bilirubin, which detects liver cell damage and cholestasis. Elevated levels suggest viral or alcoholic hepatitis.
- Liver enzymes like ALT and AST reflect hepatocyte damage, while alkaline phosphatase, GGT, and 5'NT indicate cholestasis.
- Prothrombin time evaluates synthetic function and is a marker of severity in acute liver disease.
- Albumin reflects synthetic capacity but has a long half-life. Prealbumin and coagulation factors are more sensitive markers.
- Transient elastography can stage fibrosis non-invasively
The document discusses anemia, defining it as a hemoglobin level below 130g/L for men and 120g/L for women. Anemia is initially classified based on erythropoiesis, which involves EPO production, iron availability, bone marrow proliferative capacity, and red blood cell maturation. Causes of anemia include blood loss, hemolysis, bone marrow diseases, and deficiencies. Evaluation involves history, exam, blood tests of cell counts and indices, smear examination, iron studies, and bone marrow analysis. Treatment depends on the underlying cause.
Dynamic endocrine tests involve stimulating or suppressing hormonal axes to assess endocrine function. Dr. Sahana discusses several key dynamic tests, including:
1. The Insulin Tolerance Test which triggers GH and ACTH release to assess pituitary function.
2. The Synacthen Test which uses ACTH to assess adrenal response and diagnose adrenal insufficiency.
3. Growth Hormone stimulation tests like the Insulin Tolerance Test which provoke GH release to diagnose growth hormone deficiency.
4. The Water Deprivation Test which restricts fluid intake to raise osmolality and assess ADH response, diagnosing diabetes insipidus.
This document discusses anemia and iron deficiency anemia. It defines anemia as a low level of hemoglobin and classifies it as mild, moderate, or severe based on hemoglobin levels. Iron deficiency anemia is described as the most common type worldwide, caused by too little iron in the body. Symptoms, causes like blood loss or poor diet, diagnostic tests, and iron metabolism are summarized. Iron is stored in the liver and spleen and transported by transferrin to support erythropoiesis when needed.
A 22-year-old male presented with jaundice, fatigue, and muscle pain for 6 months. Liver tests showed elevated bilirubin, AST, and prolonged PT/INR, suggesting a chronic liver disease. A 19-year-old female with history of chicken pox 8 months ago developed jaundice. Liver tests showed direct hyperbilirubinemia, elevated AST and markedly elevated ALP, indicating a cholestatic picture with ongoing activity. A 32-year-old alcoholic male with known cirrhosis showed mild elevation of AST and direct hyperbilirubinemia, with AST/ALT ratio of 3:1, consistent with alcoholic liver disease with ongoing activity.
An overview about approach to diagnosis of anemia for new learners. It is not all about approach to anemia, approach to anemia really needs a lot of knowledge about each groups of anemia such as microcytic, normocytic and macrocytic anemia.
Thalassemia is an inherited blood disorder caused by reduced or absent production of hemoglobin subunits (globin chains). There are two main types: alpha thalassemia involves a deficiency of alpha globin chains, while beta thalassemia involves a deficiency of beta globin chains. The severity of symptoms depends on how many globin genes are affected. Alpha thalassemia ranges from silent carrier state with no symptoms to hydrops fetalis, which is fatal if untreated.
Evaluation of liver function tests pptDhiraj Kumar
The document discusses liver function tests used to evaluate liver disease. It provides details on various tests including:
- Serum bilirubin, which detects liver cell damage and cholestasis. Elevated levels suggest viral or alcoholic hepatitis.
- Liver enzymes like ALT and AST reflect hepatocyte damage, while alkaline phosphatase, GGT, and 5'NT indicate cholestasis.
- Prothrombin time evaluates synthetic function and is a marker of severity in acute liver disease.
- Albumin reflects synthetic capacity but has a long half-life. Prealbumin and coagulation factors are more sensitive markers.
- Transient elastography can stage fibrosis non-invasively
The document discusses anemia, defining it as a hemoglobin level below 130g/L for men and 120g/L for women. Anemia is initially classified based on erythropoiesis, which involves EPO production, iron availability, bone marrow proliferative capacity, and red blood cell maturation. Causes of anemia include blood loss, hemolysis, bone marrow diseases, and deficiencies. Evaluation involves history, exam, blood tests of cell counts and indices, smear examination, iron studies, and bone marrow analysis. Treatment depends on the underlying cause.
Dynamic endocrine tests involve stimulating or suppressing hormonal axes to assess endocrine function. Dr. Sahana discusses several key dynamic tests, including:
1. The Insulin Tolerance Test which triggers GH and ACTH release to assess pituitary function.
2. The Synacthen Test which uses ACTH to assess adrenal response and diagnose adrenal insufficiency.
3. Growth Hormone stimulation tests like the Insulin Tolerance Test which provoke GH release to diagnose growth hormone deficiency.
4. The Water Deprivation Test which restricts fluid intake to raise osmolality and assess ADH response, diagnosing diabetes insipidus.
This document discusses anemia and iron deficiency anemia. It defines anemia as a low level of hemoglobin and classifies it as mild, moderate, or severe based on hemoglobin levels. Iron deficiency anemia is described as the most common type worldwide, caused by too little iron in the body. Symptoms, causes like blood loss or poor diet, diagnostic tests, and iron metabolism are summarized. Iron is stored in the liver and spleen and transported by transferrin to support erythropoiesis when needed.
Hereditary hemochromatosis, also known as Celtic Curse or Bronze Diabetes, is an autosomal recessive genetic disorder characterized by abnormal iron accumulation in organs. It is most commonly caused by mutations in the HFE gene and results in increased intestinal iron absorption. Symptoms include liver disease, arthritis, diabetes, skin pigmentation changes and heart/endocrine issues. Diagnosis involves blood tests showing elevated iron levels. Treatment is regular phlebotomy to reduce iron stores to normal levels and prevent organ damage. Screening of at-risk family members allows early detection before complications arise.
This document provides an overview of how to approach and evaluate anemia. It begins by defining anemia and describing a complete blood count. It then discusses evaluating the size, hemoglobin content, and distribution of red blood cells to classify anemia as microcytic, normocytic, or macrocytic. For each type of anemia, the document lists potential causes and recommends further tests. It also covers evaluating reticulocyte count, peripheral smear, and bone marrow biopsy findings to determine if anemia is caused by blood loss, increased destruction, or decreased production of red blood cells. The goal is to systematically narrow down the cause of anemia through a series of blood tests and examinations.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Basic approach on short stature in childrenAzad Haleem
This document provides an overview of short stature, including definitions, types, diagnostic principles, causes, and management. It defines short stature as height below the 3rd percentile and discusses types such as familial short stature. Diagnosis involves accurate height measurements, bone age assessment, mid-parental height comparison, and medical investigations. Causes include growth hormone deficiency, Turner syndrome, and small size at birth. Management consists of dietary counseling, growth hormone injections, and limb lengthening procedures depending on the underlying cause.
This document discusses the pathogenesis and laboratory diagnosis of sickle cell anemia and thalassemia. It describes how abnormal red blood cells are destroyed in the spleen, releasing hemoglobin. The heme portion of hemoglobin is broken down into bilirubin and stored iron, while the globin portion is recycled to amino acids. This leads to anemia. Specific tests are used to diagnose these conditions based on abnormal hemoglobin levels, types or variants seen on electrophoresis or peripheral smears. Genetic testing can also identify mutations that cause these hemolytic anemias.
This document discusses renal tubular acidosis (RTA). It defines RTA as a metabolic acidosis with a normal anion gap due to bicarbonate loss in the setting of normal kidney function. It describes the different types of RTA, including proximal (type II) RTA which is caused by impaired bicarbonate reabsorption in the proximal convoluted tubule. Cystinosis, an inherited disorder, is mentioned as a common cause of proximal RTA. Clinical features, diagnosis, and management of proximal RTA and cystinosis are covered.
- 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.
This document provides an overview of evaluating and diagnosing liver disease. It discusses classifying liver diseases as hepatocellular, cholestatic, or mixed based on etiology and evaluating disease severity and stage. Common symptoms, diagnostic tests, clinical findings, and classifications such as Child-Pugh staging for cirrhosis are outlined.
This document discusses laboratory tests for serum iron, total iron binding capacity (TIBC), transferrin, ferritin, vitamin B12 and serum folate. It provides objectives, principles, methodologies, normal ranges and limitations for each test. The tests are useful in diagnosing iron deficiency anemia and vitamin deficiencies. Sample collection and handling factors that could impact results are also outlined.
Sodium homeostasis and the regulation of serum sodium concentration is essential for normal physiological functioning. Hyponatremia occurs when there is a relative excess of water compared to sodium, decreasing the plasma sodium concentration below 135 mmol/L. It can be hypo-osmolar, euvolemic, or hypervolemic depending on water and sodium levels. Treatment involves correcting the underlying cause, restricting water intake, and sometimes using hypertonic saline or vaptans. Rapid correction of sodium levels can have neurological consequences, so changes should be gradual. Hypernatremia is less common but also dangerous, defined as a sodium level over 145 mmol/L.
This document defines megaloblastic anemia, its causes from vitamin B12 or folate deficiency, and symptoms. Vitamin B12 deficiency can result from pernicious anemia where antibodies block absorption in the stomach and small intestine. It may also be caused by other conditions affecting absorption like gastric surgery or diseases. Left untreated, B12 deficiency can cause neurological issues like numbness, weakness, and problems with memory and walking. Treatment involves replacing the deficient vitamins through supplements.
This document discusses folic acid and vitamin B12, including their structure, dietary sources, absorption, metabolism, recommended daily allowances, deficiencies, clinical manifestations, laboratory assessments, and toxicity. Folic acid and vitamin B12 play important roles in one carbon metabolism and the synthesis of DNA, RNA, and proteins. Deficiencies can cause megaloblastic anemia and neurological issues. Testing includes serum levels of cobalamin, methylmalonic acid, and homocysteine. Treatment involves vitamin supplementation and dietary changes.
Dr. Arun Karmakar presented on hyponatremia. Hyponatremia is defined as a serum sodium below 135 mmol/L and is the most common electrolyte disorder. It is clinically important because acute severe hyponatremia can cause morbidity and mortality, and outcomes are worse in hyponatremic patients with underlying diseases. Hyponatremia can be hypovolemic, euvolemic, or hypervolemic depending on water and sodium levels. Treatment depends on the severity and cause of hyponatremia, with aggressive correction for symptomatic cases and slower correction for chronic cases to avoid osmotic demyelination syndrome.
This document discusses calcium homeostasis and hypercalcemia. It explains that blood calcium levels are tightly regulated by the parathyroid hormone (PTH), vitamin D, gut, bone and kidneys. The main causes of hypercalcemia are primary hyperparathyroidism, malignancy-related hypercalcemia from bone metastases, and hypervitaminosis D from excessive vitamin D intake or production. The document provides details on the pathophysiology, clinical evaluation and management of hypercalcemia.
billirubin production billirubin transport and metabolism, different laboratory methods of billirubin estimation ,normal and abnormal levels of billirubin, different classification and types of jaundice and liver diseses, liver functioning, enterohepatic circulation, billirubin production and degradation, benefits and diseases of abnormal level of billirubin
This document summarizes several glycogen storage diseases and lysosomal storage diseases. For glycogen storage diseases, it lists the enzyme deficiency, symptoms such as hypoglycemia and hepatomegaly, and mnemonics to remember each disease. For lysosomal storage diseases, it provides the deficient enzyme, accumulated substrate, inheritance pattern, and key findings for each condition. It concludes by highlighting some distinguishing features between similar diseases, such as neurological symptoms in Niemann-Pick versus Gaucher's, and differences between Hunter's and Hurler's syndromes.
This document discusses methods for assessing renal function and damage, including estimated glomerular filtration rate (eGFR) and albuminuria. It describes the functions of the nephron including filtration, reabsorption, and secretion. Endogenous and exogenous markers for measuring GFR are discussed, along with the limitations of creatinine as an endogenous marker. Different formulas for estimating GFR, such as Cockcroft-Gault, MDRD, and CKD-EPI, are summarized along with their derivation populations. The performance of estimating equations compared to direct measurement of GFR is also reviewed.
This document discusses hemolytic anemia and focuses on sickle cell disease. It defines hemolytic anemia as increased destruction of red blood cells outside the bone marrow. Key diagnostic findings include increased reticulocyte count, hyperbilirubinemia, decreased haptoglobin, and increased lactate dehydrogenase. Hemolytic anemias are classified as hereditary defects within red blood cells or acquired external causes. Sickle cell disease results from a hereditary hemoglobinopathy and causes chronic hemolytic anemia. Complications include infections, acute chest syndrome, stroke, leg ulcers, splenic sequestration, and retinopathy. Diagnosis is made by finding sickle cells on peripheral smear and abnormal hem
Hypernatremia is defined as a serum sodium level above 145 mmol/L. It can be caused by excessive sodium intake, decreased water intake, or increased water loss through renal or non-renal routes. Signs and symptoms range from tremulousness and irritability to coma. Treatment involves slow correction of extracellular fluid volume and hypertonicity by oral or IV administration of water, with the rate of sodium level correction not exceeding 1 mmol/L per hour to avoid cerebral edema. The underlying cause, such as central diabetes insipidus, nephrogenic diabetes insipidus, or salt excess/gain must also be treated.
The document discusses disorders of water and electrolyte metabolism. It covers homeostasis of water and electrolytes, common electrolyte imbalances seen in disease, and key mechanisms that regulate fluid and electrolyte balance in the body, including thirst, antidiuretic hormone, aldosterone, and osmoreceptors.
Hereditary hemochromatosis, also known as Celtic Curse or Bronze Diabetes, is an autosomal recessive genetic disorder characterized by abnormal iron accumulation in organs. It is most commonly caused by mutations in the HFE gene and results in increased intestinal iron absorption. Symptoms include liver disease, arthritis, diabetes, skin pigmentation changes and heart/endocrine issues. Diagnosis involves blood tests showing elevated iron levels. Treatment is regular phlebotomy to reduce iron stores to normal levels and prevent organ damage. Screening of at-risk family members allows early detection before complications arise.
This document provides an overview of how to approach and evaluate anemia. It begins by defining anemia and describing a complete blood count. It then discusses evaluating the size, hemoglobin content, and distribution of red blood cells to classify anemia as microcytic, normocytic, or macrocytic. For each type of anemia, the document lists potential causes and recommends further tests. It also covers evaluating reticulocyte count, peripheral smear, and bone marrow biopsy findings to determine if anemia is caused by blood loss, increased destruction, or decreased production of red blood cells. The goal is to systematically narrow down the cause of anemia through a series of blood tests and examinations.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Basic approach on short stature in childrenAzad Haleem
This document provides an overview of short stature, including definitions, types, diagnostic principles, causes, and management. It defines short stature as height below the 3rd percentile and discusses types such as familial short stature. Diagnosis involves accurate height measurements, bone age assessment, mid-parental height comparison, and medical investigations. Causes include growth hormone deficiency, Turner syndrome, and small size at birth. Management consists of dietary counseling, growth hormone injections, and limb lengthening procedures depending on the underlying cause.
This document discusses the pathogenesis and laboratory diagnosis of sickle cell anemia and thalassemia. It describes how abnormal red blood cells are destroyed in the spleen, releasing hemoglobin. The heme portion of hemoglobin is broken down into bilirubin and stored iron, while the globin portion is recycled to amino acids. This leads to anemia. Specific tests are used to diagnose these conditions based on abnormal hemoglobin levels, types or variants seen on electrophoresis or peripheral smears. Genetic testing can also identify mutations that cause these hemolytic anemias.
This document discusses renal tubular acidosis (RTA). It defines RTA as a metabolic acidosis with a normal anion gap due to bicarbonate loss in the setting of normal kidney function. It describes the different types of RTA, including proximal (type II) RTA which is caused by impaired bicarbonate reabsorption in the proximal convoluted tubule. Cystinosis, an inherited disorder, is mentioned as a common cause of proximal RTA. Clinical features, diagnosis, and management of proximal RTA and cystinosis are covered.
- 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.
This document provides an overview of evaluating and diagnosing liver disease. It discusses classifying liver diseases as hepatocellular, cholestatic, or mixed based on etiology and evaluating disease severity and stage. Common symptoms, diagnostic tests, clinical findings, and classifications such as Child-Pugh staging for cirrhosis are outlined.
This document discusses laboratory tests for serum iron, total iron binding capacity (TIBC), transferrin, ferritin, vitamin B12 and serum folate. It provides objectives, principles, methodologies, normal ranges and limitations for each test. The tests are useful in diagnosing iron deficiency anemia and vitamin deficiencies. Sample collection and handling factors that could impact results are also outlined.
Sodium homeostasis and the regulation of serum sodium concentration is essential for normal physiological functioning. Hyponatremia occurs when there is a relative excess of water compared to sodium, decreasing the plasma sodium concentration below 135 mmol/L. It can be hypo-osmolar, euvolemic, or hypervolemic depending on water and sodium levels. Treatment involves correcting the underlying cause, restricting water intake, and sometimes using hypertonic saline or vaptans. Rapid correction of sodium levels can have neurological consequences, so changes should be gradual. Hypernatremia is less common but also dangerous, defined as a sodium level over 145 mmol/L.
This document defines megaloblastic anemia, its causes from vitamin B12 or folate deficiency, and symptoms. Vitamin B12 deficiency can result from pernicious anemia where antibodies block absorption in the stomach and small intestine. It may also be caused by other conditions affecting absorption like gastric surgery or diseases. Left untreated, B12 deficiency can cause neurological issues like numbness, weakness, and problems with memory and walking. Treatment involves replacing the deficient vitamins through supplements.
This document discusses folic acid and vitamin B12, including their structure, dietary sources, absorption, metabolism, recommended daily allowances, deficiencies, clinical manifestations, laboratory assessments, and toxicity. Folic acid and vitamin B12 play important roles in one carbon metabolism and the synthesis of DNA, RNA, and proteins. Deficiencies can cause megaloblastic anemia and neurological issues. Testing includes serum levels of cobalamin, methylmalonic acid, and homocysteine. Treatment involves vitamin supplementation and dietary changes.
Dr. Arun Karmakar presented on hyponatremia. Hyponatremia is defined as a serum sodium below 135 mmol/L and is the most common electrolyte disorder. It is clinically important because acute severe hyponatremia can cause morbidity and mortality, and outcomes are worse in hyponatremic patients with underlying diseases. Hyponatremia can be hypovolemic, euvolemic, or hypervolemic depending on water and sodium levels. Treatment depends on the severity and cause of hyponatremia, with aggressive correction for symptomatic cases and slower correction for chronic cases to avoid osmotic demyelination syndrome.
This document discusses calcium homeostasis and hypercalcemia. It explains that blood calcium levels are tightly regulated by the parathyroid hormone (PTH), vitamin D, gut, bone and kidneys. The main causes of hypercalcemia are primary hyperparathyroidism, malignancy-related hypercalcemia from bone metastases, and hypervitaminosis D from excessive vitamin D intake or production. The document provides details on the pathophysiology, clinical evaluation and management of hypercalcemia.
billirubin production billirubin transport and metabolism, different laboratory methods of billirubin estimation ,normal and abnormal levels of billirubin, different classification and types of jaundice and liver diseses, liver functioning, enterohepatic circulation, billirubin production and degradation, benefits and diseases of abnormal level of billirubin
This document summarizes several glycogen storage diseases and lysosomal storage diseases. For glycogen storage diseases, it lists the enzyme deficiency, symptoms such as hypoglycemia and hepatomegaly, and mnemonics to remember each disease. For lysosomal storage diseases, it provides the deficient enzyme, accumulated substrate, inheritance pattern, and key findings for each condition. It concludes by highlighting some distinguishing features between similar diseases, such as neurological symptoms in Niemann-Pick versus Gaucher's, and differences between Hunter's and Hurler's syndromes.
This document discusses methods for assessing renal function and damage, including estimated glomerular filtration rate (eGFR) and albuminuria. It describes the functions of the nephron including filtration, reabsorption, and secretion. Endogenous and exogenous markers for measuring GFR are discussed, along with the limitations of creatinine as an endogenous marker. Different formulas for estimating GFR, such as Cockcroft-Gault, MDRD, and CKD-EPI, are summarized along with their derivation populations. The performance of estimating equations compared to direct measurement of GFR is also reviewed.
This document discusses hemolytic anemia and focuses on sickle cell disease. It defines hemolytic anemia as increased destruction of red blood cells outside the bone marrow. Key diagnostic findings include increased reticulocyte count, hyperbilirubinemia, decreased haptoglobin, and increased lactate dehydrogenase. Hemolytic anemias are classified as hereditary defects within red blood cells or acquired external causes. Sickle cell disease results from a hereditary hemoglobinopathy and causes chronic hemolytic anemia. Complications include infections, acute chest syndrome, stroke, leg ulcers, splenic sequestration, and retinopathy. Diagnosis is made by finding sickle cells on peripheral smear and abnormal hem
Hypernatremia is defined as a serum sodium level above 145 mmol/L. It can be caused by excessive sodium intake, decreased water intake, or increased water loss through renal or non-renal routes. Signs and symptoms range from tremulousness and irritability to coma. Treatment involves slow correction of extracellular fluid volume and hypertonicity by oral or IV administration of water, with the rate of sodium level correction not exceeding 1 mmol/L per hour to avoid cerebral edema. The underlying cause, such as central diabetes insipidus, nephrogenic diabetes insipidus, or salt excess/gain must also be treated.
The document discusses disorders of water and electrolyte metabolism. It covers homeostasis of water and electrolytes, common electrolyte imbalances seen in disease, and key mechanisms that regulate fluid and electrolyte balance in the body, including thirst, antidiuretic hormone, aldosterone, and osmoreceptors.
Hyponatremia is a condition where the blood sodium level is abnormally low, below 135 mEq/L. It occurs when sodium levels in fluids outside cells drop, causing cells to swell with too much water. The main cause is syndrome of inappropriate antidiuretic hormone (SIADH), where excess antidiuretic hormone causes the body to retain too much water. SIADH can be caused by conditions like meningitis, encephalitis, brain tumors, or medications. Symptoms include nausea, vomiting, confusion and seizures. Diagnosis involves blood tests measuring sodium, potassium, chloride and osmolality levels. Treatment focuses on fluid restriction or medications to inhibit antidiuretic hormone.
This document provides information about sodium and its effects on health. It begins by defining sodium and where it is commonly found in foods, especially processed foods where it is often added to preserve or enhance flavor. It then discusses the roles of sodium in the body, such as regulating blood pressure and fluid balance. The document recommends a daily sodium intake of less than 2,300mg and identifies high-risk groups like those with kidney disease. It concludes by offering tips to reduce sodium intake through food choices and preparation.
Manejo de la hiponatremia e hipocaliemia en elResidentes1hun
Este documento resume la fisiopatología, diagnóstico y tratamiento de la hiponatremia e hipocaliemia. Define estas condiciones como sodio sérico <130 mmol/L y potasio sérico <3.6 mmol/L respectivamente. Explica su importancia clínica y las causas más comunes. Describe las complicaciones neurológicas y cardíacas potenciales y los cambios electrocardiográficos. Finalmente, resume las estrategias de tratamiento agudo y crónico para corregir los déficits de electrolitos de man
This document discusses hypernatremia, which is defined as a serum sodium level exceeding 145 mEq/liter. Sodium levels are normally regulated by ADH and the thirst mechanism, but hypernatremia can occur when there is a loss of hypotonic fluid and impaired access to water, such as in infants, elderly patients, or those who are unconscious. This leads to cellular dehydration and neurological issues if sodium levels rise too high. Causes include excessive sodium intake, water loss from vomiting/diarrhea, and certain drugs. Signs may include thirst, lethargy, seizures, or coma depending on the severity. The diagnosis involves checking serum and urine osmolality and electrolyte levels.
This document discusses hyponatremia, defined as a plasma sodium concentration less than 135mM. Hyponatremia is common, occurring in up to 22% of hospitalized patients and 15% of general admissions. It can be associated with poor outcomes if left untreated. The mechanism is usually an increase in arginine vasopressin leading to water retention. Causes include SIADH, heart failure, liver cirrhosis, and use of certain drugs. Treatment involves restricting water intake, replacing sodium deficits, and treating the underlying cause. Rapid correction of sodium levels should be avoided to prevent neurological complications.
This patient presented with altered mental status and hypernatremia. Initial workup found a serum sodium of 151 mEq/L, urine sodium of 20 mEq/L, and a urine osmolality less than 1%. A water deprivation test confirmed the diagnosis of central diabetes insipidus, as the patient continued to produce dilute urine despite becoming hypernatremic and hyperosmolar. Central diabetes insipidus was likely caused by damage to the hypothalamus preventing adequate release of antidiuretic hormone.
Hypernatremia is defined as a plasma sodium concentration >145 mEq/L. It is usually caused by a water deficit rather than sodium gain. Common causes include impaired thirst, diarrhea, insensible losses from fever/ventilation, and renal losses from osmotic diuresis or diabetes insipidus. Symptoms range from none in chronic cases to neurologic issues like altered mental status. Treatment involves gradually correcting the sodium level by about 10-12 mEq/L/day using oral or IV water while monitoring for complications like cerebral edema. Replacing volume deficits and identifying underlying causes are also important.
Sodium and Potassium Homeostasis in NeonatesKing_maged
This document discusses sodium and potassium homeostasis and management in infants. It covers sodium requirements, causes and treatment of hyponatremia and hypernatremia. It also discusses potassium requirements and causes and treatment of hypokalemia and hyperkalemia. Key points include maintaining serum sodium between 135-145 mEq/L, restricting free water intake to treat dilutional hyponatremia, and slowly correcting chronic hypernatremia to avoid brain edema. The document also outlines serum potassium goals and risks of rapid changes in potassium levels.
This document discusses sodium metabolism and disorders of sodium balance. It covers:
- Physiology of sodium distribution and regulation in the body
- Mechanisms of sodium regulation in the kidneys, including reabsorption along the nephron and role of hormones like aldosterone and ANP
- Causes, evaluation, and treatment of hyponatremia and hypernatremia, including use of fluid restriction and hypertonic saline. Chronic asymptomatic hyponatremia is usually treated conservatively while more severe or symptomatic cases require rapid correction.
The document discusses atrio-ventricular (AV) block, which refers to delays or interruptions in the conduction pathway between the atria and ventricles of the heart. There are several types of AV block defined by the degree of conduction block, including first-degree, second-degree Mobitz types I and II, and third-degree AV block. The causes, ECG characteristics, and descriptions of each type of AV block are provided. The document emphasizes practicing ECG interpretation to determine the type of cardiac dysrhythmia.
Caso clinico Medicina Interna sesion general 15 mayo 2014Ricardo Mora MD
Caso clinico Medicina Interna, Sesion General, HGZ 06 IMSS Ciudad Juarez, Chihuahua; 15/Mayo/2014; para ver y revisar dicha presentación solo es necesario la utilizacion del mouse, NO USAR LAS FLECHAS, ESPACIO U OTRA FORMA PARA AVANZAR EN LAS DIAPOSITIVAS, ya que la presentación cuenta con vinculos, podra avanzar y regresar utilizando el icono inicio o bien la "casita", cualquier duda o sugerencia mandar un msj, saludos!
Este documento trata sobre la hiponatremia en pediatría. Explica la fisiopatología, causas, diagnóstico y tratamiento de la hiponatremia. Describe las diferentes causas de hiponatremia como hipovolémica, euvolémica e hipervolémica. Explica que el tratamiento depende de si es aguda o crónica, sintomática o asintomática, y del estado de volumen. La corrección debe hacerse lentamente para evitar la mielinolisis osmótica.
This document discusses the definition, diagnosis, complications, and treatment of myocardial infarction. Some key points include:
- Myocardial infarction is defined as myocardial necrosis due to ischemia that is detected by elevated cardiac biomarkers and clinical signs.
- Common complications include arrhythmias, mechanical issues like septal rupture, heart failure, and reinfarction. Electrical complications are usually treated with medications while mechanical issues often require surgery.
- Proper rehabilitation and long-term follow-up is important to monitor for complications in post-infarction patients. Anticipating complications can help ensure early detection and management.
El documento proporciona información sobre el balance hidroelectrolítico. Explica los ingresos y egresos de agua, sodio, potasio y cloro en el cuerpo, así como las causas y tratamiento de la hiponatremia hipotónica. También describe los efectos de la hiponatremia en el cerebro y las respuestas adaptativas, así como las consideraciones para la corrección de este trastorno electrolítico.
Traumatismo craneoencefálico grave en pediatriaDavid Barreto
Este documento describe el manejo del traumatismo craneoencefálico grave en niños y adolescentes. Explica que este tipo de traumatismo ocurre cuando la escala de coma de Glasgow es de 8 o menor después de la reanimación. Describe las causas más comunes, el manejo en urgencias pediátricas incluyendo el monitoreo, la vía aérea, el estado cardiovascular y la reanimación con líquidos. También cubre procedimientos como la osteoclisis para obtener acceso intravenoso cuando no es posible por vía periférica.
GMEC - Fluid and Electrolyte Imbalances in Emergency NursingOpen.Michigan
This document provides an overview of fluid and electrolyte imbalances in emergency nursing, focusing on sodium imbalances. It defines electrolytes and explains their importance in bodily functions. Reasons for electrolyte imbalances include kidney dysfunction, dehydration, diarrhea, and medication side effects. The document discusses sodium in detail, including its normal levels, foods high in sodium, and causes and signs of hyponatremia (low sodium). It explains that hyponatremia can be hypovolemic, euvolemic, or hypervolemic, and provides examples of signs and symptoms for hypovolemic and hypervolemic hyponatremia.
Slideshow is from the University of Michigan Medical School's M2 Endocrine sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Endo
09.30.08(a): Physiology of Water MetabolismOpen.Michigan
Slideshow is from the University of Michigan Medical School's M2 Renal sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Renal
This document provides an overview of fluid and electrolyte imbalance. It defines key terms related to fluid balance and distribution in the body. It describes the regulation of fluid balance through hormones like aldosterone and ADH. Common fluid and electrolyte abnormalities are explained such as dehydration, edema, and various electrolyte imbalances. Treatment approaches are briefly outlined. Overall, the document serves as an introductory seminar covering the basics of fluid and electrolyte balance and potential imbalances in the human body.
Seminar on fluid and electrolyte imbalanceaneez103
This document provides an overview of fluid and electrolyte balance and imbalance. It defines key terms related to fluids, electrolytes, and body composition. It describes the normal regulation of fluids and electrolytes in the body, including through passive and active transport mechanisms, hormones, and the sensation of thirst. It then discusses various abnormalities in fluid and electrolyte balance that can occur, including deficits, excesses, and shifts of extracellular fluid as well as various electrolyte imbalances.
This document discusses fluid and electrolyte imbalances. It begins by outlining how water enters and leaves the body, and the mechanisms that maintain homeostasis of total fluid and electrolyte volume, including the endocrine, gastrointestinal, renal, and nervous systems. It then discusses fluid volume deficit/hypovolemia and excess/hypervolemia, their causes and nursing considerations. Next, it covers sodium, potassium, chloride, and calcium imbalances, outlining the normal levels and causes of deficits and excesses for each electrolyte. Nursing interventions are provided for managing various electrolyte imbalances.
Hyponatremia is very common in critically ill children, occurring in 20-45% of PICU admissions. It is usually caused by impaired free water excretion leading to dilutional hyponatremia from water retention and intake of hypotonic fluids. Other potential causes include inappropriate vasopressin secretion, redistribution of sodium and water in conditions like sepsis, use of hypotonic intravenous fluids, and underlying illnesses or medications. The diagnosis involves measuring plasma and urine osmolality and sodium levels, and clinically assessing volume status, to determine if the hyponatremia is hypovolemic, hypervolemic, or euvolemic in nature.
This document discusses water and electrolyte balance, focusing on sodium balance. It covers:
- Body fluid compartments and volumes, with two thirds of total body water located intracellularly.
- Factors regulating fluid movement between compartments, including osmolality and oncotic pressure.
- Mechanisms maintaining water and sodium balance, such as thirst, ADH release, and renal reabsorption.
- Common disorders of water and sodium balance like dehydration, edema, hyponatremia, and hypernatremia.
Hyponatremia occurs when someone drinks too much water, diluting the sodium levels in their blood and potentially causing fatal brain swelling. It results from an imbalance where water levels in the body are too high compared to sodium. Symptoms range from mild like nausea and fatigue, to severe like seizures and coma if not treated by restoring electrolyte balance through intravenous saline solutions.
This document provides an overview of principles of haemodialysis. It describes the components of haemodialysis including the blood circuit, dialysate circuit and dialyzer. It explains how diffusion and convection work to remove solutes and fluid across the dialyzer membrane. High water purity standards are required for patient safety. Haemodiafiltration combines diffusive and convective clearances and may provide benefits over standard haemodialysis.
Disturbances of fluid and electrolyte balance can cause serious health issues if not properly maintained. The body works to keep fluid volumes and electrolyte concentrations in balance through mechanisms like osmosis and hormone regulation. Imbalances can result from losses or gains of fluids and electrolytes. Common causes of imbalances include dehydration, overhydration, changes in sodium or potassium levels, and issues with antidiuretic hormone regulation. Symptoms vary depending on the type of imbalance but may include altered mental status, heart problems, and neurological issues. Treatment focuses on replacing lost fluids and electrolytes at appropriate rates to restore normal balances.
This document defines various fluid and electrolyte terminology and discusses different fluid and electrolyte imbalances. It describes extracellular fluid volume deficit, excess, and shift. It also covers intracellular fluid volume excess and specific electrolyte imbalances like hyponatremia. Fluid and electrolyte imbalances can have various causes and clinical manifestations. Assessment findings help diagnose the issue, and medical management focuses on correcting the underlying cause and restoring normal fluid and electrolyte balance.
1. Hyponatremia is defined as a plasma sodium concentration less than 135 mEq/L. It can be caused by an increase in circulating antidiuretic hormone (ADH) and water intake.
2. Hyponatremia is classified based on volume status and can be hypovolemic, euvolemic, or hypervolemic. Common causes include diuretic use, vomiting, cirrhosis, and heart failure.
3. SIADH is a frequent cause of euvolemic hyponatremia and results in inappropriate water retention due to abnormal ADH secretion or action. Pseudo hyponatremia can occur due to errors in sodium measurement
The document provides an overview of kidney anatomy and physiology. It describes the functions of the kidney which include regulating fluid balance, electrolytes, acid-base balance, and excreting waste. It details the structures of the nephron, the functional unit of the kidney, and its role in filtering blood to form urine through processes like filtration, reabsorption, secretion, and the countercurrent multiplier system. Key hormones involved in osmoregulation like renin, angiotensin, aldosterone, and ADH are also discussed.
Slideshow is from the University of Michigan Medical School's M2 Musculoskeletal sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Muscu
This document discusses fluids and electrolytes, covering several key points in 3 sentences or less:
Fluids and electrolytes are essential for maintaining homeostasis, as water makes up 50-60% of the human body and is needed for transport of nutrients, wastes, and substances. Fluids enter and leave the body through various avenues like the intestines, kidneys, and skin and are regulated by mechanisms such as ADH and aldosterone to control water resorption and excretion. Imbalances in fluids can cause deficits or excesses that disrupt homeostasis and must be managed through monitoring intake and output, administering IV fluids, and addressing the underlying causes.
The document provides information on pediatric fluids and electrolytes. It discusses how a child's body composition changes with age, describing them as having higher percentages of total body water when younger. It also outlines the three main components of fluid therapy: maintenance fluids, deficit fluids, and replacement fluids. Methods for calculating fluid rates are presented, including the Holliday-Segar method. Types, degrees, and treatment approaches for dehydration are defined. Oral and intravenous rehydration protocols are described for various clinical scenarios.
The document discusses body water composition and electrolyte balance. It notes that 60% of body weight is water, with two thirds being intracellular and the rest extracellular in the interstitial and intravascular compartments. The major electrolytes in the intracellular fluid are potassium, phosphate and magnesium, while the major electrolytes in the extracellular fluid are sodium, chloride, bicarbonate and calcium. Common electrolyte abnormalities in hospitalized patients include hyponatremia, hypernatremia, hyperkalemia and hypokalemia.
Similar to 09.30.08(b): Approach to the Patient with Disorders of Osmoregulation (20)
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Jim Holliman, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Alterations in Body Temperature: The Adult Patient with a Fever- Reside...Open.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Rapid Sequence Intubation & Emergency Airway Support in the Pediatric E...Open.Michigan
This is a lecture by Michele Nypaver, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This document provides an overview of ocular emergencies. It begins with an introduction to the Project: Ghana Emergency Medicine Collaborative and author information. The bulk of the document consists of slides reviewing various eye conditions and emergencies, including styes, chalazions, conjunctivitis, iritis, orbital cellulitis, subconjunctival hemorrhages, and scleritis. Treatment approaches are provided for many of the conditions. The document concludes with a discussion of the eye examination approach and areas to be reviewed.
GEMC- Disorders of the Pleura, Mediastinum, and Chest Wall- Resident TrainingOpen.Michigan
This document provides an overview of disorders of the pleura, mediastinum, and chest wall. It discusses several topics in 1-3 sentences each, including costochondritis (inflammation of the costal cartilages), mediastinitis (infection of the mediastinum), mediastinal masses, pneumothorax (air in the pleural space), and catamenial pneumothorax (recurrent pneumothorax associated with menstruation). The document aims to enhance understanding of the major clinical disorders commonly encountered in emergency medicine involving the pleura, mediastinum, and chest wall.
GEMC- Dental Emergencies and Common Dental Blocks- Resident TrainingOpen.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Arthritis and Arthrocentesis- Resident TrainingOpen.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Bursitis, Tendonitis, Fibromyalgia, and RSD- Resident TrainingOpen.Michigan
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC- Right Upper Quadrant Ultrasound- Resident TrainingOpen.Michigan
This is a lecture by Jeff Holmes from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
The document summarizes cardiovascular topics including pericardial tamponade, pericarditis, infective endocarditis, hypertension, tumors, and valvular disorders. It provides details on the causes, signs and symptoms, diagnostic studies, and management of these conditions. The document also includes bonus sections on cardiac transplant patients, pacemakers and ICDs, and EKG morphology.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC: Nursing Process and Linkage between Theory and PracticeOpen.Michigan
This is a lecture by Jeremy Lapham from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
2014 gemc-nursing-lapham-general survey and patient care managementOpen.Michigan
This is a lecture by Dr. Jeremy Lapham from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This document discusses the evaluation and management of patients with kidney failure presenting to the emergency department. It covers causes of acute kidney injury including pre-renal, intra-renal and post-renal failure. It also discusses evaluation of kidney function, risks of intravenous contrast, dialysis indications and complications in chronic kidney disease patients including infection, cardiovascular issues and electrolyte abnormalities. Special considerations are outlined for resuscitating, evaluating and treating kidney failure patients in the emergency setting.
GEMC: The Role of Radiography in the Initial Evaluation of C-Spine TraumaOpen.Michigan
This is a lecture by Dr. Stephen Hartsell from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
This is a lecture by Dr. Jim Holliman from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
"Learn about all the ways Walmart supports nonprofit organizations.
You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
हिंदी वर्णमाला पीपीटी, hindi alphabet PPT presentation, hindi varnamala PPT, Hindi Varnamala pdf, हिंदी स्वर, हिंदी व्यंजन, sikhiye hindi varnmala, dr. mulla adam ali, hindi language and literature, hindi alphabet with drawing, hindi alphabet pdf, hindi varnamala for childrens, hindi language, hindi varnamala practice for kids, https://www.drmullaadamali.com
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
How to Setup Warehouse & Location in Odoo 17 Inventory
09.30.08(b): Approach to the Patient with Disorders of Osmoregulation
1. Author(s): Michael Heung, M.D., 2009
License: Unless otherwise noted, this material is made available under the terms of
the Creative Commons Attribution–Noncommercial–Share Alike 3.0 License:
http://creativecommons.org/licenses/by-nc-sa/3.0/
We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use,
share, and adapt it. The citation key on the following slide provides information about how you may share and adapt this
material.
Copyright holders of content included in this material should contact open.michigan@umich.edu with any questions,
corrections, or clarification regarding the use of content.
For more information about how to cite these materials visit http://open.umich.edu/education/about/terms-of-use.
Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a
replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your
physician if you have questions about your medical condition.
Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers.
2. Citation Key
for more information see: http://open.umich.edu/wiki/CitationPolicy
Use + Share + Adapt
{ Content the copyright holder, author, or law permits you to use, share and adapt. }
Public Domain – Government: Works that are produced by the U.S. Government. (17 USC § 105)
Public Domain – Expired: Works that are no longer protected due to an expired copyright term.
Public Domain – Self Dedicated: Works that a copyright holder has dedicated to the public domain.
Creative Commons – Zero Waiver
Creative Commons – Attribution License
Creative Commons – Attribution Share Alike License
Creative Commons – Attribution Noncommercial License
Creative Commons – Attribution Noncommercial Share Alike License
GNU – Free Documentation License
Make Your Own Assessment
{ Content Open.Michigan believes can be used, shared, and adapted because it is ineligible for copyright. }
Public Domain – Ineligible: Works that are ineligible for copyright protection in the U.S. (17 USC § 102(b)) *laws in your
jurisdiction may differ
{ Content Open.Michigan has used under a Fair Use determination. }
Fair Use: Use of works that is determined to be Fair consistent with the U.S. Copyright Act. (17 USC § 107) *laws in your
jurisdiction may differ
Our determination DOES NOT mean that all uses of this 3rd-party content are Fair Uses and we DO NOT guarantee that
your use of the content is Fair.
To use this content you should do your own independent analysis to determine whether or not your use will be Fair.
3. Approach to the Patient with
Disorders of Osmoregulation
Michael Heung, M.D.
M2 Renal Sequence
Fall 2008
4. Objectives
• Know how to calculate plasma osmolality and
understand why sodium is a surrogate measure
• Understand the concept of an osmolar gap
• Understand the mechanisms of hypernatremia
development and know the differential diagnosis
• Be able to distinguish between various polyuric states
• Know the different types of hyponatremia and develop
an approach to determining etiology
• Be able to interpret the urine osmolality in the setting
of hyponatremia
• Understand the principles of hypo- and hypernatremia
management
5. Yes, this slide again
• Sodium balance is the critical determinant of fluid
compartment size
Therefore, alterations in sodium balance are detected
as changes in extracellular volume
• Alterations in water balance are critical for the
determination of fluid compartment composition
Therefore, alterations in water balance are manifest as
changes in plasma osmolality and are measured as
changes in plasma sodium concentration
6. Further Elaborated
• Although sodium is a determinant of volume,
measurement of the plasma sodium concentration
reflects a ratio of solute and water.
• Therefore, sodium concentration does not correlate
with the volume of the extracellular compartment. A
hyponatremic patient may be hypovolemic,
euvolemic, or hypervolemic.
7. Plasma Osmolality
• The primary solutes that are measured in the clinical lab
that contribute to the plasma osmolality are sodium,
glucose and urea
• Therefore an approximation of the plasma osmolality can
be obtained by the following formula:
Posm = (2 X [Na+]) + (glucose/18) + (urea/2.8)
* Na measured in mEq ! mmol; glucose measure in mg/dL; urea measure in mg/dL
• Normal serum osmolality is maintained between 280-290
mosm/kg water
• Under normal conditions the osmolar contributions of
glucose and urea are less than 10 mOsm/kg water; thus
plasma sodium is the primary determinant of osmolality
8. Measured Plasma Osmolality
• Measured osmolality is typically higher than
calculated osmolality due to the presence of
unmeasured osmoles in plasma (e.g. phosphate,
sulfate, amino acids, calcium, etc.)
• The difference between the measured and
calculated osmolality is termed the osmolar gap
– The osmolar gap is normally <10mosm/L
9. High Osmolar Gap:
A Diagnostic Clue
Effective Osmoles!
!Mannitol!
!Glycine!
!
Ineffective Osmoles!
!Ethanol!
!Methanol!
!Ethylene glycol!
!Isopropyl alcohol! Polar Antifreeze by Idiolecter
! Disinfected Kitty
by Knitty Cent
11. Case 1: Dehydration
A 72 year old male resident of a skilled nursing facility is brought to the
emergency department with poor responsiveness. The facility reports that he
recently had a urinary tract infection which was being treated with antibiotics.
He has also had diarrhea the past few days.
PMHx: Alzheimer s dementia, CAD, HTN
PE: BP 90/60, P 110 reg
HEENT: mucous membranes dry
Chest: clear
CV: RRR, weak peripheral pulses
Ext: no edema
Neuro: minimal responsiveness to voice
Labs: Sodium 162mEq/L, Plasma osm 332mosm/kg,
Source Undetermined
Urine osm 745mosm/kg
What factors contributed to the development of hypernatremia in this
patient?
12. Causes of Hypernatremia
Water loss in excess of sodium
– Insensible losses (skin, Normal
respiratory, fever)
– Renal losses (DI, osmotic diuresis)
Pure
– Extrarenal losses (diarrhea) water
Requires an impairment in the loss
thirst mechanism
Hypotonic
fluid
loss
Sodium gain in excess of water
– Administration of hypertonic
solutions
Most frequently iatrogenic
Hypertonic
fluid
(Why would we do this?) gain
Adapted from NEJM, Hypernatremia
13. Who Develops Hypernatremia?
• An intact thirst mechanism can almost always
compensate for water losses, even in the
complete absence of ADH
• At-Risk Populations:
– Impaired thirst sensation
• Elderly
• Hypothalamic lesions
• Psychosis
– Impaired access to water
• Dementia, delirium
• Infants
Infant Smile by Mehregan Javanmard, Wikimedia
Commons
14. Case 2: Polyuria
You are asked to evaluate a 24 yr old previously healthy male who was
admitted to the orthopedics service following a skiing accident in
which he fractured his pelvis. He underwent 6 hours of surgery
yesterday. Over the past 24 hrs he has been noted to have a urine
output of 4L. The patient is sedated with pain medications, but his
girlfriend notes that he always urinates a lot .
PE: BP 120/70, P 85, wt 80kg
HEENT: mucous membranes dry
CV: RRR
Ext: no edema
Neuro: somnolent
Labs: Sodium 152mEq/L, Plasma osm 315mosm/kg,
Urine osm 105mosm/kg
What is the diagnosis? Treatment?
Source Undetermined
15. Diabetes Insipidus
• Defined by a defect in renal water
conservation
– diabainein (Greek): “to pass through”
– insipidus (Latin): “flavorless”
Central DI: Impaired synthesis, transport, Peeing Men by gennie catastrophe,
Flickr.com
storage, or release of ADH from the hypothalamus and pituitary
– Can be hereditary or result from infection, trauma, ischemia, neoplasm
or granulomatous disease
Nephrogenic DI: Reduced response to ADH in the collecting tubule
– Hereditary or acquired (eg. renal failure, hypercalcemia, drugs)
How could you distinguish between central and nephrogenic DI?
16. Distinguishing Polyuric States
Increase in Urine
Urine osm Following
osm with Exogenous
Water Deprivation
ADH
Normal >800 Little or no increase
Complete central
<300 Substantial (>600)
diabetes insipidus
Partial central >10% following water
300-800
diabetes insipidus deprivation
Nephrogenic
<300-500 Little or no increase
diabetes insipidus
Primary Polydipsia >500 Little or no increase
M. Heung
17. Correction of Hypernatremia
• Over-aggressive
correction of
hypernatremia can
result in cerebral
edema and death
• Unless it is acute/
symptomatic,
correction should
occur gradually:
0.5 mEq/L per hour,
or 10 mEq/L per day
NEJM, Hypernatremia
18. Correction of Hypernatremia
• Estimating the free water deficit:
Current TBW = (140/[Na]) x normal TBW
Water deficit = normal TBW - current TBW
= 0.6 x weight (kg) x (1 – 140/[Na])
Case 2 Example: Na 152, weight 80kg
Water deficit = 0.6 x 80kg x (1-140/152) = 3.8L
Target correction at rate of 0.5mEq/hr = 24hrs
Therefore, need to give 158.3mL of free water/hr
(plus ongoing free water losses!
• Formula assumptions: - No sodium deficit
– Total body water distribution
– Steady state
19. Correction of Hypernatremia
• Formulas are just an estimate to
get you started!
• Clinical Pearls: Solution
Osm
Free Water
(mL per L
(mosm/L)
– Monitor your progress and solution)
adjust appropriately
– Err on the side of slow correction 0.9% NS 308
– Account for ongoing losses (eg.
urine, insensible) 0.45% NS 154
– Know how much free water
you are giving D5W 0
20. Hyponatremia Basics
• The most common electrolyte disturbance
• Symptoms are primarily neurologic and
depend on severity and rapidity of
development
– Acute: confusion, disorientation " seizures,
coma, death
– Chronic: usually asymptomatic until <125mEq/L
• Management depends on underlying etiology
21. A Systematic Approach
• Three main etiologies (by mechanism):
1. Non-hypoosmolar: pseudohyponatremia or hyperosmolar
2. Hypoosmolar hyponatremia with normal renal water
excretion
3. Hypoosmolar hyponatremia with impaired renal water
excretion
• Ask 3 questions:
1. Is the patient hypo-osmolar? Serum osm (corrected for
urea)
3. Are the patient’s kidneys responding appropriately to
clear free water? Urine osm
2. Does the patient have an adequate effective
intravascular volume? Urine Na >20, Physical exam
22. Why Not Urea?
Posm = (2 X [Na+]) + (glucose/18) + (urea/2.8)
In clinical practice:
Posm = (2 X [Na+]) + (glucose/18)
or = Measured osm - (urea/2.8)
Urea is an ineffective osmole and therefore does not
cause water shifting or contribute to disorders or
osmoregulation.
23. Case 3
An elderly woman with a history of diabetes mellitus presents to
her physician with complaints of fatigue and dizziness following
a recent bout of the flu. Her food intake has been decreased
so she has only taken half of her usual dose of insulin.
Labs: Sodium 128mEq/L Plasma osm 320mosm/kg
Urea 30mg/dL (corrected for urea ~ 310)
Glucose 800mg/dL
1. Is the patient hypo-osmolar?
Why is she hyperosmolar?
24. Non-Hypoosmolar Hyponatremia
Pseudo-Hyponatremia (Isoosmolar)
– Hyperlipidemia
– Hyperparaproteinemia
– Primarily of historical interest only
Source Undetermined
Iso- or Hyperosmolar Hyponatremia
• Due to shifting of water from intracellular to extracellular
compartments
• Occurs only with effective osmoles
– Glucose: for every 100mg/dL above
100, [Na] falls by 1.6 mEq/L
– Mannitol
Adapted from NEJM, Hyponatremia
25. Case 4
A 35 year old male is admitted to the closed psychiatry ward for auditory
and visual hallucinations. He has been on psychotropic drugs for the last
5 years. The renal consultant is called 5 days into the admission when
the patient s plasma sodium is noted to be 125 mEq/L on routine
chemistries.
Labs: Sodium 125mEq/L Plasma osm 268mosm/kg
Glucose 90mg/dL (corrected for urea ~265)
Urea 10mg/dL Urine osm 80mosm/kg
1. Is the patient hypo-osmolar?
2. Are the patient s kidneys responding appropriately to clear
free water?
What is the best approach to correcting his hyponatremia?
26. Hyponatremia With
Normal
Renal Water Excretion
• Primary Polydipsia: Water ingestion
overcomes the free water clearance
capacity of the kidneys
– Psychogenic polydipsia: thirst defect?
– Manage with water restriction
Source Undetermined
• Reset Osmostat: Normal response to changes in
plasma osmolality but at a reduced threshold
– Sodium is low but stable
– Seen in malnutrition, psychosis, pregnancy, malignancy
– Treat underlying cause, no specific therapy for hyponatremia
27. Case 5
A 50 year old woman is newly diagnosed with essential
hypertension by her internist. She is placed on
hydrochlorothiazide (25 mg/d) and returns one week later with
complaints of light-headedness and is found to be orthostatic.
Labs: Sodium 110mEq/L Plasma osm 238mosm/kg
Glucose 108mg/dL (corrected for urea ~235)
Urea 10mg/dL Urine sodium 30mEq/L
Urine osm 300mosm/kg
1. Is the patient hypo-osmolar?
2. Are the patient s kidneys responding appropriately to
clear free water?
3. Does the patient have an adequate effective intravascular
volume?
29. Case 6
A 65 year old male with a 10 year history of coronary artery disease
presents to his physician with progressive dyspnea on exertion, and
difficulty climbing stairs. He notes that he sleeps in a reclining chair and
often awakens 2 hours after falling asleep with difficulty breathing.
PE: BP 170/95, P 90 reg, RR 24.
Chest: bibasilar crackles 1/3 up.
CV: JVD to jaw, PMI displaced to post ax line, +S3
Ext: 3+ edema to knees
Labs: Sodium 125mEq/L Plasma osm 265mosm/kg
Urea 40mg/dL (corrected for urea ~ 251)
Glucose 105mg/dL Urine sodium <10mEq/L
Urine osm 350mosm/kg
1. Is the patient hypo-osmolar?
2. Are the patient s kidneys responding appropriately to
clear free water?
3. Does the patient have an adequate effective intravascular volume?
30. Hyponatremia Due to
Appropriate ADH
Low effective intravascular volume leads to ADH release and
stimulation of thirst
– Urine sodium can be helpful diagnostically
Total Body Volume Up
• Edematous states:
– Congestive heart failure
– Cirrhosis
Free water restriction
Total Body Volume Down
• Renal Losses
Source Undetermined
• Extra-renal Losses (GI, skin)
Correction of volume status results in cessation of ADH release
31. Case 7
A 52 year old male with a 50 pack-yr smoking history presents to the
emergency department for evaluation of hemoptysis. On further
questioning, he has unintentionally lost 20 lbs over the past 3 months.
PE: BP 140/90, P 80, no orthostatic changes
HEENT: bitemporal wasting
Chest: diminished breath sounds R upper lobe
Ext: no edema
Labs: Sodium 118mEq/L Plasma osm 250mosm/kg (corr 245)
Urea 15mg/dL Urine osm 600mosm/kg
Glucose 90mg/dL Urine sodium 32mEq/L
CXR: solid mass in R upper lobe
1. Is the patient hypo-osmolar?
2. Are the patient s kidneys responding appropriately to clear free water?
3. Does the patient have an adequate effective intravascular volume?
32. Syndrome of Inappropriate ADH
Non-physiologic secretion of ADH with resulting impaired water excretion in
the setting of normal sodium excretion
– Diagnosis of exclusion
Increased Hypothalamic Production
– CNS disorders (meningitis, CVA, trauma, tumors)
– Pulmonary disease (pneumonia, TB, asthma)
– HIV
– Nausea, pain (post-op)
– Drugs The Anatomy of the Nervous System: From the
Standpoint of Development and Function by SW
Ectopic Production Ranson, Wikipedia
– Small cell lung cancer
ADH Potentiation
– Drugs (carbamazepine, chlorpropamide)
– Psychosis
Source Undetermined
33. Management of SIADH
• Treat reversible underlying cause(s)
• Free water restriction
• Hypertonic saline (eg. 3% NS, 513mEq/L) +/- furosemide
• Demeclocycline
• V2 receptor antagonists
Giving 0.9% NS (154mEq NaCl/L, 300 mosm/kg) can actually
worsen the hyponatremia of SIADH. How?
Eg. Na 118, Posm 250, Uosm 600
! 1L of 0.9% NS contains 308mosm
! this patient will excrete that solute load in ~500mL of urine
! the remaining 500mL is kept as free water
34. General Management of Hyponatremia
Acute and Symptomatic
• Correct quickly by up to 5%
and then slowly
Chronic
• Limit rate of correction to
<0.5 mEq/L per hour or
<10mEq/L per day
Clinical Pearls
• Know the etiology and treat
any reversible processes
• Follow your progress and
NEJM, Hyponatremia
adjust accordingly
• Know what s coming out (urine osm)
• Err on the side of slow correction
35. Summary: Hyponatremia
Type of Serum Osm Urine Osm
Primary Urine Na Volume
Hypo- (mosm/kg (mosm/kg Therapy
Defect (mEq/L) Status
natremia water) water)
Pseudo Lab effect Normal
Varies >15 Normal none
Hyperosm Osmotic effect or High
Intact
renal Water Free water
Low <100 >15 Normal
water intoxication restriction
clearance
Free water
ADH Low >100 <15 High
restriction
Impaired
renal Volume
water ADH Low >100 <15 Low
repletion
clearance
Free water
ADH Low >100 >15 Normal
restriction
M. Heung
36. Low Plasma Sodium
1. Is Patient Hypoosmolar?
(i.e. urea-corrected P osm < 280)
Iso- or Hyperosm
Yes No (Posm>280) - Effective osm (glucose, mannitol)
2. Is Renal Water Excretion Intact?
Yes (Uosm<100) No (Uosm>100)
- Primary polydipsia
Water restrict
3. Is There Adequate Effective Circulating Volume?
Yes (UNa>20) No (UNa<20, physical exam)
- SIADH
An Algorithmic Water restrict
Approach to Volume Up Volume Down
Hyponatremia Water restrict Volume replace
M. Heung
37. Pop Quiz
Posm
Na+ K+ Cl- HCO3- Glucose BUN Uosm UNa
(corr)
A 125 3.5 80 35 90 30 268 450 5
B 128 4.0 88 28 85 14 310 250 30
C 125 3.8 90 24 90 8 260 90 25
D 120 4.2 90 20 88 14 260 350 40
Which patient has psychogenic polydipsia?
What labs are consistent with SIADH?
Which labs are those of the dehydrated man who has been vomiting?
Who is the cardiac catheterization patient who received mannitol?
39. Additional Source Information
for more information see: http://open.umich.edu/wiki/CitationPolicy
Slide 9: Polar Antifreeze by Idiolecter, http://www.flickr.com/photos/26506346@N00/15205401, Disinfected Kitty by Knitty Cent,
http://www.flickr.com/photos/knittycent/3603549561/
Slide 11: Source Undetermined
Slide 12: Adapted from NEJM, Hypernatremia, H. Anrogue, N. Madias
Slide 13: Infant Smile by Mehregan Javanmard, Wikimedia Commons, http://commons.wikimedia.org/wiki/File:Infant_smile.jpg
Slide 14: Source Undetermined
Slide 15: Peeing Men by gennie catastrophe, Flickr.com, http://www.flickr.com/photos/83478340@N00/3330474579
Slide 16: Michael Heung
Slide 17: Source Undetermined
Slide 24: Source Undetermined; Adapted from NEJM, Hyponatremia, H. Anrogue, N. Madias
Slide 26: Source Undetermined
Slide 30: Source Undetermined
Slide 32: The Anatomy of the Nervous System: From the Standpoint of Development and Function by SW Ranson, Wikipedia,
http://en.wikipedia.org/wiki/File:Vertebrate-brain-regions.png; Source Undetermined
Slide 34: NEJM, Hyponatremia, H. Anrogue, N. Madias
Slide 35: Michael Heung
Slide 36: Michael Heung