paracetamol ferrous sulfate and paclitaxel
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Hypercalcemia ,causes and treatment
This document discusses hypercalcemia, which is defined as a serum calcium level above 10.5 mg/dl. It outlines the causes of hypercalcemia including primary hyperparathyroidism, certain cancers, and excessive vitamin D or calcium supplementation. Signs and symptoms are noted such as abdominal pain, nausea, weakness and cardiac issues. Diagnostic testing including PTH, calcium, and phosphate levels as well as imaging are covered. Treatment focuses on rehydration, bisphosphonates, glucocorticoids, calcitonin, surgery if needed, and addressing the underlying cause. Complications of untreated hypercalcemia include osteoporosis, kidney stones, and kidney failure.
Hpercalcemia & its Management
Malignant hypercalcemia is caused by excess calcium mobilization from bone that exceeds renal excretion thresholds. It is often seen in patients with bone metastases from breast, lung, kidney and multiple myeloma cancers. Treatment involves aggressive hydration, decreasing bone resorption with bisphosphonates, calcitonin, or corticosteroids, and in some cases antitumor therapy.
Hpocalcemia
Hypocalcemia is a low level of calcium in the blood. Calcium is essential for nerve impulse conduction, muscle contraction, and other cellular functions. Hypocalcemia can be caused by low albumin, low parathyroid hormone, vitamin D deficiency, or other factors. Symptoms include neuromuscular irritability, tetany, seizures, and EKG changes. Treatment involves oral calcium and vitamin D supplements to replace calcium and maintain adequate blood levels. Intravenous calcium may be needed for severe acute hypocalcemia.
Calcium disorder
Calcium levels in the body are tightly regulated through the actions of parathyroid hormone (PTH), vitamin D, and other factors. Disorders can cause either hypercalcemia (high calcium levels) or hypocalcemia (low calcium levels). Primary hyperparathyroidism, where the parathyroid glands overproduce PTH, is a common cause of hypercalcemia and may require parathyroid surgery. Malignancy is another major cause through the action of PTH-related peptide. Severe hypercalcemia requires rehydration and drugs to reduce bone resorption and calcium levels. Hypocalcemia can result from hypoparathyroidism or resistance to PTH/vitamin D
Hypocalcemia and Polyuria
Hypocalcemia refers to low calcium levels in the blood and can range from asymptomatic to life-threatening depending on severity and onset. It is caused by insufficient calcium entering the bloodstream or too much calcium loss. Common causes include hypoparathyroidism, vitamin D deficiency, kidney failure, pancreatitis, cancer metastases, and sepsis. Symptoms include seizures, dementia, emotional issues, movement disorders, and papilledema. Chronic hypocalcemia is treated with calcium and vitamin D supplements to raise blood calcium levels to around 8 mg/dL to minimize symptoms while avoiding hypercalciuria.
Hypercalcemia final
This document discusses hypercalcemia, defined as a serum calcium level above 10.3 mg/dl. It lists the main causes as primary hyperparathyroidism, malignancy like multiple myeloma and breast cancer, and excess vitamin D. Symptoms involve the renal, musculoskeletal, gastrointestinal and neurological systems and include nephrolithiasis, bone pain, nausea and confusion. Emergency treatment involves rehydration with IV saline and bisphosphonates while medical management focuses on fluid intake, diet modification and exercise. Specific treatments address the underlying cause such as surgery for primary hyperparathyroidism or treating the malignancy.
Hypercalcemia, causes and treatment
This document discusses hypercalcemia, which is defined as a serum calcium level above 10.5 mg/dl. It outlines the various causes of hypercalcemia including primary hyperparathyroidism, certain cancers, granulomatous diseases, and certain medications. The clinical presentation of hypercalcemia can include symptoms affecting the stones, bones, abdominal organs, psyche, and other nonspecific symptoms. Diagnosis involves blood tests to measure calcium and PTH levels along with imaging tests. Treatment focuses on rehydration, bisphosphonates, glucocorticoids, calcitonin, surgery, and dialysis depending on the severity and underlying cause of the hypercalcemia.
Hyperammonemia
Hyperammonemia is a medical condition characterized by an abnormally elevated level of ammonia in the bloodstream. It is caused by defects in the urea cycle which is responsible for detoxifying ammonia produced from protein catabolism. Symptoms range from lethargy and vomiting to seizures and coma. Diagnosis involves tests of blood and urine amino acid and organic acid levels as well as genetic testing. Treatment focuses on restricting protein intake, supplementing with alpha-ketoacid derivatives, and administering drugs to conjugate ammonia into excretable compounds to lower blood ammonia levels.
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Hypercalcemia ,causes and treatment
This document discusses hypercalcemia, which is defined as a serum calcium level above 10.5 mg/dl. It outlines the causes of hypercalcemia including primary hyperparathyroidism, certain cancers, and excessive vitamin D or calcium supplementation. Signs and symptoms are noted such as abdominal pain, nausea, weakness and cardiac issues. Diagnostic testing including PTH, calcium, and phosphate levels as well as imaging are covered. Treatment focuses on rehydration, bisphosphonates, glucocorticoids, calcitonin, surgery if needed, and addressing the underlying cause. Complications of untreated hypercalcemia include osteoporosis, kidney stones, and kidney failure.
Hpercalcemia & its Management
Malignant hypercalcemia is caused by excess calcium mobilization from bone that exceeds renal excretion thresholds. It is often seen in patients with bone metastases from breast, lung, kidney and multiple myeloma cancers. Treatment involves aggressive hydration, decreasing bone resorption with bisphosphonates, calcitonin, or corticosteroids, and in some cases antitumor therapy.
Hpocalcemia
Hypocalcemia is a low level of calcium in the blood. Calcium is essential for nerve impulse conduction, muscle contraction, and other cellular functions. Hypocalcemia can be caused by low albumin, low parathyroid hormone, vitamin D deficiency, or other factors. Symptoms include neuromuscular irritability, tetany, seizures, and EKG changes. Treatment involves oral calcium and vitamin D supplements to replace calcium and maintain adequate blood levels. Intravenous calcium may be needed for severe acute hypocalcemia.
Calcium disorder
Calcium levels in the body are tightly regulated through the actions of parathyroid hormone (PTH), vitamin D, and other factors. Disorders can cause either hypercalcemia (high calcium levels) or hypocalcemia (low calcium levels). Primary hyperparathyroidism, where the parathyroid glands overproduce PTH, is a common cause of hypercalcemia and may require parathyroid surgery. Malignancy is another major cause through the action of PTH-related peptide. Severe hypercalcemia requires rehydration and drugs to reduce bone resorption and calcium levels. Hypocalcemia can result from hypoparathyroidism or resistance to PTH/vitamin D
Hypocalcemia and Polyuria
Hypocalcemia refers to low calcium levels in the blood and can range from asymptomatic to life-threatening depending on severity and onset. It is caused by insufficient calcium entering the bloodstream or too much calcium loss. Common causes include hypoparathyroidism, vitamin D deficiency, kidney failure, pancreatitis, cancer metastases, and sepsis. Symptoms include seizures, dementia, emotional issues, movement disorders, and papilledema. Chronic hypocalcemia is treated with calcium and vitamin D supplements to raise blood calcium levels to around 8 mg/dL to minimize symptoms while avoiding hypercalciuria.
Hypercalcemia final
This document discusses hypercalcemia, defined as a serum calcium level above 10.3 mg/dl. It lists the main causes as primary hyperparathyroidism, malignancy like multiple myeloma and breast cancer, and excess vitamin D. Symptoms involve the renal, musculoskeletal, gastrointestinal and neurological systems and include nephrolithiasis, bone pain, nausea and confusion. Emergency treatment involves rehydration with IV saline and bisphosphonates while medical management focuses on fluid intake, diet modification and exercise. Specific treatments address the underlying cause such as surgery for primary hyperparathyroidism or treating the malignancy.
Hypercalcemia, causes and treatment
This document discusses hypercalcemia, which is defined as a serum calcium level above 10.5 mg/dl. It outlines the various causes of hypercalcemia including primary hyperparathyroidism, certain cancers, granulomatous diseases, and certain medications. The clinical presentation of hypercalcemia can include symptoms affecting the stones, bones, abdominal organs, psyche, and other nonspecific symptoms. Diagnosis involves blood tests to measure calcium and PTH levels along with imaging tests. Treatment focuses on rehydration, bisphosphonates, glucocorticoids, calcitonin, surgery, and dialysis depending on the severity and underlying cause of the hypercalcemia.
Hyperammonemia
Hyperammonemia is a medical condition characterized by an abnormally elevated level of ammonia in the bloodstream. It is caused by defects in the urea cycle which is responsible for detoxifying ammonia produced from protein catabolism. Symptoms range from lethargy and vomiting to seizures and coma. Diagnosis involves tests of blood and urine amino acid and organic acid levels as well as genetic testing. Treatment focuses on restricting protein intake, supplementing with alpha-ketoacid derivatives, and administering drugs to conjugate ammonia into excretable compounds to lower blood ammonia levels.
Alcoholic liver disease new 20-6-2016
Excessive alcohol consumption can lead to alcoholic liver disease (ALD), which progresses through three main stages: 1) Hepatic steatosis or fatty liver, which is reversible, 2) Alcoholic hepatitis characterized by hepatocyte damage and inflammation, and 3) Cirrhosis, the final irreversible stage involving liver fibrosis and formation of regenerative nodules. ALD is diagnosed based on excessive drinking history and lab tests showing abnormalities in liver function. Over time, if alcohol use continues, the disease progresses from an enlarged fatty liver to scarring and shrinkage of the liver in cirrhosis.
Hypercalcemia
Hypercalcemia was causing the patient's acute renal failure. Treatment for hypercalcemia included intravenous fluids, furosemide, steroids, bisphosphonates, and dialysis which lowered the calcium levels and improved renal function. The underlying cause of hypercalcemia could not be determined after extensive testing, but was likely a malignancy given the persistent pancytopenia. Hypercalcemia can directly damage the kidneys by decreasing medullary osmolality and inducing nephrogenic diabetes insipidus, nephrolithiasis, and renal tubular acidosis. It also causes vasoconstriction and activation of the calcium-sensing receptor which stimulates renin release and worsens volume
Haemochromotosis brief overview
Haemochromatosis is an autosomal recessive condition characterized by excessive iron accumulation in the body. It affects around 0.5% of Caucasians and usually presents in the 40s-50s with a triad of pigmentation, diabetes mellitus, and hepatomegaly. Diagnosis involves blood tests showing elevated serum iron, transferrin saturation over 50%, and elevated serum ferritin. Liver biopsy can confirm iron deposition and damage. Treatment aims to reduce iron stores through weekly venesection of 1 unit of blood for 6-12 months followed by maintenance venesection.
Hypercalcemia atee
Hypercalcemia is a common condition seen in up to 4% of hospitalized patients. The most common causes are primary hyperparathyroidism and malignancy-associated hypercalcemia. Hypercalcemia occurs when calcium influx into the extracellular fluid exceeds renal excretory capacity. It is defined as a total serum calcium level greater than 10.2 mg/dL. Treatment involves stabilizing the patient with intravenous fluids, promoting calcium excretion with diuretics, and administering bisphosphonates to reduce bone resorption in malignancy-associated cases. Surgical removal of parathyroid adenomas is required for symptomatic primary hyperparathyroidism.
Seminar on calcium
This document discusses calcium metabolism and provides details on calcium homeostasis, absorption, excretion, and the roles of parathyroid hormone and vitamin D. It also covers hypocalcemia and hypercalcemia, defining each condition and describing causes, clinical manifestations, diagnostic workup, and treatment approaches. Hypocalcemia can result from neonatal issues, vitamin D deficiency, hypoparathyroidism, or other causes. Hypercalcemia has causes including parathyroid hormone excess, malignancy, vitamin D excess, and genetic conditions.
Hypercalcemia
This document presents a case study of a 41-year-old woman diagnosed with hypercalcemia caused by milk alkali syndrome. She was brought to the emergency department with nausea, vomiting, and altered mental status. Tests found her blood calcium level to be very high. Her history of consuming large amounts of antacids containing calcium and sodium bicarbonate led to the diagnosis of milk alkali syndrome. Milk alkali syndrome occurs when excessive oral intake of calcium and alkali impairs the kidney's ability to excrete calcium, resulting in hypercalcemia. The document then provides background information on calcium regulation and the various causes, symptoms, diagnostic evaluation, and treatment approaches for hypercalcemia.
Hypercalcaemia
Hypercalcemia is elevated calcium levels in the blood. Normal calcium levels are 2.12-2.65 mmol/L. It is uncommon, affecting 4 in 100,000 people per year, and more common in females ages 50-60. Signs and symptoms include bone pain, kidney stones, constipation, fatigue, and renal failure. Causes include primary hyperparathyroidism, malignancy, certain drugs, and granulomatous diseases. Diagnosis involves blood and imaging tests. Treatment consists of IV fluids, correcting electrolyte imbalances, diuretics, treating the underlying cause, bisphosphonates, steroids, and calcitonin. Untreated severe hypercalcemia can lead to osteop
Crf
This document discusses chronic renal failure (CRF). CRF is characterized by the progressive and irreversible deterioration of renal function due to the slow destruction of renal tissue, eventually leading to death when enough nephrons have been damaged. CRF is caused by conditions like diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. It progresses through stages of decreased renal reserve, renal insufficiency, renal failure, and end-stage kidney disease. Medical management of CRF focuses on controlling blood pressure and reducing edema, gastrointestinal side effects, and pruritis.
Endocrine system
This document discusses polyuria and hypercalcemia. It defines polyuria as excessive urination of over 2.5L per day. Polyuria can be caused by diabetes insipidus, diabetes mellitus, diuretics, or renal failure. Nocturnal polyuria is a key symptom affecting the elderly. Hypercalcemia is defined as high blood calcium levels, which can be caused by primary hyperparathyroidism or other factors like cancer. Symptoms include nausea, vomiting, and weakness. Treatment involves lowering calcium through surgery, medication or IV fluids.
Calcium Metabolism and Hypocalcemia
Calcium Metabolism - sources, physiology (absorption, hemostasis), functions.
Hypocalcemia - causes (PTH absent, PTH ineffective, PTH overwhelmed), treatment.
A Short Presentation on Hypercalcaemia
This document presents a case study of a 49-year-old male who presented with hypercalcemia. His investigations revealed a calcium level of 3.2 mmol/L. He had symptoms of abdominal discomfort, fatigue, and increased thirst. His examination and tests ruled out various potential causes of hypercalcemia. He was found to have elevated PTH, consistent with primary hyperparathyroidism. He was treated with IV fluids and bisphosphonates and will likely require parathyroidectomy surgery to address the underlying cause of his hypercalcemia.
An introduction to alcoholic liver disease part 2
This document provides an overview of alcoholic liver disease (ALD) in multiple parts. It begins by discussing how alcohol is metabolized in the liver and can cause liver dysfunction by damaging hepatocytes and producing toxic byproducts. The major manifestations of ALD are then described, including jaundice, coagulopathy, and encephalopathy, which result from impaired bilirubin metabolism, clotting factor synthesis, and other liver functions. The document outlines the spectrum of ALD from fatty liver to alcoholic hepatitis to cirrhosis. Diagnosis involves assessing alcohol use history and liver enzymes/function. The characteristics of fatty liver, alcoholic hepatitis, and cirrhosis are summarized.
Approach to patient with hypo/hyper calcaemia
This document discusses calcium homeostasis and disorders of calcium metabolism. It begins by describing the functions of calcium in the body and where calcium is stored. It then discusses calcium regulation by parathyroid hormone, vitamin D, and calcitonin. Causes, signs and symptoms, and treatment approaches for hypercalcemia and hypocalcemia are reviewed. The key points are that calcium levels are tightly controlled by hormones to maintain levels between 2.25-2.62 mmol/L and that disorders can result from excess or deficiencies of these regulating hormones.
Hypercalcemia
Hypercalcemia is commonly caused by primary hyperparathyroidism or malignancy. It can be life-threatening in severe cases. Diagnosis involves measuring serum calcium, PTH, and assessing for underlying causes. Treatment depends on the underlying condition but may involve surgery for hyperparathyroidism or addressing the malignancy. Complications can impact the kidneys, GI tract, cardiovascular system, muscles and bones.
Hypercalcaemia of Malignancy
1) A 10-year-old Labrador presented with PU/PD, lethargy, weight loss, and anorexia. Biochemistry revealed hypercalcemia.
2) Thoracic radiographs and ultrasound identified a cranial mediastinal mass. FNA was non-diagnostic but PCR suggested a mixed population of T-cells, consistent with mediastinal lymphoma.
3) The diagnosis was stage Vb mediastinal T-cell lymphoma, causing hypercalcemia of malignancy through PTHrP secretion and increased bone resorption. Treatment was palliative with steroids to reduce hypercalcemia and improve appetite.
Approach to Hypercalcemia
This document discusses calcium homeostasis and hypercalcemia. It notes that calcium is critical for many physiological functions and is mainly stored in bones. Hypercalcemia can be caused by primary hyperparathyroidism, vitamin D excess, certain malignancies, and other conditions. The diagnostic approach involves distinguishing between hyperparathyroidism and hypercalcemia of malignancy based on lab tests. Treatment focuses on rehydration, increasing calciuresis, and decreasing bone resorption or intestinal calcium absorption using medications like calcitonin, bisphosphonates, glucocorticoids, or dialysis depending on the severity of hypercalcemia.
Serum Electrolytes
This document discusses sodium and potassium levels in the body. It begins by outlining the distribution of sodium, potassium, and water in the body and their roles in homeostasis. It then describes pathological conditions that can result from imbalances in sodium and potassium levels. Various techniques for estimating serum sodium and potassium are also outlined, including ion selective electrodes, atomic absorption spectroscopy, and flame emission photometry.
Calcium metabolism & hypercalcemia
This document discusses calcium homeostasis and hypercalcemia. It notes that approximately 99% of calcium in the body is stored in bones and teeth, with the remaining 1% distributed in the extracellular fluid, intracellular fluid, and soft tissues. Hypercalcemia is defined as a serum calcium level above 10.5 mg/dL. Causes include primary hyperparathyroidism in about 50% of cases of hypercalcemia, as well as malignancy, vitamin D toxicity, hyperthyroidism, and certain genetic conditions. Symptoms range from being mild or absent with mild increases in calcium to severe symptoms like confusion and coma with rapid or large rises in calcium levels.
Adverse drug reaction drugs
This document summarizes the adverse reactions, mechanisms, and management of several common drugs including paracetamol, acetylsalicylic acid, and others. It specifically discusses paracetamol toxicity occurring through generation of a toxic metabolite in the liver. Management includes decontamination and antidote therapy with N-acetyl cysteine. Aspirin toxicity is also reviewed, noting effects from salicylate-induced oxidative phosphorylation and metabolic acidosis. Treatment focuses on gastric lavage, fluid replacement, hemodialysis, sodium bicarbonate, and activated charcoal.
Hypocalcemia
This document discusses hypocalcemia, defined as a serum calcium level below 8.5 mg/dl. It may be caused by low or high parathyroid hormone levels. Causes of low PTH include parathyroid gland agenesis, destruction, or dysfunction. Causes of high PTH include vitamin D deficiency, kidney disease impairing vitamin D activation, or drugs. Symptoms include increased neuromuscular excitability. Investigations include calcium, albumin, phosphorus, magnesium and PTH levels. Treatment involves vitamin D, calcium supplements, and magnesium as needed.
Drug treatment of iron deficiency anaemia
This document discusses iron deficiency anemia and its treatment. It defines anemia and identifies iron deficiency as a common cause. It describes how iron is used to form hemoglobin and the signs and symptoms of iron deficiency anemia. The document outlines dietary iron requirements and food sources of iron. It provides details on oral and parenteral iron therapy, including dosages, formulations, and potential adverse effects. It also discusses intravenous iron preparations and the use of desferrioxamine for acute iron poisoning.
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Alcoholic liver disease new 20-6-2016
Excessive alcohol consumption can lead to alcoholic liver disease (ALD), which progresses through three main stages: 1) Hepatic steatosis or fatty liver, which is reversible, 2) Alcoholic hepatitis characterized by hepatocyte damage and inflammation, and 3) Cirrhosis, the final irreversible stage involving liver fibrosis and formation of regenerative nodules. ALD is diagnosed based on excessive drinking history and lab tests showing abnormalities in liver function. Over time, if alcohol use continues, the disease progresses from an enlarged fatty liver to scarring and shrinkage of the liver in cirrhosis.
Hypercalcemia
Hypercalcemia was causing the patient's acute renal failure. Treatment for hypercalcemia included intravenous fluids, furosemide, steroids, bisphosphonates, and dialysis which lowered the calcium levels and improved renal function. The underlying cause of hypercalcemia could not be determined after extensive testing, but was likely a malignancy given the persistent pancytopenia. Hypercalcemia can directly damage the kidneys by decreasing medullary osmolality and inducing nephrogenic diabetes insipidus, nephrolithiasis, and renal tubular acidosis. It also causes vasoconstriction and activation of the calcium-sensing receptor which stimulates renin release and worsens volume
Haemochromotosis brief overview
Haemochromatosis is an autosomal recessive condition characterized by excessive iron accumulation in the body. It affects around 0.5% of Caucasians and usually presents in the 40s-50s with a triad of pigmentation, diabetes mellitus, and hepatomegaly. Diagnosis involves blood tests showing elevated serum iron, transferrin saturation over 50%, and elevated serum ferritin. Liver biopsy can confirm iron deposition and damage. Treatment aims to reduce iron stores through weekly venesection of 1 unit of blood for 6-12 months followed by maintenance venesection.
Hypercalcemia atee
Hypercalcemia is a common condition seen in up to 4% of hospitalized patients. The most common causes are primary hyperparathyroidism and malignancy-associated hypercalcemia. Hypercalcemia occurs when calcium influx into the extracellular fluid exceeds renal excretory capacity. It is defined as a total serum calcium level greater than 10.2 mg/dL. Treatment involves stabilizing the patient with intravenous fluids, promoting calcium excretion with diuretics, and administering bisphosphonates to reduce bone resorption in malignancy-associated cases. Surgical removal of parathyroid adenomas is required for symptomatic primary hyperparathyroidism.
Seminar on calcium
This document discusses calcium metabolism and provides details on calcium homeostasis, absorption, excretion, and the roles of parathyroid hormone and vitamin D. It also covers hypocalcemia and hypercalcemia, defining each condition and describing causes, clinical manifestations, diagnostic workup, and treatment approaches. Hypocalcemia can result from neonatal issues, vitamin D deficiency, hypoparathyroidism, or other causes. Hypercalcemia has causes including parathyroid hormone excess, malignancy, vitamin D excess, and genetic conditions.
Hypercalcemia
This document presents a case study of a 41-year-old woman diagnosed with hypercalcemia caused by milk alkali syndrome. She was brought to the emergency department with nausea, vomiting, and altered mental status. Tests found her blood calcium level to be very high. Her history of consuming large amounts of antacids containing calcium and sodium bicarbonate led to the diagnosis of milk alkali syndrome. Milk alkali syndrome occurs when excessive oral intake of calcium and alkali impairs the kidney's ability to excrete calcium, resulting in hypercalcemia. The document then provides background information on calcium regulation and the various causes, symptoms, diagnostic evaluation, and treatment approaches for hypercalcemia.
Hypercalcaemia
Hypercalcemia is elevated calcium levels in the blood. Normal calcium levels are 2.12-2.65 mmol/L. It is uncommon, affecting 4 in 100,000 people per year, and more common in females ages 50-60. Signs and symptoms include bone pain, kidney stones, constipation, fatigue, and renal failure. Causes include primary hyperparathyroidism, malignancy, certain drugs, and granulomatous diseases. Diagnosis involves blood and imaging tests. Treatment consists of IV fluids, correcting electrolyte imbalances, diuretics, treating the underlying cause, bisphosphonates, steroids, and calcitonin. Untreated severe hypercalcemia can lead to osteop
Crf
This document discusses chronic renal failure (CRF). CRF is characterized by the progressive and irreversible deterioration of renal function due to the slow destruction of renal tissue, eventually leading to death when enough nephrons have been damaged. CRF is caused by conditions like diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. It progresses through stages of decreased renal reserve, renal insufficiency, renal failure, and end-stage kidney disease. Medical management of CRF focuses on controlling blood pressure and reducing edema, gastrointestinal side effects, and pruritis.
Endocrine system
This document discusses polyuria and hypercalcemia. It defines polyuria as excessive urination of over 2.5L per day. Polyuria can be caused by diabetes insipidus, diabetes mellitus, diuretics, or renal failure. Nocturnal polyuria is a key symptom affecting the elderly. Hypercalcemia is defined as high blood calcium levels, which can be caused by primary hyperparathyroidism or other factors like cancer. Symptoms include nausea, vomiting, and weakness. Treatment involves lowering calcium through surgery, medication or IV fluids.
Calcium Metabolism and Hypocalcemia
Calcium Metabolism - sources, physiology (absorption, hemostasis), functions.
Hypocalcemia - causes (PTH absent, PTH ineffective, PTH overwhelmed), treatment.
A Short Presentation on Hypercalcaemia
This document presents a case study of a 49-year-old male who presented with hypercalcemia. His investigations revealed a calcium level of 3.2 mmol/L. He had symptoms of abdominal discomfort, fatigue, and increased thirst. His examination and tests ruled out various potential causes of hypercalcemia. He was found to have elevated PTH, consistent with primary hyperparathyroidism. He was treated with IV fluids and bisphosphonates and will likely require parathyroidectomy surgery to address the underlying cause of his hypercalcemia.
An introduction to alcoholic liver disease part 2
This document provides an overview of alcoholic liver disease (ALD) in multiple parts. It begins by discussing how alcohol is metabolized in the liver and can cause liver dysfunction by damaging hepatocytes and producing toxic byproducts. The major manifestations of ALD are then described, including jaundice, coagulopathy, and encephalopathy, which result from impaired bilirubin metabolism, clotting factor synthesis, and other liver functions. The document outlines the spectrum of ALD from fatty liver to alcoholic hepatitis to cirrhosis. Diagnosis involves assessing alcohol use history and liver enzymes/function. The characteristics of fatty liver, alcoholic hepatitis, and cirrhosis are summarized.
Approach to patient with hypo/hyper calcaemia
This document discusses calcium homeostasis and disorders of calcium metabolism. It begins by describing the functions of calcium in the body and where calcium is stored. It then discusses calcium regulation by parathyroid hormone, vitamin D, and calcitonin. Causes, signs and symptoms, and treatment approaches for hypercalcemia and hypocalcemia are reviewed. The key points are that calcium levels are tightly controlled by hormones to maintain levels between 2.25-2.62 mmol/L and that disorders can result from excess or deficiencies of these regulating hormones.
Hypercalcemia
Hypercalcemia is commonly caused by primary hyperparathyroidism or malignancy. It can be life-threatening in severe cases. Diagnosis involves measuring serum calcium, PTH, and assessing for underlying causes. Treatment depends on the underlying condition but may involve surgery for hyperparathyroidism or addressing the malignancy. Complications can impact the kidneys, GI tract, cardiovascular system, muscles and bones.
Hypercalcaemia of Malignancy
1) A 10-year-old Labrador presented with PU/PD, lethargy, weight loss, and anorexia. Biochemistry revealed hypercalcemia.
2) Thoracic radiographs and ultrasound identified a cranial mediastinal mass. FNA was non-diagnostic but PCR suggested a mixed population of T-cells, consistent with mediastinal lymphoma.
3) The diagnosis was stage Vb mediastinal T-cell lymphoma, causing hypercalcemia of malignancy through PTHrP secretion and increased bone resorption. Treatment was palliative with steroids to reduce hypercalcemia and improve appetite.
Approach to Hypercalcemia
This document discusses calcium homeostasis and hypercalcemia. It notes that calcium is critical for many physiological functions and is mainly stored in bones. Hypercalcemia can be caused by primary hyperparathyroidism, vitamin D excess, certain malignancies, and other conditions. The diagnostic approach involves distinguishing between hyperparathyroidism and hypercalcemia of malignancy based on lab tests. Treatment focuses on rehydration, increasing calciuresis, and decreasing bone resorption or intestinal calcium absorption using medications like calcitonin, bisphosphonates, glucocorticoids, or dialysis depending on the severity of hypercalcemia.
Serum Electrolytes
This document discusses sodium and potassium levels in the body. It begins by outlining the distribution of sodium, potassium, and water in the body and their roles in homeostasis. It then describes pathological conditions that can result from imbalances in sodium and potassium levels. Various techniques for estimating serum sodium and potassium are also outlined, including ion selective electrodes, atomic absorption spectroscopy, and flame emission photometry.
Calcium metabolism & hypercalcemia
This document discusses calcium homeostasis and hypercalcemia. It notes that approximately 99% of calcium in the body is stored in bones and teeth, with the remaining 1% distributed in the extracellular fluid, intracellular fluid, and soft tissues. Hypercalcemia is defined as a serum calcium level above 10.5 mg/dL. Causes include primary hyperparathyroidism in about 50% of cases of hypercalcemia, as well as malignancy, vitamin D toxicity, hyperthyroidism, and certain genetic conditions. Symptoms range from being mild or absent with mild increases in calcium to severe symptoms like confusion and coma with rapid or large rises in calcium levels.
Adverse drug reaction drugs
This document summarizes the adverse reactions, mechanisms, and management of several common drugs including paracetamol, acetylsalicylic acid, and others. It specifically discusses paracetamol toxicity occurring through generation of a toxic metabolite in the liver. Management includes decontamination and antidote therapy with N-acetyl cysteine. Aspirin toxicity is also reviewed, noting effects from salicylate-induced oxidative phosphorylation and metabolic acidosis. Treatment focuses on gastric lavage, fluid replacement, hemodialysis, sodium bicarbonate, and activated charcoal.
Hypocalcemia
This document discusses hypocalcemia, defined as a serum calcium level below 8.5 mg/dl. It may be caused by low or high parathyroid hormone levels. Causes of low PTH include parathyroid gland agenesis, destruction, or dysfunction. Causes of high PTH include vitamin D deficiency, kidney disease impairing vitamin D activation, or drugs. Symptoms include increased neuromuscular excitability. Investigations include calcium, albumin, phosphorus, magnesium and PTH levels. Treatment involves vitamin D, calcium supplements, and magnesium as needed.
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Iron sulphate
Iron(II) sulfate is produced as a byproduct from passing steel through sulfuric acid pickling baths during processing. It is also commercially prepared by oxidizing pyrite. Iron(II) sulfate has been used as a photographic developer, to color wood, and stain concrete. While it is mainly used now as a precursor to other iron compounds, it was also historically used in inks and to reduce chromate in cement. Side effects can include constipation.
Penicillin allergy
1. Penicillin is the most prevalent reported medication allergy, though up to 90% of reported allergies are inaccurate due to factors like mislabeling or reactions caused by underlying infections rather than the drug.
2. Penicillin allergy diagnosis requires consideration of the chemical structure of penicillin and related drugs, the mechanisms of cross-reactivity, and test methods like skin testing and drug provocation.
3. Skin testing with penicillin reagents including the major determinant (benzylpenicilloyl-polylysine) and minor determinant mixture is currently the most reliable diagnostic method for evaluating IgE-mediated penicillin allergy.
Pharmacology kinetic and clearance
This document discusses pharmacokinetics and the movement of drugs through the body over time. It covers the typical processes of absorption, distribution, metabolism and elimination that drugs undergo. It also describes various routes of drug administration including oral, parenteral, inhalation and others. Factors that influence drug absorption like pH, blood flow, surface area and contact time are also examined.
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FDA advises healthcare professionals and patients about serious skin reactions induced by Paracetamol.
Terpenes
Plants produce terpenes as secondary metabolites to defend against herbivores and pathogens. Terpenes are the largest class of plant secondary metabolites and are formed from polymerization of isoprene units. They include mono-, sesqui-, and diterpenes. Many terpenes have antimicrobial or insecticidal properties and are toxic to herbivores. Some terpenes produced as essential oils in plants can act as feeding deterrents. Terpenes also play roles in plant growth and development. Additionally, some terpene compounds released from forests can increase cloud thickness and reflect sunlight, acting as a natural cooling mechanism for the planet.
TRITERPENOIDS
Terpenoids are regarded as derivatives of polymers of isoprene ,joined head to tail and widely distrubuted in plant kindom.
Terpenes
Terpenes are secondary metabolites formed by joining isoprene units together. Isoprene, which has the formula C5H8, is considered the basic building block of terpenes. Terpenes are unsaturated hydrocarbons that vary in structure and size depending on the number of isoprene units linked together. They are used widely in fragrances, essential oils, and medicines. Terpenoids refer to oxygenated terpenes that result when terpenes are oxidized.
Iron Salt Comparison New
The document discusses newer aspects of iron supplementation. It summarizes that iron amino acid chelate, or ferrous bis glycinate, has advantages over other forms of iron supplementation, including being non-buffered in the stomach, non-precipitated in the intestine, not antagonized by phytates, and having superior and dependable bioavailability due to its unique chelate design, which potentially allows for smaller doses with fewer side effects. The document examines what is known, unknown, and needs to be known about different forms of iron supplementation and their absorption parameters.
Paracetamol overdose
A 34-year-old British woman presented to the emergency department 30 minutes after ingesting approximately 100 acetaminophen tablets with alcohol in a suspected suicide attempt. She was treated with activated charcoal and intravenous N-acetylcysteine. On the first day of admission she developed abdominal pain and vomiting. Her liver function tests remained normal during her 3-day admission before she discharged herself against medical advice to return to the UK. Paracetamol overdose is commonly seen and requires prompt treatment with N-acetylcysteine to prevent liver damage from toxic metabolite accumulation if ingestion exceeds toxic thresholds.
Iron deficiency anemia.
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This document discusses acute kidney injury (AKI), formerly known as acute renal failure, in pediatrics. It defines AKI, describes the causes and pathophysiology, presents approaches to evaluation and management, and outlines treatment of complications. The key points are:
- AKI is defined as an abrupt reduction in kidney function over 48 hours, seen as a rise in creatinine or decrease in urine output.
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paracetamol ferrous sulfate and paclitaxel
- 1. TOXICITY FOR • FERROUS SULPHATE • PARACETAMOL • PACLITAXEL EDITED BY MR MOMPATI LETSWELETSE (CPhT) SECOND YEAR STUDENT
- 2. PARACETAMOL:Mechanism of toxicity• Paracetamol is metabolized to N-acetyl-p-benzoquinone imine (NAPQI).NAPQI is extremely toxic to the liver, as a result of covalent binding to proteins and nucleic acids. However, NAPQI is rapidly detoxified by interaction with glutathione . Overdoses of acetaminophen deplete hepatic glutathione stores and allow liver injury to occur. • Signs and symptoms • PHASE ONE(<24hrs):nausea,vomiting,pallor,sweating • PHASE TWO(24-72hrs):signs of increasing liver damage(one may experience upper-quadrant pain)In some cases, acute kidney failure maybe the clinical manifestation. • PHASE THREE(3-5days):complications of massive hepatic necrosis leading to hepatic failure with complications,coagulation defects,hypoglycemia,kidney failure,cerebral edema,sepsi,multiple organ failure and death
- 3. SIGNS AND SYMPTOMS Anorexia(lack or loss of appetite for food) nausea, or vomiting hepatic necrosis becomes evident Acute renal failure
- 4. DIAGONOSIS Liver function tests: Liver function tests can show if your liver is working properly. Prothrombin time (PT) and INR rates: These tests measure how long it takes for your blood to clot. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, liver transaminases, and prothrombin time
- 5. ANTIDOTE: ACETYLCYSTEINE • Acetylcysteine works to reduce paracetamol toxicity by replenishing body stores of the antioxidant glutathione. Glutathione react with the toxic NAPQI metabolite so that it does not damage cells and can be safely excreted.
- 6. SAFETY PROFILE • Safe and can be used in pregnancy..it causes no harm to the baby, • Contra indicated in allergic patients , asthma and post surgery patients.
- 7. FERROUS SULPHATE:MECHANISM OF TOXICITY • Local • Direct corrosive effect on the gastrointestinal(GI) mucosa manifests with symptoms ranging from vomiting and diarrhea to haematemesis (the vomiting of blood).and melaena(the production of dark sticky faeces containing partly digested blood, as a result of internal bleeding).Large GI fluid losses may contribute significant hypovolaemia. Systemic toxicity does not occur in the absence of GI symptoms When the absorbed iron is not bound to protein, it produces a variety of harmful free radicals. Acute iron toxicosi causes both a direct corrosive effect on the gastrointestinal tract and cellular damage due to circulating unbound iron.
- 8. SIGNS AND SYMPTOMS • Low blood pressure • Fast and weak pulse • Hepatorenal failure • Coma • Hypoglycaemia (deficiency of glucose in the bloodstream.) • Metabolic acidosis due to disruption of cellular metabolism • Acute hepatic failure with jaundice
- 9. DIAGONOSIS • Elevation of the white blood count (> 15,000) or blood glucose (> 150 mg/dL) or visible radiopaque pills on abdominal x-ray also suggests significant ingestion
- 10. ANTIDOTE: DESFERRIOXAMINE • Desferrioxamine is a chelating agent it binds with free iron in the bloodstream and forms a water soluble desferroxamine-iron complex.
- 11. Safety Profile • Desferrioxamine -iron complex is renally excreted. If oliguria(the production of abnormally small amounts of urine) or anuria develop, peritoneal dialysis or haemodialysis may become necessary to remove ferrioxamine
- 12. PACLITAXEL :MECHANISM OF TOXICITY • Paclitaxel may induce bradyarrhythmia(is a slow heart rate) and conduction defects directly through action on the purkinje system or indirectly through its vehicle, polyoxythylated castor oil. When used in combination with doxorubicin, Paclitaxel appears to enhance cardio toxicity by altering doxorubicin pharmacokinetics and increasing the myocyte formation of doxorubicinol, the major metabolite of doxorubicin
- 13. SIGNS AND SYMPTOMS • Severe hypersensitivity reactions, including death, reported. Hypotension, bradycardia, ECG abnormalities, conduction abnormalities may occur. Fatal myocardial infarction 15 h into infusion reported.
- 14. Signs and symptoms sinus bradycardia Heart block Premature ventricular contraction Ventricular tachycardia severe hypotension bone marrow suppression peripheral neurotoxicity and mucositis.
- 15. ANTIDOTE • There is no known antidote. There is no specific antidote for overdose. Supportive therapy will help sustain the patients in toxicity. Resuscitate if indicated