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1. The document discusses electrolyte management focusing on potassium and calcium. It covers the physiology, causes, signs and symptoms, and treatment of hyperkalemia, hypokalemia, hypercalcemia, and hypocalcemia. 2. Treatment for hyperkalemia includes calcium gluconate to stabilize the myocardium as well as sodium bicarbonate, nebulized albuterol, and insulin with dextrose. Hypokalemia treatment involves potassium supplementation via infusion. 3. Calcium physiology is discussed along with caution that aggressive calcium repletion can cause circulatory shock due to intracellular calcium overload. Treatment is indicated for symptomatic hypocalcemia or ionized
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This document summarizes key points about the management of acute pancreatitis. It discusses the epidemiology, etiology, clinical presentation, diagnostic evaluation, determination of severity, treatment approaches, and complications of acute pancreatitis. Management depends on determining if the pancreatitis is mild, moderate, or severe based on the presence of organ failure or local complications on imaging. Nutritional support, antibiotics, and drainage of fluid collections are addressed.
Vitamin k MUHAMMAD MUSTANSAR
Vitamin K is essential for blood clotting as it is required for the production of proteins involved in coagulation like prothrombin. There are two forms - K1 derived from plants and K2 produced by intestinal bacteria. Vitamin K acts as a cofactor for the gamma carboxylation of glutamic acid residues in clotting factors to enable their biological activity in clot formation. A deficiency can result in bleeding issues as it decreases the synthesis of factors II, VII, IX and X.
Hypocalcemia
Hypocalcemia has various presentations and can lead to significant morbidity if left untreated. The most common cause is hypoalbuminemia from conditions like cirrhosis or malnutrition that lower serum calcium levels. Other potential causes include vitamin D deficiency, parathyroid issues, medications, and critical illnesses like sepsis. Treatment involves identifying and addressing the underlying cause, as well as replacing calcium, often intravenously, to resolve symptoms and normalize calcium levels. Calcium levels must be closely monitored during treatment until stabilized.
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.
Hypocalcemic tetany
Calcium is essential for nerve conduction, muscle contraction and bone formation. Hypocalcemia can result from inadequate intake, impaired absorption or increased excretion of calcium. It causes symptoms like muscle cramps, tetany and convulsions. Hypocalcemia is commonly caused by hypoparathyroidism, magnesium depletion, vitamin D deficiency or disorders affecting its metabolism. Treatment depends on severity and cause but generally involves calcium and vitamin D supplementation intravenously or orally.
VITAMIN K, [MEDICINAL CHEMISTRY] BY P.RAVISANKAR,STRUCTURES OF VITAMIN K1 AND...
VITAMIN K, [MEDICINAL CHEMISTRY] BY P.RAVISANKAR,STRUCTURES OF VITAMIN K1 AND K2, CHEMISTRY, RECOMMENDED DIETARY INTAKE, SOURCES OF VITAMIN K, BLOOD COAGULATION, ROLE OF VITAMIN K, FUNCTIONS, MECHANISM OF ACTION, VITAMIN K DEFICIENCY, DURG INTERACTIONS, SUMMARY.
BY P. RAVISANKAR, VIGNAN PHARMACY COLLEGE, VADLAMUDI, GUNTUR, A.P, INDIA.
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Hypocalcemia
This document discusses hypocalcemia in neonates. It defines hypocalcemia and describes the importance of calcium for biochemical processes. It outlines the risk factors for early and late onset neonatal hypocalcemia. Early onset can present within 72 hours and is often seen in preterm infants, infants of diabetic mothers, and those with perinatal asphyxia. Symptoms include neuromuscular irritability, seizures, and cardiac involvement. Treatment involves calcium supplementation, either prophylactically for high-risk infants or through IV bolus or continuous infusion for symptomatic cases. Late onset hypocalcemia presents after 7 days and may be caused by hypomagnesemia, high phosphate load, or vitamin D deficiency.
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This document summarizes hypocalcemia in goats and sows. It describes the condition as acute hypocalcemia around the time of parturition, characterized by nervous system signs like ataxia and recumbency. Causes include low serum calcium due to heavy lactation demands, low parathyroid function, and estrogen effects. Treatment involves calcium supplementation, such as calcium borogluconate intravenously. Prevention focuses on dietary calcium intake and vitamin D supplementation in the weeks before parturition.
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Alterations of-potassium-metabolism
Potassium is the most abundant cation in the human body, located mainly intracellularly. Serum potassium levels are tightly regulated between 3.5-5 mEq/L through hormones like insulin and mechanisms in the kidneys and digestive tract. Alterations in potassium levels can cause neuromuscular and cardiac issues due to potassium's role in cell excitability. Hypokalemia is a serum potassium below 3.5 mEq/L and can be caused by excessive losses or intracellular shifts, presenting as muscle weakness. Hyperkalemia, above 5 mEq/L, is more serious as it can cause fatal arrhythmias and is due to excess intake or intracellular shifts, initially showing peaked T waves on ECG.
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This document discusses alterations in potassium metabolism, including hypokalemia and hyperkalemia. It covers the physiological considerations of potassium regulation in the body, with 98% located intracellularly and serum levels normally between 3.5-5 mEq/L. Rapid regulation of potassium involves the sodium-potassium pump and hormones like insulin and catecholamines. Causes, clinical presentations, and treatments are described for both hypokalemia and hyperkalemia. Hypokalemia can result from excessive losses or intracellular shifts, while hyperkalemia involves a positive potassium balance or rapid extracellular shifts. Treatments aim to correct the underlying cause, stabilize cardiac function, shift potassium intracellularly, and promote excretion.
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This document discusses hypokalemia and hyperkalemia. It defines normal potassium levels and factors that influence potassium levels. Hypokalemia is defined as a potassium level below 3.5 mEq/L and can be caused by decreased intake, shifts of potassium into cells, or increased excretion. Hyperkalemia is a potassium level above 5.5 mEq/L and can result from increased intake, decreased excretion, or shifts of potassium out of cells. Clinical features and treatment approaches are described for both hypokalemia and hyperkalemia.
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This document discusses potassium disorders including hypokalemia and hyperkalemia. It defines normal potassium levels and factors that can decrease or increase potassium levels. For hypokalemia, it describes clinical features and recommendations for oral or IV potassium replacement depending on severity. For hyperkalemia, it outlines causes such as decreased excretion or increased intake, describes ECG changes, and recommends emergency treatments like calcium gluconate or glucose/insulin to stabilize the myocardium followed by potassium-shifting therapies.
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THIS SEMINAR GIVES THE BASIC OVERVIEW THAT HOW YOU CAN MANAGE THE PATIENT WHO COMES TO YOU A FLUID AND ELECTROLYTE IMBALANCE . AND BASIC MECHANISM OF HOMEOSTASTIS
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This document discusses electrolyte imbalances and their management. It focuses on potassium, magnesium, calcium, and their hypo- and hyper- conditions. For each electrolyte, it covers normal levels and functions, causes of imbalance, clinical features, and treatment approaches. Treatment involves identifying and correcting the underlying cause, restoring electrolyte levels, and addressing any associated abnormalities through oral or IV supplementation depending on severity. The key is balancing replacement while monitoring for side effects like arrhythmias.
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This document discusses intravenous fluid therapy and electrolyte balance. It begins by describing the body's water content and distribution between intracellular and extracellular fluid compartments. It then reviews daily water intake and losses. Key electrolytes like sodium, potassium, calcium and chloride are described along with normal levels and effects of disturbances. Various intravenous fluid types are outlined including crystalloids like normal saline and lactated ringer's, as well as colloids. Guidelines for intravenous fluid maintenance, deficit replacement and third spacing losses are provided.
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This document discusses hyperkalemia and hypokalemia in neonates. Hyperkalemia is defined as a serum potassium level greater than 5.5 mEq/L and can be caused by increased potassium load, impaired renal excretion, or transcellular shifts. It presents clinically with muscular or respiratory paralysis and arrhythmias. Treatment focuses on cardiac stabilization, shifting potassium intracellularly, enhancing excretion, and treating underlying causes. Hypokalemia is a serum potassium level below 3.5 mEq/L and can result from decreased intake, extrarenal losses, or tubular defects. It presents with muscle weakness and cardiac arrhythmias. Treatment involves replacing potassium orally or intravenously depending on severity
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This document discusses calcium imbalances, including hypercalcemia and hypocalcemia. It begins with introducing calcium, its functions, and homeostasis. Hypercalcemia is defined as a calcium level above 10.5 mg/dL and can be caused by primary hyperparathyroidism, malignancy, or excessive vitamin D and calcium supplementation. Clinical features of hypercalcemia include neurological, cardiovascular, and renal symptoms. Treatment involves rehydration, bisphosphonates, calcitonin, surgery for severe cases. Hypocalcemia is a calcium level below 8.5 mg/dL and can result from vitamin D deficiency, kidney disease, or certain drugs. Symptoms include numbness and tetany. Treatment focuses on calcium and
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This document discusses potassium metabolism and the approach to hyperkalemia. It begins with an introduction to potassium physiology and homeostasis. The kidney plays a key role in potassium excretion, reabsorbing 85-90% in the distal tubules where regulation occurs. Hyperkalemia is defined as a serum potassium over 5.5 mEq/L and can be caused by increased potassium load, impaired excretion, or transcellular shifting. Treatment focuses on stabilizing cardiac cells, rapidly lowering potassium levels, and enhancing elimination while addressing the underlying cause. Emergency therapies include calcium gluconate, insulin therapy, beta agonists, and sodium polystyrene sulfonate.
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This document discusses potassium metabolism and the approach to hyperkalemia. It begins with an introduction to potassium physiology and homeostasis. The kidney plays a key role in potassium excretion, reabsorbing 85-90% in the distal tubules where regulation occurs. Hyperkalemia is defined as a serum potassium over 5.5 mEq/L and can be caused by increased potassium load, impaired excretion, or transcellular shifting. Treatment focuses on stabilizing cardiac cells, rapidly lowering potassium levels, and enhancing elimination while addressing the underlying cause. Emergency therapies include calcium gluconate, insulin therapy, beta agonists, and sodium polystyrene sulfonate.
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This document discusses hyperkalemia and its management. It defines hyperkalemia as a potassium level greater than 5.5 meq/L. It describes the symptoms and signs of hyperkalemia including cardiac arrhythmias and EKG abnormalities. It discusses various treatments for acute hyperkalemia including calcium gluconate, sodium bicarbonate, insulin with glucose, beta-2 agonists, dialysis, and potassium-binding resins. It also addresses approaches to evaluating the underlying cause of hyperkalemia such as assessing renal potassium handling and aldosterone function.
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This document discusses hyperkalemia and its management. It begins with definitions of potassium levels and types of hyperkalemia. Mechanisms of hyperkalemia include extracellular shifts, reduced renal excretion, and decreased gastrointestinal secretion. Clinical signs include cardiac and neuromuscular symptoms. Management focuses on stabilizing the myocardium, shifting potassium into cells, and promoting excretion. Strategies include calcium gluconate, sodium bicarbonate, insulin with glucose, beta-agonists, dialysis, and cation exchange resins. Addison's disease and progesterone are also discussed in relation to potassium handling.
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Shock is a clinical condition caused by inadequate tissue perfusion leading to cellular ischemia. The main causes of death in surgical patients are from shock. Shock can be classified as cardiogenic, hypovolemic, distributive, or obstructive. The key features of shock are hypotension, tachycardia, altered mental status, and signs of poor peripheral perfusion. Treatment involves rapid fluid resuscitation to restore perfusion, with blood products as needed. Ongoing fluid needs and use of vasopressors depends on the type and severity of shock. Monitoring includes vital signs, urine output, lactate, and base deficit to guide resuscitation efforts until tissues are fully resuscitated.
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This document discusses potassium disorders and their causes, signs, and treatments. It covers the following key points:
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This document discusses electrolyte disturbances, focusing on sodium, potassium, and calcium. It provides normal levels, causes of hypo- and hyper- conditions, signs and symptoms, diagnostic tests, and treatment approaches for each electrolyte. For sodium, it describes hyponatremia and hypernatremia in detail. For potassium, it addresses hypokalemia and hyperkalemia. For calcium, it discusses hypocalcemia and the key roles of calcium in the body. The document is intended as an educational reference for electrolyte abnormalities.
Electrolyte disorder
1. Electrolyte imbalances are common in hematology patients due to the underlying disease or drug therapy. Common imbalances include hyponatremia, hypokalemia, hypercalcemia, and pseudohyponatremia.
2. Accurate assessment of fluid and electrolyte status involves clinical examination, fluid balance charts, lab tests of electrolytes, and prescribing appropriate IV fluid replacement as needed.
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Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
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The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
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Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
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Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
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Electrolitos
- 1. Manejo de Transtorno Hidroelectrolìticos: Potasio y Calcio Evelin Mejìa Escobar MR2 Anestesiologia HASS
- 6. Hyperkalemia Hyperkalemia > 5.5 mEq/L
- 11. Hypokalemia Hypokalemia < 3.5 mmol
- 17. CALCIO
- 20. Cifras normales de calcio en la sangre
- 24. Hypocalemia
Editor's Notes
- La pendiente de la curva disminuye en el lado de deficit de la grafica lo cual indica que el cambio es mucho menor cuando hay deficit de este elemento que cuando se acumula En el caso de deficit de potasio la cuantia debe ser el doble que en el exceso de K para que produzca cambio significativo
- If the serum potassium concentration continues to increase, the inward movement of sodium (phase 0) and calcium (phase 2) will diminish;
- La hipercalcemia suele acompañarse de hipercalciuria, que provoca una diuresis osmotica, esta dara posteriormente hipovolemia, con descenso de la excrecion urinaria de calcio y rapido aumento de Ca en el suero por lo tanto el aporte de volumen para corregir la hipovolemia es el primer objetivo en el tratamiento de la hipercalcemia Furosemida para favorecer la excecion urinaria de calcio Calcitonina: Inhibe la resorcion osea Hidrocortisona: Dificulta el creciemirnto del tejido linfoide neoplasico y reforzar las acciones de la vit D Pamidronato + Plicamicina : Inhiben la resorcion osea Dialisis en enf renal Por lo tanto el aporte de volumen para
- El deficit de Mg favorece la hipocalcemia al inhibir la secrecion de paratormona La hipocalcemia por deficit de Mg: Se corrige a menudo sin necesidad de aportar Calcio Alcalosis favorece la fijacion de Ca a la Albumina Las perfusiones de bicarbonato tambien pueden ocasionar hpocalcemia pues el Ca se une al bicarbonato perfundido