AMMONIA TOXICITY PowerPoint presentation
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COPPER METABOLISM
Copper is an essential trace element that is present in all tissues, especially the liver, kidneys, heart and skeletal muscles. It serves as a cofactor for several enzymes involved in processes like iron transport, collagen crosslinking, melanin synthesis and oxidative phosphorylation. Copper deficiency can result in neutropenia, anemia, bone abnormalities and neurological issues. Menkes and Wilson's diseases are genetic disorders of copper metabolism that involve defects in copper transport and result in copper accumulation in tissues.
HYPOKALEMIA .pptx
This document discusses the physiology and pathophysiology of hypokalemia. It covers the normal distribution and regulation of potassium in the body, as well as causes of hypokalemia including decreased intake, extrarenal losses, and renal losses. Types of renal tubular acidosis that can cause hypokalemia are described. The approach to hypokalemia involves considering underlying causes like Bartter syndrome, Gitelman syndrome, Liddle's syndrome, and hypomagnesemia. Treatment principles for correcting hypokalemia are provided.
Fluid and Electrolyte Management in Surgery.ppt
This document provides an outline and introduction to fluid and electrolyte management in surgery. It discusses the normal distribution and balance of body water and electrolytes like sodium, potassium, calcium and magnesium. It describes various fluid and electrolyte disorders that can occur including volume disturbances, concentration disturbances and composition disturbances. It covers causes, clinical features and treatment of conditions like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia and acid-base imbalances. The document emphasizes the importance of fluid and electrolyte management in the perioperative care of surgical patients.
Electrolytes Disturbances
This document discusses various electrolyte disturbances and their causes and effects. It covers sodium, potassium, magnesium, and trace elements. Key points include:
- Sodium is a major extracellular cation and is lost through sweat, GI tract, and urine. Hyponatremia can result from GI loss or inappropriate ADH secretion and causes neurological symptoms.
- Potassium is an important intracellular cation and is lost through the GI tract. Hypokalamia can result from GI loss and causes neuromuscular and cardiac issues.
- Magnesium is mainly stored in bone and muscles. Hypomagnesemia can block PTH and cause hypocalcemia and hypokalemia. It causes neurological
2disorders of potassium balance 2
The document discusses disorders of potassium balance, including hypokalemia (low potassium levels) and hyperkalemia (high potassium levels). It covers the normal regulation and distribution of potassium in the body, causes and manifestations of hypokalemia and hyperkalemia, ECG changes associated with each, and their treatment approaches.
lecture 6 copper.pptx
Copper is an essential micronutrient that is a component of many metalloenzymes. It is present in high concentrations in the liver and kidney. Dietary copper is absorbed in the duodenum and transported to the liver bound to albumin or caeruloplasmin. In the liver, copper is incorporated into newly synthesized caeruloplasmin and exported into the bloodstream or tissues. Genetic disorders that impact copper transport, such as Menkes disease and Wilson's disease, can result in copper accumulation or deficiency in tissues with neurological or hepatic symptoms.
urea cycle.pptx
The document outlines key aspects of amino acid metabolism and the urea cycle. It begins by describing the breakdown of muscle proteins and the transport of amino acids between tissues like liver and muscle. It then details the formation of ammonia from amino acid catabolism and its detoxification via the urea cycle in the liver. The summary concludes by mentioning several urea cycle disorders that can result from deficiencies in cycle enzymes, causing hyperammonemia.
Potassium disorders-hypokalemia and hyperkalemia
This document summarizes potassium disorders including hypokalemia and hyperkalemia. It discusses the normal physiology of potassium regulation and mechanisms that can lead to imbalances. For hypokalemia, causes include decreased intake, redistribution into cells, and increased loss from the kidneys or gastrointestinal tract. Hyperkalemia can result from shifts of potassium into the extracellular space, inadequate renal excretion, and excessive potassium intake. Clinical features and treatment approaches focusing on antagonizing cardiac effects, redistributing potassium into cells, and removing excess potassium are outlined.
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COPPER METABOLISM
Copper is an essential trace element that is present in all tissues, especially the liver, kidneys, heart and skeletal muscles. It serves as a cofactor for several enzymes involved in processes like iron transport, collagen crosslinking, melanin synthesis and oxidative phosphorylation. Copper deficiency can result in neutropenia, anemia, bone abnormalities and neurological issues. Menkes and Wilson's diseases are genetic disorders of copper metabolism that involve defects in copper transport and result in copper accumulation in tissues.
HYPOKALEMIA .pptx
This document discusses the physiology and pathophysiology of hypokalemia. It covers the normal distribution and regulation of potassium in the body, as well as causes of hypokalemia including decreased intake, extrarenal losses, and renal losses. Types of renal tubular acidosis that can cause hypokalemia are described. The approach to hypokalemia involves considering underlying causes like Bartter syndrome, Gitelman syndrome, Liddle's syndrome, and hypomagnesemia. Treatment principles for correcting hypokalemia are provided.
Fluid and Electrolyte Management in Surgery.ppt
This document provides an outline and introduction to fluid and electrolyte management in surgery. It discusses the normal distribution and balance of body water and electrolytes like sodium, potassium, calcium and magnesium. It describes various fluid and electrolyte disorders that can occur including volume disturbances, concentration disturbances and composition disturbances. It covers causes, clinical features and treatment of conditions like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia and acid-base imbalances. The document emphasizes the importance of fluid and electrolyte management in the perioperative care of surgical patients.
Electrolytes Disturbances
This document discusses various electrolyte disturbances and their causes and effects. It covers sodium, potassium, magnesium, and trace elements. Key points include:
- Sodium is a major extracellular cation and is lost through sweat, GI tract, and urine. Hyponatremia can result from GI loss or inappropriate ADH secretion and causes neurological symptoms.
- Potassium is an important intracellular cation and is lost through the GI tract. Hypokalamia can result from GI loss and causes neuromuscular and cardiac issues.
- Magnesium is mainly stored in bone and muscles. Hypomagnesemia can block PTH and cause hypocalcemia and hypokalemia. It causes neurological
2disorders of potassium balance 2
The document discusses disorders of potassium balance, including hypokalemia (low potassium levels) and hyperkalemia (high potassium levels). It covers the normal regulation and distribution of potassium in the body, causes and manifestations of hypokalemia and hyperkalemia, ECG changes associated with each, and their treatment approaches.
lecture 6 copper.pptx
Copper is an essential micronutrient that is a component of many metalloenzymes. It is present in high concentrations in the liver and kidney. Dietary copper is absorbed in the duodenum and transported to the liver bound to albumin or caeruloplasmin. In the liver, copper is incorporated into newly synthesized caeruloplasmin and exported into the bloodstream or tissues. Genetic disorders that impact copper transport, such as Menkes disease and Wilson's disease, can result in copper accumulation or deficiency in tissues with neurological or hepatic symptoms.
urea cycle.pptx
The document outlines key aspects of amino acid metabolism and the urea cycle. It begins by describing the breakdown of muscle proteins and the transport of amino acids between tissues like liver and muscle. It then details the formation of ammonia from amino acid catabolism and its detoxification via the urea cycle in the liver. The summary concludes by mentioning several urea cycle disorders that can result from deficiencies in cycle enzymes, causing hyperammonemia.
Potassium disorders-hypokalemia and hyperkalemia
This document summarizes potassium disorders including hypokalemia and hyperkalemia. It discusses the normal physiology of potassium regulation and mechanisms that can lead to imbalances. For hypokalemia, causes include decreased intake, redistribution into cells, and increased loss from the kidneys or gastrointestinal tract. Hyperkalemia can result from shifts of potassium into the extracellular space, inadequate renal excretion, and excessive potassium intake. Clinical features and treatment approaches focusing on antagonizing cardiac effects, redistributing potassium into cells, and removing excess potassium are outlined.
Mineral metabolism
This document discusses mineral metabolism and provides details on specific minerals including sodium, potassium, chloride, sulfur, and calcium. It covers their sources, absorption, functions, normal levels, and clinical conditions related to abnormal levels. For each mineral, absorption and excretion processes are described along with roles in the body. Causes and symptoms of both hypo- and hyper- conditions are outlined.
COPPER METABOLISM
This document discusses copper metabolism and abnormalities in copper metabolism. It covers the following key points:
1. Copper is an essential mineral that is involved in many enzyme functions and metabolic reactions. It is absorbed in the small intestine and transported to tissues bound to proteins like albumin and ceruloplasmin.
2. Abnormal copper metabolism can result in Menkes kinky hair syndrome or Wilson's disease. Menkes syndrome is caused by a genetic defect impairing intestinal copper absorption. Wilson's disease results from a genetic defect impairing liver copper transport and ceruloplasmin secretion.
3. Wilson's disease causes copper accumulation in the liver and brain, leading to cirrhosis and neurological symptoms.
Inborn errors of protein metabolism
Inborn errors of metabolism
Definition:- Inborn errors of metabolism occur from a group of rare genetic disorders in which the body cannot metabolize food components normally.
These disorders are usually caused by defects in the enzymes involved in the biochemical pathways that break down food components.
Mineral_ Metabolism_Coppermineralss.pptx
This document provides information about mineral metabolism and copper. It begins with definitions of minerals and their classification as macrominerals or trace elements. It then focuses on copper, discussing its distribution in the body, copper-containing enzymes and their functions, recommended dietary intake, sources, absorption, deficiency disorders like Menkes and Wilson's disease, and conditions associated with copper levels. Menkes disease is an X-linked recessive disorder causing copper deficiency due to problems with intestinal absorption and transport. Wilson's disease results from a genetic defect impairing copper excretion from the liver, leading to copper deposition and damage in various organs.
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.
Renal function
1. The kidneys maintain water and electrolyte balance, blood pH, excrete waste products and toxins, filter the blood, produce erythropoietin, and reabsorb desirable elements.
2. Renal function can be impaired acutely (acute renal failure) or chronically (chronic renal failure). Tests like urea, creatinine, and uric acid help diagnose and monitor kidney function.
3. Kidney diseases include acute tubular necrosis, renal calculi, and gout caused by uric acid crystals. Treatment depends on the underlying cause but may include fluid management, dialysis, and transplantation.
Calcium disturbaces
Calcium metabolism can be disrupted, resulting in hypercalcemia or hypocalcemia. Hypercalcemia is caused by increased bone resorption, GI absorption, or decreased renal excretion and may be due to primary hyperparathyroidism, certain cancers, or excessive vitamin D intake. Hypocalcemia occurs when ionized calcium levels decrease below normal due to hypoparathyroidism, vitamin D deficiency, or other conditions. Symptoms of hypercalcemia include fatigue, nausea, and renal problems while hypocalcemia causes muscle spasms, tingling, and seizures. Treatment depends on the underlying cause and severity but aims to restore normal calcium levels through rehydration, diuretics, bisphosphonates
biochem.pptx
Calcium and phosphorus metabolism are regulated by hormones like calcitriol, parathyroid hormone, and calcitonin to maintain normal levels in the body. Calcium is important for bone health, muscle function, and other cellular processes. The majority of calcium is stored in bones. Phosphorus also has important roles in energy storage and cellular processes. Both are absorbed in the small intestine and levels are regulated by hormones and excretion through the kidneys. Abnormal levels can cause diseases like rickets, osteomalacia, and osteoporosis. Dental issues may also arise from metabolic bone diseases like brown tumors and osteitis deformans.
approach causes management of HYPOKALEMIA.pptx
This document discusses hypokalemia, defined as a low level of potassium in the blood. It covers the normal range of potassium, causes of hypokalemia including decreased intake, redistribution into cells, and increased losses through the kidneys or gastrointestinal tract. Symptoms are related to effects on the cardiovascular, muscular, and endocrine systems. Diagnosis involves measuring potassium levels in blood and urine and considering factors like diuretic use, vomiting, malabsorption issues. Treatment focuses on replacing potassium stores through supplementation or decreasing ongoing losses.
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The document discusses iron metabolism disorders and anemia. It notes that anemia is a decrease in circulating red blood cells, which can be caused by blood loss, decreased red blood cell production, or increased red blood cell destruction. Decreased production of red blood cells can result in normocytic or microcytic anemia depending on whether it impacts the cytoplasmic production of protein or nuclear division/maturation, respectively. Causes of decreased cytoplasmic protein production include disorders of globin synthesis, heme synthesis, and decreased iron availability or utilization. Iron deficiency anemia specifically occurs when iron is not available in its ferrous form needed for electron transport and oxygen carriage.
Sodium homeostasis
This document discusses sodium metabolism and disorders of sodium balance. It begins by outlining the normal functions of sodium in the body, including determining membrane potential and acid-base balance. It then describes normal sodium metabolism, handling, and regulation by factors like the kidneys, aldosterone, and antidiuretic hormone. The document also summarizes approaches to diagnosing and managing sodium imbalances like hyponatremia and hypernatremia. It stresses the importance of first assessing a patient's volume status and correcting deficits or excesses slowly to avoid complications in conditions like cerebral edema or encephalopathy.
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FLUID AND ELECTROLYTE BALANCE AND IMBALANCE.pptx
This document provides an overview of fluid and electrolyte balance, including:
1) It defines key terms like osmolality, electrolytes, and classifications of body fluids and fluid compartments.
2) It describes common electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia, and hyperkalemia and their causes and treatments.
3) It discusses fluid volume disturbances and conditions like edema, and summarizes signs and symptoms of volume deficits and excesses.
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Chronic renal failure
Chronic renal failure (CRF) or end stage renal disease (ESRD) is an irreversible deterioration of renal function that results in uremia or azotemia. It is caused by a progressive reduction in kidney function such that the kidneys can no longer maintain homeostasis. This leads to decreased glomerular filtration rate, hypertrophy of remaining nephrons, inability to concentrate urine, further nephron loss, and loss of excretory and non-excretory renal functions. Management of CRF focuses on preserving renal function, alleviating extra-renal manifestations through medications and dialysis, and improving body chemistry through diet and medication.
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This document discusses iron in health and disease. It begins by stating that iron is an essential nutrient that plays a vital role in physiological functions. Iron deficiency is the most common micronutrient deficiency globally, affecting around 24% of the world's population. The document then discusses dietary sources of iron, requirements by age group, iron's distribution and functions in the body, absorption and transport processes, storage, and excretion. It also covers factors that affect absorption and the signs and stages of iron deficiency and anemia. Treatment options including oral iron therapy, parenteral therapy, and blood transfusion are summarized. The document concludes by mentioning hereditary forms of iron toxicity like neonatal hemochromatosis and hereditary hemochrom
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Mineral metabolism
This document discusses mineral metabolism and provides details on specific minerals including sodium, potassium, chloride, sulfur, and calcium. It covers their sources, absorption, functions, normal levels, and clinical conditions related to abnormal levels. For each mineral, absorption and excretion processes are described along with roles in the body. Causes and symptoms of both hypo- and hyper- conditions are outlined.
COPPER METABOLISM
This document discusses copper metabolism and abnormalities in copper metabolism. It covers the following key points:
1. Copper is an essential mineral that is involved in many enzyme functions and metabolic reactions. It is absorbed in the small intestine and transported to tissues bound to proteins like albumin and ceruloplasmin.
2. Abnormal copper metabolism can result in Menkes kinky hair syndrome or Wilson's disease. Menkes syndrome is caused by a genetic defect impairing intestinal copper absorption. Wilson's disease results from a genetic defect impairing liver copper transport and ceruloplasmin secretion.
3. Wilson's disease causes copper accumulation in the liver and brain, leading to cirrhosis and neurological symptoms.
Inborn errors of protein metabolism
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Definition:- Inborn errors of metabolism occur from a group of rare genetic disorders in which the body cannot metabolize food components normally.
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This document provides information about mineral metabolism and copper. It begins with definitions of minerals and their classification as macrominerals or trace elements. It then focuses on copper, discussing its distribution in the body, copper-containing enzymes and their functions, recommended dietary intake, sources, absorption, deficiency disorders like Menkes and Wilson's disease, and conditions associated with copper levels. Menkes disease is an X-linked recessive disorder causing copper deficiency due to problems with intestinal absorption and transport. Wilson's disease results from a genetic defect impairing copper excretion from the liver, leading to copper deposition and damage in various organs.
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.
Renal function
1. The kidneys maintain water and electrolyte balance, blood pH, excrete waste products and toxins, filter the blood, produce erythropoietin, and reabsorb desirable elements.
2. Renal function can be impaired acutely (acute renal failure) or chronically (chronic renal failure). Tests like urea, creatinine, and uric acid help diagnose and monitor kidney function.
3. Kidney diseases include acute tubular necrosis, renal calculi, and gout caused by uric acid crystals. Treatment depends on the underlying cause but may include fluid management, dialysis, and transplantation.
Calcium disturbaces
Calcium metabolism can be disrupted, resulting in hypercalcemia or hypocalcemia. Hypercalcemia is caused by increased bone resorption, GI absorption, or decreased renal excretion and may be due to primary hyperparathyroidism, certain cancers, or excessive vitamin D intake. Hypocalcemia occurs when ionized calcium levels decrease below normal due to hypoparathyroidism, vitamin D deficiency, or other conditions. Symptoms of hypercalcemia include fatigue, nausea, and renal problems while hypocalcemia causes muscle spasms, tingling, and seizures. Treatment depends on the underlying cause and severity but aims to restore normal calcium levels through rehydration, diuretics, bisphosphonates
biochem.pptx
Calcium and phosphorus metabolism are regulated by hormones like calcitriol, parathyroid hormone, and calcitonin to maintain normal levels in the body. Calcium is important for bone health, muscle function, and other cellular processes. The majority of calcium is stored in bones. Phosphorus also has important roles in energy storage and cellular processes. Both are absorbed in the small intestine and levels are regulated by hormones and excretion through the kidneys. Abnormal levels can cause diseases like rickets, osteomalacia, and osteoporosis. Dental issues may also arise from metabolic bone diseases like brown tumors and osteitis deformans.
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This document discusses hypokalemia, defined as a low level of potassium in the blood. It covers the normal range of potassium, causes of hypokalemia including decreased intake, redistribution into cells, and increased losses through the kidneys or gastrointestinal tract. Symptoms are related to effects on the cardiovascular, muscular, and endocrine systems. Diagnosis involves measuring potassium levels in blood and urine and considering factors like diuretic use, vomiting, malabsorption issues. Treatment focuses on replacing potassium stores through supplementation or decreasing ongoing losses.
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The document discusses iron metabolism disorders and anemia. It notes that anemia is a decrease in circulating red blood cells, which can be caused by blood loss, decreased red blood cell production, or increased red blood cell destruction. Decreased production of red blood cells can result in normocytic or microcytic anemia depending on whether it impacts the cytoplasmic production of protein or nuclear division/maturation, respectively. Causes of decreased cytoplasmic protein production include disorders of globin synthesis, heme synthesis, and decreased iron availability or utilization. Iron deficiency anemia specifically occurs when iron is not available in its ferrous form needed for electron transport and oxygen carriage.
Sodium homeostasis
This document discusses sodium metabolism and disorders of sodium balance. It begins by outlining the normal functions of sodium in the body, including determining membrane potential and acid-base balance. It then describes normal sodium metabolism, handling, and regulation by factors like the kidneys, aldosterone, and antidiuretic hormone. The document also summarizes approaches to diagnosing and managing sodium imbalances like hyponatremia and hypernatremia. It stresses the importance of first assessing a patient's volume status and correcting deficits or excesses slowly to avoid complications in conditions like cerebral edema or encephalopathy.
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This document discusses various minerals including sodium, potassium, magnesium, chloride, calcium, and selenium. It provides details on their roles, normal levels, and consequences of deficiency or excess. Sodium, potassium, chloride, and calcium are classified as macro-minerals that are essential for fluid balance, muscle and nerve function. Magnesium and selenium are micro-minerals that serve important roles in enzyme reactions and antioxidant defense. The document outlines conditions like hypernatremia, hypokalemia, hypomagnesemia that can result from imbalances in these important minerals.
FLUID AND ELECTROLYTE BALANCE AND IMBALANCE.pptx
This document provides an overview of fluid and electrolyte balance, including:
1) It defines key terms like osmolality, electrolytes, and classifications of body fluids and fluid compartments.
2) It describes common electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia, and hyperkalemia and their causes and treatments.
3) It discusses fluid volume disturbances and conditions like edema, and summarizes signs and symptoms of volume deficits and excesses.
WILLIAM__FLUID_AND_ELECTROLYTE[1].pptx
This document provides an overview of fluid and electrolyte management. It discusses the anatomy of body fluids and electrolyte composition. It describes average fluid intake and output in healthy adults and the distribution of electrolytes in extracellular fluid and intracellular fluid. It then classifies disturbances in fluid volume and concentration/composition. Specific electrolyte abnormalities like sodium, potassium, calcium, magnesium, phosphate and acid-base disorders are explained in detail, along with their causes, signs/symptoms, and management approaches.
Chronic renal failure
Chronic renal failure (CRF) or end stage renal disease (ESRD) is an irreversible deterioration of renal function that results in uremia or azotemia. It is caused by a progressive reduction in kidney function such that the kidneys can no longer maintain homeostasis. This leads to decreased glomerular filtration rate, hypertrophy of remaining nephrons, inability to concentrate urine, further nephron loss, and loss of excretory and non-excretory renal functions. Management of CRF focuses on preserving renal function, alleviating extra-renal manifestations through medications and dialysis, and improving body chemistry through diet and medication.
Iron in health and disease
This document discusses iron in health and disease. It begins by stating that iron is an essential nutrient that plays a vital role in physiological functions. Iron deficiency is the most common micronutrient deficiency globally, affecting around 24% of the world's population. The document then discusses dietary sources of iron, requirements by age group, iron's distribution and functions in the body, absorption and transport processes, storage, and excretion. It also covers factors that affect absorption and the signs and stages of iron deficiency and anemia. Treatment options including oral iron therapy, parenteral therapy, and blood transfusion are summarized. The document concludes by mentioning hereditary forms of iron toxicity like neonatal hemochromatosis and hereditary hemochrom
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Identification and nursing management of congenital malformations TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
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The Electrocardiogram - Physiologic Principles
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Identification and nursing management of congenital malformations .pptx
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AMMONIA TOXICITY PowerPoint presentation
- 1. AMMONIA TOXICITY Eric Mbindo Njunju Bsc; Msc
- 2. • Breakdown of amino acids and nucleic acids
- 3. Liver • Filters ammonia out of blood • Renders it inert • Converts to urea • Eliminated in urine Importance of a Healthy Liver
- 4. • Normal <50µmol/L • 100µmol/L- disturbance in consciousness • 200µmol/L -coma and convulsions • Tremors, slurring speech, blurring vision
- 5. • Liver converts ammonia into urea- urine • Impaired liver function- excessive concentrations of ammonia in blood (ammonia toxicity)-fatal
- 6. • In CNS the brain’s defense is severely challenged – Short circuit of transport of K+ into brain cells – Cells absorb excessive amounts of K+ and cl-
- 7. • Reductive amination of α-ketoglutarate- limits Krebs cycle- reduction in levels of ATP and NADH
- 8. • Acquired hyperammonemia-formation of collateral circulation- liver cirrhosis, hepatitis, biliary obstruction- detoxification of ammonia severely impaired
- 9. • Inherited hyperammonemia-genetic deficiencies of any of the 5 enzymes of the urea cycle • Prevalence 1 in 30,000 live births • Inability to synthesize urea- mental retardation
- 10. UREA CYCLE
- 11. • Converts highly toxic ammonia to urea for excretion • 1st metabolic cycle to be discovered