A 15-year-old girl presented with lower limb deformity and abnormal gait for 5 years. Laboratory tests found elevated calcium and PTH levels, indicating primary hyperparathyroidism. Primary hyperparathyroidism causes oversecretion of PTH by the parathyroid glands, leading to increased bone resorption and osteopenia on radiographs. Characteristic findings include subperiosteal bone resorption, especially of the fingers, though findings are nonspecific. While imaging has limited diagnostic value, subperiosteal resorption suggests primary hyperparathyroidism.
skeletal disorders of metabolic and endocrine originyashovrattiwari1
Metabolic bone diseases encompass a spectrum of disorders characterized by abnormalities in bone metabolism, structure, and mineralization. These conditions often result from disturbances in the intricate balance between bone formation and resorption, leading to weakened bones prone to fractures, deformities, and other complications. This comprehensive exploration will delve into the pathophysiology, clinical manifestations, diagnostic approaches, and management strategies for various metabolic bone diseases, shedding light on these complex yet fascinating conditions.
Introduction to Metabolic Bone Diseases
The skeleton serves as the structural framework of the body, providing support, protection, and mobility. Maintaining the integrity and strength of bones relies on a delicate equilibrium between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Disruptions in this equilibrium can give rise to metabolic bone diseases, which can be classified broadly into two categories: disorders of bone remodeling and mineralization.
Disorders of Bone Remodeling
Osteoporosis
Osteoporosis stands as the most prevalent metabolic bone disease, characterized by decreased bone mass and microarchitectural deterioration, predisposing individuals to increased fracture risk, particularly in the hip, spine, and wrist. Postmenopausal women and elderly individuals are at heightened risk due to hormonal changes and age-related bone loss. Contributing factors include inadequate calcium and vitamin D intake, sedentary lifestyle, smoking, and excessive alcohol consumption. Dual-energy X-ray absorptiometry (DXA) is the gold standard for diagnosing osteoporosis, and management strategies focus on lifestyle modifications, calcium and vitamin D supplementation, and pharmacological interventions to mitigate fracture risk.
Osteogenesis Imperfecta (OI)
OI, often referred to as brittle bone disease, encompasses a group of genetic disorders characterized by fragile bones prone to fractures, skeletal deformities, and short stature. Mutations affecting the synthesis or structure of type I collagen, the primary protein component of bone, underlie this condition. OI exhibits considerable clinical heterogeneity, ranging from mild forms with few fractures to severe cases associated with significant morbidity and mortality. Management involves a multidisciplinary approach, encompassing supportive measures, physical therapy, and surgical interventions to optimize bone health and function.
Paget's Disease of Bone
Paget's disease represents a disorder of excessive bone remodeling, marked by focal areas of increased bone resorption and disorganized bone formation, resulting in enlarged and weakened bones. Though the exact etiology remains elusive, environmental and genetic factors likely contribute to its pathogenesis. Affected individuals may present with bone pain, deformities, and complications such as fractures, nerve compression, and secondary osteoarthritis.
skeletal disorders of metabolic and endocrine originyashovrattiwari1
Metabolic bone diseases encompass a spectrum of disorders characterized by abnormalities in bone metabolism, structure, and mineralization. These conditions often result from disturbances in the intricate balance between bone formation and resorption, leading to weakened bones prone to fractures, deformities, and other complications. This comprehensive exploration will delve into the pathophysiology, clinical manifestations, diagnostic approaches, and management strategies for various metabolic bone diseases, shedding light on these complex yet fascinating conditions.
Introduction to Metabolic Bone Diseases
The skeleton serves as the structural framework of the body, providing support, protection, and mobility. Maintaining the integrity and strength of bones relies on a delicate equilibrium between osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Disruptions in this equilibrium can give rise to metabolic bone diseases, which can be classified broadly into two categories: disorders of bone remodeling and mineralization.
Disorders of Bone Remodeling
Osteoporosis
Osteoporosis stands as the most prevalent metabolic bone disease, characterized by decreased bone mass and microarchitectural deterioration, predisposing individuals to increased fracture risk, particularly in the hip, spine, and wrist. Postmenopausal women and elderly individuals are at heightened risk due to hormonal changes and age-related bone loss. Contributing factors include inadequate calcium and vitamin D intake, sedentary lifestyle, smoking, and excessive alcohol consumption. Dual-energy X-ray absorptiometry (DXA) is the gold standard for diagnosing osteoporosis, and management strategies focus on lifestyle modifications, calcium and vitamin D supplementation, and pharmacological interventions to mitigate fracture risk.
Osteogenesis Imperfecta (OI)
OI, often referred to as brittle bone disease, encompasses a group of genetic disorders characterized by fragile bones prone to fractures, skeletal deformities, and short stature. Mutations affecting the synthesis or structure of type I collagen, the primary protein component of bone, underlie this condition. OI exhibits considerable clinical heterogeneity, ranging from mild forms with few fractures to severe cases associated with significant morbidity and mortality. Management involves a multidisciplinary approach, encompassing supportive measures, physical therapy, and surgical interventions to optimize bone health and function.
Paget's Disease of Bone
Paget's disease represents a disorder of excessive bone remodeling, marked by focal areas of increased bone resorption and disorganized bone formation, resulting in enlarged and weakened bones. Though the exact etiology remains elusive, environmental and genetic factors likely contribute to its pathogenesis. Affected individuals may present with bone pain, deformities, and complications such as fractures, nerve compression, and secondary osteoarthritis.
Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets.
Vitamin D helps your child's body absorb calcium and phosphorus from food. Not enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets.
Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets is due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery.
Rare inherited disorders related to low levels of phosphorus, the other mineral component in bone, may require other medications.
Products & Services
Book: Mayo Clinic Family Health Book, 5th Edition
Symptoms
Signs and symptoms of rickets can include:
Delayed growth
Delayed motor skills
Pain in the spine, pelvis and legs
Muscle weakness
Because rickets softens the areas of growing tissue at the ends of a child's bones (growth plates), it can cause skeletal deformities such as:
Bowed legs or knock knees
Thickened wrists and ankles
Breastbone projection
Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets.
Vitamin D helps your child's body absorb calcium and phosphorus from food. Not enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets.
Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets is due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery.
Rare inherited disorders related to low levels of phosphorus, the other mineral component in bone, may require other medications.
Products & Services
Book: Mayo Clinic Family Health Book, 5th Edition
Symptoms
Signs and symptoms of rickets can include:
Delayed growth
Delayed motor skills
Pain in the spine, pelvis and legs
Muscle weakness
Because rickets softens the areas of growing tissue at the ends of a child's bones (growth plates), it can cause skeletal deformities such as:
Bowed legs or knock knees
Thickened wrists and ankles
Breastbone projection
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Plain Radiological findings of Primary Hyperparathyrodism.pptx
1.
2. Case
15 yr old, girl.
Referred to Dr. Wade for LL deformity &
abnormal gait for the last 5 yrs
Increasing with time, associated with generalized
bone pain.
V/S stable … Afebrile.
CBC: N RP: N Ca: 3,39
Al. Ph.: 300 PTH: 1092
3.
4.
5.
6. Overview
Parathyroid glands function
Maintain serum calcium concentrations
Regulate bone metabolism.
PTH secretion stimulated by a fall in the
extracellular calcium concentration
Hydroxylation of 25-hydroxy-vitamin D at the
proximal convoluted tubule in the kidney
Increases renal & GI calcium reabsorption.
Increases bone resorption through stimulation of
osteoclast-activating factors from osteoblasts.
7. Overview
Calcium
At parathyroid gland, Binds to the calcium receptor
PTH secretion and parathyroid cell growth are
inhibited.
At the kidney, inhibits the 1-hydroxylation of 25-
hydroxy-vitamin D.
At thyroid C cells, stimulating calcitonin release
regulate bone resorption.
8.
9. Classification
Primary hyperparathyroidism
Oversecretion of PTH due to gland pathology.
Secondary hyperparathyroidism
Reaction of the parathyroid glands to a hypocalcaemia
caused by something other than a parathyroid
pathology, e.g. chronic renal failure.
Tertiary hyperparathyroidism
Hyperplasia of the parathyroid glands and a loss of
response to serum calcium levels.
Seen in patients with chronic renal failure and is an
autonomous activity.
11. Radiological Findings
Plain-film radiography has limited diagnostic
value, especially in the early stages of the disease.
Normal findings do not rule out
hyperparathyroidism.
Most of findings on radiographs are not specific.
12. Radiological Findings (1)
Osteopenia is one of the most common findings
Fine trabeculations are initially lost, ended with
ground appearance in the trabeculae.
14. Subperiosteal Bone Resorption
An early and pathognomonic sign.
Can affect many sites, the most common site is
the middle phalanges of the index and middle
fingers, on the radial aspect.
24. Radiological Findings (3)
Rugger-jersey spine.
Ill-defined bands of increased bone density
adjacent to the vertebral endplates
More common in secondary disease
25. Radiological Findings (4)
Brown tumors
Well-circumscribed lytic lesions of bone that
represent the osteoclastic resorption of an area of
bone with fibrous replacement.
Consist of fibrous tissue, woven bone and supporting
vasculature, but no matrix.
Single or multiple, present in any site, usually
occur in cortical bone.
Become sclerotic on radiographs.
33. Take Home Massage
Elevated serum Ca levels & PTH levels, diagnosis
of primary hyperparathyroidism is certain.
Radiologic features of primary
hyperparathyroidism are similar to secondary
form of the disease.
The most common radiologic finding in primary
hyperparathyroidism is osteopenia
Radiographic findings of subperiosteal resorption
should prompt consideration of the primary
hyperparathyroidism
Editor's Notes
Severe osteopenia may be complicated by pathologic fractures.
Radiograph of the proximal tibia and fibula. Diffuse demineralization attributed to trabecular resorption is the most common plain radiographic sign of primary hyperparathyroidism
Anteroposterior radiographic view of the right hand in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) and primary hyperparathyroidism (same patient as in Image 2). This image shows subperiosteal bone resorption along the radial aspects of the middle phalanges (arrows).
Bilateral anteroposterior (AP) radiographic views of the hands in a patient with multiple endocrine neoplasia syndrome type 1 (MEN 1) and primary hyperparathyroidism. These images show subperiosteal bone resorption along the radial aspects of the middle phalanges.
Radiograph of the phalanges in a patient with primary hyperparathyroidism. This image demonstrates subperiosteal resorption that has resulted in severe tuftal resorption
Anteroposterior radiographic view of the left shoulder in external rotation in a patient with primary hyperparathyroidism. This image shows the healing stage of marked subperiosteal resorption (arrow) of the medial aspect of the proximal humerus.
Radiograph of the shoulder in a patient with primary hyperparathyroidism. This image depicts subperiosteal distal clavicular resorption (arrows).
Radiograph of the shoulder in a patient with primary hyperparathyroidism. This image demonstrates distal clavicular resorption
Radiograph of the middle phalanges in a patient with primary hyperparathyroidism. This image demonstrates subperiosteal resorption that has resulted in severe tuftal resorption (white arrows). Also, note the subperiosteal and intracortical resorption of the middle phalanges (black arrows).
Anteroposterior radiographic view of the top of the calvarium in a patient with primary hyperparathyroidism. This image shows trabecular bone resorption that has resulted in the salt-and-pepper appearance of the calvarium.
Radiograph of the femur in primary hyperparathyroidism (same patient as in Image 10). This image shows scalloped defects along the inner margin of the femoral cortex (arrows), which denote endosteal resorption.
Anteroposterior radiographic view of the clavicles. This image shows symmetric subchondral bone resorption of the acromioclavicular joints. Distal clavicular resorption can be subperiosteal or subchondral, but this finding is not specific for primary hyperparathyroidism.
Posteroanterior (PA) chest radiograph in a 60-year-old woman shows subligamentous bone resorption of the inferior surface of the lateral ends of the clavicles.
Posteroanterior (PA) chest radiograph shows multiple expansile brown tumors in the medial border of the left scapula and in several of the ribs (black arrows). Also note subperiosteal bone resorption along one of the rib margins (white arrow).
Radiograph of the humerus in a patient with primary hyperparathyroidism. This image depicts a brown tumor. Note the osseous expansion and lucency of the proximal humerus. Brown tumors can have varied appearances.
Radiograph of the mid femoral diaphysis in a patient with primary hyperparathyroidism. This image depicts brown tumors. Note the eccentric (arrowheads) and central positions (arrow) of the lesions.
Radiograph of the pelvis in a patient with primary hyperparathyroidism. Note the presence of brown tumors in the pelvis
Radiograph in a 53-year-old woman with nutritional osteomalacia shows a brown tumor in the region of the tibial tuberosity (left) and healing of the lesion after vitamin D therapy (right). Also note improved mineralization of the bones.
Radiograph of both hands of a 36-year-old woman receiving long-term hemodialysis shows subperiosteal bone resorption affecting the radial aspect of the middle phalanges of the fingers. Note the extensive digital arterial calcification.