achondroplasia is genetic disorder that results in dwarfism
problem is not in forming cartilage but in converting it to bone.
This disorder usually results in the following: An average-size trunk; Short arms and legs, with particularly short upper arms and upper legs; Short fingers.
Mutation in FGFR3 on chromosome 4 is responsible for achondroplasia.
achondroplasia is genetic disorder that results in dwarfism
problem is not in forming cartilage but in converting it to bone.
This disorder usually results in the following: An average-size trunk; Short arms and legs, with particularly short upper arms and upper legs; Short fingers.
Mutation in FGFR3 on chromosome 4 is responsible for achondroplasia.
Skeletal Imaging of Nutritional Disorders in Children_Crimson PublishersCrimsonpublishersNTNF
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Imaging of skeleton plays a major role in the diagnosis of nutritional disorders in children. The disorders can be1) Deficiency and2) Toxic (Overdose). The common deficiency disorders include rickets, scurvy, osteoporosis and anemias. Conventional radiology is adequate in the diagnosis, except in the grading of diagnosis of degrees of osteoporosis. The differential diagnosis is also discussed.
Vitamin D deficiency remains the most common cause of Osteomalacia & rickets.
My first presentation prepared by me as a first year family medicine board resident. đ
Report Back from SGO 2024: Whatâs the Latest in Cervical Cancer?bkling
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Are you curious about whatâs new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Womenâs Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Tom Selleck Health: A Comprehensive Look at the Iconic Actorâs Wellness Journeygreendigital
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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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
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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, Ganongâs 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
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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, Ganongâs 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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
Bowmanâs 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
New Drug Discovery and Development .....NEHA GUPTA
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The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
2. Plan
⢠Introduction â Defining the subject
⢠(1): Pathogenesis
⢠(2): Clinical Presentation and Diagnosis
⢠(3): Treatment and Prevention
⢠Conclusion
3. Defining the disease
⢠Rickets â wordâs orginin is unknown
â Maybe Rucket â to breath with difficulty, Dorset
word
â Or Rhakhis â Spine, Rhachitis ââinflammation of
spineââ
Definition: A deficiency disease resulting from a lack of
vitamin D or calcium and from insufficient exposure to
sunlight, characterized by defective bone growth and
occurring chiefly in children. Also called rachitis.
The American HeritageÂŽ Dictionary of the
English Language
4. Normal Bone Processes
⢠Calcium and Phosphate
â Constitutes the crystalline component of bone
⢠Deficiency leads to disease (i.e., Rickets and/or
osteomalacia)
⢠Rickets:
â Deficient mineralization at growth plate
⢠Osteomalacia:
â impaired mineralization of the bone matrix.
⢠Open plates: Occur in Osteomalacia and rickets.
⢠Closed plates: Happens in osteomalacia only!
5. Mineralization Defects
⢠Classified according to Predominant mineral
deficiency:
â 1) Phosphopenic (hypophosphatemic) rickets
⢠Primarily caused by phosphate deficiency
â 2) Calcipenic (hypocalcemic) rickets
⢠Primarily caused by calcium deficiency
Associated with decrease levels of phosphorus or
calcium, respectively.
6. Pathogensis
⢠Growth Plate thickens:
â Chondrocytes grow and hypertrophy
â Vascular invasion of growth plate into primary bone
⢠Vascular invasion requires mineralization of the growth plate
cartilage
⢠Can be delayed or prevent by deficiency of calcium or
phosphorous
⢠In such circumstances growth plate cartilage accumulates
and thickens. In addition, the chondrocytes of the growth
plate becomes disorganised, losing their regular straight
columned orientation.
7. The Pathogenic processes..
Osteoid Accumulation in metaphysis
Decreased biochemical resistance of the
invovled skeletal sites
ď 2nd-ary inc- diameter of the growth plate.
Compensatory mechanism due to decrease
strenght by increase size
Bone stability is compromised -ď if such
condition does not improve, bowing occurs.
8. Pathogenesis (Normal) [2]
Proliferation of
chondrocytes
Calcification and
vascular invasion
Reserve
zone
Maturation
zone
Proliferative
zone
Hypertrophic
zone
Primary
spongiosa
2. Shapiro IM, Boyde A. Mineralization of normal and rachitic chick growth cartilage: vascular canals, cartilage
calcification and osteogenesis. Scanning Microsc 1987; 1:599.
9. Pathogenesis (Rickets) [3-6]
Proliferation of
Thick + Disorganized
chondrocytes
cartilage
Less calcification and
vascular invasion
Hypertrophic
zone
3. Lacey DL, Huffer WE. Studies on the pathogenesis of avian rickets. I. Changes in epiphyseal and metaphyseal vessels in hypocalcemic and hypophosphatemic rickets.
Am J Pathol 1982; 109:288.
4. Huffer WE, Lacey DL. Studies on the pathogenesis of avian rickets II. Necrosis of perforating epiphyseal vessels during recovery from rickets in chicks caused by
vitamin D3 deficiency. Am J Pathol 1982; 109:302.
5. Takechi M, Itakura C. Ultrastructural studies of the epiphyseal plate of chicks fed a vitamin D-deficient and low-calcium diet. J Comp Pathol 1995
6.. Rauch F. The rachitic bone. Endocr Dev 2003; 6:69.
10. Clinical manifestation
⢠Usually @
distal forearm, knee, and costochondral
junctions.
⢠Typically @
Sites of rapid bone growth, where large
quantities of calcium and phosphorus are
required for mineralization.
11. Clinical Manifestations (Skeletal) [13]
1. Delay in closure of the fontanelles
2. Parietal & frontal bossing (due to excess osteoid)
3. Craniotabes ( soft skull bones)
4. Enlargement of the costochondral junction
(rachitic rosary)
5. The development of Harrison sulcus ( caused by pull of the diaphragmatic attachments
to the lower ribs)
6. Pigeon chest deformity (The weakened ribs bend inwards due to the pull of respiratory
muscles, causing anterior protrusion of sternum)
7. Enlargement of the wrist + ankle & bowing of the distal radius & ulna
8. Genus Valgus (knocked), Genus Verus (bowleg), or Windswept deformity (combination
of valgus deformity of 1 leg with varus deformity of the other leg)
13. Misra M, Pacaud D, Petryk A, et al. Vitamin D deficiency in children and its management: review of current
knowledge and recommendations. Pediatrics 2008; 122:398.
Pictures from http://www.thachers.org
12. Clinical Manifestations (Extra-Skeletal)
⢠Depends upon the type of ricket
⢠Hypoplasia of the dental enamel is typical for hypocalcemic rickets,
whereas abscesses of the teeth occur more often in phosphopenic rickets.
⢠Hypocalcemic seizures, decreased muscle tone leading to delayed motor
milestones, recurrent infections, increased sweating
13. Clinical Manifestations
⢠GENERAL Failure to thrive; Protuding abdomen;
Muscle weakness (especially proximal); Fractures
⢠HEAD Craniotabes; Frontal bossing; Delayed
fontanelle closure; Delayed dentition; caries
⢠CHEST Rachitic rosary; Harrison groove; or
Respiratory infections
⢠BACK Scoliosis ,Kyphosis ,Lordosis
⢠EXTREMITIES Enlargement of wrists and ankles;
Valgus or varus deformities Windswept deformity
(combination of valgus deformity of 1 leg with
varus deformity of the other leg); Anterior bowing
of the tibia and femur; Leg pain.
⢠HYPOCALCEMIC SYMPTOMS Tetany, Seizures;
Stridor due to laryngeal spasm
14. Chest radiograph of a patient with rickets,
demonstrating a "rachitic rosary". Observe the
opaque, bulbous indentations of the lung
adjacent to the enlarged costochondral
junctions (arrows).
Bilateral, symmetric bowing of the
femurs and tibias.
15. Radiography
⢠Best visualised @ growth plate of rapidly
growing bones.
â Upper limb ď distal Ulna
â Knee ď Metaphyses above and below
16. As disease progresses:
Disorganization of the growth plate becomes
more apparent:
1) with cupping,
2) splaying,
3) formation of cortical spurs
4) stippling.
20. Biochemical Findings in Rickets
⢠Alkaline phosphatase: âin all forms of rickets
⢠Serum phosphorus: â in both hypocalcemic and phosphopenic rickets (normal 5-
7mg/dl)
⢠Serum Ca+2: âin hypocalcemic rickets (normal 9-11mg/dl)
⢠Serum PTH: âin hypocalcemic rickets, but normal in hypophosphatemic rickets
⢠25-OH vitamin D reflect the amount of vitamin D stored in the body, and is âin
vitamin D deficiency.
⢠1,25-OH2 vitamin D can beâ, N or âin hypocalcemic rickets and usually is N or
slightly âin phosphopenic rickets
21. Labs
⢠Alkaline phosphatase is increased markedly
over the age-specific reference range.
⢠Excellent marker â participates in mineralization of
bone and growth plate cartilage.
22.
23. Evaluation
⢠A child with clinical signs of rickets should
include dietary history with particular
attention to given calcium and vitamin D
intake
⢠Medication history
⢠Measurement of serum creatinine and live
enzymes
24. Treatment of Rickets
⢠EITHER: Vitamin D. stoss therapy: 300,000-600,000 IU orally or IM in 2-4
divided doses over one day
⢠OR: High dose vit D 2000-5000 IU orally for 4-6wks followed by 400 IU
daily orally as maintenance
⢠OR: (5000-10,000 U) is given daily for 2-3 months until healing and alkaline
phosphatase concentration is approaching to the normal
⢠Adequate dietary Calcium & phosphorus provided by milk, formula &
other dairy products
⢠Symptomatic hypocalcaemia need IV CaCl as 20mg/kg or Calcium
gluconate as 100mg/kg as a bolus, followed by oral calcium tapered over
2-6 weeks
25. PREVENTION
1.Exposure to sunlight (ultraviolet light)
Early morning and evening 15 minutes per day
2. Lactating mothers should receive supplemention
with milk or vitamin D to ensure prevention of rickets in
their babies.
3. Sun exposure to mothers
26. Prevention
4. Vitamin D supplementation (careful of toxicity):
In prematures, twins and weak babies, give Vitamin D
800IU per day
For term babies and infants the demand of Vitamin D
is 400IU per day
28. Outcome
⢠Good news:
â Mostly reversible
â Some deformities might persist
29. Conclusion
⢠Rickets refers to the changes at the growth
plate caused by deficient mineralization of
bone. Happens only before growth plates
closure.
⢠2 types of rickets
⢠Skeletal findings + Extra skeletal findings
⢠Certain radiographic findings