Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. The disease develops when vitamin D levels are too low to absorb calcium and phosphate from the intestines, causing these minerals to be lost from the bones. Symptoms include bowed legs, soft skull, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels and high alkaline phosphatase. X-rays show widened growth plates and fraying and cupping of the bone. Treatment involves high dose vitamin D and calcium supplementation to strengthen the bones.
INTRODUCTION — Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. • Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus growth plate cartilage accumulates and the growth plate thickens. • In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. • In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
INTRODUCTION — Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. • Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus growth plate cartilage accumulates and the growth plate thickens. • In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. • In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
Prepared by MD, PhD., Associate Professor, Marta R. Gerasymchyk, pathophysiology department of Ivano-Frankivsk National Medical University, Ukraine.
For medical students
Calcium metabolism disorders
1. CALCIUM METABOLISM DISORDERS
2. OVERVIEW: Calcium definition and requirement . Calcium metabolism regulators : VD , PTH and calcitonin. Functions of calcium. Calcium metabolic bone diseases. Calcium metabolism disorders. CASE !!
3. WHAT IS CALCIUM? Calcium is a mineral that is essential to bone health, cardiovascular health, muscle maintenance, circulatory health, and blood clotting. Calcium also acts as an enzyme activator. While calcium is found in milk and dairy products, it is also available from other food sources, such as green leafy vegetables, seafood (eating salmon with the bones provides an even greater dose), almonds, blackstrap molasses, broccoli, enriched soy and rice milk products, figs, soybeans and tofu.
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s 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 Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
ASA GUIDELINE
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
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.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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, 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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. Rickets is a childhood disorder
involving softening and
weakening of the bones.
It is primarily caused by lack of
vitamin D, calcium, or
phosphate.
3. Vitamin D is a fat-soluble vitamin that may be absorbed
from the intestines or may be produced by the skin when
the skin is exposed to sunlight (ultraviolet light of sunlight
helps the body to form vitamin D).
The absorbed vitamin D is converted into its active form to
act as a hormone to regulate calcium absorption from the
intestine and to regulate levels of calcium and phosphate in
the bones.
If there is a deficiency of Vitamin D, the body is unable to
properly regulate calcium and phosphate levels. When the
blood levels of these minerals become too low, it results in
destruction of the support matrix of the bones.
4. In rickets, another mechanism in the body works to increase
the blood calcium level. The parathyroid gland may increase
its functioning rate to compensate for decreased levels of
calcium in the bloodstream.
To increase the level of calcium in the blood the hormone
destroys the calcium present in the bones of the body and
this results in further loss of calcium and phosphorous from
the bones. In severe cases, cysts may develop in the bones.
5. Environmental conditions where sunlight exposure
is limited like indoor confinement or working
indoors during daylight hours may reduce source
of vitamin D;
Inadequate daily consumption - a lack of vitamin D
in the diet, a dietary lack of calcium and
phosphorous may also play a part in nutritional
causes of rickets, have trouble digesting milk
products, people who are lactose intolerant;
Liver Failure;
Dark Pigmentation
7. Cholecalciferol (vitamin D-3) is formed in the skin from
7-dehydrotachysterol. This steroid undergoes hydroxylation in 2 steps.
Pathophysiology - Metabolism of vitamin D
• The first hydroxylation occurs at position 25 in the liver,
producing calcidiol (25-hydroxycholecalciferol), which
circulates in the plasma as the most abundant of the vitamin D
metabolites and is thought to be a good indicator of overall
vitamin D status.
8. Cholecalciferol (vitamin D-3) is formed in the skin from
7-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps.
Pathophysiology
• The second hydroxylation step occurs in the kidney at the 1 position,
where it undergoes hydroxylation to the active metabolite calcitriol
(1,25-dihydroxycholecalciferol - DHC). This cholecalciferol is not a
vitamin, but a hormone.
9.
10. Calcitriol acts on regulation of
calcium metabolism:
Calcitriol promotes absorption of calcium and
phosphorus from the intestine,
increases reabsorption of phosphate in the kidney,
acts on bone to release calcium and phosphate;
Calcitriol may also directly facilitate calcification.
Calcitriol (1,25-DHC) – acts as a hormone rather than a
vitamin, endocrine and paracrine properties
11. •These actions increase the concentrations of calcium
and phosphorus in extracellular fluid.
• The increase of Ca and
P in extracellular fluid,
in turn, leads to the
calcification of osteoid,
primarily at the
metaphyseal growing
ends of bones but also
throughout all osteoid
in the skeleton.
• Parathyroid hormone
facilitates the 1-hydro-
xylation step in
vitamin D metabolism
12. In the vitamin D deficiency state,
hypocalciemia develops, which
stimulates excess parathyroid
hormone, which stimulates renal
phosphorus loss, further
reducing deposition of calcium
in the bone.
Excess parathyroid hormone
also produces changes in the
bone similar to those occurring
in hyperparathyroidism.
13. Early in the course of rickets, the
calcium concentration in the
serum decreases.
After the parathyroid response, the
calcium concentration usually
returns to the reference range,
though phosphorus levels remain
low.
Alkaline phosphatase, which is
produced by overactive osteoblast
cells, leaks to the extracellular fluids
so that its concentration rises to
anywhere from moderate elevation
to very high levels.
14. The history in patients with rickets may include the
following:
The infant's gestational age, diet and degree of
sunlight exposure should be noted.
A detailed dietary history should include specifics of
vitamin D and calcium intake.
A family history of short stature, orthopedic
abnormalities, poor dentition, alopecia, parental
consanguinity may signify inherited rickets.
Evaluation
15. Rickets is a systemic disease with skeletons
involved most, but the nervous system,
muscular system and other system are also
involved.
16. Generalized muscular hypotonia is observed in the most
patients with clinical signs of rickets.
Craniotabes manifests early in infants, although this
feature may be normal in infants, especially for those
born prematurely.
Clinical signs
• If rickets occurs at a later age,
thickening of the skull
develops. This produces
frontal bossing and delays
the closure of the anterior
fontanelle.
17. • Skeletal
deformities
including Bow legs,
Forward projection of
the breastbone -
pigeon chest or pectus
carinatum),
Funnel chest
(pectus excavatum),
"Bumps" in the rib
cage (rachitic rosary)
and asymmetrical or
odd-shaped skull;
19. Clinical signs
In the chest, knobby
deformities results in the
rachitic rosary along the
costochondral junctions.
The weakened ribs
pulled by muscles also
produce flaring over the
diaphragm, which is
known as Harrison sulcus.
The sternum may be
pulled into a pigeon-chest
deformity.
Rib beading
(rachitic rosary)
22. The ends of the long bones demonstrate that same
knobby thickening. At the ankle, palpation of the tibial
Clinical signs
malleolus gives
the impression
of a double
epiphysis
(Marfan sign).
23. Increased tendency toward
bone fractures. Because the
softened long bones may
bend, they may fracture
one side of the cortex
(greenstick fracture).
In the long bones, laying
down of uncalcified osteoid
at the metaphyses leads to
spreading of those areas,
producing knobby
deformity (cupping and
fraying of the metaphyses).
24. Spine deformities
(spine curves abnormally,
including scoliosis or
kyphosis).
In more severe instances
in children older than 2
years, vertebral softening
leads to
kyphoscoliosis
25. Pain in the bones of Arms, Legs, Spine, Pelvis.
Dental deformities
Delayed formation of teeth
Defects in the structure of teeth
Holes in the enamel
Increased incidence of cavities in the teeth (dental caries)
26. Progressive weakness
Decreased muscle tone (loss of muscle
strength)
Muscle cramps
Impaired growth
Short stature (adults less than 5 feet tall)
Clinical signs
27. In children with rickets,
complete physical and
dental examinations should
be performed. The entire
skeletal system must be
palpated to search for
tenderness and bony
abnormalities.
Rickets should be
suspected in older
bowlegged children and in
cases associated with
asymmetry, pain, or
progression in severity. a
Physical examination
28. .Gait disturbances and neurologic abnormalities (such as
hyperreflexia) in all children should be
sought.
. The review of systems should focus on growth and
orthopedic concerns and signs and symptoms of
hypocalcemia, such as muscle cramps, numbness,
paresthesias, tetany and seizures.
29. Laboratory findings
Laboratory investigation may include:
serum levels of calcium (total and ionized with
serum albumin),
phosphorus,
alkaline phosphatase (ALP)
parathyroid hormone,
calcidiol
urine studies include urinalysis and levels of
urinary calcium and phosphorus.
30. Decrease
in serum calcium,
serum phosphorus,
calcidiol, calcitriol,
urinary calcium.
The most common laboratory findings in
nutritional rickets are:
Parathyroid hormone,
alkaline phosphatase,
urinary phosphorus
levels are elevated.
31. Early on in the course of rickets, the calcium (ionized fraction)
is low; however it is often within the reference range at the
time of diagnosis as parathyroid hormone levels increase.
Calcidiol (25-hydroxy vitamin D) levels are low, and
parathyroid hormone levels are elevated; however,
determining calcidiol and parathyroid hormone levels is
typically not necessary.
Calcitriol levels may be normal or elevated because of
increased parathyroid activity.
The phosphorus level is invariably low for age.
Alkaline phospohatase levels are elevated.
A generalized aminoaciduria occurs from the parathyroid
activity; aminoaciduria does not occur in familial
hypophosphatemia rickets (FHR).
Laboratory Studies
32. Classic radiographic findings
include:
widening of the distal epiphysis,
fraying and cupping of the
metaphysis, and angular
deformities of the arm and leg
bones.
33. Classic radiographic findings include
Anteroposterior and lateral radiographs of the wrist of an 8-year-
old boy with rickets demonstrates cupping and fraying of the
metaphyseal region
34. Rickets in wrist - uncalcified lower ends of bones
are porous, ragged, and saucer-shaped
(A) Rickets in 3 month old infant
(B) Healing after 28 days of
treatment
(C) After 41 days of
treatment
A
B C
35. Radiographic image of wrist and
forearm showing pathologic
fractures of radius and ulna with
rachitic changes of distal end of
radius and ulna.
37. Early stage
Usually begin at 3 months old
Symptoms: mental psychiatric symptoms
Irritability, sleeplessness
Signs: occipital bald
Laboratory findings: Serum Ca, P normal or
decreased slightly, ALP normal or elevated
slightly, 25(OH)D3 decreased
X-ray changes: normal or slightly changed
38. Advanced stage
On the basis of early rickets, osseous changes
become marked and motor development becomes
delayed.
1. Osseous changes:
1) Head: craniotabes, frontal bossing, boxlike
appearance of skull, delayed closure of anterior
fontanelle
2) Teeth: delayed dentition with abnormal order,
defects
3) Chest: rachitic rosary, Harrison’s groove, pigeon
chest, funnel-shaped chest, flaring of ribs
39. 4) Spinal column: scoliosis, kyphosis, lordosis
5) Extremities: bowlegs, knock knee,
greenstick fracture
6) Rachitic dwarfism
2. Muscular system: potbelly, late in standing and
walking
3. Motor development: delayed
4. Other nervous and mental symptoms
40. Laboratory findings:
Serum Ca and P decreased
ALP elevated
X-ray changes:
Wrist is the best site for watching the changes
Widening of the epiphyseal cartilage
Blurring of the cup-shape metaphyses of long bone
41. Healing stage:
Symptoms and signs of Rickets alleviate or
disappear by use of appropriate treatment.
The blood investigations become normal, except
ALP, that may be slightly elevated.
Sequelae stage:
All the clinical symptoms and signs disappear.
Blood investigations and X-ray changes are
recovered, but osseous deformities may be left.
Usually seen in children after 3 years old.
42. I Mild form: small changes of nervous system,
changes of one part of the skeleton;
II Moderate form: changes of all organs and
systems, changes of two parts of the skeleton;
III Severe form: damaging function of all
organs and systems, changes of three parts of
the skeleton;
Classification
44. Vitamin D dependent
Vitamin D-dependent rickets, type I is secondary to a
defect in the gene that codes for the production of renal
25(OH)D3-1-alpha-hydroxylase.
Vitamin D-dependent rickets, type II is a rare autosomal
disorder caused by mutations in the vitamin D receptor.
Type II does not respond to vitamin D treatment;
elevated levels of circulating calcitriol differentiate this
type from type I.
45. Vitamin D resistant
Rickets refractory to vitamin D treatment may be caused
by the most common heritable form, known as vitamin
D-resistant rickets or familial hypophosphatemic rickets.
Because of mutations of the phosphate-regulating gene
on the X chromosome, renal wasting of phosphorus at
the proximal tubule level results in hypophosphatemia.
Normal levels of calcitriol are found in this disorder.
46. Other Conditions That Can Cause Rickets
Medications
Antacids
Anticonvulsants
Corticosteroids
Loop diuretics
Malignancy
Prematurity
Diseases of organs associated with vitamin D and calcium
metabolism
Kidney disease
Liver and biliary tract disease
Malabsorption syndromes
Celiac disease
Cystic fibrosis (rare)
47. Assessed according to the followings:
1. History
2. Physical examination
3. Laboratory findings
4. X-ray changes
48. The replacement of Vitamin D may correct rickets using
these methods of ultraviolet light and medicine. Rickets
heals promptly with 4000 IU of oral vitamin D per day
administered for approximately one month.
Parents are instructed to take their infants outdoors for
approximately 20 minutes per day with their faces
exposed. Children should also be encouraged to play
outside.
Foods that are good sources of vitamin D include cod
liver oil, egg yolks, butter and oily fish. Some foods,
including milk and breakfast cereals, are also fortified
with synthetic vitamin D.
49. 1. Special therapy: Vitamin D therapy
A. General method: Vitamin D 2000-4000 IU/day
for 2-4 weeks, then change to
preventive dosage – 400 IU.
B. A single large dose: For severe case, or Rickets with
complication, or those who can’t bear oral therapy.
Vitamin D3 200000 – 300000 IU, im,
preventive dosage will be used after 2-3 months.
50. 4. Calcium supplementation: Dosage: 1-3 g/day
only used for special cases, such as baby fed
mainly with cereal or infants under 3 months of
age and those who have already developed
tetany.
5. Plastic surgery:
In children with bone deformities after 4 years
old plastic surgery may be useful.
52. 1. Pay much attention to the health care of
pregnant and lactating women, instruct them to
take adequate amount of vitamin D.
2. Advocate sunbathing
3. Advocate breast feeding, give supplementary
food on time
53. Vitamin D supplementation:
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,
For those babies who can’t maintain a daily
supplementation, inject muscularly
Vitamin D3 100000-200000 IU.