Vitamin D deficiency can cause rickets in children and osteomalacia in adults. It is caused by lack of vitamin D from diet and sun exposure. The body synthesizes the inactive form cholecalciferol from cholesterol in skin upon sun exposure and the active form calcitriol is produced in the kidneys. Vitamin D plays a key role in calcium absorption and bone mineralization. Deficiency is highly prevalent in India due to low dietary intake and sun exposure. It is associated with many systemic disorders including musculoskeletal, autoimmune, cardiovascular and infectious diseases.
Chemistry of Vitamin K, Biochemical role of Vitamin K, Recommended dietary allowance of Vitamin K, Dietary sources of Vitamin K, Deficiency symptoms of vitamin K, Hypervitaminosis of vitamin K, Toxicity of Vitamin K
Chemistry of Vitamin K, Biochemical role of Vitamin K, Recommended dietary allowance of Vitamin K, Dietary sources of Vitamin K, Deficiency symptoms of vitamin K, Hypervitaminosis of vitamin K, Toxicity of Vitamin K
Vitamin A-intoduction, functions, sources, storage, WHO statistics, deficiency, treatment, prevention and control of deficiencies, Vit. A deficiency in India, assessment of Vit. A deficiency, recommended allowances, toxicity.
vitamin d is one of the fat soluble vitamin on which there is great emphasis in the present scenario. it is present in breast milk in very minute amount so it is recommended that it must be supplemented right after birth to prevent it deficiency which in children can result in rickets. if not diagnosed and treated in time it may result in number of bony deformities . in adults besides oesteomalacia it is associated with n umber of non communicable diseases.
B vitamins are a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, research shows that they are chemically distinct vitamins that often coexist in the same foods. In general, supplements containing all eight are referred to as a vitamin B complex. Individual B vitamin supplements are referred to by the specific name of each vitamin (e.g., B1, B2, B3 etc.).
Vitamin k is a group of lipophilic hydrophobic vitamins. Fat soluble compound necessary for the synthesis of several proteins required for blood clotting.
Occurs in several forms:
Vitamin K1 (Phylloquinone)
Vitamin K2 (Menaquinone)
Vitamin K3 (Menadione) – synthetic form
Chemistry, and biochemical role, rda, vitamin dJasmineJuliet
Vitamin D - Chemistry,n Metabloism, Biosynthesis in our skin, Recommended dietary Allowance, Dietary sources of vitamin D, Deficiency symptoms of vitamin D, Hypervitaminosis of vitamin D.
Friend or Foe: The Microbiome in Autoimmunity DrBonnie360
Content and Visual Design by Tiffany Simms
DrBonnie360 presents The Microbiome: Sorting the Hype from the Hope at Cambridge Healthtech Institute's 23rd International Molecular Med TRI-CON 2016 in San Francisco, March 6, 2016.
Bringing two scientists from the Sonnenburg and Knight Lab, and four microbiome companies, DrBonnie360 moderates a short course on all you need to know about the microbiome and whether it will be your best friend or your worst enemy.
As DrBonnie360's work surrounds autoimmune diseases, the microbiome proves to be one of the lifelines autoimmunity could use to cross the autoimmune abyss. Presented in this slideshare is a carefully curated set of research on autoimmune and the microbiome.
Vitamin A-intoduction, functions, sources, storage, WHO statistics, deficiency, treatment, prevention and control of deficiencies, Vit. A deficiency in India, assessment of Vit. A deficiency, recommended allowances, toxicity.
vitamin d is one of the fat soluble vitamin on which there is great emphasis in the present scenario. it is present in breast milk in very minute amount so it is recommended that it must be supplemented right after birth to prevent it deficiency which in children can result in rickets. if not diagnosed and treated in time it may result in number of bony deformities . in adults besides oesteomalacia it is associated with n umber of non communicable diseases.
B vitamins are a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, research shows that they are chemically distinct vitamins that often coexist in the same foods. In general, supplements containing all eight are referred to as a vitamin B complex. Individual B vitamin supplements are referred to by the specific name of each vitamin (e.g., B1, B2, B3 etc.).
Vitamin k is a group of lipophilic hydrophobic vitamins. Fat soluble compound necessary for the synthesis of several proteins required for blood clotting.
Occurs in several forms:
Vitamin K1 (Phylloquinone)
Vitamin K2 (Menaquinone)
Vitamin K3 (Menadione) – synthetic form
Chemistry, and biochemical role, rda, vitamin dJasmineJuliet
Vitamin D - Chemistry,n Metabloism, Biosynthesis in our skin, Recommended dietary Allowance, Dietary sources of vitamin D, Deficiency symptoms of vitamin D, Hypervitaminosis of vitamin D.
Friend or Foe: The Microbiome in Autoimmunity DrBonnie360
Content and Visual Design by Tiffany Simms
DrBonnie360 presents The Microbiome: Sorting the Hype from the Hope at Cambridge Healthtech Institute's 23rd International Molecular Med TRI-CON 2016 in San Francisco, March 6, 2016.
Bringing two scientists from the Sonnenburg and Knight Lab, and four microbiome companies, DrBonnie360 moderates a short course on all you need to know about the microbiome and whether it will be your best friend or your worst enemy.
As DrBonnie360's work surrounds autoimmune diseases, the microbiome proves to be one of the lifelines autoimmunity could use to cross the autoimmune abyss. Presented in this slideshare is a carefully curated set of research on autoimmune and the microbiome.
D is for Debacle - The Sun, Vitamin D, 25(OH)D and HealthIvor Cummins
The Story of Vitamin D, and the Debacle of Human Health Impact that has unfolded over the past 50 years, as we allowed the population necessary levels to collapse. For individuals, parents, families, mothers - don't miss this understanding - this is probably the most important single factor for your health and longevity.
an overall overview in corticosteroids and its application in oral and maxillofacial diagnostic medicine and pathology drawing to the conclusions of the limitations and drawbacks of these medicines. i have also included the precautions to be taken in dental therapeutic procedures fo
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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.
- 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
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
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
2. INTRODUCTION
Vitamin D is an Fat-soluble vitamin .It is present in
animals, plants and yeast & has several important
functions in the body.
Technically it should be considerd as Hormone
( Secosteroid ) because -
-It is synthesized by the body(skin) from sunlight
(UV-B ray, wave band-290-315 nm),
-It is transported by blood, activated & then acts on
specific receptors in the target tissue.
-Feedback regulation of Vit D activation occure by
plasma Ca level & by active form of Vit D.
3. HISTORYCAL BACKGROUND
In1919 it was established that Ricket was due to
deficiency of a diatery factor & lack of sunlight.
American researchers Elmer McCollum and
Marguerite Davis in 1922 discovered a substance in
cod liver oil & its struture is determined in1935.
He called it vitamin D because it was the fourth
vitamin to be named.
Sunshine
vitamin
Sunshine
vitamin
4. WHAT IS VITAMIN D
Chemistry: There are two chemical forms of vitamin D,
-Vitamin D2 (Ergocalciferol) and
-Vitamin D3 (Cholecalciferol).
The natural form of vitamin D for animals and man is
vitamin D3; it can be produced in their bodies from
cholesterol and 7-dehydrocholesterol.
An alternative vitamin D2 is commercially prepared
from ergosterol that is present in yeast.
Cholesterol in animals and man is a precursor
substance for all steroid hormones as well as vitamin D3.
The molecular structure of vitamin D is closely allied
to that of the classical steroid hormones,
6. SOURCES OF VITAMIN D
2 sources
- 90% synthesised in skin via UVB light exposure
Cholecalciferol (vitD3 = inactive)
- 10% from food – Ergocalciferol (vit D2= inactive)
Sunshine
vitamin
Sunshine
vitamin
7. DIETARY SOURCES
Fatty fish, like tuna, mackerel, and salmon.
Cod liver oil
Foods fortified with vitamin D, like some dairy
products, orange juice, soy milk, and cereals.
Beef liver.
Cheese.
Egg yolks
8 oz milk = 115 IU
8 oz juice = 100 IU
1 egg = 29 IU
3 oz smoked salmon
= 583 IU
RICHEST SOURCE - FISH LIVER OIL
CHEAPEST SOURCE - SUNLIGHT
8. DAILY REQUIRMENT
Children & adults –400IU(10µg/day)
Pregnancy and lactation – 400IU(10µg/day)
Over 70years- 800IU (20µg/day)
1microgram of vitamin D = 40 International Units
16. Mineralization of
bone at low doses
Mobilization of
calcium from bone at
high doses
Increased
reabsorption of
calcium and
phosphorus
Decreased
excretion of calcium
and phosphorus
Increases the
intestinal absorption
of calcium and
phosphate
by increased
synthesis of calcium
binding protein
(calbinding D28k)
17. PTH EFFECTS
Increases tubular reabsorption of
calcium and stimulates the kidney to
produce 1,25 OH vitamin D3.
Stimulates the activation of osteoclasts,
which dissolve mineralized collagen matrix
in the bone, causing osteopenia and
osteoporosis and increasing the risk of
fracture.
Causes phosphaturia. A low Ca-Phos
product leads to decreased mineralization
of the collagen matrix= rickets in kids and
osteomalacia in adults
19. VITAMIN D DEFICIENCY
VITAMIN D STATUS- 25(OH)D LEVEL (ng / ml)
Normal level of vitamin D - > 30
Vitamin D insufficiency -- 21-29
Vitamin D deficiency -- < 20
Severe deficiency -- <10
Exact cuts-off value for ‘deficiency’ & ‘insufficiency’ remain
controversial.
Researchers concluded that having low levels of vitamin D
(<17.8 ng/mL) was independently associated with an increase in all-
cause mortality in the general population.
20. RISK FACTORS FOR VITAMIN D
DEFICIENCY
Elderly Individuals older than 65 years
Dark skin
No sun exposure
Strict vegan diet
Obesity
Nursing home residents
Patients on medications that
induce P-450 enzyme activity.
Individuals with kidney disease (CRF)
Individuals with low bone mass or osteoporosis
Individuals with nonvertebral or hip fractures
Individuals with a history of falls
21. CAUSES OF VITAMIN D DEFICIENCY
The main reasons for low levels of vitamin D are:
Lack of vitamin D in the diet, often in
conjunction with inadequate sun exposure.
Inability to absorb vitamin D from the
intestines.
Inability to process vitamin D due to kidney
or liver disease.
22. CAUSES OF VITAMIN D DEFICIENCY. CONTD.
Inadequate sun exposure
Sunscreen with SPF 15+ blocks 99% vitamin D synthesis
Pigmented skin
Aging (older than 65 years)
Winter season
Physical agents blocking UVR exposure,clothing, season,
air pollution, cloud cover, latitude & altitude.
Decreased absorption
Bowel bypass surgery
Crohn’s disease
Celiac disease
Fat and cholesterol absorption inhibitors.
23. CAUSES OF VITAMIN D DEFICIENCY. CONTD.
Inability to process vitamin D
Impaired production of 25hydroxy vitamin D3 -
Liver disease
Impaired production of 1,25 dihydroxy vitaminD3 -
Kidney disease,
Hypoparathyroidism,
Oncogenic osteomalacia,
X-linked hypophosphatemic rickets.
24. CAUSES OF VITAMIN D DEFICIENCY. CONTD
Other Causes
Breastfeeding
Medications;
- Steroids decrease half life of vitamin D.
- Barbiturates, Phenytoin, and Rifampin can induce
hepatic p450 enzymes to accelerate the catabolism of
vitamin,
- Ketoconazole impaired 25-hydroxylation.
- Increased degradation of 25 (OH) D -Drugs such as,
Rifampicin, Isoniazid, Phenytoin, Glucocorticoids.
Target organ resistance- Vitamin D receptor
mutation.
25. VITAMIN D DEFICIENCY: INDIAN
SCENARIO
India is a country with abundant sunshine but still a
high prevalence (> 70%) of Vitamin D deficiency has
been documented.
Subclinical Vit D deficiency is very common in India in
all the age groups and both sexes across the country.
Skin complexion, poor sun exposure, vegetarian food
habits and lower intake of vitamin D fortified foods
could be attributed to the high prevalence of VDD in
India
Malabsorption is the commonest cause of Vit.D
deficiency in India
Vitamin D deficiency is likely to play an important role
in the very high prevalence of rickets, osteoporosis,
cardiovascular diseases, diabetes, cancer and infections
such as tuberculosis in India.
28. VITAMIN D DEFICIENCY RELATED
SYSTEMIC DISORDER. CONTD..
6. Musculoskeletal system
Rickets & Osteomalasia
Osteoporesis & fracture
Myopathy
Fibromyalgia
7. Malignancy-
Breaast Ca
Colon Ca
Pancreatic Ca
Ovarian Ca
Prostate Ca
30. RICKETS in Children
OSTEOMALACIA in Adults
Increase the risk of Osteoporosis .
31. Rickets and osteomalacia are disorders of the
mineralization of newly synthesized bone
matrix(osteoid).
In children, defects occur in the growth plate
and in the mineralization of cartilage, leading to
characteristic deformities; ie. Rickets.
In adults, it occurs after epiphyseal closure, &
involves only bone; ie. Osteomalasia.
32. Age incidence- 4m-2y
Clinical Feature:
Symptom-
• Irritability & restlessness
• Rocking of head in pillow & sweating
of forehead
• Delayed dentation & Delayed milestones
Sign-
• Craniotabes - Pot belly
• Frontal bossing - Harrison’s sulcus
• Rickety rosary -Pegion chest
• Bowed legs or Knocked knee
• Delayed closure of ant. frontanelle
33. Radiological changes:
Cupping widening & fraying
of lower end of radius & ulna.
Widening of wrist (soft tissue shadow)
o Biochemical changes
Increased alkaline phosphatase
Hypophosphataemia
Hypocalcimia
Decreased plasma 25(OH)D3 level
o Treatment- 6 lakhs IU of Vit-D3 oraly or im induce
rapid healing within 3-4 wks & then 400IU per day.
35. VITAMIN D RESISTANT
RICKETS
Vitamin D-resistant rickets type I
Autosomal recessive.
Failure of 1,25 vitamin D synthesis due to inactivating mutation
in renal 25(OH)D-1-alpha hydroxylase enzyme.
Clinical features are similar to those of infantile rickets .
Diagnosis is usually first suspected when the patient fails to
respond to vitamin D supplementation.
Biochemical features of type I disease are similar to vitamin D
deficiency, except that levels of 25(OH)D are normal.
Treated with the active vitamin D metabolites, 1,25 (OH)2D3
(calcitriol) with or without calcium supplements. Initial doses
are 0.25–2 μmg/day.
36. VITAMIN D RESISTANT RICKETS. CONTD..
Vitamin D-resistant rickets type II
Autosomal recessive.
Defect in the vitamin D receptor which impair its ability to
activate transcription & impaired response to 1,25(OH)2D3.
Most patients present during infancy although less severely
affected patients may not be diagnosed until adulthood.
Approximately 50–70% of children have alopecia which tends to
be associated with a more severe form of the disease.
Here 25(OH)D is normal but PTH and 1,25(OH)2D3 values
are raised.
It is extremely difficult to treat but some times responds partially
to very high doses of active vitamin D metabolites and calcium
and phosphate supplements.
37. HYPOPHOSPHATAEMIC RICKETS
(X-LINKED DOMINANT)
The disorder is inherited in an X-linked dominant manner.This
means the defective gene is located on the X chromosome.
It is associated with mutations in PHEX, FGF23 & DMPA1 gene.
Only one copy of the defective gene is sufficient to cause the
disorder when inherited from a parent who has the disorder.
Males are normally hemizygous for the X chromosome,having only
one copy. As a result, X-linked dominant disorders usually show
higher expressivity
in males than
females.
38. HYPOPHOSPHATAEMIC RICKETS. CONTD..
Defects in phosphate and pyrophosphate metabolism.
The most apparent abnormality is decreased renal
tubular reabsorption of phosphate.
The diagnosis is made on the basis of the early age
at onset and presence of hypophosphataemia with
renal phosphate wasting in the absence of vitamin D
deficiency.
Treatment is with phosphate supplements (1–4 g
daily) and active metabolites of vitamin D to promote
intestinal calcium and phosphate absorption.
39. Osteomalacia is the softening of the bones caused by
defective bone mineralization secondary to
hypocalcemia , hypophosphatemia & vitamin D
deficiency.
The causes of adult osteomalacia are varied, but
ultimately result in a vitamin D deficiency:
Even in the presence of normal calcium and phosphate
levels, chronic acidosis and drugs such as
bisphosphonates (etidronate ) & phosphate-binding
antacids can lead to osteomalacia.
Demineralization occurs mainly in spine, pelvis &
lower extremities.
40. It manifest with bone pain, severe malaise, proximal
muscle weakness & waddling gait.
Radiological feature -Pseudo fracture- or
Looser’s Zones of decalcification along the
course of major arteries.
Biochemical changes -
Decreased serum calcium or phosphorus.
Decreased serum 25-hydroxyvitamin D .
Increased Serum ALP & PTH.
Treatment - Vit D deficiency corrected by 60000 IU
once weekly for 4-6 wk. followed by once a month.
41.
42. DIAGNOSIS OF VITAMIN D
DEFICIENCY
The key diagnostic test in vitamin D deficiency is
demonstration of a decreased serum 25(OH)D3 value.
Low values of 1,25(OH)2D3 and normal levels of
25(OH)D3 suggest a defect in 1-hydroxylase that may
be genetic or acquired as a result of loss of renal function
or tumor-induced osteomalacia.
High levels of 1,25(OH)2D3 and normal levels of
25(OH)D3 are seen in patients with vitamin D
receptor defects.
43. TREATMENT: VITAMIN D
DEFICIENCY
Treatment of vitamin D deficiency should be directed at
the underlying disorder & severity of the condition.
Vitamin D should always be repleted in conjunction with
calcium supplementation since most of the consequences
of vitamin D deficiency are a result of impaired mineral
ion homeostasis.
In patients in whom 1α-hydroxylation is impaired,
metabolites that do not require this activation step are
the treatment of choice. They include 1,25(OH)2D3
[calcitriol , 0.25–0.5 g/d] and 1α-hydroxyvitamin D2 ( 2.5-
5 g/d).
44. TREATMENT: VITAMIN D DEFICIENCY.
CONTD.
If the pathway required for activation of vitamin D is
intact, severe vitamin D deficiency can be treated with
initially 50,000 IU of Vit D weekly for 3–12 weeks,
followed by maintenance therapy (800 IU daily).
Calcium supplementation should include 1.5–2 g/d of
elemental calcium. Normocalcemia is usually observed
within one week of the institution of therapy, although
increases in PTH and alkaline phosphatase levels may
persist for three to six months.
45. MONITORING OF TREATMENT
The most efficacious methods to monitor treatment of
vitamin D deficiency are serum and urinary calcium
measurements.
In patients who are vitamin D replete and are taking
adequate calcium supplementation, the 24-hour
urinary calcium excretion should be in the range of
100–250 mg/ 24 hours.
Lower levels suggest problems with adherence to the
treatment regimen or with absorption of calcium or
vitamin D supplements.
Levels >250 mg/24 hours predispose to nephrolithiasis
and should lead to a reduction in vitamin D dosage
and/or calcium supplementation.
46. TOXICITY
Side effects of vitamin D are uncommon
unless the 25(OH)D level becomes very
elevated (>100ng/ml or 250 mmol/L) and
the person is taking high dose calcium supplement.
Avoid taking multiple products that contain vitamin D
(eg, multivitamin and vitamin D).
The upper limit of intake has been set at 4000IU/day.
Toxic feature:
Anorexia, nausea , vomiting
Deposition of calcium in soft tissue like kidney, arteries
Kidney stone , Metastatic calcification
o Treatment: stop vitamin D & calcium , low calcium
diet, acidify the urine and steroids.
47. VITAMIN D PREPARATIONS
CALCIFEROL (Vit D2)
Dose- 12,000 to 500,000 IU cap daily.
CHOLECALCIFEROL (Vit. D3)
Dose- 400 to 1000 IU orally/day or 6,00000 IU orally/inj.
every 3-4 wks. Interval.
CALCITRIOL (1,25(OH)2D3).
Dose- 0.25-1ug daily / alternate day orally / inj.
ALFA CALCIDOL (1 alfa (OH)D3 )- Prodrug rapidly
hydrolysed in liver to Calcitriol /1,25(OH)2D3.
Dose-1-2ug/day orally.
DIHYDROTACHYSTEROL- A synthetic analogue of
Vit. D2. Dose- 0.25-0.5 mg/day.
48. PREVENTION OF VITAMIN D
DEFICIENCY
Sensible sun exposure- 5-30 minutes of exposure of arms
and legs between 10 am and 3 pm twice a week is often
adequate.
To prevent vitamin D deficiency, the American Academy
of Pediatrics (AAP) recommends that infants and
children receive at least 400 IU per day from diet and
supplements.
All pregnant & lactating mother should take 400IU
vitamin D supplements daily
Evidence shows that vitamin D supplementation of at
least 700 to 800 IU per day reduces fracture and fall
rates in adults.
Fortification of food with Vitamin D such as milk, butter
chapatiflour, maida, cereals etc.
49. REFFERENCE :
Harrison’s Principles Of Internal Medicine , 18th
ed, chapter 352
Williams Textbook of Endocrinology, 10th ed.
Davidson’s Principles and Practice of Medicine 21st
ed, chapter25
Medical Pharmacology 6th
edition , chapter24
Manual of practical medicine, Alagappan, 5th
ed , chapter 2
Bedside clinics in medicine part I , 6th
ed.
Evaluation, Treatment, and Prevention of Vitamin D Deficiency:-
Journal of Clinical Endocrinology & Metabolism, July 2011,
Vitamin D Status in India – Its Implications and Remedial
Measures http://www.japi.org/january_2009
http://www.uptodate.com/contents/vitamin-d-deficiency-beyond-the-basic
http://emedicine.medscape.com/article/128762-overview
http://www.medicinenet.com/vitamin_d_deficiency/related-conditions/ind
Editor's Notes
A secosteroid is a type of steroid with a &quot;broken&quot; ring
Vitamin D plays an important role in many places throughout the body, including the development and calcification of the bones.
Adequate exposure to sunlight and the use of dairy products with vitamin D have significantly reduced the incidence of vitamin D deficiency. However, vitamin D deficiency is still a common problem in many populations, particularly older adults.
It helps to absorb dietary calcium and phosphorus from the intestines.
It suppresses the release of parathyroid hormone, a hormone that causes bone resorption.
Any organic compounds which are essential for normal growth and nutrition and are required in small quantities in the diet because they cannot be synthesized by the body is called vitamin.
A hormone is a class of signaling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviou
Multiple studies show decreased vit D at end of Winter
IS AN ALFA GLOBULIN SYNTHESIZED IN LIVER
A reduction in the serum calcium below ∼2.2 mmol/L (8.8 mg/dL) prompts a proportional increase in the secretion of parathyroid hormone (PTH) and so mobilizes additional calcium from the bone. PTH promotes the synthesis of 1,25(OH)2D in the kidney, which in turn stimulates the mobilization of calcium from bone and intestine and regulates the synthesis of PTH by negative feedback.
Calcitriol increases blood calcium levels ([Ca2+]) by promoting absorption of dietary calcium from the gastrointestinal tract and increasing renal tubular reabsorption of calcium, thus reducing the loss of calcium in the urine. Calcitriol also stimulates release of calcium from bone by its action on the specific type of bone cells referred to as osteoblasts, causing them to release RANKL, which in turn activates osteoclasts
Osteopenia is a condition in which bone mineral density is lower than normal. It is considered by many doctors to be a precursor to osteoporosis. However, not every person diagnosed with osteopenia will develop osteoporosis. More specifically, osteopenia is defined as a bone mineral density T-score between -1.0 and -2.5
Parathyroid hormone (PTH), is secreted by the chief cells of the parathyroid glands. It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium concentration.
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means more phosphate is excreted through the urine.
However, PTH enhances the uptake of phosphate from the intestine and bones into the blood.
Endocrine system refers to the collection of glands that secrete hormones directly into the circulatory system to be carried towards a distant target organ.
PARACRINE Function is an endocrine function in which effects of a hormone are localized to adjacent or nearby cells.
Intracrine refers to a hormone that acts inside a cell, regulating intracellular events. Steroid hormones act through intracellular (mostly nuclear) receptors and, thus, may be considered to be intracrines
Different kinds of medicines to control cholesterol.
HMG-CoA Reductase Inhibitors(also called Statins)
Bile Acid Sequestrants
Fibrates
Niacin
Cholesterol Absorption Inhibitors
Omega-3 Fatty Acid
Vitamin D fortified milk from Amul® (an Indian dairy cooperative, located in Anand, Gujarat, India) is the only fortified milk product found in the general market’
Kellogg’s breakfast cereals fortified with vitamin D along with other micronutrients are also available. However, the exorbitant prices of these products are essentially prohibitive for consumption by the common people of India
Vitamin D deficiency activates the renin-angiotensin-aldosterone system and can predispose to hypertension and left ventricular hypertrophy.
Proposed mechanism: The 1,25 OH vitamin D produced in the kidney enters the circulation and stimulates insulin secretion in the islet cells of the pancreas
Additionally, vitamin D deficiency causes an increase in parathyroid hormone, which increases insulin resistance secondary to down regulation of insulin receptors and is associated with diabetes, hypertension, inflammation, and increased cardiovascular risk.
Metabolic syndrome is a cluster of conditions —(HTN+DM+OBESITY) increased blood pressure, a high blood sugar level, excess body fat around the waist and abnormal cholesterol levels — that occur together, increasing your risk of heart disease, stroke and diabetes
The probable mechanism is that colon, prostate and breast express 25-OH vitamin D 1-alpha hydroxylase and produce 1,25 OH vitamin D locally to control genes that help prevent cancer by limiting cellular proliferation and differentiation by inhibiting angiogenesis and inducing apoptosis
Multiple sclerosis (MS), also known as disseminated sclerosis or encephalomyelitis disseminata, is an inflammatory disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged
Prolonged inadequate intake of vitamin D will lead to impaired bone metabolism. In children, under mineralization of bone causes soft and deformed bones and can lead to the condition known as rickets. Rickets is rare in the US today, but was fairly common as recently as 100 years ago. When children developed rickets, their legs were too weak to hold their weight, resulting in bowed legs, which often persisted into adulthood. Osteomalacia is the adult form of rickets, and leads to impaired mobility and bone fractures. And osteoporosis, a condition that leads to weak and porous bones.
Craniotabes -earliest manifestation.
Harrison’s sulcus- linear transvers depression by the side of the xiphoid process.
fraying –saucer deformity.
If mother is affected chance of affection is equal among boy & girl, but if father is affected boys are escaped, only girl childs are affected.
Expressivity-The term is analogous to the severity of a condition in clinical medicine.
Tumor-induced osteomalacia is usually referred to as a paraneoplastic phenomenon. osteosarcoma and fibrosarcoma produce FGF23 (fibroblast growth factor 23) which inhibits phosphate transport in the renal tubule and reduces calcitriol production by the kidney.
The 1,25(OH)2D levels may be normal in vitamin D deficiency, because of a maximal stimulation of 1-hydroxylase by the low serum phosphorus and high PTH levels.
ALFA CALCIDOL – it does not requre hydroxylation at position 1, limiting step in the active form of vitD take place in kidney. So it is used in- Renal bone disease ,vitD resistant Ricket. Hypoparathyroidism ( ie. Indication of Calcitriol) & osteoporesis.