Vitamins UNIT-7 biochemistry and clinical pathology, D.Pharm 2nd year.pptxAanchal Gupta
Vitamins, unit-7 for D.Pharm second year, According to PCI syllabus.
Definition and classification with examples
Sources, chemical nature, functions, coenzyme form, recommended dietary requirements, deficiency diseases of fat-and water-soluble vitamins
The word "vitamin" comes from the Latin word “vita”, means "life". Vitamins are organic components in food that are required in very small amounts for growth and for maintaining good health. Vitamins are chemicals found in very small amounts in many different foods Vitamins and minerals are measured in a variety of ways. The most common are:
mg – milligram (a milligram is one thousandth of a gram)
mcg – microgram (a microgram is one millionth of a gram. 1,000 micrograms is equal to one milligram)
IU – international unit (the conversion of milligrams and micrograms into IU depends on the type of vitamin or drug)
Hello
This ppt were on the basic information for synthesis of vitamin D and vitamin K in our body.
Along with their RDA , Source , biochemical function and disease state.
Thank you
This presentation provides knowledge about Calcium, its role in human body, homeostasis, factors affecting calcium absorption, drugs affecting calcium regulation, various endogeneous & exogeneous substances, recent research. This ia an assignment in the subject Advanced Pharmacology -II, 1st year M.Pharm, 2nd semester.
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
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
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Drug Discovery and Development .....NEHA GUPTA
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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
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
- 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
2. Table of Contents
Parathyroid Glands...............................................................................................................3
Calcitonin.............................................................................................................................5
Vitamin D.............................................................................................................................9
Forms..................................................................................................................................10
Biochemistry......................................................................................................................11
Production in the skin.........................................................................................................11
Synthesis Mechanism.........................................................................................................13
Mechanism of action..........................................................................................................14
Deficiency..........................................................................................................................15
Emiology........................................................................................................................16
Presentation....................................................................................................................17
Diagnosis........................................................................................................................17
General characteristics...................................................................................................18
Clinical features..............................................................................................................18
Biochemical findings......................................................................................................18
Causes.............................................................................................................................18
People at risk of low vitamin D levels...............................................................................19
............................................................................................................................................20
Vitamin D3 Cholecalciferol...............................................................................................21
Properties ...........................................................................................................................21
Forms..................................................................................................................................21
Metabolism.........................................................................................................................22
Regulation of metabolism..................................................................................................22
2
3. Parathyroid Glands
The parathyroid glands are small endocrine glands in the neck that produce
parathyroid hormone. Humans have four parathyroid glands, which are usually
located behind the thyroid gland, and, in rare cases, within the thyroid gland or
in the chest. Parathyroid glands control the amount of calcium in the blood and
within the bones.
The sole function of the
parathyroid glands is to
maintain the body's calcium
level within a very narrow
range, so that the nervous
and muscular systems can
function properly.
When blood calcium levels
drop below a certain point,
calcium-sensing receptors in
the parathyroid gland are activated to release hormone into the blood.
Parathyroid hormone (PTH, also known as parathormone) is a small protein that
takes part in the control of calcium and phosphate homeostasis, as well as bone
physiology. Parathyroid hormone has effects antagonistic to those of calcitonin.
PTH increases blood calcium levels by stimulating osteoclasts to break down
bone and release calcium. PTH also increases gastrointestinal calcium absorption
by activating vitamin D, and promotes calcium uptake by the kidneys.
3
4. — Single most important hormone in the control of blood [Ca2+].
— Stimulated by decreased blood [Ca2+].
— Promotes rise in blood [Ca2+] by acting on bones, kidney and intestines.
— Promotes formation of 1,25 vitamin D3.
4
5. Calcitonin
Calcitonin is a 32-amino acid linear polypeptide hormone that is produced in
humans primarily by the parafollicular (also known as C-cells) of the thyroid,
The hormone participates in calcium (Ca2+) and phosphorus metabolism. In many
ways, calcitonin counteracts parathyroid hormone (PTH).
To be specific, calcitonin affects blood Ca2+ levels in three ways:
• Inhibits Ca2+ absorption by the intestines
• Inhibits osteoclast activity in bones
• Inhibits Ca2+ and phosphate reabsorption by the kidney tubules
Its actions, in a broad sense, are:
• Bone mineral metabolism:
- Protect against Ca2+ loss from skeleton during periods of Ca2+ stress such
as pregnancy and lactation
• Serum calcium level regulation
- Prevent postprandial hypercalcemia resulting from absorption of Ca2+
from foods during a meal
- Vitamin D regulation
• A satiety hormone:
- Inhibit food intake in rats and monkeys
- May have CNS action involving the regulation of feeding and appetite
5
6. — Works with PTH and 1,25 vitamin D3 to regulate blood [Ca2+].
— Stimulated by increased plasma [Ca2+].
— Inhibits the activity of osteoclasts.
— Stimulates urinary excretion of Ca2+ and P043- by inhibiting reabsorption.
— Physiological significance in adults is questionable.
6
9. Vitamin D
Vitamin D is a group of fat-soluble prohormones, the two major forms of which
are vitamin D2 (or ergocalciferol) and vitamin D3 (or cholecalciferol). The term
vitamin D also refers to metabolites and other analogues of these substances.
Vitamin D3 is produced in skin exposed to sunlight, specifically ultraviolet B
radiation.
Vitamin D plays an important role in the maintenance of organ systems.
• Vitamin D regulates the calcium and phosphorus levels in the blood by
promoting their absorption from food in the intestines, and by promoting
re-absorption of calcium in the kidneys, which enables normal
mineralization of bone and prevents hypocalcemic tetany. It is also needed
for bone growth and bone remodeling by osteoblasts and osteoclasts.
• In the absence of vitamin K or with drugs (particularly blood thinners) that
interfere with Vitamin K metabolism, Vitamin D can promote soft tissue
calcification.
• It inhibits parathyroid hormone secretion from the parathyroid gland.
• Vitamin D affects the immune system by promoting phagocytosis, anti-
tumor activity, and immunomodulatory functions.
Vitamin D deficiency can result from inadequate intake coupled with inadequate
sunlight exposure, disorders that limit its absorption, conditions that impair
conversion of vitamin D into active metabolites, such as liver or kidney disorders,
or, rarely, by a number of hereditary disorders. Deficiency results in impaired
bone mineralization, and leads to bone softening diseases, rickets in children and
osteomalacia in adults, and possibly contributes to osteoporosis. However,
sunlight exposure, to avoid deficiency, carries other risks, including skin cancer;
this risk is avoided with dietary absorption, either through diet or as a dietary
supplement.
10. Forms
Several forms (vitamers) of vitamin D have been discovered. The two major
forms are vitamin D2 or ergocalciferol, and vitamin D3 or cholecalciferol. These
are known collectively as calciferol.
Chemically, the various forms of vitamin D are secosteroids; i.e., steroids in
which one of the bonds in the steroid rings is broken.[7] The structural difference
between vitamin D2 and vitamin D3 is in their side chains. The side chain of D2
contains a double bond between carbons 22 and 23, and a methyl group on
carbon 24.
Vitamin D2 is derived from fungal and plant sources, and is not produced by the
human body. Vitamin D3 is derived from animal sources and is made in the skin
when 7-dehydrocholesterol reacts with UVB ultraviolet light at wavelengths
between 270–300 nm, with peak synthesis occurring between 295-297 nm.
These wavelengths are present in sunlight when the UV index is greater than 3.
At this solar elevation, which occurs daily within the tropics, daily during the
spring and summer seasons in temperate regions, and almost never within the
arctic circles, adequate amounts of vitamin D3 can be made in the skin after only
ten to fifteen minutes of sun exposure at least two times per week to the face,
arms, hands, or back without sunscreen. With longer exposure to UVB rays, an
equilibrium is achieved in the skin, and the vitamin simply degrades as fast as it
is generated.
In humans, D3 is as effective as D2 at increasing the levels of vitamin D hormone
in circulation, although others state that D3 is more effective than D2. However, in
some species, such as rats, vitamin D2 is more effective than D3. Both vitamin D2
and D3 are used for human nutritional supplementation, and pharmaceutical
forms include calcitriol (1alpha, 25-dihydroxycholecalciferol), doxercalciferol and
calcipotriene.
10
11. Biochemistry
Vitamin D is a prohormone, meaning that it has no hormone activity itself, but is
converted to the active hormone 1,25-D through a tightly regulated synthesis
mechanism. Production of vitamin D in nature always appears to require the
presence of some UV light; even vitamin D in foodstuffs is ultimately derived
from organisms, from mushrooms to animals, which are not able to synthesize it
except through the action of sunlight at some point in the synthetic chain. For
example, fish contain vitamin D only because they ultimately exist on calories
from ocean algae which synthesize vitamin D in shallow waters from the action of
solar UV.
Production in the skin
The skin consists of two primary layers: the inner layer called the dermis,
composed largely of connective tissue, and the outer, thinner epidermis. The
epidermis consists of five strata; from outer to inner they are: the stratum
corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum
basale.
Vitamin D3 is produced photochemically in the skin from 7-dehydrocholesterol.
The highest concentrations of 7-dehydrocholesterol are found in the epidermal
layer of skin, specifically in the stratum basale and stratum spinosum. The
production of pre-vitamin D3 is therefore greatest in these two layers, whereas
production in the other layers is less.
Synthesis in the skin involves UVB radiation which effectively penetrates only the
epidermal layers of skin. While 7-Dehydrocholesterol absorbs UV light at
wavelengths between 270–300 nm, optimal synthesis occurs in a narrow band of
UVB spectra between 295-300 nm. Peak isomerization is found at 297 nm. This
narrow segment is sometimes referred to as D-UV. The two most important
11
12. factors that govern the generation of pre-vitamin D3 are the quantity (intensity)
and quality (appropriate wavelength) of the UVB irradiation reaching the 7-
dehydrocholesterol deep in the stratum basale and stratum spinosum.
A critical determinant of vitamin D3 production in the skin is the presence and
concentration of melanin. Melanin functions as a light filter in the skin, and
therefore the concentration of melanin in the skin is related to the ability of UVB
light to penetrate the epidermal strata and reach the 7-dehydrocholesterol-
containing stratum basale and stratum spinosum. Under normal circumstances,
ample quantities of 7-dehydrocholesterol (about 25-50 µg/cm² of skin) are
available in the stratum spinosum and stratum basale of human skin to meet the
body's vitamin D requirements, and melanin content does not alter the amount of
vitamin D that can be produced. Thus, individuals with higher skin melanin
content will simply require more time in sunlight to produce the same amount of
vitamin D as individuals with lower melanin content. As noted below, the amount
of time an individual requires to produce a given amount of Vitamin D may also
depend upon the person's distance from the equator and on the season of the
year.
12
13. Synthesis Mechanism
1. Vitamin D3 is synthesized from 7-dehydrocholesterol, a derivative of
cholesterol, which is then photolyzed by ultraviolet light in 6-electron
conrotatory electrocyclic reaction. The product is pre-vitamin D3.
2. Pre-vitamin D3 then spontaneously isomerizes to Vitamin D3
3. Whether it is made in the skin or ingested, vitamin D3 (cholecalciferol) is
then hydroxylated in the liver to 25-hydroxycholecalciferol (25(OH)D3 or
calcidiol) by the enzyme 25-hydroxylase produced by hepatocytes, and
stored until it is needed.
13
14. 4. 25-hydroxycholecalciferol is further hydroxylated in the kidneys by the
enzyme 1α-hydroxylase, into two dihydroxylated metabolites, the main
biologically active hormone 1,25-dihydroxycholecalciferol (1,25(OH)2D3 or
calcitriol) and 24R,25(OH)2D3. This conversion occurs in a tightly
regulated fashion, with renal 1α-hydroxylase being stimulated by either
parathyroid hormone or hypophosphatemia.
Calcitriol is represented below right (hydroxylated Carbon 1 is on the lower ring
at right, hydroxylated Carbon 25 is at the upper right end).
Mechanism of action
Once vitamin D is produced in the skin or consumed in food, it is converted in the
liver and kidney to form 1,25 dihydroxyvitamin D, (1,25(OH)2D) the
physiologically active form of vitamin D (when "D" is used without a subscript it
refers to either D2 or D3). This metabolically active form of vitamin D is known as
calcitriol. Following this conversion, calcitriol is released into the circulation, and
by binding to a carrier protein in the plasma, vitamin D binding protein (VDBP), it
is transported to various target organs.
The hormonally active form of vitamin D mediates its biological effects by binding
to the vitamin D receptor (VDR), which is principally located in the nuclei of
target cells. The binding of calcitriol to the VDR is involved in calcium absorption
in the intestine.
14
15. The Vitamin D receptor belongs to the nuclear receptor superfamily of
steroid/thyroid hormone receptors, and VDR are expressed by cells in most
organs, including the brain, heart, skin, gonads, prostate, and breast. VDR
activation in the intestine, bone, kidney, and parathyroid gland cells leads to the
maintenance of calcium and phosphorus levels in the blood (with the assistance
of parathyroid hormone and calcitonin) and to the maintenance of bone content.
The VDR is known to be involved in cell proliferation, differentiation. Vitamin D
also affects the immune system, and VDR are expressed in several white blood
cells including monocytes and activated T and B cells.
Deficiency
Deficiency of vitamin D can result from a number of factors including: inadequate
intake coupled with inadequate sunlight exposure, disorders that limit its
absorption, conditions that impair conversion of vitamin D into active
metabolites, such as liver or kidney disorders and body characteristics such as
skin color and body fat. Rarely deficiency can result from a number of hereditary
disorders. Deficiency results in impaired bone mineralization, and leads to bone
softening diseases including:
• Rickets, a childhood disease characterized by impeded growth, and
deformity, of the long bones.
15
16. Rickets is a softening of bones in children potentially leading to fractures and deformity.
Rickets is among the most frequent childhood diseases in many developing countries. The
predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may
also lead to rickets (cases of severe diarrhea and vomiting may be the cause of the
deficiency). Although it can occur in adults, the majority of cases occur in children suffering
from severe malnutrition, usually resulting from famine or starvation during the early stages of
childhood. Osteomalacia is the term used to describe a similar condition occurring in adults,
generally due to a deficiency of vitamin D.[1] The origin of the word "rickets" is probably from
the Old English dialect word 'wrickken', to twist. The Greek derived word "rachitis" (meaning
"inflammation of the spine") was later adopted as the scientific term for rickets, due chiefly to
the words' similarity in sound. In many languages it is known as "English disease".
Emiology
Those at higher risk for developing rickets include:
• Breast-fed infants whose mothers are not exposed to sunlight
• Breast-fed infants who are not exposed to sunlight
• Individuals not consuming fortified milk, such as those who are lactose intolerant
Individuals with red hair have been speculated to have a decreased risk for rickets due to
their greater production of vitamin D in sunlight.
It should also be noted that new-born infants can even have rickets at birth, if the mother had
low vitamin D levels during pregnancy, often referred to as Congenital Rickets
16
17. Presentation
Signs and symptoms of rickets include:
• Bone pain or tenderness
• dental problems
• muscle weakness (rickety myopathy or "floppy baby syndrome" or "slinky
baby" (where the baby is floppy or slinky like))
• increased tendency for fractures (easily broken bones), especially greenstick
fractures
• Skeletal deformity
o Toddlers: Bowed legs (genu varum)
o Older children: Knock-knees (genu valgum) or "windswept knees"
o Cranial, spinal, and pelvic deformities
• Growth disturbance
• Hypocalcemia (low level of calcium in the blood), and
• Tetany (uncontrolled muscle spasms all over the body).
• Craniotabes (soft skull)
• Costochondral swelling (aka "rickety rosary" or "rachitic rosary")
• Harrison's groove
• Double malleoli sign due to metaphyseal hyperplasia
• Widening of wrist raises early suspicion, it is due to metaphysial cartilage
hyperplasia.
An X-ray or radiograph of an advanced sufferer from rickets tends to present in a
classic way: bow legs (outward curve of long bone of the legs) and a deformed chest.
Changes in the skull also occur causing a distinctive "square headed" appearance.
These deformities persist into adult life if not treated.
Long-term consequences include permanent bends or disfiguration of the long bones,
and a curved back.
Diagnosis
A doctor may diagnose rickets by:
• Blood tests:
o Serum calcium may show low levels of calcium, serum phosphorus
may be low, and serum alkaline phosphatase may be high.
• Arterial blood gases may reveal metabolic acidosis
• X-rays of affected bones may show loss of calcium from bones or changes in
the shape or structure of the bones.
• Bone biopsy is rarely performed but will confirm rickets.
17
18. • Osteomalacia, a bone-thinning disorder that occurs exclusively in adults
and is characterized by proximal muscle weakness and bone fragility.
Osteomalacia is the general term for the softening of the bones due to defective bone mineralization.
Osteomalacia in children is known as rickets, and because of this, osteomalacia is often restricted to
the milder, adult form of the disease. It may show signs as diffuse body pains, muscle weakness, and
fragility of the bones. A common cause of the disease is a deficiency in Vitamin D,
Osteoporosis is a disease of bone that leads to an increased risk of fracture. In osteoporosis
General characteristics
the bone mineral density (BMD) is reduced, bone microarchitecture is disrupted, and the amount
and variety of non-collagenous proteins in bone is altered. Osteoporosis is defined by the World
Osteomalacia in the adult is most commonly found in mineral density 2.5 standard deviations below
Health Organization (WHO) in women as a bone confined, dark-skinned, or diet-disbalanced
subjects. Many mass (20-year-old healthy female average) as measured by osteoporosis, but the two
peak bone of the effects of the disease overlap with the more common DXA; the term
diseases are significantly different. Osteomalacia is specifically a defect in [1] Osteoporosis isthe protein
"established osteoporosis" includes the presence of a fragility fracture. mineralization of most
framework known as osteoid.menopause, when it is called postmenopausalby lack in vitamin D.may
common in women after This defective mineralization is mainly caused osteoporosis, but
also develop in men, and may occur in anyone in the presence of particular hormonal disorders
Osteomalacia chronic diseases or as osteo refers to bone, and malacia means softness. In the past,
and other is derived from Greek: a result of medications, specifically glucocorticoids, when the
the disease was also steroid- ormalacosteon and its Latin-derived equivalent, mollities ossium. its
disease is called known as glucocorticoid-induced osteoporosis (SIOP or GIOP). Given
influence on the risk of fragility fracture, osteoporosis may significantly affect life expectancy and
quality of life.
Clinical features
Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and
thighs, spreading later to the arms and ribs. Pain is non-radiating, symmetrical, and accompanied by
tenderness in the involved bones. Proximal muscles are weak, and there is difficulty in climbing up
stairs and getting up from a squatting position.
Due to demineralization bones become less rigid, physical signs include deformities like triradiate
pelvis and lordosis. The patient has a typical "waddling gait". However that physical signs may derive
from a previous osteomalacia state, since bones don't regain the original shape after they're deformed.
Pathologic fractures due to weight bearing may develop. Most of the time, the only alleged symptom is
chronic fatigue and bone aches are not spontaneous but only revealed by pressure or shocks.
Biochemical findings
Biochemical features are similar to rickets.The major fact is a collapsed vitamin D rate in blood or
serum. The major findings are 1 The serum calcium is low 2 urinary calcium is low 3 serum phosphate
is low except in cases of renal osteodystrophy 4 serum alkaline phosphate is high the technetium bone
scan will show increased activity
Causes
The causes of adult osteomalacia are varied.
• Insufficient sunlight exposure, especially in dark-skinned subjects
• Insufficient nutritional quantities or faulty metabolism of vitamin D or phosphorus
• Renal tubular acidosis
• Malnutrition during pregnancy
• Malabsorption syndrome
• Chronic renal failure
• Tumor induced osteomalacia
• Therapy with Fumaderm
• Celiac disease
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19. Vitamin D malnutrition may also be linked to an increased susceptibility to several
chronic diseases such as high blood pressure, tuberculosis, cancer, periodontal
disease, multiple sclerosis, chronic pain, seasonal affective disorder, peripheral
artery disease and several autoimmune diseases including type 1 diabetes. There
is an association between low vitamin D levels and Parkinson's disease, but
whether Parkinson's causes low vitamin D levels, or whether low vitamin D levels
play a role in the pathogenesis of Parkinson's disease has not been established.
People at risk of low vitamin D levels
— Older people in residential care
— Older people admitted to hospital
— Patients with hip fracture
— Dark-skinned men and women (particularly if veiled)
— Mothers of infants with rickets
— People unable to obtain regular sun exposure
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21. Vitamin D3 Cholecalciferol
Cholecalciferol is a form of Vitamin D,
also called vitamin D3 or calciol.
It is structurally similar to steroids such
as testosterone, cholesterol, and cortisol
One gram of pure vitamin D3 is 40 000
000 (40x106) IU, or, in other words, one
IU is 0.025 μg.
Properties
Molecular formula C27H44O
Molar Mass 384.64 g/mol
Appearance White, needle-like crystals
Melting point 83–86 °C
Forms
Vitamin D3 has several forms:
• Cholecalciferol, (sometimes called calciol) which is an inactive,
unhydroxylated form of vitamin D3)
• Calcidiol (also called 25-hydroxyvitamin D3), which is the form measured in
the blood to assess vitamin D status
• Calcitriol (also called 1,25-dihydroxyvitamin D3), which is the active form
of D3.
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22. Metabolism
7-Dehydrocholesterol is the precursor of vitamin D3 and forms cholecalciferol only
after being exposed to solar UV radiation.
Cholecalciferol is then hydroxylated in the liver to become calcidiol (25-
hydroxyvitamin D3).
Next, calcidiol is again hydroxylated, this time in the kidney, and becomes
calcitriol (1,25-dihydroxyvitamin D3). Calcitriol is the most active hormone form of
vitamin D3.
Regulation of metabolism
• Cholecalciferol is synthesized in the skin from 7-dehydrocholesterol under
the action of ultraviolet B light. It reaches an equilibrium after several
minutes depending of several factors including conditions of sunlight
(latitude, season, cloud cover, altitude), age of skin, and color of skin.
• Hepatic hydroxylation of cholecalciferol to calcidiol (25-
hydroxycholecalciferol) is loosely regulated, if at all, and blood levels of
this molecule largely reflect the amount of vitamin D3 produced in the skin
or the vitamin D2 or D3 ingested.
• Renal hydroxylation of calcidiol to calcitriol by 1-alpha-hydroxylase is
tightly regulated (stimulated by either parathyroid hormone or
hypophosphatemia) and serves as the major control point in production of
the most active circulating hormone calcitriol (1,25-dihydroxyvitamin D3).
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