This document discusses calcium and phosphate metabolism. It provides information on:
1. Calcium and phosphate are important minerals that are required for bone formation and strength. Their absorption is regulated by hormones including vitamin D, parathyroid hormone, and calcitonin.
2. Vitamin D helps regulate calcium and phosphate levels by increasing their absorption in the intestine and reabsorption in the kidneys. Parathyroid hormone also increases calcium levels by stimulating vitamin D and calcium reabsorption. Calcitonin decreases calcium levels by acting on bones and kidneys.
3. Other factors like diet, pregnancy, and growth can also influence calcium and phosphate absorption in the body. A balanced ratio of calcium to phosphate
This is a PPT of calcium and phosphate metabolism. Clinical correlation are not included. Hope it is useful to you all. Please Like and Share it with your friends
This seminar includes sources,daily requirement,metabolism i.e absorption and excretion of calcium and phosphate and various factors associated due to increase or decrease in the levels of calcium and phosphate within the body
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
This is a PPT of calcium and phosphate metabolism. Clinical correlation are not included. Hope it is useful to you all. Please Like and Share it with your friends
This seminar includes sources,daily requirement,metabolism i.e absorption and excretion of calcium and phosphate and various factors associated due to increase or decrease in the levels of calcium and phosphate within the body
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
This presentation deals with the physiological aspect of Calcium and phosphate metabolism, it's relationship with the various types of rickets and possible remedies
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Biochemistry of Calcium metabolism covering the source, factors effecting absorption, normal level of calcium, regulation of the calcium, hypercalcemia, hypocalcemia, disorders related to calcium and bone markers.
Useful for students of MBBS, BDS, BSc, MSc, MLT, Physiotherapy (BPT), Nursing etc.
This presentation deals with the physiological aspect of Calcium and phosphate metabolism, it's relationship with the various types of rickets and possible remedies
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Biochemistry of Calcium metabolism covering the source, factors effecting absorption, normal level of calcium, regulation of the calcium, hypercalcemia, hypocalcemia, disorders related to calcium and bone markers.
Useful for students of MBBS, BDS, BSc, MSc, MLT, Physiotherapy (BPT), Nursing etc.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Calcium and phosphate metabolism / orthodontics diploma coursesIndian dental academy
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
CALCIUM METABOLISM:
VITAMIN D-PARATHYROID-CALCITONIN ROLE
(Rickets,Osteoporosis,Renal Osteodystrophy)
Prevention Dr.Sandeep C Agrawal Agrasen Hospital Gondia India
Metabolic Bone Diseases:phosphorus,magnesium and other minerals ,Calcium and vitamin D rich diets,Sunlight exposure,vitamin D synthesis,Osteoporosis prevention and diet
Calcium and phosphorous metabolism/ rotary endodontic courses by indian denta...Indian dental academy
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Minerals are inorganic compounds that are required for the body as one of the nutrients.
The inorganic elements (minerals) constitute only small potion of body weight.
Human body needs number of minerals for its functioning.
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.
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.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
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.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
5. Most common metal in many animals and in the human body.
Ancient Romans prepared lime- calcium oxide. 975 AD -plaster
of Paris (calcium sulfate)was used for setting broken bones.
Sir Humphry Davy Isolated calcium(1808)
Calcium
6. Phosphorus –
Due to its use in explosives, poisons -"the Devil's element".
In human body Phosphorus is present as phosphates (compounds
containing the phosphate ion, PO4
−3
)
The first form of elemental phosphorus to be produced (white
phosphorus, in 1669) by Greek .
Hennig Brand(1669) discovered.
7. ROLE OF CALCIUM IN BODY
Affects nerve and muscle physiology
Intracellular signal transduction pathways.
Co-factor in blood clotting cascade.
Constituent of bone and teeth.
Major structural element in the vertebrate skeleton (bones and teeth) in the form of
calcium phosphate (Ca10(PO4)6(OH)2 known as hydroxyapatatite
Maintain all cells and connective tissues in the body.
Essential component in production of enzymes and hormones that regulate
metabolism
Stimulation of muscle
action potential is
generated
Contraction of muscle
8. Role of phosphate
Key constituent of bone and teeth.
Component of intra cellular buffering. Forms energy rich bonds in ATP.
Forms co-enzymes.
Regulates blood and urinary pH.
Forms organic molecules like DNA & RNA
Cellular energy metabolism.
Constituent of macro molecules like nucleic acids, phospholipids and
phosphoproteins.
9. DISTRIBUTION
1000-1500gm
(1.5% of the body weight)
99%
Bones
1%
ECF
Plasma
500-800gm
80-90%
Bones
Teeth
10%
RBC
Plasma
Total calcium Total phosphorus
10. PLASMA CALCIUM AND PHOSPHATE
Normal plasma levels
9-11mg/dl(calcium)
Normal plasma levels
2.5-4.5mg/dl(phosphorous)
Ionized Unionized
( 5 mg/dl) (4mg/dl)
organic Inorganic
(0.5-1mg/dl) (Adults:3-4mg/dl)
(children:5-6mg/dl)
12. CALCIUM PHOSPHATE RATIO
Calcium : Phosphate ratio normally is 2:1
Increase in plasma calcium levels causes corresponding
decrease in absorption of phosphate.
This ratio is always constant.
13. SOURCES OF CALCIUM
Calcium is present in variable amounts in all the foods
and water we consume, although the main sources
are dairy products and vegetables.
14. Milk-good sources of calcium
Calcium content of cow’s milk- 100mg/ml
Best source
Hard cheese
Milk
Dark green leafy vegetables
Good source
Ice-cream
Broccoli
Baked beans
Dried legumes
Dried figs
Fair source
String beans
Eggs
Bread
RDA OF CALCIUM
Average adult-800 mg/ day
Infants: <1yr- 360-540mg
1-10yr- 800mg
11-18yr- 1200mg
During pregnancy & lactation-1200mg/ day
osteoporosis-Women> men
Post menopause women start to lose more bone
Pregnant and breast feeding women must intake
adequate amount as the baby relies on only her
mother to get his supply of calcium.
A child with early childhood caries, in whom diet
management has to be considered. Milk with sugar
can be replaced (with flavoured lassi or a custard
pudding or kheer) rather than total stoppage of milk.
16. Absorption of Calcium
Absorbed from the gastrointestinal tract in to blood
Two mechanisms have been proposed for the absorption
of calcium
→ Active absorption(Proximal portion of the duodenum
→ Passive absorption(In the remainder of the small intestine)
17. PHOSPHORUS ABSORPTION
50-70%- absorbed
Small intestine- soluble inorganic phosphate
Excess calcium, iron or aluminum- interferes absorption
18. FACTORS CONTROLLING ABSORPTION
Factors are classified into
1. Those acting on the mucosal cells
2. Those affecting the availability of
calcium and phosphates in the gut.
19. Amount of dietary calcium and
phosphates:
Rottenson -1938-amount of calcium stored in body is directly
proportional to amount of calcium absorbed in body
• Increased level of calcium and phosphate in diet increases their
absorption however up to a certain limit.
• This is because the active process of their absorption can bear
with certain amounts of load beyond which the excess would
pass out into faeces
20. • During later stages of pregnancy, greater amount
of calcium absorption is seen.
• 50% of this calcium is used for the development of
fetal skeleton and the rest is stored in the bones to
act as a reserve for lactation.
• This is due to the increased level of placental
lactogen and estrogen which stimulates
increased hydroxylation of vitamin D.
• In growth there is a increased level of growth hormone.
GH acts by increasing calcium absorption. It also
increases the renal excretion of calcium and
phosphates.
Pregnancy and growth:
The rise in maternal obesity highlights that maternal and newborn
vitamin D deficiency will continue to be a serious public health
problem until steps are taken to identify and treat low 25(OH)D.
Bodnar LM, Catov JM, Roberts JM, Simhan HN. Prepregnancy obesity predicts
poor vitamin D status in mothers and their neonates. The Journal of nutrition.
2007 Nov 1;137(11):2437-42.
21. HORMONAL CONTROL OF CALCIUM & PHOSPHATE
METABOLISM
Three hormones regulate calcium and
phosphate metabolism.
Vitamin D
PTH
Calcitonin
22. Vitamin D
Cholecalciferol / D3
Ergocalciferol / D2
Can be called as hormone as it is produced in the skin
when exposed to sunlight.
Vitamin D has very little intrinsic biological activity.
Vitamin D itself is not a active substance, instead it must
be first converted through a succession of reaction in
the liver and the kidneys to the final active product 1, 25
di hydroxycholecalciferol,
23. VITAMIN-D(sun-shine vitamin)
Studies conducted by Cheng et al,2003 and Strushkevich et al in
2008 suggested that Vitamin D is converted in the liver to
25(OH)D, a process carried out by CYP2R1.
The crystal structure of CYP2R1 has been determined with vitamin
D in the active site, and the enzyme has been shown to
metabolize both vitamin D2 and vitamin D3 equally efficiently.
24. Action on bone:
In the osteoblasts of bone calcitriol stimulates ca
uptake for deposition as capo4
Action on kidney:
It is involved in minimizing the excretion of ca&p
through kidney by decreasing their excretion and
enhancing reabsorption
25. Dietary sources
Cod liver oil
Fish- Salmon
Egg, liver
Mean action of vitamin D is to increase the plasma level of
calcium.
Increases intestinal Ca&P absorption.
Increases renal reabsorption of Calcium and
phosphate.
27. Parathyroid Hormone
(PTH)
Secreted by parathyroid gland
Glands are four in number
Present posterior to the thyroid gland
Formed from third and fourth branchial pouches
Combined weight of 130mg with each gland weighing between 30-
50mg.
Histologically – two types of cells
Chief cells (forming PTH)
Oxyphilic cells (replaces the chief cells
stores hormone)
28. • Parathyroid hormone is one of the main hormones
controlling Ca+2
absorption.
• It mainly acts by controlling the formation of 1,25 DHCC,
which is active form of Vit. D, which is responsible for,
increased Ca+2
absorption.
NORMAL PTH LEVEL IN SERUM – 10-60ng/L
PARATHYROID HORMONE
29. Parathyroid Hormone
Single chain polypeptide
Molecular weight 9000
Consist of 84 amino acids
Plasma half life – 20-30 minutes
Plasma concentration – 10-50ug/ml
Measured by immunoassay .
30. Actions of PTH
The main function is to increase the level of Ca in
plasma within the critical range of 9 to11 mg.
Parathormone inhibits renal phosphate reabsorption in
the proximal tubule and therefore increases phosphate
excretion
Parathormone increases renal Calcium reabsorption in
the distal tubule, which also increases the serum calcium.
Net effect of PTH ↑ serum calcium
↓ serum phosphate
31. Stimulation for PTH secretion
The stimulatory effect for PTH secretion is low level
of calcium in plasma.
Maximum secretion occurs when plasma calcium
level falls below 7mg/dl.
When plasma calcium level increases to 11mg/dl
there is decreased secretion of PTH
32. CALCITONIN
Minor regulator of calcium & phosphate
metabolism
Secreted by parafollicular cells or C-cells of
thyroid gland.
Also called as thyrocalcitonin.
Single chain polypeptide
Molecular weight 3400
Plasma concentration – 10-20ug/ml
33. Action of Calcitonin
Net effect of calcitonin decreases Serum Ca
Target site
Bone (osteoclasts)
Kidney
Intestine
34. Calcitonin is a Physiological Antagonist to PTH with respect to
Calcium.
With respect to Phosphate it has the same effect as PTH i.e. ↓
Plasma Phosphate level
35. OTHER HORMONES on CALCIUM
METABOLISM
GROWTH HORMONE
INSULIN
TESTOSTERONE & OTHER HORMONES
LACTOGEN & PROLACTIN
STEROIDS
THYROID HORMONES
36. Increases the intestinal absorption of calcium and
increases its excretion from urine
Stimulates production of insulin like growth factor in
bone which stimulates protein synthesis in bone
GROWTH HORMONE
37. TESTOSTERONE
Testosterone causes differential growth of cartilage
resulting to differential bone development
Acts on cartilage & increase the bone growth.
INSULIN
It is an anabolic hormone which favors bone formation
38. Thyroid Hormone
In infants stimulation of bone growth
In adults
increased bone metabolism increased calcium
mobilization
39. Glucocorticoids
Anti vitamin D action, decrease absorption of calcium in
intestine
Inhibit protein synthesis and so decrease bone formation
Inhibit new osteoclast formation & decrease the activity of
old osteoclasts.
40. Factors affecting availability of Calcium and
Phosphates in gut.
pH of the intestine
Amount of dietary calcium and phosphates
Phytic acid and Phytates
Oxalates
Fats
Proteins and amino acids
Carbohydrates
Bile salts
41. pH of intestine:
• Acidic pH in the upper intestine (deodenum) increases
calcium absorption by keeping calcium salts in a soluble
state.
• In lower intestine since pH is more alkaline, calcium salts
undergoes precipitation
42. Phytic acid and phytates:
• present in oatmeal, meat and cereals and are considered anti-
calcifying factors as they combine with calcium in the diet thus
forming insoluble salts of calcium
Oxalates:
• present in spinach and rhubarb leaves. They form oxalate
precipitates with calcium present in the diet thus decreasing their
availability.
Fats:
• combines with calcium and form insoluble calcium ,
thus decreasing calcium absorption.
Xiao et al(2010) have demonstrated that a duodenal
oxidation state induced by a high fat diet could significantly
down regulate the expression of CB9k, PMCA1b, and NCX,
as well as inhibiting intestinal calcium absorption.
They demonstrated that type diabetes mellitus transientlyⅠ
inhibits intestinal Ca2+ absorption.
43. Bile salts:
• increases calcium absorption by promoting metabolism
of lipids.
Protein and aminoacids:
• increases calcium absorption as protein forms soluble
complexes with calcium and keeps calcium in a form
that is easily absorbable.
Carbohydrates:
• lactose promotes calcium absorption by creating the
acidity in the gut as they favours the growth of acid
producing bacteria.
44. Concept of Calcium Balance
Defined as the net gain or loss of calcium by the body
over a specified period of time
Calculated by deducting calcium in faeces and urine
from the calcium taken in diet.
Positive calcium balance in growing children
Negative calcium balance in aging adults.
45. Excretion of Calcium and
Phosphorous
Calcium is excreted in the urine, bile, and digestive
secretions.
The renal threshold for serum ca is 10 mg/dl.
70-90% of the calcium eliminated from the
body is excreted in the feces.
The daily loss of calcium in sweat is about 15 mg.
While passing through the kidney, large quantity of
calcium is filtered in the glomerulus. From the
filtrate, 98 to 99% of calcium is reabsorbed in the
renal tubules in to blood and only small quantity is
excreted through urine.
46. Daily turnover rates of Ca in an adult are as
follows:
Intake 1000mg.
Intestinal absorption 350mg
Secretion in GI juice 250mg
Net absorption over secretion 100mg
Loss in the faeces 200mg
Excretion in the urine 80-100mg
47. Phosphorous Excretion
Phosphorous is excreted primarily through the urine.
Almost 2/3rd
of total phosphorous that is excreted is found
in the urine as phosphate of various cations
phosphorous found in the faeces is the non-absorbed
form of phosphorous.
48. OSTEOPOROSIS
• An atrophy of bone
• Bone resorption>bone deposition
• Calcium or hormonal deficiencies
• Older people- women>60yrs
• c/f: loss of height- shortening of the trunk &collapse of the vertebrae
Deformed thoracic cage
Bone pain-due to fracture
• Radiographically: loss of bone density
Thinning of cortex
Trabaculae-reduced
49. ASSOCIATION OF MENOPAUSE,
OSTEOPOROSIS AND
PERIODONTAL DISEASES
OSTEOPOROSIS &
PERIODONTAL DISEASE
>40yrs-decline in the estrogen levels due to decrease
in the ovarian functions.
All these hormonal changes will lead to
psychological, oral and systemic health changes.
Oral changes that can be seen may include: thinning
of oral mucosa, desquamation of gingival epithelium,
burning mouth, gingival recession, xerostomia and
alveolar bone loss & ridge resorption
Since both osteoporosis and
periodontal diseases are bone
resorptive diseases,
It has been hypothesized that
osteoporosis could be a risk factor for
the progression of periodontal disease
Heaney et al(2011)-comparison of pre and post-menopausal women found
that calcium balance fell significantly in post-menopausal women and that
this was due to both a reduction in calcium absorption and an increase in
urinary calcium loss.
50. RICKETS
Softening of the bones in children potentially leading to fractures and deformity.
Due to def. of vit.D causing deficiency in Ca & phosphate
CLINICAL FEATURES
Femoral and tibial bowing
Growth retardation
weakness
tetany
Susceptibility to fracture
Irritability
Longo, Dan L. et al. (2012). Harrison's principles of internal medicine. (18th
ed. ed.). New York: McGraw-Hill. ISBN 978-0-07174889-6.
51. Oral manifestation:
Sir Edward Mellanby (1884-1955)- 1st
to report the effect of
rickets on the teeth.
1.Development abnormalities of dentine & enamel,
2.Delayed eruption
3.Malalignment of the teeth in the jaws
4.High caries index
5.Abnormally wide predentine zone
6.Interglobular dentine
Many reports-rickets linked with hypoplasia
52. TREATMENT:
Diet and sunlight
Recommendations are for 400 international units (IU) of vitamin D a day for
infants and children. Children who do not get adequate amounts of vitamin D are
at increased risk of rickets. Vitamin D is essential for allowing the body to uptake
calcium for use in proper bone calcification and maintenance.
According to the American academy of paediatrics (AAP),
all infants, including those who are exclusively breast-
fed, may need Vitamin D supplementation until they
start drinking at least 17 US fluid ounces (500 ml) of
vitamin D-fortified milk or formula a day.
Gartner LM, Greer FR (April 2003). "Prevention of rickets and vitamin D deficiency: new guidelines for
vitamin D intake". Pediatrics. 111 (4 Pt 1): 908–10.
53. • A female, aged 2 years and 6 months, was referred by her general dentist to British Columbia's Children's
Hospital dental department with facial pain and swelling. Oral antibiotics had been prescribed and the
symptoms were improving when the child was first seen
• Preoperative assessment by the pediatrician revealed a waddling gait, and a hip radiograph (not shown)
showed normal acetabular angles, metaphyseal lucency, and medial beaking. Hemoglobin was within
normal limit
• clinical examination confirmed a complete primary dentition and a discharging sinus in the buccal sulcus
associated with the carious maxillary right primary first molar. Carious lesions were noted in the
following teeth: all maxillary primary incisors, all primary first molars, and the mandibular primary
central incisors.
• The medical, hematological, and radiological investigations reported nutritional rickets.
• Intraoral dental radiographs (Fig 1) illustrate the extent of the carious lesions and the large size of the
pulp chambers with pulpal horn extension close to the dentoenamel junction, especially in the
mandibular primary first molars. Hypoplasia was not evident in the unerupted teeth. The bone
trabeculation in the anterior mandible and maxilla was very sparse. The lamina dura and the crypts of
the developing teeth were present, but attenuated. On the left side, the cortices of the inferior alveolar
canal were evident and the inferior cortex of the mandible appeared thinned, but the other side was not
available for comparison
• Oral vitamin D and Calcium Sandoz (Sandoz Canada Inc., Dorval, QB) were prescribed. An initial drop in
the serum calcium level was easily corrected by adjusting the medication.
Nutritional rickets in a 2-year-old child: case report Donal McDonnell, BDS, FFD, MSc,
FRCD(C) Gary Derkson, DMD
54. OSTEOMALACIA
Softening & distortion of skeleton
Oral manifestation:
Taylor & day-50% incidence of severe periodontitis in a
series of 22 Indian women
Clinical features
Bone pain and tenderness
Peculiar waddling or “penguin”gait
Tetany
Greenstick bone fractures
Myopathy
56. HYPOPHOPHATASIA
• Def. of enzyme alkaline phophatase
• Excretion of phosphoethanolamine in the urine
• c/f:
Infantile form
Severe rickets
Bone abnormalities
Failure to thrive
Childhood
Loss of primary teeth
Increased infection
Growth retardation
Rachitic like deformation,
lung., renal, GI disorders
Adult
Spontaneous fracture
57. Oral manifestations:
Premature loss of primary teeth
Gingivitis
Dental roentgenogram:
Hypocalcification
Large pulp chambers
Alveolar bone loss
58. HYPOCALCEMIA
<8.8 mg/dl
<8.5mg/dl- mild tremors
<7.5mg/dl- life threatening
condition will result- TETANY
Symptoms
muscle cramps
Paresthesia
Neuromuscular irritability
muscle twitching
Tetany
Seizures
Bradycardia
Causes
Hypoparathyroidism
Vit. D deficiency
Increased calcitonin
Deficiency of calcium, magnesium
Hypoalbuminemia
59. TETANY
Manifestations: Carpopedal spasm
Laryngismus stridor
Chvostek’s sign Trousseu’s sign
Treatment:
Oral calcium with vitamin d
supplementation.
Underlying cause should be treated.
Tetany needs IV calcium.
61. Adequate hydration, IV normal saline
Furosemide IV to promote calcium excretion
Steroids, if there is calcitriol excess
Definitive treatment for the underlying disorder
MANAGEMENT OF HYPERCALCEMIA
62. Periodontal disease due to Dietary
calcium deficiency and/ or dietary
phosphorous excess
Henrickson suggested:
High incidence of periodontal disease in natives of India-attributed in part to
their low dietary calcium intake.
Labile for Resorption- Alveolar bone
Vertebrae
Ribs
Long bones
Nutrition and Immunology: Principles and Practice edited by M. Eric Gershwin, J. Bruce German, Carl L. Keen
63. Lutwak et al- demineralization of alveolar bone in humans
was reversed by daily dietary calcium supplements over a
period of a year.
Hypothesized: periodontal bone loss was a direct result of
calcium deficient diet leading to secondary
hyperparathyroidism and the reversal of this condition is by
dietary calcium supplements
Journal of PeriodontologyOctober 1974, Vol. 45, No. 10, Pages 739-745 , DOI 10.1902/jop.1974.45.10.739 (doi:10.1902/jop.1974.45.10.739)
64. Effect of calcium, phosphorus imbalances &
vitamin D deficiency on dental caries incidence
Variation in ca:p Ratios in experimental diets
Quite cariogenic, because the carbonate level of the tooth was
increased.
Relatively acid soluble
Highly susceptible to dental decay
65. NUTRITIONAL FACTORS ASSOCIATED WITH DENTAL
ENAMEL HYPOPLASIA
Some studies shown that rickets during the time of tooth formation is the most common cause
of enamel hypoplasia.
Shelling & Anderson- in rachitic children:43% of teeth showed hypoplasia.
Type- pitting variety
71. REFERENCES
1. Textbook of medical biochemistry-DM
Vasudevan
2. Textbook of medical physiology-Rodney
3. Textbook of medical physiology-Sembulingam
4. Harper’s biochemistry- 25th
edition
5. Shafer’s oral pathology- 5th
edition
6. Internet sources
Editor's Notes
Calcium is one of the interesting items that you can find in many products such as cheese, milk, and other types of food. Consuming sufficient calcium is great for the body.
The word calcium is derived from the Latin world called as calcis.
Calcium is not only found in some important foods like milk and cheese. The buyer can also get this element located on the earth crust.
Calcium is as essential element for the plants and animals living surrounding your house. It can strengthen the muscle and form the new skeletal system. Moreover, the animal can form the bio chemical reaction for some purposes.
Many people have recognized about the benefit of calcium to the plants, human and animals. In 1808, this element can be purified by the man called as Si Humphrey Davy. He came from England.
The benefit of calcium in manufacturing process is big enough. It can be used as a reduction magnet for making other types of metal in the factories. You can also use it to make cheese, making cement, or even eliminating the nonmetallic impurities ingredients in the alloys.
he name calcium as I have stated before is derived from Latin word. Can you guess the meaning of calcis. It is lime. That’s why the ancient Roman uses calcium dioxide to make a liquor or a lime drink.
Phosphorus was the 13th element to be discovered. For this reason, and also due to its use in explosives, poisons and nerve agents, it is sometimes referred to as &quot;the Devil&apos;s element&quot;.[34] It was the first element to be discovered that was not known since the ancient times. The discovery of phosphorus is credited to the German alchemist Hennig Brand in 1669, although other chemists might have discovered phosphorus around the same time.[35] Brand experimented with urine, which contains considerable quantities of dissolved phosphates from normal metabolism.[11] Working in Hamburg,
IN BONE- HYDROXY APPETITE CRYSTAL
In growth there is a increased level of growth hormone. GH acts by increasing calcium absorption. It also increases the renal excretion of calcium and phosphates.
The positive balance is obvious in growing child, about 0.1 gm being retained each day in the growing & mineralizing skeleton
The Negative balance arises in later decades of age 50 yrs or more, this can be detected as a loss of skeletal tissue, not merely a reduction in the proportion of mineralization.
In osteoporosis, the cortex becomes thinner and more brittle, while
the inner trabecular bone develops larger holes.
Mature adult bone is continually being remodelled. Specialised cells
called osteoclasts absorb old bone and other cells called osteoblasts
create new, strong, bone. In this way, bone retains its strength and
density.
Normally in the adult skeleton, about 3%of ‘cortical’ bone – the outer
hard part – and 25% of ‘trabecular’ bone – the inner, honeycomb part
– is remodelled each year. For this process to work properly we need
the minerals calcium and phosphorus from which bone is made (these
come from our diet) and a range of hormones and vitamins which drive
the process.
As we grow, our bone mass steadily increases; more bone is made than
is absorbed. By early adulthood, we reach what is known as peak bone
mass, which is the maximum density achieved by our bones. After
about 35 years of age, even though bone formation still occurs, our
bone mass slowly declines as more is absorbed than is added. The
cortex becomes thinner and more brittle, while the inner trabecular
bone develops larger holes.
In women after menopause, absorption and thinning of bones occurs
even more rapidly. As bone is lost, the skeleton becomes progressively
more and more osteoporotic and prone to bone fracture. While almost
everyone loses bone, some people are less likely to suffer from
osteoporosis until they are very old (if at all).
In some cases, osteoporosis is caused by a deficiency of these hormones
or vitamins. Osteoporosis accelerates in women after menopause.
That’s because after menopause, levels of the sex hormone oestrogen
fall. Oestrogen is thought to play a role in maintaining bone mass by
slowing the process of bone breakdown by osteoclasts.
People who don’t have enough calcium in the diet are prone to
osteoporosis. Failure to absorb calcium properly from the gut can also
play a role. This may be due to a disease of the small bowel (where
calcium is absorbed) or a deficiency in vitamin D, which is needed for
calcium absorption.
Osteoporosis isn’t an inherited disease, but it tends to run in families.
So it’s more likely if there’s someone else in the family that has it.
Symptoms
The problem with osteoporosis is that it’s a silent condition; bone loss
is gradual and invisible. People may not know they have osteoporosis
until their bones become so weak that a sudden strain, bump, or fall
causes fracture which wouldn’t have happened in a person with normal
strong bones.
Fractures are most common in the wrist, hip, spine, pelvis and upper
arm – but any bone can fracture. People with smaller, lighter frames
are more likely to suffer a fracture than larger, taller people because
they have less bone mass to start with, so are more likely to get a
fracture for the same degree of bone demineralisation.
When a fracture occurs it can be quite serious. It often requires
hospitalisation – in the case of a fractured hip for example – and then
a prolonged period of rehabilitation.
Osteoporosis in the spine may cause collapse of the spinal vertebrae
resulting in severe back pain, spinal deformities, loss of height,
kyphosis of the spine or ‘dowagers hump.
Periodontitis and Osteoporosis:
Association and Mechanisms
The risk factors for osteoporosis include many risk factors associated with advanced periodontal disease. Since both osteoporosis and
Dr. Hayder A. Alwaeli
(Figure 1)
(Figure 2)
Smile Magazine
09
periodontal diseases are bone resorptive diseases, it has been hypothesized that osteoporosis could be a risk factor for the progression of periodontal disease.
(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. 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.
“rachitis” The “wrist widening” of rickets
Epidemiology
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 a decreased risk for rickets due to
their greater production of vitamin D in sunlight.
Etiology
Vitamin D is required for proper calcium absorption from the gut. In
the absence of vitamin D, dietary calcium is not properly absorbed,
resulting in hypocalcemia, leading to skeletal and dental deformities
and neuromuscular symptoms, e.g. hyperexcitability.
Presentation
Radiograph of a two-year old rickets sufferer, with a marked genu
varum (bowing of the femurs) and decreased bone opacity, suggesting
poor bone mineralization.
Signs and symptoms of rickets include:
1) Bone pain or tenderness
2) dental problems
3) muscle weakness (rickety myopathy or “floppy baby syndrome”)
4) increased tendency for fractures (easily broken bones),especially
greenstick fractures
5) Skeletal deformity
*Toddlers: Bowed legs (genu varum)
*Older children: Knock-knees (genu valgum) or “windswept knees”
*Cranial, spinal, and pelvic deformities
6) Growth disturbance
7) Hypocalcemia (low level of calcium in the blood), and
8) Tetany (uncontrolled muscle spasms all over the body).
9) Craniotabes (soft skull)
10) Costochondral swelling (aka “rickety rosary” or “rachitic rosary”)
11) Harrison’s groove
12) Double malleoli sign due to metaphyseal 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.
READ SHAFER
SHAFER
Due accidental surgical removal of parathyroid glands
Auto immune disease