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
Overall description of bone metabolism.
Introduction
Types of bone tissue
Composition of bone
Cells of bone
Regulators of bone metabolism
Calcium and phosphate balance
Calcium and phosphate
Parathyroid hormone
Calcitonin
Vitamin D
Fibroblast growth factor
Growth hormone and IGF-1
Thyroid hormone
Estrogens, progesterone and androgens
Cortisol and related glucocorticoids
Disorders of bone metabolism
Orthodontic considerations
Bone physiology and calcium homeostasisAbdulla Kamal
Bone is a highly specialized supporting framework of the body, characterized by its rigidity, hardness, and power of regeneration and repair.
It protects the vital organs, provides an environment for marrow ,acts as a mineral reservoir for calcium homeostasis and a reservoir of growth factors and cytokines, and also takes part in acid–base balance.
Bone constantly undergoes modeling (reshaping) during life to help it adapt to changing biomechanical forces, as well as remodeling to remove old, micro-damaged bone and replace it with new, mechanically stronger bone to help preserve bone strength.
Calcium metabolism disorders
1. CALCIUM METABOLISM DISORDERS
2. OVERVIEW: Calcium definition and requirement . Calcium metabolism regulators : VD , PTH and calcitonin. Functions of calcium. Calcium metabolic bone diseases. Calcium metabolism disorders. CASE !!
3. WHAT IS CALCIUM? Calcium is a mineral that is essential to bone health, cardiovascular health, muscle maintenance, circulatory health, and blood clotting. Calcium also acts as an enzyme activator. While calcium is found in milk and dairy products, it is also available from other food sources, such as green leafy vegetables, seafood (eating salmon with the bones provides an even greater dose), almonds, blackstrap molasses, broccoli, enriched soy and rice milk products, figs, soybeans and tofu.
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
Overall description of bone metabolism.
Introduction
Types of bone tissue
Composition of bone
Cells of bone
Regulators of bone metabolism
Calcium and phosphate balance
Calcium and phosphate
Parathyroid hormone
Calcitonin
Vitamin D
Fibroblast growth factor
Growth hormone and IGF-1
Thyroid hormone
Estrogens, progesterone and androgens
Cortisol and related glucocorticoids
Disorders of bone metabolism
Orthodontic considerations
Bone physiology and calcium homeostasisAbdulla Kamal
Bone is a highly specialized supporting framework of the body, characterized by its rigidity, hardness, and power of regeneration and repair.
It protects the vital organs, provides an environment for marrow ,acts as a mineral reservoir for calcium homeostasis and a reservoir of growth factors and cytokines, and also takes part in acid–base balance.
Bone constantly undergoes modeling (reshaping) during life to help it adapt to changing biomechanical forces, as well as remodeling to remove old, micro-damaged bone and replace it with new, mechanically stronger bone to help preserve bone strength.
Calcium metabolism disorders
1. CALCIUM METABOLISM DISORDERS
2. OVERVIEW: Calcium definition and requirement . Calcium metabolism regulators : VD , PTH and calcitonin. Functions of calcium. Calcium metabolic bone diseases. Calcium metabolism disorders. CASE !!
3. WHAT IS CALCIUM? Calcium is a mineral that is essential to bone health, cardiovascular health, muscle maintenance, circulatory health, and blood clotting. Calcium also acts as an enzyme activator. While calcium is found in milk and dairy products, it is also available from other food sources, such as green leafy vegetables, seafood (eating salmon with the bones provides an even greater dose), almonds, blackstrap molasses, broccoli, enriched soy and rice milk products, figs, soybeans and tofu.
Introduction to calcium
Sources of calcium
Dietary requirement of calcium
Calcium absorption
Biochemical function of calcium
Calcium in blood
Calcium estimation
Factors regulating calcium level in blood
Disease states of calcium
This presentation deals with the physiological aspect of Calcium and phosphate metabolism, it's relationship with the various types of rickets and possible remedies
Calcitonin: A peptide hormone secreted by the thyroid gland, tends to decrease plasma calcium concentration.
Secretion of calcitonin occur in the parafollicular cells, or C cells, lying in the interstitial fluid between the follicles of the thyroid gland.
These cells constitute only about 0.1 percent of the human thyroid gland and are the remnants of the ultimobranchial glands of lower animals, such as fish, amphibians, reptiles, and birds.
Calcitonin is a 32-amino acid peptide with a molecular weight of about 3400.
The primary stimulus for calcitonin secretion is increased extracellular fluid calcium ion concentration. This contrasts with PTH secretion, which is stimulated by decreased calcium concentration.
In young animals, but much less so in older animals and in humans, an increase in plasma calcium concentration of about 10 percent causes an immediate twofold or more increase in the rate of secretion of calcitonin, which is shown by the blue line in Figure 79-12.
This provides a second hormonal feedback mechanism for controlling the plasma calcium ion concentration, but one that is relatively weak and works in a way opposite that of the PTH system.
In some young animals, calcitonin decreases blood calcium ion concentration rapidly, beginning within minutes after injection of the calcitonin, in at least two ways.
The immediate effect is to decrease the absorptive activities of the osteoclasts and possibly the osteolytic effect of the osteocytic membrane throughout the bone, thus shifting the balance in favor of deposition of calcium in the exchangeable bone calcium salts. This effect is especially significant in young animals because of the rapid interchange of absorbed and deposited calcium.
The second and more prolonged effect of calcitonin is to decrease the formation of new osteoclasts. Also, because osteoclastic resorption of bone leads secondarily to osteoblastic activity, decreased numbers of osteoclasts are followed by decreased numbers of osteoblasts. Therefore, over a long period, the net result is reduced osteoclastic and osteoblastic activity and, consequently, little prolonged effect on plasma calcium ion concentration. That is, the effect on plasma calcium is mainly a transient one, lasting for a few hours to a few days at most.
The reason for the weak effect of calcitonin on plasma calcium is twofold. First, any initial reduction of the calcium ion concentration caused by calcitonin leads within hours to a powerful stimulation of PTH secretion, which almost overrides the calcitonin effect.
Rates of absorption and deposition of calcium are small, and it is also slowed by calcitonin.
In children it is much greater because bone remodeling occurs rapidly with absorption and deposition of calcium which is 5 grams or more per day which is equal to 5 to 10 times the total calcium in extracellular fluid.
Paget's (PAJ-its) disease of bone interferes with your body's normal recycling process, in which new bone tissue.
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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.
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:
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2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
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2. INTRODUCTION
• Total body calcium level is apprx. 1000gm –
1200mg.
• Apprx. 99% calcium remains in bones as
reservoir.
• Apprx 1% in the intracellular and 0.1% in
extra cellular fluids.
• Plasma calcium level is 9mg – 11mg/dl (2-
2.5 mmol/dl).
4. FUNCTIONS OF CALCIUM:
1. Skeletal muscle contraction.
2. Smooth muscle contraction.
3. Transmission of nerve impulse.
4. Skeletal bone and teeth
formation.
5. Acts as a second messenger or
some hormonal regulation.
6. Blood coagulation system.
5. HYPOCALCEMIA
• Nerve and muscle cells become
hyper excitable.
• Paresthesia or tingling
sensation.
• Tetany- latent or manifest.
• Muscle cramps carpopedal
spasms, intestinal spasm,
bronchospasm, laryngospasm,
stridor etc.
• Seizures- local or generalized.
• Cardiac rhythm disturbance
(prolong QT interval).
7. CALCIUM HOMEOSTASIS
• must be tightly regulated to maintain
physiological stability.
• Two system involve:
A)Major organ system i.e. intestine,
kidney and bone.
B)Major hormones involved are,
parathyroid hormone, active vitamin
D3 and calcitonin.
10. Calcium flux INTO and OUT of blood
• “IN” FACTORS: Intestinal absorption, Bone
resorption.
• OUT” FACTORS: Renal excretion, Bone
formation (Ca incorporation into bone).
• Balance between “IN” AND “OUT” factors
done by :
• ORGAN PHYSIOLOGY OF GUT, BONE, AND
KIDNEY
• HORMONE FUNCTION OF PTH AND
VITMAMIN D, CALCITONIN.
11. CALCIUM HOMEOSTASIS
DIETARY CALCIUM
INTESTINAL ABSORPTION
ORGAN PHYSIOLOGY
ENDOCRINE PHYSIOLOGY
DIETARY HABITS,
SUPPLEMENTS
BLOOD CALCIUM
BONE
KIDNEYS
URINE
THE ONLY “IN”
THE PRINCIPLE “OUT”
ORGAN PHYS.
ENDOCRINE PHYS.
ORGAN,
ENDOCRINE
12. INTESTINAL HANDLING OF CALCIUM
• Approx 1000 mg calcium ingested per
day.
• Approx.250 -350 mg(20%-30%) is
absorbed and others secreted through
faces.
• Absorption mainly occurs in duodenum
& jejunum.
• Absorption is both passive and active.
13. PASSIVE ABSORPTION OF Ca
• Paracellular route, non saturable.
• 5 % ingested Ca absorbed by this
route.
• Indirectly influenced by calcitriol.
1,25(OH)2 D
Activates protein kinase C
Loosen tight junction
Ca movements
14. ACTIVE ABSORPTION OF Ca
• Transcellular, receptor mediated, 25%
ingested Ca absorbed.
• 1,25(OH)2D mainly controls.
• Calcium is rapidly and reversibly bound
to the calmodulinactin- myosin I
complex.
15. ACTIVE ABSORPTION OF Ca
• Calcium binds to calbindin.
• calbindin-calcium complex
dissociates, the free intracellular
calcium is actively extruded
from the cell by Na-Ca
exchanger.
18. RENAL HANDLING OF CALCIUM
• The ultra filterable calcium
equals the total of the ionized
and complexed fractions.
• 10 g of calcium is filtered per
day.
• urine excretion 100 to 200 mg
per 24 hours.
20. CALCIUM REABSORPTION IN PCT.
• parallels that of Na⁺
and H₂O.
• 80% by passive
diffusion.
• PTF : GF is 1:1.2.
• Active absorption10-
15% ⁺
PTH, CT
21. CALCIUM REABSORPTION IN ALH.
• 20%-25% is
reabsorbed.
• both active and
passive routes.
• Active pathway
proportional to the
transtubular
electrochemical
driving force.
22. Cont…
• apical NKCC2 and the
ROMK channel
generate the “driving
force”.
• cinacalcet increases
the abundance of
claudin-14 in tight
junction.
• ALH is also influenced
by the CaSR.
23. Effect of diuretics on renal calcium
handling:
• Furosemide
NKCC2
ROMK
NK
ATPase
Na
2Cl
K
CALCIUM CALCIUM
TALH
lumen blood
24. CALCIUM REABSORPTION IN DCT
• 8% - 10% is reabsorbed.
• exclusively via transcellular
route.
1st step: through apical
membrane via TRPV5.
2nd step: binding with
calbindin28k.
3rd step: extruded via sodium-
calcium exchanger NCX1 and
the plasma membrane
calcium-ATPase PMCA1b.
26. Influence of thiazide diuretics
• calcium reabsorption.
• 1st hypothesis:
• 2nd hypothesis: increased
NaCa exchanger in BL
membrane of DCT & CNT.
Not proved.
ECF depletion
calcium filtrate
H₂O& Na absorption in PCT
driving Ca absorption in PCT
28. PARATHYROID HORMON (PTH)
• FOUR parathyroid glands
located behind the thyroid
gland.
• Two types of cells
1. Chief cells
2. Oxyphil cells
• Normal plasma PTH
10 -55 pg / mL
• Half life – 10 mins
29. ACTIONS OF PTH
I. Increases calcium and
phosphate absorption
from the bones.
II. Decreases excretion
of calcium by the
kidneys.
III. Increases the
excretion of
phosphate by the
kidneys.
IV. Increases intestinal
absorption of calcium
and phosphate.
30. BONE RESORPTION INFLUENCED BY
PTH:
• Bone resorption occurs in two phases:
• Rapid phase: osteocytic osteolysis.
Transfer calcium from canaliculi to the ECF from
bone fluid via osteocytic membrane by
osteocytes.
Does not affect bone mass.
Transfer calcium from most recently formed
calcium crystals.
• Slow phase: done by osteoclast resorption.
31. RAPID PHASE - OSTEOLYSIS
BONE
ECF
OSTEOCYTIC MEMBRANE
OCTEOCYTES
BONE FLUID
B.FL BECF O.M
33. Slow phase of osteolysis
• Done by OSTEOCLAST.
• Activated by unknown mechanism
Suspected signal by osteocytes and
osteoblasts.
• Involves two stages
Activation of present osteoclasts
Formation of new osteoclasts
• Observed after several days of PTH
stimulation.
• Long lasting effect can weaken bone.
34. Vitamin D.
• Vitamin D3 (cholecalciferol) is a fat-soluble steroid that
is present in the diet and also can be synthesized in the
skin from 7-dehydrocholestrol(3.2mcg/g skin) in the
presence of uv light.
35. MECHANISM OF ACTION
• 1,25 – dihydroxy cholecalciferol is a
steroid compound (secosteroid)
• Acts via the steroid receptor super family.
• Exposes the DNA – binding domain and
results in increased transcription of some
mRNAs.
38. Calcitonin
• Produced by the parafollicular cells
/ C cells of thyroid gland.
• STIMULUS : Increased plasma
calcium
Others: β adrenergic agonists,
dopamine and estrogen, GASTRIN,
glucagon..
39. Cont..
• ACTIONS:
Decreases absorptive action of
osteoclasts
Deposits exchangeable Ca in bone salts
Decreases the formation of osteoclasts
• CLINICAL USE: Used in the treatment of
PAGET’S DISEASE.
Hypercalcaemia together with
bisphophonate.