1 / 111

PARATHYROID GLAND PHYSIOLOGY

PARATHYROID GLAND PHYSIOLOGY. 99% calcium of our body is in the crystalline form in the skeleton and teeth Of the remaining 1% 0.9% intracellular less than 0.1% in the ECF. The extracellular fluid calcium concentration is about 9.4 mg/dl.

cameron-adams
Télécharger la présentation

PARATHYROID GLAND PHYSIOLOGY

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. PARATHYROID GLAND PHYSIOLOGY

  2. 99% calcium of our body is in the crystalline form in the skeleton and teeth • Of the remaining 1% 0.9% intracellular less than 0.1% in the ECF

  3. The extracellular fluid calcium concentration is about 9.4 mg/dl

  4. Calcium in Plasma and Interstitial Fluid • 41% of the calcium is bound with plasma proteins(non-diffusible) • 9% bound with anionic substances(citrate, phosphate(diffusible, non-ionized) • Remaining 50% calcium is both diffusible and ionized

  5. Hypocalcemia(low blood calcium) • Fall in free calcium results in over excitability of nerves and muscles • Decrease in free calcium increases neuronal sodium permeability with resultant influx of sodium moving the resting potential closer to threshold

  6. Tetany • Hypocalcemia causes tetany • At plasma calcium ion concentration about 50% below normal the peripheral nerve fibers become so excitable that they begin to discharge spontaneously • Tetany usually occurs at calcium conc of 6 mg/dl from normal value of 9 mg/dl

  7. Hypercalcemia (elevated blood calcium) • Depresses neuro-muscular excitability • Depressive effects begin to appear at calcium concentration of 12mg/dl (constipation, poor appetite, decreased QT interval)

  8. Role of Free Fraction of ECF Calcium • Neuromuscular excitability Even minor variations in concentration of free ECF calcium have profound and immediate impact on the sensitivity of excitable tissues

  9. Excitation-contraction coupling in cardiac and smooth muscles

  10. Stimulus-secretion coupling The entry of calcium into secretory cells which results from increased permeability to calcium in response to appropriate stimulation triggers the release of secretory product by exocytosis

  11. Excitation-secretion coupling In pancreatic beta cells calcium entry from the ECF in response to membrane depolarization leads to Insulin secretion

  12. Maintenance of tight junctions between cells (part of intercellular cement) • Clotting of blood (acts as a co-factor)

  13. Intracellular Calcium • Second messenger • Involved in cell motility • Calcium in Bone and teeth(structural and functional integrity)

  14. Absorption of Calcium • Calcium is absorbed from duodenum by carrier mediated active transport and in the rest of small intestine by facilitated diffusion (poorly absorbed) • Vitamin D is essential for absorption of calcium from GIT

  15. Calcium Excretion • 98-99% of the filtered calcium is reabsorbed from renal tubules into blood • 90% of the filtered calcium is reabsorbed from the proximal tubule, loop of Henle and early distal tubule • Remaining 10% is reabsorbed selectively from the late distal tubule and early collecting ducts depending on calcium conc in blood

  16. Calcium Homeostasis & Calcium Balance • Urinary excretion of calcium is hormonally controlled • Absorption of Calcium from intestine is also hormonally controlled and depends on the calcium status of body • Bones are the large reservoirs of calcium and exchange of calcium between ECF and bone is also subject to hormonal control

  17. Calcium Homeostasis • Regulation of calcium homeostasis involves the immediate adjustments required to maintain a constant free plasma calcium concentration on a minute-to-minute basis. • This is mainly accomplished by rapid exchanges between the bone and the ECF and to a lesser extent by modifications in urinary excretion of calcium

  18. Calcium Balance • Regulation of calcium balance involves the slowly responding adjustments required to maintain a constant total amount of calcium in the body. Calcium is maintained by adjusting the extent of intestinal calcium absorption and urinary calcium excretion

  19. Phosphate • The average total quantity of phophorus represented by both the ionic forms is 4mg/dl (3-4mg/dl in adults and 4-5mg/dl in children) • Good Intestinal absorption • Excretion in faeces in combination with unabsorbed calcium • Remaining absorbed in blood and excreted in urine

  20. Excretion of Phosphate • Renal phosphate excretion is controlled by an over-flow mechanism • When phosphate conc in the plasma is below the critical value of 1mmol/L, all the phosphate in the glomerular filtrate is reabsorbed • But above this conc the rate of phosphate loss is directly proportional to the additional increase

  21. Bone • Tough organic matrix strengthened by deposits of calcium salts • 30% matrix, 70% salts • Newly formed bone has a higher percentage of matrix than salts

  22. Organic Matrix • 90-95% collagen fibers(tensile strength) and the remaining homogeneous gelatinous medium called ground substance (ECF plus proteoglycans)

  23. Bone Salts • Are crystalline salts containing calcium and phosphorus • Major crystalline salt is Hydroxyapatite • Magnesium, sodium, potassium and carbonate ions etc are also conjugated

  24. Collagen fibers and the crystalline salts together give the bony structure extreme tensile and compressional strength

  25. Hydroxyapatite does not precipitate in the extracellular fluid although the conc of calcium and phosphate ions is considerably greater than those required to cause precipitation of hydroxyapatite • Role of pyrophosphate (inhibitor of precipitation)

  26. Bone Calcification • Secretion of collagen molecules (monomers) and ground substance by osteoblasts • Polymerization of collagen monomers to form collagen fibers (osteoid) • As osteoid is formed some of the osteoblasts become entrapped in it and become silent (osteocytes)

  27. Calcium salts begin to precipitate on the surfaces of collagen fibers • The initial calcium salts are not hydroxyapatite crystals but are amorphous compounds • By process of substitution, addition, reabsorption these salts are converted into hydroxyapatite crystals over a period of weeks or months

  28. Some of the salts remain in the amorphous form • The osteoblasts supposedly secrete a substance into the osteoid that neutralizes the pyrophosphate

  29. Calcium Exchange Between Bone and ECF • Most of the exchangeable calcium is in the bone • This exchangeable calcium is in equilibrium with the calcium ions in the extracellular fluid • The exchangeable calcium provides a buffering mechanism to keep the calcium ion conc in the ECF from rising to excessive levels or falling to low levels

  30. Remodeling of Bone • Deposition of bone by Osteoblasts • Absorption of bone by Osteoclasts

  31. Bone deposition and absorption are normally in equilibrium

  32. Value of Continual Bone Remodelling • Bone can adjustits strength in proportion to the degree of bone stress. • The shape of the bone can be rearranged for proper support of mechanical forces by deposition and absorption of bone in accordance with stress patterns • When old bone becomes brittle and weak new organic matrix is laid downand normal toughness of bone is maintained

  33. HORMONAL REGULATION OF CALCIUM AND PHOSPHATE HOMEOSTASIS • PTH • Vitamin D • Calcitonin

  34. PARATHYROID GLANDS • Four glands located on the posterior surface of the thyroid gland • Derived from the 3rd and 4th pharangeal pouches • Chief cells secrete the polypeptide hormone PTH

  35. TARGET ORGANS FOR PTH • Bone • Kidney

  36. Hyperfunction of Parathyroid gland-------Hypercalcemia • Hypofunction of Parathyroid gland---------Hypocalcemia

  37. Effect of PTH on Calcium and Phosphate Concentrations in ECF

  38. Rise in calcium levels is due to • Effect of PTH to increase calcium and phosphate absorption from bone • Rapid effect of PTH to decrease the excretion of calcium by kidneys

  39. The decrease in Phosphate conc is due to • Effect of PTH to increase renal phosphate excretion

  40. ACTIONS OF PTH ON BONE • Rapid Phase - osteocytic osteolysis • Slow Phase - osteoclastic osteolysis

  41. Osteocytic Osteolysis • The calcium ion conc in the blood begins to rise with in minutes • There is removal of bone salts • From the bone matrix in the vicinity of osteocytes • In the vicinity of osteoblasts along the bone surface

  42. Osteocytic Membrane System • Long processes extend from osteocyte to osteocyte through out the bone structure and theses processes also connect with the surface osteocytes and osteoblasts • This membrane separates the bone from ECF • Between the processes and the bone there is small amount of bone fluid

  43. Osteolysis • The osteocytic membrane pumps calcium ions from bone fluid into ECF • When it becomes excessively activated the bone fluid calcium conc falls and calcium and phosphate salts are absorbed from the bone (osteolysis) • When the pump is inactivated the bone fluid calcium conc rises and calcium and phosphate salts are deposited in the bone

  44. The cell membranes of both osteoblasts and osteocytes have receptors for binding PTH • PTH strongly stimulates Calcium pump by increasing the calcium permeability of bone fluid side of osteocytic membrane

  45. Slow phase of bone absorption and calcium phosphate release • Immediate activation of already formed osteoclasts • Increased osteoclastic size and number • Increased osteoclastic collagenase and lysosomal enzyme activity • Increased osteoclastic acid phosphatase,carbonic anhydrase,lactic acid and citric acid concentrations • Increased bone resorption

  46. Osteoclasts do not have membrane receptors for PTH. • The activated osteoblasts and osteocytes send secondary "signals" to the osteoclasts (OPGL)

  47. Activation of Osteoblats • Excess PTH stimulated osteoclastic resorption of bone can lead to weakened bones and secondary stimulation of the osteoblasts that attempt to correct the weakened state

More Related