Disorder of Ca Metabolism         DR ROHANI     MODERATOR: DR ROZI
Calcium Present in the body greater amounts than  any other mineral Distribution:2 major pools     Readily exchangable ...
   Total plasma ca consists :     Ca bounds to alb (40%)     Ca complexed with citrate and phosphorus      (10%)     F...
   Only unbound ca (free/ ionized)    biologically active:     serum level must be adjusted for abnormal      albumin le...
Biochemical function of Calcium   Membrane excitation:     Excitable membrane of nerve and muscle      contain specific ...
   Excitation-secretion process     Influxof ca req for secretion both endocrine &      exocrine organs     Ca: necessa...
Ca Metabolism   Regulate by 3 hormones:     Parathyroid     Calcitonin     Vitamin   D   Act on bone, kidney and inte...
Absorption Gastrointestinal          tract Passive:     Depends   plasma calcium concentration   Active :     Stimula...
 Kidney Influence by PTH Filtered at glomerulus (98%) Reabsorbed   Proxtubule(60 %)   Loop and distal tubule (40%)
Parathyroid hormone (PTH) Produced by 4 small glands (parathyroid  glands) Contain 2 cell types:     Chiefcells: sectre...
   Synthesis PTH controlled by extracellular    ionized ca     Decreased extracellular ionized ca increases      PTH syn...
PTH   Increase rate bone resorption     Stimulate    activity of osteocytes and osteoclast        Raise   se ca concent...
Calcitonin Secreted by parafollicular (C) cell in the  thyroid gland Single chain polypeptide Secretion calcitonin incr...
ActionDecreases plasma calcium and phosphate levels :direct inhibition of osteoblasts Increases renal excretion of phosp...
Vitamin D Steroid compound derived from  cholecalciferol (D3) 25-Hydroxycalciferol: circulating form  (inactive) 1,25-D...
 Cholecalciferol (D3): produced in the skin  from 7-dehydrocholesterol by UV light Liver : D3 hydroxylated to 25-  hydro...
Action of Vit D   1,25-dihydroxycholecalciferol     Act on small intestine: promote absorption of      calcium and phosp...
Disorders of calcium metabolism Hypercalcemia Hypocalcemia
Hypercalcemia Serum calcium level greater than 10.5 mg/dL  (>2.5 mmol/L) Mild: Total Ca 10.5-11.9 mg/dL (2.5-3 mmol/L)  ...
Hypercalcemia   Causes:      Hyperparathyroidism     Malignancy     Excessive vit D intake     Granulomatous d/o (sar...
Clinical manifestations: CVS: hypovolaemia, Ecg:     Shortened   QT interval CNS: confusion, drowsiness, weakness Ren...
   Treatment     Symptomatic:    req rapid treatment     Initial rx: rehydration f/b brisk diuresis (U/O:      200-300 ...
 Additional therapy with bisphosphonate /  calcitonin may be req esp severe hyperca (ca  > 15 mg/dL) Bisphosphonates    ...
   Corticosteroids     Useful in hypervitaminosis D, bone mets and      sarcoidosis     Ineffective with hyperparathyro...
 Additional treatment depends on underlying  cause 90% of hypercalcemia d2 malignancy/  hyperPTH     Lab test: double a...
ANAESTHETIC CONSIDERATION Ionized ca monitored closely Saline diuresis should be cont intraop with  great care to avoid ...
HYPERPARATHYROIDISM   PTH : principal regulator of ca    homeostasis     Increase   se ca:        Promoting   bone reso...
   Causes     Primary   hyperparathyroidism:       Adenoma,  carcinoma and hyperplasia of        parathyroid gland    ...
Effects of hyperparathyroidism CVS: HPT, ventricular arrythmias, ECG  changes (shortened QT interval) Renal :       Hyp...
Hypocalcemia   Hypoparathyroidism   Pseudohypoparathyroidism   Vit D Def       Nutritional       Malabsorption   Hyp...
   Clinical manifestations     CNS:        Muscle spasm        Carpopedal spasm, laryngeal spasm        Trosseau’s si...
 Circumoral numbness     Convulsions, depression and dementia   CVS:     Prolonged    QT and non-spesific t-wave      ...
   Treatment     Medical emergency     Treated with:        Calcium chloride 3-5 ml of 10% solution       Calcium glu...
   Severe sx:     IV 20-40 ml Ca gluconate or 10 ml CaCL in      100 ml infused over 2-5 min     f/up with 20-60 ml Ca ...
   Anaesthetic considerations     Should   be corrected preoperatively     Serial ionized ca level should be monitored ...
REFERENCES emedicine.medscape.com PRINCIPLES OF PHYSIOLOGY FOR  ANAESTHETIST: IAN POWER & PETER  KAM Bedside ICU Handbo...
Disorder of ca metabolism
Disorder of ca metabolism
Disorder of ca metabolism
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Disorder of ca metabolism

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Disorder of ca metabolism

  1. 1. Disorder of Ca Metabolism DR ROHANI MODERATOR: DR ROZI
  2. 2. Calcium Present in the body greater amounts than any other mineral Distribution:2 major pools  Readily exchangable comprising 1 % of total body ca: act as immediate reserve for sudden change in plasma ca  Not readily exchangeable comprising 99 % & consist of bone Normal plasma concentration:  8-10 mg/dL (2.0-2.5 mmol/L)
  3. 3.  Total plasma ca consists :  Ca bounds to alb (40%)  Ca complexed with citrate and phosphorus (10%)  Freely diffusible ionized ca (50%) Ionized conc also depends on arterial pH
  4. 4.  Only unbound ca (free/ ionized) biologically active:  serum level must be adjusted for abnormal albumin levels. 1-g/dL drop in serum alb below 4 g/dL, measured serum ca decreases by 0.8 mg/dL Corrected Ca =total Ca in mmol/L + [0.02 x (40-alb in g/dL)]
  5. 5. Biochemical function of Calcium Membrane excitation:  Excitable membrane of nerve and muscle contain specific Ca ionic channels  Control membrane excitability  Influx of ca ion occurs during excitation of nerves and muscle Haemostasis : activation of clotting factors in plasma Muscle contraction
  6. 6.  Excitation-secretion process  Influxof ca req for secretion both endocrine & exocrine organs  Ca: necessary for release of neurotransmitter Structural support  Bound cell surfaces, important for membrane stability & intercellular adhesion  Important component of bone
  7. 7. Ca Metabolism Regulate by 3 hormones:  Parathyroid  Calcitonin  Vitamin D Act on bone, kidney and intestine
  8. 8. Absorption Gastrointestinal tract Passive:  Depends plasma calcium concentration Active :  Stimulated by 1:25-dihydroxycalciferol
  9. 9.  Kidney Influence by PTH Filtered at glomerulus (98%) Reabsorbed  Proxtubule(60 %)  Loop and distal tubule (40%)
  10. 10. Parathyroid hormone (PTH) Produced by 4 small glands (parathyroid glands) Contain 2 cell types:  Chiefcells: sectrete PTH  Oxyphil cell: unknown function
  11. 11.  Synthesis PTH controlled by extracellular ionized ca  Decreased extracellular ionized ca increases PTH synthesis Action PTH  Increases plasma ca and lowers plasma phosphate concentration  Act on bone, kidney and GIT (indirectly`)
  12. 12. PTH Increase rate bone resorption  Stimulate activity of osteocytes and osteoclast  Raise se ca concentration
  13. 13. Calcitonin Secreted by parafollicular (C) cell in the thyroid gland Single chain polypeptide Secretion calcitonin increased when extracellular ca rises to 2.4 mmol/L Parafollicular C have ca-sensing receptor When ca binds to these receptor stimulates calcitonin secretion
  14. 14. ActionDecreases plasma calcium and phosphate levels :direct inhibition of osteoblasts Increases renal excretion of phosphate and calcium
  15. 15. Vitamin D Steroid compound derived from cholecalciferol (D3) 25-Hydroxycalciferol: circulating form (inactive) 1,25-Dihydroxycholecalciferol: active form
  16. 16.  Cholecalciferol (D3): produced in the skin from 7-dehydrocholesterol by UV light Liver : D3 hydroxylated to 25- hydroxycholecalciferol Kidney:  convert 25-hydroxycholecalciferol to 1,25- dihydroxycholecalciferol  By action of renal 1-hydroxylase  Stimulated by PTH
  17. 17. Action of Vit D 1,25-dihydroxycholecalciferol  Act on small intestine: promote absorption of calcium and phosphate  Facilitate bone mineralization by increasing ECF concentration of ca and phosphate  Increase synthesis ca-binding protein: promote ca absorption  With PTH mobilizes ca and phosphate from bone  Important for bone remodelling
  18. 18. Disorders of calcium metabolism Hypercalcemia Hypocalcemia
  19. 19. Hypercalcemia Serum calcium level greater than 10.5 mg/dL (>2.5 mmol/L) Mild: Total Ca 10.5-11.9 mg/dL (2.5-3 mmol/L) or Ionized Ca 5.6-8 mg/dL (1.4-2 mmol/L) Moderate: Total Ca 12-13.9 mg/dL (3-3.5 mmol/L) or Ionized Ca 5.6-8 mg/dL (2-2.5 mmol/L) Hypercalcemic crisis: Total Ca 14-16 mg/dL (3.5- 4 mmol/L) or Ionized Ca 10-12 mg/dL (2.5-3 mmol/L)
  20. 20. Hypercalcemia Causes:  Hyperparathyroidism  Malignancy  Excessive vit D intake  Granulomatous d/o (sarcoidosis, tuberculosis)  Chronic immobilization  Milk-alkali syndrome: Excess ca intake  Drug induced:  Thiazide diuretics  Lithium
  21. 21. Clinical manifestations: CVS: hypovolaemia, Ecg:  Shortened QT interval CNS: confusion, drowsiness, weakness Renal : polyuria d2 nephrogenic diabetes insipidus GIT: epigastric pain, nausea, vomiting, constipation
  22. 22.  Treatment  Symptomatic: req rapid treatment  Initial rx: rehydration f/b brisk diuresis (U/O: 200-300 ml/h)  Hydration: IV infusion D5%, o.45 % NaCl or NS > 3L at 250- 500ml/h to correct hypovol  Frusemide : to induce diuresis and reduce ca reabsorption  Hydration and diuresis may remove potential risk of CVS and neurological cx , usua se ca remains elevated
  23. 23.  Additional therapy with bisphosphonate / calcitonin may be req esp severe hyperca (ca > 15 mg/dL) Bisphosphonates  Binds hydroxylapatite in bone matrix and inhibit osteoclastic act  Iv pamidronate 60mg in 50-500 ml NS over 4-24H  Onset effect in 24H , peak effect 5-6 days  Mg –checked: avoid hypomagnesaemia  Clodronate  Iv 300 mg in 500 ml NS at least 2h for 7-10 days/ PO 1.6 -3.2 g/d in 1-2 devided doses Calcitonin  IV 5-10 U/ kg in 100 ml NS over 6-24h/ IM/SC/ intranasal 200-400 U/d in 2-4 devided doses
  24. 24.  Corticosteroids  Useful in hypervitaminosis D, bone mets and sarcoidosis  Ineffective with hyperparathyroidism  Onset within hours but efficacy min Mithamycin (plicamycin)  Insevere hyperca, unresponsive to above measures  Severe adverse effect:  Bone marrow suppresion, hepatic and renal toxic effect  Rapidly reduces osteoclastic activity
  25. 25.  Additional treatment depends on underlying cause 90% of hypercalcemia d2 malignancy/ hyperPTH  Lab test: double anti body PTH assay  Se PTH concentration:  SUPRESSED: MALIGNANCY STATE  ELEVATED: HYPERPARATHYROIDISM
  26. 26. ANAESTHETIC CONSIDERATION Ionized ca monitored closely Saline diuresis should be cont intraop with great care to avoid hypovolemia Central venous and pulm artery pressure monitoring advisable –pts with decreased cardiac reserve Avoid acidosis
  27. 27. HYPERPARATHYROIDISM PTH : principal regulator of ca homeostasis  Increase se ca:  Promoting bone resorption  Limiting renal excretion  Indirectly enhancing GI absorption (effect on vit D met)
  28. 28.  Causes  Primary hyperparathyroidism:  Adenoma, carcinoma and hyperplasia of parathyroid gland  secondary hyperparathyroidism  Adaptive response to hypocalcemia  Renal failure/ intestinal malabsorption syndrome  Ectopic hyperparathyroidism  Production of PTH by tumour outside parathyroid gland  Mostclinical manifestations d2 hypercalcaemia
  29. 29. Effects of hyperparathyroidism CVS: HPT, ventricular arrythmias, ECG changes (shortened QT interval) Renal :  Hyperchloremic met acidosis  Poluria, dehydration, polydipsia, renal stone GIT:  Ileus, N & V, PUD, Panvreatitis Musculoskletal : muscle weakness, osteoporosis Neurologic : mental status change (e.g: delirium, psychosis, coma)
  30. 30. Hypocalcemia Hypoparathyroidism Pseudohypoparathyroidism Vit D Def  Nutritional  Malabsorption Hyperphosphatemia Precipitation of calcium  Pancreatitis  Rhabdomyolysis  Fat embolism Chelation of calcium  Multiple rapid red blood transfusion or rapid infusion of large amounts of albumin
  31. 31.  Clinical manifestations  CNS:  Muscle spasm  Carpopedal spasm, laryngeal spasm  Trosseau’s sign: inflate BP cuff 10 mmHg above SBP for 3 min: postive if flexion metocarpophalangeal jt & extension interphalangeal jt  Chovstek’s sign: tap facial nerve at ant border masseter ms, 2 cm in front of ear lobe  Positive : twitching of upper lip
  32. 32.  Circumoral numbness  Convulsions, depression and dementia CVS:  Prolonged QT and non-spesific t-wave changes  Hypotension d2 decrease cardiac contractility
  33. 33.  Treatment  Medical emergency  Treated with:  Calcium chloride 3-5 ml of 10% solution  Calcium gluconate 10-20 ml 10 % solution  10 ml 10% CaCl = 272 mg of ca  10 ml calcium gluconate =93 mg of ca  To avoid precipitation: should not be given with bicarbonate / phosphate containing solutions
  34. 34.  Severe sx:  IV 20-40 ml Ca gluconate or 10 ml CaCL in 100 ml infused over 2-5 min  f/up with 20-60 ml Ca gluconate / 20-40 ml CaCl in 500 ml infusedd over 6 H SX mild -oral elemental Ca 1-3 gm /d in 3 devided dose
  35. 35.  Anaesthetic considerations  Should be corrected preoperatively  Serial ionized ca level should be monitored intraoperatively in pt’s with hx hypoca  Avoid alkalosis: prevent further decrease in ca  IV ca may necessary following rapid transfusions of citrated blood products/ large vol of albumin  Responses to NMBAs are inconsistent and req close monitoring with nerve stimulator
  36. 36. REFERENCES emedicine.medscape.com PRINCIPLES OF PHYSIOLOGY FOR ANAESTHETIST: IAN POWER & PETER KAM Bedside ICU Handbook : Tan Tock Seng Hospital

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