1. OSTEO- POROSIS

2. OSTEO- POROSIS Dr.Abdullah Al-Omran

3. NOTE : THIS PRESENTATION DOES NOT REPLACE ATTENDANCE OR INFORMATION GIVEN IN THE LECTURE.IT IS INTENDED AS A HIGHLIGHT FOR THE TOPIC NOTE : THIS PRESENTATION DOES NOT REPLACE ATTENDANCE OR INFORMATION GIVEN IN THE LECTURE.IT IS INTENDED AS A HIGHLIGHT FOR THE TOPIC

4. OSTEOPOROSIS OSTEOPOROSISDEFINITION WHO Definition 1994: A skeletal disease characterized by low bone mass and deterioration of the microarchitecture of bone tissue with a consequent increase in bone fragility and susceptibility to low trauma fractures. Why? Imbalance between osteoblast & osteoclast function

5. OSTEOPOROSIS

6. OSTEOPOROSIS OSTEOPOROSIS INCIDENCE: 1 in 3 women and 1 in 12 men. TYPES : I. (postmenoposal): thin trabicular bone 55-75y 55-75y f:m 6:1 f:m 6:1 II. Senile : thin both trabicular & cortical bone 70-85 y 70-85 y 2:1 2:1

7. OSTEOPOROSIS RISK FACTORS + CAUSES :! I.POST MENOPOSAL & SENILE (primary) -sessation of estrogen or androgen -sessation of estrogen or androgen - bad nutritional habits during productive years (15-45yr) - bad nutritional habits during productive years (15-45yr) (low calcium content food, smoking,alcohol,soda drinks. (low calcium content food, smoking,alcohol,soda drinks. - genetics (inheritance) & race (cocasian female) - genetics (inheritance) & race (cocasian female) II.Secondary : 1.medications: steroids,chronic heparin use,anticonvusants,chemotherapy. 2.immobilisation 3. Medical conditions: Anorexia Nervosa, RA, Early menopause,Hyperthyroidism, hyperparathyroidism, hypogonadism Transplantation, Cushings disease/syndrome, Chronic kidney, lung or GI diseases

11. OSTEOPOROSIS Clinically:P?P?

12. OSTEOPOROSIS

13. OSTEOPOROSIS INVESTIGATIONS 1. History for risk factors 2. Physical examination 3. X-ray of lumbar and thoracic spine. Although >30 % of bone loss required to be visible on X-ray, there may be some asymptomatic wedge #s 4. Bone mineral Density measurement 5. Blood tests, FBC, ESR, serum biochemistry 6. Testosterone and Gonadotrophin levels in men

14. OSTEOPOROSIS The Gold standard test in clinical practice is measurement of Bone Mineral Density (g/cm3), of the vertebral spine and the hip. This is as recommended by the National Osteoporosis society. Only vertebral measurements can be used to assess effectiveness of treatment at present. 1. DEXA scans 2. Radiographic Absorptiometry 3. Single Photon X-ray absorptiometry (SPA) 4. Quantitative Computer tomography 5. Quantitative Ultrasound

15. OSTEOPOROSIS

16. OSTEOPOROSIS PREVENTATIVE MEASURES Aims- to achieve an adequate peak bone mass, by ?

17. OSTEOPOROSIS TREATMENT OF ESTABLISHED OSTEOPOROSIS: CALCIUM + VIT. D SUPPLEMENTS Minimum daily intake of calcium should be achieved. Should only be prescribed if this is not achieved by diet. Vit D in all elderly institutionalized osteoporotics is recommended. Vit D in all elderly institutionalized osteoporotics is recommended. RDA Calcium = 1400 mg RDA Vit. D = 600-800 IU.

18. biphos OSTEOPOROSIS HRT (OESTROGEN): Prevent osteoporosis and slows or reverses progression. Given at doses equivalent to 0.625mg of Premarin, it will increase bone density by 2% per year. Given for 5-10 years almost halves the risk of fractures. Has a role in corticosteroid induced osteoporosis Contraindications: Endometrial carcinoma, Breast cancer, undiagnosed vaginal bleeding. Other benefits: loss of menopausal symptoms, cardiovascular protection.

19. OSTEOPOROSIS BISPHOSPHONATES: Synthetic analogues of inorganic pyrophosphate. Inhibit bone resorption by osteoclasts Alendronate (Fosamax) Reduces the incidence of hip, wrist and vertebral fractures in postmenopausal women (statistically significant) Contraindications-Abnormalities of oesophagus, renal problems Dose -10mg daily at least 30 mins before breakfast and sit upright for at least 30 mins Disodium Etidronate (Didronel) Etidronate is effective in reducing vertebral fracture (statistically significant). Dose- disodium etidronate 400mg once daily.

20. OSTEOPOROSIS OESTROGEN RECEPTOR MODULATORS (Raloxifene) Work like oestrogen at bone without other harmful effects. Can increase post menopausal symptoms so not to be given within 5 years of menopause Can increase post menopausal symptoms so not to be given within 5 years of menopause CALCITONIN Non sex, non steroid hormone Reduces resorption of bone Nasal form at dosages of 200 units per day Can be used for analgesia CALCITRIOL (1,25 DIHYDROXYCHOLECALCIFEROL) The active metabolite of vit D. 0.25 microg o.d. may reduce risk of vertebral #. Need monitoring of plasma calcium

21. RICKETS & OSTEOMALACIA Def.: reduction in bone mineralization !

23. OSTEOMALACIA,RICKETS Normal bone metabolism CALCIUM 99% in bone. Main functions- muscle /nerve function, clotting. Plasma calcium- 50% free, 50% bound to albumin. CALCIUM 99% in bone. Main functions- muscle /nerve function, clotting. Plasma calcium- 50% free, 50% bound to albumin. Dietary needs- Kids- 600mg/day, Adolesc.-1300mg/day, Adult-750mg/day, Pregnancy-1500mg/day, Breastfeeding-2g/day, Fractures- 1500mg/day Dietary needs- Kids- 600mg/day, Adolesc.-1300mg/day, Adult-750mg/day, Pregnancy-1500mg/day, Breastfeeding-2g/day, Fractures- 1500mg/day Absorbed in duodenum (active transport) and jejunum (diffusion), 98% reabsorbed in kidney prox. tubule, may be excreted in stool. Absorbed in duodenum (active transport) and jejunum (diffusion), 98% reabsorbed in kidney prox. tubule, may be excreted in stool.

24. OSTEOMALACIA,RICKETS Normal bone metabolism PHOSPHATE 85% in bone. Functions-metabolite and buffer in enzyme systems. PHOSPHATE 85% in bone. Functions-metabolite and buffer in enzyme systems. Plasma phosphate mainly unbound. Daily requ. 1-1.5g/day Plasma phosphate mainly unbound. Daily requ. 1-1.5g/day

25. OSTEOMALACIA,RICKETS Regulation of Calcium & Phosphate Metabolism: Peak bone mass at 16-25 years. Bone loss 0.3- 0.5% per year (2-3% per year after 6 th decade). 1. Parathyroid Hormone (PTH) 2. Vitamin D3 3. Calcitonin 4. Other Hormones: Estrogen: Prevents bone loss Corticosteroids: Increases bone loss Thyroid hormones: Leads to osteoporosis Growth hormones: Cause positive calcium balance Growth factors

28. RICKETS, OSTEOMALACIA PATHOLOGY: Sufficient osteoid, poor mineralization Sufficient osteoid, poor mineralization (Rickets is found only in children prior to the closure of the growth plates, while OSTEOMALACIA occurs in persons of any age. Any child with rickets also has osteomalacia, while the reverse is not necessarily true).

29. RICKETS, OSTEOMALACIA CAUSES: 1. Nutritional deficiency 1. Nutritional deficiency 1. Vit D 2. chelators of calcium- phytates, oxalates, phosphorous 3. Antacid abuse, causing reduced dietary phosphate binding 2. GI Absorption defects 1. Post gastrectomy 2. Biliary disease (reduced absorption of Vitamins ) 3. Small bowel disease 4. liver disease 3. Renal tubular defects 4. Renal osteodystrophy 5. Miscellaneous causes

30. RICKETS, OSTEOMALACIA CLINICAL FEATURES: Rickets - Tetany, convulsions, failure to thrive, restlessness, muscular flaccidity. Flattening of skull (craniotabes), Thickening of wrists from epiphyseal overgrowth, Stunted growth, Rickety rosary, spinal curvature, Coxa vara, bowing, # of long bones Rickets - Tetany, convulsions, failure to thrive, restlessness, muscular flaccidity. Flattening of skull (craniotabes), Thickening of wrists from epiphyseal overgrowth, Stunted growth, Rickety rosary, spinal curvature, Coxa vara, bowing, # of long bones Osteomalacia, - Aches and pains, muscle weakness loss of height, stress #s. Osteomalacia, - Aches and pains, muscle weakness loss of height, stress #s.

31. RICKETS, OSTEOMALACIA XRAY FINDINGS: RICKETS Thickening and widening of physes, Cupping of metaphysis, Wide metaphysis, Bowing of diaphysis, Blurred trabeculae.

32. RICKETS, OSTEOMALACIA XRAY FINDINGS: OSTEOMALACIA Loosers zones - incomplete stress # with healing lacking calcium, on compression side of long bones. Loosers zones - incomplete stress # with healing lacking calcium, on compression side of long bones. Codfish vertebrae due to pressure of discs Trefoil pelvis, due to indentation of acetabulae stress #s

33. RICKETS, OSTEOMALACIA INVESTIGATIONS: BLOOD TESTS Calcium Reduced, Phosphate reduced Alkalline Phosphatase increased Urinary excretion of calcium diminished Calcium phosphate products (= serum [Ca] x serum [PO4]) normally 30. In rickets and osteomalacia is less than 24 Calcium phosphate products (= serum [Ca] x serum [PO4]) normally 30. In rickets and osteomalacia is less than 24

34. RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Nutritional Vitamin D deficiency Dietary chelators of calcium Phytates Phytates Oxalates Phosphorus deficiency (unusual) Oxalates Phosphorus deficiency (unusual) Antacid abuse Antacid abuse  Treatment- vitamin D (5000u) and Calcium (3g/day)

35. RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Gastro-intestinal absorption defects Post-gastrectomy Biliary disease Enteric absorption defects Short bowel syndrome Short bowel syndrome Rapid onset (gluten-sensitive enteropathy) Inflammatory bowel disease Rapid onset (gluten-sensitive enteropathy) Inflammatory bowel disease Crohns Crohns Celiac Celiac

36. RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Renal tubular defects Vitamin D dependant type I type I type II type II Treatment; High levels of vit D Treatment; High levels of vit D Vitamin D resistant (familial hypophosphatemic rickets) Vitamin D resistant (familial hypophosphatemic rickets) Treatment; Phosphate 1-3 gm daily, Vit D3 high dose Fanconi syndrome I, II, III Renal tubular acidosis Treatment; Phosphate 1-3 gm daily, Vit D3 high dose Fanconi syndrome I, II, III Renal tubular acidosis

37. RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Renal Osteodystrophy – in chronic renal failure Miscellaneous Hypophosphatasia Anticonvulsant therapy SURGERY For deformities