Osteo porosis
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OSTEO- POROSIS. OSTEO- POROSIS Dr.Abdullah Al-Omran. NOTE : THIS PRESENTATION DOES NOT REPLACE ATTENDANCE OR INFORMATION GIVEN IN THE LECTURE.IT IS INTENDED AS A HIGHLIGHT FOR THE TOPIC. OSTEOPOROSIS. OSTEOPOROSIS DEFINITION WHO Definition 1994:

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Osteo porosis

OSTEO-POROSIS


Osteo porosis dr abdullah al omran

OSTEO-POROSISDr.Abdullah Al-Omran


Osteo porosis

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


Osteoporosis

OSTEOPOROSIS

OSTEOPOROSIS

DEFINITION

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


Osteoporosis1

OSTEOPOROSIS


Osteoporosis2

OSTEOPOROSIS

OSTEOPOROSIS

INCIDENCE:1 in 3 women and 1 in 12 men.

TYPES :

  • (postmenoposal): thin trabicular bone

    55-75y

    f:m 6:1

  • Senile : thin both trabicular & cortical bone

    70-85 y

    2:1


Osteoporosis3

OSTEOPOROSIS

RISK FACTORS + CAUSES :!

I.POST MENOPOSAL & SENILE (primary)

-sessation of estrogen or androgen

- bad nutritional habits during productive years (15-45yr)

(low calcium content food , smoking,alcohol,soda drinks.

- 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


Osteoporosis4

OSTEOPOROSIS

Clinically:

P?

P?


Osteoporosis5

OSTEOPOROSIS


Osteoporosis6

OSTEOPOROSIS

INVESTIGATIONS

  • History for risk factors

  • Physical examination

  • 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

  • Bone mineral Density measurement

  • Blood tests, FBC, ESR, serum biochemistry

  • Testosterone and Gonadotrophin levels in men


Osteoporosis7

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.

  • DEXA scans

  • Radiographic Absorptiometry

  • Single Photon X-ray absorptiometry (SPA)

  • Quantitative Computer tomography

  • Quantitative Ultrasound


Osteoporosis8

OSTEOPOROSIS


Osteoporosis9

OSTEOPOROSIS

PREVENTATIVE MEASURES

Aims- to achieve an adequate peak bone mass, by ?


Osteoporosis10

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.  

RDA Calcium = 1400 mg

RDA Vit. D = 600-800 IU.


Osteoporosis11

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.


Osteoporosis12

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.


Osteoporosis13

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  

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


Rickets osteomalacia

RICKETS & OSTEOMALACIA

Def.: reduction in bone mineralization !


Osteomalacia rickets

OSTEOMALACIA,RICKETS

Normal bone metabolism

  • 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

  • Absorbed in duodenum (active transport) and jejunum (diffusion), 98% reabsorbed in kidney prox. tubule, may be excreted in stool.


Osteomalacia rickets1

OSTEOMALACIA,RICKETS

Normal bone metabolism

  • PHOSPHATE 85% in bone. Functions-metabolite and buffer in enzyme systems.

  • Plasma phosphate mainly unbound. Daily requ. 1-1.5g/day


Osteomalacia rickets2

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 6th decade).

  • Parathyroid Hormone (PTH)

  • Vitamin D3

  • Calcitonin

  • Other Hormones: Estrogen: Prevents bone loss Corticosteroids: Increases bone loss Thyroid hormones: Leads to osteoporosis Growth hormones: Cause positive calcium balance Growth factors


Rickets osteomalacia1

RICKETS, OSTEOMALACIA

PATHOLOGY:

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).


Rickets osteomalacia2

RICKETS, OSTEOMALACIA

CAUSES:

  • Nutritional deficiency 

    • Vit D

    • chelators of calcium- phytates, oxalates, phosphorous

    • Antacid abuse, causing reduced dietary phosphate binding

  • GI Absorption defects

    • Post gastrectomy

    • Biliary disease (reduced absorption of Vitamins )

    • Small bowel disease

    • liver disease

  • Renal tubular defects

  • Renal osteodystrophy

  • Miscellaneous causes


Rickets osteomalacia3

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

  • Osteomalacia, - Aches and pains, muscle weakness loss of height, stress #s.


Rickets osteomalacia4

RICKETS, OSTEOMALACIA

XRAY FINDINGS:

RICKETS Thickening and widening of physes, Cupping of metaphysis, Wide metaphysis, Bowing of diaphysis, Blurred trabeculae.


Rickets osteomalacia5

RICKETS, OSTEOMALACIA

XRAY FINDINGS:

OSTEOMALACIA

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


Rickets osteomalacia6

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


Rickets osteomalacia7

RICKETS, OSTEOMALACIA

MANAGEMENT:

Depends on the cause

Nutritional Vitamin D deficiency Dietary chelators of calcium

Phytates

Oxalates Phosphorus deficiency (unusual)

Antacid abuse

  • Treatment- vitamin D (5000u) and Calcium (3g/day)


Rickets osteomalacia8

RICKETS, OSTEOMALACIA

MANAGEMENT:

Depends on the cause

Gastro-intestinal absorption defects Post-gastrectomy Biliary disease Enteric absorption defects

Short bowel syndrome

Rapid onset (gluten-sensitive enteropathy) Inflammatory bowel disease

Crohns

Celiac


Rickets osteomalacia9

RICKETS, OSTEOMALACIA

MANAGEMENT:

Depends on the cause

Renal tubular defects Vitamin D dependant

type I

type II

Treatment; High levels of vit D

Vitamin D resistant (familial hypophosphatemic rickets)

Treatment; Phosphate 1-3 gm daily, Vit D3 high dose Fanconi syndrome I, II, III Renal tubular acidosis


Rickets osteomalacia10

RICKETS, OSTEOMALACIA

MANAGEMENT:

Depends on the cause

Renal Osteodystrophy – in chronic renal failure

Miscellaneous Hypophosphatasia Anticonvulsant therapy

SURGERY

For deformities


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