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2017 Dr. Iin SLIDE KULIAH Osteoporosis Osteomalacia Rickettsia
2017 Dr. Iin SLIDE KULIAH Osteoporosis Osteomalacia Rickettsia
POROSIS
OSTEO-
POROSIS
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
OSTEOPOROSIS
OSTEOPOROSIS
OSTEOPOROSIS
II.Secondary :
1.medications: steroids,chronic heparin use,anticonvulsants,chemotherapy.
2.immobilisation
3. Medical conditions: Anorexia Nervosa, RA, Early
menopause,Hyperthyroidism, hyperparathyroidism, hypogonadism
Transplantation, Cushings disease/syndrome, Chronic kidney, lung or GI
diseases
OSTEOPOROSIS
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, ESR, serum biochemistry
6. Testosterone and Gonadotrophin levels in men
OSTEOPOROSIS
PREVENTATIVE MEASURES
Aims- to achieve an adequate peak bone mass, by ?
OSTEOPOROSIS
■ PHOSPHATE 85%
in bone. Functions-
metabolite and buffer in enzyme systems.
■ Plasma phosphate mainly unbound.
Daily requ. 1-1.5g/day
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).
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
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, OSTEOMALACIA
CAUSES:
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
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
XRAY FINDINGS:
RICKETS
Thickening and widening of
physes,
Cupping of metaphysis,
Wide metaphysis,
Bowing of diaphysis,
Blurred trabeculae.
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, OSTEOMALACIA
INVESTIGATIONS:
BLOOD TESTS
Calcium Reduced,
Phosphate reduced
Alkalline Phosphatase increased
Urinary excretion of calcium diminished
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, OSTEOMALACIA
MANAGEMENT:
Depends on the cause
MANAGEMENT:
Depends on the cause
Renal tubular defects
Vitamin D dependant
type I
type II
Treatment; High levels of vit D
MANAGEMENT:
Depends on the cause
SURGERY
For deformities