sem osteoporosis(edit)

8/12/2019 Sem Osteoporosis(Edit)

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DEFINITION

A systemic skeletal disease characterized

by reduce bone mass and micro-

architectural deterioration of bone tissuewith consequent of increase in bone

fragilityand susceptible to bone fracture

Normal bone Osteoporotic bone


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CLASSIFICATION

OSTEOPOROSIS

LOCAL

Disuse of limb(paralysis)

Nearbyinflammation

GENERALIZED(Metabolic Bone

Disease)

Primary Secondary


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Primary Osteoporosis

1) Postmenopausal Osteoporosis (Type 1)

Usually affecting female ages : 55 65 years old

Related loss of estrogens protective effect on bone

Results in trabecular bone loss and some corticalbone loss

Clinical features :

- Acute back pain (vertebra compression)- Progressive kyphosis (d/t repeated minor #)

- Liable to sustain a fracture (Colles #)


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2) Senile Osteoporosis (Type 2)

All aging individuals (men/women)

Ages : over 70 years old

Clinical features : - Femoral neck #- Proximal end of humerus #

- History of previous #

3) Idiopathic Osteoporosis

Rarely

Affect children and adult


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Secondary OsteoporosisNutritional

-Malabsorption

-Malnutrition

-Scurvy

Endocrine disorders

-Hyperparathyroidism

-Gonadal insufficiency

-Cushings disease

-Thyrotoxicosis

Inflammatory disease

-Rheumatoid arthritis

-Ankylosing spondylosis

-Tuberculosis

Malignant disease

-Multiple myeloma

-Carcinomatosis

-Leukemia

Drug-induced

-Corticosteroids

-Heparin

-Anticonvulsants

-Immunosuppressant

Others

-Osteogenesis imperfecta

-Chronic renal disease

-Smoking


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RISK FACTORS


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Non-modifiable Risk Factors

Gender.Women get osteoporosis more often than men.

Age.The older you are, the greater your risk ofosteoporosis.

Body size.Small, thin women are at greater risk.

Ethnicity. White and Asian women are at highest risk.Black and Hispanic women have a lower risk.

Family history.Osteoporosis tends to run in families. If afamily member has osteoporosis or breaks a bone,there is a greater chance that you will too.

Rheumatoid arthritis, liver disease, IBD


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Modifiable Risk Factors

Low calcium and Vitamin D diet

Certain meds, such as glucocorticoids andanticonvulsants

Inactive lifestyle; extended bed rest

Cigarette smoking

Excessive alcohol use.


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Due to imbalance between bone resorptionandbone deposition rate

-increase osteoclastic activity

-reduce osteoblastic activity

In early menopause, bone loss is caused by

excessive osteoclast-mediated resorptionIn late post-menopause, bone loss is causedby supression of ostoeblast activity

PATHOGENESIS


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CLINICAL MANIFESTATIONAssymptomatic until the later stage

Fracture after minor trauma

Most frequent fracture associated with osteoporosis includefracture of:

- Vertebral body- Proximal femoral- Distal radius- Pelvis

- Proximal humerus

May have vague complaints related to aging process:- Stiffness- Pain- Weakness


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COMPLICATIONS

1. Fractures most common at vertebra, femoral

neck and distal radius

2. Progressive kyphosis loss of height

3. Chronic back pain due to compression fracture


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DIAGNOSIS

The diagnosis of primary osteoporosis is made afterexcluding secondary causes of bone loss.

A clinical evaluation, which includes history, physicalexamination and appropriate laboratory investigations, ismandatory.

Multiple risk factor assessment for further investigation.

When a patient presents with a low trauma fracture,osteoporosis is a presumptive diagnosis.

Gold standard for diagnosis of osteoporosis remainsmeasurement of BMD using DEXA.

Patients such as those over 65 years of age with multiple riskfactors who are at sufficiently high risk for osteoporosis, canbe started on treatment even without BMD measurement.


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INVESTIGATION

Aims of investigation:-

1) To confirm the diagnosis of osteoporosis

2) To assess fracture risk

3) To exclude other causes


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Initial Investigations1. Full blood count

2. Serum Ca, phosphate, albumine3. Alkaline phosphatase

4. Renal function test

5. Biochemical marker for bone formation/resorption-biomarkers of type-1 collagen breakdown product

(Urinary deoxypyridinoline (DPD) )

6. Other investigation :- Serum estrogen / testosteron /FSH/TSH/T4

7. Plain X-rays - Lateral thoracolumbar spine/hip

- Osteoporosis apparent in plain X-ray

only after 30% bone loss occurred


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Specific Investigations

1.BONE MINERAL DENSITY TESTING

a) Dual energy X-ray absorptiometry (DEXA)

b) Quantitative computed tomography (QCT)

c) Single energy X-ray absorptiometry (SXA)

2.Quantitative ultrasound (QUS) - For screening


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Dual energy X-ray absorptiometry (DEXA)

Gold standard for diagnosis of osteoporosis

Measure bone mineral density

Predict the risk for fracture

As monitoring to assess the response to treatmentMeasured at lumbar spine and proximal femur

Result are reported as:

-T-scores (comparison with the young adult mean)

-Z-scores (comparison with the mean of individualsof the same age)


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Expression of Bone mineral

Density as measured by DEXA


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Normal Bone mineral density (BMD) within 1 SD of youngadult reference range(T score > 1)

Osteopenia(Low bone mass)

BMD is between 1 and 2.5 SD below the young adultmean (T score between 1 and 2.5)

Osteoporosis BMD value of 2.5 SD below the young adult mean (Tscore < 2.5)

Severe/

Establishedosteoporosis

BMD value of 2.5 SD below the young adult mean with

the presence of 1 or more fragility fractures

The lower the T-score, the lower your BMD, and the higher yourfracture risk


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Indication BMD measurement1. Presence of strong risk factors

Oestrogen deficiency

-Premature menopause (< 45years of age) including

-Surgical menopause

-Prolonged secondaryamenorrhoea

-Hypogonadism

Glucocorticoid therapy (equivalentto > 7.5 mg prednisolone daily for>

1 year)

Maternal family history of hipfracture

Low body mass index (


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MANAGEMENT

Goal:

1. To control bone loss

2. Prevent additional fracture

3. Control pain

Treatments:

Non pharmacology

Pharmacology


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Lifestyle Modification

ExercisePhysical activity can stimulate normalbone remodelling

Diet - Proper nutrition includes a diet sufficient incalcium and vitamin D & adequate protein and

energy

Stop unhealthy habit stop smoking and avoid

alcohol intake


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Pharmacological


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Hormone Replacement Therapy With estrogen and progesterone

As prevention and treatment of postmenopausalosteoporosis.

Can be started at any time from the perimenopausalperiod till late postmenopausal.

Inhibit bone loss and prevent the occurrence of the

fracture Decrease bone resorption and increase bone mass.

A full gynaecological assessment is mandatory prior tostarting HRT and at regular intervals while on HRT. Abreast examination should be conducted annually

Contraindication: -undiagnosed vaginal bleeding

-severe liver disease

-a hx of venous thromboembolism

(within the past 12 months)


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Selective Estrogen Receptor

Modulators (SERMs) Raloxifene at 60 mg daily

Suitable alternative for women who are unable orunwilling to take HRT.

Improves and preserves bone density at both thespine and hip

With a reduction in the risk of breast cancer

Side effects : hot flushes and leg cramps. Both raloxifene and estrogen are associated with

a slightly increased risk of deep vein thrombosis


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Biphosphanates

Bisphosphonates are potent inhibitors of boneresorption

Alendronate

Increases lumbar spine BMD by up to 8.8% andfemoral neck BMD by 5.9%

Prevent postmenopausal bone loss with similarefficacy to HRT

Side effects : Gastro-intestinal - nausea Proper administration of alendronate will reduce the

small risk of oesophagitis or oesophageal ulceration.


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Calcitonin

Anti-resorptive agent.

A daily intranasal dose of 200 IU,

Increase lumbar spine BMD and reduce vertebral

fracture rates

Calcitonin has also been shown to have ananalgesic effect for acute pain relief in osteoporosis

related fractures. Side effects: nausea, flushing, vomiting and nasal

irritation.


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Calcium and Vitamin D

Activated Vit D (calcitriol/alfacalcidol) use incombination with Calcium

Increase BMD in those with established osteoporosis

and reduce vertebral fractures. All patients on activated Vitamin D should avoid

taking excessive calcium supplements to reduce therisk of hypercalcemia and renal stone disease.

Serum and urinary calcium should be monitoredperiodically, 6 weeks after initiation of therapy andat 3 to 6 monthly intervals thereafter.


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