Kuliah Osteoporosis Yarsi

7/30/2019 Kuliah Osteoporosis Yarsi

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OSTEOPOROSIS

Dr. Zulfan, SpPD

Bagian Penyakit Dalam

FK Universitas YARSI


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Osteoporosis is a major public health problem, and

postmenopausal osteoporosis constitutes as a major part

of the problem.

Claus Christiansen, Am J Med 1993

Hip fractures will increase sharply in the next half

century, especially in Asia, making osteoporosis a trulyglobal issue.

WHO 1998

EPIDEMIOLOGY


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Introduction

Osteoporosis is a disease characterized

by low bone mass and microarchitecturaldeterioration of bone tissue, leading toenhance bone fragility and a consequentincrease in fracture risk

(WHO)


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Osteoporosis is a skeletal disorders

compromised bone strength,

predisposing in an increase risk

of fracture


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Rigg and Nelson divided into :

A/. Primary osteoporosis1. Post menopause osteoporosis

2. Senile osteoporosis

B/. Secondary osteoporosisOsteoporosis due to other condition

of disease such as metabolic,endocrine or malignancy


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Post menopausal osteoporosis

Most common in woman 15 20 year after menopause

Mostly affects trabecular bone, increasing patient

susceptibility to vertebral compression fractures,

distal radial fractures and intertrochanteric fractures.

Esterogen deficiency plays a primary role


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Senile Osteoporosis Occurs in men and women over the age of

70 years with female to male ratio of 2:1

It affects : cortical and trabecular boneequally, predisposing patient to multiplewedges vertebral and femoral neck

fracturesAging and long-term calcium deficiency is

more important.


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Primary osteoporosis mostly are old and

elderly people complaining of mild

backache but may also a sudden pain

with only a mild injury due to a

compression fractures of the vertebrae.


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Before it reaches the threshold of fractures,

usually the height of patient reduces beside

deformity (kyphotic deformity)


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It is a silent disease, meaning there is

no significant signs and symptoms

caused by osteoporosis


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Etiology :

General factor predictive of osteoporosis :

1. Peak bone mass at maturity :

General / familialNutritionalPhysical (activity status, exercise, etc)Life style (alcohol, cigarettes, caffeine)

Medical (chronic disease, hypogonadal states, etc)Iatrogenic (corticosteroid, anticonvulsant, etc)

Orthopaedics Study Guide, Metabolic Bone Disease, 1999, p.885-889


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20 40 8060

BoneMass

Peak Bone Mass

male

female

Menopause

Bone Loss

Bone Mass Development

ageAge (year)


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2. Post menopausal bone loss

Accelerated trabecular bone loss for 3to 10 years post menopausal

Due to increased bone resorptionsecondary to estrogen loss

Loss of normally 1 to 2% per year to

a maximum of 10%

Orthopaedics A Study Guide, Metabolic Bone Disease, 1999, p.885-889


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3. Age-related (involutionall) bone loss

Starts at age 35 40 years in both sexes,continues for 30 to 40 years

Subtle uncoupling of rates of bone formationand resorption

Both cortical and trabecular bone affectedLoss normally less than 0.5% per year to a

maximum of 20 %



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4. Risk factors

Genetic, life style, Medical, Iatrogenic


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Risk factors for bone loss :

1. Genetic :

- Female sex- Caucasian / Asian ethnicity- Family history of osteoporosis



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2. Life Style :

- Low calcium intake- Excessive alcohol use

- Cigarette smoking- Excessive caffeine use- Extreme or insufficient athlecity- Excessive acid ash diet (high protein /

soft drink intakes)



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3. Medical :

- Early menopause- Gonadal hormone deficiency states

- Eating disorders- Chronic liver / kidney disease- Malabsorption syndrome



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4. Iatrogenic :- Corticosteroids- Excessive thyroid hormone

- Chronic heparin therapy- Radiotherapy to skeleton- Long-term anticonvulsants

- Loop diuretics



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Bone is the most dynamic tissue.

Metabolism of catabolism and anabolism

as the activity of osteoclast and osteoblast

as a process of bone remodeling or

bone turn over


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Degeneration occurs as an aging process

where the activity of osteoclast is not able

to compensate by the activity of osteoblast.

As a result bone mineral density decrease


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The main problem of osteoporosis

lies in the effectiveness of intervention-prevention and treatment


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Osteoporosis is preventable if prevention

starts during the childhood and adolescence

when bone reaches maturity at the end

of 3rd decade to achieve maximum

Peak Bone Mass


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After the 3rd decade all organ include skeletal /bone will degenerate, the speed ofdegeneration, differs for different organ.

In general organ will loose function

1% every year (the rule of 1% of Andreas

and Tobin)


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Diagnosis should include differential diagnosis ofprimary and secondary osteoporosis by :

o Taking a good history

o Physical examination

o Laboratory examination

o Imaging examination


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DIAGNOSIS

History :

o ras, sex and age

o health status

o life style (alcohol, smoking)

o physical activity (sports)

o history of previous disease including administration of

drugs, previous fracture.


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Physical Examination :

Body weight and height (BMI)

Extremities and spine including :

deformity, MMT and ROM


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Laboratory findings :

o blood serum

o hormone

o Urine


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LABORATORY FINDINGS :

Routine:

- Serum :- Complete blood counts

- Electrolytes, creatinine, blood urea, nitrogen calcium

- Phosphorus, protein, albumin, alkaline phosphatase,

liver enzyme

- Protein electrophoresis

- Thyroid function tests

- Testoterone (men only)- 24 hours urine :

- calcium

- Pyridinium cross-links


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LABORATORY FINDINGS :

Spesial :

- Serum:

- 25 hydroxyvitamin D3

- 1,25 hydroxyvitamin D3

- intact parathyroid hormone

- osteocalcium (bone Gla protein)

- Urine :

- Immunoelectrophoresis

- Bence-Jones protein


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IMAGING :Radiology : plain X-ray

(especially the spine, hip and wirst)

The spine : - the ballooning disc

- deformity of vertebral body

(wedge, fish tail)

The Hip : - Singh Index

The Wirst : - Porotic / thinning cortex


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The general diagnostic categories

established in woven : (WHO working group)

Normal : Bone Mass Density (BMD)or

Bone Mineral Content (BMC)-1 SD from T Score of the young

adult reference mean

Osteopenia : BMD or BMC 1 SD to 2.5 SD

Osteoporosis : BMD or BMC

2.5 SD

(severe osteoporosis when there is followed a fracture)


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Prevention and Treatment

T-score Fracture risk Teatment

> +1 very low no treatment densitometry with indication

-1 s/d 0 low no treatment densitometry after 5 years

- 1 s/d +1 low no treatment densitometry after 2 years

-1s/d -2,5 midle prevention densitometry after 1 years

< - 2,5 high osteoporosis treatment

no fracture continue prevention densitometry after 1 years

< - 2,5 very high osteoporosis treatmentWith fracture continue prevention

surgery with indication densitometry after within6 month1 years


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Prevention

Aging process is a natural process of a persongetting old

3 steps of osteoporosis prevention :I. Up to the end of 3rd decadewhere Peak Bone Mass should be achieved

II. After the 3rd decade up to menopause /Andropause

III. Senile, prevent from minor injury / accident


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Goal of Osteoporosis Prevention

Optimising skeletal developmentNutritionPhysical activityLife style changesMinimize medical / iatrogenic factors

Minimize postmenopausal bone loss

Early identification of patients at riskReduced risk factorsHormone replacement therapy (HRT)Other agents pre-emptively if HRT contraindicatedraloxifene, alendronate

Minimize age-related bone lossIdentification of patients at riskReduce risk factorsFull prevention and exercise program (physical therapy)



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1st Prevention :

Good nutrition

Life style and physical exercise

To achieve maximum Peak Bone Mass


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2nd Prevention

Early diagnose of osteoporosis The same prevention as 1st prevention In female patient after menopause with HRT Prevention of the use of medication

consist steroid etc


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3rd Prevention

Prevent from accident

(minor injury could cause fracture) Care giver especially after fracture Operative intervention and bracing


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Treatment

Nowadays there is a lot of medicationFor osteoporosis such as :- calcium and vitamin D- calcitriol- calcitonin

- bisphosphonate : generation : I

IIIsuch as (clorodronate, alendronate, and

risedronate (actonel))- hormone : - anabolic

- sex hormone

- SEMs (Selective Modulator)- SERM (Selective Estrogen Reseptor

Modulator : Raloxifene(analogue of tamosifene)

SURGERY


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Calcium : 1500 mg / day

Vitamin D : 500 mg / day

Calcitonin (myacalcic : Nasal spray: 200 mg / daily)


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HRT :establish approach for osteoporosis prevention

and treatment.

But what after WHI report ????

SERM :Raloxifene : Evista : 60 mg/daily

- the goal is to increase bone benefits and decrease

deletterious affects on breast and endometrim.

- decrease breast cancer : 76 %

- 60 % women, 2 years : BMD increase 1-2 %

Dr. C. Deeply


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DIET CUKUP KALSIUM DAN VIT. D4 SEHAT 5 SEMPURNA

KEBUTUHAN KALSIUM

Balita 400 700 mg / hari Remaja 1000 1500 mg / hari Dewasa 750 1000 mg / hari Hamil 1500 mg / hari Menyusui 2000 mg / hari Sebelum menopause 800 1000 mg / hari Selama menopause 1000 1200 mg / hari Setelah menopause 1200 1500 mg / hari

BAHAN MAKANAN


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BAHAN MAKANAN

Per Ons Teri nasi mengandung 1000 mg Kalsium

Per Ons Kepiting 210 mg

Per Ons Kerang 133 mg

40 gr Dencis kaleng 200 mg

Per Ons Kuning telur ayam 147 mg

Per Ons Tempe 129 mg

Per Ons Tahu 124 mger Ons Emping 100 mg

Per Ons Bayam merah 347 mg

Per Ons Kacang panjang 347 mg

Per Ons Daun singkong 165 mg

1 gelas Susu kental manis 275 mg1 gelas Susu segar 380 mg

1 gelas susu krim penuh 290 mg

1 gelas Susu non fat 480 mg

1 gelas yurgort 200 mg

20 gr keju 100 mg

PREPARAT KALSIUM YANG TERSEDIA DI PASARAN


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PREPARAT KALSIUM YANG TERSEDIA DI PASARAN

No. Jenis Kalsium Nama Dagang Kalsium(mg)

1. Kalsium karbonat Ca-C 100 Sandoz 327

Calsan 1250

Caxon-F 250

Calsium Sandoz 300

Epocaldi 400

2. Kalsium Laktas Ca-C 1000 Sandoz 1000

Calcidin 100

Calsium Sandoz 2940

3. Kalsium fosfat Calcidin 200

Calcalcin 800

Catatan : Kalsium karbonat mengandung 40 % kalsium

Kalsium laktas mengandung 13 % kalsium

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Kuliah Osteoporosis Yarsi