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osteoporosis

Intan Rahmania Eka D

Osteoporosis
The term osteoporosis is derived from the Greek
words osteon (bone) and poros (pore). Although
osteoporosis has many definitions, the World Health
Organization (WHO) defines it as a disease
characterized
by
low
bone
mass
and
microarchitectural deterioration of bone tissue,
leading to enhanced bone fragility and a
consequent increase in fracture risk

Epidemiologi
Currently affecting more than 10 million people in
the United States.
osteoporosis is projected to impact approximately
14 million adults over the age of 50 by the year
2020.
Worldwide, approximately 200 million women
have osteoporosis.

Osteoporosis
PRIMER
bila sebabnya tidak
diketahui

Tipe
TipeI I
Pada
Padawanita
wanita umur
umurantara
antara51
51
75
75tahun,
tahun,&&berhubungan
berhubungan
dengan
berkurangnya
dengan berkurangnyaestrogen
estrogen
pada
padamasa
masatransisi
transisi
menopause.
menopause.
Tipe
TipeIIII(Senile
(SenileOsteoporosis)
Osteoporosis)
Sering
Seringterjadi
terjadipd
pdumur
umur>
>60
60
thn.
thn.Pd
Pd&&
mempunyai
mempunyai
patofisiologi
patofisiologiyang
yangberbeda,
berbeda,
meskipun
meskipunestrogen
estrogenmungkin
mungkin
memegang
memegangperanan
perananpd
pdtipe
tipeIIII
osteoporosis.
osteoporosis.

SEKUNDER
bila sebabnya
diketahui
Osteoporosisyang
yang
Osteoporosis
didasarisuatu
suatu
didasari
penyakitatau
atau
penyakit
pengobatan,yang
yang
pengobatan,
merusaktulang.
tulang.
merusak

Bone remodeling

Estrogen
supresing production and defferentiation of
osteoclast
increasing osteoclast apoptosis
decrease production of several cytokin (IL 1, IL 6,
TNF)
decrease production of RANKL (inhibit mature of
osteoclast)
decrease of osteoprotegerin (OPG)

Vit D, Parathyroid
Hormon, and calcium
vit D and parathyroid hormon work to maintain calcium
homeostasis.
UV B7-Dehidrocholesterol (skin) cholecalciferol (vit
D3)
From dietary cholechalciferol (Vit D3 ) + ergocalciferol
(vit D2)
cholechalciferol (Vit D3 ) + ergocalciferol (vit D2)25
hydroxyvitaminD (25(OH)D) (liver)

PTH via 25(OH)vit D 1


hydroxylase
25 hydroxyvitamin D
1,25dihidroxyvit D (calcitriol) (kidney)
Calcitriol bind to intestinal reseptor and increase
absorbtion of calcium n phosphorus

Calcium Homeostasis

Etiology

Risk Factor

Clinical Manifestation
many patients are unware and present only after
fracture
pain, immobility, depression, fear, and low self esteem
from physical limitation and deformities
sign : shortened statur, kyphosis, or lordosis
fracture
low bone density or radiography
Laboratory : CBC, Cr , Ca, Posphate, ALP, Albumin, TSH,
25 (OH) vit D, 24-H urine concentration of Ca n Phospate
Pemeriksaan :
DXA (dual energy x ray absorbtiometry
Vertebra Fracture Assesment with DXA
technology
Radiograph

Treatment
Non pharmacology Therapy :
Diet : Alcohol, caffein dan carbonate cola
beverage
calcium supplement

Vit D
Vit K osteocalcin bone formation
Isoflavon phytoestrogen
Exercise : jogging, golf, walking 30 min/day at
least 2/weeks
Fall prevention

Pharmacology
combination calcium, vit D suplement and
biphosphonate is drug of choice.
E-BOOK\__Pharmacotherapy__8th_Edition__2011_
.chm

Biphosphonate
(Alendronate,
Risedronate, and
ibandronate)

bone resorption inhibitor


blocking and inhibiting triphosphatase-signaling protein
osteoclast maturation, number, bone adhesion, and
life span.

Alendronate : 5 mg/day, or 35 mg/weekly (prevention), 10


mg/day or 70 mg with vit D 2800, 5600 U.

Patients should not lie down, but should stay fully upright for at
least 30 minutes (60 minutes for ibandronate) after ingesting
an oral bisphosphonate to prevent esophageal irritation or
ulceration and to ensure appropriate bioavailability
Patients should ingest adequate calcium and vitamin D, but
should not take the calcium or vitamin D at the same time as
the alendronate
jika pasien lupa 1 hari tidak minum obat boleh dilanjutkan dosis
selanjutnya, jika lupanya lama maka tunggu 7 hari sebelum
pemakaian berikutnya.

Mixed Estrogen
agonis/antagonist/Selective Estrogen
Receptor Modulators
Raloxifene has estrogen agonist in bone and
antagonist action in breast and uterine tissue
decrease vertebral fracture and increase spine
and hip BMD.
Hot flushed greater likehood women finishing
menopouse or discontinue estrogen therapy
benefit for women who has osteoporosis and
breast cancer risk
decrease LDL, neutral for HDL, increase TG
contraindicated for patient who has VTE
Cholestyramine, when coadministered with
raloxifene, may decrease raloxifene absorption by
60% because of its effects on enterohepatic
cycling

Calcitonin
third line terapies
less benefit than antiresorptive therapies
is an endogenous hormon released from thyroid
gland when calcium is elevated
Calcitonin has been studied for the prevention of
glucocorticoid-induced osteoporosis as well

Denosumab
dosis : 60 mcq subcutaneously every 6 months
fully monoclonal antibody bind RANKL inhibitor
osteoclastogenesis and promote osteoclast
apoptosis
Adverse effect : back, extrimity, and
musculoskeletal pain, ,hipercholesterolemia.

Testosteron
Decrease testosteron concentrations are seen
with certain gonadall disease, eating disorder,
glucocorticoid therapy, oophorectomi and also
menopouse andandropouse.

Anabolic Therapies
increase bone formation
Recombinan product representing at the first 34
amino acid in PTH
Teriparatide
Transient hipercalcemia
Strontium ranelate has antiresorptive and mild
anabolic effects. The exact mechanism of action
remains unknown
Nausea and vomiting have been associated with
oral dissolved strontium, which abated after 3
months of therapy.

Medications

Comments

AIDS/HIV medications

Nucleoside reverse transcriptase inhibitors (antiretroviral


therapy, ART) (zidovudine, didanosine, lamivudine)

BMD (ART > PI), no fracture data; increased osteoclast


activity and decreased osteoblast activity

Protease inhibitors (PI) (nelfinavir, indinivir, saquinavir,


ritonavir, lopinavir)

Anticonvulsant therapy (phenytoin, carbamazepine,


phenobarbital, valproic acid)

BMD and fracture risk; increased vitamin D metabolism


leading to low 25(OH) vitamin D concentrations

Aromatase inhibitors (e.g., letrozole, anastrozole)

BMD and fracture risk; reduced estrogen concentrations

Furosemide

fracture risk; increased calcium renal elimination

Glucocorticoids (long-term oral therapy)

BMD and fracture risk; dose and duration dependent; see


special populations section

Gonadotropin-releasing hormone (GnRH) agonists or


analogs (e.g., leuprolide, goserelin)

BMD and fracture risk; decreased sex hormone production

Heparin (unfractionated, UFH) or low molecular weight


heparin (LMWH)

BMD and fracture risk (UFH >>>LMWH) with long-term use


(e.g., >6 mo); decreased osteoblast function and increased
osteoclast function

Medroxyprogesterone acetate depot administration


(DMPA)

BMD, no fracture data; possible BMD recovery with


discontinuation; central DXA monitoring of BMD
recommended with 2 years of use; decreased estrogen
concentrations

Proton pump inhibitor therapy (long-term therapy)

vertebral and hip fracture risk; possible calcium


malabsorption secondary to acid suppression for carbonate
salts

Selective serotonin reuptake inhibitors

hip fracture risk; decreased osteoblast activity

Thiazolidinediones (TZDs) (pioglitazone, rosiglitazone)

BMD and fracture risk; risk may be greater in women than


men; decreased osteoblast function

Thyroidexcessive supplementation

BMD and fracture risk (> in men); risk increases with TSH
concentration <0.1 IU/mL (<0.1 mIU/L); possible increase in
bone resorption

Vitamin Aexcessive intake (1.5 mg of retinol form)

BMD and fracture risk; decreased osteoblast activity and


increased osteoclast activity