OSTEOPOROSIS
BY:
Mrs.Keerthi Samuel,
Asst.Professor,
Vijay Marie CON.
INTRODUCTION
• Osteoporosis is a disease in which bone weakening increases the risk of
a broken bone.
• It is the most common reason for a broken bone among the elderly.
• Bones that commonly break include the vertebrae in the spine, the bones of
the forearm, and the hip.
• Until a broken bone occurs there are typically no symptoms.[3] Bones may
weaken to such a degree that a break may occur with minor stress or
spontaneously.
• After a broken bone, Chronic pain and a decreased ability to carry out normal
activities may occur.[
.
DEFINITION
• Osteoporosis is a metabolic skeletal disease characterized
by low bone density and microarchitectural deterioration of
bone tissue which results in increased bone fragility and
susceptibility to fracture. The vertebrae ,wrists ,and hips are
the most common sites of fractures.
• According to WHO osteoporosis is when the BMD is 2.5 SD.
.
INCIDENCE
 1 in 3 women over 50 years suffer from
osteoporosis.
 1 in 5 men over 50 years suffer
from osteoporosis.
 15% - 30% men and 30%- 50%
women suffer fractures related to
osteoporosis in their life time.
 Peak incidence : Western (70-80) and
in India ( 50-60 years)
.
INCIDENCE
 It is three times more common in
women than men as :
1.Low peak bone mass (PBM)
2.Hormonal changes at
menopause
3.Live longer thanmen
 Vertebrae and wrist are the more
common sites in women.
.
CLASSIFICATION
I. NORDINS CLASSFICATION
• Generalized: primary and secondary
• Localized
II. RIGGS AND MELTON
CLASSIFICATION
• Primary osteoporosis –
• Type 1 postmenopausal
• Type 2senile
• Secondary osteoporosis
• Osteogenesis imperfecta
• Idiopathic juvenile osteoporosis
GENERALIZED
OSTEOPOROSIS
• Primary osteoporosis is bone loss that
occurs during the normal human aging
process.
• Secondary osteoporosis is defined as bone
loss that results from specific, well-defined
clinical disorders and medical conditions
that cause bone resorption
• Localized osteoporosis in the
context used
indicates osteoporosis affecting
either part of one bone or several
bones in a chain.
LOCAIZED
OSTEOPOROSIS
NORDINS CLASSIFICATION
TYPE -I
OSTEOPOROSIS/POST
MENOPAUSAL
OSTEOPOROSIS
• Usually effects females ages 51-75
• Related to the loss of estrogens
protective effect on bone.
• Results in trabecular and some
cortical bone loss.
• Vertebral and wrist fractures are
common
• Trabecular and cortical bone loss
• Occurs most commonly in ages 70-
85.
• Fractures of proximal humerus,
proximal tibia, femoral neck and
pelvis.
TYPE -II
OSTEOPOROSIS/
SENILE
OSTEOPOROSIS
RIGGS & MILTON- PRIMARY OSTEOPOROSIS
SECONDARY
OSTEOPOROSIS
Itis defined as low bone mass leading
to fragility fractures in the presence of
an underlying disease like
hyperthyroidism, vit-D deficiency or
medication
• (OI) is a group of genetic disorders
that mainly affect the bones due to
imperfect bone formation. People with
this condition have bones that break
(fracture) easily, often from mild
trauma or with no apparent cause.
OSTEOGENESIS
IMPERFECTA
RIGGS & MILTON- SECONDARY OSTEOPOROSIS
IDIOPATHIC JUVENILE
OSTEOPOROSIS
Idiopathic juvenile osteoporosis (IJO) is
a primary condition of bone
demineralization that presents with pain
in the back and extremities, walking
difficulties, multiple fractures, and
radiological evidence of osteoporosis.
RIGGS & MILTON- PRIMARY OSTEOPOROSIS
ETIOLOGY
-
THREE MAIN
REASONS
• When rate of bone absorption is
less than bone resorption-loss of
one mass.
• Loss of calcium and phosphate-
porous and brittle bones.
• menopause
ETIOLOGY-RISK FACTORS
• Caucasian/ asian
• Female
• Family history
• Small frame
GENETICS- low
bone mass
• Post menopause
• Advanced age
• Low testosterone
in men
• Less calcitonin
AGE-hormonal
changes
• Low calcium and
Vit-D diet.
• High
phosphate(carbona
ed drinks
• Less calories
NUTRITION-for
remodelling
• Sedentary
• Lack of weight
bearing excersices
• Low weight and
BMI
EXCERCISES-
bone needs
stress for
maintainence
• Caffeine
• Alcohol
• Smoking
• Lack of exposure
to sunlight
LIFESTYLE-
reduces
osteogeneis in
remodelling
• Corticosteroids
• Antiseizure
medicines
• Heparin'
• Thyroid hormones
• Comorbidities like
RF,Hyperthyroidism
MEDICATIONS-
affects Ca
metabolism
.
PATHOPHYSIOLOGY
Bone undergoes a constant
remodelling directed by a balance
between Osteoblasts and
Osteoclasts.
Osteoblasts take longer to produce bone
than Osteoclasts take to resorb bone, so
anything that increases Osteoclast activity
or increases bone remodelling (e.g.
increased remodelling right after
menopause) in general increases bone
resorption over time.
.
PATHOPHYSIOLOGY
Furthermore, when remodeling is
rapid, the new bone may not fully
mineralized and so is more fragile
This balance is influenced by multiple
factors such as androgens, Vitamin
D,PTH, prostaglandins, TGF, IGF-I and
–II IL-1
.
Estrogen deficiency
accelerates bone loss in men
and women via multiple
mechanisms
Aging is associated with a
decrease in the supply of
IL-1 increase production of
osteoclasts
Vitamin D deficiency can lead to
secondary hyperparathyoidism and
break-down of bones to maintain
[Ca] in the bloodstream
.
FACTORS
AFFECTING
BONE MASS
CLINICAL
FEATURES
common
fracture sites
Osteoporosis is called
SILENT DISEASE
because the bone mass is
lost over many years
without signs and
symptoms.
1.FRACTURES
• Common symptom.
• Acute and chronic pain often attributes to fractures which can lead to
mortality and morbidity.
• Common sites-wrist, hip, spine, shoulder.
• vertebrae collapse leading to dowager’s hump(postural kyphosis).
The signs of sudden vertebral collapse are sudden back pain,
radicular pain ( shooting pain)rarely with cauda equina syndrome.
• Multiple vertebral fractures leads to stooped posture , loss of height
and chronic pain.
CLINICAL FEATURES
DOWGARS HUMP
VERTEBRAL
COLLAPSE
CLINICAL
FEATURES
VERTEBRAL FRACTURES
• Two thirds are asymptomatic.
• Acute onset back pain after bending, lifting, coughing
which resolves in 4-6 weeks but can have chronic
multiple fractures with kyphosis.
• Sharp nagging or dull Pain that may radiate to the
abdomen
LONG TERM OUTCOMES
• Progressive kyphosis with short stature
• Reduce pulmonary function
• Dependence of pain medications.
• Decreased quality of life ,depression, loss of
independence
CLINICAL
FEATURES
HIP FRACTURES
 Groin, posterior buttock, anterior or medial
thigh and/or medial knee pain after weight-
bearing or attempted weight-bearing
 Decreased range of motion in the hip
 Hips externally rotate in the resting position
LONG TERM OUTCOMES
 50% permanently disabled
 20% long-term home
 25% mortality in first year
2.RISK OF FALLS
• There is increased risk of falls with aging which can cause increased
damage to wrist, spine, knee, foot and ankle.
• Collapse( transient loss of postural tone with or without loss of
consciousness.
• Syncope is one of the reason for the falls
DIAGNOSTIC TESTS
1. CONVENTIONAL RADIOGRAPHY
2. DUAL ENERGY X-RAY (DEXA)
3. BIOMARKERS
4. OTHER MEASURING TOOLS
DIAGNOSTIC TESTS
1. CONVENTIONAL RADIOGRAPHY:
 It is useful in conjunction with CT or MRI.
 The main radiographic features of generalized osteoporosis are
cortical thinning and increased radiolucency.
 Spiral X ray can help in vertebral fractures, vertebral height
measurements such as height loss together with area reduction,
particularly when there is vertical deformity in T4-L4
DIAGNOSTIC TESTS
2. DUAL ENERGY X RAY ABSORPTIOMETRY –( DEXA):
• gold standard in the diagnosis.
• The diagnosis is confirmed when the bone mineral density is
below or equal to 2.5standard deviations which is the ‘T’ scores.
Category T-score range % young women
Normal T-score ≥ −1.0 85%
Osteopenia
−2.5 < T-score <
−1.0
14%
Osteoporosis T-score ≤ −2.5 0.6%
Severe osteoporosis
T-score ≤ −2.5 with
fragility fracture
DIAGNOSTIC TESTS
3. BIOMARKERS:
• Chemical biomarkers are useful tool in detection of bone degradation.
• An enzyme cathepsin K breaks down type-I collagen, an important constituent in bone
• Prepared antibodies can recognize the resulting fragment called a NEOEPITOPE as a
way to diagnose osteoporosis
• Increased urinary excretion of C-telopeptide, a type-I collagen breakdown product,
also serves as a biomarker for osteoporosis.
4. OTHER TESTS: used to assess cortical and trabecular bone.
• Quantitative computed tomography
• Quantitative ultrasound
MANAGEMENT
• The main goal of treatment is to prevent development of
osteoporosis and to stabilize remaining bone mass.
• The management can be a combination of Lifestyle modifications
and drug therapy.
1. LIFESTYLE:
 Weight bearing endurance exercises to strengthen muscle
and improve bone strength
 Aerobics, weight bearing and resistance exercises maintain
or increase BMD in menopausal woman.
 Hip protectors are available to protect from hip fractures.
MANAGEMENT
2. MEDICATIONS:
• BIPHOSPHOSPHONATES are useful in preventing fractures in
clients who already have osteoporosis.
• This benefit is present when taken for three to four years. They do not
appear to change the overall risk of death
• There are concerns of atypical femoral fractures and osteonecrosis of the
jaw with long-term use, but these risks are low. With evidence of little
benefit when used for more than three to five years and in light of the
potential adverse events, it may be appropriate to stop treatment after this
time.
MANAGEMENT
2. MEDICATIONS:
• ALENDRONATE decreases fractures of the spine but does not
have any effect on other types of fractures. Half stop their
medications within a year. When on treatment with
bisphosphonates rechecking bone mineral density is not needed
• FLUORIDE SUPPLEMENTATION does not appear to be effective
in postmenopausal osteoporosis, as even though it increases bone
density, it does not decrease the risk of fractures.
• TERIPARATIDE (a recombinant parathyroid hormone) has been
shown to be effective in treatment of women with postmenopausal
osteoporosis.
MANAGEMENT
• Some evidence also indicates STRONTIUM RANELATE is
effective in decreasing the risk of vertebral and nonvertebral
fractures in postmenopausal women with osteoporosis.
• HORMONE REPLACEMENT THERAPY, while effective for
osteoporosis, is only recommended in women who also have
menopausal symptoms. It is not recommended for osteoporosis by
itselfSelective Estrogen Receptor Modulators are used.
• Raloxifene, while effective in decreasing vertebral fractures, does not
affect the risk of nonvertebral fracture. And while it reduces the risk
of breast cancer, it increases the risk of blood clots and strokes.
MANAGEMENT
• CALCITONIN while once recommended is no longer due to the
associated risk of cancer and questionable effect on fracture risk.
• ALENDRONIC ACID/COLECALCIFEROL can be taken to treat
this condition in post-menopausal women.
• Certain medications like alendronate, etidronate, risedronate,
raloxifene, and strontium ranelate can help to prevent osteoporotic
fragility fractures in postmenopausal women with osteoporosis.
• Tentative evidence suggests that Chinese herbal medicines may
have potential benefits on bone mineral density.
PREVENTION
1) A CALCIUM RICH DIET ESPECIALLY IN
CHILDHOOD.
• Adolescents may need 1200mg and
postmenopausal women may need
1500mg daily.
• Milk, cheese and yogurt are rich in
calcium.
• Elderly should be advised to take 400-
800 units ofVit. D daily
Comes (from 2 sources : the sun and
Fortified dairy products, egg yolks,
saltwater fish, and liver)
PREVENTION
3. EXERCISE:
• Exercising regularly in childhood and
adolescence can ensure that you will reach
peak bone density.
(4) Alcohol , caffeine intake should be avoided.
(5) Women with low body w.t (those with eating
disorders) should receive appropriate
evaluation, Rx and dietary counseling.
RANKL
• A number of agents are currently undergoing
assessment for the treatment of osteoporosis.
• These include new selective oestrogen receptor
modulators, calcium sensing receptor antagonists,
inhibitors of sclerostin, a protein produced by
osteocytes that inhibits bone formation.
• A human monoclonal antibody to RECEPTOR
ACTIVATOR OF NFKB LIGAND (RANKL), a cytokine
that stimulates osteoclast development and activity,
has been shown in phase III trials to reduce vertebral,
non-vertebral and hip fractures and is currently being
evaluated by the regulatory authorities.
• It is administered once every six months by
subcutaneous injection.
RECENT
ADVANCEMENTS
IN MANAGEMENT
OF
OSTEOPOROSIS
From:
Recent advances in the
management of
osteoporosis
2009 dec; 9(6): 565–569,
JOURNAL OF CLIICAL
MEDICINE, ROYAL
COLLEGE OF PHYSICIANS
Nursing process
assessment
History:
• Profile: Age & gender
• Risk factor
• Secondary causes
• Symptoms related
• Past medical Hx
• Family Hx
• Social Hx
19
PHYSICAL EXAMINATION
• General:
- decreasing height greater > 1.5inches
- dorsal kyphosis
- exaggerated cervical lordoisis
- low body weight.
• Assessed for:
- localized pain
- muscle spasm
- neurologic deficit (risk of spinal cord compression)
- loss of strength
- range of motion in the affected area
• Fractures most commonly occur in the vertebral bodies,
wrist, humerus, hip. rib and pelvis (in that order).
Nursing diagnosis:
• acute pain
• Impaired physical mobility
• self-care deficit (Dressing or grooming)
• Imbalanced nutrition: Less than body
requirement
• Risk for impaired skin integrity
• Risk for injury
• Risk for constipation RT immobility
• Deficient knowledge about the osteoporosic
process and treatment regimen.
Goals:
-relieving pain
-improve self-care.
-improve nutritional status.
-improve physical mobility.
-prevent injury. (no new fracture)
-improving bowel elimination.
-promoting understanding of osteoporosis and
the treatment regimen.
Intervention
-consume adequate dietary calcium and vit D.
-encourage to increase level of exercise.
-modify lifestyle choices: avoid smoking, alcohol,
carbonated beverages.
-maintain optimal body wt.
-creates safe home environment.
-adheres to prescribe screening and monitoring
prcedures.
-take prescribed medication as instruction.

Osteoporosis keerthi

  • 1.
  • 2.
    INTRODUCTION • Osteoporosis isa disease in which bone weakening increases the risk of a broken bone. • It is the most common reason for a broken bone among the elderly. • Bones that commonly break include the vertebrae in the spine, the bones of the forearm, and the hip. • Until a broken bone occurs there are typically no symptoms.[3] Bones may weaken to such a degree that a break may occur with minor stress or spontaneously. • After a broken bone, Chronic pain and a decreased ability to carry out normal activities may occur.[ .
  • 3.
    DEFINITION • Osteoporosis isa metabolic skeletal disease characterized by low bone density and microarchitectural deterioration of bone tissue which results in increased bone fragility and susceptibility to fracture. The vertebrae ,wrists ,and hips are the most common sites of fractures. • According to WHO osteoporosis is when the BMD is 2.5 SD. .
  • 5.
    INCIDENCE  1 in3 women over 50 years suffer from osteoporosis.  1 in 5 men over 50 years suffer from osteoporosis.  15% - 30% men and 30%- 50% women suffer fractures related to osteoporosis in their life time.  Peak incidence : Western (70-80) and in India ( 50-60 years) .
  • 6.
    INCIDENCE  It isthree times more common in women than men as : 1.Low peak bone mass (PBM) 2.Hormonal changes at menopause 3.Live longer thanmen  Vertebrae and wrist are the more common sites in women. .
  • 9.
    CLASSIFICATION I. NORDINS CLASSFICATION •Generalized: primary and secondary • Localized II. RIGGS AND MELTON CLASSIFICATION • Primary osteoporosis – • Type 1 postmenopausal • Type 2senile • Secondary osteoporosis • Osteogenesis imperfecta • Idiopathic juvenile osteoporosis
  • 10.
    GENERALIZED OSTEOPOROSIS • Primary osteoporosisis bone loss that occurs during the normal human aging process. • Secondary osteoporosis is defined as bone loss that results from specific, well-defined clinical disorders and medical conditions that cause bone resorption • Localized osteoporosis in the context used indicates osteoporosis affecting either part of one bone or several bones in a chain. LOCAIZED OSTEOPOROSIS NORDINS CLASSIFICATION
  • 11.
    TYPE -I OSTEOPOROSIS/POST MENOPAUSAL OSTEOPOROSIS • Usuallyeffects females ages 51-75 • Related to the loss of estrogens protective effect on bone. • Results in trabecular and some cortical bone loss. • Vertebral and wrist fractures are common • Trabecular and cortical bone loss • Occurs most commonly in ages 70- 85. • Fractures of proximal humerus, proximal tibia, femoral neck and pelvis. TYPE -II OSTEOPOROSIS/ SENILE OSTEOPOROSIS RIGGS & MILTON- PRIMARY OSTEOPOROSIS
  • 12.
    SECONDARY OSTEOPOROSIS Itis defined aslow bone mass leading to fragility fractures in the presence of an underlying disease like hyperthyroidism, vit-D deficiency or medication • (OI) is a group of genetic disorders that mainly affect the bones due to imperfect bone formation. People with this condition have bones that break (fracture) easily, often from mild trauma or with no apparent cause. OSTEOGENESIS IMPERFECTA RIGGS & MILTON- SECONDARY OSTEOPOROSIS
  • 13.
    IDIOPATHIC JUVENILE OSTEOPOROSIS Idiopathic juvenileosteoporosis (IJO) is a primary condition of bone demineralization that presents with pain in the back and extremities, walking difficulties, multiple fractures, and radiological evidence of osteoporosis. RIGGS & MILTON- PRIMARY OSTEOPOROSIS
  • 14.
    ETIOLOGY - THREE MAIN REASONS • Whenrate of bone absorption is less than bone resorption-loss of one mass. • Loss of calcium and phosphate- porous and brittle bones. • menopause
  • 15.
    ETIOLOGY-RISK FACTORS • Caucasian/asian • Female • Family history • Small frame GENETICS- low bone mass • Post menopause • Advanced age • Low testosterone in men • Less calcitonin AGE-hormonal changes • Low calcium and Vit-D diet. • High phosphate(carbona ed drinks • Less calories NUTRITION-for remodelling • Sedentary • Lack of weight bearing excersices • Low weight and BMI EXCERCISES- bone needs stress for maintainence • Caffeine • Alcohol • Smoking • Lack of exposure to sunlight LIFESTYLE- reduces osteogeneis in remodelling • Corticosteroids • Antiseizure medicines • Heparin' • Thyroid hormones • Comorbidities like RF,Hyperthyroidism MEDICATIONS- affects Ca metabolism .
  • 16.
    PATHOPHYSIOLOGY Bone undergoes aconstant remodelling directed by a balance between Osteoblasts and Osteoclasts. Osteoblasts take longer to produce bone than Osteoclasts take to resorb bone, so anything that increases Osteoclast activity or increases bone remodelling (e.g. increased remodelling right after menopause) in general increases bone resorption over time. .
  • 17.
    PATHOPHYSIOLOGY Furthermore, when remodelingis rapid, the new bone may not fully mineralized and so is more fragile This balance is influenced by multiple factors such as androgens, Vitamin D,PTH, prostaglandins, TGF, IGF-I and –II IL-1 .
  • 18.
    Estrogen deficiency accelerates boneloss in men and women via multiple mechanisms Aging is associated with a decrease in the supply of IL-1 increase production of osteoclasts Vitamin D deficiency can lead to secondary hyperparathyoidism and break-down of bones to maintain [Ca] in the bloodstream . FACTORS AFFECTING BONE MASS
  • 19.
    CLINICAL FEATURES common fracture sites Osteoporosis iscalled SILENT DISEASE because the bone mass is lost over many years without signs and symptoms.
  • 20.
    1.FRACTURES • Common symptom. •Acute and chronic pain often attributes to fractures which can lead to mortality and morbidity. • Common sites-wrist, hip, spine, shoulder. • vertebrae collapse leading to dowager’s hump(postural kyphosis). The signs of sudden vertebral collapse are sudden back pain, radicular pain ( shooting pain)rarely with cauda equina syndrome. • Multiple vertebral fractures leads to stooped posture , loss of height and chronic pain.
  • 21.
  • 22.
    CLINICAL FEATURES VERTEBRAL FRACTURES • Twothirds are asymptomatic. • Acute onset back pain after bending, lifting, coughing which resolves in 4-6 weeks but can have chronic multiple fractures with kyphosis. • Sharp nagging or dull Pain that may radiate to the abdomen LONG TERM OUTCOMES • Progressive kyphosis with short stature • Reduce pulmonary function • Dependence of pain medications. • Decreased quality of life ,depression, loss of independence
  • 24.
    CLINICAL FEATURES HIP FRACTURES  Groin,posterior buttock, anterior or medial thigh and/or medial knee pain after weight- bearing or attempted weight-bearing  Decreased range of motion in the hip  Hips externally rotate in the resting position LONG TERM OUTCOMES  50% permanently disabled  20% long-term home  25% mortality in first year
  • 25.
    2.RISK OF FALLS •There is increased risk of falls with aging which can cause increased damage to wrist, spine, knee, foot and ankle. • Collapse( transient loss of postural tone with or without loss of consciousness. • Syncope is one of the reason for the falls
  • 27.
    DIAGNOSTIC TESTS 1. CONVENTIONALRADIOGRAPHY 2. DUAL ENERGY X-RAY (DEXA) 3. BIOMARKERS 4. OTHER MEASURING TOOLS
  • 28.
    DIAGNOSTIC TESTS 1. CONVENTIONALRADIOGRAPHY:  It is useful in conjunction with CT or MRI.  The main radiographic features of generalized osteoporosis are cortical thinning and increased radiolucency.  Spiral X ray can help in vertebral fractures, vertebral height measurements such as height loss together with area reduction, particularly when there is vertical deformity in T4-L4
  • 29.
    DIAGNOSTIC TESTS 2. DUALENERGY X RAY ABSORPTIOMETRY –( DEXA): • gold standard in the diagnosis. • The diagnosis is confirmed when the bone mineral density is below or equal to 2.5standard deviations which is the ‘T’ scores. Category T-score range % young women Normal T-score ≥ −1.0 85% Osteopenia −2.5 < T-score < −1.0 14% Osteoporosis T-score ≤ −2.5 0.6% Severe osteoporosis T-score ≤ −2.5 with fragility fracture
  • 30.
    DIAGNOSTIC TESTS 3. BIOMARKERS: •Chemical biomarkers are useful tool in detection of bone degradation. • An enzyme cathepsin K breaks down type-I collagen, an important constituent in bone • Prepared antibodies can recognize the resulting fragment called a NEOEPITOPE as a way to diagnose osteoporosis • Increased urinary excretion of C-telopeptide, a type-I collagen breakdown product, also serves as a biomarker for osteoporosis. 4. OTHER TESTS: used to assess cortical and trabecular bone. • Quantitative computed tomography • Quantitative ultrasound
  • 31.
    MANAGEMENT • The maingoal of treatment is to prevent development of osteoporosis and to stabilize remaining bone mass. • The management can be a combination of Lifestyle modifications and drug therapy. 1. LIFESTYLE:  Weight bearing endurance exercises to strengthen muscle and improve bone strength  Aerobics, weight bearing and resistance exercises maintain or increase BMD in menopausal woman.  Hip protectors are available to protect from hip fractures.
  • 32.
    MANAGEMENT 2. MEDICATIONS: • BIPHOSPHOSPHONATESare useful in preventing fractures in clients who already have osteoporosis. • This benefit is present when taken for three to four years. They do not appear to change the overall risk of death • There are concerns of atypical femoral fractures and osteonecrosis of the jaw with long-term use, but these risks are low. With evidence of little benefit when used for more than three to five years and in light of the potential adverse events, it may be appropriate to stop treatment after this time.
  • 33.
    MANAGEMENT 2. MEDICATIONS: • ALENDRONATEdecreases fractures of the spine but does not have any effect on other types of fractures. Half stop their medications within a year. When on treatment with bisphosphonates rechecking bone mineral density is not needed • FLUORIDE SUPPLEMENTATION does not appear to be effective in postmenopausal osteoporosis, as even though it increases bone density, it does not decrease the risk of fractures. • TERIPARATIDE (a recombinant parathyroid hormone) has been shown to be effective in treatment of women with postmenopausal osteoporosis.
  • 34.
    MANAGEMENT • Some evidencealso indicates STRONTIUM RANELATE is effective in decreasing the risk of vertebral and nonvertebral fractures in postmenopausal women with osteoporosis. • HORMONE REPLACEMENT THERAPY, while effective for osteoporosis, is only recommended in women who also have menopausal symptoms. It is not recommended for osteoporosis by itselfSelective Estrogen Receptor Modulators are used. • Raloxifene, while effective in decreasing vertebral fractures, does not affect the risk of nonvertebral fracture. And while it reduces the risk of breast cancer, it increases the risk of blood clots and strokes.
  • 35.
    MANAGEMENT • CALCITONIN whileonce recommended is no longer due to the associated risk of cancer and questionable effect on fracture risk. • ALENDRONIC ACID/COLECALCIFEROL can be taken to treat this condition in post-menopausal women. • Certain medications like alendronate, etidronate, risedronate, raloxifene, and strontium ranelate can help to prevent osteoporotic fragility fractures in postmenopausal women with osteoporosis. • Tentative evidence suggests that Chinese herbal medicines may have potential benefits on bone mineral density.
  • 36.
    PREVENTION 1) A CALCIUMRICH DIET ESPECIALLY IN CHILDHOOD. • Adolescents may need 1200mg and postmenopausal women may need 1500mg daily. • Milk, cheese and yogurt are rich in calcium. • Elderly should be advised to take 400- 800 units ofVit. D daily Comes (from 2 sources : the sun and Fortified dairy products, egg yolks, saltwater fish, and liver)
  • 37.
    PREVENTION 3. EXERCISE: • Exercisingregularly in childhood and adolescence can ensure that you will reach peak bone density. (4) Alcohol , caffeine intake should be avoided. (5) Women with low body w.t (those with eating disorders) should receive appropriate evaluation, Rx and dietary counseling.
  • 38.
    RANKL • A numberof agents are currently undergoing assessment for the treatment of osteoporosis. • These include new selective oestrogen receptor modulators, calcium sensing receptor antagonists, inhibitors of sclerostin, a protein produced by osteocytes that inhibits bone formation. • A human monoclonal antibody to RECEPTOR ACTIVATOR OF NFKB LIGAND (RANKL), a cytokine that stimulates osteoclast development and activity, has been shown in phase III trials to reduce vertebral, non-vertebral and hip fractures and is currently being evaluated by the regulatory authorities. • It is administered once every six months by subcutaneous injection. RECENT ADVANCEMENTS IN MANAGEMENT OF OSTEOPOROSIS From: Recent advances in the management of osteoporosis 2009 dec; 9(6): 565–569, JOURNAL OF CLIICAL MEDICINE, ROYAL COLLEGE OF PHYSICIANS
  • 39.
    Nursing process assessment History: • Profile:Age & gender • Risk factor • Secondary causes • Symptoms related • Past medical Hx • Family Hx • Social Hx
  • 40.
    19 PHYSICAL EXAMINATION • General: -decreasing height greater > 1.5inches - dorsal kyphosis - exaggerated cervical lordoisis - low body weight. • Assessed for: - localized pain - muscle spasm - neurologic deficit (risk of spinal cord compression) - loss of strength - range of motion in the affected area • Fractures most commonly occur in the vertebral bodies, wrist, humerus, hip. rib and pelvis (in that order).
  • 41.
    Nursing diagnosis: • acutepain • Impaired physical mobility • self-care deficit (Dressing or grooming) • Imbalanced nutrition: Less than body requirement • Risk for impaired skin integrity • Risk for injury • Risk for constipation RT immobility • Deficient knowledge about the osteoporosic process and treatment regimen.
  • 42.
    Goals: -relieving pain -improve self-care. -improvenutritional status. -improve physical mobility. -prevent injury. (no new fracture) -improving bowel elimination. -promoting understanding of osteoporosis and the treatment regimen.
  • 43.
    Intervention -consume adequate dietarycalcium and vit D. -encourage to increase level of exercise. -modify lifestyle choices: avoid smoking, alcohol, carbonated beverages. -maintain optimal body wt. -creates safe home environment. -adheres to prescribe screening and monitoring prcedures. -take prescribed medication as instruction.