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Musculoskeletal Disorders Part I
Degenerat ve eta o c one sor ers
Maria Carmela L. Domocmat, RN,MSNInstructor
School of NursingNorthern Luzon Adventist CollegeArtacho, Sison, Pangasinan
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Overview
Part 1: Degenerative & Metabolic bone disorders OA Gout and gouty arthritis
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s eoporos s Pagets dse
Osteomalacia
Part 2: Bone infections
Part 3: Muscular disorders Part 4: Disorders of the hand Part 5: Spinal column deformities Part 6 : Disorders of foot
Part 7: Sports Injuries
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SkeletonThe skeleton consists of groups of bones
which protect and move the body.
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Osteoporosis risk factors mnemonic
ACCESS:
Alcohol
Calcium low
Estrogen low
Smoking
Sedentary lifestyle
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http://www.myphysio.ca/site_assets/www.myphysio.ca/images/dynamic/osteoporosis.jpg
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http://healthinfo.fitnessguide101.com/wp-content/uploads/2010/10/Boneloss.jpg
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http://images.emedicinehealth.com/images/SlideShow/Osteoporosis_s1_bone_density.jpg
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Osteoporosis Symptoms: Stress FractureA fracture that occurs during the course of normal activity iscalled a minimal trauma fracture or stress fracture. Forexample, some patients with osteoporosis develop stressfractures of the feet while walking or stepping off a curb.
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OsteoporosisSymptoms: Hip Fracture
Hip fractures typically occuras a result of a fall. Withosteoporosis, hip fracturescan occur as a result oftrivial accidents. Hipfractures may also bedifficult to heal after surgicalrepair because of poor bonequality
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Orthotics (thoracolumbosacral
orthosis)
decrease flexionforces
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of kyphosis reduce pressure on
fracture sites
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Osteomalacia
Osteomalacia means "soft bones". is softening of the bones due to a lack of vitamin
'
down and use this vitamin.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001414/
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Osteomalacia
characterized by incomplete mineralization ofnormal osteoid tissue following closure of the
.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001414/
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Osteoid bone protein matrix, composed primarily of type 1 collagen. When there is insufficient mineral or osteoblast
d sfunction the osteoid does not mineralize ro erl andit accumulates.
When the newly formed bone of the growth plate doesnot mineralize, the growth plate becomes thick, wide andirregular. This results in the clinical diagnosis of rickets,and is seen only in children because adults no longer
have growth plates. When the remodeled bone does notmineralize, osteomalacia occurs, and this happens in allages. Most of the hereditary causes of osteomalaciaappear during childhood and cause rickets.
http://courses.washington.edu/bonephys/hypercalU/opmal2.html
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http://www.moondragon.org/health/graphics/osteomalaciaadult.jpg
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Loosers zone
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xray showing a pseudofracture(red arrow) from an adult whohas x-linked
This is an xray of a child withbowed legs due to rickets
.
This is a classic pseudofractureand is pathognomonic forosteomalacia.
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Treatment
vitamin D, calcium, and phosphorussupplements, taken by mouth.
needed for people who cannot properly absorbnutrients into the intestines.
Regular blood tests may be needed to monitor
blood levels of phosphorus and calcium inpersons with certain underlying conditions.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001414/
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Recommended Dietary Allowances
(RDAs) for Vitamin D
Age Male Female Pregnancy Lactation
012 months*400 IU
10 mc400 IU
10 mc
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http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/
113 years 600 IU(15 mcg) 600 IU(15 mcg)
1418 years600 IU
(15 mcg)600 IU
(15 mcg)600 IU
(15 mcg)600 IU
(15 mcg)
1950 years600 IU
(15 mcg)600 IU
(15 mcg)600 IU
(15 mcg)600 IU
(15 mcg)
5170 years600 IU
(15 mcg)600 IU
(15 mcg)
>70 years800 IU
(20 mcg)
800 IU
(20 mcg)
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Tolerable Upper Intake Levels (ULs) for
Vitamin D
Age Male Female PregnancyLactation
1 000 IU 1 000 IU
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(25 mcg)
(25 mcg)
712 months1,500 IU(38 mcg)
1,500 IU(38 mcg)
13 years2,500 IU(63 mcg)
2,500 IU(63 mcg)
48 years3,000 IU(75 mcg)
3,000 IU(75 mcg)
9 years4,000 IU
(100 mcg)4,000 IU
(100 mcg)4,000 IU
(100 mcg)4,000 IU
(100 mcg)
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Selected Food Sources of Vitamin DFood
IUs per
serving*
Percent
DV**Cod liver oil, 1 tablespoon 1,360 340
Swordfish, cooked, 3 ounces 566 142
Salmon (sockeye), cooked, 3 ounces 447 112
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http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/
, , ,
Orange juice fortified with vitamin D, 1 cup (check product labels, as amountof added vitamin D varies) 137 34
Milk, nonfat, reduced fat, and whole, vitamin D-fortified, 1 cup 115-124 29-31
Yogurt, fortified with 20% of the DV for vitamin D, 6 ounces (more heavilyfortified yogurts provide more of the DV)
80 20
Margarine, fortified, 1 tablespoon 60 15Sardines, canned in oil, drained, 2 sardines 46 12
Liver, beef, cooked, 3 ounces 42 11
Egg, 1 large (vitamin D is found in yolk) 41 10
Ready-to-eat cereal, fortified with 10% of the DV for vitamin D, 0.75-1 cup
(more heavily fortified cereals might provide more of the DV)
40 10
Cheese, Swiss, 1 ounce 6 2
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Expectations (prognosis)
Improvement can be seen within a few weeks insome people with vitamin deficiency disorders.
months.
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001414/
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Prevention
diet rich in vitamin D get plenty of sunlight
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Paget's disease
AKA: Osteitis deformans is a disorder that involves abnormal bone
,
deformity. there is an abnormal breakdown of bone tissue,
followed by abnormal bone formation. The new
bone is bigger, but weakened and filled with newblood vessels.
/ /i l
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Pagets disease
Sir James Paget first described chronicinflammation of bone as osteitis deformans in
.
Paget disease, as the condition came to beknown,
second most common bone disorder
(after osteoporosis) in elderly persons.
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Pagets Disease (Osteitis Deformans)
Excess of bone destruction & unorganized boneformation and repair.
nd . .
etiology is unknown
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s/s
Usually affects the axial skeleton, vertebrae andskull, although the pelvis, tibia, femur are the
.
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Symptoms
Most persons are asymptomatic & diagnosis isincidental.
Old Hat dont fit an more!
hat gets tighter head diameter becomes larger
pathologic fractures congestive heart failure hearing loss dysesthesias and weakness due to nerve-root
compression.
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Symptoms
Bone pain (may be severe and persistent) Bowing of the legs and other visible deformities Enlarged head rac ure
Headache Hearing loss Joint pain or stiffness Neck pain Reduced height Skull deformities Warmth of skin over the affected bone
Note: Most patients have no symptoms.
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S/s
Vascularity is increased in affected portions ofthe skeleton. Lesions ma occur in one or more bones does not
spread from bone to bone.
Deformities & bony enlargement often occur. Bowing of the limbs & spinal curvature in persons
with advanced disease.
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S/s
Bone pain- is the most common symptom. usually worse with ambulation or activity but may
also occur at rest. Involved bones may feel spongy & warm because
of increased vascularity. Skull pain is usually accompanied with headache,
warmth, tenderness & enlargement of the head.
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Dx
Bone scan Bone x-ray
instance, N-telopeptide) Elevated serum alkaline phosphatase
This disease may also affect the results of the
following tests:ALP (alkaline phosphatase) isoenzyme
Serum calcium
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Dx
Pathologic fractures- because of the increasedvascularity of the involved bone-bleeding is a
.
Alkaline phosphatase levels- markedly elevatedas the result of osteoblast activity.
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Dx
Serum calcium are normal except withgeneralized disease or immobilization.
of increased bone activity, which causes anincrease in nucleic acid catabolism.
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Dx
Radiograph reveals radiolucent areas in thebone, typical of increased bone resorption.
.
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Management
Not all patients need treatment. For example, patients who have abnormal blood
tests only may not need treatment.
People with Paget's disease who are commonlytreated include:
Patients with deformities Patients with no symptoms when certain bones
(such as weight-bearing bones) are involved,especially if the bony changes are progressingquickly, to reduce the risk of fractures
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Management
Patients with symptoms Bisphosphonates Alendronate (Fosamax) Etidronate (Didronel) Pamidronate (Aredia)
Risedronate (Actonel) Tiludronate (Skelid) Zoledronic acid (Zometa)
Calcitonin Intranasal (Miacalcin) Subcutaneous (Calcimar)
Plicamycin (Mithracin) Analgesics or nonsteroidal anti-inflammatory medications
(NSAIDs)
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Management
Goals of the treatment- to relieve pain & preventfracture & deformities.
osteoclastic activity. Bisphosphonates & calcitoninare effective agents to decrease bone pain & bone
warmth & also relieve neural decompression, jointpain & lytic lesions.
Use of analgesics & NSAIDs. Assistive devices,including cane, walker.
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Management
Deformities may be corrected by surgicalintervention (osteotomy).
.
The patient may benefit from a PT referral. Local application of ice or heat may help
alleviate pain.
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Management
A regular exercise should be maintained;walking is best. Avoid extended periods of
.
A nutritionally adequate diet is recommended.Assistance in learning to use canes or otherambulatory aids.
The Arthritis Foundation & Paget Foundationare useful resources for patients & their families.
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Treatment
Patients with symptoms Drug therapy helps prevent further bone breakdown.Currently, there are several classes of medications used totreat Paget's disease. These include:
Bisphosphonates -- the first-line treatment; help increase bone
density. Calcitonin hormone involved in bone metabolism. Plicamycin (Mithracin) Analgesics or nonsteroidal anti-inflammatory medications
(NSAIDs) - for pain.
Localized Paget's disease needs no treatment, if there areno symptoms and no evidence of active disease.
Orthopedic surgery may be needed to correct a deformityin severe cases.
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Outlook (Prognosis)
Disease activity and symptoms can generally becontrolled with current medications.
cancer of the bone called osteosarcoma. Some patients will need joint replacement
surgery.
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Possible Complications
Bone fractures Deafness
Heart failure Paraplegia
Spinal stenosis
http://orthoinfo.aaos.org/topic.cfm?topic=A00076
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Left, Paget's disease of the spine. The white, patchy appearance of the bone onthis X-ray is characteristic of the dense but disordered bone in this disease.Right, Paget's disease of the pelvis. The bone is thick, wide, and patchy.
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