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Musculoskeletal System

Lydia Booher, MSN, RNNursing Education

O th di & Rh t l i I tit t

DOS CME Course 20111 Oxtober 20101Confidential© Cleveland Clinic 2011

Orthopedic & Rheumatologic Institute

Musculoskeletal System

2 DOS CME Course 2011

URL:www.merckmanuals.com/media/home/figures/MMHE_...

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Overview

Bones

Muscles

Tendons

Ligaments

Joints

Cartilage

Bursae


URL:img.webmd.com/.../achilles_tendon.jpg

Synovial Joint


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Terminology

Articular Structures Nonarticular StructuresJ i t l P i ti l li t• Joint capsule

• Articular cartilage• Synovium• Synovial fluid• Intra-articular ligaments• Juxta- articular bone

• Periarticular ligaments• Tendons• Bursae• Muscle• Fascia• Bone• Nerve• Overlying skiny g

Bickley, 2007


Joint Pain

Localized or widespreadp

Acute or chronic

Inflammatory or noninflammatory

Articular or nonarticular

Joint pain with systemic features


URL:medicalworld.in/.../2010/02/joint-pain.jpg

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Joint Pain Nonarticular•Myalgia

•Arthralgia•Tenosynovitis

•Sprains

•Trauma•Nongonococcal

A h i iLocalized

Diffuse

Monoarticular

Polyarticular

Arthritis•Tendinitis•Bursitis

Migratory Pattern

•Rheumatic Fever•Gonoccocal Arthritis

Systemic

Polyarticular

Progressive AdditivePattern

•Rheumatoid Arthritis


Digging Deeper

Timing - Rapid or slow onset, constant or intermittent

Predisposing Factors – Trauma or overuse of body part

Quality – Sharp, dull, throbbing or aching pain

Aggravating Factors – Movement or exercise

Relieving Factors – Rest, heat or cold


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History & Physical – H&P

History:

Chief complaintp

Past medical history

Social History

Physical:

Inspection Inspection

Palpation

Range of motion


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Articular Origin Nonarticular Origin

Assessment

Pain

Swelling

Loss of active &passive motion

“Locking” deformity

Tenderness outsidethe joint

Loss of active but not passive motion

No locking deformity Locking deformityg y


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Case Study

Mr. Jackson is a 30 year old male who presents with pain and swelling to his right ankle. He slipped and fell while jogging this morning.

On examination there is moderate swelling to the ankleOn examination, there is moderate swelling to the ankle, ecchymotic, tender to touch, unable to bear weight with limited range of motion.

What are the questions we need to ask?


Every Life Deserves World Class CareEvery Life Deserves World Class Care

DOS CME Course 201112

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Osteoarthritis-OA

Pathophysiology:

Cartilage degeneration

Thickening of subchondral boneg

Formation of osteophytes

Cause:

No single cause

Idiopathic or Secondary

Risk Factors:

Age, Sex hormones, Genetic

Modifiable - ↑ weight, ↓ activity


URL:www.runningbarefootisbad.com/wp-content/uploa

OA- Clinical Manifestations

Joint Pain - 1° SymptomLocalized, asymmetricalIncreases with useIncreases with use

Stiffness - GellingImproves with activity, <30 minsMay have crepitus, effusion

Joint DeformityyHeberdens, BouchardsLeg deformities


Mosby, 2008

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Diagnosis

H & P – Most often sufficient to diagnose OAto diagnose OA

Labs – CBC Renal & Liver panelRF & ESR

X-Ray - Osteophytes, narrowing joint space g j p

MRI


URL:img.medscape.com/.../336139-392096-3991.jpg

OA - Management

Exercise – Walking, swimming, water aerobics, Yoga

Activity Modification – Periods of activity followed by rest

Weight Reduction

Heat & Cold

Pharmacologic – Acetaminophen recommendedNSAIDS – SalicylatesCOX-2 InhibitorsIntra-articular Corticosteroids

Surgical - Osteotomy, Arthrodesis, Arthroplasty

.


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Case Study

Mr. Jones is a 70 year old male who presents with complains of pain

to both knees for 2 years. The pain is worse on the right knee compared to the left. His knees are stiff for 15-20 minutes when he wakes up in the morning He has difficulty walking for long periods ofwakes up in the morning. He has difficulty walking for long periods of time and has to rest frequently.

Mr. Jones is 6 feet tall and weighs 250 lbs. He is a retired teacher and lives alone.

On examination, there is no evidence of effusion, crepitus present.

What are the questions we need to ask?


f ld lEvery Life Deserves World Class Care


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Septic Arthritis

Pathophysiology

Inflammation of joints secondary to infection

Gonococcal or nongonococcal

Infection can spread through

Direct inoculation

Infected periarticular tissue

Bloodstream


URL:eso-cdn.bestpractice.bmj.com/best-practice/im...

Septic Arthritis - Causes

Pyogenic bacteria: Staphylococci, Streptococci Trauma Prosthetic joints – Intraoperative contamination

Bacteremia Osteomyelitis Cellulitis Abscess Tenosynovitis


Septic Bursitis Miscellaneous – Fungal, Viral

URL:i.ehow.co.uk/images/a05/94/q6/infectious-arth...

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Joint PainLocalized, asymmetrical, rapid onsetExtremely painful Tender to touch

Clinical Manifestations

Extremely painful, Tender to touch

Range of Motion

Active & passive ROM

Redness, warmth, swelling

Effusion – Usually large


Fever- Low grade - <102

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Septic Arthritis - History

Present History – Rapid onset, Constant pain, pain with activityUsually monoarticular

Past medical – Sexually Transmitted DiseaseLyme diseaseRheumatoid arthritisIntraarticular joint injectionsImmunosuppressive drugsDiabetes mellitus, Chronic renal failure

Social History – IV drug use, alcohol abuse


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Diagnosis

Synovial Fluid CultureGram stainAerobic & anaerobic Cell countCell count

LabsESRCRPWBC

X-Ray

MRIMRI

Zeller, J et al. (2007). Septic Arthritis. The Journal of the American medical association, 297 (13), 1510


Septic Arthritis - Treatment

Administration of appropriate antibiotic

Aspiration of purulent synovial fluid Aspiration of purulent synovial fluid

Arthroscopic irrigation & debridement

Prosthetic infections – Removal of hardware

Antibiotic therapy x 6 weeksPlace new hardware


URL:us.123rf.com/400wm/400/400/shaday365/shaday36

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Case Study

Mrs. Smith is a 55 year old female who presents with left knee pain, swelling and fever for 2 days.

PMH:

Ri ht T t l k l t (TKA) i 2008Right Total knee replacement (TKA) in 2008.

Right knee infection in 2009, underwent hardware removal, insertion of antibiotic spacer, followed by Revision of Right TKA 3 months later.

In 2010, Patient underwent another Revision of Rt. TKA. Positive for MRSA.

Physical Exam:

On examination, left knee was erythamatous, edematous & warm to touch

What are the next steps?


Every Life Deserves World Class Care


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Back Pain


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Overview of the Spine

Vertebrae & Intervertebral discs Vertebrae & Intervertebral discs

Ligaments between:Anterior & posterior vertebraeSpinous processes lamina of two adjacent vertebrae

Muscles: Large superficialDeep intrinsicpAbdominal

.


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Bony Structures of the vertebra


Mosby, 2008

Low Back Pain- LBP

2nd most common patient complaint in the outpatient settingthe outpatient setting

Occupational risk factor – Prolonged sittingLiftingBendingTwistingReaching

Common cause of disability – Especiallyl th 45 ldamong nurses less than 45 yrs old


URL:www.pyroenergen.com/articles08/images/lumbago.jpg

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LBP - Pathophysiology

Spine-Bony structures, joints & ligaments


URL:www.hughston.com/hha/b_12_1_1a.jpg

LBP - Causes

Ligamentous-Muscular Injuryg j y- Muscle Strain

Degeneration of Spine - OA

Herniated disc

Spinal Stenosis

Spondylolisthesis Spondylolisthesis

Fractures


URL:www.popovic.com.au/imgs/disc-problems.jpg

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Terminology

Muscle Strain – Overstretched musclePain, swelling, muscle spasms, limited ability tomove affected muscles

Disc Degeneration – Mechanical low back painAggravated by activity Relieved by rest

Disc Herniation – Nerve root irritation & compression“Sciatica’’, Paresthesia,

Spinal Stenosis – Narrowing of the spinal canalSpinal Stenosis – Narrowing of the spinal canal

Pressure on spinal cord – pain, numbness or weakness

Spondylolisthesis – Forward slippage of vertebra - Step-offs


Assessment - LBP

History Chi f l i t Chief complaint Present illness Past medical history Family history Occupational history Social history


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Clinical Manifestations

PainOnset Quality Severity- Onset, Quality, Severity,

Consistency, Location, Timing

Aggravating & Alleviating factors

Associated Symptoms- Bowel or bladder problems- Numbness & Tingling


URL:www.severelowerbackpain.net/wp-content/upload

Assessment

Inspection Observe gait

Curvature of spine

Palpation Spinous processes Sacroiliac joint Sciatic notch Paraspinal musculature

Range of Motion L t l b d Lateral bends Back extension Toe touch


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Assessment

Straight leg raiseg g Place patient in supine position Raise leg until pain occurs Dorsiflex the foot

Pain

Radiculopathy due tolumbosacral disc herniation

Mosby, 2008


Assessment

Nordin & Anderson, 1997


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Diagnosis

H & P - <50 yrs old

X-Ray to rule outy- Malignancy- Compression fracture- Ankylosing spondylitis- Chronic osteomyelitis

MRI- To pinpoint source- To pinpoint source

of radiculopathy


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Management

Acute Low Back Pain Measures to decrease inflammation

Analgesics – TylenolNSAIDS - COX-2 InhibitorsNSAIDS COX 2 InhibitorsMuscle relaxant – Flexeril, zanaflex

Bed Rest – Short term

Heat & Cold

Exercises – AerobicsAbdominal strengthening

Physical Therapy –

Reconditioning Exercises

Walking

Acupuncture


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Management

Surgical Interventions

Laminectomy

Spinal Fusion

Microdiskectomy


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Case Study

Mr. Ray is a 40 year old male who presents with left sided low back pain which radiates to his left leg and foot for 2 weeks. He fell few months back and did not have major problems at that time.

He tried heat and cold applications, and over the counter analgesics for pain and did not have any relief.

What are the questions we will ask him to arrive at a diagnosis?

Type of occupation?

?

??


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References

• Bickley, L.S. (2007) Bate’s guide to physical examination andy ( ) g p yhistory taking. (9th. Ed). Philadelphia, PA: Lippincott Williams


Accessed through Mosby’s Nursing Consult

Bryant: Acute and Chronic Wounds, 3rd ed.

Buttaro: Primary Care, 3rd ed.

References: Denise Smith-Hauser

y ,

Chavez - Journal for Nurse Practitioners - June-2009; 5(6): Supplemen

Ferri's Clinical Advisor. 2011, 1st ed.

Goldman: Cecil Medicine, 23rd ed.

Habif: Clinical Dermatology, 5th ed

Journal for Nurse Practitioners. Volume 5 • Number 6 Suppl 1 • June, 2009.


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Accessed through Mosby’s Nursing Consult

Knudston - Journal for Nurse Practitioners - June-2009; 5(6): Supplement

References: Denise Smith-Hauser

Meiner: Gerontologic Nursing, 4th ed.

Moser & Riegel: Cardiac Nursing, 1st ed

National Osteoporosis Foundation (NOF)

Salvarani C - Lancet - 01-JAN-2008; 372(9634): 234-245

Swearingen: Manual of Medical-Surgical Nursing Care, 6th ed.

Thompson: Mosby's Clinical Nursing, 5th ed.




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Giant Cell ArteritisGiant Cell Arteritis

DOS CME Course 201147 Oxtober 201047Confidential

Denise Smith-Hauser, NP-CDepartment of RheumatologyOrthopedic and Rheumatologic Institute

© Cleveland Clinic 2011

• Referred to as temporal arteritis or cranial arteritis

• Giant cell arteritis (GCA) is a segmental systemic granulomatous arteritis affecting medium and large

t i

Giant Cell Arteritis (GCA)

arteries

• Inflammation of lining of artery

• primarily targets extracranial blood vessels, and although the carotid system is usually affected, pathology in the posterior cerebral artery has been reported

• 15% of cases involves the aorta and branches of aortic arch


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• Age 60-80

• 200 cases per 100,000 persons

• US 52 per 100,000 persons > 50 yrs – increases with age

GCA Epidemiology & Demographics

p , p y g

• Prevalence is @ 0.5 – 0.7% US

• Internationally – Scandinavian – highest rates

• Female> Male (twofold to fourfold)


• GCA can present with the following clinical manifestations:– Headache (often associated with marked scalp tenderness)

– Constitutional symptoms (fever weight loss anorexia fatigue)

GCA Clinical Presentation

Constitutional symptoms (fever, weight loss, anorexia, fatigue)

– Polymyalgia syndrome PMR (aching and stiffness of the trunk and proximal muscle groups)

– Visual disturbances (transient or permanent monocular visual loss)

– Intermittent claudication of jaw and tongue on mastication


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• Vascular examination:– tenderness, decreased pulsation, and nodulation of temporal

t i

GCA Physical findings

arteries

– diminished or absent pulses in upper extremities


GCA Tongue Claudication


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• Clinical history and vascular examination are cornerstones of diagnosis.

• Age of onset >50 yr

GCA Diagnosis

• New-onset or new type of headache

• Temporal artery tenderness or decreased pulsation

• Erythrocyte sedimentation rate (ESR) elevated (typically >50 mm/hr)

• Jaw claudication• Jaw claudication


• Temporal artery biopsy with vasculitis and mononuclear cell infiltrate or granulomatous changes

• Skipped nature of the pathologic inflammatory lesions in th l ll 20 t 30% f bi

GCA Diagnosis

the vessel wall, as many as 20 to 30% of biopsy specimens may be normal despite an overwhelming diagnostic likelihood of GCA

• Outpatient biopsy should be performed on the symptomatic side of the head– preferably including inflamed areas with tenderness or nodularity

and

– incorporating 2 to 3 cm of vessel.

– Multiple sections should be requested because of the segmental nature of the disease process.


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• Other vasculitic syndromes

• Nonarteritic anterior ischemic optic neuropathy (AION)

• Primary amyloidosis

GCA Differential Diagnosis

y y

• TIA/CVA

• Infection

• Occult neoplasm, multiple myeloma


• ESR elevated– up to 22.5% patients with GCA have normal ESR before treatment

• C-reactive protein

GCA Diagnostic Testing

– may have greater sensitivity than ESR

• Mild to moderate anemia– normochromic normocytic


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• Reliability of color duplex US of temporal artery is controversial because it is believed to not improve diagnostic accuracy over careful physical examination.

Fl i i f hth l i l b

GCA Diagnostic Studies

• Fluorescein angiogram of ophthalmic vessels may be warranted to differentiate between arteritic AION (i.e., GCA) and nonarteritic AION

• MRI/angiography

• PET


• IV methylprednisolone (250 to 1000 mg qd for 3 to 5 days)– indicated in those with significant clinical manifestations (e.g.,

visual loss)

GCA Treatment-Acute General RX

)

• Oral prednisone (1 mg/kg/day)– High-dose oral regimen should be continued at least until

symptoms resolve and ESR returns to normal

– Prednisone treatment may last up to 2 yr and is tapered over several weeks to months

– Other immunosuppressive agents may be used when steroids are pp g ycontraindicated.

– GCA highly responsive to prednisone

– that an immediate and dramatic improvement in GCA symptoms within 1 to 3 days after steroid institution supports the diagnosis


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• If steroid therapy is initiated early, GCA has excellent prognosis

• once there is visual loss, improvement is dismal

GCA Prognosis

• In one study only 4% of eyes improved in both visual acuity and central visual field

• Taper steroids by 5-10 mg q 7-10 days


• Surgical referral for biopsy of temporal artery

• Ophthalmology referral in patients with visual disturbances and after initiation of corticosteroid th

GCA Referral

therapy

• Rheumatology referral for patients in whom steroids are contraindicated


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• The diagnostic utility of temporal artery biopsy is not compromised if performed within days of starting steroid therapy.

Th l ti b t l l i h ti d GCA i

GCA Considerations

• The relation between polymyalgia rheumatica and GCA is unclear, but the two frequently coexist

• Clinical picture rather than ESR should be the prime yardstick for continuing prednisone therapy

• A rising ESR in a clinically asymptomatic patient with normal hematocrit should raise suspicion for alternatenormal hematocrit should raise suspicion for alternate explanations (e.g., infections, neoplasm)


• GCA is associated with a markedly increased risk for the development of aortic aneurysm, which is often a late complication and may cause death.

A l h t di h i h i CGA ti t h

GCA Considerations

• Annual chest radiograph in chronic CGA patients has been suggested, as well as emergent chest CT or MRI for clinical suspicion


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75 y/o pleasant WF presents with following:

Stiffness to upper back radiating around neck and worse in temporal arteries

GCA Case Study

ROS:

HA at nighttime only – better during day

No fevers/vision changes/no other joint pains

Jaw/tongue pain with eating

Osteoporosis x 2 years

Hyperlipidemia x 2 years

FH:

Cardiac/Cancer


VS: B/P: 100/62, HR: 84, T: 99.1, weight: 117 lb

MEDS: Flexeril 5 mg qhs

Actonel 35 mg qwk

GCA: Case Study

Calcium carbonate 400 mg chewable qd

MVI qd

PE:

A&O x3, Heart: RRR, Lungs: CTA, M/S: no, synovitis, mild discomfort to R) shoulder


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LABS:

WSR 58 (0-30)

CRP (25.1) (1-1.0)

GCA Case Study

CBC: Anemia

CMP: wnl

Diagnosis: ???


Diagnosis:

GCA

Treatment:

GCA

-consult to vascular for TAB (confirmed GCA)

-begin prednisone 60 mg daily

-calcium/vit D (check vit d level)

-f/u in 1 wk

Follow up: -feels much better

Labs: 1 wk: CRP 2.6, 3 wk: 1.5

WSR: 34, 3 wk 5


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OsteoporosisOsteoporosis

DOS CME Course 201170 Oxtober 201070Confidential

Denise Smith-Hauser, NP-CDepartment of RheumatologyOrthopedic and Rheumatologic Institute

© Cleveland Clinic 2011

36

• Osteoporosis is characterized by increased bone fragility and increased susceptibility to fracture

• This increased bone fragility results from decreases in b d d t i ti f b i hit t

Osteoporosis

bone mass and deterioration of bone microarchitecture that occur as the result of estrogen deficiency and aging

• Osteoporotic fractures are more common than heart attack, stroke, or cancer

• In 2005, osteoporosis was responsible for an estimated two million fractures and $19 billion in coststwo million fractures and $19 billion in costs

• By 2025, experts predict that osteoporosis will be responsible for approximately three million fractures and $25.3 billion in costs each year


• @ 10 million Americans have the disease.

• @ 34 million are at risk.

• Estimates suggest that about half of all women older than

Osteoporosis

gg50 will break a bone

• Up to one in four men will break a bone

• Defined by World Health Organization (WHO), as a bone mineral density (BMD) of 2.5 SD or less below the young normal mean (i.e., T-score ≤-2.5)


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• Bone provides a supportive and protective framework for the body.

• Bone serves as a large calcium reservoir

Osteoporosis Pathophyiology

– Calcium is necessary for proper neural, M/S & cardiac function

• Bone remodeling has two main phases: bone resorption and bone formation

• Normal bone remodeling allows both access to the calcium reservoir and replacement and repair of old and damaged bonedamaged bone

• Peak bone mass occurs between the ages of 18-25– Critical years of bone building teens-early/mid 20’s


• Bone resorption (Osteoclasts)– releases calcium into the circulation

– removal of damaged or old bone

– cells derived from macrophages and monocytes

Osteoporosis Pathophyiology

cells derived from macrophages and monocytes

– process is rapid and occurs in a matter of days to weeks

– Osteoblasts in response to parathyroid hormone (PTH) and other cytokines, secrete RANK ligand (receptor activator of nuclear factor kappa beta) and mCSF (monocyte-colony stimulating factor), which cause monocytes and macrophages to differentiate into osteoclasts and proliferate

Osteoclasts produce powerful degradative enzymes such as– Osteoclasts produce powerful degradative enzymes, such as cathepsin K, to break down bone, releasing calcium, phosphorus, and type I collagen crosslinked products into the circulation


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• Bone formation (Osteoblasts)– lay down osteoid, an organic matrix composed of type I collagen

and other proteins

– Bone formation, occurring over months, is a slow process.

Osteoporosis Pathophysiology (con’t)

, g , p

– It is estimated that the skeleton is completely replaced over approximately 4 years

– responsible for mineralizing the bone, depositing calcium and phosphorus into the osteoid.

–This process depends on the presence of adequate amounts of calcium and phosphorus and alkaline phosphatase activity.

Poor bone mineralization leads to osteomalacia a painful– Poor bone mineralization leads to osteomalacia, a painful softening of the bone


• Normally, bone resorption and bone formation proceed at equal rates

• In osteoporosis, however, the rate of bone resorption d th t f b f ti d i t l f

Osteoporosis Pathopysiology (con’t)

exceeds that of bone formation, producing a net loss of bone

• This uncoupling of bone resorption and bone formation is a consequence of estrogen deficiency– most pronounced in the first 5 -10 years after menopause


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Osteoporosis Risk Factors

• UNMODIFIABLE– Advanced age

– Female gender

– Caucasian or Asian raceCaucasian or Asian race

– Personal history of fracture

– History of fracture in a first-degree relative

– Dementia


• MODIFIABLE– Hypogonadism

– Current cigarette smoking

– Excessive alcohol or caffeine use

Osteoporosis Risk Factors (con’t)

Excessive alcohol or caffeine use

– Low calcium intake

– Low body weight (>58 kg [127 pounds])

– Inadequate physical activity

– Visual impairment

– Glucocorticoid or anticonvulsant use

– ThyrotoxicosisThyrotoxicosis

– Recurrent falls

– Poor health or frailty


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• Silent– unless there is a fracture present

– If pain is present – r/o fx

BMD (b i l d it t )

Osteoporosis Clinical Presentation

• BMD (bone mineral densitometry)

• The presence of a typical osteoporotic fracture in a postmenopausal woman is usually sufficient to diagnose osteoporosis

• The typical sites of fractures include the vertebrae/distal wrist/proximal femur/ribsp

• Even with a diagnosed fx, the diagnosis of osteoporosis is often missed and treatment is never initiated

• Consider secondary causes of OP for men/premenopausal women


• Medical history

• Physical examination– “dowager's hump” – OP with fx

Osteoporosis Physical Exam

–T spine kyphotic deformity that occurs with multiple vertebral compression fractures.

– Vertebral compression fractures may also lead to scoliosis and height loss

• Bone density test

• FRAX® scoreFRAX® score

• Laboratory tests


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– CBC and differential

– Serum electrolytes/BUN and creatinine

– LFTs

– Serum calcium with albumin

Osteoporosis Diagnostics Labs

– Serum phosphorus

– 25-Hydroxyvitamin D

– Intact parathyroid hormone

– TSH

– Serum and urine protein electrophoresis

– 24-Hour urine calcium

– 24-Hour urine free cortisol

– Urinary N-telopeptides

– Serum testosterone

– tissue transglutaminase antibody


• IMAGING– Bone densitometry (definitive method for dx OP)

–Dual energy xray absorptiometry of hip & LS (wrist in obese or if cannot use hips ie: THR)

Osteoporosis Diagnostics

p )

– Bone scan

– X-ray

– Vertebral fracture assessments (VFAs)

– CT

– MRI

• Bone biopsy• Bone biopsy


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• WOMEN– 65 years or more

– Postmenopausal age of less than 65 years with risk factors

– Postmenopausal status with a fracture

Osteoporosis Indications for DEXA

– Considering osteoporosis therapy

– Receiving long-term hormone replacement therapy

• MEN– 70 years or more

– Low trauma fractures

– Hypogonadism

Prevalent vertebral deformities– Prevalent vertebral deformities

– Radiographic osteopenia

• BOTH:– Hyperparathyroidism

– Chronic glucocorticoid therapy


• According to NOF recommendations:

• Adults under age 50 need a total of 1,000 milligrams (mg) of calcium from all sources and 400 - 800 i t ti l it (IU) f it i D d il

Osteoporosis Prevention (Calcium)

international units (IU) of vitamin D daily

• Adults age 50 and older need at total of 1,200 mg of calcium from all sources and 800 - 1,000 IU of vitamin D daily


43

• Fat soluble vitamin– D3 (cholecalciferol)

– D2 (ergocalciferol)

Vit i D d d f l i b ti

Osteoporosis Prevention – Vit D

• Vitamin D needed for calcium absorption

• Skin makes vitamin D when exposed to sun – @30,000 IU in 20-30 minutes of exposure

• Foods (1 cup of milk=98 IU)

• Adults under age 50 should get between 400 and 800 g gInternational Units (IU) of vitamin D every day

• >age 50 and older should get between 800 and 1,000 IU of vitamin D every day


• DEXA results =Osteopenia

• Fracture risk assessment- FRAX– tool (uses bone density and other risk factors to estimate 10-year

f t i k ti t d % h f b ki b ithi th

Osteoporosis Treatment Guidelines - FRAX

fracture risk estimate and % chance of breaking a bone within the next 10 years

– Assists with decision making on taking an osteoporosis medicine.


44

Osteoporosis FRAX

Source: www.sheffield.ac.uk/FRAX/


• National Osteoporosis Foundation recommends BMD testing for:– Woman >/= age 65, Men >/=70

– Postmenopausal woman men age 50-70 with risk factors

OP NOF Guidelines When to Tx

Postmenopausal woman, men age 50 70 with risk factors

– Woman or Men whom have experienced a fracture

• Initiate therapy in those with:

• A prior vertebral or hip fx

– BMD T Scores of </= -2.5

– BMD scores between -1.0 and -2.5 with FRAX 10 year probability of hip fracture > 3% and /or osteoporosis related fx > 20

• Individual clinical judgment is important


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• Alendronate– (Generic Alendronate and Fosamax® Oral (tablet) Daily/Weekly

– Alendronate Fosamax Plus D™ (with 2,800 IU or 5,600 IU of Vitamin D3) Oral (tablet) Weekly

OP Tx options: Bisphosphonates

– Alendronate Fosamax® Oral (liquid solution) Weekly

• Ibandronate Boniva– Oral (tablet) Monthly

– Ibandronate Boniva® Intravenous (IV) injection Four Times per Year

• Risedronate Actonel– Oral (tablet) Daily/Weekly/Twice Monthly/MonthlyOral (tablet) Daily/Weekly/Twice Monthly/Monthly

– Risedronate Actonel® with Calcium Oral (tablet) Weekly

• Zoledronic Acid Reclast– Intravenous (IV) infusion One Time per Year/Once every two years


• Calcitonin– Calcitonin Fortical® Nasal spray Daily

– Calcitonin Miacalcin® Nasal spray Daily

– Calcitonin Miacalcin® Injection

OP Tx options: (con’t)

Calcitonin Miacalcin® Injection

• Estrogen*– Estrogen Multiple Brands Oral (tablet) Daily

– Estrogen Multiple Brands Transdermal (skin patch) Twice Weekly/Weekly


46

• Estrogen Agonists/Antagonists (Selective Estrogen Receptor Modulators -SERMs)– Raloxifene Evista® Oral (tablet) Daily

P th id H

OP Tx options: (con’t)

• Parathyroid Hormone– Teriparatide Forteo® Injection Daily

• RANK ligand (RANKL) inhibitor– Denosumab ProliaTM Injection Every 6 Months


• Anabolic Medicines– Forteo

– increase rate of bone formation

A ti ti M di i

Osteoporosis Medicines

• Antiresportive Medicines– Bisphosphonates, calcitonin, denosumab, estrogen and SERMS

–Decrease bone loss


47

• Exercise– Weight bearing long bones

– Severe OP – avoid yoga/pilates/tennis/golf d/t twisting/bending

Di t

Osteoporosis Non Pharmacologic

• Diet– Nutritionally balanced

– Caffeine/alcohol moderation

• -PT– Fall prevention

– Correct body alignments (ie: sneeze – support back)Correct body alignments (ie: sneeze support back)

• Modifiable changes


VS: B/P 114/66, HR 62, Wt: 104 lb (47.174 kg), BMI: 17.8 Ht: 162 cm (5’4”)

11/26/2010 DEXA:

Osteoporosis Case Study: 54 y/o WF

L/S: T-Score -2.8

L) Femoral neck T-sore -2.3

Total hip T score -2.8

PMH:

Stress fx to L) ankle in college – soccer) g

ROS: unremarkable

Meds: Citracal 600 mg daily

Recent: Vit D3 50,000 IU twice weekly x 12 weeks


48

LABS:

Vit D level 12.4 (31-80 ng/mL)

CBC/CMP/TSH/PTH/UA wnl

Osteoporosis Case Study


Risk Factors:

PMP

FH of OP fx (Mother) hip


Hx of Tobacco use

3 cups caffeine/qd

Low body weight <127/lb

Personal hx of stress fx (not fragility)

Low calcium intake (doesn’t like milk, rare yogurt/cheese)

What to do?

FRAX??


49

What to do?

Urine ntx ordered for baseline and to monitor tx

DX: Osteoporosis (based on DEXA)


p ( )

Increase calcium to 600 mg bid

Con’t with vit D – recheck vit d level after tx and adjust dose accordingly

Begin bisphosphonate tx

? Other options: HRT/SERMS

?Forteo/Prolia

Exercise/Monitor caffeine intake



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