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Musculoskeletal System
Presenter: Denise Smith-Hauser, NP-C
Department of Rheumatology
Orthopedic and Rheumatologic Institute
DOS CNE Course 20111 Oxtober 20101Confidential© Cleveland Clinic 2011
p g
Presentation by: Lydia Booher MSN, RN
Clinical Nurse SpecialistNursing Education
Orthopedic & Rheumatology Institute
Musculoskeletal System
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Overview
Bones –skeletal framework,
blood cell formation, osteoblasts, osteoclasts
Muscles- skeletal, cardiac
and smooth
Tendons- muscles to bone
Ligaments- bone to bone
Joints- synovial, cartilagionous, skull
Cartilage- hyaline(joints), elastic (outer ear), fibrocartilage (intervertebral discs)
Bursae- synovial sacs
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Synovial Joint
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Joint Pain
Localized or widespreadp
Acute or chronic
Inflammatory or noninflammatory
Articular or nonarticular
Joint pain with systemic features
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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
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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 (ACL)• Juxta- articular bone
• Periarticular ligaments• Tendons• Bursae• Muscle• Fascia• Bone• Nerve• Overlying skiny g
Bickley, 2007
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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, meds
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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
30 y/o WM presents with pain and swelling to R) ankle30 y/o WM presents with pain and swelling to R) ankle
Slipped and fell while jogging this am
On exam: Moderate swelling, ecchymotic, tender to touch, unable to bear weight with limited ROM
What are the questions we need to ask?
How would we diagnose?
Treatment? RICE: rest/ice/compression/elevation
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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
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OA- Clinical Manifestations
Joint Pain - 1° SymptomLocalized, asymmetricalIncreases with useIncreases with use
Stiffness - GellingMay have crepitus, effusion
Joint DeformityHeberdens, Bouchards,Leg deformities
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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
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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 y/o M
c/o b/l knee pain x 2 years –p y
Hx of HTN
Wt: 250 lbs, Ht: 6’
How to diagnose?
Treatment?
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Septic Arthritis
Pathophysiology
Inflammation of joints secondary to infection
Gonococcal (50% affected can develop) (W>M) or nongonococcal
Infection can spread through:
Direct inoculation –open fx, surgery
Infected periarticular tissue: bursitis/tendonitis Infected periarticular tissue: bursitis/tendonitis
Bloodstream - bacteremia
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Septic Arthritis - Causes
Pyogenic bacteria: Staphylococci, Streptococci Trauma Prosthetic joints – Intraoperative contamination
Bacteremia Osteomyelitis Cellulitis Abscess Tenosynovitis
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Septic Bursitis Miscellaneous – Fungal, Viral
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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
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Fever- Low grade - <102
Septic Arthritis - History
Present History – Rapid onset, Constant pain, pain with activityUsually monoarticular (80% of time)
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
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Septic Arthritis - Treatment
Administration of appropriate antibiotic-started after
specimen sent to labspecimen sent to lab
Aspiration of purulent synovial fluid
Arthroscopic irrigation & debridement
Prosthetic infections – Removal of hardware
Antibiotic therapy x 6 weeks
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Place new hardware
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Case Study
55 y/o AAF presents with c/o fever, malaise, L) knee pain and swelling x 2 days
Wt: 297 Ht: 5’4” Hx of HTN, DM 2
Underwent a TKR 3 months prior
Exam: L) knee erythematous, edematous, warm. T: 101.4
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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
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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
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LBP - Pathophysiology
Spine-Bony structures, joints & ligaments
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LBP - Causes
Ligamentous-Muscular Injuryg j y- Muscle Strain
Degeneration of Spine - OA
Herniated disc
Spinal Stenosis
Spondylolisthesis Spondylolisthesis
Fractures
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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 -
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Assessment - LBP
History Chi f l i t Chief complaint Present illness Past medical history Family history Occupational history Social history
Bending
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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
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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 herniation90% L4, L5, S1
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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
Compression fracture
- To pinpoint source of radiculopathy
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Management
Acute Low Back PainMeasures to decrease inflammation
Analgesics – TylenolNSAIDS - COX-2 InhibitorsNSAIDS COX 2 InhibitorsMuscle relaxant –
Bed Rest – Short term 2-3 days
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
Jane is a 40 y/o WF whom works as an RN
She presents today with c/o LBP – R) sidedp y )
Lifted a pt this morning and states she felt pain following
What to do?
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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
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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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DOS CNE Course 201147
OsteoporosisOsteoporosis
DOS CNE Course 201148 Oxtober 201048Confidential
Denise Smith-Hauser, NP-CDepartment of RheumatologyOrthopedic and Rheumatologic Institute
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• 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
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• @ 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
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• 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
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• 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
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• 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
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• 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
– Urinary N-telopeptides
– Serum testosterone
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• 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
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• 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
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• 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
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• 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.
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Osteoporosis FRAX
Source: www.sheffield.ac.uk/FRAX/
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• 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
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• 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
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• 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
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• 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
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• 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
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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
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LABS:
Vit D level 12.4 (31-80 ng/mL)
CBC/CMP/TSH/PTH/UA wnl
Osteoporosis Case Study
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Risk Factors:
PMP
FH of OP fx (Mother) hip
Osteoporosis Case Study
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??
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What to do?
Urine ntx ordered for baseline and to monitor tx
DX: Osteoporosis (based on DEXA)
Osteoporosis Case Study
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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Giant Cell ArteritisGiant Cell Arteritis
DOS CME Course 201176 Oxtober 201076Confidential
Denise Smith-Hauser, NP-CDepartment of RheumatologyOrthopedic and Rheumatologic Institute
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• 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
• Internationally – Scandinavian – highest rates
• Female> Male (twofold to fourfold)
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• 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
– 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
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GCA Tongue Claudication
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GCA Physical findings
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GCA Physical findings
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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
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• 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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• 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
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• 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
• Taper steroids by 5-10 mg q 7-10 days
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• 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)
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• 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
DOS CME Course 20119191 DOS CNE Course 2011
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
DOS CME Course 20119292 DOS CNE Course 2011
47
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.
Temporal artery palpation tenderness with scalp tendernessTemporal artery palpation tenderness with scalp tenderness
DOS CME Course 20119393 DOS CNE Course 2011
LABS:
WSR 58 (0-30)
CRP (25.1) (1-1.0)
GCA Case Study
CBC: Anemia
CMP: wnl
Diagnosis: ???
DOS CME Course 20119494 DOS CNE Course 2011
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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
DOS CME Course 20119595 DOS CNE Course 2011
DOS CNE Course 201196