Skeletal Diseases Flashcards
Osgood-Schlatter
Inflammation of the patellar tendon corresponding small subacute avulsion fractures of the tibial tuberosity due to repetitive use of the quads and knee
Onset: Late childhood or adolescence; more common in males
Pain last into evening after activity subsides
Diagnosis: clinical or X-ray
Treatment: self limiting and resolves with maturity, use rest, less activity, knee imobilizer, isometric and flexibility exercises, Rarely surgery
Osteoarthritis
Etiology: mechanical-joint wear and tear destroys articular cartilage (asymetric joint narrowing)
pathogenesis: progressive breakdown of articular cartilage with remodeling of subchondral bone
Joint Findings: Subchondral cysts, sclerosis, osteophytes (bone spurs)
Eburnation (polished, ivory appearance of bone), Heberden nodes (DIP), and bouchard nodes (PIP). NO MCP involvement
Predisposing factors: age, obesity, joint deformity, trauma
Clinical features:
Boney hypertrophy, crepitance, reduced range of motion, hammertoe
Classic Presentation: slow onset, Pain in weight bearing joints after use, improving with rest, knee cartilage loss beings medially (bowlegged), short morning stiffness, limb and axial distribution
Noninflammatory
No systemic symptoms
Treatment: NSAIDS, intraarticular glucocorticoids, heat, short acting narcotics, SSRI, GABA inhibitor, Tricyclic anitdepressant, long acting narcotics Activity modification and weight loss Joint stabilization (strengthening, orthoticcs, bracing, heel wedge), increase flexibility supportive muscles-ligaments Surgery-total joint arthroplasty>arthroscopy
NO cartilage stabilizing disease modifying agent
Rheumatoid arthritis
Etiology: Autoimmune-inflammatory destruction of synovial joints. Mediated by IgM against Fc portion of own IgG (rheumatoid factor)-activates complement
Type III and IV hypersensitivity reactions
Joint findings: pannus formation in joins (MCP, PIP)
Subcutaneous rheumatoid nodules (fibrinoid necrosis), ulnar deviation of fingers, subluxation
Baker cyst in poplitieal fossa
No DIP involvement
Pencil-in-cup deformity
Predisposing factors: females>males
80% are positive for rheumatoid factor
Anti-cyclic citrullinated peptide Ab is more specific
Strong association with HLA-DR4
Ethinicity: greatest in Northern European ancestry
Age of onset 20-60 can follow giving birth
More common in smokers
Classic presentation: Morning stiffness lasting > 30 mins
and improving with use, symmetric joint narrowing, systemic symptoms (fever, fatigue, pleuritis, pericarditis), soft tissue swelling (periarticular), osteopersosis (decreased bone density periarticular)
Develop secondary osteoarthritis
Treatment: NSAIDS, glucocorticoids, disease modifying agents (methotrexate, sulfasalazine, TNF-alpha inhibitors
Adaptive shoes and othotics, splints bracing and heel wedge
pacing, prioritizatin, positioning, incremental goal setting
Avascular necrosis injuries
Scaphoid, Talus, Femoral neck (most common-medial circumflex), Navicular
ischemic necrosis of bone and bone marrow
Infarcts can be subchondral or intramedullary
Causes include: trauma or fracture, steroids, sickle cell anemia, caisson disease (gas emboli), lupus, high dose corticosteroids, alcoholism
Osteoarthritis and fracture are major complications
usually very painful
Gout
Uric acid buildup
Diagnosis: arthrocentesis of single painful swollen joint
Needle shaped, negatively birefringent monsodium urate crystals (yellow under polarized light)
Due to:
Underexcretion of Uric acid (90%): idiopathic or thiazide diuretics
Overproduction of uric acid (10%): Lesch-Nyhan syndrome, PRPP excess, increased cell turnover (tumor lysis syndrome), Von Gierkes disease
Triggered by dehydration, diuretics, joint trauma, large meal, alcohol intake (alcohol metabolites share same excretion site in kidney as uric acid)
Presents with single acutely swollen joint (great toe)
max inflammation in 1 day (neutrophil response)
Redness over joint-MTP and tarsus most common
tophi (ear, olecranon bursa, or Achilles’ tendon)
Serum uric acid>7
Synovial fluid culture=negative
Asymptomatic hyperurecmia to acute intermittent gout to chronic tophaceous gout
WBC=20,000 to 50,000
Treatment: NSAIDs (acute), glucocorticoids (elderly), Colichine, febuxostat (peptic ulcer disease or other CI)
Pseudo-gout
Calcium pyrophosphate buildup
Intra-PMN (neutrophils), romboidal shaped, postiviely bi-refringent
Clinical features:
Acute joint swelling especially in knees>wrists>shoulder>elbow
Triggered by joint trauma, acute medical illness or surgery
Occasionally associated with hyperparathryoidism (increase of calcium), hypoparathyroidism and hemochromatosis
Calcification of cartilage on X-ray Intracellular CPPD in joint fluid during attack Synovial fluid culture=negative \+ bifrngent Crystals are blue when parallel to light
Treatment: NSAIDS (acute), steroids and colcichine
WBC= 20,000 to 50,000
Systemic Lupus Erythematosis
Acute onset, chronic, remitting and relapsing Injury to skin, joints kidney and serosal membranes
Affects childbearing-age African American and Hispanic women most (sex hormones associated)
Failure of mechanisms that maintain self tolerance
Antinuclear antibodies DNA (sensitive), anti-histones (drug induced), nonhistone proteins bound to RNA, nucleolar Ags Abs to dsDNA (specific) and smith Ag (snRNPs), anti cardiolipin (syphilis FP) are diagnostic
May have false positive for syphillis due to cardiolipin Ag produced
Have hypercoagulability state despite slow PTT test
HLA-DQ gene linked to production of anti-dsDNA, anti smith antigen and anti phospholipid Abs
Inherited defienciencies of C1q, C2, or C4 associated with lupus-defective clearance of apoptotic cells
SLE also has hypocomplimentemia of C3, C4 and CH50
Exposure to Uv light exacerbates the disease-induces apoptosis, changes DNA to be immunogenic, or stimulating keratinocytes to produce Il-1
Hydralazine, isoniazid and procainamide associated with drug induced lupus (antihistone Ab)
Failure of self tolerance of B cells
Clinical: fever, weight loss, fatigue, raynaud phenomenon, Butterfly rash upon sunlight exposure, anemia (type II hypersensitivity)
Painless oral or nasopharyngeal ulcers Arthritis (>2 joints) Serotitis (pleuritis and pericarditis) Psychosis and seizures Renal damage (glomerulonephritis) Anemia, thrombocytopenia, or leukopenia (type II hypersensitivy)
Sterile deposits on both sides of mitral valve (lib man sacks valvular endocarditis)-can lead to MI or thrombus
Death: renal failure or accelerated coronary atherosclerosis
Treatment: NSAIDs, immunosuppressants, hydroxychloroquine
Spondyloarthropathritis
Age of onset: teens to 40
Ethinicity: Northern European
Associated with HLA B27-HLA MHC class I
mucosal infection can predispose you to spondyloarthritis
Pathogenesis: Immune response to unknown Ag which cross reacts with native Ag in the synovium or enthesis (tendon or ligament insertion)
IL-23/IL-17 are central to pathogensis
Clinical features (P.E.A.R.) Psoriatic arthritis Enteric arthritis/Irritable bowel syndrome-Crohn's disease Ankylosing Spondylitis Reactive Arthritis
Common features: asymmetric oligoarthritis, enthesitis, dactylitis, sacroiliitis (sclerosis, erosion, narrowin-fusion) spondylitis (vetebral squaring, marginal eroion, vertical bridging osteophytes) and iritis
Treatment: NSAIDS Oral injectable steroids Topical: steroids and retinoids, tar based creams phototherapy (Psoriasis) Sulfasalazine, methotrexate, leflunomide TNF blockers IL-12/23 blocker IL-17 blocker
Psoriatic arthritis
Part of spondyloarthropathies Joint pain and stiffness associated with psoriasis Assymetric and patchy involvment Dactylitis (sausage fingers) Pencil-in-Cup deformity
Psoriasis: Salmon colored plaques with silvery scale
on elbows, knees, gluteal cleft, lumbrosacral area, glans penis, and scalp
Nails have yellow brown discoloration with pitting, thickening or crumbling
Ankylosing spondylitis
Chronic inflammatory disease of spine and sacroiliac joints leading to ankylosis (stiff spine due to fusion of joints)
uveitis and aortic regurgitation
Bamboo spine
3 months
Improves with exercise
Peripheral enthesitsi (tendon inflammation)
Limits chest wall expansion
Morning stiffness and lower back pain
Inflammatory bowel disease
Crohn disease and ulcerative colitis accompanies by ankylosing spondylitis or peripheral arthritis
Reactive arthritis
Classic triad: conjuctivitis, urethritis, Arthritis
Can’t pee, can’t see, can’t climb a tree
Post GI (Shigella, Salmonella, Yersinia, Campylobacter) or Chlamydia infections
Also hyperkeratotic vesicles on palms and soles
Annular dermatitis of glans penis
Sterile joints-large joints affected
Cauda Equina syndrome
Acute loss of function of the nerve roots in the Cauda equina usually due to tumor, trauma, herniated lumbar disk
Patients present with lower extremity weakness and bowel and bladder incontinence
Best assessed by MRI
Neurosurgical or radiation therapy emergency
Red flags: bladder/bowel dysfunction-urinary overflow incontinence Saddle anesthesia: numb where you sit Bilateral sciatica Leg muscle weakness Surgical emergency
Piriformis syndrome
Piriformis compresses or irritates sciatic nerve
Buttock pain radiating down the posterior leg
Overlaps in symptoms with sciatica
Herniated Disk
Red flags:
Pain in back down the leg in the sciatic distribution frequently to the foot and ankle (worse than back pain)
Not compression of sciatic nerve but pressure on L5 or S1 nerve roots
Tingling or weakness in ankle dorsifleors, toe extension
Can increase with coughing, sneezing, valasalva
L1-L3: nerve roots radiates to hip and/or anterior thigh
L4-S1 below the knee
Osteoporosis
Decrease in trabecular bone mass resulting in porous bone with an increased risk for fracture (decreased interconnections)
Peak bone mass is achieved during young adulthood determined by genetics, physical activity, diet and hormonal state
Aging causes decreased replicative activity of progenitor cells, decreased activity of osteoblasts, and decreased physical activity
Menopause causes estrogen deficiency leading to increased IL-1, IL-6, TNF, RANK, RANK-L and osteoclast acitivity
Risk factors: family history, thin body, poor nutrition, Caucasian or Asian, decreased physical activity, aging, estrogen deficiency, smoking, alcohol, corticosteroisd
Clinical: early is asymptomatic
Skeletal integrity declines, fractures with minimal trauma, vetebral compression fractures are most common-hip and wrist fractures major problem, femoral neck fracturse
End stage-marked dorsal kyphosis and bone pain
Diagnosis: plain films provide a very poor assessment
Bone densitometry measurements (DEXA scan)
T score=2.5 SDs below the mean for young normal or fragility fracture regardless of T-score
Osteopenia=-1 to -2.5 SD
Calcium, phosphate, PTH, and alkaline phosphate will be normal-helps distinguish between osteoporosis and osteomalacia
Prevention: adequate calcium and vitamin D in susceptible individuals
avoid hypogonadism, add weight bearing exercise
Treatment: bisphosphonates, PTH, SERMS, calcitonin, denosumab
Osteomalacia and rickets
Inadequate mineralization of osteoid (rickets is prior to closure of growth plates)-increased unmineralized osteoid and widening between osteoid seams
Vitamin D deficiency or resistance is due to inadequate intake, inadequate sunlight exposure, malabsorption, severe liver disease, renal failure or hereditary syndromes
Phosphate deficiency occurs as a result of renal tubular disorders tumor associated osteomalaxia, X-linked hypophosphatemia, or phosphate binders
Vitamin D deficiency leads to decreased absorption of calcium and phosphate by the GI tract-leads to secondary hyperparathyrodism
Elevated PTH levels maintain the serum calcium but the cost is phosphaturia, hypophosphatemia and increased bone reabsorption-low serum phosphate results in inadequate bone mineralization and a decrease in bone density
Clinical: bone pain and pathologic fractures, decreased bone density, increased PTH, increased alkaline phosphatase and hypophosphatemia
Children: bowing of legs, pigeon breast deformity, frontal bossing and rachitic rosary with osteoid deposition, sofetining of skull, indentations of ribs
Diagnosis: Low levels of 25-hydroxyvitamin D or 1, 25 (OH) D
Paget disease of bone
Increased bone turnover
May be preceded by childhood infection of paramyxovirus
Over the age of 55
Localized does not involve the entire skeleton
3 phases
1) osteoclastic (increased RANK and NFkB) 2) mixed osteoblastic/clastic 3) osteoblastic (hypovascular separated by cement lines)
End result is thick, sclerotic bone that fractures easily
Biopsy reveals mosaic pattern of lamellar bone
Axial skelton or proximal femur is involved
Clinical: Many asymptomatic
Causes bone pain and deformity (bowing)
fractures, increased hat size, hearing loss, lion like faces arthritis, excessive bleeding with orthopedic surgery
Complications: osteosarcoma, high output cardiac failure due to formation of AV shunts in bone
Diagnosis: isolated increased alkaline phosphatase, characteristic radologic apperance: mixed lytic/sclerotic lesions, cotton wool appearance, pseudofractures) bone scan to determine extent
Serum Ca2+, phosphorus and PTH are normal
Treatment: bisphosphonates (very effective) calcitonin (less effective)
Osteomyelitis
Infection of marrow and bone that usually occurs in children
Bacteria arises via hematogenous spread
Bacteremia seeds metaphysis in children and open wound bactermia seeds epiphysis in adults
Clinical: bone pain with systemic signs of infection, lytic focus (abscess), surrounded by sclerosis of bone on X-ray
Diagnosis: blood culture
Fracture healing
Need skeletal progenitor cells, ECM matrix scaffolding, Vasculature
Step 1: hematoma (1-7 days): matrix factors are released and inflammation is initiated
Immune cells infiltrate releasing cytokines
FGFs and BMPs increase stem cell, fibroblast, chondrocyte, and osteoblast proliferation and differentiation. FGFs are also angiogenic
Step 2: Callus (soft, 2-5 weeks) stem celsl differentiate into chondrocytes which form cartilage to stabilize the joint (endochondrial bone fomration) moderately stable
Step 3: Callus (hard, 6-12 weeks): osteoclasts absorb the cartialge callus which is converted to woven bone. TGFs, BMPs and IGFs promote osteogenesis Both intramembranous (bone periphery/periosteum) and endochondrial bone formation are involved
Step 4: remodeling (18 wks-years): woven bone becomes lamellar with time and the mature bone is indistinguishable from the surrounding bone
Failure to heal: soft callus breaks down due to too much movement, too much stress on woven bone, inadequate or over stabilization (excessive or too little cartilage formation), interruption of blood supply, bone cell death, malnutrition, smoking (decreased formation, vasoconstriction), diabetes (collagen defects, decreased formation), anti inflmmatories
Knee injury
Presents with acute knee pain and signs of joint instability/injury
Anterior drawer sign (pull forward)-ACL injury
Posterior drawer sign (push in)-PCL injury
Abnormal passive abduction (of leg/foot-varus stretch)-LCL injury
Pain on external rotation-medial meniscus
Pain on internal rotation-lateral meniscus
ACL/PCL refer to tibial attachment
ACL inferior attachment is away from fibula
PCL inferior attachment is same side as fibula
ACL connects lateral femoral condyle to antermodeal tibial head
Prevents anterior motion of tibia with respect to femur
Unhappy triad
common injury in contact sports due to lateral force applied to a planted leg
Damage to ACL, MCL and medial meniscus
HOWEVER lateral meniscus is more commonly injured
Rotator Cuff Muscles/Injury
Primarily innervated by C5-C6
Supraspinatus (Suprascapular nerve)-Abducts arm initially (before the action of deltoid)
Most common rotator cuff injury-impingement trauma between humeral head and acromion
Simulataneous abduction and flexion of the arm at the shoulder can cause inflammation leading to fibrosis
Empty Can test: abduct arm 90 and flex thaem at 30 with thumbs down-90% specific for supraspinatus
Infraspinatus (suprascapular nerve)-laterally rotates arm Pitching injury (pitch an INning)
Teres minor-(axillary nerve)-adducts and laterally rotates arm
Subscapularis (subscapular nerve)-medially rotates and adducts arm
Radial head subluxation
Most common injury in children 1-4
Sharp pull of hand when forearm is pronated and elbow extended
Annular ligament tears from periosteal attachement at radial neck and slides into radiohumeral joint
Children present with arm held close to body with elbow extended and forearm pronated
No distress until attempt to move arm
reduction accomplished by supinating forearm followed by fully flexing the elbow
