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224 Cards in this Set

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what are routine tests of synovial fluid?
WBC count and differential, crystal analysis, mucin clot, culture, Gram stain
How are monosodium urate crystals characterized?
(1) Needle-shaped (monoclinic) crystal
(2) Special polarization shows negative birefringence.
o Crystal is yellow when parallel to the slow ray
How are calcium pyrophosphate crystals characterized?
(1) Monoclinic-like or triclinic (rhomboid) crystals
(2) Special polarization shows positive birefringence.
o Crystal is blue when parallel to the slow ray.
How are mucin clots characterized? what does it evaluate? How are they caused? What is the normal joint fluid composed of? What does poor clot formation mean?
(1) Evaluates joint viscosity
(2) Acid added to synovial clots hyaluronic acid
o Hyaluronic acid is the normal joint lubricant
(3) Poor clot formation reflects decreased hyaluronic acid
o Sign of joint inflammation
How are group I joint disorder classified? What are examples?
noninflammatory

osteoarthritis, neuropathic joint
How are group II joint disorders classified? what are examples?
inflammatory

rheumatoid arthritis, gout
How are group III joint disorders classified? What are examples?
septic

Lyme disease, disseminated gonococcemia
How are group IV joint disorders classified? What are examples?
hemorrhage

trauma, hemophilia A and B
What is arthritis?
pain associated with joint swelling, tenderness, warmth
How is morning stiffness defined? What diseases does it occur in?
1) Pain in the joints that lasts >30 minutes
2) Rheumatoid arthritis (RA)
3) Polymyalgia rheumatica
4) Systemic lupus erythematosus (SLE)
A hot joint could be from what?
septic arthritis
What is joint crepitus? What causes it?
crackling feeling

osteoarthritis
What is another name for Ochronosis? What causes it? What is the disease process? What is the characteristic finding?
1) alkaptonuria
2) autosomal recessive disease caused by deficiency of homogentisic acid oxidase
3) there is accumulation of homogentisic acid (urine turns black when oxidized). Homogentisic acid deposits in the intervertebral disks, causing osteoarthritis and other systemic findings
What is the most common debilitating joint disease? Is it inflammatory/noninflammatory? Does it occur more in men or women? What age?
1) osteoarthritis
2) Noninflammatory joint disease
3) No sex predilection
4) Almost universal >65 years of age
What are secondary causes of osteoarthritis?
(1) Legg-Calvé-Perthes disease (degenerative disease of the hip joint)
(2) Osteochondritis dissecans (blood deprivation in the subchondral bone causes cracks)
(3) Obesity, trauma, neuropathic joint
(4) Meniscus injuries, hemochromatosis
Where are the most common sites of osteoarthritis? What is exception and what forms here?
femoral head, knee, cervical/lumbar vertebrae, hands

Less common sites:
1) Shoulder
2) Elbow
3) Feet with exception of first metatarsophalangeal joint
where bunion forms
What provides elasticity in articular cartilage? What about tensile strength? How are these elements degraded?
1) Proteoglycans that provide elasticity
2) Type II collagen that provides tensile strength
3) Cytokines activate metalloproteinases
What is the pathogenesis of osteoarthritis? What forms at joint margins? Are there cysts? is there ankylosing? What are joint mice?
1) Erosion and clefts in articular cartilage
2) Reactive bone formation at joint margins (osteophytes)
o Causes a slight increase in serum alkaline phosphatase
3) Subchondral cysts
4) Bone eventually rubs on bone.
o Produces dense, sclerotic bone
5) No ankylosis (fusion) of the joint
6) Joint mice
o Fragments of articular cartilage that break free into the joint space
What is the most common complaint in osteoarhritis? Where does hip pain refer to? When does joint stiffness occur? What happens at the hands? Is there pain with passive motion? What occurs at the vertebrae?
1. Pain is the most common complaint from Osteophytes irritating synovial lining; bone rubbing on bone
2) Hip OA may refer pain to the groin
3) Joint stiffness after inactivity
* Waking up in morning
* After sitting
3) Aggravated by activity
4) Hand involvement
a. Enlargement of distal interphalangeal joints (DIPs) called Heberden's nodes (osteophytes)
5) Enlargement of proximal interphalangeal joints (PIPs)
o Called Bouchard's nodes (osteophytes)
6) Pain with passive motion of the joint
* Due to secondary synovitis
7) Vertebral findings
* Degenerative disk disease and compressive neuropathies
Where do Bouchard's nodes occur? What are they?
osteophytes in PIPs of someone with osteoarthritis
What are Heberden's nodes? Where do they occur?
osteophytes at DIP in osteoarthritis
How is osteoarthritis treated?
1) Heat; decrease weight bearing; range of motion exercises
2) Use of a cane
3) Analgesics (NSAIDs, acetaminophen)
4) Viscosupplementation
* Oral chondroitin sulfate, glucosamine
5) Joint replacement
Neuropathic arthropathy is also known as? Is it an inflammatory or non-inflammatory disease? what is lost at the joint?
1) Charcot's joint
2) Noninflammatory joint disease
3) Secondary to a neurologic disease with loss of proprioception and deep sensation leading to recurrent trauma
What are common causes of Charcot's joint? What joint does each disease typically effect?
1. Diabetes mellitus (15%)
* Primarily affects the tarsometatarsal joint

2. Syringomyelia (20-25%) - a cyst or cavity forms within the spinal cord
* Primarily affects the shoulder, elbow, wrist joints

3. Tabes dorsalis (10-20%) - degenerating nerves are in the posterior columns
* Primarily affects the hip, knee, ankle joints
who does RA primarily occur in? What gene is associated with it? What organisms can cause?
1) Occurs more often in women 30 to 50 years of age
2) HLA-DR4 association
3) Epstein-Barr virus, parvovirus, human herpesvirus 6, Mycoplasma
What is the pathogenesis of RA? What type of hypersensitivity? Is there ankylosis?
1) B and T cells are activated leading to damage of synovial cells
2) Synovial cells express an antigen that triggers B cells to produce rheumatoid factor (RF).
3) RF is an IgM autoantibody that has specificity for the Fc portion of IgG.
4) RF and IgG join together to form immunocomplexes (type III hypersensitivity).
5) Immunocomplexes activate the complement system to produce C5a, a chemotactic agent for neutrophils and other leukocytes to enter the joint space.
6) Chronic synovitis and pannus formation eventually occur
7) Pannus is granulation tissue that is formed within the synovial tissue by fibroblasts and inflammatory cells
8) Pannus proliferates and releases cytokines that eventually destroy the articular cartilage leading to fusion of the joint by scar tissue (called ankylosis).
what joints are involved in RA of the hand? Is ulnar deviation B/L or unilateral? Besides the hands what other joints are involved?
symmetric involvement of second/third MCP and PIP joints.

B/L

(a) Knees, cervical spine, hips
(b) Shoulders, elbows
What deformities occur in the hands of someone with RA?
1) Swan neck deformity
(a) Flexion of DIP joint
(b) Extension of PIP joint
2) Boutonnière deformity
(a) Extension of DIP joint
(b) Flexion of PIP joint
What happens to the lungs in RA? to the blood?
1) Chronic pleuritis with effusions, interstitial fibrosis
2) ACD, AIHA, Felty's syndrome (autoimmune neutropenia, splenomegaly)
What happens to the cervical spine in RA? What happens to the wrists
subluxation atlantoaxial joint; cord/vertebral artery compression

carpal tunnel syndrome
where do rheumatoid nodules occur? How do they present? What do they correlate with?
1) Extensor surface of the forearm, lungs
2) Fibrinoid necrosis present in center of nodule
3) Correlates with very high titers of RF
What is Caplan syndrome? What are symptoms?
rheumatoid nodules in lung plus pneumoconiosis.

1) cough and shortness of breath in conjunction with features of rheumatoid arthritis such painful joints and morning stiffness.
2) tender, swollen MCP joints and rheumatoid nodules; auscultation of the chest may reveal diffuse râles that do not disappear on coughing or taking a deep breath.
What happens to the cardiovascular system in Lyme disease? What is a Bakers cyst? What is commonly confused with?
pericarditis, aortitis, vasculitis

popliteal cyst is an outpouching of posterior joint space in knee
1) Sometimes ruptures and dissects into the calf
* Frequently misdiagnosed as deep venous thrombosis
2) Sometimes confused with popliteal artery aneurysm
What are common lab findings in RA? What happens to total protein and C3? What is seen on protein electrophoresis?
1) Positive serum antinuclear antibody (ANA) test (30%)
2) Positive serum RF (70-90%)
3) Normal to increased serum C3
4) Decreased synovial C3
5) Increased serum total protein
a. Due to increase in γ-globulins (IgG) in chronic inflammation
b. Polyclonal gammopathy on serum protein electrophoresis
How is RA treated?
1. Physical therapy emphasizing movement of joints
* Swimming pool exercises are very useful.
2. Initial treatment with NSAIDS
3. Early treatment with disease-modifying drugs
a) Methotrexate (most commonly used agent)
b) Cyclosporine; corticosteroids; hydroxychloroquine; gold compounds
c) Tumor necrosis factor (TNF)-α blockers effective if disease-modifying drugs ineffective
Who does sjogrens commonly occur in? What is attacked?
women

Autoimmune destruction of minor salivary glands and lacrimal glands
What are clinical findings in sjogrens?
1. Rheumatoid arthritis
2. Keratoconjunctivitis sicca
a) Dry eyes described as "sand in my eyes"
b) Due to autoimmune destruction of lacrimal glands
3. Xerostomia or dry mouth
a) Autoimmune destruction of minor salivary glands
4. Dental caries

(Dry mouth dry eyes = sicca)
"Doctor, I can't swallow dry crackers." What's your diagnosis?
sjorgrens

Sjögren's syndrome: dry eyes; dry mouth
What are laboratory findings in sjogrens?
1. Positive serum ANA in most cases
2. Positive serum RF (90%)
3. Anti-SS-A antibodies (Ro; 70-95%)
4. Anti-SS-B antibodies (La; 60-90%)
What is anti-SS-A also known as? what about anti-SS-B?
Ro

La
How is sjogrens treated?
1. Artificial tears
2. Pilocarpine (non-selective muscarinic receptor agonist) or cyclosporine eye drops
3. Cevimeline (cholinergic agent with muscarinic agonist activity
* Used for dry mouth
when does juvenile RA occur? Is it more common in boys or girls? Is RF present?
1. Occurs in children < 16 years of age
2. More common in girls
3. RF is usually absent.
What is Still's disease? How is it characterized? How does it frequently present? It accounts for 20% of cases of what disease?
1. Commonly presents as an "infectious disease"
2. Fever, rash, polyarthritis
3. Generalized lymphadenopathy
4. Neutrophilic leukocytosis
5. JRA
polyarticular arthritis accounts for 40% or JRA cases. How is it characterized?
Disabling arthritis predominates
Pauciarticular JRA accounts for 40% of JRA. how does it present?
1. Arthritis limited to a few joints.
2. Uveitis with the potential for blindness
Who does gouty arthritis occur in?
1 Occurs more often in men > 30 years of age (95%).
2 Uncommon in women before menopause (5%)
What occurs in primary gout? what is cause?
Primary gout arises from inborn errors of metabolism involving purine metabolism.
* Example-deficiency of hypoxanthine-guanine phosphoryltransferase (HGPRT) in Lesch-Nyhan syndrome
What occurs in secondary gout? What is cause?
Secondary causes are more common
1) Underexcretion of uric acid in kidneys (80-90%)
o Examples-lead poisoning; alcoholism; diets rich in red meat, seafood, beer
2) Overproduction of uric acid (increased nucleated cell turnover; 10-20%)
o Examples-treating leukemia; psoriasis
What are clinical conditions associated with gout?
1) Urate nephropathy, renal stones
2) Hypertension, coronary artery disease
3) Lead poisoning
o Produces interstitial nephritis, which interferes with uric acid excretion
What is podagra? what precipitates it?
acute Gout flare-up that most commonly involves the first metatarsophalangeal joint

Often precipitated by dietary indiscretions, illness, exercise, emotional stress
What does uric acid in the joint do?
1) Activate synovial cells, leukocytes, and the complement cascade, the latter releasing C5a, which attracts neutrophils into the joint producing acute inflammation
* Neutrophils also phagocytose uric acid crystals.
What are 2 common sites for an acute gout attack?
number 1 is the first metatarsophalangeal joint

Another common site for acute gout is the extensor tenosynovium on the dorsum of the midfoot
How does an acute gout attack present?
1) Sudden onset of severe pain in the big toe
2) Joint is hot, red, and swollen
3) Fever, tachycardia, and other constitutional signs
What are lab findings in acute gout in both men and women?
1) Hyperuricemia
o (a) Increased serum uric acid > 7 mg/dL in men
o (b) Increased serum uric acid > 6 mg/dL in women
2) Absolute neutrophilic leukocytosis
3) Joint aspiration is confirmatory.
o Negatively birefringent MSU crystals
Does hyperurecemia define gout?
No must confirm with joint aspiration; hyperuricemia does not define gout
What structures form in chronic gout? Why? What cells are crystals seen in? What is end result of crystals?
1) Tophy Due to MSU crystals leaking into the soft tissue around the joint
2) MSU excites a brisk granulomatous reaction in the periarticular tissue.
o Microscopic sections reveal numerous multinucleated giant cells within which are MSU crystals that have negative birefringence.

3 Tophi destroy subjacent bone causing erosive arthritis.
What is non-pharmacologic treatment of gout? with drugs? prevention of acute gout with chronic drug therapy?
1) eliminate high-purine diet; moderation in alcohol intake
2) NSAIDs or colchicine
3) b) Uricosuric agents for underexcretors (e.g., probenecid)
* If 24-hour urine collection of uric acid < 700 mg
c) Allopurinol (xanthine oxidase inhibitor) for overproducers
* If 24-hour urine collection of uric acid > 900 mg
What occurs in Calcium pyrophosphate dihydrate deposition (CPPD) disease?
Deposition of calcium pyrophosphate in cartilage (called chondrocalcinosis)
* Less commonly in tendons, ligaments, synovial tissue, bursa
What predisposes someone to developing CPPD?
1) Hemochromatosis, hemosiderosis
a) Pyrophosphate inhibitor is increased in these diseases.
b) Causes an increase in inorganic pyrophosphate concentration
2) Primary hyperparathyroidism (HPTH)
o Increase in calcium is responsible.
What is the most common variant of CPPD associated with? Who is it most common in? What is the most common joint involved? What happens to the cartilage? What type birefringence is observed?
1) OA Most common in elderly population
* Present in 50% of patients who are 85 years old
2) Degenerative arthritis with symptoms similar to OA
(3) Most common joint involved is the knee.
4) Calcium pyrophosphate crystals deposit in articular cartilage (usually knee).
a) Crystals produce linear deposits in articular cartilage
b) Called chondrocalcinosis when it deposits in articular cartilage
5) Crystals phagocytosed by neutrophils show positive birefringence
How is CPPD treated?
NSAIDs; colchicine; arthroscopic surgery
What are the characteristics of Seronegative spondyloarthropathies (spondyloarthritis)? what joints are involved? More in male or females? What genetic association is present?
1. Rheumatoid factor (RF) negative (meaning of seronegative)
2. Involve the axial skeleton (spondylitis)
3. Individuals HLA-B27 positive
4. Male dominant
5. Sacroiliitis with or without peripheral arthritis
What are the types of sponyloarthritis?
1. Ankylosing spondylitis
2. Reiter's syndrome
3. Psoriasis
4. Enteropathic
* Associated with ulcerative colitis, shigellosis
Where and in who does ankylosing spondylitis occur? How are the vertebral column, cardiovascular system and eyes effected?
1) Initially targets sacroiliac joint in young men
* Bilateral sacroiliitis with morning stiffness
*Eventually involves the vertebral column
2) Fusion of vertebrae ("bamboo spine") causes forward curvature
* Kyphosis interferes with chest wall movement.
* Nonpulmonary restrictive lung disease
3) Schober test evaluates degree of restriction to forward bending.
4) Aortitis with aortic regurgitation
5) Anterior uveitis (20%)
a. Blurry vision
b. Potential for blindness
how is ankylosing spondylitis treated?
1) NSAIDs
2) Disease-modifying agents
o Methotrexate, cyclosporine, corticosteroids
3) TNF-α inhibitors
o Extremely effective in slowing down progression of the disease
What causes Reiters syndrome? What is affected? What is confirmatory sign?
1. Urethritis due to Chlamydia trachomatis (intracellular gram -)
2. Arthritis and Achilles tendon periostitis
* Achilles tendon periostitis is a confirmatory radiologic sign.
3. Conjunctivitis (noninfectious)
How is psoriatic arthritis characterized? What do radiographs show?
1. Sausage-shaped DIP joints (finger or toe)
2. Radiographs show erosive joint disease.
* "Pencil-in-cup" deformity
3. Extensive nail pitting
What is the most common cause of nongonnococcal septic arthritis? How is it treated?
S aureas

Treatment
* Nafcillin + cephalosporin (third generation)
What is the most common cause of septic arthritis in urban populations? Who is it more common in? What is deficient? What happens to skin, tendons, joints? How is it treated?
N gonorrhea
1) More common in young women
o Deficiency of C6-C9 predisposes to dissemination
2) Septic arthritis (knee)
3) Tenosynovitis (wrists and ankles)
4) Dermatitis (pustules on wrists or ankles)
5) Treatment is ceftriaxone.
What causes lyme disease and how is it transmitted? What is the reservior? What occurs at bite site? What occurs in late infection?
1) Transmitted by bite of Ixodes tick; Borrelia burgdorferi (spirochete)
2) White-tailed deer is a reservoir for the organism.
3) Erythema chronicum migrans develops at tick bite site
* Red, expanding lesion with concentric circles ("bull's-eye" lesion)
(3) Pathognomonic lesion of Lyme disease
Late disease
1) Disabling arthritis (usually involves the knee)
2) Bilateral Bell's palsy
3) Myocarditis and pericarditis
How is lyme disease diagnosed and treated?
1) ELISA testing first as screen is highly sensitive
2) Western blot assay for equivocal or positive ELISA test
o High specificity (94-96%)
3) PCR test is also available

Treatment
1) Adults-doxycycline or amoxicillin or erythromycin or ceftriaxone
2) Child-amoxicillin
What is babeosis? How is transmitted? What can disease can also be present? What are the symptoms? How is it treated?
1) Intraerythrocytic protozoal disease due to Babesia microti
2) Secondary infection transmitted by Ixodes
o Often presents concurrently with Lyme disease
3) Fever, headache, hemolytic anemia
4) Diagnosis
(a) Wright- or Giemsa-stained peripheral smear to look for organisms
(b) Serologic testing
5) Treatment
o quinine, clindamycin
Note: have maltese cross and ring forms
What causes Septic arthritis and tendinitis due to cat/dog bite? What are the different types of infections it causes? How long after a bite do symptoms present? How is it treated?
1. Causal agent is Pasteurella multocida.
2. Most common infection secondary to animal injury
3. Types of infection
* (1) Cellulitis (most common)
* (2) Septic arthritis/tendinitis
* (3) Osteomyelitis
* (4) Endocarditis, meningitis
4. Rapid onset of infection at the bite site (usually within 24 hours)
5. Treatment
* Amoxicillin-clavulanate
What is a ganglion cyst? Where do they mostly occur? How are they felt? What are they called when felt behind knee?
1) small multiloculated, cystic lesion in connective tissue joint capsules
2) favored location is small joints of wrist
3) felt as firm pea-sized nodules
4) bakers cyst
"brittle bone" disease is also called? Which type is the worst? What is defective produ
1) osteogenesis imperfecta
2) type II = babies are crushed, lethal
3) type I collagen
How does type I osteogenic imperfecta present? What are the genetics? Is it life long?
1) AD
2) fractures
3) hearing loss
4) blue sclera
5) mild at birth, progressively worse, normal lifespan
Why do the sclera appear blue in osteogenesis imperfecta? How can osteogenesis imperfecta be treated?
1) underlying choroidal veins are seen from lack of type I collagen
2) Bisphosphonates to increase bone mineralization
What are the genetics of achondroplasia? Which chromosome? What is impaired?
1) AD
2) mutation in FGFR3 gene on chromosome 4p16.3
3) Gene mutations increase with paternal age
4) Impaired proliferation of cartilage at the growth plate
What are clinical findings in achondroplasia? How are GH and IGF-1 effected?
1. Normal-sized head and vertebral column
2. Shortened arms and legs
3. Normal growth hormone and insulin growth factor-1 levels
"marble bone" disease is also known as? What are genetics?
1) osteopetrosis or albers-schonberg disease
2) Autosomal recessive (severe in infancy)
3) Autosomal dominant (less severe in adults)
4) deficiency of carbonic anhydrase II
Pathologically what is occurring in osteopetrosis?
1. Deficiency osteoclasts
2. Normal balance of osteoblasts making bone and osteoclasts breaking down bone is disrupted favoring increased bone formation.
3. Overgrowth and sclerosis of cortical bone ("too much bone")
Clinically how does osteopetrosis present?
1. Pathologic fractures
2. Anemia
a. Replacement of marrow cavity
3. Cranial nerve compression
a. Visual and hearing loss
4. cranial nerve entrapment
Note: x-rays show erlenmyer flask bones that flare out
Note: genetic deficiency of carbonic anhydrase II
How do bacteria get to bones to cause osteomyelitis? What is most common site?
1) Most commonly due to sepsis with subsequent spread to bone
2) Metaphysis is the most common site.
a. Favors the tibia and fibula in children
In children what is the most common cause of osteomyelitis? What are common causes in newborns?
1) S aureus (#1), Streptococcus pyogenes, Haemophilus influenzae
2) group B beta hemolytic strep and E. coli
What is the most common cause of osteomyelitis in a IV drug user? In someone with sickle cells disease?
1) pseduomonas
2) Most often due to Salmonella paratyphi
How does tuberculosis osteomyelitis spread to the bones? Which bones does it go to?
1) vertebrae (Potts disease)
2) hip
3) long bones (femur and tibia)
4) hands and feet
5) spreads via blood
Osteomyelitis Most often due to puncture of foot through rubber footwear is caused by?>
pseudomonas aeurginosa
What is the pathogenesis of osteomyelitis?
1) Neutrophils enzymatically destroy bone
2) Devitalized bone is called sequestra.
3) Chronic disease produces reactive bone formation in periosteum.
a. Called involucrum
4) Draining sinus tracts to the skin surface often occur.
If a sinus tract forms in someone with osteomyelitis what are they at risk of developing?
Danger of squamous cell carcinoma developing at orifice of sinus tract
necrotic bone in osteomyelitis is known as what? what is a sleeve of new bone formation called? If new bone has surrounding granulation tissue what is it called?
1) sequestrum
2) involucrum
3) brodie abscess
How is osteomyelitis caused by staph treated? by salmonella paratyphi?
1. Surgical débridement
2. Staphylococcus aureus: vancomycin + ceftazidime
3. Salmonella paratyphi (sickle cell): ciprofloxacin
what is the Most common metabolic abnormality of bone? How is it characterized?
1) osteoporosis
2) Loss of both organic bone matrix and minerals
a. Decreased bone mass and density
2) Radiograph shows osteopenia (washed out appearance).
3) Decreased thickness of cortical and trabecular bone
4) loss of mineralized bone + organic bone matrix (osteoid)
Why in part do more women have osteoporosis than men? compare fractures related to men and women over 65 with osteoporosis?
1) Men have greater bone mass to begin with; takes longer to develop osteoporosis
2) 50% in women > 65 years old
3) 20% in men > 65 years old
What are secondary causes of osteoporosis?
(a) Underlying disease (e.g., hypercortisolism)
(b) Drugs (e.g., heparin)
(c) Hypogonadism (e.g., hypopituitarism)
(d) Malnutrition (e.g., anorexia nervosa)
(e) Space travel
** Lack of gravity reduces bone stress
Why is there osteoporosis after menopause?
1) Due to estrogen deficiency
a. Increased resorption of bone by osteoclasts
b. Decreased formation of bone by osteoblasts
What are clinical findings in osteoporosis?
(1) Compression fractures of vertebral bodies
a. Most common fracture
(2) Colles' fracture of distal radius
(3) Dowager's hump (similar to kyphosis)
How is osteoporosis diagnosed?
1) Dual-photon absorptiometry
a. Noninvasive test that evaluates bone density
How is osteoporosis prevented?
(1) Role of estrogen replacement is being reevaluated.
(2) Calcium and vitamin D supplements
(3) Stop smoking (inhibits osteoblast activity)
(4) Weight-bearing exercise
(a) Weight lifting; vigorous walking
(b) Excludes swimming, which decreases bone stress
How is osteoporosis treated?
(1) Bisphosphonates inhibit bone resorption.
a. First-line treatment
(2) Calcitonin inhibits osteoclasts.
Why does senile osteoporosis occur?
Decreased ability of osteoblasts to divide and produce osteoid
What are causes of avascular necrosis?
(1) Corticosteroids (35%) most common cause of avascular necrosis
(2) Alcohol (22%)
(3) Other causes (43%)
(a) Idiopathic
(b) Fractures
where are common sites for aseptic necrosis of bone?
(1) Femoral head and condyle
(2) Humeral head
(3) Scaphoid (navicular) and lunate bones in wrist
(4) Talus bone
a. Located between the calcaneus and the tibia and fibula
In an elderly person what is the difference between a pertrochanteric fracture and subcapsular fracture of femoral head?
1) Pertrochanteric fracture is extracapsular and does not compromise blood supply to the femoral head; hence, no aseptic necrosis
2) Subcapsular fracture disrupts blood supply (retinacular arteries from medial circumflex femoral artery); hence, aseptic necrosis occurs.
Why is the scaphoid bone prone to avascular necrosis?
(1) Located on the thumb side of the wrist
(2) Most common bone in the wrist that is fractured
(3) Normally has a poor blood supply
dactylitis is a type of avascular necrosis seen in what?
sickle cell disease
What are clinical findings in aseptic necrosis?
1. Asymptomatic
2. Localized pain exacerbated by movement
3. Functional limitation of activity
What is most sensitive test for avascular necrosis?
1) MRI
2) Early finding-margin of low signal and inner border of high signal produce a "double line sign."
3) Most sensitive test (75-100%) for early detection of aseptic necrosis
What does a bone scan and x-ray show in aseptic necrosis?
a. Bone scan
(1) Early-shows no uptake (cold area; sensitivity 70%)
(2) Later-increased uptake (result of bone remodeling)

b. X-ray study
(1) Most insensitive test in early phases
(2) Early-may show osteopenia (radiolucency)
(3) Later-flattening, collapsed bone
How is aseptic necrosis treated?
1) Core decompression
2) bone graft
3) joint replacement
What is osteochondrosis? Who does it occur in? what is disease called?
1) Aseptic necrosis of ossification centers in children
2) Legg-Calvé-Perthes disease
a. Aseptic necrosis involving the femoral head ossification center
b. Occurs most often in boys 3 to 10 years of age
c. Presents with pain in the knee or a limp
d. Secondary osteoarthritis is common
In growing children what is avascular necrosis of the femoral head called? of the tibial tubercle? of the navicular bone?
1) legg-calve perthes disease
2) osgood-schlatter disease
3) Kohler bone disease
what is osteochondritis dissecans a variant of?
a. Variant of osteochondrosis limited to the articular epiphysis
1. Articular epiphyses fail as a result of compression.
2. Trauma is the primary insult.
3. Ischemia is a secondary injury.
4. Portion of cartilage and underlying subchondral bone separates.
when does Osteochondritis dissecans occur? More common in males or females? what is the most common joint? What are other joints?
1) Occurs between 10 and 50 years of age
2) No sex predilection
3) Most common joint is knee.
a. Lateral surface of the medial femoral condyle is the most frequent site.
b. Cartilage may become detached.
3) Other sites
a. Capitellum of humerus
b. Dome of talus bone in foot
c. Shoulder, hip, elbow
What are clinical findings in Osteochondritis dissecans? What is a complication of the disease?
1. Localized pain, stiffness, swelling
2. Locking of joint by loose body
3. Tenderness at site of lesion
4. complication is Osteoarthritis
Who does Osgood-Schlatter disease occur in? How is it characterized?
1) Affects physically active boys 11 to 15 years of age
2) Painful swelling of tibial tuberosity
a. Inflammation of proximal tibial apophysis at insertion of patellar tendon
How does Osgood-Schlatter present clinically? What is effect on bone growth?
1) Pain aggravated by
a. Squatting
b. Walking upstairs
c. Extending knee with resistance
2) Permanent knobby-appearing knees
3) No effect on bone growth
Paget's disease of bone is also known as? Who does it occur in? What is cause? which bones effected?
1) osteitis deformans
2) Primarily occurs in men > 50 years of age
3) Cause unknown (? virus-slow virus, respiratory syncytial virus)
4) Targets the pelvis, skull (enlarged), and femur
what is the pathogenesis of Pagets disease of bone? What marker is elevated?
1. Early phase of osteoclastic resorption of bone
a. Causes shaggy-appearing lytic lesions
2. Late phase of increased osteoblastic bone formation
a. Markedly increased serum alkaline phosphatase
b. Production of thick, weak bone (mosaic bone)
What are clinical findings in Pagets disease of bone?
1. Bone pain is the most common complaint.
2. Headaches, hearing loss if it affects skull
3. Increased hat size with skull involvement
What are complications of osteitis deformans?
1. Pathologic fractures
2. Risk for developing osteogenic sarcomas
3. Risk for developing high-output heart failure
a. Due to arteriovenous connections in vascular bone
4. long bone chalk-stick fractures
How is osteitis deformans diagnosed? How is it treated?
1. Radiographs show thickened bone with shaggy areas of radiolucency.
2. Markedly increased serum alkaline phosphatase with normal serum calcium and phosphorus
Treatment:
1. Bisphosphonates
2. Calcitonin
In Osteitis deformans what do osteoclasts show under microscope?
intranuclear inclusions suggesting a viral cause such as with a paramyxovirus
How are alkaline phosphatase, PTH, Ca2+ and phosphate seen on blood chem in someone with Pagets disease of bone?
1) alk phosphatase increased
2) normal Ca2+ and phosphate and PTH
Note: hearing loss is seen in this condition from bone thickening
How is fibrous dysplasia characterized?
1) Defect in bone-forming mesenchyme with replacement of medullary bone by fibrous tissue
a. Defect in osteoblastic differentiation and maturation
2) Cysts may develop in the fibrous tissue matrix that manifests as a defect in osteoblastic differentiation and maturation
When and who does fibrous dysplasia of bone occur?
1) May involve single (monostotic; 70-80%) or multiple bones (polyostotic)
2) No sex predilection
3) Occurs between 10 and 30 years of age
Where are the most common locations for fibrous dysplasia of bone?
1. Ribs (28%)
2. Femur (23%)
3. Tibia or craniofacial bones (10-25%)
a. In craniofacial bone, it produces cherubism
4. Humerus, vertebra
when fibrodysplasia is polyostotic what is it associated with?
McCune-Albright's syndrome:
1) polyostotic bone involvement
2) café au lait spots
3) precocious puberty
What are complications of fibrous dysplasia?
1) pathologic fracture
2) osteogenic sarcoma
3) fibrosarcoma
McCune-Albrights syndrome presents how? in who?
1) polyostotic fibrous dysplasia
2) precocious puberty
3) cafe-au-lait spots
4) occurs in YOUNG GIRLS
McCune-Albrights causes a skin disorder that is likened to the "coast of main". Why? what is the genetic cause of the disease?
1) cafe-au-lait spots have irregular borders
2) postzygotic somatic cell mutation of GNAS1 which codes for a G protein (note it is NOT hereditary)
Metastasis is the most common malignancy of bone. Where is most common primary site?
breast
What are primary malignant tumors of bone in decreasing frequency?
1) Multiple myeloma
2) osteogenic sarcoma
3) chondrosarcoma
4) Ewing's sarcoma
What is the most common benign bone tumor?
Osteochondroma
What is Von Recklinghausen disease of bone also called? what causes it?
1) osteitis fibrosa cystica
2) primary or secondary hyperparathyroidism
How does osteitis fibrosa cystica characterized?
1) brown tumor of bone
2) cystic spaces lined by multinucleated osteoclasts and filled with vascular fibrous stroma
3) brown color is from hemorrhage
Note: von recklinghausen disease of bone
How is von Recklinghausen diagnosed? What disease can it mimic?
1) has diffuse radiolucency mimicking osteoporosis
2) blood chem shows:
a. high Ca2+
b. low phosphorous
c. high alkaline phosphatase
d. high PTH
What is the cause of osteomalacia? who does it occur in? what is seen on x-ray?
1) vitamin D deficiency in adults
2) defective calcification showing radiolucency resembling osteoporosis
If osteomalacia is secondary to renal disease what is it called?
renal osteodystrophy
What occurs pathologically in rickets?
1) decreased vit D in kids
2) low Ca2+ and excess accumulation of osteoid lead to increased thickness of epiphyseal growth plates and skeletal deformities
What are clinical manifestations of Rickets?
1) craniotabes = thinning and softening of occipital and parietal bones
2) late closing of fontanelles
3) RACHITIC ROSARY = thickening of the costochondral junctions that results in a string of beads appearance
4) HARRISON GROOVE = depression along the line of insertion of diaphragm into rib cage
5) pigeon chest
6) decreased height
How do the following effected in osteoporosis?
1) Ca2+
2) Phosphorous
3) AP
4)
1) normal
2) normal
3) normal or decreased
4) normal
How do the following effected in von Recklinghausen disease of bone?
1) Ca2+
2) Phosphorous
3) AP
4) PTH
1) Ca2+ = high
2) Phosphorous = low
3) AP = high
4) PTH = high
Note: this is a brown tumor
How do the following effected in osteomalacia and rickets?
1) Ca2+
2) Phosphorous
3) AP
4) PTH
1) Ca2+ = low
2) Phosphorous = low
3) AP = norm
4) PTH = increased
How do the following effected in paget disease of bone?
1) Ca2+
2) Phosphorous
3) AP
4) PTH
1) normal
2) normal
3) markedly increased AP
4) normal
How does scurvy manifest?
1) subperiosteal hemorrhage (painful)
2) osteoporosis (especially at metaphyseal ends)
3) epiphyseal cartilage not replaced by osteoid
who does osteochondroma occur in? Where in body? how is it characterized?
1) Males, 10-30 yr
2) Solitary or multiple
3) Metaphysis of distal femur or upper end of tibia
4) Outgrowth of bone (exostosis) capped by benign cartilage
5) Most common benign tumor
Who does endochondroma occur in? where in body? What is there increased risk of?
1) Equal distribution, 20-50 yr
2)Solitary or multiple
3) Medullary location
4) Small tubular bones in hands and feet
5) Multiple enchondromas = Risk for chondrosarcoma
Note chondrosarcomas occur in proximal bone locations
Who does Osteoma occur in? Where in body? What is it associated with?
1) Males, any age
2) Facial bones and can protrude into paranasal sinuses
3) Associated with Gardner's polyposis syndrome
Who does Osteoid osteoma occur in? where in body? what is x-ray finding?
1) Males, 10-20 yr
2) Cortex of proximal femur or proximal tibia
3) Radiographic finding: radiolucent focus surrounded by sclerotic bone
4) neoplastic proliferation of osteoid and fibrous tissue
Who does Osteoblastoma occur in? where in body? what is it similar to?
1) Males, 10-20 yr
2) Vertebra
3) Similar to osteoid osteoma (interlacing trabeculae of woven bone surrounded by osteoblasts)
Who does Giant cell tumor occur in? Where in body? What is cell type is present?
1) Females, 20-40 yr
2) Epiphysis of distal femur or proximal tibia
3) Reactive multinucleated giant cells resemble osteoclasts
4) Neoplastic mononuclear cells
Who does Chondrosarcoma occur in? where in body? Where does it metastisize?
1) Males, 30-60 yr
2) Pelvic bones, proximal femur, ribs and vertebrae
3) Grade determines biologic behavior
4) Metastasizes to lungs
Note: expansile glistening mass in medullary cavity
Who does osteogenic sarcoma occur in? What are risk factors?
1) Males, 10-25yr
2) Risk factors:
a.Paget's disease
b. familial retinoblastoma
c. irradiation
d. fibrous dysplasia
e. bone infarcts
Where does does osteogenic sarcoma occur in body? how is it described?
1) Metaphysis of distal femur, proximal tibia
2) osteoid and bone producing neoplasm
3) Most common primary bone cancer (some authors say multiple myeloma)
Note: codman's triangle or sunburst pattern on xray from periosteum elevation
What are radiographic signs of Osteosarcoma (osteogenic sarcoma) Where does it metasisize?
1) "sun-burst" appearance (spiculated pattern from calcified malignant osteoid)
2) "Codman's triangle" (tumor lifting the periosteum)
3) Metastasizes to lungs
Who does Ewing Sarcoma occur in? Where in body? How do cells look? what are radiologic findings? what are other findings?
1) Males, 10-20yr
2) Pelvic girdle, diaphysis and metaphysis of proximal femur or rib
3) Small, round cell tumor
4) Radiographic finding: "onionskin" appearance around bone (periosteal reaction)
5) Possible fever and anemia
Note: this a small blue tumor
A soap bubble appearance on x-ray is characteristic of what tumor? sunburst pattern and codman triangle indicate what tumor, and what blood value is elevated?
1) giant cell tumor
2) osteosarcoma has elevated AP
Familial retinoblastoma predisposes someone to what? Where is mutation?
1) first have ocular tumor
2) later in life develop osteosarcoma
3) Rb on chromosome 13
small blue cell malignant tumor is which cancer? What can it mimic in early stages? what translocation? What tumors does it resemble?
1) ewing sarcoma
2) mimics acute osteomyelitis
3) 11;22 translocation identical to that found in peripheral neuroectodermal tumor and olfactory neuroblastoma
Note: develops onion skin appearance of bone
what are the 3 malignant bone tumors?
1) osteosarcoma
2) chondrosarcoma
3) ewing sarcoma
What are the 3 histiocytosis X variants?
1) letterer-siwe disease
2) hand-schuller christian disease
3) eosinophilic granuloma
Describe the cells that are in histiocytosis X variants?
1) resemble Langerhans cells of epidermis
2) contain BIRBECK GRANULES
3) tennis racket shaped cytoplasmic structures
How is Letterer-siwe disease characterized? who does it occur in?
1) aggressive and fatal disease of young infants and small children
2) Features:
a. eczema
b. hepatosplenomegaly
c. lymphadenopathy
d. pancytopenia
e. recurrent infections
f. pulmonary involvement
Who does hand-schuller-christian disease occur in? what are features of disease?
1) children less than 5
2) Features:
a. mixed inflammatory cell infiltrate in bone especially skull, liver, spleen
b. triad of skull lesions, diabetes insipidus, exopthalmos
3) Fever
4) Localized rash on scalp and in ear canals
Eosinophilic granuloma has best prognosis. How does it present?
1) solitary bone lesion with extraskeletal involvement limited to lung
2) mixed inflammatory cells with macrophages, lymphocytes and eosinophils
What determines muscle fiber type?
1) the muscles innervation
How are type I muscle fibers characterized?
1. Slow-twitch (red) fibers
a. Slow contraction but repetitive
b. Do not fatigue easily
c. Example-long muscles in the back
2. Rich in mitochondria, myoglobin, and oxidative enzymes
3. Weak in ATPase enzymes
How are type II muscle fibers characterized?
1. Fast-twitch (white) fibers
a. Fast contraction, but fatigue easily
b. Specialized for fine, skilled movement
c. Examples-extraocular muscles, some muscles in the hand
2. Poor in mitochondria, myoglobin, oxidative enzymes
3. Rich in ATPase enzymes
How does someone acquire trichonella spiralis? What type of organism?
1) nematode
2) Eating raw or poorly cooked pork containing the encysted larvae in muscle
3) Common on pig farms where pigs are fed uncooked garbage
4) Bear and seal meat are other sources
What is pathogenic process of trichonella spiralis?
1) Larva excyst and develop into adult worms within small intestine mucosa.
2) Eggs hatch within the adult female worm.
3) Larvae are released into the blood stream.
4) Larvae encyst in striated muscle.
a. Commonly undergo dystrophic calcification; visible on x-ray
5) Larvae die if deposited in other sites
How does trichinosis present?
(1) Muscle pain
(2) Periorbital edema (larva)
(3) Splinter hemorrhages in nails
What are complications of trichinosis?
1) Complications
a. Myocarditis
b. encephalitis
2) Diagnosis
a. Pronounced eosinophilia
b. muscle biopsy
3) Treatment is albendazole.
How do group A strep effect muscles and fascia?
(1) Necrotizing fasciitis
(2) Myositis
(3) Streptococcal toxic shock syndrome (STSS)
Note: bacitracin sensitive, beta hemolytic and catalase negative
What toxins does group A strep produce that lead to pathogenesis?
1) Pyrogenic exotoxin A
a. Superantigen associated with STSS
2) Exotoxin B
a. Protease that destroys tissue associated with necrotizing fasciitis
How is invasive strep pyogenes treated?
(1) Intravenous penicillin G + clindamycin
(2) Intravenous immunoglobulin
(3) Death rates range from 20% to 100%
What are the genetics and incidence of duchennes muscular dystrophy?
1) X-linked recessive (XR)
2) Incidence 1:3500 male births
What is the pathogenesis of duchennes muscular dystrophy?
(1) Absence of dystrophin
a. Dystrophin normally anchors actin to membrane glycoprotein.
b. Becker's type has deficiency/defective dystrophin.
(2) Progressive degeneration of type I and II fibers
(3) Fibrosis and infiltration of muscle tissue by fatty tissue
a. Produces pseudohypertrophy of calf muscles
What is the Most common childhood muscular dystrophy?
duchennes muscular dystrophy
Clinically what is seen in Duchennes muscular dystrophy?
(1) Symptoms occur between 2 and 5 years of age.
(2) Weakness and wasting of pelvic muscles
a. Child places hands on the knees for help in standing (Gower's maneuver)
a. Waddling gait (duck-like)
(3) Cardiac involvement may be present.
(4) Death usually occurs by 20 years of age from pneumonia
What are lab markers that are eleveated in Duchennes?
(1) Serum creatine kinase (CK) is increased at birth.
a. Progressively declines as muscle degenerates
(2) Female carriers have increased levels of serum CK
How is Duchennes diagnosed and treated?
(1) Muscle biopsy
(2) DNA testing available
(3) Western blot
o Diagnosed prenatally via chorionic villous sampling
3) Treatment:
a. Corticosteroids improve muscle strength and function
How does Duchennes initially present? how do muscles then change?
1) proximal extremity muscle weakness
2) develop compensatory hypertrophy of distal sites like calves
3) eventual pseudohypertrophy which is fibrosis and adipose infiltrate
What is beckers muscular dystrophy?
1) mild form of duchennes
2) abnormal truncated dystrophin
What is facioscapulohumeral muscular dystrophy?
1) AD
2) slow progression and non-disabling
3) normal life-expectancy
4) sequentially involves muscles of face, scapular area, and humerus
What is limb-girdle dystrophy?
1) AR
2) involves proximal muscles of shoulder, pelvic girdle or both
What are genetics of mytonic dystrophy? What muscle type is effected?
(1) Autosomal dominant
(2) Most common adult muscular dystrophy
(3) Trinucleotide repeat (CTG) disorder
(4) Selective atrophy of type I fibers
Note: exhibits ANTICIPATION
What is the most common muscular dystrophy of adult? children?
1) myotonic dystrophy
2) duchennes
What are clinical and lab findings in myotonic dystrophy?
(1) Facial muscle weakness
a. Sagging face; problem in closing the mouth
(2) Percussion and grip myotonia
a. Inability to relax muscles (sustained grip)
(3) Frontal balding; cataracts
(4) Testicular atrophy; glucose intolerance
(5) Cardiac involvement (conduction defects)
(6) Increased serum CK
When are men effected by MG? women?
(1) Afflicts men in sixth and seventh decades of life
(2) Afflicts women in second and third decades of life
Pathologically what is occurring in MG? What type of hypersensitivity? Where in body are antibodies produced?
(1) Autonomic disorder of postsynaptic neuromuscular transmission
(2) Autoantibody against acetylcholine receptors
a. Type II hypersensitivity reaction
b. Antibodies inhibit or destroy the receptors.
c. Decrease in functional ACh receptors
d. Antibody is synthesized in the thymus.
3) Thymic hyperplasia with germinal follicles (85% of cases)
Clinically how does MG present?
1) Fluctuating muscle weakness
a. Worsened with exercise, improved with rest
2) Ptosis is the most common initial finding
a. Diplopia is due to eye muscle weakness.
3) Weakness in proximal muscles, diaphragm, neck extension (85%)
4) Dysphagia for solids and liquids
a. Occurs in the upper esophagus (striated muscle)
5) Normal reflexes, sensation, and coordination
6) Increased risk for developing a thymoma (15%)
How is MG diagnosed?
(1) Tensilon (edrophonium) test
a. Inhibits acetylcholinesterase
b. Increase in acetylcholine reverses muscle weakness
(2) Single-fiber electromyography (abnormal in 95% of MG)
How is MG treated? Which drugs should be avoided?
1) Avoid certain medications
a. β-Blockers
b. aminoglycosides
c. quinolone antibiotics
d. class 1 antiarrhythmics
(2) Pyridostigmine (acetylcholinesterase inhibitor)
(3) Immunosuppressive drugs
a. Corticosteroids
b. azathioprine
c. mycophenolate mofetil
d. cyclosporine
(4) Plasmapheresis (short-term treatment; removes antibodies)
(5) Thymectomy (removes site for antibody production)
An older male shows frontal balding, drooping of the eyelids, sagging of the facial muscles, and atrophy of the sternocleidomastoid muscles. What do you suspect?
myotonic dystrophy
Denervation atrophy effects both type I and II muscle fibers. What are histologic features of denervation?
1) tartget fibers which have a central darker area reminiscent of the bull's-eye of a target
After reinnveration occurs what happens in the muscle cell?
1) fiber-type grouping where a cluster of type I and a cluster of type II fibers may be seen
2) this is in contrast to normal muscle where a mixture of individual not clusters of fibers are seen
What are 3 congenital myopathies? How are they often characterized?
1) central core disease
2) nemaline myopathy
3) mitochondrial myopathies
Note: ALL can present as floppy baby syndrome with marked hypotonia at birth and generally have normal creatine kinase levels
What is central core disease?
1) congenital myopathy
2) loss of mitochondria and other organelles from type I muscle fibers
What is nemaline myopathy?
1) tangles of rod shaped granules are seen in type I fibers
2) can be mild and nonprogressive or severe with death of respiratory failure
3) note this a congenital myopathy
What occurs in mitochondrial myopathy? What is an example?
1) non-Mendilian inheritance
2) maternal inheritance
3) children have ragged red appearance of muscle fibers
4) Kearns-sayre syndrome is characterized by opthalmoplegia, pigmentary retinopathy, heart block, cerebellar ataxia
What causes Lambert-Eaton syndrome?
1) para-neoplastic syndrome usually small cell carcinoma of lung
2) defect in release of acetylcholine
3) autoantibodies react with presynaptic voltage-gated Ca2+ channels
What is fibromatosis?
1) Non-neoplastic, proliferative connective tissue disorder
2) Fibrous tissue infiltrates tissue (usually muscle)
Where does dupuytrens contracture occur? what is it associated with?
1. Fibromatosis involving palmar fascia
2. Causes contraction of single or multiple fingers
3. Associated with alcoholism
Where does a desmoid tumor occur? In who? what is it associated with?
1. Fibromatosis of the anterior abdominal wall in women
2. Associated with previous trauma
3. Associated with Gardner's polyposis syndrome
What is the most common benign soft tissue tumor? where do they mostly occur?
1) lipoma
2) Trunk, neck, proximal extremities
3) Arises in subcutaneous tissue
4) No clinical significance
What is the most common adult sarcoma?
1) liposarcoma - malignant tumor of adipose tissue
2) Thigh, retroperitoneum
3) Lipoblasts identified with fat stains
where are fibrosarcomas common? What can do they occur after?
1) Thigh, upper limb
2) May arise after irradiation
3) malignant fibroblasts with spindle-shaped cells and herringbone pattern
Where do dermatofibromas occur? How are they characterized?
1) Lower extremities
2) Benign, nonencapsulated proliferation of spindle cells confined to the dermis
3) Red nodule that umbilicates (has a central dimple) when squeezed
Where do Malignant fibrous histiocytomas occur? what are they associated with?
1) Retroperitoneum, thigh
2) Associated with radiation therapy and scarring
Rhabdomyomas occur where? What are they associated with?
1) Heart, also tongue and vagina 2) Benign heart tumor associated with tuberous sclerosis
Where does Embryonal rhabdomyosarcoma occur? who is most common in? How does it present?
1) Penis and vagina
2) Most common sarcoma in children
3) Grape-like, necrotic mass protrudes from penis or vagina
What is the most common benign tumor of GI tract? Where else can this tumor occur?
1) leiomyoma
2) uterus
what is the Most common sarcoma of gastrointestinal tract and uterus?
leiomyosarcoma
where do synovial sarcomas occur? what type of growth pattern in present?
1) Does not arise from synovial cells in joints but from mesenchymal cells around joints
2) Biphasic pattern: epithelial cells forming glands + intervening spindle cells
How does a colles fracture occur? what is damaged?
1) Common fracture when falling on outstretched hand
2) Fracture of distal radius with or without fracture of ulnar styloid
where is tennis elbow pain located? when is pain present?
1) Pain where extensor muscle tendons insert near the lateral epicondyle (lateral epicondylitis)
2) pain when gripping something
Where does pain occur with golfers elbow? what movements aggravate it?
1) Pain where the flexor muscle tendons insert near the medial epicondyle (medial epicondylitis)
2) Pain duplicated by flexing hand muscles and supinating the arm (arm wrestling movement)
How does DeQuervain's tenosynovitis develop? where is pain? what test is used to diagnose?
1) Chronic stenosing tenosynovitis of the first dorsal compartment of the wrist
2) overuse of the hands and wrist
3) first dorsal compartment has abductor pollicis longus and extensor pollicis brevis
4) Excessive friction thickens tendon sheath causing stenosis of the osseofibrous tunnel
5) Pain on the radial aspect of the wrist aggravated by moving the thumb
6) Finkelstein's test: patient puts thumb in the palm, closes fist, tilt hand toward little finger (ulnar deviation); pain occurs in first dorsal compartment
Where and in who do ganglion cysts occur?
1) Bulge on the dorsum of the wrist when the wrist is flexed
2) More common in women than in men
3) Cyst communicates with synovial sheaths on the dorsum of the wrist
what are the 5 p's of compartment syndrome?
1) pain
2) paresthesias
3) pallor
4) paralysis
5) pulselessness
What is Volkmann's ischemic contracture?
1) displaced supracondylar fracture of distal humerus causing compression of brachial artery and median nerve
2) forearm muscles (superficial and deep flexor muscles) may undergo contracture
3) although most of the muscles are innervated by the median nerve, the flexor carpi ulnaris is innervated by the ulnar nerve
How does carpal tunnel syndrome present?
1) Pain, numbness, or paresthesias in the thumb, index finger, 2nd finger, 3rd finger, and the radial side of 4th finger
2) thenar atrophy produces "ape hand" appearance
Herniation of L3-L4 disk causes loss of what reflex? Herniation of L4-L5 disk? Herniation of L5-S1 disk?
1) loss of knee jerk (femoral nerve L2-L4)
2) no loss of reflexes (ankle and knee reflexes intact)
3) loss of ankle reflex (tibial nerve L4-S3)
Who does idiopathic scoliosis commonly occur in? which way is curve usually?
1) usually affects adolescent girls between 10 and 16 years of age
2) usually a right thoracic curve
3) forward bending causes a paraspinous prominence on the right from a hump in the ribs due to a rotational component of the vertebra