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Trauma, Infection, & Disease
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disorders of musculoskeletal system
bone diseases
diseases of skeletal muscle
soft tissue injuries
osteomyelitis
severe infection of bone & local tissue in which organisms reach bone
needs urgent care
ways organisms reach bone in osteomyelitis
bloodstream
adjacent soft tissue
direct introduction of organism
bloodstream / hematogenous osteomyelitis
most common
infectious agent introduced by blood from infection elsewhere in body
adjacent soft tissue / contiguous focus
caused by burns, sinus disease, trauma, malignant tumor, necrosis, periodontal infection, infected pressure ulcer
ex: bedsores (prolonged pressure on skin)
direct introduction of organism
direct infection causes open fracture, penetrating wounds, surgical contamination, or insertion of screws/metal plates
osteomyelitis usually occurs in
children < 16 y/o (mean age 6 y/o) & elderly
IV drug users
indwelling intravascular catheters / central line
diseases (sickle cell anemia; chronic granulomatous disease)
long bones (metaphysis/rich in bone marrow 4 child)
diseases that can lead to osteomyelitis
sickle cell anemia
chronic granulomatous diseases
sarcoidosis
chron’s dx
TB
pathogens associated with osteomyelitis
staph. aureus (most common)
strept. pneumoniae
H. influenzae (rare b/c vaccination)
clinical manifestations of osteomyelitis in children
high fever & pain at site of bone involvement
signs of inflammation (redness; swelling; heat)
brodie abscess (subacute osteomyelitis)
brodie abscess / subacute osteomyelitis
localized infection enclosed by fibrotic tissue
clinical manifestations of osteomyelitis in adults
fever; malaise; anorexia; night sweats; weight loss
result of healing complications of osteomyelitis if not managed or treated sufficiently
necrotic bone leads to dead segments in healthy bone
abscess or chronic infection
involucrum
involuvrum (result of healing complication of osteomyelitis)
prevents successful effects of antibiotics
treatment of osteomyelitis
4-6wks of antibiotic IV therapy
abscess formation = debridement
amputation
scoliosis
lateral curvature of spine ≥ 10˚
S or C shaped
2-4% of US population
= for men & women
etiology & pathogenesis of scoliosis
idiopathic (majority)
consequence of:
congenital disorder (hemi-vertebrae)
connective tissue disorder (marfan’s sx)
neuromuscular disorder (cerebral palsy)
congenital disorder related to scoliosis
hemi-vertebrae
connective disorder related to scoliosis
marfan’s sx
neuromuscular disorder related to scoliosis
cerebral palsy
clinical manifestations of scoliosis
present AFTER puberty
asymmetry of shoulders, hips, chest wall
possible respiratory problems
GI dysfunctions
nonstructural scoliosis
RESOLVES when patient bends to the affected side
NO VERTEBRAL ROTATION / bony deformity of vertebrae
related to postural problems, inflammation, or compensation due to leg discrepancy
not progressive
structural scoliosis
fails to correct itself on forced bending against the curvature
VERTEBRAL ROTATION
involves deformity of vertebrae & asymmetric changes in hip, shoulder, & rib cage positions
progressive
treatment of scoliosis
bracing
exercises
surgical interventions w/ spinal alignment if ≥ 40-50˚ curve
most common metabolic bone disease & cause of broken bone among elderly
osteoporosis
osteoporosis
bone reabsorption greater than that of bone formation
greater in female than male
osteoClastic balance is DISRUPTED but NORMAL osteoBlastic activity
mineral & protein matrix components are decreased
cancellous bone lost faster than cortical bone
rate of bone loss is influenced by
age; genetics; estrogen level; family history (major risk factor)
risk factors of osteoporosis
family history (MAJOR); estrogen deficiency; white or asian race; menopause;
small frame (less bone tissue & faster bone loss)
disease (cushing dx; scurvy (vit. c def.))
clinical manifestations of osteoporosis
muscle wasting; back muscle spasms; difficulty bending over
fractures [fx] (colles fx of wrist; vertebral compression fx)
kyphosis (thoracic spine: DOWAGER’S HUMP)
shortened stature
how much height loss is normal
½ inch every 10 years after age 40
diagnosis of osteoporosis
based on bone mineral density (BMD)
measured by dual energy x-ray absorptiometry (DEXA)
T score: ≤ -2.5
T score that indicates osteopenia ranges between
-1.0 & -2.5
treatment for osteoporosis
calcium & vit. D supplements
exercise
bisphosphonates = antiresorptive agent (not for long term use/5 years)
recombinant human parathyroid hormone (2 years ONLY)
exercise best for increasing bone density
weight bearing exercise
rickets/osteomalacia (same disorder just called different based on age)
both involve vit. D deficiency that leasts to soft osteopenic bone
in children = rickets
in adults = osteomalacia
clinical manifestations of rickets/osteomalacia
kyphosis
genu valgum (knock knee)
genu varum (bowleg)
pain in adults
rickets
deficits in mineralization of newly formed bone matrix in GROWING skeleton (children)
osteomalacia
deficits in mineralization of newly formed bone matrix in MATURE skeleton (adults)
etiology of rickets/osteomalacia
inadequate concentration of:
vit. D
calcium or phosphorus
poor vit. D metabolism
renal disease
treatment for rickets/osteomalacia
vit. D
calcium
phosphorus supplementation
most common primary tumor of bone
multiple myeloma or sarcoma
multiple myeloma
slow growing bone marrow malignancy
etiology & pathogenesis of multiple myeloma
neoplastic proliferation of a single clone of plasma cells
usually in elderly
affects kidneys; immune system; circulatory system
clinical manifestations of multiple myeloma
BONE PAIN in predominant symptom
pathologic fractures & HYPERCALCEMIA
kidney dysfunction
neurologic symptoms
UNEXPLAINED ANEMIA
fatigue; weakness
diagnosis of multiple myeloma
homogenous immunoglobulin present in urine & serum (bence hones proteins)
BONE MARROW ASPIRATION & biopsy
imaging tests
bone destruction = lytic bone lesions
treatment of multiple myeloma
aggressive combination chemotherapy
local radiation
survival > 2-3 years (< 10%)
muscular dystrophy
group of GENETICALLY determined myopathies characterized by progressive muscle weakness & degeneration
muscle tissue is replaced by fat & fibrous connective tissue
muscular dystrophy is classified by the pattern of
inheritance
age of onset
distribution of muscular weakness
duchenne muscular dystrophy
most common & most severe form
inherited as X-linked trait (AFFECTS ONLY MEN)
muscle cells deficient in the protein dystrophin
muscle necrosis & degeneration
rod-shaped cytoplasmic protein
clinical manifestations of duchenne muscular dystropphy
disease begins at brith & is usually apparent by age 3
calf muscles enlarged
distal muscle involvement
dies by 20
calf muscles enlarged in duchenne muscular dystrophy due to
infiltration of fat cells
degeneration of muscle fibers
distal muscle involvement in duchenne muscular dystrophy leads to
frequent falling by age of 5 or 6
by age 12-14 yrs most children are confined to a wheelchair
treatment of duchenne muscular dystrophy
appropriate education of patient & family
corticosteroid therapy & preservation of function
myasthenia gravis
chronic autoimmune disease
affects neuromuscular function of voluntary muscles
acetylcholine receptor antibodies destroy/block receptors = profound muscle weakness & fatigability
myasthenia gravis risk factors
women > men
peak onset 20-30 y/o
rapid diagnostic of myasthenia gravis
ice bag test or edrophonium test
clinical manifestations of myasthenia gravis
ptosis (drooping or falling of upper eyelid)
painless muscle weakness
improves by rest & exacerbated by repetitive use
treatment of myasthenia gravis
antiacetycholinesterase / acetylcholinesterase inhibitors
coricosteroids
IV immune globin
plasmapheresis
immunosuppressive agents
thymectomy if not responsive to meds
[faulty treatment of myasthenia gravis] myasthenia crisis results from
INSUFFICIENT medication; emotional stress; trauma; infection; surgery; sudden increase in BP & pulse
[faulty treatment of myasthenia gravis] cholinergic crisis / SLUDGE syndrome results from
excessive medication; fasciculations (especially around mouth)
SLUDGE syndrome
salivation
lacrimation
urination
defecation/diarrhea
gastrointestinal distress
emesis