exam #4 - MSK Flashcards
factors that influence bone growth
nutrition - vit D, calcium
age - >30 more growth than destruction
hormones - calcitonin, estrogen (inhibits bone breakdown, stimulates bone formation) testosterone stimulates muscle growth - puts stress on bones, facilitates bone formation
inhibitors of bone growth/ factors that increase risk for fractures
smoking, obesity, age, anti-inflammatory or cytotoxic medications, steroids, excess alcohol/caffeine/ carbonated soft drinks, eating disorders, hyperthyroid, hyperparathyroidism (causes excess Ca to be reabsorbed from bone)
hormones - postmeno women - osteoclasts>osteoblasts - steady decrease in bone mass with age
stress fracture
repetitive fracture - more stress than bone is able to absorb - no acute trauma. xray may not show fracture first 2-4 weeks
fracture healing - step 1
fracture and inflammatory phase - hematoma
bleeding into tissue, inflammation to encourage WBCs
lasts hours to days
fracture healing 2
granulation tissue formation. fibrblasts attracted to area, growth of vascular tissue - 2 weeks
fracture healing 3
bony callus formation - closed in, well vascularized, spongy bone created healing outside. eventually will be replaced by mature bone. cannot weight bear
3-4 weeks post injury
fracture healing 4
lamellar bone deposition - ossification is beginning - callus replaced by lamallae of mineralize bone
fracture healing 5
remodeling - bony callus, dead portions of bone removed by osteoclasts, compact bone replaces spongy bone, excess material removed
what determines dx of fractures
location, type, direction/pattern
amount of soft tissue damage
complications of fractures
bleeding, nerve damage, nonunion/malunion, infection (osteomyelitis), thromboemboli (dvt or PE), fat embolism, compartment syndrome, fracture blister
osteomyelitis
bone infection - bacteria (common staph). can be exogenous or endogenous. 3 types
CM - chills, fever, tenderness, erythema, edema, pain without movement of infected extremity, loss of ROM. Dx is difficult
hematogenous osteomyelitis
osteomyelitis where bone becomes invaded with bacteria that is present in bloodstream, forms an abscess, bone becomes necrotic
contiguous osteomyelitis
direct bacterial infection or extension of an adjacent soft tissue infection - seen with trauma or surgery. common with older adults, PVD, diabetes
chronic osteomyelitis
infection persists longer than 6-8 weeks, fails to respond to antibiotic therapy. key feature - development of necrotic bone tissue that distinctly separates from surrounding living bone
DVT
Virchows triad - venous stasis, hypercoagulability, injury to vessel wall. common complication of orthopedic surgery
warm, edematous, +homans sign (pain in calf with dorsiflexion)
Dx - d-dimer, prothrombin time, fibrinogen level, ultrasound
Fat embolism
travelling fat thought to originate from fracture site
CM: resp failure, cerebral dysfunction, skin and mucosal petechial
within 12-72 hours of long bone/pelvic fracture
dx - ABG
compartment syndrome
common in anterior compartment of leg, after surgery or soft tissue injury
tissue pressure exceeds perfusion pressure - generally due to inflammation
5 Ps: pallor, paresthesia, paresis, pulseless, pain
tight and shiny skin
treatment - cut open fascia to allow for swelling
can lead to loss of limb, rhabdo, renal failure, death
strain vs sprain
strain - overuse/improper use - low back and hamstrings
patho: stretching injury to muscle/tendon - causing spasm
sprain - quick twist or pull or a force that displaces joint from normal alignment- common location ankle
patho: ligament injury - overstretched
3 grades - grade 3 full thickness, 2 partial, 1 stretchin, small tears
healing of sprains and strains
1) inflammatory exudate
2) granulation tissue frows
3) collagen formation
can take up to 3 months to regain mechanical stability of joint
CM: pain, swelling, changes in tendon or ligament contour, dislocation/subluxation of bones, decreased ROM, instability, weakness
tendinopathy
aka tendinitis (wrong because inflammation not central to pathological process - instead failed healing from overuse)
patho - failed healing process of tendons, tendon thickening, inflammatory response (minimally present if chronic overuse tendinopathy)
rhabdomyalosis
eti- crush injuries, burns, drugs, muscular contraction
breakdown of muscle that causes release of protein myoglobin into bloodstream. SO much breakdown clogs kidney -> renal failure. Elevated K+ and phosphate and CK >1000, could be >5000.
CM - pain weakness dark urine
osteoarthritis
excess pressure + inflammation causes degradation of cartilage causing narrowing of joint space, and exposing bone. Chondrocytes synthesize proteoglycans in repair effort -> excess fluid -> swelling. as disease process goes on, less proteoglycans
slow progressive degenerative inflammatory disease. Risk factors: obesity, athletics, heavy occupational work
common >40yo, equal occurences f/m
Osteoporosis
low bone density, prolonged negative calcium balance. hormonal disorders or drugs. linked to gender (women>men), genetics, age, nutritional deficiency of calcium or vitamin d
dexa scan/vitamin D test
RA
Autoimmune - synovial inflammation/destruction of joint cartilage, genetic predisposition
seen in all ages (book says 20-40), differences depending on age (women>men)
worse in the morning, improves with movement
symmetrical involvement
can have systemic manifestations
Systemic Lupus Erythematosus (SLE)
autoimmune
>women >african americans
autoantibodies & immune complexes -> direct tissue damage
arthralgias/arthritis common early sx, facial butterfly rash
hard to dx
Gout
inc serum uric acid - deposit in joints and kidneys
primary- overproduction or poor elimination
secondary-due to prior diease (eg. renal failure or cancer)
joint - red, warm swollen (big toe - 80% of flareups)
fluid sample from joint - dx
untreated can lead to chronic arthritis
factors that delay wound healing
age
tissue oxygen tension/hypoxia
vascular insufficiency
severe anemia
infection
edema
smoking
pain/stress
nutrition deficiencies
bacterial colinization
chronic diseases/DM
Pressure
medications (eg steroids)
tissue repair
- primary intention - no tissue loss
surgical incision
infection could turn into secondary intention - secondary intention - tissue loss, increased scar tissue
burns
slower healing –> larger scar formation
steps of wound healing
hemostasis (5-15 minutes)
inflammatory phase (1st 24-48 hrs to 2wks) - platelet derived chemoattractands and growth factors, neutrophils and macrophages (clean, remove debris, release cytokines and growth factors)
prolipherative phase (3-4 days - 21 days) - granulation +angiogenesis
remodeling phase (few days -2 years)- collagen/ECM organization
(key - overlap)
stepwise:
1.bleeding, mast cells and damaged cells release histamine
2. increased blood flow
3. blood clot formed (loosely knit)
4. surface dries/hardens to from scab
5. macophages cleaning up beneath scab
6. formation of granulation tissue/angiogenesis
7. fibroblasts deposit collagen
8. epithelial cells migrate into wound bed beneath scab
9. slough off of scab
ideally acute wound will heal within 3 weeks
acute-> chronic - interuption of inflammatory and/or proliferation phase (inadequate blood supply, stalled immune response, bioburden (excess bacteria), inefficient host response
CM of wound infection
fever, elevated WBC
inc amount/type wound drainage
inc pain, heat
regression of wound healing
education - nurses tell pts to watch out for after surgery
Basal Cell Carcinoma
75% of all skin CA
slow growing
wide and deep
rarely metastasize
lesions on face, neck
pearly or ivory, slightly elevated
Squamous cell carcinoma
tumor of epidermis
more malignant if left untreated
sun exposed areas
premalignant lesions (actinic keratosis), whitish discolored areas
Melanoma
tumor of the melanocytes, rapid progress malignant
sun/UV exposure, family history (fair freckled skin)
90% on sun exposed skin for white ppl
darker skinned - occur in non sun exposed areas, such as mucous membranes
CM- erythema, inflammation, tenderness, ulcerate, bleed
ABCDE
asymmetry, border irregularity, color, diameter (1/4 inch), evolution
Contact dermatitis
type 4 hypersensitivity rxn
caused by synthetics, alloy, poison ivy, medications
cell-mediated, inc in igE - t-cells become sensitized to antigen and release inf. cytokines
CM: erythema, pruritis, edema
dx -patch testing
Contact dermititis (irritant)
non-immunological inflammation of the skin such as diaper dermatitis - contact with urine, feces, chemicals, soaps, detergents
patho - disruption in epidermal barrier, damage to cell membranes leads to cytotoxic effect of keratinocytes- activates innate immunity - inflammation
dx - patch testing to determine antigen
can look similar to candida albicans, or turn into candida infection if untreated
tinnea capitis
ringworm! fungal
sharing of combs/brushes, poor hygiene
most common in children 2-10 years
circular lesion
capitis - ringworm of the scalp
tinnea manus, tinnea unguium etc
scabies
mite - burrows into epidermis
survival several days without blood supply
epi - poverty, malnutrition, sexual promiscuity
folds of skin, nipples, genitalia
Lice (pediculosis capitis)
large affinity for skin covered by hair
males, black children less affected
female produces 100s of nits every 2 weeks
Herpes zoster
shingles - reactivation of the varizella zoster virus
>50 yo, stress
zostavax vaccine 50% effective, shingrix 90% effective
travels up nerves
course is 4-5 weeks, along dermatomes, flu-like sx
can cause blindness, damage nerves
