Unit 21 Flashcards
osteoporosis
atrophy of bone or l/o bone mass,composition, matrix
what does fragile bones in OP mean
physiologic stress may fracture bones
et OP
aging
genetic predisposition related to pbm
endorcine changes rt age
what endocrine changes occur with age in relation to op
no E prod in menopausal women -> E is supportive of bone and limits osteoblast prod
2 risk for op
low pbm
low e rt menopause
low bpm
more bone is being removed then put in, negative reinforcment
what does dec E in OP mean
inc bone loss
what age do we normally reach pbm
30
what happens after age 30 in OP
we slowly begin to loose bone mass (negative reinforcement)
how can we inc pbm and cause a more gradual dec after age 30
healthy lifestyel
when does longitudinal bone growth stop
20yo
what is negative reinforcement of pbm talking about
resportion is > then formation
what type of changes occur to bone with dec pbm
architectural (visible)
microscopic (microdamage)
what is the first sign (usually) of OP
fracture
which 2 areas of bone are most affected in OP
vertabrae
maxilla/mandible
what happens when vertabrae are affected by OP
hunched stature, change in height
breathing problems rt spine distortion
what happens when the maxilla/mandible is affected by OP
atrophy of bone -> incompetent dentition (teeth fall out, pt cannot eat)
what are some complications of maxilla/mandible affected by OP
change in nutrtion and change in metb
dx OP
xray (only visible in late stages)
bone density scan
bone density scan
light absorption (no light shines thru) and transmission (light shines thru) to see density of bone
what 3 areas are usually selected to perform bone density scans
lumbar spine
radius
neck of femur
why are a variety of areas used to perform bone scans
to scan both compact and spongy bone
results of bone scan
called t score. associated with numbs 1-2.5. lower number means more OP
tx for OP
prevent fractures dec pain inc weight bearing activity resportive agents anabolic agents diet
why is there pain in OP
force of m. on weak bone causes MS pain
purpose of weight bearing activity
promotes bone remodelling
fx of resorptive agents
dec breakdown, limit osteoclast activity
fx of anabolic agents
inc bone building, osteoblasts
what do we need to make sure occurs in diet for OP
adeq protein, ca, vit d
Osteoarthritis
degen joint disease
what breaks down in OA
cart break down of subchondral cart in joints
what happens when subchondral cart is broken down in OA
bone on bone lt erosion and inc in friciton
where does OA occur first
large, weight bearing joints
what type of issue may we confuse OA with?
inflm. IT is NOT an inflm issue although damage -> inflm
priarmy OA
related to age
secondary OA
inc in young adults, inc joint use leading to damage
primary OA et
idipathic rt wear and tear
genetic dispostion
what genetic def may occur in primary oa
some genes code for proteins that assist with cart remodelling. pts with OA may not have this gene -> cart is easier to damage and harder to repair
secondary oa et
injury, repetitive movement at time of injury
obesity (inc mass on joints -> inc weawr, metb link rt joint)
fx of articular cart
smooth, wt bearing, dissipates force evently to bone
what cells maintain cart
chondrocytes
when does comp and properties of cart change
when chondrocytes are altered (genes?)
what is released when chondrocytes are altered
cells rls cytokines (interlukin, TNF)
what happens in joitns when chondrocytes rls cytokines
cells begin to rls proteases causing destr of cart/chondrocytes
how to chondrocytes change once they are affected by proteases
inability to maintain and heal cart
what happens to bone when there is no cart to protect it
beings to scleros (harden)
cysts and fissures appear as synovial fluid enter cracks
osteophyte formation
osteophyte
enlargement and deformation of joints
what actions stimulate response from chondrocytes
mechanical injury
destr of joint strs by protease rls/subchondrol bone destr
when do osteophyts form
when subchondrol bone is destroyed
main features of early disease in OA
narrowing joint spaces and cart breakdown
main features of late disease in OA
sev cart loss and osteophyte fomration
how does force spread in a normal joint
maximizing contact area by causing joint deformation
how does force spread in a joint with OA
no deformation with load -> force spread unevenly so its more conc causing damage
initial complaints in mnfts of oa
non localized aching pain
late complaints in mnfts of oa
localized pain rt activity and use of joint
weight bearing crepitus
what does inc use of joints in oa cause
pain
what does dec use of joints in oa cause
dec mobility and stiffening plus inflm
dx oa
presentation
xray (only with inc damage)
labs (to exclude other forms of arthritis
tx for oa
pain releif only
rehab
artificial joints
initial tx for oa
mono tx for pain
what drugs do we use for inital tx for oa
first choice: tylenol
2nd choice: cyclognease )COX ex inhibitor
fx of cox inhibitior
inhibits the ez that does 2 things
1) enhances inflm
2) forms prostalglandins
sev tx for oa
intra articular injection of steroids
rhumatoid arthritis incidence
1-2% of adults, 80% is women
what else does RA affect
synovial joints
CT
where does ra begin
non weight bearing joints
et of ra
complex et
hla autoimmunity
viral trigger
what virus may trigger ra
epstein barr
main patho of ra
alt t cell response -> targets synovial joint membs (CT) -> inflm/joint damage
what abn abs occur in 75% of pts with ra
rhumatoid factors, RF
what causes RF prod in ra
alt b cells cause ab to form rf
what type of rxn is ra
type 3 h
what happens in type 3 h rxn in ra
Rf forms IC ->deposition of IC in synovial membs -> inflm
what happens in RA with repetitive inflm
abn pathologic deform
what abn deposit forms in joints in RA
pannus
pannus
vascular granulation tissue
what does pannus rls
destr ez that targets cart
what does pannus contain
inflm cells with inc mediators that damage -> dec joint motility
systemic mnfts of ra
neck pain, eye lesions, low grade fever/fatigue, weakness, lymphandenopathy, splenomeglay, ulnar deviation
mnfts of ra
not restr to joints extra articular / articular mgnt subtle onset am joint pain non articular issues
what subtle onset occurs with ra
malaise
low grade fever
gen m. pain
inc fatigue with time
what may subtle onset of mnfts of ra be rt to
viral triggeR?
why does AM joint pain occur in RA
dec utlization of joints over night
what non articular issues occur with ra
issues with heart, blood vessels, skin, lung, eyes
dx ra
xr,
labs (RF, ana1)
tx for ra
limit progression using immune modulatores
manage pain
eye tx
what drugs are used to manage pain in ra and what are their fxs
meloxicam
matrosym
begin to destr ez’s
fx of plaquenil
antiparasitic
tx of inflam disorders
eye exam q8-12mo
what combo tx is usually used for ra
sulfasalazine
methotrexate
what labs are associated with combo tx of ra
monthly cbc, liver ez, creatinine
gout
crystal dep in joints -> crystal induced joint disease
what is there an inc in blood in gout
uric acid
primary gout
most prevelant form
metb disrder rt abn or inc form of uric acid
affects mostly men
secondary gout
build up of uric acid rt azotemia or se of other med -> inc cell turnover and destr
what may inc build up of uric acid be rt (secondary gout_
cell destr
abn renal fx
other - alcohol, chemo pts
altered break down of what leads to asymptomatic hyper uricemia rt inability of kindey to cope
purine
how are purine and uric acid related
uric acid is a byprod of alt purine breakdown
what cell response occurs initially when crystals begin to deposit in synovial joints
wbc influx and complement activation
what happens when wbc phagocytize crystals (ingestthem) in gout
wbc necrosis
why does ez damage occur in gout
wbc necrosis lt -> rls of lysosomal ez causing ez damage
what causes tophi formation in gout
recurrent, cyclic attacks (acute)
tophi/tophus
lesion with inc uric acid crystals in joint
what happens when tophi form in joint
dec joint mobility rt accum and form of hard mass
first stage of gout
asympt hyperuricemia
2nd stage gout
pt gets up at night with single, very painful joint rt acute inflm
which joints are usually first affected in gout
distal joints, large toe
what does second stage gout normally follow
bing drinking beer
ing eating (esp protein rich food)
excessive exercise
why does binge drinking beer potentially result in gout
beer has inc purine content
why may eating large means with protein rich food cause gout
protein breaks down into purine
why may excessive exercise cause gout
inc damage to proteins rt uric acid rls as prod of protein catabolism
why does gout form in distal joints
uric acid has dec solubility in dec temps, so the further blood with inc [uric acid] moves away from the core, the more likely it is this will crystalize
why does gout usually form at night
blood remains in distal body parts longer when pt lays still for long amount of time eg night
3 stage gout
inflm subsites within a week
how long may gout be asymptomatic after 3rd stage gout
mo-yrs
what happens in stage 4/5 of gout
freq+recurrent attacks in multi joints -> perm damage
dx gout
serum and urine for inc uric acid content (not ideal for only dx.
confirm hyperuricemia in joints via xr
tx gout (acute attacks)
tx pain and inflm with
NSAIDS
colchine
steroids
colchine
targets movement of luekocytes -> joints
tx of gout (long term)
dec hyperuricemia by inc uric acid excer
no alcohol
dec protein diet
are tophus permanent
yes
