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PAtho > Unit 21 > Flashcards

Unit 21 Flashcards

1
Q

osteoporosis

A

atrophy of bone or l/o bone mass,composition, matrix

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2
Q

what does fragile bones in OP mean

A

physiologic stress may fracture bones

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3
Q

et OP

A

aging
genetic predisposition related to pbm
endorcine changes rt age

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4
Q

what endocrine changes occur with age in relation to op

A

no E prod in menopausal women -> E is supportive of bone and limits osteoblast prod

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5
Q

2 risk for op

A

low pbm

low e rt menopause

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6
Q

low bpm

A

more bone is being removed then put in, negative reinforcment

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7
Q

what does dec E in OP mean

A

inc bone loss

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8
Q

what age do we normally reach pbm

A

30

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9
Q

what happens after age 30 in OP

A

we slowly begin to loose bone mass (negative reinforcement)

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10
Q

how can we inc pbm and cause a more gradual dec after age 30

A

healthy lifestyel

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11
Q

when does longitudinal bone growth stop

A

20yo

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12
Q

what is negative reinforcement of pbm talking about

A

resportion is > then formation

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13
Q

what type of changes occur to bone with dec pbm

A

architectural (visible)

microscopic (microdamage)

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14
Q

what is the first sign (usually) of OP

A

fracture

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15
Q

which 2 areas of bone are most affected in OP

A

vertabrae

maxilla/mandible

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16
Q

what happens when vertabrae are affected by OP

A

hunched stature, change in height

breathing problems rt spine distortion

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17
Q

what happens when the maxilla/mandible is affected by OP

A

atrophy of bone -> incompetent dentition (teeth fall out, pt cannot eat)

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18
Q

what are some complications of maxilla/mandible affected by OP

A

change in nutrtion and change in metb

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19
Q

dx OP

A

xray (only visible in late stages)

bone density scan

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20
Q

bone density scan

A

light absorption (no light shines thru) and transmission (light shines thru) to see density of bone

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21
Q

what 3 areas are usually selected to perform bone density scans

A

lumbar spine
radius
neck of femur

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22
Q

why are a variety of areas used to perform bone scans

A

to scan both compact and spongy bone

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23
Q

results of bone scan

A

called t score. associated with numbs 1-2.5. lower number means more OP

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24
Q

tx for OP

A 
prevent fractures
dec pain
inc weight bearing activity
resportive agents
anabolic agents
diet
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25
Q

why is there pain in OP

A

force of m. on weak bone causes MS pain

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26
Q

purpose of weight bearing activity

A

promotes bone remodelling

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27
Q

fx of resorptive agents

A

dec breakdown, limit osteoclast activity

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28
Q

fx of anabolic agents

A

inc bone building, osteoblasts

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29
Q

what do we need to make sure occurs in diet for OP

A

adeq protein, ca, vit d

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30
Q

Osteoarthritis

A

degen joint disease

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31
Q

what breaks down in OA

A

cart break down of subchondral cart in joints

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32
Q

what happens when subchondral cart is broken down in OA

A

bone on bone lt erosion and inc in friciton

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33
Q

where does OA occur first

A

large, weight bearing joints

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34
Q

what type of issue may we confuse OA with?

A

inflm. IT is NOT an inflm issue although damage -> inflm

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35
Q

priarmy OA

A

related to age

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36
Q

secondary OA

A

inc in young adults, inc joint use leading to damage

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37
Q

primary OA et

A

idipathic rt wear and tear

genetic dispostion

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38
Q

what genetic def may occur in primary oa

A

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

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39
Q

secondary oa et

A

injury, repetitive movement at time of injury

obesity (inc mass on joints -> inc weawr, metb link rt joint)

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40
Q

fx of articular cart

A

smooth, wt bearing, dissipates force evently to bone

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41
Q

what cells maintain cart

A

chondrocytes

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42
Q

when does comp and properties of cart change

A

when chondrocytes are altered (genes?)

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43
Q

what is released when chondrocytes are altered

A

cells rls cytokines (interlukin, TNF)

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44
Q

what happens in joitns when chondrocytes rls cytokines

A

cells begin to rls proteases causing destr of cart/chondrocytes

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45
Q

how to chondrocytes change once they are affected by proteases

A

inability to maintain and heal cart

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46
Q

what happens to bone when there is no cart to protect it

A

beings to scleros (harden)
cysts and fissures appear as synovial fluid enter cracks
osteophyte formation

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47
Q

osteophyte

A

enlargement and deformation of joints

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48
Q

what actions stimulate response from chondrocytes

A

mechanical injury

destr of joint strs by protease rls/subchondrol bone destr

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49
Q

when do osteophyts form

A

when subchondrol bone is destroyed

50
Q

main features of early disease in OA

A

narrowing joint spaces and cart breakdown

51
Q

main features of late disease in OA

A

sev cart loss and osteophyte fomration

52
Q

how does force spread in a normal joint

A

maximizing contact area by causing joint deformation

53
Q

how does force spread in a joint with OA

A

no deformation with load -> force spread unevenly so its more conc causing damage

54
Q

initial complaints in mnfts of oa

A

non localized aching pain

55
Q

late complaints in mnfts of oa

A

localized pain rt activity and use of joint

weight bearing crepitus

56
Q

what does inc use of joints in oa cause

A

pain

57
Q

what does dec use of joints in oa cause

A

dec mobility and stiffening plus inflm

58
Q

dx oa

A

presentation
xray (only with inc damage)
labs (to exclude other forms of arthritis

59
Q

tx for oa

A

pain releif only
rehab
artificial joints

60
Q

initial tx for oa

A

mono tx for pain

61
Q

what drugs do we use for inital tx for oa

A

first choice: tylenol

2nd choice: cyclognease )COX ex inhibitor

62
Q

fx of cox inhibitior

A

inhibits the ez that does 2 things

1) enhances inflm
2) forms prostalglandins

63
Q

sev tx for oa

A

intra articular injection of steroids

64
Q

rhumatoid arthritis incidence

A

1-2% of adults, 80% is women

65
Q

what else does RA affect

A

synovial joints

CT

66
Q

where does ra begin

A

non weight bearing joints

67
Q

et of ra

A

complex et
hla autoimmunity
viral trigger

68
Q

what virus may trigger ra

A

epstein barr

69
Q

main patho of ra

A

alt t cell response -> targets synovial joint membs (CT) -> inflm/joint damage

70
Q

what abn abs occur in 75% of pts with ra

A

rhumatoid factors, RF

71
Q

what causes RF prod in ra

A

alt b cells cause ab to form rf

72
Q

what type of rxn is ra

A

type 3 h

73
Q

what happens in type 3 h rxn in ra

A

Rf forms IC ->deposition of IC in synovial membs -> inflm

74
Q

what happens in RA with repetitive inflm

A

abn pathologic deform

75
Q

what abn deposit forms in joints in RA

A

pannus

76
Q

pannus

A

vascular granulation tissue

77
Q

what does pannus rls

A

destr ez that targets cart

78
Q

what does pannus contain

A

inflm cells with inc mediators that damage -> dec joint motility

79
Q

systemic mnfts of ra

A

neck pain, eye lesions, low grade fever/fatigue, weakness, lymphandenopathy, splenomeglay, ulnar deviation

80
Q

mnfts of ra

A 
not restr to joints
extra articular / articular mgnt
subtle onset
am joint pain
non articular issues
81
Q

what subtle onset occurs with ra

A

malaise
low grade fever
gen m. pain
inc fatigue with time

82
Q

what may subtle onset of mnfts of ra be rt to

A

viral triggeR?

83
Q

why does AM joint pain occur in RA

A

dec utlization of joints over night

84
Q

what non articular issues occur with ra

A

issues with heart, blood vessels, skin, lung, eyes

85
Q

dx ra

A

xr,

labs (RF, ana1)

86
Q

tx for ra

A

limit progression using immune modulatores
manage pain
eye tx

87
Q

what drugs are used to manage pain in ra and what are their fxs

A

meloxicam
matrosym
begin to destr ez’s

88
Q

fx of plaquenil

A

antiparasitic
tx of inflam disorders
eye exam q8-12mo

89
Q

what combo tx is usually used for ra

A

sulfasalazine

methotrexate

90
Q

what labs are associated with combo tx of ra

A

monthly cbc, liver ez, creatinine

91
Q

gout

A

crystal dep in joints -> crystal induced joint disease

92
Q

what is there an inc in blood in gout

A

uric acid

93
Q

primary gout

A

most prevelant form
metb disrder rt abn or inc form of uric acid
affects mostly men

94
Q

secondary gout

A

build up of uric acid rt azotemia or se of other med -> inc cell turnover and destr

95
Q

what may inc build up of uric acid be rt (secondary gout_

A

cell destr
abn renal fx
other - alcohol, chemo pts

96
Q

altered break down of what leads to asymptomatic hyper uricemia rt inability of kindey to cope

A

purine

97
Q

how are purine and uric acid related

A

uric acid is a byprod of alt purine breakdown

98
Q

what cell response occurs initially when crystals begin to deposit in synovial joints

A

wbc influx and complement activation

99
Q

what happens when wbc phagocytize crystals (ingestthem) in gout

A

wbc necrosis

100
Q

why does ez damage occur in gout

A

wbc necrosis lt -> rls of lysosomal ez causing ez damage

101
Q

what causes tophi formation in gout

A

recurrent, cyclic attacks (acute)

102
Q

tophi/tophus

A

lesion with inc uric acid crystals in joint

103
Q

what happens when tophi form in joint

A

dec joint mobility rt accum and form of hard mass

104
Q

first stage of gout

A

asympt hyperuricemia

105
Q

2nd stage gout

A

pt gets up at night with single, very painful joint rt acute inflm

106
Q

which joints are usually first affected in gout

A

distal joints, large toe

107
Q

what does second stage gout normally follow

A

bing drinking beer
ing eating (esp protein rich food)
excessive exercise

108
Q

why does binge drinking beer potentially result in gout

A

beer has inc purine content

109
Q

why may eating large means with protein rich food cause gout

A

protein breaks down into purine

110
Q

why may excessive exercise cause gout

A

inc damage to proteins rt uric acid rls as prod of protein catabolism

111
Q

why does gout form in distal joints

A

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

112
Q

why does gout usually form at night

A

blood remains in distal body parts longer when pt lays still for long amount of time eg night

113
Q

3 stage gout

A

inflm subsites within a week

114
Q

how long may gout be asymptomatic after 3rd stage gout

A

mo-yrs

115
Q

what happens in stage 4/5 of gout

A

freq+recurrent attacks in multi joints -> perm damage

116
Q

dx gout

A

serum and urine for inc uric acid content (not ideal for only dx.
confirm hyperuricemia in joints via xr

117
Q

tx gout (acute attacks)

A

tx pain and inflm with
NSAIDS
colchine
steroids

118
Q

colchine

A

targets movement of luekocytes -> joints

119
Q

tx of gout (long term)

A

dec hyperuricemia by inc uric acid excer
no alcohol
dec protein diet

120
Q

are tophus permanent

A

yes

PAtho (31 decks)

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