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Flashcards in Unit 21 Deck (120):
1

osteoporosis

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

2

what does fragile bones in OP mean

physiologic stress may fracture bones

3

et OP

aging
genetic predisposition related to pbm
endorcine changes rt age

4

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

5

2 risk for op

low pbm
low e rt menopause

6

low bpm

more bone is being removed then put in, negative reinforcment

7

what does dec E in OP mean

inc bone loss

8

what age do we normally reach pbm

30

9

what happens after age 30 in OP

we slowly begin to loose bone mass (negative reinforcement)

10

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

healthy lifestyel

11

when does longitudinal bone growth stop

20yo

12

what is negative reinforcement of pbm talking about

resportion is > then formation

13

what type of changes occur to bone with dec pbm

architectural (visible)
microscopic (microdamage)

14

what is the first sign (usually) of OP

fracture

15

which 2 areas of bone are most affected in OP

vertabrae
maxilla/mandible

16

what happens when vertabrae are affected by OP

hunched stature, change in height
breathing problems rt spine distortion

17

what happens when the maxilla/mandible is affected by OP

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

18

what are some complications of maxilla/mandible affected by OP

change in nutrtion and change in metb

19

dx OP

xray (only visible in late stages)
bone density scan

20

bone density scan

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

21

what 3 areas are usually selected to perform bone density scans

lumbar spine
radius
neck of femur

22

why are a variety of areas used to perform bone scans

to scan both compact and spongy bone

23

results of bone scan

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

24

tx for OP

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

25

why is there pain in OP

force of m. on weak bone causes MS pain

26

purpose of weight bearing activity

promotes bone remodelling

27

fx of resorptive agents

dec breakdown, limit osteoclast activity

28

fx of anabolic agents

inc bone building, osteoblasts

29

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

adeq protein, ca, vit d

30

Osteoarthritis

degen joint disease

31

what breaks down in OA

cart break down of subchondral cart in joints

32

what happens when subchondral cart is broken down in OA

bone on bone lt erosion and inc in friciton

33

where does OA occur first

large, weight bearing joints

34

what type of issue may we confuse OA with?

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

35

priarmy OA

related to age

36

secondary OA

inc in young adults, inc joint use leading to damage

37

primary OA et

idipathic rt wear and tear
genetic dispostion

38

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

39

secondary oa et

injury, repetitive movement at time of injury
obesity (inc mass on joints -> inc weawr, metb link rt joint)

40

fx of articular cart

smooth, wt bearing, dissipates force evently to bone

41

what cells maintain cart

chondrocytes

42

when does comp and properties of cart change

when chondrocytes are altered (genes?)

43

what is released when chondrocytes are altered

cells rls cytokines (interlukin, TNF)

44

what happens in joitns when chondrocytes rls cytokines

cells begin to rls proteases causing destr of cart/chondrocytes

45

how to chondrocytes change once they are affected by proteases

inability to maintain and heal cart

46

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

47

osteophyte

enlargement and deformation of joints

48

what actions stimulate response from chondrocytes

mechanical injury
destr of joint strs by protease rls/subchondrol bone destr

49

when do osteophyts form

when subchondrol bone is destroyed

50

main features of early disease in OA

narrowing joint spaces and cart breakdown

51

main features of late disease in OA

sev cart loss and osteophyte fomration

52

how does force spread in a normal joint

maximizing contact area by causing joint deformation

53

how does force spread in a joint with OA

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

54

initial complaints in mnfts of oa

non localized aching pain

55

late complaints in mnfts of oa

localized pain rt activity and use of joint
weight bearing crepitus

56

what does inc use of joints in oa cause

pain

57

what does dec use of joints in oa cause

dec mobility and stiffening plus inflm

58

dx oa

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

59

tx for oa

pain releif only
rehab
artificial joints

60

initial tx for oa

mono tx for pain

61

what drugs do we use for inital tx for oa

first choice: tylenol
2nd choice: cyclognease )COX ex inhibitor

62

fx of cox inhibitior

inhibits the ez that does 2 things
1) enhances inflm
2) forms prostalglandins

63

sev tx for oa

intra articular injection of steroids

64

rhumatoid arthritis incidence

1-2% of adults, 80% is women

65

what else does RA affect

synovial joints
CT

66

where does ra begin

non weight bearing joints

67

et of ra

complex et
hla autoimmunity
viral trigger

68

what virus may trigger ra

epstein barr

69

main patho of ra

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

70

what abn abs occur in 75% of pts with ra

rhumatoid factors, RF

71

what causes RF prod in ra

alt b cells cause ab to form rf

72

what type of rxn is ra

type 3 h

73

what happens in type 3 h rxn in ra

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

74

what happens in RA with repetitive inflm

abn pathologic deform

75

what abn deposit forms in joints in RA

pannus

76

pannus

vascular granulation tissue

77

what does pannus rls

destr ez that targets cart

78

what does pannus contain

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

79

systemic mnfts of ra

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

80

mnfts of ra

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

81

what subtle onset occurs with ra

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

82

what may subtle onset of mnfts of ra be rt to

viral triggeR?

83

why does AM joint pain occur in RA

dec utlization of joints over night

84

what non articular issues occur with ra

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

85

dx ra

xr,
labs (RF, ana1)

86

tx for ra

limit progression using immune modulatores
manage pain
eye tx

87

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

meloxicam
matrosym
begin to destr ez's

88

fx of plaquenil

antiparasitic
tx of inflam disorders
eye exam q8-12mo

89

what combo tx is usually used for ra

sulfasalazine
methotrexate

90

what labs are associated with combo tx of ra

monthly cbc, liver ez, creatinine

91

gout

crystal dep in joints -> crystal induced joint disease

92

what is there an inc in blood in gout

uric acid

93

primary gout

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

94

secondary gout

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

95

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

cell destr
abn renal fx
other - alcohol, chemo pts

96

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

purine

97

how are purine and uric acid related

uric acid is a byprod of alt purine breakdown

98

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

wbc influx and complement activation

99

what happens when wbc phagocytize crystals (ingestthem) in gout

wbc necrosis

100

why does ez damage occur in gout

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

101

what causes tophi formation in gout

recurrent, cyclic attacks (acute)

102

tophi/tophus

lesion with inc uric acid crystals in joint

103

what happens when tophi form in joint

dec joint mobility rt accum and form of hard mass

104

first stage of gout

asympt hyperuricemia

105

2nd stage gout

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

106

which joints are usually first affected in gout

distal joints, large toe

107

what does second stage gout normally follow

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

108

why does binge drinking beer potentially result in gout

beer has inc purine content

109

why may eating large means with protein rich food cause gout

protein breaks down into purine

110

why may excessive exercise cause gout

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

111

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

112

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

113

3 stage gout

inflm subsites within a week

114

how long may gout be asymptomatic after 3rd stage gout

mo-yrs

115

what happens in stage 4/5 of gout

freq+recurrent attacks in multi joints -> perm damage

116

dx gout

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

117

tx gout (acute attacks)

tx pain and inflm with
NSAIDS
colchine
steroids

118

colchine

targets movement of luekocytes -> joints

119

tx of gout (long term)

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

120

are tophus permanent

yes