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Patient > Introduction to joint disease > Flashcards

Introduction to joint disease Flashcards

1
Q

when does oesteoperosis start?

A

disease of old age but starts early on in life

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2
Q

osteoporosis is more common in….

A

women

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3
Q

OP results in what?

A

fractures

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4
Q

what are the most common fractures associated with OP?

A

hip, wrist and spine

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5
Q

which fractures go largely unnoticed? why?

A

spine

dont report to health professionals

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6
Q

__% die from complications from hip fractures. such as….?

A

20

prolonged hospital stay- infections

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7
Q

1 in __ women over 50

1 in ___ men over 50

A

2

5

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8
Q

TF: bone is the same your entire life

A

FALSE

is constantly turned over and remodelled

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9
Q

how long does the turnover of bone take

A

3 months

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10
Q

what do oestoblasts do?

A

BUILD new bone

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11
Q

what do oesteoclasts do?

A

break down old bone

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12
Q

what is breaking down old bone by oestoclasts also known as?

A

resorption

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13
Q

OP is caused by reduced _____ activity

A

oestoblast

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14
Q

what is the cortex?

A

which outer shell of bone

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15
Q

what is trabecular bone?

A

meshwork of bone inside cortex

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16
Q

what happens to trabecular bone in OP

A

BECOMES HOLEY AND WEAKER

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17
Q

when does your bone density decrease

A

1% per year after you reach peak bone mass

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18
Q

TF: putting stress on skeleton when younger is good to prevent OP?

A

TRUE

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19
Q

what is the WHO definition for OP

A

osteoporosis is a generalized skeletal disorder of low bone mass (thinning of the bone) and deterioration in its architecture (middle bit of bone becomes weaker), causing susceptibility to fracture.

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20
Q

bone takes about ____ days to be remodelled

A

100

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21
Q

what is bone turnover influenced by?

A

hormones- oestrogen, testosterone, cytokines, PGs

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22
Q

if oestrogen and testosterone is low, you are ____ likely to develop OP

A

MORE

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23
Q

what happens when insult activated osteoclasts

A

in response to insult activation is triggered
osteoclasts will start the resorption process
then the reversal phase- holes that need filling
oestroblasts are triggered to fill the hole

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24
Q

signs and symptoms of OP?

A

fracture is usually the first presentation
DXA scan shows reduced bone density
pain
reduced mobility
Kyphosis where the spine starts curving- in vertebral fractures:
Reduction in height
Indigestion (more pressure on stomach)

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25
Q

what is a DXA scan?

A

high intensity X-ray
calculates bone density to see if you are progressing to OP
compares to what you should be at that age

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26
Q

are DXA scans commonly used?

A

NO
very expensive
only high risk patients

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27
Q

what is kyphosis?

A

Kyphosis where the spine starts curving- in vertebral fractures:
Reduction in height
Indigestion (more pressure on stomach)

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28
Q

vertebral fractures can result in a height reduction of….

A

10-20cm

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29
Q

what problems can vertebral fractures cause?

A

indigestion
neck weakness
back pain
loss of mobility

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30
Q

TF: bone density changes throughout life

A

true

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31
Q

when do you peak in bone mass?

A

25-40

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32
Q

what happens at menopause for women? why

A

steep decline in bone density

due to loss of protective effect of oestrogens

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33
Q

what can you do in life to optimise peak bone mass?

A

healthy balanced diet- Ca and Vitamin D

weight bearing exercise early on in life

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34
Q

what about a DXA scan tells us you have OP?

A

get a T score

if the T score is <2.5

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35
Q

what is the most reliable part of the body to scan in DXA scans?

A

hip/ lower spine

36
Q

risk factors for OP

A 
history of fracture 
smoking 
low body weight 
female 
oestrogen deficiency (e.g. menopause) 
corticosteroid use
white 
age 
Ca intake low 
alcohol 
no exercise 
falls 
dementia 
poor health
37
Q

primary prevention for OP?

A

lifestyle changes

try to reduce fall risks- chair lift

38
Q

secondary prevention for OP

A 
pharmacological management: 
Calcium 
Vitamin D
Calcitriol 
HRT 
SERMS
Bisphosphonates 
Calcitonin 
Strontium 
PTH 
Senosumab
39
Q

what is osteoarthritis?

A

disease of ware and tare

limited to 1-2 joints due to damage and stress

40
Q

TF: OA is a disease of all joints

A

FALSE- 1 or 2

41
Q

how do you manage OA?

A

difficult

many need surgery

42
Q

OA affects ___% of >65 year olds

A

12

43
Q

onset of OA is common…

A

40-60 year olds

44
Q

OA is more common in:

men or women

A

women

45
Q

why can obesity increase OA risk?

A

carrying more weight

bigger strain on joints

46
Q

do we know what triggers off OA?

A

no we only know the risks

47
Q

clinical features of OA?

A

joint pain that’s worse at the end of the day
swelling- not always
early morning stiffness for about 30 minutes

48
Q

FT: OA is alway accompanied by swelling?

A

FALSE

49
Q

pathogenesis of OA?

A

Cartilage which protects the ends of the bone at a joint gradually roughens and becomes thin
Thickening of underlying bone
Formation of osteophytes- bony spurts at the edge of a joint= uncomfortable
Thickening & inflammation of synovium
Thickening and contraction of ligament round the outside of the joint

50
Q

can joints in OA repair themselves?

A

Some joints repair themselves, others don’t- if a little bit the body can manage

51
Q

ligaments attach….

A

bone to bone

52
Q

tendons attach…

A

bone to muscle

53
Q

features of mild OA?

A

cartilage is starting to ware away
formation of oestophytes
inflammation

54
Q

features of severe OA?

A

two bones dont have cartilage to cushion between them
bones move closer together
when bones touch opposing bone it rubs and is painful
joint deformity

55
Q

what is needed when someone has severe OA?

A

probably a joint replacement

56
Q

goals of OA management?

A

reduce pain
optimise mobility
minimise joint deformity
patient education

57
Q

normal joint pathophysiology?

A

Cartilage protects the bone
Round the side of the joint= capsule and synovium (membrane round the joint which protect everything) white space- synovial fluid which lubricates

58
Q

non pharmacological management for OA?

A 
weight reduction 
physiotherapy 
exercise plan 
heat or cold packs 
psychological support 
occupational therapy review
59
Q

when will a patient get an occupational therapy review?

A

if mobility is limited

advice on how to independently manage is needed

60
Q

pharmacological managements of OA?

A

ANALGESICS- codeine, paracetamol etc
NSAIDS- if we know there inflammation
corticosteroids- injections into the joints, never oral
chondroprotective agents

61
Q

TF: Oral corticosteroids can be used to treat OA?

A

NO

injected into joints

62
Q

rheumatoid arthritis is a ______ condition

A

systemic

63
Q

can arthritis occur in young children?

A

yes

juvenile arthritis

64
Q

why are there more management options for RA than OA?

A

as we know RA is an autoimmune condition

65
Q

RA affects ___% of the population

A

1-3

66
Q

RA most common ones age?

A

30-50 years

67
Q

what is key for RA?

A

Early intervention

68
Q

why do people with RA have a reduced life expectancy?

A

not from the condition, from cardiac, liver and respiratory conditions

69
Q

are females more likely to get RA than males

A

3:1

70
Q

aetiology of RA?

A

unknown

71
Q

clinical features of RA?

A

slow progressive symmetrical polyarthiritis
pain and stifness in small joints of hands and feet
nearly alway associated with early morning stiffness

72
Q

extra-articular symptoms of RA?

A

Sjogren’s syndrome- reduced secretions- dry eyes and mouth
Vasculitis- inflammatory condition of vessels
Neuropathy- can cause circulation problems
Subcutaneous nodules- painful build-up of tissue over joints effected- can need surgery to remove
Lymphadenopathy- enlargement of lymph nodes
Cardiovascular disease
Depression
Respiratory disease

73
Q

What is sjogrens syndrome?

A

reduced secretions- dry eyes and mouth

74
Q

what is vasculitis

A

inflammatory condition of the vessels

75
Q

what are subcutaneous nodules?

A

painful build up of tissue over joints

need surgery to remove

76
Q

what is lymphadenopathy

A

enlargement of lymph nodes

77
Q

___% of patients have mild RA and respond well to first treatment

A

20

78
Q

__% RA patients develop severe disease which can lead to being in a wheelchair

A

5

79
Q

how many patients have relapsing remitting RA? what does this mean?

A

3/4

flare up for a while and then settles with treatment

80
Q

pathogenesis of RA?

A

Lymphocytes (inflammatory cytokines) infiltrate synovial membrane, causing inflammation & thickening- almost always
Formation of pannus over cartilage causes erosion into bone which causes:
Eventual degeneration of cartilage & joint
Eventually permanent joint damage and deformity

81
Q

What stage of RA does pharmacological intervention become hard

A

once there’s already erosions in the joints

82
Q

goals of RA management?

A

relief of pain and inflammation
prevention of joint damage
improvement in movement ability
maintenance of lifestyle

83
Q

pharmacological management of RA?

A 
analgesics 
NSAIDs
conventional DMARDs 
biological DMARDS
steroid- po/ IM/ injection into joint
84
Q

what are conventional DMARDs

A

disease modifying medicines e.g. methotrexate, sulfasalazine

85
Q

when should conventional DMARDs be given?

A

ideally within 3 months of diagnosis

86
Q

how are Biological DMARDs administered

A

self injection

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