Musculoskeletal Flashcards
1
Q
What is osteoarthritis?
A
A degenerative joint disorder caused by a breakdown of cartilage in a (usually sinovial) joint
2
Q
What makes up the articular capsule of a sinovial joint?
A
fibrous capsule
synovial membrane
3
Q
What joints are affected by osteoarthritis?
A
affects weight-baring joints asymmetrically
e.g. knees, hips, neck, hands, feet
4
Q
What are the risk factors for osteoarthritis?
A
- age > 50
- female
- obesity
- previous joint injury
- leg abnormality (e.g. bow legs, knock knees)
- family history
5
Q
Describe the classification of osteoarthritis.
A
PRIMARY (idiopathic)
no preceding injury, usually due to old age
SECONDARY
due to congenital abnormality
trauma
inflammatory arthropathy
6
Q
What is the clinical presentation of osteoarthritis?
A
pain:
- worse at end of the day
- exacerbated by exercise and relieved by rest
stiffness (especially after rest)
malalignment of joint- if osteoarthritis is severe may have Genu Varus (bow legs) and Gent Valgus (knock knees)
tenderness on joint palpation
decreased range of motion
Bouchard’s/ Heberden’s nodes
7
Q
What are the true names for bow legs and knock knees?
A
bow legs- genu varus
knock knees- genu valgus
8
Q
What are Bouchard’s and Heberden’s nodes?
A
bony swellings of the hand typical of osteoarthritis
Bouchard’s are proximal and Herbenden’s are distal
9
Q
What is the differential diagnosis for osteoarthritis?
A
- gout/ pseudogout
- rheumatoid arthritis
- psoriatic arthritis
- bursitis
- avascular necrosis
- internal derangements
10
Q
What is bursitis?
A
inflammation of fluid filled sacs (bursa) in the joints
11
Q
What investigations are used to diagnose osteoarthritis?
A
X-RAY pneumonic: LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
Serum CRP and serum ESR may also be elevated in osteoarthritis
12
Q
What is the conservative management of osteoarthritis?
A
weight loss
less sport, more rest
physio- muscle strengthening
walking aids, supportive footwear, home modifications
13
Q
What is the medical management of osteoarthritis?
A
- Analgesia:
- paracetamol
- NSAIDS (ibuprofen, naproxen)
- capsaicin cream - Joint injection:
- steroids (hydrocortisone)
14
Q
What is capsaicin derived from?
A
chilli peppers
15
Q
What is the surgical management of osteoarthritis?
A
- arthroscopy: visualise damage and remove any lost bodies
- arthroplasty: joint replacement
- osteotomy: cut bone to change shape/ length
- fusion
16
Q
Describe the pathophysiology of osteoarthritis.
A
- Degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage and the inflammatory cells in the surrounding tissue
- Release of enzymes from these cells break down collagen and proteoglycans, destroying the articular cartilage
- The exposure of the underlying subchondral bone results in sclerosis, followed by active remodelling changes that lead to the formation osteophytes and subchondral bone cysts
- The joint space is collectively lost over time
17
Q
What is the most common type of arthritis?
A
Osteoarthritis
18
Q
What are DMARDS used to treat?
A
rheumatoid arthritis
ankylosing spondylitis
psoriatic arthritis
systemic lupus erythematosus
19
Q
What is rheumatoid arthritis?
A
chronic inflammatory, autoimmune condition primarily affecting small joints of the hands and feet symmetrically
20
Q
What genes are associated with rheumatoid arthritis?
A
most associated: HLA-DR4
others:
STAT4
TRAF1
PTPN22
21
Q
Describe the involvement of big joints in rheumatoid arthritis.
A
no spinal involvement
big joints can be affected later down the line, but it is a bad prognostic sign if they are affected on presentation
22
Q
What % of the population are affected by rheumatoid arthritis?
A
1%
23
Q
What % of the population are affected by osteoarthritis?
A
10% of men
18% of women
24
Q
What are the risk factors for rheumatoid arthritis?
A
- 3 times more common in females
- family history
- smoking
- middle aged
25
What is the clinical presentation of rheumatoid arthritis?
- morning stiffness
- systemic presentations: scleritis, pleural effusions, pericarditis
- deformities of the hand (ulnar deviation, swan neck deformity, boutonniere deformity)
- pain in affected joints
26
What are the investigations for rheumatoid arthritis?
- X-Ray (LOES):
Loss of joint space
Osteopenia
Erosion of bone
Swelling of soft tissue
- Rheumatoid factor (positive in 60-70% of cases)
- Anti-cyclic citrullinated peptide (Anti-CCP) antibody (positive in 70% of cases)
27
What is the DIAGNOSTIC CRITERIA for rheumatoid arthritis?
Symptoms lasting more than 6 weeks, plus > 4 of:
- rheumatoid factor present
- finger/ hand/ wrist involvement
- rheumatoid nodules present
- involvement of 3 or more joints
- stiffness in the morning for > 1 hour
- erosions seen on x-ray
- symmetrical involvement
28
What is the medical management of rheumatoid arthritis?
1. DMARD
2. DMARD + biologic
During a flare up: NSAID + PPI (e.g. ibuprofen + omeprazole)
29
What is a DMARD?
disease-modifying anti-rheumatic drugs
30
What DMARDS and biologics are prescribed for rheumatoid arthritis?
DMARDS: methotrexate, sulfasalazine, hydroxychloroquine
biologics: infliximab, rituximab
31
What must be prescribed alongside DMARDs for rheumatoid arthritis?
should give a glucocorticoid (e.g. prednisolone) as this further slows progression of RA
for methotrexate specifically must prescribe folic acid supplements to protect body's healthy cells and prevent D+V
32
What is the mechanism of action and side effects of methotrexate?
MECHANISM OF ACTION:
inhibits enzymes involved in purine metabolism which inhibits T cell action
SIDE EFFECTS:
mouth ulcers
hair loss
diarrhoea
33
What is the mechanism of action and side effects of sulfasalazine?
MECHANISM OF ACTION:
inhibits inflammatory molecules (e.g. inhibits COX which is the enzyme involved in prostaglandin synthesis)
SIDE EFFECTS:
dry cough
diarrhoea
headaches
34
What is the mechanism of action and side effects of hydroxychloroquine?
MECHANISM OF ACTION:
suppresses TOLL-like receptors which stops activation of innate immune response and autoimmune disease
SIDE EFFECTS:
abdo pain
dizziness
eye oedema/ disorders
35
Describe the mechanism of action and side effects of glucocorticoids as a supplementary treatment for rheumatoid arthritis.
MECHANISM OF ACTION:
they are immune-suppressants that cause vasodilation and decreased leukocyte migration + reduced permeability of capillaries to sites of inflammation
SIDE EFFECTS:
weight gain
easy bruising
muscle weakness
mood changes
insomnia
36
Describe the mechanism of action and side effects of infliximab in the treatment of rheumatoid arthritis.
MECHANISM OF ACTION:
inhibits tumour necrosing factor- alpha
inhibits immune response
SIDE EFFECTS:
increased risk of infection
fever
headache
skin reaction at injection site
37
Describe the mechanism of action and side effects of rituximab in the treatment of rheumatoid arthritis.
MECHANISM OF ACTION:
inhibits CD20- stops cell lysis and reduces inflammation
SIDE EFFECTS:
back pain
bloating
blood in urine/ stool
38
In the case of a rheumatoid arthritis flare up, why must you prescribe a PPI with the NSAID?
to protect the gastric mucosa
39
What are the non-surgical/ non-pharmacological interventions for rheumatoid arthritis?
physiotherapy
occupational therapy
podiatry
transcutaneous electrical nerve stimulation (TENS machine)
40
What are the possible surgical interventions for rheumatoid arthritis?
- finger/ hand/ wrist surgery to correct joint malformation
- arthroscopy
- joint replacement
- joint fusion
41
What is the differential diagnosis for rheumatoid arthritis?
psoriatic arthritis
infectious arthritis
gout
SLE
osteoarthritis
42
What is gout?
a type of inflammatory arthritis caused by deposition of irate crystals in the joint
43
Describe the epidemiology of gout.
- most common cause of acute joint swelling
- more common in males and elderly
- uncommon in female under 50
- increasing frequency due to aging population
44
Describe the pathogenesis of gout.
underlying hyperuricaemia
- plasma is super saturated at 6.8mg/dL which leads to uric acid crystal formation, clustering, propagation...
- cold and trauma may alter crystal solubility
uricase is not present in humans so the uric acid crystals are insoluble
symptoms are caused by inflammatory response to irate deposition in joint
45
Describe the pattern of gout symptoms.
an individual with chronic gout with have episodes of acute gout attacks then recover and so on
46
What are the stages of gout symptoms?
4 stages:
1. asymptomatic hyperuricaemia
2. acute gout
3. inter critical gout
4. chronic tophaceous gout
47
What is the inter critical gout stage?
acute gout has been resolved and treatment is geared towards prevention of further attacks
48
What are the acute symptoms of gout?
rapid onset of severe pain
acute monoarthritis
classical podagra- gout of the big toe
general malaise
low grade fever
swelling of the joint
erythema
shiny overlaying skin
49
What is the chronic symptom of gout?
tophi
50
What are tophi?
stone-like deposits of monosodium urate in the soft tissues, synovial tissues, or in bones near the joints
51
What are the risk factors for gout?
high beer intake
intake of high purine foods
family history
age
male
menopause
52
What are the investigations for gout?
BEST TEST= joint aspiration and polarised light microscopy
serum uric acid levels
x-ray- normal in an acute attack but useful when investigating chronic gout
53
How do gout crystals appear on joint aspiration and polarised light microscopy?
needle shaped
negatively birefringent
54
How does gout affect serum uric acid levels?
chronic gout suffers have generally high serum uric acid
during an acute attack the uric acid from the blood migrates to joints which lowers the serum uric acid to either normal or below normal
therefore serum uric acid test should only be done outside of an acute attack as a diagnostic tool
55
How does chronic gout appear on an x-ray?
complete loss of joint space
soft tissue swelling
junta articular erosions (rat bite erosions)
56
What is the treatment for an acute gout attack?
ADVICE:
rest
ice the joint
stay hydrated
continue urate lowering therapy
MEDICATION:
NSAIDS/ COX-2 inhibitors
colchicine
prednisolone
IF ELDERLY +/- CKD
reduced dose colchicine
prednisolone
AVOID NSAIDS/ COX-2
57
What is the prophylactic treatment for chronic gout?
ADVICE:
dietary modification: reduce alcohol, lose weight, reduce purine rich foods and fructose containing drinks
MEDICATION:
allopurinol
febuxostat if allopurinol intolerant/ inefficacy (CKD)
benzbromarone
PLUS...
colchicine 500micrograms OD for up to 6 months as allopurinol can cause an acute attack when started
also need a CV risk assessment and treatment
58
What's the differential diagnoses for gout?
pseudogout
septic arthritis
trauma
RA
reactive arthritis
psoriatic arthritis
59
What is the true medical term for pseudo gout?
calcium pyrophosphate deposition
60
Gout and pseudo gout are what type of condition?
crystal arthropathies
61
What is the name for the thumb to hand-base joint?
1st carpo-metacarpal joint
62
In what disease do you see mobile, subcutaneous nodules at points of pressure?
rheumatoid arthritis
63
Why does higher diary intake improve gout?
promotes excretion of uric acid into the urine
64
Which inflammatory diseased increase the risk of osteoporosis and why?
inflammatory cytokines increase bone resorption
includes:
rheumatoid arhtritis
seronegative arthritis
connective tissue disease
IBD
65
Which endocrine conditions increase risk of osteoporosis and why?
- hyperthyroidism and primary hyperparathyroidism
because thyroid hormone and parathyroid hormones increase bone turnover
- Cushing's syndrome,e because cortisol increases bone resorption and induces osteoblast apoptosis
- early menopause/ male hypogonadism because oestrogen and testosterone control bone turnover
66
Which medications increase the risk of osteoporosis?
glucocorticoids
depo-provera
aromatase inhibitors
GnRH analogues
androgen deprivation
67
What is osteoporosis?
a systemic skeletal disease characterised by low bone mass and micro architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture
68
What % of women over the age of 50 will have an osteoporotic fracture?
40%
69
What is a T score?
a measure of bone density
it is a standard deviation score
the score is compared with a gender-matched young adult average
70
What are the three most common fractures resulting from osteoporosis?
hip, wrist, vertebral
71
What has the biggest influence on peak bone mass?
genetic factors
72
What are the risk factors for osteoporosis?
low BMI
family history
female
rheumatoid arthritis
heavy drinking and smoking
sedentary lifestyle
73
What are the causes of osteoporosis?
ENDOCRINE: Cushing's, parathyroid overactivity
HAEM: myeloma
GI: malabsorption
Iatrogenic: steroid use
74
Descrie post-menopausal osteoporosis.
loss of restraining effects of oestrogen on bone turnover
characterised by:
- high one turnover (resorption > formation)
- predominantly cancellous bone loss
- micro architectural disruption
75
How can post-menopausal osteoporosis be prevented?
oestrogen replacement
76
Describe the changes seen in trabecular architecture with aging.
- decrease in trabecular thickness, more pronounced for non load-bearing horizontal trabeculae
- decrease in connections between horizontal trabecular
- decrease in trabecular strength and increased susceptibility to fracture
77
How is osteoporosis diagnosed?
bone densitometry can be used to assess fracture risk
patient will be sent for DEXA scan to measure bone density
T score will be calculated and diagnosis made as a result
78
What does DEXA stand for?
dual energy x-ray absorptiometry
79
Why are DEXA scans useful other than for diagnostic reasons?
DEXA scans only use a low radiation dose so it can be used for children and for research/ screening
80
Describe how a T score is used in the classification of osteoporosis.
bone mass density of spine, hip, femoral neck and forearm taken
T scores:
> -1.0 = normal
-1.0 to -2.5 = osteopenia
< -2.5 = osteoporosis
< -2.5 plus fracture = sever osteoporosis
81
What is osteopenia?
low bone density, but not so low that a diagnosis of osteoporosis is appropriate
82
What are the signs and symptoms of osteoporosis?
usually a broken bone is the first sign
83
When is osteoporosis treated?
only when there's a high fracture risk
84
What drugs are used to treat osteoporosis?
ANTI-RESORPTIVE- decreases osteoclast activity and bone turnover:
- bisphosphonates
- HRT
- denosumab
ANABOLIC- increases osteoblast activity and bone formation
- teriparatide
85
What is the first line treatment for osteoporosis?
bisphosphonates - as they are cheap and effective
given orally or intravenously
86
Which oral bisphosphonates can be given for osteoporosis?
alendronate (daily/ weekly)
risedonate (daily/ weekly)
ibandronate (monthly)
87
Which intravenous bisphosponates can be prescribed for osteoporosis?
ibandronate (3-montly)
zoledronate (annually)
