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Phase 2a BASICS > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What is osteoarthritis?

A

A degenerative joint disorder caused by a breakdown of cartilage in a (usually sinovial) joint

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2
Q

What makes up the articular capsule of a sinovial joint?

A

fibrous capsule
synovial membrane

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3
Q

What joints are affected by osteoarthritis?

A

affects weight-baring joints asymmetrically

e.g. knees, hips, neck, hands, feet

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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
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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

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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

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7
Q

What are the true names for bow legs and knock knees?

A

bow legs- genu varus
knock knees- genu valgus

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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

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9
Q

What is the differential diagnosis for osteoarthritis?

A
  • gout/ pseudogout
  • rheumatoid arthritis
  • psoriatic arthritis
  • bursitis
  • avascular necrosis
  • internal derangements
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10
Q

What is bursitis?

A

inflammation of fluid filled sacs (bursa) in the joints

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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

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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

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13
Q

What is the medical management of osteoarthritis?

A
  1. Analgesia:
    - paracetamol
    - NSAIDS (ibuprofen, naproxen)
    - capsaicin cream
  2. Joint injection:
    - steroids (hydrocortisone)
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14
Q

What is capsaicin derived from?

A

chilli peppers

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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
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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
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17
Q

What is the most common type of arthritis?

A

Osteoarthritis

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18
Q

What are DMARDS used to treat?

A

rheumatoid arthritis
ankylosing spondylitis
psoriatic arthritis
systemic lupus erythematosus

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19
Q

What is rheumatoid arthritis?

A

chronic inflammatory, autoimmune condition primarily affecting small joints of the hands and feet symmetrically

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20
Q

What genes are associated with rheumatoid arthritis?

A

most associated: HLA-DR4

others:
STAT4
TRAF1
PTPN22

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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

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22
Q

What % of the population are affected by rheumatoid arthritis?

A

1%

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23
Q

What % of the population are affected by osteoarthritis?

A

10% of men
18% of women

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24
Q

What are the risk factors for rheumatoid arthritis?

A
  • 3 times more common in females
  • family history
  • smoking
  • middle aged
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25
Q

What is the clinical presentation of rheumatoid arthritis?

A
  • morning stiffness
  • systemic presentations: scleritis, pleural effusions, pericarditis
  • deformities of the hand (ulnar deviation, swan neck deformity, boutonniere deformity)
  • pain in affected joints
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26
Q

What are the investigations for rheumatoid arthritis?

A
  • 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)
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27
Q

What is the DIAGNOSTIC CRITERIA for rheumatoid arthritis?

A

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
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28
Q

What is the medical management of rheumatoid arthritis?

A
  1. DMARD
  2. DMARD + biologic

During a flare up: NSAID + PPI (e.g. ibuprofen + omeprazole)

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29
Q

What is a DMARD?

A

disease-modifying anti-rheumatic drugs

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30
Q

What DMARDS and biologics are prescribed for rheumatoid arthritis?

A

DMARDS: methotrexate, sulfasalazine, hydroxychloroquine

biologics: infliximab, rituximab

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31
Q

What must be prescribed alongside DMARDs for rheumatoid arthritis?

A

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

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32
Q

What is the mechanism of action and side effects of methotrexate?

A

MECHANISM OF ACTION:
inhibits enzymes involved in purine metabolism which inhibits T cell action

SIDE EFFECTS:
mouth ulcers
hair loss
diarrhoea

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33
Q

What is the mechanism of action and side effects of sulfasalazine?

A

MECHANISM OF ACTION:
inhibits inflammatory molecules (e.g. inhibits COX which is the enzyme involved in prostaglandin synthesis)

SIDE EFFECTS:
dry cough
diarrhoea
headaches

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34
Q

What is the mechanism of action and side effects of hydroxychloroquine?

A

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

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35
Q

Describe the mechanism of action and side effects of glucocorticoids as a supplementary treatment for rheumatoid arthritis.

A

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
Q

Describe the mechanism of action and side effects of infliximab in the treatment of rheumatoid arthritis.

A

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
Q

Describe the mechanism of action and side effects of rituximab in the treatment of rheumatoid arthritis.

A

MECHANISM OF ACTION:
inhibits CD20- stops cell lysis and reduces inflammation

SIDE EFFECTS:
back pain
bloating
blood in urine/ stool

38
Q

In the case of a rheumatoid arthritis flare up, why must you prescribe a PPI with the NSAID?

A

to protect the gastric mucosa

39
Q

What are the non-surgical/ non-pharmacological interventions for rheumatoid arthritis?

A

physiotherapy
occupational therapy
podiatry
transcutaneous electrical nerve stimulation (TENS machine)

40
Q

What are the possible surgical interventions for rheumatoid arthritis?

A
  • finger/ hand/ wrist surgery to correct joint malformation
  • arthroscopy
  • joint replacement
  • joint fusion
41
Q

What is the differential diagnosis for rheumatoid arthritis?

A

psoriatic arthritis
infectious arthritis
gout
SLE
osteoarthritis

42
Q

What is gout?

A

a type of inflammatory arthritis caused by deposition of irate crystals in the joint

43
Q

Describe the epidemiology of gout.

A
  • 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
Q

Describe the pathogenesis of gout.

A

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
Q

Describe the pattern of gout symptoms.

A

an individual with chronic gout with have episodes of acute gout attacks then recover and so on

46
Q

What are the stages of gout symptoms?

A

4 stages:

  1. asymptomatic hyperuricaemia
  2. acute gout
  3. inter critical gout
  4. chronic tophaceous gout
47
Q

What is the inter critical gout stage?

A

acute gout has been resolved and treatment is geared towards prevention of further attacks

48
Q

What are the acute symptoms of gout?

A

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
Q

What is the chronic symptom of gout?

A

tophi

50
Q

What are tophi?

A

stone-like deposits of monosodium urate in the soft tissues, synovial tissues, or in bones near the joints

51
Q

What are the risk factors for gout?

A

high beer intake
intake of high purine foods
family history
age
male
menopause

52
Q

What are the investigations for gout?

A

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
Q

How do gout crystals appear on joint aspiration and polarised light microscopy?

A

needle shaped
negatively birefringent

54
Q

How does gout affect serum uric acid levels?

A

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
Q

How does chronic gout appear on an x-ray?

A

complete loss of joint space
soft tissue swelling
junta articular erosions (rat bite erosions)

56
Q

What is the treatment for an acute gout attack?

A

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
Q

What is the prophylactic treatment for chronic gout?

A

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
Q

What’s the differential diagnoses for gout?

A

pseudogout
septic arthritis
trauma
RA
reactive arthritis
psoriatic arthritis

59
Q

What is the true medical term for pseudo gout?

A

calcium pyrophosphate deposition

60
Q

Gout and pseudo gout are what type of condition?

A

crystal arthropathies

61
Q

What is the name for the thumb to hand-base joint?

A

1st carpo-metacarpal joint

62
Q

In what disease do you see mobile, subcutaneous nodules at points of pressure?

A

rheumatoid arthritis

63
Q

Why does higher diary intake improve gout?

A

promotes excretion of uric acid into the urine

64
Q

Which inflammatory diseased increase the risk of osteoporosis and why?

A

inflammatory cytokines increase bone resorption

includes:
rheumatoid arhtritis
seronegative arthritis
connective tissue disease
IBD

65
Q

Which endocrine conditions increase risk of osteoporosis and why?

A
  • 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
Q

Which medications increase the risk of osteoporosis?

A

glucocorticoids
depo-provera
aromatase inhibitors
GnRH analogues
androgen deprivation

67
Q

What is osteoporosis?

A

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
Q

What % of women over the age of 50 will have an osteoporotic fracture?

A

40%

69
Q

What is a T score?

A

a measure of bone density
it is a standard deviation score

the score is compared with a gender-matched young adult average

70
Q

What are the three most common fractures resulting from osteoporosis?

A

hip, wrist, vertebral

71
Q

What has the biggest influence on peak bone mass?

A

genetic factors

72
Q

What are the risk factors for osteoporosis?

A

low BMI
family history
female
rheumatoid arthritis
heavy drinking and smoking
sedentary lifestyle

73
Q

What are the causes of osteoporosis?

A

ENDOCRINE: Cushing’s, parathyroid overactivity
HAEM: myeloma
GI: malabsorption
Iatrogenic: steroid use

74
Q

Descrie post-menopausal osteoporosis.

A

loss of restraining effects of oestrogen on bone turnover

characterised by:
- high one turnover (resorption > formation)
- predominantly cancellous bone loss
- micro architectural disruption

75
Q

How can post-menopausal osteoporosis be prevented?

A

oestrogen replacement

76
Q

Describe the changes seen in trabecular architecture with aging.

A
  • 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
Q

How is osteoporosis diagnosed?

A

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
Q

What does DEXA stand for?

A

dual energy x-ray absorptiometry

79
Q

Why are DEXA scans useful other than for diagnostic reasons?

A

DEXA scans only use a low radiation dose so it can be used for children and for research/ screening

80
Q

Describe how a T score is used in the classification of osteoporosis.

A

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
Q

What is osteopenia?

A

low bone density, but not so low that a diagnosis of osteoporosis is appropriate

82
Q

What are the signs and symptoms of osteoporosis?

A

usually a broken bone is the first sign

83
Q

When is osteoporosis treated?

A

only when there’s a high fracture risk

84
Q

What drugs are used to treat osteoporosis?

A

ANTI-RESORPTIVE- decreases osteoclast activity and bone turnover:
- bisphosphonates
- HRT
- denosumab

ANABOLIC- increases osteoblast activity and bone formation
- teriparatide

85
Q

What is the first line treatment for osteoporosis?

A

bisphosphonates - as they are cheap and effective
given orally or intravenously

86
Q

Which oral bisphosphonates can be given for osteoporosis?

A

alendronate (daily/ weekly)
risedonate (daily/ weekly)
ibandronate (monthly)

87
Q

Which intravenous bisphosponates can be prescribed for osteoporosis?

A

ibandronate (3-montly)
zoledronate (annually)

Phase 2a BASICS (6 decks)

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