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Phase 2A conditions > MSK conditions > Flashcards

MSK conditions Flashcards

1
Q

What is osteoarthritis?

A

Degenerative joint disorder resulting from a loss of cartilage and bone

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2
Q

What is the pathophysiology of OA?

A
  • failure to maintain balance between cartilage synthesis and degradation leads to exposure of subchondral bone: sclerosis, fractures and cyst formation
  • attempts of repair results in osteophytes
  • mediated by cytokines and driven my mechanical forces
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3
Q

What is the aetiology of OA?

A

multifactorial and driven by mechanical factors

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4
Q

What are the RF of OA?

A

age, female, obesity (inflammatory component), genetic, trauma, smoking, physically demanding sport or occupation

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5
Q

How does OA present?

A

Presents with pain on movement, functional difficulties, less than 30 min of morning stiffness, crepitus, bony deformities, asymmetrical, heberden’s nodes

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6
Q

Which joints can you find OA in?

A

commonly in knee, hip, hands (DIP, PIP and base of thumb)

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7
Q

what tests would you order for OA?

A

Order X-ray, serum CRP+ESR, RF, and anti CCP antibody

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8
Q

What do you expect to see on an xray for OA?

A

LOSS on xray:

loss of joint space, osteophytes, subchondral sclerosis, subchondral cysts

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9
Q

What are differentials of OA?

A

RA, gout

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10
Q

What are consequences of OA?

A

Reduced mobility and functional decline, spinal stenosis

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11
Q

How do you treat OA?

A
  1. topical analgesic and conservative measures (exercise, weight loss, physio, walking aids)
  2. analgesic ladder: topical, oral, transdermal
  3. steroid injections
  4. If debilitating consider surgery i.e. joint replacement or arthroscopy
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12
Q

What is Rheumatoid arthritis?

A

Inflammatory condition of synovial joints

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13
Q

What is the pathophysiology of RA?

A
  1. inflammation of synovial membrane causes it to thicken and infiltration of inflammatory cells
  2. synovial becomes hyperplasic due to proliferation and a pannus (granulation tissue) grows over cartilage.
  3. Underlying cartilage is damaged because nutrition is cut off, cartilage thins and exposes bone leading to erosions
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14
Q

What is the aetiology of RA?

A

infections and genetics (HLA-DR4 and DR8)

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15
Q

What are RF of RA?

A

female, infections, genetics, family history, smoking, stress

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16
Q

How does RA present?

A

Insidious onset: joint pain and swelling that improved with use, morning stiffness, warm and red joints, deformities, rheumatoid nodules, symmetric

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17
Q

What deformities can you see in RA?

A

ulnar deviation (fingers bend), swan neck (PIP hyperextension and DIP flexion) and Boutonniere deformity (opposite to swan neck)

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18
Q

What labs would you order for RA?

A

RF, anti-cyclic citrullinated peptide antibody (Anti-CCP), xray, MRI and FBC

RF is less specific than anti-CCP

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19
Q

What would you expect to see on an xray with RA?

A

LESS: loss of space, erosions, soft tissue swelling, soft bones

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20
Q

What are differentials of RA?

A

SLE, gout and psoriatic arthritis

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21
Q

What are consequences of RA?

A

CV disease, work disability, depression, interstitial lung disease

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22
Q

How do you treat RA?

A
  • Treat with DMARD’s (methrotextrate, hydroxychloroquine or sulfasalazide)
    + NSAIDS and corticosteroids
  • more severe etanercept (TNF alpha inhibitor)
  • physio and occupational therapy
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23
Q

What is osteoporosis?

A

Low bone mass and deterioration of bone tissue resulting in fragility and fractures

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24
Q

What’s the pathology of osteoporosis?

A

imbalance in remodelling and inadequate peak bone mass

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25
Q

What is the precursor of osteoporosis called?

A

osteopenia

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26
Q

What are causes of primary osteoporosis?

A

Age (decrease in trabecular thickness) and menopause (oestrogen deficiency increases osteoclast activity through RANKL)

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27
Q

What are causes of secondary osteoporosis?

A

SHATTERED: steroid use, hyperthyroidism, alcohol, thin, testosterone low, early menopause, renal or liver failure, erosive bone disease, dietary calcium

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28
Q

what are RF for osteoporosis?

A
  1. patient (age, post menopausal, female, low BMI, calcium deficiency, alcohol), 2. drugs (steroids, oestrogen inhibition), 3. disease (cushing’s, hyperthyroidism, renal)
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29
Q

How and where does osteoporosis present?

A

Asymptomatic until fracture:

neck of femur, wrist or vertebrae

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30
Q

What tests do you order for osteoporosis?

A

DEXA scan, xray, FBC and do a fracture risk assessment (FRAX 10 years probability of fracture: age, sex, BMI, no of RF)

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31
Q

What are the DEXA scores for osteoporosis and osteopenia?

A

DEXA score below -2.5 is OP, below -1 is osteopenia

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32
Q

What are differentials of OP?

A

MM, osteomalacia

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33
Q

How do you treat osteoporosis?

A

oral biphosphonates (aledronic acid) and calcium/vitamin D supplements

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34
Q

What are preventative measures for osteoporosis?

A

hormone replacement, weight bearing exercise, prophylactic bidphosponates when giving steroids

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35
Q

What is gout?

A

Episodic disease: Hyperuricaemia and depositions of urate crystals in joints

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36
Q

What is the physiopathlology of gout?

A
  1. Purines in diet - xanthine - uric acid - excreted in kidneys
  2. problems cause hyperuricaemia - monosodium rate precipitates which forms crystals that deposit in joints (collection = tophi)
  3. crystals can trigger inflammatory response by inducing TNF alpha and causing neutrophil adhesion
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37
Q

What is the aetiology of Gout?

A

diopathic hyperuricaemia, impaired excretion (CKD, diuretics) or overproduction (diet, high turn over)

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38
Q

What are RF for gout?

A

male, older age, post-menopausal, alcohol, meat, seafood, family history, obesity, Diabetes M, diuretics

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39
Q

How and where does gout present?

A

Rapid onset and severe pain: joint stiffness and swelling, joint tenderness, tophi

metatarsalphalangeal joint of the big toe

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40
Q

what labs do you order for gout?

A

arthrocentesis with synovial fluid analysis , serum uric acid levels, xray and ultrasound

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41
Q

What do the crystals look like in gout?

A

negative birefringent needle shaped crystals

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42
Q

What lab results would you expect in gout?

A

WBC over 2, increased serum urate (can be normal), xray shows punched erosions around joint, US shows tophi

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43
Q

What are differentials for gout?

A

pseudo-gout, septic arthritis, trauma, RA

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44
Q

What are consequences of Gout?

A

kidney stones and infection

45
Q

How do you treat Gout?

A

Treat acutely with NSAIDs and lifestyle factors

- if happens more than once: colchicine
- preventative: allopurinol with colchicine
46
Q

What drug class is allopurinol?

A

xanthine-oxidase inhibitor

47
Q

What is the difference between seropositive and seronegative RA?

A

Whether there is RF and anti-CCP in the blood. This doesn’t alone diagnose RA but normally seropositive is more common, severe and has complications

48
Q

What 5 traits do all Spondyloarthropathies have?

A

axial inflammation, asymmetric arthritis, absence of RF, inflammation of enthisis and HLA-B27 association

49
Q

What is pseudo gout and what is the pathology?

A

Deposition of calcium phosphate crystals in joints:

Excess calcium and pyrophosphate in blood leads to depositions of calcium pyrophosphate crystals in articular cartilage

50
Q

What are the different types of pseudo gout?

A
  • A: acute
  • B: chronic
  • C+D: with osteoarthritis
  • E
51
Q

What contributes to the development of pseudo gout?

A

dehydration, steroids and hyperparathyroidism

52
Q

What are RF for pseudo gout?

A

old age, female, hyperparathyroidism, family history, previous joint injury

53
Q

How does pseudo gout present?

A

Often asymptomatic: painful and tender joints, synovitis, similar to osteoarthritis

54
Q

What joints does pseudo gout affect?

A

affects larger joints such as knees, wrists and shoulders

55
Q

What tests do you order and what results do you expect to see?

A

arthrocentesis, X-rays, serum calcium and CT scan

elevated calcium, xray shows chonedrocalcinosis (cartilage calcification

56
Q

what do pseudo gout crystals look like?

A

positively birefringent rhomboid shaped crystals

57
Q

What are differentials of pseudo gout?

A

Gout, septic arthritis, OA

58
Q

How do you treat pseudo gout?

A

Treat depending on involvement:

- mono articulate: intraarticular steroids if accessible otherwise NSAIDs
- polyarticulate: NSAIDs (colchicine 2nd line)
- chronic: DMARDs, surgery
59
Q

what is ankylosing spondylitis?

A

Inflammation of the axial skeleton leading to syndesmophytes and vertebrae fusion

60
Q

What is the pathology of AS?

A

cartilage erosion and joint/bone destruction due to osteoclasts. Fibrin replaces the damage which limits range of motion and ossification causes syndesmophytes (bony growths):
Ankylosis of spine (stiffness) and vertebrae fusion (bamboo spine)

61
Q

How does AS present?

A

back pain, morning stiffness in back and buttocks that improved with exercise,
progressive loss of spinal movement:
1. loss of lumbar lordosis (straight spine) and 2. increased kyphosis (upper spine bending forward)

62
Q

what tests would you order for AS and what do you expect to see?

A

pelvic xray, MRI and spine xray: sacroilitis, erosions and bamboo spine

63
Q

How do you treat AS?

A

NSAIDs and physio

chronic: TNF alpha inhibitor (adakimumab)

64
Q

What is psoriatic arthritis and what is its pathology?

A

Inflammatory joint disease associated with psoriasis:

angiogenic growth factors are over expressed and with TNF they contribute to vascular and bone changes

65
Q

How does PA present?

A

Usually starts with rash then presents with joint pain/swelling/stiffness, nail changes, dactylics and mild arthritis in less than 5 joints

66
Q

What labs would you order for psoriatic arthritis?

A

hand and feet xray, CRP+ESR, RF and anti CCP, synovial fluid aspiration

67
Q

What deformity would you expect in advanced PA?

A

pencil in cup deformities (end of bone like a sharp pencil)

68
Q

What lab results would you expect in PA?

A

Early PA may not have radiological changes, DIP erosions, new bone formation, osteolysis, can have raised inflammatory markers

69
Q

How do you treat psoriatic arthritis?

A

NSAIDs and physio (2nd line TNF alpha inhibitor)

70
Q

What is reactive arthritis?

A

Inflammatory arthritis following GI or urogenital infection

71
Q

What is the Aetiology of reactive arthritis?

A
  • Enteric: campylobacter, salmonella, shigella

- STI: chlamydia trachomatis

72
Q

how does reactive arthritis present?

A

Presents 2-4 weeks after infection with acute onset: fatigue, fever, lower back pain, painful and swollen joints

73
Q

What is renters triad?

A

Seen in reactive arthritis:

conjunctivitis, urethritis and oligoarthritis

74
Q

What labs would you order and what results do you expect for reactive arthritis?

A

inflammatory markers, ANA antibodies, RF, urogenital and stool culture, serum antibodies:

raised inflammatory markers, if tested early the cultures may show, sterile synovial fluid

75
Q

What is a complication of reactive arthritis?

A

destructive enthesitis (inflammation where tendons insert onto bone)

76
Q

How do you treat reactive arthritis?

A

antibiotics for causative agents and then NSAIDs+steriods+physio

77
Q

What is septic arthritis and what is the pathology?

A

Infection of one or more joints caused by inoculation of microbes:
nvasion directly or through haematogenous spread which causes bone and cartilage necrosis

78
Q

What organisms can cause septic arthritis and who would you see them in?

A
  • Staph. aureus is most common
  • Neisseria gonorrhoea in young and sexually active
  • Steph. epidermis in joint replacement
  • E.coli and klebsiella in immunocompromised
  • Gram-ve are more common in older and compromised patients
79
Q

What are RF for septic arthritis?

A

elderly (80), prosthetic joint, immunocompromised, underlying joint disease, IVDU, diabetes mellitus, skin lesions, recent surgery

80
Q

How does septic arthritis present?

A

swollen, warm and tender joint, pain, restrictive movement and fever

81
Q

What tests would you order for septic arthritis?

A

Orthopaedic emergency so do a urgent aspiration!!!

then blood cultures, U+E, inflammatory markers, xray

82
Q

what results would you expect for septic arthritis?

A

inflammatory markers elevated, yellow synovial fluid, WCC increased and cultures show bacterium

83
Q

What complications come with septic arthritis?

A

osteomyelitis, joint destruction and LT disability

84
Q

How do you treat septic arthritis?

A 
empirical antibiotics (flucloxacillin) and stop immunosuppressants
    - analgesia and splinting
85
Q

what is osteomyelitis?

A

Infection and inflammation of the bone marrow that is localised to the bone

86
Q

what is the physiological classification of osteomyelitis?

A
  • A: no cormorbidities
  • B: comorbidities directly affecting wound healing
  • C: treatment for harmful than condition
87
Q

What is the anatomical classification of osteomyelitis?

A
  • I: medullary and endosteal bone
  • II: superficial
  • III: medullary and cortical involvement
  • IV: entire bone circumference
88
Q

What organisms cause osteomyelitis?

A

S.aureus, salmonella (sickle cell) and coagulase negative staphylococci

89
Q

What are the RF for osteomyelitis?

A

previous osteomyelitis, trauma, surgery, diabetes, immunosuppression, sickle cell, prosthetics

90
Q

How does osteomyelitis present?

A

Presents with dull pain at site, fever, weakness, reluctant to weight bear, swelling and warm
chronic may present with ulcers that fail to heal

91
Q

What tests would you order and what results do you expect for osteomyelitis?

A

Order FBC (increased inflammatory), xray (osteopenia, loss of trabecular architecture), blood cultures, bone biopsy, MRI

92
Q

What are complications of osteomyelitis?

A

fractures and growth disturbances

93
Q

How do you treat osteomyelitis?

A

immobilising site, then give broad spectrum empiric antibiotics until culture results
- surgery to remove debris and dead bone

94
Q

What is SLE?

A

Remitting and relapsing multisystem autoimmune disorder and most common form of lupus

95
Q

What is the pathology of SLE?

A

Autoantibodies produced by B-cells target autoantigens and form immune complexes which activate compliment system leading to an influx of neutrophils and inflammation

96
Q

What are the RF for SLEß

A

pre-menopausal women, family history, genetics, smoking, drugs, UV light

97
Q

How does SLE present?

A

non-specific symptoms: fever, fatigue, weight loss, rash and skin problems

98
Q

What tests do you order for SLE?

A

FBC, inflammatory markers, ANA, double stranded DNA antibody, compliment levels

99
Q

How do you diagnose SLE?

A

need at least 4: butterfly rash on face, discoid rash (photosensitive), oral ulcers, arthritis, serositis, photosensitivity, blood disorders (low), renal disease, ANA positive, neurological disorder or Anti-ds DNA

100
Q

What complications does SLE have?

A

pericarditis, blood disorders, lupus nephritis

101
Q

How do you treat SLE?

A

high factor sunscreen and DMARD’s

- maintain:NSAIDs and hydroxychlocoquine
- Flares: prednisolone
102
Q

What is osteomalacia?

A
  • poor bone mineralisation leading to soft bones

adult form of rickets: lack of calcium

103
Q

what is fibromyalgia?

A

non specific muscular disorder with unknown cause: widespread MSK pain (other diseases excluded), symptoms for at least 3 months and pain at 11/18 tender point sites

104
Q

How does fibromyalgia present?

A

widespread muscle pain for at least 3 months, morning stiffness, poor sleep, poor concentration

105
Q

What are primary benign bone tumours?

A

osteochondroma, giant cell, osteoblasts

106
Q

What are malignant bone tumours?

A

osteosarcoma, ewing’s sarcoma

107
Q

What is paget’s disease?

A

Chronic disorder where bone remodelling is out of balance, resulting in brittle and abnormaly shaped bone

108
Q

What is Ehler dances syndrome?

A

Inherited condition that affects connective tissue

Phase 2A conditions (7 decks)

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