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Phase 2 > MSK > Flashcards

MSK Flashcards

1
Q

Brief pathology of osteoarthritis

A

Degenerative progressive destruction of cartilage from repeated mechanical forces
Disruption of chondrocytes prevents rebuilding
Usually in synovial joints

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2
Q

Why is obesity considered a pro-inflammatory state?

A

Bc it releases IL1, TNF and adipokines

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3
Q

RF of osteoarthritis

A

Older age
High intensity labour
Joint hypermobility
Diabetes
F > M
Obesity

COL2A1 collagen type 2 gene plays a role

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4
Q

Why is age a risk factor for OA?

A

Cumulative effect of traumatic insult and ↓ of neuromuscular function

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5
Q

Main pathological features of OA

A

Loss of cartilage
Disordered bone repair

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6
Q

Key Presentation - OA

A

Painful joints, stiffness < 30 mins in morning
Worse throughout the day
Occurs at PIP (Bouchard) and DIP (Heberden)

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7
Q

What effects do oestrogen have on bone turnover?
And hence, what is a RF for MSK diseases e.g. osteoporosis, OA?

A

Oestrogen has restraining effect on bone turnover
∴ EARLY MENOPAUSE results in ↓ trab. Th, strength and bone connections

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8
Q

List 4 other signs/symptoms of OA

A

Joint pain on movement
Tenderness
Crepitus
Asymmetrical joint involvement

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9
Q

Ix Osteoarthritis

A

XRAY - LOSS

Loss of joint space
Osteophytes
Subchondral sclerosis (more white on XR)
Subchondral cysts

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10
Q

DDx OA

A

RA
Gout
Psoriatic arthritis

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11
Q

Tx OA

A

1. Px education & lifestyle changes
(weight loss if obese, physiotherapy, occupational therapy)

2. Analgesic ladder
a). Paracetamol, topical NSAIDs, topical capsaicin
b). Oral NSAIDs (+ PPI)
c). Opiates e.g. codeine, morphine

also, intra-articular steroid injections - hyaluronic acid

If extreme, joint replacement
(avoid steroids before surgery bc immunosuppressive)

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12
Q

What type of hypersensitivity reaction is RA?

A

Type III

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13
Q

RF RA

A

Female! (premenopausal women 3x more affected than men)
HLA-DR4 and HLA-DRB1 (more susceptible, associated w/ ↑ severity)
FHx
Stress
Infection
Smoking

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14
Q

What are the diagnostic criteria for RA?

A

Need 4/7 to be diagnostic

Rheumatoid nodules
Rh factor POS
Radiographic changes (XR LESS)
Arthritis of hand joints
Morning stiffness > 30 mins
Symmetrical

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15
Q

State and describe hand deformities found w/ RA

A

Ulnar deviation
Boutonniere deformity - PIP flexion, DIP hyperextension
Swan neck deformity - PIP hyperextension, DIP flexion

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16
Q

State 10 other signs/symptoms of RA

A

Digital infarcts along nail bed
Anaemia - normochromic/cytic
Palpable lymph nodes
Bursitis
Tenosynovitis
Warm, red, tender joints
Joint pain worse in mornings/cold
Loss of function
Popliteal cyst
Rheumatoid nodules at pressure points
Sicca
Carpal tunnel syndrome
Fatigue and malaise
Symmetrical
DIPs are usually spared!

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17
Q

Ix RA

A

FBC/Bloods
Rh factor POS (sensitive)
Anti-CCP POS (specific, not routine)
↑ ESR, ↑ CRP, ↑ Platelets

XR - LESS

Loss of joint space
bone Erosions
Soft tissue swelling
Soft bones (osteopenia)

Genetic testing

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18
Q

State some extra-pulmonary manifestations of RA

A

Caplan’s syndrome (esp in coal miners)
Felty’s syndrome
Anaemia of chronic disease
Lymphadenopathy
2° Sjogren’s syndrome
Amyloidosis

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19
Q

DDx RA

A

Psoriatic arthritis
OA
Symmetrical seronegative spondyloarthropathies

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20
Q

Tx RA

A

MDT treatment!

  1. NSAIDs (+PPI)
    Steroids initially, for flare ups to settle
  2. DMARDs e.g. methotrexate, leflunomide, sulfasalazine hydroxychloroquine (mildest DMARD ∴ preferential if disease isn’t too severe)

a) one of above
b) 2 of above
c) Methotrexate + TNF inhibitor
d) Methotrexate + biologic e.g. Rituximab

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21
Q

Remember :

A

OA less convincing response to NSAIDs than RA
RA - worse w rest, better w movement. OA is opposite
RA - symmetrical, OA - not

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22
Q

At what age, is the peak bone mass?

A

29 years

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23
Q

State 1° causes of osteoporosis

A

Post-menopause
Age

bc oestrogen protects bone!

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24
Q

State 2° causes of osteoporosis

A

SHATTERED

Steroid use
Hyperthyroidism/hyperparathyroidism
Alcohol/Smoking
Thin (low BMI < 22)
Testosterone low
Early menopause
Renal or liver failure
Erosive / inflammatory bone disease
Dietary calcium low

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25
Q

Key presentation of osteoporosis

A

Fractures!
Esp if happens when/where it shouldn’t happen

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26
Q

Ix Osteoporosis

A

DEXA Scan BMD measurement
T score (esp at hip)

(then compared against gender-matched YA average)
> -1 normal
Between -1 and -2.5 = Osteopenia
<-2.5 = Osteoporosis

ALSO : FRAX score - 10 year probability of major fracture

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27
Q

When ↓ seru Ca2+,

A

Parathyroid gland secretes PTH
∴ ↑ bone resorbtion and Ca2+ released into blood stream

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28
Q

When ↑ serum Ca2+,

A

Parathyroid gland produces calcitonin,
inhibits PTH secretions,
↑ bone formation and Ca2+ absorbed from bloodstream

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29
Q

What happens to trabecular architecture with age?

A

↓ Trab Th
↓ Connections between horizontal trabeculae
∴ ↓ Trab strength (∴ ↑ risk of fractures)

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30
Q

Why are horizontal trabeculae so important?

A

Makes bones a LOT stronger
Eular-Buckling theory

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31
Q

During bone turnover due to oestrogen deficiency, what type of bone is mostly lost?

A

Cancellous bone

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32
Q

What occurs if there’s too much mineralisation in bones?

A

Become stiff and shatter

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33
Q

What occurs if there’s too little mineralisation in bones?

A

Bones aren’t strong and break

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34
Q

What occurs if there’s too little mineralisation in bones?

A

Bones aren’t strong and break

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35
Q

What do bloods show in osteoporosis?

A

Ca2+, phosphate, alkaline phosphate are all normal

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36
Q

Tx Osteoporosis

A

Lifestyle changes - Avoid falls!!
Quit smoking, ↓ alcohol, healthy weight
Adcal D3 (Vit D + Calcium)

  1. Oral bisphosphonate (↓ osteoclastic activity)
    e.g. alendronate (10mg daily), risendronate (5mg daily)
  2. Denosumab or Strontium ranelate or Teriparatide

ALSO : consider Hormone Replacement Therapy in young post-menopausal women

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37
Q

What does ESR stand for?

A

Erythrocyte Sedimentation Rate

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38
Q

Define ESR

A

Measure of how quickly erythrocytes will fall to bottom of tube

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39
Q

What does ESR measure?

A

Fibrinogen values
Rise w/ inflammation bc erythrocytes stick together and ∴ fall faster

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40
Q

How does ESR rise and fall?

A

Rises and falls SLOWLY (days to weeks)

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41
Q

What causes ESR to rise falsely? (False positives)

A

Female
Age
Obesity
SE Asian
Hypercholestrolaemia
High Immunoglobulin (myeloma)

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42
Q

Full form of CRP

A

C-Reactive Protein

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43
Q

Define CRP

A

Acute phase protein, released in inflammation

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44
Q

Where is CRP produced?

A

In liver in response to IL-6

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45
Q

How does CRP rise and fall?

A

QUICKLY - high at 6 hours, peaks at 48 hours
∴ if patient has infection in 24 hours, ESR won’t have risen but CRP will have

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46
Q

SPINEACHE go

A

Sausage digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAID good response
Enthesitis (heel)
Arthritis
Crohn’s / Colitis / ↑CRP (but CRP can be normal)
HLA B27
Eye (uveitis)

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47
Q

What joint do Spondyloarthropathies typically affect?

A

Spinal and sacroiliac joints

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48
Q

Spondyloarthropathies are _____

A

seronegative (no RhF)

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49
Q

HLA-B27 encoded by

A

Major histocompatibility complex on chromosome 6

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50
Q

Why does HLA-B27 cause disease?

A

Causes autoimmune disease by molecular mimicry
Infection occurs and infection agents have peptides v similar to HLA-B27
∴ immune system launches attack on HLA-B27

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51
Q

Epidemiology of Ankylosing Spondylitis

A

*More common and severe in Males
*Presents in late teens/20s
↓ Incidence in African and Japenese people
Native NA ↑ incidence

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52
Q

Ix Ankylosing Spondylitis

A

Bloods -
HLA-B27 positive
↑ CRP, ↑ ESR
Normocytic anaemia

XR
MRI

Schober’s test!

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53
Q

Why can you perform an MRI for ankylosing spondylitis?

A

Bc before bamboo spine, bone marrow oedema occurs first - showed by MRI

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54
Q

What XR signs are there in Ankylosing spondylitis?

A

Sacroiliitis
Enthesitis
Dagger sign
Syndesmophytes
BAMBOO SPINE

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55
Q

Ankylosing Spondylitis, diagnose if :

A

Age at onset < 45 years
At least 3 months back pain
XR/MRI shows sacroiliitis + at least 1 SPINEACHE feature

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56
Q

State some other signs/symptoms of Ankylosing Spondylitis

A

Worse with rest
Slow onset morning stiffness > 30 mins
Fatigue
Buttock/thigh pain - sacroiliac joints
Rashes/skin changes

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57
Q

Describe Schober’s test

A

Make a point at L5
Put a finger 10cm above and 5cm below
Px bends forwards
If distance between 2 fingers is < 20 cm, supports a diagnosis of Ankylosing Spondylitis

58
Q

Rf for Ankylosing Spondylitis

A

HLA-B27!
Environment : Klebsiella, Salmonella, Shigella

59
Q

Differences between Ankylosing Spondylitis and RA

A

RA affects smaller joints and is usually symmetrical
AS affects spine and is asymmetrical

60
Q

Is HLA-B27 diagnostic for ankylosing spondylitis?

A

NO!

61
Q

Red flags for back pain

A

TUNA FISH

Trauma, TB
Unexplained weight loss & night sweats
Neurological deficits, bowel/bladder incontinence
Aage <20 and > 55

Fever
IVDU
Steroid use or immunosuppressed
History of cancer, early morning stiffness

62
Q

What is Scleroderma?

A

Multi-system disease w/ involvement of skin. Vascular damage (fibrosis) of small arteries, arterioles and capillaries.

63
Q

Epidemiology of Scleroderma

A

Female!
30 - 50 years
Rare in children

64
Q

RF Scleroderma

A

Exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
Drugs - bleomycin
Genetics

65
Q

Types of Scleroderma

A
  1. Diffuse - CREST + organ problem
  2. Limited - just CREST
66
Q

What are the FIRST symptoms usually in Scleroderma?

A

Raynaud’s
Sclerodactyly

67
Q

Ix Scleroderma

A

Bloods - norm anaemia
RhF+
For limited : Anti-centromere antibodies
For diffuse : Anti-topoisomerase-1 (anti SCL-70) antibodies & anti-RNA polymerase III

CXR - exclude other causes
Hand XR - see calcium deposits
Barium swallow - confirm oesophageal dysmotility

68
Q

What systemic effects can Scleroderma have?

A

GI - heartburn, dysphagia, malabsorption, pseudo-obstruction
Renal - AKI, CKD, acute hypertensive crisis
Lung - fibrosis, pul HTN
Heart - arrhythmias

69
Q

Tx Scleroderma

A

No cure. Immunosuppressants used to slow progression - cyclophosphamide

MDT - physio

Treat symptoms
Raynaud’s : vasodilators - nifedipine
Analgesia
PPI for reflex
Pul HTN - sildenafil
etc

70
Q

Prognosis Scleroderma

A

~ 12 years after diagnosis (avg)
However, if limited, could have normal lifespan

71
Q

Complications of Sjorgren’s

A

B-Cell lymphoma !!!!!!

72
Q

A patient comes in with a red, hot, swollen joint. What do you do?

A

ASPIRATE IT ALWAYS !!!!!!!!!!!!!!
COULD BE SEPTIC ARTHRITIS

73
Q

Causes of Septic arthritis

A

S. Aureus

Neisseria gonorrhoea - sexually active, young
Staph. Epidermis - prosthetic joint
E.coli / Klebsiella - immunocomp

H. influenzae - infants, but rare bc immunisation now

74
Q

RF Septic Arthritis

A

> 80 years, infants (always suspect in ANY joint problem in children)
Pre-existing joint disease
DM
Prosthetic joints
Immunosuppress
Penetrating trauma

75
Q

Key presentation Septic Arthritis

A

*Knee, hip, shoulder
Acute, painful, red, hot, swollen joint
SEPTIC UNTIL PROVEN OTHERWISE

76
Q

Other signs/symptoms of septic arthritis

A

Fever
Impaired range of motion
Refusing to bear weight
Monoarthritis

77
Q

Ix Septic Arthritis

A

ALWAYS ASPIRATE FIRST -> GS !!

FBC - ↑ WBC, neutrophilia
Blood cultures
Polarised light microscopy - exclude gout/pseudogout

78
Q

What would you see in the aspirate of a patient with Septic Arthritis?

A

Turgid fluid - non-transparent
Leukocytes
Send for gram-stain

Normal = yellow, clear, thin

79
Q

Why is Septic Arthritis a medical emergency?

A

Can destroy joint in under 24 hours !!!!!!!!

80
Q

Tx Septic Arthritis

A

Stop immunosuppressive drugs (e.g. methotrexate) and anti-TNF for as long as on Abx

ANTIBIOTICS !
Empirical e.g. flucloxacillin
then pathogen-directed, 3-6 weeks

(IF on steroids, double dose. If not, then don’t give steroids)

81
Q

What Abx against S. Aureus?

A

Flucloxacillin
Erythromycin
Doxycycline
Tetracycline

82
Q

Causes of Osteomyelitis

A

Staph. Aureus
Salmonella - if sickle cell anaemia
Staph - coagulase neg (epsa)
H. influenzae

83
Q

How does bacteria reach the joints to cause septic arthritis?

A

Direct inoculation or via haematogenous spread

84
Q

Key presentation of OM

A

Dull pain at site of OM
Onset - several
Non-specific tenderness and pain
Reluctance to weight bear

85
Q

Name some systemic symptoms of OM

A

Fever
Rigors
Sweat
Malaise

86
Q

Ix OM

A

FBC - ↑ ESR, ↑ CRP, ↑ WBC, but can be normal in chronic
XR - can see periosteal reaction, low sensitivity/specificity for OM i.e. cannot exclude

GS : Bone biopsy (but must be done thru not infected tissue)

MRI - best imagine to establish diagnosis
must be done after XR

Blood cultures

87
Q

Tx OM

A

Antibiotics - tailored to culture
If vascular disease, less reliable Abx penetration ∴ longer duration

Surgery if severe

88
Q

DDx OM

A

Charcot joint! - damage due to sensory nerves affected by DM
Gout
Fracture

89
Q

Ix Psuedogout

A

Joint aspirate and polarised light - rhomboid crystals, positively birefringent, no bacterial growth

GS : XR - Chondrocalcinosis

90
Q

Hidden sites for psoriasis

A

Behind ear/inside ear
Scalp
Pitting in nails/ onokylisis
Umbilicus
Penile
Natal cleft

91
Q

State the types of Psoriatic Arthritis

A

5 patterns of disease

  1. Asymmetrical oligoarthritis
  2. Symmetrical seronegative polyarthritis
  3. Spondylitis
  4. Distal interphalangeal arthritis
  5. Arthritis mutilans
92
Q

Describe symmetrical polyarthritis

A

Females
Hands, wrists, ankles and DIP joints
MCP less common (∴ unlike RA but otherwise v similar)

93
Q

Describe asymmetrical oligoarthritis

A

Mainly fingers, toes and feet
Only a few joints

94
Q

Describe spondylitic psoriatic arthritis

A

Males
Back stiffness, sacroiliitis, alanto-axial joint involvement.
Can also affect - spine, achilles tendone, plantar fascia

95
Q

Key presentation of Psoriatic Arthritis

A

Plaques of psoriases - in hidden areas
Onycholysis
Dactylitis
Enthesitis

96
Q

Ix Psoriatic Arthritis

A

Bloods - HLA-B27, ↑ ESR
NEG RhF and NEG anti-CCP

GS : XRAY
Erosion in DIP, periarticular new bone formation
Oateolysis
Pencil-in-cup deformity

97
Q

Tx Psoriatic Arthritis

A

Similar to RA -

NSAIDs
DMARDs - methotrexate, sulfasalazine, leflunomide
TNF-i or monoclonal antibodies - etanercept, infliximab, adalimumab
Steroid injection
Physio

98
Q

Complications of Psoriatic Arthritis

A

Arthritis mutilans
Most severe form
Occurs in phalanxes
Osteolysis of bones around joint - causes progressive shortening
Skin folds as digit shortens - telescopic finger

99
Q

Ix Anti-phospholipid Syndrome

A

Anti-cardiolipin antibody test
Anti-B2-glycoprotein test
Lupus anticoagulant test

^ All 3 are needed to diagnose
Positive test on at least 2 ocassions 12 weeks apart

100
Q

What does the anti-cardiolipin antibody test test for?

A

IgG or IgM antibodies that bind to cardiolipin (neg charged phospholipid)

101
Q

What does the lupus anticoagulant test detect?

A

Changes in ability of blood to clot

102
Q

Tx Anti-Phospholipid Syndrome

A

Manage risk factors e.g. smoking

Long term warfarin (LMWH if trying to conceive)

Prophylaxis e.g. for stroke - aspirin or clopidogrel

103
Q

Anti-Phospholipid Syndrome causes

A

CLOTs

Coagulation defect
Livedo reticularis
Obstetric issues
Thrombocytopenia

104
Q

Key presentation of Anti-Phospholipid Syndrome

A

Thrombosis !!!!!!!!!
e.g.
Arteries - stroke, MI, TIA
Veins - Budd-chiari syndrome, DVT, PE
Miscarriage !!

105
Q

Cause of Anti-Phospholipid Syndrome

A

HLA-DR7 mutation + Environmental trigger
e.g. infection (malaria), drugs (CV drugs - propranolol, anti-psychotic - phenytoin)

106
Q

How soon after an infection do clinical signs of reactive arthritis occur?

A

1-4 weeks

107
Q

What is small vessel vasculitis called?

A

Granulomatosis with Polyangiitis
aka Wegener’s Granulomatosis

108
Q

RF Psuedogout

A

Females > 70years
Hyperthyroidism
Hyperparathyroidism
XS iron or calcium

109
Q

RF Gout

A

Middle-age
Overweight
High purine diet (red meat, seafood)
Alcohol
Diuretics
FHx
Renal disease/existing CVD

110
Q

RF RA

A

Middle age
Female! (3x more common)
FHx
Other autoimmune diseases

111
Q

RF OA

A

High intensity labour
Older age
Obesity
Trauma
Female
FHx

112
Q

What vessels does Giant Cell Arteritis affect?

A

Aorta and/or its major branches (carotid and vertebral arteries)
Often temporal artery!

113
Q

RF Giant Cell Arteritis

A

> 50 years
Northern European
Females! (2-3x more common)
Hx of polymyalgia rheumatica
(RA, SLE, scleroderma)

114
Q

Key presentation of Giant Cell Arteritis

A

Headache! new onset, unilateral over temporal area
Scalp tenderness (hurts to brush hair)

115
Q

Other signs/symptoms of Giant Cell Arteritis

A

Jaw claudication
Visual disturbances! - blurred vision, diplopia, amaurosis fugax, blindness
On palpitation, temporal arteries tender and thickened
Pulse may be diminished

116
Q

What type of vessels does Takayasu’s arteritis affect?

A

Large

117
Q

What type of vasculitis affects medium-sized vessels?

A

Polyarteritis nodosa (PAN)

118
Q

What type of vasculitis affects small vessels?

A

Granulomatosis with polyangiitis

119
Q

Ix Giant Cell Arteritis

A

Bloods - ↑ ESR +/- ↑ CRP (v sensitive)
ANCA neg
ESR > 50 mm/hour
Ultrasound - Halo sign of temporal and axillary artery

GS : TEMPORAL ARTERY BIOPSY
shows giant cells, granulomatous inflammation

120
Q

Tx Giant Cell Arteritis

A

High dose prednisolone (40-60mg) then gradual reduction
Long-term (12-18 months) ∴ give GI and bone protection -> Lansoprazole, alendronate, Ca2+, Vit D

if visual change - emergency! IV methylprednisolone

121
Q

What locations does Polyarteritis Nodosa occur?

A

Medium muscular arteries, esp at branch points
Skin, GI tracts, kidneys, heart

NOT veins

122
Q

RF Polyarteritis Nodosa

A

Associated with Hep B! (and Hep C, HIV)
More common in LICs

123
Q

DDx Giant Cell Arteritis

A

Migraine
Tension headache
Trigeminal neuralgia
Polyarteritis nodosa

124
Q

Presentation of Polyarteritis Nodosa

A

Cutaneous/subcutaneous nodules
Unilateral orchitis
Peripheral neuropathy - mononeuritis
Abdo pain
Livedo reticularis
HTN

125
Q

Ix Polyarteritis Nodosa

A

Bloods - ↑ ESR +/- ↑ CRP
HBsAG
ANCA neg

Biopsy - transmural fibrinoid necrosis

126
Q

Tx PAN

A

If Hep B neg - corticosteroids + immunosuppressant (cyclophosphamide)
If Hep B pos - corticosteroids, then antivirals, plasma exchange

Control BP - ACEi

127
Q

Complications PAN

A

GI perforation & haemorrhages
Arthritis
Renal infarcts
Strokes
MI

128
Q

Age of presentation of Granulomatosis with Polyangiitis

A

Late teenage years - early adulthood

129
Q

Key presentation of Granulomatosis with Polyangiitis

A

Saddle shaped nose
Epistaxis (nosebleed)
Crusty nasal/ear secretions - hearing loss
Sinusitis
Cough, wheeze, haemoptysis

130
Q

DDx Granulomatosis with Polyangiitis

A

Pneumonia (esp bc cough, wheeze, haemoptysis)

131
Q

Ix Granulomatosis with Polyangiitis

A

Bloods - ↑ Eosinophils
c-ANCA !!!!!!!!!!
Histology - granulomas

132
Q

Tx Granulomatosis with Polyangiitis

A

Corticosteroids
Cyclophosphamide

133
Q

Complications of Granulomatosis with Polyangiitis

A

Glomerulonephritis

134
Q

Describe Churg-Strauss

A

P-ANCA
No nasopharyngeal involvement
No granuloma

Small vessels?
check

135
Q

Paget’s disease

A

Raised ALP

136
Q

Ix Sjogren’s

A

Anti-Ro and Anti-La antibodies
Schirmer’s test

137
Q

Tx Sjogren’s

A

Artificial tears, artificial saliva, vaginal lubricants
Hydroxychloroquine used to halt progression

138
Q

What is Sjogren’s?

A

Autoimmune condition that affects exocrine glands

139
Q

Difference between primary and secondary Sjogren’s

A

1º - condition occurs in isolation
2º - related to SLE or RA

140
Q

RF Sjogren’s

A

FHx (first degree relative = 7x higher risk)
Female
> 39 years

Phase 2 (24 decks)

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