Loco rheumatology Flashcards

1
Q

Cause of excessive thoracic kyphosis

A

Fracture of anterior part of vertebrae

Treatment = kyphoplasty

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2
Q

Sheuermann’s disease

A

Adolescent kyphosis
Thoracic bones grow more posteriorly due to growth plate damage
Xray = Schmori’s nodes

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3
Q

Muscles imbalances in lumbar lordosis

A

Weak lower abdominals, gluteals and hamstrings
Tight psoas major and quadriceps
–> anterior pelvic tilt

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4
Q

Flat back syndrome

A

Tight hamstrings and paraspinals

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5
Q

Where is disc herniation most common?

A

L4/L5 and L5/S1 as largest vertebrae

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6
Q

Symptoms of cauda equina syndrome

A
Lower back pain 
Sciatica 
Saddle anaesthseia 
Bladder and bowel weakness 
Sexual dysfunction 
Lower limb weakness 
Reduced reflexes
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7
Q

Treatment of cauda equina syndrome

A

Laminectomy

Discectomy

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8
Q

Which area if most commonly affected by burst fracture?

A

Thoracolumbar junction

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9
Q

What gives bamboo spine appearance

A

AK

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10
Q

Peak age of onset of AK

A

20s

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11
Q

Which gender is affected more by AK?

A

Males

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12
Q

What HLA molecule is associated with AK?

A

HLA B27

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13
Q

Mechanisms of septic arthritis

A

Haematogenous spread
Disseminated osteomyelitis
Spread from adjacent soft tissues
Penetrating trauma

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14
Q

Septic arthritis pathogens

A

Most common = S. aureus
Common in middle age = gonococcus
Common in infants = staph, strep and haemophilus

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15
Q

Reactive arthritis pathogens

A

Chlamydia
Campylobacter
Salmonella

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16
Q

Reactive arthritis genetics

A

HLA B27

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17
Q

Mechanisms of osteomyelitis

A

Haematogenous spread
Spread from adjacent soft tissues
Direct trauma

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18
Q

Special antibiotic forms for OM

A

Vancomycin cement beads

Clindamycin foam

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19
Q

Complications of OM

A

Squamous cell carcinoma

Amyloidosis

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20
Q

Common sites of tendonitis

A

Lateral epicondyle
Achilles tendon
Supraspinatous

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21
Q

How can inflammation lead to ossification

A

PGE2 and COX-2 though to favour chondrocyte differentiation which can lead to ossification

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22
Q

How do tendons heal?

A

Within sheath = intrinsic from own fibroblasts

Outside sheath = from external fibroblasts

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23
Q

Types of enthesis

A

Fibrous

  • for long tendons
  • weaker
  • Sharpey’s fibres

Fibrocartilagenous

  • for short tendons that are at strong angles
  • stronger
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24
Q

AS treatment

A

Sulfasalazine
Methotrexate
Anti-TNF therapies

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25
Q

De Quervain’s tenosynovitis

A

Fibrosis and narrowing of tendon sheath surrounding extensor policis bravis and abductor pollicis
Due to rubbing over radial styloid process

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26
Q

Trigger finger

A

Nodule forms on finger flexor tendon and makes extension hard

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27
Q

Antibodies present in SLE

A

ANA

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28
Q

Presentation of SLE

A

Butterfly rash
Arthralgia of small joints of hands
Photosensitivity
Renal disease

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29
Q

Treatment for SLE

A
NSAIDs 
Cyclophosphamide 
Biologicals against B and T cells 
Steroids 
IV immunoglobulins
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30
Q

Gout pathophysiology

A

Purines –> uric acid
Uric acid normally insoluble or coated in apo E and B so inert
If levels rise too much –> crystals form and trigger immune reaction
Phagocytes engulf crystals –> lysis
Release of enzymes and acid content

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31
Q

Gout causes

A
Overproduction 
- excessive meat, beer, red wine, shellfish intake 
- tumour lysis syndrome 
- Lesch-Nyhan syndrome 
Under-excretion 
- diuretics 
- renal insufficiency 
- dehydration
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32
Q

Common locations for tophi

A
Ear cartilage 
Toes and fingers 
Olecranon bursa 
Achilles tendon 
Kidney
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33
Q

Histology of tophi

A

Fibrous tissue
Ring of foreign body giant macrophages
Ring of lymphocytes

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34
Q

Normal uric acid level

A

<6.8mg/dL

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35
Q

Crystals in gout

A

Monosodium urate
Needle shaped
Strong negative birefringence

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36
Q

X-ray in gout

A

Rat bite erosions

Soft tissue swelling

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37
Q

Gout treatment for acute attacks

A

Analgesics
Calchicine = anti-mitotic to prevent neutrophil proliferation
Corticosteroids
Anti-IL-1 biologicals = anakinra, rilonacept, canakinumab

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38
Q

Chronic gout treatment

A

Xanthine oxidase inhibitors = allopurinol, oxypurinol, febuxostat
Probenecid = increases uric acid secretion (urisuric)
Rasburicase = uric acid –> allantoin (inert)
Other urosurics = vitamin C, losartan

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39
Q

Crystals in pseudogout

A

Calcium pyrophosphate
Rhomboid shaped
Weak positive birefringence

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40
Q

X-ray of pseudogout

A

Calcification of soft tissues

Especially menisci of the knees and wrists

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41
Q

Nodes in OA

A
DIP = Herberden's 
PIP = Bouchard's
42
Q

Joints affected in nodal generalised OA

A
DIP and PIP
1st CMC 
Hallux valgus (1st MTP)
Hallux rigidus (1st MTP) 
Knee
43
Q

Apatite associated destructive arthritis

A

Due to hydroxyapatite crystals in joint space
Can cause severe joint erosions
Mainly affects hip and shoulder (Milwaukee shoulder)

44
Q

Erosive OA

A

Cartilage destruction + synovial inflammation
Affects DIP, PIP and 1st CMC
Gull wings appearance from central erosions
Ankylosis common

45
Q

OA of premature onset causes

A

Previous meniscectomy
Perthes
Haemochromatosis

46
Q

Rate of bone loss

A

After 40 = 0.7% per year

After menopause = 2-9% per year

47
Q

T scores

A

> -1 = normal
-1 to -2.5 = osteopenia
< -2.5 = osteoporosis

48
Q

Causes of secondary osteoporosis

A
Steroids 
Anorexia 
Chronic malabsorption diseases 
Malignancy 
Thyrotoxicosis 
Hypogonadism
49
Q

Too much Th1

A

Autoimmunity

50
Q

Too much Th2

A

Allergy

51
Q

Too much Th17

A

Chronic inflammation

52
Q

Too much Treg

A

Cancer

53
Q

Too little Treg

A

Autoimmunity and inflammation

54
Q

Eye problems in RA

A

Keratoconjunctivitis sicca = dry eyes
Scleritis
Scleromalacia perforans

55
Q

Complications of RA

A
Carpal tunnel 
AAS
Osteoporosis 
Pericarditis 
Pleuritis
56
Q

Signs of scleroderma

A

Thickened waxy appearance of skin

Digital ischaemia

57
Q

Signs of dermatomyositis

A

Purple rash on eyelids, backs of hands, chest, neck, back

Proximal muscle weakening

58
Q

Signs of reactive arthritis

A

Conjuntivitis
Skin rash
Sausage toe
Arthritis

59
Q

Paget’s disease phases

A

Increased rate of resorption = large numbers of osteoclasts break down bone
Compensatory phase = osteoblasts produce large amounts of disorganised bone
Sclerotic = left with hyper cellular bone with hyper vascular bone marrow

60
Q

Which bones are affected in Paget’s?

A

Pelvis
Femur
Skull
Vertebrae

61
Q

Complication of Paget’s disease?

A

Osteosarcoma

62
Q

Paget’s treatment

A

Bisphosphonates = slow resorption
Calcitonin = inhibits osteoclasts
Calcium and vitamin D

63
Q

Sclerostin mAb

A

Romosozumab

64
Q

How many fibres in a motor unit?

A

5-200

65
Q

Which muscle fibres appear darker with ATPase staining?

A

Type 2 fast fibres

66
Q

Antibody in dermatomyositis

A

ANA

Anti-Jo1

67
Q

EMG in myositis

A

Low grade irritability
Fibrillations
Early recruitment and low amplitude

68
Q

Biopsy of myositis

A
Variation in fibre size with central nuclei 
Necrosis 
Inflammatory cell infiltration 
- mainly connective tissue 
- mainly CD8 T cells
69
Q

Polymyositis vs dermatomyositis

A
Polymyositis = endomysium 
Dermatomyositis = perimysium
70
Q

Treatment for dermatomyositis

A

Azathioprine
Methotrexate
Rituximab
Infliximab

71
Q

What causes death in dermatomyositis

A

Malignancy

Pulmonary fibrosis

72
Q

Inclusion body myositis muscles affected

A

Quads
Wrist flexors
Oesophagus

73
Q

Biopsy of inclusion body myositis

A

Fibres contain empty vacuoles
Stain for beta amyloid
Variation in fibre size
Central nuclei

74
Q

Genetics of DMD

A

X linked recessive

75
Q

Presentation of DMD

A

Proximal muscle weakness

Unable to walk by age 7

76
Q

Causes of death in DMD

A

Respiratory failure due to diaphragm damage

Dilated cardiomyopathy

77
Q

Biopsy of DMD

A
Fibre size variability 
Splitting of muscle fibres 
Large fibres with central nuclei 
Endomysial fibrosis 
Muscle tissue gradually replaced by fibrous and adipose tissue in late stages
78
Q

Pathophysiology of DMD

A

Absence of dystrophin needed to link muscle membrane and sarcomeric proteins

79
Q

What does excessive corticosteroid use do to muscle fibres?

A

Degeneration of type 2 dark fibres

80
Q

What does excessive statin use do to muscle fibres?

A

Rhabdomyolysis

Myoglobin release can cause kidney problems

81
Q

What is elevated in DMD?

A

Creatine kinase

82
Q

What is raised in myositis?

A

Creatine kinase

83
Q

What does excessive alcohol intake do to muscle fibres?

A

Type 2 fibre loss
Acute session = rhabdomyolysis
Chronic = proximal weakness

84
Q

Antibodies in fibromyalgia

A

Antipolymer

85
Q

Articular cartilage layers

A
Top = tangential 
Middle = transitional 
Deep = radial
86
Q

Gene that increases OA risk

A

HMGB2

Usually expressed in superficial zone to protect cells

87
Q

3 macroscopic changes in OA

A

Fibrillation
Cracking
Eburnation

88
Q

Microscopic changes in OA

A
Chondrocyte necrosis 
Isogenic clusters of chondrocytes remaining 
Hyaline --> fibrocartilage 
Type II --> I collagen 
Duplicated tidemark
89
Q

Neutraceuticals for OA

A

Chondroitin sulphate

Glucosamine

90
Q

Capsaicin

A

Topical chill for analgesia

91
Q

Microfracture vs chondrocyte graft

A

Microfracture –> fibrocartilage

Chondrocyte graft –> hyaline cartilage

92
Q

Where to perform osteotomy for varus deformity

A

Tibia

93
Q

Types of synoviocytes

A
A = macrophages 
B = fibroblasts
94
Q

Distance between joint surfaces

A

50um

95
Q

Volume of synovial fluid in knee

A

1-2ml

96
Q

String test

A

Should be 4-6cm

97
Q

Mucin clot test

A

Add 2-5% acetic acid

Should form solid clot

98
Q

Finkelstein’s test

A

De Quervains tenosynovitis

99
Q

When to avoid joint injection

A

Olecranon bursitis –> infection

Achilles tendon –> rupture

100
Q

When do you inject directly into the enthesis?

A

Tennis elbow

101
Q

Which movements are limited in frozen shoulder?

A

External rotation > internal rotation > abduction

102
Q

Tests for impingement

A

Painful arc = pain most at 90 degrees abduction

Painful resisted abduction