rheumatology/MSK Flashcards

1
Q

MSK complaint epidemiology

A

1/4 GP consultations
more common cause of severe long term pain and disability
prevalence increases with age

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2
Q

inflammatory vs. degenerative: stiffness

A

inflammatory- early morning/at rest, usually >60mins

degenerative- morning/evening, <30 mins

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3
Q

inflammatory vs. degenerative: presentation

A

inflammatory: swelling= synovial joints, can be bony, hot/red
degenerative- no swelling

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4
Q

inflammatory vs. degenerative: patient demographics

A

inflammatory: young, psoriasis, family history

degenerative- older, prior occupation/sport

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5
Q

inflammatory vs. degenerative: NSAIDS

A

inflammatory: responds

degenerative- no response

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6
Q

bone pain- patterns of pain

A

pain at rest and night

usually tumour/infection/fracture

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7
Q

inflammatory arthritis patterns of pain

A

pain and stiffness in morning/at rest

inflammatory/infection

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8
Q

osteoarthritis patterns of pain

A

pain on use/at end of day

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9
Q

neuralgic patterns of pain

A

pain and paraesthesia in dermatomal distribution, worsened by specific activity
root or peripheral nerve compression

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10
Q

joint distribution in rheumatoid arthritis

A

bilateral
symmetrical
hands and feet

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11
Q

joint distribution in osteoarthritis

A
1st metacarpal joint (base of thumb)
distal interphalangeal joint
hips
knees
large toe
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12
Q

joint distribution in psoriatic arthritis

A

joints
enthesitis
dactylitis- sausage digit

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13
Q

rheumatoid arthritis presentation

A
symmetrical
polyarthritis
deformity
erosion of bone on x-ray
bone nodules
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14
Q

osteoarthritis presentation

A

bouchard’s nodes- proximal interphalangeal joints
heberden’s nodes- distal interphalangeal joints
bowed legs

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15
Q

connective tissue disease presentation

A
non-erosive arthritis
butterfly rash
photosensitivity 
mouth ulcers
raynaud's- circulatory changes in response to temperature changes
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16
Q

inflammatory markers

A

erythrocyte sedimentation rate

C reactive protein

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17
Q

erythrocyte sedimentation rate

A

rises with infection/inflammation

fibrinogen=RBCs stick together=fall faster so ESR rises

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18
Q

inflammatory markers: C reactive protein

A

acute phase protein
released in inflammation/infection
produced in liver in response to IL-6

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19
Q

auto-antibodies in inflammatory joint pain

A

immunoglobulins that bind to self-antigens
rheumatoid arthritis
systemic lupus erythematosus

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20
Q

systemic lupus erythematosus auto-antibodies

A

ANA- anti nuclear antibody, binds to antigens with cell nucleus, most people test positive

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21
Q

rheumatoid arthritis auto-antibodies

A

RF- IgM or IgG

CCP

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22
Q

seronegative spondyloarthropathies

A

umbrella term for inflammatory disease that involve joints and entheses

axial inflammation, asymmetrical peripheral arthritis, no RF, association with HLA-B27

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23
Q

seronegative spondyloarthropathies: conditions

A
ankylosing spondylitis
acute anterior uveitis
psoriatic arthritis
enteropathic arthritis (crohn's/UC)
JIA
undifferentiated SpA
reactive arthritis
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24
Q

seronegative spondyloarthropathies: HLA-B27

A

class I surface antigen (on all cells except RBCs)
immunity and self-recognition
either HLA +ve or -ve
main theory is infection triggers immune response and infectious agent has peptides similar to HLA so auto-immune response against it

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25
Q

seronegative spondyloarthropathies: SPINEACHE

A
Sause digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAID=good response
Enthesitis 
Arthritis
Crohn's/colitis/elevated CRP
HLA-B27
Eye (uveitis)
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26
Q

ankylosing spondylitis

A

chronic inflammatory disorder of the spine, ribs and sacroiliac joints
ankylosis= abnormal stiffening and immobility of a joint due to new bone formation

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27
Q

ankylosing spondylitis: epidemiology

A

more common and severe in males
presents at 16 y/o, <30 y/o
88% are HLA-B27 +ve

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28
Q

ankylosing spondylitis: risk factors

A

HLA-B27
klebsiella
salmonella
shigella

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29
Q

ankylosing spondylitis: pathophysiology

A

local erosion of bone and its attachments

syndesmophyte: new bone formation and vertical growth from anterior vertebral corners
sacroilitis: sclerosis, loss of joint space, joint fusion

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30
Q

ankylosing spondylitis: typical patient

A

man, <30 y/o
gradual onset of lower back pain
worse at night with morning spinal stiffness
relieved by exercise

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31
Q

ankylosing spondylitis: presentations

A

episodic inflammation of sacroiliac joint in late teens
pain radiates from sacroiliac to hips and improves through the day
progressive loss of spinal movement
asymmetrical joint pain

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32
Q

ankylosing spondylitis: spinal abnormalities

A

loss of lumbar lordosis and increased kyphosis (curvature of C spine/ upper T)
limitation of lumbar spine mobility in sagital and frontal planes

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33
Q

ankylosing spondylitis: enthesitis

A

inflammation at site of insertion of a tendon or ligament into bone

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34
Q

ankylosing spondylitis: investigations

A

blood: ESR raised, CRP raised (can be normal), normocytic anaemia, HLA
Xray- can be normal, erosion, blurring of vertebral rims, new bone formation, fusion of sacroiliac joints
MRI- shows early sacrolitis

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35
Q

ankylosing spondylitis: treatment

A
treat quickly to prevent irreversible syndesmophyte formation
morning exercise to maintain posture
NSAIDS
methotrexate 
steroid injections
surgery
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36
Q

psoriatic arthritis: epidemiology

A

can occur without psoriasis

occurs in 10-40% of those with psoriasis and can present before skin changes

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37
Q

psoriatic arthritis: risk factors

A

family history of psoriasis

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38
Q

psoriatic arthritis: 5 patterns of disease

A
asymmetrical oligoarthritis
symmetrical seronegative polyarthritis 
spondylitis 
distal interphalangeal arthritis
arthritis mutilans
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39
Q

psoriatic arthritis: spondylitis

A

unilateral or bilateral sacrolitis and early cervial spine involvement
similar to AS but only 50% are HLA-b27 +ve

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40
Q

psoriatic arthritis: distal interphalangeal arthritis

A

DIPJs involvement only
often adjacent with nail dystrophy, reflecting enthesitis extending into nail root
dactylitis- an entire digit is swollen

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41
Q

psoriatic arthritis: arthritis mutilans

A

5% of those with PA

causes periarticular osteolysis (bone resorption) and shortening (telescope fingers)

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42
Q

psoriatic arthritis: hidden sites

A

behind/inside ear
scalp
pitting nails
umbilicus

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43
Q

psoriatic arthritis: diagnosis

A

xray- it is erosive but central in the joint, pencil in cup deformity

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44
Q

psoriatic arthritis: treatment

A
similar to rheumatoid arthritis
NSAIDS
DMARDS
methotrexate and ciclosporin 
anti-tnf alpha
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45
Q

reactive arthritis

A

sterile inflammation of synovial membrane, tendons and fascia
triggered by infection at distant site (GI/GU)
typically lower limb

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46
Q

reactive arthritis: epidemiology

A

males HLA-B27 positive (30-50 fold increased risk)

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47
Q

reactive arthritis: causes

A
GI infections (salmonella, shigella)
STIs
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48
Q

reactive arthritis: pathophysiology

A

bacterial antigens or bacterial DNA found in inflamed synovium of affected joints
persistent antigenic material is driving inflammatory response

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49
Q

reactive arthritis: classic triad

A

arthritis, 2 days- 2 weeks post infection
conjunctivitis
urethritis

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50
Q

reactive arthritis: skin lesions

A

circinate balantis- ulceration of glans of uncircumcised penis, in circumcised it is raised, red and scaly
keratoderma blennorrhagica- skin of feet and hands, similar to pustular psoriasis

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51
Q

reactive arthritis: investigations

A
ESR and CRP raised
culture stool if diarrhoea
sexual health review
aspirate spinal fluid 
xray
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52
Q

reactive arthritis: treatment

A

NSAIDS for joint inflammation
treat infection
screen sexual partners
relapse- methotrexate

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53
Q

rheumatoid arthritis: epidemiology

A

1% of population affected
peak prevalence 30-50 y/o
not seen as much in elderly compared to OA
more common in females

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54
Q

rheumatoid arthritis: risk factors

A

female
family history
smoking

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55
Q

rheumatoid arthritis: inflammation

A

chronic inflammatory reaction

infiltration of lymphocytes, macrophages and plasma cells

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56
Q

rheumatoid arthritis: proliferation

A

tumour like mass- pannus

grows over articular cartilage

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57
Q

rheumatoid arthritis: bone loss

A

focal erosion
periarticular osteoporosis
generalised osteoporosis in skeleton

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58
Q

rheumatoid arthritis: cartilage loss

A

joint space narrows due to loss of cartilage

TNF and IL-1 release proteinases with damages cartilage

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59
Q

rheumatoid arthritis: clinical manifestations

A

symmetrical, swollen painful, stiff joints
usually warm
morning stiffness >30 mins
hand deformities

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60
Q

rheumatoid arthritis: soft tissue manifestations

A

nodules
bursitis
tenosynovitis
muscle wasting

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61
Q

rheumatoid arthritis: lung manifestations

A

pleural effusions

pneumoconiosis

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62
Q

rheumatoid arthritis: cardiac manifestations

A

rare
pericarditis
raynaud’s

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63
Q

rheumatoid arthritis: eye manifestations

A

dry eyes, episcleritis

scleritis

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64
Q

rheumatoid arthritis: neurological manifestations

A

peripheral sensory neuropathies
compression/entrapment neuropathies
cord compression

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65
Q

rheumatoid arthritis: kidney manifestations

A

amyloidosis
nephrotic syndrom
CKD

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66
Q

rheumatoid arthritis: skin manifestations

A

subcut nodules

vasculitis

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67
Q

rheumatoid arthritis: haematological manifestations

A

lymph nodes palpable
spleen enlargement
anaemia

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68
Q

rheumatoid arthritis: blood tests

A

normochromic normocytic anaemia
ESR/CRP raised
RF factor
anti CCP

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69
Q

rheumatoid arthritis: radiology

A

xray

MRI

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70
Q

rheumatoid arthritis: anti-CCP

A

marker of disease
presents early in disease
those who are positive have worse prognosis

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71
Q

rheumatoid arthritis: treatment

A
no cure
lifestyle modification
pain management
corticosteroids
DMARDS
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72
Q

DMARDS

A

inhibit inflammatory cytokines
this suppresses immune system so risk of infection
take 6 weeks to start working
regular blood tests required

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73
Q

methotrexate

A

gold standard drug
contraindicated in pregnancy due to reducing folate
nausea, mouth ulcers, diarrhoea, neutropenia, renal impairment

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74
Q

biological therapy

A
expensive
TNF-alpha blockers (infliximab)
B-cell inhibitor (rituximab)
interleukin blockers
T cell activation blockers
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75
Q

vasculitis

A

inflammation and necrosis of blood vessel wall with subsequent impaired blood flow

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76
Q

vasculitis damage

A

vessel wall destruction- aneurysm, rupture, stenosis

endothelial injury- thrombosis, ischaemia, infarction

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77
Q

vasculitis classification

A
by blood vessel involved
size of vessel
presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA)
target oran
primary vs. secondary
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78
Q

vasculitis histology

A

vessel wall infiltration
neutrophils, mononuclear cells and or giant cells
fibrinoid necrosis
leukocytoclasis (dissolution of leukocytes)

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79
Q

infective conditions associated with vasculitis

A

subacute infective endocarditis

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80
Q

non infective conditions associated with vasculitis

A
SLE
scleroderma
polymyositis 
inflammatory bowel diseases
RA
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81
Q

primary large vessel vasculitis

A
giant cell (temporal) arteritis 
takayasu's arteritis
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82
Q

giant cell arteritis

A

inflammatory granulomatous arteries of large cerebral arteries as well as other large vessels such as aorta

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83
Q

giant cell arteritis: epidemiology

A

primarily in those >50
incidence increases with age
more common in females

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84
Q

giant cell arteritis: risk factors

A

over 50
female
RA, SLE, scleroderma

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85
Q

giant cell arteritis: pathophysiology

A

arteries inflamed and thicker
obstruction in blood flow
particularly cerebral and ophthalmic arteries

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86
Q

giant cell arteritis: presentation

A
headaches
tenderness of scalp
claudication of jaw
sudden painless vision loss (emergency)
malaise
weak pulses
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87
Q

giant cell arteritis: signs

A

temporal arteries- palpable, tender, reduced pulsation

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88
Q

giant cell arteritis: differential diagnosis

A

migraine
tension headache
trigeminal neuralgia

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89
Q

giant cell arteritis: investigations

A

3 or more of: >50, new headache, temporal artery tenderness, ESR raised, abnormal artery biopsy

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90
Q

giant cell arteritis: temporal artery biopsy

A
definitive diagnostic test
should be done before taking high dose corticosteroids
lesions are patchy so large biopsy
inflammatory infiltrates present
breaking up of internal elastic lamina
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91
Q

giant cell arteritis: treatment

A

high dose corticosteroids
bone protection, bisphosphantes, ca2+ and vit d
monitor treatment progress

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92
Q

primary small vessel vasculitis

A

granulomatosis with polyangiitis
eosinophilic granulomatosis with polyangiitis
microscopic polyangiitis

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93
Q

granulomatosis with polyangiitis

A

necrotising granulomatous vasculitis of arterioles, capillaries and post capillary venules
associated with ANCAs

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94
Q

granulomatosis with polyangiitis: epidemiology

A

age 25-60 y/o

prevalence 5-7/100,000

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95
Q

granulomatosis with polyangiitis: vasculature affected

A

all organ systems but limited if no renal involvement
resp tract (sinusitis, nasal bleeding, pulmonary haemorrhage)
kidneys (glomerulonephritis)
skin (purpura/ulcers)

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96
Q

granulomatosis with polyangiitis: eye disease

A

scleritis
granulomatous orbital disease
marked bilateral periorbital oedema

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97
Q

granulomatosis with polyangiitis: investigations

A

bloods- ESR, CRP, anaemic, renal impairment, ANCA

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98
Q

granulomatosis with polyangiitis: treatment

A

untreated mortality= 90% at 2 years
severe= high dose steroids
non-end organ threatening= moderate dose steroids and methotrexate

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99
Q

osteoarthritis

A

cartilage loss with periarticular bone response

non-inflammatory degenerative arthritis

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100
Q

osteoarthritis: epidemiology

A
most common type of arthritis
all tissues of joint involved
increases with age
majority= primary, no obvious cause
secondary= obesity or occupational
after age of 55 more common in females
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101
Q

osteoarthritis: risk factors

A
hypermobile joints
insufficient joint repaire
diabetes
increasing age
female
obesity
manual labour/farming
trauma
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102
Q

osteoarthritis: pathophysiology

A

balance between cartilage degradation and production is lost
focal erosion of cartilade occurs and surface becomes fibrillated and fissured
ulceration exposes underlying bone to increased stress- microfractures

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103
Q

osteoarthritis: main pathological features

A

loss of cartilage

disordered bone repair

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104
Q

osteoarthritis: presentation

A
joint pain worse on movement
stiff after rest
distal interphalangeal joints
muscle wasting
nodes
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105
Q

osteoarthritis: investigations

A

deformity and bone enlargement of joints
CRP may be elevated
RF and antinuclear antibodies are negative
MRI to see cartilage injury

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106
Q

osteoarthritis Xray- LOSS

A

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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107
Q

non- pharmacological treatment of osteoarthritis

A
exercise to improve muscle strength
lose weight 
local heat or ice packs
bracing devices
walking aids
phsyio
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108
Q

pharmacological treatment of osteoarthritis

A

paracetamol before NSAIDs
weak opioids
corticosteroid injections

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109
Q

surgical treatment of osteoarthritis

A

arthroscopy
arthroplasty
osteotomy
fusion

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110
Q

inherited connective tissue diseases

A

Marfan

Ehlers-danlos

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111
Q

auto-immune connective tissue diseases

A

systemic lupus erythematosus
systemic sclerosis
primary sjogren’s
polymyositis

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112
Q

systemic lupus erythematosus

A

inflammatory, multisystem autoimmune disorder with arthralgia and rashes

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113
Q

systemic lupus erythematosus: epidemiology

A

more common in females
peak age of onset is 20-40 years
more common in African-Caribbean’s and asians

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114
Q

systemic lupus erythematosus: risk factors

A

cause unknown
family history
UV light triggers flare ups

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115
Q

systemic lupus erythematosus: pathophysiology

A

cell apoptosis- cell remnants appear on cell surface as blebs (self antigens)
removal of blebs by phagocytosis is inefficient so transferred to lymph tissues to be taken up by APCs
the blebs are presented to B/T cells so autoantibodies produced

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116
Q

systemic lupus erythematosus: joint presentation

A

90% of cases

similar to RA

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117
Q

systemic lupus erythematosus: skin presentation

A
85% of cases
erythemia in butterfly distribution
vasculitis on fingertips and nails
photosensitive rash
alopecia
raynaud's
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118
Q

systemic lupus erythematosus: lung presentation

A

50% of cases
recurrent pleural effusions and pleurisy
pulmonary fibrosis rarely

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119
Q

systemic lupus erythematosus: cardiac presentation

A

25% of cases

pericarditis and pericardial effusions

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120
Q

systemic lupus erythematosus: CNS presentation

A
60% cases
depression
epilepsy
migraines
psychosis
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121
Q

systemic lupus erythematosus: eye presentation

A

15% cases

retinal vasculitis

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122
Q

systemic lupus erythematosus: kidney + GI presentation

A
kidney= 30% of cases, glomerulonephritis with persistent proteinuria
GI= mouth ulcers
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123
Q

systemic lupus erythematosus: tests

A

ESR raised, CRP normal
leukopenia, lymphopenia, thrombocytopenia
anaemia

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124
Q

systemic lupus erythematosus: autoantibodies

A

anti-nuclear antibodies, 95% +ve
raised anti-double strand DNA antibody is specific but positive in 60%
RF +ve 40%

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125
Q

systemic lupus erythematosus: treatment

A
reduce sunlight exposure
reduce CVD risk factors
NSAIDS 
topical corticosteroids for rashes
treat anaemia
immunosuppressants
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126
Q

systemic lupus erythematosus: treating severe

A

immunosuppressants
high dose oral corticosteroids
treat renal or cerebral disease and anaemia

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127
Q

systemic sclerosis

A

multisystem disease with involvement of skin and Raynaud’s (100% of cases)
distinct from localised sclerosis that do not involve internal organ disease

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128
Q

systemic sclerosis: epidemiology

A

highest case of mortality of any autoimmune rheumatic disease
occurs worldwide
more common in females
peak incidence 30-50 y/o

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129
Q

systemic sclerosis: risk factors

A

exposure to vinyl chloride, silica dust, adulterated rapeseed oil
bleomycin
genetic

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130
Q

systemic sclerosis: pathophysiology

A

widespread vascular damage
continued vascular damage and increased vascular permeability
uncontrolled and irreversible proliferation of connective tissue and thickening of vascular walls with narrowing of the lumen

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131
Q

systemic sclerosis: limited cutaneous scleroderma

A

70% cases
skin involvement limited to hands, face, feet and forearms
tight over fingers and produces flexion deformities
GI involvement is common with oesophageal dysmotility

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132
Q

systemic sclerosis: diffuse cutaneous scleroderma

A

30% cases
skin changes develop more rapidly
early involvement of other organs (GI, renal, lung, cardiac)

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133
Q

systemic sclerosis: blood tests

A

normochromic normocytic anaemia
microangiopathic haemolytic anaemia
urea and creatine rise

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134
Q

systemic sclerosis: autoantibodies

A

limited= speckled or anti-centromere antibodies, 70% cases
diffuse= anti-RNA polymerase 20%, anti-topoisomerase-1 antibodies, 30% cases
RF +ve in 30%

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135
Q

systemic sclerosis: imaging

A

CXR to exclude other pathology
hand xr- calcium deposits
barium swallow- confirms impaired oesophagus
high res CT- fibrotic lung

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136
Q

systemic sclerosis: treatment

A
no cure
treat raynaud's 
lansoprazole for oesophageal involvement
nutritional supplements
prevention of renal crisis- ACE inhibitors, ramipril
immunosuppressants
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137
Q

Sjogren’s syndrome

A

chronic inflammatory autoimmune disorder

characterised by immunologically mediated destruction of epithelial exocrine glands

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138
Q

primary Sjogren’s syndrome: epidemiology

A

dry eyes in absence of other autoimmune disease
more common in females
onset in 40s/50s

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139
Q

secondary Sjogren’s syndrome: epidemiology

A

associated with connective tissue disease

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140
Q

Sjogren’s syndrome: pathophysiology

A

lymphocytic infiltration and fibrosis of exocrine glands, especially lacrimal and salivary glands

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141
Q

Sjogren’s syndrome: presentations

A
dry eyes
dry mouth
salivary and parotid gland enlargement
dryness of skin and vagina
fatigue
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142
Q

Sjogren’s syndrome: systemic presentation

A
arthralgia
raynaud's
other autoimmune diseases
renal tubular defects
vasculitis
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143
Q

Sjogren’s syndrome: investigations

A

schirmer tear test
rose bengal staining
raised Ig levels, RF +ve, ANA in 80%, anti-Ro Ab in 60-90%

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144
Q

Sjogren’s syndrome: treatment

A

artificial tears and saliva replacement

NSAIDS

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145
Q

polymyositis/dermatomyositis

A

PM rare muscle disorder of unknown aetiology, inflammation and necrosis of skeletal muscle fibres
when skin is involved it is DM

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146
Q

polymyositis/dermatomyositis: epidemiology

A

rare
adults and children
more common in females

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147
Q

polymyositis: presentation

A

symmetrical progressive muscle weakness and wasting affecting proximal muscles of shoulder and pelvic girdle
difficulty squatting, going upstairs and standing from sitting involvement of resp and laryngeal muscles- dysphagia and resp failure

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148
Q

dermatomyositis: presentation

A

heliotrope (purple) skin, discolouration of eyelids and plaques on knuckles
arthralgia, dysphagia from oesophageal muscle involvement
increased incidence of underlying malignancy

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149
Q

polymyositis/dermatomyositis: investigations

A

muscle biopsy
muscle enzymes
ESR not usually raised

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150
Q

polymyositis/dermatomyositis: serum antibodies

A

ANA positive in DM
RF +ve in 50%
myositis-specific antibodies

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151
Q

polymyositis/dermatomyositis: treatment

A

bed rest with exercise
oral prednisolone for at least 1 month after it is enzymatically inactive
hydroxychloroquine or topicals to help with skin
relapse: oral- methotrexate, ciclosporin

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152
Q

Raynaud’s

A

intermittent spasm of arteries supplying fingers and toes
no underlying cause- raynaud’s disease
underlying cause- phenomenon

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153
Q

Raynaud’s: epidemiology

A

5% of population

more common in females

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154
Q

Raynaud’s: risk factor

A

the cold

smoking can aggravate symptoms

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155
Q

Raynaud’s: pathophysiology

A

peripheral digit ischaemia due to vasospasm

usually bilateral and fingers affected more than toes

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156
Q

Raynaud’s: presentation

A

skin pallor followed by cyanosis, then redness due to hyperaemia (white, blue then red)
duration is variable
numbness, burning and pain

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157
Q

Raynaud’s: when it can exhibited

A

connective tissue disorders (SLE, systemic sclerosis, RA)
vibrational tools
beta blockers, smoking

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158
Q

Raynaud’s: treatment

A

avoid cold by wearing gloves
stop smoking and beta blockers
vasodilators

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159
Q

high risk activities for MSK problems

A
heavy manual handling >20kg
lifting above shoulder 
lifting from below knee
incorrect handling techniques
forceful repetitive work
160
Q

work related MSK conditions of the arm

A
tennis elbow
golfers elbow
tenosynovitis 
carpal tunnel
hand-arm vibration
seamstress' finger
RSD
161
Q

carpal tunnel syndrome: epidemiology

A

0.6% men, 8% women

associated with obesity, pregnancy, diabetes, hypothyroidism and RA

162
Q

carpal tunnel syndrome: pathology

A

compression of median nerve by flexor tendons

seen in jobs with forceful, repetitive work done with abnormal wrist postures

163
Q

carpal tunnel syndrome: presentation

A

pain, numbness, tingling, weakness and wasting of muscles supplied by median nerve

164
Q

carpal tunnel syndrome: investigation

A

Tinel’s and Phalen’s provoking tests

165
Q

hand-arm vibration syndrome

A

aka raynaud’s phenomenon of industrial origin

eligible for state benefit

166
Q

hand-arm vibration syndrome: pathology

A

excessive exposure to hand transmitted vibration

chain saws, grinders, jack jammers and drills

167
Q

hand-arm vibration syndrome: presentation

A

blanching

tingling, numbness and loss of dexterity

168
Q

hand-arm vibration syndrome: investigation

A

distinguish from primary raynaud’s and other secondary causes
exclude neuropathy in hands

169
Q

tenosynovitis: epidemiology

A

more common in females

jobs that have forceful and repetitive hand movements- hammering

170
Q

tenosynovitis: pathology

A

local tenderness and swelling of the wrist

inflammation of APL and EPB tendon sheath

171
Q

tenosynovitis: presentation

A

crepitus- crackling of tendons

pain on resisted movements

172
Q

tenosynovitis: investigations

A

Finkelstein’s test

173
Q

tenosynovitis: treatment

A

NSAIDs, steroid injection and rest

change job

174
Q

medial epicondylitis: presentation

A

golfer’s elbow
common flexor tendon
pain against resisted flexion of wrist

175
Q

lateral epicondylitis: presentation

A

tennis elbow
common extensor tendon
pain against resisted extension of wrist

176
Q

medial and lateral epicondylitis: pathology

A

repetitive bending and straightening of elbow

177
Q

medial and lateral epicondylitis: investigations

A

Cozen’s test

178
Q

medial and lateral epicondylitis: treatment

A

NSAIDs, steroid injection and rest

179
Q

Repetitive strain disorder

A

non specific pain in hand

180
Q

Repetitive strain disorder: treatment

A

rest breaks
job rotation
ergonomically neutral postures

181
Q

thoracic outlet syndrome: presentation

A

pain or tingling down arms or blanching of fingers related to posture of arm
wasting of hands
Roo’s sign

182
Q

thoracic outlet syndrome: pathology

A

compression of trunks of brachial plexus
may be due to a cervical rib, cervical band or other abnormal anatomy in the neck
poor posture, loading of shoulders and working at a keyboard

183
Q

thoracic outlet syndrome: investigations

A

neck x ray

MRI scan

184
Q

thoracic outlet syndrome: treatment

A

surgery

185
Q

rotator cuff tendonitis: pathology

A

rotator cuff tendon tears leading to swelling

usually supraspinatus tendon

186
Q

rotator cuff tendonitis: presentation

A

painful arc

jobs include those with heavy manual handling, throwing and lifting above shoulders

187
Q

rotator cuff tendonitis: investigations

A

Hawkin’s sign

188
Q

mechanical back pain: epidemiology

A

associated with:

heavy manual handling, stooping and twisting while lifting, whole body vibration and smoking

189
Q

mechanical back pain: pathology

A

normal MRI findings:
disc degeneration
bulging discs

190
Q

mechanical back pain: investigations

A

distinguish from sciatica

191
Q

mechanical back pain: treatment

A

avoid prolonged inactivity and maintain normal activity within limits of pain
analgesics or NSAIDs

192
Q

mechanical lower back pain

A

common and self-limiting

traumatic or work related

193
Q

mechanical lower back pain: red flags

A
onset <20 y/o or >55y/o
violent trauma
constant and progressive pain
thoracic pain
steroids, drug abuse or HIV
unwell/weight loss
restriction of lumbar flexion
structural deformity
194
Q

mechanical lower back pain: epidemiology

A

common in 20/55 y/o

heavy manual handling, stooping and twisting

195
Q

mechanical lower back pain: causes

A
lumbar disc prolapse
osteoarthritis
fractures
spondyloisthesis 
heavy manual handling
196
Q

mechanical lower back pain: risk factors

A
psychosocial distress
smoking
female
increasing age
fibromyalgia
197
Q

mechanical lower back pain: presentation

A

stiff and scoliosis may be present when standing
muscle spasm can be visible or palpable
pain is often unilateral and helped by rest
sudden onset
pain worse in evening
morning stiffness is absent

198
Q

mechanical lower back pain: pathophysiology

A

spinal movement occurs at the disc and posterior fact joints
stability is achieved by spinal ligaments and muscles
any of those structures can be a source of pain

199
Q

mechanical lower back pain: lumbar spondylosis

A

most common site= L5/S1 and L4/5
discs become thin and less compliant with age
circumferential bulging of the ligaments
reactive changes occur in adjacent vertebrae- bone becomes sclerotic and osteophytes form around rim of vertebra

200
Q

mechanical lower back pain: facet joint syndrome

A

pain is worse on bending backwards and straightening from flexion
can be unilateral or bilateral, radiates to buttock
facet joints well seen on MRI and may show osteoarthritis, effusion or ganglion cyst
treat with corticosteroid injections and physio

201
Q

mechanical lower back pain: fibrositic nodulosis

A

uni/bilateral pain in low back/buttock
tender nodules in upper buttock along iliac crest
treat with intralesional corticosteroid injections

202
Q

mechanical lower back pain: pregnancy

A

common
reflects altered spinal posture and increase ligamentous laxity
weight control and exercises help
pain settles after delivery

203
Q

mechanical lower back pain: investigations

A

spinal xrays for red flags
MRI
bone scans

204
Q

mechanical lower back pain: treatment

A

urgent neurosurgical referral if any neuro deficit
analgesia
avoid excessive rest
training in manual handling

205
Q

bone and joint infections

A

usually caused by bacteria and rarely fungi

206
Q

septic arthritis

A

medical emergency
acutely inflamed joint which can be destroyed in under 24 hours
knee affected in >50% of cases

207
Q

septic arthritis: epidemiology

A

increases with age

45% >65 y/o

208
Q

septic arthritis: causes

A

staph aureus = most common causes
streptococci
gonorrhoea

209
Q

septic arthritis: risk factors

A
pre-existing joint disease
diabetes
immunosuppression 
renal failure
joint surgery
prosthetic joints
IV drug abuse
210
Q

septic arthritis: presentation

A

painful, red, swollen, hot joint
fever
mechanical dysfunction

211
Q

septic arthritis: differential diagnosis

A

gout

psuedogout

212
Q

septic arthritis: investigation

A
joint aspiration
check for gout
gram stain and culture
inflammation markers
Xray
skin wound swabs
213
Q

septic arthritis: treatment

A
stop any  methotrexate and anti-TNF alpha
if on prednisolone, double dose
double any steroids
joint drainage
NSAIDS
IV antibiotics
214
Q

septic arthritis: IV arthritis

A
only start after aspiration
flucloxacillin- gram -ve, e.coli
erythromycin- if allergic to penicillin
vancomycin for MRSA
cefotaxime- gram -ve or gonococcal
215
Q

gonococcal arthritis

A
one or several joints, secondary to genital, rectal or oral infection
gram -ve neisseria gonorrhoea
most common cause in fit young adults
fever and pustules on distal limbs
culture blood to diagnose
216
Q

meningococcal arthritis

A

complicates meningococcal septicaemia and presents as migrating polyarthritis
deposition of circulating immune complexes and containing meningococcal antigens
treat with penicillin

217
Q

tuberculous arthritis

A

1% of those with TB have joint/bone involvement
caseating granulomas and rapid destruction of cartilage and adjacent bone
fever, night sweats, weight loss

218
Q

joint infection in infants

A

haemophilus influenzae was most common, now rare in infants due to standard childhood immunisation in UK

219
Q

osteomyelitis

A

infection localised to bone

either due to metastatic haematogenous spread or local infection

220
Q

osteomyelitis: epidemiology

A

predominantly occurs in children, especially acute
adults tend to get secondary due to infection or trauma
increasing incidence

221
Q

osteomyelitis: causes

A

staph aureus, 90%
coag -ve staphylococci
haemophilus influenzae

222
Q

osteomyelitis: risk factors

A
diabetes
peripheral vascular disease
malnutrition
inflammatory arthritis
immunosuppression
sickle cell
trauma
223
Q

osteomyelitis: entering bone

A
direct inoculation of infection into bone through trauma or surgery (easy)
contiguous spread into bone (medium)
haematogenous seeding (hard)
224
Q

osteomyelitis: contiguous spread into bone

A

no breaking of skin
infection of adjacent soft tissue spreads to bone
seen in elderly who have diabetes, ulcers, vascular disease or joint replacements

225
Q

osteomyelitis: haematogenous seeding

A

where bone has large blood supply
infection from skin spreads to blood then to bone
in children tend to be long bones in metaphysis
in adults it is vertebra

226
Q

osteomyelitis: acute changes, histopathology

A

inflammatory changes
oedema
vascular congestion
small vessel thrombosis

227
Q

osteomyelitis: chronic changes, histopathology

A

necrotic bone
new bone formation
neutrophil exudates
lymphocytes and histiocytes

228
Q

osteomyelitis: process of pathology

A

inflammatory exudate in the marrow leads to increased intramedullary pressure with extension of exudate into bone cortex
rupture through the periosteum and interruption of periosteal blood supply
necrosis leaves separated dead bone known as sequestra

229
Q

osteomyelitis: presentation

A

dull pain at site
fever, sweats, rigors and malaise
can present as septic arthritis

230
Q

acute osteomyelitis: presentation

A

tenderness
warmth
erythema
swelling

231
Q

chronic osteomyelitis: presentation

A
tenderness
warmth
erythema
swelling
draining sinus tract which is associated with deep ulcers that fail to heal
232
Q

osteomyelitis: differential diagnosis

A
charcot joint- damage due to sensory nerves affected by diabetes
soft tissue infection
avascular necrosis of bone
gout
fracture
malignancy
233
Q

osteomyelitis: blood investigations

A

blood culture to determine aetiology
ESR and CRP raised
acute has raised WCC
chronic can have normal WCC

234
Q

osteomyelitis: imaging investigations

A

plain xray to show osteopenia
MRI may show marrow oedema
bone scan helpful

235
Q

osteomyelitis: treatment

A

immobilisation
antimicrobial therapy
surgical debridement

236
Q

prosthetic infections

A

most serious complication of arthroplastic surgery

hips and knees

237
Q

prosthetic infections: epidemiology

A

increasing due to increasing age, diabetes and obesity

238
Q

prosthetic infections: causes

A

staph. aureus
coag -ve staphylococci
gram +ves mainly

239
Q

prosthetic infections: risk factors

A

poor infection control
old age
diabetes
obesity

240
Q

prosthetic infections: presentation

A

majority aren’t acutely infected
systemically well
tender, hot, swollen joint

241
Q

prosthetic infections: investigations

A
joint aspiration
tissue sample 
x-ray
inflammation marker
alpha defensin- 95% sensitive
242
Q

prosthetic infections: joint aspiration

A

gold standard diagnostic
identifies organism and antibiotic sensitivities
must be done with patient off antibiotics for 2 weeks minimum

243
Q

prosthetic infections: aim of treatment

A

eradicate sepsis
relieve pain
restore function

244
Q

prosthetic infections: treatments

A
antibiotic suppression
debridement and retention of prosthesis 
excision arthroplasty 
one stage arthroplasty exchange 
two stage arthroplasty exchange
amputation
245
Q

prosthetic infections: antibiotic suppression

A

if they’re unfit for surgery
multiple prosthetic infections
does not eliminate sepsis

246
Q

prosthetic infections: debridement and retention of prosthesis

A

for early post-op infections

not for chronic infections

247
Q

prosthetic infections: excision arthroplasty

A

for high risk, frail and multiple co-morbidities whose infection is not controlled by antibiotic suppression

248
Q

prosthetic infections: one stage arthroplasty exchange

A
radical debridement
implantation of new prosthesis with antibiotic cement
systemic and local antibiotics
avoids bone grafts
85% success
249
Q

prosthetic infections: two stage arthroplasty exchange

A

radical debridement
local antibiotic spacer with systemic antibiotics
interval stage
implantation of new prosthesis with antibiotic cement
90-95% success

250
Q

prosthetic infections: amputation

A

if severe infection

if all else fails

251
Q

fibromyalgia: definition

A

widespread musculoskeletal pain when other diseases have been excluded
symptoms present for at least 3 moths with pain at 11 or 18 tender point sites on digital palpation

252
Q

fibromyalgia: epidemiology

A

can develop any age, often over 60 y/o
more common in females
12% with RA have fibromyalgia

253
Q

fibromyalgia: associations

A

depression
chronic headache
IBS
chronic fatigue syndrome

254
Q

fibromyalgia: risk factors

A
female
middle age
low household income
divorced
low educational status
255
Q

fibromyalgia: presentation

A

chronic pain
non-restorative sleep
fatigue
anxious

256
Q

fibromyalgia: non-restorative sleep

A
frequent waking during night
waking unrefreshed
poor concentration and forgetfulness
low mood, irritable, weepy
lack of non-REM sleep causes functional pain
257
Q

fibromyalgia: pain

A

chronic- >3months
widespread
aggravated by stress, cold and activity
associated with morning stiffness

258
Q

fibromyalgia: areas that pain focuses on

A
lower front of neck 
base of skull
upper edge of breast
neck and shoulder
upper, inner shoulder
upper, outer buttock
hip
upper, inside knee
259
Q

fibromyalgia: differential diagnosis

A
hypothyroidism
SLE
polymyalgia rheumatics
high calcium
low vitamin D
inflammatory arthritis
260
Q

fibromyalgia: investigations

A
digital palpation of 18 tender point sites
thyroid function test
ANAs and DsDNA to exclude SLE
ESR and CRP
Ca2+
Vit D
261
Q

fibromyalgia: treatment

A

educate patient on pain doesn’t always mean damage
avoid unnecessary investigations
correct sleep
low dose antidepressants such as amitriptyline

262
Q

fractures: pattern

A

transverse, oblique and spiral= low energy
comminuted= high energy
torus and greenstick= common in children

263
Q

fractures: joint involvement

A
extra-articular= not involving joint
intra-articular= involving joint
264
Q

fractures: skin involvemnet

A

open- breach in skin

265
Q

fractures: management

A
analgesia
neurovascular examination- pre and post immobilisation
reduce
immobilise
rehabilitate
266
Q

fractures: immobilisation techniques

A

cast, splint, brace, halo

internal- wires, screws, plates, nails

267
Q

fractures: healing stages

A

haematoma
fibrocartilaginous callus formation
bony callus formation
bone remodelling

268
Q

fractures: haematoma

A
hours
bleeding as endosteal and periosteal vessels torn
decreased blood blow
periosteal stripping
osteocyte death due to ischaemia
269
Q

fractures: inflammation

A

days
fibrin clot organisation
neurovascularisation
cellular invasion

270
Q

fracture healing: inflammation and cellular invasion

A

haematopoieitic cells- clear debris and express repair cytokines
osteoclasts- resorb dead bone
mesenchymal stem cells- building cells for repair

271
Q

fractures: repair

A

hard callus formation- reduces movement
fibroblasts produce fibrous tissue, chondroblasts cartilage and osteoblasts osteoid
progressive matrix mineralisation
high vascularity

272
Q

fractures: remodelling

A
months- years
woven bone replaced by lamella bone
increased bone strength
vascularity returns to normal
healing without scar
273
Q

vertebral disc degeneration

A

prolapse of intervertebral disk resulting in acute back pain

274
Q

vertebral disc degeneration: epidemiology

A

disease of younger people, 20-40 y/o as degenerated discs in elderly cannot prolapse

275
Q

vertebral disc degeneration: presentation

A

sudden onset of severe back pain, often following strenuous activity
muscle spasm leads to sideways tilt when standing
radiation of pain and findings depend on disc affected
most common to be affected are the lower 3 discs (L4-S1)

276
Q

vertebral disc degeneration: investigations

A

Xrays often normal

MRI when surgery considered

277
Q

vertebral disc degeneration: treatment

A

acutely= bed rest on firm mattress, analgesia and epidural corticosteroid injection
surgery for severe or increasing neurological impairments
physio in recovery phase

278
Q

Root lesion @ L4: pain, reflex lost and other signs

A

pain= lateral aspect of thigh and medial side of calf
reflex lost= knee jerk
positive femoral stretch test

279
Q

Root lesion @ L5: pain, reflex lost and other signs

A

pain= buttock to lateral aspect of leg and top of foot
no reflex lost
diminished straight leg rising

280
Q

Root lesion @ S1: pain, reflex lost and other signs

A

pain= buttock down back of thigh to ankle/foot
reflex lost= ankle jerk
diminished straight leg rising

281
Q

chronic disc disease

A

associated with degenerative changes in lower lumbar discs and facet joints
pain is mechanical
sciatic radiation may occur with pain in buttocks radiating into posterior thigh

282
Q

chronic disc disease: treatment

A

NSAIDS, physio and weight reduction

surgery can be done if pain arises from a single identifiable level

283
Q

bone tumours: epidemiology

A

the most common tumours are metastases from other cancers

primary bone tumours are rare and usually only seen in children or young adults

284
Q

bone tumours: presentation

A

symptoms usually related to anatomical position of tumour with local bone pain
systemic= malaise, pyrexia, aches and pains- related to hypercalcaemia

285
Q

bone tumours: red flag signs

A
rest pain
night pains 
lump present
loss of function
neurological symptoms
weight loss
286
Q

bone tumours: benign vs. malignant examples

A
benign= osteoid osteoma, osteoblastoma, osteochondroma
malignant= osteosarcoma
287
Q

cartilage tumours: benign vs. malignant examples

A
benign= enchondroma, chondroblastoma
malignant= chondrosarcoma
288
Q

fibrous tumours: benign vs. malignant examples

A
benign= fibrous dysplasia, non- ossifying fibroma
malignant=  fibrosarcoma
289
Q

cystic tumours examples

A

unicameral bone cyst

aneurysmal bone cyst

290
Q

bone tumours with unknown aetiology: benign vs. malignant examples

A

giant cell tumour
ewing tumour
adamantinoma

291
Q

osteoid osteoma

A

bone-forming lesion in the young
localised pain and self-limiting <7yrs
produces high levels of prostaglandin E2
proximal femur, tibial diaphysis, spine

292
Q

osteoid osteoma: investigation

A

x-ray: active reactive bone and nidus (5-10mm)

best appreciated on CT

293
Q

osteoid osteoma: treatment

A

medical- NSAIDs are 50% successful

surgical- radiofrequency ablation

294
Q

osteoblastoma

A

rare bone producing tumour

spine lesions can present with neurology

295
Q

osteoblastoma: epidemiology

A

M:F=3:1

296
Q

osteoblastoma: presentation

A

pain
not self-limiting
spine, proximal humerus and sacrum

297
Q

osteoblastoma: investigation

A

X rays- bone destruction surrounded by reactive new bone

histology- interlacing trabeculae and loose fibrovascular stroma

298
Q

osteoblastoma: treatment

A

excision with at least a marginal line of excision

299
Q

osteosarcoma

A

spindle cell neoplasms that produce osteoid

300
Q

osteosarcoma: types

A

intramedullary osteosarcoma- high grade
parosteal osteosarcoma- low grade
periosteal sarcoma- high grade
telangiectatic osteosarcoma

301
Q

secondary osteosarcomas: causes

A

Paget’s
post radiation
fibrous dysplasia

302
Q

osteosarcoma: secondary to Paget’s

A

older population
paget’s is present in 0.7-0.9% so it is rare
high risk for pulmonary metastasis

303
Q

osteosarcoma: secondary to irradiation

A

60-70% survival for extremity lesions, 27% for axial
children treated with high dose radiotherapy are greatest risk
high grade tumours, high risk of pulmonary mets

304
Q

high grade intramedullary osteosarcoma: presentation

A

most common type
in the knee, proximal humerus and proximal femur
children and young adults
90% are high grade and penetrate cortex early

305
Q

osteosarcoma: management

A

multi-agent chemo, pre-op for 8-12 weeks

aims to reduce or treat pulmonary mets

306
Q

osteosarcoma: current survival

A
if untreated it is fatal
with treatment: 
-overall= 60-70% for 5 years
-if tumour necrosis is >90% after chemo, 5 yr survival is 80-90%
-if necrosis is <90%, 5 yr survival <15%
307
Q

enchondromas

A

lesions tend to occur in small bones- hand and feet, but can occur anywhere
do not destroy bone

308
Q

enchondromas: investigations

A

x-ray for metaphyseal popcorn

histology- island of cartilage

309
Q

aneurysmal bone cyst

A

always biopsy if large or any doubt
usually <20 y/o
metaphyseal and eccentric

310
Q

aneurysmal bone cyst: investigation

A

x ray- eccentric, lytic and expansile lesion

MRI- fluid levels

311
Q

aneurysmal bone cyst: treatment

A

simple curettage has 86% success

312
Q

giant cell tumours

A

locally destructive neoplasm with poorly defined cells
20-40 y/o, F>M
benign but 2% metastasise to lungs

313
Q

giant cell tumours: presentation

A

lesions are 50% in knee, 30% vertebrae and sacrum

314
Q

giant cell tumours: investigation

A

histology shows multinucleated cells

x rays- destructive lesion, no sclerotic rim

315
Q

giant cell tumours: treatment

A

curettage, wash out, dental burr- 90% success rate

316
Q

Ewing’s sarcoma

A

small round cell tumour
arise from neural crest cells
children and young adults

317
Q

Ewing’s sarcoma: lesion types

A

classic= diaphyseal lesion, commonly on femur, also pelvis, tibia and humerus
destructive lytic lesion= periosteum may be lifted off in multiple layers giving an onion skin appearance

318
Q

Ewing’s sarcoma: bone marrow biopsy

A

monotonous blue cell tumour
indistinct cell borders
no matrix production by tumour cells

319
Q

Ewing’s sarcoma: treatment

A

chemo, radiotherapy and surgical excision/reconstruction

320
Q

Ewing’s sarcoma: prognosis

A

poor if large tumour/pelvic/mets and Dx

70% survival overall, 30% if mets present

321
Q

bony metastasis: most common tumours

A
breast
lung
prostate
kidney
thyroid
322
Q

bony metastasis: presentation

A

bone pain
generally unwell
pathological fracture

323
Q

bony metastasis: management

A

correct metabolic abnormalities
full length x rays
liase with oncology

324
Q

crystal deposition

A

local inflammatory response and tissue damage
joints= crystal arthopathies
kidney and gallbladder= stones

325
Q

crystal arthropathy

A

arthritis caused by crystal deposition in joint lining

326
Q

crystal arthropathy: presentation

A

acutely hot and swollen joints

chronically with longer term damage

327
Q

crystal arthropathy: diagnosis

A

history, pattern and aspiration of joint

328
Q

gout

A

inflammatory arthritis associated with hyperuricaemia and intra-articular monosodium urate crystals

329
Q

gout: epidemiology

A

common
more common in males
most common arthritis in men >40 y/o

330
Q

gout: risk factors

A
high alcohol intake
purine rich food
high saturated fat intake
low-dose aspirin
ischaemic heart disease
family history
331
Q

gout: serum uric acid levels increase with..

A
age
obesity
diabetes
ischaemic heart disease 
hypertension
332
Q

gout: pathogenesis

A
renal excretion reduced
excessive urate
urate crystals
phagocyte activation
inflammation
333
Q

gout: joint involvement

A
big toe
ankle/foot
knee
finger
elbow
wrist
334
Q

gout: precipitants of an attack

A

aggressive introduction/cessation of hypouricaemic therapy
alcohol/shellfish binges
sepsis/MI/severe illness

335
Q

acute gout: presentation

A

sudden onset of agonising pain, swelling and redness of first MTP joint
usually one joint affected but can be multiple

336
Q

chronic gout: presentation

A

rare except in elderly- on long term diuretics in renal failure of if they started on allopurinol too soon

337
Q

gout: differential diagnosis

A

exclude septic arthritis

338
Q

gout: investigations

A

joint fluid aspiration
serum uric acid levels
creatinine

339
Q

gout: lifestyle treatment

A

lose weight
less alcohol
avoid purine rich food
increase dairy

340
Q

gout: medical treatment

A

NSAIDS- naproxen or ibuprofen

if they’re not tolerated then colchicine or prednisolone

341
Q

gout: prevention

A

stop diuretics
allopurinol
febuxostat

342
Q

gout: allopurinol

A

inhibits xanthine oxidase so less uric acid production

side effects are rash, fever and low WCC

343
Q

gout: febuxostat

A

non-purine xanthine oxidase inhibitor

use when allopurinol is contraindicated or because of it’s side effects

344
Q

pseudogout

A

deposition of calcium pyrophosphate crystals on joint surface

345
Q

pseudogout: epidemiology

A

affects elderly women

346
Q

pseudogout: risk factors

A
old age
diabetes
osteoarthritis
joint trauma
hyperparathyroidism
347
Q

pseudogout: pathophysiology

A

deposition of calcium pyrophosphate in articular cartilage and periarticular tissue producing radiological appearance of chonedrocalcinosis

348
Q

pseudogout: triggers of acute attack

A
direct trauma
intercurrent illnesses
surgery- parathyroidectomy
blood transfusion
T4 replacement
joint lavage
most are spontaneous
349
Q

pseudogout: presentation

A

resembles acute gout but more common in elderly women and affects knee or wrist

350
Q

pseudogout: diagnosis

A

joint aspiration
xray
bloods- raised WCC

351
Q

pseudogout: joint aspiration

A

small rhomboidal crystals

positively bifringent

352
Q

pseudogout: treatment

A

high dose NSAIDs
colchicine if NSAIDs not tolerated
prednisolone
joint aspiration

353
Q

pseudogout: treatment

A

high dose NSAIDs
colchicine if NSAIDs not tolerated
prednisolone
joint aspiration

354
Q

osteoporosis definition

A

systemic skeletal disease characterised by low bone mass and amicro-architectural deterioration of bone tissue
consequent increase in bone fragility and susceptibility to fracture

355
Q

osteopenia definition

A

pre cursor to osteoporosis characterised by low bone density

356
Q

osteoporosis: T score definition

A

standard deviation score ascertained using a dual energy x ray absorptiometry (DEXA) scan

357
Q

osteoporosis: T score ranges

A

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

358
Q

osteoporosis: epidemiology

A

> 50 y/o and females= more common

caucasian and asian races are particularly at risk

359
Q

osteoporosis: risk factors

A
old age
women
family history
previous bone fracture
smoking/alcohol
360
Q

osteoporosis: SHATTERED (risk factors)

A
Steroid use
Hyperthyroidism/hyperparathyroidism
Alcohol/tobacco
Thin, BMI<22
Testosterone decreased
Early menopause
Renal/liver failure
Erosive/inflammatory bone disease
Dietary calcium decrease/diabetes
361
Q

osteoporosis: pathophysiology

A

start to lose bone mass after the age of 25
increased breakdown by osteoclasts and decreased formation by osteoblasts
genes involved= callagen type A1, vitamin D receptor and oestrogen receptor genes
nutritional factors, sex hormone status and physical activity

362
Q

osteoporosis: bone strength determinants

A

BMD
bone size
bone quality

363
Q

osteoporosis: bone strength and BMD

A

how much mineral is in bone

determined by the amount gained during growth and amount lost during ageing

364
Q

osteoporosis: bone strength and bone size

A

short and fat is stronger than long and thin

distribution of cortical bone

365
Q

osteoporosis: bone strength and bone quality

A

bone turnover, architecture and mineralisation
not enough mineral= break easy
too many minerals= too stiff and shatter

366
Q

osteoporosis: oestrogen deficiency

A

postmenopausal osteoporosis
results in increased numbers of remodelling units (osteoclasts), premature arrest of osteoblastic synthetic activity and perforation of trabeculae with a loss of resistance to fracture

367
Q

osteoporosis: changes in trabecular architecture

A

decrease in trabecular thickness

strain on bones is head to toe so we preserve vertical trabeculae and lose horizontal ones

368
Q

osteoporosis: presentation

A

fracture is the only cause of symptoms

369
Q

osteoporosis: investigations

A

xray- fractures
bloods- Ca, phosphate and alkaline phosphate all normal
DEXA

370
Q

osteoporosis: DEXA scan

A

low radiation dose
measures important fracture sites (lumbar spine and proximal femur)
gold standard for measuring bone density and diagnosing osteoporosis

371
Q

osteoporosis: liftestyle management

A

quite smoking and reduce alcohol consumption
weight bearing exercise
calcium and vitamin D rich diet
balance exercises

372
Q

osteoporosis: bisphosphonate treatment

A

1st line treatment
inhibit bone resorption through inhibiting an enzyme- reduces osteoclast activity
oral aldendronate= most common
should be taken fasting with a large drink of water

373
Q

osteoporosis: denosumab treatment

A

osteoblasts produce RANK to activate osteoclasts and thus resorption
this is a monoclonal antibody that inhibits RANK signal
reduces fracture risk

374
Q

osteoporosis: HRT treatment

A

2nd line- used in menopausal women
reduces fracture risk and stops bone loss
prevents hot flushes and other menopausal symptoms

375
Q

osteoporosis: raloxifene treatment

A

selective oestrogen receptor modulator- activates oestrogen receptor on bone whilst having no stimulatory effect on endometrium

376
Q

osteomalacia

A

normal amount of bone but mineral content is low
defective mineralisation after fusion in epiphyses
clinical manifestation of profound vitamin D deficiency

377
Q

osteomalacia: aetiology

A

hypophosphataemia due to hyperparathyroidism , secondary to vitamin D deficiency
liver/renal disease
drugs
tumour induced

378
Q

osteomalacia: caused by liver disease

A

leading to reduced hydroxylation of vitamin D to 25-hydroxy vitamin D

379
Q

osteomalacia: caused by drugs

A

anticonvulsants may induce liver enzymes- breakdown of 25-hydroxy vitamin D
rifampicin (antibiotic)

380
Q

osteomalacia: caused by renal disease

A

renal failure means there is inadequate conversion of 25-hydroxy vitamin D to 1,24- hydroxy vitamin D

381
Q

osteomalacia: caused by vitamin D deficiency

A

malabsorption since vitamin D is fat soluble
poor diet- not enough oily fish or egg yolks
lack of sunlight

382
Q

osteomalacia: presentation

A

muscle weakness
widespread bone pain
bone tenderness
fractures, especially femoral neck

383
Q

rickets presentation

A

growth retardation
knock knees, bowed legs
widened epiphyses at wrists
hypocalcaemic tetany

384
Q

osteomalacia: investigations

A

bloods
biopsy- gold standard as shows incomplete mineralisation, but not practical
Xray

385
Q

osteomalacia: blood test results

A

low Ca2+ and phosphate
raised serum alkaline phosphatase
elevated parathyroid hormone
low 25-hydroxy vitamin D

386
Q

osteomalacia: treatment

A

Vitamin D:

  • dietary insufficiency= calcium D3 forte
  • malabsorption/hepatic disease= oral ergocalciferol or IM calcitriol
  • renal disease- alfacidol or calcitriol
387
Q

Paget’s disease of bone

A

aka osteitis deformans

focal disorder of bone remodelling

388
Q

Paget’s disease of bone: epidemiology

A

increases with age, rare under 40
10% of those aged 90
UK has highest prevalence in the world
F>M

389
Q

Paget’s disease of bone: risk factors

A

may result from latent viral infection but aetiology unknown

390
Q

Paget’s disease of bone: pathophysiology

A

increased osteoclast bone resorption followed by weaker new bone
new woven bone is weak and leads to deformity and increased fracture risk

391
Q

Paget’s disease of bone: presentation

A

pelvis, lumbar spine, femur, thoracic spine, skull and tibia are common sites
60-80% asymptomatic
bone/joint pain

392
Q

Paget’s disease of bone: neurological complications

A

never compression- deafness from 8th cranial never involvement. paraparesis, partial paralysis of lower limbs

hydrocephalus due to blockage of aqueduct of sylvius

393
Q

Paget’s disease of bone: investigations

A

increased serum alkaline phosphatase with normal calcium and phosphate shows increased bone turnover
urinary hydroxyproline excretion is raised

394
Q

Paget’s disease of bone: radiography investigations

A

x ray- localised bony enlargement and distortion, sclerotic changes, osteolytic areas
isotope bone scans- determine skeletal involvement

395
Q

Paget’s disease of bone: treatment

A

bisphosphonates
NSAIDS
monitor disease activity

396
Q

Rickets definition

A

Rickets is defective mineralisation during bone growth at the epiphyseal growth plate
clinical manifestation of profound vitamin D deficiency