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Phase 3 > Week 11 > Flashcards

Week 11 Flashcards

1
Q

Describe tendinopathy

A

chronic tendon injury of over use - repetitive loading
degeneration, disorganisation of collagen fibres
increased cellularity
little inflammation
loss of balance between micro damage from overuse and reparative mechanisms

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2
Q

What are the risk factors for tendinopathy?

A 
age
chronic disease
diabetes
rheumatoid arthritis
adverse biomechanics
repetitive exercise
recent increase in activity 
quinolone antibiotics
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3
Q

Describe the pathology of tendinopathy

A

deranged collagen fibres/regeneration with a scarcity of inflammatory cells
increased vascularity around the tendon
failed healing response to micro tears
inflammatory mediators release IL-1, NO, PG’s cause apoptosis, pain and provoke degeneration through release of MMPS

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4
Q

What are common tendinopathies?

A 
achilles 
rotator cuff
tennis elbow (lateral epicondylitis 
golfers elbow (medial epicondylitis)
patella 
hamstring
adductor
plantar fasciitis
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5
Q

What are the clinical features of tendinopathy?

A 
pain
swelling
thickening
tenderness
provocation tests
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6
Q

How is tendinopathy diagnosed?

A

clinical history
ultrasound
MRI - best seen on T1

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7
Q

What are the non operative treatments of tendonopathy?

A 
NSAIDs
activity modification
physiotherapy
GTN patches
PRP injection
prolotherapy 
extracorporeal shockwave therapy 
topaz - radiofrequeny collation
steroid injection
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8
Q

Describe physiotherapy in the treatment of tendonopathy

A

eccentric loading

contraction of the musculotendinous unit whilst it elongates

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9
Q

Describe operative treatment of tendonopathies

A

debridement
excision of diseased tissue
possible to deride 50% of tendon without loss of function

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10
Q

Describe compartment syndrome

A

elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise
common sites - leg, forearm, thigh

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11
Q

What are the causes of compartment syndrome?

A

increased internal pressure - bleeding, swelling, iatrogenic inflammation
increased external compression - casts, bandages, full thickness burns
combinations

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12
Q

Describe the pathophysiology of compartment syndrome

A 
decreased perfusion
muscle ischaemia
muscle swelling
increased permeability - fluid leaks into interstitial space
increased pressure
autoregulatory mechanisms overwhelmed
muscle necrosis and myoglobin release
loss of function, extremity or loss of life
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13
Q

Describe the end stage of compartment syndrome

A

stiff fibrotic muscle compartments
impaired nerve function
clawing of limbs
loss of function

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14
Q

What are the clinical features of compartment syndrome?

A

pain - out of proportion to that expected from the injury
pain on passive stretching of the compartment
pallor
parathesia
paralysis
pulselessness

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15
Q

How is compartment syndrome diagnosed?

A 
site 
swelling
shiny ski
autonomic responses - sweating, tachycarida
pulses present until late stages
deep nerves affected first - 1st dorsal web space - deep perineal nerve
normal pressure 0-4mmHg
DBP-CP <30mmHg
CP>30mmHg
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16
Q

What is the treatment of compartment syndrome?

A 
open any constricting dressings / bandages
reassess
surgical release
later wound closure
skin grafting / plastic surgery input
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17
Q

Describe surgical release in compartment syndrome

A

full length decompression of all compartments
excise any dead muscle
leave wounds open
repeat debridement until pressure dow and all dead muscle excised

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18
Q

Describe the preoperative care in compartment syndrome

A 
adequate hydration
fluid loss
monitor and regulate electrolyes
correct acidosis
myoglobinuria
renal function
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19
Q

Describe the treatment in late presentation of compartment syndrome

A

irreversible damage already present
fasciotomy will predispose to infection
consider non-operative treatment
splint in position of function

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20
Q

What is vasculitis?

A

inflammation of the blood vessels

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21
Q

What are the main secondary causes of vasculitis?

A

infection
underlying disease - cancer, autoimmune diseases such as RA, SLE or IBD
cold injury
drugs

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22
Q

What are the main infectious causes of vasculitis?

A

meningococcal septicaemia

streptococcus

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23
Q

Describe cryoglobulinaemia

A

cold causes antibodies to acitivate
these antibodies attack, clump and destroy red blood cells
this blocks and irritates the vessels
peripheral are worst affected

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24
Q

What drugs can cause vascultits?

A 
anti thyroid drugs (carbimazole)
micocyclin
hydralazine
penicillamine
antibiotics
anticonvulsants
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25
Q

What are the general features for all primaries vasculitis?

A

systemic inflammation -fever, malaise, weight loss, myalgia, arthralgia, night weats

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26
Q

What does large vessel vasculitis cause?

A

end organ ischaemia or infarction

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27
Q

What does medium vessel vasculitis cause?

A

localised ischaemia or infarction

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28
Q

What does small vessel vasculitis cause?

A

organ specific inflammation

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29
Q

What are the 2 main types of large vessel vasculitis?

A 
giant cell (common)
takayasu (rare)
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30
Q

What are 2 types of medium vessel vasculitis?

A 
polyarteritits nodosa (PAN)
Kawasaki disease (children only)
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31
Q

What are the 2 types of small vessel vasculitis?

A

immune complex mediated vasculitis

ANCA associated vasculits

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32
Q

What types of immune complex mediated vasculitis are there?

A

HSP

cryoglobulinaemia

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33
Q

What are the ANCA associated vasculitis?

A

microscopic polyangitis
granulomatosis with polyangitis (Wegener’s)
eosinophilic granulomatosis with polyangitis (churn-strauss disease)

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34
Q

Describe giant cell arteritis

A

elderly
common
women

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35
Q

What re the clinical features of giant cell arteritis?

A 
fatigue
headaches
jaw claudication
scalp tenderness
test - very high ESR
definitive test - biopsy
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36
Q

What is the sudden blindness associated with giant cell arteritis called?

A

amaurosis fugax

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37
Q

Describe polymyalgia rheumatica

A

considered related disorder to giant cell
elderly, mainly women
pain is the main symptom
pain and stiffness in muscles of neck, shoulder and pelvis
not particularly weak
high ESR
better with steroids

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38
Q

Describe takayasu’s arteritis

A

pulseless disease or aortic arch syndrome
very rare
younger women (15-25)
systemic features come early and may resolve by diagnosis
late features of vascular insufficiency in aorta and large tributaries
- bruits, absent or reduced pulses
claudication - arms, legs, spine, gut
ischameic heart disease, heart failure, pulmonary hypertension
headaches and amaurosis fugax
BP variability - syncope, hypertension, variable BP between limbs
diagnosis - imaging, angiography, CT

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39
Q

Describe polyarteritis nodosa

A

medium vessel
fever and weight loss
malaise and myalgia
organs generally - infarction or ischaemia - gut,
brain
angina
liver
skin - gangrene, purpura, nodules
peripheral nervous system - pain in distribution of nerve, loss of sensory/motor
limbs - claudication
kidney - infarction, renal artery stenosis, renal aneurysms, hypertension

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40
Q

Describe kawasaki disease

A

only in children
aneurysm found in medium to large sized arteries
coronary arteries - MI
axillary, iliac and popliteal arteries
early features - high fever, miserable, mucositis, conjunctivitis

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41
Q

Describe HSP

A 
commonest vasculitis in childhood 
less common in adults
possible infective tirgger
palpable purpura (extensor surfaces, starts peripherally)
abdominal pain
arthritis 
complicated by - renal involvement, intersucception / infarction
pain
misery
testis pain/infarction
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42
Q

What does ANCA stand for?

A

anti-neutrophil cytoplasmic Ab

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43
Q

What are the 2 types of ANCA?

A

cytoplasmic c-ANCA

perinuclear p-ANCA

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44
Q

When is cANCA positive?

A

very specific for granulomatous polyangitis (Wegener’s )

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45
Q

when is pANCA and MPO positive?

A

microscopic polyangitis
crescentic glomerulonephritis
eosinophilic granulomatous polyangitis

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46
Q

When is pANCA positive and MPO negative?

A

IBD
RA
sclerosing cholangitis

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47
Q

Describe granulomatous polyangitis

A

Wegener’s

classically involves URT, LRT and kidneys

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48
Q

Describe eosinophilic angitis

A 
churg strauss
asthma
eosinophilic infiltrates
eosninophilia
eosinophil rich granulomata 
peripheral neuropathy
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49
Q

Describe microscopic polyangitis

A 
small and medium sized vessels 
chronic inflammation
5 most common clinical manifestations of MPA are kidney glomerulonephritis 
weight loss
skin lesions
peripheral neuropathy, mononeuritis multiplex
fevere
no granuloma
pANCA 75%
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50
Q

What is the treatment of primary vasculitis?

A

corticosteroids

other immune suppression

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51
Q

What is the commonest cause of vasculitis in children?

A

henoch scholein purpura

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52
Q

What are 3 ANCA associated vasculitis?

A

microscopic polyangitis
granulomatosis with polyangitis
eosinophilic grnulomatosis with polyangitis

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53
Q

Describe septic arthritis

A

pain, fever, swollen joint, loss of function
staph.aureas, neisseria gonorrhoea, haemophilus influenza (children)
increased risk if steroids, RA
suspected septic arthritis is a medical emergency

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54
Q

How can bacteria infect a joint space?

A

hematogenous
dissemination from osteomyelitis
spread from adjacent soft tissue infection
medical procedures
penetrating damage by puncture or traumaa

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55
Q

What investigations should be carried out for septic arthritis?

A

joint aspirate - microbiology from gram stain and culture
blood culture
FBC -leukocytosis
xray - no value

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56
Q

What affect can septic arthritis have in the joint if it is not treated?

A

synovial inflamed with fibrin exudation and numerous neutrophil polymorphs
loss of articular cartilage may lead to secondary osteoarthritis

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57
Q

What are other types of septic arthritis?

A

lyme disease - borrelia burgdoferi
brucellosis
syphilitic arthritis - congenital and acquired

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58
Q

What types of crystal arthropathy are there?

A

gout and pseudogout

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59
Q

Describe gout

A

excess levels of uric acid - leads to deposition of urate crystals in joints or soft tissue (top)
acute - precipitation in joint stimulates acute inflammatory process
chronic gout - top formation

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60
Q

how is gout diagnosed?

A

aspirate - negatively befringement needle shaped crystals on polarised microscopy
serum urate levels and U&Es

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61
Q

What can cause primary gout?

A

hyperurciaemia due to genetic predisposition – Lesch Nyhan syndrome

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62
Q

What can cause secondary gout?

A

myeloproliferative disorder
leukaemia treated with chemo
thiazides
chronic renal disease

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63
Q

What tend to raise uric acid levels?

A 
increasing age
obesity 
high alcohol intake
high protein diet
diabetes mellitis
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64
Q

What is the management of gout?

A

NSAIDs
alternatives - colchicine, corticosteroids
if repeated - allopurinol - xanthine oxidase inhibitor
uricosuric agent (probenecid) increased secretion of uric acid in the urine

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65
Q

Describe pseudogout

A

calcium pyrophosphate crystal deposition
synovial
cartilage and extra-articular tissues (chondorcalcinosis)
acute or chronic
primary or secondary (hyperparathyroidism, haemochromatosis)
positively befringement rhomboid shaped crystals on aaspiration

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66
Q

What is the management of pseudo gout?

A

aspiration helps to reduce pain and swelling
NSAIDs
colchicine

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67
Q

Describe reactive arthritis

A

sterile synovitis which occurs following an infection

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68
Q

What are the common trigger organisms for reactive arthritis?

A

salmonella, shigella, yersinia, chlamydia thachomatis

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69
Q

What are the clinical features of reactive arthritis?

A

acute, asymmetrical lower limbs arthritis
more common in men
days-weeks post infection
also - enthesitis (plantar fasciitis), sacroiliitis, spondylitis anterior uveitis, conjungtivism keratoderma blenorrhagia

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70
Q

What is the management of reactive arthritis?

A

little evidence of treating the triggering infection alters the course of the disease
pain control - NSAIDs, intra-articular steroids

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71
Q

Describe enteropathic arthritis

A

form of reactive synovitis seen in association with UC and crohns disease
an asymmetrical lower limb arthritis
treatment of bowel disease and NSAIDs

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72
Q

Describe osteoarthritis

A 
degenerative joint disease
commonest form of arthritis 
middle aged / elderly 
weight bearing joints - hip, knee
pathology - disorder of articular cartilage
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73
Q

What can cause secondary osteoarthritis?

A 
fracture
previous sepsis
RA
osteonecrosis
gout
haemochromatosis
ochronosis
peripheral neuropathy
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74
Q

What can be seen on xray of an osteoarthritic joint?

A

narrowed joint space loss of cartilage

bony spurs

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75
Q

Describe the pathophysiology of OA

A

loss of articular cartilage, exposure of underlying bone subchondral cysts and sclerosis, osteophytes
synovium becomes hyper plastic, mild inflammation, bony detritus

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76
Q

What is the most common primary bone tumour?

A

myeloma

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77
Q

Which cancers most commonly metastasise to bone?

A

bronchus, breast, prostate, kidney, thyroid (follicular)

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78
Q

Which childhood cancers often metastasise to bone?

A

neuroblastoma

rhabdomyosarcoma

79
Q

What are the effects of metastases to bone?

A 
often asymptomatic 
bone pain
bone destruction
long bones - pathological fractures
spinal metastases- vertebral collapse, spinal cord compression, nerve root compression, back pain
hypercalcaemia
80
Q

What is the most common type of bone metastasis?

A

lytic

81
Q

How is the bone destroyed in lytic tumours?

A

osteoclasts, not tumour cells
stimulated by cytokines from tumour cells
inhibit by biphosphonates

82
Q

How are sclerotic bone metastases formed?

A

reactive - osteoblasts induced by tumour cells

83
Q

Which cancers sometimes lead to solitary bone metastases?

A

renal and thyroid
often long survival
surgical removal often valuable

84
Q

Describe myeloma

A

commonest malignant primary bone tumour
monoclonal proliferation of plasma cells
solitary (plasmacytoma) or multiple myeloma
orthopaedic and medical consequences

85
Q

Describe the clinical effects of myeloma

A

bone lesions - punched out lytic foci, generalised osteopenia
marrow replacement - anaemia, infections
immunoglobulin excess - ESr > 100
serum electrophoresis - monoclonal band
urine - immunoglobulin chains (bence jones protein)

86
Q

Name 3 benign primary bone tumours

A

osteoid osteoma
chondroma
giant cell tumour

87
Q

name 3 malignant primary bone tumours

A

osteosarcoma
chondrosarcoma
ewing’s tumour

88
Q

Describe osteoid osteoma

A

a small, benign osteoblastic proliferation
common any age, especially male adoslescents
any bone - especially long bones and spine
pain worse at night, relieved by aspirin, scoliosis
junta-articular tumours - sympathetic synovitis

89
Q

Describe osteosrcoma

A 
a malignant tumours whose cells form osteoid or bone
peak 10-25
metaphysics of long bones 
mainly around knee
male predominance 
early lung metastases
90
Q

Describe paget’s disease

A 
common in elderly
anglo-saxon origin
excessive bone turnover
increased osteoclasts, increased bone formation, structurally weak bone
disorganised architecture
vertebrae, pelvis, skull, femur
91
Q

What are the results of paget’s disease?

A 
bone pain
deformity
pathological fracture
osteoarthritis
deafness
spinal cord compression
high cardiac output- HF
paget's sarcoma
92
Q

Describe paget’s sarcoma

A 
second osteosarcoma peak in elderly
usually lytic
long bones >spine
very poor prognosis
early metastases to lung and bone
93
Q

Describe enchondroma

A

lobulated mass of cartilage within medulla
common
any age
>50% hands and feet, long bones
often asymptomatic in long bones
hands - swelling
low cellularity, often surrounded by plates of lamellar bone

94
Q

Describe osteocartilaginous exostosis

A

bengin outgrowth of cartilage with endochondral ossification
probably derived from growth plate
very common- usually in adolescent
metaphysis of long bones - not craniofacial

95
Q

What is the genetic condition associated with oesteocartilaginous exostosis?

A

multiple diaphyseal aclasis

autosomal dominant

96
Q

Describe chondrosarcoma

A

primary or from pre-exisitng enchondroma or exostosis
central, within medullary cavity or peripheral on bone surface
predominantly middle aged and elderly
more males
axial skeleton, pelvis, ribs , shoulder girdle, proximal femur, humerus.
rare in hands or feet

97
Q

Describe Ewing’s sarcoma

A 
peak 5-15 years
long bones
flat bones of limb girdles 
early metastases to lung, marrow and bone
(22:11) balanced translocation
98
Q

Name 2 types of autoimmune myositis

A

polymyositis

dermatomyositis

99
Q

Describe polymyositis

A

chronic inflammation of striated muscle

100
Q

Describe dermatomyositis

A

chronic inflammation of striated muscle with a rash
elderly - associated with malignancy
children - not malignant

101
Q

What are the diagnostic features of polymyositis and dermatomyositis?

A 
painful proximal myopathy with weakness
evidence of inflammation in muscle - biopsy, MRI
elevation of muscle enzymes 
characteristic EMG patten
characteristic JDM rash
102
Q

Describe the rash in dermatomyositis

A 
heliotrope rash - purple hue on eyelids
butterfly distribution
vasodilated capillaries
gottron's papuls
nailfold features
103
Q

what are the investigations in JDMS?

A

muscle enzymes - CK, ALT, LDH
MRI
muscle biopsy
clinical monitoring - FVC, power testin

104
Q

Describe the systemic involvement in lupus

A 
dermatitis
renal
liver
spleen
lymph nodes
CNS
systemic vasculitis
serositis - pleurisy, pericarditis, peritonitis
arthritis 
failure to thrive
105
Q

What is included the the diagnosis criteria for SLE?

A 
malar rash
discoid rash
photosenstiivty
oral ulcers
arthrits 
serositis
renal disorder
neurological disorder
haematolgical disorder
immunological dirorder
ANA
106
Q

Describe ANA testing for lupus

A

sensitive but not specific
many causes of positive ANA including; other AI conditions, drug induced, hepatic disease, pulmonary disease, malignant etc

107
Q

Descrbir anti-dsDNA

A

specific but not sensitive

108
Q

Describe the investigation of SLE

A 
FBC
renal Ix
acute phase response 
ANA
dsDNA
Ro/La
low complement
excess total immunoglobulins
109
Q

What organs can systemic scleroderma affect?

A

lung
renal
GIT
joints

110
Q

How can inflammation be controlled in connective tissue disease?

A

steroids
DMARDS
biologics

111
Q

In what ways are steroids excellent immunosuppressants?

A

rapid onset
easy to administer
able to treat wide variety of inflammatory conditions

112
Q

Why are steroid sparing agents used?

A 
steroids cause - 
weight gain and fluid retention
glaucoma
osteoporosis
infection
hypertension
hypokalaemia
peptic ulceration and GI bleed 
psychological and psychiatric symptoms
113
Q

Which immunosuppressants are inhibits of DNA synthesis?

A

methotrexate
azithioprine
mycophenolate

114
Q

which immunosuppressant drugs are lymphocyte signalling inhibitors?

A

cyclosporin
tacrolimus
sirolimus
leflunomide

115
Q

What are the adverse effects of methotrexate?

A

GI -nausea, vomiting, diarrhoea, hepatitis, stomatitis
haematological - leukopenia
others - frequent infections, pulmonary fibrosis

116
Q

Describe methotrexate in practise

A

mostly used for RA and psoriatic arthritis
steroid sparing agent in giant cell arteritis
given once a week with folic acid 4 days later
normally orally
takes weeks to work
blood monitoring

117
Q

How does azathioprine work?

A

converted within cells into a nucleoside analog
incorporated into DNA and RNA chains leading to termination of nucleic acid strands
cell growth and metabolism halts
preferential action of lymphocytes as other cells have purine salvage pathway

118
Q

Which enzyme must be checked before starting azathioprine?

A

TPMT

119
Q

Describe azathioprine in practise

A 
mostly used for IBD
and Myasthenia gravis, eczema
orally on a daily basis 
takes several weeks to work
monthly bloods
120
Q

How does cyclosporin work?

A

small molecule inhibitor of calcineurin
effect of inhibiting signal transduction from the activated TCR complex
profound inhibition of T cell activation

121
Q

What are the adverse effects of cyclosporin?

A 
nephrotoxicity
hypertension
hepatotoxicity
anorexia and lethargy
hirsutism
paraesthesia 
does not suppress bone marrow
122
Q

Describe tacrolimus

A

different class of drug but similar mechanism of action as cyclosporin
more potent activity
very similar use to cyclosporin but may be better tolerated

123
Q

What is cyclosporin used for?

A 
organ transplantation or some inflammatory conditions 
orally daily
therapeutic drug monitoring 
P450 enzymes 
blood tests regularly
124
Q

What are the disadvantages of immunosuppressants?

A 
often insufficient to control inflammatory disease with subsequent progression
slow onset
significant toxicities 
bone marrow suppresison
frequent infections
125
Q

Describe biologic therapies

A

able to target specifically designated components of the immune systems
able to do so with minimal off target effects
usually parenteral route
relatively favourable side effect profile

126
Q

What are the side effects of biologic therapy?

A

hypersensitivity reactions
infusion reactions
mild GI toxicity

127
Q

What infection is more likely with anti-TNF therapy?

A

TB
particularly disseminated TB
also salmonella and listeria

128
Q

What infection is more likely with rituximab?

A

generalised risk of serious infection

high risk of hep B reactivation

129
Q

What infections are more likely with abatacept?

A

pneumonia and respiratory tract infections

130
Q

What infections are more likely with anti IL-1 therapy?

A

RTIs and pneumonia

131
Q

Describe the burdens of back pain

A 
financial - work, expenses
insomnia
emotional stress
relationship breakdowns
severe emotional distress for partners
limitations in fulfilling family tasks
132
Q

What are the 3 broad categories of back pain?

A

mechanical - non specific low back pain
systemic
referred

133
Q

Describe mechanical back pain

A

onset at any age, variable rate
generally worsens with movement or prolonged standing
better at rests
early morning stiffness <30 minutes

134
Q

What are the causes of mechanical back pain?

A

lumbar strain/sprain
degenerative discs / facet joints
disc prolapsed, spinal stenosis
compression fractures

135
Q

Describe degenerative disc disease

A

spondylosis
many asymptomatic
increase with flexion, sitting, sneezing

136
Q

Describe degenerative facet joint disease

A

more localised

increased with extension

137
Q

Describe the management of non-specific LBP

A 
keep diagnosis under review
reassurance - careful with terminology
education, promote self management
advise to stay active
exercise programme and physiotherapy
analgesics as appropriate (avoid opiates)
also acupuncture 
avoid infections, traction, lumbar supports
138
Q

Describe raduculopathy

A 
disc prolapse
herniated nucleus pulposis
may be acute, increase cough
more leg pain than back - sciatica
straight leg testing positive
reduced reflexes
most resolve within 12 weeks
wait with investigations - MRI
<10% need surgery (helps leg, not back pain)
139
Q

Describe spinal stenosis

A 
anatomical narrowing of spinal canal
congenital and / or degenerative
often presents with "claudication" in legs/calves
worse walking, rest in flexed position
natural history variable
investigations xray, MRI 
surgery generally high risj
140
Q

Describe cauda equina syndrome

A 
spinal cord ends at L1/2
neuropathic symptoms - bilateral sciatica, saddle anaestehsia
bladder or bowel dysfunction
reduced anal tone
usually large prolapsed disc
urgent neurosurgical review
141
Q

What is spondylolisthesis?

A 
"slip" of one vertebra on the one below 
mainly asymptomatic
pain may radiate to posterior thigh
increase with extension
rarely needs surgery (if severe)
142
Q

Describe compression fractures

A

elderly patient
sudden onset, severe
radiates in “belt” around chest / abdomen
most pain settles in 3 months
associated osteoporosis - risk of recurrence is high
investigations xray, DEXA scan
treatment - conservative, calcitonin, vertebroplasty or kyphoplasty

143
Q

What can cause referred pain in the back?

A

aortic aneurysm
acute pancreatitis
peptic ulcer disease
acute pyelonephritis / renal colic

144
Q

What are the causes of systemic back pain?

A

infection - discitis, osteomyelitis , epidural abscess
malignancy
inflammatory

145
Q

Describe infective discitis

A

fever, weight loss
constant back pain - rest, night pain
immunosuppressed, diabetes, IV drug use

146
Q

What is the diagnosis / treatment of discitis?

A 
bloods - FBC, ESR, CRP, blood cultures
imaging - Xray, MRI
radiology guided aspiration
most common staph aureas
IV antibiotics &amp; surgical debridement
look for source
147
Q

Describe malignancy as a cause of back pain

A 
history of malignancy 
LP thomas knows best 
lung, prostate, thyroid, kidney, breast
onset >50
constant pain, often worse at night
systemic symptoms, primary tumour signs &amp; symptoms 
Xray, MRI, bone scan
look for primary
148
Q

Describe inflammatory back pain

A 
onset <45 years, often teens
early morning stiffness >30 minutes
back stiff after rest and improves with movement
may wake 2nd half of night
family history
149
Q

Describe the overall approach to back pain

A

history - red flags
examination - back, neuro, abdomen
most = non specific LBP = no further investigation
keep diagnosis under review - investigate if unusual
imaging - xray, MRI
bloods - if suspect infective / inflammatory / myeloma screen

150
Q

What are the red flag symptoms of back pain?

A 
new onset <16 or >50
following significant trauma
previous malignancy
systemic - fevers, malaise, weight loss
previous steroid use
IV drug abuse, HIV or immunocompromised 
recent significant infection
urinary retention
non-mechanical pain (worse at rest "night pain"
thoracic spine pain
151
Q

What are the red flag signs in back pain?

A 
saddle anaesthesia
reduced anal tone
hip or knee weakness
generalised neurological deficit
progressive spinal deformity
152
Q

What are the yellow flags in back pain?

A 
attitudes
beliefs
compensation
diagnosis
emotions
family
work relationship
153
Q

What are the symptoms of axial spondyloarthritis?

A 
inflammatory back pain
fatigue
arthritis in other joints
inflammation outside joints - uveitis, psoriasis, IBD, other- heart, lungs, osteoporosis
family history of above
154
Q

What gene is thought to be involved in axSpA and AS?

A

HLA-B27

155
Q

What is physical activity?

A

any bodily movement produced by skeletal muscles that requires energy expenditure
includes broad range of activities - everyday activities,
household chores
occupational tasks
leisure time physical activity
exercise

156
Q

What is FITT?

A 
energy expended
frequency
intensity 
time
type
157
Q

What is exercise?

A

physical exercise that is planned, structures, repetitive and purposeful (aimed at improving or maintaining on or more component of physical fitness)

158
Q

What is meant by physical fitness?

A

a set of attributes that people have or achieve that relates to the ability to perform physical activity

159
Q

What types of physical fitness are there?

A

cardiorespiratory endurance
muscular strength
balance and coordination
flexibility

160
Q

Describe traumatic sports injuries

A

fractures and dislocations
major muscle - ligament-tendon injuries
head and spinal injuries
chest and abdominal injuries

161
Q

What are the types of fractures?

A

transverse, oblique, spiral, comminuted, avulsion - a piece of bone attached to tendon or ligament is torn away

162
Q

What are the clinical features of a fracture?

A

pain, tenderness, localised bruising, swelling, deformity, restriction of movement

163
Q

Describe injuries to articular cartilage

A

associated with soft tissue injuries (ACL rupture)
initial xray often normal - suspect if sprain remains painful and swollen longer than expected
diagnose on MRI
arthroscopy to confirm and remove loose fragments
may predispose to premature osteoarthritis
do not usually heal fully - variety of treatment to improve healing - perforation, alteration of joint loading, cell transplantation

164
Q

What is dislocation?

A

trauma produces complete dissociation of the articulating surfaces

165
Q

What is subluxation?

A

some contact of articulating surfaces remains

166
Q

What are the complications of joint dislocations / subluxations?

A

associated nerve or blood vessel damage

xray to exclude fracture

167
Q

What is the treatment of joint dislocations / subluxations?

A 
reduction
muscle relaxants may be required 
protect to allow soft tissue to heal
early protected mobilisation
rebuild muscle strength
168
Q

Describe strain / tear of muscle

A

occur when demands exceed muscle capacity
common if cross 2 joints - hamstrings, quadriceps and gastrocnemius
common during sudden acceleration or deceleration

169
Q

What is the management of strains / tears of muscle?

A 
first aid to minimise bleeding, swelling and inflammation 
electrotherapy 
soft tissue therapy 
stretching
strengthening
170
Q

What are the predisposing factors to muscle tears?

A 
inadequate warm up
insufficient joint range of motion 
excessive muscle tightness
fatigue/ overuse / inadequate recovery 
muscle imbalance 
previous injury
poor technique
altered biomechanics
171
Q

What is the treatment of achilles tenonopathy

A

active rest
alter training schedule - no hills / decrease pace
heal wedge
NSAID
immobilisation
surgery for chronic tendonitis or rupture
no steroid injections

172
Q

Give an overview of RA

A 
chronic multisystem disease
autoimmune
hallmark is synovitis 
affecting any synovial joint
small joint predominance but distal sparing
multiple extra-articular manifestations
173
Q

Describe the aetiology of RA

A 
HLA-DR4 and other genetic factors
shared epitope 
smoking 
infection (EBV, TB, porphyromonas gigivalis)
hormonal
174
Q

Describe the pathophysiology of RA

A

synovitis - immune cells invading a normally relatively acellular synovial in the form of a pannus

175
Q

What is a pannus?

A

hyperplastic, invasie tissue leading to cartilage breakdown, erosions and consequent reduced function

176
Q

What are the clinical features of RA?

A

synovitis
symmetrical
small joints in hands and feet early on : shoulder/hip at onset rare
inflammatory -pain, eryhtema, swelling, EMS
tenosynovitis, bursitis, CTS
constitutional - fatigue, weakness, low grade fever, weight loss, anorexia

177
Q

What are the classical joint features in late RA?

A 
boutonniere
swan neck
Z-thumb
volar subluxation of wrist
ulnar deviation digits
radial deviation wrist
piano key ulnar head
178
Q

What systemic effects can RA have?

A 
respiratory 
cardiac
dermatological
opthalmic 
neurological
haematological
179
Q

What investigations should be done for RA?

A 
FBC
U&amp;Es 
LFTs
ESR / CRP
RF
ACPA
(ANA)
180
Q

Describe rheumatoid factor

A 
autoantibody again Fc portion of IgG
usually IgM against IgG
60% sensitive, 80% specific 
other conditions - SLE, SBE, SScl, SjS, TB, EBV, healthy controls etc
part of assessment, not diagnostic
181
Q

Describe anti CCP

A

sensitive 60%, specific 80-90%
picks up those who may be RF negative
predictor of worse prognosis, more erosions, resistant disease
linked with smoking (increases citrullination)

182
Q

Describe imagine in RA

A

Xrays - soft tissue swelling, joint space narrowing, erosions, periarticular OP
USS: more sensitive for synovitis and erosions
MRI -bone marrow oedema

183
Q

What are the differentials for RA?

A 
OA
SLE
PMR
psoriatic arthropathy
sponyloarthropathies
reactive arthritis
sarcoid
CPPD (calcium pyrophosphate)
Lyme's
184
Q

What are the non-pharmacological treatments of RA?

A

OT/PT - mobility Ax and preservations, work assessment, walking aids
podiatrists - foot clinics, foot wear assessments etc

185
Q

What are the pharmacological treatments of RA?

A

symptomatic
NSAIDS, analgesics etc
DMARDS - glucocorticoids, methotrexate, sulfasalazine
biologics - anti TNF (etanercept, infliximab) , anti CD20, anti IL16 etc

186
Q

Describe juvenile idiopathic arthritis

A

chronic inflammatory arthropathy
commonest rheumatic disease in childhood
clinical diagnosis with no diagnostic tests
group of diseases
overlap with adult inflammatory arthropathies
important differences in children

187
Q

What name is given to RA in children?

A

rheumatoid factor positive polyarthritis

188
Q

What name is given to ankylosing spondylitis I’m children?

A

enthesitis related arthritis

189
Q

What is an enthesis?

A 
insertion of - tendon
ligament
joint capsule
fascia
- to bone
190
Q

What is associated with reactive arthritis?

A

conjungtivitis
urethritis
plantar fasciitis
arthritis

191
Q

Describe seronegative arthritis

A

asymmetrical
large lower limb weight bearing joint
(AS/ERA/Reactive / OBD
large and small joint (psoriatic)

192
Q

Describe seropositive arthritis

A

symmetrical
large and small joints
wrists and MCPS
often widespread

193
Q

What tests should be carried out in JIA?

A

FBC and differential
acute phase response
MRI
think why before - X-rays, synovial biopsies, ANA, rheumatoid factor

194
Q

What does tiny TIM for?

A

Trauma
inflammation - infecition, autoimmmune JIA
Malignancy -leukaemia, bone tumours

Phase 3 (15 decks)

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