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Week 11 Flashcards

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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
What are the general features for all primaries vasculitis?
systemic inflammation -fever, malaise, weight loss, myalgia, arthralgia, night weats
26
What does large vessel vasculitis cause?
end organ ischaemia or infarction
27
What does medium vessel vasculitis cause?
localised ischaemia or infarction
28
What does small vessel vasculitis cause?
organ specific inflammation
29
What are the 2 main types of large vessel vasculitis?
``` giant cell (common) takayasu (rare) ```
30
What are 2 types of medium vessel vasculitis?
``` polyarteritits nodosa (PAN) Kawasaki disease (children only) ```
31
What are the 2 types of small vessel vasculitis?
immune complex mediated vasculitis | ANCA associated vasculits
32
What types of immune complex mediated vasculitis are there?
HSP | cryoglobulinaemia
33
What are the ANCA associated vasculitis?
microscopic polyangitis granulomatosis with polyangitis (Wegener's) eosinophilic granulomatosis with polyangitis (churn-strauss disease)
34
Describe giant cell arteritis
elderly common women
35
What re the clinical features of giant cell arteritis?
``` fatigue headaches jaw claudication scalp tenderness test - very high ESR definitive test - biopsy ```
36
What is the sudden blindness associated with giant cell arteritis called?
amaurosis fugax
37
Describe polymyalgia rheumatica
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
38
Describe takayasu's arteritis
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
39
Describe polyarteritis nodosa
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
40
Describe kawasaki disease
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
41
Describe HSP
``` 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 ```
42
What does ANCA stand for?
anti-neutrophil cytoplasmic Ab
43
What are the 2 types of ANCA?
cytoplasmic c-ANCA | perinuclear p-ANCA
44
When is cANCA positive?
very specific for granulomatous polyangitis (Wegener's )
45
when is pANCA and MPO positive?
microscopic polyangitis crescentic glomerulonephritis eosinophilic granulomatous polyangitis
46
When is pANCA positive and MPO negative?
IBD RA sclerosing cholangitis
47
Describe granulomatous polyangitis
Wegener's | classically involves URT, LRT and kidneys
48
Describe eosinophilic angitis
``` churg strauss asthma eosinophilic infiltrates eosninophilia eosinophil rich granulomata peripheral neuropathy ```
49
Describe microscopic polyangitis
``` 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% ```
50
What is the treatment of primary vasculitis?
corticosteroids | other immune suppression
51
What is the commonest cause of vasculitis in children?
henoch scholein purpura
52
What are 3 ANCA associated vasculitis?
microscopic polyangitis granulomatosis with polyangitis eosinophilic grnulomatosis with polyangitis
53
Describe septic arthritis
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
54
How can bacteria infect a joint space?
hematogenous dissemination from osteomyelitis spread from adjacent soft tissue infection medical procedures penetrating damage by puncture or traumaa
55
What investigations should be carried out for septic arthritis?
joint aspirate - microbiology from gram stain and culture blood culture FBC -leukocytosis xray - no value
56
What affect can septic arthritis have in the joint if it is not treated?
synovial inflamed with fibrin exudation and numerous neutrophil polymorphs loss of articular cartilage may lead to secondary osteoarthritis
57
What are other types of septic arthritis?
lyme disease - borrelia burgdoferi brucellosis syphilitic arthritis - congenital and acquired
58
What types of crystal arthropathy are there?
gout and pseudogout
59
Describe gout
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
60
how is gout diagnosed?
aspirate - negatively befringement needle shaped crystals on polarised microscopy serum urate levels and U&Es
61
What can cause primary gout?
hyperurciaemia due to genetic predisposition -- Lesch Nyhan syndrome
62
What can cause secondary gout?
myeloproliferative disorder leukaemia treated with chemo thiazides chronic renal disease
63
What tend to raise uric acid levels?
``` increasing age obesity high alcohol intake high protein diet diabetes mellitis ```
64
What is the management of gout?
NSAIDs alternatives - colchicine, corticosteroids if repeated - allopurinol - xanthine oxidase inhibitor uricosuric agent (probenecid) increased secretion of uric acid in the urine
65
Describe pseudogout
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
66
What is the management of pseudo gout?
aspiration helps to reduce pain and swelling NSAIDs colchicine
67
Describe reactive arthritis
sterile synovitis which occurs following an infection
68
What are the common trigger organisms for reactive arthritis?
salmonella, shigella, yersinia, chlamydia thachomatis
69
What are the clinical features of reactive arthritis?
acute, asymmetrical lower limbs arthritis more common in men days-weeks post infection also - enthesitis (plantar fasciitis), sacroiliitis, spondylitis anterior uveitis, conjungtivism keratoderma blenorrhagia
70
What is the management of reactive arthritis?
little evidence of treating the triggering infection alters the course of the disease pain control - NSAIDs, intra-articular steroids
71
Describe enteropathic arthritis
form of reactive synovitis seen in association with UC and crohns disease an asymmetrical lower limb arthritis treatment of bowel disease and NSAIDs
72
Describe osteoarthritis
``` degenerative joint disease commonest form of arthritis middle aged / elderly weight bearing joints - hip, knee pathology - disorder of articular cartilage ```
73
What can cause secondary osteoarthritis?
``` fracture previous sepsis RA osteonecrosis gout haemochromatosis ochronosis peripheral neuropathy ```
74
What can be seen on xray of an osteoarthritic joint?
narrowed joint space loss of cartilage | bony spurs
75
Describe the pathophysiology of OA
loss of articular cartilage, exposure of underlying bone subchondral cysts and sclerosis, osteophytes synovium becomes hyper plastic, mild inflammation, bony detritus
76
What is the most common primary bone tumour?
myeloma
77
Which cancers most commonly metastasise to bone?
bronchus, breast, prostate, kidney, thyroid (follicular)
78
Which childhood cancers often metastasise to bone?
neuroblastoma | rhabdomyosarcoma
79
What are the effects of metastases to bone?
``` often asymptomatic bone pain bone destruction long bones - pathological fractures spinal metastases- vertebral collapse, spinal cord compression, nerve root compression, back pain hypercalcaemia ```
80
What is the most common type of bone metastasis?
lytic
81
How is the bone destroyed in lytic tumours?
osteoclasts, not tumour cells stimulated by cytokines from tumour cells inhibit by biphosphonates
82
How are sclerotic bone metastases formed?
reactive - osteoblasts induced by tumour cells
83
Which cancers sometimes lead to solitary bone metastases?
renal and thyroid often long survival surgical removal often valuable
84
Describe myeloma
commonest malignant primary bone tumour monoclonal proliferation of plasma cells solitary (plasmacytoma) or multiple myeloma orthopaedic and medical consequences
85
Describe the clinical effects of myeloma
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
Name 3 benign primary bone tumours
osteoid osteoma chondroma giant cell tumour
87
name 3 malignant primary bone tumours
osteosarcoma chondrosarcoma ewing's tumour
88
Describe osteoid osteoma
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
Describe osteosrcoma
``` 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
Describe paget's disease
``` common in elderly anglo-saxon origin excessive bone turnover increased osteoclasts, increased bone formation, structurally weak bone disorganised architecture vertebrae, pelvis, skull, femur ```
91
What are the results of paget's disease?
``` bone pain deformity pathological fracture osteoarthritis deafness spinal cord compression high cardiac output- HF paget's sarcoma ```
92
Describe paget's sarcoma
``` second osteosarcoma peak in elderly usually lytic long bones >spine very poor prognosis early metastases to lung and bone ```
93
Describe enchondroma
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
Describe osteocartilaginous exostosis
bengin outgrowth of cartilage with endochondral ossification probably derived from growth plate very common- usually in adolescent metaphysis of long bones - not craniofacial
95
What is the genetic condition associated with oesteocartilaginous exostosis?
multiple diaphyseal aclasis | autosomal dominant
96
Describe chondrosarcoma
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
Describe Ewing's sarcoma
``` peak 5-15 years long bones flat bones of limb girdles early metastases to lung, marrow and bone (22:11) balanced translocation ```
98
Name 2 types of autoimmune myositis
polymyositis | dermatomyositis
99
Describe polymyositis
chronic inflammation of striated muscle
100
Describe dermatomyositis
chronic inflammation of striated muscle with a rash elderly - associated with malignancy children - not malignant
101
What are the diagnostic features of polymyositis and dermatomyositis?
``` painful proximal myopathy with weakness evidence of inflammation in muscle - biopsy, MRI elevation of muscle enzymes characteristic EMG patten characteristic JDM rash ```
102
Describe the rash in dermatomyositis
``` heliotrope rash - purple hue on eyelids butterfly distribution vasodilated capillaries gottron's papuls nailfold features ```
103
what are the investigations in JDMS?
muscle enzymes - CK, ALT, LDH MRI muscle biopsy clinical monitoring - FVC, power testin
104
Describe the systemic involvement in lupus
``` dermatitis renal liver spleen lymph nodes CNS systemic vasculitis serositis - pleurisy, pericarditis, peritonitis arthritis failure to thrive ```
105
What is included the the diagnosis criteria for SLE?
``` malar rash discoid rash photosenstiivty oral ulcers arthrits serositis renal disorder neurological disorder haematolgical disorder immunological dirorder ANA ```
106
Describe ANA testing for lupus
sensitive but not specific many causes of positive ANA including; other AI conditions, drug induced, hepatic disease, pulmonary disease, malignant etc
107
Descrbir anti-dsDNA
specific but not sensitive
108
Describe the investigation of SLE
``` FBC renal Ix acute phase response ANA dsDNA Ro/La low complement excess total immunoglobulins ```
109
What organs can systemic scleroderma affect?
lung renal GIT joints
110
How can inflammation be controlled in connective tissue disease?
steroids DMARDS biologics
111
In what ways are steroids excellent immunosuppressants?
rapid onset easy to administer able to treat wide variety of inflammatory conditions
112
Why are steroid sparing agents used?
``` steroids cause - weight gain and fluid retention glaucoma osteoporosis infection hypertension hypokalaemia peptic ulceration and GI bleed psychological and psychiatric symptoms ```
113
Which immunosuppressants are inhibits of DNA synthesis?
methotrexate azithioprine mycophenolate
114
which immunosuppressant drugs are lymphocyte signalling inhibitors?
cyclosporin tacrolimus sirolimus leflunomide
115
What are the adverse effects of methotrexate?
GI -nausea, vomiting, diarrhoea, hepatitis, stomatitis haematological - leukopenia others - frequent infections, pulmonary fibrosis
116
Describe methotrexate in practise
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
How does azathioprine work?
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
Which enzyme must be checked before starting azathioprine?
TPMT
119
Describe azathioprine in practise
``` mostly used for IBD and Myasthenia gravis, eczema orally on a daily basis takes several weeks to work monthly bloods ```
120
How does cyclosporin work?
small molecule inhibitor of calcineurin effect of inhibiting signal transduction from the activated TCR complex profound inhibition of T cell activation
121
What are the adverse effects of cyclosporin?
``` nephrotoxicity hypertension hepatotoxicity anorexia and lethargy hirsutism paraesthesia does not suppress bone marrow ```
122
Describe tacrolimus
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
What is cyclosporin used for?
``` organ transplantation or some inflammatory conditions orally daily therapeutic drug monitoring P450 enzymes blood tests regularly ```
124
What are the disadvantages of immunosuppressants?
``` often insufficient to control inflammatory disease with subsequent progression slow onset significant toxicities bone marrow suppresison frequent infections ```
125
Describe biologic therapies
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
What are the side effects of biologic therapy?
hypersensitivity reactions infusion reactions mild GI toxicity
127
What infection is more likely with anti-TNF therapy?
TB particularly disseminated TB also salmonella and listeria
128
What infection is more likely with rituximab?
generalised risk of serious infection | high risk of hep B reactivation
129
What infections are more likely with abatacept?
pneumonia and respiratory tract infections
130
What infections are more likely with anti IL-1 therapy?
RTIs and pneumonia
131
Describe the burdens of back pain
``` financial - work, expenses insomnia emotional stress relationship breakdowns severe emotional distress for partners limitations in fulfilling family tasks ```
132
What are the 3 broad categories of back pain?
mechanical - non specific low back pain systemic referred
133
Describe mechanical back pain
onset at any age, variable rate generally worsens with movement or prolonged standing better at rests early morning stiffness <30 minutes
134
What are the causes of mechanical back pain?
lumbar strain/sprain degenerative discs / facet joints disc prolapsed, spinal stenosis compression fractures
135
Describe degenerative disc disease
spondylosis many asymptomatic increase with flexion, sitting, sneezing
136
Describe degenerative facet joint disease
more localised | increased with extension
137
Describe the management of non-specific LBP
``` 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
Describe raduculopathy
``` 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
Describe spinal stenosis
``` 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
Describe cauda equina syndrome
``` 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
What is spondylolisthesis?
``` "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
Describe compression fractures
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
What can cause referred pain in the back?
aortic aneurysm acute pancreatitis peptic ulcer disease acute pyelonephritis / renal colic
144
What are the causes of systemic back pain?
infection - discitis, osteomyelitis , epidural abscess malignancy inflammatory
145
Describe infective discitis
fever, weight loss constant back pain - rest, night pain immunosuppressed, diabetes, IV drug use
146
What is the diagnosis / treatment of discitis?
``` bloods - FBC, ESR, CRP, blood cultures imaging - Xray, MRI radiology guided aspiration most common staph aureas IV antibiotics & surgical debridement look for source ```
147
Describe malignancy as a cause of back pain
``` 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 & symptoms Xray, MRI, bone scan look for primary ```
148
Describe inflammatory back pain
``` 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
Describe the overall approach to back pain
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
What are the red flag symptoms of back pain?
``` 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
What are the red flag signs in back pain?
``` saddle anaesthesia reduced anal tone hip or knee weakness generalised neurological deficit progressive spinal deformity ```
152
What are the yellow flags in back pain?
``` attitudes beliefs compensation diagnosis emotions family work relationship ```
153
What are the symptoms of axial spondyloarthritis?
``` inflammatory back pain fatigue arthritis in other joints inflammation outside joints - uveitis, psoriasis, IBD, other- heart, lungs, osteoporosis family history of above ```
154
What gene is thought to be involved in axSpA and AS?
HLA-B27
155
What is physical activity?
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
What is FITT?
``` energy expended frequency intensity time type ```
157
What is exercise?
physical exercise that is planned, structures, repetitive and purposeful (aimed at improving or maintaining on or more component of physical fitness)
158
What is meant by physical fitness?
a set of attributes that people have or achieve that relates to the ability to perform physical activity
159
What types of physical fitness are there?
cardiorespiratory endurance muscular strength balance and coordination flexibility
160
Describe traumatic sports injuries
fractures and dislocations major muscle - ligament-tendon injuries head and spinal injuries chest and abdominal injuries
161
What are the types of fractures?
transverse, oblique, spiral, comminuted, avulsion - a piece of bone attached to tendon or ligament is torn away
162
What are the clinical features of a fracture?
pain, tenderness, localised bruising, swelling, deformity, restriction of movement
163
Describe injuries to articular cartilage
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
What is dislocation?
trauma produces complete dissociation of the articulating surfaces
165
What is subluxation?
some contact of articulating surfaces remains
166
What are the complications of joint dislocations / subluxations?
associated nerve or blood vessel damage | xray to exclude fracture
167
What is the treatment of joint dislocations / subluxations?
``` reduction muscle relaxants may be required protect to allow soft tissue to heal early protected mobilisation rebuild muscle strength ```
168
Describe strain / tear of muscle
occur when demands exceed muscle capacity common if cross 2 joints - hamstrings, quadriceps and gastrocnemius common during sudden acceleration or deceleration
169
What is the management of strains / tears of muscle?
``` first aid to minimise bleeding, swelling and inflammation electrotherapy soft tissue therapy stretching strengthening ```
170
What are the predisposing factors to muscle tears?
``` inadequate warm up insufficient joint range of motion excessive muscle tightness fatigue/ overuse / inadequate recovery muscle imbalance previous injury poor technique altered biomechanics ```
171
What is the treatment of achilles tenonopathy
active rest alter training schedule - no hills / decrease pace heal wedge NSAID immobilisation surgery for chronic tendonitis or rupture no steroid injections
172
Give an overview of RA
``` chronic multisystem disease autoimmune hallmark is synovitis affecting any synovial joint small joint predominance but distal sparing multiple extra-articular manifestations ```
173
Describe the aetiology of RA
``` HLA-DR4 and other genetic factors shared epitope smoking infection (EBV, TB, porphyromonas gigivalis) hormonal ```
174
Describe the pathophysiology of RA
synovitis - immune cells invading a normally relatively acellular synovial in the form of a pannus
175
What is a pannus?
hyperplastic, invasie tissue leading to cartilage breakdown, erosions and consequent reduced function
176
What are the clinical features of RA?
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
What are the classical joint features in late RA?
``` boutonniere swan neck Z-thumb volar subluxation of wrist ulnar deviation digits radial deviation wrist piano key ulnar head ```
178
What systemic effects can RA have?
``` respiratory cardiac dermatological opthalmic neurological haematological ```
179
What investigations should be done for RA?
``` FBC U&Es LFTs ESR / CRP RF ACPA (ANA) ```
180
Describe rheumatoid factor
``` 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
Describe anti CCP
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
Describe imagine in RA
Xrays - soft tissue swelling, joint space narrowing, erosions, periarticular OP USS: more sensitive for synovitis and erosions MRI -bone marrow oedema
183
What are the differentials for RA?
``` OA SLE PMR psoriatic arthropathy sponyloarthropathies reactive arthritis sarcoid CPPD (calcium pyrophosphate) Lyme's ```
184
What are the non-pharmacological treatments of RA?
OT/PT - mobility Ax and preservations, work assessment, walking aids podiatrists - foot clinics, foot wear assessments etc
185
What are the pharmacological treatments of RA?
symptomatic NSAIDS, analgesics etc DMARDS - glucocorticoids, methotrexate, sulfasalazine biologics - anti TNF (etanercept, infliximab) , anti CD20, anti IL16 etc
186
Describe juvenile idiopathic arthritis
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
What name is given to RA in children?
rheumatoid factor positive polyarthritis
188
What name is given to ankylosing spondylitis I'm children?
enthesitis related arthritis
189
What is an enthesis?
``` insertion of - tendon ligament joint capsule fascia - to bone ```
190
What is associated with reactive arthritis?
conjungtivitis urethritis plantar fasciitis arthritis
191
Describe seronegative arthritis
asymmetrical large lower limb weight bearing joint (AS/ERA/Reactive / OBD large and small joint (psoriatic)
192
Describe seropositive arthritis
symmetrical large and small joints wrists and MCPS often widespread
193
What tests should be carried out in JIA?
FBC and differential acute phase response MRI think why before - X-rays, synovial biopsies, ANA, rheumatoid factor
194
What does tiny TIM for?
Trauma inflammation - infecition, autoimmmune JIA Malignancy -leukaemia, bone tumours

Phase 3 (15 decks)

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