Arthropathies/Muscular/Neuromuscular/ Back Pain/ Spine/ Spinal conditions Flashcards
(181 cards)
1
Q
Neuromyotonia (NMT, Isaac’s syndrome)
A
> Multiple disorders of skeletal muscle function
- cramps
- stiffness
- slow relaxation (myotonia)
- muscle twitches
> Acquired form (commonest) - autoimmune origin
- autoantibodies against voltage activated K+ channels in motor neurone
- disrupts function resulting in hyper excitability (repetitive firing)
TREATMENT
- Anti convulsants (carbamazepine, phenytoin) which block voltage-activated Na+ channels
2
Q
Lambert-Eaton Myasthenic Syndrome (LEMS)
A
> Muscle weakness in limbs
> Rare
> Associated with Small Cell carcinoma of the lung
> Autoimmune. Autoantiboides against voltage activated Ca2+ channels in the motor neurone terminal –> reduced Ca2+ entry in response to depolarisation and hence REDUCED VESICULAR RELEASE OF ACh
3
Q
Myasthenia gravis (MG)
A
> Progressively increasing muscle weakness during periods of activity (fatiguability).
> Often weakness of the eye and eyelid muscles
> Autoantiboides against nicotinic ACh receptors in the endplate result in reduction in number of functional channels and hence reduction in amplitude of e.p.p.
Treatment
Anticholinesterases (edrophonium for diagnosis, pyridoosigmine for long term)
Immunosuppressants - azathioprine
4
Q
Botulinum Toxin
A
> Clostridium botulinum
> Potent exotoxin that acts at motor neurone terminals to irreversibly inhibit ACh release
> Enters presynaptic nerve terminal
> Enzymatically modifies proteins involved in “docking” of vesicles containing ACh
> High mortality
5
Q
Clinical uses of botulinum toxin?
A
> Low dosage botulinum haemaglutin complex can be administered by intramuscular infection to treat OVERACTIVE MUSCLES (dystonia)
- extra ocular muscles (strabismus, squints)
- Smoothing out age related wrinkles
6
Q
Curare-like compounds (alkaloid arrow poisons)
A
> Interfere with the postsynaptic action of acetylcholine by acting as competitive antagonists of the nicotinic ACh receptor (e.g. vecuronium, atracurium)
> reduce amplitude of the endplate potential (e.p.p.) to below threshold for muscle fibre action potential generation
> Used to induce reversible muscle paralysis in certain types of surgery
7
Q
Congenital Insensitivity to Pain
A
Results due to loss of function mutations (missense, in frame, deletions) in gene SC9A that encodes a particular voltage activated Na+ channel (nA 1.7)
Na 1.7 is highly expressed in nociceptive neurones
> Lip and tongue injury > Bruises and cuts > Multiple scars > Bone fractures > Joint deformity > Premature mortality due to multiple injuries/infections.
8
Q
Rheumatoid arthritis - definition
A
(can be )Autoimmune disorder (HLA-DR4 mediated)
SYMMETRICAL inflammation arthritis
Pain, swelling and stiffness.
Joints feel spongy
Affects mainly peripheral joints
Affect both articular and extra-articular structures
Loss of function and increased morbidity.
Can occur at any age.
Women 3x more likely
9
Q
What part of the spine can rheumatoid arthritis sometimes affect?
A
C1 and C2 spine.
10
Q
Which HLA/MHC complex is rheumatoid arthritis mediated by?
A
HLA-DR4
Infections, stress and cigarette smoking are potential triggers
11
Q
Main structure involved in rheumatoid arthritis?
A
Synovium.
Lines inside of synovial joint capsules and tendon sheaths
Becomes hypertrophic and inflamed –> joint damage and swelling, pain
12
Q
What is the hallmark sign of RA?
A
Synovitis
13
Q
Rheumatoid arthritis Pannus
A
Abnormal layer of granulation tissue/fibrovascular tissue.
T cells activated –> inflammatory cascade
14
Q
What do the joints feel like in RA (on palpation)?
A
Spongy
15
Q
Early rheumatoid arthritis
A
Defined as less than 2 years since symptom onset
16
Q
What is the therapeutic window of opportunity in early rheumatoid arthritis?
A
First 3 months.
17
Q
ACR/EULAR Classification of RA
A
Joint Distribution (0-5)
Serology (0-3)
Symptom duration (0-1)
Acute phase reactants (0-1)
18
Q
Diagnosis of RA
A
Hx and clinical exam.
Routine blood testing - anaemia of chronic disease, raised platelets
Inflammatory markers (CRP, ESR, Plasma viscosity)
Autoantibodies - Anti CCP, (anti RF - less so)
Imaging
19
Q
When is stiffness the worst in RA?
A
In the morming
Lasting longer than 30 minutes
20
Q
Normochromic anaema
A
Blood cells are normal but there are just not enough of them.
21
Q
Rheumatoid - clinical features/ presentation
A
Features//
Prolonged morning stiffness - MORE than 30 minutes
Involvement of small joints of hands and feet
Symmetrical distribution
Positive compression tests of metacarpophalangeal (MCP) and metatarsophalangeal joints
SORE to squeeze the joints
Presentation//
PIP, MCP, wrist, MTP synovitis
Monoarthritis
Tenosynovitis
Trigger finger
Carpal tunnel syndrome
Polymyalgia rheumatica
Palindromic rheumatism
Systemic symptoms
Poor group strength
22
Q
Palindromic rheumatism
A
rare episodic form of inflammatory arthritis – meaning the joint pain and swelling come and go. Between attacks, the symptoms disappear and the affected joints go back to normal, with no lasting damage.
Hydroxychloroquine
23
Q
Auto antibodies in RA
A
> Rheumatoid factor (rheumatoid IgM)
> Antibodies to cyclic citrullinated peptide (Anti-CCP antibodies) - highly specific (90-99%)
30% of patients will still have rheumatoid without the antibodies
absence of Anti-CCP does NOT exclude the disease.
24
Q
Anti-CCP antibodies
A
Can be present for several years prior to articular symptoms
Co relates with disease activity
Associated with current or previous smoking history
More likely to be associated with erosive damage.
Absence does not exclude the disease
25
Imaging for Rheumatoid arthritis?
What is the GOLD standard?
> Plain x-rays of hands and feet
- - cheap, reproducible
- - soft tissue swelling
- - periarticular osteopenia
- - erosions
However, absence of findings in early disease
> US scanning
- - synovitis in early disease
- - can detect MCP erosions better than X ray
- - useful in making treatment changes
> MRI scans
- - bone marrow oedema
- - integrity of tendons can be assessed
- - distinguish synovitis from effusions
- - monitor disease activity
-- LIMITED BY COST $$$
MRI scans are the GOLD STANDARD
26
DAS28 score
Disease Activity score
Assessment of disease
28 joints counted
Lower score = better.
less than 2.6 = remission
2. 6-3.2 = low level activity
3. 2 -5.1 = moderate disease
>5.1 = active disease
27
A DAS28 score of less than than 2.6 for rheumatoid arthritis indicates?
Remission
28
Management of RA
Early recognition & diagnosis
Early treatment with Disease modifying anti-rheumatic drugs
Target of remission or low disease activity
Use of NSAIDs & steroids only as adjuncts
Patient education
29
Treatment of RA
```
1. Aspirin/NSAIDs
+ steroids
+ DMARD #1
+ DMARD #2(?)
+ DMARD #3(?)
```
Gradually withdraw treatment after remission is achieved
30
Rheumatoid arthritis - steroids
Improve symptoms and reduce radiological damage
Used in combination with DMARDs - never used on their own
Can be given orally, IA or IM
Intra articular injection if fewer than 5 joints affected?
31
Are steroids ever given on their own in RA?
NO, NEVER.
Only given in combo with DMARDs.
32
DMARDs
Disease Modifying Anti-Rheumatic Drugs
Methotrexate (1st line)
Sulfasalazine
Hydroxychloroquine
Combo therapy with MTX, SASP & HCQ
Leflunomide
Gold injections
Peniciilamne
Azathioprine
Bone marrow suppression
Infection
Liver function derangement
33
Methotrexate
1st line DMARD for Rheumatoid arthritis?
15mg/week with rapid escalation
Max does 25mg/week
Folic acid 24 hours after MTX dose
---
However is teratogenic
Allergic reaction in lungs --> PNEUMONITIS
34
Hydroxychloroquine
Does not prevent erosions
If above 2, it does not work.
35
What lung condition can methotrexate cause?
Pneumonitis
36
What should be taken with methotrexate?
Folic acid
37
DMARDs combination
Combination therapy-SASP 40mg/kg/day plus methotrexate 15mg/week plus hydroxychloroquine 200-400 mg/day plus steroids.
Hydroxychloroquine for palindromic RA.
Regular monitoring of LFTS,FBC.
38
When should sulfasalazine be avoided?
Co trimoxazole allergy
G6PD deficiency
39
Biological agents used in RA
Anti TNF agents- Infliximab,Etanercept,Adalimumab,
Certolizumab,Golimumab
T cell receptor blocker-Abatacept.
B cell depletor-Rituximab
IL-6 blocker-Tocilizumab.
JAK 2 inhibitors-Tofacitinib.
However, risk of severe infection
e.g. reactivation of TB.
----
Only use when patient has failed to respond to 2 DMARDs including methotrexate and DAS28 greater than 5.1 on two occasions 4 weeks apart.
Methotrexate co prescribed.
Screen for latent or active TB, Hep B,c; HIV, Varicella zoster
Avoid live attenuated vaccines
40
Untreated RA - complications
Joint damage and deformities
Boutonniere deformity of thumb
Ulnar deviation of Metacarpophalangeal joints
Swan neck deformity of fingers
Subluxatiion of toes downwards - feels like "walking on pebbles"
Atlanto-axial subluxation
- c2 moves under C1
- erosion of odontoid peg
- spinal cord compression
- perform a FLEXION & EXTENSION x ray
41
Osteoarthritis
Most common form of arthritis.
Progressive degenerative condition
Affects joint due to gradual thinning of cartilage, loss of joint space and formation of bony spurs (osteophytes)
High impact - running, sports
Once it starts its always there
42
Osteoarthritis pathogenesis
Loss of matrix of the cartilage
Release of cytokines (IL-1, TNF, metalloproteinases, prostaglandins) by chondrocytes
Fibrillation of the cartilage surface and attempted repair with oesteophye formation
43
Osteoarthritis symtpoms
> Gradual onset (months --> yrs)
> NO REDNESS OR HOTNESS
> MECHANICAL pain ie worse on activity, worse end of day
> Relieved by rest
> Crepitus (grinding/creaking on movement)
> Stiffness (<30 minutes) inactivity gelling
> Bony swelling and joint deformity - hard and bony (unlike rheumatoid)
> Effusions and soft tissue swelling
> Loss of function and mobility
44
Joints most affected by osteoarthritis
Neck
```
Lower back
Hips
Base of thumb
Ends of fingers
Knees
Base of big toe
```
45
Osteoarthritis - hands, knee, hip, spine
Hands//
DIP, PIP and 1st CMC joints
Bony enargements may be seen at DIPs (Heberden's nodes)
& @ IPIs (bouchards nodes)
Squaring of the thumb
Knee//
Osteophytes, effusions, crepitus,
restriction of movement
Genu varus (bow legged)
Gen valgus (knock kneed)
Baker's cyst
Hip//
Pain may be felt in groin or radiating to knee
Pain may be radiating from back
Hip movement restricted
Spine//
Cervical - pain and restriction of movement
Osteophytes may impinge on nerve roots
Lumbar - osteophytes can cause spinal stenosis if encroach on spinal canal.
46
Osteoarthritis - risk factors
> Age (mid-late 40s >)
> Gender - commoner in women
> Genetic factors
> Previous injury/joint abnormality
> Obesity
> Other underlying conditions
-- Acromegaly, gout, arthritis
47
Osteoarthritis - Ix
Bloods - inflam markers usually normal
X rays showing:
joint space narrowing
Subchondral sclerosis
Bony cysts
Osteophytes
---
Rheumatoid factor negative
Anti-CCP antibody negative
Normal ESR and C reactive protein
48
Osteoarthritis - management
> Non pharma
> Pharma
Non pharma//
- education
- physiotherapy, muscle strengthening, proprioceptive
- weight loss
- footwear
- aids: walking stick, jar openers
- LOW impact exercise
Pharma//
- analgesia: paracetamol, compound analgesics, topical
- NSAIDs: symptomatic relief, short stint
- Pain modulators: tricyclics e.g. amitriptyline; anti convulsants, gabapentin
- Intraarticular steroids: only short term
----
Surgery
- arthroscopic washout, loose body, soft tissue trimming
- joint replacement
when the OA is at a point where they have constant pain
49
Crystal arthropathies - main conditions
1. Gout (monosodium urate)
| 2. Pseudogout (calcium pyrophosphate dihydrate/ CPPD)
50
Gout
INFLAMMATORY arthritis
Associated with monosodium urate crystal deposition
Most common inflammatory arthritis in men.
51
Foods to avoid in gout
```
Beer and wine
Red meat
Shellfish/oily fish
Game
Offal
```
Eat other foods in moderation.
52
Gout Pathogenesis
Aspects of diet and DNA/RNA
Production of purines
Hypoxanthine --> xanthine --> plasma urate --> urine, uric acid
--> deposition in joints and crystallisation
--> Gout
53
Hyperuricaemia
Serum uric acid > 7mg/dL
or 0.42mmol/L
Risk of developing gout related to degree of hyperuricaemia
54
Gout - overproduction and/or underexcretion of uric acid
OVERPRODUCTION//
Genetic-
Lesch- Nyhan (hypoxanthine guanine phosphoribosyltransferase deficiency), Von Gierke (glucose 6 phosphotase deficiency)
High cell turnover-
Psoriasis, Myeloproliferative and lymphoproliferative disorders, Chemotherapy, haemolytic and pernicious anaemia, bleeding, excessive exercise, obesity, infection,
Overconsumption of foods rich in purines (red meat, offal, shellfish, sardines, dried peas, legumes)
UNDERSECRETION//
```
Renal insufficiency
Starvation
Dehydration
Hypothyroidism
Hyperparathyrodism
Drugs (diuretics, levodopa, cyclosporin A, pyrazinamide)
Alcohol abuse
```
55
Does high serum uric acid indicate gout?
No.
| Not everyone with high serum uric acid will develop gout
56
Diagnosis of gout
Based on identification of crystals or classic radiographic findings, not hyperuricaemia alone
Level of uric acid does not actually precipitate the gout
ACUTE CHANGES in the level of uric acid causes gout
Serum urate can be normal in 25% of acute attacks.
DO NOT TREAT HYPERURICAEMIA ON ITS OWN
57
Best time to measure serum urate?
2 weeks following acute attack
58
Urea - clinical presentation
Acute monoarticular gout
Rapid onset (hours, often overnight)
Red, hot joint
Severe pain
Duration - up to 2 weeks
Site - first metatarsal phalangeal joint > ankle > knee > upper limb joints > spine
59
Podagra
gout of the foot
60
Gout - differential
Septic arthritis
Trauma
Seronegative arthritis (psoriatic arthritis, Reiter's -- but need to ask regarding associated symptoms e.g. skin psoriasis, eye symptoms, urethritis)
61
Chronic polyarticular gout
Chronic joint inflammation
Usually after having recurrent acute attacks> 10 years
Often diuretic associated
High serum uric acid
Tophi
May get acute attacks
62
Gout - investigations
- Gold standard
> Inflammatory markers (CRP, PV/ESR) - RAISED.
> WCC may be raised (difficult to differentiate from infection)
> X ray
- normal in acute attack
- chronic/ repeated attack
- erosions, overhanging osteophytes, joint destruction
> JOINT ASPIRATE (Gold standard) -- needle shaped crystals
63
Management of Gout
Acute attack//
- NSAIDs if no contraindicaiton
- Colchicine (too much can lead to diarrhoea)
- Corticosteroids (oral/ intra-articular, IM)
Other analgesia e.g. opiates, paracetamol.
Really really sore
----
Lifestyle modification
- restrict red meat, offal, beans, shellfish
- reduce alcohol
- lose weight
- fluids: 2L/day; dehydration triggers acute attack
- start 2-4 weeks after acute attack.
- start low dose and titrate
- aim for target urate <0.30mmol/L
64
Gout - prophylactic treatment s
> Indications: >2 attacks, top, erosions on x ray, renal stones
> Urate lowering therapy:
- Allopurinol/Febuxostat (blocks xanthine oxidase)
- start 2-4 weeks after acute attack
- Start low dose and titrate
- Aim for target serum urate <0.30mmol/L
(British Society of Rheumatology guidelines
65
Pseudogout (Calcium Pyrophosphate Dihydrate Deposition Disease - CPPD)
More common in elderly
Calcium deposition in the cartilage.
Chondrocalcinosis increases with age
Related to osteoarthritis
Affects fibrocartilage - knees, wrists, ankles
Rhomboid crystals
66
Calcium pyrophosphate disease association s
```
Aging
Hyperparathyroidsim
Familial hypocalciuric
hypercalcaemia
Haemochromatosis
Haemosiderosis
Hypophosphatasia
```
```
Hypomagnesaemia
Hypothyroidism
Neuropathic joints
Trauma
Amyloidosis
Gout
```
67
Pseudogout treatment
NSAIDs
Colchicine
Steroids
Rehydration
68
Hydroxyapatite
Crystal arthropathy
Milwaukee shoulder
Hydroxyapatite crystal deposition in or around the joint.
Acute and rapid deterioration
Females
Crystals not detected under light or polarised microscopy - alizarin stain show red clumps
69
Spondyloarthropathy - general definition
Family of inflammatory arthritis characterised by involvement of both the spine and joints, principally genetically predisposed.
70
HLA-B27
Associated with many spondyloarthropathies
Ankylosing spondylitis; reactive arthritis; Crohn's disease; Uveitis
More common in northern hemisphere
Not a useful screening tool as it is common in the general population.
71
Spondyloarthritis disease sub groups
> Ankylosing spondylitis
> Psoriatic arthritis
> Reactive arthritis
> Enteropathic arthritis
72
Mechanical back pain
Worsened by activity
Worse at end of day
Better with rest
73
Inflammatory back pain
Worse on rest
Better with activity
Significant early morning stiffness (>30 minutes)
74
Shared rheumatological & extra articular features of the sponyloarthropathies
> Sacroiliac and spinal involvement
> Enthesitis: inflammation at insertion of tendons into bones eg Achilles tendinitis, plantar fasciitis…
> Inflammatory arthritis:
- - Oligoarticular
- - Asymmetric
- - Predominantly lower limb
> Dactylitis (“sausage” digits)- inflammation of entire digit
-----
Extra-articular features
> Ocular inflammation (anterior uveitis, conjunctivitis, scleritis)
> Mucocutaneous lesions
> Rare aortic incompetence or heart block
> No rheumatoid nodules
75
Enthesis
Site of insertion of a tendon, ligament or articular capsule into bone
76
Ankylosing spondilitis
> Chronic systemic inflammatory disorder that primarily affects the spine.
> Hallmark- Sacroiliac joint involvement (sacroiliitis) . Pain around buttocks; stiff, painful.
>Peripheral arthritis uncommon (shoulder and hip)
> Enthesopathy
> Late adolescence or early adulthood
> More common in men 3-5:1
ASAS classification criteria
77
Ankylosing Spondylitis - clinical features
> Back pain (neck, thoracic, lumbar)
> Enthesitis
> Peripheral arthritis (shoulders,hips) – rare
> Extra articular features:
- Anterior uveitis
- Cardiovascular involvement (aortic valve/root )
- Pulmonary involvement (fibrosis upper lobes)
- Asymptomatic enteric mucosal inflammation
- Neurological involvement (Rarely A-A subluxation)
- Amyloidosis
Straightening of lumbar lordosis
Pronounced cervical kyphosis
Syndesmophytes - fusion of vertebrae
78
Ankylosing Spondylitis - "A" Disease
- Axial Arthritis
- Anterior Uveitis
- Aortic Regurgitation
- Apical fibrosis
- Amyloidosis/ Ig A Nephropathy
- Achilles tendinitis
- PlAntar Fasciitis
Which of the following is involved with ankylosing spondylitis?
Classic Q
79
Syndesmophytes
Fusion of spinal vertebrae
Ankylosing spondylitis
80
Ankylosing spondilitis - diagnosis
```
> History
> Exam
-- tragus/occiput to wall
-- chest expansiion
-- modified Schober test
```
> Bloods
- inflammatory parameters (ESR, CRP, PV)
- HLA B27
> X rays
- sacroilitis
- syndesmophwytes
- "bamboo" spine
> MRI imaging is GOLD standard.
-- best in showing early radiological changes
-- bone marrow oedema, enthesitis
81
Ankylosing Spondylitis - Treatment
> Physiotherapy; stretching
> Occupational therapy
> NSAID (first line)
> Disease modifying drugs. SZP, MTX – if also peripheral joint involvement
>Anti TNF treatment – Infliximab, Certolizumab, Adalimumab and Etanercept in severe AS
> Secukinumab (anti-IL17)
82
Psoriatic arthritis
> Inflammatory arthritis associated with psoriasis, but 10 -15% of patients can have PsA without psoriasis
> No Rheumatoid nodules
> Rheumatoid factor negative
83
Psoriatic Arthritis - clinical features
> Inflammatory Arthritis (5 subgroups/ presentations)
> Sacroiliitis:
- - often asymmetric
- - may be associated with spondylitis
> Nail involvement (Pitting, onycholysis, hyperkeratosis)
> Dactylitis
> Enthesitis:
- - Achilles tendinitis
- - Plantar fasciitis
> Extra articular features (eye disease)
84
Clinical subgroups of psoriatic arthritis (5)
1. Confined to distal interphalangeal joints (DIP) hands/feet
2. Symmetric polyarthritis (similar to RA)
3. Spondylitis (spine involvement) with or without peripheral joint involvement
4. Asymmetric oligoarthritis with dactylitis
5. Arthritis mutilans
85
Psoriatic arthritis - diagnosis
```
> History
> Examination
> Bloods:
-- Inflammatory parameters (raised)
-- Negative RF
```
> X-rays
- - Marginal erosions and “whiskering”
- - “Pencil in cup” deformity
- - Osteolysis
- - Enthesitis
86
Psoriatic arthritis - treatment
Pharma//
- NSAIDs
- Corticosteroids/joint injections
- Disease Modifying Drugs (Methotrexate, Sulfasalazine, Leflunomide)
- Anti TNF in severe disease unresponsive to NSAIDs & Methotrexate
- Secukinumab (anti-IL17)
Non-pharma//
- physiotherapy
- OT
- orthotics, chiropodist
87
Reactive Arthritis
Infection-Induced systemic illness characterised by an inflammatory SYNOVITIS from which viable microorganisms CANNOT be cultured
Symptoms 1-4 weeks after infection
Most common infections
-- urogenital (chlamydia)
-- enterogenic (salmonella, shigella, yersinia)
> Young adults
> Equal sex distribution
> HLA B27 pos.
88
Reiter's syndrome
Form of reactive arthritis
Triad:
- Urethritis
- conjunctivitis
- arthritis
Not a separate diagnosis
89
Reactive arthritis - Clinical features
> General symptoms (fever fatigue, malaise)
> Assymetrical monoarthritis or oligoarthritis
> Enthesitis
> Mucocutaneous lesions
- keratoderma blenorrhagica
- circinate balanitis
- painless oral ulcers
- hyperkeratotic nails
> Ocular lesions (uni/bilateral)
- - conjunctivitis
- iritis
> Visceral manifestations
- - mild renal disease
- - carditis
90
Reactive arthritis - diagnosis
```
> History & exam
> Bloods
- eSR, CRP, PV
- FBC, U&Es
- HLA B27
```
> Cultures (blood, urine, stool)
> Joint fluid analysis
> X ray of affected joints
> Ophthalmology opinion
91
Reactive arthritis - treatment
Spontaneous resolution with 6 months (90%)
PHARMA//
```
NSAIDs
Corticosteroids
-- intra articular (once sepsis ruled out)
-- oral
-- eye drops
```
Abx for underlying infection
DMARDs (SZP) - if resistant, chronic
Non Pharma//
- physiotherapy
- Occupational therapy
92
Enteropathic arthritis
> Associated w/ IBS
- - Crohn's
- - UC
> Present w/ arthritis in several joints
-- esp knees, ankles, elbows and wrists (spine, hips or shoulders)
> Sacroilitis
> WORSENING of symptoms during flare ups of inflammatory bowel disease.
93
Enteropathic arthritis - clinical symptoms
GI- loose, watery stool with mucous and blood)
- Weight loss, low grade fever
Eye involvement ( uveitis)
Skin involvement ( pyoderma gangrenosum)
Enthesitis
Achilles tendonitis, plantar fasciitis, lateral epicondylitis)
Oral- aphthous ulcers
94
Enteropathic arthritis - Ix
Upper and lower GI endoscopy with biopsy showing ulceration/ colitis
Joint aspirate- no organisms or crystals
Raised inflammatory markers- CRP, PV
X ray/ MRI showing sacroiliitis
USS showing synovitis/ tenosynovitis
95
Enteropathic Arthritis - Treatment
Treat IBS in order to control arthritis
NSAID usually not good idea as may exacerbate inflammatory bowel disease
Normal analgesia - paracetamol, co codamol
Steroids (oral, IA, IM)
DMARDs - methotrexate, sulfasalazine, azathioprine) - decided in conjunction w/ gastroenterologists
Anti TNF - Infliximab, adalimumab
96
Which group of drugs shouldn't;t you use in enteropathic arthritis?
NSAIDs
May exacerbate inflammatory bowel disease
97
Suspicious features (red flags) for back pain
Non-mechanical pain (doesn't vary with time of day; troublesome at night)
Systemic upset
Major, new, neurological deficit (things like drop foot isn't so urgent)
Saddle anaesthesia ± bladder or bowel upset --> surgical emergency
98
Neurological examination of the back
> Myotomes
> Dermatomes
> Reflexes
> Nerve irritation
- - straight leg raise
- - femoral stretch test for the femoral roots
- - bowstring test (pressure behind the knee)
99
Myotome for hip flexion
L1/L2
Ask the patient to push up against your hand
100
Knee extension myotome
L3/4
Ask patient to straighten their knee against your hand
101
Foot dorsiflexion and Extensor Hallicus longus Myotome
L5
Dorsiflexion against hands of clinician
102
Ankle plantarflexion
S1/2
Plantarflexion of the foot
Very powerful movement and the deficit needs to be gross before you pick it up.
More subtle deficits can be detected by asking the patient to stand on tip toe.
103
Overt pain behaviour
```
Guarding
Bracing
Rubbing
Grimacing
Sighing
```
104
Waddell Behavioural Signs
> Superficial / non anatomical tenderness
> Simulation – axial loading / rotation
> Distraction – SLR (straight leg raise)
> Over-reaction to examination
> Regional – sensory disturbance
-- giving way
---
```
Pain at tip of coccyx
whole leg pain
whole leg numbness
whole leg giving way
absence of pain free spells
intolerance of treatment
emergency admission
```
105
High intensity zone - white triangle on an MRI of the spine. What does this indicate?
Annular tear of disc
106
Sciatica - surgeon's definition
Buttock and/or leg pain in a specific dermatomal distribution accompanied by neurological disturbance
107
Disc prolapse - common presentation
> EPISODIC back pain
> Onset of leg pain ± neurology
> Leg pain becomes dominant
> Myotomes and dermatomes
> not an emergency
> vast majority settle without surgery
> Many settle within 3 months
> Consider more treatment if not resolved after 3 months.
-----
large spectrum
108
When is a disc prolapse considered an emergency?
If the patient is displaying symptoms of cauda equina syndrome.
109
Disc prolapse treatment
> Conservative treatment first
> Consider surgery if not resolving after 3 months
> Long term results (2,5,10 yrs) - same whether operated or not
> Short term benefits
110
Management of backache
> SHORT bed rest (debatable)
> Anti-inflammatory ± muscle relaxant
> Mobilise thereafter
> Place of physical therapies
> Return to normal activity
---
2nd line
> Education/instruction/reassurance
> Physiotherapy
> Osteopathy/chiropractic
> TENS/psychology/ pain clinic
> complementary therapies
> surgery
111
Adjacent Segment Disease
a broad term encompassing many complications of spinal fusion, including listhesis, instability, herniated nucleus pulposus, stenosis, hypertrophic facet arthritis, scoliosis, and vertebral compression fracture
Increasing problem
8-10 years after 2 level fusion
18 months after 3 level fusion
112
Chronic pain syndromes
Central pain perception
Dorsal horn - NMDA receptors
Mid-brain
Anterior cingulate region
Cord changes
Pain and psychosocial stimuli
113
Stress & distress
Stress - normal emotion in response to life
Distress - excessive or abnormal stress response.
Increasing evidence of link between chronic pain and childhood abuse
PTSD
White coat distress
114
Causes of Back Pain
```
> Muscular strain
> Ligamentous disruption
> Facet arthropathy
> Disc degeneration
> Internal disc disruption
> Segmental instability
> Tumours
> Fractures
> Gynaecological
> Psychological
> God Only Knows
```
115
Social implications of Back Pain
Major cause of disability
Loss of job - can't pay bills, mortgage...
Vicious cycle
Workdays lost due to back pai
116
Back pain is a complex interaction of multiple physical and non-physical components
Social Environment
Illness behaviour
Psychological distress
Attitudes and beliefs
Pain
117
Approximately (%), how many back pain referrals end up needing surgery?
2. 5%
| i. e. 97.5% of back pain patients have a non-surgical condition.
118
Spinal claudication - presentation
Age 50+
More males than females
Manual workers (obesity now a major contributor)
Limited walking capacity
Stoop/sit/lean forward to relieve symptoms
Heavy or tired legs
119
How do those with spinal claudication relieve their symptoms?
Stooping/sit/ leaning forward
Stopping and standing still does not relieve the pain
120
Spinal Claudication features
| vs Vascular claudication
Relieved by flexing
Walking up hill is often not bad (flexing)
Trouble walking downhill (extending)
Cycling is easy
-----
Vascular claudication
- relieved by standing
- uphill ba
- cycling bad
121
Discogenic Pain
Segmental instability - background ache with exacerbations and remissions superimposed
Worse as day goes on
Worse on flexion
Worse with activity
Deep seated central lower back pain
122
Facet Arthropathy
Stiff in the morming
"loosen up routine" - 20 minutes
restless
Difficulty sitting, driving and standing for extended periods of time
Worse with extension
Better with activity
Often radiates to the buttocks and legs
---
Excision of facets and fusion can treat it
123
What kind of symptoms do people with Back Ache come to the GP with?
> Pain
- - localised
- - lumbar
Type? - radiates, localised
> Referred pain
-- sciatica
```
> Stiffness
> Loss of sleep
> Loss of function
-- walking
-- lifting
-- carrying
```
try to find out how the problem affects the individual
> Trauma - recent/past
> Previous surgery
> Symptoms suggesting other pathology
- urinary tract
- GI
- Resp
- Systemic illness
124
Main red flag for back pain?
Known/ history of Cancer.
125
When to use MRI with back pain
Only if red flags or if considering surgery
126
LOSS acronym - X ray features of osteoarthritis
Loss of joint space
Osteophytes
Sclerosis
Subarticular cysts
127
Back pain - red flags
Age <20 or >50
Thoracic pain
Previous carcinoma (breast, bronchus, prostate)
Immunocompromise (steroids, HIV)
Feeling unwell
Weight loss
Widespread
neurological symptoms - saddle anaesthesia/parasthesia ± loss of bowel or bladder control
Structural spinal deformity
Severe pain longer than 6 months
128
"Yellow" flags for chronic back pain
```
> Low mood
> High levels of pain/disability
> Belief that activity is harmful
> Low educational level
> Obesity
> Problem with claim/compensation (secondary gain)
```
> Job dissatisfaction
> Light duties not available at work
> Lot of lifting at work
129
Management of back pain
Reassurance
Encourage to mobilise
Cultivate positive mental attitude
Analgesics - paracetamol, co- analgesics, opiates
NSAIDs - short term (if they don't change within a few weeks, consider different treatment)
Muscle relaxants
Physio
Osteopahty and chiropractic
Referral
130
Emergency back pain
Cauda equina syndrome
Fracture with deteriorating neurology
131
Spinal cord injury pattern
ASIA grading
Complete
Incomplete
- central cord
- brown sequard (damage to half spinal cord)
- anterior cord
---
ASIA grading
I - complete motor and sensory loss
ii - complete motor and incomplete sensory
iii - incomplete motor - no practical use
iv - useful motor and incomplete sensory
v - normal motor and sensory function
132
Central cord injury
Typically hyperextension injury
Incomplete spinal cord injury patterns
Arms worse than legs
Prognosis variable
133
Brown Sequard
Incomplete Spinal cord injury
Paralysis on ipsilateral side
Hypaesthesia on contralateral side
Associated with fracture.
134
Anterior Cord injury
Incomplete spinal cord injury
Motor loss
Loss of pain and temperature sense
Deep touch, position and vibration PRESERVED
May have traumatic or VASCULAR insult
Prognosis is poor
Complication of AAA repair
135
Secondary Cord Damage
```
Stretching
Compression
Undue movement
Hypotension/Hypoxaemia***
Inappropriate surgery
Infection
```
136
Paraplegia
Partial or total control of limbs
NOT the arms
137
Tetraplegia
Partial or total loss of function/control of all limbs
138
Thoracolumbar Fractures
Complete paraplegia
Decompression doesn't help
Stability is good due to the rib cage
139
Thoracolumbar fractures - partial cord damage
Mechanically unstable fracture --> stabilisation
Decompression by anterior route
controversial – some believe it helps, others that it creates more trauma in an already compromised area and it’s best to let the cord recover on it’s own.
140
When should spinal surgery (for likes of Thoracolumbar fractures) be performed?
Within 7-10 days.
NOT immediately because that is when swelling, tissue compromise and hypoxia are at their worst
High risk of secondary cord damage
Better to let swelling and tissue perfusion improve
141
Ring epiphysis in chldren
Damage to the growth plate can cause premature fusion and cessation of growth.
In the spine this can lead to Kyphosis.
142
Ankylosing spondylitis - cervical spine injury
How should you immobilise the patient?
Dangerous and unstable injury
May be made WORSE by collars..
Immobilise in "natural" position.
i.e. if AS patient has kyphosis, support their head in this manner. Do not try and force it into a brace as this may cause even more problems.
143
Scoliosis
- categories
- complex deformity
Complex deformity
- rotational component
- lateral bend component
- rib deformities
- visceral abnormalities
-----
Congenital
Early onset idiopathic
Late onset idiopathic
Secondary
144
Congenital scoliosis
Imbalance in the number of growth plates
Greater the imbalance, the worse the potential deformity
e.g.
Unilateral partial failure of vertebrae formation
Unilateral failure of segmentation
Bilateral failure of segmentation (of vertebrae)
145
Secondary Scoliosis
Neuromuscular
Tumours
Spina bifida
Treat the underlying cause
146
Non operative management of Scoliosis
Serial corrective casts
Bracing
Corrective exercises
Electrical stimulation
Results are variable for all.
147
Spondylosis
Defect in the pars interarticularis of the vertebra
DOnt mix up with spondylolisthesis
148
Sponylolisthesis
Forward slippage of one vertebra on another
Don't mix up with spondylosis
149
Meyerding Grading for Spondylolisthesis
method of grading spondylolisthesis is the Meyerding classification, based on the ratio of [overhanging part of the superior vertebral body] to [anteroposterior length of the adjacent inferior vertebral body]:
grade I: 0-25%
grade II: 26-50%
grade III: 51-75%
grade IV: 76-100%
grade V (spondyloptosis): >100% (traumatic subluxation of a vertebral body in sagittal or coronal plane)
150
Spondylolisthesis Grade 1 or 2
Abnormal neighbouring discs
Posterolateral stabilisation in situ
L4/S1 fusion
151
Spondylolisthesis Grade 3+
Combined discogenic + nerve root problem
One stage combined anterior and posterior stabilisation
152
Early osteoarthritis - non operative treatments
Weight loss, stick, exercise, analgesics, activity modification.
Steroid injection only for acute flare ups
Osteotomy can be useful in varus knee with isolated early medial compartment OA
-good for heavy manual workers.
153
Osteogenesis Imperfecta
Brittle bone disease
> Thin, osteopoenic bones
> Defect in type 1 collagen synthesis
> Different types - varying severity
Milder - autosomal dominant with multiple fragility fractures, blue sclerae, hearing loss
Rarer cases - autosomal recessive and may be fatal in perinatal period or associated with severe scoliosis and deformity
Fractures heal with abundant callus
Deformity may need osteotomies.
154
Osteogenesis imperfecta - defect in synthesis of?
Type I collagen
155
Skeletal Dysplasias
- what kind of treatment is provided?
Genetic disorder
Leads to short stature
May/may not be associated with learning difficulties, spine deformity, hyper mobility, facial or skull deformity, skin abnormalities, tumour formation, intra-uterine or premature death.
Supportive treatment:
- prevent spinal cord/ nerve compression
- joint instability
- deformity
Achondroplasia is the most common type (autosomal dominant)
GROWTH HORMONE IS INEFFECTIVE
156
In skeletal dysplasias, is growth hormone effective?
No.
It is generally ineffective.
157
Most common skeletal dysplasia?
Achondroplasia is the most common type
| autosomal dominant
158
Connective tissue is an umbrella term for?
Tendons, ligaments, cartilage and bone
Mesoderm
159
Marfan's syndrome
Autosomal dominant / sporadic mutation of fibrillin gene
Tall stature
Long limbs
Hypermobility
Arachnodactyly
----
Associated with:
```
> High arched palate
> Scoliosis
> Pectus excavatum
> Lens dislocation
> Aortic aneurysm
> Cardiac valve incompetence.
> Spontaneous pneumothorax
> Joint dislocations
```
160
Fibrillin is required for?
Scaffolding for elastin
Fibrillin gene is defective in Marfan's
161
Ehlers-Danlos Syndrome
Autosomal dominant defect of one of number of genes involved in collagen and elastin formation
Joint hyper mobility and dislocations
Early onset osteoarthritis
Atrophic scars, poor wound healing
Ease of bruising
Scoliosis, kyphosis, cardiac abnormalities
Occipito-atlantal instability, myelopathy, spinal cord tethering.
---
That guy in the Guinness world records with really stretchy skin.
162
Down Syndrome
Trisomy 21
Joint laxity predisposes to recurrent dislocations and OA
Atlanto-axial instability --> spinal cord compression (myelopathy)
163
Duchenne Muscular Dystrophy
X-linked recessive (boys only)
Defect in dystrophin calcium transport gene --> progressive muscle weakness as boys grow older.
Gowers sign on standing raised.
Scoliosis
Progressive cardiac & respiratory failure
Usually death in early 20s
164
Becker's muscular dystrophy
Milder form of Duchenne Muscular Dystrophy
Survival into 30s and 40s
165
Gower's sign
Medical sign that indicates weakness of the proximal muscles, namely those of the lower limb.
The sign describes a patient that has to use their hands and arms to "walk" up their own body from a squatting position due to lack of hip and thigh muscle strength.
166
Talipes Equinovarus
Clubfoot
50% cases bilateral.
Abnormal alignment of talus, calcaneus and navicular --> ankle plantar flexion, supination and varus of forgot with contractures tendons, ligaments and capsule.
More boys
Risk: +ve family history, breech; oligohydramnios (low amniotic fluid volume)
Generalised skeletal dysplasia
Higher risk DDH
-----
Ponseti Technique
casting for around 9 weeks.
Boots and bar 23 hours per day/3 months then night time up to 4 years.
Risk of recurrence
167
Ponseti technique
Used to treat clubfoot (Talipes Equinovarus)
Casting for around 9 weeks
Boots and bar 23 hrs per day 3 months then night time up to 4 years
168
When is there a developing limb bud in gestation?
Around 4-6 weeks
169
Syndactyly
Commonest limb malformation.
Failure of separation of the digits
May only be skin
Can be bone & joint involvement
Surgical separation required at age 3 or 4
170
Polydactyly
Extra digit
Treatment by surgical removal.
171
Fibular hemimelia
Partial or complete ABSENCE of the fibula
Shortening of leg, bowing of tibia and deformity of ankle
---
Treatment
> Mild cases
-- limb lengthening with circular frame external fixator
> Severe -- amputation at 10 months to 2 years.
172
Radial club hand
Congenital difference occurring in a longitudinal direction resulting in radial deviation of the wrist and shortening of the forearm.
Minor anomaly to complete absence of the radius, radial side of the carpal bones and thumb
173
Proximal focal femoral deficiency
Is a rare, non-hereditary birth defect that affects the pelvis, particularly the hip bone, and the proximal femur. The disorder may affect one side or both, with the hip being deformed and the leg shortened.
absence or shortening of a leg bone (fibular hemimelia) and the absence of a kneecap.
Dislocation or instability of the joint between the femur and the kneecap, a shortened tibia or fibula, and foot deformities.
174
Obstetric Brachial Plexus Injury
2/1000 births
Most common with large babies (macrosomia, diabetes)
Twin deliveries
Shouder dystocia
Nerves stretched as the shoulder is stuck behind th mother's pelvic bone on delivery
Erb's palsy (upper brachial plexus C5&C6 roots)
Klumpke's Palsy (lower brachial plexus injury from traction on abducted arm)
175
Erb's Palsy
Congenital defect
Upper brachial plexus (C5 & 6 roots)
176
Klumpke's Palsy
Lower brachial plexus injury due to traction on abducted arm
--> Paralysis intrinsic hand muscles ± finger and wrist flexors
Prognosis poorer than for Erb's
177
Cerebral palsy
Due to insult to the immature brain before 3 years of age.
Often intrauterine - genetic abnormalities, brain malformation, intrauterine infection
1 in 10 hypoxia at birth
Some due to meningitis at early age.
Variable expression depending on area of brain affected.
- may affect one limb, 2 limbs, all 4 or total body involvement
- learning difficulties and developmental delay
---
Different types:
Spastic (80%) – motor cortex affected
Ataxic (cerebellum)
Athetoid – uncontrolled writhing (basal ganglia)
Dystonic – Repetitive movements (basal ganglia)
Spastic : One limb = monoplegic, ipsilateral arm & leg = hemiplegic, Legs only = diplegic, all 4 limbs = quadriplegic
UMN problem weakness, spasticity, hyperreflexia
178
Types of cerebral palsy
Different types:
Spastic (80%) – motor cortex affected
Ataxic (cerebellum)
Athetoid – uncontrolled writhing (basal ganglia)
Dystonic – Repetitive movements (basal ganglia)
Spastic : One limb = monoplegic,
ipsilateral arm & leg = hemiplegic,
Legs only = diplegic,
all 4 limbs = quadriplegic
UMN problem --> weakness, spasticity, hyperreflexia
179
Cerebral palsy -
| spasticity/ joint contractures/ hip dislocation treatment
Baclofen
Botox injection
Neurosurgical procedures (rhizotomy)
Joint contractures --> surgical release, fusions
Hip dislocations --> THR, osteotomy, excision, arthroplasty
180
Spina bifida
Mild
Severe
Failure of fusion of posterior vertebral arch
Mild - spina bifida occulta
--- may be brith mark, skin tag, lipoma or hairy patch
-- can cause tethering of spinal cord and roots
- pes cavus (high arch) and clawing of toes
- bladder/bowel problems
----
Severe - spina bifida cystica
Herniation of meninges (meningocele) or roots of cauda equina (myelomeningocele)
Meningocele usually no neurological deficit
Myelomeningocele usually motor and sensory deficit below level of lesion – most never walk independently
May be associated with hydrocephalus (build up of CSF in brain – treatment = shunt)
Treatment early closure within 48hrs birth.
May need scoliosis correction, procedures for hips, release contractures, foot surgery
181
Polio (poliomyelitis)
> Viral infection of anterior horn cells in spinal cord or brainstem
--> LMN deficit – weakness, reduced tone, loss of reflexes
> Entry via GI tract, flu like illness and subsequent paralysis of group of muscles one or more limbs within 2-3 days
> Recovery may occur – may be residual permanent deficit. Sensation is preserved
> Limb may be weak and short, joint deformities can occur
> Vaccination has eradicated in developed countries
----
Splint/brace/caliper may help
Tendon transfers
Joint fusions
Leg lengthening.
