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MSK > Arthropathies/Muscular/Neuromuscular/ Back Pain/ Spine/ Spinal conditions > Flashcards

Arthropathies/Muscular/Neuromuscular/ Back Pain/ Spine/ Spinal conditions Flashcards

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
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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

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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

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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

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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
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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

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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.
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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

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9
Q

What part of the spine can rheumatoid arthritis sometimes affect?

A

C1 and C2 spine.

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10
Q

Which HLA/MHC complex is rheumatoid arthritis mediated by?

A

HLA-DR4

Infections, stress and cigarette smoking are potential triggers

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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

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12
Q

What is the hallmark sign of RA?

A

Synovitis

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13
Q

Rheumatoid arthritis Pannus

A

Abnormal layer of granulation tissue/fibrovascular tissue.

T cells activated –> inflammatory cascade

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14
Q

What do the joints feel like in RA (on palpation)?

A

Spongy

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15
Q

Early rheumatoid arthritis

A

Defined as less than 2 years since symptom onset

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16
Q

What is the therapeutic window of opportunity in early rheumatoid arthritis?

A

First 3 months.

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17
Q

ACR/EULAR Classification of RA

A

Joint Distribution (0-5)

Serology (0-3)

Symptom duration (0-1)

Acute phase reactants (0-1)

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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

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19
Q

When is stiffness the worst in RA?

A

In the morming

Lasting longer than 30 minutes

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20
Q

Normochromic anaema

A

Blood cells are normal but there are just not enough of them.

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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

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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

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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.

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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

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25
Q

Imaging for Rheumatoid arthritis?

What is the GOLD standard?

A

> 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

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26
Q

DAS28 score

A

Disease Activity score

Assessment of disease

28 joints counted

Lower score = better.

less than 2.6 = remission

  1. 6-3.2 = low level activity
  2. 2 -5.1 = moderate disease

> 5.1 = active disease

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27
Q

A DAS28 score of less than than 2.6 for rheumatoid arthritis indicates?

A

Remission

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28
Q

Management of RA

A

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

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29
Q

Treatment of RA

A 
1. Aspirin/NSAIDs
\+ steroids
\+ DMARD #1
\+ DMARD #2(?)
\+ DMARD #3(?)

Gradually withdraw treatment after remission is achieved

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30
Q

Rheumatoid arthritis - steroids

A

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?

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31
Q

Are steroids ever given on their own in RA?

A

NO, NEVER.

Only given in combo with DMARDs.

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32
Q

DMARDs

A

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

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33
Q

Methotrexate

A

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

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34
Q

Hydroxychloroquine

A

Does not prevent erosions

If above 2, it does not work.

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35
Q

What lung condition can methotrexate cause?

A

Pneumonitis

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36
Q

What should be taken with methotrexate?

A

Folic acid

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37
Q

DMARDs combination

A

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.

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38
Q

When should sulfasalazine be avoided?

A

Co trimoxazole allergy

G6PD deficiency

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39
Q

Biological agents used in RA

A

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

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40
Q

Untreated RA - complications

A

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
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41
Q

Osteoarthritis

A

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

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42
Q

Osteoarthritis pathogenesis

A

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

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43
Q

Osteoarthritis symtpoms

A

> 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

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44
Q

Joints most affected by osteoarthritis

A

Neck

Lower back
Hips
Base of thumb
Ends of fingers
Knees
Base of big toe
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45
Q

Osteoarthritis - hands, knee, hip, spine

A

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.

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46
Q

Osteoarthritis - risk factors

A

> Age (mid-late 40s >)

> Gender - commoner in women

> Genetic factors

> Previous injury/joint abnormality

> Obesity

> Other underlying conditions

– Acromegaly, gout, arthritis

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47
Q

Osteoarthritis - Ix

A

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

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48
Q

Osteoarthritis - management

> Non pharma
Pharma

A

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

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49
Q

Crystal arthropathies - main conditions

A
  1. Gout (monosodium urate)

2. Pseudogout (calcium pyrophosphate dihydrate/ CPPD)

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50
Q

Gout

A

INFLAMMATORY arthritis

Associated with monosodium urate crystal deposition

Most common inflammatory arthritis in men.

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51
Q

Foods to avoid in gout

A 
Beer and wine
Red meat
Shellfish/oily fish
Game 
Offal

Eat other foods in moderation.

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52
Q

Gout Pathogenesis

A

Aspects of diet and DNA/RNA

Production of purines

Hypoxanthine –> xanthine –> plasma urate –> urine, uric acid

–> deposition in joints and crystallisation

–> Gout

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53
Q

Hyperuricaemia

A

Serum uric acid > 7mg/dL

or 0.42mmol/L

Risk of developing gout related to degree of hyperuricaemia

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54
Q

Gout - overproduction and/or underexcretion of uric acid

A

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
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55
Q

Does high serum uric acid indicate gout?

A

No.

Not everyone with high serum uric acid will develop gout

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56
Q

Diagnosis of gout

A

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

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57
Q

Best time to measure serum urate?

A

2 weeks following acute attack

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58
Q

Urea - clinical presentation

A

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

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59
Q

Podagra

A

gout of the foot

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60
Q

Gout - differential

A

Septic arthritis

Trauma

Seronegative arthritis (psoriatic arthritis, Reiter’s – but need to ask regarding associated symptoms e.g. skin psoriasis, eye symptoms, urethritis)

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61
Q

Chronic polyarticular gout

A

Chronic joint inflammation

Usually after having recurrent acute attacks> 10 years

Often diuretic associated

High serum uric acid

Tophi

May get acute attacks

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62
Q

Gout - investigations

  • Gold standard
A

> 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

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63
Q

Management of Gout

A

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
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64
Q

Gout - prophylactic treatment s

A

> 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
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65
Q

Pseudogout (Calcium Pyrophosphate Dihydrate Deposition Disease - CPPD)

A

More common in elderly

Calcium deposition in the cartilage.

Chondrocalcinosis increases with age

Related to osteoarthritis

Affects fibrocartilage - knees, wrists, ankles

Rhomboid crystals

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66
Q

Calcium pyrophosphate disease association s

A 
Aging
Hyperparathyroidsim
Familial hypocalciuric
     hypercalcaemia
Haemochromatosis
Haemosiderosis
Hypophosphatasia
Hypomagnesaemia
Hypothyroidism
Neuropathic joints
Trauma
Amyloidosis
Gout
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67
Q

Pseudogout treatment

A

NSAIDs
Colchicine
Steroids
Rehydration

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68
Q

Hydroxyapatite

A

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

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69
Q

Spondyloarthropathy - general definition

A

Family of inflammatory arthritis characterised by involvement of both the spine and joints, principally genetically predisposed.

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70
Q

HLA-B27

A

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.

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71
Q

Spondyloarthritis disease sub groups

A

> Ankylosing spondylitis

> Psoriatic arthritis

> Reactive arthritis

> Enteropathic arthritis

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72
Q

Mechanical back pain

A

Worsened by activity

Worse at end of day

Better with rest

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73
Q

Inflammatory back pain

A

Worse on rest

Better with activity

Significant early morning stiffness (>30 minutes)

74
Q

Shared rheumatological & extra articular features of the sponyloarthropathies

A

> 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
Q

Enthesis

A

Site of insertion of a tendon, ligament or articular capsule into bone

76
Q

Ankylosing spondilitis

A

> 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
Q

Ankylosing Spondylitis - clinical features

A

> 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
Q

Ankylosing Spondylitis - “A” Disease

A
  • 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
Q

Syndesmophytes

A

Fusion of spinal vertebrae

Ankylosing spondylitis

80
Q

Ankylosing spondilitis - diagnosis

A 
> 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
Q

Ankylosing Spondylitis - Treatment

A

> 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
Q

Psoriatic arthritis

A

> Inflammatory arthritis associated with psoriasis, but 10 -15% of patients can have PsA without psoriasis

> No Rheumatoid nodules

> Rheumatoid factor negative

83
Q

Psoriatic Arthritis - clinical features

A

> 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
Q

Clinical subgroups of psoriatic arthritis (5)

A
  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
Q

Psoriatic arthritis - diagnosis

A 
> History
> Examination
> Bloods:
-- Inflammatory parameters (raised)
-- Negative RF

> X-rays

    • Marginal erosions and “whiskering”
    • “Pencil in cup” deformity
    • Osteolysis
    • Enthesitis
86
Q

Psoriatic arthritis - treatment

A

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
Q

Reactive Arthritis

A

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
Q

Reiter’s syndrome

A

Form of reactive arthritis

Triad:

  • Urethritis
  • conjunctivitis
  • arthritis

Not a separate diagnosis

89
Q

Reactive arthritis - Clinical features

A

> 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
Q

Reactive arthritis - diagnosis

A 
> History &amp; exam
> Bloods 
- eSR, CRP, PV
- FBC, U&amp;Es
- HLA B27

> Cultures (blood, urine, stool)
Joint fluid analysis
X ray of affected joints
Ophthalmology opinion

91
Q

Reactive arthritis - treatment

A

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
Q

Enteropathic arthritis

A

> 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
Q

Enteropathic arthritis - clinical symptoms

A

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
Q

Enteropathic arthritis - Ix

A

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
Q

Enteropathic Arthritis - Treatment

A

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
Q

Which group of drugs shouldn’t;t you use in enteropathic arthritis?

A

NSAIDs

May exacerbate inflammatory bowel disease

97
Q

Suspicious features (red flags) for back pain

A

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
Q

Neurological examination of the back

A

> Myotomes

> Dermatomes

> Reflexes

> Nerve irritation

    • straight leg raise
    • femoral stretch test for the femoral roots
    • bowstring test (pressure behind the knee)
99
Q

Myotome for hip flexion

A

L1/L2

Ask the patient to push up against your hand

100
Q

Knee extension myotome

A

L3/4

Ask patient to straighten their knee against your hand

101
Q

Foot dorsiflexion and Extensor Hallicus longus Myotome

A

L5

Dorsiflexion against hands of clinician

102
Q

Ankle plantarflexion

A

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
Q

Overt pain behaviour

A 
Guarding 
Bracing
Rubbing
Grimacing
Sighing
104
Q

Waddell Behavioural Signs

A

> 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
Q

High intensity zone - white triangle on an MRI of the spine. What does this indicate?

A

Annular tear of disc

106
Q

Sciatica - surgeon’s definition

A

Buttock and/or leg pain in a specific dermatomal distribution accompanied by neurological disturbance

107
Q

Disc prolapse - common presentation

A

> 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
Q

When is a disc prolapse considered an emergency?

A

If the patient is displaying symptoms of cauda equina syndrome.

109
Q

Disc prolapse treatment

A

> 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
Q

Management of backache

A

> 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
Q

Adjacent Segment Disease

A

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
Q

Chronic pain syndromes

A

Central pain perception

Dorsal horn - NMDA receptors

Mid-brain

Anterior cingulate region

Cord changes

Pain and psychosocial stimuli

113
Q

Stress & distress

A

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
Q

Causes of Back Pain

A 
> Muscular strain
> Ligamentous disruption
> Facet arthropathy
> Disc degeneration
> Internal disc disruption
> Segmental instability 
> Tumours
> Fractures
> Gynaecological 
> Psychological 
> God Only Knows
115
Q

Social implications of Back Pain

A

Major cause of disability

Loss of job - can’t pay bills, mortgage…

Vicious cycle

Workdays lost due to back pai

116
Q

Back pain is a complex interaction of multiple physical and non-physical components

A

Social Environment

Illness behaviour

Psychological distress

Attitudes and beliefs

Pain

117
Q

Approximately (%), how many back pain referrals end up needing surgery?

A
  1. 5%

i. e. 97.5% of back pain patients have a non-surgical condition.

118
Q

Spinal claudication - presentation

A

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
Q

How do those with spinal claudication relieve their symptoms?

A

Stooping/sit/ leaning forward

Stopping and standing still does not relieve the pain

120
Q

Spinal Claudication features

vs Vascular claudication

A

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
Q

Discogenic Pain

A

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
Q

Facet Arthropathy

A

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
Q

What kind of symptoms do people with Back Ache come to the GP with?

A

> 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
Q

Main red flag for back pain?

A

Known/ history of Cancer.

125
Q

When to use MRI with back pain

A

Only if red flags or if considering surgery

126
Q

LOSS acronym - X ray features of osteoarthritis

A

Loss of joint space
Osteophytes
Sclerosis
Subarticular cysts

127
Q

Back pain - red flags

A

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
Q

“Yellow” flags for chronic back pain

A 
> 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
Q

Management of back pain

A

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
Q

Emergency back pain

A

Cauda equina syndrome

Fracture with deteriorating neurology

131
Q

Spinal cord injury pattern

ASIA grading

A

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
Q

Central cord injury

A

Typically hyperextension injury

Incomplete spinal cord injury patterns

Arms worse than legs

Prognosis variable

133
Q

Brown Sequard

A

Incomplete Spinal cord injury

Paralysis on ipsilateral side

Hypaesthesia on contralateral side

Associated with fracture.

134
Q

Anterior Cord injury

A

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
Q

Secondary Cord Damage

A 
Stretching 
Compression
Undue movement 
Hypotension/Hypoxaemia***
Inappropriate surgery
Infection
136
Q

Paraplegia

A

Partial or total control of limbs

NOT the arms

137
Q

Tetraplegia

A

Partial or total loss of function/control of all limbs

138
Q

Thoracolumbar Fractures

A

Complete paraplegia

Decompression doesn’t help

Stability is good due to the rib cage

139
Q

Thoracolumbar fractures - partial cord damage

A

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
Q

When should spinal surgery (for likes of Thoracolumbar fractures) be performed?

A

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
Q

Ring epiphysis in chldren

A

Damage to the growth plate can cause premature fusion and cessation of growth.

In the spine this can lead to Kyphosis.

142
Q

Ankylosing spondylitis - cervical spine injury

How should you immobilise the patient?

A

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
Q

Scoliosis

  • categories
  • complex deformity
A

Complex deformity

  • rotational component
  • lateral bend component
  • rib deformities
  • visceral abnormalities

Congenital
Early onset idiopathic
Late onset idiopathic
Secondary

144
Q

Congenital scoliosis

A

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
Q

Secondary Scoliosis

A

Neuromuscular

Tumours

Spina bifida

Treat the underlying cause

146
Q

Non operative management of Scoliosis

A

Serial corrective casts

Bracing

Corrective exercises

Electrical stimulation

Results are variable for all.

147
Q

Spondylosis

A

Defect in the pars interarticularis of the vertebra

DOnt mix up with spondylolisthesis

148
Q

Sponylolisthesis

A

Forward slippage of one vertebra on another

Don’t mix up with spondylosis

149
Q

Meyerding Grading for Spondylolisthesis

A

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
Q

Spondylolisthesis Grade 1 or 2

A

Abnormal neighbouring discs

Posterolateral stabilisation in situ

L4/S1 fusion

151
Q

Spondylolisthesis Grade 3+

A

Combined discogenic + nerve root problem

One stage combined anterior and posterior stabilisation

152
Q

Early osteoarthritis - non operative treatments

A

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
Q

Osteogenesis Imperfecta

A

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
Q

Osteogenesis imperfecta - defect in synthesis of?

A

Type I collagen

155
Q

Skeletal Dysplasias

  • what kind of treatment is provided?
A

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
Q

In skeletal dysplasias, is growth hormone effective?

A

No.

It is generally ineffective.

157
Q

Most common skeletal dysplasia?

A

Achondroplasia is the most common type

autosomal dominant

158
Q

Connective tissue is an umbrella term for?

A

Tendons, ligaments, cartilage and bone

Mesoderm

159
Q

Marfan’s syndrome

A

Autosomal dominant / sporadic mutation of fibrillin gene

Tall stature

Long limbs

Hypermobility

Associated with:

> High arched palate
> Scoliosis
> Pectus excavatum 
> Lens dislocation
> Aortic aneurysm
> Cardiac valve incompetence.
> Spontaneous pneumothorax
> Joint dislocations
160
Q

Fibrillin is required for?

A

Scaffolding for elastin

Fibrillin gene is defective in Marfan’s

161
Q

Ehlers-Danlos Syndrome

A

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

That guy in the Guinness world records with really stretchy skin.

162
Q

Down Syndrome

A

Trisomy 21

Joint laxity predisposes to recurrent dislocations and OA

Atlanto-axial instability –> spinal cord compression (myelopathy)

163
Q

Duchenne Muscular Dystrophy

A

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
Q

Becker’s muscular dystrophy

A

Milder form of Duchenne Muscular Dystrophy

Survival into 30s and 40s

165
Q

Gower’s sign

A

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
Q

Talipes Equinovarus

A

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

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
Q

Ponseti technique

A

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
Q

When is there a developing limb bud in gestation?

A

Around 4-6 weeks

169
Q

Syndactyly

A

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
Q

Polydactyly

A

Extra digit

Treatment by surgical removal.

171
Q

Fibular hemimelia

A

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
Q

Radial club hand

A

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
Q

Proximal focal femoral deficiency

A

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
Q

Obstetric Brachial Plexus Injury

A

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
Q

Erb’s Palsy

A

Congenital defect

Upper brachial plexus (C5 & 6 roots)

176
Q

Klumpke’s Palsy

A

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
Q

Cerebral palsy

A

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
Q

Types of cerebral palsy

A

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
Q

Cerebral palsy -

spasticity/ joint contractures/ hip dislocation treatment

A

Baclofen

Botox injection

Neurosurgical procedures (rhizotomy)

Joint contractures –> surgical release, fusions

Hip dislocations –> THR, osteotomy, excision, arthroplasty

180
Q

Spina bifida

Mild
Severe

A

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
Q

Polio (poliomyelitis)

A

> 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.

MSK (11 decks)

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