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ΩΩ 2a Bateman - Systems Based > Musculoskeletal System > Flashcards

Musculoskeletal System Flashcards

1
Q

What are the scans in a trauma series?

A

3 X-rays

  1. AP chest
  2. AP pelvis
  3. Lateral cervical spine
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2
Q

What complex imaging can be ordered after a trauma series?

A
  1. CT head
  2. CT abdo
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3
Q

What is HLA B27 associated with?

A

Spondyloarthritis (SpA) such as:

Ankylosing spondylitis

Psoriatic arthritis

Reactive arthritis

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4
Q

WHAT IS ANKYLOSING SPONDYLITIS OR “AXIAL SPONDYLOARTHRITIS”?

A
  1. Inflammatory arthritis of the spine, rib cage and sacroiliac joints
  2. Eventually leading to new bone formation and fusion of the joints
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5
Q

When does ankylosing spondylitis start?

A

Typically starts in late teenage years/ 20s.

More common in Men.

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6
Q

What are the clinical features of ankylosing spondylitis?

A
  1. Low back pain – particularly at night - improves with activity not improved with rest
  2. Morning stiffness
  3. Inflammatory arthritis of the “axial skeleton”, which results in new bone formation and “fusion” of the vertebrae/costovertebral
  4. Enthesitis (inflammation of junction between ligament/ tendon and bone),
  5. Acute anterior uveitis (irits) ie inflammation of the anterior chamber of the eye
  6. Peripheral arthritis (often large joint oligoarthritis but in PsA can be small joint just like RA)
  7. Skin psoriasis
  8. May also have (sub-clinical) inflammatory bowel disease
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7
Q

What does SPINEACHE help with and what does it represent?

A
  • *S**ausage digit (dactylitis)
  • *P**soriasis - Onycholysis
  • *I**nflammatory back pain
  • *N**SAID good reponse
  • *E**nthesitis (heel)
  • *A**rthritis
  • *C**rohn’s/ Colitis/ elevated CRP*
  • *H**LA B27
  • *E**ye (uveitis)

Symptoms of SpA.

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8
Q

What are Syndesmophytes?

A

Bone growth originating inside ligaments.

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9
Q

What is the proposed method for Ankylosing spondylitis?

A

Delayed damage theory”

ie once inflammation has occurred – new bone formation is inevitable, therefore once treatment started, new bone continues to form for some time after

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10
Q

What are the tests for ankylosing spondylitis?

A
  1. Diagnosis is clinical, supported by imaging
  2. MRI is most sensitive and better at detecting early disease.
  3. Sacroiliitis is the earliest X-ray feature, but may appear late: look for irregularities, erosions, or sclerosis affecting the lower half of the sacroiliac joints, especially the iliac side.
  4. Syndesmophytes common later stages on radiography
  5. Apical fibrosis - Chest X-ray
  6. ‘Bamboo spine’ In later stages, calcification of ligaments with ankylosis lead to this
  7. FBC (normocytic anaemia), increased ESR, increased CRP, HLA B27+ve (not diagnostic).
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11
Q

What is the ASAS criteria used for? What does the criteria require?

A
  1. Ankylosing spondylitis.
  2. Confirmation of sacroiliitis on imaging plus more than or equal to 1 SpA feature
  3. or HLA-B27 plus more than or equal to 2 SpA features.
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12
Q

What is the treatment for ankylosing spondylitis?

A

Exercise

NSAIDS

  1. Ibuprofen or Naproxen.

TNF alpha blockers

  1. Golimumab
  2. Infliximab
  3. Etanercept

Local steroid injections

Surgery includes hip replacement/spinal osteomy

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13
Q

WHAT IS PSORIATIC ARTHRITIS?

A

Psoriatic arthritis is a form of arthritis affecting the joints in people with the skin condition psoriasis

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14
Q

What are the clinical manifestations of disease for Psoriatic Arthritis?

A
  1. Sarcoilitis (Similar to AS)
  2. Arthritis mutilans
  3. DIPJ only, (Distal interphalangeal joint)
  4. Oligoarthritis (2-4 joints in first 6 months) (Like RA) Large joint - Asymmetrical
  5. Polyarthritis = >5 joints RA like (Asymmetrical small joint).

Also
Dactylitis
Nail changes

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15
Q

What is arthritis mutilans?

A

An extremely severe form of chronic rheumatoid or psoriatic arthritis characterized by resorption of bones and the consequent collapse of soft tissue.

When this affects the hands, it can cause a phenomenon sometimes referred to as ‘telescoping fingers.’

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16
Q

What are the investigations for psoriatic arthritis?

A
  1. ‘Pencil-in-cup’,
    • ​​Erosive changes, with deformity in severe cases.
  2. Nail changes in 80%
  3. Synovitis (dactylitis)
  4. Rashes
    • Acneiform rashes and palmo-plantar pustulosis.
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17
Q

What is the treatment for Psoriatic Arthritis?

A

Similar to RA

  1. NSAIDs
    • ​​For mild peripheral/arthritis/mild axial disease
  2. DMARDs
    • Methotrexate, ciclosporin
  3. IL12/23 blockers
    • Ustekinumab
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18
Q

What are patients with psoriatic arthritis likely to develop?

A

Cardiovascular disease

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19
Q

WHAT IS REACTIVE ARTHRITIS?

https://www.youtube.com/watch?v=dzQwIqc6dQE

A

Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually gastro-intestinal or genital.

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20
Q

What is the epidemology of reactive arthritis?

A

Mostly Male

20-40

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21
Q

What are some causes of reactive arthritis?

A

Gut associated infections
Salmonella
Shigella

Sexually acquired infection (NSU)
Chlamydia
Ureaplasma urealyticum.

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22
Q

What is Reiter’s syndrome?

A

Classical triad of

Arthritis (large joints)

Urethritis.

Conjunctivitis

CANT PEE, CANT SEE, CANT CLIMB A TREE

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23
Q

What are some symptoms of reactive arthritis?

A

Iritis

Keratoderma blenorrhagica
Brown, raised plaques on soles and palms

Circinate Balanitis
Painless penile ulceration secondary to Chlamydia

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24
Q

What are some differential diagnosis of reactive arthritis?

A

Hot swollen joint

Think

  1. Septic arthritis.
  2. Gout.
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25
Q

What are some tests for reactive arthritis?

A
  1. Blood test
    • Raised ESR/CRP
  2. Aspirate joint
    • To exclude infection/crystals.
  3. Urethral swab, stool culture
    • Show infection.
    • Contact tracing if necessary.
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26
Q

What is the management for reactive arthritis?

A
  1. Symptomatic
    • Analgesia, NSAIDS, intra-articular steroid
    • Symptoms rarely last more than 12 months
    • Oral prednisolone if not responding to NSAIDS and polyarthropathy
  2. Sulfasalazine or methotrexate
    • If symptoms >6 months. (Consider)

Treating the original infection may make little difference to the arthritis.

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27
Q

WHAT IS BEHCET’S SYNDROME?

A

Behcet’s syndrome is a complex multisystem disorder associated with presumed autoimmune-mediated inflammation of the arteries and veins. The precise aetiology has yet to be elucidated however.

The classic triad of symptoms are

  1. Oral ulcers
  2. Genital ulcers
  3. Anterior uveitis
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28
Q

WHAT IS ENTEROPATHIC ARTHRITIS?

A

Inflammatory arthritis associated with the occurrence of an inflammatory bowel disease (IBD), the two best-known types of which are ulcerative colitis and Crohn’s disease.

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29
Q

What are the symptoms of enteropathic arthritis?

A
  1. Peripheral synovitis
  2. Asymmetric lower limb arthritis
  3. Apthous ulceration
  4. Uveitis
  5. Erythema Nodosum
  6. AS occurs in 7% of patients with IBD.
  7. 50% of patients with IBD and HLA-B27 +ve develop sacroiliitis
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30
Q

What are the investigations for enteropathic arthritis?

A
  1. Leucocytosis
  2. HIGH - ESR + CRP
  3. Hypergammaglobulinaemia
  4. Negative RF
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31
Q

What are the treatments for enteropathic arthritis?

A

No specific cure

  1. Splint joints
  2. NSAIDS or local steroid injections
  3. Underlying bowel disease treated
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32
Q

What are some examples of inflammatory joints?

A
  1. Auto-immune.
  2. Crystal arthritis.
  3. Infection.
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33
Q

WHAT IS RHEUMATOID ARTHRITIS?

https://www.youtube.com/watch?v=6ylzE5usu7o

A

Auto-immune inflammatory disease affecting joints and other systems

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34
Q

What is the epidemology of rheumatoid arthritis?

A
  1. Most common inflammatory arthritis~1% population
  2. Women more common
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35
Q

What are the properties of an inflammatory joint disorder?

A

Pain eases with use

Stiffness
Significant (>60 mins)
Early morning/ at rest (evening)

Swelling Synovial +/- bone

Pt demographics
Eg young, psoriasis, family history

Joint distribution
Eg hands & feet

Responds to NSAIDs

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36
Q

What are the properties of a degenerative arthritis?

A
  1. Pain increases with use
    • Clicks/ clunks
  2. Stiffness
    • Not prolonged (<30 mins)
    • Morning/ evening
  3. Swelling
    • None, bony
    • Not clinically inflamed
  4. Pt demographics
    • Eg older, prior occupation/ sport
  5. Joint distribution
    • Eg 1st CMCJ, DIPJ, knees
  6. Less convincing response to NSAIDs
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37
Q

What is the cause of rheumatoid arthritis?

A

Combination of genetic and environment

  1. HLA DR4
  2. Ciagrette smoke or infection
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38
Q

What are the symptoms of rheumatoid arthritis?

A
  1. Joint pain often worse in morning
    • (may improve with activity)
  2. Morning stiffness-several hours
  3. Loss of function
  4. General-fatigue, malaise
  5. Extra-articular involvement.
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39
Q

What is some signs of rheumatoid arthritis?

A

Symmetrical small joints
MCP
PIP

  1. Ulnar deviation of the fingers.
  2. Boutonnière and swan-neck deformities of fingers or Z-deformity of thumbs occur.
  3. Baker (poploteal cyst)
  4. Larger joints can be involved - atlanto-axial joint subluxation may threaten the spinal cord (rare).
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40
Q

What are some eye involvements of rheumatoid arthritis?

A

Sicca (dry eyes)

Secondary Sjorgren’s syndrome

Episcleritis

Scleritis (corneal ulceration).

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41
Q

What are some investigations for rheumatoid arthritis?

A
  1. Blood tests
    • Rheumatoid Factor - 80% - NEGATIVE MEANS GOOD PROGNOSIS
    • Anti-Cyclic Citrullinated Peptide (Anti-CCP) antibody c - 80% - MARKER OF PROGNOSIS
    • High ESR/CRP
    • Anti-nuclear antibody (ANA) < 50%
  2. X-Ray
    • Loss joint space
    • juxta-articular osteopenia
    • Soft tissue swelling
    • Sublaxation
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42
Q

What are the management for rheumatoid arthritis?

A
  1. DMARDS
    • Methotrexate - FIRST LINE WITH STEROIDS
    • Can switch sulfasalazine - close allergy to aspirin caution!
  2. NSAIDS
    • Symptom relief, no efect on disease progression
    • Paracetamol and weak opiates are rarely effective
    • Physio- and occupational therapy, eg for aids and splints
  3. TNF-inhibitors
  4. Acute Flares
    • Methylprednisolone
    • Rapidly reduce symptoms and inflammation
  5. Rituximab - B cells
  6. Abatacept - T cells
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43
Q

What does a rheumatoid arthritis patient need to have before going for surgery?

A
  1. Anteroposterior and lateral cervical spine radiographs
  2. Incase of atlantoaxial subluxation
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44
Q

WHAT IS FELTY’S SYNDROME?

A
  1. RA
  2. Splenomegaly
  3. Low white cell count
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45
Q

WHAT IS A VASCULITIS?

https://www.youtube.com/watch?v=ise3cEqmEqU

A

Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow

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46
Q

What is the cause of vasculitis?

A

Autoimmune disease, confusing part of the blood vessel as foregin

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47
Q

How do you classify vasculitis?

A

Size of vessel
Small – medium - large vessel disease

Target organ(s)

Anti-neutrophil cytoplasmic antibodies (ANCA)
Present or not

Primary vs secondary

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48
Q

What are the different classifications of vasculitis?

What are some examples?

A

Large

Medium

Small

ANCA +ve vasculitis

ANCA –ve vasculitis

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49
Q

How does vasculitis present?

A

No single typical presentation

Systemically unwell
Fever
Arthralgia/arthritis
Rash
Weight loss
Headache
Footdrop
Major event eg stroke, bowel infarction.

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50
Q

What are some common tests for vasculitis?

A

ESR/CRP increase. ANCA may be +ve.

Increase in Creatinine if renal failure.

Urine: proteinuria, haematuria, casts on microscopy.

Angiography ± biopsy may be diagnostic.

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51
Q

What is ANCA-associated vasculitis?

A

Antineutrophil cytoplasmic antibodies

Small/medium vessel vasculitis

Specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes.

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52
Q

What are the investigations for ANCA-associated vasculitis? What are the two major patterns?

A

Detected with indirect immunofluorescence microscopy

Two major patterns

Cytoplasmic ANCA (c-ANCA) Major antigen Proteinase 3

Peri-nuclear ANCA (p-ANCA) Major antigen Myeloperoxidase (MPO)

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53
Q

WHAT IS GIANT CELL (TEMPORAL) ARTERITIS?

https://www.youtube.com/watch?v=ise3cEqmEqU

A

Granulomatous arteritis of aorta + larger vessels-extracranial branches of carotid arteries

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54
Q

What is the epidemology of Giant cell arteritis?

A
  1. Primarily>50yrs old
  2. Incidence increases with age
  3. Twice as common in women
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55
Q

How does giant cell (temporal) arteritis present?

A
  1. Headache
  2. Scalp tenderness
  3. Jaw claudication
  4. Acute blindness
  5. Non specific malaise
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56
Q

What does the American College of Rheumatology Diagnostic criteria require for GCA?

A

3 or more of:

  1. Age>50
  2. New headache
  3. Temporal artery tenderness or decreased pulsation
  4. ESR > 50 mm/h
  5. Abnormal artery biopsies showing necrotizing arteritis with mononuclear infiltrate or granulomatous inflammation
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57
Q

What is AION(Arteritic) anterior ischemic optic neuropathy ?

A

Sudden, painless, monocular and severe visual loss.

May be preceded by transient visual loss

The optic disc becomes pale and swollen, often with flame-shaped haemorrhages at the margin.

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58
Q

What are the tests for giant cell arteritis?

A
  1. Raised inflammatory markers
    • ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
    • CRP may also be elevated
  2. Temporal artery biopsy
    • Skip lesions may be present
  3. Note creatine kinase and EMG normal
  4. VISION TESTING
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59
Q

What is the treatment for GCA?

A

Corticosteroids
Prednisolone

Prophylaxis of osteoporosis
Lifestyle advice
Calcium/Vitamin D + Bisphosphonate
DEXA scan

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60
Q

WHAT IS POLYARTERITIS NODOSA (PAN)?

https://www.youtube.com/watch?v=ise3cEqmEqU

A

PAN is a necrotizing vasculitis that causes aneurysms and thrombosis in medium-sized arteries

Leading to infarction in affected organs, with severe systemic symptoms.

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61
Q

What is the cause of polyarteritis nodosa?

A

Some associated with Hep B

Others unknown

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62
Q

What is the pathology of polyarteritis nodosa?

A

Immune cells confuse the vessel wall with hep B virus

Causes transmural inflammation
All layers die

Fibosis as vascular wall heals

This process is fibrinoid necrosis

Anneurysms occur through weakness of artery

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63
Q

What are the symptoms of polyarteritis nodosa?

A
  1. Typically systemic features
    • Fever, malaise, weight-loss, arthralgia, myalgia
  2. Skin
    • Rash and ‘punched out’ ulcers
  3. Renal
    • Hypertension
  4. Cardiac
    • Angina or MI
  5. GI
  6. GU
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64
Q

What are the tests for polyarteritis nodosa?

A
  1. Gold standard = biopsy
  2. Often WCC increase
  3. Normocytic Anaemia
  4. ESR increase
  5. Angiography
    • String of beads
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65
Q

What is the treatment of PolyArteritis Nodosa?

A
  1. Control BP
  2. Corticosteroids
    Prednisolone
  3. Cyclophosphamide/Azathioprine
  4. Hepatitis B should be treated with an antiviral after initial treatment with steroids.
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66
Q

WHAT IS POLYMYALGIA RHEUMATICA (PMR)?

A

Polymyalgia rheumatica is a disease of the muscles and joints characterized by muscle pain and stiffness, affecting both sides of the body, and involving the shoulders, arms, neck, and buttock areas.

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67
Q

What disease is common with polymyalgia rheumaticia?

A

PMR and GCA share the same demographic characteristics and, although separate conditions, the two frequently occur together

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68
Q

What is the epidemology of polymyalgia rheumatica (PMR)?

A

Over 50 years olds

Women more than men

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69
Q

What is the pathogenesis of Polymyalgia rheumatica (PMR)?

A

Unknown

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70
Q

What are the symptoms of polymyalgia rheumatica?

A
  1. Rapid onset <1 month
  2. Tenderness and morning stiffness
  3. Bilateral aching
  4. Tenosynovitis
  5. Carpal tunnel syndrome
  6. B symptoms
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71
Q

What are the investigations for polymyalgia rheumatica?

A
  1. Note creatinine kinase levels are normal (helping to distinguish from myositis/myopathies)
  2. EMG normal
  3. CRP increased
  4. ESR increased
  5. ALP is increased
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72
Q

What are the treatment options for polymyalgia rheumatica?

A

Corticosteroids
Prednisolone

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73
Q

What is osteoarthritis?

https://www.youtube.com/watch?v=sUOlmI-naFs&t=63s

A

A non inflammatory disorder

Deterioration of articular cartilage

Formation of new bone of the joint surfaces and margins

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74
Q

What is the cause of osteoarthritis?

A

Unknown but risk factors have a big impact

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75
Q

What is the prevalence of osteoarthritis?

A

Commonest joint disorder

M=F

<45yrs prevalence greater in males

>55yrs prevalence greater in females

Common in Caucasians

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76
Q

What are the different classifications of osteoarthritis?

A

Primary or idiopathic
No identifiable predisposing cause

Secondary
When an underlying cause is implicated

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77
Q

What does osteoarthritis look like on examiantion?

A
  1. Squaring of the thumb
  2. Swelling
  3. Muscle wasting
  4. Deformity
  5. Decreased ROM
  6. Crepitus (cracking or clicking of joint movement)
  7. Osteophytes palpable
  8. Joint instability (later on)
  9. Heberdens
  10. Bouchards
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78
Q

What are Heberdens and Bouchards?

A

Heberden’s nodes are hard or bony swellings that can develop in the distal interphalangeal joints (DIP)

Bouchard’s nodes are hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints

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79
Q

What investigations can you do for osteoarthritis?

A

Imaging
X-RAY DIAGNOSTIC

Laboratory Tests
Blood & Synovial Fluid

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80
Q

What are you looking for in a X-ray of osteoarthritis?

A

Loss of joint space

Osteophytes (bony projection associated with the degeneration of cartilage at joints.)

Subarticular sclerosis (denser area of bone just under the cartilage in your joint, appearing as abnormally white bone along the joint line)

Subchondral cysts (The cartilage tries to repair itself, the bone remodels, the underlying (subchondral) bone hardens, and bone cysts form.)

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81
Q

What labratory tests could you do for osteoarthritis?

A

Blood
ESR, FBC, Rh Factor, Calcium, ALP, Electrophoresis
All Normal

Synovial Fluid Analysis
Non specific in OA

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82
Q

What are the different types of management of osteoarthritis?

A
  1. All patients should be offered help with weight loss, given advice about local muscle strengthening exercises and general aerobic fitness
  2. FIRST LINE
    • Paracetamol and topical NSAIDs are first-line analgesics. Topical NSAIDs are indicated only for OA of the knee or hand
  3. SECOND-LINE
    • Oral NSAIDs/COX-2 inhibitors, opioids, capsaicin cream and intra-articular corticosteroids. A proton pump inhibitor should be co-prescribed with NSAIDs and COX-2 inhibitors. These drugs should be avoided if the patient takes aspirin
  4. non-pharmacological treatment options include supports and braces, TENS and shock-absorbing insoles or shoes
  5. if conservative methods fail then refer for consideration of joint replacement
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83
Q

WHAT IS SYSTEMIC LUPUS ERYTHEMATOSUS?

https://www.youtube.com/watch?v=0junqD4BLH4

A

SLE is a multisystemic autoimmune disease in which autoantibodies are made against a variety of autoantigens (eg ANA).

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84
Q

What is the epidemology of systemic lupus erythematosus?

A

Women of child bearing age

Genetic Association:

HLA: DR2, DR3
C4 A Null Allele

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85
Q

What are the clinical features of SLE?

A
  • *S**erositis (pleuritis, pericarditis)
  • *O**ral ulcers
  • *A**rthritis
  • *P**hotosensitivity
  • *B**lood (all are low - anaemia, leukopemnia, thrombocytopenia)
  • *R**enal (protein)
  • *A**NA
  • *I**mmunologic (DSm DNA)
  • *N**eurologic (psych,seizures)
  • *M**alar rash
  • *D**iscoid Rash
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86
Q

What immunology/testing can be done for SLE?

A
  1. Double stranded DNA antibody (Anti-dsDNA)
    • MOST Specific
  2. Anti-nuclear antibody
    • ​​Not specific for lupus (screening test), 99% present though - RULE OUT
  3. Other antibodies:
    • Rheumatoid factor
    • Cardiolipin antibodies, Anti Ro, La, Sm, RNP
    • ESR increase but normal CRP
  4. HIGH CRP INDICATES UNDERLYING INFECTION
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87
Q

What does the SLE : ACR 1982 Classification Criteria
require for diagnosis of SLE?

A

Four or more of the following.

  1. Malar rash
  2. Discoid rash
  3. Photosensitivity
  4. Oral ulcers
  5. Arthritis
  6. Serositis
  7. Renal disorder
  8. Neurological disorder
  9. Haematological disorder
  10. Immunological disorder
  11. Anti-nuclear antibody
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88
Q

What is the management for SLE?

A
  1. Topical steroids and sunblock
    • Rashes
  2. NSAIDS and Hydroxychloroquine (retinal problems)
    • Joint and skin symptoms.

If internal organ involvement

  1. Steroids
    • Suppress immune syste
  2. Immunosupressants
    • ​​Azathiprine, methotrexate and mycophenolate are used as steroid-sparing agents.
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89
Q

What are the causes of drug induced lupus?

What is the antibody associated with this?

A
  1. Procainamide
  2. Hydralazine
  3. Anti-histone
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90
Q

WHAT IS ANTIPHOSPHOLIPID SYNDROME?

A

Antibodies against protein in the phospholipid membrane

Associated with Lupus

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91
Q

What does antiphoshpholipid syndrome cause?

A

Antiphospholipid antibodies (anticardiolipin & lupus anticoagulant) cause CLOTS:

  1. Coagulation defect - Prolonged APTT
  2. Livedo reticularis (mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin)
  3. Obstetric (recurrent miscarriage)
  4. Thrombocytopenia (reduced platelets)
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92
Q

How do you diagnose antiphospholipid syndrome?

A
  1. Lupus anticoagulant

And/or

  1. Cardiolipin Antibodies

Positive on 2 occasions 12 weeks apart

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93
Q

How can you treat antiphospholipid syondrome?

A

Primary thromboprophylaxis

  1. Low-dose aspirin

Secondary thromboprophylaxis

  1. Initial venous thromboembolic events:
    Lifelong warfarin with a target INR of 2-3
  2. Recurrent venous thromboembolic events:
    Lifelong warfarin; if occurred whilst taking warfarin then consider adding low-dose aspirin, increase target INR to 3-4
  3. Arterial thrombosis
    Should be treated with lifelong warfarin with target INR 2-3
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94
Q

WHAT IS RAYNAUD’S PHENOMENON?

https://www.youtube.com/watch?v=n809IRTYYeU

A

Discoloration of the fingers and/or the toes

After exposure to changes in temperature or emotional events.

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95
Q

What are the colour changes of Raynaud’s?

A

Fingers or toes ache and change colour:

pale (ischaemia) to

blue (deoxygenation) to

red (reactive hyperaemia)

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96
Q

How is Raynaud’s phenomenon caused?

A

Primary
Raynaud’s disease

Secondary
Connective tissue diseases e.g. SLE
Drugs - Beta Blockers
Vascular damage
Raynaud’s syndrome

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97
Q

What are the symptoms of raynaud’s?

A

Colour changes

Numbness, tingling and pain

Could cause tissue death

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98
Q

What is the diagnosis of raynaud’s phenomenom?

A
  1. Description of episodes
  2. Explore underlying condition
  3. Nailfold capillary microscopy
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99
Q

What is the treatment for Raynaud’s phenomenon?

A
  1. Vasodilators
    • Calcium channel blockers - Nifedipine
    • Sildenafil
  2. IV prostacyclin infusions
  3. Avoid triggers
  4. Stop smoking
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100
Q

WHAT IS SYSTEMIC SCLEROSIS?

https://www.youtube.com/watch?v=ErchMUH0oXY

A

Autoimmune disease of the connective tissue

Thickening of the skin caused by accumulation of collagen

And by injuries to small arteries

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101
Q

What are the different types of systemic sclerosis?

A
  1. Limited cutaneous
  2. Diffuse cutaneous
  3. Scleroderma
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102
Q

What does limited systemic sclerosis show?

A

Mainly affects face and sital limbs predominately

  1. Calcinosis (calcium deposits form in the skin)
  2. Raynaud’s phenomenon
  3. Oesophageal reflux, strictures
  4. Sclerodactyly (localized thickening and tightness of the skin of the fingers or toes)
  5. Telangectasia (widened venules (tiny blood vessels) cause threadlike red lines or patterns on the skin.)
  6. Pulmonary arterial hypertension
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103
Q

What is the antibody for limited systemic sclerosis?

A

Anti-centromere

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104
Q

What does diffuse (skin) systemic sclerosis show?

A

Mainly affects trunk and proximal limbs predominately

Diffuse affects organs too

  1. Proximal scleroderma
  2. Pulmonary fibrosis
  3. Bowel involvement
  4. Myositis
  5. Renal crisis: hypertension
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105
Q

What is the antibody for diffuse systemic sclerosis?

A
  1. Antibodies
    • Scl-70
    • Nucleolar
    • RNA polymerase
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106
Q

What are the investigations for systemic sclerosis?

A
  1. Immunological tests
    • Anti-nuclear antibodies ++
    • Anti-Scl-70, anti-centromere & anti-nucelolus +
  2. Haematological
    • Normocytic anaemia
    • High ESR
  3. Radiological
    • X-rays - calcium in skin of fingers
    • Barium swallow - oesophageal involvement
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107
Q

What is the management of systemic sclerosis?

A
  1. NO CURE
  2. Supression of immune system with
    • Cyclophosphamide
  3. Treat symptoms
    • Raynaud’s phenomenon
    • Oesophageal reflux
    • Sjogren’s syndrome
  4. Kidney problems
    • ACE inhibitor
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108
Q

WHAT IS SJÖGREN’S SYDROME?

https://www.youtube.com/watch?v=d3qPMecBrY0

A

Primary Sjogren’s syndrome is the association of

keratoconjunctivitis sicca and/or xerostomia, with

rheumatoid arthritis or other connective tissue disorder

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109
Q

Which glands are mainly affected in sjorens?

A
  1. Lacrimal and salivary glands (parotid)
  2. T cell mediated
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110
Q

What are some systemic involvements of sjorens?

A

Polyarthritis/arthralgia

Raynaud’s

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111
Q

What are the features of Sjögren’s Syndrome?

A

Sicca complex:
Dry eyes
Dry mouth
Enlarged salivary glands

Systemic features
InflammatoryArthritis
Rash (sub-acute lupus)
Neuropathies
Vasculitis
Neonatal lupus

ASSOCIATED WITH LYMPHOMA

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112
Q

What would the tests show to diagnose Sjögren’s Syndrome?

A
  1. Schirmer’s test
    Conjunctival dryness
  2. Biopsy
    Lymphocyte infiltration in glands
  3. Auto-antibodies
    ANA (in most) 70%
    Rheumatoid factor 50%
    Anti-Ro 70%
    Anti-La 30%
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113
Q

What is the management of Sjogren’s?

A
  1. Tear and saliva replacement
    • Artifical saliva and tears
    • Pilocarpine may stimualte saliva production
  2. Immuno-suppression for systemic complication
    • ​Prednisolone
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114
Q

WHAT IS DERMATOMYOSITIS/POLYMYOSITIS?

A

Systemic connective tissue diseases which are characterised by acute and chronic inflammation of striated muscle.

In dermatomyositis there is an accompanying dermatitis

Assocaited with malignancy

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115
Q

What is affected most in Dermatomyositis/Polymyositis?

A

Muscle and skin mainly affected: rash and muscle weakness

Lungs can be affected (Interstitial lung disease)

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116
Q

What the differences between polymyositis vs dermatomyositis?

A

Polymyositis tends to have a chronic natural history and is less responsive to therapy

Dermatomyositis can be life-threatening, but is more responsive to treatment

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117
Q

What are the symptoms for myosits?

A
  1. Muscle tenderness
  2. Proximal, symmetrical muscle weakness
  3. May present as difficulty rising from a chair or climbing stairs
  4. Dysphagia
  5. Dysphonia
  6. Respiratory failure
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118
Q

What are the extra symptoms for dermatomyositis?

A
  1. Macular rash
  2. Rash on eyelids - Heliotrope rash
  3. Hand Rash - Gottron’s papules
  4. Nails - Periungal telangectasias + Cuticular hypertrophy with punctate infarcts
  5. Neck - poikiloderma
  6. Spots - Calcinosis cutis
119
Q

What investigations can you do for Dermatomyositis/Polymyositis?

A
  1. Muscle enzymes (serum creatinine kinase + serum aldolase)
  2. EMG to identify to do
    • –> Muscle/skin biopsy - muscle necrosis, phagocytosis of muscle fibres + inflammatory infiltrate
  3. Autoantibodies such as ANF and RF are often positive
  4. ANA positive
120
Q

What is the management for Dermatomyositis/Polymyositis?

A
  1. Steroids - Prednisoline - 20-60mg daily
  2. Immunosuppressive drugs - azathioprine 150mg/day
  3. Hydroxychloroquine (skin rash)
121
Q

WHAT IS LOWER BACK PAIN?

A

Pain of the lower back

122
Q

When does mechanical lower back pain present?

A

Ages of 20-55.

123
Q

Where is lower back pain?

A

Located in lumbrosacral region, buttocks and tighs.

124
Q

What are the red flags for possible serious spinal pathology?

A
  1. Age on onset less than 20 or greater than 55.
  2. Violent trauma e.g. fall from a heigh
  3. Constant progressive, non-mechanical back pain
  4. Thoracic pain
  5. PMH carcinoma, systemic steroids, drug abuse, HIV
  6. Systemically unwell, weight loss
  7. Persisting servere resistriction of lumbar flexion
  8. Structural deformity
125
Q

What examination would you do for a patient with lower back pain?

A

With the patient standing, gauge the extent and smoothness of lumbar forward/ lateral flexion and extension.

Clinical tests for sacroiliitis: direct pressure, lateral compression, sacroiliac stretch test (pain on adduction of the hip, with the hip and knee flexed).

Signs of generalized disease—eg malignancy. Examine other systems (eg abdo- men) as pain may be referred.

126
Q

What are the causes of lower back pain?

A

15–30yrs:
Prolapsed disc, trauma, fractures, ankylosing spondylitis, spondylolisthesis (a forward shift of one vertebra over another, which is congenital or due to trauma), pregnancy.

30–50yrs:
Degenerative spinal disease, prolapsed disc, malignancy (primary or secondary from lung, breast, prostate, thyroid or kidney ca).

>50yrs:
Degenerative, osteoporotic vertebral collapse, Paget’s, malignancy, myeloma, spinal stenosis.

127
Q

How can a person damage their lower back?

A

SIngle excessive force

Static loading

Repetative wear and tear

A bit of reality

128
Q

What investigations can you do for back pain?

A

Arrange relevant tests if you suspect a specific cause, or if red flag symptoms:

FBC,
ESR and CRP (myeloma, infection, tumour), U&E, ALP (Paget’s), serum/urine electrophoresis (myeloma), PSA.

X-rays
Exclude bony abnormality but are generally not indicated.

MRI
Is the image of choice and can detect disc prolapse, cord compression (fig 1), cancer, infection or inflammation (eg sacroiliitis).

129
Q

What is the management for back pain?

A
  1. For non-specific back pain, focus on education and self-management.
  2. Continue with normal activites and be active.
  3. Manage pain
    • NSAIDS - FRIST LINE
    • Codeine
  4. Physiotherapy, acupuncture or an exercise programme if not improving.
  5. Psychosocial issues
  6. Surgery
130
Q

WHAT IS OSTEOMYELITIS?

https://www.youtube.com/watch?v=kta5vCz_8Lw

A

Infection localized to bone

Metaphysis - Kids

Epiphysis - Adults

131
Q

What are the different types of osteomyelitis? Which bacteria are involved?

A
  1. Pyogenic (involving or relating to the production of pus)
    • S. aureus
    • Salmonella in sickle cell patients
  2. Non-pyogenic
    • M. tb
132
Q

How can the infection of bone take place?

A
  1. Direct
  2. Contiguous
  3. Haematogenous
133
Q

What are the host factors for osteomyelitis?

A
  1. Behavioural factors
    • I.e. risk of trauma
  2. Vascular supply
    • Arterial disease
    • Diabetes mellitus
    • Sickle cell disease
  3. Pre-existing bone / joint problem
    • Inflammatory arthritis
    • Prosthetic material
  4. Immune deficiency
134
Q

What are the chronic changes occur to the bone as a result of osteomyelitis?

A
  1. Chronic changes
    • Necrotic bone ‘sequestra’
    • New bone formation ‘involucrum’
    • Neutrophil exudates
    • Lymphocytes & histiocytes
135
Q

How are sequestra and involucrum produced?

A

Interruption of periosteal blood supply causing necrosis.

Leaves pieces of separated dead bone ‘sequestra’

New bone forms here ‘involucrum’.

136
Q

What are the signs and symptoms of osteomyelitis?

A

Systemic:
Fever, rigors, sweats, malaise

Local:
Acute OM
Tenderness, warmth, erythema, and swelling

Chronic OM
Tenderness, warmth, erythema, and swelling
Draining sinus tract
Deep / large ulcers
Non-healing fractures

137
Q

What tests can you do for osteomyelitis?

A
  1. MRI - INVESTIGATION OF CHOICE FOR OSTEOMYELITIS
  2. X-rays
  3. Aspiration of pus + culture
  4. FBC/WCC
    • Rasied or normal
  5. CRP/ESR
    • Raised
138
Q

What is the treatment for osteomyelitis?

A
  1. Antibiotics
    • Flucloxacillin and fusidic acid, clindamycin
  2. Surgical
  3. Splintage
  4. Supportive
139
Q

WHAT IS SEPTIC ARTHRITIS?

https://www.youtube.com/watch?v=Tz07Uqx7_VY

A

Inflammation of a joint that’s caused by infection.

140
Q

What is septic arthritis caused by? What does it affect?

A
  1. Staphylococcus aureus is the most common agent
  2. In young adults who are sexually active, Neisseria gonorrhoeae is the most common organism (disseminated gonococcal infection)

Also:

  1. Streptococcus pyogenes
  2. pneumococcus
141
Q

What are the risk factors for septic arthritis?

A

Pre-existing joint disease

Vascular e.g. diabetes mellitus,

Immunosuppression

Chronic renal failure

Recent joint surgery

Prosthetic joints, IV drug abuse, age >80yrs

142
Q

What are the symptoms for septic arthritis?

A
  1. Overlying skin is red and warm
  2. Swollen, painful joint
  3. Pain on movement - movements are always diminished and often absent if the joint is rigid due to pain and spasm
  4. General features include tachycardia and swinging pyrexia.
143
Q

What tests can you do for septic arthritis?

A
  1. Joint aspiration - FIRST LINE for synovial fluid microscopy and culture
  2. Blood cultures
  3. X-rays and CRP may be normal
144
Q

What are the differential diagnosis for septic arthritis?

A

Crystal arthropathies.

145
Q

What are the treatment options for septic arthritis?

How long is treatment?

A
  1. Antibiotics IV
    • staphylococci and streptococci in adults, and, additionally, Haemophilus in children
  2. Joint drainage
  3. Flucloxacillin
  4. Clindamycin if penicillin allergic
  5. Vancomycin IV if MRSA
  6. Cefotaxime IV if gonococcal or Gram –ve or- ganisms suspected

4-6 WEEKS OF TREATMENT

146
Q

WHAT IS BONE CANCER?

A

Cancer of the bone

147
Q

What are the red flags signs for a MSK malignancy?

A

Rest pain

Night pain

Lump present – tender, enlarging, deep to fascia, above 5cm in diameter

Loss of function

Neurological symptoms

Unwell / Weight loss

148
Q

How do you name the different types of tumour?

A
  • Prefix will be tissue of origin, for example:
  • Osteo… = Bone
  • Chondro… = Cartilage
  • Rhabdomyo… = Skeletal Muscle
  • Lipo… = Fat
  • Suffix tells you whether it is benign or malignant
  • …oma = Benign tumour
  • …sarcoma = Malignant connective tissue tumour
  • …carcinoma = Malignant epithelial/endothelial tumour

…blastoma = (Malignant) Tumour of embryonic cells

149
Q

What are the different secondary osteosarcomas?

A

Paget’s, Post-Radiation, Fibrous Dysplasia

Associated with p53 mutation

Also associated with Chondrosarcoma and STS

150
Q

What is secondary osteosarcoma secondary to?

A
  1. Paget’s Disease
  2. Fibrous Dysplasia
  3. Associated with McCune-Albright syndrome and Polyostic Fibrous Dysplasia
  4. McCune-Albright = fibrous dysplasia + café-au-lai spots + endocrine abnormalities
151
Q

What is the treatment for an osteosarcoma?

A
  • Initial treatment with multi-agent chemotherapy pre-op 8-12 weeks
  • Aims to kill tumour cells, reduce further spread, treat micro-metastases
  • Repeat procedures to Stage the Tumour
  • Limb Salvage surgery (where possible) + adjuvant chemotherapy
152
Q

What are the different surgical margins that can be achieved during oncologic surgery?

A
  • Intralesional: The plane of surgery goes through the tumour.
  • Marginal: The plane of surgery goes through the reactive zone of the lesion (the reactive zone contains oedema, tumour cells, fibrous tissue, and inflammatory cells).
  • Wide: The plane of dissection goes through normal tissue.
  • Radical: The entire anatomic compartment of the lesion is removed.
153
Q

WHAT IS A CRYSTAL IN CRYSTAL ARTHRITIS?

A

Homogenous solid
ions bonded closely in ordered, repeating, symmetric arrangement

Stable, hard, high density

154
Q

Where are crystals and what do they do?

A

All animals
Strengthen endo & exo-skeleton
Remove excess ions (surface binding)

155
Q

Why are crystals common in the gall bladder and kidney?

A

They are the two routes of excretion of uric aicd.

156
Q

What is the pathway of excretion of uric acid?

A

Purines -> HypoXanthine-> Xathine -> Uric acid -> monosodium urate

157
Q

WHAT IS GOUT?

https://www.youtube.com/watch?v=bznoU5bke4U

A

Monosodium urate crystals deposited in joints

158
Q

What is the cause of gout?

A

Hyperuricemia

Too much uric acid in the blood

159
Q

What is the pathogenesis of gout?

A
  1. Too much uric acid
  2. Formation of sharp crystals
  3. In areas of slow blood flow
  4. Joints and kidneys
  5. Overtime results in destruction of tissue leading to arthritis
  6. Inflammation from WBC releasing proinflammatory mediators
160
Q

What is the key enzyme in formation of uric acid from purines?

A

Xanthinine oxidase.

161
Q

In what food are purines rich?

A

Shellfish

Anchiovies

Red meat

Organ meat

162
Q

Where are the most common areas for gout to form?

A
  1. Occur at the first metatarsophalangeal joint of the big toe
    • This is called Podagra
  2. Other common joints are the ankle, foot, small joints of the hand, wrist, elbow or knee.
163
Q

What are the symptoms of gout?

A

Podagra

Pain

Hot

Red

164
Q

What are the investigations of gout?

A
  1. Polarized light microscopy of synovial fluid
    Shows negatively birefringent urate crystals
  2. Serum urate
    Raised
  3. Radiographs
    Soft-tissue swelling
    ‘Punched out’ erosions
    There is no sclerotic reaction, and joint spaces are preserved until late
165
Q

How do you treat the acute gout attack?

A
  1. NSAIDs or colchicine are first-line
    • NSAID should be prescribed until 1-2 days after the symptoms have settled. Gastroprotection (e.g. a proton pump inhibitor) may also be indicated
  2. Oral steroids may be considered if NSAIDs and colchicine are contraindicated. A dose of prednisolone 15mg/day is usually used
  3. If the patient is already taking allopurinol it should be continued
166
Q

What is the long term management of gout?

A
  1. Allopurinol
    • Started 2 weeks after an attack
    • Start this with NSAID or colchicine for ‘cover’
  2. Lifestyle modifications
    • Reduce alcohol
    • Lose weight
    • Change diet
167
Q

What are the triggers of the acute attack of pseudogout and gout?

A
  1. Direct trauma to the joint
  2. Intercurrent illness
  3. Surgery – especially parathyroidectomy
  4. Blood transfusion, IV fluid
  5. T4 replacement
  6. Joint lavage
  7. Most are spontaneous
168
Q

What predisposes a patinet to gout?

A

Decreased excretion of uric acid

  1. drugs*: diuretics
  2. chronic kidney disease
  3. lead toxicity

Increased production of uric acid

  1. myeloproliferative/lymphoproliferative disorder
  2. cytotoxic drugs
  3. severe psoriasis

Lesch-Nyhan syndrome

  1. hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
  2. x-linked recessive therefore only seen in boys
  3. features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation
169
Q

WHAT IS PSEUDOGOUT?

A

Calcium pyrophosphate deposition in joints

170
Q

Who are most at risk of developing pseudogout?

A
  1. Haemochromatosis
  2. Hyperparathyroidism
  3. Low magnesium, low phosphate
  4. Acromegaly, Wilson’s disease
171
Q

Where is pseudogout most common?

A

Typical distribution – (MCPs), wrists, knees, (ankles)

172
Q

What are the clincial features of pseudogout?

A

Commonly incidental finding on radiology

  1. Severe pain, stiffness, swelling
  2. Knee, wrist and shoulder more commonly affected
  3. Fever
173
Q

How do you distinguish OA from pyrophosphate arthropathy?

A
  1. Pattern of involvement
    • Wrists, shoulders, ankles, elbows
  2. Marked inflammatory component
  3. Superimposition of acute attacks
174
Q

What are the tests for pseudogout?

A
  1. Knee, wrist and shoulders most commonly affected
  2. Joint aspiration
    • Weakly-positively birefringent rhomboid-shaped crystals
  3. X-ray: chondrocalcinosis
    • In the knee this can be seen as linear calcifications of the meniscus and articular cartilage
175
Q

What is the acute management of pseudogout?

A

Acute
NSAIDs, analgesia, colchicine

Injections
Steroids

Immunosuppresants
Methotrexate and hydroxychloroquine for chronic pseudogout

176
Q

WHAT IS OSTEOPOROSIS?

A

Low bone mass and deterioration of bone tissue

Consequent increase in bone fragility and susceptibility to fracture.

177
Q

What are the different types of osteoporosis?

A

Primary (age)

Secondary (related to a condition)

178
Q

What is the epidemiology of osteoporosis?

A

1/2 women and 1/5 men over 50

179
Q

What are some causes and risk factors of osteoporosis?

A

Inflammatory disease

Endocrine disease.

Reduced skeletal loading

Medication.

Alcohol and smoking.

180
Q

What is the pathophysiology of fractures?

181
Q

How do we diagnose osteoporosis?

A

Bone densitometry
Dual energy X-ray absorptiometry. (DEXA)

Bloods
Calcium and Phosphate OFTEN NORMAL

182
Q

How does a DEXA work?

A

Uses to different beams to assess how much calcium is in the bone.

Low radiation dose

Measures important fracture sites

183
Q

What is a T-score?

A

Standard deviation score, it compares your score with gender-matched young adult average (peak bone mass)

184
Q

What do you use the T-score for?

A

Diagnose osteoporsis.

< -1.0
Normal

-1.0 to -2.5
Osteopenia

> -2.5
Osteoporosis

> -2.5 plus fracture
Severe osteoporosis

185
Q

What medications cause an increase risk of osteoporosis?

A
  1. Glucocorticoids (corticosteroids)
  2. GnRH analogues (goserelin)
  3. Androgen deprivation
186
Q

What is FRAX?

A

A genorator to see how much at risk of a fracture you are

187
Q

What are the treatment options for osteoporosis?

A

Calcium + Vitamin D

Anti-resorptive
Decrease osteoclast activity and bone turnover
Bisphosphonates
HRT
Denosumab - antibody to RANK

Anabolic
Increase osteoblast activity and bone formation
Teriparatide

188
Q

What are benefits and risks of hormone replacement therapy?

A

Benefits
Reduce the risk of fractures
Stop bone loss
Prevents hot flushes
Reduces risk of colon cancer

Risks
Breast cancer
Stroke
Cardiovascular disease

189
Q

When are bisphosphonates used and why?

What are some oral and intravenous drugs?

A

First line treatment

ORAL
Alendronate (daily or weekly)
Risedronate (daily or weekly)
Ibandronate (monthly)
Etidronate (two weeks of 13)

IV
Ibandronate (3-monthly)
Zoledronate (once yearly)

190
Q

WHAT IS OSTEOMALACIA?

A

Osteomalacia there is a normal amount of bone but its mineral content is low (there is excess uncalcified osteoid and cartilage).

191
Q

What is the cause of osteomalacia?

A

Vitamin D deficiency

Renal failure
1,25-dihydroxy-cholecalciferol deficiency

Drug-induced
Increased breakdown of 25-hydroxy-vitamin D.

Vitamin D resistance:
Osteomalacia responds to high doses of vitamin D

Liver disease
Due to reduced hydroxylation of vitamin D to 25-hydroxy-cholecalciferol and malabsorption of vitamin D, eg in cirrhosis

Tumour

192
Q

What are the signs and symptoms of osteomalacia?

A
  1. Bone pain and tenderness
  2. Fractures
  3. Proximal myopathy (waddling gait)
193
Q

What are the investigations for osteomalacia?

A
  1. Bloods
    Low vitamin D levels
    Low calcium, phosphate (in around 30%)
    Raised alkaline phosphatase (in 95-100% of patients)
  2. X-ray
    Translucent bands (Looser’s zones or pseudofractures)
194
Q

What are the treatments for osteomalacia?

A
  1. Vitamin D supplmentation
    A loading dose is often needed initially
  2. Calcium supplementation if dietary calcium is inadequate
195
Q

WHAT IS PAGETS DISEASE OF BONE?

A
  1. Increased bone turnover associated with increased numbers of osteoblasts and osteoclasts
  2. With resultant remodelling, bone enlargement, deformity, and weakness
196
Q

What is the epidemiology of Paget’s diease of bone?

A

Rare in the under-40s.

Incidence rises with age (3% over 55yrs old).

197
Q

What are the signs + symptoms of paget’s disease of bone?

A

Asymptomatic

Deep, boring pain, and bony deformity and enlargement

Classically a bowed sabre tibia

198
Q

What are the investigations for paget’s disease of bone?

A
  1. X-ray
    Localized enlargement of bone.
    Patchy cortical thickening with sclerosis, osteolysis, and deformity
  2. Blood chemistry
    Ca2+ and PO43 normal
    ALP RAISED
199
Q

What is the treatment for paget’s disease of bone?

A
  1. Analgesia - e.g. Paracetamol, NSAIDs
  2. Bisphosphonates - e.g. Alendronate
  3. Surgery - If fractures occur
200
Q

WHAT IS FIBROMYALGIA?

https://www.youtube.com/watch?v=Jyl98z07ZHM

A

Fibromyalgia is a chronic condition affecting fibrous tissue and muscle causing pain

201
Q

What is the epidemology of fibromyalgia?

A

Female more than men

202
Q

What is the cause of fibromyalgia?

A

Unknown

Thought to be caused by the way the brain receieves pain signals

203
Q

What are the risk factors for fibromyalgia?

A
  1. Genetics
  2. Environmental
    • Child abuse
    • Depression
    • Anxiety
    • Negative beliefs
204
Q

What are the symptoms of fibromyalgia?

A
  1. Chronic pain: at multiple site, sometimes ‘pain all over’
  2. Lethargy
  3. Cognitive impairment: ‘fibro fog’
  4. Sleep disturbance, headaches, dizziness are common
205
Q

What are the investigations for fibromyalgia?

A

Pain location in more than 7 areas with a symptom severity score of 5/12

OR

Pain location in more than 5 areas with a symptom severity score of 9/12

SYMPTOMS must be present for more than 3 months

NOT due to another disease

206
Q

What are the treatment options for fibromyalgia?

A
  1. Explanation
  2. Aerobic exercise
    • Has the strongest evidence base
  3. Cognitive behavioural therapy
  4. Medication
    • Pregabalin
    • Duloxetine
    • Amitriptyline
207
Q

WHAT ARE SOME VERTEBRAL DISC PROBLEMS?

A

Disorders effecting intervertebral discs: herniation, degeneration, infection.

208
Q

What is disc herniation?

A

Herniation = prolapsed vertebral disc.

209
Q

What is disc degeneration?

A

Major cause of lower back pain.

Exact cause is known

Could be natural part of ageing

Can occur in young people: genetic, environmental, traumatic, inflammatory, infectious, etc.

May lead to disc herniation.

210
Q

What is the pathophysiology of disc prolapse?

A

Nucleus pulposus herniates, it can irritate or compress the adjacent nerve root - symptoms of sciatica

211
Q

What is the presentation of a disc prolapse?

A

Symptoms of sciatica

Compress cauda equine

Nerve root compression

Symptoms can correspond to the level.

212
Q

What are the investigations for disc prolapse?

A

Symptoms may settle within 6 weeks

MRI very sensitive

CT

Plain x-rays sometimes useful

213
Q

What is the management for a disc prolapse?

A

Analgesia

Encourage to keep active

Heat and massage to relieve muscle spasm

Avoid activities that aggravate pain

Physiotherapy

Surgery.

214
Q

WHAT ARE THE SIGNS FOR A OSTEOPOROTIC VERTEBRAL FRACTURE?

A
  1. Loss of height: vertebral osteoporotic fractures of lead to compression of the spinal vertebrae hence a reduction in overall length of the spine and thus the patient becomes shorter
  2. Kyphosis (curvature of the spine)
  3. Localised tenderness on palpation of spinous processes at the fracture site
215
Q

What are the investigations for a osteoporic vertebral fracture?

A
  1. X-ray of the spine: This should be the first investigation ordered and may show wedging of the vertebra due to compression of the bone. An X-ray of the spine may also show old fractures (which can have a sclerotic appearance)
216
Q

WHAT IS DISCITIS?

A
  1. Pyogenic infection of the spine
  2. Rare
  3. Incidence ­ due to ­ life expectancy
217
Q

What is the pathopgysiology of discitis?

A

Inflammation of vertebral disc space

Can co-exist with osteomyelitis

Most commonly effects lumbar spine

Usually haematogenous spread of infection from other parts of the body

Common sources; urinary tract, lungs, soft tissues

218
Q

What is the cause of discitis?

A
  1. Bacterial
    • Staphylococcus aureus is the most common cause of discitis
    • Need to do echo to see if organism came from here
  2. Viral
  3. TB
  4. Aseptic
219
Q

What is the presentation of discitis?

A
  1. Back pain
  2. General features
    • pyrexia,
    • rigors
    • sepsis
  3. Neurological features
    • e.g. changing lower limb neurology
    • if epidural abscess develops
220
Q

What are the investigations for discitis?

A
  1. Imaging: MRI has the highest sensitivity
  2. CT guided biopsy may be required to guide antimicrobial treatment
221
Q

What is the management for discitis?

A
  1. Antibiotics (adjusted after culture results)
  2. Immobilization (2 weeks bed rest, then immobilization with brace)
  3. Surgery if neurological deficit, deformity or lack of response tp antibiotics.
222
Q

WHAT IS COMPARTMENT SYNDROME?

A

Raised pressure within a closed anatomical space.

The raised pressure within the compartment will eventually compromise tissue perfusion resulting in necrosis.

The two main fractures carrying this complication include supracondylar fractures and tibial shaft injuries.

223
Q

What are the features of compartment syndrome?

A
  1. Pain, especially on movement (even passive)
    • excessive use of breakthrough analgesia should raise suspicion for compartment syndrome
  2. Parasthesiae
  3. Pallor may be present
  4. Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
  5. Paralysis of the muscle group may occur
224
Q

What is used for diagnosis of compartment syndrome?

A
  1. Is made by measurement of intracompartmental pressure measurements. Pressures in excess of 20mmHg are abnormal and >40mmHg is diagnostic
  2. Compartment syndrome will typically not show any pathology on an x-ray
225
Q

What is the treatment for compartment syndrome?

A
  1. This is essentially prompt and extensive fasciotomies
  2. In the lower limb the deep muscles may be inadequately decompressed by the inexperienced operator when smaller incisions are performed
  3. Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these patients require aggressive IV fluids
  4. Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation may have to be considered
  5. Death of muscle groups may occur within 4-6 hours
226
Q

WHAT IS THE TYPICAL PRESENTATION OF A SCAPHOID FRACTURE?

A

Fall onto an outstretched hand

227
Q

What are the features of a scaphoid fracture?

A
  1. Compromise of the dorsal carpal arch of the radial artery
  2. Pain along the radial aspect of the wrist, at the base of the thumb
  3. Loss of grip / pinch strength
  4. Point of maximal tenderness over the anatomical snuffbox
    • This is a highly sensitive (around 90-95%), but poorly specific test (<40%)in isolation
  5. Wrist joint effusion
    • Hyperacute injuries (<4hrs old), and delayed presentations (>4days old) may not present with joint effusions.
  6. Pain elicited by telescoping of the thumb (pain on longitudinal compression)
  7. Tenderness of the scaphoid tubercle (on the volar aspect of the wrist)
  8. Pain on ulnar deviation of the wrist
228
Q

What are the investigations of a scaphoid fracture?

A
  1. Imaging
    • X-ray
    • CT
    • MRI - definitive and exclusive
  2. Repeated 7-10 days if first x-ray is normal
229
Q

What is the management of a scaphoid fracture?

A
  1. Immobilisation with a Futuro splint or standard below-elbow backslab
  2. Undisplaced fractures of the scaphoid waist
    • Cast for 6-8 weeks
  3. Displaced scaphoid waist fractures
    • requires surgical fixation
  4. proximal scaphoid pole fractures
    • require surgical fixation
230
Q

WHAT ARE THE FEATURES OF A HIP FRACTURE?

A
  1. Pain
  2. The classic signs are a shortened and externally rotated leg
  3. Patients with non-displaced or incomplete neck of femur fractures may be able to weight bear
231
Q

What is a common complication of a hip fracture?

A

Avascular necrosis

232
Q

What are the different types of hip fracture?

A
  1. Intracapsular (subcapital): from the edge of the femoral head to the insertion of the capsule of the hip joint
  2. Extracapsular: these can either be trochanteric or subtrochanteric (the lesser trochanter is the dividing line)
233
Q

What system is used to classify hip fractures?

A

The Garden system is one classification system in common use.

  1. Type I: Stable fracture with impaction in valgus
  2. Type II: Complete fracture but undisplaced
  3. Type III: Displaced fracture, usually rotated and angulated, but still has boney contact
  4. Type IV: Complete boney disruption

Blood supply disruption is most common following Types III and IV.

234
Q

What is the treatment for an intracapsular fracture?

A
  1. Undisplaced Fracture:
    • Internal fixation, or hemiarthroplasty if unfit.
  2. Displaced Fracture:
    • NICE recommend replacement arthroplasty (total hip replacement or hemiarthroplasty) to all patients with a displaced intracapsular hip fracture
    • Total hip replacement is favoured to hemiarthroplasty if patients:
      • Were able to walk independently out of doors with no more than the use of a stick and
      • Are not cognitively impaired and
      • Are medically fit for anaesthesia and the procedure.
235
Q

What is the treatment of an extracapsular fracture?

A
  1. Stable intertrochanteric fractures: dynamic hip screw
  2. If reverse oblique, transverse or subtrochanteric fractures: intramedullary device
236
Q

What are the complications of total hip replacements?

A
  1. Perioperative
    • venous thromboembolism
    • intraoperative fracture
    • nerve injury
    • surgical site infection
  2. Leg length discrepancy
  3. Posterior dislocation
    • may occur during extremes of hip flexion
    • typically presents acutely with a ‘clunk’, pain and inability to weight bear
    • on examination there is internal rotation and shortening of the affected leg
    • Aseptic loosening (most common reason for revision )
  5. prosthetic joint infection
237
Q

What would the leg look like with a posterior dislocation?

A

Leg shortening and internal rotation

238
Q

What would the leg look like in an anterior hip dislocation?

A

Hip adduction and external rotation

239
Q

WHAT IS ADHESIVE CAPSULITIS?

A
  1. Common in middle-age and diabetics
  2. Characterised by painful, stiff movement
  3. Limited movement in all directions, with loss of external rotation and abduction in about 50% of patients
240
Q

WHAT IS SUPRASPINATUS TENDONITIS?

A
  1. Rotator cuff injury
  2. Painful arc of abduction between 60 and 120 degrees
  3. Tenderness over anterior acromion
241
Q

WHAT IS CUBITAL TUNNEL SYNDROME?

A

Cubital tunnel syndrome occurs due to compression of the ulnar nerve as it passes through the cubital tunnel

242
Q

What are the features of cubital tunnel syndrome?

A
  1. Tingling and numbness of the 4th and 5th finger which starts off intermittent and then becomes constant.
  2. Over time patients may also develop weakness and muscle wasting
  3. Pain worse on leaning on the affected elbow
  4. Often a history of osteoarthritis or prior trauma to the area.
243
Q

what are the investigations for cubital tunnel syndrome?

A
  1. the diagnosis is usually clinical
  2. however, in selected cases nerve conduction studies may be used
244
Q

What is the management for cubital tunnel syndrome?

A
  1. Avoid aggravating activity
  2. Physiotherapy
  3. Steroid injections
  4. Surgery in resistant cases
245
Q

WHAT ARE THE DIFFERENT FRACTURE TYPES?

246
Q

What do you need to do to a displaced fracture before anything else?

A

Reduce the fracture

247
Q

WHAT IS ILIOTIBIAL BAND SYNDROME?

A

Iliotibial band syndrome is a common cause of lateral knee pain in runners, occurring in around 1 in 10 people who run regularly.

248
Q

What are the features of iliotibial band syndrome?

A
  1. Tenderness 2-3cm above the lateral joint line
249
Q

What is the management of iliotibial band syndrome?

A
  1. activity modification and iliotibial band stretches
  2. if not improving then physiotherapy referral
250
Q

WHAT IS RHABDOMYLOLYSIS?

A

Rhabdomyolysis will typically feature in the exam as a patient who has had a fall or prolonged epileptic seizure and is found to have an acute kidney injury on admission.

251
Q

What are the features of rhabdomyolysis?

A
  1. acute kidney injury with disproportionately raised creatinine
  2. elevated creatine kinase (CK)
  3. Tubular cell necrosis
  4. myoglobinuria
  5. hypocalcaemia (myoglobin binds calcium)
  6. elevated phosphate (released from myocytes)
  7. hyperkalaemia (may develop before renal failure)
  8. metabolic acidosis
252
Q

What are the causes of rhabdomyolysis?

A
  1. seizure
  2. collapse/coma (e.g. elderly patients collapses at home, found 8 hours later)
  3. ecstasy
  4. crush injury
  5. McArdle’s syndrome
  6. drugs: statins (especially if co-prescribed with clarithromycin)
253
Q

What is the management of rhabdomyolysis?

A
  1. IV fluids to maintain good urine output
  2. urinary alkalinization is sometimes used
254
Q

WHAT IS OLECRANOIN BURSITIS?

A

Swelling over the posterior aspect of the elbow. There may be associated pain, warmth and erythema. It typically affects middle-aged male patients.

255
Q

WHAT ARE THE FEATURES OF AN ANTERIOR SHOULDER DISLOCATION/GLENOHUMERAL DISLOCATION?

A
  1. External rotation and abduction
  2. 35-40% recurrent (it is the commonest disorder)
  3. Associated with greater tuberosity fracture, Bankart lesion, Hill-Sachs defect
256
Q

WHAT ARE THE FEATURES OF ACROIMIOCLAVICULAR JOINT DISLOCATION?

A

Acromioclavicular joint (ACJ) dislocation normally occurs secondary to direct injury to the superior aspect of the acromion. Loss of shoulder contour and prominent clavicle are key features. Note; rotator cuff tears rarely occur in the second decade.

257
Q

WHAT ARE THE RISK FACTORS FOR ACHILLES TENDON RUPTURE?

A
  1. Quinolone use (e.g. ciprofloxacin) is associated with tendon disorders
  2. Hypercholesterolaemia (predisposes to tendon xanthomata)
258
Q

What is done in investigations for achilles tendon rupture?

A
  1. An examination should be conducted using Simmond’s triad, to help exclude Achilles tendon rupture.
  2. This can be performed by asking the patient to lie prone with their feet over the edge of the bed.
  3. The examiner should look for an abnormal angle of declination; Achilles tendon rupture may lead to greater dorsiflexion of the injured foot compared to the uninjured limb.
  4. They should also feel for a gap in the tendon and gently squeeze the calf muscles if there is an acute rupture of the Achilles tendon the injured foot will stay in the neutral position when the calf is squeezed.
259
Q

What is the imaging of choice for achilles tendon rupture?

A

Ultrasound is the initial imaging modality of choice for suspected Achilles tendon rupture

260
Q

WHAT IS CHARCOT JOINT?

A
  1. A Charcot joint is also commonly referred to as a neuropathic joint.
  2. It describes a joint which has become badly disrupted and damaged secondary to a loss of sensation.
  3. In years gone by they were most commonly caused by neuropathy secondary to syphilis (tabes dorsalis) but are now most commonly seen in diabetics.
261
Q

What are the features of charcot joint?

A
  1. Charcot joints are typically a lost less painful than would be expected given the degree of joint disruption due to the sensory neuropathy. However, 75% of patients report some degree of pain
  2. The joint is typically swollen, red and warm
262
Q

WHAT ARE THE FEATURES OF SPINAL STENOSIS?

A
  1. Usually gradual onset
  2. Unilateral or bilateral leg pain (with or without back pain), numbness, and weakness which is worse on walking. Resolves when sits down. Pain may be described as ‘aching’, ‘crawling’.
  3. Relieved by sitting down, leaning forwards and crouching down
  4. Clinical examination is often normal
263
Q

What is the investigation for spinal stenosis?

264
Q

WHAT ARE THE FEATURES OF A POSTERIOR SHOULDER DISLOCATION?

A

Posterior shoulder dislocation is more likely associated with seizures and electric shock. It presents with unilateral shoulder deformity. While anterior instability and dislocations are still more common in seizures, a shoulder locked in an internally rotated position is highly suggestive of a posterior dislocation.

265
Q

WHAT ARE THE FEATURES OF A ROTATOR CUFF TEAR?

A
  1. Rotator cuff tears are common in elderly people and may occur following minor trauma or as a result of long standing impingement. Tears greater than 2cm should generally be repaired surgically
  2. Passove movement still works
266
Q

WHAT IS THE WEBER CLASSIFICATION?

A
  1. Related to the level of the fibular fracture.
    • Type A is below the syndesmosis
    • Type B fractures start at the level of the tibial plafond and may extend proximally to involve the syndesmosis
    • Type C is above the syndesmosis which may itself be damaged
267
Q

What is the treatment of a type A weber fracture?

A

Weber A fractures – patients with minimally displaced, stable fractures may weight bear as tolerated in a CAM boot

268
Q

What is the treatment for a weber type C fracture?

A

Open reduction and external fixation would only be necessary for unstable injuries such as a Weber C fracture.

269
Q

WHAT IS A BUCKLE FRACTURE?

A

Buckle, or torus, fractures are incomplete fractures of the shaft of a long bone that is characterised by bulging of the cortex. They typically occur in children aged 5-10 years.

As they are typically self-limiting they do not usually require operative intervention and can sometimes be managed with splinting and immobilisation rather than a cast.

270
Q

WHAT IS A GREENSTICK FRACTURE?

A

The radiograph shows a fracture involving the palmar surface of the distal radius, with minimal dorsal angulation and no disruption of the dorsal cortex. The growth plate appears normal.

271
Q

WHAT IS A GALEAZZI FRACTURE?

A
  1. Radial shaft fracture with associated dislocation of the distal radioulnar joint
  2. Occur after a fall on the hand with a rotational force superimposed on it.
  3. On examination, there is bruising, swelling and tenderness over the lower end of the forearm.
  4. X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to dislocation of the inferior radio-ulnar joint.
272
Q

WHAT IS THE MANAGEMENT OF A PATELLAR FRACTURE?

A
  1. Undisplaced fractures
    • ​​particularly vertical fractures with an intact extensor mechanism can be managed non-operatively in a hinged knee brace for 6 weeks and patients allowed to fully weight bear.
  2. Displaced fractures and those with loss of extensor mechanisms
    • should be considered for operative management with either tension band wire, inter-fragmentary screws or cerclage wires.
    • Again, patients are placed in a hinged knee brace for 4 to 6 weeks and allowed to fully weight bear.
273
Q

WHAT IS THE TREATMENT FOR AN ANTERIOR SHOULDER DISLOCATION?

A
  1. Kocher-technique reduction
274
Q

WHAT IS THE MANAGEMENT OF AN ANKLE FRACTURE?

A
  1. All ankle fractures should be promptly reduced to remove pressure on the overlying skin and subsequent necrosis
  2. Young patients, with unstable, high velocity or proximal injuries will usually require surgical repair. Often using a compression plate.
  3. Elderly patients, even with potentially unstable injuries usually fare better with attempts at conservative management as their thin bone does not hold metalwork well.
275
Q

WHAT IS OSTEOCHONDRITIS DISSECANS?

A

Osteochondritis dissecans (OCD) is a pathological process affecting the subchondral bone (most often in the knee joint) with secondary effects on the joint cartilage, including pain, oedema, free bodies and mechanical dysfunctions

276
Q

WHAT ARE THE FEATURES OF OSTEOCHONDRITIS DISSECANS?

A
  1. Knee pain and swelling, typically after exercise
  2. Knee catching, locking and/or giving way: more constant and severe symptoms are associated with the presence of loose bodies
  3. Feeling a painful ‘clunk’ when flexing or extending the knee - indicating the involvement of the lateral femoral condyle
277
Q

HOW DO AC JOINT INJURIES NORMALLY OCCUR?

A

Injury to the AC joint is relatively common and typically occurs during collision sports such as rugby following a fall on to the shoulder or a FOOSH (falls on outstretched hand).

278
Q

How are the different grades of AC joint injury treated?

A
  1. Grade I and II injuries are very common and are typically managed conservatively including resting the joint using a sling.
  2. Grade IV, V and VI are rare and require surgical intervention.
  3. The management of grade III injuries is a matter of debate and often depends on individual circumstances.
279
Q

WHAT ARE THE SYMPTOMS OF L3 NERVE ROOT COMPRESSION?

A
  1. Sensory loss over anterior thigh
  2. Weak quadriceps
  3. Reduced knee reflex
  4. Positive femoral stretch test
280
Q

What are the symptoms of L4 nerve root compression?

A
  1. Sensory loss anterior aspect of knee
  2. Weak quadriceps
  3. Reduced knee reflex
  4. Positive femoral stretch test
281
Q

What are the symptoms of L5 nerve root compression?

A
  1. Sensory loss dorsum of foot
  2. Weakness in foot and big toe dorsiflexion
  3. Reflexes intact
  4. Positive sciatic nerve stretch test
282
Q

What are the symptoms of S1 nerve root compression?

A
  1. Sensory loss posterolateral aspect of leg and lateral aspect of foot
  2. Weakness in plantar flexion of foot
  3. Reduced ankle reflex
  4. Positive sciatic nerve stretch test
283
Q

WHAT IS DE QUERVAIN’S TENOSYNOVITIS?

A

De Quervain’s tenosynovitis is a common condition in which the sheath containing the extensor pollicis brevis and abductor pollicis longus tendons is inflamed. It typically affects females aged 30 - 50 years old.

284
Q

What are the features of De Quervain’s tenosynovitis?

A
  1. pain on the radial side of the wrist
  2. tenderness over the radial styloid process
  3. abduction of the thumb against resistance is painful
  4. Finkelstein’s test: the examiner pulls the thumb of the patient in ulnar deviation and longitudinal traction. In a patient with tenosynovitis this action causes pain over the radial styloid process and along the length of extensor pollisis brevis and abductor pollicis longus
285
Q

What is the management of De Quervain’s tenosynovitis?

A
  1. analgesia
  2. steroid injection
  3. immobilisation with a thumb splint (spica) may be effective
  4. surgical treatment is sometimes required
286
Q

WHAT IS OSTEOGENESIS IMPERFECTA?

A
  1. Osteogenesis imperfecta (more commonly known as brittle bone disease) is a group of disorders of collagen metabolism resulting in bone fragility and fractures.
  2. The most common, and milder, form of osteogenesis imperfecta is type 1
287
Q

What are the features of osteogenesis imperfecta?

A
  1. presents in childhood
  2. fractures following minor trauma
  3. blue sclera
  4. deafness secondary to otosclerosis
  5. dental imperfections are common
288
Q

What are the investigations for osteogenesis imperfecta?

A
  1. Adjusted calcium
  2. Phosphate
  3. Parathyroid hormone amd
  4. ALP results are usually normal in osteogenesis imperfecta
289
Q

WHAT IS AVASCULAR NECROSIS OF THE HIP?

A
  1. Avascular necrosis (AVN) may be defined as death of bone tissue secondary to loss of the blood supply.
  2. This leads to bone destruction and loss of joint function.
  3. It most commonly affects the epiphysis of long bones such as the femur.
290
Q

What are the causes of avascular necrosis of the hip?

A
  1. long-term steroid use
  2. chemotherapy
  3. alcohol excess
  4. trauma
291
Q

What are the investigations for avascular necrosis of the hip?

A
  1. plain x-ray findings may be normal initially. Osteopenia and microfractures may be seen early on. Collapse of the articular surface may result in the crescent sign
  2. MRI is the investigation of choice. It is more sensitive than radionuclide bone scanning
292
Q

What is the management for avascular necrosis of the hip?

A
  1. joint replacement may be necessary
293
Q

WHAT IS A MONTEGGIA’S FRACTURE?

A
  1. Dislocation of the proximal radioulnar joint in association with an ulna fracture
  2. Fall on outstretched hand with forced pronation
  3. Needs prompt diagnosis to avoid disability
294
Q

WHAT NERVE DOES PRONATION OF THE HAND?

ΩΩ 2a Bateman - Systems Based (11 decks)

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