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Sharon's Phase 2a Medicine Revision > Musculoskeletal and rheumatology > Flashcards

Musculoskeletal and rheumatology Flashcards

1
Q

Define osteoarthritis

A

It is a degenerative joint disorder affecting the synovial joints most common form of arthritis and typically affects the knees, hips, hands, and spine (cervical and lumbar).

“Wear and tear” condition

Not an inflammatory condition like rheumatoid arthritis.

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2
Q

What is the aetiology of osteoarthritis?

A

Osteoarthritis is thought to result from an imbalance between the degradation of cartilage and the chondrocytes repairing it, leading to structural issues in the joint.

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3
Q

What are the risk factors for developing osteoarthritis?

A
  • Obesity
  • Age (>50)
  • Occupation (overusing joints)
  • Trauma
  • Female
  • Family history.
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4
Q

What joints are most commonly affected by osteoarthritis?

A
  • Hips
  • Knees
  • Sacro-iliac joints (hips)
  • Distal-interphalangeal joints in the hands (DIPs)
  • Carpometacarpal joint (CMC)
  • Wrist
  • Cervical spine (cervical spondylosis)
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5
Q

What signs and symptoms might a patient with osteoarthritis present with?

A

The most common symptoms are joint pain and stiffness.

Signs:

  • Bulky, bony enlargement of the joint
  • Restricted range of motion
  • Crepitus on movement (popping)
  • Effusions (fluid) around the joint
  • Hand signs (see next flashcard)
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6
Q

How does the pain experienced by patients in osteoarthritis differ to inflammatory arthritis?

A

In osteoarthritis: pain and stiffness tend to be worse with activity and at the end of the day,

inflammatory arthritis - activity improves symptoms and the symptoms tend to be worse first thing in the morning.

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7
Q

What are the hand signs in a patient that could indicate osteoarthritis?

A
  • Heberden’s nodes (in the DIP joints)
  • Bouchard’s nodes (in the PIP joints)
  • Squaring at the base of the thumb at the carpometacarpal joint
  • Weak grip
  • Reduced range of motion
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8
Q

What investigations/tests are used to diagnose osteoarthritis?

A

OA is essentially a clinical diagnosis, but the following investigations can be considered:

  • XR of affected joints

Joint x-rays: X-rays of the affected joint usually demonstrate the radiological hallmarks of osteoarthritis

  • Reduced joint space
  • Osteophytes
  • Subchondral cysts
  • Subchondral sclerosis

Serum CRP + ESR elevated in inflammation to rule out inflammatory arthritis

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9
Q

What is the management plan for OA?

A

First line: topical analgesia e.g. capsaicin + non-pharmacological approaches such as weight loss, physiotherapy, occupational therapy, orthotics, e.g. knee braces)

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10
Q

Why are NSAIDs used with caution for pain management in OA?

A

NSAIDs are very good at controlling pain, however, long-term use can cause GI, renal, and cardiovascular side-effects and exacerbate asthma.

Also need to be careful in elderly patients + patients on anticoagulants

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11
Q

What are the differential diagnoses for OA?

A
  • Gout
  • Pseudogout
  • Rheumatoid arthritis
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12
Q

Define rheumatoid arthritis

A

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease.

This leads to a deforming, symmetrical inflammatory arthritis of the small joints, which progresses to involve larger joints and other organs of the body, e.g. skin and lungs

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13
Q

What is the aetiology of RA?

A

Unknown but thought to be an interplay between genetic, environmental factors which lead to an immune response against self-peiptides:

Genetic factors thought to be involved:

  • HLA DR4 (a gene often present in RF positive patients)
  • HLA DR1 (a gene occasionally present in RA patients)
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14
Q

What is the pathophysiology of RA?

A

Rheumatoid factor (RF) - autoantibodies present in around 70% of RA patients

RF targets the Fc portion (present on all antibodies to bind cells of the immune system) of the patient’s own IgG antibody > activation of the immune system against the IgG > systemic inflammation

RF are usually IgM, but can be any class

Anti-cyclic citrullinated peptide antibodies (anti-CCP antibodies) - autoantibodies that are more specific to rheumatoid arthritis than RF

Anti-CCP antibodies indicate the development of rheumatoid arthritis as it comes before the symptoms.

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15
Q

What are the risk factors for developing RA?

A

1% in the UK and the most common inflammatory arthritis.

  • Age: peak onset = 30-50 years of age
  • Female gender: 2-4x more common in women
  • Family history
  • Smoking
  • Infections
  • Hormones: increased risk post-menopause > decreased oestrogen levels
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16
Q

What symptoms might a patient with RA present with?

A

Symptoms:

  • Morning stiffness: > 30 mins and improves throughout the day with activity
  • Malaise
  • Myalgia
  • Low-grade fever
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17
Q

What hand signs might a patient with RA present with?

A
  • Symmetrical polyarthritis: swollen and tender small joints of the hands and feet (MCP, PIP, MTP) > progresses to larger joints
  • Boutonniere deformity: PIP flexion and DIP hyperextension
  • Swan-neck deformity: PIP hyperextension and DIP flexion
  • Z-thumb deformity: hyperextension of the thumb IP joint with flexion of the MCP joint.
  • Ulnar deviation of the fingers
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18
Q

What are some extra-articular signs might a patient with RA presents with?

A
  • Lungs (fibrosis, effusion)
  • Eyes (keratoconjunctivitis sicca - dry eye (most common))
  • Kidneys (CKD)
  • Skin (rheumatoid nodules)
  • Anaemia of chronic disease
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19
Q

What investigations/tests are used to diagnose RA?

A
  • Rheumatoid factor - positive
  • Anti-CCP antibodies - positive

Diagnostic criteria - patient scored on:

  • The joints that are involved (more and smaller joints score higher)
  • Serology (presence of rheumatoid factor and anti-CCP)
  • Inflammatory markers (abnormal ESR and CRP - 1)
  • Duration of symptoms (more (1) or less than 6 weeks (0))

≥ 6 indicates a diagnosis of rheumatoid arthritis.

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20
Q

What is the management plan for RA?

A

Disease-modifying anti-rheumatic drug (DMARD):

1st line = monotherapy with methotrexate or sulfasalazine.

2nd line: 2 of these used in combination.

If DMARD fails > biologics:

3rd line: methotrexate plus infliximab (anti-TNF alpha)

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21
Q

What are the main differential diagnoses of RA?

A
  • Psoriatic arthritis
  • Infectious arthritis
  • Gout
  • Systemic lupus erythematosus
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22
Q

What is the management for RA flare-ups?

A
  • NSAIDs
  • Glucocorticoids (prednisolone): intra-articular therapy.
  • Or intramuscular steroids or oral prednisolone as alternative
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23
Q

Define gout

A

Gout is an inflammatory arthritis caused by the deposition of monosodium urate crystals within joints, most commonly the first metatarsophalangeal joint (MTP) - base of big toe.

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24
Q

What are the risk factors for developing gout?

A
  • Male sex
  • > 40 (peak incidence 40 - 60)

Uric acid overproduction:

  • Purine-rich diet - meat, seafood, alcohol
  • Obesity
  • Haematological malignancies - increased cell turnover

Reduced uric acid excretion:

  • CKD
  • Diuretics
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25
Q

What is the aetiology/pathophysiology of gout?

A

High blood uric acid level means urate crystals are deposited in the joint causing it to become hot, swollen and painful.

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26
Q

What signs and symptoms might a patient with gout present with?

A

Symptoms

  • Relapsing/remitting - patients present with recurrent episodes of red, hot, tender joints
  • Asymptomatic between flares - remission can last months
  • Rapid onset severe joint pain
  • Joint stiffness

Signs:

  • Joint inflammation: tenderness, erythema and swelling
  • Monoarticular or oligoarticular (≤ 4 joints):

1st MTP most commonly affected in a first presentation (70%); ankle, wrist and knee

Gouty tophi: nodular masses of urate crystals form, usually as a late complication

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27
Q

What are the most commonly affected joints in gout?

A
  • Base of the big toe (metatarsophalangeal joint)
  • Wrists
  • Base of thumb (carpometacarpal joints)
  • Large joints like the knee and ankle.
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28
Q

What investigations/tests are used to diagnose gout?

A

1st line: joint aspiration: confirm the diagnosis and exclude septic arthritis - negative birefringent needle-shaped monosodium urate crystals under polarised microscopy

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29
Q

What is the management plan for gout?

A

Dietary changes: decreased meat, increased dairy as protective against gout

Acute flare:

1st line: NSAIDs/colchicine + corticosteroids + PPI to protect stomach

Prevention - urate-lowering therapy:

All patients given this after acute episode
1st line: allopurinol - xanthine oxidase inhibitors

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30
Q

What is an important differential diagnosis of gout?

A

Septic arthritis

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31
Q

Define pseudogout

A

Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals.

Calcium pyrophosphate crystals are deposited in the joint, causing synovitis.

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32
Q

What joints are most commonly affected by pseudogout?

A

Knees, shoulders and wrists

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33
Q

What are the risk factors for pseudogout?

A
  • Elderly (70+)
  • Female
  • Diabetes
  • Osteoarthritis
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34
Q

What signs and symptoms might a patient with pseudogout present with?

A

Symptoms:

  • Rapid onset severe joint pain: knee, shoulder and wrist are most commonly affected
  • Joint stiffness

Signs:

  • Joint inflammation: pain, erythema and swelling
  • Monoarticular or polyarticular
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35
Q

What investigations/tests are used to diagnose pseudogout?

A

1st line:
Joint aspiration: confirms the diagnosis and rules out septic arthritis, weakly-positive birefringent rhomboid-shaped crystals under polarised microscopy

Joint X-ray: chondrocalcinosis (calcification of articular cartilage) in 40% of cases

  • In the knee, this is seen as linear calcifications of the articular cartilage and meniscus
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36
Q

WHat is the management plan for pseudogout?

A

Similar treatment to gout with NSAIDs and corticosteroids

Anti-inflammatory: NSAIDs or colchicine

Corticosteroid:
Monoarticular: intra-articuar
Polyarticular: systemic steroids

Joint replacement: only indicated in chronic, recurrent cases with severe joint degeneration

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37
Q

What is an important differential diagnosis for pseudogout if a patient presents with hot, tender and red joints?

A

Septic arthritis - medical emergency!

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38
Q

Define osteoporosis

A

Osteoporosis is the reduction in trabecular bone mass/density and disruption of bone architecture, resulting in porous bone with increased fragility and fracture risk.

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39
Q

What is the aetiology of osteoporosis?

A

Osteoporosis is caused by a prolonged imbalance of bone remodelling where resorption (osteoclastic activity) exceeds formation (osteoblastic activity).

A combination of environmental and genetic factors involved

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40
Q

What are the risk factors for osteoporosis?

A

Fight Me!

  • Female
  • post-Menopausal

SHATTERED

  • Steroids
  • Hyper/hypothyroidism
  • Alcohol + smoking
  • Thin (low BMI)
  • Testrosterone (low)
  • Early menopause (decreased oestrogen)
  • Renal/liver failure
  • Erosive/inflammatory disease
  • DMT1 or malabsorption
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41
Q

What investigations/tests are used to diagnose osteoporosis?

A
  • 1st line + gold standard: Dual X-ray absorptiometry (DEXA) - T- and Z-score
  • Diagnosis = T-score ≤-2.5
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42
Q

What signs and symptoms might a patient with osteoporosis present with?

A

Asymptomatic until fragility fractures occur

Signs:

Evidence of acute fracture:

  • Pain
  • Acute bony deformity
  • Inability to weigh bare

Evidence of previous fractures:

  • Kyphosis (curvature of spine)
  • Chronic bony deformity
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43
Q

Describe the DEXA scan, T- and Z-scores in more detail

A

Z-scores compare the patient’s bone density against age-matched controls

T-scores compare the patient’s bone density against healthy adults at peak bone density

T-score ≤-2.5 = osteoporosis

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44
Q

What is the management for osteoporosis?

A

Conservative:

  • Weight-bearing exercise
  • Dietary sources of vitamin D and calcium
  • Smoking cessation
  • Reduce alcohol consumption

Medical:

  • Men and women with fragility fracture of DEXA T-score <2.5:

1st line:

Bisphosphonates - reduce osteoclast activity through the inhibition of enzyme (Farnesyl Pyrophosphate synthase) e.g. alendronic acid

Calcium and vitamin D supplements: adcal D3

Denosumab: post-menopausal women at high risk of fracture

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45
Q

What is osteopenia?

A

It is a less severe loss of bone density compared to osteoporosis. Reduced bone density means bones are not as strong and are more prone to fractures

Defined as a T-score of -1 to -2.5

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46
Q

Define fibromyalgia

A

A syndrome characterised by widespread pain and tender points at specific anatomical sites. It is often accompanied by depression, fatigue and sleep disturbance.

MSK equivalent of IBS

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47
Q

What is the pathophysiology of fibromyalgia?

A

CNS pathology (i.e., brain and spinal cord) and involves a problem with pain processing and pain/sensory amplification (increased pain response to painful stimuli and pain response to non-painful stimuli)

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48
Q

What are the risk factors for developing fibromyalgia?

A
  • Female sex: x1.5 more likely to be diagnosed
  • Family history of fibromyalgia

Aged 30-60 - peak onset of symptoms and diagnosis

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49
Q

What signs and symptoms might a patient with fibromyalgia present with?

A

Symptoms:

  • Chronic pain
  • Fatigue
  • Sleep disturbances
  • Headaches
  • Difficulties with concentration

Signs:

Specific tender points throughout the body suggest fibromyalgia (see next flashcard)

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50
Q

What are the 18 tender points that suggest fibromyalgia (see OneNote for diagram)?

A
  • Occiput (base of skull)
  • Low cervical region (C3 - C7)
  • Trapezius (shoulder muscle)
  • Supraspinatus (shoulder muscle)
  • Second rib
  • Lateral epicondyle (outside of elbow)
  • Gluteal region
  • Greater trochanter (hip)
  • Knees

Tenderness to these areas bilaterally was previously used as a diagnostic criterion for fibromyalgia.

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51
Q

How is fibromyalgia diagnosed?

A

Clinical diagnosis

Diagnosis = presence of chronic, widespread body pain for > 3 months and associated symptoms such as fatigue and sleep disturbance

A 31-point questionnaire assessing patients on:

  • A widespread pain index (WPI), body divided into 19 regions, patients report painful areas
  • A symptoms severity score (SS) assesses fatigue, sleep and cognitive symptoms

Diagnosis is made if 3 conditions are met:

  • WPI ≥7 and SS ≥5 or WPI 3 - 6 and SS ≥9
  • Symptoms ≥ 3 months
  • Other conditions that might cause the pain excluded

Other tests are used to exclude other diagnoses.

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52
Q

What tests are used to exclude DDx for fibromyalgia?

A

TFTs: hypothyroidism

Erythrocyte sedimentation rate +/- autoimmune screen: inflammatory arthropathy

Creatine kinase: inflammatory myopathy

Bone profile & LFTs: hyperparathyroidism and osteomalacia

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53
Q

What is the management plan for fibromyalgia?

A

Difficult and tailored to each patient

First-line:

  • Patient Education
  • Physical therapy: individualised graded physical exercise, particularly aerobic exercise
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54
Q

Define Sjogren syndrome

A

Systemic auto-immune disorder

Characterised by dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) caused by lymphocytic infiltration into the lacrimal and salivary glands

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55
Q

What are the two different types of Sjogren syndrome?

A

Primary Sjogren’s - occurs in isolation

Secondary Sjogren’s - related to SLE or RA

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56
Q

What signs and symptoms might a patient with Sjogren syndrome present with?

A

Symptoms

  • Fatigue
  • Dry eyes
  • Dry mouth

SIgns

  • Vasculitis (skin rash)
  • Dental caries
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57
Q

What investigations and tests are used to diagnose Sjogren syndrome?

A
  • Schirmer’s test - filter paper inserted under the lower eyelid hanging over the eyelid.

Test positive if <5mm paper is wetted after 5 mins (normal ~15mm)

  • Serology - anti-Ro and anti-La antibodies test
  • anti-Ro and anti-La autoantibodies associated with autoimmune diseases, present in around 90% patients with Sjogren’s syndrome
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58
Q

What is the management plan for Sjogren’s syndrome?

A

1st line: Artificial tears, artificial saliva, vaginal lubricants

Hydroxychloroquine might be considered by doctor to halt progression

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59
Q

Define giant cell arteritis (GCA)

A

Large vessel vasculitis, the most common type to affect adults

Usually affects branches of the carotid artery:

  • Superficial temporal artery
  • Mandibular artery
  • Ophthalmic artery

Aka temporal arteritis

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60
Q

What is the pathophysiology of giant cell arteritis (GCA)?

A

Granulomatous inflammation along the affected vessel walls > intimal thickening and narrowed lumen > affects blood flow

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61
Q

What are the risk factors for developing GCA?

A

Rare, ~0.5% population

  • Age: > 50
  • Female
  • Caucasians
  • Polymyalgia rheumatica (PMR) - condition that causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips
  • Family history
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62
Q

What signs and symptoms might a patient with GCA present with?

A

Depends on the artery affected

Symptoms

  • Superficial temporal artery:

Headache and scalp pain when combing hair

  • Mandibular artery:
    Jaw claudication
  • Ophthalmic artery:
    Visual loss due to retinal ischaemia

Signs

  • Superficial temporal artery tenderness
  • Absent temporal artery pulse
  • Reduced visual acuity
  • Pallor of the optic disc
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63
Q

What investigations/tests are used to diagnose GCA?

A

Temporal artery biopsy: definitive test for diagnosis

A positive biopsy = presence of granulomas

Skip lesion - so take a large chunk otherwise could result in negative biopsy

ESR: a value ≥ 50mm/h = 1 of 5 diagnostic criteria

CRP - elevated

FBC - normochromic, normocytic anaemia

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64
Q

What are the diagnostic criteria for GCA?

A

3 or more criteria need to be met for a diagnosis of GCA.

  • Age ≥ 50
  • New-onset headache
  • Temporal artery abnormality: e.g. tenderness on palpation or decreased pulsation
  • Elevated ESR ≥ 50mm/h
  • Abnormal temporal artery biopsy
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65
Q

What is the management plan for GCA?

A

1st line - Corticosteroid:

  • Prednisolone
  • IV methylprednisolone for visual symptoms
  • Oral aspirin: 75mg daily - may protect against cranial ischaemia

Urgent ophthalmology review: if there is evidence of visual compromise

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66
Q

What are the main DDx for GCA?

A
  • Polymyalgia rheumatica - mainly causes stiffness and aching in shoulders and proximal limb muscles in morning
  • Solid organ caners and haematological malignancies
  • Takayasu’s arteritis (main difference is TA age onset younger at 20 -30 and affects mainly women)
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67
Q

What is polymyalgia rheumatica (PMR)?

A

A chronic inflammatory rheumatic condition of unknown cause.

Closely associated with GCA, 2 in 5 people with GCA develop PMR.

Patients commonly present with bilateral pain, and stiffness in the shoulders + hips (>45 mins in morning/rest)

Diagnosis of exclusion: ESR raised >40 mm/hr while creatine kinase (CK), rheumatoid factor (RF) normal

Treatment = oral prednisolone then reduce dose weekly

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68
Q

What complications can arise from GCA?

A
  • Ischaemic cranial complications: visual loss and cerebrovascular accidents (stroke)
  • Aortic aneurysms
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69
Q

Define granulomatosis with polyangiitis (GPA)

A

Granulomatosis with polyangiitis (Wegener’s granulomatosis) is a systemic vasculitis affecting small and medium vessels.

The classic triad of organ systems affected:

  • Upper respiratory tract
  • Lower respiratory tract
  • Renal with pauci-immune glomerulonephritis (small vessel vasculitis that leads to renal failure)
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70
Q

What signs and symptoms might a patient with GPA present with?

A

Upper respiratory tract:

  • Nose bleeds (epistaxis)
  • Saddle-shaped nose due to perforated nasal septum
  • Hearing loss
  • Sinusitis

Lungs:

  • Cough
  • Wheeze
  • Haemoptysis (coughing up blood)

Kidneys
Rapidly progressing glomerulonephritis

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71
Q

What investigations and tests are used to diagnose GPA?

A

Anti neutrophil cytoplasmic antibodies (ANCA) - definitive blood test in vasculitis

The test is positive for c-ANCA

  • Urinalysis and microscopy - haematuria, proteinuria, dysmorphic RBCs, RBC casts
  • CT chest - lung nodules, infiltrates
  • FBC and differential - anaemia
  • Inflammatory markers (CRP and ESR) elevated
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72
Q

What is the management plan for granulomatosis with polyangiitis?

A

1st line:

  • Corticosteroids, e.g. prednisolone
  • Immunosuppressant - severe disease = rituximab (anti-B-lymphocyte mAb), non-severe disease = methotrexate
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73
Q

What conditions are part of the group of conditions known as seronegative spondyloarthropathy?

A
  • Ankylosing spondylitis (AS)
  • Reactive arthritis
  • Psoriatic arthritis

They are associated with the HLA B27 gene

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74
Q

What are the general features of spondyloarthropathies?

A

Mnemonic: SPINE-ACHE

S - Sausage fingers (dactylitis)
P - Psoriasis
I - Inflammation + backache
N - NSAIDs- good response
E - Enthesitis (inflammation where tendons and ligaments attach to bones) - plantar fasciitis, inflamed knee tendon)
A - Arthritis
C - Crohn’s or colitis
H - HLAB27
E - Eyes > uveitis

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75
Q

Define Ankylosing spondylitis (AS)

A

An inflammatory condition mainly affecting the spine.

  • Causes progressive stiffness and pain.
  • Part of the seronegative spondyloarthropathy group of conditions relating to the HLA B27 gene
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76
Q

What is the aetiology of AS?

A

Strong link with the HLA B27 gene.

  • ~90% of patients with AS have the HLA B27 gene
  • ~2% of people with the gene will get AS

This number is higher (around 20%) if they have a first-degree relative that is affected.

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77
Q

What is the pathophysiology of AS?

A

Key joints affected:

  • Sacroiliac joints
  • Vertebral column joints
    The inflammation causes pain and stiffness in these joints.

It can progress to the fusion of the spine and sacroiliac joints - “bamboo spine” on spinal x-ray

78
Q

What signs and symptoms might a patient with AS present with?

A

Typical presentation in exams - young adult male in his late teens/the early 20s

Although studies show it affects men and women in similar numbers

Symptoms:

  • Lower back pain, stiffness, reduced spinal movement
  • Worse with rest, improves with movement
  • Worse at night
  • Painful red eye

Signs:

  • Sacroiliac pain in the buttock region
  • Uveitis
  • Schober’s Test shows decreased spine flexion (<20cm) when patient tries to touch their toes while standing

Symptoms can fluctuate with “flares” of worsening symptoms and other periods where symptoms improve.

79
Q

What investigations and tests are used to diagnose AS?

A
  • 1st line: spinal x-ray/MRI - sacroiliitis (inflammation of sacroiliac joint) and bamboo spine (fused spine)
  • Inflammatory markers (CRP and ESR) elevated
80
Q

What is the management plan for AS?

A
  • 1st line: regular exercise regime and NSAIDS as it stops new spinal bone formation
  • Steroids - used during flares to control symptoms
  • DMARD if NSAIDs ineffective - anti-TNF-alpha (proinflammatory cytokine) medications, e.g. infliximab
81
Q

What is a key complication of AS?

A

Vertebral fractures

82
Q

What are the main DDx for AS?

A
  • Osteoarthritis
  • Psoriatic arthritis
  • Reactive arthritis
83
Q

Define psoriatic arthritis

A

Psoriatic arthritis is an inflammatory arthritis associated with psoriasis.

Can be mild with stiffening and soreness in the joint

Severe: arthritis mutilans where joints are completely destroyed

10-20% of patients with psoriasis within 10 years.

84
Q

What signs and symptoms might a patient with psoriatic arthritis present with?

A

Symptoms:

  • Painful, swollen, stiff joints

Signs:

  • Psoriatic plaques on the skin
  • Pitting of the nails
  • Onycholysis (separation of the nail from the nail bed)
  • Dactylitis (inflammation of the full finger)
  • Enthesitis (inflammation of the entheses, which are the points of insertion of tendons/ligaments into bone)
85
Q

What sign is seen in a patient with arthritis mutilans?

A

Telescopic finger - osteolysis (destruction) of the bones around the joints in the digits leads to the shortening of the digits

86
Q

What investigations and tests are used to diagnose psoriatic arthritis?

A

X-ray of hands and feet - erosion of DIP joints and classic sign is “pencil-in-cup appearance” of digit joints

87
Q

What is the management plan for psoriatic arthritis?

A

1st line:
- NSAIDs for pain and inflammation
- Physiotherapy

Patients with joint erosion/polyarthritis

  • Disease-modifying antirheumatic drugs (DMARDs) (e.g. methotrexate)
  • Anti-TNF medications (e.g. infliximab) if DMARDs fail
88
Q

DDx for psoriatic arthritis

A
  • Rheumatoid arthritis (RA)
  • Gout
  • Erosive osteoarthritis
89
Q

Define reactive arthritis

A

Reactive arthritis is where synovitis occurs in the joints as a reaction to certain recent gastrointestinal and genitourinary infections.

90
Q

What are the most common infections that trigger reactive arthritis?

A
  • Gastroenteritis or sexually transmitted infection.
  • Chlamydia is the most common STI cause
  • Gonorrhoea commonly causes gonococcal septic arthritis.

Think of reactive arthritis + septic arthritis if someone had a recent STI

91
Q

What is a good way to remember the symptoms/signs of reactive arthritis?

A

Can’t see - Uveitis (middle layer of eye inflammation)
Can’t pee - Urethritis (inflammation of urethra)/ Balanitis (inflammation of penis head)
Can’t climb a tree - arthritis

92
Q

What is an important DDx for reactive arthritis?

A

Septic arthritis - if a patient presents with acute warm, swollen, painful and hot joints, give Abx until excluded as cause

93
Q

What investigations/tests are used to diagnose reactive arthritis?

A

Joint aspiration - the absence of microorganisms excludes septic arthritis. Raised WCC will be seen

Swab from the infected site: urethral, cervical or rectal swab to demonstrate evidence of an STI

Stool sample: if the history is consistent with infective gastroenteritis as a precipitant

94
Q

What is the management plan for a patient with reactive arthritis?

A
  • NSAIDs
  • Intra-articular steroid injections into affected joints if monoarticular
  • Systemic corticosteroids when polyarticular
  • Abx for STI
  • Most resolve within 6 months and don’t recur.
95
Q

Define septic arthritis

A

Septic arthritis describes an infection of a joint. Septic arthritis must be considered a medical emergency due to the risk of permanent joint destruction, osteomyelitis and sepsis.

96
Q

What is the aetiology of septic arthritis?

A

Up to 90% of cases are caused by staphylococci or streptococci, often as a complication of other pathologies such as cellulitis, chronic osteomyelitis, or IV drug abuse.

97
Q

What are some other causes of septic arthritis?

A

Staphylococcus epidermidis - Prosthetic joints

Streptococcus pyogenes - Children under 5 years old

Neisseria gonorrhoeae - Young, sexually-active adults

98
Q

What signs and symptoms might a patient with septic arthritis present with?

A

Symptoms:

  • Fever
  • Difficulty weight bearing on affected side
  • Typically affects a single joint

Signs:

  • Hot, tender, erythematous, swollen joint
  • Very limited range of movement
99
Q

What investigations and tests are used to diagnose septic arthritis?

A

Definitive investigation: joint aspiration (arthrocentesis) before starting antibiotics, synovial fluid sent to the lab for culture and microscopy:

  • Colour: yellow and cloudy (normally clear)
  • WBC/ul: >50,000
  • PMN cells (e.g. neutrophils): >50%

Blood cultures: should be performed on all patients before commencing antibiotics

  • FBC: leukocytosis
  • CRP and ESR: elevated
100
Q

What is the Kocher criteria?

A

Used in children to diagnose septic arthritis in the hip, each criterion gives 1 point:

Non-weight bearing

Temp > 38.5

ESR > 40mm/hr

WCC > 12 x 109/L

  • score ≥ 3 = 93% probability
101
Q

What is the management plan for septic arthritis?

A

Combination of antibiotics and joint aspirations to dryness:

Abx: IV 2 weeks then oral 4 weeks

  • 1st line: flucloxacillin
  • Penicillin allergy: clindamycin
  • MRSA: vancomycin
  • Gonococcal arthritis or gram-negative infection: cefotaxime or ceftriaxone
102
Q

What are some complications that can arise from septic arthritis?

A

Osteomyelitis: the spread of infection from the joint to the surrounding bone

Permanent joint destruction

Sepsis

103
Q

DDx for septic arthritis

A
  • Osteoarthritis
  • Psoriatic arthritis
  • Rheumatoid arthritis
104
Q

Define osteomyelitis (OM)

A

Osteomyelitis (OM) is an inflammatory condition affecting any bone in the skeleton, usually as a result of bacterial infection

105
Q

What is the pathophysiology of OM?

A

The underlying infection may occur due to haematogenous spread from, e.g. septic arthritis or direct penetration by a causative microorganism e.g. trauma.

OM can be both acute or chronic in its presentation.

106
Q

What is the aetiology of OM?

A

The most common causative microorganism:

  • Staphylococcus aureus: most common (90%)
  • Salmonella species: most common cause in sickle-cell disease patients
107
Q

What are the risk factors for developing OM?

A
  • Penetrating injury
  • Intravenous drug use: S. aureus, Pseudomonas
  • Diabetes mellitus - particularly if foot ulcers present
  • Sickle cell disease
  • Rheumatoid arthritis
108
Q

What signs and symptoms might a patient with OM present with?

A

Symptoms:

  • Fatigue - especially with chronic OM
  • Fever
  • Pain at infection site
  • Reduced range of movement

Signs:

  • Puncture wound: may be visibly infected
  • Not weight-bearing (common in children)
  • Local inflammation
  • Local erythema
  • Swelling
  • Vertebral osteomyelitis
  • Ulceration or Charcot foot: diabetics
109
Q

What investigations/tests are used to diagnose OM?

A
  • FBC: raised in acute infection, may be normal in chronic osteomyelitis
  • ESR: raised in acute, often normal in chronic
  • CRP: raised in acute, often normal in chronic
  • Blood cultures: to identify causative microorganism and microbial sensitivities
  • X-ray of the affected area:
  • Osteopenia
  • Bone destruction
110
Q

What is the treatment for acute OM?

A

Sepsis - treat immediately!

Acute OM:

  • 1st line: IV flucloxacillin
  • Suspected MRSA infection: vancomycin
  • Supportive therapy: analgesia, hydration
  • Acute OM in a patient with diabetic foot:

MDT referral (diabetologist, orthopaedic surgery, podiatry, microbiology)

111
Q

What is the treatment for vertebral osteomyelitis

A

Vertebral osteomyelitis:
Referral to infectious diseases team and spinal surgery

If neurological involvement, progressive disease or spinal instability: surgery

No neurological involvement: broad spectrum IV abx - vancomycin and ceftriaxone

Supportive therapy: analgesia, hydration

112
Q

What is the treatment for chronic OM?

A

Chronic osteomyelitis = >3 months

Diabetic foot ulcer infection > osteomyelitis

  • MDT referral: diabetologist, orthopaedic surgery, podiatry, microbiology
  • Consideration for surgery
  • Optimisation of contributing co-morbidities: diabetes, nutrition, sickle cell disease
  • Treat acute flares: IV antibiotics.
113
Q

Define systemic lupus erythematosus (SLE)

A

SLE is a chronic systemic autoimmune condition caused by a type 3 hypersensitivity reaction (immune complexes) - IgG mediated.

Apoptotic debris is poorly cleared > activates an immune response -producing antibody-antigen complexes (IgG antibodies against double-stranded DNA)

immune complex deposit in tissues > complement activation > tissue inflammation & damage

Immune complex deposition can affect any organ, such as the skin, joints, kidneys, heart and brain.

114
Q

What are the risk factors for developing SLE?

A
  • Middle-aged: peak onset age - 15 and 45
  • Female gender: x12 more likely
  • African and Afro-Caribbean - more prevalent and severe
  • Family history

Drugs: procainamide, isoniazid, hydralazine may cause drug-induced Lupus

115
Q

Genetics is thought to play a role in the aetiology of SLE. What genes are associated with SLE?

A

HLA genes: HLA-B8, HLA-DR2, HLA-DR3

116
Q

What are the most common symptoms/signs of SLE?

A

SLE is a multi-system disorder which most commonly affects the joints and skin - many other signs/symptoms in other organs

Classic presentation:

  • Malar “butterfly” rash
  • Fatigue
  • Widespread MSK pain
  • Middle-aged African female
  • Relapsing/remitting with acute flares
117
Q

What are some of the other symptoms/signs of SLE?

A
  • Joint pain
  • Skin - discoid rash, photosensitive rash
  • Serositis (inflammation of serous membrane) - scleritis, pericarditis, pleuritis, oral ulcers
  • Kidneys - Glomerulonephritis with proteinuria (lupus nephritis)
  • CNS - depression, psychosis
118
Q

What investigations/tests are used to diagnose SLE?

A

FBC: anaemia, thrombocytopaenia and leukopaenia

U&E: lupus nephritis can cause chronic kidney disease

ESR raised in active disease

CRP is usually normal; raised CRP = underlying infection

Antibodies:
ANA (antinuclear antibodies): most sensitive test and present in 99% of patients - associated with autoimmune disease

Anti-dsDNA & anti-Smith - highly specific for SLE and can confirm the diagnosis

119
Q

What is the management plan for SLE?

A

Treatment for acute flares:

Mild:

  • Prednisolone (corticosteroid)
  • Hydroxychloroquine (DMARD)
  • NSAIDs

Moderate/severe:

  • Prednisolone and hydroxychloroquine
  • An immunosuppressant e.g. azathioprine

Maintenance therapy:
Once patient is stable - reduce steroid dose

The goal = hydroxychloroquine alone.

Avoid the sun and use sunscreen

120
Q

Define Paget’s disease of the bone

A

Paget’s disease (or Paget’s disease of the bone) is a condition characterised by increased bone turnover due to increased osteoclast activity.

This leads to metabolic hyperactivity within the bone > patchy areas of high density (sclerosis) and low density (lysis) > long-bone and skull deformities

121
Q

What are the risk factors for developing Paget’s?

A
  • Males are slightly more at risk than females
  • Age: mean onset 55 years
  • Family history of Paget’s disease
  • Infection: paramyxoviruses
122
Q

What symptoms would a patient with Paget’s disease present with?

A
  • Asymptomatic: incidental finding on x-ray or LFT in most patients
  • Bone pain: femur/pelvis 75% of patients, skull involvement 37%
  • Facial pain: if skull disease with CN V involvement
  • Hearing loss: if skull disease with CN VIII involvement
123
Q

What signs would be present in a patient with Paget’s disease?

A
  • Bony deformities: skull bossing, bone bowing, prognatism (protrusion of lower jaw)
  • Pathological fracture
  • Reduced visual acuity: if CN II involvement (rare)
  • Local temperature rise: due to increasing metabolic activity
124
Q

What investigations and tests are used to diagnose Paget’s disease?

A

Plain film x-ray: early-stage = osteolytic lesions, fractures, late stage = sclerotic changes

Radionucleotide bone scan: to identify pagetoid bone

Liver function tests: raised ALP

Bone profile: calcium normal but sometimes raised

Vitamin D level: normal in Paget’s but decreased in osteomalacia

125
Q

What is the management plan for Paget’s disease?

A

Treatment depends on whether a patient is asymptomatic or disease is in a high-risk area of bone e.g. skull or affecting a joint

Asymptomatic:

Observation: regular follow-up, education, e.g. regarding high-risk activities

Symptomatic or high-risk:

1st line:
Bisphosphonates: alendronic acid to reduce osteoclastic activity

Severe disease:
Surgery: i.e. total hip replacement if hips affected

126
Q

What are the main DDx for Paget’s disease?

A

Osteomalacia - low vitamin D levels in osteomalacia vs normal levels in Paget’s disease

127
Q

Define antiphospholipid syndrome

A

A disorder associated withantiphospholipid antibodieswhere the blood becomes prone to clotting.

The patient is in a hyper-coagulable state.

Associated with thrombosis and pregnancy complications such as recurrent miscarriages.

128
Q

What is the pathophysiology of antiphospholipid syndrome?

A

Antiphospholipid syndrome can be primary or secondary to an autoimmune condition, particularly SLE.

It is associated with antiphospholipid antibodies:

  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein I antibodies

These antibodies interfere with coagulation and create a hypercoagulable state where the blood is more prone to clotting.

129
Q

What conditions are antiphospholipid syndrome associated with?

A
  • Venous thromboembolism - DVT, PE
  • Arterial thrombosis: strokes, MI, renal thrombosis
  • Pregnancy complications: recurrent miscarriage, stillbirth, preeclampsia
  • Thrombocytopenia (low platelets)
130
Q

What signs and symptoms might a patient with antiphospholipid syndrome present with?

A

A patient with APS usually presents with signs/symptoms of associated conditions e.g.:

  • History or current diagnosis of vascular thrombosis
  • History of pregnancy loss
  • History of SLE
  • Joint stiffness/arthritis
  • Thrombocytopenia (low platelets caused by idiopathic thrombocytopenic purpura)
131
Q

What investigations and tests are used to diagnose antiphospholipid syndrome?

A

Diagnosis based on history of thrombosis or pregnancy complication and persistent antibodies:

Lupus anticoagulant

Anticardiolipin antibodies

Anti-beta-2 glycoprotein I antibodies

132
Q

What is the management plan for antiphospholipid syndrome?

A

APS with thrombosis (non-pregnant)

  • 1st line: Low-molecular weight heparin
  • Follow-up with warfarin

APS with thrombosis (pregnant)

  • 1st line: LMWH
  • Follow-up with fetal monitoring + MDT
  • Warfarin post delivery
  • Management of risk factors (e.g. hypercholesterolemia, smoking cessation etc.)
133
Q

Define polymyositis and dermatomyositis

A

Polymyositis and dermatomyositis are autoimmune disorders with muscle inflammation (myositis). They are rare.

134
Q

What is polymyositis?

A

A condition where there is chronic inflammation of the muscles

135
Q

What is dermatomyositis?

A

A connective tissue disorder where there is chronic inflammation of the skin and muscles.

136
Q

What signs and symptoms might a patient with polymyositis present with?

A
  • Muscle pain, fatigue and weakness
  • Occurs bilaterally and mostly affects the shoulder and pelvic girdle
  • Develops over weeks

Polymyositis occurs without any skin features whereas dermatomyositis is associated with involvement of the skin.

137
Q

What signs and symptoms might a patient with dermatomyositis present with?

A

General symptoms:
Muscle pain, fatigue and weakness

Occurs bilaterally and mostly affects the shoulder and pelvic girdle

Develops over weeks

Additional skin features (signs):

  • Gottron lesions(scaly erythematous patches) on the knuckles, elbows and knees
  • Photosensitive erythematous rashon the back, shoulders and neck
  • Purple rash on the face and eyelids
  • Periorbital oedema (swelling around the eyes)
138
Q

What investigations/tests are used to diagnose polymyositis?

A
  • Clinical presentation
  • Elevated creatine kinase
  • Electromyography (EMG)
  • Muscle biopsy - definitive diagnosis
  • Autoantibodies test:

Anti-Jo-1 antibodies: polymyositis (but often present in dermatomyositis)

139
Q

What investigations/tests are used to diagnose dermatomyositis?

A

Similar to polymyositis except for different autoantibodies.

  • Clinical presentation
  • Elevated creatine kinase
  • Autoantibodies: anti-Mi-2 antibodies, anti-nuclear antibodies
  • Electromyography (EMG)
  • Muscle biopsy - definitive diagnosis
140
Q

What is the management plan for polymyositis and dermatomyositis?

A

1st line: corticosteroids

If no response to steroids:

  • Immunosuppressants (such as azathioprine)
  • IV immunoglobulins
  • Biological therapy (such as infliximab)
141
Q

What are the different types of primary bone tumours?

A
  • Osteosarcoma (most common malignancy), associated with Paget’s, most commonly onsets between 15 - 19 years old
  • Ewing’s sarcoma - from mesenchymal stem cells, 15 years old, very rare
  • Fibrosarcoma
  • Osteochondroma - Benign, very common in M < 25yo
142
Q

What causes osteochondroma?

A

Overproduction of bone which deposits on the metaphysis (growth plates)

143
Q

Where does osteosarcoma most commonly metastasise to?

A

Lungs

144
Q

What are osteolytic metastases?

A

Osteolytic metastases occur when metastatic cancer cells destroy bone, causing the bone to become weak.

Osteolytic metastases often happen when breast cancer spreads to the bone.

145
Q

WHat are osteoblastic metastases?

A

Osteoblastic metastases develop when cancer cells invade the bone and cause excess bone proliferation. The bone becomes very dense (sclerotic).

Osteoblastic metastases often happen when prostate cancer spreads to the bone.

146
Q

Which types of cancer most commonly metastasise to the bone?

A

BLT KP (bacon leuttce tomato and KP notes)

B - Breast
L - Lung
T - Thyroid
K - Kidney
P - Prostate

147
Q

What are the general symptoms of bone cancer?

A

Local

  • Severe bone pain worst at pain - enough to wake patient up
  • Reduced range of movement of vertebrates/long bones if affected
  • Pathological fractures.

Systemic - weight loss, fatigue, fever, malaise

148
Q

What investigations/tests are used to diagnose bone cancers?

A

Bloods:

FBC - normal
ALP - raised
PSA - raised in prostate cancer

Imaging:

X-rays - can show osteolysis
CT scans. -shows metastates

149
Q

What are the general treatments for bone cancers?

A
  • Pain Management
  • Bisphosphonates (e.g. alendronic acid) - slows down osteoclast activity
  • Radiotherapy
  • Chemotherapy
150
Q

Define scleroderma/CREST

A
  • Scleroderma (aka systemic sclerosis) is a multi-system, autoimmune disease.
  • Functional and structural abnormalities of small blood vessels
  • Fibrosis of skin and internal organs
  • Production of auto-antibodies.
  • Subdivided into Diffuse Cutaneous Systemic Sclerosis and Limited Cutaneous Systemic Sclerosis.
151
Q

What is Diffuse Cutaneous Systemic Sclerosis?

A

Diffuse Cutaneous Systemic Sclerosis is a subcategory of systemic sclerosis that affects multiple organ systems but no skin involvement like in systemic sclerosis

152
Q

What is Limited Cutaneous Systemic Sclerosis?

A

a subcategory of systemic sclerosis that affects fewer organs, notably sparing the kidneys and the skin on the trunk and proximal limbs

153
Q

What is CREST syndrome?

A

Another name for Limited Cutaneous Systemic Sclerosis and describes the main clinical features

154
Q

What is the aetiology of scleroderma/CREST?

A

Related to increased production of collagen in tissues.

Immunological - auto-antibodies are associated with the conditions:

  • 90% of patients are positive for Anti-Nuclear Antibodies
  • Limited sclerosis - Anti-centromere antibodies
  • Systemic sclerosis - Anti-topoisomerase I (Scl-70) antibodies
155
Q

Which population is most commonly affected by scleroderma/CREST?

A

Women aged between 30 - 50

156
Q

What signs and symptoms might a patient with Limited Cutaneous Systemic Sclerosis present with?

A

Symptoms:

Skin involvement - skin thickening distal to elbows and knees: face and distal limbs predominantly

Raynaud’s phenomenon often comes before skin changes (fingers turn cold and blue to minor triggers)

CREST syndrome:

  • Calcinosis (calcium deposits in soft tissue)
  • Raynaud’s phenomenon
  • Esophageal dysmotility
  • Sclerodactyly (hardening of the skin on hand > claw-like)
  • Telangiectasia (spider veins)
157
Q

What signs and symptoms might a patient with Diffuse Cutaneous Systemic Sclerosis preset with?

A

Skin involvement:

  • Skin thickening extends proximally: trunk and proximal limbs predominantly
  • Raynaud’s phenomenon can occur before or after skin changes

Early visceral involvement:

  • Interstitial lung disease
  • Pulmonary hypertension
  • Renal crisis: acute renal failure with hypertension
  • Hypertension
158
Q

Systemic sclerosis has characteristic dermatological features. What are they?

A
  • Sclerodactyly (prayer sign)
  • Skin tightening and fibrosis; may present as plaques (morphoea) or linear
  • Digital ulcers
  • Calcinosis: lumpy calcium deposits
  • Telangiectasia

Typical facies:

  • Perioral furrowing: wrinkles in the skin around the mouth
  • Beaked nose
  • Microstomia: tightening of the skin around the mouth
159
Q

What investigations/tests are used to diagnose scleroderma/CREST?

A

Serum auto-antibodies:

  • Anti-nuclear antibodies (ANA): positive in 90% of patients
  • Anti-centromere: more common in limited systemic sclerosis
  • Anti-Scl 70 (Anti-topoisomerase): more common in diffuse systemic sclerosis

Bloods:

  • FBC: anaemia of chronic disease (microcytic anaemia)
  • U&Es: may demonstrate evidence of renal failure
  • CRP and ESR: elevated inflammatory markers
160
Q

What is the management plan for systemic sclerosis/scleroderma/CREST?

A

There is no cure and the disease is generally progressive

  • Immunosuppressants are used to slow the disease progression - particularly cyclophosphamide
  • Physiotherapy
  • Occupational therapy
  • Symptomatic treatment for clinical features:
  • Analgesia
  • Calcium channel blockers for Raynauds (i.e. nifedipine)
  • Topic skin emollients
  • PPI for oesophageal reflux
  • Treating hypertension (bosentan, sildenafil, iloprost)
161
Q

Alendronic acid

1) Use
2) MOA
3) Side effects

A

1) osteoporosis

2) Bisphosphonate, they are adsorbed onto hydroxyapatite crystals in bone, slowing both their rate of growth and dissolution, and therefore reducing the rate of bone turnover.

3) Alopecia; anaemia; appetite decreased; arthralgia;

162
Q

Celecoxib (NSAID)

1) Use
2) MOA
3) Side effects

A

1) Ankylosing spondylitis, pain and inflammation in rheumatoid arthritis and osteoarthritis

2) Selective inhibition of cyclooxygenase-2 (COX-2), which is responsible for prostaglandin synthesis, involved in pain and inflammation

3) Angina pectoris; benign prostatic hyperplasia; cough

163
Q

Chloramphenicol

1) Use
2) MOA
3) Side effects

A

1) Superficial eye infection, outer ear infection, typhoid fever

2) Chloramphenicol is a potent broad-spectrum antibiotic.

3) With parenteral use: aplastic anaemia (rare)

Ear: blood disorder; bone marrow depression

Eye (topical): angioedema; bone marrow disorders

164
Q

Ciclosporin

1) Use
2) MOA
3) Side effects

A

1) Severe acute ulcerative colitis refractory to corticosteroid treatment, severe RA

2) Ciclosporin inhibits production and release of lymphokines, thereby suppressing cell-mediated immune response.

3) Eye inflammation, appetite decreased; diarrhoea

165
Q

Ciprofloxacin

1) Use
2) MOA
3) Side effects

A

1) Superficial eye infection, outer ear infection, corneal ulcer

2) Broad-spectrum Abx, inhibition of the enzymes topoisomerases, required for bacterial DNA replication, transcription, repair, and recombination.

3) Quinolones can cause convulsions and tendon damage

166
Q

Ethinylestradiol

1) Use
2) MOA
3) Side effects

A

1) Oestrogen deficiency, post-menopausal osteoporosis prophylaxis

2) Prevents accelerated bone loss by inhibiting bone resorption, restoring the balance of bone resorption and formation

3) Breast abnormalities; cervical mucus increased; cholelithiasis

167
Q

Methotrexate

1) Use
2) MOA
3) Side effects

A

1) Disease-modifying antirheumatic drugs (DMARD) in rheumatoid arthritis and Crohn’s

2) Immunosppredsant that inhibits the enzyme dihydrofolate reductase, essential for the synthesis of purines and pyrimidines. Thus, Methotrexate prevents nucleic acid synthesis and causes cell death.

3) Alopecia; arthralgia; bone marrow disorders, folate deficiency - patients need folic acid supplement

168
Q

Define mechanical back pain

A

Pain that is elicited with spinal motion and decreases with rest

169
Q

What are the main types of mechanical back pain?

A

1) Lumbar strain/sprain (most common 70% cases)

  • Strain - disruption of muscle fibres within the muscle belly > intense pain 24 - 48 hrs
  • Sprain - stretch of ≥ 1 spinal ligament

2) Vertebral disc degeneration

3) Herniated disc

4) Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)

5) Scoliosis (curved spine)

170
Q

What framework should you use when assessing any pain?

A

SOCRATES mnemonic:

S – Site
O – Onset
C – Character
R – Radiation
A – Associations
T – Timing
E – Exacerbating and relieving factors
S – Severity

171
Q

What symptoms should you look out for in a patient with suspected mechanical back pain that indicates a more serious underlying pathology?

A

Key symptoms:

  • Recent major trauma? (spinal fracture)
  • Stiffness in the morning or with rest (ankylosing spondylitis)
  • Age under 40 (ankylosing spondylitis)
  • Gradual onset of progressive pain (ankylosing spondylitis or cancer)
  • Night pain (ankylosing spondylitis or cancer)
  • Age over 50 (cancer)
  • Weight loss (cancer)
  • Bilateral neurological motor or sensory symptoms (cauda equina)
  • Saddle anaesthesia (cauda equina)
  • Urinary retention or incontinence (cauda equina)
  • Faecal incontinence (cauda equina)
  • History of cancer with potential metastasis (cauda equina or spinal metastases)
  • Fever (spinal infection)
  • IV drug use (spinal infection)
172
Q

What key signs (found via examination) for a patient with back pain might indicate a more serious underlying pathology?

A

Key findings on examination are:

  • Localised tenderness to the spine (spinal fracture or cancer)
  • Bilateral neurological motor or sensory signs (cauda equina)
  • Bladder distention implying urinary retention (cauda equina)
  • Reduced anal tone on PR examination (cauda equina)
173
Q

What investigations/tests are used to diagnose patients with mechanical back pain?

A

1) Mechanical/non-specific lower back pain - diagnosed clinically and warrant no further investigations

2) Spinal fractures - CT/MRI of the spine

3) Emergency MRI spine for suspected cauda equina

4) Investigations for suspected ankylosing spondylitis are:

  • Inflammatory markers (CRP and ESR)
  • X-ray of the spinal and sacrum (may show a fused “bamboo spine” in later-stage disease)
  • MRI of the spine (may show bone marrow oedema early in the disease)
174
Q

What is the STarT Back tool?

A

A tool used to assess the risk of a patient with acute back pain developing chronic back pain.

  • Total score (out of 9)
  • Subscore (psychosocial factors)

Low risk: total ≤ 3, subscore ≤ 3

Medium risk: total > 3, subscore ≤ 3

High risk: total > 3, subscore > 3

175
Q

What is the management plan for low-risk acute back pain?

A

1) First, exclude serious underlying causes.

Suspected cauda equina: same-day referral to the on-call orthopaedic team for an urgent MRI scan

Ankylosing spondyltis:

  • Inflammatory markers and an urgent rheumatology review
  • Major trauma - spinal immobilisation, admission and x-rays/CT scans

Patients at low risk of chronic back pain according to STarT back tool can generally be managed with:

  • Self-management
  • Education
  • Reassurance
  • Analgesia (1st line: NSAIDs ibuprofen/naproxen)
  • Staying active and continuing to mobilise as tolerated
176
Q

What is the additional management strategy for patients with acute back pain with a medium-high risk of developing chronic back pain?

A
  • Physiotherapy
  • Group exercise
  • Cognitive behavioural therapy
177
Q

What are the differential diagnoses for back pain?

A
  • Lumbar muscular strain/sprain
  • Herniated disc
  • Spinal stenosis
178
Q

Define degenerative cervical spine disease

A

Cervical spondylosis - osteoarthritis of the spine, which includes the spontaneous degeneration of the disc or facet joints

Most common complications:

  • Cervical spondylotic radiculopathy - arm pain pattern, mild weakness and sensory loss in muscles and skin innervated by affected nerve root
  • Degenerative cervical myelopathy (loss of neurological function from pressure on the cervical spinal cord)
179
Q

What signs and symptoms might a patient with degenerative cervical spine disease present with?

A
  • Commonly asymptomatic (look for risk factors: e.g. over 40, FHx, spinal trauma)
  • Spontaneous onset of neck pain
  • Cervical muscle pain and spasm
  • Headache or occipital pain
180
Q

What investigations/tests are used to diagnose degenerative cervical spine disease?

A

Cervical MRI - bone destruction, spinal cord or nerve compression

Cervical x-ray - presence of degenerative joint disease/degenerative disc disease, spinal canal stenosis

181
Q

What is the management plan for degenerative cervical spine disease?

A

Axial neck pain

  • 1st line: physiotherapy

Cervical spondylotic radiculopathy

  • 1st line: analgesia

Degenerative cervical myelopathy

  • If moderate/severe + fit for surgery - surgical decompression
  • Mild/not fit for surgery - immobilisation with a hard cervical collar
182
Q

What are the differential diagnoses for degenerative cervical spine disease?

A
  • Whiplash injury
  • Acute disc herianation
  • Metastatic malignancy
183
Q

Define discogenic back pain

A

Back pain where the primary source of pain is thought to be from the affected disc

It is a complex multi-factorial clinical condition characterised by low back pain in the presence of radiological confirmed degenerative disc disease

184
Q

What symptoms might a patient with discogenic back pain present with?

A
  • Persistent lower back pain - worsened with sitting or standing, improves with lying down
  • Radicular leg pain - results from nerve root compression
  • Activity-related symptoms - pain exacerbated by motion and relieved by rest
185
Q

What investigations are used to diagnose discogenic back pain?

A

Erect lumbar spine X-ray - presence of osteoporosis, features, metastasis or degenerative changes

MRI spine - signs of degeneration (appearing as black disc)

186
Q

What is the treatment for discogenic back pain?

A

1) Emergency - cauda equina syndrome send for neural decompression

2) Acute back pain < 3. months, or chronic pain exacerbation - analgesia - paracetamol/NSAIDs

3) Chronic pain > 3 months - paracetamol, NSAIDs, opioids (codeine/tramadol) for short-term use only

187
Q

What are some differential diagnoses for discogenic back pain?

A
  • Spinal tumour
  • Spinal infection
  • Postural back pain
188
Q

What is the immunological basis for Ehlers-Danlos syndrome?

A

Ehlers-Danlos syndrome (EDS) is a connective tissue disorder caused by mutations of connective tissue proteins, with collagen being the most commonly affected.

These mutations lead to weakened connective tissue in the skin, bones, blood vessels, and organs.

This results in clinical features:

  • Musculoskeletal - joint hypermobility and pain and recurrent dislocation
  • Skin - hyperelasticity, easy bruising
  • Cardiovascular - mitral valve prolapse, aortic dissection and AAA
  • Neuro - subarachnoid haemorrhage
189
Q

What is the pathophysiology of Marfan syndrome?

A

Marfan syndrome is an autosomal dominant condition caused by the fibrillin-1 gene responsible for creating fibrillin. Fibrillin is an important component of connective tissue, and the mutation affects the mechanical stability and elastic properties of connective tissue.

190
Q

What are the signs and symptoms of Marfan syndrome?

A

Results in the following features:

  • Tall stature
  • Long neck
  • Long limbs
  • Long fingers (arachnodactyly)
  • High arch palate
  • Hypermobility
  • Pectus carinatum (chest sticking out) or pectus excavatum (chest caving in)
  • Positive wrist sign - thumb and little finger overlap when hand wraps around the opp wrist
  • Positive thumb sign - when patients cross their thumb across their palm, if the thumb tip goes past the opposite edge of the hand this indicates arachnodactyly
191
Q

DDx for systemic lupus erythematosus

A
  • Rheumatic arthritis
  • Antiphospholipid syndrome

Sharon's Phase 2a Medicine Revision (10 decks)

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