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2a Medicine > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What is osteoarthritis?

A

Non-inflammatory wear and tear of joints resulting from loss of articular cartilage.
All tissues of the joint are involved.
Articular cartilage is the most affected (produced by chondrocytes).

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2
Q

Who is most commonly affected by osteoarthritis?

A

Elderly and females.

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3
Q

What reduces the risk of osteoarthritis?

A

Osteoporosis.

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4
Q

What is the pathophysiology of osteoarthritis?

A

Imbalance in process of cartilage by wear and production by chondrocytes in favour of cartilage breakdown (chondrocyte ECM breakdown). Faulty cartilage undergoes erosion so disordered repair which causes fibrillations. There is then cartilage ulceration which exposes underlying bone to increased stress and so there are microfractures and cysts. The exposed bone attempts repair and so there is abnormal sclerotic subchondral bone and overgrowth at joint margins. These cartilaginous growths become calcified (osteophytes).

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5
Q

What are the main features of osteoarthritis?

A
  • Loss of cartilage

* Disordered bone repair.

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6
Q

Which cytokines is osteoarthritis driven by?

A
  • IL-1
  • TNF-a
  • NO.
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7
Q

What are the symptoms of osteoarthritis?

A
  • Joint pain on movement (hip is groin pain) and pain at rest in severe OA
  • Pain at night
  • Crepitus: crunching sensation when moving joint
  • Functional impairment in walking and activities of daily living
  • Joint stiffness after rest.
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8
Q

What improves the pain in osteoarthritis?

A

Rest.

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9
Q

Where are the bony swellings in osteoarthritis?

A

Distal interphalangeal (Heberden’s nodes) and proximal interphalangeal (Bouchard’s nodes).

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10
Q

How long is morning stiffness in osteoarthritis?

A

< 30 minutes.

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11
Q

What is shown on an X-ray in osteoarthritis?

A 
Remember LOSS:
L oss of joint space (narrows)
O steophytes
S unchondral sclerosis
S unchondral cysts.
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12
Q

Which joints does osteoarthritis most commonly affect?

A

Big weight-bearing joints (knee, hip, vertebra), affects DIP and PIP, first carpometacarpal joints at base of thumb.

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13
Q

What will the bloods show in osteoarthritis?

A

Normal:
• CRP may be slightly elevated
• Rheumatoid factor and anti-nuclear antibodies negative.

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14
Q

What is the treatment for osteoarthritis?

A

Medical (analgesic ladder):
• Topical: NSAIDs, capsaicin
• Oral: paracetamol, NSAIDs with caution (consider PPI for long-term NSAIDs), opioids e.g. dihydrocodeine
• Transdermal patches: buprenorphine, lignocaine
• Intra-articular steroid injections: hyaluronic acid, role remains unclear
• DMARDs have a role in inflammatory OA.
Surgical:
• Osteophyte removal
• Joint replacement/fusion if severe
• Arthroscopy: only for loose bodies. Indicated in uncontrolled pain particularly at night and significant limitation.
• Osteotomy
• Arthroplasty.

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15
Q

What is rheumatoid arthritis?

A

Autoimmune inflammation of the synovial joints. Chronic systemic inflammatory disease due to deposition of immune complexes in synovial joints which causes symmetrical, deforming polyarthritis.

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16
Q

What are the antibodies present in rheumatoid arthritis?

A

Rheumatoid factor, anti-cyclic citrullinated peptide.

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17
Q

What is the pathophysiology of rheumatoid arthritis?

A

Inflammation of synovial lining of joints:
• Synovium thickens and is infiltrated by inflammatory cells (lymphocytes, macrophages, plasma cells)
• Generation of new synovial blood vessels induced by angiogenic cytokines and activated endothelial cells produce adhesion molecules which force leukocytes into the synovium and cause inflammation of synovial joints.

Proliferation:
• Tumour like mass “pannus” grows over articular cartilage and damages underlying cartilage by blocking its normal route for nutrition and by direct effects of cytokines on chondrocytes
• Cartilage becomes thin and underlying bone is exposed
• Pannus destroys articular cartilage and subchondral bone which causes bony erosions.

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18
Q

Is the arthritis in rheumatoid symmetrical or asymmetrical?

A

Symmetrical.

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19
Q

What are the hand deformities in rheumatoid arthritis?

A

Ulnar deviation, swan neck/Z thumb (PIP hyperextension and DIP flexion), Boutonniere deformity (extensor tendon splits so PIP flexion and DIP hyperextension).

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20
Q

How long is the morning stiffness in rheumatoid arthritis?

A

> 30 minutes.

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21
Q

What improves the pain in rheumatoid arthritis?

A

Use.

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22
Q

What are the joints like in rheumatoid arthritis?

A

Warm, red tender joints.

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23
Q

What joints are affected in rheumatoid arthritis?

A

Small joints (MCP, PIP, MTP of feet, DIP spared), large joints (as disease progresses, wrists, elbows, shoulders, knees, ankles).

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24
Q

What are the extra-articular manifestations of rheumatoid arthritis?

A

Pericardial effusion, pleural effusion, anaemia and uveitis.

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25
Q

Does osteoarthritis or rheumatoid arthritis respond to NSAIDs?

A

Rheumatoid.

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26
Q

What diagnostic criteria is required for rheumatoid arthritis?

A 
Need 4/7:
•	Morning stiffness
•	Arthritis of 3 or more joints
•	Arthritis of hand joints
•	Symmetrical
•	Rheumatoid nodules
•	Rheumatoid factor positive
•	Radiographic changes: LESS.
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27
Q

What are the X-ray changes in rheumatoid arthritis?

A 
Think LESS:
L oss of joint space
E rosions (peri-articular)
S oft tissue swelling
S oft bones (osteopenia).
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28
Q

What will show in the bloods in rheumatoid arthritis?

A
  • Rheumatoid factor positive in 70% of patients (non-specific)
  • Anti-CCP (anti-cyclic citrullinated protein antibody) very specific but not routinely performed
  • FBC: raised platelets, raised CRP, raised ESR, normochromic, normocytic anaemia.
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29
Q

What is the treatment for rheumatoid arthritis?

A
  • Initially NSAIDs for symptom relief
  • Disease-modifying anti-rheumatic (DMARDs) suppresses inflammation e.g. methotrexate. Must give folate supplements as methotrexate inhibits folic acid synthesis. CI in pregnancy. Can lead to malignancy, most commonly of the skin. Other examples are hydroxychloroquine, sulfasalazine
  • Biologics: e.g. rituximab, etanercept (TNF-alpha blocker), baricitinib
  • Acute exacerbations: steroids e.g. IM methylprednisolone injection
  • MDT management : rheumatologist, OT, physiotherapy, GP.
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30
Q

What is osteoporosis?

A

A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.

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31
Q

What is osteopenia?

A

Osteopenia is a precursor to osteoporosis, characterised by low bone density. Defined as bone mineral density 1-2.5 standard deviations below young adult mean value.

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32
Q

How is osteoporosis defined?

A

More than 2.5 standard deviations below young adults mean value.

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33
Q

What are the types of osteoporosis?

A

Primary: menopause and age as oestrogen protects bone. HRT after menopause.
Secondary: to disease or drugs.

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34
Q

What are the causes of osteoporosis?

A

Primary: post-menopausal.

Secondary causes: SHATTERED (increases bone turnover)
S teroid use (prednisolone)
H yperthyroidism/hyperparathyroidism
A lcohol/smoking
T hin (low BMI)
T estosterone low
E arly menopause
R enal or liver failure
E rosive/inflammatory bone disease e.g. RA, myeloma
D ietary calcium low.
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35
Q

Why are women more likely to get osteoporosis?

A

Women lose trabeculae with age whereas in men there is reduced formation but trabeculae numbers are more stable.

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36
Q

What are the risk factors for osteoporosis?

A

Patient: old, female, low BMI, alcohol and smoking, calcium deficient.
Disease: joint disease, hyperthyroidism and hyperparathyroidism, high cortisol, low oestrogen, renal disease and Vitamin D.
Medication: corticosteroids, hormonal.

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37
Q

What is the pathophysiology of osteoporosis?

A

Increased resorption by osteoclasts and decreased formation by osteoblasts. Inadequate peak bone mass. Changes in trabecular structure with ageing so decrease in trabecular thickness and decrease in connections between horizontal trabeculae which means decrease in trabeculae strength and increased susceptibility to fracture.

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38
Q

What are the symptoms of osteoporosis?

A

Asymptomatic until fracture (only cause):
• Hip: neck of femur after elderly individual falls on side or back
• Wrist: distal radius is Colle’s/Smith’s fracture after following on outstretched arm
• Vertebra: shorter and stooping posture. Sudden onset of severe pain in spine, often radiating to front. Thoracic vertebral fractures may lead to kyphosis
• Fragility fractures.

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39
Q

What are the investigations for osteoporosis?

A
  • DEXA BMD (dual energy X-ray and absorptiometry): T score is a standard deviation score. Less than -2.5 is osteoporosis, between -1 and -2.5 is osteopenia and more than -1 is normal
  • X-ray
  • FRAX (fracture assessment tool): age, sex, BMI, previous fractures, steroids
  • FBC: normal calcium phosphate and alkaline phosphate.
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40
Q

What is the first line management for osteoporosis?

A

First line treatment for osteoporosis is Alendronic acid (oral bisphosphonate) and AdCal (vit D and calcium supplement). They inhibit bone resorption through the inhibition of Farensyl Pyrophosphate synthase in the cholesterol pathway which reduces osteoclast activity by removing their ruffled border.
Second line: is the introduction of Denosumab (monoclonal antibody to RANK ligand). This inhibits osteoclast activity and bone resorption.

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41
Q

What is primary prevention for osteoporosis?

A
  • Adcal D3: vitamin D + calcium
  • Calcium-rich diet e.g. dairy or sardines, white beans
  • HRT: menopausal women
  • Corticosteroids: consider prophylactic bisphosphonates
  • Regular weight bearing exercise
  • Smoking and alcohol cessation
  • DEXA scans.
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42
Q

What is SLE?

A

Autoimmune disease is a pathological condition causes by an immune response directed against an antigen within the host i.e. a self-antigen. Heterogenous. Anti-nuclear antibodies.

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43
Q

Who is more commonly affected by SLE?

A

Females.

Peak age of onset is 20-40.

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44
Q

What conditions is SLE associated with?

A

Anti-phospholipid and Raynaud’s.

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45
Q

What causes the onset of a rash in SLE?

A

UV light.

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46
Q

What is the pathophysiology of SLE?

A

A multisystemic autoimmune inflammatory disease in which autoantibodies produced by B cells target a variety of autoantigens leading to the formation of immune complexes at various sites. This activates the complement system and causes an influx of neutrophils which causes inflammation in those types (type III hypersensitivity).

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47
Q

What are the symptoms of SLE?

A
  • Fever
  • Fatigue
  • Rash
  • Myalgia and arthralgia (symmetrical joint and muscle pain) (90%)
  • Skin problems (85%), butterfly rash
  • Lymphadenopathy
  • Weight loss.
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48
Q

What are the signs of SLE?

A 
Haematological:
•	Anaemia (haemolytic, Coombs positive)
•	Thrombocytopenia
•	Neutropenia
•	Lymphopenia.
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49
Q

What is the diagnostic criteria for SLE?

A

Diagnosis must have 4/11: remember MD SOAP BRAIN
M alar rash: butterfly rash on face
D iscoid rash
S erositis: pleuritis, pericarditis
O ral ulcers in mouth
A rthritis similar to RA
P hotosensitivity (rashes on sun exposed area)
B lood (haematological) disorder where all low so anaemia, leukopenia and thrombocytopenia
R enal disease proteinuria (glomerulonephritis)
A nti-nuclear antibody positive
I mmunological disorder anti dsDNA
N eurological disorder with seizures, cerebrovascular disease, myasthenia gravis.

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50
Q

What are the autoantibodies in SLE?

A

Autonantibodies:
• Anti-nuclear antibody: sensitive but not specific so screening test
• Double stranded DNA antibody: specific but not sensitive
• Other antibodies: RF, anti-cardiolipin antibodies, anti-RO/lupus antibody/SM/RNP.

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51
Q

What are the inflammatory markers like in SLE?

A
  • Raised ESR

* CRP may be normal.

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52
Q

What happens to the complement in SLE?

A

Decreased C3 and C4.

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53
Q

What is the management for SLE?

A

Avoid triggers: UV protection.
Lifestyle: smoking cessation and weight loss.
Topical: sun cream and steroids.
Immunosuppressives for severe: cyclophosphamide, methotrexate, ciclosporin, azathioprine, mycophenolate.
NSAIDs and corticosteroid for arthraldgi.
Anti-malarial (hydroxychloroquine) and/or steroids (prednisolone).
Anticoagulants.
Biological: rituximab (anti-CD20).
Plasmapheresis.

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54
Q

What clinical features do seronegative spondyloarthropathies share?

A
  • Axial inflammation: spine and sacroiliac joints
  • Asymmetrical peripheral arthritis
  • Absence of RF hence “seronegative”
  • Strong association with HLA-B27.
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55
Q

What is the pathophysiology of seronegative spondyloarthropathies?

A

Infection causes an immune response and infectious agent has peptides very similar to HLA B27 molecule so an auto-immune response is triggered against HLA B27. Mis-folding theory and HLA B27 heavy chain homodimer hypothesis.

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56
Q

What are the symptoms of seronegative spondyloarthropathies?

A 
Remember SPINEACHE:
S ausage digit (dactylitis): inflammation of tendon sheaths and joints in fingers
P soriasis
I nflammatory back pain
N SAID good response
E nthesitis (heel)
A rthritis
C rohn’s/colitis/elevated CRP but CRP can be normal
H LA B27
E ye (uveitis).
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57
Q

When should you think of seronegative spondyloarthropathies?

A
  • Inflammatory back pain
  • Asymmetrical large joint arthritis
  • Skin psoriasis
  • Inflammatory bowel disease
  • Inflammatory eye disease.
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58
Q

What are the 5 main traits of seronegative spondyloarthropathies?

A
  • Predilection for axial inflammation
  • Asymmetrical peripheral arthritis
  • Absence of rheumatoid factor
  • Inflammation of the enthesis
  • Strong association with HLA-B27.
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59
Q

When does ankylosing spondylitis present?

A
  • Typically starts in late teens/early 20s

* More common and severe in males.

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60
Q

What is the cause of ankylosing spondylitis?

A

Unknown, thought to involve CD8 T cells.

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61
Q

What is the pathophysiology of ankylosing spondylitis?

A

Inflammation destroys the intervertebral joints, facet joints and sacroiliac joints. Fibroblasts replace the destroyed joints with fibrin which causes formation of tough fibrin band around joints which limits range of motion. Ossification occurs (fibrous tissue turns to bone) and makes spine immobile. Syndesmophytes are new bone formation and vertical growth from anterior vertebral corners.

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62
Q

What are the symptoms of ankylosing spondylitis?

A
  • Weight loss
  • Fever
  • Fatigue
  • Buttock/thigh pain (sacroiliac joints) which improves with exercise
  • Neck or back pain/stiffness (cervical/thoracic region) which can lead to SOB.
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63
Q

What is the typical presentation of ankylosing spondylitis?

A
  • Young 20-30
  • Female
  • Seronegative spondyloarthropathy
  • Spine: sacroiliitis and spondylitis
  • Slow onset of morning back stiffness >30 minutes. Reduced range of movement. ‘Question mark pose’ (loss lumbar lordosis, buttock atrophy, exaggerates thoracic kyphosis)
  • Extra-articular: uveitis
  • X-ray syndesmophytes fusing to become ‘bamboo spine’.
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64
Q

What does an X-ray show with ankylosing spondylitis?

A
  • Sacroiliitis is the first sign on X-ray
  • Enthesitis
  • Syndesmophytes fusing to make bamboo spine
  • Dagger sign.
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65
Q

What are the symptoms of ankylosing spondylitis?

A 
Remember SPINEACHE:
S ausage digit (dactylitis): inflammation of tendon sheaths and joints in fingers
P soriasis
I nflammatory back pain
N SAID good response
E nthesitis (heel)
A rthritis
C rohn’s/colitis/elevated CRP but CRP can be normal
H LA B27
E ye (uveitis).

Slow onset morning stiffness >30 minutes.

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66
Q

What is the final stage of ankylosing spondylitis?

A

Severe kyphosis of thoracic and cervical spine. Patient is fused in this position and cannot move. Cannot look up and see the sun.

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67
Q

What are the signs of ankylosing spondylitis?

A 
Remember prism:
P ain
R ashes and skin changes
I mmune: SLE, Sjoegren’s, CREST
S wellings
M alignancy: bone pain, systemic
S ome other: dry eyes, dry mouth, sexual history or GI infections (reactive arthritis).
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68
Q

What do bloods show in ankylosing spondylitis?

A
  • HLA-B27 positive
  • Raised CRP/ESR
  • Normocytic anaemia
  • Decreased haemoglobin
  • Raised ALP.
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69
Q

What is the management of ankylosing spondylitis?

A
  • Physio and hydrotherapy
  • Long-term high dose NSAIDs e.g. ibuprofen or naproxen. Risk of peptic ulcer, vascular disease, renal damage etc.
  • DMARDs: e.g. methotrexate. Treat peripheral arthritis but not the disease
  • Biologics: specifically anti-TNFs e.g. etancercept, adalimumab. Stop syndesmophytes forming as once formed nothing can stop or reverse the process
  • Surgery: can correct spinal deformities to repair damage. Possible replacement.
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70
Q

What is psoriatic arthritis?

A

Autoimmune arthritis characterised by red scaly patches. Ranges from mildy synovitis to severe progressive erosive arthropathy.

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71
Q

What are the five patterns of disease in psoriatic arthritis?

A
  • Oligoarthritis: very mild, asymmetrical and affects <5 joints
  • Polyarticular/Rheumatoid pattern: resembles RA, symmetrical and >5 joints
  • Spondyloarthritis: asymmetrical, typically involves spine and sacroiliac joint (fusion)
  • Distal Interphalangeal predominant: affects DIP joint and can cause dactylitis (sausage digits) and nail abnormalities (onycholysis, hyperkeratosis, nail pitting)
  • Arthritis mutilans: causes periarticular osteolysis (bone resorption) and bone shortening. Destruction of small bones in hands and feet. Pencil in cup x-ray changes.
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72
Q

What are the skin signs in psoriatic arthritis?

A

Psoriatic plaques on scalp, trunk and extensor surfaces of limbs:
• Salmon pink colour with silver surface scale
• Symmetrical distribution
• Itchy
• Hidden areas e.g. in and behind ears, nails and natal cleft.

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73
Q

What do the bloods in psoriatic arthritis look like?

A
  • HLA-B27 positive
  • Raised ESR
  • RF and anti-CCP absent
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74
Q

What does an X-ray show in psoriatic arthritis?

A

Erosive changes (pencil in cup deformity), erosions are central in joint and not juxta-articular.

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75
Q

What is the management of psoriatic arthritis?

A
  • NSAIDs
  • Early intervention with DMARDs e.g. methotrexate, leflunomide, ciclosporin, sulfasalazine. DMARDs often help disease.
  • Anti TNF drugs (biologics) e.g. etanercept, adalimumab, infliximab
  • IL 12/23 blockers: ustekinumab
  • Exercise
  • Surgery: repair damage hip and knee (rare as risky).
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76
Q

What is reactive arthritis?

A

Sterile inflammation of synovial membranes, tendons and fascia following infection, typically STIs or GI infections.

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77
Q

What are the 2 causes of reactive arthritis?

A
  • GI infection e.g. shigella, salmonella, E. coli, campylobacter, Yersinia (all gram-negative) causes post-enteric
  • STI e.g. chlamydia, gonorrhoea causes post-veneral.
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78
Q

What syndrome is associated with reactive arthritis?

A

Reiter’s syndrome/triad:
• Can’t see: conjunctivitis
• Can’t pee: urethritis, circinate balanitis (painless superficial ulceration of glans penis)
• Can’t climb a tree: oligoarthritis, <6 joints.

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79
Q

How many joints are usually involved in reactive arthritis?

A

One large joint e.g. knee.

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80
Q

What are the psoriatic like skin lesions in reactive arthritis?

A
  • Keratoderma Blenorrhagica: skin rash on feet
  • Circinate balanitis: uncircumcised (painless superficial ulceration of glans), circumcised (raised, red and scaly lesions).
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81
Q

What do the bloods show in reactive arthritis?

A

HLA-B27 positive and raised ESR and CRP.

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82
Q

What would a joint aspiration show in reactive arthritis?

A

High neutrophil count. Should be sterile. If not, it is septic arthritis.

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83
Q

What does an X-ray show in reactive arthritis?

A

Enthesitis e.g. achilles, sacroiliitis.

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84
Q

What is the management for reactive arthritis?

A

Treat cause of infection with antibiotics.
NSAIDs +/- steroid joint infections. Consider use of methotrexate and sulfasalazine as steroid sparing agents if >6 months.

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85
Q

What is gout?

A

Inflammatory arthritis associated with hyperuricaemia (high levels of uric acid) and intra-articular monosodium urate crystals deposited in joints.

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86
Q

What are the risk factors for gout?

A
  • High alcohol intake: highest risk beer>spirits>wine
  • Purine rich foods: red meat e.g. liver and seafood
  • High fructose intake e.g. sugary drinks, cakes, sweets, fruit sugars
  • Family history
  • High uric acid levels: age, obesity, diabetes mellitus, IHD and HTN.
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87
Q

What are the symptoms of gout?

A

Asymptomatic hyperuricaemia.
Sudden onset of agonising pain, swelling, tenderness and redness (typically in 1st metatarsophalangeal joint of big toe), “toe on fire”.

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88
Q

What is the typical presentation of gout?

A
  • Obese man with toe pain
  • Crystal induced arthropathy: monosodium urate crystals
  • First MTP onset 24 hours, resolution in 14 days
  • Tophi, asymmetrical, chalky appearance, firm nodules
  • Raised serum urate level >4 weeks after episode
  • Joint aspiration: negatively birefringent in polarising light
  • Treatment is NSAID/colchicine
  • Prophylaxis is allopurinol.
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89
Q

What crystals are involved in gout?

A

Sodium urate.

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90
Q

What are the white deposits in skin around joints called in gout?

A

Tophi.

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91
Q

What is shown in polarised light microscopy in gout?

A

Negatively birefringent needle-shaped monosodium crystals.

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92
Q

What is shown in bloods in gout?

A

Raised serum urate.

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93
Q

What investigation should always be performed on a red, hot joint.

A

Joint aspiration to rule out septic arthritis.

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94
Q

What is prophylaxis for gout?

A

Allopurinol. (Xanthine oxidase inhibitor) or febuxostat if CI. Do not use allopurinol during an acute attack.

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95
Q

What is the first line treatment in gout?

A

NSAIDs e.g. naproxen, ibuprofen.

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96
Q

What is the second line treatment in gout?

A

Colchicine (if NSAIDs contraindicated i.e. peptic ulcer, diabetes, renal disease). Inhibits WBC migration.

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97
Q

What is the treatment for gout?

A

First-line: NSAIDs e.g. naproxen, ibuprofen.
Second line: colchicine (if NSAIDs contraindicated i.e. peptic ulcer, diabetes, renal disease). Inhibits WBC migration.

Steroids (prednisolone): most effective but can be painful.

Cover with colchicine 500ug daily or twice daily for 6 months, or NSAID for 6 weeks otherwise you may induce a gouty flare.

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98
Q

What is the crystal involved in gout?

A

Deposition of calcium pyrophosphate crystals in joints.

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99
Q

Who does pseudo gout typically affect?

A
  • Predominantly disease of the elderly (70+), typically older females
  • Overlaps with OA.
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100
Q

What is the typical distribution of psuedogout?

A

Usually affects larger joints, knee> wrist> shoulder > ankle> elbow.

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101
Q

What is the radiological appearance of pseudo gout?

A

Chondrocalcinosis (linear calcification parallel to the articular surfaces).

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102
Q

What is the typical presentation of psuedogout?

A
  • Female/male with knee pain
  • Crystal induced arthropathy: calcium pyrophosphate
  • Often asymptomatic, mono or oligoarticular
  • Knee (but any joint can be affected)
  • XR chondrocalcinosis. Weakly positive birefringent in polarizing light.
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103
Q

What is shown on polarising light in pseudo gout?

A

Positively bifringent rhomboid shaped calcium pyrophosphate crystals.

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104
Q

What do bloods show pseudogout?

A

Raised WBCs.

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105
Q

What is the acute management for pseudogout?

A
  • First line: NSAIDs
  • Second line: colchicine
  • Analgesia
  • Aspiration, steroid injection
  • Physiotherapy
  • Rest and icepacks.
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106
Q

What is the long term management for pseudo gout?

A
  • If continues inflammatory changes, trial of anti-rheumatic treatment e.g. methotrexate, hydroxychloroquine
  • Synovectomy in troublesome disease
  • Surgery.
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107
Q

What is the most common cause of septic arthritis?

A

S.Aureus.

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108
Q

What are the causes of septic arthritis?

A

• S. Aureus: most common
• N. gonorrhoea: young, sexually active
• Staph. Epidermidis: if joint replacement
• E. Coli/Klebsiella: if immunocompromised
• Mycobacterium tuberculosis.
H. influenzae now a rare cause for joint infection in infants due to the standard childhood immunisation schedule in the UK.

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109
Q

How do you treat gonococcal arthritis?

A

Oral penicillin, ciprofloxacin or doxycycline.

110
Q

How do you treat meningococcal arthritis?

A

Penicillin.

111
Q

How do you treat tuberculous arthritis?

A

Treatment same as pulmonary TB: 9 month therapy, joint rested and spine immobilised in acute phase.

112
Q

Which joint does septic arthritis most commonly affect?

A

The knee (50%), hip and shoulder.

113
Q

What would you see with a joint aspiration in septic arthritis?

A
  • Turgid fluid: yellow and non-transparent
  • Leucocytes
  • Gram stain: gram positive cocci.
114
Q

What would FBCs show in septic arthritis?

A
  • ESR and CRP elevated
  • High WBC
  • Neutrophilia.
115
Q

What is the management for septic arthritis?

A
  • Urgent aspiration
  • Antibiotics: S. Aureus sensitive to flucloxacillin, erythromycin, doxy/tetracycline
  • Stop immunosuppressive drugs e.g. methotrexate (DMARD) and anti-TNF injections (biologics) for as long as they’re on antibiotics and 2 weeks after
  • Commence IV flucloxacillin (high dose)
  • Prednisolone doubled if on long term prednisolone: glucocorticoids are body’s natural fight/flight hormone. If patient is on long term steroids then adrenal glands might be suppressed and lack the ability to raise the native level of glucocorticoid stress hormone
  • Analgesia
  • Splinting as necessary/rest/off-load with crutches.
116
Q

What is osteomyelitis?

A

Inflammation of the bone marrow (infection localised to bone).

117
Q

Who does osteomyelitis most commonly affect?

A

Bimodal age distribution. Children and older patients.

118
Q

What are the causes of osteomyelitis?

A
  • S. Aureus: most common (90% of cases). Live on skin and can invade the skin and spread contiguously to bone
  • Salmonella: complication of sickle cell anaemia
  • Coagulase negative staphylococci e.g. S. epidermidis
  • H. Influenzae
  • Others: pseudomonas (in IVDU), E. coli, streptococcus.
119
Q

What is the pathophysiology of osteomyelitis?

A

Results in inflammatory destruction of bone. When dead bone detaches from healthy, it forms a sequestrum. Large sequestrum that remains in situ acts as a focus for infection. New bone can form around this and often causes deformity.

120
Q

Where can the infection spread in osteomyelitis?

A
  • Nearby bone: knee or hip joint in young children
  • Overlying muscle
  • Skin.
121
Q

What does the FBC show in osteomyelitis?

A
  • Raised ESR and CRP

* Raised WBC: may be normal in chronic OM.

122
Q

What would be shown on an X-ray for osteomyelitis?

A 
X-ray: to see if infection is in foot:
Chronic osteomyelitis:
•	Corticol erosion
•	Soft tissue swelling
•	Periosteal elevation
•	Loss of trabecular architecture
•	Osteopenia
•	Mixed lucency
•	Sclerosis 
•	Sequesta
Poor sensitivity and specificity especially in early OM:
•	Only osteopenia initially.
123
Q

What is the management for osteomyelitis?

A

Immobilisation.
Antimicrobiral.
Surgical debridement, removal of dead bone (sequestrum), hardware placement or removal.

124
Q

What are the complications of osteomyelitis?

A
  • Bone abscess
  • Bacteraemia
  • Growth arrest
  • Chronic infection.
125
Q

What are benign primary bone tumours?

A

Osteochondroma: males <25. Develop in metaphysis of long bone.
Giant cell tumour: bone trauma, develop in epiphysis of long bones.
Osteoblastomas and osteoid osteomas: arises from osteoblasts.

126
Q

What are malignant primary bone tumours?

A

Osteosarcoma: kids, adults <20, arises from osteoblasts in metaphysis of long bones. Common site is knee. Rapid metastasise to lung.
Ewing’s sarcoma: <25, mostly hips and long bones.
Chondrosarcoma: mostly pelvis. Most common form of adult bone sarcoma.

127
Q

What is the most common primary bone malignancy in children?

A

Osteosarcoma.

128
Q

Who are primary bone tumours commonly seen in?

A

Children and young adults.

129
Q

What are risk factors for primary bone tumours?

A

Radiation e.g. X-ray and CT.

Paget’s disease.

130
Q

What is the pathophysiology of primary bone tumour?

A

Combination of oncogene (overstimulate cell growth) and mutated tumour suppressor genes (usually promote apoptosis) so leads to uncontrolled proliferation.

131
Q

What is a symptom of osteochondroma and osteoblastoma?

A

Can press on spinal cord so numbness, limb weakness and avascular necrosis.

132
Q

When is pain in osteoid osteoma worse?

A

At night.

133
Q

How do primary bone tumours present on X-ray?

A
  • Osteochondroma: exostosis
  • Giant cell tumour: soap bubble appearance
  • Osteosarcoma: sunburst appearance and Codman’s triangle
  • Ewing’s sarcoma: onion skin appearance.
134
Q

What protein is deposited in urine in myeloma?

A

Bence-Jones protein.

135
Q

How many radiograph planes do you need to image a tumour?

A

2.

136
Q

What is the management for primary bone tumour?

A

Benign: surgery.
Malignant: chemotherapy, radiotherapy, surgery.
Bisphosphonates reduces pain and fracture risk.

137
Q

Are primary or secondary bone tumours more common?

A

Secondary much more common.

138
Q

What are the five most common tumours that spread to bone?

A
  • Breast
  • Prostate
  • Kidney
  • Lung
  • Thyroid.
139
Q

What is myeloma?

A

Malignancy of plasma cells.

140
Q

What is the peak age of presentation of myeloma?

A

60.

141
Q

What is the pathophysiology of myeloma?

A

Increased RANK-L and so increased activity.
Remember CRAB:
C alcium raised
R enal failure
A naemia
B one pain lytic lesions, pepper pot skull.

142
Q

What shows on an X-ray in myeloma?

A

Pepperpot skull.

143
Q

What is the bone profile in myeloma?

A

Raised calcium, normal alkaline phosphate.

144
Q

What is the management for myeloma?

A
  • Analgesia: avoid NSAIDs due to renal failure
  • Bisphosphonates: alendronate
  • EPO/transfusions for anaemia
  • Stem cell transplant (haematopoietic stem cell)
  • Chemotherapy if unsuitable for transplant.
145
Q

What is fibromyalgia?

A

Non-specific muscular disorder with unknown cause (chronic persistent pain). No signs of inflammation. Symptoms present for at least 3 months and other causes have been excluded. Pain at 11/18 tender point sites on digital palpitation with enough pressure that the thumb blanches.

146
Q

Who does fibromyalgia most commonly affect?

A

Middle aged females.

147
Q

What is fibromyalgia most commonly associated with?

A

IBS, chronic headache, depression, chronic fatigue syndrome.

148
Q

What are the symptoms of fibromyalgia?

A
  • Pain worse with stress, cold weather activity
  • Morning stiffness < 1 hour
  • Non-restorative sleep
  • Headache/diffuse abdominal pain
  • Poor sleep
  • Fatigue
  • Mood disorder
  • Poor concentration
  • Memory.
149
Q

What are the investigations for fibromyalgia?

A
  • 9 pairs of sites to assess
  • TFTs to rule out hypothyroidism
  • ANAs and dsDNA to exclude SLE
  • ESR and CRP to exclude polymyalgia rheumatica
  • Calcium and electrolytes to exclude high calcium
  • Vitamin D to rule out low vitamin D
  • Examine patient and CRP to rule out inflammatory arthritis.
150
Q

What is the management for fibromyalgia?

A 
Non-pharmalogical:
•	Education
•	CBT
•	Exercise
•	Acupuncture.

Pharmalogical:
• Analgesia
• Sleep improvement: amitriptyline anti-depressant and serotonin-norepinephrine reuptake inhibitors (SSRIs) can raise serotonin and norepinephrine
• Anti-convulsant pregabalin.

151
Q

Where is the back pain in mechanical lower back pain?

A

Lumbosacral.

152
Q

Why is there nerve root pain in mechanical lower back pain?

A

Due to herniated discs. Could also be due to cauda equina syndrome. Causes a sharp, well localised pain, can be associated with paresthesia

153
Q

What are the symptoms of mechanical back pain?

A
  • Back pain often unilateral and helped by rest
  • Muscular spasm, causes local pain and tenderness.
  • Sudden onset
  • Worse in the evening
  • Exercise aggravates pain
  • Scoliosis, may be present when patient is sitting.
154
Q

What are the red flags in mechanical lower back pain?

A

Remember TUNAFISH:
T rauma, TB
U nexplained weight loss and night sweats
N eurological deficits, bowel and bladder incontinence
A ge <20 and > 55
F ever
I V drug user
S teroid use or immunosuppressed
H istory of cancer, early morning stiffness.

155
Q

What are the investigations in mechanical lower back pain?

A 
Unnecessary unless chronic (>12 weeks).
If young:
•	CRP/ESR to rule out myeloma, infection, tumour
•	X-Ray only if there are red flags.
MRI more preferable than CT.
Bone scans.
156
Q

What is the management for mechanical lower back pain?

A

Majority (90%) resolve after 6 weeks.
Continue normal activities and don’t rest.
Lifestyle:
• Avoid slouching
• Proper lifting technique
• Heat pads
• Swimming.
Analgesic ladder: Diazepam if insufficient
Physio, acupuncture, CBT.
Urgent neurosurgical referral if there is neurological deficit.
Muscle-relaxants.

157
Q

What is osteomalacia?

A

Inadequate mineralisation of osteoid framework. ‘Rickets in children’.

158
Q

What are the symptoms of osteomalacia?

A
  • Proximal muscle weakness and pain
  • Low bone density
  • Bowed legs and knock knees in children.
159
Q

What is the cause of osteomalacia?

A

Profound vitamin D deficiency. Lack of exposure to sunlight and/or GI malabsorption.

160
Q

What does an X-ray show in osteomalacia?

A

Defective mineralisation.

161
Q

What is the management in osteomalacia?

A

Oral calciferol.

162
Q

What is a side effect of bisphosphonates?

A

Can cause oesophagitis and so it is recommended that patients take them first thing in the morning and remain upright for at least 30 minutes.

163
Q

What drug can cause gout?

A

Methotrexate use, a DMARD used in severe Rheumatoid Arthritis. Gout can also be precipitated by thiazide and loop diuretics, a side effect of which is urinary frequency.

164
Q

What drug can cause haemolytic anaemia?

A

Side effect of sulphasalazine, a DMARD used in severe Rheumatoid Arthritis.

165
Q

What does Sjogren’s present with?

A

Arthritis, dry eyes and dry mouth.

166
Q

What is Sjogren’s?

A

The immune destruction of exocrine glands.

167
Q

Whichis the most appropriate investigation in diagnosing Sjogren’s syndrome?

A

The Schirmer test involves placing a small strip of paper in the eye to measure tear production and is used in the diagnosis of Sjogren’s, alongside lacrimal gland biopsy and antibody testing.

168
Q

What joints are spared in rheumatoid arthritis?

A

DIP.

169
Q

What is polymyalgia rheumatica?

A

Auto-inflammatory process affecting joints and muscles.

170
Q

Who does polymyalgia rheumatica most commonly affect?

A
  • Systemic disease of elderly
  • Affect those over 50
  • More common in females
  • Often co-exists with GCA.
171
Q

What are the symptoms of polymyalgia rheumatica?

A
  • Morning stiffness (>30 mins) typically in shoulders and proximal limb muscles
  • Pain more severe in morning and evening
  • Improves with activity
  • Symmetrical aching
  • Fever
  • Weight loss
  • Fatigue.
172
Q

What do the bloods show in polymyalgia rheumatica?

A
  • Raised CRP and ESR
  • ANCA negative
  • Raised alkaline phosphatase
  • Muscle enzymes: normal creatine kinase as muscles are spared.
173
Q

What is the treatment for polymyalgia rheumatica?

A
  • Steroids: prednisolone
  • Long term GI and bone protection (to prevent osteoporosis due to steroid use)
  • Lansoprazole
  • Aldendronate
  • Ca2+ and Vitamin D
  • Exercise and healthy diet.
174
Q

What is polyarteritis nodosa?

A

Necrotising vasculitis that causes aneurysms and thrombosis in medium sized vessels, leading to infarction in affected organs.

175
Q

What are the symptoms of polyarteritis nodosa?

A
  • Fever, malaise, weight loss and myalgia
  • Neurological: numbness, tingling, abnormal/lack of sensation and inability to move part of body
  • Abdominal: pain due to arterial involvement of abdominal viscera, mimicking acute cholecystitis, pancreatitis or appendicitis
  • Renal: presentation with haematuria and proteinuria. Hypertension and acute/chronic kidney disease occur
  • Cardiac: coronary arteritis leads to MI and HF
  • Skin: subcutaneous haemorrhage and gangrene.
176
Q

What would the bloods show in polyarteritis nodosa?

A
  • Anaemia
  • WBC raised
  • Raised ESR
  • ANCA negative.
177
Q

What does angiography show in polyarteritis nodosa?

A

Shows micro-aneurysms in hepatic, intestinal or renal vessels.

178
Q

What is the management for polyarteritis nodosa?

A
  • BP control: ACE-I e.g. Ramipril
  • Corticosteroids e.g. prednisolone with immunosuppressive drugs e.g. azathioprine or cyclophosphamide
  • Hep be treated with anti-viral after steroid treatment.
179
Q

What is granulomatosis with polyangiitis?

A

Wegener’s granulomatosis.

Necrotising, granulomatous vasculitis of arterioles, capillaries and post capillary venules.

180
Q

What vasculitis is ANCA positive?

A

Granulomatosis with polyangiitis (Wegener’s granulomatosis).

181
Q

What are the symptoms of granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A

Affects vasculature of all organ systems, most commonly lung, nasal passage and kidneys:
• Upper respiratory tract: Sinusitis/otitis/nasal crusting/bleeding
• Lungs: Pulmonary nodules/haemorrhage
• Kidney: glomerulonephritis (haematuria/proteinuria)
• Skin: purpura/ulcers
• Nervous system: mononeuritis multiplex/CNS vasculitis
• Eye: proptosis/scleritis/episcleritis/uveitis. Marked bilateral periorbital oedema. Chemosis (swelling of conjunctiva) of left eye secondary to local granulomatous inflammation
• Other: synovitis/pericarditis/GI/GU.

Also:
• Saddle nose deformity
• Collapsed trachea.

182
Q

What would bloods show in granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A
  • Raised ESR

* C-ANCA positive (90%).

183
Q

What investigations other than bloods are done in granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A

Biopsy of kidney, lungs, upper resp. tract etc. (see granulomas).
CXR: nodules.

184
Q

What is the management for granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A
  • High dose corticosteroids e.g. prednisolone
  • Cyclophosphamide
  • Biologics

Remember it as the rule of C’s: C in body (nose, upper resp. tract, kidneys), C-ANCA +, biopsy (Cross-section), Corticosteroids and Cyclophosphamide.

185
Q

What nerve is compressed in carpal tunnel syndrome?

A

Median.

186
Q

What are the symptoms of carpal tunnel syndrome?

A

Gives pain, numbness, tingling, weakness and muscle wasting of muscles supplied by median nerve.

187
Q

What are the investigations in carpal tunnel syndrome?

A

Tinel’s and Phalen’s provoking tests: positive if patient feels pain and/or tingling
• Tinel’s: tap over wrist with tendon hammer
• Phalen’s: ask patient to hold fixed wrist position for several minutes.

188
Q

What are prescribed diseases IIBD?

A

Carpal tunnel, tenosynovitis, repetitive strain disorder, osteoarthritis of hip if farmer >10 years, osteoarthritis of the knee for miners and carpet layers >10 years.

189
Q

What is hand-arm vibration syndrome?

A

Previously called vibration white-finger. A cause of secondary Raynaud’s phenomenon.

190
Q

What causes hand-arm vibration syndrome?

A
  • Caused by excessive exposure to hand-transmitted vibration (>2.5m/s2 per 8 hours day)
  • Chain saws, angle grinders, jack hammers, drills.
191
Q

What are the symptoms of hand-arm vibration syndrome?

A

Vascular (blanching) and neural (tingling, numbness and loss of dexterity) components.

192
Q

What is tenosynovitis?

A

Inflammation of a tendon.

193
Q

What is the cause of tenosynovitis?

A

Most commonly caused by inflammation of Abductor Pollicis Longus and Extensor Pollicis Brevis tendon-sheath.

194
Q

What is the test for tenosynovitis?

A

Finkelstein’s test: ask patient to put thumb in palm of hand and then ulnar deviate wrist, positive if patient feels pain.

195
Q

What is the management for tenosynovitis?

A
  • NSAIDs, steroid injection, rest

* Change job.

196
Q

What are the symptoms of epicondylitis?

A

Weakness of grip.

197
Q

What is the test for epicondylitis?

A

Cozen’s test: ask patient to form a fist and push back against resistance, positive if painful.

198
Q

What is the management for epicondylitis?

A

NSAIDs, steroid injection, clasp, rest, surgery.

199
Q

What is repetitive strain disorder?

A

Non-specific pain in hand. Writer’s cramp is a focal dystonia.

200
Q

What is the management for repetitive strain disorder?

A
  • Rest breaks, job rotation, reduced force, ergonomically neutral working postures
  • Ergonomic computer keyboards and mice.
201
Q

What causes rotator cuff problems?

A

Tendonitis or a tear. Usually affects supraspinatus tendon.

202
Q

What are the symptoms of rotator cuff problems?

A
  • Painful arc

* Hawkin’s sign.

203
Q

What is thoracic outlet syndrome?

A

Pain or tingling down arm or blanching of fingers related to posture of arm.

204
Q

What causes thoracic outlet syndrome?

A

• Compression of the trunks of brachial plexus or subclavian artery in the neck under the clavicle
• May be due to a cervical rib, cervical band or other abnormalities of anatomy in neck.
Associated with poor posture or loading of shoulders.

205
Q

What is the sign in thoracic outlet syndrome?

A

Roos sign.

206
Q

What is the management in thoracic outlet syndrome?

A

Surgery.

207
Q

What is osteoarthritis of the hip associated with?

A
  • Associated with CDH, slipped epiphyses, Perthe’s disease

* Occupationally associated with heavy manual work and a lot of walking e.g. farming.

208
Q

What is the management for osteoarthritis of the hip?

A
  • Weight loss, NSAIs, paracetamol, arthroplasty
  • Stick in hand contra-lateral to affected hip or knee
  • Shoe inserts to correct abnormal biomechanical loading.
209
Q

What is associated with osteoarthritis of the knee?

A
  • Associated with obesity, trauma and menisectomy
  • Occupationally associated with heavy manual work and knee flexion-extension (e.g. prolonged stair climbing, squatting, kneeling).
210
Q

What should be excluded before reconstructing a failed joint?

A

Prosthetic infection.

211
Q

What are the causes of prosthetic infection?

A
  • S. Aureus
  • Coagulase negative staphylococci e.g. S. Epidermidis (most frequent infecting organism after hip replacement)
  • Gram positives mainly.
212
Q

What does and FBC show in prosthetic infection?

A

• FBC: ESR (>30) and CRP (>10). For a single ESR and CRP reading, if increased there is 50% chance of infection and if normal, there is 90% chance not infected. For multiple CRP and ESR, if increased there is 80% chance of infection and if normal there is 95% chance not infected. Alpha defensin sensitivity/specificity is 95%.

213
Q

What investigations are done in prosthetic infection?

A

Aspiration, X-rays, FBC, microbiology culture.

214
Q

What are the aims of management in prosthetic infection?

A
  • Eradicate sepsis
  • Relieve pain
  • Restore function.
215
Q

What is the management in prosthetic infection?

A

Antibiotic suppression (will not eliminate sepsis) if:
• Patient unfit for surgery
• Multiple prosthetic joint infections
• Poor distal skin/soft tissues
• Low virulence infecting organisms
• Available oral antibiotics
• Patient tolerates antibiotics
• Prosthesis not loose.
Debridement and implant retention (DAIR) if:
• Early postoperative infections or acute haematogenous infections
• Not for chronic infections
• Prosthesis not loose.
Excision arthroplasty:
• High risk in frail, multiple co-morbidities
• Low functional demand
• Uncontrolled with antibiotic suppression
• High risk re-infection (poor skin or soft tissues)
• Food infection control (antibiotic depot and debridement)
• Poor functional outcome
One/two stage exchange arthroplasty:
• Know the organism(s) and their sensitivities
• Debridement of all infected and dead tissue
• Confirmatory intra-operative micro samples
• Appropriate and sufficient antibiotic cover
• Sufficient soft tissue cover/reconstruction
• Sufficient, stable joint reconstruction
One stage:
• Radical debridement
• Dirty to clean approach
• Implantation of new prosthesis, cemented
• Systemic and local antibiotics
• Avoid bone graft
• 85% success rate.
Two stage:
• Radical debridement
• Local antibiotic spacer ± systemic antibiotics
• Interval stage, duration
• Implantation of new prosthesis as per aseptic reconstruction
• Tissue samples for culture
• Cemented or cement less
• ±Bone graft
• Routine antibiotic prophylaxis
• 90-95% success rate.
Amputation.

216
Q

What is a fracture?

A

A soft tissue injury in which there is also a break in the continuity of a surface or substructure of bone.

217
Q

What are the types of fracture?

A

Transverse, linear, oblique non-displaced, oblique displaced (common is ankle due to axial load injury), spiral (generated from twisting injury), greenstick (specific to children, unicortical fracture in which the bone bends and breaks due to thick periosteum. Bone not completely broken), comminuted (generated from high energy impact)

218
Q

What are the most common fracture sites?

A
  • Neonates: humerus and clavicle due to fracture from birth
  • Infants: radius
  • Child: fibula, radius and femur
  • Adolescents: tibia.
219
Q

What are the stages of fracture healing?

A
  1. Haematoma formation
  2. Fibrocartilaginous callus formation
  3. Bony callous formation
  4. Bone remodelling.
220
Q

What is the management for fractures?

A
  • Reduce fracture to restore length, alignment and rotation
  • Immobilise to allow healing
  • Rehabilitate
  • Surgery for internal and external fixations.
221
Q

What are the complications of fractures?

A
  • Open fracture has an infection risk
  • Neurovascular compromise: avascular necrosis e.g. scaphoid fracture and hip fracture (head of femur)
  • Malunion: bone heals but with deformity
  • Non-union: failure of bone to heal
  • Compartment syndrome: painful condition in which the pressure within the fascia builds to dangerous levels, usually caused by bleeding within the fascia. Common in tibia, caused by cast (too tight) or post-op bleeding of fascia and treated with fasciotomy.
222
Q

What is anti-phospholipid syndrome?

A

Syndrome characterised by thrombosis (arterial or venous) and/or recurrent miscarriages with positive blood tests for anti-phospholipid antibodies (aPL).

223
Q

What causes anti-phospholipid syndrome?

A

HLA-DR7 mutation and environmental trigger:
• Infection (HIV, Malaria)
• Drugs: CV drugs (propranolol, hydralazine) and anti-psychotics (phenytoin).

224
Q

What is the pathophysiology of anti-phospholipid syndrome?

A

• Anti-phospholipid antibodies which attack phospholipids in cell membrane or proteins bound to phospholipids
• aPL play a role in thrombosis by binding to phospholipid on surface of cells such as endothelial cells, platelets and monocytes
• Once bound, this change alters the functioning of those cells leading to thrombosis and/or miscarriage
• Causes CLOTs:
C oagulation defect
L ivedo reticularis: lace-like purplish discolouration of skin
O bstetric issues i.e. miscarriage
T hrombocytopenia (low platelets).

225
Q

What are the symptoms of anti-phospholipid syndrome?

A 
Major clinical features are the result of thrombosis
•	Arteries: stroke, TIA, MI.
•	Veins: DVT, PE, Budd-Chiari syndrome
•	Placenta: miscarriage due to placental infarction
•	Kidneys: renal failure
•	Valvular heart disease
•	Migraine
•	Epilepsy
•	Thrombocytopenia.
226
Q

What are the investigations in anti-phospholipid syndrome?

A
  • Anti-cardiolipin antibody test
  • Anti-B2-glycoprotein test
  • Lupus anticoagulant test.
227
Q

What is the management of anti-phospholipid syndrome?

A
  • Manage thrombosis RFs – smoking, weight, diet, exercise, DM, HTN, hyperlipidaemia
  • Warfarin or (LMWH if trying to conceive as it can have toxic effect on fetus)
  • Prophylaxis - aspirin (antiplatelet) or Clopidogrel.
228
Q

What is Sjogren’s syndrome?

A

Autoimmune destruction of exocrine glands, especially the lacrimal (tear) and salivary glands.

229
Q

What does Sjogren’s syndrome have a strong association with?

A

Gluten sensitivity.

230
Q

What are the causes of Sjogren’s syndrome?

A
  • Primary: sicca syndrome (occurs alone)
  • Secondary: associated with other autoimmune connective tissue diseases e.g.
  • SLE
  • Rheumatoid Arthritis
  • Scleroderma
  • Primary biliary cirrhosis.
231
Q

What is the pathophysiology of Sjogren’s syndrome?

A

Lymphocytic infiltration (anti-SS-A and anti-SS-B) and fibrosis of exocrine glands, especially the lacrimal and salivary glands.

232
Q

What are the symptoms of Sjogren’s syndrome?

A

Lacrimal gland involvement: Keratoconjunctivitis (inflammation and ulceration of cornea and conjunctiva) leading to blurring of vision, itching, redness, burning.
Salivary gland involvement: xerostomia (dry mouth) so difficulty tasting and swallowing and cracks and fissure.
Nose and respiratory passages: ulceration and peroration of nasal septum so crusting and bleeding.
Larynx: difficult speaking.
Dryness of the skin and vagina.
Fatigue.
Joint pain.

233
Q

What would the bloods show in Sjogren’s syndrome?

A
  • Anti-Ro antibodies
  • Presence of anti-SS-A and anti-SS-B antibodies
  • Positive ANA
  • Positive RF
  • Negative ds-DNA
  • Raised Immunoglobulins.
234
Q

What are the investigations in Sjogren’s syndrome?

A
  • Sialometry: measures saliva flow
  • Lip biopsy: sialadenitis
  • Bloods
  • Schirmer’s tear Test: measures conjunctival dryness
  • Rose Bengal staining: staining of eyes shows punctate or filamentary keratitis
  • Ultrasound: abnormal salivary glands.
235
Q

What is the management of Sjogren’s syndrome?

A 
Sicca:
•	Artificial tears
•	Frequent drinks/artificial saliva
•	Sugar-free pastilles
NSAIDs and hydroxychloroquine for arthralgia and fatigue.
236
Q

What is systemic sclerosis?

A

Multisystem disease with involvement of the skin and Raynaud’s phenomenon occurring early.

237
Q

What causes systemic sclerosis?

A
  • Exposure to vinyl chloride, silica dust, adulterated rapeseed oil and trichloroethylene
  • Drugs e.g. bleomycin
  • Genetic.
238
Q

What is the pathophysiology of systemic sclerosis?

A

Simply: T-helper cell activation so damage to skin and blood vessels and fibrosis (FGF sensitivity).

The end result is uncontrolled and irreversible proliferation of connective tissue and thickening of vascular walls with narrowing of the lumen.
Damage to small blood vessels also produces widespread obliterative arterial lesions and subsequent chronic ischaemia.

239
Q

What are the limited symptoms of systemic sclerosis?

A

Remember CREST:
C alcinosis: calcium deposits in skin
R aynaud’s phenomenon
(O)E sophageal dysfunction: acid reflux and decrease in motility of oesophagus (can’t swallow)
S clerodactyly: thickening and tightening of skin on fingers and hands
T elangiectasias: dilation of capillaries causing red marks on surface of skin (spider veins).
Skin involvement limited to hands, face, feet and forearms (beak-like nose and small mouth (microstomia)).

240
Q

What causes Raynaud’s?

A 
Digital ischaemia due to paroxysmal vasospasm in response to cold or stress.
•	Usually bilateral
•	Fingers affected more than toes
•	Stop smoking, keep warm, CCB
•	Propranolol
241
Q

What are the colour changes in Raynaud’s?

A

White -> blue -> red as ischaemia -> deoxygenation -> reactive hyperaemia.

242
Q

What is the treatment for Raynuad’s?

A

Stop smoking, keep warm, CCB.

Propranolol.

243
Q

What are the diffuse symptoms of systemic sclerosis?

A

More rapid and widespread skin changes affecting all skin and organ fibrosis.
GI involvement with dilation and atony (loss of strength) in:
• Oesophagus resulting heartburn and dysphagia
• Small intestine resulting in bacterial overgrowth and malabsorption
• Colon resulting in pseudo-obstruction.
Renal involvement:
• Acute and chronic kidney disease
• Acute hypertensive crisis.
Lung disease:
• Fibrosis and pulmonary vascular disease resulting in pulmonary hypertension.
Myocardial fibrosis:
• Leads to arrhythmias and conduction disturbances.

244
Q

What is the management for systemic sclerosis?

A

No cure: steroids and occasionally immunosuppressants.

Raynaud’s:
• Physical protection – hand warmers
• Vasodilators: CCB e.g. nifedipine, endothelin receptor antagonist e.g. bosentan, iloprost (treats pulmonary hypertension) and sildenafil
• Fluoxetin
• Sympathectomy.
Gastro-oesophageal reflux:
• Proton pump inhibitors for life e.g. lansoprazole
Prevention of renal crisis:
• Use of ACE inhibitors e.g. Ramipril.
Early detection of pulmonary arterial hypertension:
• Annual echocardiograms and pulmonary function tests.
Pulmonary fibrosis:
• Immunosuppressant e.g. IV cyclophosphamide
• Oral prednisolone.
Treatment of skin oedema:
• No treatment
• Cytotoxic drugs
• Autologous stem cell transplant
Treatment is cyclophosphamide.

245
Q

What is dermatomyositis/ polymyositis?

A

Rare muscle disorders of unknown aetiology in which there is inflammation and necrosis of skeletal muscle fibres.
Muscle and skin mainly affected (rash and muscle weakness). Lungs can be affected (interstitial lung disease). Can present as a para-neoplastic syndrome.

246
Q

What are the causes of dermatomyositis/ polymyositis?

A
  • Viruses: Coxsackie, rubella and influenza

* Genetic predisposition: HLA-D8/DR3 appear to be at highest risk.

247
Q

What are the symptoms of polymyositis?

A
  • Symmetrical progressive muscle weakness and wasting affecting large and proximal muscles e.g. shoulders and hips
  • Patient has difficulty squatting, going upstairs, rising from a chair and raising hands above head
  • Involvement of pharyngeal, laryngeal and respiratory muscles so dysphagia, dysphonia and respiratory failure.
248
Q

What are the symptoms of dermatomyositis?

A
  • Same as polymyositis
  • Heliotrope: purple discolouration of eyelids
  • Gottron’s Sign: scaly erythematous plaques over knuckles.
249
Q

What are the investigations in dermatomyositis/ polymyositis?

A
  • Electromyography (EMG) to detect typical muscle changes
  • Antibodies: Jo-1, PM-Scl, Mi-2
  • Muscle/skin biopsy: diagnostic
  • Muscle enzymes: raised creatinine kinase, Aldolase, AST, LDH
  • Screen for malignancy
  • CXR, PFTs, high resolution CT lungs
  • MRI.
250
Q

What is the definitive investigation in dermatomyositis/ polymyositis?

A

Muscle/skin biopsy.

251
Q

What are the treatments in dermatomyositis/ polymyositis?

A
  • Corticosteroids: oral prednisolone
  • Exercise therapy
  • Hydroxychloroquine for skin rashes
  • Tacrolimus.
252
Q

What is Paget’s disease?

A

Increased bone turnover so enlarged misshapen bones.

253
Q

What is the cause of Paget’s disease?

A

Genetic component: autosomal dominance in some cases.

254
Q

What is the pathophysiology of Paget’s disease?

A

Lytic phase: increase bone resorption with abnormal osteoclast activity leads to rapid increase in bone formation by osteoblasts. New bone is mechanically weaker, more vascularised and poorly organised so pathological fractures.

255
Q

What are the symptoms of Paget’s disease?

A

Commonly asymptomatic.
When presents, it is often bone pain and/or deformity.
Localised to one or a few bones.
Bone fragility can lead to pathological fractures.

256
Q

What are the investigations in Paget’s disease?

A

X-rays: deformity.

Bloods: bone specific alkaline phosphatase raised.

257
Q

What is the management in Paget’s disease?

A

Bisphosphonates inhibit bone resorption by reducing osteoclast activity.

258
Q

What are the symptoms of degenerative disc disease?

A

Chronic low back pain, sometimes radiating to the hips or the buttocks.

259
Q

What is the pathophysiology of degenerative disc disease?

A

Simply: protrusion, spondylolysis and/or spinal stenosis.

260
Q

What is the management of degenerative disc disease?

A

Physical therapy, NSAIDs, epidural steroids.

If no effect, surgery to relieve the pain.

261
Q

What is the role of articular cartilage?

A

Reduce friction and shock absorption.

262
Q

What is the function of the synovial membrane?

A

Highly vascularised and secretes and absorbs synovial fluid.

263
Q

What is the function of synovial fluid?

A

Lubrication, shock absorption and nutrient distribution (hyaline cartilage is avascular and relies on diffusion from synovial fluid).

264
Q

What is ESR raised in?

A

Inflammation/infection e.g. SLE/

265
Q

Does ESR rise quickly or slowly?

A

Slowly (days to weeks).

266
Q

What gives false positives for raised ESR?

A

Females, age, obesity and SE Asians.

267
Q

Why does ESR rise in inflammation/infection?

A

Increased fibrinogen makes RBCs “stick together” and therefore they fall faster.

268
Q

When is CRP (C-reactive protein released)?

A

In inflammation/infection. It is an acute phase protein.

269
Q

What produces CRP?

A

Produced by liver in response to IL-6 (pro-inflammatory cytokine).

270
Q

Does CRP rise or fall rapidly or slowly?

A

Rapidly.

High at 6 hours and peaks at 48 hours. If patient has infection in 24 hours, ESR won’t have risen yet but CRP will have.

271
Q

What are auto-antibodies?

A

Immunoglobulins that bind to self-antigens.

272
Q

What are the inflammatory markers in rheumatoid arthritis?

A
  • Rheumatoid Factor (RF)

* Anti-Cyclic Citrullinated Peptide (CCP).

2a Medicine (11 decks)

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