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MBChB3 > Week 11 - Musculoskeletal > Flashcards

Week 11 - Musculoskeletal Flashcards

1
Q

What are the routes which result in septic arthritis?

A
  • Haematogenous.
  • dissemination from osteomyelitis.
  • spread from adjacent soft tissue infection.
  • diagnosis/therapeutic measures.
  • penetrating damage by puncture or trauma.
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2
Q

Types of septic arthritis.

A
  • TB.
  • Lyme disease.
  • Brucellosis.
  • Syphilitic arthritis.
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3
Q

Investigations for septic arthritis.

A
  • Joint aspirate.
  • blood culture.
  • FBC.
  • X-ray.
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4
Q

Define gout.

A

Inflammation caused by uric acid crystal deposits in the joint space or soft tissue (tophi). An attack is usually extremely painful. The uric acid crystals are deposited in the joint fluid (synovial fluid) and joint lining (synovial lining).

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5
Q

Gout risk factors (for high uric acid levels)

A

Older people, obesity, high alcohol consumption, high protein diet, diabetes mellitus.

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6
Q

Management of gout,

A

NSAIDs - high dose.
(alternatives: colchicine, corticosteroids).
Repeated attacks:
- allopurinol: xanthine oxidase inhibitor..
- uricosuric agent (probenecid): increased secretion of uric acid into urine.

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7
Q

Define pseudo-gout.

A

Inflammation of the joints that is caused by deposits of calcium pyrophosphate crystals, resulting in arthritis, most commonly of the knees, wrists, shoulders, hips, and ankles.

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8
Q

Describe the joint aspirate in gout.

A

Negatively birfringement needle shaped crystals on polarised microscopy.

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9
Q

Describe the joint aspirate in pseudogout.,

A

Positively bifringement rhomboid shaped crystals on aspiration.

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10
Q

Management of pseudogout.

A

Aspiration - reduces pain and swelling.
NSAIDs.
Colchicine.

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11
Q

Define reactive arthritis.

A

Sterile synovitis which occurs following an infection.

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12
Q

Trigger organisms for reactive arthritis.

A

Salmonella.
Shigella.
Versinia.
Chlamydia trachomatis.

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13
Q

Define enteropathic arthritis.

A

Form of reactive synovitis seen in association with UC and Crohn’s disease.
Asymmetrical lower limb arthritis.
Treatment: underlying bowel disease and NSAIDs.

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14
Q

Define osteoarthritis,

A

Degenerative joint disease affecting articular cartilage.

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15
Q

Cardinal signs of osteoarthritis on x-ray.

A

Loss of articular cartilage.
Exposure of underlying bone.
Subchondral cysts and sclerosis.
Osteophytes.

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16
Q

Define rheumatoid arthritis.

A

A chronic autoimmune disease that causes inflammation and deformity of the joints.

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17
Q

Define synovitis.

A

|Immune cells invading a normally relatively acellular synovium in the form of a pannus.

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18
Q

Define pannus,

A

Hyperplastic, invasive tissue leading to cartilage breakdown, erosion and consequent reduced function.

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19
Q

Clinical features of RA.

A 
Synovitis.
Symmetrical.
MCP/PIP's/wrists.
Inflammatory,
Tenosynovitis, bursitis, 
Fatigue, weakness, low grade fever, weight loss, anorexia.
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20
Q

Classical late joint features of RA.

A 
Boutonniere.
Swan neck.
Z-thumb (Boutonniere of thumb).
Volar subluxation of wrist.
Ulnar deviation digits.
Radial deviation wrist.
Piano key ulnar head.
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21
Q

Describe rheumatoid factor.

A

Autoantibody against Fc portion of IgG.
Positive in RA.
Not diagnostic (also positive in other conditions, e.g. SLE).

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22
Q

Describe anti-CCP/ACPA.

A

Picks up those that may be RF negative.
Predictive of worse prognosis, more erosions, resistant disease.
Linked with smoking (increased citrullination).

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23
Q

Signs of RA on x-ray.

A

Soft tissue swelling.
Joint space narrowing.
Erosions.
Periarticular OP.

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24
Q

Methotrexate.

A 
DMARD.
MOA: dihydrofolate reductase inhibitor.
Also anti-inflammatory.
Side effects: GI, hair, skin, rashes.
Concomitant folic acid.
Teratogenic in pregnancy.
Withhold during infection and if on antibiotics.
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25
Q

Sulfasalazine

A 
DMARD.
MOA: multiple but incompletely understood.
Side effects: GI, rashes.
Safe in pregnancy.
Fine in infection unless cytopenic.
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26
Q

Define indirect fracture healing.

A

Formation of bone via a process of differential tissue formation until skeletal continuity is restored.

27
Q

Describe the main stages of indirect fracture healing,

A
  1. Inflammation: fracture haematoma and inflammation.
  2. Repair: fibrocartilage (soft) callus and bony (hard) callus.
  3. Remodelling: osteoclasts remodel woven bone into compact and trabecular bone.
28
Q

Define direct fracture healing,

A

Direct formation of bone, without the process of callus formation, to restore skeletal continuity.

29
Q

Which anatomical sites are predisposed to problems with union or necrosis in the case of fractures,

A

Proximal pole of scaphoid fractures.
Talar neck fractures.
Intracapsular hip fractures.
Surgical neck of humerus fractures.

30
Q

Describe the structure of tendons.

A

Parallel collagen fibrils with tenocytes.
Surrounded by paratenon/shealth.
Largely avascular, nutrition via paratenon.

31
Q

Describe the pathology of tendinopathies.

A

Not inflammatory.
Deranged collagen fibres/degeneration with a scarcity of inflammatory cells.
Increased vascularity around the tendon.Failed healing response to micro-tears.
Inflammatory mediators released IL-1, NO, PG’s - cause apoptosis, pain and provoke degeneration through release of MMP’s.

32
Q

Define compartment syndrome.

A

Elevated interstitial pressure within a closed fasical compartment resulting in microvascular compromise.

33
Q

Pathophysiology of compartment syndrome.

A

Pressure within the compartment exceeds pressure within the capillaries.
Reduced blood flow.
Muscles become ischaemic and develop oedema through increased endothelial permeability.
Necrosis begins in ischaemic muscles after 4 hours.
Ischaemic nerves become neuropraxic.
Late compromise of arterial supply.

34
Q

Describe the features of end-stage compartment syndrome.

A

Stiff fibrotic muscle compartments.
Impaired nerve function.
Clawing of limbs.
Loss of function.

35
Q

What are the 6 P’s of compartment syndrome?

A 
Pain (out of proportion).
Pain (on passive stretching of compartment).
Pallor.
Parasthesia.
Paralysis.
Pulselessness.
36
Q

What are the 3 broad differential causes of back pain?

A
  1. Mechanical.
  2. Systemic - infection, malignancy, inflammatory.
  3. Referred - i.e. no pathology in back itself.
37
Q

What are the causes of mechanical back pain?

A

Lumbar strain/sprain.
Degenerative discs (spondylosis)/facet joints.
Disc prolapse, spinal stenosis.
Compression fractures.

38
Q

Describe cauda equina syndrome.

A

Medical emergency - urgent neurosurgical review.
Neuropathic symptoms:
- bilateral sciatica.
- saddle anaesthesia.
Bladder or bowel dysfunction - reduced anal tone.
Usually a large prolapsed disc.

39
Q

What are the causes of referred back pain?

A

Retroperitoneal structures:

  • AA.
  • Acute pancreatitis.
  • peptic ulcer disease (duodenal).
  • acute pyelonephritis/renal colic.
  • endometriosis/gynae.
40
Q

What carcinomas often metastasise to the spine?

A 
'LP Thomas Knows Best'
Lung
Prostate
Thyroid 
Kidney
Breast
41
Q

What are the red flag signs of back pain?

A 
Saddle anaesthesia.
Reduced anal tone.
Hip or knee weakness.
Generalised neurological deficit.
Progressive spinal deformity.
42
Q

Clinical and radiological criteria of Ankylosing spondylitis.

A

Clinical:
- low back pain and stiffness for >3 months, improves with exercise.
- limitation of movement of lumbar spine in sagittal and lumbar planes.
- limitation of chest expansion relative to normal values for sex and age.
Radiological:
sacroiliitis grade >2 bilaterally or grade 3-4 unilaterally..
(need radiological plus at least one clinical criteria for diagnosis).

43
Q

Define osteonecrosis.

A

Bone infarction (tissue death caused by an interruption of the blood supply) near a joint.

44
Q

Clinical presentation of osteonecrosis.

A

Asymptomatic.
Pain (worsens with weight bearing and motion).
Rest pain in 2/3 of patients; night pain in 1/3 of patients.
Limp.
Tenderness around the affected bone.
Restricted motion.

45
Q

What blood disorder has a strong association with osteonecrosis?

A

Sickle cell anaemia/haemoglobinopathies.

46
Q

What are the main risk factors for development of osteonecrosis?

A

History of trauma, esp joint dislocation.
Corticosteroid use/Cushing’s.
Alcohol abuse.
Sickle cell disease/haemoglobinopathies.

47
Q

What are the radiological features of osteonecrosis?

A

Subchondral collapse.
Bone remodelling.
Crescent sign.

48
Q

How does osteonecrosis cause arthritis?

A

Ischaemic bone doesn’t remodel.
Microdamage isn’t repaired, so mechanical properties of bone are impaired.
If enough damage accumulates, the sub-chondral bone can be weakened to the point of collapse
So the joint surface of course becomes irregular and no longer smooth.
If one side of the joint surface is not smooth it will damage the other surface.

49
Q

Pathology of osteoarthritis.

A
  • proteolytic breakdown of the cartilage matrix from an increased production of enzymes, such as metallproteinases.
  • the proteoglycan and collagen fragments released into the synovial fluid as the disease progresses; erosion to the cartilage roughens surface and fibrillation which narrows the joint space.
  • increased production of synovial metalloprotinases, cytokines and TNF that can diffuse back into the cartilage to destroy soft tissue around the knee.
50
Q

Kellgren Lawrence stages of OA on radiographs.

A

grade 0:no radiographic features of OA are present
grade 1:doubtful joint space narrowing (JSN) and possible osteophytic lipping.
grade 2:definite osteophytes and possible JSN on anteroposterior weight-bearing radiograph.
grade 3:multiple osteophytes, definite JSN, sclerosis, possible bony deformity.
grade 4:large osteophytes, marked JSN, severe sclerosis and definite bony deformity.

51
Q

Radiological signs of ankylosing spondylitis.

A

Bilateral sacro-iliitis - symmetrical.
Squaring of vertebral bodies.
Bamboo spine.
Peripheral large joint arthritis.

52
Q

Define SLE.

A

Chronic multi-system disorder that most commonly affects women during their reproductive years. Characterised by the presence of antinuclear antibodies. In addition to constitutional symptoms, it most frequently involves the skin and joints, although serositis, nephritis, haematological cytopenias, and neurological manifestations may occur during the course of the disease.

53
Q

Risk factors of SLE.

A

Female sex.
Age 15-45 yrs.
African/Asian descent in Europe and US.
Drugs.

54
Q

Signs and symptoms of SLE.

A

Malar butterfly rash.
Photosensitive rash.
Discoid rash.
Fatigue, weight loss, fever, oral ulcers.

55
Q

Investigations to consider in SLE.

A

FBC and differential.
Activated PTT.
Urea and electrolytes.
Erythrocyte sedimentation rate (ESR) and CRP.

56
Q

Treatment of SLE.

A

Steroids: oral prednisolone (used in moderate disease).
Hydroxychloroquine:
Belimumab: used in moderate disease.

57
Q

Define Sjrogen’s syndrome.

A

Chronic inflammatory and autoimmune disorder characterised by diminished lacrimal and salivary gland secretion.

58
Q

Signs and symptoms of Sjrogen’s syndrome.

A

Fatigue, dry eyes, dry mouth, vasculitis, dental caries.

59
Q

Risk factors of Sjrogen’s syndrome.

A

Female.
SLE.
RA.
Scleroderma (systemic sclerosis).

60
Q

Investigations to consider in Sjrogen’s syndrome.

A

Schirmer’s test.

Anti-60 kD (SS-A) Ro and anti-La (SS-B).

61
Q

Define systemic sclerosis (scleroderma).

A

Multisystem, autoimmune disease characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of auto-antibodies.

62
Q

Signs and symptoms of scleroderma.

A

Raynaud’s phenomenon.
Digits pits or ulcers.
Swelling of the hand and feet.
Fatigue, dry cough, decreased exercise tolerance, weight loss.

63
Q

Investigations to consider in scleroderma.

A

Serum auto-antibodies.
FBC.
Urea and serum creatinine.
ESR.

64
Q

Define myositis.

A

Idiopathic inflammatory myopathies constitute a heterogeneous group of sub-acute, chronic, and, rarely, acute diseases of skeletal muscle that have in common the presence of moderate-to-severe proximal muscle weakness and inflammation on muscle biopsy.

MBChB3 (14 decks)

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