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MSK > Lower Limb Arthritis > Flashcards

Lower Limb Arthritis Flashcards

This deck tests your knowledge of arthritis pathologies specific to the lower limbs.

1
Q

What is gout?

A

Inflammatory arthritis, arising from hyperuricemia and deposition of monosodium urate crystals in the joints

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2
Q

What causes hyperuricemia?

A
  1. Excess purines (high purine diet, enzymatic defects)
  2. Increased catabolism of nucleic acids due to high cell turnover (infections, cancer)
  3. Decreased renal excretion of uric acid
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3
Q

What are risk factors for gout?

A
  1. Male
  2. Old
  3. Diabetes, Hyperlipidemia, Hypertension
  4. Hyperuricemia-inducing drugs (thiazide/loop diuretics, ciclosporin, aspirin)
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4
Q

What is the pathophysiology of gouty arthritis?

A
  1. Hyperuricemia > precipitation of MSU crystals in bloodstream > deposition in joints and surrounding tissues
  2. Causes inflammation, releasing IL-1 to recruit neutrophils
  3. Neutrophils release inflammatory mediators to attract other phagocytes, and attempt to phagocytose crystals
  4. Phagocytes’ lysosome membranes are damaged by crystals, releasing hydrolytic enzyme content
  5. Manifests as severe, sudden inflammatory attack, esp. at MTP of big toe
  6. Over time, recurrent crystal deposition can cause firm yellow nodules (tophi) around joints and ears
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5
Q

S/S of gout?

A
  1. Needle-like crystals in joint aspirate
  2. Sudden, severe inflammatory arthritis attacks (esp. at night)
  3. Limited ROM due to pain
  4. Tophi
  5. Advanced, LT gout can cause joint destruction + hypertrophy (bony sclerosis), leading to overhanging edges in the joint
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6
Q

Treatment of gout?

A

Uric acid-lowering therapies

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7
Q

Who are uric acid-lowering therapies indicated for?

A
  1. > 65 y/o
  2. CKD
  3. > 5 gouty attacks / year
  4. Tophi
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8
Q

What is pseudogout?

A

Gout-like inflammatory arthritis, arising from deposition of calcium pyrophosphate dihydrate crystals in the joints. aka Chondrocalcinosis

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9
Q

What causes pseudogout?

A

Idiopathic; associated with trauma, hyperparathyroidism, and haemochromatosis

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10
Q

S/S of pseudogout?

A
  1. Usually asymptomatic, or similar to gout
  2. Under polarised light, joint aspirate reveals strongly birefringent, rhomboid-shaped crystals
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11
Q

How to differentiate between gout and pseudogout?

A

Joint aspirate crystals

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12
Q

What is septic arthritis?

A

Suppurative inflammatory arthritis, caused by infectious agent

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13
Q

What usually causes septic arthritis?

A
  • Streps, S. aureus, Pseudomonas, GN rods (e.g. Gonococcus)
  • Spread via blood; direct inoculation; spread from adjacent soft tissue infections / osteomyelitis
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14
Q

S/S of septic arthritis?

A
  1. Red, hot, swollen joint
  2. Rapid onset joint pain, worsened with movement
  3. Purulent fluid in joint aspirate
  4. Unilateral hip / knee joints affected
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15
Q

Unique S/S of gonococcal septic arthritis?

A
  1. Septic emboli
  2. STD / UTI symptoms, e.g. painful micturition
  3. GN rods in joint aspirate
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16
Q

Describe treatment of gonococcal septic arthritis.

A

IV/IM ceftriaxone

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17
Q

Unique S/S of S. agalactiae septic arthritis?

A
  1. Gp B Streps in joint aspirate
  2. Associated with raw fish consumption
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18
Q

What is osteomyelitis?

A

Bone infection involving cortex, medulla, and periosteum, usually caused by S. aureus

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19
Q

What usually causes osteomyelitis?

A
  • S. aureus
  • Spread via blood, direct inoculation, or from adjacent soft tissue infections
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20
Q

How do you detect osteomyelitis?

A
  1. MRI
  2. Tissue culture / Biopsy
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21
Q

How do you treat osteomyelitis?

A

Targeted, specific antibiotic therapy

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22
Q

What is suppurative osteomyelitis?

A

Acute / Acute-on-chronic pyogenic osteomyelitis

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23
Q

What is the pathogenesis of suppurative osteomyelitis?

A
  1. Infection localised in cortex, forming small abscess
  2. Abscess enlarges, and grows into sub-periosteal space
  3. Abscess may escape from bone via sinus tracts
  4. Abscess may undergo necrosis
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24
Q

What are the possible sequelae of suppurative osteomyelitis?

A
  1. Healing and resolution
  2. Subacute / Chronic suppurative osteomyelitis
  3. Abscess, necrosis
  4. Pathological fractures / deformities (proliferative periostitis, involucrum)
  5. Sinus tract formation in skin and soft tissue
  6. Secondary amyloidosis
  7. Malignant transformation to osteosarcoma (bone) / squamous cell carcinoma (sinus tract)
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25
Q

What is proliferative periostitis?

A
  • Extensive new bone formation, especially in children’s jaws (Garre’s sclerosing osteomyelitis)
  • Causes irritation, trauma, and dental infection
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26
Q

What is involucrum?

A

Sleeve of reactive woven bone tissue around necrotic native bone

27
Q

Which bones are commonly affected in children for osteomyelitis?

A

Long bones, jaw

28
Q

Which bones are commonly affected in adults for osteomyelitis?

A

Small bones of foot, femur, spine

29
Q

How do suppurative and chronic osteomyelitis differ?

A
  • Mainly chronic inflammatory infiltrate and fibrosis, with little pus
  • Sclerosis, proliferative periostitis
30
Q

Why can chronic osteomyelitis occur?

A
  1. Delayed diagnosis
  2. Inadequate treatment (antibiotics, surgical debridement of necrotic bone)
  3. Immunocompromised
31
Q

What are the possible sequelae of chronic osteomyelitis?

A
  1. Pathological fractures / deformities
  2. Secondary amyloidosis
  3. Malignant transformation to osteosarcoma (bone) / squamous cell carcinoma (sinus tract)
  4. Spread of infection
32
Q

What is tuberculous osteomyelitis?

A

A subtype of chronic osteomyelitis, caused by TB

33
Q

How does tuberculous osteomyelitis spread?

A

Via blood / lymph

34
Q

Who is more at risk of tuberculous osteomyelitis?

A

Immunocompromised patients

35
Q

Why is tuberculous osteomyelitis hard to treat?

A

Extensive necrosis, highly-destructive

36
Q

S/S of tuberculous osteomyelitis?

A
  1. Greater spinal involvement, causing compression fractures, deformities (scoliosis/kyphosis), and neurological deficits from spinal cord/nerve damage
  2. Chronic inflammatory infiltrate
  3. Epithelioid granulomas with caseating necrosis
37
Q

What is osteoarthritis?

A
  • Degenerative inflammatory joint disease
38
Q

What are the three types of osteoarthritis?

A
  1. Primary generalised OA (usually affects post-menopausal women)
  2. Erosive inflammatory OA (rapid, severely damaging)
  3. Hypertrophic OA (florid osteophyte formation, slowly-progressing bony sclerosis)
39
Q

What is the pathophysiology of osteoarthritis?

A
  1. Wear and tear causes degeneration of articular cartilage
  2. Subchondral bone exposed; osteophytes attempt to repair damage, leading to bony spur formation (further restricts movement)
  3. Mild synovial inflammation from articular cartilage breakdown also occurs
40
Q

S/S of osteoarthritis?

A
  1. Hips and knee joints affected more
  2. Joint pain (worsened on exertion)
  3. Mild inflammation, incl. morning stiffness
  4. Crepitus
  5. Bony erosion (eburnation, where surface is polished smooth; subchondral cyst)
  6. Bony spurs, sclerosis (may cause spinal nerve compression)
  7. Joint deformities (Heberden (dorsal PIPJ) and Bouchard (DIPJ) nodes)
  8. Joint space narrowing (fibrillation, thinning, erosion)
41
Q

How is osteoarthritis detected?

A

X-rays

42
Q

What is the pathophysiology of degenerative intervertebral disc?

A
  1. Nucleus pulposus loses matrix’s water content, thus reducing its shock-absorbing capability
  2. Fibrous disc annulus becomes brittle and prone to tearing due to repeat microtrauma
  3. Disc herniation may occur, where the nucleus pulposus prolapses out of the disc annulus
43
Q

What are causes of degenerative intervertebral disc?

A
  1. Wear and tear
  2. Mechanical factors (posture, trauma)
  3. Genetics
  4. Others (nutrition, metabolism, infection)
44
Q

What are complications of disc herniation from degenerative intervertebral disc?

A
  1. Posterior prolapse compresses spinal cord
  2. Posterolateral prolapse compresses spinal nerve roots
45
Q

What is rheumatoid arthritis?

A

Autoimmune attack of citrullinated proteins in the synovial membrane, leading to inflammation and thickening

46
Q

What are risk factors for rheumatoid arthritis?

A
  1. Female
  2. HLA-DRB1 gene
47
Q

Pathophysiology of rheumatoid arthritis?

A
  1. autoAbs target citrullinated proteins, which are mostly found in joints
  2. leads to synovial membrane inflammation and thickening, and a pannus may be created to invade the articular cartilage and erode the underlying bone
  3. ankylosis (abnormal fusion) may occur
48
Q

S/S of rheumatoid arthritis?

A
  1. Inflammatory joint pain w/ morning stiffness
  2. Deformities (swan neck deformity, Boutonniere’s deformity, rheumatic nodules, ankylosis)
49
Q

What is swan neck deformity?

A
  • Hyperextended PIPJ, flexed DIPJ
  • Due to imbalance between extensor and flexor tendons (from chronic synovitis)
50
Q

What is Boutonniere’s deformity?

A
  • Flexed PIPJ, hyperextended DIPJ
    – Due to imbalance between extensor and flexor tendons (from chronic synovitis)
51
Q

What are rheumatic nodules?

A
  • Granulomas with a zone of central necrosis, which manifest as firm subcutaneous nodules
  • Due to immune complex deposition
52
Q

What joints are usually affected first in rheumatoid arthritis?

A

Small joints of the hand

53
Q

What Ab are used to detect rheumatoid arthritis?

A
  1. ACPA / anti-CCP Ab
  2. RF
54
Q

What is systemic lupus erythematosus?

A

An autoimmune disease, characterised by immune complex deposition and inflammation in many tissues

55
Q

S/S of SLE?

A
  1. Butterfly-shaped malar rash
  2. Discoid lupus rash
  3. Photosensitivity rash
  4. Livedo reticularis rash
  5. Alopecia
  6. Oral ulcers
  7. Polyarthritis of small joints, with no significant erosion
  8. Lupus nephritis (glomerulonephritis)
  9. Autoimmune haemolytic anaemia
  10. Serositis
56
Q

What is Sjögren’s syndrome?

A
  • Autoimmune attack on exocrine glands, esp. salivary and lacrimal glands.
  • Associated with attack on joints
57
Q

Pathophysiology of Sjögren’s syndrome?

A
  1. AutoAbs (anti-RO and anti-LA) attack exocrine glands
  2. Lymphocytic infiltration also occurs
  3. This leads to swelling and fibrosis of the glands, esp. the parotid gland
  4. Non-erosive arthritis also occurs
58
Q

S/S of Sjögren’s syndrome?

A
  1. Usually asymptomatic until dryness is severe
  2. Dry, painful eyes > ocular lesions, blurry vision
  3. Xerostomia > dental caries, difficulty swallowing
59
Q

How do we detect Sjögren’s syndrome?

A
  1. Salivary gland biopsy to detect lymphocytic cell infiltrate
  2. Schirmer’s test, where absorbent strip of paper is placed under lower eyelid to measure tear production
60
Q

What is psoriatic arthritis?

A

Autoimmune attack of skin and joints; commonly affects joints, tendons, and entheses

61
Q

Pathophysiology of psoriatic arthritis?

A
  • Idiopathic
    1. Inflammation starts at entheses, and gradually leads to bone erosion (pannus) and hypertrophy (bony spurs, ankylosis)
62
Q

S/S of psoriatic arthritis?

A
  1. Dactylitis - red, hot, swollen (sausage-like) digits
  2. Enthesitis - pain and tenderness, esp. Achilles’ tendon
  3. Asymmetrical arthritis, esp. hands and feet
  4. Nail changes - oncholysis, pitting, hyperkeratosis
  5. Psoriatic plaques, esp. elbows, knees, and scalp
  6. Arthritis mutilans - rare deformity of fingers and toes due to severe inflammation
  7. Spinal disease - rare
63
Q

How do we detect psoriatic arthritis?

A

Imaging for pencil-in-cup deformity, where distal bone’s end is eroded into sharp tip, and proximal bone’s end is hypertrophic and concave

MSK (6 decks)

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