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Phase 1b - Musculoskeletal & Rheumatology > Inflammatory Non-Autoimmune Arthritis > Flashcards

Inflammatory Non-Autoimmune Arthritis Flashcards

Septic arthritis Gout Psudogout

1
Q

Outline the epidemiology of septic arthritis (2).

A
  • In developed countries is 6 cases per 100,000 population per year
  • In patients with underlying joint disease or with prosthetic joints the incidence increases approximately 10-fold, to 70 cases per 100,000 of the population
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2
Q

What are the risk factors of septic arthritis (6)?

A
  • Underlying joint disease
  • Prosthetic joint
  • Age
  • Immunosuppression
  • Contiguous spread
  • Exposure to ticks
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3
Q

Outline the pathogenesis of septic arthritis.

A
  • Septic arthritis is caused by the pathogenic inoculation of micro-organisms into the joint, either directly or by the haematogenous route

The predominant causative organisms of septic arthritis are staphylococci or streptococci.

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4
Q

Outline the pathophysiology of septic arthritis.

A
  • Following pathogenic inoculation into the joint, the mechanisms by which joint sepsis subsequently develops are as yet not fully understood
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5
Q

How would a patient with septic arthritis present (2)?

A
  • Hot, swollen, painful, restricted joint (inflammed)
    Acute presentation (< 2 weeks)
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6
Q

What investigations are suggested in suspected septic arthritis?

A

Synovial aspiration:
* Synovial fluid microscopy, gram stain, and polarising microscopy
* Synovial fluid culture and sensitivities
* Synovial fluid white cell count

Blood:
* Blood culture and sensitivities
* White cell count
* Erythrocyte sedimentation rate (ESR)
* CRP
* U&E
* LFTs

Imaging:
* Plain X-ray
* Ultrasound

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7
Q

What synovial aspiration investigations are suggested in septic arthritis (3)?

A
  • Synovial fluid microscopy, gram stain, and polarising microscopy
  • Synovial fluid culture and sensitivities
  • Synovial fluid white cell count
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8
Q

What would a synovial fluid microscopy, gram stain, and polarising microscopy show in a patient with septic arthritis?

A
  • Micro-organisms may be present
  • Urate or pyrophosphate crystals may be present
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9
Q

What would a synovial fluid culture and sensitivities show in a patient with septic arthritis?

A
  • Culture may reveal organism type and sensitivities to antibiotic therapy
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10
Q

What would a synovial fluid white cell count show in a patient with septic arthritis?

A
  • White cell count around 2000 to 50,000 per mm3
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11
Q

What blood investigations are suggested in septic arthritis (6)?

A
  • Blood culture and sensitivities
  • White cell count
  • Erythrocyte sedimentation rate (ESR)
  • CRP
  • U&E
  • LFTs
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12
Q

What would blood culture and sensitivities show in a patient with septic arthritis?

A
  • Presence of micro-organisms
  • Subsequent culture revealing organism type and sensitivities to antibiotic therapy
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13
Q

What would a white blood count show in a patient with septic arthritis?

A
  • May be elevated
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14
Q

What would a erythrocyte sedimentation rate (ESR) show in a patient with septic arthritis?

A
  • May be elevated
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15
Q

What would a serum CRP show in a patient with septic arthritis?

A
  • Elevated
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16
Q

What would a serum U&E show in a patient with septic arthritis?

A
  • May be normal or abnormal
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17
Q

What would an LFTs show in a patient with septic arthritis?

A
  • May be normal or raised
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18
Q

What imaging is suggested in septic arthritis (2)?

A
  • Plain X-ray
  • Ultrasound
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19
Q

What would an X-Ray of the affected joints show in a patient with septic arthritis (3)?

A
  • May reveal degenerative changes or chondrocalcinosis
20
Q

What is the management of septic arthritis?

A
  • Surgical wash-out (‘lavage’) and intravenous antibiotics
Aspiration of pus from a septic joint P.S. you should wear gloves for this!
21
Q

Outline the epidemiology of gout (4).

A
  • Gout is more prevalent in men than women, and increases with age for both groups
  • Prevalence varies geographically and racially, with the highest rates reported in Pacific countries, Australia and the US in 2017
  • Gout is rare in pre-menopausal women
22
Q

What are the risk factors of gout (7)?

A
  • Older age
  • Male sex
  • Post-menopausal
  • Consumption of meat, seafood, alcohol
  • Genetic susceptibility
  • High cell turnover rate (due to other diseases)

Dx:
* Use of diuretics
* Use of ciclosporin (cyclosporine) or tacrolimus
* Use of pyrazinamide
* Use of aspirin

23
Q

Outline the pathogenesis of gout.

A
  • There is a causal relationship between hyperuricaemia (high urate level) and gout
    • Urate is a metabolite of purines and the ionised form of uric acid (a weak acid at a physiological pH); hence, uric acid exists mostly as urate
  • Hyperuricaemia does not always lead to gout, but the incidence of gout increases with urate level
  • Hyperuricaemia is due to renal under-excretion of urate in 90% of cases and to over-production in 10%, although there is often an overlap of both
    • Aspirin, ciclosporin, tacrolimus, or pyrazinamide can raise serum uric acid level by increasing uric acid re-absorption
    • Diuretics can increase urate levels and are associated with an increased risk of gout
24
Q

Outline the pathophysiology of gout.

A
  1. High urate levels result in super-saturation and crystal formation, leading to gout
  2. Urate crystals in the joint interact with undifferentiated phagocytes and trigger an acute inflammatory response by inducing tumour necrosis factor (TNF)-alpha and activating signal pathways and endothelial cells
  3. TNF-alpha, interleukin (IL)-8, and other chemokines lead to neutrophil adhesion to endothelium, influx, and amplification, resulting in neutrophilic synovitis

Spontaneous resolution of gout attack results from clearance of urate crystals by differentiated phagocytes, coating of the crystals with proteins, neutrophilic apoptosis, and inactivation of inflammatory mediators

25
Q

How would a patient with gout present (8)?

A
  • Presence of risk factors
  • Rapid-onset severe pain
  • Joint stiffness
  • Foot joint distribution
    • Most commonly involved are joints in the feet, especially the first metatarsophalangeal, tarsometatarsal, and ankle joints
  • Few affected joints
    • Pattern is usually monoarticular or oligoarticular (< 4 joints)
  • Swelling and joint effusion
  • Tenderness
  • Tophi
Tophi are stone-like deposits of monosodium urate in the soft tissues, synovial tissues, or in bones near the joints
26
Q

What investigations are suggested in suspected gout (5)?

A
  • Arthrocentesis with synovial fluid analysis
  • Serum uric acid level
  • USS
  • Dual energy computed tomography (DECT)
  • X-ray of affected joint
27
Q

What would an arthrocentesis with synovial fluid analysis show in a patient with gout (2)?

A
  • WBC count > 2.0 x 109/L (2000/mm3 or 2000/microlitre; mean, 20,000/mm3 or 20,000/microlitre)
  • Strongly negative birefringent needle-shaped crystals under polarised light
28
Q

What would a serum uric acid level show in a patient with gout (2)?

A
  • Elevated

  • > 420 micromol/L (>7 mg/dL) in men
  • > 360 micromol/L (>6 mg/dL) in women
29
Q

What would imaging show in a patient with gout (3)?

A
  • Erosions
  • Tophi
  • Double contour line
USS
30
Q

What is the first line of treatment for gout?

A
  • Corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or colchicine are recommended first-line treatments for patients experiencing a gout flare
31
Q

Outline the epidemiology of pseudogout.

Pseudogout: Calcium pyrophosphate deposition (CPPD)

A
  • Increase in pseudogout with age
  • No clear sex predilection
32
Q

What are the risk factors of pseudogout (7)?

Pseudogout: Calcium pyrophosphate deposition (CPPD)

A
  • Advanced age
  • Injury
  • Hyperparathyroidism
  • Haemochromatosis
  • Fx of pseudogout
  • Hypomagnesaemia
  • Hypophosphatasia
33
Q

Outline the pathogenesis of pseudogout.

Pseudogout: Calcium pyrophosphate deposition (CPPD)

A
  • Aetiology of pseudogout is unkown
34
Q

Outline the pathophysiology of pseudogout.

Pseudogout: Calcium pyrophosphate deposition (CPPD)

A
  1. CPP crystals can be shed from cartilage into the articular space, where they may induce an inflammatory response and cause acute pseudogout (CPP arthritis)
  2. In addition, CPP crystals can have direct catabolic effects on articular tissues. They can elicit the production of cytokines and proteases that degrade cartilage
  3. They may also produce mechanical damage. It is likely that both inflammatory and non-inflammatory processes contribute to the severe joint degradation associated with articular CPP crystals
35
Q

How would a patient with pseudogout present (4)?

A
  • Presence of risk factors
  • Painful and tender joints
  • Osteoarthritis-like involvement of joints (wrists, shoulders)
  • Sudden worsening of osteoarthritis
36
Q

What investigations are suggested in suspected pseudogout (7)?

A
  • Arthrocentesis with synovial fluid analysis
  • X-rays of affected joints
  • Serum calcium
  • Serum parathyroid hormone
  • Iron studies
  • Serum magnesium
  • Serum alkaline phosphatase
37
Q

What would an arthrocentesis with synovial fluid analysis show in a patient with pseudogout (2)?

A
  • Intracellular or extracellular positively birefringent rhomboid-shaped crystals under polarised light confirms CPPD
  • Fluids are often bloody
38
Q

What would an X-Ray of the affected joints show in a patient with pseudogout?

A
  • Progressive rapid joint degeneration or bony collapse
Wrist radiograph from a patient with chronic calcium pyrophosphate arthritis showing severe degenerative changes

Linear, stippled radio-opaque deposits in the fibro-cartilage or hyaline articular cartilage of joints, calcified tendons, subchondral cysts,

39
Q

What would a serum calcium test show in a patient with pseudogout?

A
  • May be normal or elevated
40
Q

What would a serum parathyroid hormone test show in a patient with pseudogout?

A
  • May be normal or elevated
41
Q

What would iron studies test show in a patient with pseudogout?

A
  • May be normal or elevated
42
Q

What would a serum magnesium test show in a patient with pseudogout?

A
  • May be normal or decreased
43
Q

What would a serum alkaline phosphatase test show in a patient with pseudogout?

A
  • May be normal or decreased
44
Q

What is the 1st line of treatment of acute pseudogout (2)?

A

If joint accessible: Intra-articular corticosteroids

OR

If joint inaccessible: Non-steroidal anti-inflammatory drugs (NSAIDs)

45
Q

What is the 1st line of treatment of ongoing pseudogout (1)?

A
  • Joint relacement surgery

Phase 1b - Musculoskeletal & Rheumatology (11 decks)

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