Inflammatory Non-Autoimmune Arthritis Flashcards
Septic arthritis Gout Psudogout (45 cards)
Outline the epidemiology of septic arthritis (2).
- 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
What are the risk factors of septic arthritis (6)?
- Underlying joint disease
- Prosthetic joint
- Age
- Immunosuppression
- Contiguous spread
- Exposure to ticks
Outline the pathogenesis of septic arthritis.
- 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.
Outline the pathophysiology of septic arthritis.
- Following pathogenic inoculation into the joint, the mechanisms by which joint sepsis subsequently develops are as yet not fully understood
How would a patient with septic arthritis present (2)?
-
Hot, swollen, painful, restricted joint (inflammed)
Acute presentation (< 2 weeks)
What investigations are suggested in suspected septic arthritis?
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
What synovial aspiration investigations are suggested in septic arthritis (3)?
- Synovial fluid microscopy, gram stain, and polarising microscopy
- Synovial fluid culture and sensitivities
- Synovial fluid white cell count
What would a synovial fluid microscopy, gram stain, and polarising microscopy show in a patient with septic arthritis?
- Micro-organisms may be present
- Urate or pyrophosphate crystals may be present
What would a synovial fluid culture and sensitivities show in a patient with septic arthritis?
- Culture may reveal organism type and sensitivities to antibiotic therapy
What would a synovial fluid white cell count show in a patient with septic arthritis?
- White cell count around 2000 to 50,000 per mm3
What blood investigations are suggested in septic arthritis (6)?
- Blood culture and sensitivities
- White cell count
- Erythrocyte sedimentation rate (ESR)
- CRP
- U&E
- LFTs
What would blood culture and sensitivities show in a patient with septic arthritis?
- Presence of micro-organisms
- Subsequent culture revealing organism type and sensitivities to antibiotic therapy
What would a white blood count show in a patient with septic arthritis?
- May be elevated
What would a erythrocyte sedimentation rate (ESR) show in a patient with septic arthritis?
- May be elevated
What would a serum CRP show in a patient with septic arthritis?
- Elevated
What would a serum U&E show in a patient with septic arthritis?
- May be normal or abnormal
What would an LFTs show in a patient with septic arthritis?
- May be normal or raised
What imaging is suggested in septic arthritis (2)?
- Plain X-ray
- Ultrasound
What would an X-Ray of the affected joints show in a patient with septic arthritis (3)?
- May reveal degenerative changes or chondrocalcinosis
What is the management of septic arthritis?
- Surgical wash-out (‘lavage’) and intravenous antibiotics
Outline the epidemiology of gout (4).
- 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
What are the risk factors of gout (7)?
- 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
Outline the pathogenesis of gout.
- 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
Outline the pathophysiology of gout.
- High urate levels result in super-saturation and crystal formation, leading to gout
- 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
- 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
