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MBBS VI - SpC - Family Medicine > Rheumatology - Monoarthropathy - OA, Septic arthritis, Gout > Flashcards

Rheumatology - Monoarthropathy - OA, Septic arthritis, Gout Flashcards

1
Q

List diseases that cause monoarticular symptoms

A

Septic arthritis: Bacterial, Mycobacterial, Lyme disease…etc

Crystal deposition diseases:

  • Gout
  • Pseudogout
  • Hydroxyapatite
  • Calcium oxalate

Trauma:

  • Fracture
  • ACL/ PCL tear
  • Hemarthrosis

Others:

  • OA
  • Juvenile idiopathic arthritis
  • Coagulopathy
  • Avascular necrosis of bone
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2
Q

List polyarticular diseases that sometimes present with monoarticular onset

A

RA

JIA

Viral arthritis

Spondyloarthritis (SpA)

  • Reactive arthritis
  • Psoriatic arthritis
  • IBD associated arthritis
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3
Q

Ddx the most likely cause of monoarticular pain over minutes, hours/days, weeks

A

Pain in Seconds/ minutes: Fracture, Hemarthrosis

Hours to days: Septic arthritis, Crystal deposition disease

Weeks: Inflammatory arthritis/ SpA, Indolent infection (TB), Osteoarthritis

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4
Q

Ddx most likely causes of articular pain with recurrent acute attacks

A

Crystal arthritis: e.g. gout, pseudogout, hydroxyapatite, calcium oxalate

Inflammatory arthritis syndromes

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5
Q

Ddx most likely causes of articular pain with immunosuppression

A

Septic arthritis

Osteonecrosis

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6
Q

First-line investigations for mono-articular pain

A

Synovial fluid aspiration and analysis:

  • Gross appearance
  • Microscopy
  • Microbiology

Blood:

  • CBC with diff.
  • ESR
  • Serum uric acid level
  • Prothrombin and Partial thromboplastin time
  • ANA, ACPA, autoimmune markers

Microbiology: Blood, urine, other sample culture

Others: Arthroscopy, X-ray of joint and contralateral side, Synovial biopsy, Other imaging

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7
Q

Indications of synovial fluid aspiration and analysis

A

Clinical suspicion of:

  • Infection
  • Crystal deposition disease
  • Hemarthrosis
  • Differentiate inflammatory and non-inflammatory arthritis
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8
Q

List all tests done on synovial fluid analysis

A

Gross appearance

  • Color
  • Turbidity
  • Viscosity

Microscopy

  • Wet films
  • Cell stains and differential counts
  • Polarized light

Microbiology

  • Gram stain
  • Culture
  • Special stains: ZN stains, Fungal stains
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9
Q

Interpret the following profile of synovial fluid

High viscosity

Straw- yellow color

Transparent

WBC: 200-2000

PMN: <25%

A

Non-inflammatory arthritis/ Normal/ OA

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10
Q

Interpret the following profile of synovial fluid

Viscosity Low

Yellow color

Translucent

WBC: 2000-75000

PMN: >50%

A

Inflammatory arthritis e.g. RA, crystal deposition diseases

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11
Q

Interpret the following profile of synovial fluid

Variable viscosity, sometimes low, sometimes high

Variable color

Opaque

WBC >100,000

PMN: >75%

A

Septic arthritis

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12
Q

Interpret following synovial fluid analysis

Low viscosity

Red color

Slightly turbid

WBC: <200

PMN: <25%

A

Haemarthrosis

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13
Q

Describe the function of polarized light microscopy on synovial fluid

A

Birefringent crystal in fluid alters vector of plane polarized light

Birefringence detected by color shift to blue (Positive) or yellow (Negative) when long axis of crystal is aligned with optical axis of the first order red compensator

Blue when parallel to optical axis of red compensator = Calcium pyrophosphate

Yellow (negative) when parallel to optical axis = Monosodium urate

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14
Q

Arthroscopy

Functions

Indication

A

Functions

  • Diagnostic: directly visualize articular surface, assess cartilage damage, take synovial biopsy
  • Therapeutic: Debridement of damaged cartilage, remove loose bodies, pain relief

Indications:

  • Pain relief
  • Inflammatory arthritis needing synovial biopsy
  • Remove fractured cartilage/ loose bodies
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15
Q

Septic arthritis

  • Typical onset
  • Distribution
  • Routes of infection
A

Abrupt onset of monoarticular pain

Typically at large weight bearing joints e.g. hip, knee

Routes of infection:

  1. Hematogenous
  2. From adjacent Osteomyelitis
  3. Adjacent soft tissue infection
  4. Diagnostic/ therapeutic procedure contamination
  5. Penetrating injury by puncture or cut
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16
Q

Risk factors of septic arthritis

A

Age under 5 or over 65

Medical:

  • Chronic arthritic diseases e.g. RA, OA, Crystal deposition diseases…etc
  • Chronic skin infections
  • Chronic systemic diseases: SLE< DM, Malignancy, Immunocompromised…etc

Iatrogenic:

  • Prosthetic joints
  • Intra-articular injections or arthrocentesis

Social:

  • Parenteral/ IV drug use
  • STDs
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17
Q

Common causative bacteria for septic arthritis in:

Infant (<1 month)

Children <2 years old

A

Infants:

  • Streptococcal agalactiae
  • Gram negative bacilli e.g. E. coli
  • Staph. aureus

Children:

  • Hemophilus influenzae type B
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18
Q

Common causative bacteria of septic arthritis in:

Older children, adults, elderly, chronically ill

A

Staphylococcus auerus

Gram negative bacilli (chronically ill, elderly)

Neisseria gonorrhoeae (disseminated), Chlamydia trachomatis (reactive) (sexually active)

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19
Q

Common causative bacteria of septic arthritis in:

Prosthetic infection

Skin infection

IV drug users

Gas forming infection

A

Prosthetic: Staphylococcal aureus

Skin/ soft tissue infection: Streptococcal infection

IV DU: Gram negative bacilli, Pseudomonas aeruginosa, Staphylococcal aureus

Gas forming/ foul smelling; Anaerobes e.g. Clostridium difficile, Clostridium perfringens

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20
Q

Red flag features and approach/ first-line investigations to septic arthritis

A

Clinical Features:

  • Fever
  • Acute onset of hot, swollen and tender joint with restricted movement

Investigations:

  • Synovial fluid aspiration for microbiology: Negative gram smear or culture does not exclude sepsis
  • Blood culture, CBC, ESR, CRP
  • Electrolyte, RFT, LFT (detect end-organ damage, antibiotic use)
  • Imaging: X-ray and MRI

Promptly treat with antibiotics only AFTER joint aspiration

21
Q

Empirical antibiotics treatment for septic arthritis (typical organisms)

A

First-line: IV Flucloxacillin - 2g, 4 doses/ day

Penicillin-allergy:

  • IV Clindamycin 450-600mg QDS or
  • IV 2nd/ 3rd gen. cephalosporin
22
Q

Empirical antibiotics treatment for septic arthritis caused by:

  • Gram-negative sepsis
  • MRSA
  • Gonoccocus or meningococcus
A
  • Gram-negative sepsis: IV 2nd/ 3rd gen. cephalosporin
  • MRSA: IV Vancomycin + IV 2nd/3rd gen. cephalosporin
  • Gonoccocus or meningococcus: IV Ceftriaxone
23
Q

What conditions are associated with gram negative or MRSA spetic arthritis

A

Gram-negative: Elderly with chronic illness, Recurrent UTI, Recent abdominal surgery

MRSA: recent inpatient care, Leg ulcers, Nursing home residents, Long-term catheter insertion

24
Q

Which patient groups cannot be given empirical antibiotics for septic arthritis

A

IV Drug users

ITU/ ICU patients with known colonization of other organs

25
Surgical treatment options for septic arthritis
Acute: Arthroscopy Delayed or chronic: Open arthrotomy Repeat surgical debridement until infection is controlled
26
Intrinsic crystalline particles in crystal deposition diseases
* Monosodium Urate monohydrate * Calcium Pyrophosphate Dihydrate CPPD * Calcium phosphate compounds e.g. hydroxyapatite, tricalcium phosphate, calcium oxalate * Lipids: Cholesterol, lipid crystals, Charcot-Leyden phospholipase crystals * Cystine * Xantine, Hypoxanthine * Protein precipitates e.g. cryoglobulins
27
Extrinsic crystalline particles in crystal deposition disease
Synthetic corticosteroids Plant thorns - Semi crystalloid cellulose e.g. blackthorn, rose thorn, dried palm fronds Sea-urchin spines - Crystalline calcium carbonate
28
Gout * Demographics * Joint distribution * Presentations * Diagnostic Ix
Demographics * M:F = 8:1 * 30-60 years old Joint distribution * First MTP in 20% Presentations * Acute gouty arthritis with systemic upset * Intercritical gout * Chronic tophaceous gout Diagnostic Ix: Urate crystals in synovial fluid aspiration
29
Compare the presentation between acute, intercritical and chronic tophaceous gout
Acute: Monoarticular pain with systemic upset, Pruritus and desquamation of overlying skin Intercritical: Asymptomatic between attacks, frequency and duration increases, becomes polyarticular Chronic tophaceous gout: Late stage, continuous arthritis with superimposed acute attacks
30
Areas affected by chronic tophaceous gout
Tophi in periarticular tissues, Helix of ear, Tendon sheaths Late stage: Larynx. tongue, heart
31
Gout Associated diseases Causes of hyperuricaemia
Associated diseases: * Obesity * Alcoholism * Type IV hyperlipoproteinemia * Impaired glucose tolerance * Ischemic heart disease * Hypertension Pathogenesis: * Dietary excess of uric acid +/- Overproduction of urate Under-excretion of urate
32
Outline the production and excretion cycle of uric acid
33
34
Causes of overproduction of uric acid
Primary hyperurecaemia * Idiopathic * HGPRT deficiency - cannot convert hypoxanthine to xanthine * PRPP synthase superactivity - cannot convert 5-phosphoribosyl 1-pyrophosphate to PRPP glutamine Secondary hyperurecaemia * Excessive purine intake * Myeloproliferative/ lymphoproliferative diseases/ Hemolytic diseases - increase cell breakdown * Psoriasis * Glycogen storage diseases type 1,3,5,7
35
Causes of under-secretion of uric acid
Primary: idiopathic Secondary: * Poor renal function * Metabolic acidosis * Dehydration, Diuretics * Hypertension * Hyperparathyroidism * Drugs: Cyclosporine, Pyrazinamide, Ethambutol, Salicylate * Lead nephropathy
36
Gout Acute treatment options
Pain relief and acute management * NSAID (avoid aspirin or salicylates) * COX-2 selective inhibitors - Etoricoxib * Colchicine * Steroids * Anti-IL1 injection: Anakinra, Canakinumab
37
Describe the molecular pathway for urate crystals to trigger inflammatory response and articular damage
Signal 1 = innate immune response against pathogen TLR at plasma membrane activated \> NF-kB pathway \> inflammasome response Signal 2 = monosodium urate crystal \> engulfed by macrophage \> inflammasome \> capase 1 to cleave pro-IL1 to IL1 \> Release IL1 to extracellular space \> draw more WBC to site of infection (chemotactic factor) for inflammatory response + fever
38
Gout Long-term management objective and drug options
Prevent recurrent attacks, formation of tophi and articular damage Prophylaxis: Colchicine or NSAID for 3 months to prevent breakthrough attacks Xanthine oxidase inhibitors: (C/I Azathioprine, synergistic toxicity) * Allopurinol * Febuxostat (for impaired kidney function, C/I liver dysfunction) Uricosuric agents: * Probenecid, benzbromarone * Sulphinpyrazone Urate lowering agents: * Pegloticase (recombinant uricase) * Lesinurad: URAT1 inhibitor
39
C/I uricosuric agents
Primary overproduction of urate Gross hyperuricosuria Urolithiasis Renal insufficiency
40
Toxic S/E of drugs for long-term Gout control
TEN and vasculitis - Allopurinol Nephrotic syndrome - Probenecid Hepatitis and BM suppression - Hypouricaemic drugs
41
Indications for hypourcaemic agents (allopurinol, rasburicase…etc)
Indications for hypouricaemic drugs: * Recurrent acute attacks * Tophi, chronic joint damage (Contraindications for uricosuric agents) * Renal disease * Young patient with hyperuricaemia * Family history of renal and heart disease * Primary purine overproduction and under-secretion
42
Pseudogout/ Chondrocalcinosis Demographics Joints affected Crystal
Demographics: Elderly, M:F = 1.4:1 Joint: Knee most common Calcium Pyrophosphate - Rhomboid crystals
43
Pseudogout Causes
Hereditary Idiopathic (elderly) Metabolic diseases: * Hyperparathyroidism * Haemachromatosis * Hypothyroidism * Gout * Hypomagnesemia * Hypophosphatasia
44
Pseudogout Treatment options
Majority asymptomatic - no Tx Supportive measures: ice pack, immobilization, joint rest Joint aspiration + intra-articular glucocorticoid injection Systemic anti-inflammatory drug if \>2 joints involved: * Choice: NSAIDs (caution on C/I in elderly), colchicine (first 24h), oral steroids
45
Haemarthrosis Common causes Symptoms Diagnostic Ix Tx
Causes: 1. Trauma 2. Hemophilia 3. Acquired hemophilia 4. Anti-platelet or anti-coagulants S/S: Pain, swelling, stiffness (non-specific) Diagnostic Ix: Arthrocentesis Tx: Underlying cause
46
Xanthine oxidase inhibitor Examples MoA S/E D/D interactions
allopurinol and febuxostat Initiation: start only after resolution of flare MoA: block xanthine oxidase = increase conversion of hypoxanthine into xanthine into uric acid for urine excretion S/E: rash, leukopenia/thrombocytopenia, diarrhoea (3-5%), xanthine stones, severe cutaneous reactions, DRESS syndrome
47
Uricosuric agents Examples MoA Indications S.E
probenecid, benzbromarone MoA: inhibit PCT urate-anion exchangers → ↓urate reabsorption → ↑↑urate excretion Indication: impaired urate excretion, used in combination with XOI for refractory to monotherapy S/E: rash, precipitation of gout flare, GI intolerance, urate stone formation Probenecid S/E = Precipitation of gout, Rash, Obstruction (urate stone), Bowels (GI upset)
48
Recombinant uricase Examples MoA S/E
eg. pegloticase (for gout), rasburicase (for TLS, not for gout) → MoA: enzyme that catalyzes conversion of urate into more soluble allantoin for excretion S/E: may develop Ab vs pegloticase → ↓therapeutic response → limiting factor for long-term treatment
49
Radiological features of pseudogout
→ Chondrocalcinosis: irregular faint punctate/linear radiodensities in articular cartilage → Degenerative changes: subchondral cysts, osteophytes, ↓joint space → Other features in specific joints: - MCPJ: squared off bone ends and hook-like MPCJ - Wrist: isolated/unusually extensive radiocarpal joint narrowing - PFJ: severe space degeneration

MBBS VI - SpC - Family Medicine (42 decks)

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