Arthritides Flashcards
What is the definition of infectious arthritis?
infection of >1 joint caused by bacteria, virus, fungi, mycoplasma, rickettsiae, parasites
What is the aetiology and pathology of acute infectious arthritis?
- Bacteria: Neisseria gonorrhoea, Staph aureus
- Viruses: Epstein-Barr, hep B, HIV, rubella, mumps
- oedema, neutrophil infiltration of synovium (+ necrosis and hemorrhage)
- panes, cartilage erosion
What is the aetiology and pathology of chronic infectious arthritis?
- Mycobacterium TB
- low pathogenicity bacteria
- fungi (Candida albicans)
• lymphocytic and plasma cell infiltration, in-grown granulation tissue, fibrosis, cartilage destruction, permanent joint damage
Compare the clinical features of acute and chronic infectious arthritis?
• depends on organism and joint
Acute: fever, pain, swelling, red, warm, tender, limited ROM
Chronic: insidious pain, swelling limited ROM
What are the predisposing factors to infectious arthritis?
- prosthetic joint
- diseased joint (RA, SLE)
- STI
- trauma
- diabetes mellitus
- immunosupressed
- IV drug use
- very young/old
Explain the relationship of infective agents to joint pain. What other symptoms and signs would this explain?
- infectious arthritis: caused BY bacteria, virus, fungi, mycoplasma, riskettsiae, parasites
- reactive arthritis: autoimmune disorder as a result of an infection of genitourinary (STI) or GI (shigella flexneri, salmonella)
- with any infection you get: fever, pain, swelling, redness, warmth, tenderness, decreased ROM
- infection in the joint damages tissue (pain-sensitive)
What is the definition of reactive arthritis?
• autoimmune disorder as a RESULT of an infection (genitourinary or GIT)
What is Reiter’s syndrome?
old name for reactive arthritis
What is the aetiology of reactive arthritis?
HLA B27 positive
a) Venereal: STI origin, manifests by urethritis following sex
b) Enteric: 1-3 weeks of acute dysenteric illness of Shingella flexneri, Yersinia enterocolitica, or salmonella
What is the pathology of reactive arthritis?
- synovitis
- fibrous proliferation
- periostitis
- erosions
Spine:
• paravertebral ossification
• bones may unite
What are the clinical features of reactive arthritis?
- can’t pee, see, dance
- SIitis, uveitis, urethritis
- Hx of urinary or GI infection
- dysuria, discharge, prostatitis
- asymmetrical painful effusion
- knee, ankle, forefoot, calcaneus, low back, shoulder, wrist
- short duration (2-3months)
- recurrence
- conjunctivitis, skin lesions on soles
- mucocutaneous lesions (penis, mouth)
What are complications of reactive arthritis?
- urinary tract obstruction
- iritis
- retrobulbar neuritis
- corneal ulceration
- aortitis
- A V block
- cranial nerve paralysis
What investigations can we do for reactive arthritis?
- FBC - anaemia, leukocytosis
- ESR -increased
- 75% have HLA B27 antigen
- imaging studies
What is the definition of rheumatoid arthritis? and epidemiology?
- progressive systemic disease of synovial membranes and connective tissues
- common in hands and feet
- common
- females 3:1
- onset 35-50yrs
What is the aetiology of RA?
- multifactorial
- genetic susceptibility + infection = autoantibody (rheumatoid factor) -> synovial inflammation
- genetic, immunological, hormonal, environmental factors
List the infectious arthropathies
Septic
Reactive
List the inflammatory arthritides
Rheumatoid Psoriatic Juvenile Enteropathic Gout Calcium pyrophosphate dihydrate Crystal Deposition disease HADD
List the arthrosis’
Polyarthrosis (primary and erosive) Coxarthrosis Gonarthrosis Arthritis of 1st carpometacarpal joint Hypertrophic osteoarthrosis
How does the pathological process in RA relate to its clinical features?
Predisposition -> trigger (infection, trauma) + autoimmune reaction
-> articular:
• synovium (acute red, hot, swell, tender)
• lig and tend (chronic weak, hypermobile, deformed)
and extraarticular: • cardio (valves) • lungs (oedema) • skin (rash) • eyes (sclera)
What is the pathophysiology of RA?
Antigen + susceptibility -> activates CDa+ helped T cells and B lymphocytes -> release cytokines -> stimulate synovial macrophage and fibroblast ->
a-> activate B lymphocytes -> rheumatoid factor -> autoimmune complex deposits in tissue
b-> activate osteoclasts
c-> enzyme release
-> damage leads to panes formation, joint destruction, cartilage fibrosis
What are the articular clinical features of RA?
- insidious or acute onset
- begins with transient arthralgia or myalgia
- first fingers and toes
- spindle shaped fingers
- MTPs and PIPs
- knees, wrists, elbows, ankles, cervical spine
- warm, stuff, atrophy, reduced ROM
- deformity (fixed flexion, ulnar deviation)
arthralgia
joint pain
myalgia
muscle pain
What are the non-articular clinical features of RA?
- rheumatoid nodules
- leg ulcers
- fever
- tachycardia
- pleural, bronchial, interstitial lung (dyspnoea, cough)
- pericarditis
- rheumatoid vasculitis (cutaneous, neurological, pulmonary, GI)
- ophthalmologic (corneal, keratoconjunctivitis, scleritis, blindness)
- secondary amyloidosis
- Felty’s syndrome (splenomegaly, granulocytopenia
What is stills disease?
RA in children
Describe the course of RA
- tendency to become quiescent after remaining active for months or years
- permanent impairment of joint function
- degenerative changes are often superimposed
- permanent damage
What is the link between RA and subluxation?
- ongoing synovitis damages the attachment of surrounding ligaments at affected joints
- in cervical spine this destroys the transverse ligaments and causes Atlanta-axial subluxation
What is Felty’s syndrome?
- extra-articular complication of RA
* classic triad of RA: with splenomegaly, granulocytopenia
What are the investigations in RA?
FBC:
• Hb decreased, WCC increased (slight neutrophilia)
• increased ESR
Immunological studies: rheumatoid factor sometimes present
Synovial fluid exam
Imaging studies
What is the definition of psoriatic arthritis?
- similar to RA, but absence of rheumatoid factor
* hereditary factors
What is the pathology of of psoriatic arthritis?
- same as RA
- fibrosis tissue may produce bony ankylosis
- especially t calcaneus, hand, foot
- fusion of adjacent vertebral body
- no correlation between onset of lesions and arthritis
- develop arthritis within 5yrs of skin lesions
- joint destruction
What are the clinical features of psoriatic arthritis?
- skin lesions on extensor surfaces
- sharply demarcated, non-elevated, silvery scales
- pitting, ridging nails
- joint redness, swelling, pain
- sausage digit
- asymmetrical SIJ
What investigations do we do for psoriatic arthritis?
- increased ESR in acute phase
- negative rheumatoid factor
- maybe hyperuricemia
- maybe HLA B27 antigen
What is the pathological similarity between RA, psoriatic arthritis, and reactive arthritis?
- all same pathology
- difference is the populations at risk
Reactive: calcaneus, SI, knee, ankle, forefoot, low back
Rheumatoid: symmetrical -spindle shape fingers, MP, PIP joints, knees, wrists, elbows, ankles, cervical spine
Psoriatic: single site -PIPs and DIPs, SI, spine, calcaneous, foot
How do the clinical features of psoriatic arthritis differ from that of rheumatoid arthritis?
Psoriatic: • asymetrical • DIPs, SI, thoracic • saussage digits • pitting, ridging discoloured nails • silvery scale skin lesions
Rheumatoid:
• symmetrical
• MPs, PIPs
• spindle fingers
• knees, wrists, elbows, ankles, cervical
• fixed flexion of digits + ulnar deviation
• nodules, leg ulcers, fever, tachycardia, red lumpy rash
What is the definition of Gout?
- recurrent arthritis from deposition of sodium monourate crystals in tissues
- disorder of purine metabolism
- aggregations of crystals (trophi) in cartilage, bursae, ligaments
What id the epidemiology of gout?
- men > women
- > 40yrs
- postmenopausal women using diuretics
- family history
- Polynesian and New Zealand natives
What is the aetiology of Gout?
- hereditary
- result of hyperuricemia
- disorder of purine metabolism
Elevated uric acid levels in blood from:
- decreased renal excretion of urate (renal disease, chronic use of diuretics, chronic lead intoxication)
- increase in purine synthesis
• primary or secondary
What are some examples of diuretics that can lead to gout?
- frusemide
- aspirin
- diuretics
- nicotinic acid
What is primary gout?
- hyperuricemia is due to an overproduction or lack of excretion of uric acid due to an inborn enzymatic defect
- most common type
What is secondary gout?
• hyperuricemia develops in the course of another disease or of drug action
What is the pathology of gout?
- uric acid in plasma in solution with loose combination with proteins
- comes out of solution and deposits in crystals in connective tissues (especially injured, low blood supply)
- crystals cause inflammatory reaction
Acute: crystals soon absorbed
Chronic: disorganizes joints + trophi
What are the clinical features of acute gout?
- sudden extremely painful joint
- swollen, red, hot, tender
- 1st MTP, elbow, wrist, ankle, knee
- fever, malaise, chills
- precipitated by purine enriched foods (liver, kidneys, sweetbreads, shellfish), alcohol, excess exercise, infections, injury, surgery
- bursitis (olecranon)
Which arthritis does acute gout look like?
septic arthritis
What are the clinical features of chronic gout?
- many attacks
- when prophylactic treatment not used
- urate deposits (trophi) in cartilage of ear, joints of hands, feet, tendon sheaths, bursae
- deformity, limit ROM
- chalky eruptions of trophi
- no acute inflammatory changes
- renal calculi
What are the 4 stages of gout clinical manifestations?
1) Asymptomatic hyperuricemia
2) Acute gouty arthritis
3) Polyarticular gouty arthritis
4) Chronic tophaceous gout
At what of the 4 stages of gout is radiographic manifestations most frequently encountered?
Polyarticular gouty arthritis
What are the complications of gout?
- renal damage
- renal stones
- hypertension
- atherosclerosis
- thrombophlebitis
What investigations can we do for acute gout?
- polymorph leukocytosis
- increased ESR
- increased serum uric acid
- aspiration of swollen joints yield turbid fluid, but never organisms
- polarized light microscopy of synovial fluid reveals needle-shaped crystals
- x-rays
What is the DDx of acute gout?
- other sudden arthritis’s
- acute pyogenic arthritis
- acute pseudo gout (CPPD)
- haemophilic arthritis
- rheumatic fever
What is the DDx of chronic gout?
if involving several joints may stimulate rheumatoid arthritis
What is pseudo-gout?
another name for CPPD
What is CPPD? (definition, symptoms, aetiology, precipitating factors, age, clinical features, sites)
- Calcium pyrophosphate dehydrate crystal deposition disease
- gout-like symptoms
- unknown aetiology
- precipitating by age, genetics, coexisting disease (diabetes, gout, hyperparathyroidism)
- onset >30yrs
- peak at 60
- progressive joint pain, intermittent swelling, reduced ROM, crepitus
- knees, wrists, hands, ankles, hips, elbows
What is HADD (definition, aetiology, pathology, age, clinical features, sites)
- Hydroxyapatite deposition disease
- unknown aetiology
- following a focus of degeneration within tissue after crystals deposited
- also deposit in synovial fluid
- necrosis, fibrosis, inflammatory cell infiltrate, granular deposits
- 40-70yrs
- tendonitis, bursitis, joint pain
- single site
- often shoulder
What is the critical zone of HADD
- supraspinatus tendon is often zone for crystals
* because vascular compromised tissue
List the juvenile chronic arthritis’?
- juvenile RA seropositive
- seronegative chronic arthritis
- juvenile ankylosing spondylitis
- psoriatic
- enteropathic
- Lupus erythematosus
- Still’s disease
What is degenerative joint disease? (definition, epidemiology, age, sites)
• wear and tear process in joint • unknown exact cause • most common variety of arthritis • <45, most common in males; > 45, more females thickens, fibrosis • spine, hips, knees
What is osteoarthritis?
another name for degenerative joint disease
Which is the most common arthritis?
DJD
What is the the aetiology of DJD?
Primary: on identifiable cause Secondary: • congenital malformation • previous fracture • internal derangement (loose body, torn meniscus) • previous disease caused damaged articular cartilage • malalignment of joint (bow leg) • obesity
Is age a cause of osteoarthritis?
- alone it not a cause
- may be associated unimpaired capacity for tissue repair after injury
- may be an indirect causative factor
What is the pathology of DJD?
- discrete sequence of individual histological events which leads to cartilage destruction and secondary alterations
- degeneration starts focal, spreads -> articular cartilage worn away -> underlying bone exposed -> subchondral bone becomes hard and glossy -> weaker -> synovial fluid erodes it -> bone margins hypertrophy (osteophytes) -> capsule
- altered function of chondrocytes -> release cytokines + degenerative enzymes -> damage
What do osteophytes cause?
- deformities at joint
- limited ROM
- pressure on adjacent structures
What is DDD?
- degenerative disc disease
- damage to the annulus and faulty mechanics
- leads to degradation of nucleus pulposus
What are the clinical features of DJD?
- gradual onset of symptoms, intermittent aching joints
- pain worse by movement, better by rest
- stiffness on rest, disappears with activity
- cold and lowered barometric pressures aggravate
- crepitus, reduced ROM, palpable excrescences, muscle atrophy
- thickening on palpation (caused by osteophytes)
- no warmth
- joint instability from muscle waisting
- fixed deformity
- signs of spinal stenosis
What limits movement in DJD?
- muscle spasms
- loss of articular cartilage
- osteophytes
- effusions into joint cavity
Where does DJD target?
- C5, C6 disc spaces
- upper facet joints C2/3
- Thoracic, costovertebral joints
- L3/4/5 disc spaces and facet joints
- SIJ low 2/3s
- Hands, hips, knees, feet, elbows
What is Inflammatory Osteoarthritis?
another name for erosive osteoarthritis
What is Erosive osteoarthritis?
- variant of DJD, targeting the interphalangeal joints
- 40-50yr females
- synovial abnormalities and cartilage destruction (rheumatoid arthritis)
- bony proliferation (DJD)
- seronegative
- episodic and acute inflammation in interphalangeal joints symmetrical
- pain, oedema, redness, nodules, restricted ROM
- deformity
- develops for years
- 15% develop RA -in 12yrs becomes erosive osteoarthritis
What is hypertrophic osteoarthropathy?
- clubbing, symmetrical arthritis, periostitis
- consequence of visceral disorder (commonly bronchogenic carcinoma)
- unknown pathogenesis
- maybe humeral or visceral
Humeral: production of unidentified substance from the abnormality increases blood flow (less likely)
Visceral: afferent neural impulses from the abnormal viscus result in vagal efferent reflex vasodilation at periphery
What is synoviochondrometaplasia?
- benign metaplastic transformation of synovial tissue
- cartilaginous foci
- results in loose bodies in joint
- asymptomatic range to acute joint locking and pain
- associated with trauma
- hip and knee
What is the level of pain in acute gout? and why?
- extreme pain 10/10
- crystals cause inflammation because they are sharp and pointy
- crescendo pain: builds and builds as the crystal forms
What are the major differences between acute and chronic gout?
Acute vs Chronic:
sudden onset • repeated events
swollen, red, hot, tender • NO acute inflammation
fever, malaise, chills • top and deformity
1st MP, elbow, wrist, ankle, knee • ear, hands, feet, tendon sheaths, bursae
What is the DDx of acute gout?
Red hot tender joints: • reactive arthritis • trauma • rheumatoid arthritis • psoriatic • septic arthritis • cellulitis • pseudogout
How does HADD differ from CPPD?
HADD vs CPPD
crystal type
40-70yrs • onset 30yrs, peak at 60
supraspinatus tendon • knees, wrist, hand, ankles, hips, elbows, cervical, lumbar
What is the difference between arthrosis and arthritis?
arthrosis is cold, achy, stiff
arthritis is hot, swollen,
What is the pathophysiology of osteoarthrosis?
- excessive joint loading
- cartilage damage (not pain sensitive)
- mild inflammation (not hot, redlike arthritis)
- stiff
- time
- laxity / hypermobility
- muscle spasm, guarding + osteophytes (long term)
Why does osetoarchrosis cause discomfort?
- swelling and muscle spasm
* osteophytes put pressure on adjacent structures
Why does osetoarchrosis cause limited movement?
- muscles spasms (from altered mechanics), guarding
- lost articular cartilage
- mild inflammation - effusions into joint cavity (feeling boggy in mornings)
- osteophytes (physically block)
Why does osetoarchrosis cause swelling?
mild inflammation - effusions into joint cavity
Why does osetoarchrosis cause deformity?
- osteophytes -> hard bumps
* muscle atrophy from not using a painful joint
What are joint mice?
- loose bodies
- small pieces of bone or cartilage within joint cavity
- from trauma or wear and tear
- painful catching and locking of joint
- complications: osteoarthritis, limitation of ROM
- knees, ankle, hip, elbow
What are the onset ages of reactive arthritis, rheumatoid arthritis and psoriatic arthritis?
Reactive: 13-30
Rheumatoid: 35-50
Psoriatic: 20-50
What are the skin manifestations of psoriasis?
- silvery scaly rashes on extensor surfaces that bleed when removed
- pitting, ridging, discoloured nails
- DIP redness, swelling, (saussage digits)
- Dry, itchy cracked skin
List the areas of involvement of psoriatic arthritis
1) distal interphalangeal joints
2) sacroiliac joints
3) lower thoracic spine
4) upper lumbar
