Arthritides Flashcards
(85 cards)
1
Q
What is the definition of infectious arthritis?
A
infection of >1 joint caused by bacteria, virus, fungi, mycoplasma, rickettsiae, parasites
2
Q
What is the aetiology and pathology of acute infectious arthritis?
A
- Bacteria: Neisseria gonorrhoea, Staph aureus
- Viruses: Epstein-Barr, hep B, HIV, rubella, mumps
- oedema, neutrophil infiltration of synovium (+ necrosis and hemorrhage)
- panes, cartilage erosion
3
Q
What is the aetiology and pathology of chronic infectious arthritis?
A
- Mycobacterium TB
- low pathogenicity bacteria
- fungi (Candida albicans)
• lymphocytic and plasma cell infiltration, in-grown granulation tissue, fibrosis, cartilage destruction, permanent joint damage
4
Q
Compare the clinical features of acute and chronic infectious arthritis?
A
• depends on organism and joint
Acute: fever, pain, swelling, red, warm, tender, limited ROM
Chronic: insidious pain, swelling limited ROM
5
Q
What are the predisposing factors to infectious arthritis?
A
- prosthetic joint
- diseased joint (RA, SLE)
- STI
- trauma
- diabetes mellitus
- immunosupressed
- IV drug use
- very young/old
6
Q
Explain the relationship of infective agents to joint pain. What other symptoms and signs would this explain?
A
- 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)
7
Q
What is the definition of reactive arthritis?
A
• autoimmune disorder as a RESULT of an infection (genitourinary or GIT)
8
Q
What is Reiter’s syndrome?
A
old name for reactive arthritis
9
Q
What is the aetiology of reactive arthritis?
A
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
10
Q
What is the pathology of reactive arthritis?
A
- synovitis
- fibrous proliferation
- periostitis
- erosions
Spine:
• paravertebral ossification
• bones may unite
11
Q
What are the clinical features of reactive arthritis?
A
- 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)
12
Q
What are complications of reactive arthritis?
A
- urinary tract obstruction
- iritis
- retrobulbar neuritis
- corneal ulceration
- aortitis
- A V block
- cranial nerve paralysis
13
Q
What investigations can we do for reactive arthritis?
A
- FBC - anaemia, leukocytosis
- ESR -increased
- 75% have HLA B27 antigen
- imaging studies
14
Q
What is the definition of rheumatoid arthritis? and epidemiology?
A
- progressive systemic disease of synovial membranes and connective tissues
- common in hands and feet
- common
- females 3:1
- onset 35-50yrs
15
Q
What is the aetiology of RA?
A
- multifactorial
- genetic susceptibility + infection = autoantibody (rheumatoid factor) -> synovial inflammation
- genetic, immunological, hormonal, environmental factors
16
Q
List the infectious arthropathies
A
Septic
Reactive
17
Q
List the inflammatory arthritides
A
Rheumatoid Psoriatic Juvenile Enteropathic Gout Calcium pyrophosphate dihydrate Crystal Deposition disease HADD
18
Q
List the arthrosis’
A
Polyarthrosis (primary and erosive) Coxarthrosis Gonarthrosis Arthritis of 1st carpometacarpal joint Hypertrophic osteoarthrosis
19
Q
How does the pathological process in RA relate to its clinical features?
A
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)
20
Q
What is the pathophysiology of RA?
A
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
21
Q
What are the articular clinical features of RA?
A
- 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)
22
Q
arthralgia
A
joint pain
23
Q
myalgia
A
muscle pain
24
Q
What are the non-articular clinical features of RA?
A
- 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
25
What is stills disease?
RA in children
26
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
27
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
28
What is Felty's syndrome?
* extra-articular complication of RA
| * classic triad of RA: with splenomegaly, granulocytopenia
29
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
30
What is the definition of psoriatic arthritis?
* similar to RA, but absence of rheumatoid factor
| * hereditary factors
31
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
32
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
33
What investigations do we do for psoriatic arthritis?
* increased ESR in acute phase
* negative rheumatoid factor
* maybe hyperuricemia
* maybe HLA B27 antigen
34
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
35
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
36
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
37
What id the epidemiology of gout?
* men > women
* > 40yrs
* postmenopausal women using diuretics
* family history
* Polynesian and New Zealand natives
38
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
39
What are some examples of diuretics that can lead to gout?
* frusemide
* aspirin
* diuretics
* nicotinic acid
40
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
41
What is secondary gout?
• hyperuricemia develops in the course of another disease or of drug action
42
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
43
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)
44
Which arthritis does acute gout look like?
septic arthritis
45
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
46
What are the 4 stages of gout clinical manifestations?
1) Asymptomatic hyperuricemia
2) Acute gouty arthritis
3) Polyarticular gouty arthritis
4) Chronic tophaceous gout
47
At what of the 4 stages of gout is radiographic manifestations most frequently encountered?
Polyarticular gouty arthritis
48
What are the complications of gout?
* renal damage
* renal stones
* hypertension
* atherosclerosis
* thrombophlebitis
49
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
50
What is the DDx of acute gout?
* other sudden arthritis's
* acute pyogenic arthritis
* acute pseudo gout (CPPD)
* haemophilic arthritis
* rheumatic fever
51
What is the DDx of chronic gout?
if involving several joints may stimulate rheumatoid arthritis
52
What is pseudo-gout?
another name for CPPD
53
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
54
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
55
What is the critical zone of HADD
* supraspinatus tendon is often zone for crystals
| * because vascular compromised tissue
56
List the juvenile chronic arthritis'?
* juvenile RA seropositive
* seronegative chronic arthritis
* juvenile ankylosing spondylitis
* psoriatic
* enteropathic
* Lupus erythematosus
* Still's disease
57
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
```
58
What is osteoarthritis?
another name for degenerative joint disease
59
Which is the most common arthritis?
DJD
60
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
```
61
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
62
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
63
What do osteophytes cause?
* deformities at joint
* limited ROM
* pressure on adjacent structures
64
What is DDD?
* degenerative disc disease
* damage to the annulus and faulty mechanics
* leads to degradation of nucleus pulposus
65
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
66
What limits movement in DJD?
* muscle spasms
* loss of articular cartilage
* osteophytes
* effusions into joint cavity
67
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
68
What is Inflammatory Osteoarthritis?
another name for erosive osteoarthritis
69
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
70
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
71
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
72
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
73
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
74
What is the DDx of acute gout?
```
Red hot tender joints:
• reactive arthritis
• trauma
• rheumatoid arthritis
• psoriatic
• septic arthritis
• cellulitis
• pseudogout
```
75
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
76
What is the difference between arthrosis and arthritis?
arthrosis is cold, achy, stiff
arthritis is hot, swollen,
77
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)
78
Why does osetoarchrosis cause discomfort?
* swelling and muscle spasm
| * osteophytes put pressure on adjacent structures
79
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)
80
Why does osetoarchrosis cause swelling?
mild inflammation - effusions into joint cavity
81
Why does osetoarchrosis cause deformity?
* osteophytes -> hard bumps
| * muscle atrophy from not using a painful joint
82
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
83
What are the onset ages of reactive arthritis, rheumatoid arthritis and psoriatic arthritis?
Reactive: 13-30
Rheumatoid: 35-50
Psoriatic: 20-50
84
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
85
List the areas of involvement of psoriatic arthritis
1) distal interphalangeal joints
2) sacroiliac joints
3) lower thoracic spine
4) upper lumbar
