Medical Sciences B > Arthritides > Flashcards

Arthritides Flashcards

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1
Q

What is the definition of infectious arthritis?

A

infection of >1 joint caused by bacteria, virus, fungi, mycoplasma, rickettsiae, parasites

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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
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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

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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

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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
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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)
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7
Q

What is the definition of reactive arthritis?

A

• autoimmune disorder as a RESULT of an infection (genitourinary or GIT)

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8
Q

What is Reiter’s syndrome?

A

old name for reactive arthritis

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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

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10
Q

What is the pathology of reactive arthritis?

A
  • synovitis
  • fibrous proliferation
  • periostitis
  • erosions

Spine:
• paravertebral ossification
• bones may unite

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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)
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12
Q

What are complications of reactive arthritis?

A
  • urinary tract obstruction
  • iritis
  • retrobulbar neuritis
  • corneal ulceration
  • aortitis
  • A V block
  • cranial nerve paralysis
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13
Q

What investigations can we do for reactive arthritis?

A
  • FBC - anaemia, leukocytosis
  • ESR -increased
  • 75% have HLA B27 antigen
  • imaging studies
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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
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15
Q

What is the aetiology of RA?

A
  • multifactorial
  • genetic susceptibility + infection = autoantibody (rheumatoid factor) -> synovial inflammation
  • genetic, immunological, hormonal, environmental factors
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16
Q

List the infectious arthropathies

A

Septic

Reactive

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17
Q

List the inflammatory arthritides

A 
Rheumatoid
Psoriatic
Juvenile
Enteropathic 
Gout
Calcium pyrophosphate dihydrate
Crystal Deposition disease
HADD
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18
Q

List the arthrosis’

A 
Polyarthrosis (primary and erosive)
Coxarthrosis
Gonarthrosis
Arthritis of 1st carpometacarpal joint
Hypertrophic osteoarthrosis
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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)
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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

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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)
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22
Q

arthralgia

A

joint pain

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23
Q

myalgia

A

muscle pain

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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
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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
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