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Arthritides Flashcards

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USMLE® Step 1 flashcards
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
Q

What is stills disease?

A

RA in children

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26
Q

Describe the course of RA

A
  • tendency to become quiescent after remaining active for months or years
  • permanent impairment of joint function
  • degenerative changes are often superimposed
  • permanent damage
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27
Q

What is the link between RA and subluxation?

A
  • ongoing synovitis damages the attachment of surrounding ligaments at affected joints
  • in cervical spine this destroys the transverse ligaments and causes Atlanta-axial subluxation
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28
Q

What is Felty’s syndrome?

A
  • extra-articular complication of RA

* classic triad of RA: with splenomegaly, granulocytopenia

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29
Q

What are the investigations in RA?

A

FBC:
• Hb decreased, WCC increased (slight neutrophilia)
• increased ESR

Immunological studies: rheumatoid factor sometimes present

Synovial fluid exam

Imaging studies

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30
Q

What is the definition of psoriatic arthritis?

A
  • similar to RA, but absence of rheumatoid factor

* hereditary factors

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31
Q

What is the pathology of of psoriatic arthritis?

A
  • 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
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32
Q

What are the clinical features of psoriatic arthritis?

A
  • skin lesions on extensor surfaces
  • sharply demarcated, non-elevated, silvery scales
  • pitting, ridging nails
  • joint redness, swelling, pain
  • sausage digit
  • asymmetrical SIJ
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33
Q

What investigations do we do for psoriatic arthritis?

A
  • increased ESR in acute phase
  • negative rheumatoid factor
  • maybe hyperuricemia
  • maybe HLA B27 antigen
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34
Q

What is the pathological similarity between RA, psoriatic arthritis, and reactive arthritis?

A
  • 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

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35
Q

How do the clinical features of psoriatic arthritis differ from that of rheumatoid arthritis?

A 
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
Q

What is the definition of Gout?

A
  • recurrent arthritis from deposition of sodium monourate crystals in tissues
  • disorder of purine metabolism
  • aggregations of crystals (trophi) in cartilage, bursae, ligaments
37
Q

What id the epidemiology of gout?

A
  • men > women
  • > 40yrs
  • postmenopausal women using diuretics
  • family history
  • Polynesian and New Zealand natives
38
Q

What is the aetiology of Gout?

A
  • 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
Q

What are some examples of diuretics that can lead to gout?

A
  • frusemide
  • aspirin
  • diuretics
  • nicotinic acid
40
Q

What is primary gout?

A
  • hyperuricemia is due to an overproduction or lack of excretion of uric acid due to an inborn enzymatic defect
  • most common type
41
Q

What is secondary gout?

A

• hyperuricemia develops in the course of another disease or of drug action

42
Q

What is the pathology of gout?

A
  • 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
Q

What are the clinical features of acute gout?

A
  • 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
Q

Which arthritis does acute gout look like?

A

septic arthritis

45
Q

What are the clinical features of chronic gout?

A
  • 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
Q

What are the 4 stages of gout clinical manifestations?

A

1) Asymptomatic hyperuricemia
2) Acute gouty arthritis
3) Polyarticular gouty arthritis
4) Chronic tophaceous gout

47
Q

At what of the 4 stages of gout is radiographic manifestations most frequently encountered?

A

Polyarticular gouty arthritis

48
Q

What are the complications of gout?

A
  • renal damage
  • renal stones
  • hypertension
  • atherosclerosis
  • thrombophlebitis
49
Q

What investigations can we do for acute gout?

A
  • 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
Q

What is the DDx of acute gout?

A
  • other sudden arthritis’s
  • acute pyogenic arthritis
  • acute pseudo gout (CPPD)
  • haemophilic arthritis
  • rheumatic fever
51
Q

What is the DDx of chronic gout?

A

if involving several joints may stimulate rheumatoid arthritis

52
Q

What is pseudo-gout?

A

another name for CPPD

53
Q

What is CPPD? (definition, symptoms, aetiology, precipitating factors, age, clinical features, sites)

A
  • 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
Q

What is HADD (definition, aetiology, pathology, age, clinical features, sites)

A
  • 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
Q

What is the critical zone of HADD

A
  • supraspinatus tendon is often zone for crystals

* because vascular compromised tissue

56
Q

List the juvenile chronic arthritis’?

A
  • juvenile RA seropositive
  • seronegative chronic arthritis
  • juvenile ankylosing spondylitis
  • psoriatic
  • enteropathic
  • Lupus erythematosus
  • Still’s disease
57
Q

What is degenerative joint disease? (definition, epidemiology, age, sites)

A 
• 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
Q

What is osteoarthritis?

A

another name for degenerative joint disease

59
Q

Which is the most common arthritis?

A

DJD

60
Q

What is the the aetiology of DJD?

A 
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
Q

Is age a cause of osteoarthritis?

A
  • alone it not a cause
  • may be associated unimpaired capacity for tissue repair after injury
  • may be an indirect causative factor
62
Q

What is the pathology of DJD?

A
  • 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
Q

What do osteophytes cause?

A
  • deformities at joint
  • limited ROM
  • pressure on adjacent structures
64
Q

What is DDD?

A
  • degenerative disc disease
  • damage to the annulus and faulty mechanics
  • leads to degradation of nucleus pulposus
65
Q

What are the clinical features of DJD?

A
  • 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
Q

What limits movement in DJD?

A
  • muscle spasms
  • loss of articular cartilage
  • osteophytes
  • effusions into joint cavity
67
Q

Where does DJD target?

A
  • 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
Q

What is Inflammatory Osteoarthritis?

A

another name for erosive osteoarthritis

69
Q

What is Erosive osteoarthritis?

A
  • 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
Q

What is hypertrophic osteoarthropathy?

A
  • 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
Q

What is synoviochondrometaplasia?

A
  • 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
Q

What is the level of pain in acute gout? and why?

A
  • extreme pain 10/10
  • crystals cause inflammation because they are sharp and pointy
  • crescendo pain: builds and builds as the crystal forms
73
Q

What are the major differences between acute and chronic gout?

A

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
Q

What is the DDx of acute gout?

A 
Red hot tender joints:
• reactive arthritis
• trauma
• rheumatoid arthritis
• psoriatic
• septic arthritis
• cellulitis
• pseudogout
75
Q

How does HADD differ from CPPD?

A

HADD vs CPPD

crystal type
40-70yrs • onset 30yrs, peak at 60
supraspinatus tendon • knees, wrist, hand, ankles, hips, elbows, cervical, lumbar

76
Q

What is the difference between arthrosis and arthritis?

A

arthrosis is cold, achy, stiff

arthritis is hot, swollen,

77
Q

What is the pathophysiology of osteoarthrosis?

A
  • 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
Q

Why does osetoarchrosis cause discomfort?

A
  • swelling and muscle spasm

* osteophytes put pressure on adjacent structures

79
Q

Why does osetoarchrosis cause limited movement?

A
  • muscles spasms (from altered mechanics), guarding
  • lost articular cartilage
  • mild inflammation - effusions into joint cavity (feeling boggy in mornings)
  • osteophytes (physically block)
80
Q

Why does osetoarchrosis cause swelling?

A

mild inflammation - effusions into joint cavity

81
Q

Why does osetoarchrosis cause deformity?

A
  • osteophytes -> hard bumps

* muscle atrophy from not using a painful joint

82
Q

What are joint mice?

A
  • 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
Q

What are the onset ages of reactive arthritis, rheumatoid arthritis and psoriatic arthritis?

A

Reactive: 13-30
Rheumatoid: 35-50
Psoriatic: 20-50

84
Q

What are the skin manifestations of psoriasis?

A
  • silvery scaly rashes on extensor surfaces that bleed when removed
  • pitting, ridging, discoloured nails
  • DIP redness, swelling, (saussage digits)
  • Dry, itchy cracked skin
85
Q

List the areas of involvement of psoriatic arthritis

A

1) distal interphalangeal joints
2) sacroiliac joints
3) lower thoracic spine
4) upper lumbar

Medical Sciences B (23 decks)

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