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3 > Inflammatory arthritis > Flashcards

Inflammatory arthritis Flashcards

1
Q

Articular cartilage

A

low friction surface
no perichondrium - little capacity for healing, nutrient from synovial fluid
no innervation - significant damage when pain is felt
special collagen arrangement
arch structure

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2
Q

Collagen arrangement in articular cartilage

A

vertical near the bottom
becomes more oblique near top
arched at the top for resilience

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3
Q

Relaxation - collagen

A

cartilage is very hydrated
GAG side chains repel each other and attract water - increase in cartilage matrix volume
a point where vol is maximal based on resistance of matrix expansion by collagen arches

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4
Q

weight-bearing - collagen

A

pushes GAG side chains together, squishing water out of joint
reduces cartilage matrix volume
important for circulation of water content and nutrient throughout the joint

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5
Q

Synovium layers

A

cellular intima

subintima

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6
Q

Cellular intium of synovium

A

Synoviocytes that line inner surface of synovium
No intercellular junctions or basement membrane (not epithelium)
Type A and B synoviocytes

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7
Q

Type A synoviocytes

A 
20-30%
Monocyte derived
Phagocytosis of particles in joitn space
Prominent invaginations in plasma membrane, many lysosomes, prominent Golgi
lytic enzyme production
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8
Q

Type B synoviocytes

A

predominant
Mesenchymal derivation
modified fibroblasts
Synthesize and secrete HA and lubricin

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9
Q

Subintima of synovium

A

subsynovial

vascular CT

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10
Q

Synovial fluid production

A

Transudate from plasma

Secretion of type B synoviocytes

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11
Q

Synovial fluid from plasma

A

Transudate from subintimal fenestrated capillaries
During inflammation - capillaries become leaky
- get exudative synovial fluid
- cellular content of synovial fluid will increase, mostly PMNs

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12
Q

Type 0 synovial fluid

A

High viscosity
Colourless, transparent
<200 WBCs, mostly monocytes

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13
Q

Type 1 synovial fluid

A

non-inflammatory, e.g. OA
High viscosity
Yellow/straw coloured, translucent
<2000 WBCs, mostly monocytes

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14
Q

Type 2 synovial fluid

A

Inflammatory, e.g. RA
Low viscosity
Yellow/straw coloured, slight cloudy to cloudy
2000-100,000 >50% polys

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15
Q

Type 3 synovial fluid

A 
Septic
low viscosity
Opaque, cloudy turbid
>100,000, >75% polys
culture often +
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16
Q

Type 4 synovial fluid

A

Hemorrhagic
Viscosity - non-clotted blood
Bloody
RBCs

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17
Q

Synovial changes in OA

A

cellulra infiltration into synovium
fibrin deposition in subintima
subintimal edema
increased subintimal vascularization

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18
Q

Clinical features of RA

A 
morning stiffness - 1 hour
Preferred joints are hands, wrists, elbows, knees, ankles, feet
no DIP
Symmetric arthritis
Presence of subcutaneous rheumatoid factor-filled nodules
Ulnar deviation
Swan neck deformity
Boutinieere deformity
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19
Q

Monoarthritis

A

one joint

think of infection

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20
Q

Oligoarthritis

A

4 or fewer

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21
Q

Polyarthritis

A

5 or more

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22
Q

Arthritis of collagen vascular autoimmune disease

A

RA, seropositive

SLE

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23
Q

Seronegative inflammatory arthritis

A 
Seronegative RA
Psoriatic arthritis
Seronegative spondyloarthropathies (SSpA)
- ankylosing spondilitis
- reactive arthritis (Reiter's)
- Psoriatic spondylitis
- Arthritis of IBD
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24
Q

Arthritis of infectious causes

A

Direct septic arthritis

  • usually staph, strep, CNS
  • usually monoarthritis
  • joint aspirations and blood cultures
  • fungal and TB in immunocompromised

Indirect arthritis from bacteria - Reiter’s/reactive arthritis

Viral causes of Arthritis
Lyme disease

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25
Q

Crystal arthritis

A

Gout (uric acid crystals)
Calcium pyrophosphate dihydrate arthropathy
Calcium hydroxyapatite

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26
Q

PE features of seropositive inflammatory arthritis

A

Deformity, redness, heat, swelling
Symmetry of joints
Fullness around joint: bony - osteoarthritis
Tenderness, pain, ROM

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27
Q

SLE etiology

A 
Genetics
9:1 female to male
induced by OCP
C1q deficiency - 93% penetrance
Potentially associated with sunburns
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28
Q

SLE presentation

A 
SOAP BRAIN MD
Serositis
Oral ulcers
Arthritis
Photosensitivity, pulmonary fibrosis
Blood 
Renal consequences, Raynaud's
ANA
Immunologic (anti-Smith, anti-dsDNA, anti-phospholipid)
Neuropsychiatric
Malar rash (fixed erythema over the malar eminences, spares nasolabial folds)
Discoid rash
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29
Q

Discoid lupus

A 
FEAST, 25% SLE patients
Follicular plugging
Erythema
Atrophy
Scarring
telangiectasia
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30
Q

SLE arthritis features

A 
Non-erosive
Transient
Symmetric
affects small joints
less severe than RA
Most common presenting feature of SLE
Jaccoud's arthropathy - Non-erosive and reducible deformities
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31
Q

Neuropsychiatric consequences of SLE

A 
Behaviour, personality changes
Depression
Psychosis
Seizures
Stroke
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32
Q

CV consequences of SLE

A

Atherosclerosis
Endocarditis
Pericarditis
Myocarditis

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33
Q

Respiratory consequences of SLE

A 
Interstitial lung disease
Pneumonitis
Pleural effusions
Pulmonary hemorrhage
Pulmonary HTN
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34
Q

Hematologic disorders of SLE

A

Hemolytic anemia
Leukopenia
Lymphopenia
Thrombocytopenia

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35
Q

Lupus Nephritis

A

Class I - normal
Class II - mesangial
Class III - focal and segmental proliferative glomerulonephritis
Class IV - diffuse proliferative glomerulonephritis
Class V - membranous glomerulonephritis
Class VI - glomerular sclerosis

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36
Q

Class I lupus nephritis

A

Normal
Normal on light microscopy
Mesangial deposits on electron microscopy
Renal failure is rare

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37
Q

Class II lupus nephritis

A 
Mesangial
Mesangial proliferative
Responds to corticosteroids
20% of SLE cases
Renal failure is rare
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38
Q

Class III lupus nephritis

A

Focal and segmental proliferative glomerulonephritis
Usually responds to high dose corticosteroids
25% of SLE cases
renal failure rare

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39
Q

Class IV lupus nephritis

A

diffuse proliferative glomerulonephritis
40% SLE cases
Treat with corticosteroids and immunosuppressants
Renal failure is a common sequence

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40
Q

Class V lupus nephritis

A

Membranous glomerulonephritis
Extreme edema and protein loss
10% of SLE cases
renal failure uncommon

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41
Q

Class VI lupus nephritis

A

glomerular sclerosis

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42
Q

SLE lab workup

A 
CBC, creatinine, electrolytes, urinanalysis, albumin
CK
ANA, ENA
anti-dsDNA, C3, C4
antiphospholipid antibodies
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43
Q

SLE treatment

A 
Depends on clinical disease
Sun avoidance
NSAIDs
prednisone
Plaquenil
Azathioprine
Mycophenolate mofetil
Cyclosporine
Cyclophosphamide
Rituximab
44
Q

Undifferentiated CT disease

A 
Positive serology (ANA)
doesn't meet criteria for a specific CTD, but may progress to one
45
Q

Drug-induced lupus

A

Hydralazine, isoniazid, procainamide, chlorpromazine
No gender preference
Rarely results in nephritis/neurologic consequences
No complement abnormalities or anti-dsDNA
symptoms resolve with stopping drugs

46
Q

Neonatal lupus

A

due to maternal autoantibodies passively transferring to fetus
main concern = congenital heart block (5% of cases, monitor with cardiac US)

47
Q

Rheumatology ROS

A 
Skin - psoriasis, malar rash, photosensitivity rash, maculopapular rash
Sicca symptoms - dry mouth, dry eyes
Raynaud's syndrome
Hair loss
Recurrent mouth or nasal sores
Red painful eyes, conjunctivitis/iritis
IBD
Recent travel/dysentery
Sexual history
History of urethritis
Family history --> psoriasis
48
Q

Stiffness to differentiate the type of arthritis

A

Morning stiffness for 1 hour = cardinal symptom for inflammatory arthritis

Non-inflammatory - get stiffness with activity and usage

49
Q

Pathogenesis of RA - genetic

A

Genetic:

  • certain HLA-D alleles lead to production of MHC class II that are presented on surface of antigen-presenting cells, recognized by immune cells
  • T-cell and B-cell activation
  • HLA-DRB1, has a common 5 aa sequence
  • shared epitope theory
  • citrullination
50
Q

RA pathogenesis pathway

A

Genetics factors –> CD4+ T-cell
Macrophages produce cytokines such as TNFa, IL1, many others

Results in:
Endothelial cells upregulate adhesion molecule expression
Osteoclasts lead to bone destruction –> joint erosion
Chondrocytes and synoviocytes –> cartilage destruction, joint-space narrowing

51
Q

Shared epitope theory

A

specific aa sequence associated with RA
Shared epitope alters conformation of antigen-DR complex that is presented to the T-cell
shared epitope “welcomes” an unknown antigen

52
Q

Citrullination - RA pathogenesis

A

Modification of Arg –> Citrulline
RA linked to ACPA’s = anti-citrullinated protein antibodies
ACPAs found inside affected joints
Patients with shared epitope or ACPAs associated with more severe joint damage and disease progression

53
Q

Pathogenesis of RA - environmental

A

Female > male
Pregnancy relieves RA, flare about 6 months after delivery
Smoking - greatest known environmental risk factor
Microbiome - important role in autoimmunity, some possible infectious causes

54
Q

RA pathogenesis

A

1) genetic and environmental factors
2) T cells and inflammation
3) Angiogenesis
4) Persistent synovitis
5) cartilage destruction and bone erosion

55
Q

T cells and inflammation - RA

A

1) APCs present arthritis-associated T-cell antigens
2) Require costimulation –> potential to block costimulation and relieve RA
- Activation of T cells is most likely initiating process of rheumatoid process

3) Activation and proliferation of synovial lining
4) Recruitment of more proinflammatory cells
5) Secretion of cytokines and macrophages
6) Autoantibody production
7) B-cell role: produce antibodies, autoantibodies, cytokines

56
Q

Angiogenesis - RA

A

Early pathogenesis of RA - generation of new synovial blood vessels
Transduation of fluid, migration of lymphocytes into synovium and PMNs into synovial fluid
Eventually get mass of tissue that can’t be adequately supplied by vasculature, get ischemia

57
Q

Persistent synovitis - RA

A

Cellular expansion and cytokine production
Synovium matures - accumulation of lymphocytes, highly vascularized, becomes pannus, erodes cartilage and bone
Loss of relative balance of proinflammatory and anti-inflammatory cytokines

58
Q

TNF - RA

A

Principal cytokine in generating proliferative synovitis
Can result in bone resorption
Anti-TNF therapy important

59
Q

IL17 - RA

A

Increases bone resorption
increase COX2 and PGE2 by synovial cells and monocytes
not target for drug therapy yet

60
Q

IL6 - RA

A

drives local leukocyte activation and autoantibody production
contributes to systemic effect of RA
we have a drug to block IL6

61
Q

Intracellular kinase - RA

A

e.g. JAK

inhibitors of JAKs- helpful in blocking function of several cytokines

62
Q

Cartilage destruction and bone erosion - RA

A

synovial lining cells invade CT of cartilage and tendon, stimulate differentiation and activation of osteoclasts
Results in bone erosion
Direct invasion of synovial cells into cartilage –> release of proteases that degrade matrix (collagenases, MMP)
Subchondral bone destruction - without repair (TNF, RANKL)

63
Q

Rheumatoid factor

A

IgM antibody against Fc region of IgG antibodies
Results in circulating immune complexes
80-85% seropositive for RA (often not positive until 1-2 years into disease)
60% seropositive for CCP - highly specific

64
Q

ANA

A

Autoantibodies that bind to contents of cell nucleus
Very sensitive in SLE
Very few false negatives, but many false positives

65
Q

ENA

A

extractable nuclear antigen - Sm (SLE)
Ribonucleoprotein (SLE, MCTD)
Ro (SSA) - SLE, Sjogren’s
La (SSB) - SLE, Sjogren’s

66
Q

Anti-DNA Ab

A 
Positive in ~50% of SLE
highly specific
order when ANA positive and meaningful
can be a marker for glomerulonephritis
C3 and C4 can go down with active disease, anti-DNA up
67
Q

Radiological features of RA

A 
Joint erosions
Cysts
Progressive narrowing of joint spaces
Lack of osteophytes and subchondral sclerosis
Juxta-articular osteopenia
COncentric joint space loss
68
Q

Extra-articular features of RA

A 
More common in seropositive patients
Eyes: scleritis, keratoconjunctivitis (Sjogren's)
Pleural effusions, pleuritis
Xerostomia (Sjogren's)
Pulmonary fibrosis, nodules
Reactive lymphadenopathies
Pericardial effusions
Splenomegaly
Amyloidosis in kidney / gut
Anemia, thrombocytosis
Muscle wasting
Skin ulceration and thinning
Peripheral neuropathy
69
Q

RA management strategy

A

treat aerly
rapidly escalating methotrexate dose
combine methotrexate + DMARDs
new biologics

70
Q

Mild RA

A 
3 simultaneously affected joints
arthalgias
negative RF
negative anti-CCP
No erosions/cartilage loss
71
Q

Moderate RA

A 
6-20 affected joints
No EAFs
Elevated ESR/CRP
positive RF and anti-CCP
Osteopenia, periarticular swelling
72
Q

moderate RA Tx

A

triple therapy

MTX, SS, HCQ

73
Q

Severe RA

A 
20+ inflamed joints
declining function
elevated ESR/CRP
Hypoalbuminemia
Anemia of chronic disease
positive RF, anti-CCP
74
Q

Severe RA Tx

A

Triple therapy initially
Life-threatening disease treated with corticosteroids
add biologics

75
Q

Pharmacologic therapy for RA

A

Analgesis
NSAIDs
GCs
DMARDs

76
Q

RA analgesics

A

acetaminophen

opioids

77
Q

RA NSAIDs

A

fast-acting
no alteration in disease outcome
ineffective as sole therapy
no prevention

78
Q

RA GCs

A

fast-acting, powerful
no analgesia but reduced pain due to reduce inflammation
systemic RA effects reduced
used for treatment of life-threatening complications of RA
Use small doses, taper ASAP

oral - bridging therapy
iv - life-threatening
intra-articular - joint-specific

79
Q

DMARDs

A

preserve joint
reduce/prevent joint damage
maintain functional level

80
Q

small molecule DMARDs

A

Methotrexate
Hydroxychloroquine
Sulfasalazine

81
Q

Methotrexate

A

used in moderate-severe RA
Inhibits dihydrofolate reductase, inhibiting pyrimidine synthesis
inhibits proliferation of cells, particularly WBCs
onset: 4-12 weeks
SEs: pancytopenia, hepatitis, ILD

82
Q

Hydroxychloroquine

A

Inhibits T-cell mediated inflammation
Used in mild RA and elderly-onset RA
onset: 10-26 weeks
SEs: colour disturbances

83
Q

Biologic DMARDs

A

TNF-alpha inhibitors
IL-1 inhibitors
Rituximab (anti-CD20)
Abatacept

84
Q

TNF alpha inhibitors

A

Etanercept: recombinant soluble TNF receptor
Infliximab: Chimeric anti-TNF monoclonal antibody

Blocks TNF, which mediates inflammation; reduces neutrophil adherence and activation

85
Q

Psoriatic arthritis features

A 
Arthritis with psoriatic skin changes
- Onycholysis
Look for psoriasis behind the ears, on the scalp, on extensor aspect of elbows and knees, umbilicus, fingernails/toenails - esp scalp, gluteal crease, extensive psoriasis and nail changes
Assymetric, oligoarticular
Involves DIP
Sclerosis and periostitis rather than osteopenia
Sausage digits
Morning stiffnes
Erosions and sclerosis
Inflammatory synovial fluid
86
Q

Types of psoriatic arthritis

A

Asymmetric oligoarthritis - most common form, predilection for lower limbs
Asymmetric polyarthritis
DIP variant
Arthritis mutilans - least common form, most destructive
- get pencil in cup deformity
Spondyloarthropathy (psoriatic spondylitis)

87
Q

Psoriatic arthritis tx

A

NSAIDs, may add DMARDs

88
Q

Seronegative spondyloarthropathies

A

Inflammation in axial spine
Oligoarticular, symmetric, large joint involvement
Involves enthesis = where ligaments/tendons insert into bone

89
Q

Types of seronegative spondyloarthropathies

A

Ankylosing spondylitis
Reiter’s syndrome - reactive arthritis
Psoriatic spondyloarthropathy
Spondylitis of IBD

90
Q

Ankylosing spondylitis

A 
Syndesmophytes bridge vertebral bodies
Sacroilitis
Enthesopathy - heel spurs, ischium whiskering
Bamboo spine
Often associated with HLA B-27
No gender preference
91
Q

Ankylosing spondylitis Tx

A

Postural exercises

NSAIDs

92
Q

Reiter’s syndrome

A 
Triad:
- arthritis
- conjunctivitis
- urethritis (chlamydia)
can also be associated with dysentery - Salmonella, shigella, Yersinia, campylobacter

Molecular mimicry

93
Q

Gout risk factors

A

male, post-menopausal women
increased BMI
metabolic syndrome
rena linsufficiency
drugs: diuretics (HCT), low-dose ASA, cyclosporine
Diet - milk products, high fructose drinks, beer, organ meats

94
Q

Gout

A

most often affects the MTP joint of the first toe

Uric acid crystal deposition in joints

95
Q

Pseudogout

A

calcium hydroxyapatite crystal deposition in tendons
cause calcific tendonitis
results in chondrocalcinosis

96
Q

Acute gout tx

A

NSAIDs
Colchicine
both be careful with renal insufficiency
Prednisone

97
Q

Preventative tx of gout

A

Allopurinol
inhibits xanthine oxidase
do not use until 3 attacks, until acute attack on board

98
Q

Polymyalgia rheumatic

A

pain, stiffness, aching in hip and shoulder girdle
may be caused by temporal arteritis - 1/3 cases associated with temporal arteritis
Often have elevated ESR or CRP

99
Q

Temporal arteritis

A

Rheumatological emergency!!
Large vessel vasculitis
Inflammation of vasa vasorum of large vessels
Predominantly affects branches of external carotid
+/- swelling/tenderness of temporal arter
Jaw claudication
High ESR
Temporary artery biopsy to cover vasculitis
often requires high-dose steroids

100
Q

Fibromyalgia syndrome

A 
Non-articular rheumatism, soft tissue disorder
widespread pain
Increase in centralized pain response
Often comorbid with sleep disorders, mood/anxiety disorders
Diffuse MSK pain
no inflammation
Normal labs
11/18 painful FM tender points
101
Q

Fibromyalgia tx

A 
education, reassurance
regular aerobic exercise
CBT
psychotherapy
tricyclics for sleep
avoid opiates for pain
antidepressants
102
Q

RA diagnosis criteria

A

1) morning stiffness - 1 hour
2) arthritis in >=3 joints
3) arthritis of hand joints
4) symmetric arthritis
5) rheumatoid nodules
6) serum RF
7) radiologic changes

need >=4, 6 weeks

103
Q

RA diagnosis criteria

A

1) morning stiffness - 1 hour
2) arthritis in >=3 joints
3) arthritis of hand joints
4) symmetric arthritis
5) rheumatoid nodules
6) serum RF
7) radiologic changes

need >=4, 6 weeks

104
Q

Tocilizumab

A

anti IL6

105
Q

Tocilizumab

A

anti IL6

106
Q

DKK - RA

A

DKK inhibits Wnt

anti-TNF therapy normalizes circulating DKK level

107
Q

PGE2 - RA

A

stimulates periarticular bone resorption before erosion development

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