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Inflammatory arthritis Flashcards

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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
Crystal arthritis
Gout (uric acid crystals) Calcium pyrophosphate dihydrate arthropathy Calcium hydroxyapatite
26
PE features of seropositive inflammatory arthritis
Deformity, redness, heat, swelling Symmetry of joints Fullness around joint: bony - osteoarthritis Tenderness, pain, ROM
27
SLE etiology
``` Genetics 9:1 female to male induced by OCP C1q deficiency - 93% penetrance Potentially associated with sunburns ```
28
SLE presentation
``` 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 ```
29
Discoid lupus
``` FEAST, 25% SLE patients Follicular plugging Erythema Atrophy Scarring telangiectasia ```
30
SLE arthritis features
``` 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 ```
31
Neuropsychiatric consequences of SLE
``` Behaviour, personality changes Depression Psychosis Seizures Stroke ```
32
CV consequences of SLE
Atherosclerosis Endocarditis Pericarditis Myocarditis
33
Respiratory consequences of SLE
``` Interstitial lung disease Pneumonitis Pleural effusions Pulmonary hemorrhage Pulmonary HTN ```
34
Hematologic disorders of SLE
Hemolytic anemia Leukopenia Lymphopenia Thrombocytopenia
35
Lupus Nephritis
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
36
Class I lupus nephritis
Normal Normal on light microscopy Mesangial deposits on electron microscopy Renal failure is rare
37
Class II lupus nephritis
``` Mesangial Mesangial proliferative Responds to corticosteroids 20% of SLE cases Renal failure is rare ```
38
Class III lupus nephritis
Focal and segmental proliferative glomerulonephritis Usually responds to high dose corticosteroids 25% of SLE cases renal failure rare
39
Class IV lupus nephritis
diffuse proliferative glomerulonephritis 40% SLE cases Treat with corticosteroids and immunosuppressants Renal failure is a common sequence
40
Class V lupus nephritis
Membranous glomerulonephritis Extreme edema and protein loss 10% of SLE cases renal failure uncommon
41
Class VI lupus nephritis
glomerular sclerosis
42
SLE lab workup
``` CBC, creatinine, electrolytes, urinanalysis, albumin CK ANA, ENA anti-dsDNA, C3, C4 antiphospholipid antibodies ```
43
SLE treatment
``` Depends on clinical disease Sun avoidance NSAIDs prednisone Plaquenil Azathioprine Mycophenolate mofetil Cyclosporine Cyclophosphamide Rituximab ```
44
Undifferentiated CT disease
``` Positive serology (ANA) doesn't meet criteria for a specific CTD, but may progress to one ```
45
Drug-induced lupus
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
Neonatal lupus
due to maternal autoantibodies passively transferring to fetus main concern = congenital heart block (5% of cases, monitor with cardiac US)
47
Rheumatology ROS
``` 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
Stiffness to differentiate the type of arthritis
Morning stiffness for 1 hour = cardinal symptom for inflammatory arthritis Non-inflammatory - get stiffness with activity and usage
49
Pathogenesis of RA - genetic
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
RA pathogenesis pathway
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
Shared epitope theory
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
Citrullination - RA pathogenesis
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
Pathogenesis of RA - environmental
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
RA pathogenesis
1) genetic and environmental factors 2) T cells and inflammation 3) Angiogenesis 4) Persistent synovitis 5) cartilage destruction and bone erosion
55
T cells and inflammation - RA
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
Angiogenesis - RA
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
Persistent synovitis - RA
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
TNF - RA
Principal cytokine in generating proliferative synovitis Can result in bone resorption Anti-TNF therapy important
59
IL17 - RA
Increases bone resorption increase COX2 and PGE2 by synovial cells and monocytes not target for drug therapy yet
60
IL6 - RA
drives local leukocyte activation and autoantibody production contributes to systemic effect of RA we have a drug to block IL6
61
Intracellular kinase - RA
e.g. JAK | inhibitors of JAKs- helpful in blocking function of several cytokines
62
Cartilage destruction and bone erosion - RA
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
Rheumatoid factor
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
ANA
Autoantibodies that bind to contents of cell nucleus Very sensitive in SLE Very few false negatives, but many false positives
65
ENA
extractable nuclear antigen - Sm (SLE) Ribonucleoprotein (SLE, MCTD) Ro (SSA) - SLE, Sjogren's La (SSB) - SLE, Sjogren's
66
Anti-DNA Ab
``` 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
Radiological features of RA
``` Joint erosions Cysts Progressive narrowing of joint spaces Lack of osteophytes and subchondral sclerosis Juxta-articular osteopenia COncentric joint space loss ```
68
Extra-articular features of RA
``` 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
RA management strategy
treat aerly rapidly escalating methotrexate dose combine methotrexate + DMARDs new biologics
70
Mild RA
``` 3 simultaneously affected joints arthalgias negative RF negative anti-CCP No erosions/cartilage loss ```
71
Moderate RA
``` 6-20 affected joints No EAFs Elevated ESR/CRP positive RF and anti-CCP Osteopenia, periarticular swelling ```
72
moderate RA Tx
triple therapy | MTX, SS, HCQ
73
Severe RA
``` 20+ inflamed joints declining function elevated ESR/CRP Hypoalbuminemia Anemia of chronic disease positive RF, anti-CCP ```
74
Severe RA Tx
Triple therapy initially Life-threatening disease treated with corticosteroids add biologics
75
Pharmacologic therapy for RA
Analgesis NSAIDs GCs DMARDs
76
RA analgesics
acetaminophen | opioids
77
RA NSAIDs
fast-acting no alteration in disease outcome ineffective as sole therapy no prevention
78
RA GCs
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
DMARDs
preserve joint reduce/prevent joint damage maintain functional level
80
small molecule DMARDs
Methotrexate Hydroxychloroquine Sulfasalazine
81
Methotrexate
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
Hydroxychloroquine
Inhibits T-cell mediated inflammation Used in mild RA and elderly-onset RA onset: 10-26 weeks SEs: colour disturbances
83
Biologic DMARDs
TNF-alpha inhibitors IL-1 inhibitors Rituximab (anti-CD20) Abatacept
84
TNF alpha inhibitors
Etanercept: recombinant soluble TNF receptor Infliximab: Chimeric anti-TNF monoclonal antibody Blocks TNF, which mediates inflammation; reduces neutrophil adherence and activation
85
Psoriatic arthritis features
``` 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
Types of psoriatic arthritis
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
Psoriatic arthritis tx
NSAIDs, may add DMARDs
88
Seronegative spondyloarthropathies
Inflammation in axial spine Oligoarticular, symmetric, large joint involvement Involves enthesis = where ligaments/tendons insert into bone
89
Types of seronegative spondyloarthropathies
Ankylosing spondylitis Reiter's syndrome - reactive arthritis Psoriatic spondyloarthropathy Spondylitis of IBD
90
Ankylosing spondylitis
``` Syndesmophytes bridge vertebral bodies Sacroilitis Enthesopathy - heel spurs, ischium whiskering Bamboo spine Often associated with HLA B-27 No gender preference ```
91
Ankylosing spondylitis Tx
Postural exercises | NSAIDs
92
Reiter's syndrome
``` Triad: - arthritis - conjunctivitis - urethritis (chlamydia) can also be associated with dysentery - Salmonella, shigella, Yersinia, campylobacter ``` Molecular mimicry
93
Gout risk factors
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
Gout
most often affects the MTP joint of the first toe | Uric acid crystal deposition in joints
95
Pseudogout
calcium hydroxyapatite crystal deposition in tendons cause calcific tendonitis results in chondrocalcinosis
96
Acute gout tx
NSAIDs Colchicine both be careful with renal insufficiency Prednisone
97
Preventative tx of gout
Allopurinol inhibits xanthine oxidase do not use until 3 attacks, until acute attack on board
98
Polymyalgia rheumatic
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
Temporal arteritis
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
Fibromyalgia syndrome
``` 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
Fibromyalgia tx
``` education, reassurance regular aerobic exercise CBT psychotherapy tricyclics for sleep avoid opiates for pain antidepressants ```
102
RA diagnosis criteria
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
RA diagnosis criteria
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
Tocilizumab
anti IL6
105
Tocilizumab
anti IL6
106
DKK - RA
DKK inhibits Wnt | anti-TNF therapy normalizes circulating DKK level
107
PGE2 - RA
stimulates periarticular bone resorption before erosion development

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