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Unit 3 B&L > BL 02-18-14 8-9AM RHEUM COURSE OVERVIEW-Janson_Hirsh > Flashcards

BL 02-18-14 8-9AM RHEUM COURSE OVERVIEW-Janson_Hirsh Flashcards

1
Q

Arthritis

A

= inflammation in joints
= pain, swelling, redness, or heat
- Over time, inflammation can lead to deformity

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2
Q

Arthralgia

A

= joint hurts but no evidence of inflammation

= may represent early forms of arthritis not yet detectable by exam or may be due to a viral syndrome or other causes

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3
Q

Periarticular pain

A

= When pain actually NOT due to pain in a joint
= Instead, pain arises from structures around the joint such as tendons or bursae

Distinguished from true arthritis by:

  • lack of effusion
  • often point tenderness over immediate area of inflammation
  • pain worse w/ active compared to passive motion
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4
Q

Soft Tissue pain

A

= Pain which may be perceived as arising from the joint, but which actually arises elsewhere (in muscle, adjacent nerves, or referred)

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5
Q

ARTHRITIS - joint swelling, signs of inflammation, & ROM

A

Joint swelling can be esp. helpful in determining if pt has arthritis:

  • Joint = potential space
  • S, swelling can present as a joint effusion (important objective finding)
  • Cool swelling in non-inflammatory disease (OA)
  • Joints are usually not red, unless infected or involving crystals
  • B/c problem is in joint itself, both passive & active motion causes pain
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6
Q

Monoarticular Arthritis

A

= involvies only one joint

a. Infections, crystal-induced arthritis, or trauma.
b. –> aspirate to rule out infection
c. Untreated septic joint can destroy joint in 6 days

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7
Q

Oligoarticular Arthritis

A

= in several joints (2-4)

a. Axial arthropathies (ankylosing spondylitis, psoriatic arthritis, or reactive arthritis)
b. Often asymmetrical
c. Often involves large joints (but not invariably)

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8
Q

Polyarticular Arthritis

A

= Involves multiple joints, often symmetrically

a. Usually affects both small & large joints
b. RA, SLE, certain viral syndromes

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9
Q

Types of Joints:

A

A. Synarthrosis = interlocked bones (skull)
B. Amphiarthrosis = bones joined by fibrocartilage (rib cage w/costal cartilage)
C. Diarthrosis = synovial joint

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10
Q

Types of Diarthosis joints (based on movement / axes)

A

(1) Uniaxial or hinge joints (one plane of movement)
- – EX: elbow, knee
(2) Polyaxial joints (multiple axes of movement)
- – EX: ball & socket joint of shoulder

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11
Q

Ligaments

A

= bundles of parallel Type I collagen connecting bone to bone
—> prevent inappropriate motion (passive restraints)

*Hinge joints are commonly bordered by collateral ligaments to limit flexion & extension of the joint

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12
Q

Tendons

A

= resemble ligaments but connect muscle to bone

–> active drivers of joint motion (while ligaments are passive restraints)

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13
Q

Entheses

A

= where ligaments & tendons insert into bone
- Metabolically active (different from tendon or bone)

Important in seronegative spondyloarthropathies

  • – can inflame, erode, & eventually calcify
  • –> “enthesopathic type” arthritis
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14
Q

Bursae

A

= synovial lined sacs w/ dense regular CT support

a. Designed to slide & cushion tissues that are less forgiving during movement
b. Contains lubricating film of synovial fluid
c. Btwn tendon & bone, ligament, or tendon

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15
Q

Diarthrosis

A 
= aka synovial joint
The bone...
- articulartes
- is cushioned by hyaline cartilage
- is stabilized by ligaments
- is actively moved by muscles & tendons
- is nourished & lubricated by synovial tissues
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16
Q

Ankylosis

A

Disease process causes fibrous or bony union across joint leading to fixation of joint

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17
Q

Axial Arthropathy

A

Arthritis involving the spine.

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18
Q

Sacroiliitis

A

Inflammation of sacroiliac joint

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19
Q

Syndesmophyte

A

Calcification of ligament/tendon at site of bony insertion

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20
Q

Synchondrosis

A 
= Union btwn 2 bones formed by cartilage
Examples:  
- Pubic symphysis
- Manubriosternal joints
- Costosternal joints
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21
Q

Internal Structure of a Diarthrodial Joint

A
  • Bone’s articular surface covered by hyaline cartilage
  • Synovium
  • Subchondral bone
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22
Q

Hyaline cartilage - overview

A
  • covers articular structures of bone in diarthrodial joints
  • firm & resilient & dynamic
  • turgid gel (water + collagen + proteoglycans)
  • Contains no vessels or nerves
  • Gets nutrients from synovium via synovial fluid
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23
Q

Composition of Hyaline cartilage

A

Water (major component of cartilage)

Collagen (esp. Type II), an extremely strong protein

Proteoglycans (esp. chondroitin sulfate & keratin sulfate)

  • – hooked by link proteins to hyaluronic acid
  • – high density of fixed negative charge —> coiled spring —> gives cartilage its elastic properties
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24
Q

Embedded in the hyaline cartilage are…

A

Chondrocytes
–> produce both collagen & proteoglycans

Enzymes —> can digest these structures

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25
Q

Synovium

A

= thin layer of cells + capsule that covers all intra-articular surfaces other than articular areas of cartilage

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26
Q

Spondylitis

A

Inflammation of one or more vertebrae of the spine

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27
Q

Synovium - 2 cell types

A

Synovial cells are divided morphologically into 2 types:

  • Type A cells = macrophage-like (w/HLA-DR) & derived from bone marrow
  • Type B cells = fibroblast-like
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28
Q

Osteophyte

A

A bony outgrowth of bone

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29
Q

Pannus (and RA)

A
  • When synovium becomes diffusely inflamed & thickened, as in RA
  • Early erosions in RA occur where synovium inserts into bone b/c pannus slowly destroys bone
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30
Q

Subchondral bone (and arthritis: osteo- vs inflammatory)

A

= Area under cartilage

In OA, commonly dense or sclerotic

In inflammatory arthritis, inflammation/increased blood flow to this area
—> periarticular bone becomes less dense (osteopenic)

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31
Q

Synovium composition

A

Well-ordered matrix of microfibrils & proteoglycan aggregates with synovial cells

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32
Q

Arthritis: Diseases which characteristically present as Polyarticular Diseases

A
  • rheumatoid arthritis
  • systemic lupus erythematosus (SLE)
  • Psoriatic arthritis
  • reactive arthritis
  • hepatitis B
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33
Q

Synovitis

A

= Inflammation of synovium

—> can lead to pannus

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34
Q

Symmetric Joint Distribution - Diseases

A
  • rheumatoid arthritis

- systemic lupus erythematosus

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35
Q

Asymmetric Joint Distribution - Diseases

A
  • osteoarthritis
  • gout
  • spondyloarthropathies
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36
Q

Arthritis: Diseases which characteristically present as Monoarticular Diseases

A
  • septic arthritis
  • gout
  • pseudogout
  • traumatic arthritis
  • mechanical derangement of joint
  • osteochondritis dissecans
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37
Q

Small Joint Distribution - Diseases

A
  • rheumatoid arthritis

- systemic lupus erythematosus

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38
Q

Joints involved in Osteoarthritis

A
  • Distal interphalangeal joints (DIP)
  • Proximal interphalangeal joints (PIP)
  • 1st carpometacarpal joint (CMC)
  • Cervical & Lumbosacral spine
  • Hips
  • Knees
  • 1st metatarsophalangeal joint (MTP)
39
Q

Migratory Joint Distribution - Diseases

A
  • rheumatic fever

- disseminated gonococcemia

40
Q

Arthritis: Polyarticular Diseases which characteristically present as Monoarticular Diseases

A
  • Juvenile rheumatoid arthritis
  • Reactive arthritis
  • Sarcoid arthritis
  • Psoriatic arthritis
  • Pseudogout
41
Q

Large Joint Distribution - Diseases

A

axial arthropathies

42
Q

Additive Joint Distribution - Diseases

A
  • rheumatoid arthritis

- axial arthropathies

43
Q

Arthritis - Rapidity of Onset

A
  • Hours - septic joints & crystal diseases (gout & pseudogout)
  • Days - most chronic inflammatory diseases
44
Q

Response to rest and activity in Arthritis

A

Worse with rest or in the morning:

  • rheumatoid arthritis
  • axial arthropathies.

Worse with use:
- osteoarthritis

45
Q

Arthritis: Presentation at a young age

A
  • Rheumatoid arthritis
  • Axial arthropathies
  • SLE
46
Q

Family Hx & Rheumatoid Arthritis

A

HLAS-DR4

47
Q

Family Hx & Axial Arthropathies

A

HLA-B27

48
Q

Family Hx & Systemic Lupus Erythematosus

A

HLA-DR2
HLA-DR3
C4A null allele

49
Q

Degenerative Joint Disease (Osteoarthritis, OA)

A

= cartilage-based process (primary abnormality)
- Mostly affects big weight bearing joints, mostly

Articular cartilage loses its homogeneous nature

  • –> disrupted / fragmented with pitting, clefts, & ulcerations
  • -> uneven histochemical stain for proteoglycans in cartilage
  • -> w/ advanced disease, no cartilage remains & bare areas seen of exposed underlying bone
50
Q

Biochemical changes in Osteoarthritis

A
  • ↑ Water content of articular cartilage
  • Smaller than normal small Type II collagen fibers
  • Normally tight weave of collagen in mid-zone is slackened & distorted
  • Sharply diminished [Proteoglycan] - 50% or less
  • Less & less aggrecans present
  • Shorter & shorter glycosaminoglycan chains
  • Increased Type I collagen in cartilage covering osteophytes
51
Q

Metabolic changes in Osteoarthritis

A

Great increase of synthesis & secretion of matrix-degrading enzymes by the chondrocyte
= mainly acid & neutral proteases, esp. neutral metalloproteinases
—> Able to degrade all components of ECM

52
Q

Arthritis: Presentation in elderly

A
  • gout
  • polymyalgia rheumatica
  • pseudogout
53
Q

Etiologic factors in Osteoarthritis

A
  • greatly increases w/age

May be caused by

  • significant trauma in which joint is excessively incongruent (ex: hip disolcation)
  • unstable joint
  • impulsive loading over a lifetime
  • inflammatory arthritis (its end stage)
  • obesity
  • hereditary forms
54
Q

Clinically in OA…

A

NO systemic symptoms like morning stiffness, easy gelling (stiff w/sitting), unusual evening fatigue

Asymmetric joint involvement & cartilage loss

  • ex: hip loses cartilage more superiorly than medially
  • ex: knee more medially than laterally
  • Mild inflammation may occur, but secondary to loss of cartilage & typically later in disease course
55
Q

Non-inflammatory diseases causing secondary OA

A
  • Avascular necrosis

- Fibromyalgia

56
Q

Arthritis: Presentation in Males

A
  • gout
  • axial arthropathies
  • hemochromatosis
57
Q

Arthritis: Presentation in Females

A
  • rheumatoid arthritis
  • scleroderma
  • systemic lupus erythematosus
58
Q

Metalloproteinases

A
  1. Collagenase
  2. Stromelysin
  3. Gelatinase
59
Q

Theories for why Inflammation occurs in Joints in RA

A
  1. Abundant blood supply & rich capillary network
    - – Immune complexes might concentrate in synovium based on physical properties of vessels
  2. Joint has no epithelial tissue (different than other body spaces)
  3. Synovial lining is discontinuous w/occasional gaps & lacks formal basement membrane
  4. Joint contains some unique cell types such as synoviocytes & chondrocytes that could be targeted as privileged antigens
60
Q

Gross pathology of synovium in RA

A
  • Proliferation in pattern of villus fronds (proliferate like fern branches from common stalk to maintain contact w/synovial fluid)
  • Rheumatoid knee may have synovium that weighs 10x a normal synovium
61
Q

Synovium in RA

A
  • absolute ↑ in both Type A & Type B synovial cells
  • diverse lymphocytes (B & T), NK cells, & mast cells —> cytokines, serine proteases, histamine, rheumatoid factors
  • PGs, metalloproteases, oxygen radicals (superoxide), activated complement in synovial fluid
  • pannus —> invades & destroys adjacent cartilages / bone
62
Q

Inflammatory joint diseases - symptoms / distribution

A

Systemic symptoms such as

  • morning stiffness > 1 hr
  • easy gelling
  • unusual fatigue in afternoon & evening

Joint involvement can be

  • symmetric (RA)
  • asymmetric (axial arthropathies, septic joints)

Cartilage lost in symmetric pattern

Typically has one or more signs of inflammation

63
Q

Metabolic joint disease - Types

A
  • gout (monosodium urate disease)
  • pseudogout (calcium pyrophosphate dihydrate disease)
  • hydroxyapatite deposition disease (basic calcium phosphate deposition disease)
64
Q

Metabolic joint disease - process

A
  • Metabolic process causes crystals to form & deposit in joints
  • –> intermittent signs of inflammation
  • –> systemic symptoms
  • –> bone erosions w/out cartilage loss
65
Q

Gout

A
  • occurs after prolonged period of supersaturation of monosodium urate in serum & synovial fluid
  • Complex mechanism whereby crystals ppt in joints & induce inflammation
  • Episodic & very painful arthritis w/ swelling, redness, warmth
  • Often in lower extremities
  • May form tophi (crystalline deposits of uric acid in cartilage, joints, skin)
66
Q

Regulation of urate crystal formation in Gout

A

i. lower intraarticular temp
ii. presence of proteoglycans
iii. changes in pH
iv. reduced binding of urate to plasma protein
v. trauma
vi. aging
vii. connective tissue turnover

67
Q

Acute inflammatory response to crystals in Gout

A
  • Not fully understood
  • High level of uric acid, supersaturation & inflammatory response to crystals
  • Neutrophils appear necessary to invoke response
68
Q

Synovium in acute gout

A
  • can have clumps of crystals (tophus-like deposits) in synovium, neutrophil infiltration & some lymphocytes
  • In chronic disease, large number of lymphocytes & plasma cells are seen
69
Q

Inflammatory Joint Diseases

A

Rheumatoid Arthritis
Axial Arthropathies
Septic Joints

70
Q

Site of Inflammation in Inflammatory Joint Diseases

A

Inflammation primarily in synovium —> secondary destruction of cartilage & bone

71
Q

Rheumatoid arthritis (RA)

A

= classic example of an inflammatory arthritis

  • Can involve variety of major organ systems, but primarily a disease of the joints
  • Primarily small joints
72
Q

Acute-phase response (APR)

A
  • a large number of systemic & metabolic changes that occur with inflammation
  • may represent early defensive mechanisms or adaptations to stress of inflammatory stimulus
  • participants in innate immune response
  • can measure via ESR or CRP

Cytokines stimulate liver to produce acute phase proteins (w/ consequence of decreased albumin production)

73
Q

Spondyloarthropathies - types

A

Ankylosing spondylitis
Reactive arthritis
Psoriatic arthritis
Inflammatory bowel disease arthropathy

74
Q

C-Reactive Protein (CRP)

A

= pentameric protein that behaves as primitive Ig

  • -> can activate classic complement pathway & bind to Fcγ receptor
  • Rapidly rises 2-3 days after acute inflammatory stimulus
75
Q

Antinuclear Antibodies (ANA)

A
  • AutoAbs against cell nuclear antigens (commonly against DNA & small nuclear ribonucleoproteins - snRNPs)
  • Associated w/ SLE & others like it
76
Q

Fluorescent antinuclear antibody tests

A
  • to measure for antinuclear antibodies
  • also pick up cytoplasmic antigens
  • NONSPECIFIC - just tells pt is making autoAbs to nuclear components
77
Q

ANA profile (specific autoantigen tests)

A

Measures more specific cellular Abs

  • Originally used immunodiffusion assay
  • Includes Smith (Sm), nuclear ribonucleoprotein (snRNP), Ro/Sjogrens Syndrome Antigen (SS-A), La/SS-B, & anti-double stranded DNA (anti-ds-DNA)

More useful b/c can find specific antigens more characteristic of some diseases
EX: anti-Sm & anti-ds-DNA are relatively specific for SLE

78
Q

Organ specific autoimmunity

A
  • Immune response directed against single autoantigen or restricted group of autoantigens
  • –> destruction of specific organ or cell type
  • EX: Thrombocytopenia <— autoAbs to platelets
  • EXs: Myasthenia gravis, Type I diabetes, Pernicious anemia, Addison’s disease, & Autoimmune thyroid disease
79
Q

Spondyloarthropathies - manifestations

A

Spinal arthritis & enthesitis

Inflammatory low back pain

  • insidious onset (months)
  • prolonged morning stiffness
  • pain improves w/ exercise
  • no neurologic sequelae
80
Q

Organ damage in SLE

A

Organ damage can come about by both:
- Organ specific (type II)-mediated immunologic damage (direct Ab binding to specific cells /tissues)
OR
- Systemic autoimmunity (type III) - mediated immunologic damage (immune complexes)

81
Q

Systemic lupus erythematosus (SLE)

A

= classic autoimmune disease affecting multiple organ systems

82
Q

Categories of Vasculitis

A
  • Large vessel vasculitis affecting aorta (giant cell (or temporal) arteritis & Takayasu’s arteritis)
  • Medium vessel vasculitis (polyarteritis nodosa & Kawasaki’s disease)
  • Small vessel vasculitis (granulomatosis w/ polyangiitis (GPA; formerly known as Wegener’s) & in leukocytoclastic vasculitis)
83
Q

Erythrocyte Sedimentation Rate (ESR)

A

= most widely used measure of an APR (acute phase rxn)
Process:
- Anticoagulated blood in vertical tube –> measure rate of fall of RBCs (usually over 1 hr)
- increased acute phase proteins —> increased aggregation of RBCs (rouleaux) —> fall more rapidly

84
Q

“Pauci-immune” mechanism for vasculitis

A

<–Abs to cytoplasmic Ags found in neutrophils (antineutrophil cytoplasmic antibodies (ANCA))
- ANCAs may be directly involved in pathogenesis of pauci-immune types of vasculitis

Defined by immunofluorescent staining of ANCAs

  • Cytoplasmic staining (C-ANCA) binds to proteinase 3 (PR3) & is commonly seen in GPA
  • Perinuclear staining (P-ANCA) binds to myeloperoxidase (MPO) & is seen in microscopic polyangiitis and other diseases
85
Q

Systemic autoimmunity

A
  • Immune response against multiple autoantigens or antigens seen in most cells & not to a specific organ or cell type
  • –> affects multiple organs due to circulating immune complexes or direct immune attack
  • Seen classically in SLE
86
Q

Inheritance of MHC genes

A

Inherited co-dominantly:

  • Receive 1 allele at each locus from each parent
  • Located on short arm of chromosome 6
87
Q

Vasculitis

A
  • Heterogenous group of diseases usually categorized by size of vessels involved
88
Q

2 most common immune mechanisms to explain cause of vasculitis

A
  1. Immune complexes

2. “Pauci-immune” mechanism associated w/ antineutrophil cytoplasmic antibodies (ANCA)

89
Q

Class II region of MHC locus

A

Has HLA-DR, DP, & DQ gene loci
= only expressed in B-cells, DCs, macrophages, and thymic epithelium
= primarily involved in presentation of “exogenous” extracellular antigens (bacterial, fungi, other)

90
Q

Major Histocompatibility Complex (MHC) (Human Leukocyte Antigen [HLA] System)

A

= thought to be important hereditary component to predisposition of an autoimmune disease
= set of closely-linked genes whose products regulate recognition of foreign antigens by T cells

91
Q

Contents of MHC locus

A

Contains 3 major immunologically-important regions

  • Class I region (~universal, endogenous Ags)
  • Class II region (restricted to APC, exogenous Ags)
  • Class III region (complement, TNF, etc.)

Many autoimmune diseases are associated w/a particular MHC Class I or II allele

92
Q

Class I region of MHC locus

A

Has HLA A, B, C, & other gene loci
= expressed on all nucleated cells
= thought to be involved in presentation of “endogenous” cytoplasmic antigens (viral, tumor, etc)

93
Q

Class III region of MHC locus

A

Has gene locus for…

  • various components of complement (C4a, C4b, C2, Bf)
  • tumor necrosis factor
  • other proteins

Unit 3 B&L (18 decks)

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