Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/142

Click to flip

142 Cards in this Set

  • Front
  • Back
Two main types of joints
Solid (non-synovial: synarthroses); cavitated (synovial)
Two types of synarthroses
Fibrous synarthroses: cranial sutures, teeth/jaw; Cartilaginous Synarthroses: symphyses (manubriosternalis and pubic)
Synovial Fluid made up of:
clear, viscous, plasma filtrate containing hyaluronic acid (for lubrication and nutrition)
Hyaline Cartilage made up of:
Type II collagen, water, proteoglycans, chondrocytes
Function of water and proteoglycans in hyaline cartilage
turgor and elasticity, important in limiting friction
Chondrocyte function in hyaline cartilage
synthesize and enzymatically digest matrix
which cytokines trigger hyaline cartilage degradation?
IL-1 and TNF
Osteoarthritis characterized by:
progressive erosion of articular cartilage, intrinsic disease of cartilage
How does primary osteoarthritis initially appear?
insidously, without apparent initiating cause, as aging process (idiopathic of primary osteoarthritis)
What can cause secondary osteoarthritis?
macrotrauma, repeated microtrauma (also obesity), congenity deformity in joint, underlying system disease (diabetes, ochronosis, Wilson's disease, hemochromatosis)
Functions of normal articular cartilage (2)
friction-less motion, spreads load across joint surface in weight-bearing joints
Function of collagen II and proteoglycans in cartilage
provide elasticity and high tensile strength
evidence for role of aging and mechanical wear in osteoarthritis
increasing occurrence with age, occurrence in weight-bearing joints, increase in freq of dz in joints exposed to abnormal stresses (obesity, previous joint deformity)
Three major influences in osteoarthritis development
aging, mechanical stress, genetic factors
Cartilage changes in OA
increased water, decreased proteoglycans, weakening of collagen network (decreased collagen II production, increased breakdown), levels of IL1, TNF, NO increased, apoptosis increased
Typical age of onset of primary OA
50's and up
Characteristic symptoms of OA
deep achy pain worsening with use, morning stiffness, crepitus, limited range of movement, one or few joints involved
What are osteophytes?
bony outgrowths
Role of osteophytes in OA:
impinge on spinal foramina, cervical/lumbar nerve root compression
Which joints are involved in OA?
hips, knees, lower lumbar/cervical vertebrae, proximal/distal IP joints, first carpometacarpal and first tarsometatarsal
Heberden nodes
characteristic of OA in women, nodes on fingers representing prominent osteophytes
define ankylosis
stiffening or fixation of a joint due to a disease process, with fibrous or bony union across joint
RA progression
1) infiltration of synovium by CD4+ and B cells, 2) increased vascularity, 3) fibrin aggregation, 4) neutrophil accumulation, 5) osteoclastic activity, 6) pannus formation, destroyed cartilage, ankylosis
Skin nodules in RA
arise in regions of skin that are subjected to pressure, less commonly in viscera, firm, nontender, round to oval, in SubQ
Define Pannus
mass of synovium and synovial stroma consisting of inflammatory cells, granulation tissue, and fibroblasts
Which cells are involved in RA?
CD4+ T cells and B cells
What function to CD4+ Tcells play in RA?
RANKL and stimulate other cells in joint to produce cytokines that are mediators of synovial reaction
in RA, cytokines lead to:
synovial cell production of mediators of inflammation and matrix metalloproteases
What does RANKL do?
activates osteoclasts and promotes bone destruction
Which cells express RANKL?
T-cells and synovial fibroblasts
Which gene is linked to RA susceptibility?
HLA-DR4 at Class II HLA locus
Initial symptoms of RA:
malaise, fatigue, generalized musculoskeletal pain
Pattern of Joint Involvement in RA:
small joints affected before larger ones (generally)
Which joints involved in RA (specifically)?
MCP, PIP, MTP, followed by wrists, ankles, elbows, knees
Describe RA joints (externally)
swollen, warm, painful, stiff on arising or after inactivity
radiographic hallmarks of RA
juxta-articular osteopenia and bone erosions with narrowing of joint space
RA hand deformities (4)
radial wrist deviation, ulnar finger deviation, swan neck fingers, boutonniere fingers
boutonniere deformity
MCP extension, PIP flexion, DIP extension
swan neck deformity
PIP hyperextension, DIP flexion
RA if 4 of 7 following criteria for 6+ months
1) morning stiffness, 2) arthritis in 3 or more joints, 3) arthritis of typical hand joints, 4) symmetric arthritis, 5) rheumatoid nodules, 6) serum rheumatoid factor, 7) typical radiographic changes
3 subclasses of Juvenile Rheumatoid Arthritis
oligarticular, polyarticular, systemic
How long is a juvenile arthritis present before JRA is diagnosed?
at least 6 weeks
Five ways JRA differs from RA in clinical presentation
in JRA, 1) oligoarthritis more common, 2) systemic onset more frequent, 3) large joints affected more often than small, 4) rheumatoid nodules and factor usually absent, 5) anti-ANA+ common
Presentation of systemic JRA
can be abrupt, migratory/transient skin rash, hepatosplenomegaly, serositis
Presentation of seronegative spondyloarthropathies
inflammatory peripheral/axial arthritis, tendon inflammation
list the seronegative spondyloarthropathies (4)
ankylosing spondylitis, reactive arthritis, psoriatic arthritis, arthritis associated w/ IBD
what is ankylosing spondyloarthritis?
chronic inflammatory joint disease of axial joints (esp. sacroiliac joints)
when does ankylosing spondyloarthritis become symptomatic?
2nd/3rd decades
ankylosing spondyloarthritis disease progression
tendinoligamentous insertion site inflammation, ossification, bony outgrowths, ankylosis, spinal immobility
Definition of reactive arthritis
episode of non-infectious arthritis of the appendicular skeleton that occurs within one month of primary infection localized elsewhere in the body
Reiter Syndrome
triad of arthritis, nongonococcal urethritis/cervicitis, conjuctivitis
time course of reactive arthritis symptoms
sx develop weeks after urethritis or diarrhea, joint stiffness and low back pain are early sx, wax and wane over weeks to months
Who gets Psoriatic arthritis?
10% of patients with psoriasis
pattern of joint involvement in psoriatic arthritis?
very diverse
4 types of infectious arthritis
suppurative, tuberculous, lyme, viral
most common organisms causing acute suppurative arthritis
gonoccocus, staph, strep, h. flu, GNR
classic presentation of suppurative arthritis
sudden development of acutely painful, hot, swollen joint, restricted range of motion, fever, leukocytosis, elevated ESR
What does tuberculous arthritis accompany?
complication of osteomyelitis or hematogenous dissemination from visceral site of infection
pattern of joint involvement in tuberculous arthritis
weight bearing joints
pathogenesis of lyme arthritis
borrelia burgdorferi seeds in joints within days/weeks of primary infection
pattern of joint involvement in lyme arthritis
big joints
which viruses can cause viral arthritis?
parvovirus b19, rubella, HepC
3 crystals that can cause gout
urate, calcium pyrophosphate dihydrate, calcium phosphate (hydroxyapatite)
Gout pathogenesis
hyperuricemia, transient attacks of acute arthritis, chronic gouty arthritis, creation of tophi
what are Tophi?
large aggregates of urate crystals and the surrounding inflammatory reaction
2 causes of primary gout
overproduction with normal excretion, normal production with under excretion
3 causes of secondary gout
leukemias (overproduction of uric acid), chronic renal disease (reduced excretion), inborn error of metabolism (HGPRT deficiency)
Lesch-Nyhan Syndrome cause
x-linked complete lack of hypoxanthine guanine phosphoribosyl transferase (HGPRT)
Lesch-Nyhan Syndrome presentation
severe mental retardation, self mutilation, gouty arthritis
effect of age on Gout
rarely appears before 20-30 years of hyperuricemia
predisposing factors to gout
increased age, genetic predisposition, heavy alcohol consumption, obesity, certain drugs, lead toxicity
why gout in joints?
synovial fluid is a poorer solvent for monosodium ureate than plasma, so it preferentially precipitates there
what if acute gout untreated?
resolves in hours to weeks, complete resolution leads to asymptomatic intercritical period, recurs, with each time, next recurrence sooner
which age group gets pseudogout (CPPD)
over 50, gets up to 30-60% in 85+
crystal in pseudogout
CPPD - calcium pyrophosphate deposition disease
SLE affects more men or women?
9:1 women, esp during childbearing years
essential failure in lupus?
failure of mechanisms that maintain self-tolerance
4 categories of lupus ANAs
anti-DNA, anti-histone, anti-RNA bound proteins, anti-nucleolar antigens
Clinical lupus diagnosis?
indirect immunofluorescence that detects generic ANAs
which antibodies are diagnostic of SLE (2)?
anti-dsDNA and anti-Sm
Why do lupus patients potentially get syphilis false positives?
make anti-phospholipd (phospholipid-beta2-glycoprotein complex), which cross reacts with cardiolipin, which is the target Ag in indirect treponemal testing
explain Lupus Anticoagulant
SLE ab that interferes w/ in vitro clotting tests, but the patients suffer from a hypercoagulable state
Monoarticular Rheumatologic Diseases (3)
Gout, Infection, Reactive
Polyarticular Rheum Diseases (2)
RA, SLE
MTP Joint Distribution
Gout
DIP Joint Distribution
Osteoarthritis, Psoriatic
Which two diseases present with PIP/MCP Joint Distribution
RA, SLE
Symmetrical Rheum Diseases (2)
RA, SLE
Asymmetrical Rheum Diseases (2)
Psoriatic, Reactive
RA peak onset for women
30's to 40's
RA peak onset for men
50's to 70's
Which gene predisposes to RA?
HLA-DR4
RA disease development
genetic predisposition + environmental trigger = preclinical autoimmunity = RA
What is the major cell type found in synovial effusions?
neutrophils
Which type of T-cells found in joint?
Th1, abundant
Role of B-Cells in RA
unknown, but depleting B-cells improves clinical dz activity
Major pro-inflammatory cytokines in synovium (3)
TNF-alpha, IL-1, IL-6
Common extra-articular manifestations in RA (8)
rheumatoid nodules, sjogren syndrome, interstitial lung disease, scleritis, pleuritis/pericarditis, vasculitis, felty syndrome
Define Sjogren syndrome
autoimmune disease of lacrimal glands and parotids, leading to dry eyes and dry mouth
Lab findings in RA
mild/moderate anemia, high ESR, elevated CRP, high neutrophils in synovial fluid
Autoantibodies for RA diagnosis
Rheumatoid factor, anti-CCP (cyclic citrullinated peptides)
What is Rheumatoid Factor?
Auto antibody against Fc of IgG; not sensitive of specific for RA
Which of the two RA auto-antibodies are specific to RA?
anti-CCP
Differential Dx for RA
viral infections (parvovirus B19, HepB), SLE, Spondyloarthropathies, OA
RA Treatment
NSAIDs, glucocorticoids, DMARDs, Biologicals
NSAIDs in RA
modest symptomatic relief, but don’t prevent joint destruction, NOT GOOD FOR MONOTHERAPY
Glucocorticoids in RA
low dose, improve sx, slow dz progression, use in conjunction w/ other drugs
DMARDs in RA
slow acting (weeks to months), slow dz progression
examples of DMARDs
methotrexate, leflunomide, sulfasalazine, hydroxychloroquine
examples of Biologicals
anti-TNF: adalimumab, infliximab, etanercept; IL1 antagonist: Anakinra
Ddx for OA
psoriatic arthritis, pseudogout, neuropathic (charcot) joint, trauma
in OA, chemical shift in cartilage
less keratan sulfate and more chondroitin 4-sulfate
OA on xray
non-uniform joint space narrowing, osteophytes, subchondrial bony sclerosis, occasional bone cysts
OA treatment
px education, exercise, mescle strengthening and joint protection, NSAIDs, steroid injections
Causes of hyperuricemia (6)
overproduction, increased purine biosynthesis, increased ATP breakdown, decreased renal clearance, intrinsic renal disease, competition for excretion by organic acids
Gout pathogenesis
phagocytosis of Ig coated crystals by synovial PMNs, induce cytokine release
How to diagnose gout
aspirate synovial fluid, look for needle like birefringent crystals
Gout Treatment
don’t treat asymptomatic hyperuricemia; use NSAIDs/corticosteroids for acute attack, low doce colchicine for chronic
Pseudogout Clinical features
acute, inflammatory, gout like secondary to CPPD crystals, older px, trauma common trigger, knee is main site, + birefringent crystals
CPPD?
calcium pyrophosphate dihydrate (causes pseudogout)
pseudogout treatment
NSAIDs, low dows colchicine
Birefringent crystals
positive if: blue when parallel, yellow when perpindicular
five shared features of spondylarthropathies
axial skeleton involvement, asymmetric peripheral joint arthritis, enthesitis, seronegativity, HLA-B27 association
Genetic predisposition for spondylarthropathies
HLA-B27
is ankylosing spondy peripheral or axial?
axial
What establishes ankylosing spondy radiographically?
bilateral, symmetrical sacroiliitis
major extrauricular manifestation of ankylosing spondy?
anterior uveitis (ocular pain, photophobia) --> claucoma and posterior synechiae; GI inflammation
what do patients w/ ankylosing spondy usually present with?
low back symptoms
describe low back symptoms of ankylo spondy (7)
stiffness, dull pain, persistent, worse in AM/inactivity, better w/ activity, awakens px in night, insiduous
what are syndesmophytes?
ossification of the outer portion of the vertebral disk
pathogenesis of ankylosing spondy
squared off vertebrae (erosion of corners), syndesmophytes, bamboo spine, ankylosis
where does peripheral arthritis in akylosing spondy occur?
hips/shoulders, small bones of hands/feet, enthesopathy
Diagnosis of ankylosing spondy
inflammatory low back pain and radiographic evidence of bilateral sacroiliitis
2 spinal complications of ankylosing spondy
fractures, C1-C2 subluxation
General treatment principles of ankylosing spondy
NSAIDs, Anti-TNF, avoid systemic steroids, quick tx of anterior uveitis, physical therapy
infections known to trigger Reactive Arthritis (5)
C. trachomatis, shigella, salmonella, yersinia, campylobacter
how long after infxn does reactive arthritis appear?
1-4 weeks
are cultures of joint synovium sterile?
YES, but leftover antigenic material may still be present
clinical features of Reactive Arthritis
asymmetric oligoarth, lower extremities, enthesopathy
extrarticular manifestations of Reactive Arthritis
urethritis, cervicitis, conjuntivitis, uveitis, oral ulcers, keratoderma blenorrhagica, circinate balanitis, nail changes
what is keratoderma blenorrhagic?
hyperkeratotic, psoriatic like skin lesion, usu on soles of feet
general principles of management of reactive arthritis
NSAIDs, abx don’t help