Joint Pathology Flashcards

1
Q

What type of collagen makes up articular cartilage? Which type of nerve innervates it?

A
  • type II collagen

- lacks nerve endings! (therefore pathology of just the articular cartilage will not be painful)

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2
Q

What is degenerative joint disease? What are the three main risk factors? Is it mainly systemic or localized?

A
  • osteoarthritis
  • progressive deterioration of articular cartilage due to wear and tear
  • risk factors: old age, obesity, trauma
  • not entirely systemic; usually affects hip, lumbar spine, knees, and the DIP and PIP joints of fingers
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3
Q

How do patients with degenerative joint disease typically present? What are some complications?

A
  • patients are usually 65+ and complain of joint stiffness in the morning that WORSENS and becomes painful during the day with use
  • (joint stiffness that improves with use indicates rheumatoid arthritis)
  • when the cartilage wears away and bone rubs against bone, we get eburnation (polishing) of the subchondral bone and osteophyte (bony outgrowth/swelling) formation
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4
Q

What is rheumatoid arthritis? What is the hallmark feature of this disease? Is it mainly systemic or localized?

A
  • a chronic, systemic autoimmune disease
  • hallmark: synovitis, resulting in pannus formation (inflamed granulation tissue)
  • although systemic, it mainly affects the wrists, elbows, ankles, knees, PIP and MCP joints of fingers (bilateral, symmetrical involvement)
  • the DIPs are usually spared
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5
Q

How do patients with rheumatoid arthritis typically present?

A
  • patients are usually between 40 and 60 and complain of symmetrical joint stiffness in the morning that IMPROVES with activity
  • (movement squeezes the inflammatory debris out of the joint, relieving some of the pressure and pain)
  • (joint stiffness that worsens as the day goes on indicates degenerative joint disease)
  • systemic symptoms also present (fever, malaise, etc.)
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6
Q

What are some symptoms and complications of rheumatoid arthritis?

A
  • ankylosis (fusion) of the affected joints, osteopenia, baker cyst, vasculitis, fever, malaise, weight loss (don’t forget it’s a systemic disease)
  • complications: anemia and secondary amyloidosis
  • the ankylosis is due to the contracting nature of the myofibrils present in the pannus/inflamed granulation tissue
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7
Q

What would you expect to find in the serum of a patient with rheumatoid arthritis? In the synovial fluid?

A
  • serum: IgM and IgA antibodies against the Fc portion of IgG (this is called rheumatoid factor) + anti-cyclic citrullinated peptide antibodies (anti-CCPs, ACPAs)
  • 50-80% of patients will have one or the other or both
  • (anti-CCPs are more specific than RF for RA)
  • synovial fluid: large amounts of neutrophils and proteins
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8
Q

What percentage of rheumatoid arthritis risk is associated with genetics? Which specific gene?

A
  • about 50% is due to genetics
  • HLA-DR4
  • (there is a shared epitope in patients with RA at HLA-DR beta 1 at residues 70-74, with a positively charged residue at 71)
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9
Q

What is seronegative spondyloarthropathy? Which gene is is associated with? What are the three major types?

A
  • diseases that affect the axial skeleton and sacroiliac joints (“spondylo”) and that lack rheumatoid factor (hence the seronegative)
  • associated with HLA-B27
  • an “auto-inflammatory” disease rather than an auto-immune one
  • ankylosing spondyloarthritis, Reitier syndrome (reactive arthritis), and psoriatic arthritis (also, colitic arthritis and acute anterior uveitis)
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10
Q

Which joints are usually involved in ankylosing spondyloarthritis? What happens to these joints over time? What can patients present with?

A
  • (a type of seronegative spondlyoarthropathy)
  • involves the sacroiliac joints and spine
  • the vertebrae fuse over time (ankylosis), giving rise to “bamboo spine”
  • patients may present with lower back pain, unilateral uveitis, enthesitis, and aortitis (aortitis can increase the risk of aneurysm; an aneurysm at this location increases the risk for aortic regurgitation)
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11
Q

What is Reiter syndrome? When is classically seen?

A
  • (a type of seronegative spondlyoarthropathy)
  • a combo of arthritis, urethritis, and conjunctivitis (“can’t see, can’t pee, can’t climb a tree”)
  • classically arises in young male adults after a GIT (Campylobacter jejuni, salmonella, shigella, etc.) or chlamydia (C. trachomatis) infection
  • AKA ‘reactive arthritis’
  • can be due to an inflammatory reaction in response to infection at a distant site (so the organism is actually in the joint)
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12
Q

What is psoriatic arthritis? What is the most severe form known as?

A
  • (a type of seronegative spondlyoarthropathy)
  • arthritis of axial and peripheral joints, especially the DIP joints (results in nail changes, very common) and feet
  • this is a complication of psoriasis (10% of cases)
  • most severe and progressive form is arthritis mutilans
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13
Q

What is the most common agent of infectious arthritis in infants? In children? adults?

A
  • infants and very young children: S. aureus, group B strep, H. influenzae
  • young adults: N. gonorrhoeae (most common), S. aureus
  • older adults: S. aureus
  • (the agent is usually bacterial; S.aureus is the most common cause; septic arthritis)
  • usually due to hematogenous or traumatic route
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14
Q

How do patients with infectious arthritis typically present?

A
  • with a warm, erythematous painful joint that is limited in motion (onset is sudden)
  • (usually involves a single joint - 90% of cases involve the knee)
  • systemic signs of infection may also be present (fever, increased WBC, increased ESR)
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15
Q

What is gout? What is it due to? Which joint is most commonly affected?

A
  • deposition of MSU (monosodium urate) crystals in tissues (especially in the joints)
  • due to hyperuricemia (elevated uric acid levels)
  • very commonly affects the podagra (the MTP joint of the big toe)
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16
Q

Where does uric acid come from? What usually happens to it? Using this information, what can cause hyperuricemia?

A
  • uric acid comes from the metabolism of purines (AMP + GMP) that are digested from eaten DNA and RNA
  • uric acid usually leaves the enterocyte, enters the blood, and is excreted by the kidneys
  • hyperuricemia can therefore be caused by excess uric acid production from the diet or from a failure of renal excretion of the uric acid
17
Q

Which is more common, primary or secondary gout? What causes both?

A
  • primary gout is more common; 90% are due to underexcretion of uric acid, 10% due to overproduction of uric acid
  • secondary gout can be due to leukemia and a myeloproliferative disorder (both of these result in increased cell turnover), Lesch-Nyhan syndrome (missing an enzyme involved in purine/uric acid metabolism), or renal insufficiency
  • gout is more common in males
18
Q

What happens in an acute case of gout? What can develop in a chronic case?

A
  • acute: MSU (monosodium urate) crystals active neutrophils to trigger acute inflammation = painful arthritis
  • in chronic gout, tophi can develop (these are firm, subcutaneous deposits of urate), as can renal failure (the uric acid deposits in the tubules and damages them)
19
Q

What do we see in the serum of a patient with gout? In the synovial fluid?

A
  • serum: hyperuricemia
  • synovial fluid: needle-like crystals with a NEGATIVE birefringence under polarized light (crystals parallel with the light appear yellow, those perpendicular appear blue)
  • (under paraLLel light, MSU crystals will be yeLLow)
20
Q

What is pseudogout? What do we see in the synovial fluid of a patient with pseudogout?

A
  • clinically identical to gout, but due to calcium pyrophosphate dihydrate (CPPD) crystal deposition
  • synovial fluid: rod or square or rhombus-like crystals with weak POSITIVE birefringence under polarized light (crystals parallel with the light appear blue, those perpendicular appear yellow)
21
Q

What are some risk factors of infectious arthritis?

A
  • prosthetic joints, skin infection, joint surgery, rheumatoid arthritis, diabetes mellitus
22
Q

What is the principal site of seronegative spondyloarthropathy? (ie what part of the joint is affected?)

A
  • the enthesis (where tendons and ligaments join the bone)

- enthesitis (most common sites are the Achilles’ tendons and the plantar fascia)

23
Q

What are the four stages of gout?

A
  • asymptomatic hyperuricemia –> acute gouty arthritis (sudden, excruciating pain; 50% of cases involve the big toe) –> intercritical period (asymptomatic period, possibly with recurrent attacks) –> chronic tohpaceous gout
  • in chronic form, deposits in the ear lobe are quite common
24
Q

What is the causative agent of Lyme disease? What are the three stages of the disease? What are four major and common effects/complications?

A
  • caused by the spirochete Borrelin burgdorferi, which is transmitted by deer ticks
  • stage 1: multiplication of spirochetes at the site of tick bite; erythema chronicum migrans (expanding area of redness), fever, lymphadenopathy
  • stage 2: early disseminated stage; hematogenous spread results in skin lesions, lymphadenopathy, migratory joint pain and muscle pain, cardiac arrhythmia, meningitis (IgM and IgG appear now)
  • stage 3: late disseminated stage (2-3 years after the bite); chronic arthritis of the large joints, encephalopathy
  • major complications: bilateral facial nerve palsy, arthritis, cardiac block, erythema migrans
25
Q

What is the classic patient with ankylosing spondylitis? Why has it been so under-diagnosed?

A
  • classic patient is male less than 45 years of age (rare for older patients) complaining of back and/or buttock pain lasting longer than 3 months
  • under-diagnosed because X-rays show no signs of disease at early stage (use MRI instead!), the symptoms are commonly misdiagnosed as general back pain, and because there is a diagnostic delay of 8 to 11 years
26
Q

What percentage of patients with ankylosing spondylitis have HLA-B27? What percentage of patients with HLA-B27 have ankylosing spondylitis? What percentage of patients with other spondlyoarthropathies have HLA-B27?

A
  • 90% of patients with AS have HLA-B27, but only 5% of patients with HLA-B27 have AS
  • 50% of patients with psoriatic arthritis have HLA-B27
  • 50% of patients with colitic arthritis have HLA-B27
  • 10-60% of patients with reactive arthritis have HLA-B27
27
Q

What are the chances a relative of someone with ankylosing spondylitis developing the disease?

A
  • identical twin: 65%
  • sibling, parent, child: 8%
  • cousin: 1%
28
Q

Arthritic nodes of the DIP are known as _______; arthritic nodes of the PIP are known as ________. What diseases are these seen in?

A
  • DIP: Heberden nodes
  • PIP: Bouchard nodes
  • osteoarthritis has both; rheumatoid arthritis has only PIP (Bouchard nodes)
  • DIP involvement is also very common in psoriatic arthritis
29
Q

Other than TNF-alpha, what other inflammatory agents are associated with ankylosing spondylitis?

A
  • IL-17 and IL-23
30
Q

What four things do we use to diagnose rheumatoid arthritis?

A
  • joint involvement (usually symmetrical, commonly involves the ankles, knees, elbows, wrists, PIPs and MCPs)
  • serology (rheumatoid factor, ACPA/anti-CCP)
  • acute phase reactants (ESR and CRP)
  • duration of symptoms
31
Q

What is pseudogout associated with?

A
  • hyperparathyroidism and hemochromatosis
32
Q

Compare the synovial fluid in a normal patient, a patient with RA, a patient with gout, and in a patient with septic arthritis.

A
  • normal: clear, highly viscous, WBC less than 200
  • RA or gout: variable transparency, yellow, decreased viscosity, increased WBC (between 2,000 - 20,000)
  • septic: opaque, variable viscosity, very increased WBC (25,000 - 100,000)