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

1/94

Click to flip

94 Cards in this Set

  • Front
  • Back
Define: synarthroses
=immovable articulations, e.g. the skull
Define: amphiarthroses
=slightly movable articulations, e.g. vertebral bodies
-predominantly involved in mechanical and degeneraive arthritis
Define: diarthroses
=freely movable articulations, synovial* lined joints
-targets for inflammatory arthritis
What is the definition of arthritis?
=inflammation of the joint (literal definition)
-contemporary use applies to joint pain and joint disease, regarless of etiology
3 clinical classifications of arthritis:
1. monoarticular – 1 joint involved
2. oligoarticular – 2,3, or 4 joints involved
3. polyarthritis – more than 4 joints involved
Clinical characteristics of Arthritis:
• stiffness, pain, and tenderness arise w/in joint
• synovitis* present if etiology is inflammatory (i.e. inflamm in the joint)
• pain w/ active or passive mvmt of the joint
• disease defined by distribution of joint involvement and chronology (acute versus chronic)
***Acute Monoarticular Arthritis***
clues: male, symptoms developed in AM, drank moonshine (changes how you excrete uric acid b/c it has lead in it), and recent adjustment of diurectic
***Acute Monoarticular Arthritis***
Define acute* monoarticular arthritis:
=refers to a articular processes that present in a dramatic and sudden fashion and generally result in the pt seeking medical attention w/in 7 days*
Order of causes of ACUTE monoarticular arthritis:
1. septic – most urgent to dx
2. crystal-induced – most common
3. trauma – obvious
4. hemorrhage – may not be so obvious
5. mechanical
6. atypical polyarticular
Why is acute monoarticular arthritis important?
Represents most dramatic, potentially destructive and yet curable for of arthritis
What are the Big 3 causes of acute monoarticular arthritis?
Gout, pseudogout, septic arthritis
What is the most urgent form of arthritis to diagnose?
Septic arthritis*
What is the most common form of arthritis to diagnose?
Crystal-induced disease (gout, pseudogout, hydroxyapatite)
What symptom suggests septic arthritis?
90% of pts w/ septic arthritis have fever, but can also have it w/ severe crystal-induced disease (however, shaking chills** favors diagnosis of sepsis)
What patients have tophi?
Patients w/ chronic gout
How does acute monoarticular arthritis due to trauma, hemorrhage, pseudogout, hydroxyapatite and mechanical derangement present?
These all cause acute monoarticular arthritis without any extra-articular signs or symptoms**
What is the single most importat test for making the diagnosis of acute monoarticular arthritis?**
Synovial fluid analysis**
Cell count in synovial fluid analysis:
200 WBC is normal
2000/25% PMN or less is non-inflammatory
2000/50% PMN or greater* may be inflammatory
What 2 types of crystals are found on crystal analysis for acute monoarticular arthritis?
What do they look like/defining characteristics?
1. urate crystals: slender needles, strongly negatively birefringent** (suggests gout)
2. calcium pyrophosphate crystals: pleomorphic, rhomboid-shaped, weak positive birefringent** (suggests pseudogout)

hydroxyapatite: non-birefringence
What other test is critical to do in the case of an acute monoarticular arthritis?
Gram stain is critical!
Usefulness of blood work for acute monoarticular arthritis:
Is blood work helpful?
What will be increased in the Big 3 causes of acute monoarticular arthritis?
Does uric acid in the blood confirm a diagnosis of gout?
What does peripheral blood leukocytosis mean?
What do blood cultures show?
What does a coagulation profile show?
• Blood work is NEVER a substitue for synovial fluid!
• ESR is increased* in all of the main causes of acute monoarthritis (septic, gout, pseudogout); elevation speaks against traum or injury (this test is being replaced by CRP)
• Uric acid increase* in the blood does NOT make a diagnosis of gout nor does it rule it out!
• Peripheral blood leukocytosis – nonspecific* and does not distinguish infection from crystal disease
• Blood cultures: positive in pts w. septic arthritis BUT NOT ALWAYS
• Coagulation profile in pts with bloody tap (hemarthrosis) may indicate a bleeding diathesis
What is the usefulness of doing an X-ray when acute monoarticular arthritis is suspected?
• of little value* in diagnosis of acute monoarticular arthritis
• demonstration of chondrocalcinosis only supports* but does not confirm a diagnosis of pseudogout
• may show rapid loss of cartilage w/ joint space narrowing and bone demineralization
Why does gout get exacerbated at night?
body pH drops at night --> urate goes into synovial fluid --> nocturnal gouty attacks
**How is the diagnosis of gout made with certainty?***
gout diagnosis is made with certainty only upon the demonstration of intracellular sodium urate crystals obtained by arthrocentesis of the affected joint**
***Pathophysiology of Crystal-Induced Joint Disease***
***Pathophysiology of Crystal-Induced Joint Disease***
What is the complex series of events that results from crystals w/in the joint space?
Uric acid is released from damaged/senescent cells and then crystallizes in synovial fluid → crystals activate innate immune system via IL-1R (then NF-kB is activated) → IL-1 causes IL-8 release which recruits neutrophils to fluid space → PMNs* phagocytize crrystals (the central event which causes gout) → more IL-1, IL-8, and TNF-alpha are released from PMNs and neutrophils → more neutrophils recruited
If acute gouty arthritis goes untreated what may occur?
self-limited*
What are 6 drugs that can be used for acute monoarticular arthritis?
1. Colchicine*
2. Indomethacin*
3. Corticosteroids*
4. Allopurinol
5. Febuxostat
6. Recombinant uricase
Colchicine:
Used for?
MOA?
Side effects that have decreased its use?
Old-time remedy for gout

MOA: potently suppresses generation of inflamm molecules stimulated by interaction of PMN and MSU crystals in vitro

S/Es: GI (severe diarrhea!) and neurologic effects
Indomethacin: what class?
Potent NSAID w/ lots of side effects
Never use in elderly; almost diagnostic for gout, b/c it cures it in 2 days
What has become the treatment of choice for acute gout?**
Corticosteroids**
Allopurinol:
MOA?
Use?
MOA: xanthine oxidase inhibitor

Use: LONG-TERM suppression of uric acid synthesis (not for acute gout!)
Febuxostat:
MOA?
MOA: xanthine oxidase inhibitor (like Allopurinol, but not yet approved)
***Chronic Monoarticular Arthritis***
***Chronic Monoarticular Arthritis***
What is the definition of chronic monoarticular arthritis?
=arthritis persisting longer than 2 months
What diseases causing chronic monoarticular arthritis may be dagnosed by synovial biopsy?
1. neoplasm
2. Injection
3. Pigmented villonodular synovitis (PVS) – slow-growing benign neoplasm
4. sarcoidosis
5. plant thorn synovitis
***Acute Polyarthritis***
clues: young pregnant female, shaking chills, polyarthritis, several pustules on her right palm
***Acute Polyarthritis***
answer: gonococcal arthritis
What is acute polyarthritis?
=an inflammatory articular process involving more than 4 joints for less than 2 months in duration** (implies an abrupt onset)
Differentiating features of Acute Polyarthritis?
1. Rheumatic fever – only true migratory arthritis (w/ unique skin lesions:*erythema marginatum*)
2. Borrelia – occurs in August and September; unique skin lesion: erythema migrans
What 2 signs will a case study of acute polyarthritis show?
1. arthralgias
2. pustules on palms
How do you identify clinical subsets of acute polyarthritis?
Pattern* of evolution and distribution of joint involvement
What is migratory polyarthritis and what is the only disease it’s really seen with?
Migratory polyarthritis = a syndrome in which initially inflamed joints totally remit* while, simultaneously, other joints become inflamed

*Rheumatic fever is the ONLY disease where this realy happens*
What are the major causes of quasi-migratory polyarthritis?
1. gonococcal arthritis
2. lyme disease (Borrelia arthritis)
3. parvovirus B19 – “slapped cheek” virus
What cutaneous lesions are associated with the following causes of migratory polyarthritis?
Acute rheumatic fever?
Gonococcal arthritis?
acute rheumatic fever: erythema migrans

gonococcal arthritis: vesiculopustular lesions on erythematous base
What lab tests are assoc with the following causes of migratory polyarthritis?
Acute rheumatic fever?
Gonococcal arthritis? What if it is a recurrent syndrome?
Borrelia serologies?
Parvovirus serologies?
Acute Rheumatic fever: ASO titer*or similar test

Gonococcal arthritis: cultures* of GU tract, synovium, skin pustule, blood; if recurrent syndrome it may be terminal C deficiency
Borrelia serologies: ELISA and Western blot
Parvovirus serologies: used to detect acute* infection
What is the clinical picture for someone with gonococcal arthritis?
• Migratory polyarthritis/polyarthralgia: multiple, bilateral , symmetrical, and mainly knees, ankels, wriss, and fingers → morphs to one or 2 joints*
• Tenosynovitis (swelling of the sheaths that surround the tendons)**
• Frank purulent effusions
• Culture-negative synovial effusions in females**
• Ask: are you pregnantt; how close are you to your period*
• Late complement deficiences predispose people to repeated bouts of syndromes
What accounts for gonococci’s strain virulence?
Bacterial morphology (ex: pili) and specific OMPs
***Chronic Polyarthritis***
Case: female, AM stiffness (3 hrs or greater**), most joints affected for several months, “walking on stones” (tarsals), PIPs/MCPs/knees, can't open cans
***Chronic Polyarthritis***
Answer: almost always RA: AM stiffness** - means it is not DJD!, symmtetrical joint arthritis*
Differentiate b/w RA and OA regarding:
Soft tissue swelling?
AM stiffness?
Systemic manifestations?
Joint involvement: elbows, DIP, MCP, lumbar spine
Soft tissue swelling: RA has more
AM stiffness: always present in RA; brief in DJD
Systemic manifestations: RA has many including anemia; DJD has none
Joints*: RA never involves DIP or lumbar spine, but does involve MCP
What are the extra-articular manifestations of RA?
Nodules*
anemia
others
What is the most common cause of “noninflammatory” chronic polyarthritis in the adult?**
osteoarthritis (aka DJD)*
Definition of chronic polyarticular arthritis:
=refers to inflammatory joint disease in which more than 4 joints are involved for longer than 2 months
What is the most common cause of chronic inflamm polyarthritis in adults?**
RA*
Epidemiology of Rheumatoid Arthritis:
Worldwide
All racial groups
Women 2-4X more than men
0.2-1% prevalence
appears to be a decline in incidence and severity
50% are unable to work 10 years after diagnosis
Explain the genetic aspects of RA, including 1st –degree relatives, twins, and HLA links:
• 16X increase in 1st degree relatives
• 30% rate in twins
• linked to HLA-DR1 and DR4*
• linked to specific peptide motid in antigen binding groove
pannus?
=growth of synovial membrane which invades bone
Extra-articular manifestations of RA:
1. rheumatoid nodules*
2. Anemia – secondary to chronic inflammation
3. episcleritis
4. vasculitis
5. serositis
6. splenomegaly
What is the most important nonspecific indication of inflammation?
Morning stiffness* - duration is directly proportional to the severity and activity of the inflammatory process**
Where are rheumatoid nodules usually found?

Where are they occassionally found?
Rheumatoid nodules are comonly found over areas subject to mechanical trauma

Occassionally found in lungs and hearts
Describe the histology of rheumatoid nodules:
A central zone of fibrinoid histiocytes, lymphocytes, and plasma cells (in 20-25% of pts with RA and rarely in other diseases)
How do you diagnose RA?

What do blood tests for RA show?
Clinical diagnosis is how RA is usually diagnosed

Blood work usually NOT diagnostic*, however CCP (aka cyclic citrullinated peptide antibodies) is a new and very helpful test
What is Rheumatoid Factor?

Who has it? Is it diagnostic of RA?
RF = an autoantibody directed against the Fc portion of the IgG molecule

Found in many other diseases as well, therefore NOT diagnostic of RA
What is CCP?*
Cyclic citrullinated peptide* - highly specific for RA
What does synovial fluid analysis for RA show?
Inflammatory effusions
Are X-rays helpful for diagnosis of RA?
Erosions and periarticular osteoporosis are seen, but X-rays are suggestive, not pathognomonic
What is the cause of RA?
Who is at highest risk of getting the disease?
16X increase in 1st degree relatives
30% concurrent rate in twins
linked to DR1 and DR4 loci w/ specific binding peptide motifs
What is rheumatoid synovium characterized by?
Cellular heterogeneity and a proliferative response
What cytokine predominantes in the synovium of RA patients?
TNF-alpha** - it keeps the feedback going that creates pannus and destroys the joint
What are the basic goals of RA treatment?
Relieve pain, reduce inflammation, prevent structural damage, improve functional status
What drugs are used to treat RA?
1. NSAIDS
2. Corticosteroids – 1st mainstay of RA tx
3. DMARDS-MTX
4. Leflunomide
5. anticytokines
What are the 2 new therapies being used for RA? (TNF inhibitors*!)

How do they work?
1. false receptor that will bind TNF (i.e. IL-1 receptor antagonists)
2. monoclonal antibody that blocks TNF (anti-TNF-alpha)
*these are amazing drugs with limited S/Es, but they are incredibly exprensive!
***Osteoarthritis/Degenerative Joint Disease***
***Osteoarthritis/Degenerative Joint Disease***
Case: 66 y.o., hip pain has progresses over months, left groin pain, mild obesity
Answer: OA/DJD; predilection for weight bearing joints*
What is DJD/OA?
=form of progressive joint disease characterized by loss of articular cartilage w/ overgrowth and remodeling of underlying bone
Causes of primary OA?
No antecedent cause
What are the causes of secondary OA?
A response to a clear antecedent cause:
trauma*, prior inflamm, congenital, metabolic, avascular necrosis* (seen in weight-bearing joints in pts who have been on long-term corticosteroids), hypermobility (microtrauma)
What is the most common joint disorder?
OA – linear relationship to age and weight (leading to increased rates)
What are the 3 key symptoms of OA?
Pain worse with weight bearing
Pain better with rest
Very little AM stiffness (it is of short duration in comparison to RA)**
Signs of OA:
Joint creptius, loss of motion, bony enlargement, mild tenderness, bony angulation, soft tissue swelling
What joints are commonly affected by OA?
Cervical spine
Lumbar spine* - most common
Hands: 1st CMC joint, PIP joints, DIP joints
What lab tests are useful to aid in the diagnosis of OA?**
None!
What are the 2 mechanical functions of articular cartilage?
1. smooth, low resistance surface for movement
2. compressibility for diffusion of mechanical forces
What is the central pathological event in OA?**
=progressive deterioration and loss of articular cartilage
What are 2 reasons why articular cartilage fails?
1. overload of weight
2. lost elasticity
What 4 elements is normal cartilage composed of?
What accounts for most of the weight of cartilage in vivo? Why is this the case?
What accounts for most of the dry weight of cartilage (i.e. dehydrated)?
1. Water – 70-80% of cartilage weight in vivo
2. proteoglycans – gives cartilage its compresibility; 80% of dry weight
3. collagen – tensile strength
4. chondrocytes – responsible for keeping cartilage healthy
What type of collagen is phenotypically unique to cartilage?
Type II collagen
What’s the role of chondrocytes in cartilage?
Responsible for the production of proteoglycans, collagen, link proteins, metalloproteinases, etc.
What factors control cartilage synthesis and degradation?
IL-1 production by chondrocytes and synoviocytes, and metalloproteinases
What 2 factors strongly exacerbate the development of OA?
1. Obesity*
2. trauma*
What’s a major early change that occurs during the development of OA?
Increased water*
Once water content increases in joints, what happens to proteoglycan?
Proteoglycan aggregation defects
What happens after months of disease progression?
Focal cartilage ulceration and loss proteoglycans → worsened proteoglycan aggregation defect
What drugs have “chondroprotective” value in humans?
NO drugs have chondroprotective value!
Management of OA:
• Education
• Weight loss
• Physical therapy
• Restrained use of NSAIDS – renal problems, GI problems
• Surgery – underused; do if they have chronic pain
• Alternative therapies: glucosamine not shown effective in clinical trials