Bones, JOINTS, Soft Tissues Part 3 Flashcards

1
Q

What are the two classifications of joints?

A
  • Solid/ Nonsynovial/Synarthroses

- Cavitated/Synovial

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2
Q

Name a bunch of different kinds of arthritis?

What are 4 big ones?

A

4 big ones:

  • Osteoarthritis (DJD)
  • Rheumatoid arthritis
  • Gout
  • Calcium Pyrophosphate Crystal Deposition Disease (Pseudogout)

Others:
- Juvenile idiopathic, seronegative spondyloarthropathies,
ankylosing spondylitis, reactive, infectious, suppurative, mycobacterial, viral, lyme

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3
Q

What are some major RF for osteoarthritis (OA)?

A
  • For primary arthritis, aging is the main RF

- For secondary arthritis: Joint deformities, trauma, diabetes, ochronosis, hemochromatosis, obesity

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4
Q

What are some sx of OA?

A
  • Evening stiffness
  • Crepitus
  • Limited ROM
  • Gets worse with use (v impt distinction)
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5
Q

What are commonly affected joints in OA?

A
  • Women: Hands & knees; DIP and PIP joints affected

- Men: Hips

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6
Q

What are the nodes called in OA in the PIPs and DIPs?

A

At PIP joints they are called Bouchard’s nodes

At DIP joints they are called Heberden nodes

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7
Q

What happens to the matrix and cartilage in OA?

What does this cause the bones to do?

What can form?

A

Water content of matrix inc while concentration of proteoglycans dec leading to cracks in the matrix
- Cartilage that sloughs off: “Joint mice” or “loose bodies”

Subchondral bone is exposed and rubbed smooth leading to eburnation (bone on bone)

Microfractures develop which allows for synovial fluid into subchondral region and subchondral cysts

Osteophytes (bony outgrowths) form

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8
Q

What patient populations and ages do we see RA most commonly in?

A

Peaks in 2nd-4th decade, women more commonly than men

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9
Q

What is rheumatoid arthritis (RA)?

A

Autoimmune, nonsuppurative proliferative and inflammatory synovitis

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10
Q

What genetic markers do we see in RA?

What is a common genetic mutation seen?

A

Anti-citrullinated peptide bodies (ACPAs) and rheumatoid factor (IgM and IgA antibodies)

HLA-DR4 common allele a/w ACPA-positive RA

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11
Q

What can we see systemically in RA?

A

Extraarticular lesions in the skin, heart, blood vessels, and lungs
- Overlap w over autoimmune disorders including SL and scleroderma

Leukocytoclastic vasculitis: Acute necrotizing vasculitis of small and large arteries of heart or lungs

Ocular changes like uveitis and keratoconjunctivitis

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12
Q

What is the articular cartilage destruction like in RA?

A
  • Ankylosis or joint fusion

- Symmetrically distributed in small joints of hands and feet (PIPs and metacarpophalangeal)

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13
Q

What are some clinical symptoms of RA? What do we see happening in the joints?

A
  • Morning stiffness; does not improve w rest
  • Deformities of joints
  • Nodules
  • Pannus: Edematous and thickened hyperplastic synovium that grows over and causes erosion of articular cartilage
  • Synovial hypertrophy of villi
  • Lymphoid aggregates

After cartilage has been destroyed, pannus bridges the apposing bones to form a fibrous ankylosis which eventually ossifies and causes bon fusion

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14
Q

What deformities do we see?

  • Boutonniere
  • Swam-neck
  • Ulnar deviation
  • Radial deviation
A
  • Boutonniere: Deformity of finger, hyperextension of DIP, flexion of PIP
  • Swam-neck: Hyperextention of PIP, flexion of DIP
  • Ulnar deviation of fingers, dec joint space, bony erosions
  • Radial deviation of the wrist
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15
Q

What are rheumatoid nodules?

A

Extensor surfaces at pressure points

  • Occur in subq tissue of forearm, elbows, occiput, lumbosacral area
  • Small, firm, nontender, round to oval
  • Necrotizing granulomas w a central zone of fibrinoid necrosis
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16
Q

What is juvenile idiopathic arthritis?

What serum marker do we see?

A

Heterogeneous group of disorders of unknown cause, present w arthritis before 16 years old and persist for at least 6 weeks
- ANA seropositivity (no rheumatoid nodules)

17
Q

What are seronegative spondyloarthropathies? What serum markers and genetic mutations do we see?

A

Group of disorders unified by the following:

  • Autoimmune T cell response
  • Pathologies in the ligamentous attachments rather than synovium
  • Negative rheumatoid factor
  • HLA-B27

Ankylosing spondylitis is part of this

18
Q

What is reactive arthritis?

What is the timeline?

What other body system can be affected?

A

Part of a seronegative spondyloarthropathy

Reactive arthritis follows an infection (HLA-B27 +)

  • Triad of sx is arthritis, nongonococcal urethritis or cervicitis, conjunctivitis
  • Episodes may wax and wane for 6 months but 50% have recurrent arthritis, tendonitis, and lumbosacral pain (if longer than 6 months it is chronic)
  • May have cardiac valvular disease (aortic insufficiency)
19
Q

What is psoriatic arthritis?

A

Part of a seronegative spondyloarthropathy

Affects hands & feet, axial joints, ligaments and tendons

  • HLA-B27
  • “Pencil in cup” deformity, DIPs, can be asymmetric
  • Nails can turn thick, rough, rigid, discolored
20
Q

What is infectious arthritis?

A

Microorganism seed joints via hematogenous dissemination, direct inoculation, or contiguous spread of soft tissue abscesses or osteomyelitis
- Rapid joint destruction leading to permanent deformities

Can also have subset of mycobacterial or viral arthritis

21
Q

What is lyme disease and how does it relate to arthritis?

A

From borrelia burgdorferi (in ticks)

  • Usually tx before progressing to arthritis but if untx, migratory arthritis can develop lasting weeks to months
  • Tx w abx
22
Q

What is suppurative arthritis?

What are common agents in infants, young kids, and older kids to adults? Sickle cell? IVDU?

A

Bacteria that spreads hematogenously from distant site

  • Neonates: Contiguous spread from epiphyseal osteomyelitis
  • < 2 yo: H. flu
  • Older kids & adults: S. aureus most common, gonococcus late adolescent or early adult
  • Sickle cell diseae pts are prone to salmonella inf at any age

Acutely painful and swollen joint w restricted ROM, fever, leukocytosis, inc sed rate

Axial jont involvement w IVDU

23
Q

What are the composition of crystals that we can see in crystal-induced arthritis?

A

Crystals: Monosodium urate, calcium pyrophosphate dihydrate, calcium phosphate

24
Q

What is gout? What are some RF?

A

Transient attacks of acute arthritis initiated by crystallization of monosodium urate within and around joints
- D/t hyperuricemia (plasma level s>6.8mg/dL)

RF: Age, male, genetics, heavy alcohol consumption, obesity, certain drugs, lead toxicity

25
Q

What is acute arthritis that we see in gout?

A

Dense neurtophilic infiltrate that permeates synovium and synovial fluid; needle-shaped crystals arranged in small clusters

  • Sudden onset of excruciating joint pain, hyperemia and warmth
  • Often in big toe
  • Second attack months to years later
26
Q

What is chronic tophaceous arthritis that we see in gout?

What is an important concept to remember?

A

Repetitive precipitation of urate crystals during acute gout attacks

  • Can form pannus that destroys underlying cartilage and leads to bone erosions
  • Develops 10 years after initial attack
  • Osteoclastic bone resorption and loss of joint space (impt concept)
27
Q

What are tophi in gout?

A

Tophi are pathognomonic hallmark of gout: Large aggregations of urate crystals surrounded by foreign-body giant cells. May appear in the articular cartilage, ligaments, tendons, bursae

28
Q

What is urate nephropathy in gout?

A

Renal complications caused by urate crystals or tophi; can include uric acid nephrolithiasis and pyelonephritis

29
Q

What is calcium pyrophosphate crystal deposition (Pseudo-gout)?

What do the crystals look like?

What genes do we see?

A

Chondrocalcinosis: Calcification of hyaline or fibrocartilage

  • Crystals form that are chalky, white, friable deposits
  • Crystals are rhomboid and positively birefringent (in contrast: Gout crystals are negatively birefringent)

Can be sporadic, hereditary, or secondary types

  • ANKH
  • Secondary d/t previous joint damage
30
Q

What are some joint tumors or tumor-like conditions?

A
  • Reactive tumor-like lesions, such as ganglion cysts, synovial cysts, and osteochondral loose bodies (usually d/t trauma or degenerative processes)
  • Primary neoplasms are rare and usually benign
31
Q

What is a ganglion cyst?

A

Joint capsule or tendon sheath, 1-1.5cm cyst

  • Often on wrist
  • Firm, fluctuant pea-sized translucent nodule
  • Result of cystic or myxoid degeneration, cyst wall lacks cell linings
32
Q

What is a synovial cyst? Baker cyst?

A

Herniation of synovium through joint capsule or enlargement of bursa
- Baker cyst: Popliteal space a/w RA

33
Q

What is a tenocynovial giant cell tumor?

Tx?

A

Benign neoplasm that develops in the synovial lining of joints, tendon sheaths, and bursae
- Can be diffuse (pigmented villonodular synovitis) or localized

Tx: Surgical excision, possibly M-CSF antagonists (clinical trails show promise)

34
Q

What do we see in a diffuse tenosynovial giant cell tumor?

A

Diffuse involves large joints, can be painful w bony erosion and reoccurrence
- Red-brown to orange-yellow; tangled mat by red-brown folds, finger-like projections, and nodules
- Macrophages that may contain hemosiderin or foamy lipids and can be multinucleated
Aggressive diffuse tumors can erode into adjacent bone and soft tissues

35
Q

What do we see in a localized tenosynovial giant cell tumor?

A

Localized usually is discrete nodule attached to tendon sheath commonly in hand, can be slow-growing and painless
- Tendon sheaths along wrists and fingers

36
Q

What cytokines cause flares in gout?

A
  • IL-1 beta leads to neutrophil chemotaxis

- LTB4 leads to tissue injury (phagocytosis of crystals by neutrophils release LTB4)