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BL DD final > Rheum > Flashcards

Rheum Flashcards

1
Q

Joint involvement of OA

A

Hips and knees
Spine: cervical and lumbar
1st MTP, 1st CMC
DIP (Heberden’s), PIP (Bouchard’s)

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2
Q

OA Occupational risks:

A

Miners: OA hips, knees, shoulders
Weavers: OA hands

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3
Q

Do sports increase your risk of getting OA?

A

NO!

no increased risk; exercise may be protective

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4
Q

Secondary OA

A

Inflammatory
Metabolic: hemochromatosis,
Wilson’s disease,
ochronosis

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5
Q

What makes up Cartilage

A
  1. Collagen: predominantly type II
  2. Proteoglycans (chondroitin and keratin sulfate) linked to hyaluronic acid
  3. Matrix proteins
  4. Chondrocytes
  5. Water: 70% weight of intact cartilage
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6
Q

Cartilage in early Osteoarthritis

A

↑ chondrocytes
↑ metalloproteinases
↑ water content

↓ proteoglycan (proton weave that loves water)
↓ TIMP

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7
Q

Synovial fluid of OA

A

noninflammatory, type I fluid (200-2000 WBC/mm3)

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8
Q

Cytokines and inflammatory mediators implicated in articular cartilage destruction in OA

A
  1. Interleukin-1: stimulates MMP production, PGE2, nitric oxide (NO), IL-6
  2. Nitric oxide: increases MMP production, inhibits proteoglycan synthesis, induces chondrocyte apoptosis
  3. Prostaglandins (PGE): ↑ production and activation of MMPs
  4. Other cytokines: TNF, IL-6, IL-17, and IL-18
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9
Q

Aside from IL-1, NO, PGE, and other cytokines, what else plays a role in OA pathogenesis?

A

Complement activation

Adipokines

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10
Q

characteristics of OA in x rays

A

Joint space loss
Sclerosis
Subchondral cysts
Osteophytes

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11
Q

Which one is symmetric, RA or OA?

A

RA is.

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12
Q

RA Joint involvement:

A

Bilateral, symmetric - small joints hands + feet sparing the DIPs
Medium and large joints can be involved
X-rays: marginal joint erosions and deformities

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13
Q

Disease susceptibility of RA

A

Disease susceptibility and severity associated with shared epitope in subtypes of HLA-DR4 and HLA-DR1

RF

Anti-CCP

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14
Q

Rheumatoid factor (RF):

A

Usually IgM Antibody directed against the Fc portion of IgG

  • RF-IgG immune complexes are pathogenic
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15
Q

Anti-Cyclic Citrullinated Peptide Antibodies (Anti-CCP)

A

Autoantibodies reactive with synthetic peptides containing the unusual amino acid citrulline (modified arginine residue)

Even though RF isn’t specific for RA, A-CCP sure as hell is.
- If you have both RF AND A-CCP, hell yea, you prob gots RA

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16
Q

Pannus

  • what is it,
  • Which disorder is it usually seen in
A

Infiltrating butt ton of cells
- Lymphocytes, macrophages ect.

RA (systemic inflammatory auto imm. disorder.

17
Q

Lymphocytes in RA synovium:

A

Majority are CD4+ T cells

  • Th17 cells
  • B cells and plasma cells are present (RF, anti-CCP); no PMNs
18
Q

CD4+ memory T cells fxn in rheumatoid arthritis

A

modulation and amplification of local immune response through antigen recognition
(query altered proteoglycans or collagen; citrullinated peptides)

19
Q

The Gout

A

The result of tissue deposition of monosodium urate (MSU) crystals due to hyperuricemia (MSU supersaturation of extracellular fluids)

20
Q

Gout joint involvement

A
  • 1st MTP (podagra)
  • Cool, peripheral joints of lower and upper extremities
  • remember OA is 1st MTP too! (and 1st CMC)
21
Q

What type of Hyperuricemia is most common in Gout?

A

underexcretors (90%)

  • make it just fine, but cant get rid of it bc we lack uricase! which oxidizes uric acid into allantoin
22
Q

Uric acid is a product of what?

A

purine metabolism:

23
Q

Overproduction of uric acid

  • what is it?
  • type of genetic disorder?
  • whats wrong with the enzymes?
A

Less common type of gout
X-linked

PRPP synthetase OVERACTIVITY
HGPRT DEFICIENCY
= high uric acid

*note: the common underexcretors also result in high uric acid content

24
Q

How do you diagnose crystal arthritis in gout?

A

arthrocentesis (polarized microscopy)

aspirate or litigate!

25
Q

How would you describe MSU crystals in Gout?

A

needle-shaped, negatively birefringent (blue outline)

26
Q

Endogenous MSU crystals may act as a “danger signal”, how?

A
  • Initial recognition of naked MSU crystals by TLR2 / TLR4 critical to the inflammatory response
  • MSU crystals engage the caspase-1 activating NLRP3 inflammasome resulting in IL-1β production
27
Q

Self-limited nature of acute gouty arthritis

A
  1. Proteins coating the crystals modulate the cellular response:
  2. Phagocytosis of crystals ↓ concentration
  3. Local heat of inflammation ↑ MSU solubility
  4. ACTH secretion suppresses inflammation
  5. IL-1 and TNF are modulated by inhibitors
28
Q

How do proteins coating the crystals in gout modulate the cellular response?

A
  • IgG-coating promotes phagocytosis by PMNs
  • IgG: not specific anti-crystal antibodies
    Apolipoprotein B-coating inhibits phagocytosis
29
Q

Calcium Pyrophosphate Dihydrate Deposition Disease

A

Pseudogout

30
Q

pathology of pseudogout (whats wrong?)

A

Abnormal pyrophosphate (PPi) metabolism – not purine like gout (uric acid)– crystals are naturally in your joint and shed

31
Q

What is making more abnormal pyrophosphate (PPi) in pseudogout (CPPD)?

A

ANK and NTPPPH metabolism of nucleoside triphosphate (NTPs) from chondrocytes

32
Q

How would you describe CPPD crystals?

A

rhomboid, positively birefringent (blue outline)

Remember, in gout, crystals are needle-shaped, negatively birefringent

BL DD final (18 decks)

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