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B&L Unit 3 > Underlined Stuff from Rheum Review Session (complete) > Flashcards

Underlined Stuff from Rheum Review Session (complete) Flashcards

1
Q

Describe generally OA

A
  • Degeneration of cartilage, hypertrophy of bone

- Involves DIP (Heberden), PIP (Bouchard), 1st CMC

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2
Q

How do sports affect OA?

A
  • No increased risk

- Exercise may actually be protective

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3
Q

Describe the cartilage in OA

A

INCREASED METALLOPROTEINASES

  • also increased chondrocytes, water content
  • Decreased proteoglycan, TIMP
  • non-inflammatory synovial fluid
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4
Q

Which types of cytokines/inflammatory mediators are produced in OA?

A
  • IL-1
  • NO
  • Prostaglandins
  • Others (TNF, IL-6, 17, 18)

Complement activation

Adipokines (why obese people have ^ risk of OA)

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5
Q

Describe knees of OA

A

1) Joint space loss
2) Sclerosis (bone remodeling)
3) Subcondral cysts
4) Osteophytes

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6
Q

Describe RA

A
  • Systemic, inflammatory autoimmune
  • Unknown cause
  • peripheral, SYMMETRIC SYNOVITIS => cartilage & bone destruction
  • Joint involvement: bilateral, symmetric small joints hands (SPARES DIPS)

Overall ^ of inflammatory/cytokines causes bone and cartilage erosion

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7
Q

What is the disease susceptibility and severity associated with in RA? (think immune)

A
  • Shared epitope: short sequence in Ag binding groove

- Shared subsets: HLA-DR4 and HLA-DR1

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8
Q

What are RF-IgG immune complexes associated with?

A

They are PATHOGENIC

  • Can cause vasculitis and rheumatoid nodules over extensor surfaces
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9
Q

What are the majority of lymphocytes in RA synovium?

A
  • CD4+ T cells

- Th17 cells

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10
Q

Why are CD4+ memory T cells in the RA synovium?

A

Modulation and amplification of local immune response through Ag recognition

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11
Q

Describe THE gout

A
  • Results from tissue deposition of monosodium urate (MSU)
  • Due to hyperuricemia (MSU SUPERSATURATION of extracellular fluids)
  • Joints involved: 1st MTP, other cool peripheral joints of extremities (more likely to saturate at low temps)
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12
Q

What is the most common cause of hyperuricemia?

A

UNDER-EXCRETION of uric acid (90% of pts w/ gout)

other 10% = over-production

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13
Q

Uric acid is a a product of what?

A

Purine metabolism

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14
Q

Which enzyme do humans lack? It breaks down uric acid

A

Uricase

  • oxidizes uric acid to allantoin
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15
Q

What are two ways to overproduce uric acid?

A

1) PRPP synthetase overactivity
2) HGPRT deficiency

X-linked!!!

complete HGPRT deficiency is Lesch-Nyhan

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16
Q

How is crystal arthritis diagnosed?

A

Arthrocentesis

Crystals identified by polarized microscopy

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17
Q

What does protein coating of crystals modulate in cellular response?

A
  • IgG coating promotes phagocytosis by PMNs
  • IgG => not specific anti-crystal Abs
  • Apolipoprotein B coating INHIBITS phagocytosis
18
Q

What are the characteristics of spondyloarthropathies?

A
  • Sacroiliitis (SI joints)
  • Enthesis (inflammation where ligaments/tendons inset into bone)
  • Synovium: increased expression of TNF-alpha

Unknown infectious trigger in genetically susceptible individual => disease!

19
Q

Describe the chances of developing ankylosing spondylitis

A

THINK: HLA-B27

  • 2% if HLA-B27 positive
  • 20% if HLA-B27 positive w/ first degree relative w/ AS
20
Q

Describe reactive arthritis

A
  • H/o infectious diarrhea or urethritis

- Asymmetric, oligoarticular, LOWER EXTREMITY ARTHRITIS

21
Q

Describe systemic lupus erythematosus (SLE)

A
  • Chronic, systemic disease affecting multiple organs
  • Defect: misdirected recognition of self as foreign!!!
  • Results in autoimmune process => T cell AND B cell process
  • Ab responses to auto Ags are Ag-driven and require CD4+ T cells
  • Loss of T cell requires B cell stimulation => peripheral abnormality in self-reactive lymphocyte deletion/anergy
22
Q

Describe the genetics of SLE

A
  • POLYGENIC
  • Associated with C4A null allele

C4A null allele shows greatest risk!!!!!

23
Q

Describe antinuclear antibodies (ANA)

A
  • In SLE: >95% of pts have positive ANAs
  • Not specific for SLE
  • Abs are directed to multiple nuclear Ags
24
Q

Anti-phospholipid Abs in SLE are associated with what?

A

INCREASED clotting

  • block prothrombin activation in coag cascade
25
Q

Describe vasculitis

A

Inflammation w/in or through blood vessel wall => damage to vessel integrity/flow

26
Q

What are types of large vessel vasculitis?

A

1) Takayasu’s arteritis

2) Giant cell arteritis

27
Q

What are types of medium vessel vasculitis?

A

1) Polyarteritis nodosa

2) Kawasaki’s disease

28
Q

What are types of small vessel vasculitis that have c-ANCA?

A

1) GPA
2) Churg Strauss
3) Microscopic polyangiitis

29
Q

What are types of small vessel vasculitis that have p-ANCA?

A

1) HSP
2) Cryoglobulinemia
3) Cutaneous leukocytoclastic vasculitis

30
Q

Describe the pathophysiology of immune complexes in vasculitis

A
  • inflammation causes increased vascular permeability => IC deposition
  • Leads to palpable purpura
31
Q

Describe the pathophysiology of T cell dependent mediated endothelial cell injury in vasculitis

A

HLA-DR4 and giant cell arteritis

Suggests AG-DRIVEN vascular inflammation

32
Q

What is associated with cytoplasmic ANCA (c-ANCA)?

A
  • PROTEINASE-3 (PR3) in primary granules of PMNs
  • GPA (Wegeners)

Think 3 looks like 2 Cs and 3 on its side is a W or Wegeners

33
Q

What is associated with perinuclear ANCA (p-ANCA)?

A
  • Myeloperoxidase (MPO) in 1ary granules
  • Microscopic polyangiitis (MPA)

All the P’s!!!

34
Q

Describe polymyositis/dermatomyositis

A
  • Inflammatory myopathies
  • Muscle weakness

Present with:

  • Gottron’s papules
  • Heliotrope rash (eyeshadow rash)
  • V-sign and shawl sign
  • Mechanic’s hands
  • Periungual changes/erythema
35
Q

What is the most common presentation of anti-synthetase syndrome?

A

PM or DM presenting with:

INTERSTITIAL LUNG DISEASE (60%)

36
Q

Where are anti-synthetase Abs found?

A

Cytoplasm

37
Q

What’s another word for Anti-Jo1?

A

Anti-HISTADYL-tRNA synthetase

38
Q

Are anti-synthetase Abs pathologic?

A

NO! Not pathologic or myotoxic

They are just markers for disease

39
Q

Which inflammatory cells are associated with Polymyositis?

A

CD8+ T cells

40
Q

Which inflammatory cells are associated with dermatomyositis?

A

CD4+ T cells

41
Q

What is important to keep in mind about evidence suggesting a viral cause for PM or DM?

A

By the time a pt comes in with a disease, the virus has already been eaten up by the immune system

You won’t find the live virus, no culture

There can be evidence of the virus, but NO LIVE VIRUS

42
Q

GO REVIEW THE QUIZZES FOR RHEUM!!!

A

Apparently some of the content may be used again….

NOW GO NOW GO

B&L Unit 3 (12 decks)

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