Underlined Stuff from Rheum Review Session (complete) Flashcards Preview

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Flashcards in Underlined Stuff from Rheum Review Session (complete) Deck (42):
1

Describe generally OA

- Degeneration of cartilage, hypertrophy of bone
- Involves DIP (Heberden), PIP (Bouchard), 1st CMC

2

How do sports affect OA?

- No increased risk
- Exercise may actually be protective

3

Describe the cartilage in OA

INCREASED METALLOPROTEINASES

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

4

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

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

Complement activation

Adipokines (why obese people have ^ risk of OA)

5

Describe knees of OA

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

6

Describe RA

- 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

7

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

- Shared epitope: short sequence in Ag binding groove
- Shared subsets: HLA-DR4 and HLA-DR1

8

What are RF-IgG immune complexes associated with?

They are *PATHOGENIC*

- Can cause vasculitis and rheumatoid nodules over extensor surfaces

9

What are the majority of lymphocytes in RA synovium?

- CD4+ T cells
- Th17 cells

10

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

Modulation and amplification of local immune response through Ag recognition

11

Describe THE gout

- 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)

12

What is the most common cause of hyperuricemia?

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

other 10% = over-production

13

Uric acid is a a product of what?

Purine metabolism

14

Which enzyme do humans lack? It breaks down uric acid

Uricase

- oxidizes uric acid to allantoin

15

What are two ways to overproduce uric acid?

1) PRPP synthetase overactivity
2) HGPRT deficiency

X-linked!!!

complete HGPRT deficiency is Lesch-Nyhan

16

How is crystal arthritis diagnosed?

Arthrocentesis

Crystals identified by polarized microscopy

17

What does protein coating of crystals modulate in cellular response?

- IgG coating promotes phagocytosis by PMNs
- IgG => not specific anti-crystal Abs

- Apolipoprotein B coating INHIBITS phagocytosis

18

What are the characteristics of spondyloarthropathies?

- 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

Describe the chances of developing ankylosing spondylitis

THINK: HLA-B27

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

20

Describe reactive arthritis

- H/o infectious diarrhea or urethritis
- Asymmetric, oligoarticular, LOWER EXTREMITY ARTHRITIS

21

Describe systemic lupus erythematosus (SLE)

- 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

Describe the genetics of SLE

- POLYGENIC
- Associated with C4A null allele

C4A null allele shows greatest risk!!!!!

23

Describe antinuclear antibodies (ANA)

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

24

Anti-phospholipid Abs in SLE are associated with what?

INCREASED clotting

- block prothrombin activation in coag cascade

25

Describe vasculitis

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

26

What are types of large vessel vasculitis?

1) Takayasu's arteritis
2) Giant cell arteritis

27

What are types of medium vessel vasculitis?

1) Polyarteritis nodosa
2) Kawasaki's disease

28

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

1) GPA
2) Churg Strauss
3) Microscopic polyangiitis

29

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

1) HSP
2) Cryoglobulinemia
3) Cutaneous leukocytoclastic vasculitis

30

Describe the pathophysiology of immune complexes in vasculitis

- inflammation causes *increased vascular permeability* => IC deposition
- Leads to palpable purpura

31

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

HLA-DR4 and giant cell arteritis

Suggests AG-DRIVEN vascular inflammation

32

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

- 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

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

-Myeloperoxidase (MPO) in 1ary granules
- Microscopic polyangiitis (MPA)

All the P's!!!

34

Describe polymyositis/dermatomyositis

- 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

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

PM or DM presenting with:

INTERSTITIAL LUNG DISEASE (60%)

36

Where are anti-synthetase Abs found?

Cytoplasm

37

What's another word for Anti-Jo1?

Anti-HISTADYL-tRNA synthetase

38

Are anti-synthetase Abs pathologic?

NO! Not pathologic or myotoxic

They are just markers for disease

39

Which inflammatory cells are associated with Polymyositis?

CD8+ T cells

40

Which inflammatory cells are associated with dermatomyositis?

CD4+ T cells

41

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

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

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