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MNI (bones and joints path) > L21- Arthritis > Flashcards

L21- Arthritis Flashcards

1
Q

Synovial Joints:

  • (1) describe cells
  • cells produce (2), which has (3) functions
A

1- Synovial cells- mesenchymal cells; cuboid or fibroblast like cells, 1-4mm thick

2- Synovial fluid into joint space, hyaluronic acid, proteins

3- lubrication and nourishment to joint / articular cartilage

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2
Q

Articular cartilage is made out of (1) which is produced by (2). (2) also has (3) functions. Articular cartilage has (4) thickness.

A

1- type II collagen, proteoglycans
2- chondrocytes
3- produces matrix degrading enzymes for turnover
4- 1-4mm thick

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3
Q

Articular cartilage:

  • (1) function
  • (2) are importantly absent
  • (3) provides nourishment to cells
A

1- shock absorber, smooth / friction free movements — type II collagen disperses force across joint surface so bone absorbs most of the shock

2- BVs, nerves

3- synovial fluid

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4
Q

describe the arrangement of type II collagen in articular cartilage

A

Area closest to bone- vertical arrangements

Area furthest from bone (closest to joint)- horizontal arrangement

Functions: transmit vertical stress, resists tensile forces, disperse force across joint surface into bone

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5
Q

list the common types of arthritis

A 
osteoarthritis
rheumatoid arthritis
seronegative arthritis
crystal deposition- gouty arthritis
infectious arthritis
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6
Q

(1) is the most common type of arthritis, describe as (2).

A

Osteoarthritis: progressive destruction of articular cartilage

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7
Q

Indicate primary or secondary OA:

  • (1) older patients
  • (2) affects more joints
  • (3) more severe
A

1- primary, 80-95% are >65 y/o

2- secondary polyarticular (many joints)— primary oligoarticular (few joints)

3- secondary

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8
Q

(1) is the cause of primary OA.

(2) conditions have risks of developing secondary OA.

A

1- aging

2- DM, hemachromatosis, ochronosis, obesity, congenital deformity

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9
Q

list the three general changes seen to synovial joints in OA

A
  • changes to Articular Cartilage components
  • chondrocyte changes

-others: proinflammatory CKs –> inflammatory cells

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10
Q

describe the changes to articular cartilage in OA

A
  • altered proteoglycans => water(inc)-PG(dec) imbalance = chondromalacia-softening
  • diminished pliability of collagen due to orientation mismatch or defective structure

=> weaker articular cartilage

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11
Q

describe the changes to chondrocytes in OA

A
  • IL-1, TNF-α release –> breakdown matrix
  • inhibition of type II collagen synthesis

=> cartilage breakdown => reactive changes => inflammatory response

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12
Q

In OA there is decreased synthesis of (1) and increased activity of (2) in synovial joints. (2) occurs via (3) enzymes which regulated via (4) mediators, and (5) may be an additional factor contributing to (2).

A

1- articular cartilage

2- enzymatic breakdown

3- metalloproteins: proteoglycan breakdown, Stromelysins // collagen breakdown, Collagenases

4- IL-1, TNF-α

5- collagen gene mutations (genetic predisposition)

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13
Q

Primary OA:

  • (1) prevalence
  • (2) commonly affected joints
  • affects (males/females) more
  • (4) and (5) are major risk factors
  • (6) are secondary risk factors
A

1- 75% of all people >70y/o
2- knee, hip, spine, fingers/toes (oligoarticular)
3- females
4- obesity
5- hereditary / genetic predisposition
6- trauma, neuromuscular dysfunction, metabolic disorders

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14
Q

list the commonly affected locations of primary OA and what deviations from these locations may indicate

A

knee, hip, spine, finger/toes

-if in other locations –> investigate for secondary causes of OA

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15
Q

list the many changes seen on X-Ray for OA

A
  • dec joint space
  • erosion of articular cartilage
  • eburnation (smoothing of bone where cartilage should be via friction)
  • sclerosis
  • subchondral cysts
  • osteophytes
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16
Q

describe the development of osteophytes in OA

A
  • occurs due to reparative process occurring around articular cartilage
  • fibrocartilage deposition –> bony spur
17
Q

describe the major histological changes seen in OA

A
  • horizontal oriented type II collagen fibers destroyed (the more superficial layer)
  • vertical cracking in cartilage
  • chondrocytic proliferation => hyperplasia, hypertrophy –> degeneration / removal exposes bone
18
Q

describe the major gross changes seen in OA

A
  • Erosion of articular cartilage, could be totally absent at joint apex and intact at periphery
  • Eburnation: bone smooth due to friction
  • Subchondral Cysts: synovial fluid –> pushed into bone –> creates cyst + sclerosis reaction (denser bone)
19
Q

______ is arthritis due to an autoimmune condition

A

rheumatoid arthritis

20
Q

RA:

  • (1) general signs and symptoms (indicate common locations of arthritis)
  • (2) are the main investigatory markers / indicators of RA
A

1- Symmetrical Polyarthritis: hands/feet + ankles, wrists, elbows, shoulders
-pain, inflammation, swelling, destruction of joints

2- rheumatoid factor, ACPA (anti-citrullinated protein antibody)

21
Q

RA:

  • affects (males/females) more
  • (2) is the main risk factor
  • (3) are the main triggers
A

1- females, 2.5:1

2- HLA-DRB1 polymorphisms

3- smoking, stress, infections: EBV, E. coli

22
Q

RA:

  • genetic predisposition leads to (1)
  • environmental triggers lead to (2)
  • (1) and (2) cause a type (3) sensitivity reaction
A

1- failure of tolerance to self and unregulated lymphocyte activity

2- enzymatic modification of self-protein

3- type II (B-cells), type IV (Th1, Th17) cells

23
Q

In RA, the initiation of hypersensitivity reactions causes the proliferation of (1) cells. (1) cells will release (2) which causes (3), the main process causing RA directly. (1) cells will also release (4) in order to increase (5) activity to cause secondary osteoporosis.

A

1- fibroblasts, chondrocytes, synovial cells

2- collagenase, stromyelysin, elastase, PGE2 + other enzymes
3- Pannus formation: bone/cartilage destruction => fibrosis and ankylosis

4- IL-1 / TNF (macrophages) + RANK/RANKL (T-cells)
5- osteoclast activity

24
Q

RA histology:

  • (1) is the highlight change, describe
  • (2) are the other important cellular changes
A

1- Pannus: granulation tissue infiltration = synovial cell hypertrophy

2:

  • papillary synovial hyperplasia – multi-layered synovial cells
  • lymphocyte, plasma cell invasion: perivascular lymphoid aggregates + vascular congestion
25
Q

describe some of the major changes on radiography seen in RA

A
  • dec joint space
  • subchondral cysts – osteoporosis
  • deviation of bones due to abnormal joint
26
Q

Systemic RA symptoms:

  • (1) soft tissue
  • (2) brain
  • (3) CVS
  • (4) eyes
  • (5) lungs
  • (6) blood vessels
  • inc risk to develop (7)
A 
1- rheumatoid nodules
2- fatigue, reduced cognition
3- inc risk MI, stroke. HF (via inc inflammatory mediators)
4- uveitis (more so in juvenile RA)
5- inflammation, fibrosis
6- vasculitis
7- lymphoma
27
Q

what are the major differences in adult and juvenile RA

A

Adult: onset 20-30y/o, less risk of uveitis

Juvenile: onset <16y/o, high risk of uveitis

28
Q

Rheumatoid nodules:

  • (1) prevalence
  • (2) commonly affected areas
  • (3) describe gross features of nodule
  • (4) describe microscopic features of nodule
A

1- 25% RA Pts
2- elbows, skull/occiput, back (lumbrosacral), knees

3- non-tender firm nodule in subcutaneous fat

4- central necrosis with palisading (wall of) macrophages / inflammatory cells (like a granuloma)

29
Q

Complications of RA:

  • (1) lung
  • (2) CVS
  • (3) additional systemic syndrome
  • (4) iatrogenic
  • (5) change in life expectancy
A

1- end-stage lung disease (fibrosis, inflammation)

2- Vasculitis => MI, CVA, renal failure, mesenteric/intestinal infarction, gangrene

3- systemic amyloidosis

4- immunosuppression therapy => many complications

5- dec by 3-7 yrs

30
Q

compare morning stiffness between OA, RA

A

OA: <30mins

RA: >1hr

31
Q

compare how physical activity affects symptoms of OA, RA

A

OA: worse with activity

RA: improves with activity

32
Q

compare distribution of joints between OA, RA

A

OA, oligoarticular: weight bearing joints (knees, hips, spine), fingers (PIP, DIP)

RA, polyarticular + symmetrical: wrist, fingers (MCP, PIP)

33
Q

(OA/RA) is systemic disease with (2) as additional symptoms

A

RA- fever, weight loss

34
Q

(OA/RA) is a non-inflammatory disease

A

OA

35
Q

(OA/RA) has reparative activity leading to (2)

A

OA (RA does not) –> osteophytes, subchondral sclerosis (surrounding cysts)

36
Q

Seronegative arthritis is commonly called (1) because of (2). It presents similar to (3), with (4) as the main differences.

A

1- seronegative spondyloarthropathies
2- joints of sacrum, pelvis

3- RA
4- milder disease (although systemic), no rheumatoid factor

37
Q

Seronegative Spondyloarthropathies is related to ______ genetic change

A

HLA-B27 associated

38
Q

list the many changes and symptoms seen at the joints in Seronegative Spondyloarthropathies

A
  • Chronic synovitis + Destruction of articular cartilage and subchondral bone
  • Fibrosing ankylosis: fibrosis + narrowing of joint space
  • Bony ankylosis: ossification of fibrosis + joint immobility
  • ankylosing spondylitis is most common: sacroiliac joints and spine
39
Q

Infectious Arthritis:

  • extends from (1) infection or from (2)
  • (3) are the common organisms
A

1- osteomyelitis (bone infection spreads to joint)
2- hematogenous seeding (via blood)

3:

  • Bacteria: S. aureus (children), N. Gonnococcus (adults), Mycobacteria, Borrelia (Lyme disease)
  • Viral: parvovirus B19

MNI (bones and joints path) (10 decks)

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