inflammatory joint disease

Question 1

what is meant by primary OA

Answer 1

without any apparent cause usually as part of an aging process normally occurring later in life (>50yr)

Question 2

what is meant by secondary OA

Answer 2

pre-existing joint deformity, a previous joint injury, an underlying systemic disease like diabetes, or marked obesity that places weight-bearing joints at risk

Question 3

there are 3 stages of OA pathogenesis what are they

Answer 3

1. Chondrocyte injury, related to genetic and biochemical factors
2. Early OA, in which chondrocytes proliferate and secrete inflammatory mediators, collagens, proteoglycans, and proteases, which act together to remodel the cartilage matrix and initiate secondary inflammatory changes in the synovium and the subchondral bone
3. Late OA in which repetitive injury and chronic inflammation lead to chondrocyte drop out, marked loss of cartilage and extensive subchondral bone changes.

Question 4

what are some morphological changes seen in OA

Answer 4

1. Degradation of articular cartilage, with cartilage “fibrillation”
2. Narrowing of the joint space due to loss of cartilage
3. Mushroom-shaped osteophytes (bony outgrowths) develop at the margins of the articular surface.
4. Eburnation of the exposed underlying bone
5. Subchondral sclerosis and cyst formation in the underlying subchondral bone
6. Joint mice loose bodies made up of detached bits of cartilage and bone, resulting in pain or recurrent locking of the joint

Question 5

what should be done if a young person comes in with clinical features of OA

Answer 5

a search for some underlying cause should be made.

Question 6

what are heberden nodes

Answer 6

prominent osteophytes at the distal interphalangeal joints, are common in women (but not men)

Question 7

what is the main difference between OA and RA

Answer 7

RA is a autoimmune dissorder and OA is not

Question 8

what is the pathogenesis of RA

Answer 8

CD4+ T helper (TH)cells initiate the autoimmune response in RA by reacting with an arthritogenic agent perhaps microbial or a self-antigen.
The T cell produce cytokines that stimulate the inflammatory cells to produce tissue injury

Question 9

Why is RA an autoimmune disease and what is the related pathogenesis

Answer 9

80% of RA patients have serum IgM or IgA autoantibodies. These autoantibodies are called rheumatoid factor/Anti-cyclic citrullinated peptide (anti-CCP)
50% of the risk of developing RA is related to genetic susceptibility due to inheritance of a HLA-DRB1 allelee

Question 10

what is the morphology of RA in the joints

Answer 10

An acute and chronic inflammatory synovitis

leads to formation of “pannus” which is a vascular connective tissue in the synovium, infiltrated by acute and chronic inflammatory cells, there is no pus formation

Question 11

due to RA what morphological signs can we see physically on the patients body?

Answer 11

Skin- rheumatoid nodules

Seen in patients with severe form of the disease, arise in pressure areas such as ulnar aspect of the forearm, elbows etc.
Microscopically palisading granuloma around a central zone of fibrinoid necrosis

Question 12

what are some clinical features of RA

Answer 12

Slow and insidious in onset

Malaise, fatigue, and
generalized muskuloskeltal pain mediated by IL-1 and TNF

After several weeks to months joints become involved

Symmetric arthritis initially of small joints before large joints are involved

Usually begins in the hands (metacarpo-phalangeal [MPJ] and proximal interphalangeal joints [PIP] and feet, followed by wrists, ankles, elbows, and knees.

Question 13

what is juvenile RA

Answer 13

Rheumatoid arthritis in one or more joints beginning under age 16 and persist for at least 6 weeks
Joint involvement is usually oligoarticular
Larger joints are affected more often than small joints
Rheumatoid nodules and rheumatoid factor is usually absent, while antinuclear antibody (ANA )is often positive

Question 14

what is a Seronegative Spondyloarthropathies

Answer 14

Pathologic changes in the ligamentous attachments rather than the synovium
Involvement of the sacro-iliac joints with or without the other joints
Absence of rheumatoid factor
Association with HLA-B27
The manifestations are immune mediated and are initiated by a T cell response

Question 15

what types of Seronegative Spondyloarthropathies do you get

Answer 15

Psoriatic arthritis
Associated with psoriasis
Affects peripheral and axial joints and ligaments and tendons
Ankylosing spondylitis
causes destruction of articular cartilage and bony ankylosis, especially of the sacroiliac and apophyseal joints

Reactive arthritis
Defined by a triad of arthritis, non-gonococcal urethritis or cervicitis, and conjunctivitis.
Arthritis appears for 6 weeks to 6 months
Enteritis associated arthritis
caused by gastrointestinal infection by Yersinia, Salmonella, Shigella, and Campylobacter,
Arthritis involves both knees and ankles sometimes wrists, fingers and toes
Lasts more for about a year, then clears

Question 16

what would be your main consern if a patient came in with a plasma urate level of 6.8mg/dl or more

Answer 16

i would suspect hyperuricemia , this could lead to gout

Question 17

is gout gout run in families

Answer 17

yes it does

Question 18

how would gout present itself

Answer 18

Gout is marked by transient attacks of acute arthritis
initiated by deposition of monosodium urate crystals in and around joints
• First attack is usually monoarticular, in the first metatarso phalangeal joint

Question 19

what body part does pseudogout target

Answer 19

involves deposition of calcium phosphate crystals, usually in the knees.

Question 20

what is a tophi

Answer 20

pathognomonic hallmark of gout • These are aggregates of urate crystals
surrounded by a foreign body granulomatous inflammation