Joint

Question 1

Synovial Joint Anatomy

Answer 1

Connection between two bones. Articular surface of adjoining bones is lined by hyaline cartialage (made of collagen II) that is surrounded by a joint capsule lined with synovium that secretes hyaluronic acid that lubricates the joint

Question 2

Degenerative Joint Disease

Answer 2

Osteoarthritis is degeneration of articular cartialage due to WEAR + TEAR (increases with age, obesity, and trauma)
Affects: Hips, lower lumbar spine, knees, and Distal Interphalangeal joints (DIP), AND Proximal Interphalangeal Joints (PIP)
Joint stiffness that gets WORSE throughout the day
Pathology includes : diruption of catrialage leads to “joint mice” floating in joint space, ebuneration (polishing) of bone due to bone on bone, and osteophyte formation (classically on DIP = herben nodes and PIP = Bouchard nodes)

Question 3

Herben Node vs Bouchard Node

Answer 3

osteophyte on DIP vs PIP

Question 4

Anatomy of Rheumatoid Arthritis

Answer 4

Chronic systemic autimmune disease (so women of late childbearing age) and associated with HLA-DR4
Involves joints vis synovitis that leads to formation of a panus (inflammed granulation tissue)
The inflammed granulation tissue has myelofibroblasts that contract and can pull joints closer together and fuse them = ankylosis or pull them in different direction = bent fingers

Question 5

Ankylosis

Answer 5

Fusion of joints usually seen in Rheumatoid Arthritis as a result of myelofibroblasts in pannus

Question 6

Clinical Features of Rheumatoid Arthritis

Answer 6

Morning stiffnes that IMPROVES with activity
Symmetric involvement of PIP joints of fingers = swan neck deformity, radial deviation of wrist, elbows, ankles, knees.
DIP IS SPARED
Fever, malaise, weight loss, and myalgia
Rheumatoid nodules = central zone of necrosis by epitheliod histiocytes (in skin and visceral organs)
Vasculitis
Baker Cyst
Pleural effusions, lymphadenopathy, and interstitial lung fibrosis

Question 7

Lab findings in Rheumatoid Arthritis

Answer 7

IgM autoantibody agsint Fc portion of IgG = rheumatoid factor. Marks tissue damage and disease activity
Neutrophils and high protein in synovial fluid

Question 8

Complications of Rheumatoid Arthritis

Answer 8

Anemia of chronic disease = get acute phase reactants like hepcidin that blocks ability to use Fe stored in macrophages
SAA is another acute phase reactant that is converted to AA which depositis in tissues and causes secondary amyloidosis

Question 9

Seronegative Spondyloarthropathies

Answer 9

Joint disorders characterized by lack of rheumatoid factor (IgM to Fc portion of IgG), involve axial skeleton, and HLA-B27
Includes Ankylosing Spondyloarthritis, Reiter syndrome, and Psoriatic Arthritis

Question 10

Ankylosing Spondyloarthritis

Answer 10

young adults (usually MALE), involves sacroilliac joints and spine.  Presents with lower back pain that progresses to fusion of vertebrae (bamboo spine)
Extra articular manifestation include uveitis, and aortitis (that can lead to aortic regurge via aneurysm that pulls on aortic valve)

Question 11

Reiter Syndrome

Answer 11

Cant see (conjunctivitis), cant pee (urethritis), cant climb a tree (arthritis)
Usually young adult males weeks after GI or Chlamydia infection

Question 12

Psoriatic Arthritis

Answer 12

10% of cases of psoriasis

Axial and peripheral joitns. Most commonly DIP of hands and feet and presents as SAUSAGE fingers or toes

Question 13

Infectious Arthritis

Answer 13

Arthritis due to usuaully a bacterial infection (n gonorrhea or S aureus)
Usually involves a single joint (knee) that presents as warm, limited motion, fever, increased WBC, and elevated ESR.
Treat with antibiotic quickly

Question 14

Steps of purine metabolism

Answer 14

1) DNA+RNA
2) broken down to AMP and GMP respectively
3) Broken down to hypoxanthine and Guanine respectively
4a) can be recylced via HGPRT to be used to make DNA and RNA
4b) Converted to xanthine
5) Converted to Uric Acid via Xanthine Oxidase
6) Uric acid is pushed out of cell and filtered out by the kidney

Question 15

Gout

Answer 15

Deposition of monosodium urate (MSU) crystals in tissues especially the joints.
Due to hyperuricemia as a result of increased prodcution of Uric acid or decreased excretion

Question 16

Primary Gout

Answer 16

Unknow etiology but is most common

Question 17

Secondary Gout

Answer 17

seen in

1) Leukemia and myeloproliferative Disorders = increased cell turnover leads to hyper Uricemia
2) Lesh-Nyhan Syndrome = X linked deficiency of HGPRT so cant recycle hyp[oxanthine and guanine so get increased uric acid. Also get mental retardation and self mutilation
3) Renal Insufficency = cant excrete Uric acid and get gout

Question 18

Leukemia and myeloproliferative Disorders

Answer 18

increased cell turnover leads to hyper Uricemia leads to gout

Question 19

Lesh-Nyhan Syndrome

Answer 19

X linked deficiency of HGPRT so cant recycle hyp[oxanthine and guanine so get increased uric acid. Also get mental retardation and self mutilation

Question 20

Renal Insufficency

Answer 20

cant excrete Uric acid and get gout

Question 21

Acute Gout

Answer 21

Very painful arthritis of the great toe (podgra). Commonly seen after excessive consumption of meat or alcohol

Question 22

Chronic Gout

Answer 22

Development of tophi (white chalky aggregates of uric acid crytsals with fibrosis and giant cell reaction in soft tissue and joints
Renal failure = urate crytsals deposit in kidney tubules

Question 23

Lab Findings of Gout

Answer 23

Hyperuricemia, synovial fluid shows NEEDLE shaped crystals with negative bifringence under polarized light (look yellow)

Question 24

Pseudogout

Answer 24

Resembles gout clinically but is due to deposition of calicum pyrophosphate dihydrase (CPPD) and see RHOMBOID crystals with weakly positive birefrinegence