Joint

Question 1

What is the articular surface of adjoinging bones made up of?

Answer 1

Hyaline cartilage (Type II collagen)

Question 2

What secretes the lubricating joint fluid?

Answer 2

Synovium lining secretes fluid rich hyaluronic acid to lubricate the joint

Question 3

What is another name for Degenerative Joint Disease?

Answer 3

Osteoarthritis?

Question 4

What is osteoarthritis? Most common cause? Risk factors? Typical joints affected? Classic presentation?

Answer 4

Progressive degeneration of articular cartilage (most common arthritis); Wear and tear; >60 yo, obesity, trauma; Hips, lower L spine, knees, distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of fingers; Joint stiffness in the morning and worsening during the day.

Question 5

Pathologic features of osteoarthritis

Answer 5

Disruption of cartilage resulting in joint space filled with “joint mice”; Eburnation (polishing) of bone; Osteophyte formation classically in DIP (Heberden nodes) and PIP (Bouchard nodes)

Question 6

What is rheumatoid arthritis? Population? Marker? Observed pathology?

Answer 6

Chronic systemic autoimmune disease; Arises classically in women of late childbearing age. HLA-DR4; Hallmark is synovitis leading to formation of a pannus (inflamed granulation tissue) and eventual destruction of cartilage and ankylosis (fusion) of the joint

Question 7

RA clinical features?

Answer 7

Arthritis w/ morning stiffness that improves w/ activity -general symmetric involvement of PIP joints (swan neck deformity), wrists (radial deviation), elbows, ankles, knees; DIP usually spared; Joint space narrowing, loss of cartilage, and osteopenia seen on xray, fever, malaise, weight loss, myalgias,rheumatoid nodules (central zone of necrosis surrounded by epithelioid histiocytes in skin and viscera), vasculitis, Baker cyst, pleural effusion, lymphadenopathy, interstitial lung disease

Question 8

RA lab findings

Answer 8

IgM autoAb against Fc portion of IgG (AKA rheumatoid factor), marker of tissue damage and disease activity, Neutrophils and high protein in synovial fluid

Question 9

Complications of RA

Answer 9

Anemia of chronic disease and secondary amyloidosis

Question 10

What is Seronegative Spondyloarthropathies? Presentation? Complications?

Answer 10

Group of joint disorders without rheumatoid factor, only axial skeleton involvement (sacroiliac joints and spine) and HLA-B27 association; Classically young adult males, with low back pain and eventual vertebral body involvement; Fusion of vertebrae (bamboo spine), uveitis, aortitis;

Question 11

What is Reiter syndrome? Population?

Answer 11

Triad of arthritis urethritis and conjunctivitis; Young adult males weeks after GI or Chlamydia trachomatis infection

Question 12

Mnemonic for Reiter syndrome?

Answer 12

Can’t see, can’t pee, can’t climb a tree

Question 13

What is Psoriatic arthritis? Clinical presentation?

Answer 13

Arthritis involving 10% people with psoriasis; Axial, peripheral joints, DIP joints of hands/feet - “sausage fingers/toes”

Question 14

What are general agents that cause infectious arthritis and the associated population involved? Typical clinical presentation?

Answer 14

N. gonorrhoeae - young adults; S. aureus - older children and adults; Classically single joint; Warm joint with limited ROM; fever, increased WBC, elevated ESR

Question 15

What is Gout? Cause?

Answer 15

Deposition of monosodium urate (MSU) crystals in tissues/joints; Hyperuricemia due to increased production/decreased excretion

Question 16

From where is uric acid derived and how is it eliminated?

Answer 16

Purine metabolism to the kidneys

Question 17

What is the etiology of primary gout?

Answer 17

Etiology unknown

Question 18

What is the relationship between leukemia (myeloproliferative disorders) and gout

Answer 18

There is a lot of cellular turnover and therefore a lot of processed purines. Therefore you can relatively easily get gout

Question 19

What is the relationship between Lesch-Nyhan syndrome and gout?

Answer 19

X linked deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) leads to hyperuricemia and gout (along with mental retardation and self mutilation). Usually, the HGPRT is used to salvage purines. If you can’t perform that, purines will be metabolized to uric acid.

Question 20

Relationship between kidney failure and gout

Answer 20

Can’t excrete uric acid and therefore you get hyperuricemia

Question 21

What is the classic presentation of gout?

Answer 21

Pain in the great toe (podagra)

Question 22

What are three common causes of acute gout?

Answer 22

High protein diet, Diuretics, and alcohol

Question 23

Chronic gout leads to:

Answer 23

Tophi - white chalky aggregates of uric acid crystals with fibrosis and giant cell reaction in soft tissue and joints and renal failure - urate crystals deposit in kidney tubules

Question 24

Gout lab findings

Answer 24

Hyperuricemia, synovial fluid with needle-shaped crystals with negative birefringence under polarized light

Question 25

What is pseudogout? What is found in the synovial fluid?

Answer 25

Resembles gout but due to deposition of calcium pyrophosphate dihydrate (CPPD); Rhomboid-shaped crystals with weakly positive birefringence under polarized light

Question 26

Mnemonic for remembering gout crystals under polarized light

Answer 26

Horizontal crystals “lay LOW and are yelLOW”. Under paraLLel light, they are yeLLow;