Pathology MCQ 12:

Pathology MCQ 12:
51-year-old man has endured episodes of intense local pain involving his left foot for the past 4 months. The pain may last hours to days. Physical examination identifies the right metatarsophalangeal (MP) joint as the focus of ten￾derness and swelling, but minimal loss of joint mobility. A painless 2-cm nodule with overlying ulcerated skin is pres￾ent on the lateral aspect of the MP joint. Beneath the eroded skin is a chalky white deposit of soft material. A firm 1-cm subcutaneous nodule on the extensor surface of the left elbow is excised and has the microscopic appearance shown in the figure. Which of the following mechanisms is most important in causing joint injury in this man?

Figure: Gouty tophi histology

          

A Activation of neutrophils by phagocytosis of uratec rystals
B Release of TNF causing acute joint inflammation
C Deposition of serum cholesterol into the synovium
D Granulomatous inflammation with Mycobacterium
tuberculosis infection
E Reduced metabolism of homogentisic acid

Explanation:
The histologic picture is that of a central amorphous aggregate of urate crystals surrounded by reactive fibroblasts and mononuclear inflammatory cells. This is a gouty tophus. Tophi are large collections of monosodium urate crystals that can appear in joints or soft tissues of patients with gout. Large superficial tophi can erode the overlying skin. Precipitation of urate crystals into the joints produces an acute inflammatory
reaction in which neutrophils and monocytes can be found. Neutrophils phagocytize urate crystals, which cannot be digested, but cause release of destructive neutrophilic lysosomal enzymes and oxygen free radicals. Release of crystals from the neutrophils perpetuates this cycle of inflammatory response. Inflammation of the joints involves different mechanisms depending on the etiology.
In rheumatoid arthritis, release of tumor necrosis factor (TNF) by macrophages plays
a central role, as evidenced by the dramatic relief provided by anti-TNF agents.
Marked hypercholesterolemia, as occurs in
familial hypercholesterolemia, can lead to deposition of cholesterol in tendons and elsewhere. When deposited in tendons,
the yellowish lesions are called xanthomas; the cholesterol crystals appear microscopically as clefts in the tissue.
Extrapulmonary Mycobacterium tuberculosis infection can cause granulomatous inflammation and chronic arthritis and skin
lesions, but there is caseous necrosis with epithelioid cells and no urate crystals. Tuberculous arthritis, in contrast to gouty
arthritis, almost never begins in the MP joint. Reduced metabolic breakdown of homogentisic acid occurs in the inborn
error of metabolism known as alkaptonuria, and deposition of homogentisic acid (ochronosis) in cartilage causes an arthritis
that typically affects large joints, such as knees, intervertebral disks, hips, and shoulders, but small joints of the hands and feet are spared. So the correct option is AP. C-Easynotecard)
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