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FEEDBACK EXERCISE 1b FOR MLS 222
EXERCISE 1b: ELABORATE
PATHOLOGY
A. ACUTE NEPHRITIS as
seen in rapidly progressive
glomerulonephritis
NORMAL HISTOLOGY
PATHOLOGIC
Crescent-shaped
Crescentic glomerulonephritis (PAS stain). Note the collapsed
glomerular tufts and the crescent-shaped mass of
proliferating parietal epithelial cells and leukocytes internal
to Bowman capsule.
The hypercellularity is caused by
(1) infiltration by leukocytes, both neutrophils and monocytes;
(2) proliferation of endothelial and mesangial cells; and
(3) in severe cases by crescent formation. The proliferation
and leukocyte infiltration are typically global and diffuse,
that is, involving all lobules of all glomeruli. There is also
swelling of endothelial cells, and the combination of proliferation,
swelling, and leukocyte infiltration obliterates the capillary
lumens.
Crescents are formed by proliferation of parietal cells and
by migration of monocytes and macrophages into the urinary
space. Neutrophils and lymphocytes
may be present.
The
crescents
may
obliterate
the
urinary space and compress
the glomerular tuft. Fibrin strands are frequently prominent
between the cellular layers in the crescents; the
escape
of
procoagulant factors, fibrin and cytokines into Bowman space
may contribute to crescent formation.
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FEEDBACK EXERCISE 1b FOR MLS 222
B. FOREIGN BODY
granuloma (tophi)
Tophi are the pathognomonic hallmark of gout. They are formed by
large aggregations of urate crystals surrounded by an intense
inflammatory reaction of foreign body giant cell. Tophi may appear
in the articular cartilage, ligaments, tendons, and bursae. Less
frequently they may occur in soft tissues (earlobes, fingertips) or
kidneys. Superficial tophi can ulcerate through the overlying skin.
Amputated great toe with white tophi involving the joint and soft
tissues.
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FEEDBACK EXERCISE 1b FOR MLS 222
Gouty tophus—an aggregate of dissolved urate crystals is
surrounded by reactive fibroblasts, mononuclear inflammatory cells,
and giant cells.
C. MILIARY TUBERCULOSIS
of the lung
Miliary pulmonary disease occurs when organisms draining
through lymphatics enter the venous blood and circulate back
to the lung. Individual lesions are either microscopic or small, visible
(2-mm) foci of yellow white consolidation scattered through the
lung parenchyma (the adjective “miliary” is derived from the
resemblance of these foci to millet seeds). Miliary lesions may
expand and coalesce, resulting in consolidation of large regions or
even whole lobes of the lung. With progressive pulmonary tuberculosis,
the pleural cavity is invariably involved, and serous pleural effusions,
tuberculous empyema, or obliterative fibrous pleuritis may
develop.
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FEEDBACK EXERCISE 1b FOR MLS 222
D. CHRONIC
GLOMERULONEPHRITIS as
seen in end-stage renal
disease
“thyroidization”
The microscopic changes involve predominantly tubules and
interstitium. The tubules show atrophy in some areas and hypertrophy
or dilation in others. Dilated tubules with flattened epithelium may be
filled with casts resembling thyroid colloid (thyroidization).
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FEEDBACK EXERCISE 1b FOR MLS 222
MORPHOLOGY:
The kidneys are symmetrically contracted and have diffusely
granular cortical surfaces. On section, the cortex is thinned, and
there is an increase in peripelvic fat. The glomerular histology
depends on the stage of the disease. In early cases, the
glomeruli may still show evidence of the primary disease (e.g.,
membranous nephropathy or MPGN). However, there eventually
ensues obliteration of glomeruli, transforming them into acellular
eosinophilic masses, representing a combination of trapped plasma
proteins, increased mesangial matrix, basement membrane-like
material, and collagen. Marked atrophy of associated tubules, irregular
interstitial fibrosis, and mononuclear leukocytic infiltration of the
interstitium also occur.
REFERENCE: Robbins SL, Cotran RS, Kumar V, Abbas AK, Aster JC. Pathologic basis of disease. 9TH ed. Philadelphia, PA: Saunders Elsevier; 2015.
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