. 5
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penetrated the esophagus and is invading the aorta
from the outside.

5-20. A. Re¬‚ux esophagitis has led to ulceration of
the lower end of the esophagus with some surviving
pale islands of squamous epithelium. B. Histology of
the epithelium at the edge of the ulcerated area
shows eosinophils (circled) within the squamous
epithelium. Basal cell hyperplasia is also noted.


288 Salivary Glands and GIT

5-21. A. Esophageal surgical resection for Barrett
esophagus (pale area of mucosa) (arrows). The
external resection margins have been inked. B. His-
tology of Barrett esophagus shows the squamous
epithelium becoming almost totally replaced by
metaplastic, columnar epithelium. The diagnostic
intestinal-type goblet cells are present in the surface
epithelium. C. Low-grade dysplasia in another
patient with Barrett esophagus.


Salivary Glands and GIT 289

5-22. A. Adenocarcinoma that has arisen in an area
of Barrett esophagus is in¬ltrating the gastroe-
sophageal junction. B. Histology of the lesion shows
an invasive adenocarcinoma of intestinal type.

290 Salivary Glands and GIT


5-23. A. Acute on chronic gastritis. Note the red-
dened, granular appearance of the gastric mucosa
that also appears smoother than normal in some
areas. B. Chronic inactive gastritis. C. Histology of
chronic gastritis showing numerous mononuclear
cells (lymphocytes and plasma cells) within the gas-
tric mucosa.

Salivary Glands and GIT 291


5-24. The feature of hypertrophic gastropathy (HG) is giant cere-
briform rugal fold enlargement of the gastric mucosa. Three
conditions may produce such an appearance: M©n©trièr disease
(surface mucous cell hyperplasia with gland atrophy), hyper-
trophic-hypersecretory gastropathy (hyperplasia of parietal and
chief cells), and gastric gland hyperplasia secondary to a gastri-
noma/Zollinger“Ellison syndrome. A. Hypertrophic gastropathy
shows an exuberant expansion of rugal folds that may be mis-
taken for a neoplasm on endoscopic or radiographic examina-
tions. B. Slice of stomach showing the greatly thickened mucosal
folds of HG. C. Histology shows a marked increase in the num-
ber of the surface mucous cells consistent with M©n©trièr disease.

292 Salivary Glands and GIT
5-25. A. Lymphoid hyperplasia of the stomach pre-
senting as multiple small intramucosal nodules.
B. Multiple reactive germinal follicles are situated
in the deep aspect of the gastric mucosa adjacent to
the muscularis mucosae.


Salivary Glands and GIT 293


5-26. A. Multiple small hyperplastic polyps (cir-
cled in close-up view) of the stomach. These are the
most common type of polyp found in the stomach.
Hyperplastic polyps may occur in the atrophic body
and fundal mucosa of patients with atrophic gastri-
tis or in the antrum of patients with Helicobacter
pylori infection. These polyps have no malignant
potential (unlike adenomatous polyps). Proton pump
inhibitor therapy may lead to the formation of
benign fundic gland polyps. B. Single large hyper-
plastic polyp of the stomach. (continued on next

294 Salivary Glands and GIT

5-26. (Continued) C. Histology shows a serrated sur-
face epithelium with foveolar epithelium lining the
underlying crypts. D. Multiple tubular adenomas
(adenomatous polypi) of the stomach with atypia.
E. Histology of tubular adenoma showing mild
atypia of the surface epithelium.


Salivary Glands and GIT 295

5-27. Gastrointestinal stromal tumor (GIST) of the
stomach. A. Gastric mucosa with focal ulcerated,
excavated area (top left) overlies a submucosal
GIST. B. Transverse section of a GIST shows an area
of necrosis (left center) with ulceration of overlying
gastric mucosa.


296 Salivary Glands and GIT

5-28. A. Desmoid tumor of mesentery in Gardner
syndrome shows focal areas of necrosis and cystic
degeneration. B. Histology of desmoid tumor show-
ing interweaving fascicles of spindle-shaped cells in
a ¬brous stroma.


Salivary Glands and GIT 297

5-29. A. Acute gastric erosions (hemorrhagic gas-
tropathy) are rendered more visible by associated
super¬cial hemorrhage. B. Histology shows focal
mucosal ulceration plus intramucosal hemorrhage.


298 Salivary Glands and GIT

5-30. A. Chronic peptic ulcer of the stomach has a
sharp, punched-out edge. Probes have been inserted
into two small arteries in the ulcer base that caused
signi¬cant bleeding. B. Helicobacter pylori organ-
isms are seen on the surface epithelium. These
organisms have been implicated in the etiology of
peptic ulcers. (continued on next page)


Salivary Glands and GIT 299
5-30. (Continued) C. Healing gastric ulcer shows in-
drawing of the mucosal folds toward the ulcer mar-
gins due to contraction of ¬brous tissue. D. Healed
chronic gastric ulcer shows radiating folds pointing
to the site of the healed ulcer.


300 Salivary Glands and GIT
5-31. Massive edema of the stomach has caused
ballooning of the mucosa, and the surface has a
smoothed-out appearance. Patient had received an
excessive amount of intravenous ¬‚uids in combina-
tion with cardiac failure.

Salivary Glands and GIT 301
5-32. Foreign bodies within the stomach. A. Tri-
chobezoar (hairball) of the stomach is composed of
a mass of hairs swallowed by the patient that has
become encased by food residues and mucus. Note
that the hairball appears in the shape of a cast of
the stomach. In the Rapunzel syndrome, long
strands of hair may extend through the small gut
into the colon. (In phytobezoars, vegetable matter
takes the place of hair.) B. Left ventricular assist
device (LVAD) pump casing that eroded into and
came to occupy the lumen of the stomach. On gas-
troscopy, the endoscope viewed the serial number
of the LVAD!


302 Salivary Glands and GIT

5-33. A. Multiple small carcinoid (neuroendocrine)
tumors of the stomach. B. Histology of carcinoid
tumor showing lack of anaplasia; the size of the
tumor is more important than the histology in pre-
dicting the potential for metastasis.


Salivary Glands and GIT 303


5-34. A. This ulcerated gastric cancer has a decep-
tively sharp border suggestive of a benign gastric
ulcer. B. Section of the same lesion reveals that the
cancer is directly invading the underlying liver.
(continued on next page)

304 Salivary Glands and GIT

5-34. (Continued) C. Surgically resected gastric car-
cinoma. D. Histology of the gastric carcinoma shows
an intestinal type of adenocarcinoma. (continued on
next page)


Salivary Glands and GIT 305


5-34. (Continued) E. Diffusely in¬ltrating gastric car-
cinoma (so-called leather bottle stomach). F. Sections
of two stomachs comparing a diffusely in¬ltrating G
carcinoma (left) and a normal stomach (right). G. His-
tology shows diffusely in¬ltrating signet ring“
shaped malignant cells between smooth muscle cells
of stomach muscularis.

306 Salivary Glands and GIT

5-35. Lymphoma of the stomach. A. Mucosa shows
multiple lymphomatous nodules, some of which
have become ulcerated. (The esophagus shows glyco-
genic acanthosis.) B. Histology shows lymphoma
in¬ltrating into the mucosa from the submucosa.


Salivary Glands and GIT 307

5-36. A. Kaposi sarcoma of the stomach. The mul-
tiple highly vascular-looking tumor nodules in the
gastric mucosa should make one think of an
angiosarcoma. B. Histology shows that interweaving
fascicles of spindle-shaped cells surround many
slit-like spaces.


308 Salivary Glands and GIT


5-37. A. Duodenum contains multiple chronic pep-
tic ulcers (arrows). B. Blood cast of the duodenum
due to clotted blood from bleeding into the lumen.

Salivary Glands and GIT 309
5-38. Congenital atresia (arrow) of the duodenum:
there is no continuity between the distal stomach
(left of center) and the jejunum (far left).

5-39. Duodenal mucosa bears multiple tubular ade-
nomas (adenomatous polypi), plus an adenocarci-
noma (arrow).

310 Salivary Glands and GIT

5-40. Adenocarcinoma of the ampulla of Vater in
the second part of the duodenum. A. Tumor
obstructs the lumen of the ampulla. B. Histology
shows a well-differentiated papillary adenocarci-


Salivary Glands and GIT 311
5-41. Volvulus has led to venous infarction of the
small intestine. A. Note the purple, hemorrhagic
appearance of the dilated, necrotic gut. B. Montage
of pictures starting counterclockwise from lower
left shows (i) infarcted small gut, (ii) and (iii) his-
tologic hemorrhage ¬lling the submucosa of colon,
and (iv) extreme congestion and thrombosis of
dilated veins in bowel wall. The arteries are patent.

i ii

iii iv


312 Salivary Glands and GIT


5-42. A. Arterial ischemia of the intestine. Skip
areas of ischemic necrosis of small gut due to sys-
temic hypotension and vasoconstriction of the
splanchnic arterial bed. B. Acute necrosis of ileum
showing hemorrhagic necrosis of the mucosa.
C. Necrotizing enterocolitis due to an enterotoxin
produced by Clostridium perfringens following
ingestion of contaminated meat. This latter condi-
tion is rare in industrialized nations.

Salivary Glands and GIT 313
5-43. Diverticula of the jejunum. Diverticula may 5-44. Multiple mucosal ulcers of jejunum due to
occur anywhere in the intestines but are most com- graft-versus-host disease in a bone marrow trans-
mon in the sigmoid colon. plant recipient.

5-45. Idiopathic perforation of the ileum of a few
days™ duration showing granulation tissue and early
¬brosis at the edge of the defect.

314 Salivary Glands and GIT
5-46. Crohn disease (regional ileitis): segmental
transmural in¬‚ammation of the gut. A. Transverse
sections of ileum showing severe luminal narrow-
ing. B. Early Crohn disease with prominent in¬‚am-
mation and mucosal ulceration. C. Chronic Crohn
disease showing cobblestoning (due to edema and
in¬‚ammation) between extensive areas of linear
ulceration. (continued on next page)


Salivary Glands and GIT 315

5-46. (Continued) D. Histology of Crohn disease
showing transmural in¬‚ammation with lymphoid
germinal centers and granulomas. E. Stenosis of the
colon due to regional enteritis.

316 Salivary Glands and GIT

5-47. Ulcerative colitis (UC): chronic super¬cial
ulceration of colon and rectum. A. Erythema and
mucosal ulceration are more marked in the left colon
and rectum (right half of picture) in this total colec-
tomy specimen. Cecum and appendix are seen (bot-
tom left). B. Close-up view shows granular-looking,
acutely in¬‚amed, ulcerated surface of colon. (con-
tinued on next page)


Salivary Glands and GIT 317
5-47. (Continued) C. Histology showing a crypt
abscess (outlined in green) and basal lymphocyto-
sis. D. Rectal involvement in UC. (continued on
next page)


318 Salivary Glands and GIT
5-47. (Continued) E. Chronic UC that had biopsy-
proven multiple areas of precancerous dysplasia.
F. Pseudopolypi of the colon in UC due to nodular
regeneration of the mucosa surrounded by ulcera-
tion. G. Histology of pseudopolypi showing focally
exophytic, regenerative mucosa.


Salivary Glands and GIT 319
5-48. Intussusception of small intestine. In adults,
the condition may be precipitated by a lesion in the
bowel (e.g., Meckel diverticulum or tumor). A. Lumi-
nal obstruction has resulted from a portion of the gut
(the intussusceptum) telescoping into the surround-
ing outer portion (the intussuscipiens). B. In this
patient, the ileal intussusceptum has become
infarcted due to compression of its blood supply by
the cecal intussuscipiens. C. Intussusception of the
vermiform appendix into the cecum.



320 Salivary Glands and GIT
5-49. Meckel diverticulum (due to persistence of
the vitelline duct) is an outpouching on the antime-
senteric border of the ileum 60 to 100 cm from the
ileocecal valve. It is a true diverticulum. Rare pos-
sible complications include intussusception, bleed-
ing, in¬‚ammation (diverticulitis), perforation, and
umbilical ¬stula.

Salivary Glands and GIT 321


5-50. Masses that may protrude into the gut lumen and predispose
to an intussusception. A. Lipoma of jejunum. Yellow, fatty-looking
tumor has arisen in the submucosa and protrudes into the gut lumen.
B. Histology of lipoma shows a well-circumscribed benign tumor
composed of mature adipocytes. C. Bisected in¬‚ammatory ¬brous
tumor of small gut.

322 Salivary Glands and GIT

5-51. Dilated lacteals in ileum due to obstruction of
the lymphatic drainage. A. Dilated lacteals in the
mucosa appear as yellow nodules due to the nor-
mal absorption of lipids by the lacteals and the lym-
phatic system. If a lesion is transected, it collapses
as the obstructed lymph ¬‚uid drains away. B. His-
tology con¬rms that the lesion comprises a lacteal
distended by lymph ¬‚uid.


Salivary Glands and GIT 323
5-52. Linear distribution of ulceration of the ileum
over Peyer™s patches (mucosal lymphoid tissue) in
typhoid fever.

5-53. Circumferential ulceration of the small gut
due to tuberculous enteritis. The tuberculous infec-
tion spreads in the bowel wall via the lymphatic
drainage that is circumferentially arranged. The
probe indicates a perforation of the bowel that com-
plicated the lesion.

324 Salivary Glands and GIT

5-54. A. Radiation enteritis of the small gut. Note
the luminal narrowing and intraluminal blood clot
in the lower right picture. B. Histology of the gut
shows radiation arteriopathy, including foam cells
(ballooning degeneration of intimal cells).


Salivary Glands and GIT 325

5-55. Angiosarcoma of small intestine. A. Multiple
vascular-looking nodules are noted on the mucosal
surface and on the cut surfaces of the small gut.
B. Histology of angiosarcoma shows numerous
small vascular spaces lined by atypical-looking
endothelial cells. C. Positive CD34 staining con-
¬rms that the tumor cells are producing endothe-
lial-lined vascular spaces.


326 Salivary Glands and GIT


5-56. Intestinal atresia comes about due to vascular
compromise of a portion of the gut in utero, lead-
ing to obliteration of the bowel lumen, as well as
the gut becoming replaced by a ¬brous cord that
connects the normal proximal and distal segments.
A. Long atretic segment of small bowel comprising
a ¬brous cord devoid of any lumen. B. Short atretic
segment (arrow) separates dilated, feces-¬lled, prox-
imal segment from the distal thinner segment that
contains no fecal material.

Salivary Glands and GIT 327


5-57. Diverticular disease (diverticulosis). A. Exter-
nal appearance of colonic diverticula. B. Transverse
section showing diverticulosis. C. Histology of a
diverticulum showing herniation of mucosa through
the muscle coat. (continued on next page)

328 Salivary Glands and GIT


5-57. (Continued) D. Probe placed in a diverticulum
that has led to abscess formation as shown in the
next ¬gure. E. Pericolic abscess derived from the
in¬‚amed diverticulum shown in D. F. Healed diver-
ticulitis (top) has produced marked local ¬brosis
around the colon. The condition may mimic a
malignant stricture clinically.


Salivary Glands and GIT 329
5-58. Pseudomembranous colitis (due to Clostrid-
ium dif¬cile) following administration of antibiotics
for renal tract infection. The mucosa shows focal
super¬cial ulceration covered by a mixture of
necrotic mucosal debris and acute in¬‚ammatory

5-59. Necrotizing enterocolitis in an adult with
transmural infarction of a portion of cecum and
ascending colon due to ischemia. The bowel
mucosa is edematous and shows scattered small
ulcers with scanty-covering exudate. The condition
is more common in infants.

330 Salivary Glands and GIT
5-60. Two ischemic ulcers of the colon due to
rheumatoid vasculopathy (severe intimal thickening
of small arteries in the bowel submucosa).

5-61. Stercoral ulcers (arrows) of the colon due to
constipation; hard, dehydrated fecal material has
produced linear pressure necrosis of the colonic

Salivary Glands and GIT 331
5-62. Drug-induced toxic megacolon with focal
devitalization of the colonic wall. Toxic megacolon
may also occur in ulcerative colitis. Congenital
megacolon occurs in Hirschsprung disease.
Acquired megacolon has been associated with lax-
ative use, diabetic neuropathy, parkinsonism, sys-
temic sclerosis, and amyloidosis.

5-63. Graft-versus-host disease of the colon. Multi-
ple super¬cial mucosal ulcers are noted.

332 Salivary Glands and GIT
5-64. A. Amebic colitis has produced ulcers with a
necrotic, slough-like base, and no surrounding in¬‚am-
mation is present. (Photo courtesy of Dr. R.M. Bowen.)
B. Pathogenic amebae (Entameba histolytica) within
colonic wall deep to ulcers. The organisms produce
cytolysins that liquefy the tissue, and they also damp
down the in¬‚ammatory response. The infected colon
is very fragile and handles with the consistency of wet
blotting paper.


Salivary Glands and GIT 333
5-65. Colon-skin ¬stula (indicated by orange stick)
following abdominal trauma.

5-66. A. Candida infection of a devitalized cecum.
The ulcerated area is bile stained. B. Histology
shows Candida organisms within the necrotic cecal


334 Salivary Glands and GIT
5-67. A. Stricture (arrow) of colon due to endometrio-
sis. B. Histology shows endometrial-type glands and
stroma within the ¬brous reaction seen in A.


Salivary Glands and GIT 335

5-68. Pneumatosis cystoides intestinalis. The condi-
tion indicates the presence of gas in the bowel wall
and may affect any part of the gastrointestinal tract.
The gas may enter via a mucosal tear, be produced
by microorganisms (e.g., in neonatal necrotizing
enteritis), or be derived from an air leak in the lung
(surgical emphysema). A. Cecal mucosa bears mul-
tiple nodules due to air trapping within the mucosa.
B. Section of the cecum shows the intramucosal air
bubbles. If chronic, a giant cell response may be
elicited by the air within the tissues.


336 Salivary Glands and GIT


5-69. Polyps of the colon. A. Close-up view of mul-
tiple hyperplastic (metaplastic) polyps showing the
characteristic small, sessile, and pale appearance.
Such polyps may be found in up to 50% of colons
in adults. B. Pedunculated adenomatous polyp
(tubular adenoma). (continued on next page)

Salivary Glands and GIT 337

5-69. (Continued) C. Multiple juvenile (retention)
polyps. The two upper polyps have the typical
hyperemic, ulcerated surface of a juvenile polyp.
This patient had multiple juvenile polyposis (with
polyps distributed throughout the bowel). This con-
dition may be associated with the development of
adenomatous polypi and adenocarcinoma of the
stomach, duodenum, gut, and pancreas. D. Histol-
ogy of juvenile polyp showing cystically dilated
glands that have no epithelial atypism.

338 Salivary Glands and GIT

5-70. Familial polyposis of the colon. The diagnosis
rests on the presence of at least 100 adenomatous
polyps. A. Multiple small, widely scattered, sessile
polypi are present. B. Another patient shows more
numerous and larger adenomatous polypi. C. His-
tology of adenomatous polypi in familial polyposis.
(continued on next page)


Salivary Glands and GIT 339

5-70. (Continued) D. Surface of adenomatous polyp showing
some cellular atypism. E. Villoglandular polyp (mixed adeno-
matous and villous polyp). F. Bisected villoglandular polyp
showing central adenomatous portion (*) ringed by branching
villoglandular portion.



340 Salivary Glands and GIT
5-71. A. Villous adenoma of the colon exhibiting
the usual large, sessile, and branching appearance
of this lesion. B. Histology shows the typical
branching pattern of a villous adenoma.


Salivary Glands and GIT 341

5-72. A. Mucinous cystadenoma of the cecum. A
well-circumscribed unilocular cystic structure is
¬lled with dense mucinous material. B. Histology
shows a lining composed of benign-appearing,
columnar-shaped, mucus-secreting cells.


342 Salivary Glands and GIT

5-73. Adenomatous polyp has evolved into an ade-
nocarcinoma in the lower half of the polyp (*). This
portion of the polyp has a denser, more solid
appearance due to the increased cellular prolifera-
tion of the cancer.

5-74. A. The colon has become encircled by an ade-
nocarcinoma that is obstructing the lumen and has
invaded through the external muscle coat. B. His-
tology shows a well-differentiated adenocarcinoma.


Salivary Glands and GIT 343
5-75. A. Adenocarcinoma of the colon in a patient
with melanosis coli. The cancer contains no pig-
ment. Melanosis coli is a misnomer because no
melanin pigment is present “ the pigment is related
to lipofuscin and is derived from breakdown of cell
membranes secondary to chronic use of anthracene
laxatives. B. Histology of melanosis coli shows
macrophages in the lamina propria are ¬lled with
brown-colored lipofuscin granules.


344 Salivary Glands and GIT
5-76. Diffuse in¬ltration of colon by undifferenti-
ated signet ring cell carcinoma.

Salivary Glands and GIT 345


5-77. A. Bulky, ¬‚eshy-looking lymphoma of the colon (showing the
so-called ¬sh ¬‚esh appearance of the cut surface). B. Histology shows
a diffuse large cell lymphoma. C. Matted loops of bowel due to peri-
toneal involvement by a posttransplant lymphoma in a lung transplant
recipient. The lymphoma is related to a previous Epstein“Barr virus

346 Salivary Glands and GIT
5-79. Adenocarcinoma of the rectum.

5-78. Carcinoid tumor (arrow) of the distal ileum.

Salivary Glands and GIT 347

5-80. A. Abdominoperineal resection and left hemi-
colectomy for a cloacogenic carcinoma of the rec-
tum. This rare cancer arises from the transitional
cloacogenic zone of the anorectal junction and
behaves in an aggressive fashion. B. Histologically,
the tumor has the appearance of a basaloid squa-
mous carcinoma.


348 Salivary Glands and GIT
5-81. Malignant melanoma (arrow) of the anorectal
junction is presenting as an exophytic mass pro-
truding into the lumen.

5-82. Exomphalos (omphalocele) is a congenital
abnormality in which the abdomen fails to close
around the base of the umbilical cord producing an
umbilical hernia in which abdominal organs may
push into the umbilical cord. In this patient, small
intestine is present in the hernial sac.

Salivary Glands and GIT 349


5-83. A. Acute appendicitis with acute in¬‚amma-
tory exudate (arrow) on the serosal surface. B. Acute
appendicitis with rupture.

350 Salivary Glands and GIT
5-84. Large fecalith within a distended appendix in
a patient with cystic ¬brosis (mucoviscidosis).

5-85. Diverticulitis of the appendix with periap-
pendicular ¬brosis.

Salivary Glands and GIT 351
5-86. A. Carcinoid tumor of the distal appendix.
B. Histology shows this carcinoid tumor to be con-
¬ned to within the distal appendix.


352 Salivary Glands and GIT
5-87. Mucocele of the appendix indicates an appen-
dix whose dilated lumen is ¬lled with mucin.
Causes include proximal obstruction by a fecalith
to cystadenoma or cystadenocarcinoma. A. Inspis-
sated mucus released from an obstructed appendix
lies alongside the appendix. B. Mucinous cystade-
noma of the appendix. C. Pseudomyxoma peritonei
is compressing loops of small bowel. This condition
may result from a mucinous cystadenocarcinoma of
either the appendix or the ovary that has spread in
the peritoneal cavity.


Salivary Glands and GIT 353
5-88. Ganglioneuroma has produced thickening of
the distal portion of the appendix.

5-89. Benign cyst of the peritoneal lining of uncer-
tain origin. Peritoneal cysts may be derived from
lymphatic channels, enteric diverticula, urogenital
ridge, or healed infection.

354 Salivary Glands and GIT


5-90. Infarcted appendix epiploica may present as
a free-lying body in the peritoneal cavity. These pic-
tures show the sequence of this process. A. Twist-
ing of the base of the appendix epiploica is leading
to its infarction. B. Free-lying, infarcted, and calci-
¬ed appendix epiploica. C. Appearance of a trans-
versely sectioned appendix epiploica showing a
hollow center.

Salivary Glands and GIT 355
5-91. Foreign body in mesentery is an intrauterine
contraceptive device (arrow) that had penetrated
through the wall of the uterus to lie free in the peri-
toneal cavity.

5-92. Fibrinopurulent peritonitis in a paracolic gut-
ter secondary to bowel perforation.

356 Salivary Glands and GIT


5-93. A. Tapeworm (Taenia saginata) segments from
a stool. B. Histology shows typical ova of T. saginata
within the segments.

Salivary Glands and GIT 357
6 Female Genital Tract and Breast

6-1. Hypertrophy of the clitoris (clitoromegaly or
macroclitoris). The condition may be congenital
(e.g., due to congenital adrenal hyperplasia or due
to intersex development, graded according to
Prader) or acquired (e.g., via the administration of
androgenic anabolic steroids to females, such as the
drug Danazol given to treat idiopathic thrombocy-
topenic purpura or female bodybuilders who take
anabolic steroids). Idiopathic cases may also occur.
The normal clitoris is 4 to 5 mm long and 3 to 4
mm wide, whereas the surgically excised clitoris
shown is about 40 mm long.

6-2. A. A human papillomavirus“induced condy-
loma (arrow) is present in the short cuff of vagina
attached to a uterus that is in¬ltrated by a malig-
nant lymphoma. Note the rather ¬‚at, papillary-
appearing lesion on the vaginal lining. B. Histology
shows the typical appearance of a condyloma
acuminatum with pointed, ¬nger-like projections
covered by squamous epithelium, many of whose
cells show apoptotic changes (koilocytes).


358 Female Genital Tract and Breast

6-3. A. Bisected giant condyloma acuminatum of
Buschke“Lowenstein of the vulva (skin surface is on
the left of the specimen) due to human papillo-
mavirus infection. These large condylomata form
part of a spectrum of lesions that merge with the
concept of a verrucous carcinoma. Note how the
squamous epithelial proliferation (arrows) has pen-
etrated into the underlying vulvar soft tissue.
B. Histology shows the typical pushing margin of a
verrucous carcinoma. C. Higher-power view of the
same area shows the characteristic absence of signs
of marked anaplasia that are characteristic of an
ordinary squamous carcinoma.


Female Genital Tract and Breast 359

6-4. A. Widespread severe dysplasia and carcinoma
in situ of the vulva. The labia minora and majora
appear to be wrinkled and covered by a thicker
epithelium than normal. B. Histology shows the
junction (arrow) between normal excision margin
(left) and the carcinoma in situ (right, more
basophilic staining epithelium). Larger pink cells
overlying the midportion of the sections are squa-
mous epithelial cells probably derived from the
staining solution. C. High-power view of severe dys-
plasia of the epidermis showing an abnormal mito-
sis (center) and some super¬cial keratinization.


360 Female Genital Tract and Breast


6-5. A. Paget disease (arrows) of the vulva “ unlike the breast, there
is often no underlying neoplasm. B. Cytokeratin-stained slide
showing Paget disease of the vulva reveals malignant epithelial
cells in both the dermis and epidermis. C. Vulval excision for


. 5
( 10)