Clinical History: A 70-year-old man was referred to a gastroenterologist due to a six-month history of slowly worsening dysphagia. Esophagogastroduodenoscopy was performed and revealed a friable, necrotic, ulcerated mass. An esophagectomy was performed.
The resected esophagus contained a firm, raised, pink-gray, friable and necrotic 3.5 x 4.5 cm tumor mass, completely encircling the esophagus and producing a marked stenosis.
At one end of the section the squamous epithelium of the esophagus shows marked atypia, pleomorphism and loss of polarity, but no submucosal invasion. These changes represent carcinoma in situ. By following the mucosal lining, one comes upon an area where the cords and nests of poorly differentiated squamous cells are seen to invade the mucosa and submucosa reaching the muscular layer. At one margin of the section the tumor cells are better differentiated with production of keratin and formation of so-called epithelial pearls. Associated with the tumor are marked fibrous proliferation and intense chronic inflammatory infiltration in the stroma. The tumor invades into, but not through the muscularis externa.
For the purpose of histological descriptions, the esophagus is subdivided into upper (entirely skeletal muscle in the muscularis externa), middle (mixed smooth and skeletal muscle) and lower (entirely smooth muscle) portions. Slide UCSF 226 is from the upper 1/3; slides 126 and 153 are from the middle 1/3; and slide 155 is from the lower 1/3 (at the esophageal-cardiac junction). The esophageal epithelium[example] is the non-keratinized stratified squamous type and is supported by a connective tissue lamina propria. Note the presence of isolated lymphoid nodules[example] and scattered leukocytes in the lamina propria. A rather thick layer of longitudinally arranged smooth muscle fibers form the muscularis mucosae [example]. The connective tissue of the submucosa consists of mostly collagenous fibers with some elastic fibers and varying amounts of fat as well as submucosal sero-mucous glands which can be readily observed in both slide 126 [example] and slide 153 [example] (those in slide 155 are not very well preserved).
In the upper esophagus, as shown in Slide UCSF 226, the muscularis externa consists of both inner and outer layers of skeletal muscle only. In the middle esophagus, the muscularis externa contains a mixture of skeletal and smooth muscle as seen in slide 126[example], whereas in the lower esophagus only smooth muscle is found as seen in slide 155[example]. Present in all regions of the esophagus (upper, mid, and lower) is the myenteric (Auerbach’s) plexus[example] between the two layers of the muscularis externa (W pg 267, 14.3). For most of its extent, the esophagus is retroperitoneal, so its outermost layer consists of a connective tissue adventitia which merges with the adjacent connective tissue associated with nearby structures (such as the trachea as shown in slide 126). Below the diaphragm, however, the esophagus is suspended within abdominal cavity and is therefore covered by a connective tissue serosa as shown in slide 155.
Clinical History: A 60-year-old woman was referred to a gastroenterologist due to a one-year history of weight loss with new onset abdominal pain. Physical exam revealed occult blood present in her stool. Upper endoscopy showed a fungating, ulcerated mass in the gastric antrum and the patient underwent a partial gastrectomy.
The resected portion of the stomach showed a large fungating, partially ulcerated tumor mass in the antrum. Regional lymph nodes and a liver biopsy were free of tumor.
There is a rather abrupt change of the normal stomach mucosa to malignant tumor tissue, projecting into the lumen as a cauliflower-like mass. The tumor forms abundant irregular acini, lined by one or more layers of atypical cells with mostly large irregular nuclei and poorly defined eosinophilic cytoplasm. Atypical mitoses are moderately frequent. The tumor has infiltrated through the muscularis mucosa and the edematous submucosa and has invaded the muscle layers. The invading tumor had elicited a rather marked neutrophilic and plasma cell response.
In these slides, you can see the transition from pylorus of the stomach to duodenum of the small intestine. The pyloric region of the stomach is characterized by a thick wall due to the presence of the pyloric sphincter muscle[example], which is comprised primarily of the inner circular layer of the muscularis externa. Compare its wall thickness with that of the adjacent duodenum (W pg 273, 14.15). The pyloric glands[example] at the base of each gastric pit [ORIENTATION] are also composed again of a mostly HOMOGENEOUS population of mucous cells that are similar in appearance to those in cardiac glands although the pits are much deeper compared to cardiac glands. Present, but not seen, are stem cells and endocrine cells. An occasional parietal cell may be also found. Note that the bases of the pyloric glands abut the muscularis mucosae whereas in the duodenum, you will see abundant glands (Brunner’s glands) DEEP to the muscularis mucosae (i.e. in the SUBMUCOSA).
Clinical History: A 31-year-old woman with a ten-year history of bloody diarrhea that was adequately managed by immunosuppressant therapy presented to her primary care physician with worsening symptoms. She underwent a partial colectomy.
The mucosa showed an area of edema and hyperemia distally. This was sharply demarcated from the remainder of the colon. A superficial mucosal lesion was noted.
This section shows fulminant ulcerative colitis with areas of ulceration extending into the submucosa and also some areas of hemorrhage. While deep ulceration is seen, there is no fissuring necrosis, fibrous expansion of the submucosa, or transmural chronic inflammation, which differentiates this lesion from Crohn's disease. The base of the ulcerated area is covered by necrotic debris and fibrinopurulent or sanguinous exudate. Glands are distorted in shape, infiltrated by neutrophils, and lined by regenerating epithelium.
The colon is lined by glandular epithelium with numerous mucin secreting goblet cells. The epithelium is infolded into straight tubular glands of uniform diameter to increase the surface area available for secretion and absorption.
Clinical History: A 39-year-old man presented to his gastroenterologist with a one-day history of cramping, lower abdominal pain and bloating that he noticed about five hours after a meal. He also reported bloody diarrhea. His clinical history is significant for an 8-year history of enteritis and a one-year history of a non-healing rectal fistula. Large bowel obstruction was suspected and he underwent a partial colon resection.
The colon showed extensive ulcerations separated by pedunculated areas of hypertrophic mucosa. The intestinal wall was swollen and edematous. The serosa was thickened with fibrous adhesions.
A broad area of ulceration extends into the submucosa. The surface of the ulcer is covered by fibrinopurulent exudate overlying granulation tissue. Neutrophils infiltrate glands in the adjacent mucosa, some of which are lined by regenerating epithelium. A few crypts are distorted in shape. These features differ little from those seen in ulcerative colitis (Case No. 111). However, this section also shows transmural chronic inflammation in the form of lymphoid aggregates and granulomatous inflammation.
The colon is lined by glandular epithelium with numerous mucin secreting goblet cells. The epithelium is infolded into straight tubular glands of uniform diameter to increase the surface area available for secretion and absorption.
Clinical History: A 64-year-old woman presented to her primary care physician with a six-month history of weakness and weight loss and recent onset colicky abdominal pain and distention. Physical exam revealed occult blood in her stool and a mass was palpated in the rectum. The patient underwent total colectomy.
A tumor was present 4 cm from the anus. It was hard and had completely surrounded the bowel, reducing the lumen to less than 0.5 cm in diameter. Small tumor implants were present over the peritoneum and mesentery nearby. No distant metastases were noted.
The the lumen of the bowel can be recognized. Note the thickened bowel wall and masses of tumor surrounding fat. Under low power note the tendency in some areas toward a gland-like structure. There is considerable variation in nuclear staining, size and shape. In some areas clumps of tumor cells are in the midst of mucus which the tumor cells are producing. Note the relatively large amount of dense collagen which accompanies the tumor cells in the fat.
The colon is lined by glandular epithelium with numerous mucin secreting goblet cells. The epithelium is infolded into straight tubular glands of uniform diameter to increase the surface area available for secretion and absorption.
Absolutely critical information you must know to practice medicine is in bold font. Important information that will be needed for routine patient care is in regular font. Information about less common diseases that you may encounter in clinical practice and that will probably appear on examinations is in italics
Describe the clinical and pathologic features of disorders of the esophagus:
pathogenesis, including genetic and molecular factors
morphology, including grading and staging criteria
clinical features and course
Contrast and compare clinical and pathologic features of carcinoma of right and left colon.
Discuss carcinoid tumors of the colon, rectum, and appendix, in terms of:
pathogenesis
morphology
clinical features (including extra-colonic manifestations)
course and prognosis
Describe the etiology, pathogenesis, and morphology of appendicitis
actinomycotic appendicitis. chronic suppurative appendicitis resulting from infection by Actinomyces israelii. acute appendicitis. acute inflammation of the appendix, usually resulting from bacterial infection, which may be precipitated by obstruction of the lumen by a fecalith; variable symptoms often consisting of periumbilical, colicky pain and vomiting may be followed by fever, leukocytosis, persistent pain, and signs of peritoneal inflammation in the right lower quadrant of the abdomen; perforation or abscess formation is a frequent complication of delayed surgical intervention. bilharzial appendicitis. appendicitis caused by deposition of the eggs of the blood fluke Schistosoma mansoni in the vermiform appendix. chronic appendicitis. fibrous adhesions, scarring, or deformity of the appendix following subsidence of acute appendicitis; fibrous obliteration of the distal lumen is not abnormal in older persons; term frequently used to refer to repeated mild attacks of acute appendicitis. focal appendicitis. acute appendicitis involving only part of the appendix, sometimes at the site of, or distal to, an obstruction of the lumen. foreign-body appendicitis. appendicitis caused by obstruction of the lumen of the appendix by a foreign substance, such as a particulate foreign body. gangrenous appendicitis. acute appendicitis with necrosis of the wall of the appendix, most commonly developing in obstructive appendicitis and frequently causing perforation and acute peritonitis. left-sided appendicitis. appendicitis occurring on the left side of the abdomen, usually the left lower quadrant, due to abnormal rotation of the gut (e.g., situs inversus). lumbar appendicitis. acute appendicitis in a retrodisplaced appendix in the lumbar region. obstructive appendicitis. acute appendicitis due to infection of retained secretion behind an obstruction of the lumen by a fecalith or some other cause, including carcinoma of the cecum. perforating appendicitis. inflammation of the appendix leading to perforation of the wall of the appendix into the peritoneal cavity, resulting in peritonitis. recurrent appendicitis. repeated episodes of right lower quadrant abdominal pain attributed to recurrence of inflammation of the appendix in a person who did not have an appendectomy for prior episodes. SYN: relapsing appendicitis. relapsing appendicitis. SYN: recurrent appendicitis. stercoral appendicitis. appendicitis following a lodgment of fecal material in the appendix. subperitoneal appendicitis. appendicitis of a subperitoneally displaced appendix. suppurative appendicitis. acute appendicitis with purulent exudate in the lumen and wall of the appendix. verminous appendicitis. appendicitis caused by obstruction or in response to the presence of parasitic worms such as Ascaris lumbricoides, Strongyloides stercoralis, or the pinworm Enterobius vermicularis.
and list the most common complications.
Compare and contrast the clinical and pathologic features of
