Index to Histologic Pathology in ERG
Here are gathered the various references to illustrative examples of pathology that may be found scattered in context elsewhere in this study guide. Within each system, organs are listed from proximal to distal.
GI SYSTEM
[Tongue.] Clinically, the oral cavity provides an easy opportunity for revealing examination of a mucosal surface. For an extreme example (candidiasis), see WebPath (gross image) and WebPath (micrograph).
[Salivary glands.] Autoimmune involvement of salivary glands in Sjogren's syndrome is associated with inflammation, atrophy, and fibrosis. See WebPath or Milikowski & Berman's Color Atlas of Basic Histopathology, p. 220.
[Esophagus.] Epithelial continuity is critical for normal function. A breach in the epithelium creates an ulcer. For an image of an esophageal ulcer, see WebPath or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 162-163.
[Esophagus.] Esophageal epithelium may be transformed to a simple columnar form in the condition called Barrett's esophagus. The epithelium is variously described as resembling that of gastric mucosa (i.e., with tubular glands) or of intestinal mucosa (i.e., with goblet cells). The cause of this condition remains uncertain, but it may represent a metaplastic response to chronic inflammation (caused, e.g., by gastric reflux). Barrett's esophagus can be associated with esophageal obstruction from scarring and/or carcinoma. (For images, go to WebPath and/or see Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 234-236.)
[Esophagus.] In the esophagus, the submucosal vascular plexus includes especially large venous spaces. These may enlarge into esophageal varices, especially in cases of portal hypertension (an increase in pressure in the portal vein, due to cirrhosis). Such varices carry a substantial risk of rupture with fatal bleeding into the esophageal lumen. (For more, go to WebPath or see Robbins Pathologic Basis of Disease.)
[Esophagus.] Excessive development of collagen in esophageal submucosa, as in scleroderma, can cause a reduction in esophageal motility (see WebPath, scleroderma).
[Stomach.] Failure of the surface mucous cells to protect the stomach wall can lead to an ulcer. See WebPath (low mag), WebPath (high mag), or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 240-241.
[Liver.] Failure of adequate venous drainage from the liver leads to chronic passive congestion, with blood backing up in centrilobular areas. This gives rise to a gross appearance picturesquely labelled "nutmeg liver". For images of congested liver, see WebPath (gross) and WebPath (microscopic), or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 302.
[Liver.] A high concentration of leukocytes in portal connective tissue is a sign of inflammation, such as as in viral hepatitis (see WebPath).
[Liver.] In human liver, the appearance of connective tissue extending out from portal areas is pathological, the defining characteristic of cirrhosis. For images of cirrhosis, see WebPath or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 284ff.
[Liver.] With sufficient liver damage, many portal areas may collapse together (portal collapse, WebPath).
[Liver.] Neoplasms display abnormal architecture of hepatic parenchyma. For examples, see WebPath (hepatocellular carcinoma), WebPath (cholangiocarcinoma), and WebPath (metastatic ductal carcinoma from breast), or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 298ff.
[Gall bladder.] Inflammation of the gall bladder is a fairly common problem. For an image of cholecystitis, see WebPath or Milikowski & Berman's Color Atlas of Basic Histopathology, p. 308.
[Pancreas.] In pancreatitis, the appearance of the pancreas may be altered by inflammatory infiltrate in the stroma. In acute pancreatitis, release of pancreatic enzymes can cause proteolytic digestion and associated haemorhagic necrosis. Chronic pancreatitis can lead to atrophy and fibrosis of the parenchyma. For print images, see Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 304-306.
[Small intestine.] The structure of the intestinal mucosa may be altered by pathological processes. Examples include ischemic enteritis or necrotizing enterocolitis, both characterized by necrosis of the mucosa (see WebPath and WebPath), and malabsorption enteropathy (celiac sprue), characterized by blunting or loss of villi with concommitant loss of absorptive surface area, increased crypt length, and inflammatory infiltrate in lamina propria (see WebPath or Milikowski & Berman's Color Atlas of Basic Histopathology, p. 256, or Robbins Pathologic Basis of Disease.)
[Small intestine.] The brush border of the intestinal epithelium not only facilitates absorption, it also provides a site of attachment for pathogens. For an example (cryptosporidia), see WebPath.
[Stem cells.] The importance of stem cells in the intestinal crypts is illustrated by recovery from cholera. The cholera toxin kills the intestinal epithelium, leading to loss of bodily fluid across the mucosa, copious diarrhea, massive dehydration, and death within a few days. However, if patients can be kept hydrated for those few days, epithelial replacement by stem cell division will restore normal function.
[Appendix.] In acute appendicitis, heavy leukocyte infiltration occurs throughout the wall of the organ. For images, see WebPath (gross), WebPath (low power), WebPath (medium power), and WebPath (high power), or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 274-275.
[Colon.] For images of benign adenomatous polyps (tubular adenoma), see WebPath (gross), WebPath (low power), WebPath (medium power). Compare these growths with villous polyps, WebPath (gross), WebPath (low power); with adenocarcinomas, WebPath (gross), WebPath (low power), WebPath (medium), WebPath (high power), WebPath (higher power); and with precancerous dysplasia, WebPath. Also see Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 266-271.
[Colon.] Accumulations of lymphoid tissue are characteristic of chronic inflammatory bowel disease. For more on inflammation of the colon, see Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 258-265, or Robbins Pathologic Basis of Disease. Compare Crohn's disease, WebPath and ulcerative colitis, WebPath (low power), WebPath (high power).
MALE SYSTEM
[Testis.] Infertility due to atrophy of the testicular tubules can result from a number of causes, ranging from undescended testes (cryptorchidism) to inflammation (orchitis) to malnutrition or hormonal imbalance. For images, see WebPath and WebPath or see Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 426-427.
[Testis.] For images of tumors (seminomas and carcinomas) involving germ cells, see WebPath and WebPath or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 428-435.
[Prostate.] For lots of material related to the prostate, see the WebPath prostate tutorial. For an example of prostatic hyperplasia, see WebPath
FEMALE SYSTEM
[Fallopian tube.] For an image of salpingitis (inflammation in the fallopian tube), see WebPath.
[Cervix.] For examples of cervical dysplasia, see WebPath and WebPath.
[Breast.] For examples of breast cancer, see the WebPath and Webpath.
ENDOCRINE SYSTEM
[Pituitary.] Pituitary adenomas may be "benign" (i.e., not malignant) but can nevertheless cause significant problems either from excess hormone production or from mass effect (e.g., crowding the optic chiasm). For illustration, see WebPath.
[Thyroid.] For some examples of thyroid pathology, see WebPath (thyroiditis, inflammation), WebPath (Grave's disease, hyperthyroid), and WebPath (goiter), or Milikowski & Berman's Color Atlas of Basic Histopathology, pp. 452-461.
[Parathyroid.] For an example of parathyroid hyperplasia with prominent oxyphils, see WebPath. For a parathyroid adenoma, see WebPath.
[Adrenal.] For images of tumors leading to Cushing's disease, see WebPath (gross) and WebPath (microscopic), or Milikowski & Berman's Color Atlas of Basic Histopathology, p. 466. For gross images of adrenal hyperplasia (e.g., subsequent to Cushing's disease or ectopic ACTH production) and also adrenal atrophy, see WebPath.
[Pancreatic islets.] Diabetes may result from immunological destruction of islet cells. For images, see WebPath (diabetes I) and WebPath (diabetes II), or Milikowski & Berman's Color Atlas of Basic Histopathology, p. 469.
The following textbooks are recommended for further reading.
Color Atlas of Basic Histopathology (1997), Milikowski & Berman.
This is a picture-book, with minimal explanation, but it offers an excellent resource for images of particular pathologies.Robbins Pathologic Basis of Disease, 6th ed. (1999), Cotran, et al.
A classic textbook of pathology, which includes descriptions (but relatively few illustrations) of pathologic histology.Histology for Pathologists (1998), Sternberg.
An exceptionally detailed (and exceptionally thick) textbook of histology, with emphasis on normal structure. Although this is a reference for specialists (as the title suggests), this text is a good source for answers to details which may not be found in any of the standard introductory textbooks.
Comments and questions: dgking@siu.edu
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Last updated: 15 May 2022 / dgk