Basic Pathology lab slides
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This document contains numerous pathology slides and descriptions of different types of cell and tissue changes seen microscopically. Some key points summarized: 1) Slides show examples of necrosis, inflammation, repair processes like granulation tissue and scarring, and various neoplastic conditions including benign tumors like lipomas and malignant tumors with areas of necrosis, abnormal mitosis, and anaplasia. 2) Specific examples include liver necrosis showing pale hepatocytes without nuclei, acute bronchopneumonia with neutrophils filling alveoli, and granulation tissue forming during repair. 3) Benign tumors discussed include pleomorphic adenomas, fibroadenomas, and mature teratomas, while malignant tumors shown
Basic Pathology lab slides
- 1. Pathology slides By the Name of Allah, The Most Gracious, The Most Merciful
- 3. Many cells have died that the tissue is not recognizable. Many nuclei have become pyknotic (shrunken and dark) and have then undergone karorrhexis (fragmentation) and karyolysis (dissolution). The cytoplasm and cell borders are no longer recognizable. In this case, loss of the blood supply from a major coronary artery led to ischemia and cell death.
- 4. Necrosis
- 5. In these images you can see this preservation of architecture: this is quite recognizably liver, despite the absence of nuclei in the hepatocytes in the affected area. Notice the thread-like bacteria present in the sinusoids: these are the organism causing the lesion! Darker staining viable hepatocytes are visible around the portal regions (right) and pale, necrotic hepatocytes are visible in the central lobular zones. Hepatocytes near the blood supply have more physiologic reserve and will be more able to fend off the infection than those in the oxygen and nutrient-poor central region: but in this case the "advantage" is moot.
- 6. Caseous necrosis and granulomatosis
- 7. A typical gross pathology finding in a case like this would look similar to those you see here. At left is an example of liquefactive necrosis in the brain, as seen at autopsy in a coronal section. The area of the cerebral infarct is grossly visible at the upper left, and can be highlighted by scrolling the cursor over the image. Notice also the formation of a "clear" area (arrow) visible in the gross specimen. Liquefactive necrosis of brain tissue in the infarcted area has occurred. At right you see the clear area at low magnification in an H&E slide. The region marked by the line is that which has been destroyed by cell death. The rest of the field is normal brain tissue.
- 8. Figure 7.11 Fat necrosis, ordinary type. Multinucleated histiocytic giant cells surround a large lipid vacuole formed by fusion of destroyed adipocytes. Scattered lymphocytes and monocytes occupy expanded spaces between cells at top.
- 9. Intracellular accumulations of a variety of materials can occur in response to cellular injury. Here is fatty metamorphosis (fatty change) of the liver in which deranged lipoprotein transport from injury (most often alcoholism) leads to accumulation of lipid in the cytoplasm of hepatocytes.
- 10. • 26. Lungs: anthracotic pigment in a patient with "black lung" disease • Note the heavy deposition of black pigment in this lung (see arrow) from a patient with coal worker s pneumoconiosis (dust- related pulmonary disease). The large spaces in the apex of this lung represent emphysema secondary to damage associated to the respiratory bronchioles from the excess anthracotic pigment. "Black lung" disease is a crippling disease and is associated with an increased incidence of TB.
- 13. A Prussian blue reaction is seen in this iron stain of the liver to demonstrate large amounts of hemosiderin that are present within the cytoplasm of the hepatocytes and Kupffer cells. Ordinarily, only a small amount of hemosiderin would be present in the fixed macrophage-like cells in liver, the Kupffer cells, as part of iron recycling.
- 14. Some of these skeletal muscle fibers here show atrophy, compared to normal fibers. The number of cells is the same as before the atrophy occurred, but the size of some fibers is reduced. This is a response to injury by "downsizing" to conserve the cell. In this case, innervation to the small, atrophic fibers was lost. (This is a trichrome stain.)
- 16. Picture 2 : Dry gangrene on hand
- 18. 2- Inflammation
- 19. Inflammatory cells.neutrophils , macrophages ,lymphocytes
- 20. The neutrophils are seen infiltrating the mucosa and submucosa of the gallbladder in this patient with acute cholecystitis.
- 21. numerous neutrophils fill the alveoli in this case of acute bronchopneumonia
- 22. there is marked laryngeal edema such that the airway is narrowed. This is life- threatening. Thus, fluid collections can be serious depending upon their location.
- 24. The arm at the botton is swollen(edematous) & reddened(erythematous)
- 25. fibrin mesh in fluid with PMN's that has formed in the area of acute inflammation.
- 26. PMN's that are marginated along the dilated venule wall (arrow) are squeezing through the basement membrane (the process of diapedesis) and spilling out into extravascular space.
- 29. purulent exudate in pericardium
- 30. Friction blister
- 33. the pericardial cavity has been opened to reveal a fibrinous pericarditis with strands of stringy pale fibrin between visceral and parietal pericardium.
- 34. Microscopically, the fibrinous exudate is seen to consist of pink strands of fibrin jutting from the pericardial surface(arrows). Below this, there are a few scattered inflammatory cells.
- 35. the yellowish fluid in this opened pericardial cavity is a purulent exudate.
- 36. A purulent exudate is seen beneath the meninges in the brain of this patient with acute meningitis from Streptococcus pneumoniae infection. The exudate obscures the sulci.
- 37. extensive purulent peritonitis that resulted from rupture of the colon. A thick yellow exudate coats the peritoneal surfaces.
- 38. The white arrows mark areas of abscess formation in the upper lobe of this lung. The liquefactive necrosis of an abscess is apparent, because the purulent contents are draining out to leave a cavity.
- 39. focal abscess in the lung. The alveoli in that area have been destroyed.
- 40. abscesses
- 41. One consequence of acute inflammation is ulceration. This occurs on epithelial surfaces. Here the gastric mucosa has been lost, or ulcerated.
- 42. Below the vocal cords in this larynx are large ulcerations. Such subglottic ulcers are produced with prolonged endotracheal intubation in which the cuff of the endotracheal tube fits too tight
- 45. he end result of inflammation can be scarring. Here, the alveolar walls are thickened and filled with pink collagen.
- 46. 3- Repair
- 48. keloid
- 49. 4- Neoplasia
- 50. Colonic polyps
- 54. Fibroadenoma
- 55. Fibroadenoma
- 56. Mature teratoma
- 57. Lipoma
- 58. Lipoma
- 60. Leiomyoma
- 62. Well differentiated squamous cell carcinoma (keratin formation-arrow)
- 63. Normal colonic mucosa vs adenoma
- 66. Anaplasia
- 67. Anaplasia
- 68. Anaplastic tumor with abnormal mitosis
- 69. Abnormal mitotic figures highly suggestive of malignancy
- 70. A, Carcinoma in situ. Low-power view shows the entire thickness of the epithelium is replaced by atypical dysplastic cells. There is no orderly differentiation of squamous cells. The basement membrane is intact, and there is no tumor in the subepithelial stroma. B, High-power view of another region shows failure of normal differentiation, marked nuclear and cellular pleomorphism, and numerous mitotic figures extending toward the surface.
- 75. Fibroadenoma of breast encapsulated small tumor is sharply demarcated from the whiter breast tissue.
- 76. Uterine leiomyoma well-defined but not encapsulated
- 77. Liver Hemangioma