Basic Pathology lab slides

1. Pathology slides
By the Name of Allah,
The Most Gracious, The Most Merciful

2. 1- cell injury

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.

12. Liver hemochromatosis

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.

23. Erythema (redness)

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.

27. Pleural effusion (serous)

28. Pleural
effusion(serosanguinous)

29. purulent exudate in pericardium

30. Friction blister

31. Serous acute inflammation

32. Fibrinous pericarditis

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

44. Esophageal acute ulcer

45. he end result of inflammation can be scarring.
Here, the alveolar walls are thickened and filled
with pink collagen.

46. 3- Repair

47. Granulation tissue

48. keloid

49. 4- Neoplasia

50. Colonic polyps

51. Colonic polyps
(adenoma)

52. Pleomorphic adenoma

53. Pleomorphic adenoma
(high magnification)

54. Fibroadenoma

55. Fibroadenoma

56. Mature teratoma

57. Lipoma

58. Lipoma

59. Mature adipose tissue
(lipoma)

60. Leiomyoma

61. Leiomyoma
smooth muscle bundles

62. Well differentiated squamous
cell carcinoma (keratin
formation-arrow)

63. Normal colonic mucosa vs
adenoma

64. Moderately differentiated
adenocarcinoma

65. Moderately differentiated
Liposarcoma

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.

71. Well encapsulated
schwannoma

72. Hepatic
adenoma(encapsulated)

73. Liver adenoma(encapsulated)
low magnification

74. Liver adenoma(encapsulated)
higher magnification

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

78. Hemangioma of skin

79. Infiltrating breast carcinoma