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Cesar Forslund, Histopathology 2009/2010

1. Acute myocardial infarction (coagulative necrosis). We can see


cardiac myocytes and the cells are dead but the architecture
could be lasting for days. The cells are lacking nucleus and stain
eosinophilic. We can also see RBC and granulation tissue

2. Gangrene in lower leg: Coagulative necrosis of striated muscle


cells, inflammatory reaction with PMN cells to the necrotic tissue,
attempted regeneration. No nuclei in necrotic cells-eosinophilia.
There is giant cells (endomysial proliferation)

3. Fat necrosis in pancreas. Islets of langerhans are necrotic showing


basophilia (accumulation of calcium soaps). These are surrounded
by fibroblasts and lymphocytes.

4. Caseous necrosis in a mediastinal lymphnode. (ziehl-neelsen). Infection


with M. Tuberculosis. Lymphoid tissue, macrophages, lymphocytes.

5. Fatty change in the liver (alcoholic). Beginning of liver cirrhosis.


Fibrous septa between vacuoles.

6. Fatty change in the liver (Freezing oil red).

7. Cholesterolosis in the gall bladder mucosa. Lipid full macrophages. We


do not have any submucosa.

8. Atrophia brunea cordis. Atrophy of the myocardium, myocytes are


thinner and slender due to severe malnutrition, presence of lipofuscin
granules

Cesar Forslund, Histopathology 2009/2010


9. Simple endometrial hyperplasia. Glandular as well as stromal hyperplasia
(stratification of the nuclei) in response to estrogen. Glands are often
cystically dilated.

10. Atrophy of the endometrium and myometrium because of lack of estrogen


stimulation in postmenopausal women. Overall thinning and reduction of
cells.

11. Nodular hyperplasia of the prostate gland, normal control. Uneven


response of the gland to a troph hormone. Glandular as well as stromal
hyperplasia. Adenomatous (prostatic glands) and stromal (loose CT)
nodules.

12. Bile stasis in the liver due to extrahepatic bile obstruction. Canalicular
and intracytoplasmic accumulation of bile pigment. A few PMN
leukocytes.

13. Amyloidosis in the kidney (kongo red stain). Systemic amyolidosis,


deposition of planar congo red molecules on the amyolid filaments and
this produces birefringence and dichroism. In Glomeruli (in the
mesangium), in afferent arteriole (in the media)

14. Seborrheic keratosis of the skin with melanin hyperpigmentation. The


melanocytes are overproductive, macrophages eat it, and keratinocytes
store it.

15. Hemosiderosis (berlin-blue/preussian blue, stains inorganic compounds


like iron). Liver-lymphnode Hepatocytes/macrophages are loaded with
hemosiderin type of iron. Cirrhosis (hemochromatosis).
16. Arterial thrombus. Laminated deposition (layers of fibrin and layers of
platelets) of blood constituents forming a solid mass obliterating the
arterial lumen. Eosinophilic granular masses.

Cesar Forslund, Histopathology 2009/2010

17. End stage lesion in Buergers disease. Fibrous replacement of a secondary


thrombotic occlusion in an inflammatory vascular disease. Obliterated
artery. Internal elastic membrane shows Spanish collar due to shrinkage of
collagen in the fibrous replacement of thrombus.

18. Necrosis of the small bowel due to incarceration. Ischemic necrosis due to
strangulation (hemorrhagic type). Palely staining eosinophilic. There is no
nuclear staining in a wall of a necrotic artery.

19. Hepar moshatum adiposum Nutmeg liver. Liver congestion from right sided
heart failure, we can see a dilated sinus system (around central vein). Fatty
change (steatosis) due to ischemia and RBCs is accumulating. And also a
small biliary congestion.

20. Hemorrhagic infarct in the lung. Pulmonary arterial obstruction, ischemia


together with pulmonary congestion. Necrotic area is eosinophilic, with
focal hemorraghes. Re-canalization of the thrombus (new formed vessels).

21. Pulmonary Edema. Transudation of fluid into the alveoli due to elevated
hydrostatic pressure because of LVF. The lumen of alveoli is filled with
pale eosinophilic material (low protein content). Carbon containing
macrophages are present and hemosiderin containing macrophages
indicate chronic pulmonary congestion.

22. Acute suppurative appendicitis. Phlegmon (spreading type). Inflammatory


exudates of PMN leukocytes. Mucosal suppurative necrosis.

23. Purulent meningitis. Infiltration of leukocytes in meninges, pus forming


(empyema in an anatomical cavity). This is generally seen in sepsis. Could
be Hemophilus (in child), Neisseria in epidemic. We can also see RBCs and
fibrocytes.

Cesar Forslund, Histopathology 2009/2010

24. Septic abscesses (micro abscesses) in the myocardium due to systemic


fungal infection (PAS stain for carbohydrates in candida albicans).
Opportunistic infection. The fungal abscesses are surrounded by
inflammatory infiltrate. PMN leukocytes.

25. Chronic non-specific salpingitis, the fallopian tube. Chronic exudative


inflammation. Inflammatory infiltrate. PMN leukocytes, macrophages,
plasmacells and lymphocytes (if lymphocytes are present, it is sign of
chronic inflammation).

26. Caseous granuloma of the lung (Ziehl-neelsen). Necrotizing granuloma.


Epitheliod cells in margin of granuloma, necrotizing center. Lymphocytes
around macrophages. Highly basophilic because of calcium deposition and
calcification.

27. Foreign body granuloma (skin) probably a surgical stitch. Undegradable


material incorporated in cytoplasm, or is surrounded by the cytoplasm of
macrophages/giantcells (fusion of numerous macrophages). Tissue is necrotic
in center, inflammatory zone around.

28. Rheumatoid nodules (subcutaneous). Chronic granulomatous inflammation


around degenerate collagen. Eosinophilic mass surrounded by epitheloid cells.
We can perhaps see Langhans type of multinucleated giant cell in the zone of
granulomatous inflammation.

29. Organized pneumonia. Chronic inflammation with organized alveolar


exudates.Alveolar spaces are obliterated by fibrous granulation tissue. Fibrous
bodies made up of capillaries, fibroblast and collagen. Plasma cells

Cesar Forslund, Histopathology 2009/2010


30. Allergic vasculitis. Local arthus reaction (T III hypersensitivity). Inflammatory
infiltrate in dermis, thickened vessels (arterioles/venules). Fibrin-deposit and
exudates of PMN leukocytes with luekocytoclasia (fragmentation).

31. Polyarteritis nodosa. Vasculitis. Deposition of immune complexes in the


vessel wall, fibrinoid necrosis. The intima and media are involved. Infiltration
of PMN leukocytes and lymphocytes.

32. Chronic synovitis in rheumatoid arthritis. Synovial joint. Autoimmune early


arthritis. The synovium is covered by fibrin, the synovial lining cells show focal
hyperplasia. Increase in chronic inflammatory cells. Perivascular lymphocytic
innfiltration.
33. Polymyositis. Skeletal muscle necrosis, chronic inflammation and repair by
fibrous CT, (paraneoplastic sign). Fragmentation of sarcoplasm inflammatory
infiltration by mononuclear cells.

34. SLE lymphadenopathy. Necrosis of the lymphoid tissue, hematoxylin bodies


formation from nuclear material involved in the immune complexes.
Eosinophilic necrotic area and small basophil foci within, resembling bacterial
colonies. A lot of lymphocytes are seen.

35. Gaucher disease, lymphnode (PAS). Accumulation of glucocerebrosidase within


macrophages due to deficiency of B-glucocerebrosidase. Numerous enlarged
capsular foci with PAS positive macrophages. We can see Gaucher cells within
capsule.
36. Gouty tophus. Deposition of uric acid crystals in soft tissues due to
hyperuricemia. Surrounded by foreign body giant cells around crystals.

37. Signet ring carcinoma in the stomach (PAS). Diffuse infiltrative pattern, mucinous
carcinoma of intracellular type. Desmoplastic in stroma (growth of fibrous
connective tissue). We cannot see gastric glands because of thickened mucosa
and muscularis. Signet rings within mucosa (they have a large amount of mucin
which pushes the nucleus out towards the periphery).

Cesar Forslund, Histopathology 2009/2010


38. Krukenberg type of metastatic ovarian carcinoma. Metastatic signet ring cell
carcinoma, desmoplastia in stroma (growth of fibrous connective tissue).
Spindle cells form fascicles and pale cell groups are made up by signet ring
cells.
39. Condyloma. Benign tumor of the stratified squamous epithelium, koilocytotic
change in the keratinocytes produced by HPV infection. Growth of fingerlike
processes that is covered by hyperkeratotic cells. In the prickle cells we can see
virus associated clear spaces
40. Bowens intraepithelial squamous cell carcinoma of the vulva. Dysplasia top to
bottom Carcinoma in Situ (CIN-III). Thickening of the stratified squamous
epithelium. Mitotic figures in all layers, and we can se dyskeratotic cells
(surrounded by char halo).

41. Keratoachantoma. Pseudomalignant epidermal growth with characteristic


architecture. Central mass of keratin surrounded by invagination of squamous
epithelium (pseudo). Chronic inflammatory connective tissue underneath.
Atypical cytologic features .

42. Squamous cell carcinoma of the penis. Invasive cancer. Infiltration of chronic
inflammatory cells. Tumor cells are poorly differentiated and do not possess
tonofilaments. Focal necrosis.

43. Basal cell carcinoma of the face. Nodular. Dermal nesting by small dark cells.
Palisaded pattern and keratin cysts occasionally. Numerous mitoses in the edges
of the tumor cell clusters.

44. Compound nevus. Migration of nevus from the junctional nests into the dermis
and aggregation. Both nevus cells and melanin-laden macrophages (melanophor
cells) are seen. Melanin pigment granules.

45. Superficial spreading malignant melanoma. Flat lesion with intraepidermal spread
and microinvasion of the dermis by malignant melanocytes. Atypical melanocytes.
Melanin-laden macrophages. Pagetoid invasion (upward spreading) by single
melanoma cells in superficial epidermis.

Cesar Forslund, Histopathology 2009/2010


46. Malignant melanoma nodular type. Vertical dermal invasion, signs of a preceeding
benign melanocytic lesion (junctional nevus). Ulcerated surface. Nevus cell nests.
Heavily pigmented invasive melanocytes. Spindleshaped tumor cells, poorly
defined. Tumor cells have a prominent nucleoli and show mitotic figures.

47. Leiomyoma with bizarre foci. Myometrial smooth muscle. Focal regressive atypia
within a benign tumor (pseudosarcomatous area). Prominent nuclear enlargements.
The tumor is made up of fascicles of typical smooth muscle cells. The bizarre foci
have irregular hyperchromatic nuclei (re/de-generative atypia).
48. Schwannoma. Benign nerve sheath tumor. Nuclear palisading and biphasic structure
Antoni A/Antoni B. In Antoni A we can see Verocay bodies, hyper cellularity. In
Antoni B we can see hypo cellularity.

49. Neurofibroma. Monophasic tumor of Scwann cells and nerve sheath fibroblasts
producing collagen fibers. Intact epidermis. Few thickened nerves pass through the
tumor. We can see Schwann cells with special immuno-histochemistry reaction.

50. Embryonal rhabdomyosarcoma (botryoid type). Malignant in Vagina or ectocervix.


Derived from mesenchymal tissue. Soft tissue sarcoma with partial differentiation
towards skeletal muscle. Rhabdomyoblast are large rounded with an eosinophilic
cytoplasm. Strap cells are present.

51. Toxoplasma lymphadenitis by toxoplama gondii. Immunoreactive follicular


hyperplasia, granulomatous lymphadenitis. Enlarged secondary lymphoid follicles.
Pale eosinophilic foci in germinal centers made up of epithelioid cells. Nucleoli
containing. Langhans type multinucleated giant cells are seen occasionally.

52. Chronic lymphocytic leukemia in the Bone Marrow. Separation of lymphoid infiltrate
from hematopoietic marrow cell population. Lymphoid cells are a monotonous
population. The Hematopoetic marrow is variable. We can see erythroid islands,
megakaryocytes, granulocyte precursors and hemosiderin containing macrophages.

Cesar Forslund, Histopathology 2009/2010


53. Follicular lymphoma. The tumor is composed of follicles made up by centrocytes (dominate) and centroblasts. The follicles are surrounded by nonmalignant cells, mostly reactive T- lymphocytes. No macrophages can be seen
in germinal centres. By immunohistochemical reactions for b-cells (CD 20, Bcl-2
oncogen), and (CD 3) T-cells.

54. Diffuse large B-cell lymphoma. Anaplastic cells, centrally located prominent
nucleoli (immunoblast). Diffuse growt pattern, large cells.

55. Gastric lymphoma of MALT-origin. Non-neoplastic lymphoid follicles coexist with


lymphoma cells. Gastric mucosa is thickened, gastric glands are missing. Diffuse
Infiltration by lymphocytes. The germinal center of lymphoid follicle is rimmed by
1-2 layers of small lymphocytes belonging to the mantle zone. Neoplastic centrocyte like cells (they have irregular shaped nuclei, loose chromatin, pale cytoplasm
keeping the nuclei apart).
56. Hodkins disease (mixed cellularity type). Hodgkins cells (mononuclear) and ReedSternberg cells (polyploidy) represent the neoplastic cell population. Numerous
atypical cells and scattered lymphocytes. Immunoperoxidase (CD15).

57. Immunoblastic lymphoma of B-cell origin. Diffuse growth pattern,


large cell lymphoma. The normal structure of the lymphnode is
replaced by proliferation of large lymphoid cells.