Study guide for pathol 750: “General Pathology” goals and objectives



Download 74.88 Kb.
Page1/3
Date28.01.2017
Size74.88 Kb.
  1   2   3
STUDY GUIDE FOR PATHOL 750: “General Pathology”
GOALS AND OBJECTIVES
To synthesize characteristics of disease processes based on etiology (cause) and pathogenesis (mechanism of expression).
To understand how disease processes affect physiological function (pathophysiology)
To trace pathologic processes from a molecular event to cellular alterations and to changes in organ function and appearance

To describe the size, shape, color, consistency, and location of gross anatomic abnormalities


To recognize and describe abnormal features of gross and microscopic specimens that ares common to all organ systems, and to categorize them into the 5 major pathologic processes:

Inflammatory/Infectious/Immunologic

Vascular/Hemodynamic

Developmental/Genetic

Neoplastic

Environmental/Nutritional


To describe microscopic characteristics of individual cells (cytology) including their size, shape, and color (staining characteristics), and microscopic characteristics of groups of cells (architecture) and the relationships between individual cells and surrounding structures
To use the microscope to reinforce knowledge obtained from other sources
To distinguish preparation or fixation artifacts from abnormalities of disease

Cellular Adaptation, Injury, Death
From the PATHOL 750 teaching collection

    1. Necrosis, pancreas and fat: The underlying cause of necrosis in this tissue is the thrombosis present in the vessel at the lower left of the slide. This has led to coagulative necrosis within pancreatic tissue. Few acini are full-sized. Acini are also disrupted and infiltrated with primarily mononuclear inflammatory cells. Fat necrosis is present at the lower right of the slide. The cell membranes of necrotic adiopcytes are fuzzy, rather than sharply defined. Fat necrosis occurs when injured pancreatic acinar cells release lipolytic enzymes. These enzymes liquefy the adipocyte membranes and release fatty acids from triglycerides. The fatty acids combined with calcium to form insoluble salts that are visible as basophilic deposits on the damaged membranes.




    1. Cirrhosis, liver; Pancreas: Cirrhosis is defined by 3 characteristics, all of which are well-demonstrated in this section: 1) bridging fibrous septae that form delicate bands or broad scars that link portal tracts with one another and with the central veins; 2) parenchymal nodules that contain proliferating hepatocytes encircled by fibrosis. The diameters of the nodules can be small (<3 mm in the case of micronodular cirrhosis) to quite large (can be several cm in diameter in macronodular cirrhosis); and 3) disruption of the architecture of the entire liver. Bile duct profiles are evident within the fibrous tissue that is present between nodules. The section of pancreas on this slide is normal.




    1. Healed myocardial infarct: Infarcted myocardial tissue has been replaced by scar tissue (collagen).




    1. Recent myocardial infarction. Infarcted muscle fibers (upper left of slide) are surrounded by an inflammatory infiltrate that contains large numbers of neutrophils, dating this infarct to 1-3 days prior to death. Contraction bands are also evident in adjacent tissue. Slide 4a is a duplicate of this slide


Additional slides from the Duke Medical School teaching collection: “Pathology_200 Slides” folder

14 Acute Tubular Necrosis, Kidney

31 Recent Myocardial Infarct

35 Recent Infarct, Kidney

40 Pulmonary Edema

85 Fatty Liver (lipid accumulation)

95 Hemorrhagic Infarct, Ileum

202 Nodular hyperplasia, prostate

203 Verruca Vulgaris (hyperplasia)

286 Healed myocardial infarct

370 Infarct of Brain

429 Hyperplasia, thyroid (colloid nodule)

Inflammation and Tissue Repair
From the PATHOL 750 teaching collection

2-1: Ulcer, stomach: The gastric epithelium has been artifactually lost over both of these sections. Nonetheless, it is easy to identify the location of the ulcer, where the mucosa has been lost. The remaining tissue at the ulcer site (called the ulcer bed) is composed of granulation tissue, along with acute and chronic inflammation. Bacterial colonies are evident in tissue adjacent to the ulcer.


2-2: Bronchopneumonia: The 2 sections of lung show patchy consolidation. Affected alveoli are packed with inflammatory cells, including neutrophils. Other alveoli show evidence of edema, with pale pink-staining fluid present within the alveoli.
2-3: Ulcer, esophagus; Stomach: The section of stomach is mostly normal. Normal stratified squamous epithelium is present on one end of each of the 2 sections of esophagus, however the epithelium is absent from the middle and other end of the tissue. The tissue underlying the epithelial defect contains numerous inflammatory cells, many small blood vessels, and plump fibroblasts that are synthesizing collagen. These are characteristics of granulation tissue that characterizes the ulcer bed.
2-4: Lobar pneumonia: Alveoli are uniformly filled with an inflammatory infiltrate consisting of neutrophils, macrophages, lymphocytes, and erythrocytes.
Additional slides from the Duke Medical School teaching collection: “Pathology_200 Slides” folder

17 Proliferative Glomerulonephritis, Severe, Advanced (Chronic)

39 Bronchopneumonia

46 Organizing Bronchopneumonia

54 Acute Suppurative Appendicitis with Perforation

81 Micronodular Cirrhosis

89 Acute and Chronic Cholecystitis

93 Acute and Chronic Pancreatitis

98 Silicosis of the Lung

123 Acute and Chronic Salpingitis

143 Foreign Body Reaction

240 Chronic Gastric Ulcer

Hemodynamic and Vascular Disorders
From the PATHOL 750 teaching collection

3-1: Atherosclerosis, coronary artery. The slide contains 4 cross-sections of coronary artery that demonstrate varying degrees of lipid accumulation in the intima and calcification.


3-2: Pulmonary embolism, lung. Both sections of lung contain occlusive emboli in a large branch of the pulmonary artery.
3-3: Infarct, spleen.
3-4: Coagulative necrosis, liver. The necrosis occurs in a centrilobular pattern, with necrotic tissue present surrounding the central vein. This is the pattern typically observed when the liver experiences ischemia. The periportal areas are relatively preserved since oxygen levels are highest there.
3-5: Thrombosis, periprostatic veins. Note the laminar (many layered) nature of the clot and its adhesion to the vessel wall.
3-6: Thromboembolus in an atherosclerotic vessel, lung. Numerous macrophages filled with the golden-brown pigment hemosiderin are present within the alveoli. Cholesterol clefts are prominent in the media of the atherosclerotic vessel. A longitudinal section of embolus attached to the pulmonary artery is also present on the section.
3-7: Hemorrhage and infarction, lung. Most of the alveoli contain numerous red blood cells. Several foci of hemorrhagic infarction are present. In these areas, the outlines of the alveoli can still be discerned but the alveolar epithelial cells have experienced karyolysis. This is an example of coagulative necrosis due to infarction.
3-8: Multiple pulmonary emboli, lungs. Thromboemboli are present in many small and medium-sized vessels in all 3 sections of the lung.
3-9: Congestion and acute tubular necrosis, kidney. Tubules show coagulative necrosis as well as signs of regeneration. The medullary vessels are distended with blood (congestion).

.

Additional slides from the Duke Medical School teaching collection: “Pathology_200 Slides” folder



14 Acute Tubular Necrosis, Kidney

28 Dissecting Aneurysm, Ascending Aorta, with cystic medial necrosis

31 Recent Myocardial Infarct

35 Recent Infarct, Kidney

40 Pulmonary Edema

95 Hemorrhagic Infarct, Ileum

158 Pulmonary Embolism and Hemorrhagic Infarct

286 Healed myocardial infarct

370 Infarct of Brain Pathology of Infectious Diseases
From the PATHOL 750 teaching collection

4-1: Adenovirus infection, liver. Adenovirus replication occurred unchecked in this patient with severe combined immunodeficiency, leading to destruction of much of the liver. Hepatocytes with bizarre smudgy nuclei that are adjacent to the necrotic regions are adenovirus-infected cells.


4-2: Fungal abcess, lung. The lesion extends through the pleural surface of the lung. Note the ring of neutrophils that surround the mass of necrotic tissue. The fungal hyphae can be seen quite well, particularly at the edges of the abcess, despite the lack of specific fungal staining.
4-3: Fungal thrombosis and abcess, lung. Note the fungus-filled vessels in the center of the one of the 2 abcesses present. The accompanying methenimine silver stain highlights the fungal hyphae, but they can be seen quite well on the H & E-stained section. The section of bronchus demonstrates extensive squamous metaplasia. The remaining normal respiratory epithelial cells have enlarged nuclei, some with nuclear inclusions, consistent with viral infection. Parainfluenza virus was cultured from this patient and bronchial infection was confirmed by immunostaining.
4-4: Parainfluenza virus infection, lung. The section demonstrates areas of hemorrhage and organizing pneumonia with numerous giant cells resulting from parainfluenza virus infection. The giant cells are formed by fusion of virally-infected alveolar epithelial cells. Note on the accompanying immunostain that all giant cells do not react with the parainfluenza virus antibody. It is not known if this is artifactual or if it reflects the particular stage in the life cycle of the virus within those cells. Also note that a brown color does not always represent positive immunostaining, since hemosiderin-laden macrophages are also common in this section.
Additional slides from the Duke Medical School teaching collection: “Pathology_200 Slides” folder

39 Bronchopneumonia

281 Aspergillosis, Lung (SILVER)

451 Miliary Tuberculosis of Lung

452 Caseous Pulmonary Tuberculosis

Immunopathology
From the PATHOL 750 teaching collection

5-1: Liver with necrosis and regeneration (cirrhosis) due to autoimmune hepatitis.


5-2: Rheumatoid arthritis, synovium. The synovial lining is hyperplastic, with multiple layers of macrophage-type lining cells rather than the normal single layer of cells. The prominent mononuclear cell infiltrate contains many plasma cells. Multiple irregularly shaped dark purple calcifications are present in the tissue.
5-3: Rheumatoid arthritis, synovium. Note the prominent villous architecture containing numerous lymphoid nodules.
5-4: Rheumatoid nodule, subcutaneous tissue. Irregularly shaped regions of necrotic material are surrounded by palisading macrophages.
5-5: Thymus, spleen, and lymph node from patient with severe combined immunodeficiency (SCID), with fungal abcess present in mediastinal tissue. The thymus is markedly abnormal, consisting almost exclusively of small nests of thymic epithelial cells surrounded by adipose tissue. No Hassall’s bodies are present. Sections of 2 lymph nodes show near total absence of lymphocytes. No primary or secondary follicles are apparent. Lymph node sinuses are filled with macrophages, some of which contain ingested red blood cells (hemophagocytosis). The spleen similarly shows absence of lymphocytes and appears to be composed solely of red pulp. This profound immunodeficiency left the patient vulnerable to severe disseminated fungal infection, which was a major contributor to his death. Fungal hyphae are identifiable around the edge of the absess. Note that the abcess is surrounded by neutrophils and their debris (neutrophil function is not affected in SCID).
5-6: Hashimoto’s thyroiditis. The thyroid is enlarged and contains a large lymphoid infiltrate, arranged in nodules containing germinal centers.
Additional slides from the Duke Medical School teaching collection: “Pathology_200 Slides” folder

17 Proliferative Glomerulonephritis, Severe, Advanced (Chronic)

18 Acute Proliferative Glomerulonephritis with Crescents

19 Amyloid - Liver and Kidney

26 Polyarteritis Nodosa

111 Ulcerative colitis

121 Rheumatoid Nodule

133 Crohn’s disease

264 Hashimoto's Thyroiditis

Neoplasia
From the PATHOL 750 teaching collection

6-1: Adenomatous polyp, colon: Note the normal appearance of the colon tissue surrounding the lesion, with simple columnar epithelium containing basal nuclei that occupy ~25% of the height of the cell and abundant mucin production. This normal mucosa is present along most of the “stalk” and then transitions abruptly to adenomatous mucosa. The adenomatous changes include nuclear enlargement, such that nuclei occupy 50% or more of the height of the cell. Nuclei are hyperchromatic, have abundant nucleoli, and vary in size from cell to cell. Rather than staying close to the basal portion of the cell, nuclei may be found in the upper portions of the cell (this is loss of polarity). Note the increasingly complex foldings of the adenomatous mucosa compared with normal mucosa. This polyp is classified as demonstrating low grade dysplasia since the complex “gland within a gland” or back to back arrangement of glands characteristic of high grade dysplasia are not present. This polyp is best classified as pre-malignant, neoplastic lesion.


6-2: Invasive adenocarcinoma of the colon. A small focus of normal non-neoplastic mucosa is located on the far right of the slide. The remaining epithelium is neoplastic and located on the surface (in situ) and invading through the wall of the colon. Note the similarity of the cytologic features of the neoplastic cells to those observed in the adenomatous polyp (slide 6-1). Nuclei are enlarged (in most cells they take up more than 50% of the height of the cell), hyperchromatic with multiple nucleoli, vary in size and shape, and lack polarity. Mitotic figures and apoptotic cells are frequent. The invasive neoplastic cells form glands, so this lesion is classified as an adenocarcinoma. Many of the neoplastic glands contain necrotic material with bits of strongly basophilic material in their lumen, the so-called “dirty necrosis” that is characteristic of colon carcinomas. Note the fibrosis that accompanies invasion of the carcinoma into the submucosa (this is called a ‘desmoplastic” response). The pools of mucin containing clusters of the neoplastic cells that produced them that are present in the submucosa are also commonly observed in adenocarcinomas of the colon.
6-3: Sarcoma, metastatic to lung: The nodule of sarcoma dominates the slide, however fairly normal lung tissue can be identified to the right of the slide. The center of the lesion is necrotic (eosinophilic remnants of cell bodies remain, but nuclei are absent) due to tumor growth outstripping its blood supply. The neoplastic cells are spindle-shaped and have some resemblance to smooth muscle cells. Although this tumor is compressing the adjacent lung over most of its perimeter, foci of distinct invasion can be seen at the upper right of the slide.
6-4: Lung with adenocarcinoma. Note the large necrotic center of the tumor nodule. Invasion of the tumor cells into the surrounding lung tissue can be seen in multiple foci. The neoplastic glands are secreting large amounts of mucin.
6-5: Squamous cell carcinoma of the lung. Note the replacement of a portion of the bronchial epithelium with neoplastic squamous cells that invade deeply into the lung parenchyma in the center of the piece of tissue on the right of the slide. The neoplastic cells are present in sheets that somewhat resemble cells present in the skin, with focal secretion of keratin. However, as characteristic of neoplastic cells, the tumor cell nuclei are enlarged, hyperchromatic, and vary in size and shape. There is a desmoplastic response to the presence of tumor, with increased deposition of fibrous tissue adjacent to and between groups of tumor cells.
6-6: Leiomyoma of the uterus. This is a benign smooth muscle tumor that grows and pushes the surrounding tissue out of the way rather than invading. The cells in the leiomyoma very closely resemble their normal counterparts in the surrounding myometrium. However, their abnormal growth has resulted in the grossly apparent mass. Because the smooth muscle cells in this lesion are not incorporated into the rest of the myometrium, leiomyomas impede the contractility of the uterus.
Additional slides from the Duke Medical School teaching collection: “Pathology_200 Slides” folder

5 Adenocarcinoma of Prostate

33 Papillary Transitional Cell Carcinoma of Urinary Bladder

79 Cortical Adenoma, Adrenal

84 Adenocarcinoma of Rectum

134 Adenocarcinoma of Colon

139 Colon carcinoma, metastatic to liver

154 Squamous Cell Carcinoma of the Larynx

155 Cavernous Hemangioma of Liver

166 Tubulovillous Adenoma (Polyp) of Colon

170 Cartilaginous Hamartoma

199 Infiltrating Ductal Carcinoma of the Breast

220 Leiomyoma of Uterus

223 Osteogenic Sarcoma of Bone

227 Basal Cell Carcinoma

253 Adenocarcinoma of Stomach (Intestinal Type)

329 Medulloblastoma

427 Chromophobe Adenoma, Pituitary

430 Papillary Carcinoma of the Thyroid

Genetic and Developmental Disorders
From the PATHOL 750 teaching collection

7-1: Skin, epidermolysis bullosa. . Epidermolysis bullosa is characterized by blister formation in response to mechanical trauma. This 3 year old had blistering over 60% of her body. Note the separation of the epidermis from the dermis at the dermal-epidermal junction. A careful examination of the cleavage plane shows accumulation of fluid and necrotic material, indicating that the cleavage occurred in vivo and is not an artifact of slide preparation. Mutations in genes coding for laminin 5 subunits (3 chain, laminin 3 chain (this is the most commonly observed mutation), laminin 2 chain), collagen XVII, 6 integrin, and 4 integrin have been demonstrated to cause this form of epidermolysis bullosa.



7-2: Exocrine atrophy of the pancreas, cystic fibrosis. At first glance, this tissue looks just like adipose tissue with scattered cellular foci that could be mistaken for inflammation. However, a closer look at these foci shows that the cells have too much cytoplasm to be lymphocytes and seem to have cellular connections that are not present between leukocytes. The tissue was obtained from the normal anatomic location of the pancreas and represents end-stage atrophy of the exocrine portion of the pancreas. This results from plugging of pancreatic ducts by the highly viscous secretions that are characteristic of cystic fibrosis and self-digestion via the pancreatic enzymes.
7-3: Lung, cystic fibrosis. The greatly enlarged bronchi containing inspissated mucus are characteristic of the process of bronchiectasis and are readily visible on examination of the slide without magnification. Bronchial inflammation (acute and chronic bronchitis) and acute and chronic bronchopneumonia with scarring are also present.
7-4: Heterotopic pancreas, small bowel. This lesion was discovered incidentally at autopsy, since it resulted in a grossly detectable nodule in the wall of the small bowel. Microscopic examination reveals tortuous duct profiles, lined by normal-appearing simple columnar epithelium. Ghosts of acini formed by pancreatic secretory epithelial cells can be seen in the bowel wall, with more viable cells present closer to the serosal surface. The presence of histologically normal tissue in an unusual place is called heterotopia. It represents a developmental defect rather than a neoplasm.
7-5: Thymus, severe combined immunodeficiency. The thymus is small grossly. Microscopically, it consists of islands of thymic epithelial cells embedded in adipose tissue. Rather than the normal light lacy network of thymic epithelial cells that results from their multiple processes that enfold the developing thymocytes, these epithelial cells are in contact with each other. Some foci of epithelial cells exhibit a “pseudo-rosette” arrangement. Lymphocytes are almost totally absent. Hassall bodies form as the result of interactions between thymic epithelial cells and thymocytes, thus they are typically absent when thymopoiesis has not occurred.
7-6: Liver, Hurler’s syndrome. The liver was grossly enlarged. Many hepatocytes appear pale and vacuolated due to accumulation of storage product. Hurler’s syndrome is due to -L-iduronidase deficiency , which leads to faulty degradation of dermatan and heparan sulfate and storage of these undegraded glycosaminoglycans in organs and connective tissue. The storage product is highly water-soluble, but can be demonstrated using a colloidal iron stain.
7-7: Heart, sialic acid storage disease. The cardiac myocytes are enlarged by vacuoles that appear empty due to loss of the highly water-soluble storage product during tissue processing. The disease results from a defect in the transporter that transports sialic acid out of lysosomes following degradation of proteins that contain this molecule. The disease is fatal during infancy due to organ dysfunction that results from the sialic acid-filled lysosomes.
7-8: Skeletal muscle and cartilage, centronuclear myopathy. The striated muscle tissue on this slide clearly must be skeletal muscle, given its proximity to the cartilage (which was obtained from a rib). However, the muscle fibers are thin and poorly developed. Rather than having nuclei on the outside, between 25 and 50% of the fibers have nuclei present in their central portion. Centronuclear myopathy (also known as myotubular myopathy) is a congenital disorder with 3 subtypes based on the age of onset of clinical disease. The early or infantile form presents as a floppy infant at birth. The juvenile form is the most common and presents in late infancy with slowly progressive muscle weakness. The adult form has a relatively benign course. The infantile form of centronuclear myopathy shown here is rare, with only 15 families described in the literature by 1990 (Darnfors et al. Clin. Genetics 37:335-340, 1990). It has an X-linked recessive form of inheritance. Affected infants are severely hypotonic with respiratory distress. Prenatally, these infants exhibit polyhydramnios and weak fetal movements (Donders et al. Eur. J. Obstet. Gynecol. Reprod. Biol. 24:33-38, 1987). The neonatal mortality is 80%. The major histologic findings are muscle fibers with centrally placed nuclei in 10-50% of fibers, with perinuclear halos (Sasaki et al. Brain Develop. 11:26-32, 1989). All of these features were present in the current case.

The gene for this disorder was localized by positional cloning to Xq28, corresponding to the myotubularin locus. Myotubularin has a tyrosine phosphatase (PTP) domain and is highly conserved through evolution. A variety of mutations were discovered in patients with X-linked centronuclear myopathy, including point mutations, deletions, and splice mutations. Five point mutations were found in multiple unrelated patients, accounting for 27% of the observed mutations. The possibility of detecting mutations and determining carrier status in a disease with a high proportion of sporadic cases is of importance for genetic counselling. More than half of these mutations are expected to inactivate the putative enzymatic activity of myotubularin, either by truncation or by missense mutations affecting the predicted PTP domain.


7-9: Liver, adult polycystic kidney disease. The liver has focal steatosis. Other notable lesions are a proliferation of large often tortuous bile ducts, both on the surface of the liver and within the parenchyma. This lesions are called biliary microhamartomas or Von Meyenberg Complexes. The pathogenesis of these lesions is not well-understood, but they are commonly observed in patients with polycystic kidney disease, suggesting a defect shared between kidney tubular and biliary epithelial cells. The lung tissue that is also present on this slide shows poor aeration, but is otherwise normal.
7-10: Kidney, adult polycystic kidney disease. Grossly, the kidney contained numerous large, fluid-filled cysts that disrupted the architecture and function of the kidney. The section here shows portions of 5 or 6 different cysts. The cyst lining has a simple squamous appearance. Although many of the tubules show signs of autolysis, the glomeruli are fairly well-preserved in this kidney. This patient was asymptomatic and his polycystic kidney disease was diagnosed at autopsy after death due to an unrelated illness.
Additional slide from the Duke Medical School teaching collection: “Pathology_200 Slides” folder

1 Polycystic Kidney

Environmental and Nutritional Disorders
From the PATHOL 750 teaching collection

9-1: Skin, sun damage. The UV radiation in sunlight induces expression of matrix metalloproteinases that degrade the elastic fibers and collagen that are present in the upper dermis. The result is disorganization and basophilic degeneration of the dermal connective tissue. These changes accumulate with repeated sun exposure and are largely irreversible, resulting in wrinkling and a leather-like skin appearance.


9-2: Lung, silicotic nodule. The lung contains several discrete nodules characterized by deposition of collagen and anthracotic pigment. Few functional alveoli remain. The deposition of collagen is incited by cytokines released by macrophages after attempting to ingest particles of inhaled silica.
9-3: Lung, centrilobular emphysema. Rather than the normal polygonal pattern of alveolar walls, numerous irregular “holes” are present in this section of lung, without evidence of accompanying fibrosis. The presence of seemingly free-floating alveolar walls results from expansion of individual alveoli such that their connections to other alveoli cannot be visualized on the scale of the section. These changes are diagnostic of emphysema. In centilobular (centriacinar) emphysema, the central and proximal parts of the acini formed by the respiratory bronchioles are affected, with relative sparing of the distal alveoli. Thus normal and emphasematous airspaces typically coexist side-by-side. Because this disease occurs most commonly in heavy smokers, large amounts of anthracotic pigment may be observed in the lung tissue, as seen in this section.
9-4: Colon, diverticulosis. The section shows a segment of normal colon with an adjacent diverticulum. The mucosa of the diverticulum is somewhat flattened but otherwise normal. The muscularis propria is markedly attenuated. This allows the diverticulum to herniate below the muscularis layer when intraluminal pressure is increased during defecation to form a grossly characteristic spherical outpouching. The majority of diverticula are located in the sigmoid colon. They are rare in individuals under age 30 and are highly prevalent (~50%) in Western adult populations over age 60. The current hypothesis proposes that diverticula form when focal weakness in the colonic wall is exacerbated by straining to pass stool. Treatment is a high fiber diet to improve bowel function. See Figure 17-52 (p. 855 in Robbins 7th Edition) for excellent gross and microscopic illustrations.
Additional slides from the Duke Medical School teaching collection: “Pathology_200 Slides” folder

92 Centrilobular Emphysema

98 Silicosis of the Lung

Numerical Index of Slides from the “Pathology_200 Slides” folder

Number

Organ




Diagnosis

1

Kidney




Polycystic kidney

2

Kidney




Carcinoma, renal cell

5

Prostate




Carcinoma, adeno

9

Kidney




Pyelonephritis, acute

12

Kidney




Pyelonephritis, chronic

14

Kidney




Necrosis, acute tubular

17

Kidney




Glomerulonephritis, chronic

18

Kidney




Glomerulonephritis, acute (crescents)

19

Kidney & Liver




Amyloidosis

20

Kidney




Diabetic nephropathy

25

Heart




Rheumatic heart disease

26

Gallbladder




Polyarteritis nodosa

28

Vessel




Aneurysm, aortic, dissecting

30

Kidney




Nephrosclerosis, arteriolar

31

Heart




Infarct, recent, myocardial

33

Bladder




Carcinoma, papillary transitional cell

34

Testis




Seminoma

35

Kidney




Infarct, recent

39

Lung




Pneumonia, broncho

40

Lung




Edema, pulmonary

46

Lung




Pneumonia, broncho-, organizing

51

Lung




Pneumonia, lobar, gray hepatization

54

Appendix




Appendicitis, acute

70

Uterus




Polyp, endometrial

79

Adrenal




Adenoma, cortical

81

Liver




Cirrhosis, Laennec's

84

Colon




Carcinoma, adeno

85

Liver




Fatty metamorphosis

89

Gallbladder




Cholecystitis, acute & chronic

92

Lung




Emphysema

93

Pancreas




Pancreatitis, acute and chronic

95

Ileum




Infarct, hemorrhagic

98

Lung




Silicosis

111

Colon




Colitis, ulcerative

116

Ovary




Cystadenoma, pseudomucinous

121

Skin




Rheumatoid nodule

123

Ovary




Salpingitis, acute and chronic

126

Lung




Carcinoma, adeno

129

Esophagus




Carcinoma, squamous cell

133

Colon




Colitis, granulomatous (Crohn's Disease)

134

Colon




Carcinoma, adeno

135

Stomach




Carcinoma, adeno- (linitis plastica)

139

Liver




Carcinoma, metastatic adeno

143

Breast




Foreign body reaction

154

Larynx




Carcinoma, squamous

155

Liver




Hemangioma, cavernous

158

Lung

Embolism with hemorrhagic infarct

159

Appendix

Carcinoid

161

Lung

Sarcoma, Ewing's

166

Colon

Adenoma, tubulovillous

170

Lung

Hamartoma, cartilaginous

189

Pancreas

Carcinoma, adeno

195

Heart

Endocarditis, infective

199

Breast

Carcinoma, infiltrating ductal

200

Bone

Tumor, giant cell

202

Prostate

Hyperplasia, nodular

203

Skin

Verruca vulgaris

220

Uterus

Leiomyoma

223

Bone

Sarcoma, osteogenic

227

Skin

Carcinoma, basal cell

229

Liver

Cirrhosis, biliary

233

Cervix

Carcinoma, squamous cell

240

Stomach

Ulcer, chronic

253

Stomach

Carcinoma, adeno

264

Thyroid

Thyroiditis, Hashimoto's

281

Lung

Aspergillosis (SILVER)

286

Heart

Infarct, myocardial, healed

294

Marrow

Leukemia, chronic lymphocytic

295

Lymph node

Hodgkin's disease, nodular sclerosing

329

Brain

Medulloblastoma

370

Brain

Infarct

413

Marrow

Myeloma, multiple

427

Pituitary

Adenoma, chromophobe

429

Thyroid

Colloid nodules

430

Thyroid

Carcinoma, papillary

451

Lung

Tuberculosis, miliary

452

Lung

Tuberculosis, caseous











Descriptions for Slides from the “Pathology_200 Slides” folder
Slide 1:

Clinical History: This 15 day old female child had multiple congenital cardiac defects. In addition, bilateral abdominal masses were present.


Microscopic: This is a complete hemisection of the kidney. Examination with naked eye or inverted ocular reveals that the entire kidney has a honeycombed appearance. Microscopic examination shows the cysts to be markedly dilated tubules that contain granular eosinophilic material (probably protein) and in some cases, red blood cells. The glomeruli, in contrast to those of an adult kidney, contain peripheral rows of visceral epithelial cells. This pattern, which disappears during the course of several years, is normal for infant glomeruli. Polycystic renal disease may also present in adulthood, in which case the kidneys are often grossly enlarged and virtually replaced by cysts up to several centimeters in diameter.
DIAGNOSIS Polycystic Kidney

Slide 5:

Clinical History: This 77 year old male died from pneumococcal meningitis. The patient had a history of advanced tuberculosis, which had been successfully treated, and mild silicosis. Adenocarcinoma of the prostate with several metastases was an unexpected finding.


Gross: The prostate was quite large and firm with multiple rubbery nodules measuring 2 mm to 6 mm in diameter. Some of the nodules contain yellowish flecks. The seminal vesicles were firm bilaterally.
Microscopic: There are a number of glands shown in varied patterns. In some cases the epithelial cells are found in non-glandular masses. The epithelial cells are cuboidal or polygonal with central, round, deeply pigmented nuclei. Few, if any, mitotic figures can be seen. The presence of perineural and perivascular invasion is clearly in evidence. This is a useful diagnostic characteristic of adenocarcinoma of the prostate.
DIAGNOSIS Adenocarcinoma of Prostate

Slide 9:

Clinical History: A 51 year old male had a "neurogenic bladder", caused by a spinal cord tumor, for about 9 months. He died following an attempt at surgical excision of the spinal tumor.


Gross: The bladder was distended, with a thickened, trabeculated wall. There was a bilateral hydroureter and hydronephrosis. The left kidney was swollen, and the cut surface showed soft foci of yellow streaks extending toward the pelvis. E. Coli was cultured.
Microscopic: Naked eye examination of the slide reveals dark streaks extending from the outer cortex to the inner medulla. Microscopically these are foci of acute inflammation, including necrosis and hemorrhage, with masses of polymorphonuclear leukocytes that are also found in many tubules.
DIAGNOSIS Acute Pyelonephritis
Slide 12:

Clinical History: A 20 year old male had had a tonsillectomy. 7 days later he had a fever, pain in the region of the costovertebral angles, pyuria, and illness that disappeared after antibiotic treatment. He was rejected by the Army because of "proteinuria". Six months before death he developed impairment of his vision and was found to have severe hypertension. He was put on a rice diet and improved for several months, but finally died with uremia and pulmonary edema.


Gross: Both kidneys, distorted by multiple irregular broad scars, were small, each weighing about 60 grams.
Microscopic: The following features, present in this slide, are characteristic of severe chronic pyelonephritis.Interstitial tissue shows prominent infiltration by lymphocytes and plasma cells, and occasional polymorphonuclear neutrophils; irregular fibrous scars and periglomerular fibrosis. Tubules are dilated, many filled with eosinophilic casts giving the region a "thyroid-like" appearance. A few tubules contain polymorphonuclear neutrophils, indicating that this is an active exacerbation of a chronic pyelonephritis. Arteries are markedly thickened, with intimal proliferation resulting in narrowing of the lumen. Many arterioles show hyaline changes in their walls. Most glomeruli are replaced by fibrous tissue. A few are surprisingly normal in appearance with intact capillaries. There is a prominent peri-glomerular fibrosis in many regions with a thick rim of fibrous tissue circling the outside of Bowman's capsule.
DIAGNOSIS Chronic Pyelonephritis

Slide 14:

Clinical History: This 37 year old female ingested about a dozen tablets of mercury

bichloride (HgC12). Despite vomiting, treatment with BAL, fluids, and colonic irrigations she became anuric and died 10 days later. The small amount of urine obtained on the first day after taking the pills gave a 4+ benzidine test for occult blood.
Gross: The kidneys were both markedly enlarged and pale.
Microscopic: The tubular damage here is so severe that it is hard to identify the segment involved. However, it may be noted that most of the necrosis is in the cortex, whereas the collecting tubules in the medulla, although their lumina contain many casts, are lined by relatively intact cells. HgC12 presumably damages mainly proximal convoluted tubules because it is concentrated in this segment. Many involved tubules show marked coagulative necrosis, with sloughing of cells into the lumen. Some tubules that look more nearly normal actually have already have undergone marked necrosis and all that is left is a layer of flattened basilar cells which serve to regenerate the tubule. Regenerative changes can be recognized, including occasional mitoses in epithelial cells. The basement membrane around a few necrotic tubules is broken, and the interstitial tissue contains collections of inflammatory cells and edema fluid.
DIAGNOSIS Acute Tubular Necrosis, Kidney

Slide 17:

Clinical History: Four years before death the patient was seen in the hospital because of nausea and vomiting. He had some hematuria, proteinuria, urinary casts, and a BUN of 50 mg/dl. A diagnosis of "chronic glomerulonephritis" was made. He did well for over 3 1/2 years, his BUN varying from 50-60 mg/dl, and his blood pressure being borderline elevated (150/90). A month before death his BUN started to increase, and he died in uremia.


Gross: The kidneys were small (80 and 90 grams), and were pale and finely granular. The cortex was markedly thinned.
Microscopic: All of the 4 main constituents of the kidney (glomeruli, tubules, vessels, and interstitial tissue) are involved. Although all glomeruli are abnormal, they are not involved to the same degree; some are completely replaced by fibrous tissue, others are only partly scarred, and a few still contain patent capillary loops. The latter have increased mesangial and epithelial

cells of Bowman's capsule. The tubules are dilated; some contain red blood cells, but most contain hyaline casts. The interstitial tissue is rather diffusely infiltrated with many lymphocytes and plasma cells. There is a moderate to marked degree of arteriolarsclerosis.


DIAGNOSIS Proliferative Glomerulonephritis, Severe, Advanced (Chronic)
Slide 18:

Clinical History: This 29 year old male's illness began 10 weeks prior to death, with an episode of "flu". Two weeks later his urine became "smoky". He was found to have hematuria, albuminuria and elevated BUN (180 mg/dl).


Gross: The kidneys were enlarged (230 gm each) and smooth. The surface was covered with pinpoint hemorrhages.
Microscopic: There is marked proliferation of epithelium of Bowman's capsule producing "crescents" ("extracapillary glomerulonephritis"). In places fibrin strands are intermixed with the epithelial cells. Tubules are dilated and contain many red blood cells. There is marked interstitial edema and presence of numerous leukocytes. The presence of a large number of crescents is a bad prognostic sign.
DIAGNOSIS Acute Proliferative Glomerulonephritis with Crescents

Slide 19:

Clinical History: This 51 year old male had tuberculosis for many years, and had been a patient in a sanitarium for almost 7 years. He developed some ankle edema, and was found to have an enlarged liver and 2+ proteinuria.


Gross: The heart was large, weighing 470 grams; the liver weighed 1900 grams, and the spleen 450 grams. Both kidneys were large and pale, each weighing 450 grams, and their surfaces were irregularly scarred.
Microscopic: Liver. Most of the liver is replaced by homogenous, hyaline pink-staining amyloid which has been laid down between the sinusoids and the liver cells. This would stain with Congo red, or would be metachromatic if stained with crystal violet. The liver cords are replaced or compressed, and appear as widely separated thin cords of cuboidal cells. Bile plugs are present in the bile capillaries.

Kidney: The same type of hyaline pink material is present in the glomeruli, and is deposited between the endothelial cells and the basement membrane. In some places, it may be present in masses that encroach on the lumen of the capillary. The amyloid can also be recognized in the walls of some small arteries, and in a few places can be seen around the tubules in the interstitial tissue.


DIAGNOSIS Amyloid - Liver and Kidney
Slide 25:

Clinical History: A 9 year old female had two previous attacks of rheumatic fever. She entered the hospital for the third time with painful swollen joints, fever, and pulmonary edema. She died with signs of progressive heart failure.


Gross: Her heart weighed 380 grams (normal for this age is about 115 grams). The pericardium was covered with a shaggy, fibrinous exudate. The left ventricle was dilated and the myocardium was flabby. The mitral valve was slightly thickened as were the chordae tendinae. There was a MacCallum's patch in the left atrium. The liver weighed 780 grams (normal 750 grams). Its edges were rounded and there was centrilobular congestion ("nutmeg liver").
Microscopic: The section includes the entire thickness of the myocardium and is taken through the mitral valve so that both left atrial and left ventricular myocardium are present in the section. The epicardium shows a prominent layer of fibrin on the surface; deep to this is young connective tissue with many capillaries, fibroblasts, and chronic inflammatory cells, i.e. granulation tissue. Thus, this is an organizing fibrinous pericarditis. There is also myocarditis present. The myocardial inflammation includes Aschoff bodies of different ages. Identify very early, intermediate and healed foci. The presence of Aschoff bodies indicates that this is a rheumatic myocarditis. Note also marked endocardial thickening due to inflammation and scarring, especially in the left atrium (MacCallum's patch).
DIAGNOSIS Acute Rheumatic Fever of Heart

Slide 26:

Clinical History: This 48 year old female was admitted with a history of chills, fever, and pain in the right upper quadrant. In view of a clinical diagnosis of cholangitis and cholecystitis, the gallbladder was resected.


Gross: The walls of the gallbladder were reddish and thickened. No stones were noted.
Microscopic: The mucosa of the gallbladder is intact. The wall is markedly thickened by edema and fibrous tissue. The small arteries in the wall are involved in a necrotizing and inflammatory process which appears to be in all stages of development, resolution, and healing. The earliest change seen is an acute fibrinoid necrosis of the wall of the artery, which appears in the innermost third of the media, frequently involves the wall in an eccentric arrangement, and finally involves the entire thickness of the wall. Many of these arteries are markedly dilated with the formation of aneurysmal-like sacs. There is a marked exudation of inflammatory cells both within the wall of the artery and surrounding the artery. These cells are made up of eosinophils, neutrophils, histiocytes and lymphocytes. In some of the vessels, the process appears to be in a healing phase with the site of artery represented by fibrous scar surrounded by a chronic inflammatory exudate. Arterioles, capillaries, and veins are relatively spared in this necrotizing process.
DIAGNOSIS Polyarteritis Nodosa

Slide 28:

Clinical History: A 47 year old female with a history of hypertension of at least 8 months duration noted sudden onset of severe inter-scapular pain which rapidly radiated to base of neck but not to abdomen 7 hours prior to admission. On admission her BP was 160/130 (both arms) and pulse was 80 and equal bilaterally. No murmurs were noted. A retrograde aortogram revealed a double channel extending from the root of the aorta to the innominate artery. Aortotomy was performed for attempted repair of the dissecting aneurysm, but during the procedure there occurred an adventitial tear with subsequent hemopericardium and cardiac tamponade. The patient expired on the operating table 6 hours after surgery had begun.


Gross: The heart weight was 550 grams and there was left ventricular hypertrophy. The aorta had an intimal tear at the base of the innominate artery with dissection of the media occurring in the outer 2/3 and extending proximally to within 0.5 cm of the aortic valve. There was an adventitial tear at this point.
Microscopic: There is a blood-filled tear between the inner 2/3 and outer 1/3 of the media. Note necrosis and deposition of fibrin along the margins of the defect. The remainder of the media contains the changes of "cystic medial necrosis"
DIAGNOSIS Dissecting Aneurysm, Ascending Aorta, with cystic medial necrosis

Slide No. 30

Clinical History: This 80 year old woman had been known to be hypertensive for many years. She died of congestive heart failure, following a period of hospitalization for pneumonia.


Gross: The heart was enlarged. Both kidneys were somewhat smaller than normal (100 grams each) and were finely and diffusely granular.
Microscopic: The arterioles are prominent with hyalinized walls. Note the thickened arterioles at the vascular poles of the glomeruli, and observe the extension of the hyaline material into the glomerulus. Some glomeruli are more scarred than others. This "sclerosis" is secondary to the ischemia caused by the narrowed lumens of the arterioles. There are also scattered patches of interstitial fibrosis and chronic inflammation.
DIAGNOSIS Arteriolar Nephrosclerosis
Slide 31:

Clinical History: This 45 year old man had been well until he was awakened by chest

pain that radiated to both arms and neck and was associated with diaphoresis. His blood

pressure was 160/110. He was treated with diuretics (Lasix), but despite this he

continued to gain weight. Two days after the onset of the chest pain he had a cardiac

arrest which was preceded by third degree heart block.


Gross: The heart was slightly enlarged weighing 460gms. There was severe atherosclerosis of all the major coronary arteries with a recent thrombotic occlusion of the proximal right coronary artery. A recent transmural infarct was present in the left ventricle that involved the posterior interventricular septum and the posterior papillary muscle.
Microscopic: The slide includes a transmural section of the posterior wall of the left ventricle. Nearly the entire section is involved by infarct. However, there is a thin rim (5 to 10 cell layers) of endocardial myocytes which have survived because of diffusion of oxygen and nutrients from the ventricular cavity. Other viable myocytes can be found around larger blood vessels within the section. The intense hypereosinophilia of the necrotic myocytes can best be appreciated by comparing the thin rim of lighter staining subendocardial myocytes with the deeper cells. Note also the karyolysis that is characteristic of coagulation necrosis. In some areas there is little inflammatory response. This observation is explained by microvascular necrosis which does not allow access of circulating leukocytes to these areas. In other areas, especially in the epicardial half of the infarct, there is an intense acute inflammatory response. Many intact neutrophils can be seen. In addition, there are many nuclear fragments from lysed neutrophils. Macrophage activity is not evident. These features of the inflammatory response indicate that the infarct was approximately three to four days old. Note also that the inflammation extends to the epicardial surface and that there are deposits of fibrin on the epicardium. This is called fibrinous pericarditis. The granular grey material seen within some blood vessels is barium sulfate, which was injected to permit post-mortem study of the coronaries by radiography.
DIAGNOSIS Recent Myocardial Infarct

Slide 33:

Clinical History: This 57 year old female complained of hematuria. She was cystoscoped and found to have a papillary mass near the dome of the bladder.


Microscopic: Orient yourself by naked-eye and low power examination in regard to the 3 main layers of the bladder wall. A normal transitional epithelium lines about 1/2 of the mucosal surface. The central portion is thrown up into many fingerlike fronds (papillae). The connective tissue and vascular core is line by thickened, atypical transitional epithelium. There is a suggestion of very early invasion into the mucosa at the base of the tumor but the muscularis is uninvolved.
DIAGNOSIS Papillary Transitional Cell Carcinoma of Urinary Bladder

Slide 35:

Clinical History: This 76 year old female was discovered to have a bronchogenic carcinoma six

months prior to her death. After a right upper lobectomy she did well, but later developed an "agitated depression". Metastasis to the brain was suspected.
Gross: Recent infarcts are seen in Kidneys, Brain, Spleen
Microscopic - Kidney: There is recent infarct in this section, with a central area containing "ghosts" of tubules outlined by a marginal zone of polymorphonuclear neutrophils, necrotic debris, and hemorrhage. Some tubules immediately beneath the renal capsule are spared. An artery in the medulla contains a thrombo-embolus that presumably originated from the thrombus on the mitral valve.
DIAGNOSIS Recent Infarct, Kidney

Slide 39:

Clinical History: A 58 year old African American female had been hemiplegic on the right for a period of 3 months prior to death. She developed fever and dyspnea several days prior to death.


Gross: There was a thrombosis of the left internal carotid artery with infarction of the left cerebral hemisphere. There was a massive embolus of the right pulmonary artery. Both lungs were firm with mucopurulent exudate in and about the bronchi. The left lower lobe was firm and gray-yellow with a shaggy fibrinous exudate over the pleura. (E. Coli and Proteus mirabilis were cultured from this area).
Microscopic: Bronchi and alveoli are filled with neutrophils. There are scattered masses of fibrin.




Share with your friends:
  1   2   3


The database is protected by copyright ©dentisty.org 2019
send message

    Main page