Patho Lab Trans -butch

OS 214 Excretory Module

Pathology Department Lab Exam & Exam 2

Pathology Lab 2 part 2 OUTLINE I.

II.

Gross Specimen a. Renal Cell Carcinoma b. Wilm’s Tumor c. Renal Dysplasia d. Chronic Pyelonephritis e. Nephrolithiasis f. Kidney Hydronephrosis g. Benign Prostatic hyperplasia h. Transitional / urothelial cell carcinoma Microscopic Specimen a. Chronic protatitis b. NPH c. Prostatic adenocarcinoma d. Papillary urothelial carcinoma e. Chronic cystitis

-

-

border are areas of necrosis), areas of hemorrhage (dark areas) ** the bigger the tumor, the bigger the area of necrosis should always be correlated with clinical features clear cell CA – most common type ** the type of CA determines management and prognosis ** the type of CA cannot be determined by just looking at the gross specimen lesion during nephrectomy, blood vessel sample should also be taken invasion of gerota’s facia – malignant lesion

GROSS SPECIMEN A. Renal Cell Carcinoma May arise in any portion of the kidney Areas of ischemic, gray white necrosis; foci of hemorrhage or discoloration; areas of softening Has a tendency to involve the renal vein

Figure 2. Due to gross yellow appearance, the differential for this case is a xantho-granulomatous pyelonephritis.

Figure 3. Fungating mass, nodular in appearance, which has already invaded much of the normal kidney tissue.

Figure 1. Renal Cell Carcinoma Notes: when given a gross specimen, you have to differentiate benign from a malignant lesion. ** malignant lesions: infiltrative, irregular border, areas of necrosis, areas of hemorrhage specimen: infiltrative, irregular/ill-defined border, necrotic areas (pale areas which can be found either in the outer or inner part of the lesion, for the gross specimen shown in the lab the outer

March 11, 2009 | WED

Page 1 of 6 LEXI-ADI-GILLIAN-BUTCH

OS 214 Excretory Module

Pathology Department Lab Exam & Exam 2

Pathology Lab 2 part 2 -

due to an differentiation

abnormality

in

metanephric

Figure 4. The tumor has already spread to the perirenal fat. B. -

Wilm’s Tumor Large, solitary, well circumscribed mass On cut sections, tumor is soft, homogenous, and tan to gray with occasional foci of hemorrhage, cyst formation and necrosis On microscopic sections, classic triphasic combination of blastemic stromal and epithelial cell types

Figure 7. Renal Dysplasia Notes: congenital presence of islets of cartilage and immature collecting tubules D. -

Figure 5. Wilm’s Tumor Notes: common in children specimen: smooth, homogenous lesion occupying the entire renal parenchyma, foci of hemorrhage (minimal areas of hemorrhage as compared to the renal cell CA specimen) and cyst may be triphasic (classical type): composed of blastema, epithelial cells, stroma; biphasic; or anaplastic

Figure 6. Nephroblastoma, Differential is a neuroblastoma, Triphasic: stromal, epithelial and blastemic components, which can only be differentiated under the microscope, Circumscribed, well-demarcated, usually chromosomal, Common in children<5 C. -

Renal Dysplasia irregular shaped, multicystic cysts vary in size

March 11, 2009 | WED

Chronic Pyelonephritis kidneys are irregular scarred coarse, discrete, corticomedullary scar overlying in a dilated, blunted or deformed calyx kidneys are smaller than usual ureter is dilated and thickened, a finding consistent with chronic vesicoureteral reflux

Figure 8. Chronic Pyelonephritis Notes: specimen: granular surface with scarring, small kidney, blunting of calyx (hallmark), thickening of ureter wall due to reflux causes: recurrent UTI and chronic obstructive diseases thyroidization – lumen filled with colloid-like material kidney becomes nonfunctional requiring dialysis if both kidneys are affected -

Figure 9. Inflammation is usually caused by ascending infections due to E. coli. The corticomedullary junction has been obliterated. E.

Nephrolithiasis

Page 2 of 6 LEXI-ADI-GILLIAN-BUTCH

OS 214 Excretory Module

Pathology Department Lab Exam & Exam 2

Pathology Lab 2 part 2 -

favoured sites of formation are within the renal calyces and pelvis, thus causing dilatation and if multiple, may thin out the renal parenchyma most stone (75%) are calcium containing (calcium oxalate, calcium phosphate); 15% are so-called triple stones (magnesium ammonium phosphate).

-

weighs between 60 to 100 grams; even up to 200 or more may show a well defined bulge almost exclusively occurs in the inner aspect of the gland, in the transitional and periurethral zones Nodular enlargement may encroach the lateral walls of the urethra to compress it into a slitlike orifice

-

Figure 10. Nephrolithiasis Notes: specimen: dilated calyx, atrophic renal parenchyma which is replaced with fat types of stone: (1) calcium, (2) triple phosphate/magnesium ammonium phosphate/struvite stone treatment: laser to convert the stone into powder type of necrosis: coagulative necrosis wherein the original morphology is retained urinalysis: presence of blood (hematuria) and crystals ** renal cell CA may also present with hematuria ** how to differentiate renal cell CA and nephrolithiasis? conduct urine cytology (low sensitivity) ** urine cytology: centrifuge urine sample → get the sediments → stain with hematoxylin eosin (H&E) ureterolithiasis – kidney is still intact F. -

-

Kidney Hydronephrosis enlargement may be slight or massive kidney transformed into a thin-walled cystic structure striking parenchymal atrophy blunting of apices of the pyramids

Figure 12. BPH Notes: can weigh up to 200g usually occur in the older age group specimen: nodular lesion which may displace the urethra, dilated urethra may be due to obstruction but usually the urethra is slit-like due to impingement H. Figure 11. Kidney Hydronephrosis Notes: specimen: atrophy of parenchyma replaced with fatty tissue cause: chronic obstruction kidney may rupture from trauma which may lead to peritonitis since urine is detected as a foreign body treatment: pathologic kidney is usually removed

-

Transitional / urothelial cell carcinoma gross pattern vary: may be papillary to nodular or flat heterogenous gross appearance may fungating, necrotic or ulcerative that have unmistakably invaded deeply

G. Benign Prostatic hyperplasia

March 11, 2009 | WED

Page 3 of 6 LEXI-ADI-GILLIAN-BUTCH

OS 214 Excretory Module Pathology Lab 2 part 2

Pathology Department Lab Exam & Exam 2

Figure 15. Hyperplasia of the median lobe of the prostate produces a polypoid mass that protrudes in the bladder lumen.

Figure 13. Transitional / urothelial cell carcinoma Notes: normal bladder wall – smooth or trabeculated specimen: fungating lesion (papillary), infiltrating into the smooth muscle, black areas are due to India Ink stain which is used to determine the depth of infiltration microscopically and as surgical lining of the section; along with the specimen is the an atrophied uterus which is means the specimen came from a 50-60 year old female management: surgical removal of the bladder and creation of a neobladder from the ilium

Figure 16. The luminal contour shows tufts and papillary infoldings of glands. The tall secretory epithelial cells have pale clear cytoplasm and uniform round or oval nuclei. Prominent nucleoli are not seen. Fibromuscular stroma and any basal cells can be identified.

MICROSCOPIC SPECIMEN A. Chronic protatitis

Figure 17. BPH can involve both glands and stroma, though the former is usually more prominent. Here, a large hyperplastic nodule of glands is seen. Figure 14. A dense inflammatory infiltrate has replaced glandular epithelium which has been largely destroyed. Some cases of granulomatous prostatitis may closely mimic high-grade cancer. Small foci of cancer adjacent to foci of inflammation may sometimes be overlooked.

B.

Nodular prostatic hyperplasia

March 11, 2009 | WED

Figure 18. At higher magnification, the enlarged prostate has glandular hyperplasia. The glands are well-differentiated and still have some intervening stroma. The small laminated pink concretions within

Page 4 of 6 LEXI-ADI-GILLIAN-BUTCH

OS 214 Excretory Module

Pathology Department Lab Exam & Exam 2

Pathology Lab 2 part 2 the glandular amylacea. C.

lumens

are

known

as

corpora

Prostatic adenocarcinoma

-

invasive urothelial CA – no need to grade because regardless of a low or high grade, prognosis and management are still the same LM: fibrovascular core a.

Figure 19. High-grade prostatic intraepithelial neoplasia (PIN) consists of intermediate to large size preexisting glands with proliferative changes resulting in hyperchromatic appearance. Note the small foci of cancer adjacent to PIN on the upper left and lower right.

Figure 21. These tumors show more architectural disorder and nuclear atypia than urothelial tumors of low malignant potential. The nuclear size, shape, polarity, and chromatin show greater variability. Mitoses are still infrequent. Umbrella cells can still be seen.

b.

Figure 20. Prostatic CA Note: gross pic: asymmetrical, multilobulated nodular hyperplasia due to proliferation of stromal or/and glandular elements; glandular hyperplasia grossly appear as cystic spaces adenocarcinoma – cells are trying to form glands which fuse together gleason grading: grades 1-3 = distinct glands grade 4 = fused glands grade 5 = no glands visible score = predominating grade + second most predominant grade LM pic: pleomorphic hyperchromatic nuclei D.

Low-grade

High-grade

Figure 22. These tumors display total architectural disorganization and significant cytologic atypia of urothelium. There is loss of nuclear polarity; considerable variation in nuclear size, shape, and chromatin content; mitoses are frequent and may be abnormal. Umbrella cells are usually absent. E.

Chronic cystitis

Papillary urothelial carcinoma

Figure 21. Urothelial Carcinoma Notes: gross pic: thick, stiff, nodular wall (may be malignant)

March 11, 2009 | WED

Figure 23. Inflammation of the sub mucosa Notes: gross: unilaterally dilated ureter due to stones impacted at the outlet when evaluating the urothelium look for: number of cell layers (normal is 7 layers but if the section is tangentially cut there may be more than 7 layers), polarity, crowding of nuclei pic: stones caused inflammation of the submucosa

Page 5 of 6 LEXI-ADI-GILLIAN-BUTCH

OS 214 Excretory Module Pathology Lab 2 part 2 a.

Pathology Department Lab Exam & Exam 2

Papillary Cystitis

Figure 24. Proliferation of vessels and accumulation of edema fluid and inflammatory cells in the lamina propria has created papillary configuration focally. Distinction from papillary urothelial carcinoma is important.

Figure 25. Another example of papillary cystitis. The urothelium is hyperplastic. The lamina propria contains numerous plasma cells and delicate vessels.

Figure 27. The presence of edema fluid and inflammatory cells can be better appreciated in this image. The majority of the patients with polypoid cystitis have history of indwelling catheters.

Figure 28. The lamina propria contains eosinophils, plasma cells, lymphocytes, and rare neutrophils. The overlying urothelium is unremarkable. On cystoscopic examination, papillary and polypoid cystitis are frequently mistaken for neoplasms. Microscopic examination reveals their true nature.

b. -

Polypoid Cystitis (Robbin’s) an inflammatory condition resulting from irritation to the bladder mucosa. Although indwelling catheters are the most commonly cited culprits, any injurious agent may give rise to this lesion. The urothelium is thrown into broad, bulbous, polypoid projections as a result of marked submucosal edema. Polypoid cystitis may be confused with papillary urothelial carcinoma both clinically and histologically

-

Figure 26. The term polypoid cystitis is applied for broad-based lesions enclosing large amounts of edema fluid with scattered inflammatory cells. If the lesions are even more broad-based and larger, the term bullous cystitis may be applied.

March 11, 2009 | WED

Page 6 of 6 LEXI-ADI-GILLIAN-BUTCH