UNIVERSIDAD CENTRAL DEL CARIBE

SCHOOL OF MEDICINE
DEPARTMENT OF PATHOLOGY
THE KIDNEY - OBJECTIVES
1. Review normal histology of the kidney
2. Review the renal physiology
3. Special stains:
What is or what is the use?
a) Periodic Acid Schiff stain
b) Silver Impregnation stains
c) Immunofluorescence and immunoperoxidase
a) Electron microscopy
4. How is defined congenital anomaly of the kidney?
a) Describe agenesis of the kidney
a) Describe hypoplasia
b) What is ectopic kidneys?
c) What is a horseshoe kidney?

5. Describe the following cystic diseases of the kidney (See table 20-2, page
962 Robbins, 7 t h ed)
a) Cystic renal dysplasia
b) Autosomal dominant polycystic kidney disease
a) Autosomal recessive polycystic kidney disease
c) Cystic diseases of renal medulla
6. Describe the following glomerular syndromes:
a) Acute nephritic syndrome
b) Rapidly progressive GN
c) Nephrotic syndrome
d) Chronic renal failure
e) Asymptomatic hematuria or
proteinuria
7. What are the four basic tissue reactions?
8. What is?
a) Anti-GBM nephritis
b) Heymann's nephritis
c) Antibodies against planted antigens
 9. What is circulating immune complex nephritis?
10. What is the etiology and pathogenesis of?
( see Robbins 7 t h edTable 20-6, page 975)
a) Acute poststreptococcal glomerulonephritis (proliferative)
b) Rapidly progressive (crescentic) glomeruionephritis (RPGN)
c) Membranous glomerulonephritis
d) Minimal change disease (MCD) (LIPOID NEPHROSIS)
e) Focal segmental glomerulonephritis (FSG)
a) Membranoproliferative glomerulonephritis (MMPGN)
f) IgA Nephropathy (Berger's disease)
g) Focal proliferative and necrotizing glomerulonephritis (focal GN)
11. What is chronic glomerulonephritis?
12. What are the light, fluorescence, and electron microscopy changes of the
glomerulonephritides ?
13. What are the most frequent clinical presentation of the
glomerulonephritides ?
DISEASES AFFECTING TUBULES AND INTERSTITIUM:
1.Acute tubular necrosis (ATN)
a)What is acute tubular necrosis?
a) What are the causes?
b)What is the pathogenesis?
b) Describe the morphologic changes of ATN.

2.Tubulointerstitial nephritis:
3.What characterizes these diseases?
a) What is pyelonephritis (PN) and urinary tract infection?
a) What is the etiology and pathogenesis?

4.Describe the morphology of acute pyelonephritis, papillary necrosis, pyelonephrosis, and

perinephric abscess.
a) What are the predisposing conditions?
5. Explain chronic pyelonephritis (CPN) and reflux nephropathy. Describe the
morphology of CPN.
6. Describe tubulointerstitial nephritis (TIN) induced by drugs and toxins. Explain the
pathogenesis and the morphology.
7. What is the difference between drug-induced interstitial nephritis and analgesic abuse
 nephropathy?
8. What is Urate nephropathy?
9. What are the kidney manifestations of Multiple Myeloma?
URINARY TRACT OBSTRUCTION:
1. What are the most common congenital anomalies?
2. What is hydronephrosis?
Describe the morphology of urinary tract obstruction. Describe the clinical
course.
3. What are the causes of urolithiasis?
4. What is the pathogenesis?
5. Explain the types of renal stones
TUMORS OF THE KIDNEY:
1. Benign tumors:
a) Cortical adenoma
Morphology
What is the importance of the size?
a) Renal fibroma
b) Angiomyolipoma
What is the relationship with tuberous sclerosis?
b) Oncocytoma

2. Malignant tumors:
a) Renal cell carcinoma (Adenocarcinoma)
Whatis the morphology? Explain the difference betwen sporadic and hereditary
carcinomas.
What is the importance of the size?
What is the clinical course?
What is the cytogenetic and genetic of the renal cell carcinomas?
UROTHELIAL CARCINOMAS OF RENAL PELVIS, URINARY BLADDER, URETER AND
URETHRA.
1. Where are the locations of this type of tumors?
2. What are the environmental association with transitional cell carcinoma?
3.What is the classification and frequency of these tumors?
4.Malignant and Benign
5.Describe and explain squamous cell carcinoma of the urinary bladder.
6.What is the role of schistosoma haematobium in SCC of urinary bldder? Explain
adenocarcinoma of urinary bladder.
7.What is acute cystitis. What is
chronic cystitis?
8. What is squamous metaplasia?
9. What is glandular metaplasia?
10. What is Malakoplakia?
1. What is nephrosclerosis?
a) benign
b) malignant
2. What is renal artery stenosis?
DISEASES AFFECTING TUBULES AND INTERSTITIUM:
1. Acute tubular necrosis (ATN)
a) What is acute tubular necrosis?
b) What are the causes?
c) What is the pathogenesis?
d) Describe the morphologic changes of ATN.
2. Tubulointerstitial nephritis:
3. What characterizes these diseases?
a) What is pyelonephritis (PN) and urinary tract infection?
b) What is the etiology and pathogenesis?
4. Describe the morphology of acute pyelonephritis, papillary necrosis,
pyelonephrosis, and perinephric abscess.
a) What are the predisposing conditions?
5.Explain chronic pyelonephritis (CPN) and reflux nephropathy. Describe
the morphology of CPN.
6.Describe tubulointerstitial nephritis (TIN) induced by drugs and toxins. Explain the
pathogenesis and the morphology.
7. What is the difference between drug-induced interstitial nephritis and analgesic
abuse nephropathy?
8. What is Urate nephropathy?
9. What are the kidney manifestations of Multiple Myeloma?
10. What is nephrosclerosis?
 Universidad Central del Caribe
GLOMERULAR DISEASES
GLOMERULAR SYNDROMES:
- Acute Nephritic Syndrome-
- Hematuria, azotemia, variable proteinuria, oliguria, edema and Hypertension.
- Rapidly progressive (crescentic) glomeruionephritis( RPGN) -
Acute nephritis, proteinuria, acute renal failure

- Nephrotic Syndrome-
- > 3.5 g proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria
- Chronic Renal Failure-
- Azotemia with uremia progressing through the years
- Asymptomatic Hematuria-
- Glomerular hematuria
- Asymptomatic Proteinuria-
- Subnephrotic proteinuria
Prevalence (%) of the etiologies for Nephrotic Syndrome
Children Adults
Membranous GN 5 30
MCD or Lipoid Nephrosis 65 10
FSGS 10 35
MPGN 10 10
Other proliferative GN 10 15
Histologic Alterations
- Glomerular Hypercellularity
- four or more adjacent cells per tuft
- they may e secondary to mesangial, endothelial or epithelial cells - leukocytic
infiltration (PNHs, MO, LY
- Basement Membrane Thickening
- Special stains: PAS or PASM
- Crescents
- Are formed by proliferation of parietal epithelial cells
Intermixed with inflammatory cells and fibrin.
Acute Poststreptococcal (Proliferative) GN
- It appears 1-4 weeks after a streptococcal infection of the pharynx or skin
- It occurs most frequently in children six to ten years of age, adults of any age may be
affected.
- E&P: Most due to Group A beta-hemolytic streptococci
(Streptococcus S. Pyogenes, types 12, 4, 1 (90%); and other bacteria
- Laboratory findings:
- AS0 titers
- Complement C3
- Cryoglobulins in the serum
Post streptococcal GN
- Clinical presentation: Acute nephritic syndrome
- Pathogenesis: Antibody mediated: circulating or planted antigen
- LM: Diffuse proliferative GN, leukocyte infiltration (PMNs)
- IF: Granular IgG and C3 in GBM and Mesangium
- EM: Subepithelial humps
Goodpasture's Syndrome
- Clinical presentation: RPGN
- pathogenesis: anti-GBM COL4A3
- LM: Diffuse proliferative GN, crescents - IF: Linear IgG and
C3 in GBM
- EM: No deposits; GBM disruptions; fibrin
Idiopathic RPGN
- Clinical presentation: RPGN
- Pathogenesis" Anti-GBM immune complex; p-ANCA
- LM: Diffuse proliferative GN; focal necrosis' crescents - IF: Linear IgG and
C3 in GBM; Negative or Equivocal
- EM: Deposits may or may not be present.
No deposits
Membranous GN
- Clinical presentation: Nephrotic Syndrome
- Pathogenesis: antibody mediated
- LM: Diffuse capillary wall thickening; spikes (PASM) and domes (Trichrome)
- IF: Granular IgG and C3; diffuse
- EM: Subepithelial deposits
Focal Segmental Glomerulosclerosis (FSGSI
- Clinical presentation: Nephrotic syndrome; non-nephrotic proteinuria
- Pathogenesis: Unknown
- LM: Focal and segmental sclerosis and hyalinosis
- IF: Focal; IgM and C3
- EM: Loss of foot processes; epithelial denudation
- Membranoproliferative GN MPGN Type I
- Clinical presentation: Nephrotic Syndrome
- Pathogenesis: Immune Complex - LM: Mesangial proliferation; GBM
thickening and splitting
- IF: Granular IgG and C3; Cl and C4 in GBM
- EM: Subendothelial deposits
- Membranous Proliferative GN MPGN Type II
- Clinical presentation: Hematuria; Chronic renal failure.
- Pathogenesis: Autoantibody; alternative complement pathway activation
- LM: Mesangial proliferation; GBM thickening and splitting
- IF: Granular C3 IgG, no Cl or C4
- EM: Dense deposit disease
IgA Nephropathv (Berger's Disease)
- Clinical presentation: Recurrent hematuria and/or proteinuria
- Pathogenesis: Unknown
- LM: Focal proliferative GN' mesangial proliferative GN
- IF: Granular IgA and IgG, M, and C3 in mesangium - EM: Mesangial and
paramesangial dense deposits
Minimal Change Disease (MCD1

- Clinical presentation: Nephrotic Syndrome.

Most frequent cause of Nephrotic Syndrome in children,
- Pathogenesis: ?? ,

- LM: Normal
- IF: No deposits
- EM: Diffuse loss of foot processes of epithelial cells.

Diabetes Mellitus:
- End-stage renal disease occurs in as any as 30% of IDDM (type I) and accounts for
22% of the death in patients younger than 40 years of age
- In the renal arterioles: Arteriolosclerosis
- In the renal medulla: Papillary necrosis
Diabetic Glomerulosclerosis
- In the glomeruli:
- Capillary basement membrane thickening
7 Diffuse glomerulosclerosis: most common lesion but not pathognomonic
- Nodular glomerulosclerosis, intercapillary glomeruloscle - rosis or Kimmelstiel-Wilson:
less common lesion but it is pathognomonic of DM.
 UNIVERSIDAD CENTRAL DEL CARIBE
PATHOLOGY
THE KIDNEY
Robbins 7ed
Congenital Anomalies: congenital renal disease can be hereditary but is most often the result of
an acquired developmental defect that arises during gestation.
Agenesis
Hypoplasia - Six or fewer renal lobes and pyramids
Ectopic
Horseshoe- Fusion of the upper or lower poles- 90% fused at the lower pole; 1/500 to
1000 autopsies.
CYSTIC DISEASES OF THE KIDNEY
A heterogeneous group comprising: See table 20-2
Hereditary
Developmental but nonhereditary
Acquired
Cystic renal dysplasia abnormality in metanephric differentiationpersistence in
the kidney of abnormal structures as cartilage, undifferentiated mesenchyme, and immature
collecting ductules, and abnormal lobar organization. Unilateral or bilateral, always cystic.
Autosomal dominant (adult) Polycystic kidney disease multiple expanding
cysts of both kidneys, 1/400 to 1000 live births , 10% of cases of chronic renal failure.
Autosomal dominant with high penetrance. Usually bilateral.
Three separate genes PKD1-16p13.3 85% of cases polycystin I= complex cell membrane
protein.
PKD2 4q13-23,polycystin 2integral membrane protein
PKD3 HAS YET TO BE MAPPED.
The kidneys are usually bilaterally enlarged up to 4 kg for each kidney. The external
surface appears to be composed of a mass of cysts. They may be filled with clear serous
fluid to hemorrhagic fluid.
Some of the patients remain asymptomatic until renal insufficiency or the dilatation of the
cysts may produce pain, hematuria, protinuria, polyuria, and hypertension.
40% of patients have one to several cysts in the liver usually asymptomatic, intracraneal
berry aneurysm in the circle of Willis, and/or mitral valve prolapse.
Possible mechanism of cyq-formation in polycystic kidney disease:
Mutation in polycystin 1,2
Defects in cell-cell and cell-matrix interactions Altered
tubular epithelial zrowth and differentiation

Abnomal extracellular matrix Cell proliferation Fluid secretion

vascular damage CYST Interstitial inflammationifibrosis
Autosomal Recessive--childhood Polycystic kidney disease
The kidneys are enlarged and have smooth appearance. The cut surface shows small cysyts in
the cortex and medulla spongelike appearance. Multiple epithelium-lined cysts in the liver and
proliferation of portal bile ducts. Infantile and juvenile form may develop congenital hepatic
fibrosis. They may develop portal hypertention with splenomegaly. This condition may occurs in
the absence of polycystic kidney. It has been reported occasionally with adult polycystic - kidney.
Subcategories:
Perinatal
Neonatal Infantile
Juvenile
Cystic Disease of Renal Medulla:
Medullary sponge kidney
Nephronophthisis uremic medullary cystic disease complex
Acquired ( dialysis-associated) cystic disease
Simple - cysts
Diseases affecting tubules and interstitium
Acute renal failure = acute suppression of renal function and urine flow = < 400 ml in
24 hrs.
It can be caused by: organic vascular obstruction -
severe glomerular disease
- acute tubulointerstitial nephritis
- massive infection pyelonephritis
- disseminated intravascular coagulation -
urinary
obstruction
- acute tubular necrosis
Acute Tubular Necrosis = ATN
Clinicopathologic entitydestruction of tubular epithelial cells and clinically by acute
suppression of renal function. The most common cause of acute renal failure.
It is a reversible renal lesion and arises in different clinical settings, they have in common a
period of inadequate blood flow to the peripheral organs - hypotension and shock; this pattern
is called ischemic ATN.
nephrotoxic ATN = drugs gentamicin
radiographic contrast agents
poisons mercury
organic solvents carbon tetrachloride
Pathogenesis:
tubular cell injury
disturbances in blood flow hemodynamic alterations that cause reduced GFR
intrarenal vasoconstriction.
Morphology: Ischemic ATN is characterized by focal tubular epithelial necrosis and apoptosis
at multiple points along the nephron, with skip areas.
Eosinophilic hyaline casts and pigmented granular casts,particularly in distal tubules and
collecting ducts; Tamm-Horsfall protein, hemoglobin, myoglobin, and other plasma proteins.
Interstitial edema and accumulation of leukocytes within dilated vasa recta.
Toxic ATN - acute tubular injury most obvious in the proximal convoluted
tubules. The necrosis may be entirely nonspecific but with certain agents may be
somewhat
distinctive mercuric chloride injured cells not yet dead may contain acidophilic inclusion..
Clinical course:
Initiating phase: lasting for about 36 hrs. Slight decline in urine output with a rise in BUN.
Maintenance phase: sustained decreased in urine output to between 40 - 400 mUda, with
salt and water overload, rising BUN, hyperkalemia, metabolic acidosis...
Recovery phase: steady increased in urine volume that may reach up to 3 liter/day.
Hypokalemia. Vulnerability to infection. Most patients who reach this phase eventually recover
completely.
Up to 50% of patients with ATN may not have oliguria and may in fact have increased
urine volumes= nonliguric ATN - nephrotoxin { gentamicin, heavy metals, carbon
tetrachloride}
Tubulointerstitial Nephritis
Primarily glomerular disease
Secondary tubulointerstitial nephritis
Acute: acute clinical onset interstitial edema, often leukocyte infiltration and focal tubular
necrosis.
Chronic: infiltration of mononuclear cells, interstitial fibrosis, and widespread tubular atrophy.
Pyelonephritis and urinary tract infection 85% of cases are gram-negative bacilli that are
normal inhabitants of the intestinal tract.
Acute: bacterial infection
Chronic: bacterial infection with other factors
Etiology and Pathogenesis
hematogenous
ascending infection:
From urethra
Multiplication in the bladder
Vesicoureteral reflux
Intrarenal reflux
Acute pyelonephritis
Morphology patchy interstitial suppurative inflammation and tubular necrosis.
Neutrophilic exudate within tubules and the renal substance. The glomeruli appear to be
resistant to the infection, severe necrosis eventually destroy the glomeruli, and fungal
pyelonephritis often affects glomeruli.
Complications:
Papillary necrosis diabetics and obstruction.
 AIL
Pyonephrosis total or almost complete obstruction

Perinephric abscess extension of suppurative inflarnrnmation

through the renal capsule into the perinephric tissue.
6% of pregnant women develop bacteriuria sometime during pregnancy, and 20% to 40%
of these eventually develop symptomatic urinary infection if not treated.
Chronic pyelonephritis and reflux nephropathy
Chronic obstructive pyelonepnritis
Reflux nephropathy symmetrically scarred.
Hallmark: coarse, discrete, corticomedullary scar overlying a dilated, blunted, or deformed
calyx.
Microscopic: the tubules show atrophy, hypertrophy, or dilation. The
dilated tubules may be filled with colloid casts = thyroidization.
Focal segmental gomerulosclerosis proteinuria
Xanthogranulomatous pyelonephritis foamy macrophages with
plasma cells, lymphocytes, polymorphonuclear leukocytes, and giant cells.
Proteus infection and obstruction
Tubulointerstitial nephritis induced by drugs and toxins
Acute drug-induced interstitial nephritis
Sulfonamides, synthetic penicillin-methicillin, ampicillin- rifampin,
diuretics- thiazides- NSAIDs, cimetidine.
Fever, eosinophilia, rash, and renal abnormalities hematuria,r4ild
proteinuria, and leukocyturia.
In about 50% of the patients there is serum creatinine level or acute renal failure with
oliguria.
Analgesic abuse nephropathy a form of chronic renal disease caused by
excessive intake of analgesic mixtures and characterized morphologically by chronic
tubulointerstitial nephritis with renal papillary necrosis.
Papillary necrosis occurs first, and cortical tubulointertiital nephritis is a
secondary phenomenon.
Nephropathy associated with nonsteroidal anti-inflammatory drugs
Acute renal failure inhibition of vasodilatory prostaglandin synthesis by NSAIDs.
Acute interstitial nephritis and lipoid nephrosis
Acute hypersensitivity interstitial nephritis
Membranous glomerulonephritis unclear pathogenesis
Urate nephropahty
Hypercalcemia and Nephrocalcinosis
Multiple myeloma
UNIVERSIDAD CENTRAL DEL CARIBE
SCHOOL OF MEDICINE

Pathologic Basis of Diseases, Robbins---7 ed

Testis and Epididymis
Congenital anomalies:
Cryptorchidism: failure of descent
a. 1% of 1 year old boys ; bilateral in 25% of the cases and may result in sterility
a. most idiopathic
Genetics anomalies--Trisomy 13- Patau syndrome
c. histologic changes: as early as 2 years of age
1. Decreased germ cell development
2. Thickening of seminiferous tubular basement membrane
1. Hyalinization of seminiferous tubular basement membrane
2. Interstitial fibrosis
5. Relative sparing of Leydig cells and appear to be proruinent
d. changes may also occur in the contralateral descended testis
e. 5 to 10 fold increased incidence of testicular neoplasms
e. concomitant inguinal hernia accompanies the testis in about 10 to 20% of
cases surgical correction Orchiopexy
Risk of cancer unclear after procedure. Orchiopexy in unilateral
cryptorchidism before 10 years of age may protects against cancer. Malignant changes may
occur in the contralateral normally descended testis.
Inflammations:
Mumps: uncommon in children it develops in 20 - 30 of postpubertal males
with mumps.
Typically about one week after parotitis but may precede or occur in the
absence of it.
Is not usually associated with sterility
Tuberculosis: almost always begins in the epididymis
granulomatous inflammation with caseous necrosis.
 Syphilis: almost always begins as orchitis with secondary involvement of the
epididymis. May occur in congenital and acquired syphilis
Gummas or diffuse interstitial inflammationperivascular plasma cell
infiltration ,lymphocytic infiltration, and obliterative endarteritis.
VASCULAR DISTURBANCES -- Torsion
1. Torsion secondary to twisting of the spermatic cord--- venous obstruction
2. Typically occurs with preexisting structural lesion; generally precipitated by
trauma or violent movement
3. congestion and interstitial hemorrhage to hemorrhagic necrosis
Testicular tumors : painless enlargement of the testis
Germ cell tumors
Incidence in USA 6 / 100,000
15 to 34 year age group most common tumor - 10% of all cancer death
More common in white than in black - 5:1
Risk factors: 1. Cryptorchidism
2. Genetic factor--siblings, racial differences
3. Testicular dysgenesis: testicular feminization
Klinefelter
syndrome:
Male hypogonadism that occurs when there are two or more X chromosome and
one or more
Y chromosome.
1 / 850 live male birth. Principal cause of reduced spermatogenesis and male
infertility.
Isochromosome of the short arm of chromosome 12 is found in virtually
all germ cell tumor.
Lymphatic spread ---retroperitoneal periaortic nodes
Hematogenous spread --- lungs, liver, brain, and bones
Seminoma: 50% of all testicular germ cell tumor
Almost never occur in infant, peak in the thirties. In
the ovary = dysgerminoma
Tends to remain localized --70% present in stage I
Variants of seminoma
1. Classic = 85%
2. Anaplastic = 5 to 10 %
3. Spermatocytic 4 to 6 `',/0 see later
Morphology: classical - homogeneous gray- white lobulated cut surface. usually no necrosis or
hemorrhage.
Large and round-polyhedral cells with distinct cell membrane; clear or
watery-appearing cytoplasm; large central nucleus with one or two nucleoli.
The cytoplasm contains varying amount of glycogen, rarely lipid vacuoles.
No alpha- fetoprotein (AFP) or human chorionic gonadotropin ( HCG) in the
cells. The cells stain for placental alkaline phosphatase.
15% of the tumors contain syncytial giant cells that resemble the
syncytiotrophoblast of the placenta in that they contain HCG. In that subset
of patients , serum HCG levels are elevated. The stroma varies - scant or
abundant- well defined fibrous strands creating lobules of neoplastic cells.
T lymphocytes usually infiltrate the septa, sometimes granulomas are seen.
Anaplastic seminoma: cellular and nuclear irregularity,
we^
giant cells and many mitoses.
Spermatocytic seminoma : is a distinctive tumor clinically and histologically.
It is one of the two variant of germ cell tumor that do not arise from an
intratubular germ cell neoplasm - the other is teratoma in children-
Uncommon, 1 - 2% of all germ cell tumors.
The age over 65 years.
Small growing tumor-rarely produce metastases- excellent prognosis.
The cut surface is pale gray soft and friable. The cells are larger than the
classic seminoma.
1. Medium size - most numerous, round nucleus and eosinophilic
cytoplasm
1. Smaller cells - narrow rim of eosinophilic cytoplasm
resembling secondary spermatocyte. 3. Giant cells -scattered-
either uninucleate or multinucleate
Electron microscope tumor cells show nuclear and cytoplasmic
feature of spermatic maturation.
 Embryonal Carcinoma : 20 to 30 year age group > aggressive than seminoma
Morphology: small tumor; the cut surface is variegated, no define margins, foci of
hemorrhage and necrosis. Extension of the tumor through the tunica
albuzinea , epididymis or cord.
The cells grow in glandular, alveolar, or tubular patterns, sometimes with
papillary convolutions. Sheets of cells when undifferentiated. The cells
are large and anaplastic with an epithelial appearance with
hyperchromatic nuclei and prominent nucleoli. Mitotic figures. Giant cells.
Syncytial cells - HCG, also cells containing AFP are detected with
immunoperoxidase. The presence of these substance are indicative of a
mixed tumor.
Pure tumors = 3%
Mixed tumors = 45%
The Marker is 13 hCG
Yolk sac tumor =
infantile embryonal carcinoma or endodermal sinus tumor: Most common in
infants and children up to 3 years of age. Adults as a mixed germ
cell tumor.
Morphology: nonencapsulated, homogeneous, yellow-white, mucinous appearance. The
cells are cuboidal in a lacelike network - reticular- or solid areas or papillae.
There are structure resembling glomeruli endodermal sinus- in 50% of cases.
Eosinophilic ,hyalin globules with immunoreactive AFP and alpha I-
antitrypsin are present within and around the cells.
Teratoma: Any age. Pure forms in infants and children, second to yolk sac. Pure
teratomas rare in adults 2 to 3%. In combination with other tumor 45%.
Mature--- differentiated mesodermal { muscle, cartilage, adipose tissue)
ectodermal { skin, neural tissue }
endodermal { gut, bronchial epithelium }
Common in infants and children
Pure testicular teratoma = Caution ; malignant elements
Immature teratoma --- three germ layer in incomplete stages of differentiation
--- regarded as malignant
Teratoma with malignant transformation --- malignancy in the form of carcinoma ,
most common, developing within a mature teratoma.
Choriocarcinoma: highly malignant
Both elements: cytotrophoblastic and syncytiotrophoblastic. Similar tumors
 may occur in the ovary, placenta, or secquested rests of totipotential cells.
Pure form is rare < 1%, more common foci of the tumor in mixed tumors.
Morphology: Small tumor, no testicular enlargement. Sometimes only an area of
fibrosis; noticed only the metastases.
The cut surface shows hemorrhage and necrosis. Syncytiotrophoblastic cells
are large an irregular with a vacuolated cytoplasm--HCG is demonstrated.
Cytotrophoblastic cells are more regular and polygonal with distinct borders
and clear cytoplasm.
Mixed tumors:

60% of testicular tumors are composed of more

than one pattern.
Most common combination 14 % teratoma,
embryonal, yolk sac, and HCG containing
syncytiotrophoblast. Teratocarcinoma=
embryonal+ teratoma

Seminoma and NSGCT

Metastases may be different from that of the testicular lesion

Tumor of sex cord- gonadal stroma:

Leydig ( interstitial ) cell tumor: may elaborate androgens or /and estrogen, also
corticosteroids.
20 - 60 years of age
Testicular swelling
Gynecomastia
Sexual precocity children

Morphology: usually < 5 cm, well circumscribe, golden brown. Neoplastic

cells similar to Leydig cells rod-shaped crystalloids of Reinke
in 25 % of cases.
10% of tumors in adults are invasive and metastized.
Sertoli cell tumor Androblastoma: uncommon
 Composed of Sertoli cells or a mixture of Sertoli and
granulosa cells.
Elaborates androgens or estrogens but rarely in sufficient
amount to produced symptoms.
Morphology: gray white to yellow. Variable size.
Cells are tall, columnar cytoplasm, often forming cords
immature seminiferous tubules.
Most benign---10% show invasion and/or metastases.
Testicular lymphomas: 5% of all testicular tumors.
Most common testicular tumor in patients older than 60 yrs.
Most are diffuse, large cell non-Hodgkin lymphomas. Disseminate widely.
Prognosis poor.
PROSTATE

Nodular Hyperplasia:
20% of men 40 years; 70% of men 60 years; 90% of men 79 yrs.
Asymptomatic in most patients.
? effects of androgens--- dihydrotestosterone --- via 5 alpha -reductase.
Frequency, nocturia, difficulty starting, and stopping.
Acute retention and chronic stasis
Morphology: periurethral portion. Hyperplasia of glands and fibromuscular
stroma.
Squamous metaplasia, infarcts, and cystic dilation.
Carcinoma of Prostate
Most common form of cancer in men.
Second leading cause of cancer death among men.
Men > 50 years.
Blacks > white; rare Asian
Etiology: unknown--hormonal influences, genetic factors, and -
environmental factors-diet-.
Morphology: 70% peripheral part--- posterior region. Stony hard area
Adenocarcinomas-- well to poorly differentiated sheets and cords. Closely spaced;
single layer of epithelial cells: invasion of vascular channel and perineural spaces.
Poorly demarcated, firm, gritty foci.
Advanced cases infiltrate the seminal vesicle and urinary bladder; invasion of
the rectum uncommon
 Lymphatic metastases initially in obturator nodes. followed to perivesical.
hypogastric, iliac, presacral, and para-aortic.
Hematogenous dissemination bone osteoblastic metastases. Prostatic
intraepithelial neoplasia is common adjacent ducts, presumably precursor of invasive
carcinoma.
Grading degree of differentiation, nuclear atypia, growth pattern--
predict the biologic behavior of carcinoma; Gleason system.
Staging therapy and prognosis
DNA ploidy , additional prognostic information--- aneuploid and tetraploid worst than
diplod
Serum prostatic acid phosphatase useful in diagnosis and staging.
PSA = PROSTATIC SPECIFIC ANTIGEN elevated in localized and advanced cancer; lesser
elevation may be seen in prostatic hyperplasia. Read Robbins 7th 1053- 1058
The ratio of free PSA to that bound to alpha -antichymotrypsin is consider useful in
distinguishing carcinoma from benign diseases. The percentage of free PSA is lower in
prostatic cancer.
Revised: 2009