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Pathology II Lower Urinary and Male Genital


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Congenital Anomalies
a. double ureters
b. (UPJ) obstruction
c. Diverticular out-pouching
d. Hydroureter
1. Usually seen in infants and young children
2. More common in boys
3. Abnormal organization of smooth muscle with collagen deposits
4. Results in hydronephrosis
5. 20% of the time may be bilateral in nature
Ureteral-pelvic junction (UPJ) obstruction
usually associated with double kidneys (4 ureters, 2 kidneys)
Double ureters
When it is symptomatic it may cause an obstruction of the lower portion of the ureter.
Diverticular out-pouching of the ureteral wall
A congenital or acquired dilatation of the ureter
Represents a ureter in which there are multiple small mucosal cysts
Ureteritis cystica
Represents an accumulation of lymphocytes within the wall of the ureter presenting a fine granular appearance on the surface of the mucosa
Ureteritis follicularis
Ureteritis – chronic UTI
Ureteritis cystica
Ureteritis follicularis
Tumors and tumor like lesions: rare - Benign
Fibro epithelial polyp and leiomyoma
Tumors and tumor like lesions: rare - Malignant
Majority are transitional carcinomas
Obstructive lesions result in
Intrinsic obstructions
Blood clot
Extrinsic obstructions
In Extrinsic obstructions Inflammation is caused by?
Salpingitis or Diverticulitis
This is a fibroproliferative inflammatory response in which there is an excessive growth of inflammation and fibrosis surrounding the ureter resulting in blockade or obstruction
Sclerosing retro peritoneal fibrosis
sometimes referred to as idiopathic retroperitoneal fibrosis
Sclerosing retroperitoneal fibrosis
It occurs in middle to late age
70% are idiopathic
Associated with ergot and beta blockers
Sclerosing retro peritoneal fibrosis
It occurs in other areas such as the mediastinum (sclerosing mediastinitis)
Sclerosing retro peritoneal fibrosis
Reidel’s fibrosing thyroiditis and Crohn’s disease
Sclerosing retro peritoneal fibrosis
Nests of urothelial cells may invaginate into the lamina propria and are known as?
Cell nests of von Brunn
Due to persistent urethral obstruction e.g. BPH with resultant increased intravesicle pressure
Diverticula: Acquired

Congenital is rare
People with diverticula of the urinary bladder are more prone to develop
Urinary stasis, infection, calculus formation, predisposition to vesico-ureteral reflux
Abnormality characterized by the absence of a portion of the anterior abdominal wall, so that the urinary bladder wall is exposed to the outside.
Developmental failure of the anterior abdominal wall; bladder communicates through a large defect on the abdominal wall surface or lies as an open sac to the outside.
This represents a fistulous track between the urinary bladder and the ureter, or even the uterus.
Congenital vesico-uterine fistula
A combination between the urinary bladder and the umbilicus
A Urachus
Sometimes this urachus does not completely atrophy,so that you develop an actual fistulous track between the urinary bladder and the umbilicus
Patent urachus
Capable of urinating outside umbilicus. Subject to repeated inflammation and can undergo metaplasia which can leads to the formation of an adenocarcinoma.
Patent urachus
Causes of Acute and chronic cystitis
Age, Sex, the presence of stones or obstruction, Calculus, Infection, Hemorrhage, Radiation, or Chemotherapy
Signs and Symptoms of Acute cystitis
Fever, Abdominal Pain and Dysuria
Acute cystitis will present itself as a clinical triad, namely?
Fever, Abdominal Pain and Dysuria
Acute cystitis is usually associated with inflammatory conditions such as:
E. coli
Painful or difficult urination in the Far East
Schistosomiasis (Schistosomes)
Hemorrhagic cystitis due to?
Cytotoxic drugs
People who received irradiation
Radiation cystitis
Long-term inflammatory condition of the bladder
Chronic cystitis
Most frequently associated in the male with benign prosthetic hypertrophy BPH
Chronic cystitis
Common cause is BPH
Fibromatous hyperplasia -Histologic variants:
1. Follicular
2. Eosinophilic
As a special form of cystitis
Interstitial cystitis is sometimes called?
Hunner’s ulcer
A persistent form of cystitis that does not respond to treatment
Interstitial cystitis (Hunner’s ulcer)
It presents with painful cystitis, frequency, mucosal ulceration, hematuria, and dysuria
Interstitial cystitis (Hunner’s ulcer)
middle-aged female. Urine cultures are negative
Interstitial cystitis (Hunner’s ulcer)
An increase in number of mast cells - significant in making diagnosis.
Interstitial cystitis (Hunner’s ulcer)
Intermittent pain, urinary frequency, even blood in the urine, and painful urination
Interstitial cystitis (Hunner’s ulcer)
Hypertrophy of the bladder wall - fibrotic
Increased numbers of mast cells
Interstitial cystitis (Hunner’s ulcer)
• Chronic inflammatory disease of the urinary bladder,
• Sometimes producing ulcerations Hunner’s ulcer,
• Histologically shows the presence of increased Mast cells.
Interstitial cystitis (Hunner’s ulcer)
A vesicle inflammatory reaction showing raised soft yellow mucosal plaques
If you stain these areas they will show the presence of PAS (+) granules.
multi-nucleated giant cells & lymphocytes - Malacoplakia
These foamy macrophages will colace to form multi-nucleated giant cells and lymphocytes - What is the Condition?
The microscopic finding which is diagnostic for Malacoplakia is a body we call?
Michaelis-Gutman bodies (Calcospheroids)
These are small (little) laminated basophilic mineral concretions that you see within the walls or on the surface of the bladder.
Michaelis-Gutman bodies (Calcospheroids)
It is generally thought that Malacoplakia is related to?
A chronic bacterial infection
The other important thing to remember about Malacoplakia is that?
It has no malignant potential
It may be seen in the testis, kidney and prostate
The diagnostic finding is laminated basophilic mineral concretions called Michaelis-Gutman bodies which are found in macrophages or between cells.
Malacoplakia is thought to be related to chronic bacterial infections of?
E. coli and Proteus
It will show small yellow mucosal plaques with PAS (+) granules.
Nests of transitional epithelial cells grow down into the mucosa forming cysts & glands. With extensive intestinal metaplasia there is an increased risk of Ca.
Cystitis glandularis and Cstitis cystica
An invagination of nest of transitional epithelial cells into the underlying lamina propria, we call these: Cell nests of von Brunn and there are seen in?
Cystitis glandularis
This is the same as Cystitis glandularis but it is seen in the ureter where small little cysts are formed on the mucosal surface
Cystitis cystica
You can see ectopic endometrial tissues occurring within the wall of the urinary bladder giving rise to a chronic inflammatory reaction.
Urothelial tumors: Size, higher grade give
A worse prognosis

Deeper penetration means worse prognosis
Transitional cell tumors make up about how much % of bladder tumors?
90% of bladder tumors
The ISUP grading system (International Society of Urologic Pathologists) is used to stage the disease.
It depends on the layer into which the neoplasm has infiltrated.
Muscularis propria
Large bundles of smooth muscle cells
Muscularis mucosae
Scattered smooth muscle cells
Lamina propria; basement membrane; and mucosa
3-7 layers thick
Urothelial papilloma: Transitional cell papillomas account for what % of bladder neoplasms?
Transitional cell papillomas account for 1% of bladder neoplasms
7% of these will develop into carcinomas. A small nodule is attached to the bladder wall by a delicate stalk.
Urothelial papilloma
Invertede papillomas are similar to papillomas, but exhibit a?
Thickened mucosa with large cells penetrating the lamina propria
These lesions have a thickened epithelium with diffuse nuclear enlargement & are generally non-invasive.
Urothelial lesion of low malignant potential (TCC Grade I)
Invasion of the muscularis propria is the diagnostic finding
Urothelial lesion of low malignant potential (TCC Grade I)
With full thickness dysplasia, 50% will become malignant and invasive.
Urothelial lesion of low malignant potential (TCC Grade I)
These exhibit good polarity and cohesion and nuclear atypism at the basal cell layer.
Urothelial carcinoma - low grade (TCC Grade II)
It is usually papillary and invasion is rare, occurring in less than 10% of cases
Urothelial carcinoma - low grade (TCC Grade II)
Patients are treated with intravesicle chemotherapy, not by cystectomy.
Urothelial carcinoma - low grade (TCC Grade II)
These may be papillary, nodular, allomorphic, or anaplastic
Urothelial carcinoma - high grade (TCC Grade III)
Characterized by dys-cohesiveness with increased mitotic figures.
Urothelial carcinoma - high grade (TCC Grade III)
It may exhibit extreme anaplasia, and invasion is common, occurring in 80% of cases.
Urothelial carcinoma - high grade (TCC Grade III)
Involves the full thickness of the bladder
It is characterized by cytologic malignant cells within a flat urothelial surface & is usually not big.
The extent of the invasion is of prognostic importance
Invasive urothelial carcinoma
3%-7% of cases and almost always associated with chronic bladder infections
Squamous cell carcinoma
It shows an increased incidence with Schistomiasis infection
Squamous cell carcinoma
Is rare and is usually due to cystitis cystica or cystitis glandularis
Mesenchymal Tumors – may be very large - Benign are?
Mesenchymal Tumors: Malignant - Produce large masses of tumor(10-15 cm) that are soft and fleshy.
Adults over the age of 40 years
Seen in infancy and early childhood. They are large tumors. Biopsy will show strap cells with cross striations.
Embryonal rhabdomyosarcomas (sarcoma botryoides)
Strap cells with cross striations.
Embryonal rhabdomyosarcomas (sarcoma botryoides)
similar to that of lung cancer
Male affected more than female 3:1
Bladder cancer
Risk factors for bladder cancer
Cigarette smoking
Industrial exposures
Long-term use of analgesics
Gene mutations
Incites inflammation; there is a 3-7 X increased risk.
Cigarette smoking
Shows a 50-80% association in men who smoke.
Bladder cancer
Industrial exposures more common in the West
Alpha-napthayl amines
70% are squamous cell carcinomas
Risk factor for bladder cancer - Long term use of analgesics, especially?
Painless hematuria; also associated with frequency, urgency and dysuria
Clinical Findings in Bladder cancers
Pyelonephritis - due to urethral orifice involvement
Clinical Findings in Bladder cancers
Clinical Findings in Bladder cancers
Recurrence rate is high with anaplastic tumors 80-90%.
Clinical Findings in Bladder cancers
Grade I has a 98% 10 year survival rate
Bladder cancers
Grade III has a 40% 10 year survival rate
Bladder cancers
Squamous Cell Carcinoma - 20% dead in one year
Bladder cancers
Regarding Bladder Cancer: Early diagnosis is key to survival and is aided by?
Urine cytology – flow cytometry of urine sediment for aneuploid tumor cells (high S-phase).
Regarding Bladder Cancer: The last step of diagnosis is?
Obstructions: clinically important - Kidney
Obstructions: clinically important - Prostate gland
Obstructions: clinically important - Bladder
Obstructions: clinically important - Cystocele
Narrowing or stricture of urethra - seen in females
Obstructions: clinically important - Gross
Hypertrophy and trabeculation
Invasion of the muscularis propria
has the worst prognosis. 50% of these patients will be dead in 5 years.
Treatment for bladder cancer:
1. Cauterization of nodules
2. Interstitial chemotherapy
3. Cystectomy – removal of the bladder is the ultimate treatment
Inflammations: Urethritis is classically divided into:
1. Gonococcal
2. Non-gonococcal
3. Reiter’s syndrome
Urethritis is an early sign of
Gonococcal infection
These are often accompanied by cystitis in female and prostatitis in male
Non-gonococcal – E coli, Chlamydia, Mcoplasma infections
Arthritis, urethritis, conjunctivitis – associated with mycoplasma infection
Reiter’s syndrome
Is an inflamed painful red nodule at the external urethral meatus in female. It may ulcerate and bleed. Treatment is surgical excision.
Urethral caruncle
Occurs at external meatus. It may be viral in origin. exhibits highly vascular fibroblastic connective tissue
Usually squamous cell carcinoma. It is seen in older females, and is more aggressive than transitional cell ca.
Male Genital Tract:
Congenital disorders:
1. Hypospadias
2. Epispadias
3. Phimosis
Congenital disorder:
ventral opening (under-surface; more common)
Congenital disorder:
Dorsal Opening
Congenital disorder:
Phimosis - prepuce is too small to permit normal retraction of foreskin - risk of infections due to poor hygiene
These infections are the most common causes
Syphilis, g.c. chancroid, herpes
Inflammation of the glans and prepuce
Balanoposthitis may be caused by?
Candida and Gardnerella
Male Genital Tract:
Is caused by HPV type 6. It can be a sessile or pedunculated lesion.
Condyloma accuminata
The picture of condyloma acuminata is
Red papillary excressences showing a branching villous architecture with underlying stroma covered by epithelium and exhibits koilocytic changes (clear vacuolization of prickle cells - characteristic of HPV infection - bigger than normal cells with a central nucleus).
A squamous cell dysplasia confined to the epithelium, full thickness but without invasion.
It is considered to be pre-invasive carcinoma
Is carcinoma-in-situ occurring in men and women over 35 years of age. The lesion shows a thick grey-white membrane with shallow ulceration and crusting.
Bowen’s disease
Microscopically, there are atypical squmaous cells with increased mitoses but no invasion. 10% will develop SCC – involving the skin of penis
Bowen’s disease
(on glands penis) forms a shiny red plaque, single or multiple lesions. It is histologically indistinguishable from Bowen’s disease. Patients can develop carcinoma.
Erythroplasia of Queyrat
The lesion usually involves the surface of the glans only
Erythroplasia of Queyrat
Occurs on external genitalia in sexually active young patients and multipigmented red brown papule associated with HPV 16.
Bowenoid papulosis
It is histologically similar to BD but does not develop Ca.
Bowenoid papulosis
High rate in Asia and Africa. Circumcision protects due to better hygiene.
Carcinoma is usually?
A squamous cell carcinoma
Male Genital Tract:
Verrucous carcinoma is a giant condyloma and is also called?
(Buschke-Lowenstein tumor)
It is slow growing, with local spread to inguinal and iliac lymph nodes.
Carcinoma: Verrucous carcinoma is a giant condyloma (Buschke-Lowenstein tumor)
It is associated with HPV 16 &18 and forms a painless ulcer. There is a direct relationship to cigarette smoking.
Carcinoma: Verrucous carcinoma is a giant condyloma (Buschke-Lowenstein tumor)
A failure of the testicle to descend into the scrotal sac.
The testicle is palpable in inguinal canal, small, firm, and atrophic. It is usually unilateral.
Microscopically there is arrest of germ cell development with habitation and thickening of the basement membrane with hyalinization and obliteration, and increased interstitial cells of Leydeg.
Cryptorchidism results in?
There is a 5-10 X risk of a germ cell tumor. Treatment is by orchiplexy – surgically moving the testicle into the scrotum.
Regressive changes:
Causes may be inflammation, atherosclerosis, cryptorchdism, hypopituitarism, radiation, or estrogen therapy (prostate Ca)
Regressive changes:
Causes include GC, TB, Syphilis, Mumps.
Regressive changes:
True inflammation is?
Vascular disturbances:
Will result in infarct due to decreased oxygen, and commonly occurs in athletes.
Testicular Tumors are associated with?
The higher up the greater risk of Ca
Genetic factors - racial differences
Testicular Tumors
Testicular Tumors:
Tsticular feminization and Klinefelter’s syndrome show an increased risk of Ca
Testicular dysgenesis
Appear as painless mass and characteristically spread to the retro- peritoneal lymph nodes to the par aortic, to mediastinal lymph node, and then to supraclavicular nodes.
Testicular tumors
Testicular tumors are divided into two major types?
1. Germ cell tumors
2. Non-germ cell tumors
Testicular tumor:

Two major categories?
1. Germ Cell tumors
2. Sex-Cord Tumors
Occur in younger males, blacks more than whites. These may be of 2 types:
Germ Cell tumors
Germ Cell tumors may be of 2 types?
a. Pure or Single Histologic Pattern
b. Mixed Histologic Pattern
40% of testicular tumors
Pure or Single Histologic Pattern type.
Pure or Single Histologic Pattern:
i. Seminomatous tumors Seminomas (seminiferous tubule tumor)
ii. Non-seminatous tumors
Non-seminatous tumors -

A subcategory of Pure or Single Histologic Pattern:
1. bEmbryonal carcinoma
2. Yolk sac tumor (endodermal sinus tumor)
3. Choriocarcinoma: may be mature, immature, or malignant transformation
60% of testicular tumors. These are not as treatable as pure cell tumors.
Mixed Histologic Pattern
Embryonal carcinoma with teratoma (teratocarcinoma)

Choriocarcinoma with any other type
Mixed Histologic Pattern
Sex-Cord Tumors:
a. Leydig cell tumor
b. Sertoli cell tumor
c. Granulosa cell tumor
Are the most common form of testicular tumor with a peak age of 30 years.
They are similar to an ovarian neoplasm (dysgerminoma). There is usually no invasion.
These may be up to 10 mm, or very small and they respond well to radiation therapy.
There are 3 histologic variants of Seminomas, name them?
1. Typical seminomas
2. Anaplastic seminomas
3. Spermatocytic seminomas
85% - Homogeneous, grey white with no penetration of the tunica vaginalis and usually shows no hemorrhage or infarct.
Typical seminomas
Consist of sheets of uniform appearing cells with delicate fibers infiltrated with lymphocytes and rare mitosis
Typical seminomas
5-10% - It is a more aggressive tumor with marked cellular and nuclear changes with giant cells and many mitoses (More than 3 per high power field)
Anaplastic seminomas
4-6% - It is a distinct but uncommon tumor, usually seen over the age of 60 years and is composed of three cell types: large, small and giant cells.
Spermatocytic seminomas
They do not secrete alpha-fetoprotein or HCG. They do exhibit high levels of placental alkaline phosphatase.
Non-Seminomatous tumors:
1. Embryonal carcinoma
2. Yolk Sac tumor
3. Choriocarcinoma
4. Teratomas
5. Mixed Tumors
Most often in the 20-30 age group. Gross appearance: poorly defined tumor boundaries - usually smaller than seminomas, characterized by hemorrhage and/ necrosis. May penetrate the tunica albunigea.
Embryonal carcinoma
Microscopically, there is a glandular alveolar or tubular pattern with papillary convolutions, and frequent mitoses and giant cells. The carcinoma may show syncytial cells which may contain HCG or AFP (Mixed type)
Embryonal carcinoma
Is an infantile embryonal carcinoma or endodermal sinus tumor and is the most common testicular tumor in infants up to three years. It has a yellow-white mutinous appearance.
Yolk Sac tumor
The microscopic appearance is a micro-cystic papillary pattern containing glomerular type structures known as Schiller-Duval bodies. Within the cytoplasm of these cells are eosinophilic hyaline globules which contain alpha-fetoprotein and alpha-1-antitry
Yolk Sac tumor
occurs in 1% of these tumors, usually mixed with some other form of neoplasm. It is a highly malignant tumor which consists of both synctiotrophoblasts (large irregular hyperchromatic nuclei with eosinophilic cytoplasm) and cytotrophoblasts (regular poly
Is aggressive but remains of small size. Hemorrage and necrosis are extremely common and the tumor does produce extremely high levels of HCG.
Possess various cellular or organoid components (endoderm, ectoderm, and mesoderm) and occur at any age.are usually very large - 5-10 cm. There are multiple histologic types:
Different types of teratomas:
a. Mature teratomas
b. Immature teratomas
c. Teratomas with malignant transformation
are well differentiated cells such as nerve, muscle cartilage, squamous epithelium, thyroid, GI or brain tissue, and are usually seen in children.
Mature teratomas
Have 3 germ cell layers with incomplete differentiation.
Immature teratomas
Are clearly the appearance of a malignant neoplasm. Examples are Squamous cell Carcinoma, adenocarcinoma, or sarcoma.
Teratomas with malignant transformation
These are tumors composed of more than one type of tumor and account for 60% of testicular tumors.
Mixed Tumors
Examples of mixed tumors include
Seminoma with embryonic Carcinoma, and embryonal Carcinomas with teratoma (teratocarcinoma).
From the clinical standpoint tumors of the testis are classified into two broad categories:
1. Seminomas
2. Non-seminomatous tumors
Tend to remain local
70% stage I tumors
Mets via lymphatic
60% have advanced clinical disease
Mets via blood
Non-seminomatous tumors
Clinical Staging of Testicular tumors:
Confined to testicle
Clinical Staging of Testicular tumors:
Distant spread to retro peritoneal nodes below the diaphragm
Clinical Staging of Testicular tumors:
Distant spread above the diaphragm
Characteristic mode of spread of testicular cancer is via?
Characteristic mode of spread of testicular cancer is via lymphatic
1. Retro peritoneal (para-aortic nodes first)
2. Mediastinal
3. Supraclavicular
4. Hematogenous spread: lungs, liver, brain, bone
Biologic Markers:
A glycoprotein containing two polypeptide chains: alpha and beta, normally synthesized and secreted by placental syncytiotrophoblasts?
A serum protein synthesized in the fetal gut, liver and yolk sac. After the first year of life it is normally undetectable. It is seen in yolk sac tumors but also seen in hepatocellular carcinomas and ulcerative colitis?
Biologic Markers:
Only produced by seminomas
Placental alkaline phosphatase
Biologic Markers:
High in seminomas
Biologic Markers:
Are elevated in mixed cell tumors; (Note:Placental alkaline phosphatase and LDH are elevated in seminomas)
Biologic Markers:
Yolk sac tumors will produce?
AFP only
Biologic Markers:
Choriocarcinoma will produce?
HCG only
Value of Markers:
1. In the initial evaluation of a testicular mass
2. For staging following orchidectomy
3. LDH will asses tumor burden 6 months post-operative
4. Predict possible recurrence if levels remain elevated after surgery
Tumors of Sex cord- gonadal stroma:
1. Leydig cell (interstitial) tumors
2. Sertoli cell tumors
3. Testicular lymphomas
Are derived from stromal tissues and may elaborate androgens and/or estrogens. Patients will show enlarged testicles or gynecomastia. In children you will see precocious puberty. Microscopically there are large round to oval cells with abundant eosinophi
Leydig cell (interstitial) tumors
Are derived from sex cords. Sertoli cell tumors were previously called androblastomas. They occur in younger patients and are composed of sertoli cells which resemble semeniferous tubules. Estrogenic effect causes gynecomastia.
Sertoli cell tumors
Are usually a B-cell lymphoma, usually occurring after age 60. They are rare but very aggressive.
Testicular lymphomas
Lesions of the Tunica Vaginalis:
1. Hydrocele
2. Hematocele
3. Spermatocele
4. Varicocele
5. Chylocele
Is an accumulation of clear fluid within the scrotal sac – may be up to 10 cm in diameter. Diagnosis is by transillumination
Results from blood in the sac, usually due to trauma or torsion
Is a cyst with accumulation of spermatozoa, usually occurring due to surgery for an orchidectomy.
Dilated veins in the spermatic cord
Prostate Gland:
Inflammation (prostatis):
a. Acute bacterial prostatitis
b. Chronic bacterial prostatitis
c. Chronic abacterial prostatitis
Diagnose with urine culture. It may be a focal or diffuse suppurative inflammation, usually caused by E. coli or other gram negative rod. Symptoms are fever, chills, dysuria, and an acutely tender prostate with rectal exam.
Acute bacterial prostatitis
Presents with low back pain and dysuria. It is characterized by recurrent UTI, cystitis, and urethritis. Diagnosis: leukocytes in prostatic secretions and a positive culture.
Chronic bacterial prostatitis
Is the most common form of prostatitis. It is similar to chronic bacterial prostatitis except for negative culture and is seen commonly in sexually active individuals. Chronic abacterial prostatis may be caused by Chlamydia trachoma and Mycoplasma homini
Chronic abacterial prostatitis
Benign enlargememt:
Occurs in 20% of males over 40, 70% of males over 60, and 90% of males over 70. Is related to androgens
(prostatic hyperplasia) BPH.
Benign enlargememt:
Is a metabolite of testosterone and acts on androgen receptor sites of the prostate maintaining normal prostate function. It is 10X more potent in its effect than testosterone.
Benign enlargememt:
Estrogens induce or increase androgen receptor sites rendering the cells more susceptible to the action of DHT resulting in
Prostatic Hyperplasia
Benign enlargememt:
As males age, there is a decreased ability to detoxify
Benign enlargememt:

Gross appearance of BPH?
Is a nodular, whorled pattern
Benign enlargememt:

Microscopic appearance of BPH?
Glands exhibit a double layer of cells with inner columnar and outer cuboidal hyperplasia. BPH may be asymptomatic. There may be areas of infarct, indicated by foci of squamous metaplasia.
Clinical symptoms of BPH:
a. Compress the urethra
b. Retention of urine in bladder - thus vulnerable to infections
c. Generally considered not to be a pre-malignant process
Is the most common cancer in men. It usually occurs after 50 years. Latent ca is present at 20% in 50 year olds, and 70%= 70-80 year olds. It is rare in Asians, but has an increased incidence in blacks.
Prostate cancer
Etiology of prostate cancer is influenced by?
Age, race, family history, hormone levels, environmental factors(as evidenced by the fact that a man going from low incidence areas to high incidence areas show increased risk of developing Ca). It is thought that androgens play a part in development of prostate cancer.
Tumors of the Prostate Gland:
Morphology of Prostate cancer
70% occur peripherally, most commonly in the posterior lobe, and almost all are adenocarcinoma.
Prostate cancer spreads via:
1. Direct invasion or contiguous spread
2. Hematogeneous spread
3. Lymphatic spread
Prostate cancer:
Beginning at the base of bladder, seminal vesicles
Direct invasion or contiguous spread
Prostate cancer:
Is chiefly to bone by osteoblastic mets (more common) or osteolytic lesions. Cranial mets seen as a result of passage up the vertebral column through the paravertebral veins of Batson and invades the calvarium.
Hematogeneous spread
Prostate cancer:
Is via the obturator nodes, inguinal, and pelvic lymph nodes. Upon pelvic lymphadenectomy if there are positive Obturator lymph nodes, surgery (prostatectomy) is not done.
Lymphatic spread
Prostate cancer:
Shows malignant cells one layer thick, back to back with little stroma (normal prostatic gland arrangement is 2 layers thick. The best indication of malignancy is capsular invasion and perineural invasion
Prostate cancer:
A precancerous lesion exhibiting dysplastic cells. It is thought to be a intermediate lesion between normal and malignant tissues
Concept of PIN
Gleason’s grading system
Gleason’s grading system
There are five grades, based on the histologic pattern and degree of differentiation - assess and add to a total of ten. Assign a primary grade to the dominant cellular type and then assign a secondary grade to the sub-dominant type. Add the two together to come up with the Gleason’s grade. For example a well differentiated tumor 1+2=3; Good correlation with prognosis.
Biochemical markers:
In normal males, it is seen in small amounts (<4 ng/ml). Is organ specific but not cause specific, as it is also seen in nodular hyperplasia and prostatitis
Prostatic specific antigen (PSA), a product of prostatic epithelium.
Prostatic acid phosphatase (PAP) old type, has been supplanted by PSA.
Biochemical markers:
% free PSA - differentiates between?
Non-neoplastic and neoplastic prostatic lesions.
Biochemical markers:
Free PSA is lower in Ca. Use free PSA to test when?
Levels of PSA are in the gray zone (4-10).
Biochemical markers:
Serial measurement valuable in assessing
Response to therapy
Treatment for Prostate cancer
Surgery – transurethral prostatic resection – cauterize and remove select areas of the prostate. Over age 70, often no treatment is done.
Hormonal manipulation – useful if there is mets

Estrogen therapy

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