Lower Urinary Tract and Male Genital System

Question 1

Ureter Congenital Anomalies

Answer 1

• ureteropelvic junction obstruction = important cause of hydronephrosis in kids.
  
  • secondary to disorganized junctional smooth muscle, excess stromal matrix, or compression by renal vessels.

Question 2

Benign Ureteral Neoplasms

Answer 2

• mesenchymal.

Question 3

Fibroepithelial Polyps

Answer 3

• small intraluminal projections in kids.

Question 4

Malignant Ureteral Neoplasms

Answer 4

• urothelial carcinomas, similar to tumors in renal pelvis and bladder.

Question 5

Ureteral Obstruction

Answer 5

• can be secondary to calculi or clots, strictures, tumors, or neurogenic bladder dysfunction.
• ureteral dilation less important than secondary renal hydronephrosis or pyelonephritis.
• sclerosing retroperitoneal fibrosis = uncommon cause of obstruction having retroperitoneal inflammation and fibrosis, encases ureters and leads to hydronephrosis.
  
  • most have no cause (Ormond disease). can be from: drugs, neoplasms, inflammation.

Question 6

Diverticula

Answer 6

• outpouchings of bladder wall that arise as congenital defects or are acquired from persistent urethral obstruction (prostatic enlargement).
• urinary stasis predisposes to infection and calculi formation, also vesicoureteric reflux.
• if have carcinoma with it, is more advanced from thinned wall.

Question 7

Exstrophy

Answer 7

• due to development failure of anterior abd wall. bladder communicates directly with overlying skin or lies as exposed sac.
• complications = chronic infection and ↑ incidence of adenocarcinoma.
• can be surgically corrected.

Question 8

Other Ureteral Anomalies

Answer 8

• vesicoureteral reflux, connections btw bladder and vagina, rectum, uterus, or umbilicus.
  
  • umbilicus is from remnant fistulous tract of urachus that connected fetal bladder and allantois.
  • urachal cyst when only central portion of tract persists.

Question 9

Acute and Chronic Cystitis

Answer 9

• UTI.
• from bacteria, TB, fungi, viruses, Chlamydia, mycoplasma.
• schistosomiasis cystitis common in middle east.
• radiation and chemo can cause inflammation and hemorrhage.
• presentation: urinary frequency, lower abd pain, and dysuria.

Question 10

Interstitial Cystitis

Answer 10

• aka chronic pelvic pain syndrome.
• chronic cystitis in women, causing pain and dysuria without infection.
• punctate hemorrhages early, then localized ulceration (Hunner ulcer) with inflammation and transmural fibrosis.
• have mast cells.

Question 11

Malacoplakia

Answer 11

• in chronic bacterial cystitis (E. coli or Proteus), in immunosuppressed pts.
• lesions are 3-4cm soft, yellow, mucosal plaques made of foamy macrophages and bacterial debris.
• macrophages have intra-lysosomal laminated calcified concretions = Michaelis-Gutmann bodies.
• have defective macrophage phagocytic or degradative function.

Question 12

Cystitis Glandularis

Answer 12

• can be in normal bladder or with chronic cystitis.
• composed of Brunn nests (nests of transitional epithelium) that grow downward into lamina propria and transform into cuboidal epithelium.
• sometimes has intestinal metaplasia.

Question 13

Cystitis Cystica

Answer 13

• in normal bladder and chronic cystitis.
• made of Brunn nests (nests of transitional epithelium that grow downward into lamina propria and transform into flattened cells lining fluid-filled cysts.

Question 14

Squamous Metaplasia of Bladder

Answer 14

• in response to injury.

Question 15

Nephrogenic Adenoma of Bladder

Answer 15

• when shed tubular cells implant and proliferate at sites of injured urothelium.
• benign although can extend into superficial detrusor muscle.

Question 16

Urothelial Tumors

Answer 16

• occur anywhere from renal pelvis to distal urethra.
• precursor lesions: non-invasive papillary tumors = most common, range of atypia that can reflect biologic behavior.
  
  • carcinoma in situ = high grade lesion of malignant cells in flat urothelium. lack cohesiveness and shed into urine.
• involvement of muscularis propria (detrusor muscle) is major determinant of outcome, 50% 5 yr mortality.
• pathogenesis: 3:1 M:F. affects urban populations more. 80% btw ages 50-80 yrs.
  
  • risk factors: cigarettes, arylamines, schistosoma haematobium infection, chronic analgesic use, long term cyclophosphamide exposure, bladder radiation.
  • 30-60% have chromosome 9 mutations, affects p16 and p15. p53.
• morphology: papillary are low grade, red excrescences 0.5-5cm in size.
  
  • CIS = mucosal reddening, granularity, or thickening without evident intraluminal mass.
    
    • multifocal. untreated - 50-75% becomes invasive.
• presentation: painless hematuria, frequency, urgency, dysuria. 60% single, 70% localized at diagnosis.
  
  • develop new tumors after excision, are new or shedding/implantation.

Question 17

Exophytic Papillomas

Answer 17

• urothelium over finger-like papillae with loose fibrovascular cores.
• low incidence of progression or recurrence.
• 98% 10 yr survival.

Question 18

Inverted Papillomas

Answer 18

• bland urothelium extending into lamina propria.
• uniformly benign.
• 98% 10 yr survival.

Question 19

Papillary Urothelial Neoplasms of Low Malignant Potential

Answer 19

• slightly larger than papillomas with thicker urothelium and enlarged nuclei, rare mitoses, infrequent invasion.

Question 20

Low-Grade Papillary Urothelial Carcinomas

Answer 20

• orderly cytology and architecture with minimal atypia.
• can invade but rarely fatal.
• 98% 10 yr survival.
• transurethral resection.

Question 21

High-Grade Papillary Urothelial Cancers

Answer 21

• have discohesive cells with anaplastic features and architectural disarray.
• high risk (80%) for rogression and metastases.
• 25% mortality rate.

Question 22

Squamous Cell Carcinomas (Bladder)

Answer 22

• associated with chronic bladder infection and inflammation.
• 3-7% of bladder cancers.
• more frequent in countries with endemic schistosomiasis.

Question 23

Mixed Urothelial Carcinomas

Answer 23

• with areas of squamous carcinoma are invasive, fungating, and/or ulcerating tumors.
• more common than purely squamous cell bladder cancers.

Question 24

Bladder Adenocarcinomas

Answer 24

• rare.
• from urachal remnants or in setting of intestinal metaplasia.

Question 25

Mesenchymal Tumors of Bladder

Answer 25

• rare.
• benign = look like elsewhere. ex: leiomyomas (most common).
• sarcomas = large (10-15cm), exophytic masses.
  
  • most common in kids = embryonal rhabdomyosarcoma
  • most common in adults = leiomyosarcoma

Question 26

Urethritis

Answer 26

• either gonococcal or non-gonococcal.
  
  • men usually have prostatitis, women usually have cystitis.
  • most common non-gonococcal = E. coli and enterics.
  • Chlamydia = 25-60% NGU in men, 20% in women.
  • mycoplasma is least frequent
• Reiter syndrome = urethritis, arthritis, conjunctivitis. associated with NGU.

Question 27

Hypospadia

Answer 27

• malformations of urethral canal producing aberrant openings on ventral aspect of penis.
• associated with urogenital malformations (undescended testes).
• constriction can predispose to UTIs.
• severe displacement can cause sterility.

Question 28

Epispadia

Answer 28

• malformation of urethral canal that can produce aberrant openings on dorsal surface of penis.
• associated with urogenital malformations (undescended testes).
• constriction predisposes to UTIs.
• severe displacement can cause sterility.

Question 29

Phimosis

Answer 29

• prepuce (foreskin) orifice too small to permit normal retraction.
• usually due to inflammation.
• predisposes to secondary infections and carcinoma from chronic accumulation of secretions and other debris (smegma).

Question 30

Penile Inflammation

Answer 30

• involve both glans penis and prepuce.
• sexually transmitted = syphilis, gonorrhea, chancroid, lymphopathia venereum, herpes, granuloma inguinale.
• balanoposthitis = non-specific infection by other organisms (Candida, Gardnerella, anaerobic or pyogenic bacteria).
  
  • from poor local hygiene in uncircumcised males from smegma, can cause phimosis.

Question 31

Condyloma Acuminatum

Answer 31

• benign sexually-transmited epithelial proliferation from HPV types 6 and 11.
• recurs after excision, rarely malignant.
• morphology: single or multiple sessile or pedunculated red papillary excrescences 1-5mm. involves coronal sulcus or inner prepuce.
  
  • branching papillae covered by hyperplastic stratified squamous epithelium, with hyperkeratosis. koilocytosis common (epithelial cell vacuolation).

Question 32

Bowen Disease

Answer 32

• carcinoma in situ. involves **male or female genitalia in patients >35yrs. **
• men present with solitary or multiple thickened, gray-white or red shiny plaques on penile shaft.
  
  • marked epithelial atypia with lack of orderly maturation, no invasion.
• 10% transition to invasive squamous cell carcinoma.
• associated with HPV infection, type 16.

Question 33

Bowenoid Papulosis

Answer 33

• carcinoma in situ, associated with HPV type 16.
• multiple, pigmented papular lesions on external genitalia in younger sexually active pts.
• indistinguishable from Bowen disease.
• rarely evolves to invasive carcinoma.
• frequently spontaneously regress.

Question 34

Invasive Carcinoma

Answer 34

• penile squamous cell carcinoma <1% of cancers in american men.
• higher prevalence in uncircumcised.
  
  • related to carcinogens in smegma, HPV types 16 and 18.
• occurs in men ages 40-70yrs.
• morphology: epithelial thickening on glans or inner surface of prepuce, progreses to ulceroinfiltrative or exophytic growth eroding penile tip, shaft, or both.
  
  • histology same as squamous cell carcinoma.
  • verrucous carcinoma = uncommon well-differentiated variant, low malignant potential.
• presentation: slow growth, metastases occur in inguinal and iliac lymph nodes.
  
  • 66% 5 yr survival if only in penis. 27% with lymph node involvement.

Question 35

Cryptorchidism

Answer 35

• in 1% of 1yr old boys.
• failure of descent of testes.
• usually unilateral and isolated anomaly.
  
  • bilateral in 25%.
• testes found anywhere along normal abd to scrotal sac pathway.
  
  • 5-10% from defect in transabdominal descent (controlled by mullerian-inhibiting substance).
  • most involves abnormalities in descent through inguinal canal (controlled by androgens), usually palpable in inguinal canal.
• morphology: manifest as early as 2yrs old. decreased germ cell development, thickening and hyalinization of seminiferous tubule basement membrane, and interstitial fibrosis. sparing of Leydig cells.
  
  • deterioration in contralateral descended testes, suggests intrinsic defect in testicular development.
• presentation: associated with sterility, inguinal hernias, ↑ incidence of testicular malignancy.
  
  • most spontaneously descend within 1st year or get orchiopexy (surgery) before 2nd bday.

Question 36

Testicular Atrophy and ↓ Fertility

Answer 36

• primary = due to developmentat abdnormality (Klinefelter syndrome).
• secondary to cryptorchidism, vascular disease, inflammatory disorders, hypopituitarism, malnutrition, ↑ levels of FSH, exogenous androgenic or anti-androgenic hormones, readiation, chemo.
• morphology same as with cryptorchidism.

Question 37

Testicular and Epididymal Inflammation

Answer 37

• more common in epididymis.
• syphilis begins in testes, progresses to epididymis.

Question 38

Nonspecific Epididymitis and Orchitis

Answer 38

• from primary urinary tract infection, reaches epididymis via vas deferens or spermatic cord lymphatics.
• childhood epididymitis: associated with congenital genitourinary abnormalities and gram (-) rod infections.
• sexually active men <35yrs = C. trachomatis and N. gonorrhoeae.
• men >35yrs = common UTI agents (E. coli and Pseudomonas).
• morphology: non-specific epididymal congestion, edema, neutrophilic infiltrates.
  
  • can go to generalized suppuration. can go to testes via efferent ductules or local lymphatics, scarring can cause infertility.
  • Leydig cells not effective so testosterone normal.

Question 39

Granulomatous (Autoimmune) Orchitis

Answer 39

• presents in middle age as painless to moderately tender testicular mass, sudden onset.
• spermatic tubule granulomas.
• suspected to be autoimmune.

Question 40

Gonorrhea in Testes

Answer 40

• retrograde extension from posterior urethra to prostate, seminal vesicles, epididymis.
• untreated ⇒ testis, causes suppurative orchitis.

Question 41

Mumps in Testes

Answer 41

• uncommon in kids but develops in 20-30% of postpubertal men with mumps.
• acute interstitial orchitis develops 1 wk post parotid inflammation.

Question 42

TB in Testes

Answer 42

• begins in epididymis, secondarily involves testis.
• caseating granulomas.

Question 43

Syphilis in Testes

Answer 43

• congenital or acquired.
• isolated orchitis without involvement of adnexal structures.
• nodular gummas or diffuse interstitial inflammation with edema, lymphoplasmacytic inflammation, and obliterative endarteritis.

Question 44

Testicular Torsion

Answer 44

• twisting of spermatic cord cuts off testicular venous drainage.
• thick-walled arteries remain patent ⇒ intense vascular engorgement, may cause hemorrhagic infarction.
• neonatal = in utero or shortly after birth. lacks anatomic defect.
• adult = present in adolescence as sudden testicular pain. associated with bilateral anatomic defect giving testis increased mobility (bell-clapper abnormality).
• occurs without cause. is urologic emergency, need to untwist within 6 hrs of onset.
• orchiopexy to fix it to scrotum, prevent twisting.

Question 45

Spermatic Lipomas

Answer 45

• involve proximal spermatic cord.
• fat around cord sometimes represents retroperitoneal adipose tissue that has been pulled into inguinal canal of hernia sac.

Question 46

Adenomatoid Tumors (Male Genitalia)

Answer 46

• most common benign paratesticular neoplasm.
• small nodules of mesothelial cells near upper epididymal pole.

Question 47

Rhabdomyosarcomas

Answer 47

• most common malignant tumor in kids in spermatic cord and paratesticular area.

Question 48

Liposarcomas

Answer 48

• most common malignant tumor in adults in spermatic cord and paratesticular tumors.

Question 49

Testicular Germ Cell Tumors

Answer 49

• 95% of cases. malignant. divided into seminomas and non-seminomas.
• whites:blacks 6:1.
• most common malignancy in men btw 15-34 yrs, 10% of cancer deaths in that age range.
• pathogenesis: cryptorchidism (in 10%); testicular dysgenesis syndrome (TDS) which includes cryptorchidism, hypospadias, poor sperm quality.
  
  • TDS related to pesticides, estrogen in utero.
  • genetic = familial clustering, incidence of testicular carcinoma among brothers and sons of affected.
  • most come from intratubular germ cell neoplasia (iTGCN) that is dormant until puberty. retain expression of OCT3/4 and NANOG associated with totipotentiality. can have activating mutations of c-KIT.
• consequences: 60% have multiple cell types. usually capable of rapid, wide spread dissemination, respond to therapy.
• presentation: painless enlargement of testis.
  
  • radical orchiectomy to prevent tumor spillage.
  • lymphatic metastases first in retroperitoneal paraaortic nodes. hematogenous metastases involve lung, then liver, brain, and bone.
  • non-seminomatous more aggressive than seminomas.
    
    • seminomas radiosensitive.
    • non-seminomas radioresistant, present in advanced disease. chemo ⇒ 90% remission.
    • choriocarcinomas aggressive, extensive hematogenous metastases, poor prognosis.
  • AFP elevated in endodermal sinus tumors.
  • high hCG in choriocarcinomas, lower in seminomas.
  • lactate dehydrogenase, rough measure of tumor burden.

Question 50

Seminoma

Answer 50

• 50% of testicular germ cell tumors. peak incidence btw age 30-40yrs.
• morphology: homogeneous, lobulated, gray-white masses. Devoid of hemorrhage or necrosis. tunica albuginea intact.
  
  • made of large polyhedral seminoma cells with abundant clear cytoplasm (glycogen), large nuclei, and prominent nucleoli.
  • fibrous stroma makes irregular lobules. there is lymphocytic infiltrate.
  • positive for c-KIT, OCT2, and placental alkaline phosphatase (PLAP).
  • 15% contain syncytiotrophoblasts, hCG present.

Question 51

Spermatocytic Seminoma

Answer 51

• uncommon. In older pts (>65yrs).
• little tendency to metastasize.
• morphology: soft, gray cut surfaces some with mucoid cysts.
  
  • mixture of: small cells resembling secondary spermatocytes, medium-sized cells with round nucleus and eosinophilic cytoplasm, and scattered giant cells.

Question 52

Embryonal Carcinoma

Answer 52

• peak incidence btw 20-30yrs.
• more aggressive than seminomas.
• morphology: poorly demarcated, small, gray-white masses punctuated by hemorrhage and/or necrosis.
  
  • commonly extend through tunica albuginea into epididymis or cord.
  • primitive epithelial cells with indistinct cell borders, form irregular sheets, tubules, alveoli, and papillary structures.
  • frequent mitoses and giant cells.
  • positive for OCT3/4, PLAP, cytokeratin, and CD30.
  • negative for c-KIT.

Question 53

Yolk Sac Tumor (Endodermal Sinus Tumor)

Answer 53

• most common testicular neoplasm in pts <3yrs.
• adult cases are part of embryonal carcinoma.
• morphology: infiltrative, homogeneous, yellow-white mucinous tumor.
  
  • made of cuboidal neoplastic cells in lacelike (reticular) network. solid areas and papillae.
  • Schiller-Duval bodies = reseble primitive glomeruli.
  • eosinophilic hyaline bodies contain immunoreactive alpha-fetoprotein (AFP) and alpha-1 antitrypsin, associated with neoplastic cells.

Question 54

Choriocarcinoma

Answer 54

• highly malignant, made of cytotrophoblastic and syncytiotrophoblastic elements. <1% germ cell tumors.
• morphology: small, can be hemorrhagic or inconspicuous lesion replaced by fibrous scar.
  
  • made of polygonal, uniform cytotrophoblastic cells in sheets and cords, mixed with multinucleated syncytiotrophoblastic cells.
  • hCG present.

Question 55

Teratoma

Answer 55

• shows differentiation along endodermal, mesodermal, and ectodermal lines.
• in kids, behave as benign tumors, good prognosis.
• post-pubertal men: malignant regardless of maturity or immaturity.
• morphology: large (5-10cm), heterogeneous.
  
  • hemorrhage and necrosis suggest mixture with embryonal and choriocarcinoma.
  • haphazard array of differentiated mesodermal (muscle, cartilage, adipose), ectodermal (neural tissue, skin), and endodermal (gut, bronchial epithelium) elements.
  • mature (resemble adult tissues) or immature (embryonic or fetal tissues).
• malignant transformation signifies non-germ cell malignancy within teratoma.
  
  • spreads outside testis = no response to chemo.

Question 56

Leydig Cell Tumors

Answer 56

• 2% testicular tumors. btw 20-60 yrs old.
• can produce androgens, estrogens, and/or corticosteroids.
• most benign, 10% invade/metastasize.
• morphology: circumscribed nodules with homogeneous golden brown cut surface.
  
  • made of polygonal cells with abundant granular, eosinophilic cytoplasm and indistinct cell borders.
  • lipochrome pigment, lipid droplets, eosinophilic Reinke crystalloids common.
• presentation: testicular mass, changes from hormone elaboration (gynecomastia/sexual precocity).

Question 57

Sertoli Cell Tumors

Answer 57

• 10% malignant.
• morphology: homogeneous gray-white to yellow masses, variable size.
  
  • tall, columnar cells in trabeculae, form cords or tubules.
• presentation: testicular mass, no changes in hormones.

Question 58

Testicular Lymphoma

Answer 58

• 5% testicular neoplasms.
• most common testicular tumor in pts >60yrs.
• diffuse, large B-cell non-Hodgkin lymphomas.
• disseminate widely.
• high incidence of CNS involvment.

Question 59

Hydrocele

Answer 59

• accumulation of serous fluid within mesothelial-lined tunical vaginalis.
• due to generalized edema.

Question 60

Hematocele

Answer 60

• accumulation of blood secondary to trauma, torsion, or generalized bleeding diathesis.

Question 61

Chylocele

Answer 61

• accumulation of lymphatic fluid secondary to lymphatic obsturction (elephantiasis)

Question 62

Spermatocele

Answer 62

• local cystic accumulation of semen in dilated ductuli efferentes or rete testis.

Question 63

Varicocele

Answer 63

• dilated vein in spermatic cord.
• may be asymptomatic or contribute to infertility.

Question 64

Malignant Mesothelioma

Answer 64

• rare in tunica vaginalis.

Question 65

Acute Bacterial Prostatitis

Answer 65

• by organisms causing UTIs (E.coli and gram (-) rods, enterococci, and staph).
• from urinary reflux or lymphohematogenous seeding, catheterization or surgical manipulation.
• presentation: fever, chills, dysuria, and boggy, markedly tender prostate.
• dx: via urine culture and symptoms.

Question 66

Chronic Bacterial Prostatitis

Answer 66

• insidious, can be asymptomatic or associated with low back pain, suprapubic and perineal discomfort, dysuria.
• associated with recurrent UTI, without previous prostatitis.
• same organisms as acute bacterial prostatitis.
• dx: leukocytes and positive bacterial cultures in prostatic secretions.

Question 67

Chronic Abacterial Prostatitis

Answer 67

• most common form of prostatitis.
• presentation: insidious, asymptomatic or with low back pain, suprapubic and perineal discomfort, dysuria.
• dx: prostatic secretions contain >10 leukocytes per high power field, cultures are negative.

Question 68

Granulomatous Prostatitis

Answer 68

• from installation of BCG to treat bladder cancer.
  
  • prostatic granulomas don’t need tx.
• non-specific granulomatous prostatitis uncommon, from rxn to secretions from rupture prostatic ducts and acini.

Question 69

Benign Prostatic Hyperplasia

Answer 69

• aka nodular hyperplasia.
• common, from periurethral epithelial and stromal hyperplasia that compresses urethra.
• 20% men by age 40; 70% men by age 60; 90% by age 70.
• 50% clinically detectable, 50% have symptoms.
• 30% white Americans >50yrs have mod to severe symptoms.
• pathogenesis: mediated by dihydrotestosterone (DHT), made by stromal cells of prostate from circulating testosterone via 5alpha-reductase, type 2.
  
  • binds AR of stromal and epithelial cells, activates genes ⇒ ↑ production secondary growth factors and receptors (FGF-7 in stromal cells).
  • FGF-7 stimulates stromal cells proliferation and inhibits epithelial apoptosis.
  • FGF-1, FGF2, and TFG-beta ⇒ fibroblast proliferation.
• morphology: gland enlarged by nodules in transitional and periurethral zones. cut surface has well-demarcated nodules, vary from firm and pale gray (mostly fibromuscular stromal) to yellow-pink and soft (mostly glands).
  
  • nodules made of mixtures of proliferating glands and fibromuscular stroma. glands lined by two layers of cells: basal layer of low cuboidal epithelium and layer of columnar secretory cells.
  • can have squamous metaplasia and infarcts.
• presentation: lower urinary tract obstruction symptoms from ↑ size of prostate, extrinsic compression of urethra, and smooth muscle-mediated contraction of prostate.
  
  • bladder hypertrophy and distention, urinary retention.
  • urinary frequency, nocturia, difficulty starting and stopping, chronic urinary stasis with bacterial overgrowth and UTIs, urinary bladder diverticula and hydronephrosis.
• tx: alpha blockers, 5alpha reductase inhibitors, resection.

Question 70

Adenocarcinoma (Prostate)

Answer 70

• most common form of cancer in men. 1 in 6 lifetime risk.
• men >50yrs; 70% in men >70yrs. uncommon in Asians, more common in blacks.
• pathogenesis: risk factors = ↑ age, race, hormonal influences, genetics, enviromnent.
  
  • X-linked AR gene has CAG repeats, shorter in blacks = more sensitive, longer in Asians = less sensitive.
  • ↑ risk with first-degree relatives.
  • BRCA2 mutation ⇒ 20x risk.
  • acquired mutations: ETS next to TMPRSS2 makes more invasive; hypermethylated glutathione S-transferase downregulates expression causing ↑ susceptibility to carcinogens; ↑ expression of E-cadherin with ↓ expression EZH-2 transcription repressor.
  • ↑ risk with fat consumption, lycopenes, vitamin d, selenium, soy products.
  • precursor lesions = prostatic intraepithelial neoplasia (PIN).
• morphology: arise in peripheral zone usually in posterior prostate.
  
  • poorly demarcated, gritty, firm, yellow. may infiltrate seminal vesicles, urinary bladder. rarely invades rectum.
  • well-demarcated adenocarcinomas with small, crowded glands lined by single layer of epithelium, nuclei large and have nucleoli.
  • perineural invasion = malignancy.
  • high grade PIN = benign but cytologically atypical cells, see in 80% prostatic carcinomas.
  • Gleason system = 5 grades prostate cancer.
    
    • 1 = normal; 5 = no glandular differentiation.
    • low to mod grade = treatable; high grade = bad prognosis.
• presentation: metastases in obturator nodes, spread from there. hematogenous spread to bone causing osteoblastic metastases.
  
  • PSA for diagnosis, secreted from prostatic epithelium into semen.
    
    • measure by level, velocity (rate of change).
• tx: surgery or radiotherapy