Causes of testicular atrophy
- congenital
- cryptorchidism
- klinefelter’s
- acquired
- atherosclerosis
- inflammation
- malnutrition
- hypopituitarism
- hormone therapy
Categories of causes of males infertility
- disorders that affect spermatogenesis, sperm fxn, or ductal obstruction
- congenital causes
- acquired causes
- Hormonal causes: FSH, LH, GnRH abnormalities
- Klinefelter’s syndrome (47 XXY): sclerosing tubular degeneration
Congenital causes of male infertility
- Cryptorchidism,
- Immotile cilia syndrome
- Anorchia (absence of both testes at birth),
- Absent vas deferens
Acquired causes of male infertility
- Torsion
- Twisting of cords ==> blocks venous flow ==> swelling and infarction
- Infarction
- Varicocele = varicose veins of the pampiniform plexus
- Rare cause of infertility
- due to venous valve insufficiency
- Obstruction
- Inflammation
Nonspecific epididymitis or orchitis: causative organism
- Kids: UTI bugs: gram (-) rods
- Sexually active adults:
- STDs: Chlamydia trachomatis, N. gonorrhoeae
- Elderly: Enterobacteria
- Also E. coli and P. aeruginosa per Goljan
Nonspecific epididymitis or orchitis: basic morphology
- Direct extension from urinary tract (vas deferens or lymphatics)
- Tends to affect epididymis first with subsequent orchitis
- Quick to form abscess due to cinching off of end artery blood supply
Mumps orchitis: cause/basic morphology
- cause: mumps virus
- Inflammatory infiltrate in poorly draining region causing atrophy:
- Unilateral 70%, Mononuclear inflammatory
- infiltrate with interstitial edema +/- neutrophils,
- subsequent to parotid involvement
TB orchitis: cause/basic morphology
- cause: Mycobacterium tuberculosis
- morphology
- Epididymis → Testis
- Usually part of systemic disease
- Caseating granulomas
Syphillis: cause/basic morphology
- cause: Treponema pallidum
- Testis → Epididymis
- Congenital or acquired
- Diffuse mononuclear interstitial inflammation rich in plasma cells
- Obliterative endarteritis → downstream necrosis
- +/- gummas (a characteristic tissue nodule found in the tertiary stage of syphilis)
Seminoma:
Clinical Picture
Classification
Morphologic Findings
Staging and
Treatment
Epidemiology
- clinical = 40-50yo
- class = PLAP, but serum markers often negative
- morphologic
- Fish flesh appearance, rounded
- lymphocytes + tumor cells
- staging/tx
- Good prognosis, radiosensitive + chemosensitive
- epidemiology
- Most common GCT 30-50%
Spermatocytic Seminoma:
Clinical Picture
Classification
Morphologic Findings
Staging and
Treatment
Epidemiology
> 50 years old
Serum markers often negative
Mixture of cells resembling 1o and 2o spermatocytes in myxoid stroma (look like combo of spermatogonia + spermocytes)
Good prognosis
Older men, 1-2%
Embryonal carcinoma:
Clinical Picture
Classification
Morphologic Findings
Staging and
Treatment
Epidemiology
Third decade
Markers variable: PLAP (Placental Alk Phos), placental lactogen, β hCG
Gross → looks ugly; lobulated, fibrosis. Anaplastic Histology: Apoptosisand a lot of mitotic activity. Grows fast, necrotic, rosettes, papillae.
Chemosensitive,High likelihood of metastasis, recurrence common
Pure → 3%
Mixed → 85%
Teratoma:
Clinical Picture
Classification
Morphologic Findings
Staging and Treatment
Epidemiology
Infants and adults
Histology → look for mixed epithelial and cystic structures within mass.
_Morphology: _
Mature or immature tissue. Slow progression to malignant change.White cartilage
cysts → structures formed by mature epithelial cells (mixed type tissue: bronchial, pancreas, glandular, skeletal muscle, anything)
Staging and treatment
Malignant transformation (unlike mature teratoma in women).Chemoresistant tumor will regress but mature teratoma remains
Infants → 40% of testicular tumors
Adult: Pure → 2-3%; Mixed → 45%
Yolk sac tumor:
Clinical Picture
Classification
Morphologic Findings
Staging and
Treatment
Epidemiology
Children and adults
Most common testicular tumor in kids
Produces α fetal protein (AFP)
Net-like with tears (i.e. holes)
Embryoid bodies
Schiller-Duval bodies
Fairly good prognosis
Pure common in kids,
Mixed common in adults
Choriocarcinoma:
Classification
Morphologic Findings
Staging and
Treatment
Epidemiology
Produces β hCG at high levels
Differentiating towards placenta
Looks like a placenta grossly and microscopically
“Placenta is designed to be an invasive organ”
Aggressive
Metastasizes
Chemosensitive but worse prognosis
Pure → 0.3%
Mixed → 10%
Zonal anatomy of prostate
Central zone – an inverted cone with its base forming the base of the prostate and its apex at verumontanum; ejaculatory ducts pass through central zone
Transition zone – two “lobes” that surround the prostatic urethra laterally and anteriorly; separated (more or less) by fibrous band from peripheral zone
Peripheral zone – major portion (~70%) of gland, which surrounds transition zone posteriorly, laterally, and apically
Characteristics of acute prostatitis
- hour to days onset
- Etiology
- Infection from bladder, blood
- Iatrogenic → Foley catheter
- Usually associated with UTI: E. Coli or S. aureus
- Histologic features
- Neutrophil (PMN) inflammation,
- Focal or diffuse
Characteristics of chronic prostatitis
- Etiology:
- Unknown
- Most men > 60 have
- Could be due to long standing bacterial infections or dietary factors (charred meat in mice)
- Histologic features
- Aggregates of lymphocytes, plasma cells, and macrophages within prostatic substance
- Often associated with atrophy
- Granulomatous form may occur as well
- TB
- Eroded corpora amylacea
Characterstics of Malakoplakia
- Rare
- Plaque-like regions of histiocytes (resident phagocytes) with calcified inclusions (Michaelis-Gutmann bodies) → due to malfunction of histiocytes
- Occurs anywhere along urinary tract
Hyperplasia of the prostate: frequency & age distribution
- Frequency
- Most common prostatic disease of US males
- Blacks > whites > asians
- Age distribution
- Rule of 10’s: Age group indicates percent that have it.
- E.g. 50% of 50 yo men with histiological evidence.
Hyperplasia of the prostate: anatomical location & features
- Limited to transition zone of prostate
- No classical look. Stromal and epithelial components form nodules. Epithelial components look normal, but stromal has increased in mass.
Hyperplasia of the prostate: clinical sx, complication/prognosis, management
Lower urinary tract symptoms (LUTS): hesitancy, poor urine flow, incomplete voiding, ↑ frequency, urge incontinence, dribbling, nocturia
LUTS ↓ quality of life. Acute urinary retention, recurrent UTI and pyelonephritis, renal failure (due to pressure backflow), incontinence. No problems with ejaculation.
Management:
medical → Finasteride (5α reductase inhibitor)
minimally invasive therapy → microwave
surgery → Trans urethal resection of prostate (TURP)
Adenocarcinoma of the prostate: frequency, age distribution, anatomical location
- Frequency
- Most common non-skin cancer in adult males
- Black > white > asian
- > 200,000 new cases / year
- 20% of all male cancer
- ↑↑ prevalence in western countries
- Age
- Age is a strong risk factor
- Location
- Effect peripheral zone > transition zone
Adenocarcinoma of the prostate: features, clinical sx, complications/prognosis
- Features
- Gross: yellow mass, most of the time not evident from imaging etc, multifocal
- Microscopic: multifocal, heterogeneous, abnormal collections of atypical glands lined by single layer - loss of bilayer (basal layer) - of malignant cuboidal to columnar cells, prominent nucleoli, infiltrative pattern
- Clinical: Asymptomatic or similar to BPH
- Complications/Prognosis
- Metastasis, death, etc.
- More men die with prostate cancer than of it.
Dx of prostatic carcinoma
Diagnosis: digital rectal exam (15-20% sensitivity), Blind random biopsy: gold standard (only 50% sensitive) → most cancers detected not life threatening
Size of tumors decreasing (i.e. in regards to detection) which seems to be attributable to screening.
Tx of prostatic carcinoma
Localized: surgery, external beam radiation, or radioactive seeds (brachytherapy), cryotherapy
If progressive and metastasized tumors → Hormone ablation; most will become androgen refractory with time
Anti-androgens
5α reductase inhibitors
GnRH inhibitors
Chemotherapy
Characteristics of prostatic intraepithelial neoplasia
- Tufted, papillary or cribriform proliferations of atypical cells within ducts and acini surrounded by basal cell layer
- High grade PIN often associated with adenocarcinomas elsewhere in prostate
- Genetic and molecular changes similar to PCa
- Increases with age, peak prevalence 5-10 yrs before PCa [Sakr 1993]
- Finasteride (5α reductase inhibitor) trial - to prevent progression to PCa.
