Male genitalia path Flashcards
Penis: MalformationsHypospadias and epispadias
Urethral opening
-below tip of penis (ventral) = hypospadias
-above tip of penis (dorsal) = epispadias
may be associated with other genital abnormalities
the urethral orifice may be constricted, causing complications from urinary tract obstruction
Penis: InflammationsBalanitis
local inflammation of the glans penis
+ overlying prepuce = balanoposthitis
usually due to smegma accumulation, typically under the foreskin of uncircumcised males
-smegma = sweat, debris, desquamated epithelial cells
distal penis is red, swollen, and tender; may have purulent discharge
Penis: InflammationsPhimosis
Inability to retract the foreskin of uncircumcised penis because of scarring or adhesions, usually secondary to balanoposthitis
Interferes with cleanliness; smegma accumulation favors the development of secondary infections and possibly carcinoma
Penis: InflammationsParaphimosis
Forcible retraction of foreskin with phimosis leads to painful swelling that can obstruct the urethra
-severe cases may cause urinary retention
Penis:Neoplasms
uncommon; most originate from squamous epithelium (squamous cell carcinomas)
most cases occur in uncircumcised patients >40 yoa
risk factors:
-phimosis
-poor hygiene
-infection with HPV types 16 and 18
Penis:Squamous Cell Carcinoma
usually preceded by 1 of 3 variants of carcinoma in situ
- Bowen disease
- erythroplasia of Queryat
- bowenoid papulosis
Bowen disease
Appears as a solitary, plaque-like lesion on the shaft of the penis
most common >30 yoa
~1/3 of patients develop visceral cancers
Erythroplasia of Queyrat
variant of Bowen disease
erythematous patch on the glans penis and other mucosal surfaces
Bowenoid papulosis
venereally transmitted viral (HPV 16) lesion of the penile shaft
Patients typically younger than seen in Bowen disease
Presents with multiple reddish-brown pigmented papules (may be verrucoid)
Histologically indistinguishable from Bowen disease
virtually never develops into invasive carcinoma and may spontaneously regress
Penis:Squamous cell carcinoma
SCC of the penis is uncommon in the U.S. (<1% of male cancers)
-In some parts of Asia, South America, and Africa it comprises 10-20% of male malignancies
Usually found in patients between 40-70 yo
Is extremely rare in populations that practice circumcision
-better genital hygiene?
-decreases likelihood of HPV infection?
SSC clinical course
SCC is slowly growing, locally invasive, and probably present for a year or more before brought to medical attention
-In early stage metastasize to inguinal and iliac lymph nodes
-Widespread dissemination is uncommon, but occurs late in disease
Not painful until they undergo ulceration (may bleed) and infection
Prognosis is related to tumor stage
-In limited lesions without inguinal node involvement, there is a 66% 5-year survival rate
-Metastasis to a lymph node results in only a 27% 5-year survival rate
Cryptorchidism
Represents a complete or incomplete failure of testicular descent into the scrotal sac
-involves right testis more commonly than the left, but bilateral in 25%
-usually results in testicular atrophy and hyalinization by puberty
*4x increased risk of malignancy (less risk in the normally-descended testis)
*may result in sterility
usually occurs as an isolated anomaly, but may be associated with other malformations such as hypospadias or other congenital syndromes (e.g., Prader-Willi syndrome)
diagnosis is uncertain before 1 year of age (complete descent isn’t universally present at birth)
Epididymitis and orchitis
Commonly related to infections of the urinary tract (cystitis, urethritis, genitoprostatitis) that spread to the testis via the vas deferens and spermatic cord lymphatics
Cause varies with age
-In childhood associated with congenital abnormality and Gram Negative Bacteria
-In sexually active men 35 yo, common UT pathogens: Escherichia coli and Pseudomonas sp.
May lead to sterility if testis involved and inflammation not resolved in a timely fashion
Gonorrhea
neglected infection extends from posterior urethra to the prostate → seminal vesicles → epididymis
-results in abscesses that may destroy the epididymis
may spread to testis and produce a suppurative orchitis
Mumps
testicular involvement uncommon in school-age children, but produces orchitis in 20-30% of postpubertal males
-usually develops ~1 wk after swelling of parotid glands
Tuberculosis
believed epididymitis results from spread via prostate and seminal vesicles
caseating granulomas
Testicular Atrophy causes
Progressive atherosclerotic narrowing of the blood supply (old age)
End stage of inflammatory orchitis (by any cause)
Cryptorchidism
Hypopituitarism
Generalized malnutrition or cachexia
Irradiation
Prolonged exposure to female sex hormones
Testicular Torsion
Twisting of the spermatic cord may cut off venous drainage and arterial supply to testis
-Infarction may follow
Testicular Torsion clinical course
presents as sudden pain
intense congestion and widespread extravasation of blood into interstitial tissues
one of the few urologic emergencies
-need to be surgically resolved in <6 hours to retain testicular viability
Testicular torsion
sudden onset extreme pain elevated testicle absent cremasteric reflex age <20
Epididymitis
Hx urethritis
pyuria
tenderness, swelling
age <35
Varicocele
dilated vein within the spermatic cord
cause of infertility
-left testicle more commonly involved
-A rapidly developing variocele is suspicious for renal cell carcinoma
Hydrocele
accumulation of clear serous fluid in the tunica vaginalis causing enlargement of the scrotal sac
-may be mistaken for testicular enlargement
often occur spontaneously without any apparent cause
Diagnostic technique to detect a hydrocele = transillumination
Testicular neoplasms
neoplasms of the scrotal sac are unusual, but don’t forget the association of scrotal squamous cell carcinoma with chimney sweeps
We’ll focus here on testicular neoplasms, which are derived from -germ cells (95% of cases)
Some trends you should notice:
germ cell tumors are usually very aggressive cancers
-sex cord or stromal tumors are usually benign, but can elaborate steroids that cause interesting endocrinologic syndromes
most commonly present with painless enlargement of the testis
Biopsy of testicular neoplasm?
Biopsy of a testicular neoplasm is associated with a risk of tumor spillage which would necessitate excision of the scrotal skin in addition to orchiectomy
Standard management of a solid testicular mass is radical orchiectomy based on the presumption of malignancy!
Testicular Cancer Risk Factors
Cryptorchidism (3x-5x fold increase)
Family history (brothers 8x-10x fold increase)
Testicular dysgenesis
-feminization
-Klinefelter syndrome
Age range: 20-54, peak at 15-34
Caucasian
NO ASSOCIATION with lifestyle (smoking, obesity, etc.)
Development of cancer in one testis is associated with a markedly increase risk in contralateral testis
Testicular cancers
Seminoma Spermatocytic Seminoma Embryonal Carcinoma Yolk Sac Tumor Choriocarcinoma Teratoma Mixed Germ Cell Tumors
Seminoma
50% of germ-cell tumors
40-50 yoa
Large, soft, well-demarcated tumors
may have coagulation necrosis, but no hemorrhage
identical to ovarian dysgerminomas
large cells with clear, glycogen-rich cytoplasm; conspicuous nucleoli
Tumor marker:
10 % of patients have elevated hCG
7-24% have syncytiotrophoblast-like giant cells
seminoma prognosis
late metastases
very radiosensitive
chemosensitive
excellent prognosis
Spermatocytic Seminoma
larger than classic seminoma but uncommon pale gray, soft, mucoid cysts affects elderly (> 65 years ) best prognosis mixture of large & small tumor cells rarely metastasize
Embryonal Carcinoma
smaller than seminomas, but poorly demarcated
contains foci of hemorrhage or necrosis
poorly differentiated, pleomorphic cells in sheets or cords
cellular pleomorphism and nuclear atypia present in the tumor cells
Embryonal Carcinoma prognosis
more aggressive than seminomas
not radiosensitive
chemosensitive
early metastases
Yolk Sac Tumor
nonencapsulated, yellow-white, mucinous tumor
most common testicular tumor <3 (good prognosis)
Adult yolk sac tumors are often seen admixed with embryonal carcinoma
Yolk Sac Tumor cells
reticular network of poorly differentiated cuboidal or columnar cells
50% contain Schiller-Duval bodies
Choriocarcinoma
do not cause testicular enlargement, but metastasize rapidly
hemorrhage and necrosis common
rarest type (~1%)
20-30 yoa
100% have elevated BhCG
-The detection of βhCG after orchiectomy is an indicator of metastatic disease.
Primary tumors are small, nonpalpable lesions
Choriocarcinoma prognosis
very early and rapid metastases
not radiosensitive or chemosensitive
poor prognosis
Teratoma
large, with solid, sometimes cartilaginous, and cystic areas
in child, benign
in adult, always regarded as malignant
local resection for cure
Mixed Germ Cell Tumors
Mixed germ-cell tumors account for ~60% of testicular germ-cell neoplasms
most common is a combination of teratoma, embryonal carcinoma, and yolk sac tumors
nonseminomatous mixed germ cell tumor with various textures and colors is displayed
Tumors of Sex Cord or Stroma
Leydig Cell Tumors
Sertoli Cell Tumors
Testicular Lymphoma
Leydig Cell Tumors
may elaborate androgens, estrogens, even corticosteroids
most common 20-60 yoa
adults → gynecomastia; children → sexual precocity
excellent prognosis
~90% are benign
Steroli Cell Tumors
insufficient quantities of estrogens or androgens to cause masculinization or feminization, but sometimes gynecomastia
excellent prognosis
~90% are benign
Testicular Lymphoma
not a primary tumor, but discussed here because they account for ~5% of testicular neoplasms
most common form of testicular neoplasm in men >60 yoa
most common type = diffuse large-cell type Non-Hodgkin Lymphoma
Prostate
Nodular Hyperplasia
Adenocarcinoma
Nodular Hyperplasia
aka, benign prostatic hypertrophy (BPH) but misnomer
Extremely common disorder in men > 50 yo
Characterized by hyperplasia of stromal and epithelial cells resulting in the formation of large, discrete nodules in the periurethral (central) region of the prostate- postvoid dripping
When sufficiently large, can obstruct the urethra
Well-circumscribed, white-tan, rubbery hyperplastic nodules symmetrically on either side of the compressed urethra
Adenocarcinoma
Most common form of cancer in men and second leading cause of cancer death
Typically a disease of men > 60 yoa
Uncommon in Asians; higher incidence in African-Americans
In contrast to nodular hyperplasia, arises from the peripheral glands
no postvoid dripping
AdenocarcinomaRisk factors
Age, race, family history, hormone levels, and environmental influences
Incidence rises as people from areas of low risk move to areas of higher risk (change of diet, environmental carcinogens, etc.)
Androgens and estrogens believed to play a role (inhibition of these tumors occurs with orchiectomy)
In ~10% of white American men, prostate cancer has been linked to germ-line inheritance
-Men with one first-degree relative have a 2X higher risk of developing prostate cancer, and those with 2 first-degree relatives have a 5X higher risk
Adenocarcinoma diagnostic approach
Digital rectal exam suffers from low sensitivity and low specificity
-Imaging studies (transurethral unltrasonography [TRUS], etc.) are also of poor specificity and sensitivity
-Transperitoneal or transrectal biopsy is required for confirmation
Prostate specific antigen (PSA)
Prostate specific antigen (PSA)
Elevated blood levels occur in association with localized as well as advanced cancer
-In most labs, 4 ng/mL is the upper limit of normal
Caveats:
-PSA is organ specific but NOT cancer specific
-Nodular hyperplasia, prostatitis, infarct, instrumentation, and ejaculation increase serum PSA
-only ~2/3rds of men with localized prostate cancer have increased PSA (compared to 95% of metastatic)
Refinements in the interpretation of PSA values
The recommended age-specific upper reference ranges for serum PSA are
2.5 ng/mL for men 40-49 yoa
3.5 ng/mL for men 50-59 yoa
4.5 ng/mL for men 60 -69 yoa
6.5 ng.mL for men 70-79 yoa
Men with prostate cancer demonstrate an increased rate of rise in PSA compared to men without prostate cancer
-suspicious for prostate cancer if >0.75 ng/mL/y
measure 3x over 1.5 years
PSA controversy
serum PSA by itself cannot be used for early detection of prostate cancer
considerable controversy about continuing to promote PSA testing as a cancer screening tool:
recent studies show that it does NOT reduce prostate cancer mortality (evidence that screened men actually have higher morbidity and mortality, likely due to treatment side effects)
despite this evidence, the American Urological Association (April 2009) changed their recommendation to start PSA testing earlier (now at 40 yoa instead of 50 yoa)
in October 2011, the USPSTF released its draft recommendation that PSA screening be discouraged
Adenocarcinoma clinical course
Microscopic cancers found incidentally at autopsy or biopsies for nodular hyperplasia are asymptomatic
-Their long term significance is not clear
*autopsy studies have shown that 30% of men >50 yoa and 70% of men >70 yoa have occult prostate cancer
Prostate cancer that is local/regional has excellent prognosis!
Adenocarcinoma clinical course
Patients with clinically localized disease do not have urinary symptoms
-The lesion is discovered by digital rectal exam and/or PSA testing
Patients with clinically advanced disease have symptoms
-Some patients come to medical attention because of back pain
-The finding of osteoblastic bone disease is virtually diagnostic for this form of cancer in men
can have osteoblastic metastases from prostatic adenocarcinoma
-Osteoblastic bone disease is virtually diagnostic for prostate cancer!
hyperplasia vs adenocarcinoma location
Nodular hyperplasia typically occurs periurethrally, while adenocarcinoma tends to occur peripherally.
