Path Lut Male Ex2

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Cryptorchidism is found in approximately

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1% of 1-year-old boys.[67] This anomaly represents a complete or incomplete failure of the intra-abdominal testes to descend into the scrotal sac.
It usually occurs as an isolated anomaly but may be accompanied by other malformations of the genitourinary tract, such as hypospadias

Front 2

Even though testicular descent is controlled by hormonal factors, cryptorchidism is only rarely associated with

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a well-defined hormonal disorder. The condition is completely asymptomatic, and it is found by the patient or the examining physician only when the scrotal sac is discovered not to contain the testis.

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morphology. Cryptorchidism

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unilateral in most cases

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Cryptorchidism histologically

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arrest in the development of germ cells associated with marked hyalinization and thickening of the basement membrane of the spermatic tubules (Fig. 21-20). Eventually the tubules appear as dense cords of hyaline connective tissue outlined by prominent basement membranes

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the cryptorchid testis is

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small in size and is firm in consistency as a result of fibrotic changes. Histologic deterioration, associated with a paucity of germ cells, has also been noted in the contralateral (descended) testis in males with unilateral cryptorchidism, supporting an intrinsic defect in testicular development.

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Cryptorchidism complications

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sterility
undescended testis is at a greater risk of developing testicular cancer

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Orchiopexy (placement in the scrotal sac) of unilateral cryptorchidism before 10 years of age protects against

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cancer development

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Malignant change may occur in the

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contralateral, normally descended testis. These observations suggest that cryptorchidism is associated with a defect in testicular development and cellular differentiation that is unrelated to anatomic position.

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Benign Prostatic Hyperplasia (BPH) or Nodular Hyperplasia is an extremely common disorder in

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men over age 50.[94] It is characterized by hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the prostate.

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When sufficiently large Nodular Hyperplasia compress and narrow the

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urethral canal to cause partial, or sometimes virtually complete, obstruction of the urethra.

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Only 50% of those who have microscopic evidence of BPH have

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clinically detectable enlargement of the prostate, and of these individuals, only 50% develop clinical symptoms

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Benign Prostatic Hyperplasia (BPH) or Nodular Hyperplasia main component of the “hyperplastic” process is

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impaired cell death. t has been proposed that there is an overall reduction of the rate of cell death, resulting in the accumulation of senescent cells in the prostate

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The main androgen in the prostate, constituting 90% of total prostatic androgens, is

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dihydrotestosterone (DHT)

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DHT is not a direct mitogen for prostate cells, instead

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DHT-mediated transcription of genes results in the increased production of several growth factors and their receptors. Most important among these are members of the fibroblast growth factor (FGF) family, and particularly FGF-7 (keratinocyte growth factor

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Although the ultimate cause of BPH is unknown, it is believed that DHT-induced growth factors act by

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increasing the proliferation of stromal cells and decreasing the death of epithelial cells.

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Nodular hyperplasia of the prostate originates almost exclusively in

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the inner aspect of the prostate gland (transition zone).

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early nodules are composed almost entirely of

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stromal cells, and later predominantly epithelial nodules arise. From their origin in this strategic location the nodular enlargements may encroach on the lateral walls of the urethra to compress it to a slitlike orifice

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n some cases, nodular enlargement may project up into the floor of the urethra as a hemispheric mass directly beneath the mucosa of the urethra, which is termed

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median lobe hypertrophy by clinicians.

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Microscopically, the hallmark of BPH is

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nodularity (Fig. 21-33B). The composition of the nodules ranges from purely stromal fibromuscular nodules to fibroepithelial nodules with a glandular predominance

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The diagnosis of BPH cannot usually be made on

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needle biopsy, since the histology of glandular or mixed glandular-stromal nodules of BPH cannot be appreciated in limited samples

Front 21

BPH increased size of the gland, and the smooth muscle-mediated contraction of the prostate cause

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uretheral obstruction. The increased resistance to urinary outflow leads to bladder hypertrophy and distension, accompanied by urine retention

Front 22

Mild cases of BPH may be treated

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without medical or surgical therapy, such as by decreasing fluid intake, especially before bedtime; moderating the intake of alcohol and caffeinecontaining products; and following timed voiding schedules

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The most commonly used and effective medical therapy for symptoms relating to BPH are

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α-blockers, which decrease prostate smooth muscle tone via inhibition of α1-adrenergic receptors

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Transurethral resection of the prostate (TURP) has been the gold standard in terms of

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reducing symptoms, improving flow rates, and decreasing post-voiding residual urine. It is indicated as a first line of therapy in certain circumstances, such as recurrent urinary retention.

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Nodular hyperplasia is not considered to be a

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premalignant lesion.

Front 26

Granulomatous prostatitis In the United States the most common cause is related to

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instillation of BCG within the bladder for treatment of superficial bladder cancer. in this setting the finding of granulomas in the prostate is of no clinical significance, and requires no treatment

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Fungal granulomatous prostatitis is typically seen only in

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immunocompromised hosts

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Nonspecific granulomatous prostatitis is relatively common and represents a

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eaction to secretions from ruptured prostatic ducts and acini

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Morphology. Acute prostatitis may appear as

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minute, disseminated abscesses; as large, coalescent focal areas of necrosis; or as diffuse edema, congestion, and boggy suppuration of the entire gland.

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In men with symptoms of acute or chronic prostatitis, biopsy or surgical specimens are uncommonly examined microscopically, because

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the disease is diagnosed on clinical and laboratory findings. In fact biopsy of a man with acute prostatitis is contraindicated, as it may lead to sepsis

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It is common in prostate specimens removed surgically to find histologic evidence of acute or chronic inflammation in men with no clinical symptoms of acute or chronic prostatitis. In these instances etiologic infectious agents have

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et to be identified.[92] So as not to be confused with the clinical syndromes of acute and chronic prostatitis, these prostate specimens are instead diagnosed in descriptive terms as showing “acute inflammation” or “chronic inflammation” and not as “prostatitis.”

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Epididymitis and possible subsequent orchitis are commonly related to

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infections in the urinary tract (cystitis, urethritis, prostatitis), which reach the epididymis and the testis through either the vas deferens or the lymphatics of the spermatic cord.

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Though uncommon in children, epididymitis in childhood is usually associated with a

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congenital genitourinary abnormality and infection with gram-negative rods

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In sexually active men younger than age 35 years epididymitis is usually associated with a

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C. trachomatis and Neisseria gonorrhoeae

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Nonspecific Epididymitis and Orchitis Morphology

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he bacterial invasion induces nonspecific acute inflammation characterized by congestion, edema, and infiltration by neutrophils, macrophages, and lymphocytes

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Nonspecific Epididymitis and Orchitis complications

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inflammatory involvement of the epididymis and testis is often followed by fibrous scarring, which in many cases leads to sterility. Usually the interstitial cells of Leydig are not totally destroyed, so sexual activity is not disturbed

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Granulomatous (Autoimmune) Orchitis presents in

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middle age as a moderately tender testicular mass of sudden onset sometimes associated with fever

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Granulomatous (Autoimmune) Orchitis may appear insidiously, however, as a

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painless testicular mass mimicking a testicular tumor, hence its importance.

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Granulomatous (Autoimmune) Orchitis Histologically the orchitis is distinguished by

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granulomas restricted to spermatic tubules. The lesions closely resemble tubercles but differ in that the granulomatous reaction is present diffusely throughout the testis and is confined to the seminiferous tubules.

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Orchitis Mumps

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In postpubertal males, however, orchitis may develop and has been reported in 20% to 30% of male patients. Most often, acute interstitial orchitis develops about 1 week after the onset of swelling of the parotid glands.

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Twisting of the spermatic cord typically cuts off

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the venous drainage of the testis. The thick-walled arteries remain patent, so that the intense vascular engorgement may be followed by hemorrhagic infarction.

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two types of testicular torsion

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Neonatal torsion
Adult torsion

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Neonatal torsion

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occurs either in utero or shortly after birth. It lacks any associated anatomic defect to account for its occurrence.

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Adult torsion

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seen in adolescence presenting as sudden onset of testicular pain. It often occurs without any inciting injury; sudden pain heralding the torsion may even occur during sleep

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Torsion is one of the few urologic emergencies. If the testis is explored surgically and manually untwisted within approximately 6 hours after the onset of torsion, there is a good chance that

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the testis will remain viable

Front 46

In contrast to neonatal torsion, adult torsion results from

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bilateral anatomic defect where the testis has increased mobility, giving rise to what is termed the bell-clapper abnormality

Front 47

To prevent the catastrophic occurrence of subsequent torsion in the contralateral testis, the testis unaffected by torsion is surgically fixed to

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the scrotum (orchiopexy).

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most common form of cancer in men

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Adenocarcinoma of the prostate

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Cancer of the prostate is typically a disease of men over

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50. However, in men who are at increased risk (see “Etiology”), screening for prostate cancer is recommended to begin at age 40

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Prostatic cancer is uncommon in

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Asians and occurs most frequently among blacks. In addition to hereditary factors, environment plays a role, as evidenced by the rise in the incidence of the disease in Japanese immigrants to the United States, though not nearly to the level of that of native-born Americans.

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with respect to differences in prostate cancer risk among races, the X-linked Androgen receptor gene contains a polymorphic sequence composed of repeats of the codon CAG (which codes for glutamine). The shortest polyglutamine repeats on average are found in

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African Americans, while Caucasians have an intermediate length and Asians have the longest, paralleling the incidence and mortality of prostate cancer in these groups. More directly, the length of the repeats is inversely related to rate at which prostate cancer develops in mouse models

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most adenocarcinoma tumors eventually become resistant to

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androgen blockade. Tumors escape through a variety of mechanisms, including acquisition of hypersensitivity to low levels of androgen (e.g., through AR gene amplification); mutations in AR that allow it to be activated by non-androgen ligands; and other mutations or epigenetic changes that activate alternative signaling pathways, which may bypass the need for AR altogether

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observed most often in tumors that have become resistant to anti-androgen therapy.

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increased activation of the P1-3 kinase/AKT signaling pathway

Front 54

Compared with men with no family history, men with one first-degree relative with prostate cancer have

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twice the risk and those with two first-degree relatives have five times the risk of developing prostate cancer

Front 55

Men with germline mutations of the tumor suppressor BRCA2 have a

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20-fold increased risk of prostate cance

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risk-associated loci, including one at 8q24 that appears to selectively increase the risk among

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African American men

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common type of somatic mutation in prostate cancer gives rise to chromosomal rearrangements

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juxtaposition of the coding sequence of an ETS family transcription factor gene (most commonly ERG or ETV1) next to the androgen-regulated TMPRSS2 promoter.[110] These rearrangements place the involved ETS gene under the control of the TMPRSS2 promoter and lead to their over-expression in an androgen-dependent fashion

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Over-expression of ETS transcription factors makes normal prostate epithelial cells more

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invasive, possibly through the upregulation of matrix metalloproteases. In addition, tumors with rearranged ETS genes have certain distinctive morphologic features[111] and a different gene expression signature than those lacking ETS gene rearrangements,[112] suggesting that ETS gene rearrangements define a specific molecular sub-class of prostate cancer

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ETS rearrangements may also have implications for prostate cancer screening and early diagnosis, as it is possible to detect ETS fusion genes in

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the urine using sensitive PCR assays.

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most common epigenetic alteration in prostate cancer is

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hypermethylation of glutathione S-transferase (GSTP1) gene which down-regualtes GSTP1 expression. The GSTP1 gene is located on chromosome 11q13 and is an important part of the pathway that prevents damage from a wide range of carcinogens

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approximately 70% of cases, carcinoma of the prostate arises in the

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peripheral zone of the gland, classically in a posterior location, where it may be palpable on rectal examination

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on cross-section of the prostate the neoplastic tissue is

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gritty and firm, but when embedded within the prostatic substance it may be extremely difficult to visualize and be more readily apparent on palpation

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In contrast to benign glands, prostate cancer glands are more

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crowded, and characteristically lack branching and papillary infolding. The outer basal cell layer typical of benign glands is absent

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In approximately 80% of cases, prostatic tissue removed for carcinoma also harbors presumptive precursor lesions, referred to as

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high-grade prostatic intraepithelial neoplasia (PIN

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PIN consists of architecturally

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benign prostatic acini lined by cytologically atypical cells with prominent nucleoli. Cytologically PIN and carcinoma may be identical, yet architecturally PIN involves larger branching glands with papillary infolding, in contrast to invasive cancer that is typically characterized by small crowded glands with straight luminal borders

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Localized prostate cancer is

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asymptomatic, and is usually discovered by the detection of a suspicious nodule on rectal examination or elevated serum PSA level

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Most prostatic cancers arise peripherally away from the urethra, and therefore urinary symptoms occur

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late. Patients with clinically advanced prostatic cancer may present with urinary symptoms, such as difficulty in starting or stopping the stream, dysuria, frequency, or hematuria

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uncommon for patients to come to attention because of back pain caused by vertebral metastases. The finding of osteoblastic metastases by skeletal surveys or the much more sensitive radionuclide bone scanning is virtually diagnostic of this form of cancer in men. These patients have

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a universally fatal outcome

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to confirm digital rectal exam dx

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transrectal needle biopsy is required to confirm the diagnosis.

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n most laboratories a serum level of------is used as a cutoff point between normal and abnormal

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4 ng/mL

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PSA is organ-specific, yet not

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cancer-specific.

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Cancer of the prostate is treated by

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surgery, radiation therapy, and hormonal manipulations. More than 90% of patients who receive such therapy can expect to live for 15 yrs

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the most common treatment for clinically localized prostate cancer is

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radical prostatectomy

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Alternative treatments for localized prostate cancer are

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external-beam radiation therapy or interstitial radiation therapy

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Advanced, metastatic carcinoma is treated by

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androgen deprivation either by orchiectomy or by administration of synthetic agonists of luteinizing hormone–releasing hormone (LHRH)

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lthough anti-androgen therapy induces remissions, eventually tumors develop

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testosterone-resistance, followed by a rapid progression of disease and death.

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The incidence of testicular germ cell tumors in Finland is about

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wo times lower than in Sweden; second generation Finnish immigrants to Sweden, have a tumor incidence that approaches that of the Swedish population

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the most important risk factor of esticular germ cell tumors

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Cryptorchidism

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The relative risk of development of these tumors in fathers and sons of patients with testicular germ cell tumors is

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four times higher than normal, and is 8 to 10 times higher between brothers

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Seminomatous tumors are composed of

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cells that ressemble primordial germ cells or early gonocytes

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on-seminomatous tumors may be composed of

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undifferentiated cells that resemble embryonic stem cells, as in the case of embryonal carcinoma, but the malignant cells can differentiate into various lineages generating yolk sac tumors, choriocarcinomas and teratomas

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the most common testicular tumor.

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Seminomas

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Most testicular germ cell tumors originate from lesions called

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intratubular germ cell neoplasia (ITGCN), which is also referred to as intratubular germ cell neoplasia unclassified (ITGCNU).[76,][77] However, ITGCN has not been implicated as a precursor lesion of pediatric yolk sac tumors and teratomas, or of adult spermatocytic seminoma.

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ITGCN is believed to occur in

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utero and stay dormant until puberty

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peak incidence of Seminomas is the

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third decade and they almost never occur in infants.

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Seminomas in females is called

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dysgerminoma

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Seminomas contain an isochromosome

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2p, and express OCT3/4 and NANOG. Approximately 25% of these tumors have c-KIT activating mutations. c-KIT amplification has also been repeated, but increased c-KIT expression may occur without genetic defects.

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The classic seminoma cell is

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arge and round to polyhedral and has a distinct cell membrane; a clear or watery-appearing cytoplasm; and a large, central nucleus with one or two prominent nucleoli

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The term anaplastic seminoma is used by some to indicate

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greater cellular and nuclear irregularity with more frequent tumor giant cells and many mitoses. However, since “anaplastic seminoma” is not associated with a worse prognosis when matched stage for stage with classic seminoma and is not treated differently, most authorities do not recognize anaplastic seminoma as a distinct entity.

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Spermatocytic Seminoma

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over the age of 65 years. In contrast to classic seminoma, it is a slow-growing tumor that does not produce metastases, and hence the prognosis is excellent.

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spermatocytic seminomas lack

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lymphocytes, granulomas, syncytiotrophoblasts, extra-testicular sites of origin, admixture with other germ cell tumors, and association with ITGCN

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Spermatocytic Seminoma Morphology

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Grossly, spermatocytic seminoma tends to have a soft, pale gray, cut surface that sometimes reveal mucoid cysts

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Spermatocytic seminomas contain three cell populations,

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(1) medium-sized cells, the most numerous, containing a round nucleus and eosinophilic cytoplasm; (2) smaller cells with a narrow rim of eosinophilic cytoplasm resembling secondary spermatocytes; and (3) scattered giant cells, either uninucleate or multinucleate

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mbryonal carcinomas occur mostly in the

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20- to 30-year age group. These tumors are more aggressive than seminomas.

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Embryonal Carcinoma morphology

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Extension through the tunica albuginea into the epididymis or cord frequently occurs.

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Embryonal Carcinoma
Histologically the cells grow in

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alveolar or tubular patterns, sometimes with papillary convolutions

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Embryonal carcinomas share some markers with seminomas such as

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OCT 3/4 and PLAP, but differ by being positive for cytokeratin and CD30, and negative for c-KIT.[79]

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Yolk Sac Tumor Also known as endodermal sinus tumor, yolk sac tumor is of interest because it

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is the most common testicular tumor in infants and children up to 3 years of age. In this age group it has a very good prognosis. In adults the pure form of this tumor is rare; instead, yolk sac elements frequently occur in combination with embryonal carcinoma.

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Yolk Sac Tumor morphology

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nonencapsulated, and on cross-section it presents a homogeneous, yellow-white, mucinous appearance. Characteristic on microscopic examination is a lacelike (reticular) network of medium-sized cuboidal or flattened cells

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In approximately 50% of Yolk Sac Tumor structures resembling endodermal sinuses

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(Schiller-Duval bodies) may be seen; these consist of a mesodermal core with a central capillary and a visceral and parietal layer of cells resembling primitive glomeruli

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presence of AFP in the tumor cells is highly characteristic, and it underscores their

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differentiation into yolk sac cells.

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Teratoma may occur at

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any age from infancy to adult life. Pure forms of teratoma are fairly common in infants and children, second in frequency only to yolk sac tumors.

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Teratoma Hemorrhage and necrosis usually indicate

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admixture with embryonal carcinoma, choriocarcinoma, or both.

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Dermoid cysts and epidermoid cysts, are a form of teratoma that are common in the

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ovary, Unlike testicular teratomas, they have a uniformly benign behavior.

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“teratoma with malignant transformation

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a malignant non–germ cell tumors arises in teratoma

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The importance of recognizing a non–germ cell malignancy arising in a teratoma is that the non–germ cell component

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does not respond to chemotherapy when it spreads outside of the testis. In this case, the only hope for cure resides in the resectability of the tumor

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In the child, differentiated mature teratomas usually follow a benign course. In the postpubertal male all teratomas are

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malignant, capable of metastatic behavior whether the elements are mature or immature

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characteristic feature of germ cell neoplasms

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painless enlargement of the testis.

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iopsy of a testicular neoplasm is associated with a risk of tumor spillage, which would necessitate excision of the scrotal skin in addition to orchiectomy. Consequently, the standard management of a solid testicular mass is

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radical orchiectomy based on the presumption of malignancy.

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spread common to all forms of testicular tumors.

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Lymphatic, retroperitoneal para-aortic nodes are the first to be involved. Hematogenous spread is primarily to the lungs, but liver, brain, and bones may also be involved

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Seminomas tend to remain

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localized to the testis for a long time, and hence approximately 70% present in clinical stage I (see later).

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males with nonseminomatous germ cell tumors (NSGCTs)present with

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advanced clinical disease (stages II and III)

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Metastases from seminomas typically involve

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ymph nodes

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SGCTs not only metastasize earlier but also use the

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hematogenous route more frequently. The rare pure choriocarcinoma is the most aggressive NSGCT.

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three clinical stages of testicular tumors are defined:

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Stage I: tumor confined to the testis, epididymis, or spermatic cord
• Stage II: distant spread confined to retroperitoneal nodes below the diaphragm
• Stage III: metastases outside the retroperitoneal nodes or above the diaphragm

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Germ cell tumors of the testis often secrete polypeptide hormones and certain enzymes that can be detected in blood by sensitive assays.[81] Such biologic markers include

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HCG, AFP, and lactate dehydrogenase, which are valuable in the diagnosis and management of testicular cancer

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The elevation of lactate dehydrogenase correlates with

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the mass of tumor cells, and provides a tool to assess tumor burden

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Marked elevation of serum AFP or HCG levels are produced by

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yolk sac tumor and choriocarcinoma elements, respectively

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after orchiectomy, persistent elevation of HCG or AFP concentrations indicates

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stage II disease even if the lymph nodes appear of normal size by imaging studies.

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After eradication of tumors there is a rapid fall in serum AFP and HCG. With serial measurements it is often possible to predict recurrence before

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the patients become symptomatic or develop any other clinical signs of relapse.

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Seminoma, which is extremely radiosensitive and tends to remain localized for long periods, has the best

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prognosis

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umors of Leydig cells are particularly interesting, because they may

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elaborate androgens and in some cases both androgens and estrogens, and even corticosteroids.[83,][84] They may arise at any age, although most cases occur between 20 and 60 years of age

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Leydig Cell Tumors In children, hormonal effects, manifested primarily as

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sexual precocity, are the dominating features.

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Leydig Cell Tumors Morphology.

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form circumscribed nodules, usually less than 5 cm in diameter. They have a distinctive golden brown, homogeneous cut surface. Histologically, neoplastic Leydig cells usually are remarkably similar to their normal counterparts in that they are large and round or polygonal, and they have an abundant granular eosinophilic cytoplasm with a round central nucleus

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Leydig Cell Tumors are mostly

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benign

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Sertoli Cell Tumors

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Most Sertoli cell tumors are hormonally silent and present as a testicular mass.

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Sertoli Cell Tumors Morphology

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firm, small nodules with a homogeneous gray-white to yellow cut surface. Histologically the tumor cells are arranged in distinctive trabeculae that tend to form cordlike structures and tubules

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testicular lymphoma patients present with only a

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testicular mass, mimicking other, more common, testicular tumors.

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most common form of testicular neoplasms in men over the age of 60.

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Aggressive non-Hodgkin lymphomas account

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he most common testicular lyphomas, in decreasing order of frequency, are

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iffuse large B cell lymphoma, Burkitt Lymphoma, and EBV-positive extranodal NK/T cell lymphoma ( Chapter 13). Patients with testicular lymphomas have a higher incidence of central nervous system involvement than those similar tumors located elsewhere.

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In the external male genitalia, two distinct lesions display histologic features of CIS

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Bowen disease and bowenoid papulosis. These lesions have a strong association with infection by HPV, most commonly type 16.

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Bowen disease occurs in

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the genital region of both men and women, usually in those over the age of 35 years. In men it tends to involve the skin of the shaft of the penis and the scrotum

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Over the span of years, Bowen disease may transform into infiltrating squamous cell carcinoma in approximately 10% of patients. Bowen disease may also be associated with

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visceral cancer, such as that of the colon or breast, but not as frequently as initially reported.

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Bowenoid papulosis occurs in

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sexually active adults. Clinically, it differs from Bowen disease by the younger age of patients and the presence of multiple (rather than solitary) reddish brown papular lesions

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quamous cell carcinoma of the penis is an uncommon malignancy in the United States, accounting for fewer than 1% of cancers in males. By contrast, in some parts of Asia, Africa, and South America the incidence of squamous cell carcinoma of the penis ranges from

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10% to 20% of male malignancies. Circumcision confers protection, and hence this cancer is extremely rare among Jews and Moslems and is correspondingly more common in populations in which circumcision is not routinely practiced.

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It is postulated that circumcision is associated with

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etter genital hygiene, which, in turn, reduces exposure to carcinogens that may be concentrated in smegma and decreases the likelihood of infection with potentially oncogenic types of HPV. HPV DNA can be detected in penile squamous cancer in approximately 50% of patients

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Squamous cell carcinoma of the penis usually begins on

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the glans or inner surface of the prepuce near the coronal sulcus. Two macroscopic patterns are seen—papillary and flat

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Verrucous carcinoma is an exophytic well-differentiated variant of

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squamous cell carcinoma that has low malignant potential. These tumors are locally invasive, but they rarely metastasize

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Invasive squamous cell carcinoma of the penis is a slowly

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growing, locally invasive lesion that often has been present for a year or more before it is brought to medical attention.

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Invasive squamous cell carcinoma metastases to

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inguinal lymph nodes characterize the early stage, but widespread dissemination is extremely uncommon until the lesion is far advanced

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Clinical assessment of regional lymph node involvement is notoriously inaccurate; 50% of men with penile squamous cell carcinoma and clinically enlarged inguinal nodes have only reactive lymphoid hyperplasia when examined histologically. The prognosis is related to

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he stage of the tumor. In persons with limited lesions without invasion of the inguinal lymph nodes, there is a 66% 5-year survival rate, whereas metastasis to the lymph nodes carries a grim 27% 5-year survival.