Penis

Normal Anatomy of the Penis

• paired corpora cavernosa
• single corpus spongiosum
• Tyson’s glands produce smegma
• Glans – distal extension of corpus spongiosum – covered by prepuce
• Corpus spongiosum envelopes the penile urethra
• Normal anatomical position at erection

Pathology of the Penis

• Congenital Abnormalities

Ø  Malformations of the urethral groove and canal

¨      Hypospadia – opening of the urethra on the ventral surface

¨      Epispadias – opening of the urethra on the dorsal surface

¨      Both often assoc. with abnormal testicular descent and bladder malformations

¨      If constricted can lead to infection and sterility

Ø  Phimois

¨      Defined: prepuce too small to permit normal retraction

¨      Causes: abnormal development, scarring, inflammation

¨      Problems: bad hygeine, debris accululation, infection, and even CA

Ø  Paraphimosis

¨      Defined: forcible retraction of phimotic foreskin

¨      Causes: non-reducible constriction behind the corona

¨      Problems: pain, urinary retention due to urethral constriction

Ø  Congenital lesions

¨      Congenital absence

¨      Duplication

¨      Hypoplasia

¨      Hyperplasia

• Inflammatory and Infections

Ø  Syphilis

¨      Treponema pallidum – microaerophilic gram (-); spirochete

¨      9-90 day incubation period

¨      Penile involvement in all three stages

1)     1^o syphilis – early papule that develops into a ulcer = syphilitic chancre

2)     2^o syphilis – condyloma lata and mucus patches

3)     tertiary syphilis – gummatous inflammation (soft gummy tumor)

Ø  Herpes Simplex

¨      HSV-I – oral; HSV-2 – predominantly genital

¨      More severe in first episode

¨      Grouped discrete vesilces evolve into pustules that erode and form painful ulcer

¨      MICRO: intranuclear inclusions in multinucleated synctial giant cells

¨      Tzanck Smear

Lymphogranuloma venerum (LGV)

¨      Clamydia trachomatis – subtypes L₁, L₂, L₃

¨      3-6 week incubation

¨      Three stages

1)     primary genital stage – papule formation

2)     secondary inguinal stage – acute lymphadenitis with bubo formation

3)     chronic tertiary stage – genital ulcers, fistulas, elephantiasis, rectal strictures

¨      Inguinal Bubo – painful, unilateral enlargement which progress to abscess and then rupture

Ø  Granuloma Inguinale (Donovanosis)

¨      Calymmatobacterium donovani – gram (-) pleomorphic encapsulated intracellular

¨      Rare

¨      Incubation 8-80 days

¨      Single or multiple papules

¨      Papules form nontender indurated firm ulcer, bleeds readily

¨      Donovan Bodies – large histiocytes containing dark particulate inclusions

Ø  Non-specific bacteria

¨      Balanoposthitis

¨      Peyronie’s disease

• Proliferative lesions and tumors

Ø  Condyloma acuminatum

¨      Benign

¨      Basically genital warts

¨      Assoc with HPV type 6 and 11

Ø  Giant condyloma (of Buschke-Lowenstein)

¨      Also known as verrucous carcinoma

¨      Assoc with HPV types 6 and 11

¨      Locally invasive and recurrent

¨      Rarely metastasizes

¨      Difficult to distinguish from condyloma

Ø  Carcinoma in-situ

¨      NOT invasive but has invasive potential

¨      All associated with HPV virus

¨      Cytological evidence of the malignancy confined to the epithelium

¨      Three types listed

1)     Bowen’s Disease

-        thickened plaque like lesion occuring on the shaft

-        10% of cases (est) progress to squamous carcinoma

-        Treatment: topical, surgery

2)     Erythroplasia of Queyrat

-        red soft plaque on glans or foreskin

-        usually in uncircumcised

-        5-10% progress to squamous carcinoma

3)     Bownoid papulosis

-        multiple pigmented papular lesions

-        often appears verrucoid (mistaken for condyloma acuminatum)

• Squamous Cell Carcinoma

Ø  PROTECTION VIRTUALLY GUARRANTEED BY CIRCUMCISION

Ø  1% of all male cancers

Ø  disease of older men (40-70)

Ø  Risk factors: uncircumcised, poor hygeine, accumulation of smegma, phimosis, HPV infection, UV radiation

Ø  Treatment: surgery, local excision, partial to total peotomy (penectomy)

Ø  5 year survival rate – 77%

Ø  10 yr. – 71%

Prostate

Normal anatomy of the Prostate

• located in the retroperitoneum
• no capsule
• Glandular Prostate

Ø  Three zones

1)     Peripheral Zone (70% of normal prostate; 80% of prostate CA)

2)     Transition zone (5% of normal prostate; 10-20% of prostate CA)

• Benign Prostatic Hypertrophy occurs in the transition zone

3)     Central Zone (25% of normal prostate; 5% of prostate CA)

• Non-glandular prostate

Ø  preprostatic sphincter

Ø  anterior fibromuscular stroma

Ø  Neruovascular bundles

Pathology of the Prostate

Prostatitis (Inflammation of the Prostate)…

Acute Prostatitis

• Clinical presentation: fever, chills, boggy, markedly tender prostate
• Causative organisms: E. coli (number 1), S. aureus, Enterococcus, Gram (-)s
• Etiologies

1)     direct extension

2)     lymphatic or hematogenous seeding

3)     surgery

4)     expression of prostatic secretions contraindicated due to risk of bacteremia

Chronic Bacterial Prostatitis

• same organisms as AP
• Most common cause of relapsing UTI in men
• Diagnostic Features:

1)     white blood cells in expressed prostatic secretions

2)     positive bacterial cultures in prostatic secretions and urine

Chronic abacterial prostatitis

• MOST COMMON FORM OF PROSTATITIS
• Clinical: same as Chronic Bacterial Prostatitis w/o history of recurrent UTIs
• Diagnostic: 10-12 WBCs per high power field; negative bacterial culture

Granulomatous Prostatitis

• 2^o, non-specific granulomatous inflammation related to foreign body reaction
• Can be confused with carcinoma because of similar findings on rectal.
• Older age group
• Obstruction usually present

Tuberculous prostatitis

• confused w/ CA clinically
• 75-90% – have tuberculosis somewhere else in GU system
• involved in 3-12% of systemic tuberculosis

Benign Prostatic Hyperplasia

General

• Hesistancy, Frequency, Urgency
• Increasing frequency with age

Ø  20% of males at age 40

Ø  70% at 60

Ø  90% at 70

• Blacks affected on average 10 years earlier
• Uncertain etiology (maybe hormone)
• Can include glandular tissue or fibromuscular tissue]

Symptoms

• result from compression of the urethra
• Hesitancy, Urgency, Frequency, UTIs, cystitis
• Can result in bladder smooth muscle hypertrophy, trabeculation of the bladder wall, and diverticulum formation

Treatment

• TURP – transurethral resection of the prostate
• 5-10% of patients with BPH require surgical intervention for relief of urinary tract obstruction

Carcinoma of the Prostate

General

• most common form of cancer in males (skin #1)
• 2^nd leading cause of cancer-related death in males (lung #1)

Diagnosis

• early – asymptomatic
• late – obstruction
• PSA screening
• Ultrasound guided biopsies
• Some patients may present with symptoms related to metastases
• Rectal:

Ø  early – non-palpable

Ø  isolated, hard nodule, diffuse from regularity, asymmetric prostate

Ø  most cases in peripheral zone, esp in posterior region

• GROSS

Ø  poorly demarcated, firm, gritty, appear yellow

• MICRO

1)     most are adenocarcinoma (95%)

2)     composed mainly od small glands

3)     Gleason’s grading system – based on low power impression

• remember – grade of predominant pattern added to the 2^nd most prevalent pattern grade
• Gleason score 2-4 = good prognosis
• Gleason score 8-10 = bad prognosis

Staging of Prostate carcinoma – clinical

Stage A:          microscopic, not palpable

A1:                   focus in less than 5% of TURP tissue

A2:                   multiple areas of focus (>5%), or Gleason grade > 4

Stage B:          palpable macroscopic tumor

B1:                   < 1.5 cm in diameter; only in one lobe

B2:                   > 1.5 cm, or several nodules in both lobes

Stage C:          tumor w/ extraprostatic extension but still clinically localized

C1:                  palpably extending into seminal vesicle but not fixed to pelvic wall

C2:                  fixed to pelvic wall

Stage D:          metastatic

D1:                  metastases limited to three or less pelvic nodes

D2:                  more extensive nodal or extrapelvic metastases

Clinical Features

• minority of cases – undiagnosed
• 5-10% present with a palpable nodule – stage B
• stage C or stage D present in over 75% of patients at time of diagnosis – gives symptoms of urinary obstruction, local pain, bone pain, etc.
• Most CAs arise in the peripheral region, so urinary obstruction indicates advanced disease

Treatment

• dependent on stage
• Stage A and B

1)     surgery &/or radiotherapy

2)     10 year survival rate – 50-80%

• Stage C & D

1)     hormonal manipulation

2)     orchiectomy

3)     estrogen administration

4)     synthetic LHRH

5)     10 year survival rate 10-40%

Testis

Congenital Anomalies

Cryptorchidism = failure of one or both of the testis to descend into the scrotum

• Causes

1)     most are idiopathic

2)     mechanical (short cord, obstruction of inguinal canal)

3)     Genetic abnormalities (trisomy 13)

4)     Musculoskeletal disorders

5)     Hormonal abnormalities

• 25% of cases – bilateral
• MICRO

1)     changes in the cells can occur as early as 2 years of age

2)     can occur in contralateral normally descended testis

3)     decreased germ cell development

4)     thickening and hyalinazation of seminiferous tubular basment membrane

5)     Interstitial fibrosis

6)     Leydig Cell hyperplasia

• Clinical

1)     high prevalence of inguinal hernias

2)     Sterile

3)     KNOW FOR TEST!!! – Orchioplexy decreases the likehood of sterility if performed early, BUT DOES NOT DECREASE THE RISK OF NEOPLASIA, even in the contralateral testis.

Other Congenital Abnormalities – rare

Atrophy of the Testis

Genetic Causes – Kleinfelter’s syndrome – XXY

Secondary causes

• Cryptochidism
• Vascular disease
• Inflammatory disorders
• Hyoppituitarism
• Malnutrition
• Obstruction of outflow of semen
• Elevated femal sex hormones
• Prolonged increase of FSH
• Radiation
• Chemo

Inflammation

” Non-specific” orchitis

• source is often retrograde UTI
• Causative organisms:

Ø  Peds: gram (-) rods

Ø  Sexually active males: Chlamydia trachomatis and Neisseria gonorrhea

Ø  Males over 35: E. coli and Pseudomonas

Granulomatous orchitis

• rare cause of unilateral testicular enlargement in middle-age men
• autoimmune or trauma origin
• Clinical Presentation

Ø  Two types:

1)     Moderately tender mass of sudden onset; maybe accompanied by fever

2)     Painless testicular mass (resembles a testicular tumor)

• To differentiate from tuberculous orchitis

1)     presence of plasma cells

2)     occasional neutrophils

3)     enclosing rim of fibroblasts and lymphocytes

4)     NO CASEOUS NECROSIS

Gonorrhea

• can result in suppuration if neglected
• retrograde extension from urethra to prostate to seminal vesicles to epididymis

Mumps

• occurs in 20% of males w/ mumps
• age 10 or older more common
• unilateral in 70% of cases
• can resemble syphilis Microscopically
• MICRO

Ø  mononuclear cell infiltration

Ø  infiltrate

Ø  edema

Ø  NO OBLITERATIVE ENDARTERITIS (distinguishes from syphilis)

• usu does not lead to sterility

Tuberculosis

• usually assoc with an active TB infection elsewhere
• usu begins in the epididymis with 2^o involvement of the testis
• MICRO

1)     HAS CASEOUS NECROSIS (differentiates from Granulomatous orchitis)

2)     Granulomatous inflammation

3)     Late stages: pregressive fibrosis and calcification

Syphilis

• usu begins as orchitis and then may involve the epididymis
• MICRO:

1)     nodular gummas

2)     OBLITERATIVE ENDARTERITIS (distinguishes from Mumps)

3)     Diffuse interstitial inflammation

4)     Edema

5)     Lymphoplasmacytic inflitrate

• MAY LEAD TO STERILITY

Hematologic Spread from other systemic infections

Torsion = twisting of the spermatic cord with resultant venous obstruction

• arteries usually remain patent
• probably pretty painful
• hemorrhagic or ischemic infarction of the testis can occur
• associated with pre-existing structural lesions

Ø  incompletely descended testicles

Ø  absence of scrotal ligaments

Ø  testicular atrophy

Testicular Tumors

• 90% arise from germ cells – MOST ARE GERM CELL TUMORS
• non-germ cell tumors – usually benign; can elaborate steroids

Nonseminomatous Germ Cell Tumors

• Examples

1)     embryonal carcinoma of the testis

2)     Yolk Sac tumor

3)     Teratoma

4)     Choriocarcinoma

5)     Mixed Germ Cell Tumor

6)     Polyembryona

• Radioresistent

Sex Cord-stromal tumors

Leydig cell tumor, Sertoli cell tumor, Granulosa cell tumor,

mixed and unclassified sex cord-stromal tumor …

Germ Cell Tumors

General

Ø  Predisposing Factors

1)     Cryptorchidism

2)     Genetics

3)     Testicular dysgenesis (25% are associated with germ cell tumors

Ø  Rare

Ø  2/100,000 incidence annually

Ø  Peak incidence – 15 to 34 years of age

Clinical Features of Germ Cell Tumors

• usually presents as PAINLESS
• Metastasis (Where does it go?)

1)     retroperitoneal periaortic nodes – MOST COMMON SITE OF Lymphatic METS

2)     mediastinal and supraclavicular nodes,

3)     Lung – MOST COMMON SITE OF hematogenous METS

4)     Liver, Brain, Bone

• Seminomas tend to remain localized to the testis for a long period of time and are RADIATION SENSITIVE
• NSGCT’s are radioresistant

Intratubular Germ Cell Neoplasia

• precursor lesion of invasive germ cell tumors – seen in virtually all cases of germ cell tumors
• also seen in infertile patients, cryptorchidism, positive history of testicular cancer

Germ Cell tumors (Seminoma, Spermatic seminoma, Embryonal carcinoma, Yolk Sac tumor, Choriocarcinoma, Teratoma, Mixed.)

• Seminoma

Ø  MOST COMMON TYPE OF GERM CELL TUMOR (1/3 of all types)

Ø  Peak incidence 4^th decade

Ø  MICRO

1)     large cells with clear cytoplasm

2)     distinct cell membranes

3)     septal lymphocytic infiltrates

• Tcells and Plasma Cells

• Spermatic Seminoma

Ø  Rare

Ø  Indolent and nonmetastasizing

Ø  Larger than classic seminoma

Ø  MICRO (as compared to classic seminoma)

1)     smaller cells resembling 2^o spermatocytes

2)     larger seminoma cells

3)     LACK OF LYMPHOCYTES and

4)     MORE FREQUENT MITOSES

• Embryonal Carcinoma

Ø  20-30 year olds

Ø  AGGRESSIVE

Ø  MICRO

1)     primitive appearing pleomorphic cells

2)     indistinct cell borders

3)     hyperchromatic nuclei

4)     prominent nucleoli

• Yolk Sac Tumor

Ø  MOST COMMON testicular tumor in INFANTS AND CHILDREN

-        in this age group – good prognosis

Ø  RARE IN adults in pure form

• Choriocarcinoma

Ø  HIGHLY mALIGNANT

Ø  Composed of both cytotrophoblast and synctiotrophoblastic elements

Ø  Usually mixed form

Ø  MICRO

1)     polygonal cytotrophoblastic cells growing in sheets or cords

2)     multi-nucleated synctiotrophoblastic cells

Ø  usually detected as a small mass – by this time has already metastasized widely

Ø  PRODUCE HCG

• Teratoma

Ø  Group of neoplasms that exhibit evidence of simultaneous differentiation along three germ cell lines

1)     Endodermal – gut bronchial epithelium

2)     Mesodermal – muscle, cartilage, adipose tissue

3)     Ectodermal – neural tissue, skin

Ø  May occur at any age

Ø  3 variants

1)     Mature teratoma

-        wild array of differentiated tissue of all three germ cell lines

-        more common in infants and children – usually behave as benign tumors – good prognosis

2)     Immature teratoma

-        intermediate between mature and embryonal

-        incompletely differentiated but not obviously malignant

3)     Teratoma with malignant transformation

-        clear evidence of malignancy in at least on germ cell layer

-        MORE common in adults

• Mixed Tumors

Ø  60% of testicular tumors

Ø  most common combination (14% of all testicular tumors): teratoma, embryonal carcinoma and yolk sac tumor w/ HCG (+) synctiotrophoblast

Staging of Testicular Cancer

Stage I:            tumor confined to testis

Stage II:           distant spread to retroperitonael lymph nodes below the diaphragm

Stage III:          metastases outside the retroperitoneal nodesor above the diaphragm

• physical exam
• radiographic imaging of retroperitoneum and chest
• assay for various tumor markers AFP and HCG

Therapy

• Various combinations of

1)     surgery

2)     radiation

3)     chemotherapy

• dependent on histologic type of tumor
• NSGCT – generally treated the same as a group because the histology doesn’t matter; they all tend to act and respond the same

Non-germ Cell tumors – sex-cord stromal tumors

Leydig Cell tumor

• 2% of all testicular tumors
• most common – 20-60 years
• MAY ELABORATE ANDROGENS AND OTHER STEROIDS
• Clinical

1)     testicular mass

2)     gynecomastia

3)     sexual precocity

• 10% invade or metastasize
• MICRO

Ø  commonly contain lipochrome pigment, lipid droplets, and Reinke crystals

Sertoli cell tumors (androblastoma)

• may elaborate androgens and estrogens – usually not enough to manifest clinically
• 10% – invasion and metastasize

Lymphoma

• 5% of testicular neoplasms
• MOST COMMON neoplasm in PATIENTS over the AGE OF 60
• Most common lymphoma – diffuse large cell lymphoma

Tags: Acute Prostatitis, Balanoposthitis, Bownoid papulosis, Buschke-Lowenstein, Calymmatobacterium donovani, Carcinoma of the Prostate, Clamydia trachomatis, Congenital Abnormalities, Congenital lesions, epispadias, Erythroplasia of Queyrat, Gonorrhea, Granuloma Inguinale, Granulomatous Prostatitis, Herpes Simplex, Hypospadia, Lymphogranuloma venerum, Paraphimosis, penis anatomy, Peyronie's disease, Phimois, preprostatic sphincter, squamous cell carcinoma, syphilis, tertiary syphilis, Tuberculous prostatitis

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