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The key takeaways are that the document discusses various pathological conditions that can affect the male genital system including the prostate, testes and penis. It covers topics such as prostatitis, benign prostate hyperplasia, prostate cancer and various testicular tumors.

The main causes of prostatitis include bacterial infections similar to UTIs as well as recurrent UTIs. The clinical presentations include dysuria, frequency, urgency, lower back/pelvic pain and fever/chills for acute prostatitis and lower back pain, dysuria and discomfort for chronic prostatitis.

The main differences between benign prostate hyperplasia and prostate cancer are that BPH involves proliferation of both glandular and stromal elements, presents as nodular enlargement, and does not increase cancer risk. Prostate cancer only involves proliferation of glands, presents as a firm nodular lesion, and is malignant.

1 The Male Genital System

Male Genital System


THE PROSTATE GLAND

1. Acute Prostatitis:

Etiology:
- bacteria similar to that of a UTI (ie E.coli)

Pathogenesis:
- Intraprostatic reflux of urine from posterior urethra/ urinary bladder
- Possible seeding by lymphohematogenous routes from distant infection

Clinical:
- Dysuria, frequency, urgency, Lower back/pelvic pain
- Fever chills, leukocytosis, loss of sex drive w painful erection/ejaculations
- DRE: enlarged tender prostate

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2. Chronic Prostatitis:

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Etiology:
- Recurrent UTIs (cystitis, urethritis) by same organism.

o.
- Most antibiotics penetrate the prostate poorly so bacteria find safe haven in parenchyma & constantly seed UT
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Clinical:
- Lower back pain, dysuria, perineal and suprapubic discomfort. Can be asymptomatic
o

3. Benign Prostate Hyperplasia (BPH): NODULAR


aC s

Etiology:
vi y re

- >40yo males
- Possible low Testosterone, ⇑ estrogen upregulating DHTR on prostate
5 alpha reductase as well
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Morphology:
- Gross: Defined nodules of central, transitional & periurethral zones
ar stu

- Histological: Proliferating glandular element & fibromuscular stroma


o Gland & stroma proliferating (unlike prostate CA)
o 2 layers of cells on glands (CA will only have 1)
- Copora Amylacea: Proteinaceous material in lumen of gland (normal)
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Th

Pathogenesis:
- Testosterone ! DHT ! GFs !leads to hyperplasia
Clinical:
- Most asymptomatic
- Urethral compression: difficulty starting/stopping urination
o Dribbling, frequency, nocturia & dysuria
- Urinary retention: recurrent UTIs
- Complete urinary obstruction ! Obstructive uropathy
o Acute & chronic pyelonephritis with postrenal azotemia
o Bilateral hydronephrosis
o Bladder wall SM hypertrophy with ⇑ risk of diverticula
o Stone formation
- NO RISK OF CANCER
- DRE: nodular and rubbery prostate

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2 The Male Genital System

4. Prostate CA:
Etiology:
- 8-10X ⇑ in males >80 yo
- African/Caribbean at higher risk with low Asian risk
- HPC1: hereditary prostate cancer gene
o Linked to RNASEL gene

Morphology:
- Single layer of cuboidal cells with hyperchromatic nuclei
- Only gland proliferating NOT stroma (both in BPH) Peripheral zone
- Glands appear “back-to-back” with no basal cell layer (single layer)

Pathogenesis:
- precursor lesions: prostatic intraepithelial neoplasia levels (PIN)
o low grade ! high grade (carcinoma in situ)

Clinical:
- Hematuria, weight loss, dysuria & weakened flow

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- Later stage: bone (vertebral) pain from metastasis
o Osteoblastic metastasis: Hyperdensity on XR

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- DRE (smooth and firm nodular) & PSA screening (>10ng/ml) normal (4ng/ml)
- Transrectal ultrasound, Biopsy (6-12 in multiple locations)

o.
- Gleeson grading system
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o Prognosis: Gleason score 1-8 (architectural changes) & staging (TNM)
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TESTICULAR LESIONS
o

1. Cryptorchidism:
aC s

- Failure of testes to descend completely to scrotal position along gubernaculum


vi y re

o Upper scrotal/inguinal region (majority), higher up = worse prognosis


- More common on RIGHT side

- Etiology: Anatomical abnormalities, hormonal dysfunction


ed d
ar stu

- Complications: Germ cell tumor 3-5X risk commonly in contralateral testis


- Orchiopexy: surgery <5yo to prevent tumors & <2yo to prevent infertility

2. Testicular Atrophy:
sh is

Top:Normal seminiferous tubules with many


germ cells (blue nuclei)
Etiology:
Th

Bottom: Testicular atrophy; No germ cells


- Testicular injury, atherosclerotic narrowing (old age), inflammatory orchitis (empty lumens) with hyperplasia of Leydig cells
- Cryptorchidism, hypopituitarism, Klinefelter Syndrome,
- Cirrhosis (⇑ estrogen)

Morph/path:
- Hyalinosis of BM & thickening of spermatic tubules
- NO spermatogesis
- Hyperplasia of Leydig cells
- Testosterone DOES NOT function: No binding protein (Sertoli cells)

Clinical:
- ⇓ libido, ⇓ muscle mass, depressed mood, ⇓ energy
- ⇓ spontaneous erections, gynaecomastia

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3 The Male Genital System

3. Male Infertility:
- Testicular failure > obstruction > genetic > endocrinopathy
- Pretesticular: hypopituitarism or estrogen excess
- Testicular: Agonadism, atrophy, germ cell aplasia or maturation arrest
- Post-testicular: bilateral obstruction, infections, immotile cilia syndrome

4. Testicular inflammation:
- Epididymitis or orchitis (Testicular inflammation)
- Children: gram negative bacteria
- <35yo: STD (ie. N. gonorrhea, C. trachomatis)
- >35yo: UTI (E. coli or Pseudomonas)

5. Testicular Torsion:
- Vascular lesions: twisting of spermatic cord, obstructed venous drainage or infarction

6. Testicular Tumors:

Etiology:

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- Isochrome i(12p)
- Cryptorchidism, testicular dysgenesis (Klinefelter’s Syndrome), radiation.

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- Infant & Children: Teratoma/yolk sack (non-hemorrhagic)
- 15-30yo: Mixed germ cell tumor (hemorrhagic)

o.
- 30-50yo: Seminoma
- >60yo: Lymphoma
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- NEVER biopsy, risk of spread

Clinical:
- Unilateral mass, heaviness in scrotum, dull ache in abdomen or groin
o

- Hydrocele, testicular pain, breast enlargement, metastasis to LN


aC s
vi y re

Germ cell Tumors:

a. Seminoma:
ed d

Etiology:
ar stu

o Commonest Germ cell tumor with cryptochidism strongest factor (malignant)


o Ovary identical tumor: dysgerminoma (30-50 yrs )

Morph/Path:
sh is

o Fried Egg appearance: Sheets of cells + lymphocytic infiltrate


o Cells are large, round & have distinct cell membrane
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o Clear or watery-appearing cytoplasm


o Large central nucleus with one or two prominent nucleoli
o NO necrosis & NO visible hemorrhage
o isochromosome12p; expression of OCT3/4 & NANOG
o 25% have c-KIT activating mutations.
o lymphatic metastasis: Paraaortic lymph nodes

Clinical:
o DO NOT BIOPSY
o Bulky masses on testes, heaviness in the testes, pain due to this
o Slight ⇑ βHCG
o Radiosensitive (only one that is)

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4 The Male Genital System

b. Yolk Sac Tumor:


Etiology:
o Most common for Infants & children <3 yo

Morph/Path:
o Gross: Nonencapsulated, & on cross-section it presents a homogeneous, yellow-white, mucinous
appearance
o Schiller-Duval bodies: Structures resembling glomeruli. They consist of a mesodermal core with a central
capillary & a visceral & parietal layer of cells.
o Immunohistochemical staining: Eosinophilic, hyaline-like globules of AFP & α1-antitrypsin present
within & outside the cytoplasm
Clinical:
o ⇑ AFP

c. Embryonal Carcinoma:
Etiology:
o 2-30yo; more aggressive then seminomas

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Morph/Path:

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o More undifferentiated than seminoma lesions may display sheets of cells
o Primitive glandular differentiation. The nuclei are large & hyperchromatic

o.
Clinical:
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o Elevated AFP
o Positive for cytokeratin & CD30, & negative for c-KIT
o Hematogenous spread: Liver & lungs
o

d. Choriocarcinoma:
aC s

Etiology:
vi y re

o Rare germ cell tumor however highly malignant

Morph/Path:
o Small tumors; no testicular enlargement & detected only as a small palpable nodule.
ed d

o HCG in cytoplasm.
ar stu

Clinical:
o Early metastasis to lungs

e. Teratoma:
sh is

Etiology:
o Infants & children (benign), adults (malignant)
Th

Morph/Path:
o tumors with various normal derivatives from more than one germ layer

Non Germ Cell Tumors:

f. Leydig cell tumor:


o Androgen producing tumor: Gynacomastia in men, Early puberty in boys
o Large polygonal eosinophilic cells
o Cytoplasm: lipid granules, vacuoles, or lipofuscin pigmen
" Reinke crystals: rod-shaped crystalloids inside Leydig cells

g. Sertoli cell tumor:


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5 The Male Genital System

o Big and clear with some Ca++ in lumen

h. Testicular lymphoma:
o >60yo
o Diffuse large Bcell tumor
o Immunologically privileged area so WBC will not get in

PENILE & SCROTAL DISORDERS

1. Penile congenital abnormalities:

- Hypospadias: Malformation of urethral groove & urethral canal creating an opening at the ventral surface of penis

- Epispadias: Malformation of urethral groove & urethral canal creating an opening at the dorsal surface of penis
o Associated with: cryptorchidism, inguinal hernia, UT obstruction, recurrent UTI & infertility

- Phimosis: Orifice of prepuce too small to permit normal retraction

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o developmental issue or infection with scarring of pretutial ring
o Balanitis: inflammation of penis

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- Paraphimosis: When a phimotic prepuce is forcibly retracted of glans penis ! swelling & constriction

o.
o Balantitis & UTI
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2. Penile Neoplasms:

Etiology:
- HPV 16/18; smoking, smegma, in elderly (>60 yrs)
o

- Bowen Disease: (older men) solitary, scaly plaque like lesion on penis shaft.
aC s

o Associated w visceral malignancies (skin/mucosal surfaces) & can progress to invasive squamous cell
vi y re

carcinoma (10%)

- Eyrthroplasia of Queyrat: Solitary or multiple red/shiny patches on glans/preupuce penis ! progresses to invasive
CA
ed d
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- Bowenoid Papulosis: (younger males) Multiple reddish, brown papules on shaft; Non malignant

Clinical:
- Itching or burning under foreskin
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- Ulceration common
- Less in Jews and Muslims because of circumcision
Th

3. Scrotal disorders:

- Hematocele: blood in Tunica Vaginalis from trauma


- Hydrocele: Accumulation of fluid in Tunica Vaginalis
- Varicocele: Dilation of congested blood vessels (veins) in spermatic cord
- Chylocele: Accumulation of lymphatic fluid in Tunica Vaginalis
- Spermatocele: Dilation of epididymis with semen
- Scrotal CA: Chimney sweepers, coal, tar, skin cancer

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