ERS24 Pathology Of Male Genital Tract Flashcards

1
Q

Penis, Urethra, Scrotum pathologies

A
  1. Congenital anomalies
  2. Inflammatory lesions
  3. Tumour
    - Tumour-like lesion
    - Benign tumours
    - Malignant tumours
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2
Q

Congenital abnomalies of Penis, Urethra, Scrotum

A
  1. Hypospadia, Epispadia
    - Urethral orifice situated on anywhere along ventral / dorsal surface of penis
    —> predispose to ***UTI in infancy, childhood
    —> interfere with normal ejaculation in later life
  2. Congenital urethral valvular obstruction
    - presence of valves at urethra (e.g. membranous flap in Prostatic urethra)
  3. Phimosis (包皮過長)
    - orifice of prepuce to small for normal retract —> unable to retract to expose Glans penis
    - usually acquired (after inflammatory scarring), congenital (rare)

ALL affect flow of urine, prone to inflammation / infection?

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3
Q

Inflammation: Urethra, Scrotum

A

Non-specific inflammation (also affect other parts of body)

  1. Infection of Urinary tract, Prepuce (Posthitis), Glans (Balanitis)
    - **Pyogenic bacteria
    - **
    Candida albicans (itchy lesions)
    - Mumps (inflammation, swelling of salivary glands + testes)
    - TB (affect Epididymis first, then involve Testes)
    —> may be affected by immune status
  2. Sexually Transmitted Diseases (smear show many Polymorphs)
    —> each with different clinico-pathological characteristics

Specifically sexually transmitted

  • ***Syphilis
  • ***Gonorrhea
  • ***Chlamydial infections
  • ***Genital herpes
  • Lymphogranuloma venereum
  • Granuloma inguinale
  • Chancroid

Other infections that can be sexually transmitted

  • ***Trichomonas vaginalis (Protozoa, cause severe itchiness in women)
  • ***Condylomata acuminata (caused by HPV)
  • AIDS

Rmb:
Effects / Complications of STD ***NOT confined to genital tract
—> travel in different routes
—> implications in prevention / diagnosis

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4
Q

Complications of gonorrhoea in male patients

A
Spread of infection (upwards):
Urethra (can lead to fistula, stricture)
—> Prostate
—> Vas deferens
—> Epididymis
—> Testes (atrophy, scarring)

Chronic persistent inflammation
—> **Atrophy, **Scarring of structures (e.g. Testes)
—> ***Obstruction of tubular structures due to scarring (e.g. Urethra)

Systemic involvement:

  • Endocarditis
  • Arthritis
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5
Q

Tumour and Tumour-like lesions of Lower Male genital tract

A
  1. **Condyloma acuminata (Venereal warts)
    - tumour-like lesions
    - caused by low risk **
    HPV infection (HPV type 6, 11)
    - Gross:
    —> single / multiple **warty papillary growth on penis/scrotum
    —> may spread locally to wide areas in anogenital region
    - Histology:
    —> **
    fibroblastic branching stalk covered by acanthotic squamous epithelium
    —> finger-like projections covered by **Stratified squamous epithelium —> **Koilocytes (characteristic of HPV infection) —> ***Perinuclear halo + Smudged nuclei
    —> differentiated from squamous carcinoma by mature epithelium
  2. (Squamous) Carcinoma-in-situ
    - **white/red discolouration/papules of Glans penis
    - smooth, soft red plaques
    - may develop into invasive Squamous cell carcinoma
    - **
    NO stromal invasion
    - ↑ nucleus/cytoplasmic ratio
    - pleomorphic, hyperchromatic nuclei
    - frequent mitotic figure
  3. **Squamous cell carcinoma
    - **
    most common malignant tumour of penis
    - 50-70 yo
    - Etiology:
    —> poor personal hygiene + smegma
    —> HPV infection
    —> circumcision soon after birth (rare)
    - Gross: **Exophytic ulcerated growth / nodular plaques
    - Histology: **
    Stromal invasion
    - Spread: Regional ***LN metastasis
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6
Q

HPV and Cancer

A
  1. Cervical cancer (strongest association, >99%)
  2. Anal cancer (85%)
  3. Penile cancer (50%)
  4. Oropharyngeal (20% ↑)
  5. Larynx and Aerodigestive tract (10% ↑)
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7
Q

Prostate pathologies

A
  1. Inflammation
  • Acute / Chronic type
    —> Extend from bladder / urethra
    —> Nonspecific infection caused by Coliform bacteria / Gonococci / Chlamydia
  • Granulomatous type
    —> Specific infections e.g. TB / Syphilis
    —> Nonspecific inflammatory reaction to inspissated (thickened) secretion / Autoimmune causation
  1. ***Benign prostatic hyperplasia (Nodular prostate hyperplasia)
  2. Carcinoma of prostate
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8
Q

Benign prostatic hyperplasia (Nodular prostatic hyperplasia)

A

Tend to involve ***“inner” / Transitional zone of prostate (urethral (mucosal) / submucosal glands)
- common > 50 yo

Clinical presentation:

  1. **Retention of urine
    - Bladder distension / hypertrophy of bladder muscle wall (striation of bladder mucosa)
    - Hydroureter, Hydronephrosis (∵ obstruction of urine flow)
    - **
    Chronic renal failure (∵ obstruction of urine flow, common in the past)
  2. **Compression on Prostatic urethra —> **Obstruct urine flow
    - Difficulty urination
    - Frequency
    - Dribbling
  3. ***Superimposed infection
    - Prostatitis
    - Cystitis
  4. Asymptomatic

Gross:
Distinct **circumscribed grey white nodules in **Periurethral zone

Histology:
- **Proliferation of both Glandular + Fibromuscular stromal elements
- **
+/- Infarct, Infection, Squamous metaplasia
- Nodular configuration
(- Double layer of cells preserved (help to diagnose benign nature)
- Cystically dilated glands (some)
- Basal cells (can be highlighted by K903 Immunohistochemistry))

Treatment:
- ***Transurethral resection / curetting

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9
Q

Carcinoma of Prostate

A

Tend to involve outer zone of prostate (External / Prostatic glands proper)
—> may be ***palpable during rectal examination (hard mass)

↑ incidence in HK, uncommon in orientals

Etiology:
- Role of androgen in growth of tumour

Clinical presentation (Latent / Occult / Overt):

  1. Clinical symptoms of Prostatism (~BPH)
    - ***hard mass found during PR exam
  2. S/S of metastasis (e.g. back pain due to vertebral metastasis)
  3. Incidental finding by microscopic examination during removal of prostatic tissue for BPH
  4. Detected during autopsy with no clinical evidence of prostatic cancer

Gross:
- Yellowish, Hard, Gritty tissue

Histology:

  • ***Adenocarcinoma, usually microacini
  • ***Perineural invasion

Spread:

  1. Local
    - grow inwardly —> obstruct Prostatic urethra
    - grow peripherally —> infiltrate adjacent tissue
  2. Lymphatics
    - Presacral in pelvis, Iliac, Para-aortic LN
  3. Retrograde venous (**Prostatic venous plexus —> **Vertebral vein)
    - Vertebra (unique **osteoblastic lesion rather than destructive lesions, X-ray: **dense lesions —> bone formation)
  4. Bloodstream
    - wide spread metastases
  5. Perineural spread (Adenocarcinoma)

Treatment:
- Surgery +/- Hormonal therapy

Tumour marker:
- **Prostatic specific antigen (PSA)
—> Screening of occult / asymptomatic prostate cancer
—> Detection of recurrence
—> Detection of distant metastasis
—> **
Identify primary tumour in cases of metastasis of unknown origin (if PSA identified —> Prostate as primary site)

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10
Q

Differential diagnoses of Scrotal mass

A
  1. Testicular tumour (infrequent but always malignant)
    - ***Germ cell tumours (>90%)
    - Sex cord-Stromal tumours
    - Mixed germ cell and sex cord-stromal tumours
    - Lymphoma
    - Metastasis
    - Mixed
    - Tumours of epididymis
    - Unclassified
  2. Tumour-like conditions
    - e.g. ***Hydrocele, Haematocele (accumulation of fluid / blood in scrotal sac)
  3. Hernia
  4. ***Orchitis (inflammation of testes) / Epididymitis
    - Non-specific inflammation
    - Specific inflammation
    —> TB, Gonorrhea (epididymis first, then testes)
    —> Syphilis (testes first)
    —> Mumps (orchitis complicate 25-30% mumps in postpubertal group)
    —> Granulomatous orchitis (reaction to extravasated sperms, middle-aged men, simulate TB orchitis / testicular tumour)
  5. Torsion of Testes, Epididymis (Vascular lesions)
    - surgical emergency
    - twisting of spermatic cord —> interfere with venous drainage —> Engorgement + Haemorrhagic infarct
  6. Tumour / Tumour-like conditions of spermatic cord, testicular appendages
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11
Q

Germ cell tumours of Testes

A

Etiology:
1. Genetic
- strong familial predisposition

  1. ***Cryptorchidism
    - Abdominal vs Inguinal
    - Undescended vs Contralateral descended
    - Orchiopexy (may reduce risk of Germ cell tumours) vs No orchiopexy

***Heterogenous group of tumours (combinations may occur in a patient):
1. Seminoma
2. Embryonal carcinoma
3. Teratoma
4. Yolk sac tumour / Endodermal sinus tumour —> AFP
5. Choriocarcinoma —> HCG

Histogenesis:
Germ cell (Spermatogonia / Oogonia —> Seminoma)
—> Totipotent cell
—> (
Embryonal carcinoma: transition state between primitive / differentiated tumour)
—> Extra-embryonic tissue
1. Trophoblast (placenta) (Choriocarcinoma)
2. Yolk sac / Endodermal sinus (
Yolk sac tumour / Endodermal sinus tumour)
OR
—> Embryonic tissue (i.e. Ectoderm, Mesoderm, Endoderm) (***Teratoma)

Age and incidence:
- Neonate / infant —> Yolk sac tumour / Choriocarcinoma / Teratoma
- Middle-age —> Seminoma
- Adolescents / young adult —> Embryonal CA
- > 60 —> Lymphoma

Presentation:
- Testicular enlargement / pain
- Distant metastasis

**Spread:
1. **
Seminoma / Dysgerminoma —> Lymphatics
2. ***Choriocarcinoma —> Blood
3. Embryonal carcinoma, Yolk sac tumour, Teratoma —> Lymphatics / Blood

Treatment:
1. Surgery
2. Radiation
3. Chemotherapy

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12
Q

Cryptorchidism

A

Congenital anomalies of Testes

Complete / Incomplete failure of intraabdominal testes to descend into scrotal sac

Histology of undescended testes (Depend on age / duration of undescended testes):

  1. Interstitial fibrosis
  2. Shrinkage of organ
  3. Disappearance / ↓ of specialised spermatogenic cells (only Sertoli cells present)
  4. Progressive degenerative changes (Sertoli cells may disappear eventually)

Complications of undescended testes:

  1. Infertility if bilateral (∵ affect spermatogenesis)
  2. ***Inguinal hernia
  3. ***Testicular Germ cell tumours
  4. Risk of trauma (if inside inguinal canal)
  5. Testicular atrophy (at / after puberty)
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13
Q

Seminoma

A

“Potato tumour”

Gross appearance:
- well-demarcated tan-white ***homogeneous mass (“Potato-like”) composed of uniform cells separated by fine stroma

Histology:

  1. Large, round polyhedral tumour cells
  2. Abundant clear cytoplasm
  3. Large central hyperchromatic nuclei
  4. Prominent nucleoli
  5. Sharp cell border
  6. ***Abundant cytoplasmic glycogen

Spread:
- ***Lymphatics

Treatment:

  • ***Radiosensitive
  • favourable prognosis after Orchidectomy + Post-surgical irradiation
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14
Q

Embryonal carcinoma

A
  • ***Highly malignant tumour
  • Variable pattern

Histology:
- Cells resemble ***anaplastic epithelial cells

Spread:
- Lymphatics + Blood

Prognosis:
- ***Poor

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15
Q

Teratoma (畸胎瘤)

A
  • Histologically complex tumour composed of tissue derived from >=1 of Ectodermal, Mesodermal, Endodermal elements
  • Mature / Immature
    —> postpubertal males: capable of metastasis even if appear entirely mature
    —> infants / small children: differentiated mature, usually ***benign

Ectodermal differentiation

  1. Skin, appendages (e.g. hair)
  2. Choroid plexus (neuroectodermal differentiation)
  3. Neuroepithelium (immature tissue e.g. neuroblast arranged in tubes)

Mesodermal differentiation

  1. Cartilage
  2. Bone
  3. Smooth muscle

Endodermal differentiation

  1. Intestinal mucosa
  2. Bronchial mucosa
  3. Thyroid

Spread:
- Lymphatics + Blood

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16
Q

Yolk sac tumour / Endodermal sinus tumour

A

Demonstrable ***Alpha-fetoprotein

Gross appearance:
- ***Heterogeneous appearance (vs Homogenous in Seminoma) with patchy haemorrhage

Histology:

  • Resembling yolk sac
  • Distinctive perivascular structures
  • Hyaline globules

Spread:
- Lymphatics + Blood

17
Q

Tumour markers: Alpha-fetoprotein

A

Production site: Fetal yolk sac, GI tract, Liver

Normally low level

Raised in:

  1. ***HCC
  2. Germ cell tumour:
    - ***Yolk sac tumour
    - Embryonal carcinoma
18
Q

Choriocarcinoma

A
  • ***Highly malignant

Histology:
- Biphasic pattern with both
—> Cytotrophoblast (mononuclear) —> proliferation to implant into endometrium
—> ***Syncytiotrophoblast (multinucleated) —> produce HCG —> detected by Immunohistochemistry

Spread:
- ***Blood

Tumour markers:
Serum / Urinary HCG used as tumour markers for monitoring of Choriocarcinoma
—> if HCG remains high after surgery
—> suggest Micrometastases

HCG drop to normal —> increase back
—> suggest Recurrence

19
Q

Tumour markers: Human Chorionic Gonadotrophin (HCG)

A

Production site: Placenta (Syncytiotrophoblast)

Raised in:
1. Pregnancy

  1. Germ cell tumours:
    - ***Choriocarcinoma (particularly)
    - Embryonic carcinoma
    - Seminoma (ST) containing Syncytiotrophoblast
  2. Other epithelial malignancies (poorly differentiated carcinoma with ectopic HCG production) (occasionally)
20
Q

Summary of Tumour markers

A
  1. Yolk sac tumour (AFP +, HCG -)
  2. **Choriocarcinoma (AFP -, **HCG +)
  3. Seminoma (AFP -, HCG -)
  4. Teratoma (AFP -, HCG -)
  5. ***Embryonal carcinoma (AFP +, HCG +) (兩個都produce)

Significance:

  1. Detection of ***non-seminomatous elements (if Seminoma found but with high AFP/HCG)
  2. ***Adjunct diagnostic tool for unusual settings (e.g. Extragonadal germ cell tumour: Germ cells trapped during migration in dorsal midline e.g. near pineal gland, posterior mediastinum, retroperitoneal region)
  3. Detection of ***recurrence
  4. Detection of ***distant metastasis
21
Q

Sex cord-Stromal tumours

A
  • 5% of testicular tumours
  • Mostly Leydig cell tumours

Sex cord:

  • Sertoli cells
  • Granulosa cells

Stroma:

  • Leydig cells
  • Theca cells

These tumours can be found in BOTH testes / ovaries

E.g. Androgen secreting Sertoli Leydig cell tumour

22
Q

Lymphoma of Testis

A
  • 2-5% testicular malignancies (mostly secondary)
  • most common testicular tumour > 60 yo

Testes ***replaced / infiltrated by extensive sheets of Lymphoma cells
—> Seminiferous tubules hard to identify