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Lectures > Male GU Pathology > Flashcards

Male GU Pathology Flashcards

1
Q

Penis - congenital anomalies

A

Hypospadias - more common
- urethral opening on the ventral surface of the penis

Epispadias = uretrhal opening on the dorsal surface of the penis

  • -> Both malformations may leads to:
  • urinary tract obstruction and infections
  • ejaculation disturbance - sterility

Phimosis = orifice of the prepuce is too small to permit its retraction

  • secondary to repeated infections and scarring
  • interferes with cleanliness leading to infections
  • paraphimosis = forcible retraction - unable to replace the prepuce
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2
Q

Penis - inflammation

A

Sexually transmitted - gonorrhea, syphillis, chancroid, genital herpes, etc

Non-specific

  • balanoposthitis = infection of the glans and prepuce
  • most cases due to poor local hygiene in uncircumcised men
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3
Q

Penis - neoplasms

A

Benign = condyloma acuminatum

Malignant

  • carcinoma in situ
  • squamous cell carcinoma
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4
Q

Condyloma acuminatum

A

Genital warts - caused by HPV types 6 +11
- may recur but do not evolve into cancers

Histology - hyperchromatic nuclei with irregular nuclear membranes and with a halo around the nucleus = koilocytes (cells are infected by hpv)

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5
Q

Squamous carcinoma in situ (CIS)

A

Malignant changes are confined to the epithelium

  • no evidence of local invasion
  • no possibility of distant mets

Synonyms

  • Bowen’s disease
  • Bowenoid papulosis
  • erythroplasia of Querat

Associated with HPV - esp HPV 16

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6
Q

Squamous cell carcinoma

A

Uncommon in US, <1% of male cancers

  • occurs in 40-70 year olds
  • increased incidence in uncircumcised
  • HPV 16/18 implicated in 50% of cases

Histology - irregular nests of squamous carcinoma invading connective tissue;
- keratinization and keratin pearl formation

Slow growing, locally invasive, metastasize to inguinal and iliac lymph nodes
- prognosis related to stage

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7
Q

Verrucous carcinoma

A

Variant of SCC

  • very rare
  • very well differentiated - difficult to differentiate from condyloma
  • local invasion, no mets
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8
Q

Prostate - inflammation

A

Acute and chronic bacterial prostatitis

Chronic abacterial prostatitis

Granulomatous prostatitis

  • BCG therapy
  • fungal - in immunosuppressed
  • non-specific granulomatous prostatitis
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9
Q

Benign prostatic hyperplasia

A

Extremely common in men >50 years

  • hyperplasia of prostatic stroma and epithelial cells, forming large discrete nodules
  • predominantly involves periurethral region and compresses the urethra –> difficulty in urination, retention of urine, distension and hypertrophy or bladder + infections

Treatment
- medical - alpha blockers + DHT inhibitors

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10
Q

Prostate cancer = adenocarcinoma

A

Most common form of male cancer - second leading cause of cancer death
- older age >50 years

Etiology = multifactorial

  • environmental factors - red meat, fat
  • androgens
  • genetics –> one first degree relative = 2x risk; 2 first degree relatives = 5x risk
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11
Q

Prostate cancer

  • gross
  • histology
A

Gross

  • subtle gross findings, sometimes invisible
  • 70% arise in peripheral zone

Histology

  • most are bland - difficult to distinguish from normal prostate glands
  • small glands infiltrating through normal tissue
  • composed exclusively of malignant epithelial cells - LACK BASAL CELLS
  • cells have enlarged nuclei with large, prominent nucleoli
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12
Q

Prostate intraepithelial neoplasia

A

Presumed precursor of adenocarcinoma

  • cells have features of adenocarcinoma, but still in normal glands with basal cells
  • increased likelihood of invasive carcinoma elsewhere in prostate or in the future (1/3 in 10 years)
  • generally followed by repeat biopsy
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13
Q

Gleason grading

A

Best marker along with the stage for predicting prognosis and impacts treatment

  • stratified into 5 patterns on the basis of ARCHITECTURE (most grades are based on nuclei)
  • gleason score = sum of the 2 most predominant patterns
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14
Q

TNM staging of prostate cancer

A

T1 - clinically unapparent, non-palpable tumor
T2 - tumor confined within prostate
T3 - tumor extends beyond the prostate
T4 - tumor invades adjacent organs

N0 - no lymph node mets
N1 - regional lymph node mets

M1 - distant mets

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15
Q

Testis - congenital

A

Cryptocordism

  • 10% undescended at birth, 1% by 1 year old
  • most often unilateral, 25% bilateral
  • irreversible injury begins around 2 years of age

Complications

  • trauma
  • infertility
  • testicular cancer - 30-50x risk

Treatment = surgical by age 2

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16
Q

Testis - regressive changes

A

Atrophy - causes

  • progressive atherosclerosis
  • end stage inflammatory orchitis
  • cryptochidism
  • hypopituitarism
  • irradiation
  • prolonged administration of female sex hormones

Decreased fertility - various causes

  • hypospermatogenesis
  • maturation arrest
  • vas deferens obstruction
17
Q

Testis - inflammatory

A
  • non-specific epididymitis and orchitis
  • granulomatous/autoimmune orchitis
  • specific inflammation - gonorrhea, mumps, TB, syphillis
18
Q

Testicular torsion

A

Twisting of testis around spermatic cord - blocks venous outflow

  • surgical emergency - testicular infarction
  • most cases in first year of life, another peak around puberty
19
Q

Testicular neoplasms - classification

A

Germ cell tumors = 95%

  1. Seminoma = 33%
    - - classic
    - - spermatocytic
  2. Non-seminomatous = 62%
    - - mixed (most common)
    - - pure
    - –> teratoma
    - –> embryonal carcinoma
    - –> yolk sac tumor
    - –> choriocarcinoma

Sex cord stromal tumors (<1%)

Secondary - particularly lymphoma (5%)

20
Q

Germ cell tumors

A

About 8000 cases/year - 400 deaths/year

  • affect predominantly young patients - 15-34 most common
  • whites 5:1 vs. AA
  • presents as painless testicular enlargement
21
Q

Seminoma (classic)

A

Most common pure germ cell tumor
- peak in 30s

Gross = bulky, lobulated, homogenous, gray-white mass

Histology = recapitulates primitive germ cells

  • large polygonal cells with clear cytoplasma dn distinct cell membranes
  • large central nucleus with prominent nucleoli
  • CORDS OF CELLS DIVIDED BY FIBROUS STROMA WITH LYMPHOCYTIC INFILRATE

placental alkaline phosphatase (PLAP) positive

70% confined to testis (stage 1) at presentation

  • highly sensitive to radiation and chemo
  • 95% cure rate even if metastatic
22
Q

Spermatocytic seminoma

A

Very different from classic seminoma

  • older men - usually 55+
  • different morphology - no lymphocytes, 3 cell types
  • PLAP negative
  • much better natural history, so different treatment = orchiectomy is curative, no chemo needed
23
Q

Non-seminomatous germ cell tumors - overview (NSGCT)

A

Cell types mimic different parts/stages of embryonic development

  • most are mixed; pure are rare
  • prognosis and treatment are basically the same for all of them, but different from pure classical seminoma
  • mixed tumors may have seminoma component; still treated as NSGCT
  • mets and recurrences may have different cell types than primary tumor
24
Q

Teratoma

A

Components reminiscent of normal derivatives from more than one germ layer

  • mature - fetal/adult type tissues
  • immature - primitive embryonal tissues

Pure teratoma common in infants and children

Prognosis depends on age

  • kids - teratomas are benign
  • postpubertal males - all teratomas are malignant –> DIFFERENT THAN IN OVARY!
25
Q

Teratoma - gross and micro

A

Gross - large tumors with heterogeneous appearance

Micro - mixture of tissues from various organs
- skin, GI ,resp epithelium, thyroid, bone, muscle, etc

26
Q

Embryonal carcinoma

A

Recapitulates most primitive embryonal tissue

  • 20-30 year old
  • usually smaller than seminoma

Forms epithelial structures = alveolar or tubular pattern or sheet like growth
- epithelial appearing large anaplastic cells - looks like a really bad carcinoma

Stains with cytokeratin

27
Q

Yolk sac tumor

A

AKA endodermal sinus tumor

  • most common testicular tumor in infants and kids up to 3 yo (pure)
  • non-encapsulated, homogenous, yellow white, mucinous appearance
  • AFP useful marker in blood and on tissue

Recapitulates yolk sac

  • lace like reticular pattern
  • med sized cuboidal or elongated cells
  • 50% have schiller-duval bodies = endodermal sinuses ***
  • eosinophilic hyaline globules
28
Q

Choriocarcinoma

A

1% pure form, highly malignant, usually small

Gross = hemorrhage and necrosis common

Micro - recapitulates placental trophoblast

  • composed of both…
    1. cytotrophoblasts - polygonal cells with clear cytoplasm
    2. syncyttiotrophoblast - large multinucleated cells

HCG = useful marker in blood and tissue

29
Q

Intratubular germ cell neoplasia

A

Presumed origin of germ cell tumors

  • large, atypical cells in base of sertoli tubules
  • look like seminoma cells
  • seen adjacent to many germ cell tumors - not spermatocytic seminoma
30
Q

Germ cell tumors - mets

A

lymphocytic spread is common to

  • retroperitoneal para aortic lymph nodes
  • mediastinal lymph nodes
  • supraclavicular lymph nodes

Hematogenous spread is to lungs primarily
- also liver, brain and bones

NSGCT mets earlier, more commonly via hematogenous route than seminoma

31
Q

Stages of testicular tumors

A

Stage 1 - tumor confined to testis, epididymus, or spermatic cord

Stage 2 - distant spread confined to retroperitoneal nodes below the diaphragm

Stage 3 - mets outside the retroperitoneal nodes or above the diaphragm

32
Q

Germ cell tumors - tx

A

Standard management of solid testicular mass is radical orchiectomy

Adjuvant chemo and/or radiation

  • Seminoma particularly radiosensitive
  • Exceptions spermatocytic seminoma, teratoma in children – no adjuvant therapy

Natural history of germ cell tumors is mostly very bad – rapidly fatal

BUT they are very sensitive to therapy

  • NSGCT >90% long-term remission, most cured
  • Seminoma >95% cure
33
Q

Key points about testicular tumors

A
  • Key clinical distinction is seminoma vs other
  • Spermatocytic seminoma is totally different from classic seminoma
  • Testicular teratomas prognosis is defined by AGE. Any teratoma in a postpubertal male has malignant potential.
  • Most NSGCTs are mixed. All treated the same.
  • Mixed germ cell tumors may show different components in metastases and recurrences than in the original tumor

Lectures (46 decks)

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