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GU / GYN & Renal > Pathoma: Male Genital System > Flashcards

Pathoma: Male Genital System Flashcards

1
Q

Penis

Opening of urethra on inferior surface of penis

Gross Anatomy

A

Hypospadias

“Hypo-“ = low –> inferior surface

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2
Q

Penis

Failure of urethral folds to close

Pathophysiology

A

Hypospadias

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3
Q

Penis

Opening of urethra on superior surface of penis

Gross Anatomy

A

Epispadias

“Epi-“ = on top –> superior surface

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4
Q

Penis

  • Abnornal positioning of genital tubercle
  • Associated with baldder exstrophy

Pathophysiology

A

Epispadias

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5
Q

Penis

Benign warty growth on genital skin

Pathophysiology

A

Condyloma acuminatum

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6
Q

Penis

Cause of condyloma acuminatum

Etiology

A

Low-risk HPV types 6, 11

HPV-associated condyloma

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7
Q

Penis

Characterized by koilocytic change

Histopathology

A

Condyloma acuminatum

Koilocytes = histological hallmark of HPV

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8
Q

Penis

A

Condyloma acuminatum

Koilocytes = HPV hallmark; shriveled, raisin-like nuclei

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9
Q

Penis

  • Necrotizing granulomatous inflammation of inguinal lymphatic & lymph nodes
  • Eventually heals via fibrosis; perianal involvement may result in rectal strictures

Histopathology

A

Lymphogranuloma venereum

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10
Q

Penis

Cause of lymphogranuloma venereum

Etiology

A

Chlamydia trachomatis

L1 - L3

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11
Q

Penis

Malignant proliferation of squamous cells of penile skin

Histopathology

A

Penile SCC

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12
Q

Penis

Risk factors of penile SCC

Epidemiology

A
  • High-risk HPV types 16, 18 = 2/3 of cases
  • Lack of circumcision
    • Foreskin acts as nidus for inflammation & irritation
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13
Q

Penis

Penile SCC precursor in situ lesions

Natural History

A
  1. Bowen disease
  2. Erythroplasia of Queyrat
  3. Bowenoid papulosis
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14
Q

Penis

CIS of penile shaft or scrotum

Histopathology

A

Bowen disease

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15
Q

Penis

Presents as leukoplakia

Clinical Presentation

A

Bowen disease

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16
Q

Penis

CIS on glans

Histopathology

A

Erythroplasia of Queyrat

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17
Q

Penis

Presents as erythroplakia

Clinical Presentation

A

Erythroplasia of Queyrat

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18
Q

Penis

CIS that presents as multiple reddish papules

Clinical Presentation

A

Bowenoid papulosis

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19
Q

Penis

  • Seen in younger patients (40s) relative to Bowen disease & erythroplasia of Queyrat
  • Does not progress to invasive carcinoma

Distinctive Clinical Features

A

Bowenoid papulosis

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20
Q

Testicle

Failure of testicle to descend into scrotal sac
* Testicles normally develop in abdomen then descend into scrotal sac as fetus grows

Pathophysiology

A

Cryptorchidism

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21
Q

Testicle

Most common congenital male reproductive abnormality (1% of male infants)

Epidemiology

A

Cryptorchidism

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22
Q

Testicle

Treatment of cryptorchidism

Approach to Therapy

A
  • Most cases resolve spontaneously
  • Otherwise, orchipexy is performed before age 2
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23
Q

Testicle

  • Testicular atrophy w/ infertility
  • Increased risk for seminoma

Potential Complications

A

Cryptorchidism

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24
Q

Testicle

Inflammation of testicle

Histopathology

A

Orchitis

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25
Q

Testicle

Chlamydia trachomatis (serotypes D-K) or Neisseria gonorrhoeae

Etiology

A

Cause of orchitis
* Seen in young adults
* Increased risk of sterility
* Leydig cells are spared –> libido is not affected

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26
Q

Testicle

Escherichia coli & Pseudomonas

Etiology

A

Cause of orchitis
* Seen in older adults
* UTI pathogens spread into reproductive tract

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27
Q

Testicle

Mumps virus

Etiology

A

Cause of orchitis
* Seen in teenage males; testicular inflammation typically not seen in children < 10
* Increased risk of infertility

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28
Q

Testicle

Autoimmune orchitis

Etiology

A

Cause of orchitis
* Characterized by granulomas involving seminiferous tubules

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29
Q

Testicle

  • Twisting of spermatic cord
  • Thin-walled veins become obstructed leading to congestion & hemorrhagic infarction of testicle

Pathophysiology

A

Testicular torsion

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30
Q

Testicle

Results from congenital failure of testes to attach to inner lining of scrotum via the processus vaginalis

Etiology

A

Testicular torsion

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31
Q

Testicle

  • Presents in adolescence
  • Sudden testicular pain & absent cremasteric reflex

Clinical Presentation

A

Testicular torsion

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32
Q

Testicle

  • Presents in adolescence
  • Sudden testicular pain & absent cremasteric reflex

Clinical Presentation

A

Testicular torsion

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33
Q

Testicle

A

Testicular torsion

Hemorrhagic (red) infarct of testicle

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34
Q

Testicle

Dilation of spermatic vein due to impaired drainage

Pathophysiology

A

Varicocele

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35
Q

Testicle

Presents as scrotal swelling with “bag of worms” appearance

Clinical Presentation

A

Varicocele

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36
Q

Testicle

Seen in large percentage of infertile males

Epidemiology

A

Varicocele

Accumulation of warm blood in scrotum increases temperature in testicle

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37
Q

Testicle

Varicocele = usually left-sided

Distinctive Clinical Manifestations

A
  • Left testicular vein drains into left renal vein while right testicular vein drains directly into IVC
  • Associated with left-sided renal cell carcinoma
    • RCC often invades renal vein
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38
Q

Testicle

Fluid collection within tunica vaginalis
* Tunica vaginalis = serous membrane lining the testicle & internal surface of scrotum

Pathophysiology

A

Hydrocele

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39
Q

Testicle

Associated with incomplete closure of processus vaginalis (infatnts) / blockage of lymphatic drainage (adults)

Etiology

A

Hydrocele

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40
Q

Testicle

Presents as scrotal swelling that can be transilluminated

Clinical Presentation

41
Q

Testicle

42
Q

General

Testicular Tumors

A
  • Arise from germ cells or sex cord-stroma
  • Present as firm, painless testicular masses that cannot be transilluminated
  • Usually not biopsied due to risk of seeding scrotum; removed via radical orchiectomy
    • Most testicular tumors are malignant germ cell tumors
43
Q

Testicular Tumors

Most common type of testicular tumor

A

Germ cell tumors

> 95% of cases

44
Q

Testicular Tumors

  • Usually occur between 15-40 years of age

Epidemiology

A

Germ cell tumors

45
Q

Testicular Tumors

Major risk factors of germ cell tumors

Epidemiology

A
  1. Cryptorchordism
  2. Klinefelter syndrome
46
Q

Testicular Tumors

Subtypes of germ cell tumors

Histology

A
  1. Seminoma: 55% of cases
  2. Non-seminoma: 45% of cases
    * Majority of germ cell tumors are mixed types
47
Q

Testicular Tumors

Treatment of seminoma

Approach to Therapy

A
  • Highly responsive to radiotherapy
  • Metastasize late
  • Excellent prognosis
48
Q

Testicular Tumors

Treatment of non-seminoma

Approach to Therapy

A
  • Variable response to treatent
  • Often metastasize early
49
Q

Testicular Tumors

Malignant tumor comprised of large cells with clear cytoplasm & central nuclei
* Resemble spermatogonia (analogous to dysgerminoma)
* Homogenous mass with no hemorrhage / necrosis
* Rare cases may produce B-hCG
* Late mets, respond to radiotherapy –> good prognosis

Histopathology

A

Seminoma

“Sem-“ = semen –> sperm

50
Q

Testicular Tumors

Most common testicular tumor

Epidemiology

51
Q

Testicular Tumors

A

Seminoma

Large cells with clear cytoplasm & central nuclei

52
Q

Testicular Tumors

A

Seminoma

Homogenous mass w/ no hemorrhage, necrosis

53
Q

Testicular Tumors

Malignant tumor of immature, primitive cells
* May form glands
* Homogenous mass with necrosis
* Aggressive with early hematogenous spread
* Primitive cells = programmed to spread rapidly
* CTx may result in differentiation of tumor

Histopathology

A

Embryonal carcinoma

Non-seminoma

54
Q

Testicular Tumors

A

Embryonal carcinoma

Primitive cells forming glands

55
Q

Testicular Tumors

A

Embryonal carcinoma

Hemorrhagic mass

56
Q

Testicular Tumors

Malignant tumor that mimics yolk sac

Histopathology

A

Endodermal sinus (yolk sac) tumor

Non-seminoma

57
Q

Testicular Tumors

Most common testicular tumor in children

Epidemiology

A

Endodermal sinus tumor

58
Q

Testicular Tumors

  • Histology: Schiller-Duval bodies
  • Serum: elevated AFP

Approach to Diagnosis

A

Endodermal sinus tumor

SD bodies = histogical hallmark; AFP elevation = characteristic finding

59
Q

Testicular Tumors

A

Endodermal sinus tumor

Schiller-Duval bodies = histological hallmark; glomeruloid structure

60
Q

Testicular Tumors

Malignant tumor of syncytiotrophoblasts & cytotrophoblasts
* Placenta-like tissue, but villi are absent

Histopathology

A

Choriocarcinoma

Non-seminoma

61
Q

Testicular Tumors

Serum: elevated B-hCG

Approach to Diagnosis

A

Choriocarcinoma

B-hCG elevation = characteristic finding

62
Q

Testicular Tumors

Elevated B-hCG may lead to hyperthyroidism or gynecomastia

Potential Complications

A

Choriocarcinoma

a-subunit of hCG is similar to FSH, LH, and TSH

63
Q

Testicular Tumors

A

Choriocarcinoma

Cyto = middle; small, mononucleated; Syncytios = larger, binucleated

64
Q

Testicular Tumors

Tumor composed of mature fetal tissue derived from 2-3 embryonic layers
* Malignant in males; benign in females
* AFP or B-hCG may be elevated

Histopathology

A

Teratoma

Non-seminoma

65
Q

Testicular Tumors

Tumors that resemble sex cord-stromal tissues of the testicle; typically benign

Histopathology

A

Sex cord-stromal tumors

66
Q

Testicular Tumors

Subtypes of germ cell tumors

Histology

A
  1. Leydig cell tumors
  2. Sertoli cell tumors
67
Q

Testicular Tumors

Usually produce androgens

Pathophysiology

A

Leydig cell tumor

68
Q

Testicular Tumors

Children: precocious puberty
Adults: gynecomastia

Clinical Presentation

A

Leydig cell tumors

Due to androgen production

69
Q

Testicular Tumors

Reinke crystals

Histology

A

Leydig cell tumors

Reinke crystals = histological hallmark

70
Q

Testicular Tumors

  • Comprised of tubules
  • Usually clinically silent

Histopathology

A

Sertoli cell tumots

71
Q

Testicular Tumors

Most common cause of testicular mass in males age > 60

Epidemiology

72
Q

Testicular Tumors

  • Usually tumor composed of diffuse large B-cells
  • Often bilateral

Histopathology

73
Q

General

Prostate

A
  • Small, round organ that lies at base of bladder encircling urethra
    • Sits anterior to rectum; posterior aspect of prostate is palpable by digital rectal exam (DRE)
  • Consists of glands & stroma
    • Glands are composed of an inner layer of luminal cells & an outer layer of basal cells
      • Secrete alkaline, milky fluid that is added to sperm & seminal fluid to make semen
    • Glands & stroma are maintaine by androgens
74
Q

Prostate

A

Prostate, normal

Consits of glands (functional units) & stroma (CT)

75
Q

Prostate

Acute inflammation of prostate

Pathology

A

Acute prostatitis

76
Q

Prostate

Causes of acute prostatitis

Etiology

A

Typically bacterial infection
* Young adults: Chlamydia trachomatis & Neisseria gonorrhoeae
* Older adults: Escherichia coli & Pseudomonas
* Same as orchitis

77
Q

Prostate

  • Presents as dysuria with fever & chills
  • DRE: tender & boggy prostate
  • Prostatic secretions show WBCs; cultures reveal bacteria

Clinical Presentation

A

Acute prostatitis

78
Q

Prostate

Chronic inflammation of prostate

Pathology

A

Chronic prostatitis

79
Q

Prostate

  • Presents as dysuria with pelvic or low bck pain
  • Prostatic secretions show WBCs; cultures are negative

Clinical presentation

A

Chronic prostatitis

80
Q

Prostate

Hyperplasia of prostatic stroma & glands
* Related to dihydrotestosterone (DHT)
* Testosterone is converted to DHT in stromal cells by 5-a-reductase
* DHT acts on androgen receptors of stromal & epithelial cells
* Results in hyperplastic nodules
* Occurs in periurehtral zone of prostate

Histopathology

A

Benign prostatic hyperplasia (BPH)

81
Q

Prostate

  • Age-related change; present in most men by age of 60 years
  • No increased risk for cancer

Natural History

82
Q

Prostate

Symptoms related to urinary obstruction
* Difficulty starting & stopping urine stream
* Impaired bladder emptying
* Dribbling
* Bladder smooth muscle hypertrophy
* Microscopic hematuria may be present
* PSA is often slightly elevated due to increased number of glands

Clinical Presentation

83
Q

Prostate

BPH

Potential Complications

A
  • Increased risk for infection & hydronephrosis
    • Impaired bladder emptying
  • Increased risk for bladder diverticula
    • Bladder smooth muscle hypertrophy
84
Q

Prostate

Treatment of BPH

Approach to Therapy

A

a1-antagonist (e.g,. prazosin)
* Relaxes smooth muscle
* Relaxes VSM –> lowers BP
* Selective a1A-antagonists (e.g., tamsulosin) are used in normotensive individuals to avoid a1B effects on blood vessels

5a-reductase inhibitor
* Blocks conversion of testosterone –> DHT
* Takes months to produce results
* Useful for male pattern baldness
* Side effects: gynecomastia, ED

85
Q

Prostate

Epidemiology

A

BPH

Hydronephrosis due to impaired bladder emptying

86
Q

Prostate

Malignant proliferation of prostatic glands

Histopathology

A

Prostatic adenocarcinoma

87
Q

Prostate

Most common cancer in males

Epidemiology

A

Prostatic adenocarcinoma

88
Q

Prostate

2nd most common cause of cancer-related deaths

Epidemiology

A

Prostatic adenocarcinoma

89
Q

Prostate

Risk factors of prostatic adenocarcinoma

Epidemiology

A
  1. Age
  2. Race: Blacks > Whites > Asians
  3. Diet: high saturated fat intake
90
Q

Prostate

Most often clinically silent
* Tumors in posterior periphery of prostate
* No urinary symptoms early on

Clinical Presentation

A

Prostatic adenocarcinoma

Localized

91
Q

Prostate

A

Prostatic adenocarcinoma

Occurs in posterior periphery of prostate, away from urethra

92
Q

Prostate

Prostatic carcinoma screening

Approach to Diagnosis

A

Begins at age of 50 years with DRE & PSA
* Normal PSA increases w/ age due to BPH
* 2.5 ng/mL for ages 40-49
* 7.5 ng/mL for ages 70-79
* PSA > 10 ng/mL: concerning at any age
* Reduced %free-PSA is suggestive of cancer
* Tumor cells produce bound PSA

93
Q

Prostate

Prostatic biopsy

Approach to Diagnosis

A

Required to confirm presence of carcinoma
* Small, invasive glands w/ prominent nuclei
* Gleason GS = based on architecture alone
* Multiple regions are assessed
* Architecture varies in tumor
* Scores (1-5) are given to two distinct areas, then added for final score (2-10)
* 2 most common patterns
* Higher score = worse prognosis

94
Q

Prostate

A

Prostatic adenocarcinoma

Small, infiltrative glands; prominent nucleoli = histological hallmark

95
Q

Prostate

Spread to lumbar spine or pelvis is common
* Osteoblastic metastases
* Excessive activation of osteoblasts adjacent to tumor cells
* Results in overproduction of bone cells
* Bone becomes very dense / sclerotic
* Presents as low back pain, increased serum alkaline phosphatase (ALP), PSA, and prostatic acid phosphatase (PAP)
* ALP = marker of osteoblastic activity; elevation indicates bone formation

Clinical Presentation

A

Prostatic adenocarcinoma

Metastatic / Advanced

96
Q

Prostate

A

Prostatic adenocarcinoma

Osteoblastic metastases

97
Q

Prostate

Treatment of localized prostatic adenocarcinoma

Approach to Therapy

A

Prostatectomy

98
Q

Prostate

Treatment of advanced prostatic adenocarcinoma

Approach to Therapy

A

Hormone suppresion to reduce testosterone & DHT
* Continuous GnRH analogs: block anterior pituitary gonadotrophs; reduced LH & FSDH
* Flutamide: androgen receptor blcioker

GU / GYN & Renal (23 decks)

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