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Unit 5 > Pathology - male genital > Flashcards

Pathology - male genital Flashcards

1
Q

Hypospadias

A
  • Opening of urethra on inferior surface of penis
  • Due to failure of urethral folds to close
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2
Q

hypospadias - cause

A

Due to failure of urethral folds to close

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3
Q

Epispadias

A
  • Opening of urethra on superior surface of penis
  • Due to abnormal positioning of the genital tubercle
  • associated with bladder exstrophy
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4
Q

Epispadias - cause

A

Due to abnormal positioning of the genital tubercle

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5
Q

What is the difference between hypospadias and epispadias?

A

Hypo = low/below –> due to failure of urethral folds to close (inferior surface defect)

Epi = up/above –> due to abnormal positioning of genital tubercle (superior surface defect)

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6
Q

Condyloma acuminatum

A

Benign warty growth on genital skin

Due to HPV type 6 or 11 – characterized by koilocytic change

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7
Q

Condyloma acuminatum - what is the cause?

A

Due to HPV type 6 or 11 – characterized by koilocytic change

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8
Q

HPV - high risk vs low risk serotypes

A

High risk - 16, 18, 31, 33 –> risk for carcinoma

Low risk - 6, 11 –> usually results in benign lesions (ie condyloma acuminatum)

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9
Q

Chlamydia trachomatis - serotypes and respective diseases

A

Serotype A–C: trachoma

Serotype D–K: urogenital abnormalities & conjunctivitis

Serotype L1-L3: lymphogranuloma venereum

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10
Q

Lymphogranuloma venereum

A
  • Necrotizing granulomatous inflammation of the inguinal lymphatics and lymph nodes
  • Sexually transmitted disease caused by Chlamydia trachomatis
  • Eventually heals w/ fibrosis
  • Perianal involvement may result in rectal stricture
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11
Q

What bug is responsible for lymphogranuloma venereum?

A

Chlamydia trachomatis - serotypes L1-L3

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12
Q

lymphogranuloma venereum - prognosis

A

Eventually heals w/ fibrosis

Perianal involvement may result in rectal stricture (narrowing)

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13
Q

Squamous cell carcinoma of penis

A
  • Malignant proliferation of squamous cells of penile skin
  • Risk factors
    • high risk HPV (2/3 of cases) - 16,18,31,33
    • Lack of circumcision - foreskin acts as a nidus for inflammation and irritation if not properly maintained
  • Percursor insitu lesions
    • Bowen disease
    • Erythroplasia of Queyrat
    • Bowenoid papulosis
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14
Q

Squamous cell carcinoma of penis - risk factors

A
  • high risk HPV (2/3 of cases) - 16,18,31,33
  • Lack of circumcision - foreskin acts as a nidus for inflammation and irritation if not properly maintained
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15
Q

Why is lack of circumcision a risk factor for squamous cell carcinoma?

A

Foreskin acts as a nidus for inflammation and irritation if not properly maintained

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16
Q

Percursor in-situ lesions to squamous cell carcinoma of penis

A
  • Bowen disease - in situ carcinoma of the penile shaft or scrotum that presents as leukoplakia. Typically progresses to invasive carcinoma
  • Erythroplasia of Queyrat - in situ carcinoma on the glans that presents as erythroplakia
  • Bowenoid papulosis - in situ carcinoma that presents as multiple reddish papules
    • seen in younger patients (40s) relative to Bowen disease and erythroplasia of Queyrat
    • Does NOT progress to invasive carcinoma
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17
Q

Bowen disease

A

in situ carcinoma of the penile shaft or scrotum that presents as leukoplakia.

Typically progresses to invasive carcinoma

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18
Q

Bowen disease - clinical presentation?

A

leukoplakia of the penile shaft or scrotum

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19
Q

Erythroplasia of Queyrat

A

in situ carcinoma on the glans that presents as erythroplakia

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20
Q

What is the main difference between Bowen disease and erythroplasia of Queyrat?

A

Bowen disease - leukoplakia of the penile shaft or scrotum (base of penis)

Erythroplasia - erythroplakia of the glands of penis

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21
Q

Bowenoid papulosis

A
  • in situ carcinoma that presents as multiple reddish papules
  • seen in younger patients (40s) relative to Bowen disease and erythroplasia of Queyrat
  • Does NOT progress to invasive carcinoma
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22
Q

Difference between Bowen disease and Bowenoid papulosis?

A

Bowenoid papulosis is Bowen-like.

However, Bowenoid papulosis is:

  • seen in younger patients
  • erythroplasia instead of leukoplakia
  • Does NOT progress to invasive carcinoma
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23
Q

Testicle development

A

Develops in the abdomen and descends into the scrotal sac as the fetus grows

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24
Q

Most common congenital male reproductive abnormality

A

Cryptorchidism (failure of testicle to descend into the scrotal sac)

seen in 1% of male infants

Most cases resolve spontaneously

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25
Q

Cryptorchidism

A

Failure of testicles to descend into the scrotal sac

Most cases resolve spontaneously

Treatment is orchipexy performed before 2 years of age

Complications include testicular atrophy w/ infertility and increased risk of seminoma

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26
Q

Cryptorchidism - treatment

A

Most cases resolve spontaneously

If not, orchiopexy is performed before 2 years of age

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27
Q

Cryptorchidism - complications

A

testicular atrophy w/ infertility

increased risk for seminoma

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28
Q

Orchitis

A

Inflammation of the testicle

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29
Q

Orchitis - causes

A
  1. Chlamydia trachomatis (serotypes D-K) or Neisseria gonorrhoeae
    • Seen in young adults
    • increased risk of sterility, but libido is not affected because Leydig cells are spared
  2. Escherichia coli and Pseudomonas
    • seen in older adults
    • UTI pathogens spread into the reproductive tract
  3. Mumps virus
    • seen in teenage males
    • increased risk for infertility
      • testicular inflammation is usually not seen in children < 10 years old)
  4. Autoimmune orchitis
    • characterized by granulomas involving the seminiferous tubules
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30
Q

Orchitis cause in young adults?

A
  • Chlamydia trachomatis* (serotypes D-K) or Neisseria gonorrhoeae
  • increased risk of sterility, but libido is not affected because Leydig cells are spared
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31
Q

Orchitis cause in older adults?

A
  • Escherichia* coli and Pseudomonas
  • These are the most common UTI pathogens and cause orchitis when they spread into the reproductive tract
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32
Q

Mumps - where does it normally infection? What other tissues does it infect?

A

Normally infects the parotid gland

Occasionally infects other tissues

  1. meninges –> asceptic meningitis
  2. pancreatitis
  3. orchitis
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33
Q

If you see a granuloma in the testicle, what comes to mind?

A
  1. TB (will cause necrotizing granuloma)
  2. autoimmune orchitis (non-necrotizing granuloma)
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34
Q

Testicular torsion

A

Twisting of the spermatic cord –> leaves the artery open (thick walled), but twist closes off the vein (thin walled) –> obstruction leads to congestion and hemorrhagic infarction

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35
Q

What are 2 requirements of hemorrhagic infarction?

A
  1. Blood going into the space after the tissue dies
  2. Loosely organized tissue (so it can flow out as opposed to blowing up)
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36
Q

Testicular torsion - most common cause

A

Congenital failure of testes to attach to the inner lining of the scrotum (via the processus vaginalis) –> no anchor = easier twisting of the cord

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37
Q

Testicular torsion - clinical presentation

A

Sudden testicular pain

absent cremasteric reflex

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38
Q

Varicocele

A

Dilation of the spermatic vein due to impaired drainage

Seen in a large percentage of infertile males

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39
Q

Varicocele - presentation

A

Scrotal swelling w/ a “bag of worms” appearance

  • veins are dilated and seen ont he surface of the scrotum
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40
Q

Which side does varicocele normally present? Why? What is the association?

A

Usually left sided: left testicular vein drains into the left renal vein, while right directly drains into the IVC

Associated with left-sided renal cell carcinoma (loves to invade the renal vein)

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41
Q

Why is varicocele seen in a large percentage of infertile males?

A

Varicocele is basically the pooling of warm blood in the scrotal sac.

This warm blood heats up the testicles (which requires lower temperature to function) and will cause permanent damage to the production of sperm.

42
Q

Hydrocele

A

Fluid collection within the tunica vaginalis (serous membrane that covers the testicle as well as the internal surface of the scrotum)

43
Q

Hydrocele - common causes?

A
  • In infants: incomplete closure of the processus vaginalis leading to communication w/ the peritoneal cavity
  • In adults: blockage of lymphatic drainage
44
Q

Hydrocele - clinical presentation

A

Scrotal swelling

  • Can be transilluminated (not a mass, but rather a bag of fluid)
45
Q

Testicular tumors - clinical presentation

A

Present as a firm, painless testicular mass that cannot be transilluminated (contrasted to a hydrocele that can be transilluminated)

46
Q

Why do you not biopsy testicular cancers?

A
  1. May seed the scrotum when pulling the testicle out
  2. >95% of cases are geerm cell tumors (which are all malignant and require more than surgical removal)

This is contrary to most tumors that require a biopsy to diagnose

47
Q

Germ cell tumors (5)

A
  1. teratoma
  2. embryonal carcinoma
  3. choriocarcinoma
  4. yolk sac tumor
  5. seminoma

Teratoma + embryonal (both embryonic origin)

choriocarcinoma + yolk sac tumor (has to do with development)

seminoma (tumor of germ cells – mature cells – best prognosis)

48
Q

Age when most germ cell tumors occur?

A

15 - 40

49
Q

Germ cell tumors - risk factors

A

Cryptorchidism

Klinefelter syndrome

50
Q

Germ cell tumor - what is the main division? Why is it made?

A

Divided into seminoma and nonseminoma.

  • Seminoma (55% of cases) are highly responsive to radiotherapy, metastasize late, and have an excellent prognosis
  • Non-seminoma (45% of cases) show variable response to treatment and often metastasize early

Think of a seminoma as a cancer of mature cells (or at least the most mature of cells in the testicle) which typically results in the best prognosis

51
Q

Seminoma

A
  • malignant tumor comprised of large cells w/ clear cytoplasm and central nuclei (resemble spermatogonia)
  • forms a homogenous mass w/ no hemorrhage or necrosis
  • rare cases may produce B-hCG (classically associated w/ choriocarcinoma)
  • good prognosis – responds to radiotherapy
52
Q

What is the female equivalent of a seminoma?

A

dysgerminoma

53
Q

Most common testicular tumor

A

Seminoma

54
Q

Embryonal carcinoma

A
  • malignant tumor comprised of immature, primitive cells that may produce glands
  • Forms a hemorrhagic mass w/ necrosis
  • aggressive w/ early hematogenous spread (embryo-like: programmed to move and spread rapidly)
  • Chemotherapy may result in differentiation into another type of germ cell tumor (ie teratoma)
  • Increased AFP or B-hCG may be present
55
Q

Embryonal carcinoma - prognosis

A

Poor: aggressive tumor w/ early hematogenous spread

Chemotherapy may result in differentiation into another type of germ cell tumor (ie teratoma)

56
Q

What laboratory findings are associated w/ embryonal carcinoma?

A

Immature primitive cells that may produce glands

Hemorrhagic mass w/ necrosis

Increased AFP or B-hCG

57
Q

Yolk sac (endodermal sinus) tumor

A
  • Malignant tumor that resembles yolk sac elements
  • Most common testicular tumor in children
  • Schiller-Duval bodies (glomerulus-like structures) seen on histology
  • AFP is characteristically elevated
58
Q

Most common testicular tumor? in children?

A

Adults: seminoma

children: yolk sac (endodermal sinus) tumor

59
Q

Choriocarcinoma

A
  • Malignant tumor of syncytiotrophoblasts and cytotrophoblasts (placenta-like tissue, but villi are absent)
  • Spreads early via blood (remember these 2 types of cells are genetically programmed to find and invade blood vessels – mainly the role of syncytiotrophoblasts)
  • B-hCG is characteristically elevated –> may result in hyperthyroidism or gynecomastia (α-subunit of HCG is similar to that of FSH, LH and TSH)
60
Q

Choriocarcinoma - what is different between the cancer and the normal tissue?

A

Functional unit of the placenta = villus surrounded by syncytiotrophoblasts and cytotrophoblasts

In cancer form, the 2 cell types are there, but the villus is not present

61
Q

why does choriocarcinoma spread early?

A

The job of syncytiotrophoblasts is to invade blood vessels (minorly aided by cytotrophoblasts)

62
Q

β-hCG: what are the symptoms due to high levels? Why?

What disease(s) is elevated levels associated with?

A

Symptoms: hyperthyroidism or gynecomastia

  • the α subunit of hCG is similar to that of FSH, LH and TSH so at higher levels, there will be nonspecific activation of those receptors. FSH and LH –> gynecomastia, TSH –> hyperthyroidism

Elevated levels is classically associated with choriocarcinoma. However, it can be seen elevated in embryonal carcinomas, teratomas and rarely in seminomas.

63
Q

Teratoma

A

Tumor composed of mature fetal tissue derived from two or three embryonic layers

  • malignant in males, benign in females
  • AFP or β-hCG may be increased
64
Q

What is the difference between teratomas in male and females?

A

Malignant in males. Benign in females.

65
Q

Mixed germ cell tumors

A

Germ cell tumors are usually mixed

Prognosis is based on the worst component

66
Q

Sex-cord stromal cell types

A

Sertoli cells (lines the tubules)

Leydig cells (produces testosterone)

67
Q

Sex-cord stromal tumors

A

Tumors that resemble sex cord stromal tissues of the testicle (sertoli cells or leydig cells)

  • Leydig cell tumor
    • produces androgen –> precocious puberty in children or gynecomastia in adults
    • Characteristic Reinke crystal seen on histology
  • Sertoli cell tumor
    • comprised of tubules
    • clinically silent

Usually benign

68
Q

What cancer is associated with these crystals?

A

Reinke crystals

Classically seen in Leydig cell tumors

69
Q

Leydig cell tumor

A

produces androgen –> precocious puberty in children or gynecomastia in adults

Characteristic Reinke crystal seen on histology

70
Q

Sertoli cell tumor

A

comprised of tubules

clinically silent

71
Q

Most common cause of a testicular mass in males > 60 years old

A

Lymphoma – often bilateral

Usually diffuse large B-cell type

72
Q

How to distinguish between acute and chronic prostatitis?

A

Acute

  • due to bacteria
  • dysuria w/ fever and chills
  • prostatic secretions show WBCs – w/ + bacteria in culture

Chronic

  • dysuria w/ pelvic or low back pain
  • secretions show WBCs but negative for bacteria
73
Q

What testicular tumors are associated with elevated β-hCG?

A

Classically: choriocarcinoma

However, can also present in

  • seminoma (rare)
  • embryonal carcinoma
  • teratoma
74
Q

What testicular tumors are associated with elevated AFP levels?

A

Characteristically: yolk sac tumor

However can present in:

  • embryonal carcinoma
  • yolk sac tumor
75
Q

What testicular tumor is associated w/ production of glands?

A

Embryonal carcinoma

76
Q

Prostate

A

Consists of glands and stroma

  • glands are composed of an inner layer of luminal and an outer layer of basal cells
    • secret alkaline, milky fluid that is added to sperm and seminal vesicle fluid to make semen
  • glands and stroma are maintained by androgens

Prostate is a small, round organ that lies at the base of the bladder, encircles the urethra and sits anterior to the rectum (posterior aspect of prostate is palpable by digital rectal exam (DRE))

77
Q

Screening tools for prostate cancer? why are they used?

A
  1. DRE (digital rectal exam)
    • prostate sits anterior of the rectum. Posterior aspect of prostate is palpable by digital rectal exam
  2. PSA (prostate specific antigen)
    • PSA is made by prostatic glands to liquidify semen
    • cancer results in hyperplasia of the glands (adenocarcinoma) and will result in PSA levels > 10ng/ml
78
Q

What are the glands and stroma of the prostate maintained by?

A

Androgens

79
Q

Acute prostatitis

A

Acute inflammation of the prostate – usually due to bacteria (same bugs as orchitis)

  • Chlamydia trachomatis and Neisseria gonorrhoeae in young adults
  • Escherichia coli and Pseudomonas in older adults

Presents as dysuria w/ fever and chills

Prostate is tender and boddy on DRE

Prostate secretions show WBCs – culture will reveal bacteria

80
Q

acute prostatitis - causes

A

Same bugs as orchitis

  • Chlamydia trachomatis and Neisseria gonorrhoeae in young adults
  • Escherichia coli and Pseudomonas in older adults
81
Q

acute prostatitis - presentation

A

Dysuria w/ fever and chills

Prostate is tender and boggy on DRE

Prostatic secretions show WBCs – culture reveal bacteria

82
Q

Chronic prostatitis

A

Chronic inflammation of prostate

Presents as dysuria w/ pelvic or low back pain

Prostatic secretions show WBCs, but cultures are negative

83
Q

What happens to PSA as we age?

A

PSA will increase naturally – mainly due to benign prostatic hyperplasia (no increase in carcinoma risk)

84
Q

Benign prostatic hyperplasia (BPH)

A

Hyperplasia of prostatic stroma and glands

age-related change (present in most men by 60 years) – no increased risk for cancer

Related to DHT (dihydrotestosterone)

  • Testosterone is converted to DHT by 5α-reductase in stromal cells
  • DHT acts on the androgen receptor of stromal and epithelial cells resulting in hyperplastic nodules

Occurs in the central periurethral zone of the prostate

  • growth will cause compression of the urethra –> clinical features associated with urinary obstruction

Clinical features:

  • problems starting and stopping urine stream
  • impaired bladder emptying w/ increased risk for infection and hydronephrosis (backup of fluid into the kidney)
  • Dribbling
  • hypertrophy of bladder wall smooth muscle –> increased risk for bladder diverticula
  • microscopic hematuria may be present
  • PSA is often slightly elevated (4-10ng/ml) due to increased number of glands
    • PSA is made by prostatic glands and liquefies semen
85
Q

What chemical is responsible for benign prostatic hyperplasia?

A
  • Dihydrotestosterone (DHT)
  • Testosterone is converted to DHT by 5α-reductase in stromal cells
  • DHT acts on the androgen receptor of stromal and epithelial cells resulting in hyperplastic nodules
86
Q

where does benign prostatic hyperplasia occur? What is the location’s significance?

A

Occurs in the central periurethral zone of the prostate

This zone surrounds the prostate. Hyperplasia of growth of this zone will compress the urethra resulting in urinary obstruction (which is what the majority of BPH symptoms are a result of)

87
Q

Benign prostatic hyperplasia - clinical features

A
  1. problems starting and stopping urine stream
  2. impaired bladder emptying w/ increased risk for infection and hydronephrosis (backup of fluid into the kidney)
  3. Dribbling
  4. hypertrophy of bladder wall smooth muscle –> increased risk for bladder diverticula
  5. microscopic hematuria may be present
  6. PSA is often slightly elevated (4-10ng/ml) due to increased number of glands
    • PSA is made by prostatic glands and liquefies semen
88
Q

Hydronephrosis

A

literal translation: “water in kidney”

Typically results from urinary obstruction and causes backup of fluid into the kidney that can result in dilation and atrophy of the ureter and kidney

89
Q

Why is there hypertrophy of the bladder wall smooth muscle in benign prostatic hyperplasia? What can result due to this?

A

In BPN, there is narrowing of the urethra which causes increased tension in the bladder resulting in hypertrophy.

The high pressure generated in the bladder against the obstruction could result in diverticuli or outpouching of the bladder wall

90
Q

What is the purpose of PSA? Why is it secreted?

A

Secreted by prstatic glands to liquefy semen

91
Q

PSA levels? Normal/BPN/adenocarcinoma

A

Normal: 0-4ng/ml

BPN: 4-10ng/ml (increases with age from 2.5 at 40-49years to 7.5 at 70-79 years)

adenocarcinoma: > 10ng/ml

92
Q

Benign prostatic hyperplasia - treatment (2)

A
  1. α1-antagonist (ie terazosin) to relax smooth muscle
    • also relaxes vascular smooth muscle –> lowering BP (helps if patient also has HTN)
    • selective α1a -antagonists (ie tamsulosin) are used in normotensive individuals to avoid the α1b effects on blood vessels
  2. 5α-reductase inhibitor
    1. blocks conversion of testosterone to DHT
    2. Takes months to produce results
    3. also useful for male pattern baldness
    4. side effects are gynecomastia and sexual dysfunction
93
Q

Prostate adenocarcinoma

A
  • Malignant proliferation of prostatic glands
  • Most common cancer in men – 2nd most common cause of cancer-related death
  • Risk factors include age, race (African Americans > Caucasians > asians), and diet high in saturated fats
94
Q

Most common cancer in men

A

Prostatic adenocarcinoma

95
Q

Prostatic adenocarcinoma - clinical presentation

A

Most often clinically silent

  • Usually arises in the peripheral, posterior region of the prostate, and hence does not produce urinary symptoms early on (only if it cancer grows significantly to compress the urethra)
  • because it is silent, it requires screening (DRE and PSA)
96
Q

Prostatic adenocarcinoma - screening

A

Done with DRE (digital rectal exam) and PSA (prostatic specific antigen)

  • screening begins at age 50
  • Normal serum PSA increases w/ age due to BPH (normal: 2.5ng/ml @40-49, 7.5ng/ml @70-79)
  • PSA > 10ng/ml highly worrisome at any age
  • Cancer only makes bound PSA so decreased %free-PSA is suggestive of cancer
97
Q

What does a decreased % of free PSA mean?

A

Decreased % free PSA == highly suggestive of cancer

  • Cancer makes only bound PSA. Increased bound PSA will decrease the percentage of free PSA.
98
Q

What is required to confirm the diagnosis of prostatic carcinoma?

A

Biopsy - shows small, invasive glands w/ prominent and dark nucleoi

Graded on the Gleason grading system (based on architexture alone, and NOT on nuclear atypia)

99
Q

Gleason grading system

A
  • based on architexture alone, and NOT on nuclear atypia
  • multiple regions of the tumor are assessed because achitecture varies from area to area
  • A score of (1-5 is assigned for two distinct areas and then added to produce a final score (2-10)
  • Higher score suggests worse prognosis
100
Q

Where is prostatic adenocarcinoma likely to spread? What is the result of the spread?

A

Like to lumbar spine or pelvis is common

Results in osteoblastic metastases that present as low back pain and increased serum alkaline phosphatase, PSA, and prostatic acid phosphatase (PAP)

101
Q

prostatic adenocarcinoma - treatment

A

Prostatectomy is performed for localized disease

advanced disease is treated w/ hormone suppression to reduce testosterone and DHT

  • continuous GnRH analogs (ie leuprolide) shut down the anterior pituitary gonadotrophs (LH and FSH reduced)
    • remember prostate cancer is highly androgen dependent. The cancer loses its ability to thrive by reducing androgens
  • Flutamide acts as a competitive inhibitor at the androgen receptor
102
Q

Drugs used to treat prostatic adenocarcinoma

A

continuous GnRH analogs (ie leuprolide) shut down the anterior pituitary gonadotrophs (LH and FSH reduced)

  • remember prostate cancer is highly androgen dependent. The cancer loses its ability to thrive by reducing androgens

Flutamide acts as a competitive inhibitor at the androgen receptor

Unit 5 (5 decks)

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