Pathoma: Male Genital System Flashcards by Federico Girardi

Penis

Opening of urethra on inferior surface of penis

Gross Anatomy

Hypospadias

“Hypo-“ = low –> inferior surface

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Penis

Failure of urethral folds to close

Pathophysiology

Hypospadias

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Penis

Opening of urethra on superior surface of penis

Gross Anatomy

Epispadias

“Epi-“ = on top –> superior surface

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Penis

Abnornal positioning of genital tubercle
Associated with baldder exstrophy

Pathophysiology

Epispadias

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Penis

Benign warty growth on genital skin

Pathophysiology

Condyloma acuminatum

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Penis

Cause of condyloma acuminatum

Etiology

Low-risk HPV types 6, 11

HPV-associated condyloma

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Penis

Characterized by koilocytic change

Histopathology

Condyloma acuminatum

Koilocytes = histological hallmark of HPV

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Penis

Condyloma acuminatum

Koilocytes = HPV hallmark; shriveled, raisin-like nuclei

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Penis

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

Histopathology

Lymphogranuloma venereum

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Penis

Cause of lymphogranuloma venereum

Etiology

Chlamydia trachomatis

L1 - L3

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Penis

Malignant proliferation of squamous cells of penile skin

Histopathology

Penile SCC

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Penis

Risk factors of penile SCC

Epidemiology

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

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Penis

Penile SCC precursor in situ lesions

Natural History

Bowen disease
Erythroplasia of Queyrat
Bowenoid papulosis

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Penis

CIS of penile shaft or scrotum

Histopathology

Bowen disease

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Penis

Presents as leukoplakia

Clinical Presentation

Bowen disease

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Penis

CIS on glans

Histopathology

Erythroplasia of Queyrat

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Penis

Presents as erythroplakia

Clinical Presentation

Erythroplasia of Queyrat

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Penis

CIS that presents as multiple reddish papules

Clinical Presentation

Bowenoid papulosis

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Penis

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

Distinctive Clinical Features

Bowenoid papulosis

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Testicle

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

Pathophysiology

Cryptorchidism

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Testicle

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

Epidemiology

Cryptorchidism

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Testicle

Treatment of cryptorchidism

Approach to Therapy

Most cases resolve spontaneously
Otherwise, orchipexy is performed before age 2

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Testicle

Testicular atrophy w/ infertility
Increased risk for seminoma

Potential Complications

Cryptorchidism

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Testicle

Inflammation of testicle

Histopathology

Orchitis

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# Testicle *Chlamydia trachomatis* (serotypes D-K) or *Neisseria gonorrhoeae* | Etiology

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

# Testicle *Escherichia coli* & *Pseudomonas* | Etiology

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

# Testicle Mumps virus | Etiology

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

# Testicle Autoimmune orchitis | Etiology

Cause of orchitis * Characterized by granulomas involving seminiferous tubules

# Testicle * Twisting of spermatic cord * Thin-walled veins become obstructed leading to congestion & hemorrhagic infarction of testicle | Pathophysiology

Testicular torsion

# Testicle Results from congenital failure of testes to attach to inner lining of scrotum via the processus vaginalis | Etiology

Testicular torsion

# Testicle * Presents in adolescence * Sudden testicular pain & absent cremasteric reflex | Clinical Presentation

Testicular torsion

# Testicle * Presents in adolescence * Sudden testicular pain & absent cremasteric reflex | Clinical Presentation

Testicular torsion

# Testicle

Testicular torsion | Hemorrhagic (red) infarct of testicle

# Testicle Dilation of spermatic vein due to impaired drainage | Pathophysiology

Varicocele

# Testicle Presents as scrotal swelling with "bag of worms" appearance | Clinical Presentation

Varicocele

# Testicle Seen in large percentage of infertile males | Epidemiology

Varicocele | Accumulation of warm blood in scrotum increases temperature in testicle

# Testicle Varicocele = usually left-sided | Distinctive Clinical Manifestations

* 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

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

Hydrocele

# Testicle Associated with incomplete closure of processus vaginalis (infatnts) / blockage of lymphatic drainage (adults) | Etiology

Hydrocele

# Testicle Presents as scrotal swelling that can be transilluminated | Clinical Presentation

Hydrocele

# Testicle

Hydrocele

# General Testicular Tumors

* 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

# Testicular Tumors Most common type of testicular tumor

Germ cell tumors | > 95% of cases

# Testicular Tumors * Usually occur between 15-40 years of age | Epidemiology

Germ cell tumors

# Testicular Tumors Major risk factors of germ cell tumors | Epidemiology

1. Cryptorchordism 2. Klinefelter syndrome

# Testicular Tumors Subtypes of germ cell tumors | Histology

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

# Testicular Tumors Treatment of seminoma | Approach to Therapy

* Highly responsive to radiotherapy * Metastasize late * Excellent prognosis

# Testicular Tumors Treatment of non-seminoma | Approach to Therapy

* Variable response to treatent * Often metastasize early

# 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

Seminoma | "Sem-" = semen --> sperm

# Testicular Tumors Most common testicular tumor | Epidemiology

Seminoma

# Testicular Tumors

Seminoma | Large cells with clear cytoplasm & central nuclei

# Testicular Tumors

Seminoma | Homogenous mass w/ no hemorrhage, necrosis

# 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

Embryonal carcinoma | Non-seminoma

# Testicular Tumors

Embryonal carcinoma | Primitive cells forming glands

# Testicular Tumors

Embryonal carcinoma | Hemorrhagic mass

# Testicular Tumors Malignant tumor that mimics yolk sac | Histopathology

Endodermal sinus (yolk sac) tumor | Non-seminoma

# Testicular Tumors Most common testicular tumor in children | Epidemiology

Endodermal sinus tumor

# Testicular Tumors * Histology: Schiller-Duval bodies * Serum: elevated AFP | Approach to Diagnosis

Endodermal sinus tumor | SD bodies = histogical hallmark; AFP elevation = characteristic finding

# Testicular Tumors

Endodermal sinus tumor | Schiller-Duval bodies = histological hallmark; glomeruloid structure

# Testicular Tumors Malignant tumor of syncytiotrophoblasts & cytotrophoblasts * Placenta-like tissue, but villi are absent | Histopathology

Choriocarcinoma | Non-seminoma

# Testicular Tumors Serum: elevated B-hCG | Approach to Diagnosis

Choriocarcinoma | B-hCG elevation = characteristic finding

# Testicular Tumors Elevated B-hCG may lead to hyperthyroidism or gynecomastia | Potential Complications

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

# Testicular Tumors

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

# 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

Teratoma | Non-seminoma

# Testicular Tumors Tumors that resemble sex cord-stromal tissues of the testicle; typically benign | Histopathology

Sex cord-stromal tumors

# Testicular Tumors Subtypes of germ cell tumors | Histology

1. Leydig cell tumors 2. Sertoli cell tumors

# Testicular Tumors Usually produce androgens | Pathophysiology

Leydig cell tumor

# Testicular Tumors Children: precocious puberty Adults: gynecomastia | Clinical Presentation

Leydig cell tumors | Due to androgen production

# Testicular Tumors Reinke crystals | Histology

Leydig cell tumors | Reinke crystals = histological hallmark

# Testicular Tumors * Comprised of tubules * Usually clinically silent | Histopathology

Sertoli cell tumots

# Testicular Tumors Most common cause of testicular mass in males age > 60 | Epidemiology

Lymphoma

# Testicular Tumors * Usually tumor composed of diffuse large B-cells * Often bilateral | Histopathology

Lymphoma

# General Prostate

* 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

# Prostate

Prostate, normal | Consits of glands (functional units) & stroma (CT)

# Prostate Acute inflammation of prostate | Pathology

Acute prostatitis

# Prostate Causes of acute prostatitis | Etiology

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

# Prostate * Presents as dysuria with fever & chills * DRE: tender & boggy prostate * Prostatic secretions show WBCs; cultures reveal bacteria | Clinical Presentation

Acute prostatitis

# Prostate Chronic inflammation of prostate | Pathology

Chronic prostatitis

# Prostate * Presents as dysuria with pelvic or low bck pain * Prostatic secretions show WBCs; cultures are negative | Clinical presentation

Chronic prostatitis

# 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

Benign prostatic hyperplasia (BPH)

# Prostate * Age-related change; present in most men by age of 60 years * No increased risk for cancer | Natural History

BPH

# 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

BPH

# Prostate BPH | Potential Complications

* Increased risk for infection & hydronephrosis * Impaired bladder emptying * Increased risk for bladder diverticula * Bladder smooth muscle hypertrophy

# Prostate Treatment of BPH | Approach to Therapy

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

# Prostate | Epidemiology

BPH | Hydronephrosis due to impaired bladder emptying

# Prostate Malignant proliferation of prostatic glands | Histopathology

Prostatic adenocarcinoma

# Prostate Most common cancer in males | Epidemiology

Prostatic adenocarcinoma

# Prostate 2nd most common cause of cancer-related deaths | Epidemiology

Prostatic adenocarcinoma

# Prostate Risk factors of prostatic adenocarcinoma | Epidemiology

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

# Prostate Most often clinically silent * Tumors in posterior periphery of prostate * No urinary symptoms early on | Clinical Presentation

Prostatic adenocarcinoma | Localized

# Prostate

Prostatic adenocarcinoma | Occurs in posterior periphery of prostate, away from urethra

# Prostate Prostatic carcinoma screening | Approach to Diagnosis

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

# Prostate Prostatic biopsy | Approach to Diagnosis

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

# Prostate

Prostatic adenocarcinoma | Small, infiltrative glands; prominent nucleoli = histological hallmark

# 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

Prostatic adenocarcinoma | Metastatic / Advanced

# Prostate

Prostatic adenocarcinoma | Osteoblastic metastases

# Prostate Treatment of localized prostatic adenocarcinoma | Approach to Therapy

Prostatectomy

# Prostate Treatment of advanced prostatic adenocarcinoma | Approach to Therapy

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

Pathoma: Male Genital System Flashcards

(98 cards)