Male Reproductive Pathology Flashcards

(29 cards)

1
Q

Describe Bowen Disease

A

-Leukoplakia (white patch/plaque)

Premalignant lesion (HPV-associated carcinoma in-situ) on the penis

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2
Q

Describe Erythroplasia of Queyrat

A

-Erythroplakia (red patch/plaque)

Premalignant lesion (HPV-associated carcinoma in-situ) on the penis

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3
Q

Describe Bowenoid Papulosis

A

-Younger patients than the other 2 presentations (Bowen and Erythroplasia of Queyrat)
-Multiple reddish/brown papules on glans penis
-Usually transient, rare transformation to cancer

Premalignant lesion (HPV-associated carcinoma in-situ) on the penis

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4
Q

Describe Neoplasms (Penis)

A

-Squamous cell carcinoma
-Common in developing countries

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5
Q

Describe the clinical presentation of Neoplasms (penis)

A

-Gray, crusted, papular lesion usually on glans or prepuce
-Ulceration, induration, irregular margins
-Risk factors:
*poor hygiene (uncircumcised)
*smoking
*HPV

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6
Q

Describe Scrotal enlargement and the different types

A

Fluid accumulation in the tunica vaginalis (membrane covering the testes)
-Hydrocele: serous fluid
-Hematocele: blood accumulation
-Chylocele: lymph accumulation

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7
Q

Cryptorchidism

A

-Failure of testicular descent from the abdomen into the scrotum; most common congenital male reproductive abnormality
-Most resolve spontaneously; can be surgical repositioning (orchiopexy) if needed by 18 months
-Complications (even with unilateral cases): testicular atrophy (sterility); increased risk of testicular cancer

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8
Q

Urinary traction infection (testes)

A

May be secondary to an ascending bacterial (including STD) - swollen, tender, neutrophilic infiltrate

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9
Q

Mumps infection (testes)

A

Increased risk for infertility

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10
Q

Testicular Torsion

A

-Twisting of the spermatic cord obstructs venous drainage while arteries remain patent –> vascular engorgement and infarction
-Sudden onset of pain; urologic emergency- need to untwist within 6 hours to prevent necrosis

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11
Q

________ is the most important cause of firm, painless enlargement of the testis

A

Testes Neoplasms

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12
Q

Seminoma

A

-Most common testicular tumor (always malignant)
-Usually delayed metastasis
-Highly responsive to radiation; excellent prognosis

Testes (Neoplasms)

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13
Q

Teratoma

A

-Neoplastic germ cells from 2 or 3 embryonic layers differentiate toward multiple somatic cells
-Can be benign or malignant
-“Immature” (fetal-like tissue) or “mature” (fully differentiated tissues - i.e. teeth, hair)

Testes (Neoplasms)

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14
Q

Describe the prostate anatomy

A

-Located at the base of the bladder, encircling the urethra, anterior to the rectum such that the posterior aspect is palpable by digital rectal exam (DRE)
-Androgens maintain the glands and stroma which make a milky fluid added to sperm and fluid from the seminal vesicle to make semen

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15
Q

What does the prostate consist of histologically?

A

3 zones:
-Central zone
-Peripheral zone
-Transitional zone

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16
Q

Acute or Chronic Prostatitis

A

-Usually due to bacterial urinary tract infection
-Fever (in acute) and dysuria (painful or difficult urniation)

17
Q

Chronic pelvic pain syndrome

A

-May be inflammatory or non-inflammatory (no WBCs in urine)
-Pain localized to the perineum, suprapubic and penis; often pain during or after ejaculation
-Unknown etiology and hard to treat

Prostatitis

18
Q

Benign Prostatic Hyperplasia

A

-Very common after age 40 (90% have it at 80yrs)
-Only 10% with histologic evidence have symptoms
-Most often arises from the inner transitional or central zones (produces urinary obstruction)

19
Q

Describe the symptoms seen in Benign Prostatic Hyperplasia

A

(symptoms only seen in 10% of patients)

-Hesitancy (difficulty starting a urinary stream) and intermittent interruption of the urinary stream while voiding
-With obstruction - urgency, frequency, nocturia (irritated bladder)

20
Q

Describe the Etiology, Pathogenesis, and Treatment for Prostatic Hyperplasia

A

Etiology: Increase in androgens

Pathogenesis:
-Testosterone (converted by 5alpha reductase) –> dihydrotestosterone (DHT) –> nodular hyperplasia
-Increased estrogen may also increase expression of DHT receptors in the prostate

Treatment:
-5alpha reductase inhibitors: finasteride (Proscar, Propecia)
-alpha1-adrenergic blockers: relax prostate smooth muscle (ex: terazosin, tamulosin)

21
Q

What does Prostatic Hyperplasia look like histologically?

A

-Well-defined nodules compressing the urethra
-Variable amount of normal appearing but hyperplastic glandular and stromal components

22
Q

Prostatic Carcinoma

A

-Most common cancer in men (excluding skin SCC and BCC); much less deadly than many other cancer types
-Lifetime risk ~11%
-Age: 65-75yrs
-Highly variable disease course; can’t reliably predict which tumors will be aggressive

23
Q

What is the pathogenesis of Prostatic Carcinoma?

A

-Androgens: promote, don’t initiate, cancer growth
-Hereditary - increased risk in 1st degree relatives
-Environmental - geographic variations, diet?
-Acquired genetic aberrations:
*most often see androgen-regulated fusion genes
*inherited BRCA1, BRCA2 mutations can increase risk

24
Q

Where do Prostatic Carcinomas arise? What is typically the first sign?

A

-Often clinically silent
-Carcinomas (70-80%) arise from the peripheral zone (palpated on digital rectal exam)
-Often first sign is metastasis. Bone (osteolytic or osteoblastic) involvement is common

25
Prostate Specific Antigen (PSA)
-PSA is a normal product of prostatic epithelium, secreted in the semen - <4ng/mL is normal, >10ng/mL suggests cancer -Somewhat helpful for diagnosis when used with other procedures - not highly sensitive or specific -Very helpful for monitoring patients for progression/recurrence
26
Describe PSA screening: 2018 US Preventive Services Task Force Report for different age groups
For 55-69 years: -Net benefit is small for some men For 70+ years: -Benefits do not outweigh the expected harms Conclusion: If 55-69 years, patient-driven decision based on discussion with physician whether to screen -Benefits: Out of 1000 men screened may prevent about 3 cases of metastasis and 1.3 deaths over 13 years (small reduction in risk of death) -Risks: False positives leading to biopsy with potential overtreatment including complications: *after prostatectomy: 20% have long-term incontinence and 66% have long-term erectile dysfunction *after radiation: >50% have long-term erectile dysfunction and ~17% have bowel urgency and fecal incontinence
27
Gleason Score
-From 1 (well differentiated) to 5 (no differentiation) with the 2 most common patterns added together -Ex: Most differentiated would be (1+1=2) whereas the least differentiated would be (5+5=10). -(Add together what they have the most of and what else they have. Ex: a lot of 5 with some areas of 1 --> 5+1=6). -Gleason score given a grade group that correlates with prognosis
28
Prostatic Carcinoma Prognosis
Clinical spread and histological grade (Gleason score) correlate with prognosis
29
What is the treatment and prognosis of Prostatic Carcinoma?
Treatment: -Active surveillance (watchful waiting) -Surgery: robotic prostatectomy -Radiation therapy: external beam or brachytherapy (internal radioactive seeds) -Androgen deprivation (orchiectomy and/or medications- only for advanced metastatic disease Prognosis: -Stage T1,T2 (still in gland) - Good (90% 1- yr survival) -Disseminated disease (has spread outside the gland) - Poor (10-40% 10 yr survival)