Male Genital System Flashcards
Hypospadias and Epispadias
Hypospadias
- 1 in 250 live male births
- Abnormal opening of urethra along ventral aspect of penis - risk of UTI or UT obstruction
Epispadias
- Abnormal opening along dorsal aspect of penis
- Less common
- Associated w/ bladder extrophy (congenital malformation of bladder)
Balanitis and Balanoposthitis
Local inflammation of glans penis (and overlying prepuce)
Usually due to poor local hygiene in uncircumcised males w/ accumulation of smegma (debris, sweat, etc) acting as a local irritant.
Swollen, red, tender penis.
Phimosis - prepuce cannot be retracted easily over glans penis
When stenotic prepuce is forcibly retracted, circulation to glans may be compromised w/ resultant congestion, swelling, and pain (paraphimosis)
Genital candidiasis - fungal infection (common w/ diabetes mellitus)
Penile neoplasm
>95% of penile neoplasms are squamous epithelium
Uncircumcised patients > 40yrs old
Risk factors: Poor hygiene, smoking, uncircumcised, HPV 16 and 18
Preceded by intraepithelial neoplasia or carcinoma in situ
Bowen disease - older, uncircumcised males w/ solitary, plaquelike lesion on penile shaft (malignant cells w/o invasion). This can occur on other skin and mucosal surfaces (including vulva and mouth). 33% turn into SCC.
Erythroplasia of Queyrat - Bowen disease that presents as erythematous patch on glans penis.
Bowenoid papulosis - young, sexually active males. Presents w/ multiple reddish brown papules on glans, transient.
SCC - gray, cursted, papular lesion on glans penis or prepuce. Produces indurated, ulcerated lesion w/ irregular margins. Histologically - keratinizing squamous cell carcinoma w/ infiltrating margins (overall good survival rate)
Hydrocele
Scrotal enlargement due to accumulation of serous fluid w/i tunica vaginalis.
Hematoceles and chyloceles (accumulation fo blood or lymphatic fluid)
Extreme lymphatic obstruction can cause elphantiasis
Cryptorchidism
Failure of testicular descent into scrotum
Common feature of several congenital syndromes (Prader-Willi)
Unknown cause
Infertility
3-5x inc. risk of testicular cancer
Orchiopexy (surgical placement) decreases likelihood of testicular atrophy and risks of cancer and infertility
More often right testis
Foci of intratubular germ cell neoplasia may be present and may be source of testicular cancer
Epididymitis and orchitis
Nonspecific epididymitis and orchitis - Begins as primary UTI w/ secondary ascending infection through vas deferen or lymphatics of spermatic cord. Swollen and tender testis w/ neutrophilic inflammatory infiltrate.
Orchitis w/ mumps infection (adults) - lymphoplasmacytic infl. infiltrate.
Tuberculosis - begins as epididymitis, w/ secondary involvement of testis - granulomatous inflammation and caseous necrosis (just like in other areas)
Testicular Cancer
Arise from in situ lesions called intratubular germ cell neoplasia.
Most important cause of firm, painless enlargement of testis.
Peak age of 20-34 yrs
95% from germ cells, all malignant.
5% from Sertolie or Leydig cells and usually benign.
Risk factors: cryptorchidism, intersex syndromes (androgen insensitivity syndrome, gonadal dysgenesis), isochromosome of short arm of chromosome 12, cancer in one testis increases risk of cancer in the other., white people
Seminomas vs non-seminomatous tumors
Non-seminomatous more likely to have widespread metastases in absence of palpable lesion.
NSGCT metastasize earlier, while seminomas remain confined to testis.
Tumor markers - hCG found in mixed germ cell, choriocarcinoma, seminomas
AFP in yolk sac and mixed germ cell (RULES OUT SEMINOMA)
hCG and AFP useful for monitoring patients for recurrent tumor after therapy.
TREATMENT: chemotherapy successful!
Seminoma - radiosensitive
NSGCT - platinum-based chemo (not as radiosensitive)
Seminoma
50% of testicular germ cell neoplasm
Large, soft, well-demarcated, usually homogenous, confined by intact tunica albuginea. May have foci of coagulation necrosis (hemorrhage may indicate nonseminomatous)
Large, uniform cells w/ distinct cell borders, clear, glycogen rich cytoplasm, and round nuclei w/ conspicuous nucleoli. Lymphocytic infiltrate usually present.
25% of time, hCG elevated (these cells similar to syncytiotrophoblasts)
Spermatocytic seminoma - older patients, mix of medium-sized cells, large uninucleate or multinucleate tumor cells, and small cells like secondary spermatocytes - no metastases.
Embryonal carcinoma
Ill-defined, invasive w/ foci of hemorrhage and necrosis
Large and primitive looking cells w/ basophilic cytoplasm, indistinct cell borders, and large nuclei w/ prominent nucleoli.
Usually mixed w/ other types (yolk sac, teratoma, choriocarcinoma)
Yolk sac tumors (endodermal sinus tumors)
Most common primary testicular tumor in CHILDREN <3 yrs
Large tumors, well-demarcated.
Schiller-Duvall bodies (primitive glomeruli)
AFP (alph fetoprotein) elevated
Choriocarcinoma
Trophoblastic tumor
Small, nonpalpable lesions
Cytotrophoblastic and syncytiotrophoblastic differentiation
hCG elevated
Teratoma (testicular)
Firm masses w/ cysts and cartilage.
Mature teratoma has all kinds of differentiated tissue.
Immature teratomas are less differentiated.
Teratomas w/ somatic-type malignancies are tumors w/i tumors (squamous cell or adenocarcinoma)
Metases in 37%
Considered malignant
Mixed germ cell tumor
40% of all testicular germ cell tumors
Combination of any germ cell types - teratomas, embryonal carcinomas, yolk sac tumors, etc.
Prostatitis
Clinical Features: Dysuria, urinary frequency, lower back pain, poorly localized suprapubic/pelvic pain. Acute - fever, leukocytosis. Chronic - may be asymptomatic
Acute bacterial prostatitis - E. coli and gram neg rods, simultaneous UTI infections typical
Think neutrophils
Chronic prostatitis - Chlamydia trachomatis, Ureaplasma urealyticum can cause, usually not by bacteria (inc. # of leukocytes). Chronic bacterial prostatitis - imp. cause of recurrent UTIs
Think lymphoid infiltrate
Granulomatous prostatitis - part of other diseases (Wegener, fungal inf., sarcoidosis, diss. tuberculosis) - multinucleate giant cells and foamy histocytes.
Nodular Hyperplasia of Prostate
Clinical presentation: Lower UT obstruction (hesitancy, intermittent interruption, urgency, frequency, nocturia) - residual urine may lead to UTI - Only 10% are symptomatic
90% of all men by 8th decade
Hyperplasia occurs in inner transitional and central zone
Thought to be caused by local androgen excess
testosterone (by 5-alphareductase) -> dihydrotestosterone -> 3alphaandrostanediol stimulate stromal and glandular proliferation
DHT binds to nuclear receptors and stimulates synthesis of DNA, RNA, growth factors, cytoplasmic proteins
5-alphreductase inhibitors used as treatment.
Well-defined nodules pronounced in inner central and transitional region, causing urethra to be slit-like. Sometimes, it acts as a pedunculated mass, resulting in ball-valve urethral obstruction.
Hyperplastic glands lined by inner tall, columnar epithelial cells and peripheral outer layer of flattened basal cells (crowding of epithelium causes papillary projections in some glands).
Corpora amylacea - inspissated, proteinaceous secretory material in glandular lumina
Prostate carcinoma
Often clinically silent - local discomfort, evidence of lower UT obstruction. More aggressive cancers are discovered first by metastases (axial skeleton - commonly osteoblastic, bone producing, lesions)
Use of PSA > 10
Ages 65 - 75, >50% 80 yo or older
Blacks have more sympomatic carcinoma (difference in number of CAG repeats in androgen receptor gene)
Scandinavia
Hypermethylation of glutathione S-transferase p1 (GSTP1), a genome caretaker gene on chromosome 11, and telomere shortening are common genetic alterations (in sporadic cancer)
Overexpression of two ETS family transcription factors
70-80% in outer peripheral glands
Adenocarcinomas - glands lie back to back (unlike hyperplasia) and dissect sharply through native stroma. No basal layer around glands (single, cuboidal layer).
PIN - coexistant w/ invasive carcinoma (high and low grade depending on atypia
Gleason grading system
