Topic 90-94: Male genital tract Flashcards
list off the diseases of the penis
- malformations
- inflammatory lesions
- cancer
what are the 3 malformations of the penis?
- hypospadiac - urethra opens on the ventral surface of the penis shaft
- epispadia - opening on the dorsal surface
- phimosis - prepuce cannot retract
what are some inflammatory lesions of the penis? what are the 3 mechanisms in which this occurs?
- STDs
- Poor hygiene
- systemic disease
- -balanitis - glans penis inflammation due to poor hygiene.
- venereal warts
- urethritis
- chancre
what are the neoplasia of the penis? what cells do they originate from? what do they typically develop with?
- 95% from squamous epithelium
- most cases occur in uncircumcised men and HPV
- Bowen disease (erythroplasia of queyrat)- similar
- squamous cell carcinoma of the penis
what are some disease of the scrotum and the spermatic cord?
scrotum
- inflammation - infection, candida, eczema, jock itch
- contact dermatitis
- neoplasia
- hydrocele - most common, accumulation of serous fluid in tunica vaginalis
- vericocele
- spermatocele
- sebaceous cyst
- inguinal hernia
spermatic cord
-torsion - twisting of the spermatic cord so that the testicle rotates and cuts off circulation
What are the types of prostatitis? how common are they and what is their cause?
- acute bacterial - 5% of cases, ascending from UTI
- chronic bacterial - 5% of cases, due to urogenital dysfunction, catheters, recurrent UTI
- chronic nonbacterial - 90% of cases, no pathogen is discovered and simply high WBC count
- asymptomatic inflammatory - incidental discovery
what cells are associated with benign prostatic hyperplasia? where does hyperplasia typically develop? where does prostate cancer develop? what is the general morphology of the hyperplasia?
- the hyperplasia occurs in the prostatic acinar epithelium and stroma in the innermost transitional and central zones of the prostate. (most carcinomas are from the peripheral zones)
- generally the tissue forms nodules that contain cystic spaces and frequently corpora amylacea
How common is prostate hyperplasia? what is the general etiology?
- BPH occurs in 90% of men by 80 yo and most men by 40 yo
- hyperplasia correlates with androgen stimulation. DHT seems to affect it most in which is binds to nuclear receptor to increase growth factor production
- BPH doesn’t occur in castrated males or men with blocked androgen production
what is the main tumor of the prostate? how common is it? what are the four etiology influences?
2 cause of cancer related death/ 25% of men are affected!
Prostate adenocarcinoma
- hormones - androgens (castrated men do not get prostate adenocarcinoma)
- genetics - next card
- environment - certain factors such as western diet
- hereditary - familial
what mutations are responsible for prostate adenocarcinoma?
- a fusion gene of the androgen regulated promoter and the coding sequence of the ETS transcription factor
- – 40-50% of prostate cancers
- activation of the oncogenic p13K/akt signaling pathway
- – these mutations inactivate a tumor suppressor gene called PETN
what is the general morphology? what is the prostate cancer grading system?
- histologically the tumors form well defined glands with little pleomorphism. the epithelium is atypical cuboidal and crowded
- advanced lesions are firm nodules
-grade 1-5, grade 1 being most differentiated glandular structure and grade 5 being least
- gleason system tries to take into account all the histological patterns seen in the tissue by giving a grade (1-5) to the primary dominant pattern (more than 50% of tissue) and then a second one for the 2nd most prevalent growth pattern observed (less than 50% but more than 5%)
- –thus a score 2-10
Does prostate adenocarcinoma have certain clinical signs/complications? where does it typically metastasize? what are the anatomical staging levels?
– it can present as a hard, fixed nodule and does NOT present with urethral complications.
-bone metastases are common
T1 - T4 T1 - lesion not apparent clinically T2 - palpable lesion T3 - local prostatic extension T4 - invasion of other structures (bladder, ractum)
what are some specific and nonspecific inflammatory lesions that can occur in the testis and epididymis? how common is inflammation in either of these areas?
inflam is way more common in the epididymis than in the testis proper
Epididymis
-specific - STDs, mumps, TB
-nonspecific - ascending infection from UTI via vas deferens
testis (orchitis is enlargement and inflammation of testis)
-specific - mumps, syphilis (gumma) and TB (granuloma)
what is the condition in which the testicles fail to descend? what hormone controls this? how common is bilateral failure to descend? What are some causes?
cryptorchidism
-anti-mullerian hormones and then androgens cause the testis to descend into the scrotum (however cryptorchidism is not normally due to hormone abnormalities!)
-in 10% of cases, it is bilateral
- causes:
- hormone abnormalities, testicular abnormalities, mechanical abnormalities, congenital problems (prader willi), idiopathic (majority!!)
What are the complications of cryptorchidism? what does it look like histologically?
-histologically: atrophy of all other cells except for prominent leydig cells and hyperplastic sertoli cells
- sterility
- trauma, torsion and inguinal hernia
- 3-5x inc risk of seminoma (testicular malignancy), also inc risk of cancer in contralateral side
what is the definition of infertility? how often is it men’s fault? what are the general causes?
- the inability to get a fertile female pregnant
- It is always men’s fault. (actually 40-50%)
- pre-testicular- things that impede the testicles from functioning properly and producing sperm (hormonal deficiencies, bad health, lack of certain cells)
- testicular - conditions in which the testicles produce semen but it is bad quality despite the testicle/bodies best efforts (age, genetics, trauma, cancer, idiopathic)
- post-testicular -defects of the genital tract after sperm production/ejacualtion (impotence, vas deferens obstruction, retrograde ejacualtion)
testicular tumors most common symptom is what? when is the peak incident age? what are the two types of tumors (based on cells)? what is the general etiology?
- firm enlargement of the testis
- most commonly arise at age 15-34 but there are a few other exceptions
- Germ cell tumors (95%) - all are malignant, but still most are curable
- sex cord-stromal tumors - from sertoli and leydig cells, benign
- most have an unknown etiology! however some arise from germ cell neoplasia commonly seen in cryptorchidism and dysgenetic testis
- –there is a wide rage of abnormalities in germ cells that can cause tumors, most commonly isochromosomes of the short arm of chromosome 12
-cancer development frequently is associated with with contralateral testicular neoplasia
what is the WHO classification of germ cell tumors? what are the specific tumors in these categories?
-single histological pattern vs multiple histological pattern
single: 60%
- seminoma
- embryonal carcinoma
- yolk sac tumor
- choriocarcinoma
- teratoma
multiple 40%
-mixed germ cell tumor
what are the general features of single origin germ cell tumors? frequency, morphology, age of discovery (if not at age 15-30), prognosis
-seminoma - 50%
age 40-50, lymphocyte infiltrated tissue, sheets of uniform cells, very curable
-embryonal carcinoma - 2nd most common
poorly differentiated cells, radioresistant
-yolk sac tumor
age 1-3, poorly differentiated cells and most produce high AFP
-choriocarcinoma
atypical cytotrophoblasts and syncytiotrophoblasts
all pt have elevated hCG, very malignant
-teratoma
all ages, can be malignant
what is the general features of the multiple origin germ cell tumors? frequency, morphology, age of discovery, prognosis
mixed germ cell tumor
-age 15-30, variable morphology but usually teratoma + embryonal choriocarcinoma
90% of pts have high hCG and AFP
what is the staging and some clinical features of testicular cancer?
stage I - tumor confined to testis
stage II - regional lymph node metast
stage III - non regional lymph node or distant metastases
most frquently associated with painless enlarged ttesticles
- some tumors metastasize before they are palpable (usually non seminiferous)
- typically spread to iliac and para-aortic lymph nodes in upper lumbar region
