Topic 90-94: Male genital tract Flashcards

1
Q

list off the diseases of the penis

A
  • malformations
  • inflammatory lesions
  • cancer
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2
Q

what are the 3 malformations of the penis?

A
  • hypospadiac - urethra opens on the ventral surface of the penis shaft
  • epispadia - opening on the dorsal surface
  • phimosis - prepuce cannot retract
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3
Q

what are some inflammatory lesions of the penis? what are the 3 mechanisms in which this occurs?

A
  • STDs
  • Poor hygiene
  • systemic disease
  • -balanitis - glans penis inflammation due to poor hygiene.
  • venereal warts
  • urethritis
  • chancre
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4
Q

what are the neoplasia of the penis? what cells do they originate from? what do they typically develop with?

A
  • 95% from squamous epithelium
  • most cases occur in uncircumcised men and HPV
  • Bowen disease (erythroplasia of queyrat)- similar
  • squamous cell carcinoma of the penis
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5
Q

what are some disease of the scrotum and the spermatic cord?

A

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

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6
Q

What are the types of prostatitis? how common are they and what is their cause?

A
  • 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
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7
Q

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?

A
  • 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
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8
Q

How common is prostate hyperplasia? what is the general etiology?

A
  • 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
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9
Q

what is the main tumor of the prostate? how common is it? what are the four etiology influences?

A

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
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10
Q

what mutations are responsible for prostate adenocarcinoma?

A
  • 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
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11
Q

what is the general morphology? what is the prostate cancer grading system?

A
  • 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
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12
Q

Does prostate adenocarcinoma have certain clinical signs/complications? where does it typically metastasize? what are the anatomical staging levels?

A

– 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)
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13
Q

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?

A

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)

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14
Q

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?

A

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!!)
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15
Q

What are the complications of cryptorchidism? what does it look like histologically?

A

-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
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16
Q

what is the definition of infertility? how often is it men’s fault? what are the general causes?

A
  • 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)
17
Q

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?

A
  • 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

18
Q

what is the WHO classification of germ cell tumors? what are the specific tumors in these categories?

A

-single histological pattern vs multiple histological pattern

single: 60%
- seminoma
- embryonal carcinoma
- yolk sac tumor
- choriocarcinoma
- teratoma

multiple 40%
-mixed germ cell tumor

19
Q

what are the general features of single origin germ cell tumors? frequency, morphology, age of discovery (if not at age 15-30), prognosis

A

-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

20
Q

what is the general features of the multiple origin germ cell tumors? frequency, morphology, age of discovery, prognosis

A

mixed germ cell tumor
-age 15-30, variable morphology but usually teratoma + embryonal choriocarcinoma
90% of pts have high hCG and AFP

21
Q

what is the staging and some clinical features of testicular cancer?

A

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