MEDICAL UROLOGICAL PATHOLOGY

Question 1

Benign prostatic hyperplasia: ADENOFIBROMYOMATOUS HYPERPLASIA
Definition

Answer 1

Enlargement of the prostate, also known as nodular hyperplasia or benign prostatic hyperplasia (BPH), consists of overgrowth of the epithelium and fibromuscular tissue of the transition zone and periurethral area.
Epidemiology:

Question 2

Benign prostatic hyperplasia: Aetiology

Answer 2

Symptoms are caused by interference with muscular sphincteric function and by obstruction of urine flow through the prostatic urethra. The main component of the “hyperplastic” process is impaired cell death  overall reduction of the rate of cell death, resulting in the accumulation of senescent cells in the prostate.
Androgens (mainly DHT) which are required for the development of BPH, can not only increase cellular proliferation, but also inhibit cell death.

Question 3

Benign prostatic hyperplasia Pathogenesis

Answer 3

The normal prostate contains several distinct regions, including a central zone (CZ), a peripheral zone (PZ), a transitional zone (TZ), and a periurethral zone. Most carcinomas arise from the peripheral glands of the organ and may be palpable during digital examination of the rectum. Nodular hyperplasia, in contrast, arises from more centrally situated glands and is more likely to produce urinary obstruction early than is carcinoma.
Development of nodular hyperplasia includes three pathologic changes:
1. Nodule formation
2. Diffuse enlargement of the transition zone and periurethral tissue
3. Enlargement of nodules

Question 4

Benign prostatic hyperplasia clinical features:

Answer 4

These symptoms, referred to as lower urinary tract symptoms (LUTS), include urgency, hesitancy, diminished stream size and force, increased frequency, incomplete bladder emptying, and nocturia

Question 5

PROSTATE CANCER

Epidemiology

Answer 5

95% of prostatic malignancies, prostatic adenocarcinoma is rare in < 40 years. Over 40 years of age the incidence rises quickly. Autopsy studies of thoroughly evaluated prostates from men without clinical evidence of cancer have shown a very high level of latent cancer. The incidence of prostatic adenocarcinoma is much higher in men of African ancestry than in men of European ancestry

Question 6

Prostate cancer Aetiology

Answer 6

Age, race, family history, hormone levels, and environmental influences (e.g. increased consumption of fats) are suspected to play a role. Androgens play an important role in prostate cancer. Inherited polymorphisms: Compared with men with no family history, men with one first-degree relative with prostate cancer have twice the risk.

Question 7

Prostate cancer pathogenesis

Answer 7

Currently the only accepted grading system and the one recommended by WHO is the Gleason scoring system. Currently no screening program in UK

Question 8

Prostate cancer key clinical features

Answer 8

Cancer of the prostate is treated by surgery, radiation therapy, and hormonal manipulations. More than 90% of patients who receive such therapy can expect to live for 15 years.
Most common treatment for clinically localized prostate cancer is radical prostatectomy. The prognosis following radical prostatectomy is based on the pathologic stage, margin status, and Gleason grade.
Alternative treatments for localized prostate cancer:
1. External-beam radiation therapy: External-beam radiation therapy is also used to treat prostate cancer that is too locally advanced to be cured by surgery.
2. Interstitial radiation therapy (brachytherapy).

Question 9

TESTICULAR CANCER

Types:

Answer 9

Germ cell tumours, Sex Cord-Gonadal Stromal tumours pure forms, Miscelllaneous tumours of the Testis, Hematopoietic tumours, Mesenchymal tumours of spermatic cord and testicular adnexa, Secondary tumours of testis.
number of pre-existing conditions have been associated with the development of testicular germ cell tumours.

Question 10

Seminoma testicular cancer

Answer 10

35-45 yrs old, testicular enlargement, elevated serum PLAP

Question 11

Teratoma testicular cancer

Answer 11

most common up to 20yrs old, gradual testicular swelling, no tumour markers secreted.

Question 12

Testicular cancer aeitiology

Answer 12

Germ cell tumours of the testis (with the notable exception of spermatocytic seminoma) occur mostly in young males, with the incidence accelerating rapidly following puberty and peaking close to 30 years of age. There is a small peak in early childhood, but many of the cases of ‘testicular cancer’ in elderly men correspond to lymphomatous involvement or secondary tumours rather than to germ cell tumours

Question 13

testicular cance epidemiology

Answer 13

Testicular cancer incidence is highest among men of northern European ancestry and lowest among men of Asian and African descent

Question 14

Testicular failure

Answer 14

Primary – undescended testis, Klinefelter syndrome, hemochromatosis, mumps, orchitis, trauma, cystic fibrosis, testicular torsion and varicocele.
Secondary – pituitary failure, drugs (glucocorticoids, ketoconazole, chemotherapy, and opioids), obesity and aging.