Genitourinary II Flashcards
Renal tumours
Benign renal tumours are rare.
A benign developmental tumour of the kidney, known as an angiomyolipoma, has a characteristic CT scan appearance, due to the high fat content within the tumour, which can be used diagnostically, but in the absence of this appearance any solid lesion within the kidney should be considered as an indication for partial or total nephrectomy.
Routine biopsy of solid masses within the kidney is
not carried out, because the histology can be difficult to interpret and a benign appearance on biopsy does not exclude a malignant tumour.
Hypernephroma (renal adenocarcinoma)
The commonest renal tumour is the hypernephroma or renal cell carcinoma (renal adenocarcinoma, Grawitz tumour). The incidence of renal adenocarcinoma increases steadily above the age of 40, reaching a peak in the sixth and seventh decades of life. It is more common in men than women and may occur bilaterally.
Aetiological factors of hypernephroma (renal adenocarcinoma)
Aetiological factors include:
• Smokers
• Coffee drinkers
• Industrial exposure to cadmium, lead, asbestos,
aromatic hydrocarbons
• Development in renal cysts in end stage kidneys in dialysis patients
• Von Hippel-Lindau disease (this suggests a genetic predisposition).
Common presenting clinical features:
- Haematuria;
- Loin pain
- A palpable mass
Renal adenocarcinoma is also associated with a
number of paraneoplastic syndromes:
• Hypertension (due to renin secretion)
• Polycythaemia (due to erythropoietin secretion)
• Hypercalcaemia (due to ectopic parathyroid
hormone production).
Spread of hypernephroma occurs as follows
• Direct extension into perinephric tissues and
adjacent organs; direct extension may occur into
the renal vein and IVC; direct extension into
the left renal vein may obstruct the entry of the
testicular vein and result in rapid onset of a left
varicocele
• Lymphatic spread to the para-aortic nodes; and
• Blood spread to liver, brain, bone and lung
(cannon ball metastases).
Prognosis
In patients with no evidence of metastasis at presentation the five-year survival may be as high as 70% but falls to 20% when the renal vein is involved or there is extension into the perinephric fat.
Rarely metastases from renal adenocarcinoma can regress spontaneously after removal of the primary tumour, but this occurs in less than 1% of cases, with a limited duration for regression of those metastases in the majority of cases.
Wilms’ tumour
This is the commonest intra-abdominal malignancy in children under the age of ten years. The majority occur in the first three years of life. Less than 5% are bilateral.
The most common presentation is with an abdominal mass, but haematuria, abdominal pain, hypertension and intestinal obstruction may occur.
Metastases occur to the liver, lungs and regional nodes. Treatment is by surgical excision with aggressive chemotherapy and radiotherapy. There is an 80–90% chance of cure.
Carcinoma of the renal pelvis
These are relatively rare and are usually transitional
cell tumours, although squamous cell carcinomas
have been reported in areas of squamous metaplasia.
Transitional cell carcinomas frequently infiltrate the
wall of the pelvis and may involve the renal vein. With poorly differentiated tumours the prognosis is not good and multiple tumours may occur in the ureters and bladder.
Aetiological factors include:
• analgesic abuse
• exposure to aniline used in the dye, rubber, plastics and gas industries.
Squamous metaplasia of the urothelium may occur due to chronic irritation. This may be associated with calculi and chronic infection. Occasionally, squamous cell carcinomas arise de novo from transitional epithelium.
Squamous cell carcinomas carry a poor prognosis.
Urothelial tumours
Urothelial tumours arise in the transitional epithelium, which extends from the tips of the renal papillae to the navicular fossa in men and half way down the urethra in women, and represent an important pathological entity within urological practice.
Urothelial tumours may occur at any level within the urinary tract and are often multifocal. The majority, however, occur in the
1) Uinary bladder (90%)
2) Renal pelvic transitional cell carcinomas (9%)
3) Transitional cell carcinomas of the ureter (1%) are uncommon.
In patients with bladder transitional cell carcinoma there is a higher prevalence of coincidental upper tract tumours.
The commonest presenting feature of transitional
cell carcinoma of the bladder is painless macroscopic haematuria. A number of other lesions are identifi ed on the basis of investigation of either sterile pyuria or microscopic haematuria.
Transitional cell carcinomas
Transitional cell carcinomas of the bladder occur
primarily on the posterior and lateral walls of the
bladder in over two-thirds of cases. One-fifth of cases present with a tumour at the trigone or bladder neck and the remainder over the vault of the bladder.
Whilst diverticula are a well-recognised predisposing factor for the development of tumours, less than 5% develop in a diverticulum.
The prognosis for transitional cell carcinoma of the bladder is defi ned by its underlying histological grade, which refl ects the predilection of the tumour to aggressive behaviour. Tumours are usually
graded as well differentiated, moderately differentiated, or poorly differentiated. Carcinoma in situ, which elsewhere in the body is usually a premalignant and relatively benign condition, is quite the reverse in the bladder.
Certainly it is premalignant, but such patients have a tendency, in at least 50% of cases, to develop a poorly differentiated aggressive tumour.
Therefore, in the urinary tract, carcinoma in situ is
treated in a very proactive fashion.
Treatment of TCC
Whilst the mainstay of treatment in the UK has tended, traditionally, to be radical radiotherapy, there is an increasing trend towards radical surgery at an early stage.
Carcinoma in situ of the bladder, as mentioned above, is an indication for early intervention. Many of these patients will respond favourably to the use of intravesical BCG which acts as immunotherapy to promote the activation of T-cell mediated killing of abnormal urothelial cells.
If carcinoma in situ is widespread and does not respond to BCG, or is poorly differentiated, then most clinicians would proceed to radical treatment at an early stage.
Adenocarcinomas
Other tumours of the bladder include adenocarcinomas and squamous carcinomas. Adenocarcinomas in the UK are relatively uncommon and are usually associated with a urachal remnant on the anterior wall of the bladder, although the presence of adenocarcinoma
on histology should always raise the possibility
of the direct extension of an adenocarcinoma of the
bowel.
Squamous carcinomas
Squamous cell carcinoma is uncommon in the
UK but is most commonly associated with situations where there has been chronic stasis or irritation within the bladder and in this context is seen in patients with a previous history of tuberculosis or paraplegics.
In areas of the world where schistosomiasis is endemic, squamous cell carcinoma represents the commonest histological type and usually presents in patients from the second or third decade of life onwards. The tumour arises as a consequence of a chronic irritation within the bladder, leading on to squamous metaplasia and the subsequent development of a squamous carcinoma. This is precipitated by the parasite laying its eggs in a submucosal position.
Prostate cancer
Carcinoma of the prostate is one of the commonest
malignant tumours in the male. The majority of cases present clinically in the sixth or seventh decade of life, but it must be recognised that, if a male lives long enough, there is a high chance of him developing carcinoma of the prostate, although it may not be manifest clinically.
Indeed, postmortem series have reported a prevalence of carcinoma of the prostate in up to 80% of 80-year-old patients.
Prostate carcinomas traditionally develop in the peripheral zone of the prostate and are adenocarcinomas. Unfortunately the majority of patients presenting with carcinoma of the prostate (two-thirds) do so with either locally advanced disease or metastatic disease already present.
Spread of prostate cancer
• direct – by local extension through the prostatic
capsule to the urethra, bladder base, or seminal
vesicle;
• lymphatic – to the pelvic and para-aortic nodes
• blood-borne – via the prostatic venous plexus
to the vertebral venous plexus and to the bones
of the lumbar spine and pelvis; and to the lungs
and liver.
Clinical presentations of prostate cancer
Clinical presentations include:
• lower urinary tract symptoms – features of bladder
outflow obstruction
• routine rectal examination may reveal a hard
craggy prostate
• bony metastases – bone pain, pathological fracture
anaemia due to extensive neoplastic infi ltration of
marrow-containing bones
• lymph node metastases.
PSA
The advent of testing for prostate specifi c antigen
(PSA) has allowed the earlier diagnosis of many cases, although it must be recognised that the PSA test has a relatively low sensitivity and specifi city and a normal PSA does not exclude the presence of a coexisting prostate carcinoma, although conversely a markedly raised PSA level makes the diagnosis very likely.
Elevation of the PSA occurs following instrumentation of the prostate or can occur in association with a urinary tract infection. There is no evidence that digital rectal examination signifi cantly raises the PSA.
Diagnosing prostate cancer
The diagnosis of prostate carcinoma rests on the histological identification of prostatic adenocarcinoma on fine needle biopsy, which is usually carried out transrectally – either under digital guidance if there is a palpable abnormality or using ultrasound guidance. This technique should be carried out with full antibiotic cover because of the risk of bacteraemia
Treatment of prostate cancer I
Following the diagnosis of prostate cancer, in
addition to routine blood investigations, including a
baseline serum PSA, a bone scan is carried out, and if the tumour is considered possibly to be localised then baseline imaging with a transrectal ultrasound scan and an MRI scan to exclude local disease progression are usually the preferred staging modalities.
Treatment of prostate cancer II
The radical treatment for prostate carcinoma involves either radical radiotherapy (brachytherapy or external beam radiotherapy) or radical prostatectomy.
The latter has become increasingly popular in recent years, and recent years have also seen interest in newer therapies including cryotherapy and high-intensity focused ultrasound, although these are as yet unproven.
Radical prostatectomy should be confi ned to patients where biologically a life span of at least ten years is to be expected or where the tumour is locally confined; in support of this, results would suggest that PSA level in excess of 20 ng/mL is a relative contraindication.
Treatment of prostate cancer III
In patients where the tumour is locally advanced
or metastatic, then hormonal therapy is instituted.
The mainstay of treatment is to remove testosterone production either by surgical orchidectomy or chemical measures designed to achieve the same aim (anti-androgens and LHRH analogues).
There is no evidence that surgical orchidectomy is superior to chemical measures. The prognosis of patients with carcinoma of the prostate depends upon the stage of the tumour at presentation, and it is likely that in those where the tumour is detected at an early stage with a low tumour bulk, if a curative option such as radical surgery is carried out at an early stage then they can be cured. As a rule of thumb, patients presenting clinically with prostatic carcinoma before the sixth decade of life tend to have a more aggressive tumour which is reflected in a poorer prognosis.
Carcinoma of the testis
Tumours of the testis are relatively uncommon,
accounting for 1–2% of malignant tumours in men;
nevertheless they predominantly affect young men.
There is a well-established link between undescended testes and testicular tumour, and it has been estimated that adults with maldescent of the testes have a 20–30 fold greater incidence of developing a testicular tumour than men with a normally descended testis.
Testicular tumours may be derived from germ cells or non-germ cells. The majority (90%) are of germ cell origin. Germ
cell tumours include seminomas and teratomas.
Nongerm cell tumours include those arising from the Sertoli cells and Leydig cells.
Testicular tumour classification
Testicular tumours may be classifi ed as follows: • seminoma; • teratoma; • combined germ cell tumours (seminoma and teratoma); • malignant lymphoma; • interstitial (Leydig) cell tumour; and • Sertoli cell tumour.
The two most common types of tumour are seminoma and teratoma. Metastatic tumours are rare and include bowel, bronchus and prostate.
Clinical features of testicular tumours
Clinical features of testicular tumours include:
• unilateral painless enlargement of a testis;
• secondary hydrocele;
• retroperitoneal mass;
• lymph node metastases (occasionally in the
cervical nodes);
• symptoms from other metastases; and
• gynaecomastia from hormone-secreting interstitial
tumours.
Testicular tumour investigation
Serological tumour markers such as !FP,
beta-HCG and LDH should be estimated prior to orchidectomy. Ultrasound scanning is a non-invasive and very accurate way of defining primary testicular abnormalities.
Staging in testicular tumours
Staging of patients with a primary testicular tumour
is principally carried out on the basis of the serological tests mentioned above and also CT scanning of the abdomen and pelvis to look for lymph node extension and retroperitoneal tumour mass. With a combination of radiotherapy and chemotherapy the cure rate for the majority of patients with testicular tumours approaches 100%.
