Urology

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16 Urology

Urinary tract infections

Upper urinary tract – kidneys and ureters

Adenocarcinoma

Aetiology and pathology

This tumour is commonest in men in late middle age and often causes paraneoplastic syndromes (Table 16.1). These cancers are usually well encapsulated and contain areas of haemorrhage and necrosis. Spread is by local infiltration and blood-borne metastases. The tumour may grow into the renal veins and vena cava.

Table 16.1 Paraneoplastic syndromes in renal cell adenocarcinoma

Event Cause
Raised ESR Changes in plasma proteins
Anaemia Depressed erythropoiesis and haemolysis
Polycythaemia Erythropoietin secretion
Hypercalcaemia Tumour secretion of parathormone-like substance
Raised alkaline phosphatase concentration Secretion from the tumour
Pyrexia Circulating pyrogens
Hypertension Secretion of renin
Amyloid deposition Unknown
Peripheral neuropathy and myopathy Unknown

Stone disease

Urinary stones are common. Most are due to conditions causing high urinary calcium concentrations, or due to infections (e.g. Proteus spp.) which split urea to form ammonia, rendering the urine alkaline.

Symptoms depend on the size and position of the stone, and whether there is associated urinary infection. The classic presentation is of ureteric colic (Fig. 5.7, p. 94) (also commonly called renal colic) due to the passage of a stone along a ureter. Severe colicky pain (said to be as bad as labour pain) is felt in the loin, radiating to the groin and into the scrotum or labia. Vomiting is common. The loin may be tender but physical signs may be absent. Urine dipstix is usually positive for blood. Evidence of infection (dysuria, constant loin pain between colicky exacerbations, fever, loin tenderness) should be taken very seriously since an obstructed infected kidney may be irreparably damaged in less than 24 hours if not decompressed.

The differential diagnosis is important (Box 16.4). In particular, in individuals over 50, especially those who have never previously had urinary stones, ruptured aortic aneurysm must be considered and excluded.

Diagnosis is by intravenous urogram (IVU). CT or ultrasound may also be used.

Most stones pass spontaneously, and analgesia is all that is required. Large (>0.5 mm) obstructing stones in the upper ureter are more likely to need treatment (Box 16.5).

A patient who has formed one renal stone has a 20% chance of developing another. Recurrence may be reduced by ensuring a high fluid intake to ensure more dilute urine. Underlying metabolic abnormality must be excluded (check U&E, calcium, uric acid and ALP, and do 24-hour urine collection for calcium, uric acid and citrate).

Lower urinary tract

Bladder cancer

Benign bladder tumours are rare. Most bladder tumours are malignant growths arising from the transitional cell epithelium lining the urinary tract. Predisposing factors are male sex (5 : 1), smoking, chemical industry (rubber/dyes/pesticides) and schistosomiasis (squamous tumours).

The prostate gland

Prostate cancer

This is the commonest cancer in men, with over 27 000 new diagnoses per year in the UK. The difficulty with prostate cancer is distinguishing between those that will progress and those that are harmless. Autopsy studies on men who have died of unrelated causes demonstrate that half of all men aged 70–79 years and two-thirds of those aged 80–89 have unsuspected prostate cancer. Only around 1 in 200 of men with prostate cancer will die of it. Nonetheless prostate cancer is the fourth most common cause of cancer death in males. This confusion makes screening for prostate cancer problematic, since many cases detected would never have caused any symptoms, or shortened life, if left alone.

Investigation

PSA is secreted into blood by both normal and malignant prostate tissue. An elevated PSA may be due to a large benign gland, prostate cancer, prostate inflammation and catheterisation of the bladder. Many men with a mildly raised PSA do not have cancer; equally many men with cancer do not have markedly raised PSAs. This limits the value of PSA as a screening test. However, it is useful in monitoring progression of established disease and monitoring of treatment.

Abdominal ultrasound detects hydronephrosis due to ureteric obstruction. Trans-rectal ultrasound and biopsy establishes histological diagnosis.

Bone scanning (Fig. 16.4) may show bone metastases and MRI scanning complements EUA to establish staging, which is by the TNM classification (Table 16.4).

Table 16.4 Staging of prostate cancer

Stage Findings
T1a An incidental finding of tumour with low biological potential for aggressive behaviour in a prostate removed for clinically benign disease
T1b An incidental finding of a tumour with potentially biological aggressive behaviour found in a prostate removed for clinically benign disease (high-grade or diffuse)
T1c Tumour identified because of an elevated serum prostate-specific antigen
T2a Tumour involving half a lobe or less
T2b More than half a lobe but not both
T2c Both lobes
T3 Tumour extends through capsule and may involve seminal vesicle
T4 Tumour fixed invasive of adjacent structures other than seminal vesicle

Testes and scrotum

Testicular cancer

Testicular cancer accounts for only 1–2% of malignancy in males but is the commonest solid tumour in males aged 20–35. The cause is unknown, but maldescended testes have a much higher incidence of malignant change. Types of testicular tumours are summarised in Box 16.7. For clinical features see Table 16.5.

Table 16.5 Clinical features of testicular cancer

Symptoms Signs
Painless lump in scrotum Hard lump in body of testis
History of trauma often described Non-tender
10% of patients had previous orchidopexy 5% of tumours are bilateral
Pain/dragging sensation in scrotum Gynaecomastia (with choriocarcinoma)
Symptoms due to metastases (e.g. backache, haemoptysis)  

Investigation

Tumour markers aid diagnosis and allow monitoring of effectiveness of treatment (Table 16.6). Ultrasound is helpful in defining the nature of the lesion. CT of the chest and abdomen is required for staging (Table 16.7).

Table 16.6 Tumour markers for testicular cancer 1

Tumour marker Type of tumour
Alpha-fetoprotein and beta-HCG Teratomas
Lactate dehydrogenase Teratomas and seminomas
Placental ALP Seminomas

Table 16.7 Staging of testicular tumours (Royal Marsden Hospital Staging System)

Stage Details
Testis
I Tumour confined to testis
IM Rising concentrations of serum markers with no other evidence of metastasis
II Abdominal node metastasis
A ≤2 cm in diameter
B 2–5 cm in diameter
C >5 cm in diameter
III Supradiaphragmatic nodal metastasis
ABC Node stage as defined in stage II
M Mediastinal
N Supraclavicular, cervical or axillary
O No abdominal node metastasis
IV Extralymphatic metastasis
Lung
L1 ≤3 metastases
L2 ≥3 metastases, all ≤2 cm in diameter
L3 ≥3 metastases, one or more of which are ≥2 cm in diameter
H+, Br+, Bo+ Liver, brain or bone metastases