Transcript Prostate cancer

Prostate cancer
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•By the age of 80, >80% of men have prostate cancer
•It is the second most common cancer in men, and the 4th most common cause of death for men in England and
Wales.
•The tumours are adenomas and are usually located in the peripheral prostate.
•Spread is most commonly to bones. And prostate cancer is unusual in that it often causes an increased bone
density- osteosclerosis (most cancers cause decreased bone density).
Aetiology
•Prostate cancer is rare before the age of 40, and prevalence increases with age.
•There is also a genetic factor – similar to that in breast cancer, so if someone in your family has the disease, then
you are also more likely to have it.
•Average life-expectancy after diagnosis is approximately 5-10 years – the disease is very slow to progress.
Clinical features
•Lower Urinary tract obstruction
•Nocturia
•Poor flow of urine
•Symptoms of metastatic spread – particularly to the bones (weight loss and bony pain)
•Irregular hard prostate on DRE
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Investigations
•PSA – this likely to be markedly raised in metastatic disease (>16µg/dl). You can also have a
normal PSA and still have prostate cancer.
•DRE – it is NOT true that this elevates PSA levels
•Transrectal ultrasound of prostate (TRUS), often with biopsy. The ultrasound is useful because it
gives a more accurate estimation of size than a DRE, and can also help stage any tumour present.
You may also want to examine the upper renal tracts for signs of dilation.
•10-15% of TURP surgeries will uncover a cancer when it is only suspected to be BPH.
•Bone metastasis can be seen on X-ray as osteoscleoritc lesions.
Spread
•Bones – particularly the axial skeleton– these are detected with radionuclide bone scans
•Lymph nodes (obturator, internal iliac and presacral nodes)
•Bladder
•Rectum
•Seminal vesicles
•The scale for assessing the aggressiveness of the tumour is the Gleason score. This is a scale from
1-10, with 10 being the most aggressive cancers.
•For cancer spread, the scale of T1-4 is used.
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Treatment
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•Watching and waitng – this is the management method proposed by most clinicians. The side
effects of potential treatments are numerous and debilitating, and thus treatments are usually held
back from as long as possible
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•Radical prostatectomy – the is total removal of the prostate. It can be done ‘open’ or
laparoscopically. The cure rate is 90% for tumours confined to the prostate. At 12 months, the
incontinence rate is 7%, and impotence rate is 30%
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•Radiotherapy – this, along with prostatectomy are the only curative treatments for prostate
cancer.
◦Brachytherapy – this is where radioactive ‘seeds’ are planted in the prostate.
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The condition is only curative when confined to the prostate.
•Finasteride – a 5α-reductase drug, It inhibits the production of dihydrotestosterone from
testosterone and thus prevents growth of the prostate, however there is a high risk of sexual
dysfunction.
•Androgen suppression – this is the main treatment for non-localised disease. About 80% of
patients will show a sustained response to this treatment, but it can take 24-36 months for the
response to appear. The quicker the PSA returns to the normal range, the better the prognosis.
◦Luteinising hormone releasing hormone agonists – these stop the release of lutenising hormone,
and thus the production of testosterone.
◦Castration – many men refuse this treatment method.
Benign prostatic hypertrophy
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This occurs most commonly in men over 60
24% of those ages 40-64, and 40% of those over 65 will have the condition.
Nearly All men will develop BPH if they live long enough. About ½ of all men will have macroscopic enlargement,
and one half of these will have symptoms.
The prostate naturally grows throughout life – it grows in response to dihyrotestosterone – a breakdown product
of testosterone.
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Presentation
Frequency of urination (notably nocturia) is the most common early symptom
Hesitation in initiating urination.
Reduced force of the urinary stream
Post-void dribbling
Retention of urine resulting in overflow incontinence.
A benign prostate will always feel smooth
Size is relevant but is not always associated to the severity of the symptoms.
Investigations
PSA
PR (DRE – digital rectal examination)
Symptom score
Rectal ultrasound
Cystoscopy
Urine flow analysis
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Management
Patients with mild symptoms should perhaps not be given treatment if they feel
they can cope, due to the adverse effects many of the treatments. Sometimes
symptoms after treatment may be worse than symptoms before treatment!
Patients with moderate symptoms should be treated with drugs:
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Patients with more severe symptoms should be considered for surgery. These
symptoms may include renal damage, and upper UT dilation.
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α-blockers – alfuzosin, doxazosin, tamsulosin – these reduce smooth muscle contractions of
the bladder and urethra – they generally reduce the muscle tension in these regions. This
allows for easier passing of urine.
5α- reductase – finasteride – these reduce the conversion of testosterone to
dihyrotestosterone and thus help to shrink the size of the prostate. These take 4-6 months to
have an effect.
Combination therapy – this is a combination of the two drugs above, and most patients who
are on drugs for BPH are given this.
TURP – transurethral resection of the prostate – this is where part of the prostate is cut out via
the urethra. It can be done under general or local anaesthetic. About 14% of patients will
become impotent, and 20% of patients will need further surgery within 10 years.
In cases of acute retention, or retention with overflow, the immediate priority is to
relieve discomfort and pain, and often catheterisation is a good idea. The urethral
catheterization is not possible, then subra-pubic catheterization may be carried
out. This involves sticking a tube through the abdominal wall directly into the
bladder. It isoften done in cases where the patient needs to be catheterized for a
prolonged period.
Testicular cancer
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These are germ cell tumours. There are two main types (these account for 80% of all tumours)
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Seminoma (dysgerminoma in women). These arise from the seminiferous tubules. They are a lowgrade tumour and metastasis can occur via lymphatics and to the lungs.
Teratoma. A teratoma has a mixture of both mature and immature cells. initially they arise from
germ cells, and often contain muscle, bone, fat and a variety of all sorts of other tissue. They are
classified according to the degree of differentiation. As always, well differentiated tumours have
the best prognosis.
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Epidemiology
These account for 1-2% of all tumours
The incidence is very low, with prevalence being about 5 per 100 000
They are the most common cancer in men ages 15-35
Teratomas tend to occur in younger populations than seminomas
Presentation
Often they will be discovered incidentally as a firm lump on the testes. It may or may not be painful.
There may be some evidence of spread to para-aortic lymph node with associated back pain.
Some patients complain of a testicular ache.
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Investigation
All suspicious testicular lumps should be examined by ultrasound.
There should be tests for serum tumour markers:
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α-fetoprotein (AFP)
β-human chorionic gonadotrophin(HCG)
above markers tend to be increased more with more severe disease.
CT / MRI to check for distant metastasis (particularly in the lungs, liver, and retroperitoneally)
Treatment
Seminoma
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They are both radio and chemo sensitive. Even with stage I disease, there is a 30% chance of
recurrence.
Combination chemotherapy will cure 90% of those with metastatic disease.
5-year survival is 90-95%
Teratoma
This is mostly treated with inguinal orchiectomy. One of the testicles will be removed via the
inguinal route to minimise the risk of highly malignant cells spilling in the scrotum. The testicle and
spermatic chord are removed to as far up as the inguinal ring.
Metastatic spread commonly involves the lungs and lymph nodes.
80% of tumours will express AFP or HCG.
About 20% of men will be infertile at the time of diagnosis, but almost 100% of the rest will retain
fertility and be able to father children.
5-year survival is 60-95% depending on tumour stage and metastatic spread at the time of
diagnosis.
Haematuria
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Causes
Kidney
Trauma – mild to moderate trauma often causes this, but severe trauma may not.
Renal cell carcinoma – there may be loin pain, colic caused by a clot, an associated mass, hypertension, hypercalcemia, erythrocytosis (aka
polycythemia –increased number of RBCs)
Calculus – severe loin / groin pain, associated infection
Pyelonephritis – (rare)
TCC – painless, intermittent haematuria
Ureter
Calculus – severe loin / groin pain, associated infection
Bladder
Calculus – sudden cessation of micturition, pain in perineum and penis
TCC – painless, intermittent haematuria, history of work in the rubber / dye industries.
Acute cystits – frequency, dysuria (pain / difficulty micturating), bacteriuria
Prostate
BPH – painless, haematuria, recurrent UTI, associated obstructive symptoms.
Carcinoma – rare cause of haematuria
Urethra
Trauma
Calculus – rare
Urethritis – rare
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Investigations
FBC – to test for infection, and chronic blood loss
Clotting – to exclude an underlying bleeding cause
U+E – to assess renal function
MSU – to check for infection and parasites
Csytoscopy – if suspect a bladder cause
Autoimmune scan – if suspect glomerulonephritis
Intravenous Urography (IVU) / CT scan / ultrasound – if you suspect a renal cause
Renal cell cancer
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This is an adenocarcinoma
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Epidemiology
They are the most common renal carcinoma in adults.
They rarely present before the age of 40, and the average age of onset is 65-75
Twice as common in men as women.
Aetiology
This is largely unknown, however some factors are suspected to precipitate this disease:
Irradiation
Exposure to oestrogens
Hypertension
Smoking
Exposure to cadmium
The disease is more commonly found in urban and industrial areas than in rural areas.
Incidence is 10 per 100 000 in males, and 5 per 100 000 in females.
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Clinical Features
Often RCC is symptomless, until late stage. May be discovered incidentally.
The classic signs of this are:
Haematuria – 60%- this is caused by the spread of the tumour to the renal pelvis, which usually
occurs very early on. From here it may spread to the renal vein and IVC.
Flank/loin pain (40%)
Palpable mass (25%)
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These first three signs are the ‘classic’ ones, but actually only occur in 15% of patients.
Weight loss (30%)
Raised ESR
Polycythaemia (5%)
Hypertension (30%) – due to secretion of renin by the tumour
Anaemia (30%) – due to suppression of EPO by the tumour
Pyrexia of unknown origin (PUO) (20%)
Varicocoele (rare) – this occurs as a result of invasion of the left renal vein by the tumour, which
may then affect drainage of blood from the testes.
However, many tumours are now discovered earlier as a result of incidental, or screening USS.
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Treatment
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The only way to treat these tumours is by surgical excision.
As long as you have at least half of one fully functioning kidney, then renal function will be adequate.
During total nephrectomy, the perirenal fat and fascia will also be removed.
Even in the presence of metastasis, nephrectomy is still recommended, as in many cases there is regression of the metastasis after removal of the
kidney. In the case of a single metastasis, it is worthwhile to remove this secondary tumour as the metastasis is likely to be single due the relatively
slow growing rate of renal cell carcinomas.
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Advanced disease
For those with many metastasis, or invasion of the vena cava etc, then prognosis is generally very poor. Nephrectomy may still be performed to
provide symptomatic relief, but most patients are unlikely to live longer than a year.
Medroxyprogesterone acetate may be useful in cases of metastatic disease.
Radiotherapy is only useful in treating bone mets.
Immunotherapy has been shown to be effective – treatment with interferon and interleukin-2 in patients with extensive disease is beneficial in 1040% of cases, not necessarily ‘curing’ the disease, but it may prolong the patient’s life. In such cases, a nephrectomy will usually have been
performed previously. Metastasis in the lungs are the most likely to respond to this sort of treatment.
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Prognosis
5 year survival:
Tumours confined to kidney – 60-70%
Lymph node spread – 15-35%
Metastatic disease – 5%
Stones
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Renal stones are precipitates that form from urine due to a high concentration of
that particular precipitate in the urine. The most common (85%) precipitate is
calcium; particularly calcium oxalate, about 10% are uric acid, and 5% due to other
precipitates.
They are likely to form where there is stasis, and they form more quickly once a
nucleus has formed.
Epidemiology
More common in men
Occur in about 1/1000 individuals
By Age 70, 12% of men and 5% of women will have been affected
More common in elderly age groups – as they take years to form
Aetiology
Is generally multifactorial. It is believed that about 50% of cases are due to a
hereditary disorder – hypercalcuria which results in increased urinary
concentrations of calcium, despite normal serum ca2+ concentrations.
Hyperparathyroidism is also known to increase the risk due to its effects on
calcium metabolism.
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Presentation
Pain – a classical colicky loin pain. Patients often describe it as the worst pain they have ever felt!
Patients will typically writhe around in pain and find it difficult to get comfortable. The ureters
contract in a peristaltic manner, and move a ‘bolus’ of urine down from the pelvo-uteric junction
(PUJ) down along the ureters. The pain felt in renal colic occurs every time the ureters contract and
press onto the obstructing stone. The loin ain classically radiaties down and round (L1-L2 nerve
routes).
Nausea / Vomiting
Haematuria
Sepsis
Fever (above 38, you become impaired, above 40 you may hallucinate). You increase your
temperature to reduce the effectiveness of bacterial enzymes.
Dysuria (burning pain on micturation)
Tachycardia
Decreased blood pressure – can lead to septic shock.
Gram-negative bacteria are particularly dangerous
Differential diagnosis:
Pancreatitis
AAA
Gallstones
Musculoskeletal pain
Pyelonephritis
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Investigations
Urinalysis – haematuria is common, but unless there is accompanying sepsis, urine will likely otherwise be normal. .
CTKUB
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Management
Often conservative, especially if stone is less than 5mm.
Analgesia!
NSAIDs are useful as they aid with relaxation of ureteric smooth muscle. Diclofenac is usually the NSAID of choice a
Codeine/ morphine
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Smooth muscle relaxants
Small smooth stones may pass themselves
Stone may be passed depending on where it is, and urinary flow (which may be reduced due to renal failure)
Mid-ureter – 60% chance of passing
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Invasive management – if conservative is unsuccessful
Extracorporeal shock wave lithotripsy – using waves, break up the stone
Endoscopic – Ureteroscope
Endoscopic percutaneous
Endoscopic – laparoscopic very rare
Open operation. Very rare
Impacted stones will need intervention – this is where the contractions of the ureters will not move the stone, and this irritates with
mucosa and lead to oedema, which then makes the stone even harder to pass! This can lead to stricture.
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Good fluid intake is the best preventative measure for preventing stones.
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Complications
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Renal failure – any obstruction to the ureter will cause backflow and affect the GFR in the effected kidney. However, permanent
damage is unlikely to result from hydronephrosis unless the obstruction is present for weeks at a time.
Sepsis – is more common than renal failure, but still generally unlikely.
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TCC
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This is a tumour of the bladder and urinary tract. It can occur anywhere along the urinary tract from
the calyx, renal pelvis, ureter, bladder to the urethra.
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Epidemiology
Uncommon before the age of 40, only 5% of cases present before the age of 60.
Male to female ratio 4:1
Incidence is about 32 per 100 000 in men, and 10 per 100 000 in women.
Bladder tumours are by far the most common – 50x as common as tumours in any other region of
the UT.
Peak age of presentation is 65-69 in men and 75-79 in women.
The incidence is declining thanks to the improvement of working conditions and supervision of
workers is vulnerable occupations in the last 50 years. It is also expected that incidence will decline
in the future in the West, due to changes in attitudes to smoking.
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Aetiology
Smoking – it is thought that this accounts for 40% of cases of bladder cancer
Exposure to industrial chemical carcinogens; such as β-naphthylaminen and benzidine – these are
found in:
Chemical, cable, rubber, leather, painting and dye industries.
Exposure to certain drugs; phenacetin, cyclophosphamide
Chronic inflammation
• Clinical features
• Painless haematuria is by far the most common presentation. In
some cases, pain may occur due to clot retention.
• There may be symptoms suggestive of a UTI, but urine will be
negative for bacteria.
• TCC of the kidney and ureter may give rise to flank pain (and
haematuria) as a result of urinary tract obstruction.
• Investigations
• USS and CT
• Analysis of urine for malignant cells.
• Cystoscopy is also usually carried out, unless there is evidence that
the malignancy is in the upper UT.
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Treatment
Pelvic and ureteric tumours – are treated by nephroureterectomy. Radio and chemotherapies have
been shown to be of little value. There should be follow up cystoscopy at regular intervals because
50% of these patients will develop subsequent bladder tumours.
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Bladder tumours – treatment for these depends on the stage (described above):
pTa stage – these are treated by transurethral resection. Again, cystoscopy at regular intervals is
necessary, as 70% will reccur
pT1 stage – these tumours have already shown their invasive potential – and they are treated in an
unusual manner:
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Intravesical BCG – this is the vaccine that is given foe TB. It stands for Bacillus Calmette-Guerin. It is given in
bladder cancer as a form of immunotherapy. Even with this treatment, 50% of patients will develop
invasive disease within 5 years.
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pT2 stage and above – this is tumours that have invaded the muscle layers of the bladder or further.
In patients under 70, treatment is with radical cystectomy. In patients over 70, treatment is with
radiotherapy. Cystectomy carries a mortality risk of 2-4% which obviously rises with age. Both
treatments have their downsides:
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Prognosis
5 year survival rates:
80-90% for lesions not involving the bladder muscle
5% for those with metastatic disease
Testicular Torsion
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EPIDEMIOLOGY: Can occur at any age but most frequently among adolescents. It is rare >30 years of age. It occurs in about 1 in 160 males per year.
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RISK FACTORS
Bell-clapper deformity (this is where the testicle has formed with no attachment to its surrounding scrotal walls and so is free floating within the
tunica vaginalis – the serous sac surrounding the testicle)
An undescended testis
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DIFFERENTIAL DIAGNOSIS
Epididymitis (main differential)
Epididymo-orchitis
Incarcerated inguinal hernia
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CLINICAL PRESENTATION
Acute onset of diffuse pain – can be in the scrotum, groin, lower abdomen or the inguinal region.
Swollen testis
Testicular tenderness
Vomiting
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INVESTIGATIONS
Doppler Ultrasound Scan can be done to look at the flow of testicular blood – this helps to rule out epididymitis where the flow will be present. In
torsion, there will be absent blood flow.
Surgical exploration is mandatory unless torsion can be excluded.
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TREATMENT
Surgical emergency– immediate intervention required to detort the testis. (also fix other side)
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PROGNOSIS
If treated within 6 hours – 90% chance of survival of the testicle surviving; 12 hours – 50%; 24 hours – 10%; >24 hours – 0%.
Testicular/Scrotal lumps
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Testicular cancer
Testicular torsion
Epididymo-orchitis
Epididymal cyst
Hydrocoele
Varicocoele
Inguinal hernia