Genitourinary Flashcards
What is the most common zone of the prostate that carcinomas occur?
4 zones of the prostate
- i) Transitional zone
- ii) Central zone
- iii) Peripheral zone
- iv) Anterior fibromuscular stroma
Clinical important of zones of prostate
- Transitional zone surrounds the urethra and is the part of the prostate predominately affected by nodular hyperplasia. Only 20% of prostate carcinomas occur here
- Peripheral zone is palpable on rectal examination. 75% of prostate carcinomas occur here
Incidence of prostate cancer
- Most common cancer in Australian men, lifetime risk is 1/6
- Often occurs in men after the age of 50
- More prevalent in African men and less prevalent in oriental men
- Most commonly does not require care. Despite this prostate cancer remains the second biggest cause of male cancer death with 1/30 men dying from prostate cancer
Clinical features of prostate cancer
Early disease – asymptomatic
- Patients who present with LUTS usually have an enlarged prostate secondary to BPH though prostate cancer may co-exist
Advanced disease
- Locally advanced disease - urinary symptoms similar to those in BPH e.g. frequency, nocturia, hesitancy, poor stream, dysuria. Haematuria may be present
- Metastatic disease - bone pain, fractures, cord compression
- Generalised symptoms of malignancy - anaemia, weight loss, depression
Diagnostic tests for prostate cancer
- Digital rectal examination (DRE) – firm nodule (T2) hard, craggy prostate (T3/4)
- PSA test
- PSA rises with age so should be compared to norm for that age group
1. Trans-rectal U/S biopsy (TRUS biopsy) - Diagnostic. - Complications:
- Infection – all patients get prophylactic antibiotics but infection still occurs
- Bleeding – patients may see blood PR, have haematuria or haematospermia which may last several weeks. Serious post-biopsy bleeding can occur. _Anti-coagulating drugs must be stopped befor_e a TRUS biopsy
- Urinary retention
What is the grading score for prostate biopsy called and what type of cancer is the most common on histopathology
- Prostate biopsy – Gleason score is used for grading prostate cancer
- It gives prognostic information and indicator of tumour aggression
- Histological grading system: 1-5
- 95% of tumours are adenocarcinoma
- Gleason sum score = most common tumour pattern histologically + worst pattern in a core biopsy e.g. 3+4 = 7
What are the treatment options for prostate cancer
- Radical prostatectomy
- Indication: localized prostate cancer
- Urinary catheter is left in-situ for 10 days post-operatively and not to be removed as re-insertion may disrupt urethral anastomosis
- Complications:
- Impotence, incontinence, recurrence of disease, mortality
- Radiotherapy
-
External beam radiotherapy (EBRT)
- Given in fractions e.g. delivered over 7 weeks
- 3 dimensional conformal and intensity modulated techniques allow increased dose to be delivered to the prostate whilst minimizing dose to rectum and other structures
-
Brachytherapy
- Seed brachytherapy involves permanently implanting radioactive seeds (iodine or palladium) into the prostate
- High dose rate brachytherapy involved temporary insertion of a high dose radioactive source to give a boost of treatment to the prostate. It is usually combined with EBRT for high risk locally advanced disease
Complications include:
- Bladder and bowel irritation e.g. proctitis
- Impotence
- Disease recurrence
*Cure rate rates may be less compared to surgery though no trial has compared this properly
- Androgen suppression
- Prostate cancer is a testosterone dependent tumour
- Androgens may be suppressed by:
- Surgical castration
-
GnRH agonist e.g. Goserelin (Zoladex) and Leuprorelin (Lucrin)
- Note there will be an initial increase in serum testosterone following administration of an LHRH agonist. Therefore an anti-androgen must be co-administered initially to cover this.
- Anti-androgens e.g. cyproterone acetate, biclutamide
What % of macroscopic and microscopic haematuria end up being urothelial cancer?
- Approximately 20% of macroscopic haematuria end up being bladder cancer
- If there is microcytic haematuria (can’t see) - wait for 6 weeks and re-test, treat UTI etc. then refer to urologist (only 2% of these are cancer)
what is the most common histological bladder cancer
- More than 90% are transitional cell carcinoma
- A few are squamous cell carcinoma and adenocarcinoma
- Male > Female (2.5:1)
Risk factors for bladder cancer
- Age
- Male sex
- Smoking (500x)
- Family history
- Workers in certain industries exposed to carcinogens such as beta-naphthylamine, benzidine a rubber, textile/ dye industry, printing and metal
- Drugs - such as cyclophosphamide
Investigations for potential bladder cancer (Haematuria)
Gold standard investigations:
- Cystoscopy +/- biopsy for histology
- Urine cytology – very specific but has low sensitivity (therefore, negative result does not mean cancer is not present)
Symptoms of bladder cancer
- Painless gross haematuria through micturition (most common)
- Irritative voiding symptoms (dysuria, urinary frequency, urgency)
- Rarely bladder outlet obstruction
- Ssuprapubic/ rectal/ perianal pain
- Rarely palpable suprapubic mass (advanced)
- Features of metastasis
Treatment of bladder cancer (carcinoma in situ, stage t1 and muscle invasion)
Carcinoma in-situ
- Diagnosis by biopsy/ trans-urethral resection
- Treatment with intravesicular immunotherapy – BCG (Bacillus Calmette-Guerin) with subsequent maintenance
- Cystectomy if fails to respond to BCG
*Urothelial CIS represents a high grade risk form of urothelial cancer (unlike in-situ carcinoma in other organ sites. Though not showing invasion, it is at high risk of progression and should be aggressively managed
what is intravesicular BCG?
- Live attenuated bacillus calmette-guerin
- The BCG is instilled into the bladder via a catheter and then drained away weekly for 6 weeks and then monthly for one year
- This is a form of immunotherapy and has been shown to decrease recurrence and progression of CIS and other high risk bladder cancer
At & T1 bladder cancer
- TURBT (Transurethral resection of bladder tumour)
- Intravesicular cytotoxics – using drugs such as mitomycin
- Intravesicular immunotherapy – BCG
Muscle-invasive Bladder cancer
- Radical cystectomy
- Radiotherapy
- Combined treatments – chemotherapy followed by radical cystectomy. Radiotherapy followed by chemotherapy
Importance of multi-modal therapy à Chemo + surgery
Cystectomy
- Is a major surgery
- Requires thorough cardiovascular and respiratory system evaluation, bowel prep, blood cross-matched and stoma education pre-operatively
- An ileal segment is isolated on its mesentery and and end-to-end anastomosis is then performed to restore bowel continuity
- Both ureters are anastomosed to portion of ileum resected to form stoma
Metastatic Disease
- Systematic chemotherapy
- Palliative radiotherapy – to relieve symptoms and improve quality of life
- Palliative surgery – radical cystectomy and urinary diversion
Causes of Urinary tract obstruction
Renal
- Nephrolithiasis
- Sloughed off renal papilla (papillary necrosis in diabetes, sickle cell, pyelonephritis)
- Urothelial carcinoma
Ureters
-
Intraluminal
- Nephrolithiasis
- Blood clot
-
Intramural
- Ureteral stricture
- Accidental surgical ligation
- Urethral carcinoma
-
Extraluminal
- Pregnancy
- Neoplasm of cervix, ovaries, colon
- Aortic aneurysm
- Iliac artery aneurysm
- Tubo-ovarian masses: endometriosis, prolapse, haematoma
- Gastrointestinal mass: Crohn’s disease, diverticulitis
- Retroperitoneal fibrosis (Ormond disease)
Bladder
- Urothelial carcinoma
- Neurogenic bladder
- Spasic neurogenic bladder (UMN): detrusor-sphincter dyssynergia
- The bladder contracts against a closed urethral sphincter due to a loss of coordination between the central (pontine) and peripheral (sacral) micturition centers. Seen in spinal lesions at/above T12 (traumatic spinal cord injuries, multiple sclerosis). Patients may present with urinary retention or urge incontinence (due to recurrent detrusor contractions).
- Spasic neurogenic bladder (UMN): detrusor-sphincter dyssynergia
- Flaccid neurogenic bladder (LMN): detrosuor areflexia but intact urethral sphincter innervation
- Due to a spinal cord lesion/s at S2 or between S2–S4 or due to peripheral nerve damage. Since sympatheticcontrol of urethral tone is above the level of the lesion. (i.e., at T12–L2), the urethral function is preserved, causing a functional BOO/urinary retention.
Urethra
- Benign Prostatic Hyperplasia
- Prostatic Cancer
- Stricture
- Posterior urethral valves (congenital = children)
Mechanical
Kinked or plugged indwelling catheter
Clinical features of urinary obstruction
Acute
Upper UTO
- flank pain, haematuria
- nausea and vomiting
Lower UTO
- urinary retention
- suprapubic pain
- palpable bladder
Chronic
Upper UTO
- usually asymptomatic
- hypertension
- renal failure
Lower UTO
- LUTS
Investigations for suspected Urinary tract obstruction
Lab tests
- Urinalysis
- Proteinuria ?
- Haematuria – may indicate stone or tumour
- Crystals – may provide information about content of stone
- bacteriuria, pyuria
- UEC
- Elevated blood urea nitrogen
- Bilateral UTO in or UTO in solitary kidney - Elevated serum creatinine
-
Serum electrolytes
* Hyperkalaemia is dangerous complication of renal failure - FBC
- Leukocytosis in UTI
- Anaemia in chronic UTO
Imaging
- U/S
- CT- KUB
What are the different types of renal stones and which is most common
- Calcium oxylate (40%)
Hypercalciuria, decreased pH, radiopaque - Calcium phosphate (35%)
Hyperparathyroidism, Raised pH - Uric acid stones (10%)
High uric acid, gout, decreased pH - Struvite stones (Staghorn)
UTI with urease-producing bacteria such as Proteus mrabillis, Klebsiella, raised pH - Cystine
Clinical features of urolithiasis
Stones usually form in the collecting ducts of the kidneys but may be deposited along the entire urogenital tract from the renal pelvis to the urethra. Their localization and size determine the specific symptoms. Small kidney stones may also be asymptomatic.
- Severe unilateral and colicky flank pain (renal colic)
- Radiated anteriorly to the lower abdomen, groin labia, testicles, or perineum
- Paroxysmal or progressively worsening
- The area around the kidneys may be tender on percussion
- Haematuria
- Nausea, vomiting, reduced bowel sounds
- Dysuria, frequency, urgency
Investigations for urolithiasis
- Urine dipstick (microscopic haematuria is present in > 90%) and MSU (Urinalysis)
- Gross or microscopic haematuria
- Pyuria, positive leukocyte esterase, positive nitrites, or bacteriuria suggest UTI
- Urine pH
- >7 suggests urea-splitting organism and struvite stones
- <5 indicates uric acid stones
- Urine microscopy – may detect crystals
- Obtain a urine culture if signs of Uti
- Blood tests:
- FBC– leucocytosis concomitant UTI
- UEC – creatinine raised suggests acute kidney injury
- Calcium
- Phosphate
- Uric acid
- PTH, albumin
- Radiological tests:
- CT-KUB – gold standard
- IVU (intravenous Urethrogram)
- RCPG (Retrograde Pyelogram)
- USS renal tracts
- X-ray à radiopaque (calcium-containin stones), radiolucent (uric acid stones)
Differentials need to be rules out – leaking abdominal aortic aneurysm, perforated peptic ulcer, peritonism. If haematuria is absent, question your diagnosis.
Prevention of renal stones
- Sufficient fluid intake *>2.5L per day)
- For calcium stones
- Reduced consumption of salt and animal protein
- Reduced consumption of oxylate-rich foods and supplemental vitamin C
- Thiazide diuretics for recurrent calcium-containing stones with idiopathic hypercalciuria
- for uric acid stones à allopurinol
treatment of urolithiasis
Ask yourself is this case complicated by:
- High grade or infected hydronephrosis
- Urosepsis
- Acute kidney injury
- Intractable pain and Vomiting
*Infected obstruction is a medical emergency
Haemodynamically stable patients without complicated stone < 7mm à trial of observation with symptomatic treatment to enable spontaneous passage
Urological intervention required for stones:
- >7mm
- complications above
- failure to pass stone spontaneously in 4-6 weeks
Medical therapy
- Hydration
- Analgesia (NSAIDs, panadeine forte, indomethacin)
- Urology outpatient follow up
- Need to give dietary advice:
- Increase fluid intake
- Reduce intake of animal protein (meat, fish, poultry)
- Avoid excessive high oxalate containing foods/ drinks e.g. tea, chocolate, spinach, rhubarb, okra, eggplant
- Medical expulsive therapy: alpha-blockers (tamsulosin) or calcium-channel blockers (nifedipine)
- Antibiotics if UTI
*For uric acid stones - urine alkalinisation
Surgical intervention
- Extracoroporeal shockwave lithotripsy
- Uteroscopy/ lasertripsy
- Percutaneous nephrolithotomy
- Laproascopic removal
Risk factors for developing testicular cancer
- Cryptorchidism (Undescended testes)
- Previous history of testicular cancer
- Family history
- Atrophy e.g. mumps, orchitis, trauma
- Genetic syndromes (esp. klinefelter’s disease, down syndrome à Germ cell tumours
- Subfertiliy
classification of testicular neoplasms
Primary (usual) and secondary (rare)
Germ cell tumours (95%)
-
Seminoma (50% of cases)
* Good radiosensitivity, slow growth, late metastasis, better prognosis than non-seminomas - Non seminomatous germ cell tumours. Combination of:
-
Yolk sac (5%)
* Most common pre-pubertal testicular tumour -
Embryonal (20%)
* Usually min mixed germ cell tumours, aggressive tumour -
Teratoma (20%)
* Rare in adults, common in children -
Choriocarcinoma
* Most aggressive
Non germ cell tumours (Non-GCTs)
- Lymphoma (Common in > 50 years) usually non-hodgkin
- Leydig cell tumours (1-3%) – these produce testosterone – may produce androgenic symptoms
- Sertoli cell tumours (<1%) – these cells nourish the sperm
- Other
clinical features of testicular cancer
- Usually presents as painless lump
- Negative transillumination test
- Dull lower abdominal or scrotal discomfort more common than acute scrotal pain
- Patient frequently recalls a non-significant testicular trauma or event
- Occasionally present with acute testicular pain, hydrocele, or metastatic disease
- In metastatic disease – cough, SOB, chest pain
Investigations for testicular neoplasm
Produce characteristic serum tumour markers which should be monitored before, during and after treatment
- Tumour markers are raised in:
- 50% of tumours
- up to 90% of advanced tumours
- Alpha feto Protein
- Half-life: 5-7 days
- Produced by foetal gut, liver, yolk sak
- Elevated in liver, pancreatic, stomach and lung tumours. Also raised in normal pregnancy and benign liver disease
- B-hCG
- Half life: 24-36 hours
- It implies syncytiotrophoblastic component (choriocarcinoma)
- Produced by placental tissue
- Produced by many subtypes especially choriocarcinoma
- LDH
- Non-specific tumour marker, measures burden of metastatic disease
Imaging
- U/S
- CT chest/ abdomen/ pelvis
- Used to stage the disease
Confirmation
- Histopathological confirmation following radical inguinal orchiectomy