urology Flashcards
What may cause pseudohaematuria?
- drugs like rifampicin or methylodopa
- hyperbilirubinurea
- myoglobinurea
- beetroot and rubarb
What may cause haematuria? (give at least 5)
- infection: bladder, prostate, kidney
- malignancy: bladder, kidney, ureter, prostate
- renal calculi
- trauma, recent surgery
- radiation cystitis
- schistomiasis
- BPH
- antiplatelet or anti coag drugs (investigate as normal)
- glomerular nephritis
- recent transrectal biopsy of prostate
What are important features to ask about in haematuria presentation?
- timing in stream (total suggests bladder is source, early suggest lower tract and late suggests severe bladder irritation)
- clots vs diluted
- other syptoms: fevers, rigors, suprapubic or flank pain, weight loss, trauma
- drug history
- smoking status (++ risk urological malignancy)
- occupation (industrial carcinogens ++ bladder ca)
- travel: schistomiasis
How is haematuria initially managed/ investigated?
- urinalysis: ? infection
- bloods: u&e, fbc, clotting, psa
- urinary protein levels if renal function off
- urgent refferal if: age>45 and unexplained w/out UTI or visible that persists after UTI treatment OR age >60 w/ unexplained non visible and dysuria or raised WCC
What specialist investigations may be requested for haematuria?
- flexible cystoscopy
- urine cytology in some places
- US KUB: for non visible haematuria
- CT urogram: usually for visible haematuria
Where do RCCs tend to arise from and where do they spread to?
- arise from PCT and appear most often in upper poles of kidneys
- spread directly to perinephris tissues, adrenal gland or into renal vein (may cause tumour thrombosis), IVC, lymphatic system (pre aeortic or hilar nodes) and to bone, liver, brain and lung via the blood.
Give 5 risk factors for RCC
- SMOKING (biggest)
- industrial exposure to cadmium or aromatic hydrocarbons
- dialysis (30x increase)
- hypertension
- obesity
- APCKD
- horseshoe kidneys
- some other rarer genetic disorders
Describe the clinical features of RCC
- haematuria (usually visible, may be invisible, is most common PC)
- flank pain
- flank mass
- lethargy, weight loss, pyrexia of unknown origin
- left varicocele if impinging left testicular vein
- paraneoplastic syndrome
- hypertension
- features of mets such as haemoptysis or #
What paraneoplastic syndromes may RCC cause?
- EPO secretion-> polycythaemia
- PTH-> hypercalcaemia
- Renin-> hypertension
How is suspected RCC investigated?
- USS usually already one
- CT abdo pelvis with contrast
- CXR for mets
- Biopsy to stage
How can RCC be managed? (if small, large, unfit for surg and metastatic)
- SMALL-> partial nephrectomy
- LARGE-> radial nephrectomy
- not fit for surg-> percutaneous radiofrequency ablation, laparoscopic cyrotherappy, renal artery embolisation
- If old person + slow growing tumour+ unfit for surg-> surveillance
- METASTATIC-> immunotherapy (sunitinib) + nephrectomy +/- metastatectomy
- CHEMO CONSIDERED INEFFECTIVE
What is involved in a radical nephrectomy?
Remove the kidney, perinephric fat and local lymph nodes
How does an upper tract TCC usually present?
- haematuria (visible or invisible)
- post renal AKI +/- hydronephrosis
- loin pain
- palpable mass
What suggests a TCC is higher risk?
- hydronephrosis
- infiltrative features
- high grade
How is TCC managed? (if high and low risk)
- radical nephroureterectomy with bladder cuff excision
- lower risk TCCs can be managed more conservatively
What age and gender tends to get bladder cancer and what is the prognosis like usually?
- usually males >80
- most are superficial so have good prognosis
How are bladder cancers classified?
- non muscle invasive (papillary (Ta), into LP or subepithelial (T1))
- muscle invasive (T2)
- locally advanced (into perivesible tissues (T3) or adjacent structures (T4))
- metastatic
How do bladder cancers tend to present
- haematuria usually
- may be recurrent UTIs, LUTS, ureteric obstruction
- weightloss, PUO or mets if more advanced
How bladder cancers investigated?
- flexible cystoscopy then rigid cystoscopy if they find something
- when doing rigid cystoscopy do TURBT and histology
- CT staging before TURBT if lesion is invasive
- urine cystology is rarely used
How is non muscle invasive bladder cancer managed?
TURBT resection, higher risk disease may require adjuvant intravesicle chemo with BCG or mitomycin C or they can be offered radical cystectomy.
Theyll need cytology and cystoscopy follow up due to high recurrence rates
How is muscle invasive and locally advanced or metastatic bladder cancer managed?
- muscle invasive= radical cystectomy + neoadjuvant chemo (cisplatin) + regular CT follow up
- locally advanced or mets= chemo (cisplatin) + symptom management, usually palliative
What are the two options of urinary diversion following radical cystectomy?
- ileal conduit: urine drains into urostomy (ureters attach to small piece of bowel which is made into a stoma)
- bladder reconstruction: segment of small bowel used to form neobladder, urine drains from this out through urethra or catheter. Needs routine bloods, B12 and folate annually due to ileal resection.
What is the most common histological type of prostate cancer and from which part of the prostate do they most commonly arise?
- adenocarcinoma
- from peripheral zone
- can be acinar (most common) or ductal (grow and metastasise faster
Give 3 risk factors for prostate cancer
- old age
- black african or caribbean
- fhx (significant if in 1st degree relative younger than 60)
- BRCA1 or 2 genes
- obesity, diabetes, smoking, exercise less significant
What is PSA and what is its use?
A protease normally produced by the prostate to make semen more liquid.
Youre unlikley to have prostate can cancer if its low (85% NPV) but there are lots of causes of high PSA so isnt very specific (30% PPV). It can also be used for disease progression monitoring
Other than prostate cancer, what may cause PSA to be elevated?
- BPH
- Prostatitis
- vigerous exercise
- DRE
- ejaculation
How should suspected prostate cancer be investigated?
- DRE and PSA initially
- transperineal biopsy: under general, lower infection risk, better access to anterior prostate
- transrectal US guided biopsy: under local, 12 cores are taken, 1-2% sepsis risk
- repeat biopsy if suspicious DRE or persistently elevated PSA
- gleason score is given based off histology
- Multi parametric MRI may be used to target biopsies better
- CT CAP and bone scan done for men with intermediate and high risk disease
What does the gleason scale take account for?
most common glandular growth pattern plus the highest grade (most differentiation) seen- higher gleason = worse prognosis
What is taken into account when assessing risk of prostate cancer?
- PSA
- gleason score
- clinical stage (TNM)
How are low risk prostate cancers managed?
- active surveillance (3 monthly PSAs, 6 monthly DRE and 1-3 yrly biopsies)
- or watchful waiting (symptom and QoL guided care, used in elderly with low LE, can be offered for any stage/ risk prostate cancer)
How are intermediate and high risk and metastatic prostate cancers managed?
- radical prostatectomy (prostate, seminal vesicles, surrounding tissues and pelvic lymph node removal)
- if metastatic: chemo and chemical castration (LHRH agonists or GnRH agonists to surpress testosterone) or orchiectomy for surgical castration, new hormone therapies also available for metastatic
- external beam and brachytherapy becoming curative for localised disease
- intermediate risk sometimes managed with active surveillance
What are side effects/ risks of radical prostatectomy?
erectile dysfunction, stress incontinence and bladder neck stenosis
What types of testicular cancer are there and how common are they?
- 95% are germ cell tumours
- 5% non germ cell (leydig or sertoli, good prognosis)
- 50% germ cell tumours are seminomas
- 50% germ cell are non seminomas (yolk sac, choriocarcinoma, teratoma, usually malignant)
Give 3 risk factors for testicular cancer
- cryptoorchidism
- Fhx
- kleinfelter syndrome
What are the clinical features of testicular cancer
- unilateral painless, irregular, firm, fixed lump which doesnt transilluminate
- weightloss, back pain or dyspnoea
- lymphatic drainage is to para- aortic nodes so rarely presents with lymphadenopathy
How should suspected testicular cancer be investigated?
- beta HCG
- AFP
- LDH as surrogate marker for tumour volume
- Scrotal USS for initial assessment
- CT CAP with contrast for staging
- transcrotal percutaneous biopsy is NOT done as may cause seeding of the cancer
- Staging is with royal marsden classification
What are the use of beta HCG and AFP?
- beta HCG rasied in 60% NSGCT and 15% seminomas
- AFP raised in some NSGCT
How is testicular cancer managed? (stage 1 seminomas, higher stage seminomas, stage 1 and metastatic NSGCT)
- stage 1 seminomas-> orchidectomy
- inguinal radial orchidectomy for higher stage seminomas
- stage 1 NSGCT-> orchidectomy, if low risk the surveillance if high risk them adjuvant chemo
- metastatic NSGCT-> chemotherapy
- pre treatment fetility assessment and cryopreservation is offered usually
What is the prognosis like for testicular cancer?
very good even when metastatic
Describe what histological type penile cancer is and how it spreads
- squamous cell carcinoma
- spreads locally into corpus cavernosa and to inguinal nodes
- distant mets are uncommon
What type of renal stones can you get?
- calcium oxalate (30%)
- mixed calcium (35%)
- calcium phosphate (10%)
- struvite
- cystine
- urate
When do urate, struvite and cysteine stones tend to occur?
Urate= high levels of purine (lots of red meat or haemotological disorders) Struvite= from recurrent infections (tend to be soft and cause staghorn calculi) Cysteine= hypocystinuria (less cysteine absorbtion from bowel and kidney= less citrate which is a stone absorber)
Where are the 3 natural narrowings in the urinary system that stones tend to get stuck
- pelviureteric junction
- where the iliac vessels cross the ureter
- vesicoureteric junction