Urology - conditions Flashcards
Epididymitis pathophysiology
Usually caused by local extension of infection from the lower urinary tract either via enteric or non-enteric organisms
In males < 35 years old = sexual transmission therefore most common organisms are N. gonorrhoeae & C. trachomatis
In males > 35 years old = enteric organisms from a UTI is the more likely mechanism of the disease
Epididymitis risk factors
Non-enteric causes = MSM, multiple sexual partners/known contact of gonorrhoea
Enteric causes = recent instrumentation/catherisation, bladder outlet obstruction/an immunocompromised state
Epididymitis clinical features
Unilateral scrotal pain & associated swelling
Associated symptoms – dysuria, storage LUTS, urethral discharge
Examination – red & swollen, very tender
Cremasteric reflex which is intact in cases of epididymitis & Prehn’s sign (supine & scrotum is elevated by the examiner -> relieved by elevation)
Epididymitis investigations
Urine dipstick
First-void urine should be collected and sent for NAAT for suspected non-enteric epididymitis
Routine bloods
Imaging – typically a clinical one, however USS of the testes can be useful to confirm the diagnosis & rule out any complication
Epididymitis management
Appropriate abx therapy and provided with sufficient analgesia
- Enteric organisms: ofloxacin 200mg PO BD for 14 days/levofloxacin 500mg BD for 10 days
- STI organisms: ceftriaxone 500mg IM single dose and doxycycline 100mg PO twice daily for 10-14 days
Abstain from sexual activity
Epididymitis complications
Reactive hydrocele formation
Abscess formation
Testicular infarction
Testicular cancer risk factors
Cryptorchidism
Previous testicular malignancy
A positive family history
Caucasian ethnicity
Kleinfelter’s syndrome
Testicular cancer clinical features
Unilateral painless testicular lump
Examination – mass is typically irregular, firm, fixed & does not transilluminate
Evidence of metastasis – weight loss, back pain or dyspnoea
Testicular cancer investigations
Tumour markers can be used for both diagnostic and prognostic means – beta-hCG, AFP, LDH
Scrotal ultrasound
Disease staged via CT imaging with contrast
Trans-scrotal percutaneous biopsy should not be performed – might cause seeding of the cancer
Testicular cancer management
Discussed in a specialist MDT
Main treatment options for testicular cancer are surgery, radiotherapy & chemotherapy
Most cases – inguinal radical orchidectomy
Testicular torsion pathophysiology
Mobile testis rotates on the spermatic cord
Leads to reduced arterial blood flow, impaired venous return, venous congestion, resultant oedema & infarction to the testis
Males with a horizontal lie to their testes are more prone to developing testicular torsion
Testicular torsion risk factors
Age
Previous testicular torsion
Family history of testicular torsion
Undescended testes
Testicular torsion clinical features
Sudden onset severe unilateral testicular pain, associated N&V
Examination – testis will have a high position with a horizontal lie
Cremasteric reflex is absent & negative Prehn’s sign
Testicular torsion management
Surgical emergency – urgent surgical exploration of the testis
Strong analgesia and anti-emetics
Torsion in confirmed intra-operatively = bilateral orchidopexy
Testis is non-viable = an orchidectomy may be warranted
Testicular torsion complications
Delay in surgical exploration leading to prolonged ischaemia can result in testicular infarction
Affected testis may later undergo atrophy
Surgical complications – chronic pain, palpable suture, risk to future fertility & theoretical risk of future torsion
Bladder cancer risk factors
Smoking
Increasing age
Aromatic hydrocarbons
Schistosomiasis infection
Previous radiation to the pelvis
Bladder cancer clinical features
Painless haematuria
May also present with recurrent UTIs/LUTS
Clinical examination is typically unremarkable
Bladder cancer investigations
Urgent cystoscopy – initially via a flexible cystoscopy under local anaesthetic
If suspicion is identified -> rigid cystoscopy will be required for more definitive assessment
- Any tumour identified will require biopsy & potential resection via transurethral resection of bladder tumour (TURBT)
Imaging – CT staging
Urine cytology
Stress UI pathophysiology
Urine leakage occurring when the intra-abdominal pressure exceeds the urethral pressure
Impaired urethral support is most often due to weakness of the pelvic floor muscle
Most commonly seen post-partum, risk factors include constipation, obesity, post-menopausal/pelvic surgery
Urge UI pathophysiology
Overactive bladder (detrusor hyperactivity), which leads to uninhibited bladder contraction, leading to a rise in intravesical pressure -> leakage of urine
May be due to neurogenic causes, infection, malignancy, idiopathic, cholinesterase inhibitors
Overflow UI pathophysiology
Normally a complication of chronic urinary retention
Progressive stretching of the bladder wall leads to damage to the efferent fibres of the sacral reflex & loss of bladder sensation
As bladder fills with urine, becomes grossly distended, however intravesicular pressure builds, leading to a constant dribbling of urine
Most common cause is from prostatic hyperplasia
UI investigations
Midstream urine dipstick assessing for evidence of infection or haematuria
Post void bladder scans should also be performed routinely
Further investigations
- Unclear aetiology: urodynamic assessment
- Outflow urodynamics can then be performed
- Cystoscopy
- IV urogram
- Vaginal speculum examination
- MRI imaging
UI conservative management
Pelvic floor muscle training which should ideally last for at least 3 months, duloxetine can be trialled to cause stronger urethral contractions
Urge UI – anti-muscarinic drugs can be trialled (eg. oxybutynin or tolterodine)
Bladder training
UI surgical management
Urge UI – botulinum toxin A injections, percutaneous sacral nerve stimulation, augmentation cystoplasty, urinary diversion via ileal conduit
Stress UI – tension-free vaginal tape, open colposuspension, intramural bulking agents or an artificial urinary sphincter
Urethritis
Inflammation of the urethra most often due to infection
Either gonococcal or non-gonococcal
Urethritis risk factors
Age < 25 years
Men who have sex with men
Previous STI
Recent new sexual partner
More than one partner in the last year
Urethritis clinical features
Dysuria
Penile irritation
Discharge from urethral meatus
Urethritis investigations
Urethral gram stain under microscopy should be performed on urethral swabs – pus cells suggest urethritis
Gold standard investigation – first-void urine being sent for NAAT
Should also have mid-stream urine dipstick performed, triple site testing for culture
Consider further STI screening
Semen culture
Urethritis initial management
Abx management is the mainstay of initial management
- Gonococcal: ceftriaxone 1g IM single dose + azithromycin 1g PO single dose
- Non-gonococcal: doxycycline 100mg PO BD for 7 days/azithromycin 1g PO single dose
Urethritis long term management
Abstain from sexual activity for 7 days after abx course has finished, resolved symptoms & sexual partners have been treated
Counsel patients on condom use & advise patient to notify their sexual partners to attend GUM clinic for testing and treatment
Pyelonephritis
Inflammation of the kidney parenchyma and the renal pelvis, typically due to bacterial infection
Uncomplicated or complicated
Pyelonephritis pathophysiology
Acute pyelonephritis – results from bacterial infection of the renal pelvis and parenchyma
Bacteria can reach the kidney either by ascending from the lower urinary tract, from the blood stream or via lymph
Neutrophils cause suppurative inflammation -> often small renal cortical abscesses and streaks of pus in the renal medulla
Most common organism isolated is Escherichia coli
Pyelonephritis risk factors
1) Factors reducing antegrade flow of urine – obstructed urinary tract, including BPH
2) Factors promoting retrograde ascent of bacteria – female gender, indwelling catheter/ureteric stents, structural renal abnormalities
3) Factors predisposing to infection or immunocompromise
4) Factors promoting bacterial colonisation – renal calculi, sexual intercourse, oestrogen depletion
Pyelonephritis clinical features
Classical triad – fever, unilateral loin pain and N&V
Co-existing lower urinary tract infection
Examination – often look unwell, often pyrexial, unilateral/bilateral costovertebral angle tenderness
Assess patient’s fluid status and measure any post-void residual volumes
Pyelonephritis investigations
All patients will require urinalysis, urinary beta-hCG for women of child-bearing age, urine culture
Routine bloods
Renal US scan, if obstruction is suspected -> non-contrast CT imaging (CT KUB)
Pyelonephritis management
A to E approach
Empirical antibiotics based on local protocols & IV fluids as appropriate
Pyelonephritis complications
Severe sepsis
Multi-organ failure
Renal scarring leading to CKD
Pyonephrosis
Chronic pyelonephritis
Repeated infections can lead to chronic pyelonephritis -> fibrosis and destruction of kidney
Cases are more common in obstructed systems
Reverse any underlying causes, optimise renal function and consider prophylactic abx
Emphysematous pyelonephritis
Rare and severe form of acute pyelonephritis, caused by gas-forming bacteria
Fails to response to empirical IV abx, CT imaging will show evidence of gas within and around the kidney
Most common in diabetic patients -> high glucose allows CO2 production from fermentation by enterobacteria
Severe cases may warrant either nephrostomy insertion or percutaneous drainage of any collections present
RCC pathophysiology
Adenocarcinoma of the renal cortex, arising predominantly from the PCTs, most often appearing in the upper pole of the kidney
RCCs can spread through direct invasion in to perinephric tissues, renal vein (tumour thrombosis), IVC
Can spread via lymphatics to pre-aortic and hilar nodes or by haematogenous spread to the bones, liver, brain and lung
RCC aetiology
Smoking
Industrial exposure to carcinogens
Dialysis
Hypertension
Obesity
Anatomical abnormalities – polycystic kidneys & horseshoe kidneys
RCC clinical features
Haematuria, mass and flank pain = classical triad (15% of patients)
Non-specific symptoms
Diagnosed incidentally on abdominal imaging
Examination – large RCCs may be palpated in the flank, left-sided masses may also present with a left varicocoele
Paraneoplastic syndromes – polycythaemia due to EPO, hypercalcaemia due to PTH, hypertension due to renin, pyrexia of unknown origin, clinical features of metastasis
RCC investigations
Lab tests – routine blood tests, urinalysis and urine should be sent for cytology
Imaging – CT imaging of abdomen-pelvis pre and post contrast is gold standard
Biopsy of renal lesions
RCC management (localised disease)
Surgical management
- Smaller: partial nephrectomy may be suitable
- Larger: radical nephrectomy
Percutaneous radiofrequency ablation or laparoscopic/percutaneous cryotherapy if not suitable for surgical management
Renal artery embolization may be required for haemorrhaging disease
Surveillance imaging can be employed in patients unfit/unwilling to undergo surgery
RCC management (metastatic disease)
Nephrectomy combined with immunotherapy
Biological agents can be used in combination for metastatic disease
Metastasectomy is recommended where disease is resectable & patient is otherwise well
Renal cysts
Fluid-filled sacs found in the kidney and can be classified as simple or complex
Simple cysts – well-defined outline and homogenous features, very common in older patients
- Develop from the renal tubule epithelium in response to previous ischaemia
Complex cysts – more complicated structures, have a risk of malignancy & risk increases with its increasing complexity
Renal cysts risk factors
Increasing age
Smoking
Hypertension
Male gender
Polycystic kidney disease
ADPKD is an inherited condition caused by mutations in the PKD1 or PKD2 genes, resulting in multiple renal cysts forming in affected individuals
Condition associated with Berry aneurysm formation, mitral valve disease and liver cysts
Eventually develop end-stage renal failure & may require either dialysis/renal transplant
Renal cysts clinical features
Most likely to be found incidentally, as they are usually asymptomatic
Flank pain
Haematuria
Uncontrolled hypertension
Flank mass
Renal cysts investigations
CT/MRI imaging with pre and post enhancement scans with IV contrast
Ultrasound often picks up incidental findings of renal cysts
Patient’s serum U&Es should also be checked & monitored regularly in patients with a known genetic risk factor
Renal cysts management
Asymptomatic simple cysts – not normally need any further follow-up or treatment
Symptomatic simple renal cysts – initially with simple analgesia, needle aspiration/cyst deroofing may be warranted if significantly impacting the patient
Complex cysts managed depending on their Bosniak stage & may involve continued surveillance/surgical intervention
Renal cysts complications
Infection
Haemorrhage
Rupture
Renal tract stones compositions
Calcium – calcium oxalate, calcium phosphate or mixed oxalate & phosphate
Struvite stones – magnesium ammonium phosphate
Urate stones
Cystine stones – associated with familial disorders affecting cystine metabolism
Renal tract stones pathophysiology
Over-saturation of urine
Urate stones – high levels of purine either from diet or through haematological disorders, results in increase of urate formation & subsequent crystallisation in the urine
Cystine stones – typically associated with homocystinuria, an inherited defect that affects the absorption and transport of cystine in the bowel and kidneys
Location of ureteric stones
1) Pelviureteric junction – renal pelvis becomes the ureter
2) Crossing the pelvic brim, where iliac vessels travel across the ureter in the pelvis
3) Vesicoureteric junction – ureter enters the bladder
Ureteric stones clinical features
Loin to groin pain, sudden onset and severe
Haematuria – non-visible
Examination – only demonstrating some tenderness in the affected flank
Ureteric stones investigations
Urine dip
Routine bloods – FBC, CRP, U&E, urate and calcium levels
Imaging – non-contrast CT scan of the renal tract (gold standard), AXRs, ultrasound to assess for any hydronephrosis
Ureteric stones initial management
Adequate fluid resus
Sufficient analgesia
IV abx therapy & urgent referral to the urology team
Ureteric stones criteria for inpatient admission
Post-obstructive AKI
Uncontrollable pain from simple analgesics
Evidence of an infected stone
Large stones
Stent insertion vs nephrostomy
Retrograde stent insertion – placement of a stent within the ureter, approaching from distal to proximal via cystoscopy
- Allows the ureter to kept patent & temporarily relieve the obstruction
Nephrostomy – tube placed directly into the renal pelvis and collecting system, relieving the obstruction proximally
Ureteric stones definitive management
Can be achieved by several methods for stones that do not pass spontaneously
1) Extracorporeal shock wave lithotripsy – targeted sonic waves to break up the stone to then be passed spontaneously
2) Percutaneous nephrolithotomy – used for renal stones only, percutaneous access to the kidney is performed with a nephroscope passed into the renal pelvis -> stones can then be fragmented using various forms of lithotripsy
3) Flexible uretero-renoscopy – involves passing a scope retrograde up into the ureter, allowing stones to be fragmented through laser
Ureteric stones complications
Infection
Post-renal AKI
Recurrent renal stones -> renal scarring & loss of kidney function
Bladder stones
Typically form from urine stasis within the bladder, commonly seen in cases of chronic urinary retention
Most often present with LUTS
Definitive management is through cystoscopy, allowing the stones to drain/fragmenting them through lithotripsy if required
Can predispose to the development of SCC bladder cancer
BPH
Non-cancerous hyperplasia of the glandular-epithelial and stromal tissue of the prostate leading to an increase in its size
Most common cause of bladder outlet obstruction
BPH pathophysiology
Androgens play a role
Prostate converts testosterone to dihydrotestosterone using the enzyme 5a-reductase
DHT is more potent & prostate retains the ability to respond to testosterone so levels of DHT remain high through life
BPH risk factors
Age
Family history
Black African/Caribbean ethnicity
Obesity
BPH clinical features
LUTS – mainly voiding symptoms (hesitancy, weak stream, terminal dribbling or incomplete emptying)
Can get haematuria and haematospermia
DRE is essential – firm, smooth, symmetrical prostate
BPH investigations
Urinary frequency and volume chart
Bedside urinalysis and a post-void bladder scan
Counselled for a PSA test
Ultrasound scan of the renal tract
Urodynamic studies
BPH medical management
Alpha-adrenoreceptor antagonist (tamsulosin) – act by relaxing prostatic smooth muscle
- Provide a symptomatic benefit within a few days
For those who remain symptomatic – finasteride (5a-reductase inhibitors) are often trialled
- Act to prevent the conversion of testosterone to DHT
BPH surgical management
TURP – endoscopic removal of obstructive prostate tissue using a diathermy loop to increase the urethral lumen size
Holmium laser enucleation of the prostate – laser used to heat and dissect section of prostate into the bladder
Simple prostatectomy
Prostate artery embolisation
TURP syndrome
Life-threatening complication of TURP
Use of hypoosmolar irrigation during procedure -> significant fluid overload & dilutional hyponatraemia as the fluid enters the circulation through the expodes venous beds
Present with confusion, nausea, agitation or visual changes
Needs urgent management by addressing the fluid overload and carefully reduced the level of hyponatraemia
BPH complications
High-pressure retention
Recurrent urinary tract infections
Significant haematuria episodes
Prostate cancer pathophysiology
Adenocarcinomas – most from the peripheral zone
Often multi-focal
Can be categorised into two types:
1) Acinar adenocarcinomas – originates in the glandular cells that line the prostate gland
2) Ductal adenocarcinomas – originates in the cells that line the ducts of the prostate gland
Prostate cancer risk factors
Age
Black African/Caribbean ethnicity
Family history of prostate cancer
Other less significant modifiable risk factors – obesity, diabetes mellitus, smoking, degree of exercise
Prostate cancer clinical features
LUTS
Haematuria, dysuria, incontinence, haematospermia, suprapubic pain, loin pain & even rectal tenesmus
DRE essential for diagnosis – asymmetry, nodularity or fixed irregular mass
Prostate cancer investigations
PSA
MRI scan of prostate
Biopsies of prostate tissue:
1) Transperineal biopsy
2) Transrectal ultrasound-guided biopsy – involves sampling the prostate transrectally, usually ultrasound as guidance & sampling tissue in systematic manner
Imaging for staging – CT chest-abdomen-pelvis and PET-CT nuclear medicine scan
Prostate cancer management
MDT meeting
Watchful waiting
Radial treatments – radical prostatectomy
Radiotherapy
Chemotherapy agents & anti-hormonal agents
Prostatitis
Inflammation of the prostate gland
Comprised of acute bacterial prostatitis, chronic bacterial prostatitis (+ nonbacterial prostatitis & prostatodynia)
Prostatitis pathophysiology
Acute bacterial prostatitis – caused by ascending urethral infection
Causative organisms: E. coli, Enterobacter, serratia, pseudomonas and proteus, STIs are a rare cause
Chronic bacterial prostatitis – chronic bacterial infection of the prostate with/without prostatitis symptoms & caused by inadequately treated acute prostatitis
Prostatitis risk factors
ABP: indwelling catheters, phimosis/urethral stricture, recent surgery, immunocompromised
CBP: intraprostatic ductal reflux, neuroendocrine dysfunction, dysfunctional bladder
Prostatitis clinical features
ABP – LUTS, features of systemic infection, perineal/suprapubic pain or urethral discharge
Rectal examination – very tender and boggy prostate, associated inguinal lymphadenopathy may also be present
CBP – pelvic pain/discomfort for 3 months, alongside LUTS, perineum is the most common site for pain
Prostatitis investigations
Urine culture, abx therapy can be guided from sensitivities obtained
STI screen, routine bloods
Transrectal prostatic ultrasound
CT imaging
Prostatitis management
ABP – prolonged abx treatment (typically quinolone)
Suitable analgesia
CBP – focused on symptom control, 4-6 week trial of alpha blocker, 6 week course of abx if symptoms < 6 months
Consider referral to a chronic pain specialist (MDT approach)
