Urology

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GENITOURINARY TRACT ANATOMY AND PHYSIOLOGY

 Kidneys lie L1 (hilum at transpyloric plane), R one is lower (liver).
 Gerota’s fascia around kidney
 Hilum: A  P: AVU (renal artery, vein, pelvis/ureter).
 Right renal artery posterior to IVC (as IVC on right
of aorta
 Left renal vein anterior to aorta
1. Can be ligated from IVC (secondary to
increased collaterals: L adrenal, L gonadal,
L ascending lumbar veins).
2. RRV has no collaterals.
 Key relations (transpyloric plane, L1):
1. Anterior-right: liver, D2
2. Anterior-left: pancreas + its vessels,
spleen, descending colon
3. Posterior: diaphragm, quadratus, psoas,
transversus abdominis, 12th rib, 3 nerves:
subcostal (T12), iliohypogastric, and
ilioinguinal (both L1).
4. Medial: aorta, IVC, AVU.
5. Superior: adrenal glands
 Lymph drainage: para-aortic nodes
 Embryology: kidneys derived from urogenital
ridges (mesoderm). Pronephroi  mesonephroi
(W4)  metanephroi (5). Ureteric bud grows from Wolffian duct  branches into
collecting duct & bladder; the bud induces mesenchyme (metanephrogenic blastema)
to form the nephron; the stalk of the bud forms the ureter. Ascension + rotation of
kidney occurs from W8-9. Blood supply transits from common iliac to aorta.

 The ureters descend is marked by bony landmarks:

1. Tips L1-5 transverse processes
2. Sacroiliac joints
3. Ischial spines  pelvic floor  oblique angle into bladder
 Narrowest points are: PUJ, pelvic brim, UVJ
 Relations:
1. Abdominal ureter – right covered by origin of D2, then lies lateral to IVC,
behind posterior peritoneum (retroperitoneal). Medial edge of psoas separates
ureter and L2-5 transverse processes.
2. Pelvic ureter – cross anterior to bifurcation of iliac arteries on both side,
before entering pelvis. Left ureter enters pelvis at sigmoid mesocolon.
3. Intravesical ureter – VU reflux prevented by sphincter conferred by vesical
muscle and entry via oblique angle. Male ureter above seminal vesicle, under
vas (water under bridge). Female ureter above vaginal fornices, under broad
ligament and uterine vessels.
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 Blood supply from upper to lower: renal, gonadal, vesical arteries.
1. Nerve supply from nearby vessels also (renal, aortic, pre-sacral, pelvic plexus)
= radiating pain 1st at loin  iliac fossa  penis

 Urinary bladder is a retropubic, extraperitoenal organ.

 Posterior (base): internally = trigone.
 Trigone: triangle formed by 2 ureteric orifices (UOs) and urethral opening –
sympathetic sensory detect strong fullness.
 Peritoneum above bladder wall: sympathetic sensory also (strong fullness). It is
stripped upwards when bladder expand.
 Detrusor = bladder wall longitudinal smooth muscle. S2,3,4 (pelvic splanchnic nerves
of the inferior hypogastric plexus, parasympathetic)
 Bladder neck (intrinsic urethral sphincter = detrusor & circular smooth muscle that
relaxes when full under autonomic control: S2, 3, 4). Male bladder neck has
sympathetic motor fibres – close during ejaculation
 Male: rectovesical pouch
 Blood supply: superior and inferior vesical arteries (internal iliac)
 Drainage: vesical plexus (bladder base) to internal iliac. Male: added prostatic plexus
 Micturition is controlled cortically (when to void) and in the pons (how to void).
Spinal centres work in paraplegics, but voiding is incomplete.

 Prostatic urethra, as the name suggests, pass through prostate. The prostatic urethra
posterior wall forms a bulge into the lumen: the verumontanum.
 Prostate adds 20% secretions to seminal fluid; it is held by puboprostatic ligaments.
1. Blood supply: inferior vesical and middle rectal arteries. Venous drainage to
valveless veins of Batson (implication in CA spread) + prostatic plexus.
 The vas enters abdominal cavity at the deep inguinal ring (mid-inguinal point).
Crosses external iliac vessels. It is dilated as the ampulla posterior to the bladder.
1. Vas feels like shoe-lace – important to check for absence, and for vasectomy
2. Blood supply: artery to vas (superior vesical artery).
3. Innervation: intrapelvic = same as bladder; spermatic cord vas = same as testis

 Spermatic cord structures

1. 3 fascial layers: external spermatic (EO aponeurosis); cremasteric (IO apo +
contain cremaster); internal spermatic (TA fascia)
2. 3 nerves: cremaster (genitofemoral:
L1,2); sym T10 + T11; ilio-inguinal
(L1, on cord not in cord)
3. 3 arteries: testicular (aorta), cremasteric
(IEA), artery to vas (inferior vesical)
4. 3 veins: pampiniform plexus(right 
IVC, left  LRV); cremasteric; vas
5. 3 others: vas; lymphatics to para-aortic
LNs; +/- patent processus vaginalis
 Urology
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 Seminal vesicle has ducts that join the vas at th e prostate base  ejaculatory ducts
 pierce prostate, running obliquely through onto the veramontanum. Seminal
vesicles add 70% of secretions to seminal fluid.
1. SV blood supply: inferior vesical arteries
2. Innervation: same as bladder
 The testis is covered by tunica albuginea except posterior margin, which is
extraperitoneal. This aids the movement of spermatozoa into epididymis. It is
suspended by spermatic cord.
1. Site of spermatogenesis = seminiferous tubules of the testis. Testis produces
testosterone as well.
2. Epididymis tail connects vas deferens (body – posterior; head – superior to
testis).
3. Blood supply: testicular artery (direct AA branch); drainage: pampiniform
plexus
4. Lymph node reflects intra-abdominal embryonic origin – para-aortic.
5. Innervation: T10 sympathetic efferent (referred pain to periumbilicus)
 Scrotum encloses the testes with an incomplete midline septum. The layers are: (1)
skin; (2) Dartos; (3) cremaster + cremasteric fascia; (4) parietal + (5) visceral layer of
the tunica vaginalis; (6) tunica albuginea.
1. Innervation: anterior 1/3  ilioinguinal (nerve (L1); posterior 2/3  scrotal
branch of pudendal (S2, 3, 4)
 Penis is attached at its root to perineal membrane, and to ischiopubic rami by the
crura. It is also attached to the symphysis by suspensory ligament. Its body = 2 dorsal
corpora cavernosa + 1 ventral corpus spongiosum – which commences from perineal
membrane as the bulb, surrounded by bulbospongiosus (last drop of urine, rhythmic
ejaculation).
1. Buck’s fascia is the deep fascia of the penis. Continuous w sus lig + ext sperm
fas
2. Extravasation of urine: if Buck’s fascia intact, urethral rupture fluid limited
to penis, deep to Buck’s. If urethral injury (bulb) + tear of Buck’s fascia 
blood + urine accumulate in superficial perineal space  penis (superficial to
Buck’s), scortum, lower anterior abdominal wall (trunk shaped) – the fascia
lata is the continuation of Scarpa’s deep fascia and limits tracking of fluids
down to thighs.
 Urethra
1. Prostatic (widest) – discussed
2. Membranous (most rigid + shortest) – through the deep perineal pouch,
surrounded by EUS, and then through perineal membrane
3. Spongy (penile) – runs through corpus spongiosum to tip of glans. Lumen
transverse, except at EU meatus  spiral, continuous urine steram
 Superficial perineal pouch in the urogenital triangle contains the external genitalia
& 3 muscles (ischiocarvenosus, bulbospongiosus, superficial transverse perineal) in
males Females have additionally: Bartholin’s (greater vestibular) glands.
 Erection – parasympathetic
 Ejaculation – sympathetic
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 Male embryology: Urogenital ridges (mesoderm). Wolffian duct forms appendix
epididymis, epididymis ducts, vas, ejaculatory ducts, and SV. Endoderm outgrowths
 prostatic urethra into surrounding mesenchyme (prostate). The Sertoli cells are
form from surface epithelium, while primordial GC form the spermatogonia.
Masculinisation of indifferent gonads by testosterone from Leydig cells (gonadal
ridge mesenchyme). Labiascrotal swelling grows towards and fuse at the raphe.
Testicular descent (W26  W32) occurs as viscera grow (pressure), mesonephroi
atrophy, and testis enlarge, guided by gubernaculum which forms a path for
processes vaginalis to follow. The descent brings layer of fascia of abdominal wall =
layers of spermatic cord. The processus obliterates to form tunica vaginalis to cover
anterior and sides of testes.

CLINICAL APPROACH
 Testicular lumps

 Testicular pain
1. Age 15+ either abdominal or excruciating groin pain + absent cremasteric +
negative Prehn sign + horizontal lie  looks angry and red  Torsion
(confirm by Doppler or straight to OR)
2. Testicular pain that is exacerbated by standing or walking (+ Prehn sign) + no
horizontal lie + fever & dysuria  swollen and heavier epididymis + testis
 epididymo-orchitis  urinalysis (1st catch) +/- discharge  ABx 2-4 wk

 Flank pain (renal angle tenderness)

1. Colic & haematuria  urinary stones
2. Dysuria & feverish  pyelonephritis
3. Cancer, renal trauma/infarction/venous thrombosis, musculoskeletal, pleural
pain, retroperitoneal abscess
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 Haematuria
1. Painless  bladder cancer vs. Painful  nephrolithiasis
2. Non-visible (micro)  exercise; IF unexplained + > 50 years old or RF
(smokers, FHx) = refer under 2-week wait rule
 Retention [stasis  UTI]
1. Acute (bladder usually tender, contain ~ 600 mL)
 Prostatic obstruction (MCC male), urethral strictures, anti-cholinergics,
COX2i, opioids, alcohol, constipation, post-op infection, neurological
(cauda equina), CA, retroperitoneal Fb, catheter, (para)phimosis
 Examine abdomen, DRE, perineal sensation (cauda equina)
 Tests: MSU, U+E, FBC, (PSA). Renal US if renal impairment.
 Aiding voiding: analgesia, privacy in wards, ambulation, standing to
void, voiding to sound of taps (or in hot baths)
 If fail: catheterise + start -blocker (tamsulosin). If clot retention –
need 3-way catheter and bladder washout.
 If > 1 L residual, check U+E & monitor for post-obstructive diuresis
 After 2-3 d, TWOC can work (remove midnight / morning so can
replace by night).
 Prevent: finasteride (BPH); tamsulosin (↓ recath after acute retention)
2. Chronic
 May be more insidious + painless. Bladder capacity > 1.5 L
 Present: overflow incontinence, acute-on-chronic retention, lower abdo
mass, UTI, or renal failure (bilateral obstructive uropathy).
 Causes: prostate enlargement common, pelvic malignancy, rectal
surgery, DM, CNS disease e.g. transverse myelitis / MS, zoster (S2-4)
 Only cath if there is pain, UTI, or renal impairment
 Institute definitive Tx promptly. ISC sometimes required.
 Incontinence
1. Think twice before catheterisation!
2. DRE to exclude faecal impaction
3. Is bladder palpable after voiding (retention w overflow)?
4. Is there neurological co-morbidity e.g. PD, stroke, spinal trauma?
5. Men: enlargement of prostate (MCC) = urge incontinence or dribbling; TURP
+ pelvic surgery weakens bladder sphincter & can cause.
 Not all are prostate-related!
 Detrusor overactivity  pressure-flow studies or US (detrusor thick)
 Primary bladder neck obstruction (can’t open when void)  muscular
or neurological or fibrosis  Dx: video-urodynamics + simultaneous
P-flow measurement + visualise bladder neck during voiding  Tx:
watchful waiting, -blockers, surgery
 Urethral stricture  trauma or infection e.g. gonorrhoea = frequency +
voiding Sx, UTI, retention. Malignancy is rare cause. Imaging:
retrograde urethrogram / antegrade cystourethrogram if has existing
suprapubic cath. Tx = internal urethrotomy to release scar & hope
epithelisation ends before wound contracts; or stents (best for short
strictures in bulbar urethra = before the penile / after membranous)
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6. Women: often under-reported
 Functional  too slow in finding toilet (immobile, unfamiliar)
 Stress  incompetent sphincter (raised intra-abdo P e.g. coughing,
laughing). Increasing age + obesity are RF. Key to Dx is frequent loss
of small amount of urine during strain. Common in pregnancy and
post-partum. Occur to 50% post-menopausal. Pelvic floor weakness
e.g. uterine prolapse or urethrocele are common association.
 Urge/overactive bladder  urge to urinate followed by uncontrollable
+ sometimes complete emptying of bladder as detrusor contracts.
Precipitated by arriving home (latchkey incontinence: conditioned
reflex); cold; sound of running water; tea, coffee, cola; and obesity. Dx
= urodynamic studies. Causes = detrusor overactivity e.g. central
inhibitory pathway malformation, or sensitisation to peripheral afferent
terminals in bladder, or detrusor muscle problem. Check for organic
brain damage e.g. stroke, PD, dementia. Other causes = UTI, DM,
diuretics, atrophic vaginitis, urethritis.
7. Note in both sexes, incontinence can result from sedation or confusion.
8. Management:
 Check: UTI, DM, diuretics, faecal impaction, palpable bladder, GFR.
 Stress  pelvic floor exercises 1st line; intravaginal electrical
stimulation effective but unacceptable to many women. Ring pessary
help uterine prolapse (while awaiting surgery). Surgical options (e.g.
tension-free vaginal tape) aim to stabilise mid-urethra. Urethral
bulking also available. If can’t surgery  duloxetine (SNRI, S/E: N).
 Urge  incontinence chart to define pattern. Examine for spinal cord +
CNS signs (including cognition); and for vaginitis (if post-
menopausal). Vaginitis  topical oestrogen. Bladder training
(including pelvic floor exercises) & weight loss importance. Drugs are
often disappointing. Consider pads or condom catheter (in females).
 Do urodynamic assessment (cystometry + urine flow rate
measurement) before surgery to exclude detrusor overactivity or
sphincter dyssynergia.
Detrusor overactivity
Anti-M e.g. tolterodine S/E: dry mouth, eyes/skin, drowsy, constipation,
Alternatives: solifena-cin; tachycardia, abdominal pain, urinary retention,
oxybutynin (more SE unless oedema, sinusitis, weight gain, glaucoma ppt. Avoid in
transdermal) glaucoma + myasthenia.
Topical oestrogens Post-menopausal urgency, f + nocturia.
Mirabegron (3 agonist) Consider only if anti-M C/I. S/E: tachycardia. Caution:
renal / hepatic impairment. C/I: severe HTN.
Botox If all of the above fails
Percutaneous posterior tibial N If all else fails and Botox not wanted. Delivers
stimulation (12q1week, ½ h) or via neuromodulation to S2,3,4 = inhibit reflex detrusor
transcutaneous stimulation contraction
Surgery = “clam” ileocystoplasty / Reserved as last resort. Bladder bisected, open like
enterocystoplasty clam (bivalve), 25 cm ileum sewn in.
Urology
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ESSENTIAL UROLOGICAL SURGERY
 TURP
1. Definitive/surgical of BPH: TURP indicated when conservative Tx fails, or
recurrent UTIs, stones, haematuria, or renal insufficiency.
 Involves using cutting diathermy wire loop + resectoscope that strips
periuretheral hyperplastic prostate  chips of prostate drift into
bladder. Landmark: verumontanum. Arrest haemorrhage post-TURP
by tension (swab tying around catheter or taping cath to abdomen).
 TUR syndrome – hyponatremia  confusion and seizures (cerebral
oedema). Secondary to prolonged operation  irrigation with glycine
(hypotonic  lyses RBCs  clear view of prostate)  high
hydrostatic pressure of the irrigation pump forces uptake of fluid into
prostatic plexus. Glycine does not conduct electricity, hence used for
the diathermy.
 Retrograde ejaculation (100%), possible ED, clot retention, minor
haematuria, strictures.
 TURBT (diathermy)
1. If muscle wall not involved; if involved (i.e. > T2)  cystectomy + ileal
conduit, XRT, MVAC chemo regime.
 Suprapubic catheterisation
1. Ensure bladder palpable suprapubically (dull to percussion and non-pulsatile)
2. Previous midline scars = risk adhesion (check w US)
3. Infiltrate skin w LA 3 cm above pubic symphysis in direction of sacrum –
until aspiration shows urine
4. Apply artery forceps to needle at skin level as depth guide.
5. Make 5mm incision in skin w No. 15 blade
6. Advance SPC with is trocar in same direction until 2-3 cm deeper than depth
measured on needle.
7. Remove trocar, connect urine drainage bag, secure cath by inflating balloon,
or suturing collar to abdo wall.
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PATHOLOGY (ADULTS)
URINARY TRACT CANCERS
Pathology Features
Renal cell Incidence: #1 1o renal tumour; ~ 55 y (most
CA common kidney tumour actually from mets =
multiple, small); 15% HD develops RCC
Sex: ♂:♀ ≈ 2:1
Aetiology: PCT epithelium – necrotic +
cystic + bloody, solitary, upper pole. Main
RF: smoking
Path: spread haematogenously (thrombus) as
well as paraaortic LN (MC lung > colon)
SiSx: 10% triad – haematuria (MC) +
palpable mass + flank pain; paraneoplastic
syndromes (polycythemia – EPO, HTN –
renin, hypercalcaemia – PTHrP, Cushing –
ACTH, hypoglycaemia – insulin) ; left-sided
varicocele (LTV  LRV)
W/U and management
Tests: BP, FBC, ESR, U+E, ALP (bony
mets?). Urine = RBCs, cytology. Image =
US, CT/MRI, IVU (filling defect +/-
calcification); CXR = cannonball mets
Mayo prognostic risk score (SSIGN) –
stage, size, grade, necrosis
Tx: Radical nephrectomy (Involves
kidney, adrenal, fat, Gerota’s fascia,
regional nodes).
In general chemo + XRT resistant: use
sunitinib TKI, bevacizumab, sorafenib. 1st-
line with multiple poor-RF =
temsirolimus
Partial if pt requires dialysis post-op < 4
cm, Cr > 2.5. Nephron-sparing good for T1
+ preserve renal function.

Prognosis: 10 y survival 96.5 % (score 0-1)

to 19.2 % (score > 10).

Other types 1. Transitional cell (pelvis)  tx: radical nephroureterectomy

of kidney 2. Oncocytomas – benign (oncocytes = round nuclei + mitos-filled eosinophilic granules)
cancer 3. Angiomyolipomas – benign (hamartomas, can occur with tuberous sclerosis  seizures
+ mental retardation + cardiorhabdomyosarcoma + leaf skin patch)
4. VHL (3p) mutations  HIF  VEGF, PDGF bilateral, multifocal, recurrent RCCs +
renal cysts + CNS tumours + phaeo
5. Wilms tumour – metanephric blastema tumour (hence primitive-looking)  MCC
malignant tumour in children < 5 years. Presents with unilateral flank mass +
haematuria + HTN. Can be syndromic (e.g. WAGR – WT1 (11p); Denys-Drash –
mutations WT1; Beckwith-Widemann – imprinting loss maternal 11p WT2)
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Bladder CA Incidence + Sex: older ♂, transitional cell
(TCC) CA (90% in UK, 1 in 6000, 80% = Tis/Ta/ T1
confined to mucosa)
Aetiology: smoking, aniline dyes, chronic
cyclophosphamide & phenacetin  field
defect = multifocal + recur
Path: normally papillary (cystic +
pedunculated) = low-grade + rarely progress.
Can be flat CIS (malignant cystitis) – high-
grade, dysplastic in situ variant = more
aggressive due to early p53 mutations.
Spread local  pelvic; lymphatic  iliac and
para-aortic nodes; haematogenous  liver +
lungs.
SiSx: painless haematuria that recurs +/-
recurrent UTIs +/- dysuria +/- clot colic.
Tests: cystoscopy w Bx = Dx. Urine =
microscopy / cytology (sterile pyuria); CT
urogram = Dx + staging. MRI or
lymphangiography  pelvic nodes.
Bimanual examination under anaes (EUA)
helps assess spread:
 Tis (in situ), Ta (epi), T1 (LP) = not
felt at EUA
 T2 (superficial mm) = rubbery
thickening on EUA
 T3 (deep mm) = EUA mobile mass
 T4 (invasion beyond) = EUA fixed
Tx: Tis/Ta/T1  diathermy via TU
cystoscopy / TURBT. Mitomycin c +
doxo + cisplatin if multiple small tumours
or high-grade. Intravesical BCG (non-
specific immune response) works just as
well and less S/Es. 5 y survival = 95%.

Prognosis: once penetrate muscle (> T2),
mortality 50% at 5 years. Depends on age at
surgery + pelvic node involvement.
T2-3  radical cystectomy “gold
standard” + ileal conduit to avoid stasis
(avoid UTIs and stones – Ca reabsorption).
Alternative reconstruction = reservoir or
neobladders.

XRT worse 5y rates, salvage cystectomy if

XRT fails but poorer than primary surg.
Post-op chemo = MVAC (MTX, vin,
adriamycin = doxo, cisplatin)
Neoadjuvant = CMV (cis, MTX, vin)

T4  palliative chemo/radio, chronic cath

and urinary diversion to relieve pain
Other 1. Squamous cell CA of the bladder (arise from squamous metaplasia) secondary to
bladder diverticula, chronic cystitis (older women), Schistosoma haematobium (Egyptian male),
tumour chronic bladder calculi.

2. AdenoCA of bladder (glandular proliferation). More commonly secondary (nearby

rectum/prostate direct invasion / met). Risk factors: (1) urachal remnant; (2) cystitis
glandularis (chronic inflammation  metaplasia) e.g. chronic catheterisation in spinal
injury patients in trigone; (3) bladder extrophy.
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CALCULI
 Path: precipitation due to high concentration; stuck at points of narrowing (see anat)
 SiSx: colicky pain from loin to groin (renal angle tenderness) + haematuria +
unilateral flank tenderness, no comfortable positions.
 RF: stasis, chronic UTI, FB, diet, others (idiopathic MCC)
 Tests: urinalysis (1st-line) = blood (90%), MCS, biochem stones. FBC, U+E, Ca2+,
PO43-, glucose (DM increases risk), bicarbonate (v. low in RTA), urate. If recurrent 
metabolic workup + 24 h urinary excretion. AXR + abdo CT = radio-opaque stone +/-
hydro.
 Tx: pain relief via NSAIDs; helps w uretric spasm (do not give opioids – worsens);
remove stone if Cx occur (see bullet point 3 + certain occupations e.g. pilots)
1. Medical expulsive therapy: nifedipine or tamsulosin
2. ESWL / ureterscopy + Dormia basket: S/E of ESWL = renal injury, ↑BP, DM
3. Percutaneous nephrostomy or ureteric stent: infection + obstruction =
urgent intervention (delay kills glomeruli). Also in urosepsis, intractable
pain, impending ARF, obstruction solitary kidney, bilateral obstruction.
4. PCNL (nephrolithotomy): keyhole surgery to remove large + complex stones
 Prevent: drink plenty. Normal Ca2+ intake (low diets cause ↑ oxalate excretion).
STONES FEATURES CAUSES Tx
Calcium oxalate / MCC. Usually MCC = idiopathic hypercalciuria = Hydrochlorothiazide
phosphate adults. hypercalcemia and its related causes must be (calcium-sparing diuretics)
excluded. Also seen in Crohn’s (small bowel + potassium citrate to bind
Oxalate: absorb more oxalate as there is fat calcium  complex form is
envelope/dumbbell malabsorption and fat binds Ca2+; leaving soluble = ↓ urinary Ca2+
crystals oxalate free). Gastric bypass or terminal Low Na+ diet.
Phosphate: wedge- ileum resection (more oxalate absorption in
shaped crystals colon) same effect. Oxalate = pyridoxine + low
Ethylene glycol may also cause this. Vitamin intake can prevent.
C abuse. Hypocitriuria.
Triple (struvite): 2nd MCC. MCC = infection with urease +VE organisms Staghorn calculi in renal
Mg. Ammonium, Presents with e.g. Proteus mirabilis and Klebsiella; urea  calyces act as nidus –
Phosphate MILD flank pain NH3  alkaline urine leads to formation of eradicate pathogen (prevent
(higher up stone that may fill up entire renal pelvis. recurrence). Very large,
Coffin-lid crystals kindey); require surgical removal.
haematuria;
staghorn imaging.
Uric acid 3rd MCC. Hot, arid climates (conserve water and salt via Purely medical. Hydration
= urate + H+ Radiolucent and RAAS  H+ secreted). Low volume urine. and alkalinisation
can be very large; Acidic pH (e.g. chronic diarrhoea). Most (potassium
Rhomboid or usually at distal common stone in patients with gout or citrate/bicarbonate) of urine.
rosette crystals tubule (lowest hyperuricemia (leukaemia, myeloproliferative Allopurinol in patients with
pH) disorders, psoriasis – high turnover). gout.
Ileostomies.
Cystine Rare cause. Cystinuria = PCT defect in reabsorbing Hydration and alkalinisation
Children. COAL: decrease reabsorption of cysteine  of urine to increase
Hexagonal Radiolucent form disulphide bridges with another cysteine solubility of cystine.
(“sixtine”) crystals No history of  cystine = insoluble. Chelate with penicillamine
UTI. May form staghorn calculi. or tiopronin, given with
pyridoxine to prevent Vit
B6 deficiency.
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UTIs
 Patient: dysuria, frequency, urgency, incomplete bladder emptying (LUTS)
 Sudden onset of enuresis or incontinence in children or elderly  bladder infection
 RF: female (shorter urethra); mechanical; DM (glycosuria); neurologic (MS, DM
neuropathy); catheterisation; nephrolithiasis; reflux; pregnancy.
 Pregnancy: progestogens  dilate ureters + renal pelvis  prone to infection
 MCC: E.Coli > Staph saprophyticus (sexually active) > Klebsiella > Proteus
 Tests: MSU urinalysis (LE, nitrites +VE, urine looks cloudy)
 Tx by ABx usually nitrofurantoin; pregnant – avoid Cipro, tetra, TMP, genta – use a
cephalosporin e.g. cephradine.
 Recurrent UTIs – old (cath, incontinence, constipation), young/middle-aged ladies
(wipe wrong way, or post-sex); UTI abnormalities  stasis
 Upper urinary tract infections
 Pyelonephritis  unilateral loin + tenderness, poorly localised, dysuria +
cloudy urine +/- haematuria, pyrexia + tachy +/- sepsis
 USS, CT > IVP/flexi-cystoscopy.
 Complications: pyonephrosis (pus accumulate as PUJ obstructed); perinephric
abscess (pus forced out due to staghorn calculus blocking)  sepsis;
xanthomatous pyelo (when perinephric inflammatory mass partially resolved
 solid mass mimicking malignancy, so often explored and removed).
 Ureteral infections  gonorrhoea + chlamydia.

UT OBSTRUCTION
 May occur anywhere, can be partial or complete, uni or bilateral.
 Classified into luminal (clot, stones, sloughed papilla, tumour), mural (congenital or
acquired stricture, NM dysfunction, schisto), or extramural (abdominal/pelvic mass,
RPF, iatrogenic – post-surgery).
 Unilateral obstruction = clinical silent w normal o/p & U+E (compensation of c/l kid)
 Bilateral  urgent Tx.
 SiSx:
1. Acute upper: loin  groin pain +/- infection or enlarged kidney
2. Chronic upper: flank pain, renal failure +/- infection. Polyuria (loss
concentrating ability)
3. Acute lower: acute retention (often w severe suprapubic pain), often preceded
by BOO-LUTS. Clinically distended, palpable bladder, dull to percussion.
4. Chronic lower: LUTS + distended, palpable bladder + large prostate on PR
 Tests: bloods (U+E, Cr); urine (MCS); image (USS check hydros, then CT for level
of obstruction. Radionuclide imaging for functional assessment).
 Tx: upper  nephrostomy or stent (stent can cause significant discomfort & a-
blockers reduce stent-related pain by ↓ ureteric spasm); pyeloplasty to widen PUJ if
idiopathic PUJ obstruction. Lower  urethral or SPC, then Tx underlying cause.
Beware post-obstructive diuresis after reliving obstruction = temporal salt-losing
nephropathy (Na + HCO3) of few L/d  monitor fluid balance, U+E, weight.
1. Chronic uropathy masks acute retention
 Urology
High yields
2. Chronic uropathy  distal/type I RTA  hyperK+ respiratory compensated
metabolic acidosis
3. Get urgent US.
4. Renal function returns to baseline after catheterisation.
5. Volume out can be as high as 1.5 L
6. Do not be surprised if Cr = 1500!
7. Fluid depletion should be accounted for (replace w 1.26% Na2HCO3)

PROSTATE
Pathology Features
BPH Hyperplasia of stroma and glands,
age-related increase in 5
reductase in stroma 
dihydrotestosterone  androgen
R on stromal + epithelial cells =
hyperplasia in transitional (peri-
urethral) zone.
Hence: LUTS, nocturia, retention
+/- hydro, diverticula + trabeculae
(hypertrophy) +/- microscopic
haematuria. PSA slightly ↑
W/U and management
Tests: MSU, U+E, US (large residual, hydro), R/O
cancer – PSA, transrectual USS
Consider: lifestyle changes + bladder training
Tx: blocker (tamsulosin) relaxes SM and 5-
reductase inhibitor (finasteride) = inhibit DHT
production and hence growth (slow).
 Tamsulosin – drowsy, depress, dizzy, BP ↓ , dry
mouth, ejaculatory failure, extra-pyramidal Si,
nasal congestion, weight ↑
 Finasteride excreted in semen, so warn to use
condom. S/E: impotence, ↓ libido
Definitively: TURP = TULIP when conservative Tx
fails or recurrent UTIs, stones, haematuria, renal
failure. TUIP – less destruction, less risk to sexual
function. Small glands only.

Pre-op consent:
haematuria/haemorrhage,
haematospermia, hypothermia,
trauma/stricture, TUR syndrome,
infection, ED (10%), incontinence
(< 10%), clot retention near
strictures, retrograde ejaculation.
Post-op advice: avoid driving and sex 2 weeks after
surgery. Expect blood in urine. Expect infertility, and
sometimes ED. At first, may need to urinate more – do
not be disappointed but note 8% fail and lasting
incontinence may need repeat TURPs within 8y. If
feverish or dysuria, get sample of urine to doctor.
 Urology
High yields
Prostate MCC male malignancy; increases
adenoCA with age – 80% > 80 years.
RF: +VE FHx (2-3X risk), ↑
testosterone, Afro-cab >
Caucasians > Asians. High sat fat
diet.
Most arise in peripheral  spread
locally to SV, bladder, rectum, via
lymph, via blood (sclerotic bony
lesions)
SiSx: ASx, or LUTS, weight loss,
bone pain.
Prognosis: 10% die in 6 months,
10 % live > 10 years.
Scoring: Gleason  use 2 worst
histological sections and add them
up.
Screening: DRE + transrectal
USS only (PSA useless).
Advice to men seeking PSA
1. Test inaccurate – doesn’t
confer longer life.
2. FP test  need more tests 
more complications e.g.
bleeding/infection
3. 1/3 with high PSA have CA
4. Worried needlessly.
5. Even if cancer found, most die
with, not of cancer.
6. Treatment options + QoL
7. Ultimately, their choice.
Tests: DRE – hard, irregular prostate (loss of median
groove). Dx: PSA (30% normal in small cancers) +
transrectal USS &Bx. Image: XR + bone scan +
CT/MRI. MRI for staging (contrast-enhancing
magnetic nanoparticles increase SN to 90%).
Tx (confined to prostate, intracapsular)
 Radical prostatectomy (< 70 y  excellent DFS) –
remove prostate + prostatic urethra + SV then
vesicouretheral anastomosis
 Obturator lymphadenectomy (if Gleason > 7, PSA
> 10)
 Endopelvic fascia incision to access prostatic apex
+ membranous urethra
 Haemostatic control & division of prostatic plexus
to access membranous urethra (which is divided at
prostate apex)
 Denonvilliers fascia incised at prostatic base to
access vasa and SV
 Bladder neck divided to free prostate; neck
reconstructed to join membranous urethra
 Radical XRT + neoadjuvant & adjuvant hormone
therapy (alternative but no RCTs; can be external
beam or brachytherapy);
 Hormone therapy alone (merely delays – consider
in elderly unfit w high-risk dz);
 Active surveillance (>70 y + low-risk).
 Locally advanced = T3,4 N0M, add neoadjuvant
 Post-op complications (fluids in drain): bleeding,
anastomotic leak (urine), infection, lymphoedema
(LN dissection).
 PSA should drop to 0 after 3 weeks  if not 
BONE scan + ALP to check for met.
Tx (metastatic)
 Hormonal drugs (1-2 y benefit)
 LHRH agonist (goserelin)  abolish
pulsatility and hence gonadotropin release.
 N.B. tumour “flare” when 1st use start anti-
androgen alongside e.g. cyproterone acetate.
 The LHRH antagonist, degarelix is also used
in advanced dz.
 SxTx: analgesia, hypercalcaemia treatment,
palliative XRT for bone mets/spc compression
 Urology
High yields
TESTES & EPIDIDYMIS
Pathology Features
Testicular Excruciating groin pain (but can be referred to
torsion abdominal, T10) + vomit. May mimic urinary
colic. Absent cremasteric reflex, -ve Prehn.
Inflamed scrotum ipsilaterally.
RF: Bell-Clapper testis (suspended by spermatic
cord in a horizontal lie)  some spermatic cord
and all testes invested in tunica vaginalis 
hypermobile & can rotate by its suspensory cord
(c.f. normal testes TV invests anterolaterally)
Intravaginal torsion = twist on its pedicle
(spermatic cord)  obstruction of veins 
congestion  ischaemia  haemorrhagic
infarction. Extravaginal = occurs in infants, newly
descended testis and its investing TV mobile
(testis twist, not the spermatic cord).
Testicular Trauma + tunica albuginea split (if intact =
haematocele/ haematoma). Chronic haematocele = clot hardens
haematoma = mimic tumour.
Testicular Dilatation of pampiniform plexus due impaired
varicocele drainage  bag of worms + subfertility (warm
blood congestion). In middle-aged men, sudden
onset, worry retroperitoneal malignancy.
Testicular Primary: patent processus vaginalis (resolves 1st y
hydrocele of life) – MC, larger, younger men.
Secondary: testis tumour/trauma/infection
Epididymo- Causes: chlamydia (< 35y); E. coli; mumps; N.
orchitis gonorrhoea; TB.
Sudden-onset swelling, dysuria, sweats/fever.
Take 1st catch urine sample + look for discharge.
W/U and management
Doppler only if unequivocal Dx (can
also be misleading) – do not delay
surgical exploration. Window period
is 6 h (90-100% salvage rate). At 24 h
= 0-10 %.
Orchidectomy + bilateral fixation
(orchidopexy) – at surgery expose &
untwist testis. If colour fine, return to
scrotum + suture both of them to
scrotum or create a Dartos pouch.
Hydatid of Morgagni/appendix testis
(remnant of Mullerian duct) torsion  Sx
similar to torsion but out of proportion
pain relative to small area of infarction
(blue dot sign under scrotum); no
consequences.
Explore surgically if persistent + pain.
Tx: incise TA (haematoma) or drain w
repair of TA (haematocele)
Best palpate standing up. Repair by
surgery or embolization.
Aspiration or surgery: plicate TV
(Lord’s repair) or inverting the sac
(Jaboulay’s repair). USS if any
doubt post-aspiration.
<35 y: Doxycycline; if suspect
gonorrhoea: add ceftriaxone IM
>35 y (non-STI): try ciprofloxacin.
ABx should be used 2-4 weeks with
analgesia, scrotal support, drainage of
abscess.
 Urology
High yields
TESTICULAR TUMOURS
1. #1 cancer killer in men aged 25-35. Most testicular tumours are malignant
2. Presentation: painless, hard mass which can feel heavy O/E
3. RF: cryptorchidism ( seminomas), infection, hormonal influences, FHx, Klinefelter.
4. Trauma may make it difficult to detect (but could also make men check more often)
5. USS can help with Dx (seminomas: hypoechoic; teratoma: heterogeneous).
 LDH correlates with tumour bulk (burden). Tumour markers are non-specific.
6. Testicular mass  orchiectomy through inguinal incision (not trans-scrotal  do not want to
disrupt lymphatics, do not want to seed). The excised testes constitutes Tx and Bx
7. Chest + abdo CT to look for retroperitoneal LN involvement + met (usually lungs, liver)
8. Seminoma (40-50%, #1 tumour)
 Highly radiosensitive, chemosensitive  all stages orchiectomy + retroperitoneal XRT.
Chemo reserved for met (BEP = cisplatin, bleomycin, VP-16 = etoposide) – then
surgically resect residual disease.
 Usually localised, spread via lymphatics to para-aortic first. But met late.
 Excellent prognosis.
 Large cells with clear cytoplasm + central nuclei, resembling spermatogonia (fried egg) in
a background of lymphoid infiltrate
 Rarely (10%) produces -hCG. Should NOT have AFP elevation
9. Non-seminomas
 Younger patients and children. Variable sensitivity to chemo. Do not give XRT.
 Tx = orchiectomy + retroperitoneal LN dissection
 Chemo if stage II or greater (BEP). Then surgically resect residual disease.
 Met early.
 Embryonal carcinoma
 Immature, primitive, undifferentiated cells (“embryonal”).
 Haemorrhagic and necrosis (primitive = high cell turnover)
 Chemotherapy = can differentiate into other GC tumours e.g. teratoma
 Very aggressive, early haematogenous spread
 AFP or -hCG may be increased
 Yolk-sac tumour
 MCC testicular tumour in children
 Schiller-Duval bodies – glomerular-like structure
 AFP increased (yolk sac)
 Choriocarcinoma
 Syncytiotrophoblast + cytotrophoblast  -HCG produced
 Spread by blood (exception to the CA rule)
 -hCG  hyperthyroidism & gynaecomastia (subunit ≈ to FSH, LH, TSH)
 Teratoma
 Mature foetal tissue with 2-3 germ cell/embryonic layers
 Malignant in Males (c.f. females)
 AFP + -hCG may be increased
10. Mixed germ-cell tumour  prognosis depends on worst component
11. Non-germ cell (sex-cord) tumours
 Leydig – androgen  precocious puberty in children, gynaecomastia in adult males.
Reinke crystals.
 Sertoli – clinically silent
12. Lymphoma: Older-aged male (>60), often bilateral, usually DLBC
 Urology
High yields
EXTERNAL GENITALIA (MALE)
Pathology Features W/U and management
Phimosis Foreskin occludes meatus. In young boys, causes Circumcision is usually curative, but
recurrent balanitis and ballooning. With time + may require meatotomy +
gentle retraction, may obviate need for metatoplasty.
circumcision. In adults, painful intercourse,
infection, ulceration, associated w balanitis
xerotica obliterans (BXO) aka. Lichen sclerosis et
atrophicus (LSA)  characteristic white ring.
Paraphimosis Occurs when tight foreskin retracted and Ask patient to squeeze glans. Try
becomes irreplaceable = prevent VR = oedema + applying 50% glucose-soaked swab
ischaemia of glans. Can occur if foreskin not  act as osomotic gradient.
replaced after catheterisation. Lidocaine gel + icepack may help.
Dorsal slit/circumcision/aspiration
may be indicated.
Pyeronie’s Asymmetric fibrosis causing bending of penis on Nesbit plication = last resort.
disease affected side during erection. Associated w Alternative: excise plaques & replace
Dupuytren’s contracture w tunica vaginalis patch. May need
penile prosthesis.
Balanitis Inflammation of prepuce (glans = posthitis). ABx, circumcision, hygiene advice
Caused by STIs (or candida if
immunosuppressed). Painful discharge.
Penile CA Very rare. More common in Far East + Africa, XRT + iridium wire if early;
very rare in circumcised. Related to chronic amputation + LND if late
irritation, virus. Presents as chronic fungating
ulcer, bloody/purulent discharge but painless.
50% spread to lymph at presentation.
Priapism Prolonged erection (> 4h) due to corpora Ice packs + external compression.
caveronsum problem. Arterial (high-flow) causes Then: aspirate, inject a agonist
= artery ruptures into lacunar spaces of CC  (phenylephrine) or PO 2 agonist
painless erection; associated w trauma). Venous terbutaline.
(low-flow) causes due to veno-occlusion 
penile ischaemia +/- long-term fibrosis + pain & Last resort = surgical shunt.
impotence.
Fournier’s Necrotising fasciitis of genitalia, s/c skin, and Septic + crepitus.
scrotal perineum (testes protected by ext sperm fascia). IV ABx + surgical debridement.
gangrene RF: DM, steroids, chemo, EtOH abuse. Wound left open to heal by 2o
Underlying cause: variable – GU trauma, ureteral intention.
stricture, perirectal abscess, hydrocele.
Anaerobes (Bacteriodes, Clostridium) &
aerobes (E.coli & enterococcus) produces toxin
and spread across plane. 80% die.