Pathology Vivas (ALL)

FRACS Urology Path Exam
Part 1
Stuff put together by Conrad

Bishop
• What is this?
• What are the features?
• What is the natural history?
• What are the risk factors for recurrence
and progression?
• What is the likelihood of recurrence and
progression of a small solitary TaG1
tumour?
• What is the effect of post op mitomycin?
Low Grade Urothelial Cancer
• Histological Features
• Cellular uniformity
• Polarity of nuclei (oval, all point outwards)
• Minimal disruption of papillary architecture
• Natural History
• Tendency for recurrence and progression
Low Grade TCC
• Risk Factors for Recurrence / Progression
• Factors weighted towards recurrence
o Size >3cm
o Multiple tumours
o Recurrence <12 months
• Factors weighted towards progression
o T stage (T1+)
o High grade
o CIS
• Also
o Squamous differentiation
o Location- trigone, bladder neck
o continuing to smoke
o inadequate resection
o no BCG
Low Grade TCC
• Solitary small TaG1
• Recurrence 31% in 5 years
• Progression 1% in 5 years
• Effect of Mitomycin Post-op

• Decreases recurrence by 40% in 3 years
• Absolute risk reduction 12.5%
o (i.e. NNT = 8 to prevent one recurrence)
• No effect on progression
• Small risk of side effects- fever, UTI, frequency/urge,
extravesical spread (very dangerous)
• What irrigating fluids could you use?
• What is the difference between the use of
water and glycine for resection?
• How do you set up your fluids?
• What are the clinical features of TUR
syndrome?
• What are the causative mechanisms?
• How would you treat it?
TURP
• Irrigation Fluids
• Glycine (monopolar)
• Water (monopolar)
• Saline (bipolar)
• Water
• Hypotonic
• More freely absorbed into blood
• Cytocidal to free tumour cells
• Causes haemolysis when absorbed – hyperkalaemia
• Increased risk of TUR syndrome
• Not suitable for long resections (large tumours, TURP)
TURP
• Glycine
• 1.5% Glycine
• Hypotonic (200mOsm/L)
• Less haemolysis caused than water
• Metabolised to ammonium by liver
• May cause ammonium toxicity
• Use with caution in patients with liver failure
• Setup
• 60cm from top of bag to symphysis pubis
TURP
• Hyponatraemia
• Hypervolaemia/Hypo-osmolarity
• blood brain barrier impermeable to sodium but water
crosses freely leading to cerebral edema which can
trigger cushings reflex (HTN and bradycardia)
• Also causes red blood cell haemolysis
• Hyperglycinaemia
• Glycine is a GABA like inhibitory neurotransmitter
• Causes visual disturbance and transient blindness
• Hyperammonemia
• Glycine is metabolized by liver and kidneys to make
ammonia which can also causes CNS disturbance
TURP
• Clinical features of TUR Syndrome
• Hyponatraemia/hypervolaemia
• Restlessness and confusion
• N+V
• Brain swelling - Hypertension/Bradycardia (cushings
reflex)
• Seizures
• Irrigations
• Hypothermia
• Hyperglycinaemia
• Visual disturbances
• Fluid overload
• Respiratory difficulty, hypoxia
TURP
• Occurs in 2% TURP
• Risk factors
• gland size (>45g)
• intravesical pressures >30mmHg
• Resection time >60min
• Open venous sinuses/capsular perforation increase
risk
• Sympathetic blockage with spinal anaesthetic may
contribute to hypotension
TURP
• Treating TUR Syndrome
• High index of suspicion
• Cease resecting, switch to Saline, IDC
• O2 by mask
• ABG (Na+, O2), formal U&E
• 20-40mg IV Lasix
• Warm patient
• CXR in recovery- APO
• Slow IV Normal Saline
• HDU monitoring (darkened room)
• Check U&E 6 hours
• If not responding
o Repeat 40mg IV lasix
o Diazepam and phenytoin for seizures
o Consider IV mannitol
o Consider slow 200ml 3% saline
• What is this?
• How do you stage it?
Invasive Bladder Ca
• High grade TCC with detrusor muscle invasion
• Staging of Bladder Cancer
• Tx Primary tumour cannot be assessed
• T0 No evidence of primary tumour
• Tis CIS- Malignant cells not crossing BM
• Ta Non invasive tumour
• T1 Invades lamina propria
• T2a Invades inner half detrusor
• T2b Invades outer half detrusor
• T3a Microscopic extravesical extension
• T3b Macroscopic extravesical extension
• T4a Invades prostate, uterus, vagina
• T4b Invades pelvic wall or bone
Invasive Bladder Ca
• Nx Lymph nodes cannot be assessed
• N0 No evidence of lymph node metastasis
• N1 Mets in single LN in the true pelvis (EI, II, Obt, pre-
sacral)
• N2 Mets in multiple nodes in the true pelvis
• N3 Met(s) in common iliac nodes
• M0 No distant mets
• M1 Distant mets (including LNs above aortic bifurcation)
• What is this?
• What is the natural history?
• How do you treat it?
• What is the effect of BCG?
• How does it work?
• What are the side effects of BCG?
• What are the contraindications to BCG?
CIS
• High grade cells
• Pleomorphic
• Loss of polarity
• High nuclear / cytoplasmic ratio
• Nucleoli, clumping of chromatin
• No invasion of basement membrane
• Natural History
• Progression to invasive high grade disease
CIS
• How do you treat it
• Biopsy and fulguration followed by
• Induction and maintenance BCG
• Cystectomy for recurrent CIS
• Effect of BCG
• 80% initial response
• 50% at 4 years
• 30% at 10 years
• Progression: 20% after complete response to BCG
• Recurrence: 80% after TURBT, 30% after BCG
CIS
• Mechanism of action of BCG
• Attenuated mycobacteria
• Binds to tumour cells via fibronectin
• Stimulates immune response via cytokines (IL-2, INF-g)
• Influx of inflammatory cells (NK cells) kills tumour cells
• STRAIN
• BCG stands for Bacillus Calmette-Guerin which is a strain develop[ed form an attenuated strain
of mycobacterium bovis. Other strains have been developed. No one strain has shown
superiority.
• A batch that contains no or very few live organisms would be clinically ineffective.
• Immunosuppresion
• BCG efficacy reduced in immunosuppressed patients but evidence suggests its safe
• Warfarin and statin
• BCG less effective in patients on warfarin and statin drugs. Possible due to inhibiting
fibronectin binding required for bcg entry into the urothelium
• Antibiotics
• Quinolones, rifampicin, isoniazid are all toxic to bcg mycobacteria and may impact
effectiveness.
• Patients receiving bcg do not require antibiotics prior to administration
CIS
• Side effects of BCG
• Early
o UTI
o BCG cystitis (storage LUTS, haematuria, fatigue, low grade fever)
o High grade fever ( >38.5 degrees)
o BCG sepsis (0.4%)
o Skin rash
• Late
o Systemic inflammation
▪ Granulomatous prostatitis
▪ Epididymo-orchitis
▪ Arthritis
▪ Hepatitis
o Contracted bladder
o Ureteral obstruction
CIS
• BCG sepis
• Potentially life threatening event secondary to intravasation of intravesical bcg resulting in
cardiovascular collapse and acute respiratory distress
• Mechanism of sepsis
• Hypersensitivity reaction
• Mycobacterium bovis sepsis
• Clinical features
• Fever >38.5 within 2hr of treatment
• Hypotension/shock
• Risk factors
• Inadequate delay from turbt
• Traumatic catheterization or haematuria at time
• Treatment
• Co-ordinate with infectious disease specialist
• NSAIDS/Fluoroquinolones
• Antitubercular medication – isoniazid, rifampicin for 3-6 months
• Prednisolone recommended for septic shock/hypersensitivity reaction
• BCG sepis
• Different entity
• Refers to disseminated mycobacterial disease in patients treated with BCG with lung and liver
typically involved. But they are haemodynamically stable.
CIS
• Contraindications to BCG
• Within 2 weeks of TURBT
• Active UTI
• Frank haematuria
• Traumatic catheterisation
• Immunosuppressed –relative
• Pregnancy
• Poor performance status, unable to hold BCG
• Prior BCG sepsis
• Severe LUTS
• TB relative indication
• What is this?
• What are the sequelae?
• How is it treated
BXO
BXO (lichen sclerosis)
• Chronic incurable disease
Sequelae
• Small well defined white plaques mainly on external genitalia
• Does not affect inside of vagina (NOTE lichen planus DOES affect inside of
vagina. Typically red and raised not white and flat.
• Itchy and may cause dysuria/dyspareunia
• Meatal stenosis
• Distal urethral strictures
• Phimosis
• Malignant transformation rare (5% SCC)
• Pathophysiology
• Poorly understood, combination genetic and environmental factors
• Treatment
• Topical steroids – potent such as mometasone fumorate 0.1% nocte for
3 months
• Circumcision
• Treatment of stricture disease
• What is this?
• What causes it?
• How does it spread?
• How do you treat it?
Fournier’s Gangrene
• Features
• E. Coli, Group A strep, Staph, Anaerobes
• Speads along fascial planes – more extensive than seen
• Synergistic polymicrobial infection
• Endarteritis obliterans causes ischaemia
• Management
• Fluid resuscitation
• MDT- ICU, ID, physician, endocrinologist
• IV Meropenum and Clindamycin
• IDC
• Urgent surgical debridement
• ICU
• Second look at 48 hours
• What is this?
Bushke - Lowenstein Tumour
• Features
• Verrucous Carcinoma
• Locally aggressive, rarely metastasises
• Usually Ta
• Low grade SCC
• Treatment
• Topical treatments ineffective
• Radiotherapy ineffective, may incite malignant change
• Local excision treatment of choice
• What is the clinical syndrome?
• How is it transmitted?
• What are the manifestations?
Tuberous Sclerosis
• Picture shows adenoma sebaceum
• Autosomal dominant
• TSC1 gene chromosome 9, TSC2 Chrom 16
• Clinical Features
• Urologic
o Renal cysts
o AML’s in 60% (hamartoma)
o Increased risk of RCC (2%)
• CNS
o Hamartomas- brain, retina
o Mental retardation
o Seizures
• Skin
o Adenoma sebaceum – cutaneous angiofibromas that appear in
childhood and are red papules on the face especially on the nasolabial
folds, cheek and chin
o Ash leaf spots on trunk, buttocks (areas of hypopigmentation)
o Shagreen patches (orange-peel textures plaques on lower back)
o Periungual fibromas (flesh-coloured papules)
• Other hamartomas- lung, heart
• What is this?
• What are the predisposing factors?
• Describe the macroscopic features
• Sequelae
• How would you treat it
XGP
• Predisposing Factors
• Nephrolithiasis
• Obstruction
• Infection
• Diabetes
• Microscopic Features
• Chronic inflammation, necrosis, lipid laden foamy
macrophages
XGP
• Pathophysiology
• Stones
• Obstruction
• Infection
• Proteus mirabilis is most common organism with
E.Coli being secondary
• Pathological Features
• Xanthogranulomatous pyelonephritis
• Diffusely diseased kidney
• Cortical destruction
• Dilated calyces
• Fibrosis
• Nephrocalcification
• Plaques (containing lipid laden macrophages)
XGP
• Sequelae of XGP
• Chronic infection
• Prolonged illness
• Anaemia
• Progressive loss of renal function
• Destruction of surrounding organs
• Management
• Rarely cured with antibiotics
• Open nephrectomy, excise local fat
• IV antibiotics 4 weeks prior
• Bowel prep
• What does this show
• Causes
• Grading
Bladder Trabeculation
• Causes
• Bladder outlet obstruction
• High pressure neuropathic bladder
• Grading
• Grade 1 – thin bands
• Grade 2 – thick bands
• Grade 3 – sacculations between bands
• Grade 4 - diverticulae
• What is this?
• What are the histological features?
• What is the macroscopic appearance?
• What causes it?
Malakoplakia
• Chronic inflammatory disease, the etiology of which is uncertain but appears
related to underlying infectious process. Rare disease primarily affecting
genitourinary tract. Diagnosed by biopsy.
• Michaelis-Guttman bodies (owl eye)
• Incomplete erradication of bacteria
• Mineralised bacterial fragments
• Von Hansemann cells
• Large foamy mononuclear cells
• Macroscopic – yellow plaques in bladder

• Caused by chronic infection
• Bladder – self limiting
• May cause obstruction of upper tracts in ureter
Malakoplakia
• Goal of treatment is to stabilize the disease process by controlling UTI
• Optimal antibiotics improve intracellular killing of bacteria by
phagocytes such as fluoroquinolones, trimethoprim/sulfamethoxazole
and rifampin.
• Optimal length of abx unknown
• Surgical excision of malakoplakia lesions should be considered based on
the site affected. Upper tract malakoplakia tends to be aggressive and if
renal parenchyma should is involved should perform nephrectomy. If there
is urethral, bladder or ureteral obstruction, surgical excision or resection
should be considered.
• What is this?
• How is it commonly found?
• What is it associated with?
• What is the malignant potential?
• What is the chance of contralateral
disease?
• How may it be treated?
ITGCN
• Intratubular Germ Cell Neoplasia
• Large clear cells filling tubule
• Absence of spermatogenesis
• Found incidentally during biopsy for infertility

• Associated with intersex disorders, dysgenesis
• Overall incidence 0.8% (same as testicular ca)

• Contralateral testis in 5%
ITGCN
• Progression to Malignancy
• Chance of progression controversial
• 50% BM invasion histologically in 5 years
• Clinical significance unknown, likely much less
• Treatment
• Surveillance (maintain fertility, most ca curable if
develops)
• Orchidectomy
• Carboplatin
• Radiotherapy 20Gy
• What is this?
• Differential diagnosis
Adenomatoid Tumour
• Solid mass in tail of epididymis
• Benign
• Adenomatoid tumour
• Papillary Cystadenoma (VHL)
• Leiomyoma
• Sperm granuloma
• TB
• Malignant
• Adenocarcimoma
• Metastasis
• What is this condition?
• What are the urological manifestations?
• What are the non urological
manifestations?
• What is your initial management?
Prune Belly Syndrome (Eagle-
Barrett syndrome)
• Upper tract
• Dysplastic kidneys
• Mega ureter
• VUR
• Lower tract
• Abdominal testes
• Large hypotonic bladder
• Prostatic hypoplasia
• Megalourethra or urethral atresia
• Non Urological
• Abdominal wall defect
• Pulmonary hypoplasia --> chronic kidney disease
• Cardiac defects
• Intestinal malrotation
• Club foot, scoliosis
Prune Belly Syndrome
• Etiology
• Exact cause unknown
• Possible theory – abnormal bladder during fetal development.
Accumulate urine in distended bladder leading to hydroureter and
hydronephrosis
• Enlarged bladder causes abdominal musculature wasting which may
reduce intraabdominal pressure and the force required to push the testis
into the inguinal canal
• There is reduced urine production leading to oligohydramnios and
pulmonary hypoplasia
• An alternate theory is the muscle deficiency and urinary abnormalities
have a common cause
Initial treatment
• Neonatal ICU
• Manage respiratory failure
• Percutaneous suprapubic tube
• Prophylactic antibiotics
• US
• Check creatinine day 2
• VCUG if abnormal
• Refer to tertiary centre
• What sort of stone is this?
• What is it likely composed of?
• Chemical reactions
• What is it associated with?
• How does it present?
• How do you treat?
Staghorn Calculus
Struvite (Magnesium Ammonium Phosphate)
• (others include uric acid, oxalate, cystine)
• Associated with UTI and Alkaline urine
• Urease splitting oragnisms (Proteus, Klebs,
Pseudomonas)
• Presents with recurrent UTI’s, Non specific, renal failure
• High mortality rate 28% 10 years (Singh)
• Treat infection with antibiotics
• Determine renal function with MAG3
• PCNL plus ESWL to mop up (if functioning)
• Nephrectomy (if poorly functioning)
Staghorn Calculus
• Chemical reaction:
• Urea + water
• Ammonia + carbon dioxide
• (high pH)
• Ammonium + bicarbonate
• Hydrogen Phosphate dissociates
• Physiological magnesium
Part 2

Bishop
• Staging of Prostate Cancer
2010 TNM Staging
• TX Primary tumour cannot be assessed
• T1 Clinically unapparent tumour neither palpable nor visible by imaging
o T1a <5% of TURP
o T1b >5% of TURP
o T1c Non palpable, TRUS
• T2a Palpable < half one lobe
• T2b Palpable all one lobe
• T2c Palpable both lobes
• T3a Extracapsular extension
• T3b Seminal vesicle involvement
• T4 Bladder neck, sphincter, rectum, levator, pelvic wall
• Nx Regional LNs cannot be assessed

• N0 No positive regional LNs
• N1 positive regional LNs
• M0 No distant mets
• M1 Distant mets
o M1a Non-regional LNs
o M1b Bone
o M1c Other sites with/without bone
• What syndrome is this?
• What are its features?
• Implications for fertility
Klinefelters Syndrome
• Karyotype 47XXY
• Non-dysjunction during meiosis (sporadic)
• 1 in 1000 male births
• Features
o Hormone profile: low testosterone, high FSH, normal/high LH, high
estradiol
o Clinical manifestations
▪ Urological (sclerosis of seminiferous tubules)
▪ Small firm testes
▪ Azoospermia
▪ Non-urological
▪ Hypogonadism- tall, thin, lack secondary sexual
characteristics
▪ Gynaecomastia (high levels of oestrogen)
▪ Increased risk of breast ca and extra-gonadal germ cell
tumours
• Fertility issues
o 50-75% have viable sperm retrieved for ICSI
o Testosterone in selected cases- treats hypogonadism but worsens
fertility
• What is this?
• What is the life cycle?
• What are the urological implications?
• How do you diagnose it?
• What is the treatment?
Schistosomiasis
• Histological features
• Schistosomiasis haematobium
• S. Haematobium ova in detrusor
• Ova terminally spined
• Surrounded by granuloma
• Endemic in Northern Africa, Middle East
• Immature S.Haematobium in fresh water
penetrate unbroken skin
Life Cycle
• Ova excreted from human urine and faeces
• Fresh water Miracidium hatched
• Miracidium enter Bulinus snails
• Form Sporocysts in snails – asexual reproduction
• Cercaria released back into water
• Cercaria penetrate unbroken skin
• Mature to Schistosome worms, live in portal vein
• Adult Schistosomes migrate to perivesical veins
• Lay Ova in bladder – sexual reproduction
Urological Manifestations
• Lower tracts
• Chronic cystitis- storage LUTS, haematuria
• Bladder wall thickening and calcification
• Squamous / adenomatous metaplasia
• SCC, TCC, Adenocarcinoma
• Sandy patches – inactive disease
• Small contracted bladder
• Upper tracts
• Ureteric stricture (distal > proxiamal)
o Ureteric dilation or obstruction
o Chronic pyelonephritis
o Stones
o Renal failure
Diagnosis and Treatment
• Diagnosis
• Ova (terminally spined) in urine 10am-2pm
• Bladder biopsy / resection
• Serology Western Blot
• Radiologically – egg shell bladder
• Treatment
• Acute infection – Praziquantel for 1 day (4 doses)
• Surveillance for Ca
• Surgery for complications, Ca
• What is this?
• What causes this?
• What is the pathophysiology of renal
failure?
Hydronephrotic Kidney
• Caused by urinary tract obstruction
• Pathophysiology
• 0-1.5 hours
o Ureteral pressure increased
o Ipsilateral RBF increased
• 1.5- 5 hours
o Ureteral pressure increased
o Ipsilateral RBF decreased
o Contralateral RBF increased
• 5-18 hours
o Ureteral pressure decreased
o Ipsilateral RBF decreased
o Contralateral RBF increased
• 3-7 days dilation of collecting ducts
o Increased tubular pressure
o Decreased capillary perfusion
o Local ischaemia
• 12 days papillary necrosis and acute inflammation
• 16 days fibroblasts and collagen
• 3 weeks cortical atrophy
• 6 weeks diffuse scarring
• Risk factors
• Premalignant conditions
• Staging of penile cancer
• Indications for inguinal LND
Risk Factors for Penile Ca
• Increasing age
• Uncircumcised
• Chronic inflammation- phimosis, recurrent
balanitis, irritants
• Premalignant conditions (eg. BXO 3% vs 0.2%)
• Multiple sexual partners, HPV 16, 18
• Smoking
• Psoralen and UVA (used to treat psoriasis)
Premalignant Conditions
• CIS
o Erythroplasia of Queyrat (on glans)
o Bowens disease (on shaft)
• BXO
• Leucoplakia
• Cutaneous horn
• Condyloma (inc Bushke – Loweinstein tumour)
“2 red, 2 white, 2 horny”

Penile Ca Staging- clinical
Tx Primary tumour cannot be assessed
T0 No evidence of primary tumour
Ta non-invasive verrucous carcinoma
T1 Invasion in to lamina propria
T1a low grade and no LVI
T1b high grade or LVI
T2 Corpora spongiosum or cavernosum
T3 Urethra
T4 Adjacent structures
Nx Regional LNs cannot be assessed

N0 No palpable regional LNs
N1 Single palpable mobile inguinal node
N2 Multiple or bilateral palpable mobile inguinal nodes
N3 Fixed or pelvic nodes
M0 No distant mets
M1 Any metastases
Indications for Inguinal LND
• Palpable nodes
• Inpalpable nodes with high risk disease
(EAU guidelines)
o High grade
o T2 or above
o LVI
o Perineural invasion
o Basaloid or sarcomatoid type SCC
• What is the likely diagnosis?
• How is it diagnosed clinically?
• What are the non-urological features?
• What are the renal complications?
• How do you classify cystic diseases of the
kidney?
Adult Polycystic Kidney Disease
• Ultrasound Criteria
• Bilateral renal cysts
• 3 or more cysts in liver, pancreas, spleen
• Note number of cysts increases with age
• Family history spanning 3 generations

• Genetic testing PKD genes chromosomes 4,16
• Incidence 1 in 1000
• PKD1 (Chrom 16) or PKD2 (Chrom 4) gene defect
Adult Polycystic Kidney Disease
• Non-urological features
• Multiple cysts in liver, spleen and pancreas
• Berry aneurysms, low risk of subarachnoid
haemorrhage
• Mitral valve prolapse
• Diverticular disease
• Renal complications
• Cyst– infection, haemorrhage, rupture
• Hypertension
• Progressive renal failure – dialysis in 50’s
Juvenile Polycystic Kidney
Disease
• Autosomal recessive
• Variable penetrance and clinical spectrum
• Usually diagnoses in neonates
• Most die in first year – respiratory failure
• Bilateral renal cysts
• Congenital hepatic fibrosis
• Portal hypertension
• Pulmonary hypoplasia
• ESRF and dialysis
Classification of Cystic diseases
• Genetic
• Autosomal dominant polycystic kidney disease
• Autosomal recessive polycystic kidney disease
• Juvenile polycystic kidney disease
• VHL
• Tuberous Sclerosis
• Non-Genetic
• Congenital
o Medullary sponge kidney
o Multicystic dysplastic kidney
• Acquired
o Multiple simple cysts
o Multilocular cystic nephroma
o Aquired multicystic disease – dialysis
o Cystic RCC
• What is this?
• What are the causes?
• How is it treated?
Urethral caruncle
• Urethral caruncle is an inflammatory lesion of the distal
urethra usually in post-menopausal women
• Causes
o Post-menopausal
o Chronic irritation
• Treatment
o Medically- analgesia, topical oestogen, sitz baths
o Surgical- excision required if diagnosis in doubt (?cancer)
▪ Lesion excised- leave catheter or stay sutures
• What is this?
• Discuss the aetiology
BPH
• Aetiology
• Age- prostate tends to enlarge with age
• Hyperplasia of all cellular elements- fibrous stroma, smooth muscle,
epithelial glands
• BPH mostly due to failure of apoptosis.
• Androgens
o dihydroxytestosterone (DHT)- stimulates proliferation of prostatic cellular
elements and also inhibits cellular apoptosis
• Growth Factors
o Fibroblast growth factor (FGF) stimulates fibroblast production in the
stroma
o Epidermal growth factor (EGF) stimulates glandular formation
o Insulin like growth factor (IGF) augments the effect of DHT
o TGF-B may exert an inhibitory effect on cell proliferation and is
downregulated in BPH
• Stromal-Epithelial Interactions
o New gland formation in the hyperplastic prostate may be due to the
reactivation of an embryonic process of the prostatic stroma inducing
epithelial proliferation
o ↑ alpha-1 receptors in prostatic stroma and bladder neck with age → ↑
smooth muscle tone and contraction- contributes to dynamic obstruction
• Familial component
• What is this?
• What sort of upper tract stones do they
form?
• What are the mechanisms of their
formation and which bacteria?
Struvite
• Crystals
o Coffin lid shaped crystals
o Struvite or Magnesium Ammonium Phosphate
• Classical stone: Staghorn calculi
• Causes
• Recurrent UTIs with Urease splitting bacteria
o Proteus
o Klebsiella
o Pseudomonas
o Staph
o Serratia
• Produces alkaline urine
• What is this?
• Describe normal spermatogenesis
• What factors are required for normal
spermatogenesis?
Maturation Arrest
• Features
• Late arrest most common (spermatogonia – spermatocytes)
• Numerous spermatogonia
• Minimal spermatocytes
• No spermatozoa
• Causes of Maturation Arrest

• Hypogonadotrophic hypogonadism
• Hypothyroidism, Cushings syndrome
• Nitrofurantoin
• Chemotherapy, radiotherapy
• Orchitis
Maturation Arrest
• Normal Spermatogenesis
• Takes 74 days to complete
• From BM to lumen of seminiferous tubules
• Mitosis - spermatogonia → primary spermatocytes

• Meiosis - 2 meiotic divisions
Primary spermatocytes → secondary spermatocyte
Secondary spermatocytes → spermatids
• Spermiogenesis
Spermatids → spermatozoa
• Maturation in the epididymis
Maturation Arrest
• Normal Control of Spermatogenesis
• Intact hormonal axis (FSH)
• High intraluminal concentration testosterone
• Temperature 34 degrees
• Functioning sertoli cells for nourishment
Prostate Specific Antigen
• What is PSA?
• What does it bind to in the serum?
• What is the use of the free:total ratio for
PSA in the range 4-10 ng/ml?
Prostate Specific Antigen
• Prostate Specific Antigen
• 34 KiloDaltons glycoprotein which is a serine protease
• Member of Kallekrein family
• Made exclusively by prostate
• Prevents coagulation of sperm
• Binds in serum to:
o Alpha1-antichymotrypsin
o Alpha1-antitrypsin
o Alpha2-macroglubulin
• % free PSA relates to cancer risk
• PSA 4-10 ng/ml = 40% risk of prostate cancer
With % free < 10% 56%
10-15% 28%
15-25% 20%
>25% 8%
• What is this?
• When do you fix?
Cryptorchidism
• (Depending on age of child, could be right scrotal
mass! But that is another question)
• Failure of descent of testis from abdo to scrotum
• Occurs 3% males
• 2/3 unilateral
• Most decend spontaneously within 3 months
• Sequelae
• Infertility
o progressive loss germ cells after 6 months
o Higher the testis, greater the germ cell loss
• Testicular Ca – 40x risk
o Higher the testis, greater risk of malignancy
o Effect of orchidopexy on developing Ca unknown
• Higher rates of torsion and herniae (patent PV)
• What Gleason score is this?
• What is Gleason score and how is it determined?
Gleason Score
• Gleason 3+3 (Separate glands, architecture preserved)
• Gleason score
• Definition
o Classifies the low microscopic appearance of prostate cancer with a
score from 1-5 according to the degree of loss of normal glandular
architecture. (i.e. not cellular like most grading systems). 5 being most
poorly differentiated
• Grades
o Grade 1- small, well-formed, closely packed uniform glands
o Grade 2- larger, well-formed, slightly spaced uniform glands
o Grade 3- separate irregular glands with cells invading connecting
stroma
o Grade 4- fused very irregular glands
o Grade 5- sheets of cells, no glands
• Gleason score is sum of the two most prominent Gleason
patterns (total of 10)
o Primary- majority tumour >50% of pattern
o Secondary- next most prominent pattern <50% but >5% of tissue
o Tertiary- small component of higher grade cancer (usually 5)
Adrenal Mass
• What is the differential diagnosis of an
adrenal mass?
• What initial and further biochemical tests
would you order?
• How does imaging help?
• How do you distinguish a benign from a
malignant adrenal mass?
Adrenal Mass
• Functioning 20% vs non-functioning (80%)
• Benign vs Malignant (<4cm 2%, 4-6cm 6%, >6cm 25%)
• Benign
o Functioning adenoma
▪ Aldosterone- Conn's
▪ Cortisol- Cushings
▪ Catecholamines- pheo
o Nonfunctioning
▪ Adenoma
▪ Myelolipoma
▪ hemorrhage in to a cyst
▪ Inflammatory (infection, granuloma (TB/sarcoid))
▪ Adrenal nodular hyperplasia
• Malignant
o Primary
▪ Adrenocortical carcinoma (75% functioning if >5cm)
▪ Pheochromocytoma
o Secondary
▪ lymphoma
▪ metatastasis- GI, lung, breast, kidney, melanoma
Biochemical investigation
• Initial tests-
o 24 hour urine catecholamines- pheo
o Serum U&E- High Na+, low K+ for Conn’s
o Serum cortisol- elevated in Cushing's
• If diagnosis unclear or further suspicion of

underlying disease:
o Plasma renin / aldosterone ratio- low in Conn's
o 24 hour urine cortisol –Cushing’s Syndrome
o Low-dose dexamethasone suppression test- (suppressed if
normal, not suppressed in Cushing's syndrome)
o High-dose DST- suppresses cortisol in Cushing's disease, not
adrenal adenoma
o serum metanepfrines and 24 hour urine catecholamines- pheo
Imaging
• MRI Abdomen- imaging of choice
o Features suggestive of cancer
▪ irregular, heterogenous, necrosis, calcification
▪ "chemical shift MRI"- high signal intensity on T2 with
minimal dropout of signal on out-of-phase T1
o phaeochromocytoma will have significant signal intensity on T2
• CT Abdomen
o Features suggestive of cancer
▪ Irregular, heterogenous, necrosis, calcification
▪ contrast enhancement with initial attenuation >15
Hounsfield units (ie not fat which is adenoma) on non-
contrast scan to >25 with contrast
▪ lack of contrast washout on delayed scan (>60%) is more
suggestive of adrenal cancer
• MIBG- if suspect phaeochromocytoma- extra-adrenal
disease (10%), bilateral (10%)
• What is this?
• With what genetic condition are they
associated?
• When do you treat and why?
Angiomylolipoma
• Histological features
o Fat globules
o Large vessels
o Smooth muscle
• Associated with Tuberous Sclerosis

o 20% pts with AML have TS, 60% of TS pts have AML
• Indications for treatment- embolize

• Pregnancy or women considering pregnancy
• Risk of retroperitoneal haemorrhage increases >4cm
• Symptomatic
Part 3

Bishop
• What causes it?
• How is it treated?
• Condition
o Scrotal elephantiasis
o (Often with synergistic bacterial infection with Wolbachia)
• Causes
o Filariasis= parasitic disease caused by nemotodes (round
worms)
o Can be classified as lymphatic or non-lymphatic
o Lymphatic- Wuchereria Bancrofti- Tropics
▪ occupy the lymphatic system and lymph nodes leading to
obstruction due to worms and immune reaction
o Non-lymphatic- Onchocerca volvulus- Africa
▪ Mostly causes African river blindness (inflammation in eye)
• Life cycle
o Definitive host
▪ human
o Vector
▪ Mosquito (W.B.)
▪ Black fly (Onch)
• Treatment
o Albendazole and ivermectin
o Plus doxycycline for synergistic bacterial infection
o World wide eradication program aim for completion in 2020
• What is the condition?
• What are the urological manifestations?
• What are the non-urological
manifestations?
Bladder Exstrophy
• Urological features
o Upper tracts
▪ Upper tracts usually normal
▪ May have dysplastic kidneys, horseshoe, megaureter
▪ Abnormal distal ureteric course and VUJ
▪ Reflux in 100% (after repair)
o Lower tracts
▪ Bladder exstrophy
▪ Bladder mucosal metaplasia
▪ Wide bladder neck with urethra anterior to prostate
o Genitalia
▪ Ambiguous genitalia
▪ Male- epispadias, shortened corpora
▪ Female- shortened and vaginal stenosis. Cervix enters anterior
vagina. Bifid clitoris.
Bladder Exstrophy
• Non-urological features
o Skeletal defects- Pelvic diastasis
o Pelvic floor defects- flat rather than funnelled
pelvic floor
o Abdo wall defects- triangular fascial defect and
inguinal herniae
o Anorectal abnormalities- perineum is short and
broad with anteriorly placed anus
Bladder Exstrophy
• Initial Management
• Fluid resuscitation
• Wrap defect in plastic
• Antibiotic prophylaxis
• Don’t name child
• Refer to tertiary centre
• What stones are these?
• In what pH urine do they form?
• What condition are they commonly
associated with and how is it diagnosed?
Calcium Phosphate Stones
• Brushite (negatively birefringent unlike uric acid)
• Forms in alkaline urine

• Associated with RTA 1
• Test for RTA:

o U+E hypokalaemia, low bicarb
o 24 hour collection – hypocitraturia
o Urine pH >6.0
o First void urine >5.5
o Acid load test (complete vs incomplete) NH4Cl
Classic findings in RTA type1
• RTA1= impaired secretion of hydrogen ions in distal
nephron
• Complete (acidosis, hypokalaemia) or incomplete
(normal serum pH and K+)
• Features
o Hyperchloraemic metabolic acidosis
o Hypokalaemia (increased aldosterone)
o Urine pH >6.0
o Urolithiasis- Calcium Phosphate (or oxalate) stones
o Nephrocalcinosis
o Renal cysts
o Secondary effects of acidosis and hypokalaemia
▪ Hypocitraturia (most important cause of stone formation),
▪ Hypercalciuria
▪ hyperphosphaturia
RTA type1
• Treatment
o Oral potassium citrate or bicarb
o Survey with periodic KUB, serum Bicarb and
k+
Post Obstructive Diuresis
• What is the definition of post-obstructive diuresis?
• What are the mechanisms?
Post Obstructive Diuresis
Definition= Diuresis >200ml/hr over 2 consecutive hours
Mechanisms:
• Physiological
o Osmotic diuresis (excretion of non-absorble solutes UREA)
o Physiologic diuresis (excretion of fluid and Na+ overload)
o Increased ANP
• Pathological
o Nephrogenic diabetes insipidus- Impaired renal concentrating
ability
o Impaired proximal tubular sodium reabsorption (ATN)
Management of post-obstructive
diuresis
• Initial resuscitation- IV access, fluid resusc
• Admit to HDU for monitoring
• Multidiscplinary- Involve renal physicians with patient care
• Can drink for thirst
• Hourly Urine output and vital signs
o Fluid chase: if UO >200ml/hr → replace half urine output with IV 0.9%
saline over next hour
o Cease fluid chase when urine output <200ml per hour and euvolaemic
• Twice daily assessment
o Check U+E & Mg twice daily to monitor creatinine and electrolytes
o Clinical assessment- weight, thirst, mental state, tissue turgor, mucus
membranes, JVP
• Replace sodium, potassium, Mg and bicarb IV as required
• Consider dialysis if worsening renal impairment or electrolyte
disturbance
• Physiologic diuresis rarely lasts more than 48 hours (pathological
>48hours)
• What is this?
• Describe the grading system of
these cancers.
Clear Cell RCC
• Numerous clear cells
• Delicate fibrovascular stroma
• Fuhrman grade 1
• Fuhrman grading
o Grading system of clear cell and papillary RCCs
o Sarcomatoid = grade 4
o Tumour is assigned highest identifiable grade
o Based on nuclear characteristics (low → high grade)
▪ Size (small → large)
▪ Contour (smooth → irregular)
▪ Nucleoli (absent → present)
• What is this?
• Can they conceive?
Sertoli Cell Only
• No germ cells
• Wind swept appearance of sertoli cells. Normal Leydig
cells.
• Causes:
o Hypogonadotrophic hypogonadism
o Chemotherapy
o Radiotherapy
o Viral orchitis
o Cryptorchidism
o Y chromosome deletions
o Kleinfelters
• Fertility
o Sperm can be retrieved in 25-50% of patients
o Can do sperm retrieval and ICSI
• What is the likely organism?
• What constitutes a positive MSU?
• What is the sensitivity?
• What are the routes of infection?
• How does E.Coli survive in the bladder?
• What are the host defences?
• What are risk factors for UTI’s
UTI’s
• Organism
o Gram negative rod – E.Coli
• Definition of UTI
o Woman: Symptoms + >105 colony forming units/ml in
MSU
o Man: symptoms + >103 colony forming units/ml in
MSU
• Sensitivity
o 90% sensitivity with above. Other 10% <105 cfu/ml
• Route of infection
o Ascending – bowel, vaginal and skin reservoirs
o (NB- haematogenous spread for staph aureus and
candida)
UTI
• E.Coli virulence features:
o Bacterial adherence to urothelium via pilae
o Fimbriae
o Adhesin
o O Antigens
o K Antigens
UTI
• Host defences
o Long urethra in males
o Acidic vaginal pH (premenopausal)
o Regular flow of urine
o Acidic urine
o Hyperosmolar urine
o Urinary gylcoproteins (Tamm Horsfall protein, GAG)
o Intact immune system
o Local – IL secretion by urothelial cells
o Blood – circulating neutrophils, antibodies
Risk Factors for UTI
• Female sex (short urethra)
• Sexual activity
• Use of spermicidals (vaginal alkalinisation)
• Post menopause (vaginal alkalinisation)
• Diabetes (glucose, reduced immunity)
• Iatrogenic- IDC, instrumentation
• BOO
• Neuropathic bladder
• Anatomical anomalies (diverticulum, ureterocoele)
• Immunocompromised
• Institutionalised
• Decreased mobility
• What is this?
• What are the risk factors?
• How would you manage?
• What is the effect of BCG?
Papillary High Grade urothelial
cancer
o Bladder chip with high grade TCC (TaG3)
o Cellular and nuclear pleomorphism
o Loss of polarity of nuclei (rounded, in different directions)
o Disruption of architecture, disorganised
o Prominent nucleoli and clumped chromatin
• Risk Factors
o Smoking
o Occupational exposure to aromatic amines (dyes, textiles)
o Benzene
o Radiation
o Cyclophosphamide
o Other- Chronic inflammation/ infection (more likely SCC but can
cause TCC)
High Grade TCC
• Management
o Re-resect in 4-6 weeks (40% understaged)
o Check upper tracts with CT IVP
o BCG induction and maintenance
▪ 6 week induction
▪ 3 week maintenance (3, 6, 12 months then 6 monthly 3years-
SWOG)
• Effect of BCG
o Reduces recurrence by 40%
o Reduces progression by 27%
o Need maintenance to have effect on progression
• What do the images show?
• What is the composition?
Bladder Calculi
• Multiple bladder calculi
• Ammonium acid urate (smooth)
• +/- calcium oxalate (jackstone / spiculated)
• Causes:
o Bladder outlet obstruction
o Stasis – neuropathic bladder
o Foreign body (IDC, staples, sutures)
o Migrant stones from upper tracts
o Anatomical (diverticulum, ureterocoele)
o Recurrent infections / sediment
o Augmentation cystoplasty – bowel mucosa
o Primary idiopathic calculi in children
• Describe Virchow’s triad
• Risk factors for DVT
• Prevention of post op DVT
• Investigation and management
• Sequelae of DVT
Deep Venous Thrombosis
• Virchow’s Triad
o Stasis
o Endothelial injury
o Hypercoagulability
• Risk Factors
o Obesity
o Smoking
o Immobility
o Dehydration
o Post op (hypercoagulable) esp abdo, pelvic
o Malignancy
o Pelvic mass
• Prevention
o Minimise operative time
o Hydration
o TEDS
o Prophylactic heparin / clexane
o Early mobilisation
• Diagnosis
o High index of suspicion
o Red hot painful swollen leg
o Duplex doppler studies
o D-Dimer of no use post op (not specific)
• Management
o Involve physicians
o Below knee – aspirin
o Above knee – full anticoagulation
o IVC filter if contraindication to anticoagulation
o Monitor progress with duplex doppler
o Long term TEDS
• Sequelae
o PE
o Post thrombotic leg syndrome
• What is the likely disease?
• Associations
• What are the pathological mechanisms?
• What are the clinical features?
• How do you evaluate it?
• How is it best treated?
Peyronie’s Disease
• Peyronie’s= Fibrous plaque in the tunica
albuginea of the corpora cavernosa
• Associations
o Trauma
o Strong familial component
o Dupytrens contracture
o Plantar fascitis
o Autoimmune disease
Peyronie’s Disease
• Pathophysiology
o Unknown aetiology
o Tunical injury may be precipitating cause
o Injury at site of septal insertion
o Acute inflammatory reaction
o Migration of fibroblasts forms plaque
o Poor tunical blood flow inhibits remodelling
o Scar contraction causes deformity
o Calcification of plaque
Clinical Features of Peyronies
• Inflammatory Phase
o Lasts up to 12 months
o Pain (+ with erections)
o Progressive deformity, induration
o Erectile dysfunction
• Chronic Phase
o Usually after 12 months
o Pain subsides
o Stable deformity
o Calcification of plaque
Evaluation of Peyronies
• History
• Penile injury
• Duration of deformity ?progressing
• Painful erections
• Ability to have intercourse
• Examination
• Palpate for plaque
• Photo of erection +/- intracavernosal injection
• Investigations
• US to document presence and location of plaque
Treatment for Peyronies
• Acute phase
o Surveillance with simple analgesia
o Vitamin E cream/orally
o Colchicine
o Tamoxifen
o Intralesional Verapamil
• Late phase
o Indications for surgery
▪ Difficulty with intercourse due to deformity
▪ Stable deformity (absence of pain, stable for 6 mo, >12mo from
onset)
o Consent
▪ Shortening of penis
▪ Residual deformity
▪ Erectile dysfunction
▪ Recurrence
o Surgical Principles
▪ Erect penis – intracorporal injection of saline
▪ Nesbitt – eliptical incision and closure
▪ Plication – no need to incise plaque, reversible if not happy
▪ Vein patch (difficult, results no better)
▪ Penile prosthesis if poor erection
• What is this?
• What conditions could cause this?
• Discuss each condition.
Familial RCC
• Diagnosis
o Multiple RCCs
• Familial conditions causing multiple renal tumours
o VHL (clear cell RCC)
o Hereditary Papillary Renal Cell Carcinoma
o Hereditary Leiomatosis and Renal Cell Carcinoma
o Birt-Hogg-Dube syndrome (chromophobe and oncocytoma- ?
mixed))
o Tuberous Sclerosis (AML and RCC)
o Familial oncocytoma
VHL
• Definition
o Inherited Autosomal Dominant disorder of VHL gene
characterized by haemangioblastomas of the brain, spinal
cord, kidney, and retina
• Pathogenesis
o VHL is a tumour suppressor gene on chromosome 3p25/26
o 1 in 36 000, Mean age of Dx 37
o Absence allows Hypoxia Induced Factor to accumulate and
therefore promoting vasculogenesis
• Classification- people with VHL disease into two
groups:
▪ 1= without pheochromocytoma
▪ 2= with pheochromocytoma
▪ type 2A (with RCC) and type 2B (without RCC)
• Clinical Manifestations
o Urological
▪ RCC (50%)
▪ Renal Cysts (75%)
▪ Phaeo (15%)
Birt-Hogg-Dube Syndrome
• Definition and pathogenesis
o Autosomal dominant cancer syndrome
o BHD gene on chromosome 17p11.2
o BHD encodes ‘folliculin’ (function unknown)
o 25% develop renal tumours
▪ Oncocytoma
▪ Chromophobe RCC (often synchronous and bilateral) (Average number
tumors/kidney = 7!!!)
▪ 40% have multiple tumour histologies on path
o Cutaneous
▪ Benign cutaneous tumors (fibrofolliculomas)- Benign tumors of hair follicles
▪ Skin-colored papules on face, neck, back, upper trunk
▪ Appear in 3rd/4th decade of life
▪ Although helpful for diagnosis, skin lesions do not have to be present
in those with BHD mutation
o Pulmonary
▪ pulmonary cysts 90%
▪ spontaneous pneumothorax 20%
• Treatment
o Nephron-sparing surgery whenever possible
o Beware of pneumothorax in peri-operative period
Tuberous Sclerosis
o Autosomal Dominant Chromosomal Abnormality characterized by
hamartomas in multiple organs
o TSC1 gene Chr 9, TSC2 gene Chr 16
• Epidemiology
o Average age of appearance of first renal lesion = 7.2 yrs
o Urologic
▪ Renal cysts
▪ AML’s in 60% (hamartoma)
▪ Increased risk of RCC (2%)
o CNS
▪ Hamartomas- brain, retina
▪ Mental retardation
▪ Seizure
o Skin
▪ Ash leaf spots on trunk, buttocks (areas of hypopigmentation)
▪ Shagreen patches (orange-peel textures plaques on lower back)
▪ Periungual fibromas (flesh-coloured papules)
o Other hamartomas- lung, heart
• Follow-up
Hereditary Papillary RCC
• Hereditary Papillary Renal Cell Carcinoma (HPRCC)
• Autosomal Dominant
• Trisomy - Defects in chromosomes 7, 17, Y
• Multiple bilateral Papillary RCCs
• Hereditary Leiomatosis and Renal Cell Carcinoma (HLRCC)

• Autosomal Dominant
• Chromosome 1q 42-44
• Cutaneous leiomas
• Uterine leiomas
• Solitary unilateral Papillary RCCs (type 2 collecting duct)
• Very aggressive
• How does monopolar diathermy work?
• What is the difference between COAG and CUT?
• How is a bipolar diathermy different?
• What are the complications of diathermy?
• How can these be minimised?
Diathermy
• Diathermy (technically called electrosurgery) is the
application of high frequency electrical current to
biological tissues to cut or coagulate.
• Monopolar diathermy
o Patient is part of the circuit via electrical pad
o Frequency of current is 300-3000kHz
o Nerves and muscles respond at 50kHz – not affected
o Heat energy formed which cuts or coagulates
o Power setting = Watts (ie 40 COAG = 40 Watts)
Diathermy
• CUT
o Continuous high frequency current
o Sinusoidal waveform – continuous
o Low voltage, High current, less heat dispersion
o Causes rapid tissue heating which leads to explosive vaporization
of interstitial fluid (cut)
• COAG
o Pulsed waveform high frequency current
o Square waveform (on (4%)-off (96% of time)) 50-100 pulses per
second (but each pulse is 300-3000Hz)
o High voltage, low current, more heat dispersion
o Causes slower heating process (tissues cool in ‘off’ period)-
therefore , tissues coagulate.
• BLEND is a combination of the two
Diathermy
• Bipolar Diathermy
• Circuit formed between two electrical probes
• Patient is not part of the circuit
• Square waveform – coagulation only (less heat)
• Safer than monopolar diathermy
• Less power
• Less heat dispersion
Diathermy
• Complications of Diathermy
o Diathermy pad site burn
o Skin burns to flammable prep (alcohol based)
o Damage to surrounding tissues - bowel
o Interference with pacemakers
o Arcing current metal instruments or implants
o Channelling effect with narrow pedicle (penis)
o Ignition of bowel gas (in abdo) or hydrogen (in TUR)
o Smoke inhalation
Diathermy
• Minimising Complications
o Circuit
▪ Adequate contact of electrode pad (with gel)
▪ Full contact, clean skin, hairless, away from scars/bony
prominence
▪ Use on opposite side to THR, on back if bilateral
▪ Avoid metal contact with patient
o Electrosurgical unit
▪includes alarms for ground circuit interruption
▪ Use lowest possible setting
▪ Use bipolar where possible
▪ Ensure cable insulated correctly
o Ensure pacemaker turned off
o Avoid alcohol based skin prep
o Use with caution around bowel
o Experienced operator who is familiar with technique
Part 4

Bishop
• What is this?
Erythroplasia of Queyrat
• Erythroplasia of Queyrat
• CIS involving glans / shaft
• Management
o Biopsy to assess depth
o Topical 5FU, cryotherapy, laser
o Surgery or radiotherapy if resistant
o Moh’s surgery
• What is this?
• What condition is it associated with?
• What is the inheritance and the genes involved?
Tuberous Sclerosis
o Autosomal Dominant Chromosomal Abnormality characterized by
hamartomas in multiple organs
• Epidemiology
o Urologic
▪ Renal cysts
▪ AML’s in 60% (hamartoma)
o CNS
▪ Seizure
o Skin
• Follow-up
• What crystals are these?
• Discuss the condition
• How would you manage someone with
this condition?
Cysteine Stones
• Cysteinuria
o Autosomal recessive condition (Chrom 2 and 19)
o Defect in transport of dibasic amino acids in GIT and kidney
o (cysteine, lysine, arginine, ornithine)
o Cysteine crystallises when supersaturated in acidic urine
o Most cysteine is endogenously produced
▪ Methionine – metabolised to cysteine
o Heterozygotes tend not to from stones (i.e. AR)
• Diagnosis
o Crystals on first morning void
o Urinary cystine >400mg on 24 hour collection
o Sodium nitroprusside test (turns purple with cysteine)
Cysteine Stones
• Prevention- lifestyle
o Fluid hydration
o High citrate
o Low salt diet
o Low methionine diet (meat, poltury, eggs)
• Medical prophylaxis
o Dissolution
▪ Cysteine pKa = 8.3 aim for pH>7.5
▪ Potassium citrate, bicarbonate (Ural)
o Chelating agents
▪ Penicillamine - chelating agent, increases solubility
▪ Captopril - decreases urinary cysteine
▪ (alpha-mercaptopropionlyglycene not available in Aus)
Cysteine Stones
• Treatment of stones
o ESWL usually not effective
o Ureteroscopy and laser – stones <2cm
o PCNL for all other stones
• Surveillance
o Daily urine pH at home (aim >7.5)
o 6 monthly US – high sensitivity for renal stones, less rads
o Aim to treat stones with laser while small
• Describe this slide
• Which renal malignancy is it similar to?
• How do you distinguish them?
• What is their common cell/ tissue of
origin?
Oncocytoma
• Description
o Bivalved kidney
o Exophytic mass in midzone
o Mahogony in colour
o Central scar
o No central necrosis
• Difficult to distinguish from chromophobe

o Cellular and nuclear atypia, Necrosis, haemorrhage, cysts,
calcification, stains positive for Hale’s colloidal iron stain, many
microvessels, few mitochondria = chromophobe
• Both Oncocytoma and Chromophobe arise from
collecting ducts
• How does ESWL work?
• What are the four principle components of
an ESWL machine?
• By what four mechanisms does ESWL
break up stones?
• Describe the three different types of
ESWL
ESWL
• General Principles
o Use of focused shockwaves to break stone
o Shockwaves travel unhindered through water and human soft tissues
without damage
o Shockwaves absorbed by solids/ stones – energy expelled
o Small amount of energy per shockwave
o >1000 shockwaves to disintergrate stone
• 4 basic components
o Shockwave generator
o Focusing system
o Coupling mechanism
o Stone locator- US or fluoroscopy or both
• 4 mechanisms of stone destruction:
• Stone fragmentation incompletely understood
• Tensile forces created by:
o Cavitation (rapid collapse of micobubbles on stone
surface or within stone)
o Compressive fracture (tensile force when wave goes
from low to high density, plus this is the focus point
of maximal energy)
o Spalling (reflecting of pressure wave at back of stone
when wave goes from high to low density)
o Dynamic fatigue
• Great summary at: http://emedicine.medscape.com/article/444554-
overview#aw2aab6b2b1aa
ESWL
• Electromagnetic ESWL
o Most commonly used system today
o Dornier system – used in Australia
• Components:
o Electromagnetic coil
o 2 plates separated by a thin layer of insulation
o Fluid filled tube
o Focussing mechanism (lens or parabolic dish)
ESWL
• Electromagnetic ESWL
o Electrical current passed through coil
o Strong electromagnetic field generated
o Causes rapid separation of two metal plates
o Outer plate pushes on fluid in tube
o Shockwave generated in fluid tube
o Shockwaves are focused with either an acoustic lens (Siemens
system) or a cylindrical reflector (Storz system)
o Fluid tube compressed onto patient
o Low energy to skin (low rates external trauma)
o High energy to focal point (higher rates of haematoma)
ESWL
Types of Electromagnetic ESWL
Acoustic lens Parabolic

ESWL
• Electrohydraulic ESWL
o Original form of ESWL
• Components:
o Discharging Electrode
o Parabolic brass plate
o Fluid chamber
• Mechanism
o High-voltage electrical current passes across a spark-gap
electrode located within a water-filled container. The discharge of
energy produces a vaporization bubble, which expands and
immediately collapses, thus generating a high-energy pressure
wave.
o Focussed by brass plate
o Transmitted by fluid chamber (originally a bath)
o Variable shock strengths, short working life of electrode
ESWL
Electrohydraulic ESWL
ESWL
• Piezoelectric ESWL
o Rarely used
• Components:
o Multiple piezoceramic plates
o Spherical dish (no fluid chamber)
• Mechanism
o Electrical current causes piezoelectric plates to expand
o The alternating stress/strain changes in the material create
ultrasonic vibrations, resulting in the production of a shockwave.
o Focussed by positioning of plates on spherical dish
o Weak shockwaves only – difficulty breaking stones
o No anaesthetic needed
ESWL
Piezoelectric ESWL
• What stones are suitable for ESWL?
• What are the side effects?
• What renal histological changes may
occur?
• What are the contraindications?
ESWL
• Stones suitable for ESWL
o Most types (except too hard or too soft- cysteine, monohydrate,
matrix)
o Stones <2cm
o Stones <1cm if in lower pole calyx
o Renal and ureteric
• Side effects
o External bruising
o Haematuria, dysuria
o Steinestrasse (consider stent if >1cm)
o Sepsis if unrecognised infection
o Renal capsular haematoma (0.5 – 3.5%)
o Major renal injury requiring nephrectomy (very rare)
ESWL
• Acute histological changes
o Venous thrombosis
o Cellular necrosis
o Glomerular rupture
o Collecting duct dilation
• Chronic histological changes

o Diffuse interstitial fibrosis
o Nephron loss
o Calcium and haemosiderin deposits
o Note – clinical dose ESWL causes renal loss of approx 2%
ESWL
• Absolute Contraindications
o Pregnancy
o Anticoagulation, Bleeding diathesis
o AAA, Splenic artery aneurysm
o Infected urinary system
o Urinary obstruction
ESWL
• Relative Contraindications
o Obesity :
▪ May not fit on table or under machine
▪ Adipose tissue absorbs shockwaves – less effective
o Chronic pancreatitis
o Children – effects on developing kidney unknown
o Large stones >2cm or high stone burden
o Cysteine or monohydrate stones (>1000 HU), or matrix stones (too
soft)
o Intrarenal stones or in calyceal diverticulum
o Narrow infundibulum (<5mm width or >3cm long), ureteric stricture,
PUJ obstruction
o Infundibular – pelvic angle >90 degrees
o Anatomical abnormalities (non-dependent pelvis- Horseshoe, high
PUJ)
• Describe the specimen
• What is the differential diagnosis?
• What are the subtypes?
• What tumour markers are applicable?
• What are the pathological prognostic features?
• What is the relapse rate for T1 disease?
• Describe staging for testicular Ca
Seminoma
• Description of Specimen
o Bivalved testis
o Salmon coloured mass (buzz word for seminoma)
o Small areas of haemorrhage
o Abutting rete testis, possibly invading
o No involvement of cord
o Size unknown, probably close to 5cm
Seminoma
• Malignant Primary
o Seminoma
o NSGCT (embryonal, choriocarcinoma, teratoma, mixed)
o Sertoli or Leydig cell tumour (rarely malignant), Granulosa cell
• Secondary
o Lymphoma most common
• Benign
o Granuloma from chronic infection
o TB
Seminoma
• Classic Seminoma (85%)
o 85% all seminomas
• Anaplastic Seminoma (10%)

o This is not a separate entity- this just a poorly differentiated and
therefore more aggressive classic seminoma (not often used
these days)
o 30% seminoma deaths
o Same prognosis stage for stage (more likely metastatic)
• Spermatocytic Seminoma (5%)

o More indolent, low metastatic potential
o Cells resemble sperm in various degrees of maturation
Seminoma
• Tumour Markers
• BHCG - 10% classical seminomas have syncytiotrophoblasts
• AFP - Not elevated in pure seminoma
• LDH - May be elevated with retroperitoneal disease

Seminoma
• Pathological Prognostic Features
o Size >4cm
o Invasion rete testes
o Vascular or lymphatic invasion
o Anaplastic features
• Relapse rate of T1 disease

o 20% lifetime
o Higher if risk factors
o Reduced to 3% with carboplatin or radiotherapy
Seminoma
staging
• What is the definition of priapism?
• What are the possible causes?
• What are the types and how do you
differentiate them?
• Would you do any other investigations?
• What is stuttering priapism and how would
you treat it?
Priapism
• Definition
o An unwanted erection unrelated to, or persisting beyond sexual
stimulation
o (arbitrary 4 hours is often quoted)
• Sequelae
o Cavernosal scarring
o Time
▪ Intervention <8 hours - 50% ED
▪ Intervention >36 hours - 90% ED
Priapism
• Causes of Priapism
o Idiopathic 30%
o Medications
▪ Intracavernosal injections (Papavarine>Trimix>Caverject)
▪ Trazodone, Chlorpromazine
▪ Social drugs- cocaine, alcohol
▪ PDE5 inhibitors
▪ Cessation of warfarin
o Neurogenic
▪ Spinal cord injury/ lesion
o Malignant infiltration
▪ Prostate cancer, lymphoma
o Thrombotic disorders
▪ Leukaemia
▪ Myeloma
▪ Sickle cell disease
o Other
▪ TPN 20% lipids
Priapism
• Initial Management (<2 hours)
o Ejaculate
o Walk around block / up stairs (steal effect from gluteals)
o Cold shower
o Pseudoephidrine 30mg
Further management
• Treat underlying cause if identified
o Ask physician to help treat acute sickle crisis (hydration, alkalinize,
analgesia, oxygen by mask, +/- packed cell transfusion)
• Management is performed in a stepwise sequence until
detumescence
o Cavernosal aspiration and saline irrigation
▪ 19G needles 3 and 9 o'clock in to corpora
▪ Aspirate and flush with 10 mls saline 10x in 10 minutes
o Intracavernosal injection of metaraminol
▪ Monitored cubicle- blood pressure and ECG monitoring
▪ 10mg in 10 ml saline- give 1mg/ 5 mins (total 50 mins)
o Theatre- consent for distal and proximal shunts (risk of ED >60%)
▪ Distal shunt (Corporo-glanular shunt)
▪ Winters shunt - multiple stabs with 18G tru-cut biopsy gun through glans to
corpora
▪ El-Ghorab- 1.5cm incision 1cm distal to dorsal corona- excise 1cm square from tip
of each corpora (beware urethra)
▪ Proximal shunt
▪ Quackels shunt - create fistula between proximal corpus cavernosum and corpus
spongiosum
▪ Greyhack shunt - anastomose saphenous vein to corpus cavernosum (with
Priapism
• Other Investigations- If unsure of cause:
o Blood film
o Serum electrophoresis
o Sickle cell trait
o Urine drug screen
Priapism
• Stuttering Priapism
o Recurrent priapism over extended time
o Treat acute episodes as previously described
• Investigate cause – blood film, electrophoresis, sickle

cell
• Treatment:
o LHRH agonists
o Anti-androgens
o Self injections of phenlyephrine (best for younger patients)
Part 5

Bishop
Adrenal specimen
Adrenal specimen
• What is this?
• What are the screening and definitive
functional studies?
• What imaging would you do?
• What would you give pre-op if functional?
• What is the 10% rule?
• What conditions is it associated with?
Phaeochromocytoma
• Lots of purple = phaeo (basophilic)
• Screening tests in asymptomatic patients-

o 24hr urinary metanephrines- elevated in Pheo
o Serum U&E- High Na+, low K+ for Conn’s
o Serum cortisol- elevated in Cushing's
• If suspicion of underlying biochemical function (symptoms or +ve
screening tests):
o Plasma renin / aldosterone ratio- low in Conn‘s
o 24 hour urine cortisol –Cushing’s Syndrome
o Low-dose dexamethasone suppression test- cortisol not suppressed in
Cushing's syndrome
o High-dose DST- suppresses cortisol in Cushing's disease, not adrenal
adenoma
o Serum and 24hr urinary metanephrines- pheo
Phaeochromocytoma
• Imaging
▪Chemical shift MRI Abdomen
▪ phaeochromocytoma will have significant signal intensity
on T2
▪ Exclude malignancy which will have high signal intensity on
T2 images with minimal signal dropout on out of phase T1
images
▪MIBG- extra-adrenal disease (10%), bilateral
(10%)
• Pre op phenoxybenzamine (until postural drop)

Phaeochromocytoma
• 10% rule
o 10% malignant
o 10% bilateral
o 10% extra-adrenal (and of those 10% are extra-abdominal)
o 10% normotensive
o 10% paediatric
o 10% familial
• Associated with MEN-2, neurofibromatosis-1, familial

phaeo, VHL
• What are the MEN syndromes?
MEN syndromes
• Tumours of the endocrine glands
o Likely when two or more endocrine tumour types, known to occur as a
part of one of the defined MEN syndromes, occurs in a single patient
• MEN1
o parathyroid glands (95% of cases)
o Pancreatic tumours (30-80% of cases)-insulinoma, gastrinoma, vipoma
o anterior pituitary (15-90% of cases)
• MEN2A
o Parathyroid
o Medullary thyroid
o Phaeochromocytoma (>33%)
• MEN2B (also called MEN3)- most severe syndrome (presents <10yo)
o Medullary thyroid cancer (100%)
o Phaeochromocytoma (50%)
o Marfanoid body habitus 80%
o Multiple mucosal neuromata >95%
• Describe the coagulation cascade
• What do INR and APTT measure?
• Which pathways do heparin and warfarin
work?
• What parameters are safe to perform a
TURP?
• What products can assist with
coagulation?
• How do they work?
Coagulation
• Platelet activation
o Primary haemostasis is via platelets
o Circulating platelets bind to exposed collagen
o Form initial plug
• Intrinsic Pathway
o Stimulated by contact of factors to exposed collagen
o Minor role in overall coagulation
o Activation pathway 12-11-9-10-thrombin
o Heparin
o APTT
Coagulation
• Extrinsic Pathway
o Stimulated by Tissue Factor from damaged cells
o Major component of overall coagulation
o Activation pathway TF-7-10-Thrombin
o Warfarin
o INR
• Common Pathway
o Formation of haemostatic plug
o Thrombin - Fibrin
Coagulation
Intrinsic Extrinsic
Coagulation
• Safe Parameters for TURP
o Hb >100
o Plt > 60
o INR <1.3
• Surgicel
o Woven cellulose lattice
o Passive haemostasis
o Provides framework for platelet aggregation and clot
Coagulation
• Floseal
o Active haemostatic agent
o Human thrombin (from pooled human plasma) mixed with bovine
gelatin matrix
o Applied directly to bleeding site
o No fibrinogen – requires contact with blood
• Tisseel
o Active haemostatic agent
o Contains human thrombin and fibrinogen (fractionated from
pooled human plasma)
o Forms fibrin plug independent of patients coagulation
• NB both these products are derived from pooled human
thrombin and therefore have the potential to transmit
virus
• What is the mechanism of action of the
following anticoagulants?
• How can they be reversed?
o Warfarin
o Heparin
o Clexane
o Aspirin
o Clopidogrel
Warfarin
• Mechanism of action
o Inhibits synthesis of Vitamin K dependent coagulation factors (Factors II, VII, IX and X)
o Leads to disruption of the extrinsic pathway
o Effect measured by INR
• Reversal
o Vitamin K given orally or IV, takes >24 hours to work, not suitable if immediate surgery required
o Prothrombinex (freeze dried concentrated human factors II,IX and X)
o Fresh frozen plasma
Heparin
o Binds to antithrombin (AT)
o Potentiates AT inhibition of factor X and thrombin
o Disrupts intrinsic and common pathways
o Effect measured by APTT
• Reversal
o Effect wears off within hours of ceasing heparin infusion
o Protamine may be used if rapid reversal is required
o Fresh frozen plasma may also be used in emergency situations
Clexane (Low molecular weight heparin)

o Similar to heparin
o Binds to and potentiates action of antithrombin on factor X and thrombin
o Disrupts intrinsic and common pathways
o Effects may be measures by anti-factor Xa levels (does not affect APTT)
• Reversal
o Takes 12 hours for coagulation to normalize after last injection
o Protamine only has partial effect on reversal of clexane
o Fresh frozen plasma used in emergency situations
Aspirin
o Irreversible platelet function inhibitor
o Inhibits enzyme cyclo-oxygenase
o Inhibits formation of prostaglandins and thromboxane A2
o Thromboxane A2 required for normal platelet aggregation
• Reversal
o Aspirin has short half life, takes 5-7 days to regenerate normal
functioning platelets
o Platelet infusion may be given in emergency situations
Clopidogrel
o Irreversible platelet function inhibitor
o Binds to platelet ADP receptors
o Inhibits platelet aggregation and cross linking of fibrin
• Reversal
o The effects of clopidogrel are not reversible
o Effect on new platelets occurs even at low plasma levels, functioning
platelet regeneration requires 10-14 days
o Platelet infusion may be given during emergency situations, but
transfused platelets quickly become inhibited
• What is this?
• How do you distinguish it macroscopically from
other renal lesions?
• What condition is it associated with?
• What are the complications of this lesion?
• How do you follow them?
• What is the risk of bleeding?
• What are the indications for intervention?
Angiomyolipoma
• Macroscopically
o White lesion = AML
o Tan lesion = Clear cell or Papillary
o Brown lesion = Oncocytoma or Chromophobe
o Infiltrating/ irregular/ necrosis/ calcification= malignant
• Associated with Tuberous Sclerosis 60%, VHL
• Complications
o Retroperitoneal haemorrhage
o Pain
• Observe with US
Angiomyolipoma
• Risk of bleeding
o <4cm 10%
o >4cm 40%
• Indications for intervention
o Symptomatic
o Size >4cm
o Considering pregnancy
• Angiographic embolisation if >4cm
• What does laser stand for?
• What are the basic components?
• How do they work?
• What are the properties of laser?
• What types of lasers are used in Urology?
• What precautions are required?
Lasers
• Light Amplification by Stimulated Emission of Radiation
• Laser components
1. Gain medium
2. Laser pumping energy
3. High reflector
4. Output coupler
5. Laser beam
Lasers
• Mechanism
o gain medium inside a highly reflective optical cavity
o energy supply to the gain medium.
o cavity consists of two mirrors arranged such that light bounces back and forth,
each time passing through the gain medium.
o Typically one of the two mirrors, the output coupler, is partially transparent. The
output laser beam is emitted through this mirror.
o Light of a specific wavelength that passes through the gain medium is amplified
(increases in power); the surrounding mirrors ensure that most of the light makes
many passes through the gain medium, being amplified repeatedly.
o Part of the light that is between the mirrors (that is, within the cavity) passes
through the partially transparent mirror and escapes as a beam of light.
o The process of supplying the energy required for the amplification is called
pumping.
o The energy is typically supplied as an electrical current or as light at a different
wavelength. Such light may be provided by a flash lamp or perhaps another
laser. Most practical lasers contain additional elements that affect properties
such as the wavelength of the emitted light and the shape of the beam
o The gain medium absorbs pump energy, which raises some electrons into
higher-energy ("excited") quantum states. Particles can interact with light by
either absorbing or emitting photons. Emission can be spontaneous or
stimulated. In the latter case, the photon is emitted in the same direction as the
light that is passing by. When the number of particles in one excited state
Lasers
• Properties of laser
o Monochromicity
o Coherence
o Columnated
Lasers
• Holmium-YAG Laser
o Medium = Holmium (element) with YAG crystals
o Wavelength 2100nm (invisible to eye)
o Travels via flexible silica quartz fibres
o Pulsed waveform
o Absorbed by water
o Penetrance 0.5-1mm safe for surrounding tissues
o Photothermal energy – vaporisation tissue / stones
• Most versatile of all medical lasers, used on stones and

soft tissues
Lasers
• KTP Greenlight Laser
o Medium = Potassium Titinyl Phosphate
o Wavelength 532nm
o Green light spectrum
o Powerful 80-120 Watts
o Penetrance up to 5mm
o Absorbed by haemoglobin, not by water
o Photothermal energy vaporises tissue
o Excellent for larger areas of soft tissue - Prostate
o Does not work for hard stones
o More likely to injure ureter than Holmium
Lasers
• CO2 Laser
o Minimal urological use, fully absorbed in water
o May be used to treat penile skin lesions
• Neodymium-YAG Laser
o Wavelenght 1060nm
o Largely replaced by Holmium and KTP
o Long penetrance 4-5mm
o More dangerous in ureter than Holmium
o Slower to vaporise prostate than KTP
Lasers
• Laser Precautions
o Closed theatre
o Door signed
o No windows
o Safety goggles
o Devoted staff member to laser machine
o Put on standby when not using
o Only discharge under direct vision
o Wait for sediment to clear before re-firing
• What is the diagnosis?
• How would you classify it?
• What are the clinical associations?
• The mother requests circumcision, is this
a good idea?
Hypospadias
• Features
o Abnormal ventral opening of urethra
o Ventral chordae
o Hooded dorsal foreskin
• Commonest male congenital abnormality (1 in 250)

• Failure of folding of urethral mesoderm (prox – distal)
• Possible linked to low androgens or androgen
insensitivity
• Familial component – 8% if father affected, 14% if
sibling
Hypospadias
• Classification
• Based on site of
opening of urethra:
• Anterior
o glans, coronal,
subcoronal
• Middle
o shaft
• Posterior
o penoscrotal / perineal
Hypospadias
• Clinical Associations
o Inguinal hernia (10%)
o Cryptorchidism (10%)
o Bifid scrotum
o Intersex conditions
o Imperforate anus
o Persistent Mullarian structures (utricle)
o Upper tract abnormalities rare (PUJO, renal dysgenesis)
• Circumcision
o Best not to, may use foreskin as flap during repair
• Discuss the phases of wound healing
• What factors may lead to wound
breakdown?
Wound Healing
• Phases of Wound Healing
• 3 distinct but overlapping phases
• Inflammatory Phase (hours)

o Acute inflammation
o Mediated by cytokines
o Leakage of capillaries
o Influx of neutrophils to fight infection
o Activation of coagulation cascade
o Macrophages to remove necrotic tissue
Wound Healing
• Proliferative Phase (days - weeks)
o Angiogenesis - neovascularisation
o Proliferation and migration of fibroblasts
o Collagen (Type 3) laid down by fibroblasts
o Granulation tissue formed:
o - fibroblasts, inflammatory cells, new vessels, collagen, EC
o Re-epitheliasation
o Contraction of myofibroblasts
Wound Healing
• Remodelling Phase (months)
o Type 3 collagen degraded
o Type 1 collagen laid down (stronger)
o Cross linking of collagen (Zinc, Vit C)
o Collagen aligned for strength
o Apoptosis of neovascularisation (white scar)
o Further contraction to mature scar
Wound Healing
• Factors leading to Wound Dehiscence
o Preoperative factors
o Operative factors
o Post-operative factors
• Preoperative Factors
o Poor nutrition
o ETOH, smoking
o Obesity
o Diabetes
o Steroids
o COAD / Chronic cough
Wound Healing
• Operative Factors
o Emergency surgery
o Major operative complication
o Haemorrhage
o Poor technique
• Post-Operative Factors
o Wound infection
o Atelectasis
o Sepsis
o Prolonged ileus
o Anaemia
• What is this?
• What are the genetics involved?
• What familial syndromes may cause this?
Papillary RCC
• Note papillary architecture
• 10-15% malignant renal tumours

• Tendency for multifocal, bilateral (up to 40%)
• Associated with dialysis patients
• Prognosis Clear cell < Papillary < Chromophobe
• Mutation oncogenes chromosome 7,17, loss of Y
• Hereditary Papillary Renal Cell Carcinoma (HPRCC)

• Hereditary Leiomatosis and Renal Cell Carcinoma
(HLRCC)
• What is this?
• What is the spectrum of the disease?
• What are the urological considerations?
Spina Bifida
• Spina Bifida Occulta
o Small defect in vertebrae
o Too small for protusion of cord
• Myelomeningocoele
o Large defect in vertebrae
o Protusion of cord
o Protuding mass containing CSF, closed by skin
• Spina Bifida Cystica

o Open defect, cord visible
Spina Bifida
• Spina Bifida Occulta
o Patients often asymptomatic, unaware of defect
o Hair tuft, lipoma, cafe a lait spots over defect
o Spinal cord may tether
o Neurological abnormalities may progress with growth
• Urological features
o Neuropathic bladder (OAB or atonic bladder)
o DSD – high upper tract pressures
o Reflux
• What is the typical history?
• What are the complications?
• How and when would you treat it?
• What is the outcome of treatment?
Fractured Penis
• Ecchymosis – blood contained by Bucks fascia
• Typical of fractured penis
• Tear of tunica albuginea
• Penis angulated away from site of fracture
• History
o Usually occurs during intercourse
o Sudden onset penile pain
o Popping noise
o Rapid detumescence
o Haematuria indicates urethral injury (10%)
Fractured Penis
• Complications
o Penile pain
o Erectile dysfunction – cavernosal scarring
o Deformity – Peyronies disease
o Urethral injury / stricture
• Investigations
o All suspected fractures should be explored
o Limited role for US, MRI, urethrogram
Fractured Penis
• Surgical Exploration
o Best results if <8 hours
o Poor results if >36 hours
o Aim – minimise complications
o Counsel patient – this is not a cure
• Technique
o Flexible cystoscopy to rule out urethral injury
o Circumcision incision and deglove penis
o Repair urethral tear with monocryl interrupted over IDC
o Repair tunical tear – inverted non absorbable interrupted
o Leave IDC in until swelling subsides
Part 6

Bishop
• Describe the specimen
• Where do they arise from?
• What is the stage?
• Describe staging for RCC
Clear Cell RCC
• Partial nephrectomy specimen ?upper pole
• Bivalved
• 2.5cm exophytic solid mass
• Tan coloured
• Small area of necrosis
• Clear cell Ca
• Papillary Ca
• AML
• Metastasis, leioma, sarcoma
• Clear Cell and Papillary RCCs arise from the proximal tubules
Clear Cell RCC
• This is stage T1a (<4cm)
• T1a <4cm confined to kidney

• T1b 4-7cm confined to kidney
• T2 >7cm confined to kidney
• T3a Invades perinephric fat, adrenal NOT gerotas
• T3b Invades renal vein or IVC below diaphragm
• T3c IVC above diapragm
• T4 Invades gerotas
• N0 No lymph nodes
• N1 Metastasis in regional lymph nodes
• What are these?
• What are the properties?
• What is pKa? What is their pKa?
• What are the underlying metabolic conditions?
• How would you treat them?
Uric Acid Stones
• May be needles or plates
• Positively birefringent (2 colours on UV light)
• pKa = pH where solute is equally crystal and dissolved
• Uric acid pKa = 5.7
• Uric acid – final product in purine metabolism
• Causes
o Hyperuricosuria (>600mg / day)
o Gouty diathesis
o Diabetes
o Purine rich foods (animal products)
o Chemotherapy
o Myeloproliferative disorders
Treating Uric Acid Stones
• Unobstruct if obstructed
• Hydration
• Analgesia
• Dissolution with Ural pH>6.0 (if compliant)

• Stones dissolve 1cm / month
• Allopurinol if elevated serum uric acid / gouty diathesis

o Xanthine oxidase inhibitor (final step in purine metabolism)
• Exclude myeloproliferative disorder with blood film

• Describe the slide
• What are the differentials?
• What is it composed of?
• What symptoms would this cause?
Urethral Caruncle
• Vagina with poorly oestrogenised tissue
• Protusion from the urethra at 4 o’clock
• Small cystocoele
• Differential
o Urethral caruncle (lumen displaced)
o Urethral prolapse (lumen central)
o Paraurethral cyst
o Urethral carcinoma uncommon
Urethral Caruncle
o Often asymptomatic – picked up on routine exam
o Spotting
o Pain
o LUTS
o Thrombosis
• Composition
o Benign inflammatory tissue
Urethral Caruncle
• Treat with topical oestrogen
• Excise if refractory to oestrogen
• May have wrong diagnosis – tissue diagnosis
• Principles of Surgical Excision

o Stay sutures in urethra
o Excise with cold cut – facilitates tissue diagnosis
o Primary repair with monocryl if large defect
o Otherwise allow healing with secondary intention
o IDC for 24 hours - haemostasis
• What is the condition?
• What are the classifications?
• What are the predisposing factors?
Testicular Torsion
• Extravaginal Torsion
o Occurs in neonates
o Tunica vaginalis is not adherent to dartos
o Spermatic cord torts together with vaginalis
• Intravaginal Torsion
o Occurs in adolescents
o Tunica vaginalis fixed to dartos
o Spermatic cord torts within tunica
Testicular Torsion
• Predisposing Factors
o Bell Clapper deformity
o Cryptorchidism
• Bell Clapper deformity

o Congenital high attachment of tunica vaginalis
o Long stalk of cord within tunica vaginalis
o Hypermobile testis facilitates torsion
o Bilateral deformity
Tumour Markers
• Clinical applications of tumour markers
Tumour Markers
• Clinical Applications
o Predicting histological subtype
o Response to treatment
o Staging and prognosis
Tumour markers - AFP
• Type of protein
• Sites of normal production
• Half life
• Testicular tumour association
• Other states causing AFP rise
Tumour Markers - AFP
• Single chain glycoprotein
• Produced by
o Yolk sac
o Liver
o GIT
• Half life = 5-7 days

Tumour Markers - AFP
• Tumour Associations
o Embryonal carcinoma
o Yolk sac tumour
o Teratoma
• Other Causes
o Liver disease
o Pancreatitis
o GIT malignancy
Tumour Markers - BHCG
• Type of protein
• Sites of normal production
• Half life
• Testicular tumour associations
• Other causes of elevation
• Glycoprotein with a and B subunits
o “a” subunit resembles LH (pituitary hormone subunits)
• Secreted by syncitiotrophoblastic cells

• Usually from placental choriod villus
• Half life = 36 hours

• Tumour associations
• Choriocarcinoma
• Embryonal carcinoma
• Seminoma 10%
• Yolk sac
• Other Causes
o Hypogonadism
o Marijuana smoking
o Lung, breast, GIT malignancy
Nomograms
• What prostate ca nomograms do you
know?
• How are they helpful?
• What are the pitfalls?
Nomograms
• Kattan nomogram (MSK)
• Partin tables (John Hopkins)
• D’Amico tables
Nomograms
• Uses for Nomograms
o Risk assessment
o Predict extent of disease (nodes, T3, SV)
o Predict outcome of treatment (biochem recurrence)
o Help choose best modality of treatment
• Validated across centres

Nomograms
• Pitfalls of Nomograms
o Estimation only
o Different patient populations
o Different treating surgeons
o Different treating centres
• Should be used as a guide only

• Should not replace local experience
Urine Cytology
• What are the indications for cytology?
• How accurate is it?
• What can cause false positives?
Urine Cytology
• Indications
o Irritative LUTS
o Haematuria
o Screening in high risk groups
o Lower tract surveillance
o Upper tract surveillance
Urine Cytology
• Accuracy depends on tumour grade
• Generally poor sensitivity and high specificity
• CIS sensitivity 90%

• G3 sensitivity 60-70%
• G1 sensitivity 10-30%
• Highly specific in high grades >90%

• False +ve, BCG, infection, foreign body, stone,
instrumentation, radiological contrast
Gynaecomastia
Gynaecomastia
• Urological Causes
o Primary hypogonadism
o Secondary hypogonadism- prolactinoma
o Leydig cell tumours
o HCG secreting NSGCT
o Renal failure
o Kleinfelters syndrome
o Intersex disorders
o Drugs – LHRH agonists, finasteride
Gynaecomastia
• Non Urological Causes
o Obesity
o Idiopathic
o Liver disease
o Hyperthyroidism
o Pituitary tumours
o Paraneoplastic – lung ca
o Drugs – steroids, spirinolactone
ASAP
• Atypical Small Acinar Proliferation
o Note single layer of atypical cells
o Small gland
o Atypical cells – hyperchromatic
o Does not meet criteria for Ca
• 50% chance of prostate cancer on 2nd biopsy

• Independent of PSA and DRE findings
ASAP
• Gleason 6 prostate ca on repeat biopsy
60 sec spiels
General format
• Definition
• Pathogenesis
• Causes/Risk factors
• Presentation
• Investigation
• Treatment
• Complications
Discuss BXO
14 points to make
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
•
Discuss BXO
Definition and Pathogenesis
o Balanitis xerotica obliterans is a chronic , progressive, sclerosing inflammatory
dermatosis of the glans and foreskin in men. Can affect women.
• Aetiology/Risk factors
o Unknown. Probably multifactorial- uncircumcised, hormonal, autoimmune, genetic.
o Arises from chronic infection, trauma, inflammation
• Presentation
o Flat white patches on glans and prepuce.
o Maybe meatus and fossa navicularis. Can extend proximally up anterior urethra
o Often asymptomatic
o Pruritis, burning, painful erections in males, dyspareunia in women, urethral sx
(iritative / obstructive)
• Investigation
o If atypical- biopsy
o Urethral stricture Ax if indicated
• Treatment
o Topical steroids for itch and burning- for mild BXO without sign scarring.
o Circumcision if phimosis
o Beware high recurrence rate if local excision
o Urethra: circumferential laser vaporisation for severe meatal stenosis.
o Urethroplasty with non genital skin graft
• Complications
o Urethral stricture
o Pre-malignant condition- monitor
Discuss cystinuria
17 points- 90 secs
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss cystinuria
• Definition
o Inherited AR metabolic disorder that is characterized by the formation of cystine
stones in the kidneys, ureter, and bladder
• Pathogenesis
o 2 genes affected. Type I: chr 2; Non-type I: chr 19.
o Defect in renal transport in proximal tubule of dibasic amino acids (COLA- cysteine,
ornithine, lysine, arginine).
o Supersaturation of AAs in urine causes stones (esp in acid urine). Cystine= 2x
cysteines joined by disulfide bond
o pKa of cysteine is 8.3
o Also, cannot transport cysteine across gut. Therefore, all cysteine is endogenously
produced from dietary methionine.
• Presentation
o Urolithiasis is only known manifestation- inc staghorns
• Investigation
o Positive cyanide nitroprusside test
o Urine crystals- HEXAGONAL
o 24hr urine- >400mg cystine
o Xray for stones- “ground glass”. Hard stones (>1000 HU on CT)
• Treatment
o Clear stones- PCNL/URS (ESWL resistant)
o Dissolution therapy (pH>7.5. Ural/Sodibic)
o Prevention- fluids UO>3L/day, low Na+, low animal protein, low methionine diet
o Medical prophylaxis- ural, chelating agents (captopril, D-penicillamine, Thiola)
o Regular review to treat stones early
o Screen family members with cyanide nitroprusside test
What is the sodium nitroprusside test
• In urine also called the cyanide nitroprusside test

• Sodium cyanide is added to urine and let stand for approx 10
minutes
• In this time:
o Disulfide bonds are broken down from cystein or
homocysteine
▪Cystein (SNP) 🡪 cysteine + cysteine } Releases cysteine
• SNP then added
o If amino acids present the solution turns red / purple
Cysteine, cystine, homocysteine and homocystine all react
when present in the urine when this test is performed.
Discuss XGP
12 points
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss XGP
• Definition
o Chronic infection of the renal parenchyma that causes renal destruction
• Pathogenesis
o Chronic infection causes inflammation, necrosis, and foamy
macrophages
o Usually non-functioning kidney
o Can extend beyond parenchyma to hilum, gerotas, adjacent organs
o Proteus infection (commonly)
o Obstruction due to renal calculi
• Presentation
o Unilateral, recurrent pyelonephritis, anaemia, flank mass
• Investigation
o Cannot be distinguished from cancer on imaging (i.e. pathological Dx)
o CT- renal mass ASSOCIATED WITH STONE IN KIDNEY
o Also- culture blood and urine, FBE, U&E
• Treatment
o OPEN SURGERY- Nephrectomy and excision of all infected tissue
• Complications
o Invade adjacent organs that will need to be removed at surgery (Give
bowel prep. Pneumovax for spleen on left)
Discuss emphysematous
14 points pyelonephritis
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss emphysematous pyelonephritis
• Definition
o Severe, DIFFUSE, acute pyelonephritis characterised by gas in the renal
parenchyma
• Pathogenesis
o E. Coli commonest (also Klebsiella, proteus, pseudomonas, candida. But
rarely clostridium)
o DIABETICS (E.Coli ferments glucose to CO2 and hydrogen)
o Obstruction (non-diabetics)
• Presentation
o Middle aged/elderly diabetics without obstruction. Non-diabetics with
obstruction.
o Unilateral pyelonephritis- very sick.
• Investigation
o CT- gas in parenchyma (occasionally renal pelvis and perinephric)
• Treatment
o Broad spectrum ABx and fluid resusc
o Control BSLs
o SURGERY- nephrectomy
o ICU/HDU
o Medical management- only if stable and limited pyelonephritis. (Treatment-
ABx, relieve obstruction, BSLs, percutaneous drainage of gas/fluid
collections. Proceed to surgery if not improve promptly)
• Complications
Discuss emphysematous pyelitis
11 points
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss emphysematous pyelitis
• Definition
o Pyelonephritis characterised by gas in the collecting system (but not
the parenchyma)
• Pathogenesis
o DIABETES
o E. Coli
• Presentation
o Acute pyelonephritis (more sick than pyelonephritis but less sick than
emphysematous pyelonephritis)
• Investigation
o CT- gas and gas/fluid levels in collecting system
• Treatment
o IV ABx and fluid resusc
o BSL management
o Nephrostomy or stent if obstructed; if not obstructed, manage
medically
o ICU if unstable
• Complications
o Better prognosis than emphysematous pyelonephritis
Discuss Priapism
18 points- 90secs
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss Priapism
• Definition
o Persistent penile erection that continues beyond, or unrelated to, sexual stimulation (?
>4hrs)
• Pathogenesis
o Ischaemic (low flow) vs non-ischaemic (high flow)
o Idiopathic 30%
o Meds for erectile dysfunction
o Meds for depression (trazodone), psych (chlorpromazapine), recreational (cocaine/alcohol)
o Sickle cell
o Malignant infiltration- leukaemia
o Spinal cord lesion/injury
o Other- TPN, GA or spinal anaesthesia, hyperosmolar IV contrast
• Presentation
o Ischaemic- Painful. Non-ischaemic- painless, recent trauma.
• Investigation
o Corporal blood gas- O2, CO2, pH
o Duplex US
o Also- FBE with sickle cell prep, urine toxicology
• Treatment of ischaemic- emergency (non-ischaemic- not emergent)
o Concomitant treatment of sickle cell
o 19G needle in corpora- aspiration and saline irrigation- 10 mins
o Monitored cubicle (ECG, BP)- 10mg aramine in 10ml saline- give 1 ml/ 5mins- 50 mins
o Theatre (consent for both distal and proximal shunts)
▪ Distal shunts- Winter, El-Ghorab
▪ Proximal shunts- Quackel’s, Grayhack
• Complications
▪ Fibrotic penis
Discuss Peyronie’s
19 points- 60 secs
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss Peyronie’s
• Definition
o Fibrous plaque in the tunica albuginea of the corpora cavernosa
• Pathogenesis
o 12-18 months of inflammation, deformity, plaque remodelling then stabilizes
o Plaque calcification when remodelling complete
o Unknown. Possibly trauma.
• Presentation
o Pain
o Deformity or shortening
o Induration or plaque
o Associated with Dupuytren’s contracture
• Investigation
o US to visualise plaque
• Treatment
o Acute phase- aim to ↓pain and progression
▪ Surveillance with simple analgesia
▪ Vitamin E orally/ cream
▪ Colchicine
▪ Tamoxifen
▪ Intralesional Verapamil
o Late phase- depends on deformity and sexual function- surgery
▪ Penile plication of contralateral corpora- shortens. 70% satisfied
▪ Plaque incision + grafting ipsilateral corpora- not shorten. (± Penile prosthesis) if ED.
80% satisfied
Discuss schistosomiasis
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss schistosomiasis
Definition
• Described by Theodore Bilharz in 1800’s
• Parasitic trematode
o Endemic Middle East / Africa / South West Asia
Causes / Risk factors
• S.haematobium (bladder); S.mansoni & S.japonicum (GIT)
• Skin contact with infected fresh water Parasit
Pathogenesis ic
• Life-cycle Life
o Eggs extruded into fresh water (viable for 3/52)
o Miracidia (ciliated larvae) in H2O migrate into Bulinus snails Cycle
o Sporocytes exponentially replicate in snail
o Cercaria (free swimming infective larvae) released into fresh water
o Enters human skin: subdermal position -> migrates to lung and liver -> replication
o Settles in GIT venous plexus (mansoni / japonicum) or bladder venous plexus (haematobium)
o Persist in venules for up to 30yrs -> eggs laid within venules (200-500/d)
o Some eggs cross into the visceral lumen
** Disease results from granulomatous response to schistosome eggs
• Calcification of trapped eggs & fibrous reaction in the bladder (“sandy patches”)
Presentation / Complications
1. Acute cutaneous infection: fever / skin rash
2. Migration phase: hepatitis / fever / lymphadenopathy
3. Months / Years: haematospermia, dysuria, haematuria, chronic bacterial UTIs, obstructive uropathy
(BN / ureter), SCC bladder
Investigation
• •Bloods: eosinophilia, Fbe, Uec
• •Urine: sediment analysis of urine (11am – 2pm); consider urine cytology (EAU)
• •Imaging: bladder / ureteric calcification, hydronephrosis, bladder tumour
• •Cystoscopy: haemorrhagic areas (acute), sandy patches (fibrotic regions), SCC, BN or
ureteric stenosis
Treatment
• •Acute: anti-protozoan treatment eg praziquantal, metrifonate
• •Endoscopic: biopsy, TURBT, diathermy, BNI
• •Reconstruction: partial cystectomy, ureteric dilation / excision / reimplantation,
diversion
Discuss TB
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss Urinary Tract TB
Definition
• Infection due to Mycobacterium tuberculosis (intracellular aerobe)
• 15% cases extra-pulmonary (genitourinary tract most common)
o Can affect kidneys / ureter / bladder / genitalia
• Risk factors: immunosuppression (diabetes, alcohlic, HIV, cancer etc), prolonged exposure to infected
individual (health care workers, refugee camps), person from endemic area (Asia, Africa
Pathogenesis
• Primary infection usually related to inhalational exposure  can be dormant for years; reactivation from
immunosuppression or biological stress eg. Trauma, illness
• Genitourinary TB can occur in the absence of pulmonary TB
• Genitourinary infection
o Haematogenous: renal and genital
o ‘Downstream’ seeding: ureter and bladder
• Primarily cellular immune response to infection  results in caseating granulomas & dormancy of
infection
Presentation
** Clinical symptoms usually develop 10-15 years after the primary infection
• Hx:
o History of previous infection / origin or travel through endemic area
o Pain: flank or suprapubic
o Irritative voiding symptoms
o Infertility
o Systemic sx are unusual (eg fever, LOW, sweats
Effects on Genitourinary organs
1. RENAL:
o Papillary necrosis
o Infundibular stenosis
▪  calyceal dilation  calcification of calyceal walls  fill with caseous material =
PUTTY KIDNEY
o Renal granulomas
▪  erode into the collecting system  bacilluria  downstream seeding
2. URETER:
o Ureteral stricture
▪ VUJ most common location
Nb. Infundibular stenosis + ureteral stricture HIGHLY SUGGESTIVE OF TB
3. BLADDER:
o UO most commonly affected region  “GOLF HOLE UO”
▪ Initially oedematous  then scarring and fibrosis lead to GOLF HOLE UO
o Chronic infection  “THIMBLE BLADDER”
▪  scarred contracted bladder
4. GENITALIA (Epididymis / testis / prostate / penis / urethra):
o Most common site epididymis, remaining sites rare
o Epididymis feels like a ‘string of beads’
o TB of the genitalia leads to infertility
Diagnosis
1. URINE
o 3 consecutive early morning urine samples (acid-fast staining,
mycobacterial culture)
▪ 97% of pts with urinary TB will have 1/3 + cultures (Ostrow
1975)
2. PPD:
o Mantoux test
o QuantiFERON-TB Gold test
3. CXR / sputum and blood mycobacterial culture
Treatment
4. 6/12 of anti-tuberculous medication (R/I/P/E)
5. Ureteric stricture
o If significant obstruction; especially mid or proximal ureteric  stent or
nephrostomy  review post completion of antibiotic course
o Mild / mod distal ureteric stricture may be related to VUJ oedema  monitor
during treatment course
▪ Weekly monitoring, if no improvement or worse stent or nephrostomy
6. Surgery
• ** No elective surgery until > 6/52 TB medication
• Nephrectomy – if nonfunctioning kidney with pain / HT / persistent
infection
• Ureter – reassess & treat strictures that persist post 6/12 anti-TB
medication
• Bladder – if small scarred and contracted augmentation cystoplasty
Interpreting Mantoux Test
FALSE POSITIVE
• Previous BCG vaccination
• Non-tuberculous
mycobacterial infection
• scratching the injection site
FALSE NEGATIVE
• Immunosuppressed pt (eg
HIV with low CD4 counts)
• Tested prior to 2-12 wk
incubation period
WTF is SENSITIVITY & SPECIFICITY
• Specificity of > 95%
QuantiFERON-TB
• Sensitivity of > 92% in
infected patients
Gold Test? DISADVANTAGES

• Blood from pt mixed with • Need to analyse within 12
hrs (or WCC die)
synthetic Myco-TB antigens • Unclear spec / sens in
children, immunosuppresed
• If pt infected with M-TB pts, recent exposure to TB
• Some false positives with
their WBC release IFN in other mycobacterium

species
response to above (in vitro)

o QFN-G test based on amount
of IFN released ADVANTAGES
• Results within 24 hrs
• Tests different immune • Not affected by previous
BCG vaccination
pathway to Mantoux • Avoids interpretation bias
of Mantoux
Discuss Fournier’s gangrene
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss Fourniers Gangrene
Definition
• Necrotising fasciitis of the male genitalia and perineum (mean age 50; M:F 10:1)
• RARE, LIFE-THREATENING, SYNERGISTIC Rapidly progressive infection; affects predominantly
subcutaneous tissues  30% mortality
• Risk factors: immunosuppression (diabetes, alcohlic, HIV, cancer etc)
• Source of infection lower GIT / perineal cutaneous infection / urinary tract
• Risk factors: periurethral extravasation of urine eg stricture / instrumentation, paraphimosis, perirectal or
perianal infections, local surgery eg circumcision or herniorrhaphy
Pathogenesis
• Polymicrobial infection
• Common organisms: E coli, Klebsiella, Enterococci, Clostridium, Streptococci, Bacteriodes
• If genital origin of infection
o Infecting bacteria pass through Buck’s fascia
o Bacteria spread along fascial planes: dartos fascia (scrotum & penis)  Colles fascia (perineum) 
Scarpas fascia (anterior abdominal wall)
Presentation
• Hx: of recent perineal trauma / instrumentation / urethral stricture / fistula or fissure / local cutaneous
conditions
• Hx: pain / fever / local erythema, swelling, pain +++ / urinary sx eg dysuria, urethal discharge,
obstructive LUTS
• O/E: Fever (or hypothermia)  systemic toxicity out of proportion to local symptoms
• Swelling, crepitus, hypoaesthesia, discoloured skin, bullae, origin of infection (eg. Fissure / skin breach
etc)
• Ix: Ca2+ Plt Na+ Hb WCC / Imaging: subcutaneous gas / Biopsy: intact epidermis, dermal
necrosis, vascular thrombosis, PMN infiltration, subcutaneous tissue necrosis
Discuss Fourniers Gangrene
Management ** MULTI-DISCIPLINARY CARE (ICU / ID / General surgery / Plastics)
1. Prompt diagnosis (high degree of suspicion)
2. Resuscitation (IV fluids, IV antibiotics) / ICU
3. Broad spectrum antibiotics
o Penicillin / Imepenem or Meropenem / Gentamicin
o Other: Campbells: ampicillin, sulbactam and one of clindamycin, ceftriaxone, gentamicin) / Emedicine (see
below)
4. Urgent surgical debridement +/- diversion (catheter / stoma)
5. Reconstruction
Surgical Management
• Debride all non-viable tissue
• Orchidectomy rarely required (testes have separate blood supply and deep to
infection)
• +/- Second look surgery 24-48hrs later
Adjuncts to surgery
• Hyperbaric oxygen (improves wound healing and immune response)
Adult PCKD
• inheritance is autosomal dominant
• abnormal gene is located on the short arm of
chromosome 16.
• The defect results in excessive renal tubular cell
proliferation. Copious secretion of fluid into the
tubules as well as impaired connective tissue
support contribute to the development of cysts.
• The cysts gradually enlarge, and interfere with
renal function by compression of the normal
filtering units (nephrons). The disease is often
silent until loss of nephrons results in renal
failure, usually in adulthood.
• Complications include bleeding into the cysts and
recurrent infections, as occurred in this man.
• In about 40% of cases, there are also multiple
cysts in the liver. Less frequently, cysts occur in
the pancreas, spleen and lungs. "Berry"
aneurysms of cerebral arteries occur in 10-30%
of cases
GN Sepsis
DANGERMOUSE suggested intro ??
“LIFE THREATENING GN INFECTION
SECONDARY TO A URINARY TRACT
INFECTION
Pathophydiology related to SYSTEMIC
RESPONSE TO THE CELL WALL”
Gram Negative Sepsis:
Pathogenesis:
• EXOTOXIN
o May directly initiate septic shock
o Eg Exotoxin A (P. aeruginosa)
• ENDOTOXIN
o Gram negative cell wall components highly
antigenic
▪Lipopolysaccharide of bacterial outer membrane
▪ Triggers innate immune pathways
▪ Direct activation of coagulation / fibrinolytic systems
GN sepsis Pathogenesis:
Gram negative LPS (Lipopolysaccharide)
o These bacterial cell wall components are recognised by Toll-like receptors
o Triggers a cascade of cytokines / prostaglandins / IL etc
Result
1. Vasodilation / chemotaxis
2. Widespread endothelial cell activation
o Hypotension
o fluid shifts from increased vessel permeability
o Hypercoagulable state (DIC)
3. Metabolic effects
o Insulin resistance (high BGL), catabolic
o Acidosis
4. End organ dysfunction
o From tissue hypoxia (multi-factorial eg less perfusion, local oedema etc)
o At extreme MULTI ORGAN FAILURE
o Cardiac:  cardiac contractility and output
o Respiratory: ARDS
o Other: Renal / hepatic failure
Summary: Pathophysiology
Septic Shock
Robbins 8th Ed
• The classic clinical presentation of fever
and chills followed by hypotension is
manifest only in about 30% of patients
with gram-negative bacteremia
Principles of Management:
Urosepsis
1.Appropriate antibiotics *
o Blood / urine / line cultures
2.Life-supporting care
o Fluid resuscitation / vasopressors
o Intensive hyperglycaemic control
o Thrombosis prophylaxis
3.Relieve obstruction
Oncocytoma
• Benign renal tumour originating from the proximal convoluted
tubule (intercalated cells of the collecting duct)
• May be sporadic or associated with Birt-Hogg Dube syndrome
• DDx
o Imaging: RCC (esp if small, or with central necrosis)
o Pathology: chromophobe RCC
• Epidemiology
o 5-6% of renal neoplasms
o 60-70yrs commonest age at presentation
o M:F 1.7:1
• Frequency of central scar: 1/3

Appearance
• Gross:
o tan or mahogany brown
o Well circumscribed
o Central scar
o Can be large (eg up to 12cm)
Histological Features
• Large granular
eosinophilic cells
with small nuclei
abundant
mitochondria
• DDx: chromophobe
RCC (oncocytic
variant) which also
Caution: oncocytoma may co- has eosinophilic cells
exist with RCC in the same but a degree of
lesion nuclear atypia
Characteristic Features on CT +
MRI
• CT with contrast • MRI
o Well defined o Well defined, Smooth,
o Smooth Homogenous
o Relatively o Moderate signal
homogenous intensity
o  enhancement than o Stellate central region
normal renal of decreased signal
parenchyma
o Large lesions: central o T1: low to moderate
scar homogenous signal
intensity
** central scar NOT o T2: High signal
pathognomonic of intensity
oncocytoma
Characteristic Arteriography
Features
Discuss VHL syndrome
• 13 points
VHL
• Definition
o Inherited Autosomal Dominant disorder of VHL gene characterized by
haemangioblastomas of the brain, spinal cord, kidney, and retina
• Pathogenesis
o VHL is a tumour suppressor gene on chromosome 3p25/26
o 1 in 36 000, Mean age of Dx 37
o Absence allows Hypoxia Induced Factor to accumulate and therefore
promoting vasculogenesis
• Classification- people with VHL disease into two groups:
▪ 1= without pheochromocytoma
▪ 2= with pheochromocytoma
▪ type 2A (with RCC) and type 2B (without RCC)
• Clinical Manifestations
o Urological
▪ RCC (50%)
▪ Renal Cysts (75%)
▪ Phaeo (15%)
▪ Epididymal cystadonomas (10%), epididymal cysts (7%)
o Non-urological
▪ Haemangioblastomas (brain, spinal cord) - 60%
▪ Pancreatic cysts (75%) and adenocarcinoma
▪ Retinal Angiomas - first manifestation - 60%
▪ Endolymphatic sac tumours in ear - 10%
Tuberous Sclerosis
• 9 points
Tuberous Sclerosis
o Autosomal Dominant Chromosomal Abnormality characterized by hamartomas in
multiple organs
• Epidemiology
o Urologic
▪ Renal cysts
▪ AML’s in 60% (hamartoma) (20% of people with AML's have TS)
o CNS
▪ Seizure
o Skin
▪ sebaceous adenomata
• Follow-up
o Follow-up of children Dx’d with TS = annual U/S starting at puberty
Memory Tool "classic triad"= “twits with zits and fits” = retardation (like Joe), sebaceous
adenomas, seizures (like Claire’s dancing) (Note - only seen in 30% as a triad)
Burt Hogg Dube
Burt Hogg Dube
o Autosomal dominant cancer syndrome
o BHD gene on chromosome 17p11.2
o BHD encodes ‘folliculin’ (function unknown)
o 25% develop renal tumours
▪ Oncocytoma
▪ Chromophobe RCC (often synchronous and bilateral) (Average
number tumors/kidney = 7!!!)
▪ 40% have multiple tumour histologies on path
o Cutaneous
▪ Benign cutaneous tumors (fibrofolliculomas)- Benign tumors of
hair follicles
▪ Skin-colored papules on face, neck, back, upper trunk
▪ Appear in 3rd/4th decade of life
▪ Although helpful for diagnosis, skin lesions do not have to be
present in those with BHD mutation
o Pulmonary
▪ pulmonary cysts 90%
▪ spontaneous pneumothorax 20%
• Treatment
o Nephron-sparing surgery whenever possible
o Beware of pneumothorax in peri-operative period
Discuss 5α reductase
inhibitors
Discuss 5α reductase inhibitors
Types, dose, mechanism:
1. Finasteride (Proscar) 5mg daily (type II 5-ARI)
2. Dutasteride (Avodart) 0.5mg daily (type I and II 5-ARI)
Effects: (8 points)
1. reduce prostate volume by 25%
2. increase Qmax by 10%
3. improve Sx score by 20-30%
4. reduce risk of AUR by 50%
5. reduce need for surgical BPH therapy by 50%
6. reduce risk of BPH progression
7. decrease total PSA by > 50% after 9-12 months of treatment
8. may help stop chronic haematuria from the prostate
Adverse effects:
impotence < 5%; decreased libido <4%; decreased volume of ejaculate <3%, gynecomastia <1%
Evidence for use:
3. PLESS
1. 5-ARIs improve Sx and flow in men with prostates > 40cc and PSA > 1.4
4. MTOPS and CombAT
1. combined 5-ARI and a-blocker better than either agent alone at improving voiding Sx
AND preventing progression of BPH
2. IPSS reduced by 35%, flow increased by 1-3mL/sec
3. Benefit greatest with prostate volume > 40cc and PSA > 4
4. a-blocker can be stopped after 6-9 months combined therapy
5. SEs: retograde ejac, dizziness, floppy iris syndrome
Discuss urodynamics
Discuss urodynamics
Definition
Urodynamics is the study of micturition
Types
1. Uroflowmetry
1. Normal Qmax: male 20-25mL/sec, female 25-30mL/sec
2. suspected obstruction 10-15mL/sec
2. Cystometry
1. evaluates bladder filling (storage)
2. Used to evaluate detrusor pressure, bladder capacity, bladder compliance, LPP
3. ALPP < 60cm water = intrinsic sphincter dysfunction as cause for SUI, >100 is not
4. DLPP > 40cm water = upper tracts at risk
3. Pressure flow studies
1. evaluate bladder emptying (voiding)
2. Measures detrusor pressure and urinary flow rate
4. Electromyography
1. evaluates voluntary urinary sphincter activity
5. Cystogram
1. imaging of the bladder during filling and voiding
6. Urethral pressure profilometry
1. evaluates voluntary urinary sphincter
7. Residual urine
1. Evaluates bladder emptying, influenced by detrusor function and outlet resistance
Discuss urodynamics
When reading UDS, comment on
1. filling phase - compliance, capacity, sensation, DO, leak
2. voiding phase - Qmax, VV, PVR, Pdetmax,
3. video cystogram - contour, filling defects, VUR, bladder neck, ? urethral stricture
4. flow - Qmax, Qave, VV
Discuss PSA
Discuss PSA
What is it?
An androgen-dependent serine protease that liquefies the seminal coagulum, T1/2 of 2-3days
What can cause it to be elevated? (6 points)
1. prostate cancer
2. BPH
3. infection - cystitis, prostatitis
4. manipulation or trauma
5. recent ejaculation
6. increasing age
Clinical utility
7. prostate cancer detection
8. monitoring patients after prostatectomy or radiotherapy
PSA derivatives to aid decision-making
9. Age-specific reference ranges
1. 40-49 < 2.5, 50-59 < 3.5, 60-69 < 4.5, 70-79 < 6.5
10. PSAV
1. > 0.35/yr for PSA < 4
2. > 0.75/yr for PSA 4 - 10
11. PSADT
1. > 1 yr - local recurrence more likely
2. < 6 mo - systemic recurrence more likely
3. < 3 mo - higher risk of death from prostate cancer
12. PSAD
1. > 0.15 suggests cancer, needs TRUS volume
13. % free PSA
1. < 10% = 56% chance of cancer; 10-15% = 28%; 15-20% = 20%
Discuss Gleason grade
• 12 points
Discuss Gleason grade
• Definition
o Classifies the low microscopic appearance of prostate cancer with a
score from 1-5 according to the degree of loss of normal glandular
architecture. (i.e. not cellular like most grading systems). 5 being most
poorly differentiated
o Named after Donald Gleason, pathologist from Minneapolis in 1960s
• Useful for diagnosis, risk stratification for treatment, and prognosis
• Grades
o Grade 1- small, well-formed, closely packed uniform glands
o Grade 2- larger, well-formed, slightly spaced uniform glands
o Grade 3- separate irregular glands with cells invading connecting stroma
o Grade 4- fused very irregular glands
o Grade 5- sheets of cells, no glands
• Gleason score is sum of the two most prominent Gleason patterns
o Primary- majority tumour >50% of pattern
o Secondary- next most prominent pattern <50% but >5% of tissue
o Tertiary- small component of higher grade cancer (usually 5)
• Note- there was a change in the interpretation of Gleason grade in 1990s-
many Gleason 6s then are now Gleason 7. Important for interpretation of
trials from this period.
Discuss testicular serum tumour markers
• 13 points
Discuss testicular serum tumour markers
• Definition
o Proteins produced by certain testicular cancers and detected in the serum that are useful
for diagnosis, staging, risk stratification, and surveillance of testicular cancer
• αFP
o T1/2= 5-7 days
o Never elevated in pure choriocarcinoma, seminoma
o False positives
▪ Infants <1yo
▪ Liver dysfunction- hepatitis, cirrhosis, HCC
▪ Non-germ cell cancers- liver, pancreas, gastric lung
• βhCG
o T1/2= 1-3 days
o Produced by syncytiotrophoblasts
o Always elevated in choriocarcinoma, 10% of seminomas. Never teratoma.
o False positives
▪ Marijuana use
▪ Spurious- assay cross reacts with LH (hypergonadotrophic states)
• LDH
o T1/2= 4-4.5 days
o Elevated in seminoma or non-seminoma
• S stage is determined by nadir value of post-orchidectomy markers

• Need to wait 5 T1/2’s before reach nadir (ie 5 weeks αFP, 3 weeks LDH, 2 weeks βhCG)
• S stages
beware units are different in Australia for βhCG
Discuss CIS of the bladder
• Definition
• Pathogenesis
• Presentation
• Investigation
• Treatment
• Complications
Discuss CIS of the bladder
• Definition
o Urothelial cancer which is flat, high grade, and non-invasive
• Pathogenesis
o Severe cytologic atypia
o Loss of polarity leading to nuclear overcrowding
o The nuclei are enlarged, pleomorphic, hyperchromatic, and prominent
nucleoli.
o CIS can be multifocal
o As for UC (Smoking, aramine dyes, cyclophosphamide, phenacetin)
• Presentation
o Storage LUTS
o Haematuria- esp micro
o Associated with papillary urothelial cancer
o At cystoscopy- velvety patch but may look like normal mucosa
• Investigation
o Cytology- 95% positive (because cells are discohesive)
o Biopsy to confirm Dx
• Treatment
o Biopsy and fulguration followed by
o Induction and maintenance BCG
o Cystectomy for recurrent CIS
• Complications
o Risk factor for UC recurrence and progression
o Progression: 20% after complete response to BCG
Course of ureter and relations
• From PUJ lateral to L2 vertebral body
• Tips of transverse process
• SI joint
• Lateral to ischial spine
• Turns medially into UO
o 1cm above and lateral to pub tub
Blood supply of ureter
• 1st line:
o Abdominal ureter blood supply MEDIAL
o Pelvic ureter blood supply LATERAL
• Segmental
• Then go into details
o Abdominal
▪3: Renal, gonadal, aorta
▪Common iliac, internal iliac, superior/inferior
vesical, uterine/vaginal a, middle rectal
Hydrocele
• Definition: collection of fluid between tunica vaginalis layer of
scrotum
• Classification
o Primary
o Secondary
▪ Tumour
▪ Trauma
▪ Infection
▪ Patent processus vaginalis
• Management
o Aspiration
o Sclerosing agents
o Excision: excise tunica vaginalis, drain fluid
▪ Jaboulay’s procedure
▪ Lord’s procedure (plication)
Vasectomy consent
• Most reliable form of sterilisation success rates 99.9%
• Considered permanent form of contraception although can be
reversed
• Indication
• Procedure
• Post-op
o Immediate: bleeding/haematoma, infection
o Sperm counts
▪ 2 sperm analysis after 4 month + 24 ejaculates (BAS)
▪ >7 month + non motile sperm + >24 ejaculation: risk low, guarded clearance
▪ Motile sperm: repeat vasectomy
o Late:
▪ Sperm granuloma
▪ Pain 10-15%
▪ Recanalisation: early 1 in 500, late 1 in 5000
▪ Testicular atrophy
• Risk factors for reversal
o Age < 30 at procedure
o Change of marital status
• Factors associated with success of vas reversal
o Preop factors
▪ Short interval from vasectomy to reversal
▪ <3 yr: sperm 97%, pregnancy 70%
▪ 3-8 yr: 90%, 50%
▪ 9-14yr: 80%, 40%
▪ > 15 yr: 70%, 30%
▪ First attempt
o Intra op
▪ Presence of sperm in vasal fluid
▪ Clear vasal fluid
▪ Higher sperm quality in vasal fluid
▪ Sperm granuloma at site
▪ Distance from epididymis to vasectomy site
▪ Technique
RPF (Ormond disease)
• Characterised by sclerotic tissue (hard tissue) causing encasement of
retroperitoneal structures including ureter, aorta, IVC, manifestating with
obstructive uropathy
• Medial deviation of ureter +/- hydronephrosis
• Causes
o 70% Primary = Idiopathic (Ormond disease)
o 30% Secondary
▪ Medication eg methylsergide, methyldopa, beta blockers
▪ Malignancy: lymphoma, myeloma, pancreatic, prostate cancer
▪ Radiotherapy
▪ Trauma
▪ Surgery, aortitis
▪ IBD
o Treatment
▪ Exclude medication
▪ Relive urinary obstruction: stents
▪ Biopsy to rule out malignancy
▪ Refer to physician for trial of steroids: 60mg daily 6 weeks then wean to 10mg daily up to 6 month;
immunosuppressive agents eg cyclophosphamide, azathioprine, mycophenolate
▪ Ureterolysis: right angle along perirueteric tissue, care with not devascularising ureter, to free from
fibrosis. Wrapped in omentum. Bilateral procedure.
Horseshoe kidneys
• 1 in 400
• More common
o Infection
o Stones
o PUJ obstruction
▪ High insertion
▪ Crossing vessels
▪ Kinking at isthmus
o Injury by blunt trauma
o VUR
o Malignancy
Cytology
• Analysis of sloughed cells into urine to
assess for malignancy
• Cytology - Voided urine
o Sensitivity depends on tumour grade
▪ Grade 1 (?PUNLMP): 20%
▪ Grade 2 (Low Grade): 45%
▪ Grade 3 (High Grade): 75%
• Specificity Approximately 95%
• Cytology - Ureter - Point is = not as acurate
o False negative: 22%
o False positive: 35%
o Saline washings: better cell yield
Urine Cytology
• False Negative Rate (high grade tumors) = 20% (may
be up to 40% in modern series)
False Positive Rate = 1-12%
urothelial atypia
inflammation/infection (including stones, Foreign
body/stent/IDC)
BCG
Contrast
Radiotherapy/chemotherapy changes (changes last for ~1
year after therapy ceased)
• BTA-Stat – looks for human complement
factor H-related protein
• BTA- TRAK - looks for human
complement factor H-related protein
 NMP22 – looks for nuclear matrix protein
• All have ~80% sensitivities

Latex Fettish
• Estimated to affect 0.8-8.2% of population
• Causes 2 of the 4 types of hypersensitivity
• Type 1 - IgE = life threatening
• Proteins from rubber tree
• Diagnose with blood testing RAST
(Radioallergosorbent test)
• Type 4 - Dermatitis - delayed skin reaction
• From chemicals to process rubber
• Spina Bifida (68%) (probably why there
aren’t many spina bif porn stars?),
industrial rubber workers (10% - so 90%
can wear latex to work), health care
workers, people who have had numerous
surgical procedures as a child
• F>M
• Bananas, pineapple, avo, kiwi, strawberry
supposed to be no nos… Jos was right
Random Shit for Urine Dipstick
• Blood – normal < 3 rbcs per HPF
• Hb catalyses oxidation of orthotolidine by buffered
organic peroxide to turn stick blue reaction
• False positive - povidone iodine, sodium hypochlorite,
myoglobinuria, severe dehydration (high SG),
menstruation, bacterial contamination, XS vitamin C,
heavy exercise
• Protein – tetrabromophenol blue changes colour in
response to the presence of protein in the urine,
particularly albumin. Protein concentrations as low as
20mg/dl are detectable
• False-negative results can occur in dilute or alkaline
urine or when the protein present is not albumin. Bence-
Jones protein for instance is not detected by urinalysis
• Glucose is oxidised by glucose oxidase to form gluconic
acid and hydrogen peroxide. Hydrogen peroxide acted
upon by a peroxidase to cause oxidisation of the
chromophore causing a colour change.
• Glucose oxidase is specific for glucose; other sugars will
not cause a colour change
• Ketones – Sodium nitroprusside turns purple in the
presence of acetoacetate. Other ketones are not
detected. Useful for diabetic ketoacidosis (early sign)
and starvation
• Urobilinogen –
• Leukocytes – Leucocyte esterase is an enzyme
produced by neutrophils. Leucocyte esterase catalyses
the hydrolysis of an indoxyl carbonic acid ester to
indoxyl. Indoxyl oxidises a diazonium salt chromogen to
• Nitrites – 5 mins after dip. In the acidic environment of
urine nitrites react with the aromatic amine on the test
strip to form a coloured diazonium salt. This reacts with
a hydroxybenzoquinoline to provide a pink coloured azo
dye (Griess reaction)
• Nitrites not normally present in urine. Nearly all urinary
pathogens produce nitrites
• Campbell’s - "the specificity of the nitrite dipstick for
detecting bacteriuria is over 90%. The sensitivity of the
test, however, is considerably less, varying from 35% to
85%."
Wordy but useful… Me or the slides???

USANZ
RACS PRACTICE VIVAS
UROLOGY
TRAINEE WEEK 2007
Pathology
Slides and Questions
Prepared by Nathan Lawrentschuk
Case 1
Case questions
• What is this specimen? Point to the abnormality- (total penectomy-with invasive cancer and CIS in glans region)
• What type of cancer is this likely to be? SCC
• What are the risk factors for this cancer? increasing age, smoking, phimosis, HPV infection, and absence of neonatal
circumcision, Pre-existing penile lesion/Premalignant –CIS, Cutaneous horn, Balanitis Xerotica Oblitarans (lichen sclerosis et
atropicus) ., Leukoplakia, Bowenoid papulosis, Condyloma acuminatum, Karposi's Sarcoma, Buscheke-Lowenstein tumour
Bowens disease
• Other possible risk factors include a history of ultraviolet photochemotherapy (PUVA), a high number of sexual partners,
history of penile tears or abrasions, genetic factors, and race (Asia,africa,south america).
• If this was an SCC invading the corpora what Stage would it be? T2
• Discuss the TNM CLINICAL classification system for penile cancer? TNM Clinical Classification
– T Primary Tumour
• TX Primary tumour cannot be assessed
• Tis Carcinoma in situ
• Ta Noninvasive verrucous carcinoma
• T1 Tumour invades subepithelial connective tissue
• T2 Tumour invades corpus spongiosum or cavernosum
• T3 Tumour invades urethra or prostate
• T4 Tumour invades other adjacent structures
N — Regional Lymph Nodes
– NX Regional lymph nodes cannot be assessed
– NO No regional lymph node metastasis
– N I Metastasis in a single superficial inguinal lymph node
– N2 Metastasis in multiple or bilateral superficial inguinal lymph nodes
– N3 Metastasis in deep inguinal or pelvic lymph node(s), unilateral or bilateral
M — Distant Metastasis
– MX Distant metastasis cannot be assessed
– MO No distant metastasis
– Ml Distant metastasis
• What treatment options are available for localised penile cancer? for localized disease include the following:
• Cryotherapy, Electrosurgery (ie, curettage and electrodessication), Laser, Topical treatment (5-fluorouracil,
photodynamic therapy, or imiquimod) , Radiation therapy, Surgical excision, Mohs micro-surgery
• With invasive cancer such as this what are your principles of management? Cancer control then preservation of penile length/function or reconstruction
if possible; Staging/Treatment of nodes-inguinal and pelvic
• What would be your indication to do a partial penectomy versus total penectomy? Need to have a 2cm margin and preserve enough length to
functionally hold penis
• This gentleman had high grade SCC with T2 disease- What are the indications for lymphadenectomy in penile cancer? (high grade, T2 disease)
• Would you do anything before embarking on LN dissection? Antibiotics first and staging pelvic nodes with CT/MRI
• How extensive would your lymphadenectomy be? why?- Sup/modified versus deep b/c morbidity
Case 2
• Fibrin Glue (Tiseel)

Case 2 Q and Answers
• What are the 3 key contributors to NORMAL haemostasis?
– Vascular wall (endothelium and underlying connective tissue)
– Platelets
– Clotting Factors
• Briefly outline the coagulation cascade?
– See diagram
– Direct towards Intrinsic/Contact (Collagen, Platelets, Starts factor XII) pathway and Extrinsic/Tissue Factor (or thromboplastin) pathways (Starts Factor VII)
– Ultimately results in Prothrombin to thrombin and then Fibrinogen to fibrin formation and a stable clot
• Where does Heparin act? i.e. Which pathway (+/- factors) predominantly?
– Intrinsic Pathway
• Where does Warfarin Act? i.e Which pathway (+/- factors) predominantly?
– Extrinsic Pathway
• How do we measure clotting/coagulation and which pathway is being measured with each test?
– APTT- Intrinsic pathway
– Prothrombin Time- Extrinsic Pathway
• Turn your attention to the picture of the fibrin glue (Tisseel,NOT floseel) Fibrin sealants are becoming popular- which part of the coagulation cascade are they active
in? How do they work?
– Fibrin glue consists of two main components: fibrinogen and thrombin. These are loaded into two syringes with tips forming a common port. When injected the two
components meet in equal volumes at the point of delivery. The thrombin converts the fibrinogen to fibrin by enzymatic action at a rate determined by the concentration of
thrombin. The more concentrated thrombin solution produces a fibrin clot in about 10 seconds, and the more dilute thrombin solution forms the clot about 60 seconds after
the glue is applied to the surgical field. Both the extrinsic and the intrinsic mechanisms of blood coagulation are bypassed, but the physiological final common pathway of
coagulation is faithfully replicated. Factor XIII (present in the fibrinogen component of the glue) cross links and stabilises the clot's fibrin monomers. Some preparations of
fibrin glue contain aprotinin to delay the fibrinolytic action of plasmin
• What clotting/bleeding parameters do you consider safe to perform a TURP (Hb, platelets, INR)?
– Hb- greater than 100, Platelets Greater than 60, INR less than 1.5
• Two commercial preparations containing thrombin are used in head and neck reconstruction. One of these agents, FloSeal, consists of bovine-derived thrombin and a
bovine-derived gelatin matrix. The thrombin is mixed with the gelatin matrix immediately prior to its application to the bleeding site and is dispensed through a
single syringe. As the blood percolates throughout the matrix at the site of bleeding, the thrombin interacts with endogenous fibrinogen to produce fibrin that forms a
clot with the gelatin granules incorporated in the clot. Since FloSeal does not contain any fibrinogen, it requires contact with blood for the clot to be activated and is
ineffective in the absence of any bleeding. The other agent, Tisseel contains both thrombin and fibrinogen. The thrombin and fibrinogen components of Tisseel are in
separate syringes that simultaneously dispense their contents through a single dispensing tip. The mixture is sprayed or applied to a surgical bed. When the two
substances combine, a fibrin clot is formed. In head and neck reconstruction, these substances are used either to obtain hemostasis or as a tissue glue to bind the
tissues together. In skull base surgery, neurosurgeons routinely use fibrin glue products to reinforce or obtain a watertight closure and prevent cerebrospinal fluid
leakage.
Answer case 2
• Intrinsic/Contact Extrinisic/Tissue Factor Pathway
Pathway
Case 3
•
Case 3 questions
Describe the cystoscopic picture- good candidates pick up smooth versus spiculated- or jack stones (not essential)
• What is the typical composition of bladder calculi?
– Ammonium acid urate but may be pure or mixed, also calcium, oxalate or phosphate; uric acid
• What are risk factors for bladder calculi?
– BOO with stasis and nidus; Iatrogenic- suture, staples etc; Foreign bodies by patient
IN GENERAL-
•
What are stone promotors in the urinary tract: Low urine volume, low urine pH, calcium, sodium, oxalate, and urate.
• What are stone inhibitors? Many inorganic (eg. Citrate, magnesium) and
organic (eg. Urinary prothrombin fragment 1, glycosaminoglycans, osteopontin)
Uric acid stone
• What is the PKa of uric acid? 5.5 and 10.3
• Aetiology
– Idiopathic
– Inherited
– Primary Gout
– Diet
– Myeloproliferative disorders
– Congenital metabolic enzyme defects
– IBD (get UA abd CaOx stones)
– Renal Hypouricaemia
• Outline your treatment- unobstruct, hydration, diet, dissolution with alkaliniser and dipstick pH at 6.5-7 +/- allopurinol, Re-image +/-
ancillary procedures
• What happens if pH to high>7-7.5 risk of Ca PO4 stones
Case 4
Case 4 questions
• What is this? (Cancer that looks like PIN but is Gl 3)
• Briefly outline the Gleason system for grading prostate cancer:
– System of grading prostate cancer using the low-power appearance of the glandular
architecture
– A primary grade from 1-5 assigned to most predominant pattern and a secondary grade (1-5)
to the next most predominant pattern giving a total score out of 10.
– Good (6 or less), Intermediate (7) and Poor (8 or more)
– Gleason 1 and 2- small uniform glands, closely packed with little intervening stroma
– 3- variable sized glands percolating between normal stroma but no fusion
– 4- irregular glands with incomplete formation often appearing fused
– 5- Sheets of cells, no glandular formation
• What stage is a tumour with focal extraprostatic extension and micrometastatic disease in a single
lymph node with no evidence of bony or other metastasis?
T3a, N1(micro), M0
• What is your criterion for active surveillance? The Epstein Criteria:
– If the PSA density (PSA divided by prostate volume on ultrasound) is lower than 0.1
– no adverse findings on needle biopsy
• (Gleason score 7 or greater, or
• more than two needle biopsies containing prostate cancer, or
• more than 50 percent involvement of any core with cancer), then there is a 70 to 80
percent chance that the prostate cancer is small volume (less than 0.5 cc).
– Men in 60s or above (usually)

Case 5
1 in 250-300 births
Case 5
• 1. What is this?- Hypospadias:glanular (Ddx intersex)
• 2. Features of hypospadias:
– Ventral displacement of the urethral meatus (hypospadias).
– Incomplete formation of the prepuce (dorsal 'hooding')
– Ventral curvature (chordee).
• 3. Incidence & Outline the types of hypospadia/classification
and rough percentages of each?
• 4. Risk factors? (most no known factors)
– Family, Preterm/prem birth, growth restricted infant, parental
subfertility
• 5. Associations of hypospadias:
– The most frequently encountered anomalies are:
– • Inguinal hernia. (105)
– • Undescended testis. (10%)
– • Persistent Müllerian (paramesonephric) structures.Utricle
– • Intersex states.
– Proximal hypospadias think of
• Other organs-cardiac/anua/limb/cleft palate/pyloric stenosis
• Renal agenesis. 6. Increased risk of UTI?
• VUR.
• PUJ obstruction -No
Critical
point:circumcision
should not be
Case 6
Case 6 questions and Answers
• What is this? Cystic disease of the kidney- Autosomal Dominant Polycystic
Kidney Disease (Adult PKD)
• How do you classify cystic diseases of the kidney?
– Genetic versus non-genetic
• Genetic=
– A Dom PKD, A Rec PKD, Juvenile nephropthis, Medullary Cystic Disease, Congenital
nephrosuis, Familial Hypoplastic Glomerulocystic disease
– Multiple malformation Syndromes with renal cysts- VHL disease, TS
• Non-genetic=
– Multicystic dysplastic kidney
– Benign multilocular cyst
– Simple cysts, medullary sponge kidney
» Sporadic Glomerulocystic disease
– Acquired renal Cystic disease
– Calyceal diverticulum
– Cystic RCC
• What genitourinary complications arise with Aut Dom PKD?

– Hypertension;Bleeding cysts, Subcapslar bleeds, Infected cysts
– Renal Failure
– RCC controversially increased- may be scanning/imaging phenomenon
• What other conditions are associated with Aut Dom PKD?
– Aneurysms (Berry); Other cysts of lung, liver, pancreas, spleen
– Mitral valve prolapse, Diverticulosis
Case 7
• Case 7 Questions and Answers
This culture in the petri dish and gram stain is taken from the urinary tract- what is the likely
organism? Hint gram negative stain
– E.Coli
• What constitutes a positive MSU on culture and how sensitive/specific is this?
– If greater than 105 Colony Forming Units= 90% sensitivity/specificty but 30-50% women with classic
UTI will be missed (because may only gro 10 3 etc)
• What are the main types of organisms causing community acquired UTI in females?
– E.coli, Proteus, Klebsiella, Enterococcus faecalis, Staph saprophyticus
• How do organisms enter the urinary tract in males? Females?
• What factors allow E.COLI to enter and survive in the female urinary tract?
– Fimbriae, O Antigens, K Antigens, Alkaline vaginal mucosa (postmenopausal) kept low pH by
lactobacilli in premenopausal, Loss of estrogen- postmenopausal
• Host defence preventing UTI
– 1. Urine flow/regular micturition
– 2. Urine inhibitors- pH, urea, salts, high osmolality etc
– 3. Bladder mucosa- polysaccharides, Tamm-Horsfall protein, oligosaccharides
– 4. Immune system- uroepithelial secretion interleukins, antibodies, IGA also IgG, IgM
– 5. Good hygiene
• What are the principles of treating an uncomplicated UTI?

– Hydration, antibiotics (to culture) excreted into urinary tract- usually only 3 days required , Symptom
relief e.g Ural
Case 8
Case 8 questions
• What is this? TURBT chips (also looks like TURP chips)
• What do you want to know from pathologist?
Type, stage
• Factors in TCC leading to:
Progression/Recurrence
• E.g Stage, grade, CIS, multifocality, time to recurrence
SCC
How common western world in terms % Bladder ca? 1-7% versus 75% Egypt
• Risk Factors:
– Chronic inflammation (IDC, infections, Irritation, calculus, diverticuli)
– Schistosomiasis
– Leukoplakia
– Pelvic radiotherapy
– Cyclophosphamide
– Squamous metaplasia associated up to 20%
• Schistosomiasis- life cycle in brief (if doing well)? See over

Case 9
Case 9 questions
• Describe specimen- bi-valved kidney with well-
circumscribed mass- Dx? RCC
• Types of RCC
– Clear Cell, Papillary,Chromophobe, Coll Duct, Medullary,
Cystic, Sarcomatoid
• Prognosis
– Stage, grade, type
• Grading system- see over Grade Nuclear
Size
Nuclear Outline Nucleoli
• Staging systemPrimary tumor (T) 1 10µm Round and Absent or

• TX - Primary tumor cannot be assessed Uniform inconspicu
• T0 - No evidence of primary tumor ous
• T1 - Tumor 7 cm or smaller in greatest dimension, limited to the kidney
• T2 - Tumor larger than 7 cm in greatest dimension, limited to the kidney
• 2
T3 - Tumor extends into major veins or invades adrenal gland or perinephric tissues but not beyond the Gerota fascia 15µm Irregular Small
• T3a - Tumor invades adrenal gland or perinephric tissues but not beyond the Gerota fascia
• T3b - Tumor grossly extends into the renal vein(s) or vena cava below the diaphragm
• T3c - Tumor grossly extends into the renal vein(s) or vena cava above the diaphragm 3 20µm Irregular Prominent
• T4 - Tumor invading beyond the Gerota fascia
• Regional lymph nodes (N) - Laterality does not affect the N classification
• NX - Regional lymph nodes cannot be assessed
• N0 - No regional lymph node metastasis 4 >20µm Bizarre Prominent,
• N1 - Metastasis in a single regional lymph node heavy
• N2 - Metastasis in more than 1 regional lymph node
• Distant metastasis (M)
chromatin
• MX - Distant metastasis cannot be assessed clumps
• M0 - No distant metastasis
• M1 - Distant metastasis
Cell Type Features Growth Cell of Cytogenet
Pattern Origin ics
Clear cell Most Acinar or Proximal 3p-
common sarcomatoi tubule
Papillary Bilateral dPapillary or Proximal +7, +17, -
type I and and sarcomatoi tubule Y
IIChromop multifoca d
Chromoph Indolent Solid, Cortical Hypodiplo
hilic l
obic course tubular, or collecting id
Oncocytic Rarely sarcomatoi
Tumor duct
Cortical Undetermi
metastasi dnests collecting ned
Collecting ze
Very Papillary or duct
Medullary Undetermi
duct aggressiv sarcomatoi collecting ned
e d duct
Pathology Exam
25 March 2012
Station 1
This penile lesion has been present for 5 years without
metastasising
• What is this lesion?

• What other names?
• How does it progress?
• What are the key microscopic features?
Answer
• This penile lesion has been present for 5 years without metastasising
• Verrucous carcinoma (Not invasive SCC)
What other names?
• Giant condylomata, buschke-Lowenstein tumour
• Exophytic mass, smells, ulcerates
• How does it progress?
• Infiltrates deeply, local destruction
• Fistula into urethra
• Almost never metastasises
• What are the key microscopic features?
• Massive keratinisation
• Cells well differentiated
• Few mitoses
• Wide local excision
• Not radiotherapy (may cause increased malignant potential)
Station 2
• What is it?
• Embryology?
– Fusion of lower pole of kidney before ascent
• Associations?
– Urological
• Infection
• Stones
• PUJ obstruction
• Injury by blunt trauma
• VUR
• Malignancy
– Non-urological
• VSD
• Turner
• Down’s
Station 3
• What CT classification of renal cyst do you
know?
– Bosniak
• What is it?
• Malignant potential?
Bosniak Risk of
Radiographic Features Management
Classification Malignancy
I Water density None Only if symptomatic

Homogeneous Surveillance not necessary
No septa
No calcification
No enhancement
II Few thin septa Very rare Only if symptomatic
Fine calcification Surveillance not necessary
No enhancement
<3cm hyperdense lesion
IIF
No enhancement 5%-20% Periodic surveillance
Multiple thin septa
Thick/nodular calcification in wall/septa
>3cm hyperdense lesion
III Thick or irregular septa 50% Surgical excision
Thick or irregular calcification
Mild to moderate heterogeneity
No enhancement
IV Thick walls or nodular areas 75%-90% Surgical excision
Marked heterogeneity
Enhancement
Station 4
• What is this?
• What is this?
– Schistosome ova with terminal spine
• Aquatic
• Eggs🡪 extrude miracidia into fresh water
• Enter snails of Bulinus species
• Asexual multiplication: miracidum 🡪 sporocytes 🡪 105 cercariae
• Enter fresh water
•
• Humans
• Cercariae penetrate unbroken skin
• Matures in intrahepatic portal blood
• Adults pair off and move to pelvis where egg laying begins and is maintained until the
death of the worm.
• Male and female pair and produce 200-500 eggs per day
• 20% eggs excreted into urine/faeces
• Some microembolise to lungs/liver
• Some are destroyed by host’s granulomatous response
• Remaining entrapped eggs calcified and accumulate
• Medical
– Praziquantel (interferes with ion transport), 2 oral doses
20mg/kg, well tolerated (eTG Antibiotics 2011)
• Surgical
– Reserved for complications that did not respond to adequate
medical Rx
– Ureteral obstruction: excision, dilatation,
– Reconstructions: Leadbetter-Politano reimplants, Boari flap
– Diversion: ileal conduit, suprapubic intravesical ureterostomy
– Contracted bladder: diversion, ileo-cystoplasty, hydrodistention
Station 5
• 4 components of ESWL system
• What energy sources are used to generate shock wave
• Mechanism of stone fragmentation
• Complications
– Renal: haematoma, haematuria, infection, pain, steinstrasse
– Non renal: lung (haemoptysis), pancreatitis, bruising
• Contraindications
– AAA, infection, pregnancy, obstructed kidney, coagulopathy
Answers
• 4 features
– Energy source to generate shock wave
• Electrohydraulic
• Piezoelectric
• Electromagnetic
– Focus wave at a focal point
– Coupling medium
– Stone localisation system
• Mechanism of stone fragmentation
– Compressive fracture
• From layering of stone
– Cavitation
• Wave in fluid expands and breaks stone
– Dynamic fatigue
• Accumulated damage
– Spallation
• Reflected wave from interface causes stone breakage
• Complications
– Renal: haematoma, haematuria, infection, pain, steinstrasse
– Non renal: lung (haemoptysis), pancreatitis, bruising
– AAA, infection, pregnancy, obstructed kidney, coagulopathy
Station 6
• Pt with neurogenic detrusor overactivity
– Failed anticholinergic therapy
• What is Botox?
• How does it work?
• What dose for this indication?
• Describe the preparation and administration
• Contraindications?
• Complications?
Answer
What is it 🡪 botulinum toxin (from Clostridium botulinum)
How does botox work?
• Inhibits SNAP protein, prevent presynaptic release of Ach
Onset of action, duration? 5-7 days, 6-9 months
Dosage? 100 units non neuropathic 200 units neuropathic
How do you do it?
- Anaesthetised
- Antibiotics NOT GENT
- Rigid cystoscopy
- How to mix botox: 10ml NSaline for each vial: 10units per ml
– What degree scope: 0 degree scope
Answer
Complications from botox?
• UTI – 25% (despite prophylactic ABx)
• Urinary retention – requiring CISC 20%
• Transient flu-like symptoms
• Generalised weakness <5% (bad if quad/paraplegia)
– Lasted 2 wks – 2 months
– Systemic effect
– Decreased with careful injection technique and volume and decreased
dose.
• Visual disturbance (diplopia / blurred vision)
• Dysphagia
– Pre-existing neuromuscular conditions such as
Myasthenia gravis or Eaton Lambert syndrome.
– Infected site
– Known hypersensitivity
– Pregnancy
– May be potentiated by drugs that interfere with
neuromuscular transmission including
aminoglycosides.
Station 7
Case 3a
• What is this?
• What are the causes of this appearance?
• What investigations would you order?

Answer
• What is this? medullary nephrocalcinosis
• What are the causes of medullary nephrocalcinosis?
– Medullary Sponge Kidney
– RTA 1
– Hyperparathyroidism
– Papillary necrosis
– Sarcoidosis
– Hyperoxaluria
– Hypercalciuria
– Hypervitaminosis D
– Renal TB
– Milk-alkali syndrome
– End-stage renal vein thrombosis (small calcified kidney)
• What investigations would you order?
– Serum
• Ca++ (PTH if elevated), PO4, Alb
• U&E
• ? ACE, quantiferon gold
• ? TSH, Mg, Vit D
– Urine
• FWTU- ↑pH for RTA, leuks for chronic infection.
• 24hr urine- pH, vol, Ca, oxalate, citrate, UA, creat, protein
Station 7 – Part 2
• This is a urine microscopy of a stone former.
What are they?
• What is the condition and the metabolic
pathology? Which chromosomes?
• What investigations would you do?
• What are the principles of long term treatment
management?
Station 8
• What is TUR syndrome?
• Mechanism
• Risk factors
• Treatment
TURP syndrome
Due to entrance of hypotonic irrigation fluid into
the intravascular space
1. Dilutional Hyponatraemia
2. Fluid overload
3. Glycine toxicity
Dilutional Hyponatraemia
Mechanism Symptoms
● Excess absorption of ● Uncommon if Na+ > 120
hypotonic irrigation fluid ● Nausea (🡹 ADH),
● Osmotic diuresis (induced vomiting, headache,
by irrigating fluid)
malaise
● Solute loss
Effects of hyponatremia
● Cerebral oedema
● Seen on CT after ≤ 1L Glycine
absorption
Glycine Toxicity
TURP
• Glycine
• 1.5% Glycine
• Hypotonic (200mOsm/L)
• Less haemolysis caused than water
• Metabolised to ammonium by liver
• May cause ammonium toxicity
• Use with caution in patients with liver failure
• Setup
• 60cm from top of bag to symphysis pubis
TURP
• Clinical features of TUR Syndrome
• Restlessness and confusion

• Visual disturbances
• Hypertension
• Bradycardia
• Respiratory difficulty, hypoxia
• N+V
• Seizures
• Hypothermia
TURP
• Causative mechanisms
• Occurs in 2% TURP
• Risks- Large gland, bleeding, sinuses, prolonged resection
• Excessive absorption of hypotonic fluid leads to
o Dilutional hyponatraemia
o Hypervolaemia
o Brain swelling from hyponatraemia
o Ammonium CNS toxicity (Glycine converted ammonium- crosses
BBB)
o Hypothermia
o Pulmonary oedema (hypoxia)
TURP
• Treating TUR Syndrome
• High index of suspicion
• Cease resecting, switch to Saline, IDC
• O2 by mask
• ABG (Na+, O2), formal U&E
• 20-40mg IV Lasix
• Warm patient
• CXR in recovery- APO
• Slow IV Normal Saline
• HDU monitoring (darkened room)
• Check U&E 6 hours
• If not responding
o Repeat 40mg IV lasix
o Diazepam and phenytoin for seizures
o Consider IV mannitol
o Consider slow 200ml 3% saline
Station 9
• What is the clinical syndrome?
• What are the manifestations?
Tuberous Sclerosis
• TSC1 gene chromosome 9, TSC2 Chrom 16
• Clinical Features
• Urologic
o Renal cysts
o AML’s in 50% (hamartoma)
o Increased risk of RCC (2%)
• CNS
o Hamartomas- brain, retina
o Mental retardation
o Seizures
• Skin
o Ash leaf spots on trunk, buttocks (areas of hypopigmentation)
Station 10
• Etioogy?
• Principles of Management
Pathogenesis
• 60-70% idiopathic
• Malignancy 8-10%
• Drugs
• Periaortitis
• Radiation
• Retroperitoneal trauma
• Local inflammation
• Autoimmune connective
tissue disease
Etiology
Medication Malignancy
• Beta blockers
• Lymphoma, sarcoma,
• Methylsergide
• Methyldopa
breast, prostate, GIT,
• Amphetamines, cocaine cervix
• Phenacetin
• Pergolide • Malignant cells in
retroperitoneum →
Local inflammation exuberant desmoplastic
• Chrons disease
response
• Ulcerative colitis
• Sclerosing cholangitis
Etiology
Autoimmune disease
• Ankylosing spondylitis
• SLE
• Scleroderma
• Systemic vasculitis
– Wegener granulomatosis
– Polyarteritis nodosa
– Raynaud’s disease
• Rheumatoid arthritis
• Hashimoto’s thyroiditis
• Autoimmune glomerulonephritis
• HLA-B27 or HLA-DRB1 03 haplotype

Management
Initial mx – determined by clinical status
1. Urgent decompression – stent / neph tube

2. Delineate anatomy and establish diagnosis
• +/- biopsy (definitve diagnosis)
• Occult malignancy
3. Medical / Surgical management
Station 11
During TURBT obturator kick
experienced…
• Describe methods to reduce this risk
• Mx if perforation occurs
Station 12
Large obstructing R ureteric calculus. N
contralateral kidney
• Describe changes in R ureteric pressure over the

first 24 hours of obstruction
Pt with 2L retention 🡪 relieved with IDC
• What is post obstructive diuresis?

– Definition
– Mechanism
• Treatment
Unilateral Ureteric Obstruction
1. First 1-2 hours
– Increased renal blood flow (RBF)
– Obstruction 🡺 Increased ureteric pressure
2. 3-4 hours
– Renal blood flow decreases
– Ureteric pressure remains high
3. > 5 hours
– Further decreases RBF
– Decrease ureteric pressure
– Reduced GFR
• Cortical to medullary shift
Unilateral Ureteric Obstruction
Mechanism
1. Vasodilation
– Decreased sodium delivery to the macula densa
– PGE2 *
– NO
2. Decreased GFR
– Increased afferent resistance
– Angiotensin 2
– TXA2 / Endothelin
– Outer to inner cortical RBF shift
Postobstructive diuresis
• Postobstructive diuresis is defined as diuresis of
more than 200 mL/h for at least 2 hours. Patients
with severe diuresis should receive intravenous
fluid replacement in the form of half normal
saline at 80% of the hourly urine volume for the
first 24 hours, then 50%. Postobstructive diuresis
usually lasts 24-72 hours.
Postobstructive diuresis
• Rare in UUO
• BUO or obstruction of solitary kidney
• Mechanism
– Increased circulating fluid / solute retention / urea
nitrogen / other osmotic substances
– Dysregulated concentrating ability (ADH)
– Significantly elevated ANP (BUO vs UUO)
– Inhibition of Na transport in collecting duct
Clinical management of POD
• Supplemental fluids
– Oral fluids preferred
– IV supplementation IF required
• No role for graduated catheter release
• Serum electrolytes (12-24/24)
• Monitor in appropriate environment
Station 13
• Presentation:
• DDx:
• Treatment:
• Histology of female urethra
• Presentation (usually post meno women):
– Haematuria
– Spotting
– Pain
• DDx:
– Urethral carcinoma
– Urethral prolapse
– Periurethral gland abscess
• Treatment:
– Topical estrogen, excision
Station 14
• What is in this and mechanism of action
• What is in this and mechanism of action
Floseal
Surgicel
REGISTRAR TUTORIAL TESTIS
CANCER
• 19 yr old male presents painless right testicular
lump , otherwise well, h/o of right orchidopexy for
undescended testis age 8,
• Examination = left testis approx 10mls, mass in
right testis,(confirmed on u/s)no other abnormality
• Afp = 200 b hcg = 300
• CT normal, CXR normal
• Tell me about afp and b hcg
afp = single chain pp, mw of 70,000,
prod by tumors of hepatic, GIT and
yolk sac differentiation.
Assoc. yolk sac tumors and
embryonal ca.
half life 5-7 days
B- HCG= glycoprotein hormone
MW = 38,000
Produced by trophoblastic
tissue[placenta, syncytiotrophoblastic
cells and chorioCa.
Half life 24- 36 hrs
• Undergoes orchidectomy
• What will you do post op ?
• What is the likely pathology?
• What are important features of path report
• Post op need to be sure markers fall according to
half life and normalise
• Path must be nsgct – if pathologist says pure
seminoma = go back and look again
• Need to know whether lv invasion, T stage,
WHAT IS THIS ?
• Path = mixed nsgct, confined to testis with
vascular invasion,
• What stage is this ?
• Tell me about staging ?
• Post op markers normalise.
• What is risk of nodal mets ?
• What are treatment options?
• Staging of germ cell tumors of testis
• pT1 – confined to testis/epidid– no vascular or
lymphatic invasion ( may invade tunica
albuginea but not tunica vaginalis)
• pT2- vascular or lymphatic invasion , or invasion
into tunica vaginalis
• pT3 – invasion into spermatic cord
• pT4 – invasion scrotum
• cN1- nodal mass <2cm or multiple nodes none
>2cm (pN1 = and 5 or fewer positive nodes )
• cN2 nodal mass 2-5cm or multiple nodes
/masses none >5cm (pN2= and >5nodes positive
or extranodal extension tumor )
• pN3 nodes >5cm
• M1 = distant mets
• M1a = non regional LN’s or lung
• M1b= other sites
Clinical stage 1 nsgct
• Stage 1A = pT1, N0,M0,S0
• Stage 1B= pT 2-4 , “ “ “
• Stage 1S= any pT, N0,M0,S1-3
• RISK METS IN CLINICAL STG 1 NSGCT
• Overall = 30%
• HIGH RISK GP =50% risk
-lymphovascular invasion, (predom
embryonal,absence yolk sac elements-not indep
variables)
• LOW RISK GP = 10% risk
- 90%are pathol stg 1, ie ok for surveillance
Options high risk group
• Surveillance – 50% risk relapse , (80%of these in first
year, only 1%/yr after yr 3
- site recurrence - 60%retroperit,
15-30%chest, 10% only markers elevated
- usually low vol but 10% high vol despite adeq surveillance
- if recurrence – 3 CYCLES BEP- still 98% survival if
proper surveillance
Options high risk gp CS1 nsgct
• RPLND – rationale overall 30% pts understaged
by ct(75%low vol pN1)- 6-8% anejac
• After rplnd if :
-pN1 (stg 2A)surgery alone curative 70-90%
-pN2,3(stg 2B,C) “ “ “ 50%
If adjuvant chemo (2 BEP) for those positive nodes
= rec rate 2%
• After rplnd for CSI :
- retrperit rec v rare (<2%) ?surgical error
- rec rate approx 10% (low risk) 30% (high risk)
for path stage 1 disease - usually lungs,
mediastinum, or markers
- most relapse <2yrs
- if relapse - BEP and still 96%long term survival
Options high risk gp CSI nsgct
• Primary chemo- 2 cycles BEP-preferred rx in
europe
- Decreases risk recurrence to <5%
- BUT 50% did not need chemo –
- --etoposide causes increase risk leukaemia
- - if late failure increase difficulty salvage ie
chemoresistance
EAU GUIDELINES FOR THE TREATMENT OF NSGCT
STAGE I - CS 1
Risk-adapted treatments based on vascular invasion
CS1A (pT1, no vascular invasion): low risk

1. If the patient is willing and able to comply with a surveillance
policy and long-term (at least 5 years) close follow-up should be
recommended.
2. Adjuvant chemotherapy or nerve-sparing RPLND in low-risk
patients remain options for those not willing to undergo
surveillance. If RPLND reveals PN+ (nodal involvement) disease,
chemotherapy with two courses of PEB should be considered
CS1B (pT2-pT4); high risk

3. Primary chemotherapy with two courses of PEB should be
recommended.
Surveillance or nerve-sparing RPLND in high-risk patients remain

• For CS1 with RF – 2 cycles of BEP not 3
• What is the risk of cancer in the opposite testis ?
• What are the risk factors ?
• What is the risk of cancer in an undescended
testis ?
• Risk contralat metachronous tumor 1.5% over 5 yrs
• 5%risk of cis – risk factors for cis:
- prior infertility, cryptorchidism, testis<12ml, age
<30, microcalcification
If bx only pts with risk factors will pick up 85% of pts
with cis
If cis – 50%risk of cancer in 5yrs
If bx negative – v unlikely to develop later cis or
cancer
Treatment of CIS
• Surveillance –
• RT – 20Gy – causes loss fertility, testosterone n
in short term ?long term effect
• Orchidectomy
• Risk of cancer in undescended testis is 10 to 40
x
• Risk cancer in intraabd testis – 5%
• “ “ “ inguinal testis – 1%
25yr old male – presented with left
renal colic
Mass left testis

B hcg = 30
Afp = 2
Look at next 2 scans
How will you proceed?
• An inguinal orchidectomy is performed .
• Look at the next 2 slides .
• What type of tumor do you think this is?
• Tumor is a mixed seminoma and embryonal
carcinoma
• What are the treatment options?
Treatment options stage 2A/B nsgct
• RPLND(mainly nth america )
2A30%relapse (if v low vol and <6 nodes and neg
markers only 5% relapse ie avoid chemo)
2B – 50%relapse
-If then give 2 cycles BEP to those with positive
nodes only <2% relapse
• 3 cycles BEP –but 30%require postchemo –rplnd
for resid tumor with anejac 16%,and increase
surgical morbidity
• Pt had 3 cycles of BEP –
• What are the complications of this type of chemo
?
• COMPICATIONS OF CHEMO
• PLATINUM-nephrotoxicity(long term 10-20%
decrease of renal fn,HT in 25%long term,nausea
and vomiting, bone marrow
suppression,neurotoxicity ( high freq hearing loss,
peripheral neuropathy, tinnitus all up to 30%)
• ETOPOSIDE – bleeding, myelosuppression,
allergy, secondary leukaemia(5%).
• BLEOMYCIN-pneumonitis with late pulm fibrosis
in 5%( fatal in 3%of these) measure DLCO pre
treatment(risk factors= preexisting lung disease
smoking, male >40yrs, minor renal dysfunction),
raynauds phenomenon
• ALL – increased risk of infertility, DVT/PE
• Long term study 10 yrs post chemo :
- 80% increased chol
- 39% hypertension
- 25% raynauds
- 22% microalbunimemia
- >2x risk CV disease
• Look at next 3 scans done 6mths following
chemo .
• Markers remain normal
• What is the significance of para-aortic nodes post
chemotherapy?
• What are the options?
• If rising markers need salvage chemo.
• If normalised markers and resid mass >1cm need
PC- RPLND( can be nerve sparing in about 50%)
• Decision made to perform RPLND
• What are the principles of this operation?
• What are the issues regarding sexual function
post op?Why does this occur ?
• Boundaries rplnd – line up middle aorta, up to
renals, laterally to ureter, and down to iliac a
bifurcation . Attempt to spare front of aorta below
IMA and area betn aotic bifurcation
• Emission controlled by T12 –L3 sympathetic –
travel in lumbar sympathetic trunk- leave as
lumbar splanchnic n’s ( pre and post
ganglionic)and join intermesenteric plexus over
front of aorta which becomes the hypogastric
plexus below the ima – then pelvic n’s to organs.
• Bladder neck tightening – sympathetic
• Pudendal somatic S2-4 – relaxation ext sphincter
and contraction of bulbocav and ischiocav.
• Rplnd cause -failure emission
- failure ejaculation or retro ejac
If only unilat dissection and preserve below ima =
preserve ejac in 90% with no change recurrence
rate
For CSI almost always modified unilat rplnd
If high vol disease or macro contralat disease do
full bilat rplnd
Jetmir zarifi
• 19 yr old male presents mass left testis and
palpable mass left abdo
• LDH 1700, afp 2,300, hcg 12,000
• Orchidectomy path = embryonal involving cord
(pos margin at deep ring)
• Look at next 5 pix
• How would you manage him ?
• What is his ‘risk’ staging?
• Risk stratification for metastatic nsgct
-good prognosis-55% of patients-90%5YPFS -low
markers and no non pulm visceral mets
(afp<1000, hcg <5000, LDH<1.5xn)
-intermed prognosis-28%of pts-75%5YPFS–
intermed markers(afp1000-10,000, hcg 5,000-
50,000, LDH 1.5-10x n) and no non pulm visceral
mets
-poor prognosis-15% of pts-40% 5YPFS
liver , cns , bone , intestinal mets OR primary
mediastinal tumor, or high markers.
• For good prognosis pts 3 cycles of bep
• For intermed and poor risk pts – 4 cycles of bep
or VIP if risk of bleomycin lung toxicity
• Has 4 cycle BEP
• Markers normalise, chest ct n, f/u abd ct shows
2cm paraaortic node
• What would you advise ?
• Pt advised to have pc –rplnd
• Discuss possible path of resected nodes
• Pt refused rplnd
• 3m later presents headache, afp 10, hcg 9, abd ct
still 13mm p/a node
• Look at next 2 films – what would you advise ?
• NECROSIS 50%
• MATURE TERATOMA40%- need to fully resect
otherwise – growing teratoma synd
or malig transformation to viable gct, undiff ca,
sarcoma
If necrosis/mature teratoma – no further rx req as risk
relapse only <10%
• VIABLE TUMOR 10% - 50% relapse and therefore
need salvage chemo
• Undergoes craniotomy and post op rt
• Path = embryonal again
• Has salvage chemo with TIP(paclitaxel)
• 1yr later no evid recurrence
32 yr old male – short h/o mass right
testis, exam otherwise normal
Markers n
Abdo pelvic ct normal
Look at next 2 pictures.
What do you think this lesion is?
• Look at next slide
• What are the microscopic features of seminoma?
• The pathologist reports this as pure seminoma
however the beta HCG is 100-what do you
think?
• What if the AFP were high

• Micro features seminoma- large clear cells with
prominent fibrous septa and lymphocytic
infiltration of the septa.
• Even if b hcg 100 can be pure seminoma – may
contain syncytiotrophoblastic cells
• if AFP high ask pathologist to look for

nonseminomatous germ cell elements –
CANNOT be pure seminoma
• What staging system for seminoma do you use?
Stage 1 – confined to testis
Stage 2 –nodes under diaphragm
A = <2cm
B = 2-5cm
C= 5-10 cm
D= >10 cm
Stage 3 –nodes above diaphragm
Stage 4 – parenchymal mets
What are treatment options for stg
1(T1-4 , N0,M0) seminoma post
orchidectomy
Stg 1 seminoma
• 15-20% relapse after orchidx with no other
treatment.
• If tumor >4cm or rete invasion = 32% risk
• Otrherwise 12% risk
RADIOTHERAPY –p/a nodes –20-25gy
-1-3 %relapse rate – almost always outside
field [supraclavicular, lung, mediastinum,
bone,]
-esp first18m.Risk factors for relapse –
anaplastic, local invasion eg rete,or large
tumor
SURVEILLANCE –not commonly used
- 10-20% relapse rate-usually 12-18m, occ>4yrs ,
site relapse 90% p/a nodes
- If relapse treat with RT- but 20% risk second
relapse( always outside RT field )and require
chemo .
- 5yr relapse free survival 82%
- Drawback – must do suffic freq ct to detect
recurrences <5cm ie every 4m for 4yrs
- May still present later and more likely to need
chemo
- 70% of relapses occur <2yrs but 7% >6yrs
CHEMOTHERAPY
• 2 cycles carboplatinum- prob equivalent to rt
• LOOK AT NEXT 8 SCANS
• WHAT ARE YOU LOOKIN FOR ?
• SCANS SHOW NO LN’S BUT INCIDENTAL
HORSESHOE KIDNEY?
• INCREASES RISK OF RT !
• OPTIONS CHEMO OR WW
• WHAT ARE RX OPTIONS FOR MORE
ADVANCED SEMINOMA
Stage 2A/B seminoma
• Usually RT- approx 30Gy hockey stick to include
ipsilat iliacs
• 2A(any pT, N1) ie<2cm nodes –5YRPFS-95%
• 2B(any pT, N2) ie 2-5cm nodes –5YRPFS= 90%
• If fails consider ?nsgct elements
• If resid mass<3cm observe- only 3%progress- if
larger resect mass only 20% resid cancer
• Also 5-10% failure outside rx area
• Stage 2C seminoma (any p, N3 ie nodes
retroperit >5cm )- if only rt then 25-50%failure
rate outside rx area
• Therefore initial chemo –BEP
• Stage 3(nodes above diaphragm) or 4 ie

metastatic = BEP

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FRACS Urology Path Exam

Stuff put together by Conrad

• Effect of Mitomycin Post-op

• Macroscopic – yellow plaques in bladder

• Found incidentally during biopsy for infertility

• Overall incidence 0.8% (same as testicular ca)

Stuff put together by Conrad

• Nx Regional LNs cannot be assessed

“2 red, 2 white, 2 horny”

Nx Regional LNs cannot be assessed

• Note number of cysts increases with age

• Family history spanning 3 generations

• Causes of Maturation Arrest

• Mitosis - spermatogonia → primary spermatocytes

• If diagnosis unclear or further suspicion of

• Associated with Tuberous Sclerosis

• Indications for treatment- embolize

Stuff put together by Conrad

• Forms in alkaline urine

• Test for RTA:

• Hereditary Leiomatosis and Renal Cell Carcinoma (HLRCC)

Stuff put together by Conrad

• Difficult to distinguish from chromophobe

Acoustic lens Parabolic

• Chronic histological changes

• Anaplastic Seminoma (10%)

• Spermatocytic Seminoma (5%)

• BHCG - 10% classical seminomas have syncytiotrophoblasts

• AFP - Not elevated in pure seminoma

• LDH - May be elevated with retroperitoneal disease

• Relapse rate of T1 disease

• Investigate cause – blood film, electrophoresis, sickle

Stuff put together by Conrad

• Screening tests in asymptomatic patients-

• Pre op phenoxybenzamine (until postural drop)

• Associated with MEN-2, neurofibromatosis-1, familial

Clexane (Low molecular weight heparin)

• Most versatile of all medical lasers, used on stones and

• Commonest male congenital abnormality (1 in 250)

• Inflammatory Phase (hours)

• 10-15% malignant renal tumours

• Mutation oncogenes chromosome 7,17, loss of Y

• Hereditary Papillary Renal Cell Carcinoma (HPRCC)

• Spina Bifida Cystica

Stuff put together by Conrad

• T1a <4cm confined to kidney

• Dissolution with Ural pH>6.0 (if compliant)

• Allopurinol if elevated serum uric acid / gouty diathesis

• Exclude myeloproliferative disorder with blood film

• Principles of Surgical Excision

• Bell Clapper deformity

• Half life = 5-7 days

• Secreted by syncitiotrophoblastic cells

• Half life = 36 hours

• Validated across centres

• Should be used as a guide only

• CIS sensitivity 90%

• Highly specific in high grades >90%

• 50% chance of prostate cancer on 2nd biopsy

• In urine also called the cyanide nitroprusside test