Urology 2000 - Angelfire

38 Pages·1999·0.5 MB·English

by  Enrica Aguilera

UROLOGY
Dr. M.A.S. Jewett
Aaron J. Blumenfeld and Hao Ming Wu, editors
T.J. Lou, associate editor
HISTORY AND PHYSICAL . . . . . . . . . . . . . . . . . . . . 2 PENIS AND URETHRA. . . . . . . . . . . . . . . . . . . 28
Peyronie's Disease
KIDNEY AND URETER. . . . . . . . . . . . . . . . . . . . . . . 2 Priapism
Renal Stone Disease Phimosis
Stone Types Paraphimosis
Benign Renal Tumours Penile Tumours
Malignant Renal Tumours Erectile Dysfunction
Carcinoma of the Renal Pelvis and Ureter Urethral Syndrome
Renal Trauma Urethral Stricture
Urethral Trauma
BLADDER. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
Bladder Carcinoma HEMATURIA. . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
Neurogenic Bladder
Incontinence INFERTILITY. . . . . . . . . . . . . . . . . . . . . . . . . . . 33
Urinary Tract Infections
Recurring/Chronic Cystitis PEDIATRIC UROLOGY. . . . . . . . . . . . . . . . . . 35
Interstitial Cystitis Congenital Abnormalities
Bladder Stones Hypospadias
Urinary Retention Epispadias-Exstrophy
Bladder Trauma Antenatal Hydronephrosis
Posterior Urethral Valves (PUV)
PROSTATE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 UPJ Obstruction
Benign Prostatic Hyperplasia (BPH) Vesicoureteral Reflux (VUR)
Prostate Specific Antigen (PSA) Urinary Tract Infection
Prostatic Carcinoma Daytime Incontinence
Prostatitis/Prostatodynia Nephroblastoma
Ectopic Testes
SCROTUM AND CONTENTS. . . . . . . . . . . . . . . . . . 23 Ambiguous Genitalia
Epididymitis
Orchitis
Torsion
Testicular Tumours
Hematocele
Hydrocele
Spermatocele/Epididymal Cyst
Varicocele
Hernia
MCCQE 2000 Review Notes and Lecture Series Urology 1
HISTORY AND PHYSICAL Notes
HISTORY
o pain: location (CVA, genitals, suprapubic), onset, quality (colicky,
burning), severity, radiation
o associated symptoms: fever, chills, weight loss, nausea, vomiting
o irritative symptoms: frequency, nocturia, dysuria, urgency
o obstructive symptoms: hesitancy, straining, intermittency, decreased
force or caliber of stream, prolonged voiding, post-void dribble,
incomplete emptying
o incontinence: stress incontinence, urge incontinence, overflow
incontinence, history of neurological problems, past pregnancies and
method of delivery, past abdominal-pelvic operations
o urine: hematuria, pneumaturia, foul smell, colour (cloudy, white, orange)
o urethral discharge (colour, amount, smell), sexual history, UTIs, external
skin lesions, lymphadenopathy
o others: renal calculi, infertility, erectile dysfunction, congenital
disorders, family history of urological disease
PHYSICAL
o inspection
• abdomen: masses, scars from previous operations, suprapubic
distension, hair distribution
• penis: circumcision, phimosis/paraphimosis, epispadias,
hypospadias, urethral discharge, superficial ulcers or vesicles,
venereal warts, meatal stenosis
• scrotum: testicular atrophy, testicular asymmetry, balanitis,
dilated veins (varicocele) on standing, scrotal
erythema/edema/cysts/hemangiomas
o palpation
• examine all of the following: kidneys, bladder, penis, testes, vas
deferens, epididymis, prostate
• abdomen: masses, CVA tenderness, suprapubic distension/tenderness
(examine for dullness on percussion), lymphadenopathy
• penis: Peyronie’s plaques, penile masses, penile tenderness
• scrotum: scrotal tenderness/masses (size, consistency, location,
mobility, shape), hernia, hydrocele, spermatocele, spermatic
cord (varicocele, fusiform enlargement, thickening of the cord),
absence of vas deferens, epididymal size/induration/tenderness
• prostate (on DRE): size, consistency (rubbery, hard, boggy,
indurated), nodularity (size, location), tenderness, warmth
KIDNEY AND URETER
RENAL STONE DISEASE
Incidence
o 10% of population
o male:female ratio 3:1
o 50% chance of recurrence by 5 years
Clinical Presentation
o urinary obstruction ––> distension ––> pain
• flank pain from renal capsular distension (non-colicky)
• severe waxing and waning pain radiating from flank to groin due
to stretching of collecting system or ureter (ureteral colic)
• never comfortable, always moving
o nausea, vomiting
o hematuria, usually microscopic, occasionally gross (90%)
o symptoms of trigonal irritation (frequency, urgency), diaphoresis,
tachycardia, tachypnea
o +/– fever, chills, rigors secondary to pyelonephritis
Differential Diagnosis of Renal Colic
o other causes of acute ureteral obstruction
• UPJ obstruction
• sloughed papillae
• clot colic from gross hematuria
Urology 2 MCCQE 2000 Review Notes and Lecture Series
Notes
KIDNEY AND URETER
. . . CONT.
o radiculitis (L1 nerve root irritation)
• herpes zoster
• nerve root compression
o pyelonephritis (fever, chills, pyuria)
o acute abdominal crisis (biliary, bowel)
o leaking abdominal aortic aneurysm
Location of Stones
o calyx
• may cause flank discomfort, recurrent infection or persistent
hematuria
• may remain asymptomatic for years and not require treatment
o pelvis
• tend to cause UPJ obstruction
o renal pelvis and one or more calyces
• staghorn calculi
• often associated with infection
• infection will not resolve until stone cleared
• may obstruct renal drainage
o ureter
• < 5 mm diameter will pass spontaneously in 75% of patients
o the three narrowest passage points for upper tract stones include: UPJ,
pelvic brim, UVJ
Investigations
o screening labs
• CBC ––> elevated WBC in presence of fever suggests infection
• lytes, Cr, BUN ––> to assess renal function
o urinalysis
• routine and microscopic (WBCs, RBCs, crystals)
• culture and sensitivity
o KUB x-ray
• 90% of stones are radiopaque
o spiral CT
• no contrast, good to distinguish radiolucent stone from soft
tissue filling defect
o abdominal ultrasound
• may demonstrate stone (difficult in ureter)
• may demonstrate hydronephrosis
o IVP (see Colour Atlas M2)
• establishes diagnosis
• demonstrates
• anatomy of urine collecting system
• degree of obstruction
• extravasation if present
• renal tubular ectasia (medullary sponge kidney)
• uric acid stones ––> filling defect
o strain all urine ––> stone analysis
o later (metabolic studies for recurrent stone formers)
• serum lytes, calcium, phosphate and uric acid
• PTH if hypercalcemic
• creatinine and urea
• 24 hour urine x 2 for creatinine, Ca2+, PO4,
uric acid, magnesium, oxalate and citrate
Acute Management
o medical
• analgesic (Tylenol #3, demerol, morphine) +/– antiemetic
• NSAIDs help lower intra-ureteral pressure
• +/– antibiotics for UTI
• IV fluids if vomiting
o indications for admission to hospital
• severe persistent pain uncontrolled by oral analgesics
• fever ––> infection
• high grade obstruction
• single kidney with ureteral obstruction
• bilateral ureteral stones
• persistent vomiting
o surgical
• ureteric stent
• high grade obstruction
• single kidney
MCCQE 2000 Review Notes and Lecture Series Urology 3
Notes
KIDNEY AND URETER
. . . CONT.
o radiological
• percutaneous nephrostomy (alternative to stent)
Elective Management
o medical
• conservative if stone < 5mm and no complications
• alkalinization of uric acid and cystine stones may be attempted
(potassium citrate)
• patient must receive one month of therapy before being
considered to have failed
o surgical
• kidney
• extracorporeal shock wave lithotripsy (ESWL) if stone < 2.5 cm
• + stent if 1.5-2.5 cm
• percutaneous nephrolithotomy
• stone > 2.5 cm
• staghorn
• UPJ obstruction
• calyceal diverticulum
• cystine stones (poorly fragmented with ESWL)
• open nephrolithotomy
• extensively branched staghorn
• ureter
• ESWL is primary modality of treatment
• ureteroscopy
• failed ESWL
• ureteric stricture
• reasonable alternative for distal 1/3 of ureter
• open ureterolithotomy
• rarely necessary (failed ESWL and ureteroscopy)
Stone Pathogenesis
o factors promoting stone formation
• stasis (hydronephrosis, congenital abnormality)
• medullary sponge kidney
• infection (struvite stones)
• hypercalciuria
• increased oxalate
• increased uric acid
o loss of inhibitory factors
• Mg (forms soluble complex with oxalate)
• citrate (forms soluble complex with calcium)
• pyrophosphate
• glycoprotein
STONE TYPES
Calcium Stones
o account for 80% of all stones
o Ca2+oxalate most common, followed by Ca2+phosphate
o description
• grey or brown due to hemosiderin from bleeding
• radiopaque (see Colour Atlas M1)
Etiology
o hypercalciuria (60-70% of patients)
• 95% of these patients have normal serum calcium levels
• 5-10% of people without stones have hypercalciuria
• absorptive causes (majority of patients)
• increased vitamin D sensitivity ––> idiopathic
o hypercalciuric Ca2+stones
8
• sarcoidosis ––> production of 1,25(O8H)2vit D
• abnormal vitamin D metabolism ––> 1,25 (OH)2vit D
• excess vitamin D intake
• increased Ca2+intake (milk alkali syndrome)
9 8
• renal phosphate leak ––> PO4––> 1,25(OH)2
vitamin D ––> absorptive hypercalcemia
• treatment
• cellulose phosphate (decrease intestinal absorption
of Ca2+) or orthophosphates (inhibit vitamin D synthesis)
Urology 4 MCCQE 2000 Review Notes and Lecture Series
Notes
KIDNEY AND URETER
. . . CONT.
8
• resorptive cause (i.e. Ca2+from bones)
• hyperparathyroidism
• neoplasms (multiple myeloma, metastases)
• Cushing’s disease
• hyperthyroidism
• immobilization
• steroids
• renal leak of calcium
• distal renal tubular acidosis (RTA I) ––> 6.0 pH
9 8
+ citrate ––> CaPO4sto8nes
• treat with HCO3to citrate
• medullary sponge kidney (tubular ectasia)
• anatomic defect in collecting ducts;
5-20% of Ca2+stone formers
o idiopathic (25-40% of patients)
• normocalcemic
• normocalciuric
9 9 8 8
• may have citrate; Mg; oxalate; urine acidity; dehydration
• treatment
9
• hydrochlorothiazide (HCTZ) 25 mg PO daily ––> Ca2+in urine
• increase water intake
o hyperuricosuria (25% of patients with Ca2+stones)
• uric acid acts as nidus for Ca2+stone formation
• treatment
• add allopurinol if uric acid excretion > 5 mmol/day
o hypocitraturia (12% of patients)
• associated with type I RTA or chronic thiazide use
• treatment
• potassium citrate
o hypercalcemia (5% of patients)
}
• primary hyperparathyroidism
• malignancy 90% of cases
• sarcoidosis
• increased vitamin D
• hyperthyroidism
• milk-alkali syndrome
o hyperoxaluria (< 5% of patients)
• inflammatory bowel disease (IBD)
• short bowel syndrome
• dietary increase (caffeine, potatoes, rhubarb, chocolate, vitamin C)
• primary increase in endogenous production
• treatment
• increase water intake, avoid oxalate-containing foods
• oral calcium or cholestyramine
Struvite Stones
o etiology and pathogenesis
• account for 10% of all stones
• contribute to formation of staghorn calculi
• consist of triple phosphate (calcium, magnesium, ammonium)
• due to infection with urea splitting organisms
NH2CONH2+ H2O ––> 2NH3+ CO2
• NH4 alkalinizes urine, thus decreasing solubility
o common organisms
• Proteus
• Klebsiella
• Pseudomonas
• Provididencia
• S. aureus
• not E. coli
o treatment
• complete stone clearance (ESWL/percutaneous nephrolithotomy)
•.acidify urine, dissolve microscopic fragments
• antibiotics for 6 weeks
• follow up urine cultures
Uric Acid Stones
o account for 10% of all stones
o description and diagnosis
• orange coloured gravel, needle shaped crystals
• radiolucent on x-ray
MCCQE 2000 Review Notes and Lecture Series Urology 5
Notes
KIDNEY AND URETER
. . . CONT.
• filling defect on IVP
• radiopaque on CT scan
• visualized with ultrasound
o etiology
• hyperuricosuria (urine pH < 5.5)
• secondary to increased uric acid production, or
drugs (ASA and probenecid)
• hyperuricemia
• gout
• myeloproliferative disease
• cytotoxic drugs
• defect in tubular NH3synthesis (ammonia trap for H+)
• dehydration, IBD, colostomy and ileostomy
o treatment
• increase fluid intake
• NaHCO3
• allopurinol
• avoid high protein/purine diet
Cystine Stones
o autosomal recessive defect in renal tubular transport
o seen in children
o aggressive stone disease
o description
• yellow, hard
• radiopaque (ground glass)
• staghorn or multiple
• decreased reabsorption of “COLA”
• cystine
• ornithine }
• lysine soluble in urine
• arginine
o diagnosis
• amino acid chromatography of urine ––> see COLA in urine
o treatment
• greatly increase water intake ––> 3-4 L urine/day
• HCO3
• decrease dietary protein ––> methionine
• penicillamine chelators ––> 2 g daily, soluble complex
formed; use cautiously
• a-mercaptopropionylglycine (MPG) ––> similar action to
penicillamine, less toxic
• captopril (binds cystine)
• irrigating solutions: N-acetylcystine (binds cystine), Tromethamine-E
ultrasound
cystic solid
hypoechoic dense CT
no calcification calcified (exclude
thin wall septated angiomyolipoma)
CT large mass small mass
stop angiography (> 1.5 cm) (< 1.5 cm)
possible
aspiration or biopsy
surgery surveillance surgery possible
surveillance
Figure 1. Work up of a Kidney Mass
Urology 6 MCCQE 2000 Review Notes and Lecture Series
Notes
KIDNEY AND URETER
. . . CONT.
BENIGN RENAL TUMOURS
Angiomyolipoma (Renal Hamartoma)
o rare benign tumour
o round, oval, expansible
o characterized by 3 major histologic components: blood vessels, smooth
muscle and fat cells
o many asymptomatic, may spontaneously rupture, especially in
pregnant females
o found in approximately 45-80% of patients with tuberous sclerosis which
is characterized by
• epilepsy
• mental retardation
• sebaceous adenoma
• hamartomas of brain and kidney
o diagnose by CT ––> fat (negative density on CT)
observed in kidneys is pathognomonic for angiomyolipoma
Renal Adenoma
o commonly found incidentally at autopsy or after nephrectomy for an
unrelated disease
o 10-20% of the population
o asymptomatic
o need tissue diagnosis to definitively differentiate from renal
cell carcinoma
MALIGNANT RENAL TUMOURS
Renal Adenocarcinoma (Renal Cell Carcinoma, RCC)
o also known as hypernephroma
o eighth most common malignancy (accounts for 3% of all newly
diagnosed cancers)
o 85% of primary malignant tumours in kidney
o male:female = 3:1
o called the “internist’s tumour” because of paraneoplastic symptomatology
o etiology
• cause is unknown
• originates from proximal convoluted tubule epithelial cell
• risk factors: smoking (results in 2x increased relative risk),
cadmium exposure, employment in leather industry
• familial incidence seen with von Hippel Lindau syndrome
which is characterized by
• RCC (present in 2/3)
• headache, ataxia, and blindness due to cystic lesions
of cerebellum and retinal vessel aneurysms
o symptoms and signs
• increasingly diagnosed incidentally with U/S and CT
• poor prognostic indicators include
• weight loss
• weakness
• anemia
• bone pain
• classic triad (too late triad!) found in 10-15%
• gross hematuria 50%
• flank pain < 50%
• palpable mass < 30%
• 30% have metastases when first seen
• paraneoplastic syndromes
• hematopoietic disturbances: anemia, polycythemia;
raised ESR
• endocrinopathies: hypercalcemia, production of
other hormones including erythropoietin, renin,
prolactin, gonadotropins, TSH, insulin, and cortisol
• hemodynamic alterations: systolic hypertension (due to AV
shunting), and peripheral edema (due to caval obstruction)
• “Staufer’s syndrome”: abnormal liver function tests,
decreased WBC count, fever, areas of hepatic necrosis;
reversible following removal of primary tumour
MCCQE 2000 Review Notes and Lecture Series Urology 7
Notes
KIDNEY AND URETER
. . . CONT.
o diagnosis
• routine labs for paraneoplastic syndromes (CBC, ESR)
• urinalysis (60-75% have hematuria)
• IVP
• renal ultrasound
• CT scan
• angiography: no longer routinely done
o methods of spread
• direct
• venous
• lymphatic
o staging
• involves CT, chest x-ray, liver enzymes and functions, bone scan
• T1: tumour less than 2.5 cm, confined to renal parenchyma
• T2: tumour greater than 2.5 cm, confined to renal parenchyma
• T3: tumour extends into major veins or adrenal, but not beyond
Gerota’s fascia
• T4: tumour extends beyond Gerota’s fascia
• N0: no regional nodes
• N1: metastasis to a single node, less than 2 cm
• N2: metastasis to a single node between 2 and 5 cm or multiple
nodes, less than 2 cm
• N3: node greater than 5 cm
• M0: no evidence of metastasis
• M1: presence of distant metastasis
o treatment
• surgical (mainstay)
• radical nephrectomy
• en bloc removal of kidney, tumour, ipsilateral
adrenal gland and intact Gerota’s capsule and
periaortic lymphadenectomy
• surgical removal of solitary metastasis may be considered
• radiation for palliation
• for painful bony lesions
• chemotherapy: NOT effective
• immunotherapy: experimental
o prognosis
• stage at diagnosis is the single most important predictor of survival
• 5 year survival of T1 is 90-100%
• 5 year survival of T2-T3 is approximately 60%
• 5 year survival of patients presenting with metastasis is 0-20%
CARCINOMA OF THE RENAL PELVIS AND URETER
o incidence
• rare, accounts for 4% of all urothelial cancers
• frequently multifocal
• papillary transitional cell cancer 85%
• male:female = 3:1
o relative incidence
• bladder:pelvis:ureter = 100:10:1
o predisposing factors
• chemical exposure (industrial dyes and solvents)
• smoking
• analgesic abuse (acetaminophen, aspirin, and phenacetin)
• Balkan nephropathy
o symptoms and signs
• gross painless hematuria (70-90% of patients)
• microscopic hematuria found incidentally
• flank pain
• tenderness over kidney
• flank mass caused by either tumour or associated
hydronephrosis (10-20% of patients)
o diagnosis
• made by noting a radiolucent filling defect on IVP
• differential diagnosis of filling defect
• transitional cell carcinoma (differentiate via cytology and CT scan)
• uric acid stone (differentiate via cytology and CT scan)
• blood clot
• pyelitis cystica
• papillary necrosis
• fungus ball
• gas bubble from gas producing organisms
Urology 8 MCCQE 2000 Review Notes and Lecture Series
Notes
KIDNEY AND URETER
. . . CONT.
o treatment
• radical ureteronephrectomy with cuff of bladder
RENAL TRAUMA
o etiology: blunt (80%, MVA, assaults, falls) vs. penetrating (20%, stab and gunshots)
o history: mechanism of injury
o P/E: ABCs, renal vascular injury ––> shock
• flank contusions, lower rib/vertebral #, upper abdominal/flank
tenderness suggest blunt trauma
o U/A: hematuria, (> 5 RBC/HPF), degree of hematuria does not correlate
with the degree of injury
o imaging: IVP, CT if patient stable ––> look for renal laceration, urinary
extravasation, retroperitoneal hematoma, and associated
intra-abdominal organ injury
o classification according to severity
• minor: contusions and superficial lacerations, 90% of all blunt
traumas, surgical exploration seldom necessary
• major: laceration that extends into deep medulla and collecting
system, injuries to renal artery/vein and segmental branches
o management
• microscopic hematuria + isolated well-staged minor injuries do
not need hospitalization
• gross hematuria + contusion/minor lacerations: hospitalize,
bedrest, repeat CT if bleeding persists
o surgical management
• absolute indications: hemorrhage and hemodynamic instability
• relative indications
• nonviable tissue and major laceration
• urinary extravasation
• vascular injury
• incomplete staging
• laparotomy for associated injury
o outcome
• F/U with IVP or CT before discharge, and at 6 weeks
• hypertension in 5% of renal trauma
BLADDER
BLADDER CARCINOMA
o incidence
• male:female = 3:1
•.usually > 55 years
• may be characterized by frequent recurrences
o classification
• transitional cell carcinoma (TCC) 92%
• squamous cell carcinoma (SCC) 7%
• adenocarcinoma 1%
• others < 1%
o stages of transitional cell carcinoma at diagnosis
• superficial papillary (75%)
• 15% of these will progress to invasive TCC
• the majority of these patients will have recurrence
• invasive (25%)
• 85% have no prior history of superficial TCC
• 50% have occult metastases at diagnosis
• carcinoma in situ
• may progress to invasive TCC
o etiology
• smoking (main factor)
• chemicals
• naphthylamines, benzidine, tryptophan metabolites
• cyclophosphamide
• phenacetin metabolites
• Schistosoma hematobium(associated with SCC)
• chronic irritation (cystitis)
MCCQE 2000 Review Notes and Lecture Series Urology 9
Notes
BLADDER
. . . CONT.
o symptoms
• hematuria 85-90%
• pain 50%
• clot retention 17%
• no symptoms 20%
• occult hematuria
• irritative urinary symptoms - consider carcinoma in situ
o investigation
• history and physical
• urinalysis
• urine cytology
• ultrasound
• cystoscopy with bladder washings (gold standard)
• new advances with specific bladder tumour markers
(NMP-22, BTA, Immunocyt, FDP)
• intravenous pyelogram (IVP)
• for invasive disease
• CT, chest x-ray, liver tests
o TNM classification (see Figure 2)
• Ta noninvasive papillary carcinoma
• Tis carcinoma in situ; flat tumour
• T1 tumour invades subepithelial connective tissue
•.T2a tumour invades superficial muscle
• T2b tumour invades deep muscle
• T3 tumour invades perivesical fat
• T4a adjacent organ involvement; prostate, uterus or vagina
• T4b adjacent organ involvement; pelvic wall or abdominal wall
• N, M status: as for renal cell carcinoma
o treatment
• carcinoma in situ (CIS)
• TURBT
• intravesical immunotherapy with BCG, thiotepa, or mitomycin C
• superficial disease (Tis, Ta, T1)
• TURBT + intravesical chemotherapy or intravesical
BCG prophylaxis to decrease recurrence rate
• invasive disease (T2a, T2b, T3)
• radical cystectomy with urinary diversion and/or irradiation
• metastatic disease (T4a, T4b, N+, M+)
• irradiation +/– systemic chemotherapy
Perivesical Fat
Deep Muscle
Superficial Muscle
T2a T2b T3
T1 T4b
Ta
T4a
Pelvic Wall or
Tis Abdominal Wall
Submucosa
Prostate
Mucosa
Figure 2. Transitional Cell Carcinoma of Bladder
Drawing by Christine Kenney
Urology 10 MCCQE 2000 Review Notes and Lecture Series