- •Hematuria II: causes and investigation
- •Hematospermia
- •Lower urinary tract symptoms (LUTS)
- •Nocturia and nocturnal polyuria
- •Flank pain
- •Urinary incontinence in adults
- •Genital symptoms
- •Abdominal examination in urological disease
- •Digital rectal examination (DRE)
- •Lumps in the groin
- •Lumps in the scrotum
- •2 Urological investigations
- •Urine examination
- •Urine cytology
- •Radiological imaging of the urinary tract
- •Uses of plain abdominal radiography (KUB X-ray—kidneys, ureters, bladder)
- •Intravenous pyelography (IVP)
- •Other urological contrast studies
- •Computed tomography (CT) and magnetic resonance imaging (MRI)
- •Radioisotope imaging
- •Post-void residual urine volume measurement
- •3 Bladder outlet obstruction
- •Regulation of prostate growth and development of benign prostatic hyperplasia (BPH)
- •Pathophysiology and causes of bladder outlet obstruction (BOO) and BPH
- •Benign prostatic obstruction (BPO): symptoms and signs
- •Diagnostic tests in men with LUTS thought to be due to BPH
- •Why do men seek treatment for their symptoms?
- •Watchful waiting for uncomplicated BPH
- •Medical management of BPH: combination therapy
- •Medical management of BPH: alternative drug therapy
- •Minimally invasive management of BPH: surgical alternatives to TURP
- •Invasive surgical alternatives to TURP
- •TURP and open prostatectomy
- •Indications for and technique of urethral catheterization
- •Indications for and technique of suprapubic catheterization
- •Management of nocturia and nocturnal polyuria
- •High-pressure chronic retention (HPCR)
- •Bladder outlet obstruction and retention in women
- •Urethral stricture disease
- •4 Incontinence
- •Causes and pathophysiology
- •Evaluation
- •Treatment of sphincter weakness incontinence: injection therapy
- •Treatment of sphincter weakness incontinence: retropubic suspension
- •Treatment of sphincter weakness incontinence: pubovaginal slings
- •Overactive bladder: conventional treatment
- •Overactive bladder: options for failed conventional therapy
- •“Mixed” incontinence
- •Post-prostatectomy incontinence
- •Incontinence in the elderly patient
- •Urinary tract infection: microbiology
- •Lower urinary tract infection
- •Recurrent urinary tract infection
- •Urinary tract infection: treatment
- •Acute pyelonephritis
- •Pyonephrosis and perinephric abscess
- •Other forms of pyelonephritis
- •Chronic pyelonephritis
- •Septicemia and urosepsis
- •Fournier gangrene
- •Epididymitis and orchitis
- •Periurethral abscess
- •Prostatitis: presentation, evaluation, and treatment
- •Other prostate infections
- •Interstitial cystitis
- •Tuberculosis
- •Parasitic infections
- •HIV in urological surgery
- •6 Urological neoplasia
- •Pathology and molecular biology
- •Prostate cancer: epidemiology and etiology
- •Prostate cancer: incidence, prevalence, and mortality
- •Prostate cancer pathology: premalignant lesions
- •Counseling before prostate cancer screening
- •Prostate cancer: clinical presentation
- •PSA and prostate cancer
- •PSA derivatives: free-to-total ratio, density, and velocity
- •Prostate cancer: transrectal ultrasonography and biopsies
- •Prostate cancer staging
- •Prostate cancer grading
- •General principles of management of localized prostate cancer
- •Management of localized prostate cancer: watchful waiting and active surveillance
- •Management of localized prostate cancer: radical prostatectomy
- •Postoperative course after radical prostatectomy
- •Prostate cancer control with radical prostatectomy
- •Management of localized prostate cancer: radical external beam radiotherapy (EBRT)
- •Management of localized prostate cancer: brachytherapy (BT)
- •Management of localized and radiorecurrent prostate cancer: cryotherapy and HIFU
- •Management of locally advanced nonmetastatic prostate cancer (T3–4 N0M0)
- •Management of advanced prostate cancer: hormone therapy I
- •Management of advanced prostate cancer: hormone therapy II
- •Management of advanced prostate cancer: hormone therapy III
- •Management of advanced prostate cancer: androgen-independent/ castration-resistant disease
- •Palliative management of prostate cancer
- •Prostate cancer: prevention; complementary and alternative therapies
- •Bladder cancer: epidemiology and etiology
- •Bladder cancer: pathology and staging
- •Bladder cancer: presentation
- •Bladder cancer: diagnosis and staging
- •Muscle-invasive bladder cancer: surgical management of localized (pT2/3a) disease
- •Muscle-invasive bladder cancer: radical and palliative radiotherapy
- •Muscle-invasive bladder cancer: management of locally advanced and metastatic disease
- •Bladder cancer: urinary diversion after cystectomy
- •Transitional cell carcinoma (UC) of the renal pelvis and ureter
- •Radiological assessment of renal masses
- •Benign renal masses
- •Renal cell carcinoma: epidemiology and etiology
- •Renal cell carcinoma: pathology, staging, and prognosis
- •Renal cell carcinoma: presentation and investigations
- •Renal cell carcinoma: active surveillance
- •Renal cell carcinoma: surgical treatment I
- •Renal cell carcinoma: surgical treatment II
- •Renal cell carcinoma: management of metastatic disease
- •Testicular cancer: epidemiology and etiology
- •Testicular cancer: clinical presentation
- •Testicular cancer: serum markers
- •Testicular cancer: pathology and staging
- •Testicular cancer: prognostic staging system for metastatic germ cell cancer
- •Testicular cancer: management of non-seminomatous germ cell tumors (NSGCT)
- •Testicular cancer: management of seminoma, IGCN, and lymphoma
- •Penile neoplasia: benign, viral-related, and premalignant lesions
- •Penile cancer: epidemiology, risk factors, and pathology
- •Squamous cell carcinoma of the penis: clinical management
- •Carcinoma of the scrotum
- •Tumors of the testicular adnexa
- •Urethral cancer
- •Wilms tumor and neuroblastoma
- •7 Miscellaneous urological diseases of the kidney
- •Cystic renal disease: simple cysts
- •Cystic renal disease: calyceal diverticulum
- •Cystic renal disease: medullary sponge kidney (MSK)
- •Acquired renal cystic disease (ARCD)
- •Autosomal dominant (adult) polycystic kidney disease (ADPKD)
- •Ureteropelvic junction (UPJ) obstruction in adults
- •Anomalies of renal ascent and fusion: horseshoe kidney, pelvic kidney, malrotation
- •Renal duplications
- •8 Stone disease
- •Kidney stones: epidemiology
- •Kidney stones: types and predisposing factors
- •Kidney stones: mechanisms of formation
- •Evaluation of the stone former
- •Kidney stones: presentation and diagnosis
- •Kidney stone treatment options: watchful waiting
- •Stone fragmentation techniques: extracorporeal lithotripsy (ESWL)
- •Intracorporeal techniques of stone fragmentation (fragmentation within the body)
- •Kidney stone treatment: percutaneous nephrolithotomy (PCNL)
- •Kidney stones: open stone surgery
- •Kidney stones: medical therapy (dissolution therapy)
- •Ureteric stones: presentation
- •Ureteric stones: diagnostic radiological imaging
- •Ureteric stones: acute management
- •Ureteric stones: indications for intervention to relieve obstruction and/or remove the stone
- •Ureteric stone treatment
- •Treatment options for ureteric stones
- •Prevention of calcium oxalate stone formation
- •Bladder stones
- •Management of ureteric stones in pregnancy
- •Hydronephrosis
- •Management of ureteric strictures (other than UPJ obstruction)
- •Pathophysiology of urinary tract obstruction
- •Ureter innervation
- •10 Trauma to the urinary tract and other urological emergencies
- •Renal trauma: clinical and radiological assessment
- •Renal trauma: treatment
- •Ureteral injuries: mechanisms and diagnosis
- •Ureteral injuries: management
- •Bladder and urethral injuries associated with pelvic fractures
- •Bladder injuries
- •Posterior urethral injuries in males and urethral injuries in females
- •Anterior urethral injuries
- •Testicular injuries
- •Penile injuries
- •Torsion of the testis and testicular appendages
- •Paraphimosis
- •Malignant ureteral obstruction
- •Spinal cord and cauda equina compression
- •11 Infertility
- •Male reproductive physiology
- •Etiology and evaluation of male infertility
- •Lab investigation of male infertility
- •Oligospermia and azoospermia
- •Varicocele
- •Treatment options for male factor infertility
- •12 Disorders of erectile function, ejaculation, and seminal vesicles
- •Physiology of erection and ejaculation
- •Impotence: evaluation
- •Impotence: treatment
- •Retrograde ejaculation
- •Peyronie’s disease
- •Priapism
- •13 Neuropathic bladder
- •Innervation of the lower urinary tract (LUT)
- •Physiology of urine storage and micturition
- •Bladder and sphincter behavior in the patient with neurological disease
- •The neuropathic lower urinary tract: clinical consequences of storage and emptying problems
- •Bladder management techniques for the neuropathic patient
- •Catheters and sheaths and the neuropathic patient
- •Management of incontinence in the neuropathic patient
- •Management of recurrent urinary tract infections (UTIs) in the neuropathic patient
- •Management of hydronephrosis in the neuropathic patient
- •Bladder dysfunction in multiple sclerosis, in Parkinson disease, after stroke, and in other neurological disease
- •Neuromodulation in lower urinary tract dysfunction
- •14 Urological problems in pregnancy
- •Physiological and anatomical changes in the urinary tract
- •Urinary tract infection (UTI)
- •Hydronephrosis
- •15 Pediatric urology
- •Embryology: urinary tract
- •Undescended testes
- •Urinary tract infection (UTI)
- •Ectopic ureter
- •Ureterocele
- •Ureteropelvic junction (UPJ) obstruction
- •Hypospadias
- •Normal sexual differentiation
- •Abnormal sexual differentiation
- •Cystic kidney disease
- •Exstrophy
- •Epispadias
- •Posterior urethral valves
- •Non-neurogenic voiding dysfunction
- •Nocturnal enuresis
- •16 Urological surgery and equipment
- •Preparation of the patient for urological surgery
- •Antibiotic prophylaxis in urological surgery
- •Complications of surgery in general: DVT and PE
- •Fluid balance and management of shock in the surgical patient
- •Patient safety in the operating room
- •Transurethral resection (TUR) syndrome
- •Catheters and drains in urological surgery
- •Guide wires
- •JJ stents
- •Lasers in urological surgery
- •Diathermy
- •Sterilization of urological equipment
- •Telescopes and light sources in urological endoscopy
- •Consent: general principles
- •Cystoscopy
- •Transurethral resection of the prostate (TURP)
- •Transurethral resection of bladder tumor (TURBT)
- •Optical urethrotomy
- •Circumcision
- •Hydrocele and epididymal cyst removal
- •Nesbit procedure
- •Vasectomy and vasovasostomy
- •Orchiectomy
- •Urological incisions
- •JJ stent insertion
- •Nephrectomy and nephroureterectomy
- •Radical prostatectomy
- •Radical cystectomy
- •Ileal conduit
- •Percutaneous nephrolithotomy (PCNL)
- •Ureteroscopes and ureteroscopy
- •Pyeloplasty
- •Laparoscopic surgery
- •Endoscopic cystolitholapaxy and (open) cystolithotomy
- •Scrotal exploration for torsion and orchiopexy
- •17 Basic science of relevance to urological practice
- •Physiology of bladder and urethra
- •Renal anatomy: renal blood flow and renal function
- •Renal physiology: regulation of water balance
- •Renal physiology: regulation of sodium and potassium excretion
- •Renal physiology: acid–base balance
- •18 Urological eponyms
- •Index
664 CHAPTER 17 Basic science in urological practice
Renal physiology: regulation of water balance
Total body water (TBW) is 42 L. It is contained in two major com- partments—the intracellular fluid (ICF or the water inside cells) which accounts for 28 L and the extracellular fluid (ECF or water outside cells) representing 14 L.
ECF is further divided into interstitial fluid (ISF, 11 L), transcellular fluid (1 L), and plasma (3 L). Hydrostatic and osmotic pressures influence movement between the compartments. Water is taken in from fluids, food, and oxidation of food.
Water is lost from urine, feces, and insensible losses. Intake and losses usually balance (~2 L/day) and TBW remains relatively constant.
Antidiuretic hormone (ADH or vasopressin)
ADH is secreted from the posterior pituitary in response to stimuli from changes in plasma osmolarity (detected by osmoreceptors in the hypothalamus) or changes in blood pressure or volume (detected by baroreceptors in the left atrium, aortic arch, and carotid sinus). These changes also stimulate the thirst center in the brain.
The action of ADH on the kidney
•Increases collecting duct permeability to water and urea
•Increases loop of Henle and collecting duct reabsorption of NaCl
•Increases vasoconstriction
Conditions of water excess
Water excess occurs when body fluids become hypotonic and ADH release and thirst are suppressed. In the absence of ADH, the collecting duct is impermeable to water and a large volume of hypotonic urine is produced, thus restoring normal plasma osmolarity.
Conditions of water deficit
When body fluids are hypertonic, ADH secretion and thirst are stimulated. The collecting duct becomes permeable, water is reabsorbed into the lumen, and a small volume of hypertonic urine is excreted.
The ability to concentrate or dilute urine depends on the countercurrent multiplication system in the loop of Henle. Essentially, a medullary concentration gradient is generated (partly by the active transport of NaCl), which provides the osmotic driving force for the reabsorption of water from the lumen of the collecting duct when ADH is present.
Children have a circadian rhythm in ADH secretion—high at night and low during the day. Adults essentially have a constant ADH secretion over a 24-hour period, with slight increases occurring around mealtimes. At these times, increased ADH secretion probably acts to prevent sudden increases in plasma osmolality that would otherwise occur due to ingestion of solutes in a meal.
RENAL PHYSIOLOGY: REGULATION OF NA AND K EXCRETION 665
Renal physiology: regulation of sodium and potassium excretion
Sodium regulation
NaCl is the main determinant of ECF osmolality and volume. Osmolality = osmoles per kg water (osmol/kg). Osmolarity = osmoles per liter of solution (osmol/L.
Low-pressure receptors in the pulmonary vasculature and cardiac atria, and high-pressure baroreceptors in the aortic arch and carotid sinus recognize changes in the circulating volume. Decreased blood volume triggers increased sympathetic nerve activity and stimulates ADH secretion, which results in reduced NaCl excretion.
Conversely, when blood volumes are increased, sympathetic activity and ADH secretion are suppressed, and NaCl excretion is enhanced (natriuresis).
A variety of natriuretic peptides have been isolated that cause a natriuresis. Under physiological conditions, renal natriuretic peptide (urodilatin) is the most important of these. Atrial natriuretic hormone (ANP) may influence sodium output under conditions of heart failure.
Renin–angiotensin–aldosterone system
Renin is an enzyme made and stored in the juxtaglomerular cells found in the walls of the afferent arteriole. Factors increasing renin secretion are as follows:
•Reduced perfusion of the afferent arteriole
•Sympathetic nerve activity
•Reduced Na+ delivery to the macula densa
Renin acts on angiotensin to create angiotensin I. This is converted to angiotensin II in the lungs by angiotensin-converting enzyme (ACE). Angiotensin II performs several functions, which result in the retention of salt and water:
•Stimulates aldosterone secretion (resulting in NaCl reabsorption)
•Vasoconstriction of arterioles
•Stimulates ADH secretion and thirst
•Enhances NaCl reabsorption by the proximal tubule
Potassium regulation
K+ is critical for many cell functions. A large concentration gradient across cell membranes is maintained by the Na+-K+-ATPase pump. Insulin and adrenaline also promotes cellular uptake of K+.
The kidney excretes up to 95% of K+ ingested in the diet. The distal tubule and collecting duct are able to both reabsorb and secrete K+. Factors promoting K+ secretion include the following:
•Increased dietary K+ (driven by the electrochemical gradient)
•Aldosterone
•Increased rate of flow of tubular fluid (i.e., diuretics)
•Metabolic alkalosis (acidosis exerts the opposite effect)
666 CHAPTER 17 Basic science in urological practice
Renal physiology: acid–base balance
The normal pH of extracellular fluid (ECF) is 7.4 ([H+] = 40 nmol/L). Several mechanisms are in place to eliminate acid produced by the body and maintain body pH within a narrow range.
Buffering systems limiting [H+] fluctuation in the blood
Buffer bases that take up H+ ions in the body include the following:1
Bicarbonate buffer system |
H+ + HCO3– l H2CO3 l H2O + CO2 |
Phosphate system |
H+ + HPO4–2 l H2PO4– |
Protein buffers |
H+ + Protein– l HProtein |
The Henderson–Hasselbalch equation describes the relationship between pH and the concentration of conjugate acid and base:
From this equation, it can be seen that alterations in bicarbonate [HCO3–] or CO2 will affect pH. Metabolic acid–base disturbances relate to a change in bicarbonate, and respiratory acid–base disorders relate to alterations in CO2.
Bicarbonate reabsorption along the nephron
Bicarbonate is the main buffer of ECF and is regulated by both the kidneys and lungs; 85% is reabsorbed in the proximal convoluted tubule (Fig. 17.2).
Carbonic acid is first produced from CO2 and water (accelerated by carbonic anhydrase). The carbonic acid dissociates, and an active ion pump (Na+/H+ antiporter) extrudes intracellular H+ into the tubule lumen in exchange for Na+. Secretion of H+ ions favors a shift of the carbonic acid– bicarbonate equilibrium toward carbonic acid, which is rapidly converted into carbon dioxide and water.
CO2 diffuses into the tubular cells down its diffusion gradient and is reformed into carbonic acid by intracellular carbonic anhydrase. The bicarbonate formed by this reaction is exchanged for chloride and passes into the circulation. Essentially, with each H+ ion that enters the kidney, a bicarbonate ion enters the blood, which bolsters the buffering capacity of the ECF.
The remaining bicarbonate is absorbed in the distal convoluted tubule, where cells actively secrete H+ into the lumen via an ATP-dependent pump. The distal tubule is the main site that pumps H+ into the urine to ensure the complete removal of bicarbonate. Once the bicarbonate has gone, phosphate ions and ammonia buffer any remaining H+ ions.
1 H2O = water; CO2 = carbon dioxide; HCO3– = bicarbonate; H2CO3 = carbonic acid; H+ = hydrogen ions; H2PO42– = dihydrogen phosphate; H3PO4 = phosphoric acid.
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RENAL PHYSIOLOGY: ACID–BASE BALANCE |
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Tubule cell |
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Tubule lumen |
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H2O + CO2 |
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H2O + CO2 |
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CA |
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HCO3– |
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Cl – |
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Figure 17.2 Diagram showing bicarbonate reabsorption in the proximal convoluted tubule.
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