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DYSURIA AND LOIN PAIN

Pregnancy
Periureteral inflammation

Urinary Tract Obstruction


1. Urinary tract can be obstructed at any point between kidney and urethral
meatus, resulting in dilatation of the tract above the obstruction.
(Hydronephrosis dilatation of the renal pelvis; hydroureter dilatation of
ureter)
2. Epidemiology:
- same in men and women
- in the elderly, men>women because of incidence of bladder outflow
obstruction (prostatism)
3. Aetiology:
(a) within the lumen
(b) within the wall
(c) pressure from outside (outside the wall)
Within the Lumen
Calculus
Blood clot
Sloughed papillae (DM,
analgesia abuse, sickle
cell disease or trait)
Tumour of renal pelvis
or ureter
Bladder turmour

Within the Wall


Pelviureteric neuromuscular
dysfunction (congenital, 10%
bilateral)
Ureteric stricture (TB, esp.
after treatment; calculus; after
surgery
Ureterovesical
stricture
(congenital;
ureterocoele;
calculus; schistosomiasis)
Congenital megaureter

Pressure from Outside


Pelviureteric
compression
(bands; aberrant vessels)

Congenital
bladder
neck
obstruction
Neuropathic bladder
Urethral stricture (calculus;
conococcal;
after
instrumentation)
Congenital urethral valve
Pin-hold meatus

Retroperitoneal fibrosis

Tumours (e.g. retroperitoneal


tumour or glands; carcinoma
of colon)
Diverticulitis
Aortic aneurysm

Accidental ligation of ureter


Retrocaval ureter (right-sided
obstruction)
Prostatic obstruction
Tumours in pelvis
carcinoma of cervix)
Phimosis

(e.g

4. Ureters: major causes of obstruction


Intrinsic
Calculi

Strictures
Tumourous
masses
Blood clots
Neurogenic
causes
Extrinsic

Of renal origin, rarely 5mm diam


Larger renal stones cannot enter ureters
Impact at loci or ureteral narrowing: ureteropelvic junction, where ureters
cross pelvic junction, where ureters enter bladder.
Cause excruciating renal colic
Congenital or acquired (inflammations, sclerosing retroperitoneal fibrosis)
TCC arising in ureters
Rarely, benign tumours or fibroepithelial polyps
Massive haematuria from renal calculi, tumours, or papillary necrosis
Interruption of the neural pathways to the bladder

Endometriosis
Tumours

Physiologic relaxation of smooth muscle or pressure on


ureters at pelvic brim from enlarging fundus
Salpingitis,
diverticulitis,
peritonitis,
sclerosing
retroperitoneal fibrosis
With pelvic lesions, followed by scarring
Cancers of rectum, bladder, prostate, ovaries, uterus, cervix,
lymphomas, sarcomas
Ureteral obstruction is one of the major causes of death
from cervical carcinoma

5. Urinary bladder: obstruction


- males: most important lesion is prostate enlargement (benign nodular
hyperplasia or carcinoma)
- vesical obstruction less common in females (usually caused by
cystocoele when the bladder is protruded into the vagina, creating a
pouch, that fails to empty readily with micturition; tends to occur in
middle-aged and elderly women, where relaxation of pelvic support
leads to prolapse of the uterus, pulling with it the floor of the bladder
cystocoele)
- other infrequent causes:
congenital narrowings or strictures of urethra
inflammatory strictures of the urethra
inflammatory fibrosis and contraction of the bladder (after cystitis)
bladder tumours (benign or malignant)
secondary invasion of the bladder neck by growths arising in
perivesical structures (e.g. cervix, vagina, prostate, rectum)
mechanical obstructions (foreign bodies, calculi)
injury to innervation of bladder neurogenic or cord bladder
- early: thickening of bladder wall due to hypertrophy of smooth muscle
- progressive hypertrophy causes individual muscle bundles to enlarge
and produce trabeculation
- eventually, crypts form and may become converted into true acquired
diverticula
6. Pathophysiology: obstruction with continuing urine formation produces
- progressive in intraluminal pressure
- dilatation proximal to site of obstruction
- compression and thinning of renal parenchyma, eventually thin rim
( size of kidney)
7. Clinical features
(a) symptoms of upper tract obstruction
- loin pain (dull/sharp; constant/intermittent; aggravated by in urine
volume, eg. by high fluid intake, diuretics, alcohol)
- complete anuria (complete bilateral obstruction)
- polyuria (partial obstruction due to impairment of renal tubular
concentrating capacity)
- intermittent anuria and polyuria (intermittent complete obstruction)
- superimposed infections malaise, fever, septicaemia
(b) symptoms of bladder outflow obstruction (may be minimal)

typical features:
hesitancy
narrowing and diminished force of urinary stream
terminal dribbling
sense of incomplete bladder emptying
- overflow incontinence/retention with overflow (frequent passage of
small volumes of urine when a large volume of residual urine
remains in the bladder after urination incontinence of these
small volumes of urine
- infection (common): increased frequency, urgency, urge
incontinence, dysuria, passage of cloudy smelly urine
infection may precipitate acute retention
(c) signs
- loin tenderness
- (maybe) palpable enlarged hydronephrotic kidney
- (maybe in acute or chronic retention) enlarged bladder
(felt/percussed)
- remember to examine the genitalia, rectum and vagina, because
prostatic obstruction and pelvic malignancy are common causes of
urinary tract obstruction
apparent size of prostate on PR is a poor guide to the
presence of prostatic obstruction
8. Investigations: the usual bloods and biochemistry (but cannot diagnose
obstruction on these alone) and:
(a) ultrasonography
- reliable for ruling out upper UT dilatation (urinary tract = UT)
- however, cannot distinguish a baggy, low-pressure unobstructed
system from a tense, high-pressure obstructed one ( falsepositive scans are seen)
- a normal scan does, however, usually rule out UT obstruction
(b) radionuclide studies
- in obstructive nephropathy:
relative uptake may be normal or reduced on the side of the
obstruction
peak activity may be delayed
parenchymal (as opposed to pelvic) transit time is prolonged
- if doubt exists as to whether there is an obstruction at the
pelviureteric junction, administer frusemide satisfactory washout or radionuclide rules out obstruction, vice-versa
- absence of uptake indicates renal damage sufficiently severe to
render correction of obstruction unprofitable
(c) excretion urography (IVP)
- most widely used investigation
- can usually exclude obstruction even in the presence of severe
renal failure (as long as high dose of contrast medium, renal
tomography, and, if necessary, delayed films are employed)
-

plain film detects calcification


recent unilateral obstruction: kidney is enlarged and smooth,
nephrogram is delayed ( GFR), calyces and pelvis fill with
contrast medium later than normal side
- later, nephrogram becomes denser on affected side (prolonged
nephron transit time), (maybe) site of obstruction seen, with
dilatation of system proximal to level of block
- take full-length film after an attempt at bladder emptying:
complete
emptying
:
no
obstruction
to
bladder
outflow/intravesical pressure can be raised sufficiently to
overcome it
apparent bladder outflow impairment : patient nervousness or
embarrassment/failure to carry out X-ray before bladder has
refilled with contrast medium from above/atonic but nonobstructed bladder
vesicoureteric reflux : contrast medium returns to bladder from
above (appearance of partially full bladder)
antegrade pyelography and ureterography
- defines site and cause of obstruction
- can be combined with drainage of collecting venous system by
percutaneous needle nephrostomy
retrograde ureterography
- indicated if antegrade examination cannot be carried out or if there
is the possibility of dealing with ureteric obstruction from below at
the time of examination
- risk of introducing infection into obstructed UT
- collecting system may fill normall from below if obstruction is due
to neuromuscular dysfunction at pelviureteric junction or
retroperitoneal fibrosis
cystoscopy, urethroscopy and urethrography
- obstructing lesions in bladder and urethra can be seen directly be
endoscopic examination
- urethrography untroduction of contrast medium into bladder by
catheterisation or suprapubic bladder puncture and X-raying
during voiding to show obstructing lesions in urethra
valuable in diagnosing urethral valves and strictures
pressure flow studies
- demonstration of high voiding pressure being required for
maintenance of urine flow bladder outflow obstruction
- normally: while bladder is being filled, there is a small pressure
rise before voluntary initiation of urination
- upper motor neuron bladder neuropathy (e.g. multiple sclerosis) :
uninhibited contractions of detrusor muscle during filling
- lower motor neuron bladder neuropathy (e.g. in diabetes mellitus) :
hypotonic neuropathic bladder, readily acceptig large volumes of
fluid before initiating weak contractions at a low intravesical
pressure
-

(d)

(e)

(f)

(g)

combination with video cystography and urethrography helps


define site of obstruction, and may help in deciding whether to
operate or not
9. Treatment
- aims to relieve symptoms and preserve renal function
- involves
relieving obstruction
treating underlying cause
preventing and treating infection
- temporary external drainage of urine by nephrostomy allows time for
further investigation (e.g. uncertainty about lesion or immediate
surgery being hazardous) or for spontaneous relief (e.g. passage of
calculus).
ie. recent, complete upper UT obstruction needs urgent relief to
preserve renal function, esp. if infection is present
partial UT obstruction with spontaneous relief expected has no
immediate urgency
- surgery depends on cause of obstruction
nephrectomy or nephroureterectomy: malignancy or renal function
is irredeemable
permanent urinary diversion : obstruction cannot be relieved (e.g.
malignancy)
ureteric anastomosis to an ileal conduit opening on to the
abdominal wall
insertion of indwelling catheters/stents into ureter
permanent nephrostomy with high obstructions
- diuresis usually follows relief of obstruction; is usually self-limiting
10. Prognosis: depends on 4 factors
(a) partial/complete obstruction
(b) duration of obstruction
(c) presence/absence of infection
(d) site of obstruction
-

Congenital Vesicoureteric Reflux


1. In addition to obstruction as a predisposing factor in the pathogenesis of
ascending infection is incompetence of the vesicoureteral valve.
- normally, ureteral insertion into the bladder is a competent one-way
valve that prevents retrograde flow of urine, esp. during micturition
(when intravesical pressure rises)
- incompetence of the vesicoureteral orifice allows reflux of bladder
urine into the ureters
2. Most often due to congenital inherited absence or shortening of the
intravesical portion of the ureter. Therefore, ureter is not compressed in
micturition

3. Of the congenital anomalies of the urinary bladder, VUR is the most


common and serious anomaly. It is a major contributor to renal infection
and scarring
4. Bladder infection can cause or accentuate vesicoureteral reflux, esp. in
children
5. Acquired VUR in adults can be due to persistent bladder atony (due to
spinal cord injury)
6. VUR causes there to be residual urine in the urinary tract (favouring
bacterial growth)
7. Complications of VUR:
(a) UTI
(b) acute pyelonephritis
(c) chronic pyelonephritis
(d) renal function: analogous to that of partial ureteral obstruction in that
tubular function affected earlier than glomerular function.
Concentrating defect is inversely proportional to grade of reflux (may
be related to ADH effect of increased medullary pPGE levels in pts
with severe VUR)
(e) renal growth: small kidneys may be associated with developmental
arrest (associated with but not caused by VUR), and acquired failure to
grow related to reflux. More severe in cases with repeated UTI
(f) physical growth: children with VUR tend to be in lower-weight
percentile group. Reversible with medical or surgical treatment of VUR
(g) hypertension: greater risk of developing hypertension as young adults
(h) renal failure: develops with VUR and renal scarring. Those with
bilateral scarring and hypertension at particular risk. Up to 30%
children may have end-stage renal failure because of reflux
8. Investigations:
(a) renal US
(b) radiological cystogram (VCUG)/Nuclear cystogram (RNC): show
scarring or dilated UT, suggestive of reflux
(c) IVP: anatomical abnormalities (e.g. dilatation, filling defects)
(d) micturating cystourethrography (MCU) screen during voiding,
because reflux frequently occurs during voiding
(e) DMSA scan (technetium-99m-labelled dimercaptosuccinic acid): renal
scarring, and quantification of split renal function
Renal Colic: Calculi
1. Calculi are the commonest causes of renal colic
2. Epidemiology
- 2% of Western populations have a UT stone at any given time (more
prevalent in the Middle East)
- most stones occur in the upper UT in the West
- most stones are composed of calcium oxalate and these are more
common in men
- mixed infective stones (20% of all calculi) are more common in women
- overall, male:female = 2:1

frequently recurs: >50% pts with calculi form further stone(s) in 10


years
Type of Renal Stone
Approximate
Frequency (%)
Calcium oxalate
65
Calcium phosphate
15
Magnesium ammonium phosphate (struvite)
10-15
Uric acid
3-5
Cystine
1-2

3. Aetiology
- main causes are:
dehydration
hypercalcaemia leads to hypercalciuria (with normal GFR);
commonly caused by primary hyperparathyroidism (most
common), vitamin D ingestion, sarcoidosis
hypercalciuria
most common metabolic abnormality in calcium stone-formers
definition of pathological hypercalciuria is 24 hour calcium
excretion exceeding 7.5 mmol (males) and 6.25 mmol
(females)
kidney reabsorbs about 90% of the ionised calcium filtered;
renal tubular reabsoprtion is influenced by many hormones,
esp. PTH
filtered calcium is absorbed in proximal convoluted tubule
(65%), thick ascending limb of the loop of Henle (20%), distal
convoluted tubule and collecting ducts (15%)
cells in the thick ascending limb have calcium receptors that
control reabsorption of calcium (e.g. high luminal [Ca]
reduced calcium reabsorption)
causes of hypercalciuria: hypercalcaemia, excessive dietary
intake of Ca, excessive reabsorption of Ca from skeleton (e.g.
in prolonged immobilisation or weightlessness), idiopathic
hypercalciuria (caused by increased calcium absorption from
gut or renal tubular calcium leak with secondary compensatory
hyperabsorption of calcium from the gut)
hyperoxaluria: caused by
inborn errors of glyoxalate metabolism (cause increased
endogenous oxalate biosynthesis; type I and II) cause more
serious (but more rare cause of) hyperoxaluria. Poor prognosis
due to widespread calcium oxalate crystal deposition in the
kidneys with renal failure developing in late teens or early
twenties
(more common causes) excess ingestion of high oxalate foods
(spinach, rhubarb, tea), dietary calcium restriction with
compensatory increased reabsorption of oxalate, GIT disease

(e.g. Crohns) usually with intestinal resection, with increased


absorption of oxalate from colon.
dehydration secondary to fluid loss from gut also plays a part
hyperuricaemia and hyperuricosuria
the proportion of uric acid (UA) stones in the UK is 3-5% (c.f.
Israel: 40%)
UA is more soluble in an alkaline than an acid medium
hyperuricaemia can occur as a primary defect in idiopathic
gout or as a secondary consequence of increased cell
turnover
dehydration can cause UA stones to form
patients with ileostomies are at risk of dehydration and from
loss of bicarbonate from GIT secretions, producing an acid
urine
pts with calcium stones who also have hyperuricaemia and/or
hyperuricosuria are believed to have calcium salts precipitate
upon an initial nidus of UA
infection
mixed infective stones are composed of magnesium
ammonium phosphate with variable amounts of calcium
these stones are often large (usually responsible for staghorn
calculi)
thought to be due to infection of UT with organisms that
hydrolyse urea with formation of the strong base ammonium
hydroxide (e.g. Proteus mirabilis)
things that favour stone formation in this case: availability of
ammonium ions and alkalinity of urine
increased amount of mucoprotein from infection can create an
organic matrix on which stone formation can occur
cystinuria
obviously causes the formation of cysteine stones
renal tubular acidosis (inherited and acquired)
associated with nephrocalcinosis and stone formation, partly
due to production of a persistently alkaline urine and reduced
urinary citrate excretion
primary renal disease (polycystic kidneys, medullary sponge
kidneys)
4. Aetiology of bladder stones
- endemic in some developing countries
- unknown cause (but thought to be dietary)
- stones form in the bladder because of bladder outflow obstruction or
presence of foreign bodies
- significant bacteriuria is usually found in patients with bladder stones
- some stones are passed down from the upper UT
5. Calcium stones
- calcium oxalate and calcium phosphate

calcium oxalate stones in about 5% pts with both hypercalcaemia


and hypercalciuria
- 55% have hypercalciuria without hypercalcaemia
- more common in men, average onset in 20s
- most recur; average rate of new stone formation in pts with
previous stone is about 1 stone/2-3 years
UA stones
- common in pts with hyperuricaemia (e.g. gout 50%) and less
commonly associated with diseases involving rapid cell turnover
- about 50% of all pts with UA calculi have neither hyperuricaemia
nor increased urinary UA excretion
- usually familial with/without presence of gout
Struvite stones
- formed largely following UTI by urea-splitting (urease-producing)
bacteria (e.g. Proteus) which convert urea to ammonia
- resultant alkaline urine causes precipitation of magnesium
ammonium phosphate salts
Pathology
- stones can be single/multiple and vary in size
- found in renal parenchyma or in collecting system
- can cause direct damage to renal parenchyma by pressure necrosis
from a large calculus
- can cause obstruction (common) hydronephrosis
- can ulcerate through wall of collecting system, including ureters
- obstruction + infection acceleration of damage to kidney
Clinical features
- most people with UT calculi are asymptomatic
- pain is the most common symptom: may be sharp/dull, constant,
intermittent/colicky
- with UT obstruction, things that increase urine volume make the pain
worse (see urinary obstruction)
- physical exertion can cause mobile calculi to move precipitates pain
and (maybe) haematuria
- calyceal colic: movement of stones within calyces
- ureteric colic: when stone enters ureter and either obstructs it/causes
spasm
one of the most severe pains known
radiation from the flank to the iliac fossa and testis/labium in the
distribution of L1
pallor, sweating, vomiting
patient tends to be restless
haematuria
untreated, tends to subside after a few hours
- with concurrent infection, features of acute pyelonephritis or of a
Gram-negative septicaemia may dominate
- vesical calculi associated with bladder bacteriuria: frequency, dysuria
and haematuria
-

6.

7.

8.

9.

trigonitis (if present): introital or perineal pain


calculus at bladder neck or obstruction in urethra: bladder outflow
obstruction anuria and painful bladder distension
- physical examination should include search for corneal/conjunctival
calcification, gouty tophi and gouty arthritis and features of sarcoidosis
10. Investigations and diagnosis
- relevant history findings:
occupation and residence in hot countries (likely to be associated
with dehydration)
vit D consumption
gouty arthritis
analgesic abuse (because calcified papillae from papillary necrosis
associated with analgesic abuse can mimic ordinary calculi)
- investigations:
MSU for culture and measurement of serum urea, electrolyte,
creatinine and calcium
plain abdo XR and IVP (intravenous pyelogram): mainstay of
diagnosis
pure UA stones are radiolucent
mixed infective stones are barely radioopaque
calcium-containing and cysteine stones are radioopaque
calculi overlying bone are easily missed
staghorn calculi can be missed if plain abdo XR pre-contrast is not
checked first (can be mistaken for a post-contrast)
UA stones may present as a filling defect after injection of contrast
medium (readily seen on CT scanning)
IVP carried out during an episode of pain: if normal, it excludes the
diagnosis of pain due to calculous disease
urine of patient needs to be passed through a sieve to trap any
calculi for chemical analysis
11. Management
- analgesia (e.g. morphine 15-30 mg IV prn or NSAID)
- high fluid intake and increased physical activity (but efficacy is
doubtful)
- if stone is <0.5 cm diam, it usually passes spontaneously and can be
left. If > 1 cm, usually requires intervention
- indications for further therapy:
persistent pain, frequent bouts of severe pain or anuria
if stone is not moving but causing partial obstruction in the
absence of infection
complete obstruction or coexistence of UTI with partial obstruction
requires early intervention (risk of permanent kidney damage)
- usual intervention today: percutaneous surgery and extracorporeal
shock-wave lithotripsy
-

percutaneous nephrolithotomy involves removal of stones in the


calyces and renal pelvis by the creation of a track down to the
collecting system followed by endoscopic removal along this track
extracorporeal shock-wave lithotripsy involves focussing shock
waves on the renal calculi causing them to fragment fragments
then pass spontaneously; those that do not pass can be removed
percutaneously
- ureteric stones can be removed endoscopically or pushed up the
upper UT for percutaneous nephrolithotomy or extrcorporeal shockwave lithotripsy
- large stones need to be reduced in bulk by percutaneous means
before lithotripsy can be successful; some staghorn calculi are best
dealt with by open operation
- bladder stones can be removed endoscopically
can be dealt with by direct electrohydraulic disintegration at
cystoscopy or may be gripped in a lithotrite and crushed (stone
fragments are then washed out)
open cystotomy is for very large bladder stones
12. Investigating the cause of stone formation: in young patients and those
with recurrent stone formation:
(a) IVP: for primary renal disease predisposing to stone formation
(b) significant bacteriuria: mixed infective stone formation (but relapsing
bacteriuria may be due to stone formation rather than original cause)
(c) chemical analysis: cystinuria or UA stone formation
(d) serum calcium concentration: hypercalcaemia (should be investigated
further)
(e) serum urate concentration: elevated in UA stone-formers
(f) screening test for cysteinuria: add sodium nitroprusside to randum
unacidified urine sample purple colour indicates possible presence
of cysteinuria. Urine chromatography defines the diagnosis precisely
(g) urinary calcium, oxalate and UA output: 2 consecutive carefully
collected 24-hour urine samples, add acid to urine to prevent
crystallization of calcium salts upon the walls of the collection vessel
(which would give falsely low results for urinary Ca and oxalate)
(h) plasma bicarbonate: low in renal tubular acidosis. If urine pH does not
fall below 5.5 in the face of metabolic acidosis, this is diagnostic of
renal tubular acidosis
13. Prophylaxis: depends on age and severity of the problem
- main thing to remember is high fluid intake (works for all causes of
stone formation)
(a) idiopathic stone-formers
more than 2-2.5 L fluid/day
(b) idiopathic hypercalciuria
severe dietary calcium restriction is inappropriate. Just reduce
intake of milk, cheese, and white bread fortified with calcium and
vitamin D
high fluid intake; try to drink softened water (not hard water)

(c)

(d)

(e)

(f)

if hypercalciuria persists and stone formation continues, try a


thiazide (reduces urinary calcium excretion by direct effect on
renal tubule)
also: sodium cellulose phosphate (reduces calcium absorption
from gut but increases oxalate absorption, causes diarrhoea and is
now not used)
avoidance of high sodium intake (sodium and calcium excretion
are linked)
mixed infective stones
high fluid intake and meticulous control of bacteriuria
may require long term follow-up and long-term low-dose
prophylactic antibacterial agents
UA stones
effective prevention can be achieved with long-term use of
allopurinol
high fluid intake
UA is more soluble at alkaline pH and long-term sodium
bicarbonate supplementation (to maintain alkaline urine) is an
alternative treatment if unable to take allopurinol. However,
remember that alkalinization of urine facilitates precipitation of
calcium oxalate and phosphate
cysteine stones
obsessional attention to maintaining a high fluid intake (about 5 L
water/24 hours)
penicillamine (binds cysteine to form a more soluble compound,
but has side effects that are not uncommon, e.g. blood dyscrasias,
drug rashes, immune complex mediated glomerulonephritis. Is
also expensive. Useful in dissolution of cysteine stones already
present)
mild hyperoxaluria with calcium oxalate stones
high fluid intake
dietary oxalate restriction

Analgesic Nephropathy
1. A form of chronic renal disease caused by excessive intake of analgesic
mixtures and characterised morphologically by chronic tubulointerstitial
nephritis with renal papillary necrosis.
2. Papillary necrosis cortical tubulointerstitial nephritis (interstitial
inflammation with tubular damage).
3. Chronic consumption of large amounts of analgesics (esp. phenacetin,
also NSAIDs) is a common cause of chronic tubulointerstitial nephritis
4. Becks powder (not used anymore):
(a) Phenacetins metabolite acetaminophen injures cells by covalent
binding and oxidative damage

(b) Aspirin induces potentiating effect by inhibiting vasodilatory effects of


PG, predisposing papilla to ischaemia.
(c) Caffeine dehydrates increased concentration of other drugs
5. Epidemiology: female:male ratio = 2:1; middle age, often
depressed/neurotic
6. Presentation: anaemic, chronic renal failure, symptoms of urinary
infections, haematuria, UT obstruction, salt and water-wasting renal
disease, headaches, hypertension
7. Chronic analgesic abuse predisposes to uroepithelial tumours

8. Urinary bladder:
- 95% epithelial; 5% mesenchymal (most epithelial are TCC all notes
following are on TCC)
- 90% of all bladder tumours; most are multifocal at presentation
(a) grading systems: no uniformly accepted system (see table)
WHO grading (1972)

Papilloma

International Society
of Urological
Pathologists ISUP
(1998)
Urothelial papilloma

Transitional Cell Carcinoma


1. Where: the calyces, renal pelvis, ureters, bladder and urethra.
- primary neoplasia of the ureter is rare (more often metastatic seeding).
Cause obstruction; most frequently found in 6th to 7th decades of life
- TCCs represent >90% of all bladder tumours (and are variable: from
small benign lesions to invasive lesions that metastasise frequently)
2. Epidemiology
- 2-6% of deaths from malignancy
- usually >40 years old; 80% pts are 50-80 yoa
- male:female = 4:1
- bladder tumours most common (50x c.f. ureter/renal pelvis tumours)
3. Risk factors
- smoking: most important. Increases risk 3-7 times depending on pack
years and smoking habits. Cigars, pipes, smokeless tobacco have
smaller risk than cigarettes
- industrial carcinogens (arylamines): -naphthylamine and benzidene
(chemical, cable and rubber industries); 15-40 years after first
exposure
- drugs (phenacetin also causes analgesic nephropathy,
cyclophosphamide induces haemorrhagic cystitis, which increases
risk of bladder cancer)
- chronic inflammation (schistosomiasis, Schistosoma haematobium
usually causes squamous carcinoma 70%. 30% are TCC)
4. Presentation
- painless haematuria (most common)
if pain: clot retention, local nerve involvement
- symptoms suggestive of UTI without significant bacteriuria (frequency,
urgency, dysuria)
- symptoms due to local mets
- if in kidney/ureter: haematuria; flank pain (esp. if UT obstruction)
5. Ureteral tumours
- primary neoplasms are rare: metastases occur more than primaries
(a) small benign tumours: fibroepithelial polyps (more in ureters than
bladderm renal pelvis and urethra; L>R) and leiomyomas
(b) primary malignant tumours: mostly TCC. 50-60 yoa. Cause
obstruction. Sometimes multiple

TCC grade I

Urothelial neoplasm of
low malignant potential

TCC grade II (lower


spectrum)

Urothelial
low grade

carcinoma,

TCC grade II (higher


spectrum) and TCC
grade III

Urothelial
high grade

carcinoma,

Morphology and other things

Rare ( 1% bladder tumours). Younger


patients. Single, small (0.5-2cm),
delicate, soft structures with stalk.
Central loose fibrovascular core covered
by
transitional
epithelium.
True
recurrences are rare
Similar gross appearance to papilloma.
Some cytological and architectural
atypia, well-differentiated, mitoses rare.
Significant of cell layers, but slight loss
of polarity. Most recurrences benign; 35% recur with higher grade. All such
well-differentiated papillary neoplasms
seldome become invasive and provide
95-98% 10 year survival
Papillary (most)/flat. no. of layers,
mitoses and loss of polarity. Higher
variability in cell size, shape and
chromaticity. Low risk of progression
Papillary/flat/both.
Larger,
more
extensive, preponderance for invasion
of muscularis. Anaplastic cells; cellular
disarray
with
loosening
and
fragmentation of superficial layers of
cells. risk of invasion into muscular
layer, progression. Significant metastatic
potential

(b) invasion
high grade: 80% invasive locally; 40% spread to local lymph
nodes; haematogenous spread occurs late (liver, lungs, bone
marrow), and only for highly anaplastic tumours
(c) staging (extent of spread)
Depth of Invasion
Noninvasive, papillary
Noninvasive, flat
Lamina propria
Superficial muscularis propria
Deep muscularis propria
Perivesical fat
Adjacent structures
Lymph node metastases
Distant metastases

AJCC/UICC (American Joint Commission on


Cancer/Union Internationale Contre le Cancer)
Ta
TIS
T1
T2
T3a
T3b
T4
N1-3 (N1: regional lymph node <2cm; N2: regional
lymph nodes 2-5cm; N3: regional lymph nodes
>5cm or other lymph nodes)
M1

(d) bladder carcinogenesis: 2 models

(i)

2-pathway model: deletions of tumour suppressor genes on 9p


and 9q superficial papillary/occasionally flat tumours (a few
develop p53 mutations invasion) and p53 mutations
induction of potentially invasive tumours
(ii)
linear model of progression: inactivation of tumour suppressor
genes on chm 9 (or 14 for flat lesions) through loss of p53
function
7. Investigations
- cytology of urine
- IVP
- cystoscopy: not in males <20 yoa/females <30 yoa if they have normal
cytology and normal IVPT and infection is controlled (i.e. significant
bacteriuria with haematuria that ceases post treatment)
- otherwise, always investigate haematuria
8. Treatment
(a) pelvic and ureteric tumours: nephrouretectomy with subsequent
cystoscopy (because about 50% develop bladder tumours).
Radiotherapy and chemotherapy are of little value
(b) bladder tumours: treatment depends on stage (esp. penetration of
muscular later) and degree of differentiation. Many options: local
cystodiathermy and/or resection with cystoscopies and cytology of
urine/cystoscopy, cystectomy, radiotherapy and local and systemic
chemotherapy
9. Prognosis: depends on grade and stage at diagnosis
- whatever the grade, tend to develop new tumours after excision (may
be of higher grade): 50% of papillomas and low-grade carcinomas
recur; 80-90% of high grade tumours recur
- papillomas and Gd 1 carcinomas 98% 10 year survival regardless
of recurrences; <10% progress to higher grade
- Gd III 40% 10 year survival; 65% are progressive
- SCC (5-7% of all bladder carcinoma; more requent in Egypt and
Sudan where urinary schistosomiasis is endemic) 30% survive 1
year
- factors influencin prognosis also include expression of blood group
antigens A, B and H (good if expressed) and no. of chromosome and
gene mutations
Prostatic Enlargement
II.

Nodular Hyperplasia (Benign Prostatic Hyperplasia)

1. Pathophysiology
- testosterone dihydrotestosterone (DHT) by 5-reductase in
stromal cells
- DHT mediates prostatic growth
- DHT accumulates over time in the prostate, binding to nuclear
receptors prostatic hyperplasia

therapy with 5-reductase inhibitor s DHT content of prostate


prostatic volume and urinary obstruction
- DHT-mediated prostatic hyperplasia is aided and abetted by
oestrogens
- in aging men, oestradiol levels and possible sensitizes the
prostate to the growth-promoting effects of DHT
2. Complications: nodular hyperplasia usually originates in the periurethral
portion of the middle and lateral lobes.
(a) compression of urethra dysuria, frequency, hesitancy, postmicturitional dribbling, incomplete bladder emptying
(b) bladder hypertrophy and trabeculation
- retention of urine in the bladder with subsequent distension and
hypertrophy of the bladder
- raised level of the urethral floor due to e.g. middle lobe
enlargement: inability to empty bladder completely, considerable
amount of residual urine left after micturition, static fluid vulnerable
to infection
(c) infection cystitis and pyelonephritis
(d) bladder diverticula
- bladder diverticula = outpocketings of vesical mucosa between the
detrusor muscle bundles
- narrowing of vesical neck outflow resistance higher vesical
pressure required to void hypertrophy of vesical and trigonal
mm may lead to development of bladder diverticula
(e) hydronephrosis or acute urinary retention with secondary UTI
- if severe, can develop azotemia or uraemia
(f) calculi: infected residual urine may contribute to calculi formation
(g) hydroureteronephrosis: hypertrophic trigone functional obstruction
of intravesical ureter
-

II.

Adenocarcinoma of Prostate

1. Risk factors
(a) age (10% of men in 50s have adenocarcinoma; 80% in their 80s)
(b) race: US blacks>US whites>Japanese>HK
(c) family history
(d) hormone levels
(e) environmental influences
2. Pathophysiology: neoplastic epithelial cells possess androgen receptors;
however, androgens only play a permissive role in carcinogenesis.
Androgens are required for maintenance of the prostatic epithelium, which
is then transformed by agents not yet characterised
3. Complications: 70% of prostate cancer arises in the peripheral zone of the
gland, typically a posterior location

(a) prostatism: difficulty startying or stopping stream, poor stream, dysuria,


frequency, or haematuria. Because of location of cancer, urinary
symptoms occur late
(b) pain: involvement of capsular perineural spaces (late). Back pain from
vertebral metastases (usually osteosclerotic)
(c) ureteral obstruction: spread by direct local invasion to involve seminal
vesicles and base of bladder causeing ureteral obstruction
III.

Prostate-Specific Antigen (PSA)

1. PSA: product of prostatic epithelium, normally secreted in human serum. Is


a serine protease; cleaves and liquifies seminal coagulum formed after
ejaculation. Normally present in minute amounts in circulation
2. Increased in:
(a) localised prostatic cancer
(b) advanced prostatic cancer
(c) benign prostatic hyperplasia (but lesser extent)
(d) prostatitis
- PSA levels are proportional to volume of tumour
- cancerous tissue yields higher levels of serum PSA than nodular
hyperplasia for a given volume of tissue because of greater diffusion of
PSA from malignant acini to the stromal blood vessels (not so much
related to production of PSA)
3. PSA density = PSA levels per unit of prostate volume determined by
transrectal US. Increases specificity of mild elevations of serum PSA levels
4. Detection and monitoring of prostatic carcinoma
- combined with PR and TRUS (transrectal US), measurement of PSA
antigen levels is useful in detecting early cancers
- monitoring serum PSA levels is useful in assessing response to
therapy
- immunohistochemical localisation of PSA is helpful in determining
whether a metastatic tumour originated in the prostate
Urinary Tract Infection
1. Pathogenesis: most often via ascending transurethral route (3 steps)
(a) heavy colonisation of vaginal and periurethral area
- diaphragm/spermicidal jelly
- hormone-deficient vaginal atrophy
- systemic antibiotic treatment for non-UTI
(b) urethra bladder
- catheterisation
- sexual intercourse
(c) establishment and multiplication of bacteria in bladder
- flow rate
- infrequency and poor bladder emptying
2. Natural history: isolated, rarely repeated event

(a) complicated (abnormal UT or associated diseases that cause kidney


damage or may be made worse with infection) vs. uncomplicated
(functionally normal UT with normal IVP)
(b) acute pyelonephritis
- fever, loin pain, tenderness, significant bacteriuria
- morphology:
macro : small renal cortical abscesses and streaks of pus in
renal medulla (no cortical loss, smooth outline, cupped calyces
on IVP)
micro : focal infiltration by PMN (and also in tubular lumina)
- chronic pyelonephritis does not developt from this in adults with
normal UT anatomy and no complicating conditions
- chronic pyelonephritis does not develop as a result of repeated
infection
(c) chronic pyelonephritis/atrophic pyelonephritis/reflux nephropathy
- develops from VUR and infection acquired early in infancy/early
childhood
- papillary damage, interstitial nephritis and cortical scarring next to
clubbed calyces
- uni/bi lateral; all/part of kidney
- Ix: IVP (irregular renal outline, clubbed calyces, in size) and
micturating cystourethrography - MCU (reflux)
- development: reflux ceases at puberty. Damage done persists with
progressive rena fibrosis and loss of function even without further
infection
- remember: does not develop without reflux and does not begin in
adulthood
- prognosis: predisposition to hypertension. If severe, is a common
cause of end-stage renal failure in childnood/adult life
- hence, early detection and treatment of infections with/without
ureteral reimplantation can prevent further scarring normal
growth of kidneys
(d) reinfection vs. relapsing infections
- relapse = recurrence of bacteriuria within 7 days of completion of
treatment by the same organism
failure to eradicate infection ( usually in conditions where
eradication is difficult: stones, polycystic kidneys, scarred
kidneys, bacterial prostatitis)
- reinfection = absence of bacteriuria after treatment for >14 days
followed by recurrence of infection with same/different organisms
reinvasion of susceptible tract with new organisms
responsible for about 80% of recurrent infections
3. Symptoms and signs
(a) bladder and urethra inflammation (cystitis)
- frequency, dusuria, suprapubic pain and tenderness, haematuria,
smelly urine
(b) pelvis and kidney (pyelitis/pyelonephritis)

- loin pain, tenderness, fever and systemic upset


can have minimal or no symptoms
can have atypical symptoms (abdo pain, fever, haematuria without
frequency or dysuria)
4. Diagnosis
(a) symptomatic young woman
(i)
102 coliform organisms/mL urine + pyuria OR
(ii)
105 any pathogenic organism/mL urine OR
(iii)
any growth of pathogenic organism in urine by suprapubic
aspiration
(b) symptomatic male: 103 pathogenic organisms/mL urine
(c) asymptomatic patients: 105 pathogenic organisms/mL urine on 2
occasions
- dipstick tests: if both nitrates (gram negative organisms present) and
leucocyte esterase (pyuria) are positive acute infection
- urethral syndrome or abacteriuric frequency/dysuria
post-coital bladder trauma
vaginitis
atrophic vaginitis/urethritis in elderly
interstitial cystitis (Hunners ulcer)1

in symptomatic young wome: Chlamydia, TB


5. Special investigations
(a) IVP: if further attacks/abnormal post-treatment urinalysis/male/children
(b) plain abdo XR and US: most renal stones, upper UT obstruction,
scars, bladder emptying. Useful for acute pyelonephritis
(c) micturating cystourethrography (MCU): only children with abnormal
excretion urograms/IVPs and (maybe) abnormal bladder emptying at
any age. Otherwise no value in UTI management
(d) cystoscopy (limited role): abnormal bladder emptying.ureteral
emptying; haematuria in baceteriuric female over 40 years (bladder
cancer is suspect); abacteriuric frequency/dysuria
6. Bacteriuria in pregnancy
- always culture the urine of pregnant women: 2-6% have asymptomatic
bacteriuria
- acute pyelonephritis is a frequent occurrence under these
circumstances (cf. in the non-pregnany female, asymptomatic
bacteriuria seldom leads on to acute pyelonephritis and does not often
require treatment)
- failure to treat may severe symptomatic pyelonephritis later in
pregnancy with possible premature labour
- asymptomatic bacteriuria in the presence of previous renal disease
may predispose to pre-eclamptic toxaemia, anaemia of pregnancy and
small/premature babies
-

Females, over 40 years; uncommon. Frequency dysuria, severe


suprapubic pain. Cystoscopy: typical inflammatory changes with
ulceration of bladder base. Cause unknown, possibly autoimmune

always treat bacteriuria and show it to be eradicated. Avoid


tetracycline, trimethoprim, sulphonamides and 4-quinolones in
pregnancy; safer drugs to use are amoxycillin and ampicillin,
nitrofurantoin and oral cephalosporins
7. Urinary infections in the presence of an indwelling catheter
- common after being catheterised for a few days
- antibiotic treatment is likely to be ineffective as long as the bladder
catheter is in situ; continued treatment might result in development of
resistance
- treat (if patient has symptoms or evidence of infection) and replace
catheter
- bladder stones may form in patients with long-term indwelling
catheters
- prolonged catheterisation Candida (frequent complication)
-

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