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Pregnancy
Periureteral inflammation
Congenital
bladder
neck
obstruction
Neuropathic bladder
Urethral stricture (calculus;
conococcal;
after
instrumentation)
Congenital urethral valve
Pin-hold meatus
Retroperitoneal fibrosis
(e.g
Strictures
Tumourous
masses
Blood clots
Neurogenic
causes
Extrinsic
Endometriosis
Tumours
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)
-
(d)
(e)
(f)
(g)
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
6.
7.
8.
9.
(c)
(d)
(e)
(f)
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
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
TCC grade I
Urothelial neoplasm of
low malignant potential
Urothelial
low grade
carcinoma,
Urothelial
high grade
carcinoma,
(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
(i)
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
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