Bladder and urethra

What it normally does

• The bladder wall muscle (detrusor) stretches to hold roughly 400 to 600 mL while the pressure inside barely rises (compliance), then squeezes when parasympathetic nerves from S2 to S4 (pelvic splanchnic) release acetylcholine onto muscarinic receptors. M2 receptors outnumber M3 on the detrusor by roughly three to one, but it is M3 that does most of the contracting, so M3 is the drug target.

  storing and voiding are two separate jobs done by one muscle — so a drug that blocks M3 quietens an overactive bladder and, in the same breath, weakens the pump in a man whose outlet is already narrowed.

• There are two taps. The inner one (internal urethral sphincter) is smooth muscle at the bladder neck held shut by noradrenaline on alpha-1 receptors, and it is not under conscious control. The outer one (external urethral sphincter) is striated muscle you hold shut yourself through the pudendal nerve, backed up by the pelvic floor.

  blocking alpha-1 opens the outlet without touching the bladder wall, and damage to the pelvic floor lets the outer tap leak when abdominal pressure spikes.

• Stretch receptors report filling; the pontine micturition centre then runs one coordinated void — the sphincters relax and the detrusor contracts as a single sequence. The frontal cortex vetoes the reflex until you decide otherwise.

  where a neurological lesion sits decides the bladder problem: a lesion in the cortex or anywhere above the pons removes the veto but leaves coordination intact (an overactive, reflex bladder), while a lesion between the pons and the sacral cord leaves the sacral reflex running with no coordination, and a lesion at or below S2-S4 knocks the reflex out altogether (a flaccid, poorly emptying bladder).

• Bladder urine is normally free of pathogens — it carries at most a low-biomass resident flora, not an infection — and the defences are largely mechanical: emptying completely flushes bacteria out, and the urethra is a physical barrier about 4 cm long in women and around 18 to 20 cm in men.

  anything that leaves residual urine behind, or bypasses the urethra entirely with a catheter, removes the defence — and it is part of why women get far more urinary infections than men.

What goes wrong

• Overactive bladder (urge incontinence)← from “The bladder wall muscle (detrusor) stretches t…”

  The detrusor contracts during filling instead of waiting for permission. Either the cortical veto is weakened — stroke, dementia, Parkinson disease — or the muscle itself is irritable with no cause found. An unwanted contraction can drive bladder pressure above what the sphincters can hold, so the urge is sudden and the leak may arrive before the toilet does.

  Detrusor contracting during storage. Urgency, frequency, nocturia, normal post-void residual. Infection, diabetes and (in men) obstruction are excluded before calling it idiopathic; first-line treatment is bladder training and fluid/caffeine advice, not a drug.

  You would find: A sudden desperate urge, small frequent volumes, waking at night to pass urine, leaking on the way to the toilet. The bladder empties normally — a bladder scan shows a normal post-void residual, and the dipstick shows no evidence of infection.

• Bladder outlet obstruction and urinary retention← from “There are two taps. The inner one (internal ur…”

  An enlarging prostate (benign prostatic hyperplasia) squeezes the urethra, and alpha-1 driven smooth muscle tone at the bladder neck and within the gland tightens it further. The detrusor thickens to push past the obstruction, then decompensates and stops emptying fully. A trigger — an anticholinergic drug, constipation, alcohol, an anaesthetic — tips a marginal bladder into complete retention.

  Slow stream, rising residual, palpable bladder. Painful acute retention versus painless chronic retention with renal impairment. Anticholinergics precipitate it.

  You would find: An older man with hesitancy, a weak stream and terminal dribbling. In acute retention the bladder is painful and palpable suprapubically, and a catheter relieves it. Chronic retention is painless with a large residual and a bladder that can reach up towards the umbilicus, and the back pressure can swell the kidneys (hydronephrosis) and raise the creatinine; after decompressing a chronically distended bladder, a post-obstructive diuresis is the thing to watch for.

• Stress incontinence← from “There are two taps. The inner one (internal ur…”

  Childbirth, pelvic surgery and the fall in oestrogen after menopause weaken the pelvic floor and the support under the external sphincter. Coughing transmits abdominal pressure to the bladder but no longer to the closing mechanism, so pressure inside briefly beats the outlet and a small volume escapes. In pure stress incontinence the detrusor itself behaves normally — though mixed stress and urge incontinence is common.

  Leak on effort, no urge, normal residual. Mechanical failure of the outlet, so the answer is mechanical: pelvic floor training, then continence pessary or surgery.

  You would find: A small leak with a cough, sneeze, laugh or lift, and no urge beforehand. It can be demonstrated by asking the patient to cough with a comfortably full bladder. Supervised pelvic floor muscle training is the first-line treatment — there is no good drug for it, which is worth saying out loud: systemic oestrogen (menopausal hormone therapy) does not treat it and can make incontinence worse, and duloxetine is not TGA-approved for this indication in Australia.

• Urinary tract infection (cystitis)← from “Bladder urine is normally free of pathogens — …”

  Gut bacteria, most often Escherichia coli, climb the short urethra and stick to the bladder lining. The inflamed urothelium becomes irritable, so the bladder contracts on tiny volumes. Residual urine or a catheter biofilm removes the flushing defence, which is why obstruction and catheters convert an occasional infection into a recurrent one.

  Dysuria, frequency, suprapubic pain, positive nitrites. Bacteria in the urine with no symptoms (asymptomatic bacteriuria) is generally not treated — the usual exceptions are pregnancy and before a urological procedure that will breach the mucosa.

  You would find: Burning on passing urine, frequency, urgency and suprapubic pain, with nitrites and leucocyte esterase on dipstick — nitrites are specific but insensitive, so a nitrite-negative dipstick does not exclude infection (Enterococcus and Staphylococcus saprophyticus are typically nitrite-negative). Fever, rigors and loin pain mean the infection has reached the kidney and is a different, more serious problem. Roughly half of women have at least one urinary infection in their lifetime; catheter-associated infection is a leading healthcare-associated infection in Australian hospitals and the commonest device-associated one; and Aboriginal and Torres Strait Islander Australians are hospitalised for urinary infection at higher rates, with remote-community access to care and washing facilities part of the reason.

• Neurogenic bladder after spinal cord injury← from “Stretch receptors report filling; the pontine …”

  Immediately after injury there is spinal shock: the bladder is areflexic and overfills, so it needs draining. Weeks later, a cord lesion above the sacral segments has cut the bladder off from the pons but left the sacral reflex arc intact. Reflex voiding returns without coordination, so the detrusor contracts hard against a sphincter that stays shut (detrusor-sphincter dyssynergia). Pressures inside the bladder climb, urine is forced back up the ureters, and the kidneys can be damaged silently.

  Lesion above the sacral cord equals reflex bladder plus dyssynergia plus high pressure; a sacral (S2-S4) or cauda equina lesion equals a flaccid bladder with overflow. The threat to the kidney, not the incontinence, is what matters most.

  You would find: Poor emptying with high bladder pressures after a cord injury, and hydronephrosis on imaging. With lesions at T6 or above, a blocked catheter or full bladder can trigger a pounding headache, a surging blood pressure and flushing above the lesion (autonomic dysreflexia) — the immediate steps are sitting the patient upright and relieving the bladder, before any antihypertensive.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.