Micturition Flashcards
Label the key structures of the male urinary tract
Label the key structures of the female urinary tract. What are the main differences when compared to the male?
- No internal sphincter
- no prostate gland
- Shorter urethra
Which receptors would you find on the bladder, internal sphincter and external sphincter of the urinary system?
Bladder: M3 Muscurinic receptor, B3 adrenergic receptor
Internal sphincter: Alpha 1 receptors
External sphincters: Nicotininc receptor
Somatic fibres in the pudendal nerve travel from Onuf’s nucleus. Fibres from the storage pons stimulate onuf’s nucleus, thereby favouring ??? of urine.
Storage
Onuf’s nucleus is a distinct group of neurones in the ??? horn of the ??? region.
anterior
sacral.
Damage to the CNS above the pons (suprapontine) leads to coordinated voiding. However, damage to level below the pons leads to discoordinated voiding.
There are various neurological conditions that can effect bladder functions. S2/S3 and S4 cord segents typically originate at the level of T12. Therefore, lesions at T11, are called????, lesions at L1 are called ?????, and T12 lesions are ????.
Neurological conditions can be classified depepdning on either where the lesion is, or the functional affect of the condition.
Location of defect:
- Sacral
- Infrasacral
- Pontine
- Suprapotine
Functional effect:
- Detrusor (overactive, normoactive, underactive)
- Sphincter (overactive, normoactive, underactive)
There are various neurological conditions that can effect bladder functions. S2/S3 and S4 cord segents typically originate at the level of T12. Therefore, lesions at T11, are called suprasacral lesions at L1 are called infrasacral, and T12 lesions are variable.
Neurological conditions can be classified depepdning on either where the lesion is, or the functional affect of the condition.
Location of defect:
- Sacral
- Infrasacral
- Pontine
- Suprapotine
Functional effect:
- Detrusor (overactive, normoactive, underactive)
- Sphincter (overactive, normoactive, underactive)
Consequences of different types of lesions on bladder function:
- Detrusor hyperrflexia is excessive contraction of the bladder muscle - can result in urgency (when you need to pee but cannot)
- Synergic striated sphincter - means sphincter contracts and relaxes when it should
- Detrusor sphincter dyssnergia - means the shpincter is often contraction when it shouldn’t - this can lead to pressure build up, as when bladder contracts you get even more pressure build up which can transfer to the kidneys
- Areflexic bladder - does not contract properly
- low compliance with open bladder neck - does not contract properly and has tendency to leak
Supraponine lesions (basically anything that affects brain), what can cause this? You would have overactive bladder with intact sphincter behaviour
Dementia
parkinsons
Stroke
Examples of suprasacral lesions
Suprasacral spinal cord injury - can cause failure of sphincter to relax
Multiple sclerosis
Causes of infrasacral lesions
Define obstructive uropathy
Damage to renal parenchyma resulting from obstruction to flow of urine
Obstructive neuropathy most commonly associated with high pressure chronic reternion (HPCR). What is this?
- Some voiding still occurs, but bladder volume remains at over 800mls, with high intra-vesical pressure. often accompanied by hydronephrosis
What is hydroneprhosis?
Hydronephrosis refers to dilation of the renal pelvis and calyces, with accompanying atrophy of the parenchyma, caused by obstruction to the outflow of urine. The obstruction may be sudden or insidious, and it may occur at any level of the urinary tract, from the urethra to the renal pelvis.
Bilateral hydronephrosis occurs only when the obstruction is below the level of the ureters. If blockage is at the ureters or above, the lesion is unilateral. Sometimes obstruction is complete, allowing no urine to pass; usually it is only partial.
How is hydronephrosis caused?
The unusually high pressure thus generated in the renal pelvis, as well as that transmitted back through the collecting ducts, causes compression of the renal vasculature. Both arterial insufficiency and venous stasis result, although the latter probably is more important. The most severe effects are seen in the papillae, because they are subjected to the greatest increases in pressure. Accordingly, the initial functional disturbances are largely tubular, manifested primarily by impaired concentrating ability. Only later does glomerular filtration begin to diminish. Experimental studies indicate that serious irreversible damage occurs in about 3 weeks with complete obstruction, and in 3 months with incomplete obstruction. In addition to functional changes, the obstruction also triggers an interstitial inflammatory reaction, leading eventually to interstitial fibrosis.
How does high pressure chronic retention present?
Red flag is nocutrnal uresis.
Hypertensive due to increased fluid load.
In HPCR, the bladder fills and empties in a cylical fasion at an abnormally raised pressure. Even when some urination occurs, the pressure does not drop as much as it would in a healthy patient.
As ureters begin to dilate due to obstruction, peristalsis of the ureters is lost, meaning drainage is reliant on gravity. Pressure in normal patients rises to value less than 25cmh20 (weird old fashioned pressure reading). More than 25 post-void is bad, and coincides with rapid impairment of renal function and raises in serum creatinine.
immediate Management for high pressure chronic retention?
After patient has bladder drained - there is something called post-obstructive diuresis.
Long term management of HPCR
