Micturition and defecation Flashcards
Reflexes
Stretch reflex
Flexor reflex
CNS descending control
Descending control from the CNS
→ elicits voluntary control of somatic nervous system
Elicits heightened stretch reflex responses
→ due to reduced descending inhibition by CNS
Comparison of ANS and somatic NS
1)
→ Synapse at ganglion
→ No synapse outside CNS
2)
→ Post-ganglionic neurons not myelinated
→ motor neurons myelinated
3)
→ Multiple neurotransmitters and multiple receptor types at effector cells
→ ACh stimulates nicotinic receptors at neuromuscular junctions
4)
→ Effectors can receive multiple synaptic inputs
→ skeletal muscle receives only one synaptic input
5)
→ Excitatory or inhibitory effects at effector tissue
→ excitatory effects only at the muscle
6)
→ multiple effector organs innervated
→ skeletal muscle only
ANS vs somatic synapse
Somatic synapse:
→ axons of somatic neurons form a single close synaptic contact
→ with a single skeletal myocyte at neuromuscular junctions
ANS neuroeffector junction:
→ axons of postganglionic neurons of the ANS have thickenings called variocosities
→ allowing them to make ‘passing’ synapses all along the axon
→ these allow a single axon to make multiple contact with cells
Smooth muscle contraction
Slow, maintained contraction to pressurise hollow organs (eg. Bladder)
ANS + endocrine
→ Ca2+
→ Ca2+ + calmodulin
→ activates MLCK
→ phosphorylates myosin heads
→ cross bridge cycling
Calponin unblocks binding sites on actin
Congenital central hypoventilation syndrome
→ Importance of ANS-mediated reflexes
→ ANS reflexes have wider impact than somatic reflexes
→ deficient autonomic central control of ventilation
→ mutation in the transcription factor Phox2b
→ diaphragmatic pacing
(No reflex stimulating breathing)
What muscle contracts to get urine out of bladder?
Detrusor
What type of muscle are the internal and external urethral sphincters?
Internal urethral sphincter
→ smooth muscle (involuntary)
External urethral sphincter
→ skeletal muscle (voluntary)
Innervation of the bladder
Pelvic nerve (parasympathetic)
→ M3-AChR
→ detrusor contraction
Hypogastric nerve (sympathetic)
→ B3-adrenoreceptor = inhibit detrusor contraction
→ A1-adrenoreceptor = contract internal urethral sphincter
Pudendal nerve (somatic)
→ nicotinic receptors = contract external urethral sphincter
Parasympathetic nervous system with micturition
→ muscarinic-3 receptor
→ acetylcholine
→ detrusor muscle (contraction)
→ internal sphincter (relaxation)
→ internal sphincter opens
→ voiding of bladder
Sympathetic nervous system with micturition
Detruser Muscle:
→ B3 receptor
→ noradrenaline
→ detrusor muscle (relaxation)
Internal Sphincter:
→ A1 receptor
→ noradrenaline
→ internal sphincter (contraction)
→ internal sphincter closes
—> urine retention
Micturition reflex initiated by bladder filling
1)
→ Bladder stretch receptors (particularly in trigone region) detect distension
→ release ATP from uro-epithelium
→ activates afferent nerve fibres
2)
→ Sensory pathways from uroepithelium
(cerebral cortex → pontine micturition centre in dorsal pons)
3)
→ Hypogastric nerve (sympathetic) stimulated
→ Relaxes smooth muscle via B2-B3- adrenoreceptors
→ and stimulates internal sphincter contraction via a1-adrenoreceptors (storage)
OR
3)
→ Pelvic nerve (parasympathetic) stimulated
→ Contraction of smooth muscle via M3 and M2 muscarinic receptor (voiding)
4)
→ Pudendal nerve (somatic) innervates external urethral sphincter (can decide to wee or not)
Urine storage
→ Filling phase
→ low level firing of afferent neurons
→ (pontine storage centre)
→ trigger spinal guarding reflex
→ trigger activation of somatic motor neurons (pudendal nerve) and contraction of external urethral sphincter
OR
→ trigger sympathetic stimulation (hypogastric nerve) of internal urethral sphincter and inhibits contraction of detrusor muscle
→ urine storage
Urine voiding
Voiding is urinating:
→ voiding is mediated by spinobulbospinal reflex
Brainstem switch for micturition:
→ input from various centres change the threshold level of afferent firing required for periaqueductal gray (PAG) activation of pontine micturition centre (PMC)
→ High-level afferent firing
→ triggers activation of PMC via the PAG
→ sends descending inhibitory control
→ blocks inhibitory sympathetic input to detrusor muscle
OR
→ inhibits somatic motor neuron activation
→ relaxation of external urethral sphincter
→ urine voiding OR activation of PMC causes activation of PNS innervation of detrusor muscle contraction (via ACh release)
→ and internal urethral sphincter relaxation through release of non-adrenergic, non-cholinergic transmitter, nitric oxide
—> urine voiding
Co transmitters
Autonomic neurons can stimulate cells using non-adrenergic, non-cholinergic pathways.
This is done by release of co-transmitter substances such as:
→ ATP
→ NO
→ neuropeptide Y
→ vasoactive intestinal peptide
Brainstem switch for micturition
Threshold level between storage and voiding is variable.
Preiaqueductal grey (PAG) activation of the PMC is controlled by input from a number of central centres.
These change the threshold level of afferent firing required for PMC activation.
Voluntary assistance
Other voluntary events assist micturition and defecation especially Valhalla manoeuvre:
→ laryngeal cavity closed
→ air retained in thorax
→ fixed diaphragm
→ contraction of abdominal wall
→ increase in intra-abdominal pressure
Spinal cord injury - autonomic bladder
→ Spinal cord injury above sacrum
→ interruption of spinobulbospinal reflex but PNS innervation (pelvic nerve) from sacrum preserved
→ early - ‘spinal shock’ inhibits micturition reflex. Requires catherisation to avoid bladder damage
→ later - micturition reflex re-establishes itself with no descending control
→ loss of bladder sensation and emptying controlled by micturition reflex alone
Spinal cord injury - atonic bladder
→ spinal cord damage of sacrum leading to loss of sensory input
→ damage to sacrum prevents transmission of stretch signals from bladder
→ loss of bladder sensation and control - no reflex contraction of detrusor or relaxation of internal sphincter
→ loss of micturition reflex leads to bladder becoming abnormally distended as it fills uncontrollably
—> overflow incontinence
Hematuria
→ blood in urine
→ anywhere from urinary tract to- anatomically the source of the haematuria could be the upper tract (kidneys of ureters) or the lower urinary tract (bladder, prostate or urethra)
→ aetiologoically the possible causes include tumours, stones or infections in the urinary tract
→ Drug abuse with ketamine is becoming increasingly common of haematuria in younger patients
Defecation
Defecation requires control of both skeletal and smooth muscles
Enteric nervous system
Split into 2 plexuses
→ Myenteric plexus - controls GI motility
→ Submucosal plexus - controls both GI motility and secretion
Parasympathetic
→ promotes motility/secretion
Sympathetic
→ inhibits motility/secretion and contracts sphincters
Peristalsis
Peristalsis is an intrinsic local reflex (ENS-mediated stretch reflex)
→ helps move food through the GI tract towards the anus
Gut stretch afferents
→ Wall stretch
→ intra-ganglionic laminar endings (IGLES) (stretch receptor for spinal reflex)
→ trigger mechanosensitive channels
→ trigger increased entry on Na+ and Ca2+
→ increased firing of intraganglion afferents
→ spinal reflex that co-ords with peristaltic reflexes
Control of motility by long-range reflexes
Gastrocolic/duodenocolic reflexes, where food entering the stomach or duodenum promotes the motility of the colon:
→ initiates mass movement after a meal
→ mediated by vagus nerve (ANS) following distension (or irritation) of stomach and duodenum
Defecation reflex part 1
Intrinsic (peristalsis) reflex mediated by ENS in rectal wall:
→ faeces enters rectum
→ distension of rectal wall
→ afferent signals spread through myenteric plexus
→ peristaltic waves in descending colon, sigmoid and rectum
→ forcing faeces to anus
→ internal anal sphincter is relaxed by inhibitory signals from myenteric plexus
Parasympathetic spinal reflex (sacral segments of spinal cord):
→ stimulation of nerve endings in rectum
→ signals transmitted to spinal cord
→ reflex back to descending colon, sigmoid, rectum and anus via pelvic nerves (PNS)
→ PNS signals intensify peristaltic waves and relax internal anal sphincter (strengthening intrinsic myenteric defecation reflex)
Defecation reflex part 2
→ the distal colon has limited peristaltic activity. Therefore, food only begins to move into the rectum when motility is stimulated by the gastrocolic and duodenocolic reflex
→ this stretches the rectum ad causes a reflex which can trigger either if we chaise to hold on or if we choose to defecate.
→ if we choose to hold on- the reflex contraction of the external anal sphincter prevents defecation. Relaxation of the rectum removes the stimulus for the reflex
→ if we choose to defecate - the brain sends inhibitory signals to the spinal cord to prevent the reflex contraction of the external anal sphincter. This allows the sphincter to relax and allow defecation
Rectal stretch reflex
Stretch of rectum triggers:
→ increased local peristalsis elicited through ENS
→ increased regional peristalsis via spinal activation of PNS
→ relaxation of internal anal sphincter
→ contraction of external anal sphincter
→ conscious awareness
Spinal cord injury - reflex bowel
→ spinal cord damage above T12
→ loss of bowel sensation
→ loss of descending control from brain
→ defecation reflex intact
→ sphincters retain some tone
Spinal cord injury - flaccid bowel
→ spinal cord damage below T12
→ loss of bowel sensation
→ loss of descending brain control
→ loss of defecation reflex
→ loss of reflex tone of sphincters
Autonomic dysreflexia
→ noxious stimuli induce uncontrolled sympathetically-mediated spinal reflexes which trigger severe hypertension
→ SNS response is exaggerated due to lack of compensatory descending PNS stimulation - impaired baroreflex response
→ a medical emergency for spinal cord injury patient
Diarrhoea and type of diarrhoea
→ diarrhoea is impaired GI water absorption
→ osmotic diarrhoea - non-absorbable solute accumulates within the small intestine. Solutes in the lumen create osmotic pressure, retaining water in GIT —> distension of intestine + inflammatory irritation of the intestinal wall —> ENS and vagovagal reflexes —> increased intestinal motility (eg. Lactase deficiency
→ secretory diarrhoea - reduced ion absorption or increased intestinal ion secretion (eg. Bacterial toxins)
→ exudative diarrhoea - inflammatory damage to intestinal mucosal cells. Inflammation around mucosal pathogens obstructs the absorptive surface and leaves solutes in the intestinal lumen that would normally be absorbed (eg. IBD)
→ abnormal intestinal motility - increased transit in the small bowel or colon (eg. Diabetes mellitus)
