Micturition and defecation

Question 1

Reflexes

Answer 1

Stretch reflex
Flexor reflex

Question 2

CNS descending control

Answer 2

Descending control from the CNS
→ elicits voluntary control of somatic nervous system

Elicits heightened stretch reflex responses
→ due to reduced descending inhibition by CNS

Question 3

Comparison of ANS and somatic NS

Answer 3

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

Question 4

ANS vs somatic synapse

Answer 4

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

Question 5

Smooth muscle contraction

Answer 5

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

Question 6

Congenital central hypoventilation syndrome

Answer 6

→ 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)

Question 7

What muscle contracts to get urine out of bladder?

Answer 7

Detrusor

Question 8

What type of muscle are the internal and external urethral sphincters?

Answer 8

Internal urethral sphincter
→ smooth muscle (involuntary)

External urethral sphincter
→ skeletal muscle (voluntary)

Question 9

Innervation of the bladder

Answer 9

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

Question 10

Parasympathetic nervous system with micturition

Answer 10

→ muscarinic-3 receptor
→ acetylcholine
→ detrusor muscle (contraction)
→ internal sphincter (relaxation)
→ internal sphincter opens
→ voiding of bladder

Question 11

Sympathetic nervous system with micturition

Answer 11

Detruser Muscle:
→ B3 receptor
→ noradrenaline
→ detrusor muscle (relaxation)

Internal Sphincter:
→ A1 receptor
→ noradrenaline
→ internal sphincter (contraction)
→ internal sphincter closes

—> urine retention

Question 12

Micturition reflex initiated by bladder filling

Answer 12

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)

Question 13

Urine storage

Answer 13

→ 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

Question 14

Urine voiding

Answer 14

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

Question 15

Co transmitters

Answer 15

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

Question 16

Brainstem switch for micturition

Answer 16

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.

Question 17

Voluntary assistance

Answer 17

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

Question 18

Spinal cord injury - autonomic bladder

Answer 18

→ 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

Question 19

Spinal cord injury - atonic bladder

Answer 19

→ 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

Question 20

Hematuria

Answer 20

→ 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

Question 21

Defecation

Answer 21

Defecation requires control of both skeletal and smooth muscles

Question 22

Enteric nervous system

Answer 22

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

Question 23

Peristalsis

Answer 23

Peristalsis is an intrinsic local reflex (ENS-mediated stretch reflex)

→ helps move food through the GI tract towards the anus

Question 24

Gut stretch afferents

Answer 24

→ 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

Question 25

Control of motility by long-range reflexes

Answer 25

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

Question 26

Defecation reflex part 1

Answer 26

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)

Question 27

Defecation reflex part 2

Answer 27

→ 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

Question 28

Rectal stretch reflex

Answer 28

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

Question 29

Spinal cord injury - reflex bowel

Answer 29

→ spinal cord damage above T12 → loss of bowel sensation → loss of descending control from brain → defecation reflex intact → sphincters retain some tone

Question 30

Spinal cord injury - flaccid bowel

Answer 30

→ spinal cord damage below T12 → loss of bowel sensation → loss of descending brain control → loss of defecation reflex → loss of reflex tone of sphincters

Question 31

Autonomic dysreflexia

Answer 31

→ 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

Question 32

Diarrhoea and type of diarrhoea

Answer 32

→ 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)