Lower GI Physiology/Motility Flashcards
explain the pH control of pancreas/SI secretions
pancreatic fluid is alkaline (HCO3), neutralises chyme for optimal enzyme function
explain how glucose is digested in the SI
pancreatic a-amylase breaks a1-4 bonds in starch forming maltose/maltotriose/limit dextrin
broken down to glucose by maltase/isomaltase (intestinal wall epithelia)
explain how lactose, cellulose, raffinose and stachyrose are broken down in the SI
lactose - b-galactosidase (reduced production with age)
cellulose - not broken down
raffinose/stachyrose - metabolised anaerobically (colonic bacteria)
explain how fats are digested in the SI
pancreatic lipase/bile degrades lipids
lipase degrades lipids to mono/diacelglycerols and fatty acids
then emulsified and coated with bile salts (inhibits lipase activity unless co-lipase protein present)
explain how proteins are digested in the SI
proteins digested by gastric pepsin (40%) and pancreatic/SI endo/exopeptidases
trypsin, chymotrypsin and elastase break peptide bonds
explain chronic pancreatitis
diseases pancreas glands (alcohol excess/gallstones)
reduction in fat/protein digestion/absorption
diagnosed by faecal elastase test/CT
patients require synthetic pancreatin
describe SI motility
MMC in fasting conditions
optimised to digest/absorb food (post-prandial)
consists of segmentation and peristalsis
explain SI segmentation
ring-like contractions along SI length
contracted areas relax (& vice versa)
chyme moves backwards & forwards for mixing/absorption
explain SI peristalsis
propagates chyme movement distally
LM contracts shortening gut, CM contracts pushing chyme downstream
describe acute post-operative ileus
constipation/intolerance of oral intake after previous obstruction after surgery
lasts 24h in SI, 48h in stomach, 72h in colon
risk factors: open surgery, prolonged pelvic/ab surgery, delated enteral nutrition, peri-operative complications
what contributes to the intake and absorption in the colon
intake: diet (1.5l), saliva (1.5l), gastric juice (2l), pancreatic juice (1.5l), bile (0.5l), intestinal secretions (1.5l)
absorption: SI (7l), colon (1.25l)
faecal loss (0.25l)
explain colonic motility
mostly ring-like contractions of both muscle layers
contractions may move any direction
proximal colon: backwards movement for mixing
sigmoid: tonic contractions to hold faeces back for water absorption
explain the timing of colonic motility
quiescent at night
wakening/meals major stimuli
short spike electrical bursts in proximal colon last ~5s (haustral contraction)
long spike electrical bursts (~10s) cause mass movement/propulsion in colon
(propels faeces into rectum)
explain colonic transit
length of time (usually ~78h) for 50% of ingested radio-opaque markers to be expelled
prolongued by low fibre diet and drugs
what drugs reduce colonic motility?
anticholinergics and opiates
loperamide (Mu receptor agonist):
- decreases myenteric plexus tone
- slows transit and increases water absorption
- used for symptomatic diarrhoea management
what drugs increase colonic motility?
stimulant laxatives (alter gut electrolyte transport)
prucalopride (5HT4 receptor agonist)
- increases gut motility
- used in chronic constipation
explain the action of linaclotide
guanylate C receptor agonist
increases chloride/HCO3 into lumen
increases intestinal fluid
increases colonic transit
used in IBS treatment
explain the sphincter function of the anus
internal:
- SM (involuntary)
- provides greatest contraction when resting
external:
- skeletal (voluntary)
- recruited in cough/sneeze reflex
explain defecation
rectum = faeces resevoir
rectal distension -> rectal wall reflex contraction -> IAS relaxation
defecation only occurs if puborectalis muscle and EAS relaxed
explain how incontinence occurs
excessive rectal distension:
- acute/chronic diarrhoea
- chronic constipation
anal sphincter weakness:
- muscle/sphincter damage
- pudendal nerve damage
what can cause anorectal constipation?
- hirschrung’s disease (children)
- obstructive defecation (paradoxical contraction of puborectalis/EAS)
- rectocoele
- anal fissure (associated defecation pain)
how can a spinal cord injury T12 or above impact colonic motility
reflex bowel (upper motor neuron damage)
reflex arc intact, bowel opens spontaneously but no control
reflex initiated by rectal stimulation (suppository)
how can a sacral nerve spinal cord injury impact defecation?
lower motor neuron injury
flaccid bowel (no reflex arc), incontinence
slow stool propulsion through colon
management - manual stool evacuation (stoma)
