Lower GI Physiology/Motility

Question 1

explain the pH control of pancreas/SI secretions

Answer 1

pancreatic fluid is alkaline (HCO3), neutralises chyme for optimal enzyme function

Question 2

explain how glucose is digested in the SI

Answer 2

pancreatic a-amylase breaks a1-4 bonds in starch forming maltose/maltotriose/limit dextrin
broken down to glucose by maltase/isomaltase (intestinal wall epithelia)

Question 3

explain how lactose, cellulose, raffinose and stachyrose are broken down in the SI

Answer 3

lactose - b-galactosidase (reduced production with age)
cellulose - not broken down
raffinose/stachyrose - metabolised anaerobically (colonic bacteria)

Question 4

explain how fats are digested in the SI

Answer 4

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)

Question 5

explain how proteins are digested in the SI

Answer 5

proteins digested by gastric pepsin (40%) and pancreatic/SI endo/exopeptidases
trypsin, chymotrypsin and elastase break peptide bonds

Question 6

explain chronic pancreatitis

Answer 6

diseases pancreas glands (alcohol excess/gallstones)
reduction in fat/protein digestion/absorption
diagnosed by faecal elastase test/CT
patients require synthetic pancreatin

Question 7

describe SI motility

Answer 7

MMC in fasting conditions
optimised to digest/absorb food (post-prandial)
consists of segmentation and peristalsis

Question 8

explain SI segmentation

Answer 8

ring-like contractions along SI length
contracted areas relax (& vice versa)
chyme moves backwards & forwards for mixing/absorption

Question 9

explain SI peristalsis

Answer 9

propagates chyme movement distally
LM contracts shortening gut, CM contracts pushing chyme downstream

Question 10

describe acute post-operative ileus

Answer 10

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

Question 11

what contributes to the intake and absorption in the colon

Answer 11

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)

Question 12

explain colonic motility

Answer 12

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

Question 13

explain the timing of colonic motility

Answer 13

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)

Question 14

explain colonic transit

Answer 14

length of time (usually ~78h) for 50% of ingested radio-opaque markers to be expelled
prolongued by low fibre diet and drugs

Question 15

what drugs reduce colonic motility?

Answer 15

anticholinergics and opiates

loperamide (Mu receptor agonist):
- decreases myenteric plexus tone
- slows transit and increases water absorption
- used for symptomatic diarrhoea management

Question 16

what drugs increase colonic motility?

Answer 16

stimulant laxatives (alter gut electrolyte transport)

prucalopride (5HT4 receptor agonist)
- increases gut motility
- used in chronic constipation

Question 17

explain the action of linaclotide

Answer 17

guanylate C receptor agonist
increases chloride/HCO3 into lumen
increases intestinal fluid
increases colonic transit
used in IBS treatment

Question 18

explain the sphincter function of the anus

Answer 18

internal:
- SM (involuntary)
- provides greatest contraction when resting

external:
- skeletal (voluntary)
- recruited in cough/sneeze reflex

Question 19

explain defecation

Answer 19

rectum = faeces resevoir
rectal distension -> rectal wall reflex contraction -> IAS relaxation
defecation only occurs if puborectalis muscle and EAS relaxed

Question 20

explain how incontinence occurs

Answer 20

excessive rectal distension:
- acute/chronic diarrhoea
- chronic constipation

anal sphincter weakness:
- muscle/sphincter damage
- pudendal nerve damage

Question 21

what can cause anorectal constipation?

Answer 21

• hirschrung’s disease (children)
• obstructive defecation (paradoxical contraction of puborectalis/EAS)
• rectocoele
• anal fissure (associated defecation pain)

Question 22

how can a spinal cord injury T12 or above impact colonic motility

Answer 22

reflex bowel (upper motor neuron damage)
reflex arc intact, bowel opens spontaneously but no control
reflex initiated by rectal stimulation (suppository)

Question 23

how can a sacral nerve spinal cord injury impact defecation?

Answer 23

lower motor neuron injury
flaccid bowel (no reflex arc), incontinence
slow stool propulsion through colon

management - manual stool evacuation (stoma)