3. Control pathways
Both hormonal and neural
Short pathways: involves automatic regulation within the enteric
system itself
Long pathways: involves the CNS (somatic and autonomic)
Three phases: cephalic, gastric and intestinal phases
4. Cephalic phase: salivary and gastric secretions
Salivary secretion stimulated by
parasympathetic NS by odors,
sight, taste saliva fluid and
rich in enzymes
Stimulated by sympathetic NS
thick secretion, rich in
proteins
Gastric secretion: increase acid
and enzymes secretion in
response to sight, smell and
taste of food
5. Gastric phase
Stimuli: presence of
food in the stomach
(both distention and
nutrients)
Stimulation of the
parasympathetic NS
and secretion of gastrin
(hormone)
Response: increased
motility and juice
secretion
6. Intestinal phase
Arrival of nutrients in duodenum decreased gastric
secretion and motility
Promotes secretion of cholecystokinin (CCK) and secretin
- CCK promotes:
- increased pancreatic enzyme secretion
- gallbladder contraction and sphincter of Oddi
relaxation
- secretin promotes:
- bicarbonate ion secretion (pancreas)
- bile secretion
7. Peristalsis:
Waves of contraction of longitudinal muscle fibers
moving down the GI tract
Segmentation:
In small intestine for mixing chyme
9. Control mechanisms
During fasting, ghrelin and peptide YY (PYY)
concentrations are abnormal
Nutrient-stimulated concentrations of CCK
and PYY are markedly elevated delayed
gastric emptying
10. Motility in the small intestine
Segmentation and peristalsis increased by distention
of the wall
Intestino-intestinal reflex:
Severe distention or injury inhibits motility in the region
Ileo-gastric reflex:
Distension of ileum inhibits gastric motility
Gastro-ileal reflex:
Presence of chyme in stomach increases motility in ileum
11. Motility in the colon
Haustration:
Like segmentation
Colono-colonic reflex:
Distension in one part of the colon induces relaxation in other parts
Gastro-colic reflex:
A meal in the stomach increases colonic motility
Defecation:
Triggered by distention of the rectal wall
Signal sent to sacral parasympathetic and cortex
Smooth muscle of anal sphincter open
If the person decides to go to the bathroom open
voluntary muscle sphincter
12. Migrating motor complexes (MMCs):
☆Phase I:
Quiescence
☆Phase II:
Variable period of irregular contractile
activity
☆Phase III:
Short period (5~10 min) of intense, frequent, regular
contractions (motilin receptor) clear bowel
13.
14. Gastric emptying in the critically ill
Delayed gastric emptying is more frequent in:
☆Burns
☆Multiple trauma
☆Severe sepsis
►80% of head injuries
►Hyperglycemia delays gastric emptying
(pre-existing DM doesn’t affect)
15. Drugs administered in ICU, particularly inotropes
and those used for sedation
Opiates μ-receptors
16. High levels of circulating catecholamines commonly seen
negative effect
Adrenaline reduces gastric emptying by a β-adrenergic effect
Dopamine reduces antral contractions and slows orocaecal
transit
High-dose catecholamines may reduce the prokinetic effect of
erythromycin
Anticholinergics and calcium channel blockers
17. Intestinal absorption in critically ill
Glucose absorption is substantially reduced
Fat absorption may also be reduced
The reasons for impaired absorption are unclear
18.
19. Agents that enhance coordinated
contraction of the antrum & duodenum
Increases gastric emptying
Relief of gastric stasis
Decreases reflux oesophagitis / heart burn
Decreases regurgitation of gastric contents
& emesis
20. Achalasia (esophagus spasm, lower
esophageal sphincter (LES) fails to relax)
GERD (gastroesophageal reflux disease)
(insufficient LES pressure)
Gastroparesis (delayed gastric emptying,
often occurs in people with diabetes due to
vagus nerve damage)
23. Metoclopramide
D2 antagonist
5-HT4 agonist
5-HT3 antagonist
Widely used in ICU
Antagonizes the inhibitory effect of dopamine on motility
Crosses the blood brain barrier
Hyperprolactinemia
Anti-emetic effect
With repeated administration tachyphylaxis develops
Ineffective and contraindicated in patients with head injuries
24. Domperidone
D2 selective antagonist
Does not cross blood brain barrier
CNS related symptoms are least
Causes hyperprolactinemia
25. Cisapride
5-HT4 agonist
Acetylcholine increase in enteric nervous system
(parasympathomimetic) increase esophageal
sphincter tone and gastric emptying
Has no D2 receptor activity, no CNS related side effects
No hyperprolactinemia, no anti-emetic effect
Causes upper G.I. motility, promote colonic hypermotility
Relieves constipation
Causes ventricular arrhythmia by torsades de pointes
Block K+ channels in the heart & GIT
26. • Erythromycin
Macrolide antibiotic & acts as a motilin agonist
Low doses (1~3 mg/kg IV) of erythromycin act as a motilin
agonist, triggering phase III activity in the stomach and small
intestine
In critically ill, it increases antral motility, accelerates gastric
emptying and improves the success of feeding
Efficacy reduced after 7-day use
Cardiac toxicity and bacterial resistance
27. Combination therapy
Combination of erythromycin and
metoclopramide for failure of nasogastric
feeding, is superior to either drug alone and
with less tachyphylaxis
30. Elevated cholecystokinin levels slow gastric emptying
and motility and are associated with feed intolerance in
critically ill patients
☆Dexloxiglumide
Selective and highly potent CCK-1 receptor antagonist
Inhibits gall bladder contraction
Improves lower oesophageal sphincter function
Hastens colonic transit
31. μ Receptor Antagonists
Opiates slow gastric emptying opiate
antagonist
☆Naloxone
administered directly into the gut avoid
antagonism of the central effects of parenteral
opiates
improves the success of feeding and reduces
pneumonia
32. ☆Alvimopan
High affinity for μ receptors
Does not cross the blood–brain barrier
No effect on gastric emptying
hastened gut recovery and shortened time
to hospital discharge in patients after
bowel resection or hysterectomy