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3002 > 15 GI tract motility: motility of stomach, small and large intestine > Flashcards

15 GI tract motility: motility of stomach, small and large intestine Flashcards

1
Q

What is are the major functions of gastric motility? (3)

A
  1. Allows stomach to act as a reservoir for the large volume of food ingested at a single meal (receptive relaxation)
  2. Breaks food into smaller particles and mixes with gastric secretions
  3. Empties gastric contents into duodenum at controlled rate
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2
Q

Smooth muscle of the stomach:
• 3 layers?
• Change in thickness?

A

3 layers:
• Outer= Longitudinal
• Middle= Circular
• Inner= Oblique

Muscle wall thickness increases from proximal to distal

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3
Q

What does contraction in the caudad region do?

A

Mix food and propel it into the small intestine

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4
Q

List the innervation of the stomach (3)

A
  1. Extrinsic nerves
    • Parasympathetic
    • Sympathetic
  2. Enteric nervous system
    • Myenteric plexus
    (a) parasympathetic via vagus
    (b) sympathetic via coeliac ganglion
  3. Sensory nerve fibres
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5
Q

What are the extrinsic nerves that innervate the stomach?

A
  1. Parasympathetic - stimulate gastric smooth muscle motility and secretions
  2. Sympathetic - inhibit motility and secretions
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6
Q

What is the enteric nervous system that innervates the stomach?

A

Myenteric plexus:

  1. Parasympathetic innervation via vagus
  2. Sympathetic innervation via coeliac ganglion
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7
Q

What are the sensory afferent fibres that innervate the stomach?

A
  • Between sensory receptors and the ENS (pressure, distension, pH, pain)
  • Centrally via the vagal and splanchnic nerves
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8
Q

Discuss the receptive relaxation of the stomach and its functions

A

Orad region has a thin muscular wall:

  • Distension of the lower oesophagus induces relaxation of the lower oesophageal sphincter and the road region of stomach
  • Reduces pressure and increases volume of the stomach (1.5 L)
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9
Q

What nerve fibres are involved in vagovagal reflex?

A

Afferent and efferent nerve fibres in the vagus

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10
Q

Discuss the afferent information in vagovagal reflex

A

Mechanoreceptors associated with chewing, oesophageal and stomach distension relay information to CNS via sensory neurons

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11
Q

Discuss the efferent information in vagovagal reflex

A

Efferent information from CNS causes oral relaxation:

• Neurotransmitter - VIP (vasoactive intestinal peptide): released from postganglionic peptidergic vagal neurons is responsible for orad relaxation

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12
Q

What substance is responsible for orad relaxation?

A

Neurotransmitter: VIP (vasoactive intestinal peptide)

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13
Q

Describe the muscle layers and type of contractions in the fundus and body of the stomach

A
  • Muscle layers are thin

* Weak contractions - contents settle into layers based on density

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14
Q

Which region of the stomach is responsible for mixing?

A
  • Thick muscular wall of caudad region is responsible for mixing
  • Contraction waves begin in the middle of the body, move distally with increasing strength towards the pylorus
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15
Q

Describe the movement patterns in the stomach

A
  1. Propulsion - bolus is pushed toward the closed pylorus
  2. Grinding - antrum churns the trapped material
  3. Retropulsion - bolus is pushed back into the proximal stomach
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16
Q

What occurs in retropulsion?

A

Propels the gastric contents back for further mixing in the stomach

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17
Q

What is the slow wave frequency in the stomach?

A

3 - 5 per minute

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18
Q

Control of slow wave frequency in the stomach?

A
  • Neural hormonal input
  • Hormonal input
  • Parasympathetic stimulation
  • Gastrin
  • Motilin
  • Sympathetic stimulation
  • Secretin
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19
Q

What does not affect slow wave frequency in the stomach but does affect action potential frequency?

A
  • Neural input

* Hormonal input

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20
Q

What increases action potential frequency (and force of contraction) in slow wave frequency in the stomach

A
  • Parasympathetic stimulation
  • Gastrin
  • Motilin
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21
Q

What decreases action potential frequency in slow wave frequency in the stomach?

A
  • Sympathetic stimulation

* Secretin

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22
Q

What is the activity of the stomach during fasting?

A

Periodic gastric contractions (MMCs)

• Migrating myoelectric complexes:
– Mediated by motilin: released from endocrine cells in the upper GI tract
– 90 minute intervals

• Clear stomach of residue remaining from previous meal

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23
Q

After a meal, how much solids, liquids and gastric secretions are contained in the stomach?

A

1.5 L

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24
Q

How long does it take to empty gastric contents?

A

~ 3 hours

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25
Q

Why is the rate of gastric emptying regulated?

A

To ensure that gastric H+ is neutralised in the duodenum and there is adequate time for digestion and absorption of nutrients

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26
Q

What type of meal has the quickest gastric emptying time?

A
  1. Saline meal (fastest emptying time)
  2. Acid meal
  3. Oleate meal
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27
Q

What physical factors affect gastric emptying? (3)

A
  1. Liquids empty more rapidly than solids
  2. Isotonic fluids empty more rapidly than hypo - or (especially) hypertonic fluids
  3. Solids must be reduced to particles < 1mm^3 or less: retropulsion continues until this is achieved
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28
Q

What chemical factors inhibit gastric emptying?

A

Presence of fat and H+ ions in the duodenum

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29
Q

Presence of fat inhibits gastric emptying. What is fat mediated by?

A

Cholecystokinin - secreted when fat reaches the duodenum

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30
Q

Presence of H+ ions inhibits gastric emptying. What is H+ mediated by?

A
  • Reflexes in the enteric nervous system
  • H+ receptors in the duodenum detect low pH and relay information to the gastric smooth muscle via interneurons in the myenteric plexus
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31
Q

3 functions of the motility of the small intestine

A
  1. Mixes chyme with digestive enzymes and pancreatic secretions
  2. Exposes nutrients to the intestinal mucosa for absorption
  3. Propels unabsorbed chyme into large intestine
32
Q

Parasympathetic innervation of small intestine:
• Nerve?
• Action?
• Neurotransmitter?

A
  • Nerve - vagus
  • Action - increases contraction
  • Neurotransmitter -
  1. ACh
  2. Motilin
33
Q

Sympathetic innervation of small intestine:
• Nerve?
• Action?
• Neurotransmitter?

A
  • Nerve - coeliac and superior mesenteric ganglia
  • Action - decreases contraction
  • Neurotransmitter - NA
34
Q

What is the slow wave frequency in the small intestine?

A
  • Duodenum - 12 per minute

* Ileum - 9 per minute

35
Q

How often does migrating myoelectric complexes occur in the small intestine? What is its function?

A
  • Every 90 mins

* Clear small intestine of residual chyme

36
Q

In the small intestine, what are the 2 types of contractions coordinated by ENS and their functions?

A
  1. Segmental - responsible for mixing

2. Peristalsis - create forward movement

37
Q

What substances cause orad contraction?

A
  • ACh

* Substance P

38
Q

What substances cause caudad relaxation?

A
  • VIP

* Nitric oxide

39
Q

What is the structure of the colon?

A

Longitudinal muscle concentrated in 3 bands:

• Taeniae (tenia) coli

40
Q

What is the innervation of the colon?

A
  1. Parasympathetic:
    (a) Vagus
    • Caecum, ascending colon and transverse colon
    • Stimulation causes segmental contractions of the proximal colon

(b) Pelvic nerves
• Descending and sigmoid colon, rectum and anal canal
• Stimulation causes expulsive contractions of the distal colon

  1. Sympathetic:
    • Simulation stops colonic movements
41
Q

Segmental contractions in caecum and proximal colon?

A
  • Contractions mix contents

* Reverse peristalsis and segmental propulsion towards the caecum can occur (retention favours Na+ and water absorption)

42
Q

Large intestinal motility?

A
  • Material not absorbed in the small intestine enters the large intestine - faeces destined for excretion
  • After contents of of the small intestine enter the caecum and proximal colon, the ileoceacal sphincter contracts. Faecal material moves from the caecum, through the colon to the rectum and on to the anal canal
  • Colon receives 500 - 1500 ml of chyme per day but most of the salt and water are absorbed (100 ml per day lost in faeces)
  • Contractions associated with sac-like segments called haustra (haustrations)
43
Q

How much chyme does the colon receive per day?

A

500 - 1500 ml

• Most of salt and water are absorbed (100 ml lost)

44
Q

What are haustra?

A

Sac-like segment in colon associated with contraction

45
Q

What does poor motility in colon result in?

A
  • Causes greater absorption

* Hard faeces in transverse colon causes constipation

46
Q

What does excess motility in colon result in?

A
  • Less absorption

* Diarrhoea or loos faeces

47
Q

Describe mass movements in the colon

A
  • Caused by gastrocolic and duoedenocolic reflexes
  • Move contents of large intestine over long distances (20 cm)
  • Occur 1-3 times per day
  • After water is absorbed in distal colon, the faeces is semi solid
  • Final mass movement propels faecal content into rectum
48
Q

What is gastrocolic reflex? What are the afferent and efferent limbs mediated by?

A
  • Distension of the stomach by food increases the motility of the colon and the frequency of mass movements in the large intestine
  • Afferent limb in the stomach mediated by the parasympathetic nervous system
  • Efferent limb of reflex increasing colon motility is mediated by CCK and gastrin
49
Q

What is rectosphincteric reflex?

A

As rectum fills with faeces, the smooth muscle of the rectum contracts and the internal snap sphincter relaxes

50
Q

Muscle relaxation and contraction process of defecation?

A
  • Rectosphincteric reflex
  • External anal sphincter (composed of striated muscle and under voluntary control) remains tonically contracted
  • External anal sphincter is relaxed voluntarily, the smooth muscle of the rectum contracts and the pressure forces faeces through the anal canal
51
Q

Vomiting:
• Centre where?
• Afferent information?
• Efferent response?

A
  1. Vomiting centre in the medulla
2. Afferent information:
• Vestibular system
• Back of throat
• GI tract
• Chemoreceptor trigger zone in the 4th ventricle
  1. Efferent information:
    • Reverse peristalsis in small intestine
    • Relaxation of the stomach and pylorus
    • Forced inspiration to increase abdominal pressure
    • Relaxation of the lower oesophageal sphincter
    • Forceful expulsion of gastric and duodenal contents
52
Q

What may newborns vomit in the 1st few hours after birth? Why?

A
  • May vomit mucus, occasionally blood-streaked in the 1st few hours after birth
  • Rarely persists after the 1st few feedings (irritation of the gastric mucosa by material swallowed during delivery)
53
Q

Why do newborns in neonatal period vomit?

A

• Relatively frequents symptom

  • Regurgitation from overfeeding
  • Failure to permit infant to educate swelled air
54
Q

When voimiting occurs shortly after birth and is persistent, what must be considered?

A

Possibilities of:

  • Intestinal obstruction
  • Increased intracranial pressure
55
Q

What does a history of maternal hydramnios suggest?

A

Upper gastrointestinal (oesophageal, duodenal, ileal) atresia

56
Q

What does bile stained emesis suggest?

A

Intestinal obstruction beyond the duodenum and requires investigation

57
Q

How to diagnose duodenal atresia in an upright abdominal film?

A

Characteristic “double-bubble” sign

  • Dilated stomach
  • Dilated proximal duodenum
58
Q

What is normal gut rotation?

A
  • In normal embryo, physiologic herniation of the gut through umbilicus at 6 weeks is accompanied by a 270° counterclockwise rotation of the developing intestine around the superior mesenteric artery
  • By 10 - 12 weeks, the intestine returns to the abdomen and assumes its normal adult anatomic position
  • Normal small bowel mesentery has a broad attachment stretching diagonally from the duodenojejunal junction (LUQ) to caecum (RLQ)
59
Q

The physiologic herniation of the gut through the umbilicus, accompanied by a 270° counterclockwise rotation of the developing intestine around SMA occurs when in an normal embryo?

A

6 weeks

60
Q

When does the intestine return to the abdomen in an normal embryo?

A

10 - 12 weeks

61
Q

What are the broad attachments of normal small bowel mesentery?

A

From duodenojejunal junction (in LUQ) to caecum (in RLQ)

62
Q

Malrotation intestinal obstruction may result in what 3 things?

A
  1. Obstruction of the duodenum may result from congenital peritoneal bands (Lads bands) which run over the duodenum from the caecum in the RUQ
  2. Midgut volvulus
  3. Internal hernia in
    the mesentry
63
Q

What causes malrotation of the intestine?

A
  • Results when the normal embryologic sequence of bowel development and fixation is interrupted
  • Malrotated bowel is prone to torsion, resulting in midgut volvulus
64
Q

Vomiting may occur from what disturbances that don’t obstruct the digestive tract?

A
  • Milk allergy
  • Adrenal hyperplasia of the salt - losing variety
  • Galactosaemia
  • Hyperammonaemias
  • Organic acidaemias
  • Increased intracrhail pressure
  • Septicaemia
  • Meningitis
  • Urinary tract infections
65
Q

What are valvulae conniventes/ Kerckring folds/ plicae circulares/ small bowel folds?

Where do they start and end? Size?

A

• Mucosal folds of small intestine

  • Starts from 2nd part of duodenum
  • Large and thick at jejunum and considerably decrease in size distally in the ileum to disappear entirely in the distal ideal bowel loops
66
Q

What is the % of mechanical intestinal obstruction that is caused by small or large bowel obstruction?

A

• 80% - small bowel obstruction

20% - large bowel obstruction

67
Q

Small bowel obstruction can be divided into what types?

A
  1. Congenital
  2. Acquired:
    • Extrinsic causing compression
    • Intrinsic
    • Luminal
68
Q

What are the most common cause of small bowel obstruction in developed and developing countries?

A

• Developed countries:
~ 75% - adhesions

• Developing countries:
- 80% - incarcerated hernias

69
Q

What is the structure of large intestine?

A
  • 1.5 m muscular tube
  • Extends from caecum to rectum
  • Has 3 outer longitudinal muscular layers called taenia coli - 30 cm shorter than the length of the large bowel (causes characteristic sacculations interrupted by incomplete rings called haustra)
70
Q

What are the causes of large bowel obstruction?

A
  • Underlying aetiology is age-dependent
  • In adulthood, most common cause:
  1. Colonic cancer (50-60%) typically in sigmoid
  2. Acute diverticulitis (involving sigmoid colon)

• Adhesions don’t tend to cause large bowel obstruction unlike small bowel obstruction

71
Q

What is Hirschsprung disease?

A
  • Most common cause of neonatal colonic obstruction
  • Commonly characterised by a short segment of colonic aganglionosis affecting term neonates (esp. boys)
  • Affects ~ 1:5000 - 8000 live births
  • Never seen in premature infants
72
Q

How is Hirschsprung disease diagnosed and treated?

A
  • Condition typically presents in term neonates with failure to pass meconium in the first 1-2 days after birth
  • Definitive diagnosis requires a full thickness rectal biopsy
  • Surgical treatment is by removal of affected portion of the colon
73
Q

Why can Hirschsprung disease have high mortality rates?

A
  • Mortality rates can be as high as 30% due to enterocolitis

* In surgical removal m 3-4% of cases colonic perforation complicates the presentation

74
Q

What is paralytic ileus?

A

Functional intestinal obstruction without an actual physical obstruction

75
Q

What causes paralytic ileus?

A
  • Multifactorial malfunction in the nerves in the intestine and subsequent impairment in intestinal peristalsis
  • Mneumonic - 5 Ps:
  1. Postoperative
  2. Peritonitis
  3. Potassium - low
  4. Pelvic and spinal fractures
  5. Parturition
76
Q

How do patients with paralytic ileus present?

A
  • With symptoms similar to a mechanical bowel obstruction e.g. nausea/ vomiting, distension, and reduced or absent bowel movements
  • Bowel sounds will be decreased/ absent whereas they are increased in mechanical obstruction
  • On radiographs: generalised, uniform, gaseous distension of the large and small bowel

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