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Gastrointestinal System > 50-53. Structure and functions of enteric nervous system. Normal movements of GI system. Control of GI functions. Common disorders of gut motility and their causes. > Flashcards

50-53. Structure and functions of enteric nervous system. Normal movements of GI system. Control of GI functions. Common disorders of gut motility and their causes. Flashcards

1
Q

Which structures along the GI tract are under voluntary control? (2)

A

Upper oesophageal sphincter

External anal sphincter

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2
Q

Name the plexus of the

a) submucosa
b) Muscularis externa

A

a) submucosal (Meissner’s plexus)

b) Myenteric (Auerbach’s plexus)

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3
Q

Which cells mediate enteric neurotransmission between the smooth muscle cells and the enteric neurons?

A

Interstitial cells of Cajal

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4
Q

What is the function of the enteric nervous system?

A

Mediates reflex activity between meals in the absence of CNS input

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5
Q

What two intrinsic factors affect the enteric nervous system?

A
  1. Vagal control - excitatory to non-sphincteric muscle

2. Sympathetic control - inhibitory to non-sphincteric muscle, excitatory to sphincteric muscle

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6
Q

What are the three other neurohormonal influences on gut motility?

A

Motilin
Serotonin (5HT)
Opiod receptors

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7
Q

What are the two measurements of gut motility?

A
  1. Pressure (easiest at bottom and top of gut) - circular muscle function
  2. Transit - radio labelled isotopes, dynamic contrast radiology
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8
Q

What is the general nervous supply to the oesophagus?

A

Very complex (may be due to types of muscle at different parts)
Sympathetic trunk
Parasympathetic via vagus nerve

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9
Q

On high resonance manometry, what part of the oesophagus shows high enteric pressure?

A

Upper oesophageal sphincter which relaxes upon swallowing

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10
Q

In a patient with hiatus hernia, what change can be seen in high resonance manometry?

A

Contractions of the crural diaphragm become visible, resulting in two separate zones of different pressures

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11
Q

What is achalasia?

A

A rare disorder of oesophageal motility
Lower oesophageal sphincter cannot relax in response to a swallow
No peristalsis
frequently regurgitating food - therefore facing malnourishment
Dilated oesophagus detectable by transit barium swallow

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12
Q

How long does it normally take for contents of the oesophagus to empty into the stomach?

A

8 seconds

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13
Q

What treatment options are available for achalasia?

A

Baloon dilatation - inflate with air/contrast medium
Laroscopic Heller’s Myotomy - fixed sphincter not as tight as before
Per Oral Endoscopic Myotomy (POEM)

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14
Q

Briefly describe issues with the oesophagus in scleroderma and how it can be treated

A 
Connective tissue disorder resulting in lower oesophageal sphincter weakness
absent peristalsis
severe oesophagitis
Without operation - forms achalasia
Use proton pump inhibitors
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15
Q

What is nutcracker oesophagus?

A 
Associated with dysphagia (pain upon swallow)
Very high pressures in oesophagus
benign prognosis
no evident therapies
have a functional swallow
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16
Q

What is a diffuse oesophageal spasm?

A

Uncordinated contractions of the oesophagus which may cause difficulty swallowing and regurgitation

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17
Q

When does the migrating motor complex (MMC) occur?

A

Every 90-120 minutes during the interprandial (fasting) period

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18
Q

What regulated the MMC?

A

Motilin

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19
Q

What is the role of the MMC?

A

Cleanse the stomach and intestine

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20
Q

What are the 4 phases in the MMC?

A
  1. Prolonged period of quiescence
  2. Increased frequency of contractility
  3. A few minutes of peak electrical and mechanical activity
  4. Declining activity merging to next phase 1
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21
Q

What is motilin and where is it produced? How often is it secreted?

A

A polypeptide hormone produced by M cells of the small intestine
Secreted at 90 minute intervals

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22
Q

What are M cells and their function?

A

Specialised epithelial cells of the mucosa-associated lymphoid tissue of the Peyer’s patches in the ileum
Transport antigens from the lumen to the cells of the immune system

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23
Q

What is the function of motilin?

A

Stimulates contraction of the gastric fundus and enhances gastric emptying

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24
Q

What is an agonist of motilin?

A

Erythromycin

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25
Q

What % of gastric secretion happens in the cephalic phase?

A

20%

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26
Q

What mediates gastric secretion in the cephalic phase?

A

Vagus nerve

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27
Q

What controls the frequency and direction of muscular contractions within the proximal gastric body?

A

Gastric pacemaker

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28
Q

What happens to the proximal gastric tone and fundus with regards to GI movement in the beginning of the gastric phase?

A

Proximal gastric pressure reduces and fundus expands to accommodate meal

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29
Q

As food enters the stomach, there is expansion. Does this cause an increase in pressure?

A

No

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30
Q

What type of contractions replace those of MMC during the gastric phase?

A

Contractions of variable amplitude and frequency to allow mixing and digestion

31
Q

What is the role of the gastric pacemaker?

A

Generates rhythmic depolarisations at a frequency of 3 cycles per minute
Only triggers smooth muscle contractions with additional neurohumoral input

32
Q

How long does it take for solids and liquids to empty from the stomach?

A

Inert liquids - 20 minutes

Solids - 3-4 hours - digestible food particles leave when reduced to 2mm, undergo mixing and churning

33
Q

Explain how gastric emptying of inert liquids obeys first order kinetics?

A

The volume of fluid exiting the stomach remains a constant fraction of the fluid remaining in the stomach

34
Q

Nutrient content slows down gastric emptying. At what rate to liquid foods empty from the stomach (kCal/hour)

A

200kCal/hour

35
Q

What phases characterise the gastric emptying of digestible solids?

A

Initial lag phase - little chyme is delivered to duodenum

Followed by linear emptying phase with a fixed slope

36
Q

What are two causes of accelerated gastric emptying?

A

Diarrhoea

Dumping syndrome

37
Q

What is dumping syndrome?

A

Can develop after surgery to remove all/part of the stomach or to bypass the stomach

38
Q

What are five causes of delayed gastric emptying?

A 
Abdominal pain
Vomiting
Poorly controlled gastro-oesophageal reflux
Malnutrition
Gastroparesis
39
Q

What are the 4 causes of gastro-paresis?

A

Idiopathic
Post viral - subgroup of idiopathic gastroparesis
Drugs - opiates - many opiate receptors along the GI tract
Longstanding diabetes with macrovascular disease - over time, high glucose levels can damage vagus nerve

40
Q

What are the symptoms of gastro paresis? (3)

A

Abdominal pain
Nausea and often delayed vomiting
Weight loss

41
Q

What are the ways gastro paresis can be managed through diet?

A

Small meals frequently
Liquid food tolerated better than solid
Nutritional support (post-pyloric feeding)

42
Q

What are the ways gastro-paresis can be improved with relation to the underlying cause?

A

Post viral - may improve over time
Diabetes - improve diabetic control?
Opiates - limit use of opiates or other triggering medication

43
Q

In what ways can patients with gastro paresis be fed surgically?

A

Gastrostomy - patient fed directly into stomach - formal surgery
Percutaneous endoscopic gastrostomy - endoscopy
Jejunostomy - formal surgery or endoscopy

44
Q

How can gastroparesis be medically treated?

A

(Prokinetics)
5HT4 agonists e.g. metoclopramide
D2 antagonists (dopamine inhibits motility) e.g. domperidone
Motilin agonists - erythromycin

45
Q

What medication can be given endoscopically to treat gastro paresis?

A

botulinum toxin injection to pyloric sphincter

46
Q

What is the role of gastric electrical stimulation in the management of gastro paresis?

A

Electrodes 9cm away from the pylorus, in the greater curvature generate high frequency, low amplitude contractions
Is a gastric neurotransmitter which can be implanted to generate mild electrical impulses
Does NOT improve gastric emptying
Improves N&V
Used more in diabetic aetiology

47
Q

Describe the rate of small intestinal transit of both liquids and solids

A

Travel at the SAME rate, but liquids enter the caecum first due to quicker rate of gastric emptying

48
Q

How long does it take for liquid to reach the caecum from the small intestine?

A

30 minutes

49
Q

How long does it take for half the chyme to traverse the small intestine?

A

150 minutes

50
Q

What type of movement causes the chyme to move from the ileum to caecum in boluses?

A

Prolonged propagated contraction

51
Q

Name two disorders of small intestinal transit

A

Chronic intestinal pseudoobstruction

Acute post-operative ileus - lack of digestive propulsion

52
Q

What are the signs and symptoms associated with chronic intestinal pseudo-obstruction? What are it’s usual aetiologies?

A 
chronic abdominal pain
constipation
vomiting
weight loss
Usually neuropathic or myopathic
Primary neuropathy or myopathy
Secondary - all other causes
53
Q

What can acute post-operative ileus cause? How long does it last?

A

Constipation and intolerance of oral intake in the absence of mechanical obstruction after surgery

0-24 hours in small intestine
24-48 hours in stomach
48-72 hours in colon

54
Q

What are the risk factors for prolonged ileus?

A 
Open surgery
Prolonged abdominal or pelvic injury
Delayed enteral nutrition
Peri-operative complications
Peri-operative opiate analgesia
55
Q

What are the myopathic causes for chronic intestinal pseudo-obstruction?

A

Scleroderma - immune system attacks connective tissue

Amyloidosis

56
Q

What is a neuropathic cause of chronic intestinal pseudo-obstruction?

A

Parkinson’s disease

57
Q

What are endocrine causes of chronic intestinal pseudo obstruction?

A

Diabetes mellitus

Severe Hypothyroidism

58
Q

Management of chronic intestinal pseudo obstruction

A

Nutritional - enteral feeding/parenteral feeding
Antibiotics for small bowel bacterial overgrowth
In stubborn cases, small bowel transplantation

59
Q

What is acute colonic pseudoobstruction?

A

Large bowel parasympathetic dysfunction
Commonest after cardiothoracic or spinal injury
Risk of caecal perforation

60
Q

Management of acute colonic pseudoobstruction

A

Gut rest, IV fluids, nasogastric decompression
IV neostigmine
Colonoscopic decompression
Surgery

61
Q

What are the functions of the colon?

A

Mix chyme without propulsion
Storage
Cause aboral movement of content
Expel faeces

62
Q

What contractions take place in the colon?

A

No pacemaker activity

mixture of short and long duration contractions

63
Q

How long does transit from caecum to rectum take, and at what area is transit the longest duration?

A

1-2 days

Caecum

64
Q

Is colonic transit longer in duration in men or women?

A

Longer in women

Shorter duration in men, therefore increased faecal weight due to higher water content

65
Q

When viewing X-rays while using radio-opaque markers to determine colonic transit, what would be visible in:

a) normal transit
b) pelvic outlet obstruction
c) slow transit constipation

A

a) no markers left
b) markers gathered at rectosigmoid
c) markers scattered throughout

66
Q

Which drugs can reduce colonic motility?

A

Opiates
Anticholinergics
Loperamide - gut selective opiate Mu receptor agonist
- decreases tone and activity of myenteric plexus
- slows colonic transit so more water absorption
- used for symptomatic management of diarrhoea

67
Q

What drugs can increase colonic motility?

A

Stimulant laxitives - increase motility, alter electrolyte transport (short action, dramatic effects!)

Prucalopride - gut selective 5HT4 receptor angonist
- used in chronic constipation in UK

Linaclotide - minimally absorbed guanylate C receptor agonist

  • increases intestinal fluid and colonic transit
  • licensed for treatment of IBS-constipation in UK
68
Q

What is the role of the internal anal sphincter?

A

Smooth muscle - involuntary control

When relaxed, provides greatest component of contraction

69
Q

What is the role of the external anal sphincter?

A

Skeletal muscle - voluntary

recruited in reflex reaction to coughing/sneezing

70
Q

What are two causes of incontinence?

A

Excessive rectal distension

  • acute or chronic diarrhoea
  • chronic constipation

Anal sphincter weakness

  • muscle damage
  • damage to pudendal nerve
71
Q

What can cause anorectal constipation?

A

Hirsprung’s disease (children) - nerve cells failed to migrate

Obstructive defacation - paradoxical contraction of puborectalis muscle and external sphincter during contraction

Rectocoele - protrudes into posterior wall of vagina, often associated with prolapsed uterus

Anal fissure - associated pain on defacation

72
Q

At what level of spinal cord injury does the colon become affected? What effects can this have?

A 
T12 or above
Reflex bowel
damage to upper motor neurons
reflex arc intact
tonic anal sphincter

Bowel opens spontaneously but without control
Reflex can be initiated by rectal stimulation (e.g. suppositories)

73
Q

What are the 4 steps in “reflex bowel”

A
  1. Rectum gets full, stretches and pushes on area of nerves
  2. Impulses sent from bowel to sacral nerves then to spinal cord
  3. Impulses loop around in the spinal cord setting off a reflex
  4. Reflex tells sphincter muscle near anus to open and release stool
74
Q

What can be caused by damage to sacral nerve roots?

A 
LMN injury
"flaccid bowel"
No reflex arc
Slow stool propulsion through colon
Flaccid anal sphincter -> incontinence

Gastrointestinal System (29 decks)

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