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Year 2 - GI System > Gut Motility > Flashcards

Gut Motility Flashcards

1
Q

Name the plexus’ found in the gut wall

A

Sub-mucosal plexus (between the sub mucosa and the circular muscle layer) and the myenteric plexus (between the longitudinal and circular muscle layers)

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2
Q

What nervous system controls smooth muscles?

A

Enteric nervous system

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3
Q

What is the function of the interstitial cells of Cajal?

A

They mediate enteric neurotransmission

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4
Q

What are the pacemaker cells of the enteric nervous system?

A

The interstitial cells of Cajal

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5
Q

What does the enteric nervous system do?

A

Mediates reflex action in the absence of CNS input (a.k.a. During the interprandial period)

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6
Q

What influences the enteric nervous system?

A

Extrinsic factors

  • Vagal control (excites non-sphincteric muscle)
  • Sympathetic control (inhibits non-sphincteric muscle and excites sphincteric muscle)
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7
Q

What are the neurohormones that have an effect on the enteric nervous system?

A

5-hydroxylation-tryptamine (5-HT)
Motilin
Opioid receptor

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8
Q

Name two ways motility can be functionally measured.

A

Pressure - measuring circular muscle function

Transit - measuring how fast food passes out of the stomach

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9
Q

Describe scintigraphy.

A

This is when radiolabelled isotopes are swallowed, and the radiation produced is measured outside the body with a gamma camera

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10
Q

Name the nerve that supplies the striated muscle, on the upper third of the oesophagus.

A

The vagus nerve

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11
Q

What nerve allows motor functions of the smooth muscle of the oesophagus?

A

Parasympathetic branches of the vagus nerve

- this synapses with both the submucosal and myenteric plexus’

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12
Q

Where do the vasomotor sympathetic fibres that supply the oesophagus arise from?

A

T1-4/6

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13
Q

Name an oesophageal disorder that only affects striated muscle.

A

Polio

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14
Q

What problems can occur when the oesophageal smooth muscle stops working?

A

The transition of the bolus from the mouth to the stomach is affected

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15
Q

What is achalasia?

A

An oesophageal disorder that results in peristaltic failure, causing the LOS to remain contracted and eventually causes dilation of the oesophagus

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16
Q

How is achalasia treated?

A
  • Dilation of the LOS with a ballon

- Myotomy (from the outside of the person)

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17
Q

What happens to the oesophagus in scleratoma?

A

The connective tissue under the mucosa thickens. The LOS becomes weak due to a constant low pressure. This, combined with an absence of peristalsis can cause severe oesophageal reflux and therefore oesophagitits

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18
Q

Describe nutcracker oesophagus.

A

This is a very high pressure in the oesophagus and causes pain on swallowing (though swallowing is functional)
It’s a benign prognosis

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19
Q

What is a diffuse oesophageal spasm?

A

When the peristalsis moves faster than the food

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20
Q

Name the four phases of the interprandial stage.

A

1) quiescense - a prolonged period
2) contractility frequency increases
3) peak electrical and mechanical activity
4) declining activity

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21
Q

Which phase does motilin affect, and what is its nickname?

A

Motilin stimulates stage three and it’s called the housekeeper because it cleanses the stomach

22
Q

What is MMC?

A

The MMC is the cyclic series of contractions that occurs down the gut every 90 mins

23
Q

What is the action of motilin?

A

Motilin is a polypeptide hormone that is produced by the M cells of the small intestine. It stimulates contraction of gastric fundus and enhances gastric emptying

24
Q

Name the three phases of digestion

A

Cephalic
Gastric
Intestinal

25
Q

What does the stomach do during the gastric phase?

A

The proximal stomach tone decreases and the fundus expands, allowing room for food without an increase in pressure

26
Q

What controls the frequency and direction of the new contractions needed for the gastric phase?

A

The cells from the gastric pacemaker zone in the proximal stomach

27
Q

What do the pacemaker cells do?

A

They undergo rhythmic depolarisations three times a minute, triggering smooth muscle contractions with additional neurohormonal input

28
Q

How long does it take liquids to leave the stomach?

A

Around 20 mins

29
Q

How long does it take solids to leave the stomach and why?

A

Solids take between 3-4 hours because they have to be broken down to less than 2mm in diameter by constant churning and mixing.
Has a lag phase.
Fatty meals take longer to leave the stomach

30
Q

What can disorders of gastric emptying result in?

A 
Accelerated emptying can cause
- dumping syndrome 
- diarrhoea 
Delayed emptying can cause
- abdominal pain
- vomiting/nausea 
- malnutrition 
- poorly controlled gastro-oesophageal reflux
31
Q

Name some causes of gastric emptying.

A

Idiopathy
Diabetes mellitus
Drugs (opiates)
After a virus

32
Q

How to manage delayed gastric emptying

A 
Dietry
- small, infrequent meals
- lipids are tolerated best
Treat the cause
- improve DM control
- take less opiates 
Medicine (prokinetics)
- 5HT4 agonists (cisapride)
- D2 antagonists 
- motilin agonist (erythromycin)
Endoscopic therapy 
- toxin injection into the pyloric sphincter 
Gastric electrical stimulation
- improves nausea and vomiting
33
Q

Which food moves faster in the small intestine, liquid or solid?

A

They both move at the same speed because they have been combined to make chyme.

34
Q

What action facilitates bolus movement from the ilium to the caecum?

A

The prolonged propagated contraction (intermittent movements)
Takes 30 minutes or more

35
Q

Name two disorders of small intestine transit

A

Chronic intestinal pseudo-obstruction

Acute post-operative ileus

36
Q

Describe chronic intestinal pseudo-obstruction.

A

This is when there are signs of mechanical obstruction without and physical occlusion.
Symptoms are chronic abdominal pain, constipation, vomiting and weight loss.
It can be attributed to neuropathic or myopathic aetiology

37
Q

What could cause myopathic, neuropathic, endocrine or drug induced reasons for chronic intestinal pseudo-obstruction (respectively?)

A

Myopathic - scleroderma and amyloidosis
Neuropathic - Parkinson’s disease
Endocrine - bad hypothyroidism and diabetes mellitus
Drug induced - phenothiazines and anti-parkinson drugs

38
Q

How do you manage chronic intestinal pseudo-obstruction?

A

Nutritionally by parenteral/enteral feeding
Antibiotics for small intestine bacteria overgrowth
Small bowel transplantation

39
Q

Describe post-operative ileus.

A

Symptoms include constipation and intolerance of oral intake.
Is only diagnosed in the absence of mechanical obstruction after surgery
Physiogical ileus lasts for 0-24 hours in the small intestine
Risk factors include open surgery and delayed enteral nutrition

40
Q

What is the function of the colon?

A

The colon must mix materials without propulsion (to allow water absorption), act as a storage site and expel feaces.
All without pacemaker activity

41
Q

What is the gastro-colic reflex?

A

Increase in colonic motility seen after a meal

42
Q

How long does it take food to travel from the caecum to the rectum?

A

1-2 days
This is shorter in men, so they have an increased feacal weight (contains more water, because there is less time for it to be absorbed)
Food moves slowest through the ceacum

43
Q

How is colonic transit measured?

A

Serial X-Ray’s with radio-opaque markers

  • lack of markers means normal transit
  • markers in the retero-sigmoid means pelvic outlet obstruction
  • scattered markers mean slow transit constipation
44
Q

What drugs affect colonic motility?

A

Drugs that reduced colonic motility are
- opioids (Mu receptors)
- anticholinergics
- loperamide
Drugs that increase colonic motility are
- stimulant laxatives (increase gut electrolyte transport)
- prucalprides (gut selective 5HT4 agonists)
- linadolides (minimally absorbed granulate C receptor agonists and they also increase Cl and HCO3 secretion into the lumen

45
Q

Describe the action of loperamide (a drug that decreases colonic motility)

A

It’s a gut selective opiate Mu receptor agonist
- it decreases the tone and activity of the myenteric plexus
- slowed colonic transport leads to increased water reabsorption
It’s commonly used to treat diarrhoea

46
Q

What are the differences between the internal and external anal sphincters?

A

The internal is smooth muscle and is involuntary (contracted at rest)
The external is striated muscle and under voluntary control (but is alos involved in a reflex reaction while coughing and sneezing)

47
Q

Name four problems with anorectal function.

A

Incontinence
Constipation
Colon in spinal cord injury (T12 or above)
Colon in spinal cord injury (sacral nerve roots)

48
Q

How is incontinence caused?

A

Excessive rectal distension caused by acute or chronic diarrhoeal illness or chronic constipation.
Anal sphincter weakness can be caused by damage to the pudendal nerve

49
Q

How is constipation caused?

A

Hirschrugs disease in children
Obstructive defecation
A rectocele
An anal fissure - associated pain on defecation

50
Q

What happens to the colon in a spinal cord injury above the level of T12?

A

Its caused by damage to the upper motor neurons (intact reflex arc)
This causes the bowel to open spontaneously and without control
This reflex can be initiated by rectal stimulation.

51
Q

What happens to the colon in a spinal cord injury to the sacral nerve roots?

A

Caused by damage to the lower motor neurons (no reflex arc).

This causes flaccid bowel (slow stool propulsion through the colon) and a flaccid anal sphincter

Year 2 - GI System (18 decks)

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