GI Physiology and Motility Flashcards

1
Q

What is the muscular structure of GI tract?

A

Outer Myenteric plexus - longitudinal

Inner submucosal plexus- Circular

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2
Q

Describe the parasympathetic innervation of the GI tract

A

Vagus nerve for as far as ‘Canon’s point’ of descending colon for non-sphinteric muscles

Pelvic nerves (S2-4) for descending colon, rectum, bladder and urethral sphincter

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3
Q

Describe the sympathetic innervation of GI tract

A

3 prevertebral ganglia - coeliac, superior mesenteric and inferior mesenteric.

These then travel in splanchnic nerves with long post-ganglionic fibres

Sympathetic control inhibits non-sphinteric muscles and excites sphinteric muscles

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4
Q

What is the result of sympathetic innervation and how does it occur?

A

Vasoconstriction bu inhibiting cholinergic post-ganglionic neurones. The neurotransmitter aerosols out from variscotes so it is a slow process

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5
Q

What innervates the salivary glands?

A

parasympathetic division of CN7 and CN9

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6
Q

What makes up saliva? and what are functions of each component

A

Hyptonic NaCl and Mucus - lubrication
Salivary amylase - digestion (and cleans teeth)
Bacteriocidal agents such as SCN, Iodide and lysosome
Bacteria which produce Hydrogen ions

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7
Q

How can hydrogen producign bacteria cause damage?

A

Attack hydroxyappetite of enamel dentine, leading to carices, infected pulp and enterococous faecalis infection - can cause endocarditis- can cause ludwig angina

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8
Q

What is achlasia, how does it present and how can it be treated?

A

Thickening of / absence of relaxation of circular muscle layers - spasm due to peristaltic failure.

Will prevent bolus travelling forward unless with large drink - shows as birds beak on LOS x-ray

Treat with rigiflex balloon dilation, or per oral endoscopic myotomy

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9
Q

What is the muscular make up of the oesophagus and how can each be pathologically affected?

A

Upper 1/3 striated muscle- polymyositis and myasthenia gravis

Lower 2/3 smooth muscle- achlasia and Scleroderma (thickening of tissue under dermis, causing weak LOS, absent peristalsis and oesophagitis)

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10
Q

How is enteric neurotransmission mediated?

A

Interstitial cells of Cajal- mediate reflex activity in absence of CNS

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11
Q

Name two other neuro-hormonal influences on gut motility

A

Motilin and opioid receptors

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12
Q

What is the migratin gmotor complex and when is it present?

A

The MMC is a cyclic contraction sequence occurring every 90 minutes when in the interprandial (fasting) period, acting to cleanse the stomach and intestine in 4 phases:

 1. Prolonged period of quinescece
2. Increased frequency of contractility
3. Few minutes of peak electrical and mechanical activity
4. Decline in activity to merge into the next phase 1
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13
Q

How is the MMC regulated?

A

Motilin is a polpeptide hormone produced by M cells in small intestine. It is secreted at 90 minute intervals to facilitate MMC. It also causes contraction of gastric fundus, enhancing gastric emptying.

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14
Q

What drug mimics the action of motilin?

A

Erythromycin

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15
Q

How does gut motility change after a meal?

A
  1. The cehalic phase is the secretory phase, where the vagus nerve causes secretion of enzymes due to sight, smell or taste of food.
  2. In the Gastric Phase, gastric tone reduces and the fundus expands, in order to accomodate the meal. MMC is replaced by contractions of varyign amplitude and frequency, allowing for mixing and digestion.
  3. The Intestinal Phase sees solids and liquids transported at same rate but as liquids leave solids first, these reach caecum first
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16
Q

How are gastric contractions controled

A

Frequency and direction of gastric muscular contractions is controlled by gastric pacemaker zone within proximal gastric body. This generate rhythmic depolarisations, 3 cycles per minute

17
Q

What is gastroparesis and how is it caused?

A

Delayed Gastric emptying, causing abdominal pain, malnutrition, vomiting and gostro-oesophageal reflux.
Can be caused by DM or opiate use

18
Q

How can gastroparesis be treated?

A

5HT4 agonist - cisapride or metoclopramide
D2 agonist - meto-opramidem omeperidone
Motilin agonist - erythromycin
Botulinum injection into pyloric sphincter will open it
Gastric electrical stimulation

19
Q

Describe colonic motility

A

Mixture of long and short contractions to mix material for water absorption, without propulsion in order to store.

20
Q

What happens to colonic motility after a meal

A

There is a marked increase due to gastro-colic reflex - makes way for arrival of new food

21
Q

How can colonic motility be reduced?

A

Opiates, via Mu receptor
Anticholinergics
Loperamide - gut selective opiate Mu recepeptor agonist which decreases tone and activity of myenteric plexus, slowign transit and therefore increasing water absorption, so can treat diarrhoea

22
Q

How can colonic motility be increased?

A

stimulant laxatives
prucalopride - gut selective 5HT4 recepor agonist
linaclotide - guanylate C receptor agonist to increase secretion of chloride and bicarbonate ions, increasing intestinal fluid and therefore increase motility

23
Q

Describe the muscular structure of the anal sphincter

A

Internal anal sphincter - smooth muscle

External anal sphincter - skeletal muscle

24
Q

How can anal incontinence be caused

A

excessive rectal distension

Anal sphincter weakness (e.g. damage)

25
Q

How can constipation be caused?

A

anorectal fissure
obstructive defeacation
Hirshsprungs disease

26
Q

What is Hirschsprungs Disease?

A

enlarged descending colon in children, causing collapsed rectum with no nerves

27
Q

What happens to the bowel if there is an injury at T12 or above?

A

Reflex bowel - refelx arc still in tact so bowel opens sporadically

28
Q

How can reflex bowel be controlled

A

Can be stimulated and controlled by suppositries

29
Q

What happens to the bowel if there is an injury to sacral nerve roots?

A

flaccid bowel - no reflex arc, resulting in flaccid anal sphincter so therefore incontinence