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Year 1 NME > Motility of the lower GIT > Flashcards

Motility of the lower GIT Flashcards

1
Q

In the GIT which organs are accessory organs?

A
  • those involved in secretion purposes
  • liver
  • pancrease
  • gallbladder
  • oral salivary glands and the tongue
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2
Q

What is the classification of the lower GIT?

A
  • inferior to the suspensory muscle of the duodenum
  • ligament of Treitz
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3
Q

What are the 4 main components of the lower GIT?

A

1 - small intestines

2 - large intestines

3 - rectum

4 - anus

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4
Q

What are the 3 parts of the small intestines, from top to bottom?

A

1 - duodenum = shortest

2 - jejunum = medium

3 - ileum = longest

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5
Q

Generally how long does digestion in the small intestines take?

A
  • 3-5 hours
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6
Q

The small intestines (SI) has adapted and evolved to maximise digestion and absorption. How has the surface of the SI adapted to increase its surface area and this absorption?

A
  • brush border micro villi
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7
Q

There are 2 types of motility in the small intestines, what are they?

A

1 - segmentation which is mixing and circulation providing maximum exposure to villi

2 - peristaltic contractions to propel chyme

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8
Q

During segmentation contractions of the GIT, what happens?

A
  • mixing of chyme
  • stretch receptors trigger myenteric muscle contraction
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9
Q

During segmentation contractions of the GIT, is there any net movement or is segmentation just to mix digesta?

A
  • no net movement
  • mixing only
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10
Q

During propulsive peristalsis of the GIT, is there any net movement or is segmentation just to mix digesta?

A
  • movement of chyme through the digestive tract
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11
Q

During propulsive peristalsis how does the GIT know to contract and move chyme?

A
  • stretch receptors trigger myenteric plexus stimulation of muscle contraction
  • net movement forwards
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12
Q

In addition to stretch receptors activiting propulsive peristalsis, what else can contribute to GIT motility?

A
  • hormones
  • excitation via gastrin, CCK, insulin, motilin
  • inhibition via secretin and glucagon
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13
Q

There are a number of propulsive peristalsis reflexes that are triggered once chyme enters the lower GIT, stretches the GIT and stimulates the mysenteric plexus. Gastroenteric reflex is one of those reflexes, what is this?

A
  • gastric distention activates myenteric plexus
  • this promotes peristalsis with small intestine
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14
Q

There are a number of propulsive peristalsis reflexes that are triggered once chyme enters the lower GIT, stretches the GIT and stimulates the mysenteric plexus. Gastroileal reflex is one of those reflexes, what is this?

A
  • food in the stomach is recognised
  • causes peristalsis in the ileum
  • ileocecal valve opens and contents enter the large intestine
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15
Q

There are a number of propulsive peristalsis reflexes that are triggered once chyme enters the lower GIT, stretches the GIT and stimulates the mysenteric plexus. The migrating motor complex s one of those reflexes, what is this?

A
  • a pattern of electrical activity in the lower GIT
  • purpose is to move SI contents
  • occur between meals (around every 90 minutes)
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16
Q

There are a number of propulsive peristalsis reflexes that are triggered once chyme enters the lower GIT, stretches the GIT and stimulates the mysenteric plexus. The migrating motor complex (MMC) is one of those reflexes. How is the MMC contriolled?

A
  • intrinsic enteric control (no external stimulus needed)
  • hormone motilin can also contribute
17
Q

There are a number of propulsive peristalsis reflexes that are triggered once chyme enters the lower GIT, stretches the GIT and stimulates the mysenteric plexus. The migrating motor complex (MMC) is one of those reflexes. The MMC is not only important for movement of chyme, but it also has another important purpose, what is this?

A
  • ensure there is no bacterial overgrowth
18
Q

The enteric nervous system (ENS) is the intrinsic nervous system of the GIT and ensure mixing and peristalsis contractions. What are 2 alternative pathways that are able to module the mixing and peristaltic contractions of the large intestines?

A

1 - neural via autonomic nervous system

2 - hormonal secretions

19
Q

How often does the large intestine have mass movement peristaltic contractions per day?

A
  • 2-3 times per day
  • moves stool into rectum
20
Q

As the chyme moves through the large intestines, what is the large intestines doing to the properties of the chyme?

A
  • extracting H2O
  • changes chyme from liquid to faeces
21
Q

What strutctural aspect of the large intestines are involved in the mixing of the chyme?

A
  • haustra bulges
22
Q

If there is poor motility of too much motility what can this do to the stool and symptoms for the patient?

A
  • poor motility = constipation
  • fast motility = diarrhea
23
Q

Mass movements of the large intestines (LI) are facilitated by reflexes in the upper GIT. What 2 reflexes, that are triggered by stretch receptors in the upper GIT contribute to mass movements every 2-3 hours in the large intestines?

A

1 - gastro-colic reflexes

  • food stretches stomach and initiates contraction of LI

2 - duodeno-colic reflexes

  • duodenum is stretched with food and signals the LI
24
Q

What is the defecation reflex?

A
  • movement of faeces into the rectum (normally empty)
  • rectum is stretched and activates the enteric nervous system (submucosa and myenteric plexus)
  • stretch receptors also signal parasympathetic nervous system
25
Q

Once the stretch receptors of the rectum are activated due to the prescence of faeces, is it efferent or afferent nerve fibres that feed this information to the parasympathetic nervous system?

A
  • afferent nerve fibres are sensory
  • efferent nerve fibres elicit an effect
26
Q

Once the stretch receptors of the rectum are activated due to the prescence of faeces, afferent nerve fibres feed this information to the parasympathetic nervous system, and then what happens?

A
  • efferent nerve fibres of parasympathetic nervous system are stimulated
  • they provide stimulus for the internal anal sphincter
27
Q

There is the internal and external anal sphincter, which one comes under voluntary and involuntary control?

A
  • internal = involuntary
  • external = voluntary
28
Q

The internal anal sphincter is under involuntary control, but what stops us from losing control of our defacation?

A
  • external anal sphincter
  • skeletal muscle under voluntary control
  • relaxing of this allows control of defacation
29
Q

What is the prupose of emesis, more commonly known as vomiting?

A
  • removal of dangerous ingested toxins from the GIT
30
Q

How many phases of emesis (vomiting) are there, and what are they called?

A

1 - nausea phase

2 - retching phase

3 - expulsive phase

31
Q

The first phase of emesis (vomiting) is nausea, what is this?

A
  • unpleasant feelings, unease, and distress
  • feeling of the need to vomit.
32
Q

The second phase of emesis (vomiting) is retching, which normally elicits the act of vomiting, what is this?

A
  • laboured respiratory movements
  • abdominal, thoracic and diaphram muscle (s) contract
  • diaphragm contraction downwards generates a pressure gradient to permit emesis
33
Q

The third phase of emesis (vomiting) is expulsion, which normally, what is this?

A
  • involuntary emptying of gastric contents
  • emptying is due to pressure gradient caused by diaphragm
  • lower oesophageal sphincter
34
Q

In the final phase of vomitting, what happens to ensure, or at least minimise vomit entering the trachea or nasopharynx?

A
  • epiglottis covers trachea
  • soft palate cover nasopharynx
35
Q

Where is the vomiting centre in the brain located and are adrenoreceptors or muscarinic receptors able to stimulate this?

A
  • medulla oblongata
  • muscarinic as its involuntary (parasympathetic)
36
Q

What is the chemoreceptor trigger zone?

A
  • area of the medulla oblongata
  • located ventrally to 4th ventricle
  • receives inputs from blood-borne drugs or hormones, and communicates with other structures in the vomiting center to initiate vomiting
37
Q

What is able to innervate the chemoreceptor trigger zone?

A
  • dopamine
  • serotonin (5HT) receptors
38
Q

In addition to receiving inputs from blood-borne drugs or hormones, and communicates with other structures in the vomiting center to initiate vomiting, motion sickness is also able to eleicti vomiting. How does this work?

A
  • labyrinth (inner ear-vestibular system) balance centre
  • innervates the chemoreceptor trigger zone (via cranial nerve 8)
  • 5HT innervates via serotonin

Year 1 NME (61 decks)

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