39 Gastrointestinal motility Flashcards

1
Q

What are the 3 layers of GI smooth muscle?

A

Thin muscularis mucosae, Thick contractile muscle, Longitudinal muscle of externa layers

remember:
mucosae always thin, and
thick to contract,
longitudinal muscle of externa

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2
Q

Smooth muscles make up all the contractile tissue of the GI tract except:

A

the pharynx, upper 1/3 of the esophagus and external anal sphincter

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3
Q

What are the 3 regulatory control mechanisms of gut motility?

A
  1. Neural control (ANS + ENS)
  2. Hormonal control (GI peptides)
  3. Myogenic control system
    (intrinsic spontaneous electrical activity of the smooth muscle, independent of external stimuli)
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4
Q

In terms of neural control, what kind(s) of nerve terminals exert excitatory and inhibitory influences on gut motility?

A

Cholinergic, adrenergic and NANC nerve terminals

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5
Q

Sensory receptors in the smooth muscle make the initiation of
A. Short reflex (within the GI tract)
B. Long reflex (goes back to CNS and to ENS via ANS)
C. All of the above
D. None of the above

A

C

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6
Q

In terms of hormonal control of gut motility, the GI peptides are in form of:
A. Endocrine only (e.g. CCK)
B. Paracrine only (e.g. VIP)
C. Endocrine and paracrine

A

C

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7
Q

Myogenic control system is influenced by
A. External stimuli
B. Neural system
C. Hormonal system

A

B and C

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8
Q

What are the 2 types of myogenic control system in controlling gut motility?

A
  1. Slow waves

2. Action potentials

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9
Q

What does slow waves and action potentials determine respectively?

A

Slow waves: frequency
Action potential: Magnitude of the contraction force

  • SW itself doesnt cause contraction, it is the basic electrical rythem (BER): sponataneous depolarization and repolarization cycles

Absence of SW and AP can develop a weak tension, affecting basal muscle tone (when dead, gut length is doubled as the SM is no longer controlled)

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10
Q

Slow waves: constant, only affected by basal temperature and metabolic activity
The threshold for contraction is usually _____mV, while the resting membrane potential is _______mV, and the spikes created by AP will not overshoot _____mV.

A

-40
-50
0

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11
Q

Spikes causing depolarization is stimulated by

  1. stretch
  2. acetylcholine
  3. parasympathetics
  4. GI hormones/paracrines
  5. Noradrenaline
  6. Sympathetics
A

1-4

5 &6 stimulates hyperpolarization, which is the opposite way

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12
Q

Name the 2 types of GI movement and state their functions.

A
  1. Segmentation (non-propulsive annular contraction) - for mixing
  2. Peristalsis (sequential annular contraction) - for propulsing bolus
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13
Q

Peristaltic reflex occurs when food bolus is stretched/ stimulation of sensory receptors of ENS > motor neurons

Name the 4 regulatory mechanisms of peristaltic reflex.

A
  1. Ascending (oral) excitatory pathway
    - above point of stimulation, causes contraction
  2. Descending (anal) inhibitory pathway
    - below point of stimulation, causing relaxation
  3. Tonic contraction
    - complete tonic contraction occurs at GI sphincters only.
    (e. g. LES, pyloric sphincter, ileocaecal sphincter)
  4. Migrating motor complex (MMC) - occurs and repeats after (before??) arrival of next meal
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14
Q

In the ascending/oral excitatory pathway, the excitatory motor neurons are stimulated by potent constrictors like:

A

Acetylcholine and Substance P (neurocrine)

cause contraction

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15
Q

In Descending (anal) inhibitory pathway, the inhibitory motor neurons are stimulated by potent vasodilators like:

A

VIP and NO (neurocrines)

cause relaxation

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16
Q

What is the importance of tonic contraction at the GI sphincters?

A

Restrictive actions of sphincters allow luminal content to pass at proper times + aids mixing

Spasm: when tonic contraction occurs at somewhere other than sphincters

17
Q

The MMC (migrating motor complex ) is initiated by the amino acid GI peptide __________.

A

motilin

18
Q

What are the 2 housekeeping functions of MMC?

A
  1. Propel residue or previous meal

2. Control bacterial overgrowth

19
Q

What are the 3 motor functions of esophagus?

A
  1. Serves as a conduit to propel swallowed material to stomach
  2. Prevents entry of air at its upper end by upper esophageal sphincter (UES)
  3. Prevents reflux of gastric content at its lower end by lower esophageal sphincter (LES)
20
Q

UES is anatomically identified as the part where thickening of circular muscles are present, how about LES?

A

LES cannot be anatomically identified, but it exists functionally as there is elevated pressure

21
Q

What is primary and secondary peristalsis?

A

Primary peristalsis: occurs after swallowing

Secondary peristalsis: occurs in absence of swallowing and distension of food bolus (e.g. in stroke patients will still occur)

they are regulated by ENS together with the vagus nerve

22
Q

What fibers innervate the LES?

A
  1. Vagal excitatory fibers (VEF) and vagal inhibitory fibers (VIF)
23
Q

What are the contracting factors that act on VEF and the relaxing factors that act VIF?

A

VEF: Acetylcholine
VIF: NO and VIP

Normal: net stimulation og VIF for food to enter stomach

GERD: acts on VIF excessively, thus reflux of gastric content cannot be prevented.

24
Q

What are the 3 motor functions of the stomach?` (Gastric motility)

A
  1. Stomach muscle relaxes to accommodate large volumes
  2. Receptive relaxation: mix with gastric juice, facilitate digestion
  3. Mixing and propulsion: regulate rate to provide optimal time for intestinal digestion and absorption
25
Q

Gastric emptying is regulated at an optimal rate depends on the physcial and chemical compositions of gastric contents.
The condition in which the emptying is too slow is called _______, while it is called _______when it is too fast.

A
  1. Gastroparesis (delayed emptying)

2. Dumping syndrome (rapid emptying)

26
Q

Briefly describe how gastric emptying is regulated

A

Receptors in stomach and duodenum senses distension, triggers neural and hormonal pathways to regulate gastric emptying.

27
Q

Hormonal pathway of inhibiting gastric emptying:
Acid, Fat digestion produces and Hyperosmotic solutions stimulates endocrine cells in duodenal mucosa .
What cells are activated and what substances are prodcued? (3 kinds)

A
  1. S cells secrete secretin
  2. K cells secrete GIP (gastric inhibitory peptide)
  3. I cells secrete CCK

-> decreased gastric emptying (less acid, stay longer)

28
Q

Neural pathway of inhibiting gastric emptying:

  1. Short reflex at ENS via ________.
  2. Long reflex at ANS to the ______.
A
  1. Gastrointestinal nerve plexus

2. CNS

29
Q

Intestinal motility involves segmentation, peristalsis and MMC. Slow wave gradient = frequency of the slow wave declines progressively from proximal to distal region. What is the importance of this?

A

To ensure the contraction waves propagate only to the anal direction