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(OMS1) GIGU Exam > Lecture 5: Motility of the GI tract > Flashcards

Lecture 5: Motility of the GI tract Flashcards

1
Q

Layers of the GI tract (luminal to deep)

A 
(Lumen)
Epithelium
Lamina propia
Muscularis mucosae
Submucosa
Submucosal plexus
Circular muscle
Myenteric plexus
Longitudinal muscle
Serosa
(Blood)
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2
Q

What is the significance of the muscularis mucosae?

Whatis the significance of the muscularis propia?

A
  • in the mucosa layer, smooth muscle contractions here directly influence epithelium
  • has the circular and longitudinal smooth muscles
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3
Q

Circular muscle vs. Longitudinal muscle

A

C: decreases diameter of contracting segment
L: decreases length of contracting segment

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4
Q

What are slow waves and how are they different from APs?

A

shows depolarization and re-polarization of the membrane

  • slow waves are simply oscillations of voltage > changes are enough to generate tension/contraction the SM in the GI tract, which usually follows the slow wave
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5
Q

Phasic vs Tonic

A

P: periodic contractions followed by relaxation (waves)
T: constant contraction with no relaxation (plateau)

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6
Q

What is the relationship of AP to slow waves?

A

The more AP generated the stronger the contraction in the GI tract

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7
Q

What elements stimulate GI motility (more slow waves)?

A

Stretch
Ach
Parasympathetics

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8
Q

What elements inhibit GI motility (less slow waves)?

A

NE

Sympathetics

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9
Q

What is the significance of the Enteric Nervous system?

A

-have pacemaker regions that control slow wave activity without needing nervous system input

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10
Q

as parts of the ENS, what is the role of the submucosal plexus and the myenteric (auerbach’s) \plexus?

A

S: controls GI secretions and blood flow
M: controls GI movements

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11
Q

Explain how slow waves are spontaneously generated

A

Interstitial cells of Cajal (ICC) serves as pacemaker that regulate electrical activity > spreads impuse via gap junctions > smooth muscle cells respond by opening Ca2+ voltage channels > more contraction

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12
Q

What controls mastication?

A
  • CN V

- chewing is essentially a reflex caused by presence of food in mouth = triggers digestion process as well

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13
Q

Describe the physiology of swallowing
Oral phase
Pharyngeal phase
Esophageal phase

A

Oral phase: voluntary initiation of swallowing

Pharyngeal phase: soft palate ascends > epiglottis moves/vocal cords block trachea > upper esophageal sphincter relaxes > peristalsis in the pharyngeal constrictors pushing food down into esophagus

Esophageal phase: peristaltic waves controlled by the ENS and the swallowing reflex (backup plan 2ndary wave that pushes food down if not successful)

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14
Q

How does the swallowing reflex work?

A

Food in pharynx > CN IX/X detection > swallowing center in medulla > brainstem nuclei > efferent input to pharynx

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15
Q

Primary vs. Secondary peristaltic wave

A

Primary: esophageal constriction controlled by the medulla > goal is to bring food into gastric organs
-cannot happen after vagotomy

Secondary: triggered if esophagus failed to bring food into gastric organ controlled by ENS and medulla
-can happen after vagotomy

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16
Q

What does a manometry study show?

A
  • changes in pressure in thorax/abdomen at different parts of the esophageal tract
  • contraction means blocking, relaxation means allowing food to come in = results in “wave” down the GI tract = peristalsis
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17
Q

How does the GI tract prevent backflow?

A

UES (pharynx to esophagus) and LES (esophagus to stomach) - closed and contracted except when food has to pass through

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18
Q

Achalasia
Causes
Clinical

A
  • myenteric plexus ganglion cells reduced, esophageal nerve damage
  • more elevated LES resting pressure compared to normal = reduced relaxation of LES during swallowing = impaired peristalsis leading to regurgitation, dysphagia, heartburn and chest pain
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19
Q

GERD
Cause
Clinical

A
  • abnormally low pressure in the LES making it prone to relaxing instead of contracting, reflux of acid, pepsin and bile into esophagus
  • heartburn, regurgitation , GI bleeding, esophagitis, Barrett’s esophagus
20
Q

What controls motility in the stomach?

A

-Extrinsic innervations: sympathetic and parasympathetic

Intrinsic innervations: ENS (Myenteric and submucosal plexus)

21
Q

What happens at the LES/Orad junction when there is food present?
What hormone acts on this region and what does it do?

A

vagovagal reflex causing receptive relaxation (low pressure/high volume)
-Cholecystokinin (CKK) from SI decreases contractions and increases gastric distensibility

22
Q

What happens at the Caudad region of the stomach?

A

-contractions increase (n force and velocity in this area > has to be strong enough to actually push food down and open the pyloric sphincter

23
Q

What happens at the antrum region?

A
  • Contraction at the pyloric sphincter only allows small amount of food through into the duodenum, retropulsion of food occurs and backflows into stomach
  • (process is gradual, repetitive peristalsis to push food through not all at once; most of the food pushed out 3-4 hours later)
24
Q

What are the parasympathetic effectors of gastric contraction?

Sympathetic?

A

P: gastrin and motilin (increase AP and contraction force)

S: secretin and GIP (decrease AP and contraction force)

25
Q

What factors increase gastric emptying?

A
  • decreased distensibility in orad, pyloric tone and segmenting contractions in proximal duodenum
  • increased peristaltic force in caudad and diameter of proximal duodenum

(triggered after a meal)

26
Q

What factors decrease gastric emptying?

A
  • increase in segmentation contractions in duodenum and pyloric tone
  • decrease peristaltic force and distensibility (contraction) of orad
  • Enterogastric reflex (negative feedback from duodenum)
27
Q

How does the entero-gastric reflex work via acid, fat and hypertonicity?

A
  • Acid in duodenum > secretin release > inhibit gastrin > inhibit motility in stomach
  • Fats in duodenum > CKK and GIP > inhibit stomach motility
  • Hypertonicity also inhibits, hormone unk
28
Q

Gastroparesis
Causes
Clinical

A
  • DM 2, vagus n. injury

- n,v, bloating, weight loss, fullness

29
Q

Common causes of gastric motility issues

Common treatments

A
  • scarring (ulcer), obstruction (cancer), eating disorders, vagotomy
  • pyloroplasty, balloon dilation
30
Q

What is the MMC?

What mediates it?

A
  • Migrating myoelectric complex
  • periodic, bursting contractions during fasting that empties undigested residue from stomach
  • Motilin
31
Q

SIBO

What role does MMC play in preventing this?

A

Small intestinal bacterial overgrowth - overabundance of colonic bacteria in SI which disturbs small bowel movements > nausea, anorexia, bloating

MMC performs cleansing mechanisms in the small intestine

32
Q

How does the small intestine maximize nutrient absorption?

A
  • mixing chyme with digestive enzyme and pancreatic secretions that exposes as much of the nutrients to the mucosa that will absorb it
  • also pushes unabsorbed chyme to the large intestine
33
Q

What is the difference between segmentation contractions and peristaltic contractions?

A
  • SI contractions that separates the bolus to mix it as much as possible (same action)
  • done by circular and longitudinal muscles propel food forward (opposite actions, contraction behind the bolus, relaxation in front of the bolus)
34
Q

How is the generation of contractions different in the SI compared to stomach?

A

Stomach does not need spike potential AP to initiate contraction
-slow waves not enough to initiate it, but sets the maximum frequency of SI contractions (decreases the further food goes down the SI)

35
Q

Describe the pathway of the regulation of the peristalsis in the SI (include role of myenteric and Meissner plexus)

A

Meissner plexus are the sensory neurons: 5HT (serotonin) released by smooth muscle on IPAN > interneuron > excitatory motor neuron in Myenteric plexus > effector substances released to contract smooth muscle

36
Q

What neural effectors contract/excite the small intestine?

What neural effectors relax/inhibit the small intestine?

A
  • Ach, Substance P

- VIP, NO

37
Q

What hormones stimulate SI contractions?

What hormones inhibit SI contractions?

A
  • serotonin, prostaglandins, gastrin, CKK, motilin, insulin

- epinephrine, secretin, glucagon

38
Q

How does the vomiting reflex work?

A

Vagus/sympathetic afferents > medulla (vomiting center)

efferents induce: reverse peristalsis in SI > pyloric relaxation > forced inspiration to increase abd. pressure > LES relaxes/glottis closes > gastric expulsion of food = vomiti

39
Q

How is the bolus propelled into the colon from the SI?

A

bolus accumulation > distension of the ileum > causing relaxation of the ileocecal sphincter > bolus flows into colon

*distension of the colon causes the sphincter to close to block more bolus from entering

40
Q

What innervates the two types of anal sphincters?

A

Internal: Pelvic splanchnic ns. (involuntary)

External: pudendal n. (somatic/voluntary)

41
Q

What parts of the colon does ….. innervate ?

ENS (myenteric plexus)
PNS
SNS
Pudendal ns. (somatic)

A

-muscle layers of the colon

-cecum, ascending and transverse colon (via CN X)
descending, sigmoid and rectum (Pelvic splanchnic Ns.)

-Proximal regions (via superior mesenteric ganglion)
Distal regions (via inferior mesenteric ganglion)
Distal rectum and anal canal (via hypogastric plexus)

-external anal sphincter

42
Q

What characterizes bolus motility in the colon?

A

-mass movements = large distances to stimulate the defecation reflex and absorption of the water and electrolytes back into blood

43
Q

How does colon motility result in constipation and diarrhea?

A

Constipation: poor motility = slower passage = too much time for absorption = dry poop

Diarrhea: high motility = faster passage = too little time for absorption = loose poop

44
Q

What characterizes motility in the rectum and anal canal?

A

-colon’s mass movements propel feces into rectum > distension stimulates the rectosphincteric reflex

45
Q

How does the rectosphincteric reflex work?

What can lead to fecal incontinence?

A

feces fills the rectum > rectal distension > smooth muscle wall contracts and internal anal sphincter relaxes
external anal sphincter closed unless opened voluntarily

-inability to sense rectal distension or loss of voluntary control of the External anal sphincter

46
Q

What happens to GI motility control in Hirschsprung disease?

A

lack of ganglion cells in some segment of the colon > low VIP levels > no relaxation/SM constriction > colon contents accumulate

(OMS1) GIGU Exam (40 decks)

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