57 - GI Introduction Flashcards

1
Q

How is the GI system regulated by the parasympathetic, sympathetic, and enteric branches of the ANS?

A

A. ENS allows GIT to function independently form the rest of the body (distention is a key stimulator)
B. Some information is relayed to the CNS
C. Parasympathetic and sympathetic can regulate GIT directly and indirectly – modulating at the endocrine level or directly at level of smooth muscle.

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2
Q

What is the key difference between the sympathetic and parasympathetic system in the GI in relation to ENS neurons?

A

Sympathetics have postganglionic fibers that interact with ENS neurons where parasympathetics have pre-ganglionic fibers that interact with ENS neurons.

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3
Q

What neurotransmitters do the sympathetic/parasympathetic nervous system use in the GI tract?

A

Mainly Ach and NE

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4
Q

What neurotransmitters does the ENS use in the gut?

A

ENS uses Ach, Serotonin, Dopamine, NO, and VIP

VIP = vasoactive intestinal peptide

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5
Q

Regulation of GI via ACh

A

A. Ach – excitatory – vasodilates, increase secretion, smooth muscle contraction

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6
Q

Regulation of GI via NE

A

B. NE (lesser Epi, and Dopamine) – inhibitory – vasoconstrict, inhibit smooth muscle contraction, decrease secretion.

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7
Q

Regulation of GI via serotonin

A

Serotonin – excitatory – same as Ach but mainly for interneuron communication

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8
Q

Regulation of GI via dopamine

A

Dopamine – inhibits ENS neuron firing via D2 receptors

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9
Q

Regulation of GI via NO

A

NO – inhibitory – causes smooth muscle relaxation (vascular and GI)

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10
Q

Regulation of GI via VIP

A

Vasoactive intestinal peptide (VIP) – inhibitory – same as NO.

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11
Q

How does CO2 regulate blood flow to the GI tissues?

A

In vasculature, lack of blood flow or increased metabolic demand can result in CO2 buildup – this results in increased amount of blood flow to the tissue requiring oxygenation and nutrients by vasodilation

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12
Q

Do vascular and GI smooth muscle constrict and contract together?

A

No - Vascular smooth muscle behaves differently than GI smooth muscle does.

This is clearly illustrated by Ach, which contracts GI smooth muscle but relaxes vascular smooth muscle. This disparity can be explained more easily in terms fight or flight vs. rest and digest

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13
Q

Factors that increase blood flow in GI tract

A
  • PNS stimulation (rest and digest)
  • Neurotransmitters like VIP
  • Low Oxygen
  • Hyperosmolarity
  • Postprandial hyperemia (increase in blood flow post-meal by 8 fold for 2-4 hours)
  • Sequential dilation along the GI tract (peristalsis)
  • Flow is regulated to muscularis layers (primary) and through villi and submucosa
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14
Q

Factors that decrease blood flow to GI tract

A

SNS cuts vascular smooth muscle blood flow via NE (alpha adrenergic)

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15
Q

Describe the basic mechanism of GI smooth muscle contraction

A
  • Membrane potential is not constant – oscillates regularly (maintained by Migrating motor complex – MMC)
  • Intermittent peaks are spike potentials that elicit contractions
  • These are generated by stimuli (one of the key ones is distention)
  • Primary regulators of the GI smooth muscle are Ach, VIP and NO
  • Greater spike potential means greater tension
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16
Q

Describe the coordination of smooth muscle contraction in the GI tract

A

Remember – these processes are not working against each other. They work with each other in order to get the bowels moving

For example, in peristalsis, contraction upstream and relaxation downstream moves food further down the gut tube

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17
Q

Types of GI motor activity

A
  • Segmental contractions (for mixing via intermittent contraction)
  • Peristaltic contractions (for moving)
  • Reverse peristalsis (storing, emptying and vomiting)
  • MMC (migrating motor complex)
18
Q

What is the role of motilin?

A

An amino acid peptide hormone that is secreted by endocrine M cells (found in crypts of small intestine) and function in the MMC (migrating motor complex)

19
Q

Where does vagus (CN X) have the greatest role in GI innervation?

A

Stomach and duodenum

20
Q

Striated muscle sphincters include…

A
  • Upper Esophageal (UES),
  • Upper 1/3 of esophagus
  • External anal sphincter
21
Q

Describe the innervation and action of motor sphincters

A
  • Controlled by somatic neurons hence you can control swallowing and pooping
  • Sphincters are rings involved in antegrade and retrograde movement
22
Q

Upper esophageal sphincter

A

Striated muscle that separates pharynx and upper esophagus. Closed during inspiration to prevent swallowing air

23
Q

Lower esophageal sphincter

A

Separates esophagus from stomach, permits movement of food into stomach and prevents reflux into esophagus (Barrett’s esophagus)

24
Q

Pyloric sphincter

A

Pyloric (PS) - Separates stomach and duodenum and regulates gastric emptying

25
Q

Ileorectal sphincter

A

Separates ileum from cecum. Ileum distention relaxes the sphincter (distention due to buildup, this makes sense). Ascending colon distention causes contraction (also makes sense because that means there’s a backup in the colon).

26
Q

Internal anal sphincter

A

Involuntary control. Rectal distention relaxes the sphincter. Notice that the buildup that would cause IS to contract also causes IAS to relax. This probably gives us the urge to go – all fitting in with the idea of peristaltic contractions in the GI tract

27
Q

External anal sphincter

A

Striated muscle under voluntary and involuntary control. Involuntary reflex contracts EAS if defecation is not desired. If defecation is desired, EAS can be voluntarily or involuntarily contracted. Voluntary EAS contraction can override defecation reflex.

28
Q

What is the function of the hormone CCK in regulating the GI tract?

A

Cholecystokinin

  • Made in duodenum – targets pancreas, gallbladder, stomach, and sphincter of Oddi.
  • Functions: increase enzyme secretion and relaxation while decreasing emptying and contraction
  • CCK facilitates digestion.
29
Q

What is the function of the hormone gastrin in regulating the GI tract?

A
  • Made by stomach G cells to promote gastric acid secretion

- Targets parietal cells, ECL, and D cell

30
Q

What is the function of the hormone motilin in regulating the GI tract?

A
  • Made by upper GI targeting stomach and duodenum.
  • Function is to increase smooth muscle contraction – increased contractility works in conjunction with CCK to promote stomach emptying and duodenum filling.
31
Q

What is the function of the hormone peptide YY in regulating the GI tract?

A

Made by ileum and colon to target pancreas – decreases enzyme and fluid secretion.

32
Q

What is the function of the hormone secretin in regulating the GI tract?

A

Secretin

  • Made by duodenum to cause pancreas and stomach to increase bicarb secretion, decrease acid secretion, and delay gastric emptying
  • This reduces amount of chyme released into the duodenum – impacts filling as well as acidity
  • Remember the duodenum is basic relative to the stomach
33
Q

What is the function of the hormone somatostatin in regulating the GI tract?

A
  • Made by stomach, duodenum and pancreatic cells.
  • Targets stomach, intestine, pancreas and liver resulting in decreased acid secretion, increased fluid absorption, decreased smooth muscle contraction, decreased secretion, decreased bile flow.
34
Q

What is the role of the paracrine regulator prostaglandin in GI function?

A
  • Targets stomach and intestine
  • Made in stomach, intestine/immune cells
  • Functions in increased blood flow (remember how NSAIDS resulted in kidney damage for this reason as well), decrease acid secretion, increase mucus/bicarb secretion, increase motility and increase fluid secretion
35
Q

What is the role of the paracrine regulator histamine in GI function?

A
  • Targets stomach and intestines
  • Made in stomach, intestine/immune cells.
  • Functions to increase acid secretion and increase fluid secretion.
36
Q

Case #1

A

Go read case #1

37
Q

What are the causes of vomiting?

A

Vomiting can be indicative of obstruction, GI irritation due to acidity, foot toxicity, etc.

38
Q

What neurotransmitters play an important role in regulating an emetic response in the CNS and gut?

A

Ach, VIP and NO are the primary regulators of GI smooth muscle

39
Q

What does non-bilious vomiting indicate?

A

This indicates location of the irritation or blockage. Lack of bile means this occurs prior to the major duodenal papilla – child may have pyloric stenosis

40
Q

Deficiency in which neurotransmitters my result in this patient’s presentation?

A

Deficiency of contractile inhibitors would result in a stenosis of the pylorus. This means NO and VIP