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Gastrointestinal Biology > GB 6. GIT Function I: Introduction and Gastric Function > Flashcards

GB 6. GIT Function I: Introduction and Gastric Function Flashcards

1
Q

What regulates digestive function? [4]

A

[1] Intrinsic Nerve Plexuses (Enteric Nervous System, ENS)
[2] Extrinsic Nerves (Autonomic Nervous System, ANS)
[3] Autonomous Smooth Muscle Function
[4] Gastrointestinal Hormones

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2
Q

What are the 2 branches of the Extrinsic Nervous System of the gut?

A

[1] Sympathetic
- mainly inhibitory
[2] Parasympathetic
- mainly excitatory

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3
Q

What are the 3 main components of the intrinsic nerve plexus (enteric nervous system)? What are the functions of each?

A

[1] Sensory Neurons (intrinsic primary afferent)

  • receives info from sensory receptors in mucosa + muscle
  • info on gut contents + state of wall
  • responds to stretch, tension, chemical nature of contents

[2] Motor Neurons (intrinsic primary efferent)

  • controls GI motility + secretion
  • activates intestinal functions (causes muscles to contract, vessels to dilate and electrolytes to be transported)

[3] Inter-Neurons
- integrates info from sensory neurons and provides it to enteric motor neurons

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4
Q

What are the 2 major networks of nerve fibres that are a part of the Enteric Nervous System? What are the functions of each?

A

[1] Submucosal (Meissner’s) Plexus
- intestinal secretions + local absorptive environment

[2] Myenteric (Auerbach’s) Plexus
- regulates intestinal smooth muscle

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5
Q

Does the extrinsic nervous system and intrinsic nervous system interact with one another?

A
  • not entirely
  • the enteric nervous system consists of cell bodies that receive inputs from the extrinsic nerves (sympathetic + parasympathetic)
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6
Q

The enteric nervous system is regulated by both excitatory and inhibitory nerves. Give some examples of both types.

A

Excitatory - ACh

Inhibitory - NO, VIP

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7
Q

Explain the extrinsic innervation (autonomic nervous system) of the gut. Some general functions, where they are located…

A
  • not essential for motility
  • nerves end mainly on plexus
  • modify ongoing activity of ENS
  • alters the level of hormone secretion
  • can act directly on smooth muscle + glands
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8
Q

What does the parasympathetic nervous system (extrinsic innervation) effect GI activity?

A
  • from VAGUS NERVE

- increases GI activity (gastrointestinal secretion, motor activity, sphincter and blood vessel contraction)

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9
Q

What does the sympathetic nervous system (extrinsic innervation) effect GI activity?

A
  • from PREVERTEBRAL GANGLIA

- decreases GI activity (gastrointestinal secretion, motor activity, sphincter and blood vessel contraction)

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10
Q

What nerve does the parasympathetic nervous system come from?

A

VAGUS NERVE (+ pelvic nerves)

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11
Q

What nerve does the sympathetic nervous system come from?

A

PREVERTEBRAL GANGLIA

- coeliac, superior mesenteric + inferior mesenteric nerves

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12
Q

What is the main neurotransmitter of the parasympathetic nervous system? Describe the innervation of the upper and lower GIT

A
  • ACh (excitatory!)

UPPER GIT:

  • rich vagal innervation
  • esophagus, stomach, small intestine + colon (up until splenic flexure)

LOWER GIT:

  • rich pelvic innervation
  • distal colon, rectum
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13
Q

Which innervation is more important in the GIT? Parasympathetic or sympathetic?

A

Parasympathetic is more important

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14
Q

What neurotransmitter is involved with the sympathetic nervous system in the GIT?

A

NA - inhibitory to GIT!

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15
Q

What are the interstitial cells of Cajal?

A

the pacemaker cells of the GIT

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16
Q

What is the location of the Interstitial Cells of Cajal, what do they do? How are they connected to smooth muscle?

A
  • located in boundary of longitudinal and circular smooth muscle layers
  • it leads to slow changes in resting membrane potential of GIT smooth muscle (cyclic slow wave activity)
  • connected to smooth muscle by NEXI or GAP JUNCTIONS
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17
Q

What are slow waves? Describe how they work.

A
  • they are spontaneous changes in resting membrane potential
  • they bring the membrane closer or further from threshold potential
  • amplitude of slow waves may reach a certain threshold in combo (through) mechanical, neural or hormonal factors
  • when this happens, membrane Ca2+ channels are activated, resulting in calcium influx
  • DEPOLARISATION RESULTS IN REPEATED RHYTHMICAL MUSCLE CONTRACTION
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18
Q

If the amplitude of the slow waves reach the threshold potential, what happens?

A

DEPOLARISATION OCCURS AND RESULTS IN REPEATED RHYTHMICAL MUSCLE CONTRACTION

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19
Q

What are slow waves not?

A

they are not action potentials!

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20
Q

What effect does the frequency of slow waves have on smooth muscle contraction?

A

as the frequency of slow waves increase, the frequency of smooth muscle contraction increases
- ultimately dependent on pacemaker cells

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21
Q

As the number of action potentials at the crest of the depolarisation phase increases, so does what?

A
  • the strength of contraction increases
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22
Q

What are the 3 main enteric reflexes of the GIT? (just name them)

A

[1] Peristaltic Contraction (Peristalsis)
- slow waves of muscle contraction occur in the absence of the extrinsic nervous (vagal) influences

[2] Regulation of Gastric Emptying (Neural [Enterogastric] Reflex)

[3] Gastroileal Reflex (Hormonal)

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23
Q

Explain the enteric reflex - Neural (Enterogastric) Reflex.

A
  • it is triggered by the presence of food in the duodenum (due to distension) [this is sensed by chemoreceptors + stretch receptors]
  • results in inhibition of gastric motility and reduced rate of emptying of the stomach

ULTIMATELY - SLOWS DOWN ARRIVAL OF FOOD IN DUODENUM WHEN DUODENUM IS FULL

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24
Q

Explain the enteric reflex - Gastroileal Reflex (Hormonal).

A
  • it is triggered by the presence of chyme in stomach (due to distension) and gastric peristalsis
  • this leads to RELEASE OF GASTRIN
  • contractions of the ileum + relaxation of the ileocaecal sphincter
  • gastrin is a hormone that relaxes the sphincter

ALLOWS EMPTYING OF THE ILEAL CONTENTS INTO LARGE INTESTINE - PREPARES FOR INCOMING CHYME

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25
Q

What is the main function of the proximal stomach?

A

Storage - which is characterized by RELAXATION

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26
Q

What are the 3 ways that the proximal stomach relaxes?

A

[1] Receptive Relaxation
- food enters, muscles relax to accomodate

[2] Adaptive Relaxation (Reflex Relaxation)

  • distension of stomach causes reflex relaxation
  • involves nerve reflex (local + central)
  • involves inhibitory neurotransmitter
  • allows for prolonged storage for breakdown

[3] Feedback Relaxation

  • signals triggered by nutrients in the duodenal lumen
  • results in relaxation of gastric fundus
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27
Q

What is the main function of the distal stomach?

A

Mixing + Emptying

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28
Q

What is involved with mixing in the distal stomach?

A

[1] Spontaneous Electrical Activity
- Interstitial Cells of Cajal (gastric slow waves)

[2] Depolarizing Agents
- e.g. Vagus Nerve (ACh), Hormones (e.g. gastrin) and Stretch (distension + enteric reflex)

[3] Contractins

  • they mix and propel food towards duodenum
  • segmentation (local contractions causing constriction)
  • propulsive movements
29
Q

Explain the process of the emptying of the distal stomach.

A
  • the narrow pyloric sphincter only allows a small amount of food to enter the duodenum with each contraction
  • the basal electrical rhythm (BER) is initiated by pacemaker cells (of Cajal)
  • vigorous peristalsis occurs near pylorus
  • chyme either delivered to duodenum or forced back into stomach for further mixing
30
Q

What are the 3 main MOTOR gastric functions?

A

[1] Proximal Stomach (Storage)
[2] Distal Stomach (Mixing)
[3] Distal Stomach (Emptying)

31
Q

What cells (glands) are the gastric secretions secreted from?

A

Oxyntic Glands (proximal and part of distal stomach)

32
Q

List the secretions that are secreted from the oxyntic glands. [5]

A

[1] Pepsinogen

  • secreted from peptic (chief cells)
  • protein digestion

[2] HCL (Intrinsic Factor)

  • secreted from oxyntic (parietal) cells
  • kills bacteria, low pH for pepsin
  • vitamin B12 absorption

[3] Mucus + Bicarbonate

  • secreted from mucous neck cells
  • protects stomach epithelium from acid

[4] Histamine

  • secreted from enterochromaffin-like cells (mast-like cells)
  • stimulates gastric acid secretion (vasodilation, increased blood flow aids increased acid secretion)

[5] Somatostatin

  • secreted from D-cells
  • inhibits gastric acid secretion
33
Q

Where is pepsinogen secreted from?

A

peptic (chief) cells

34
Q

What is the function of pepsinogen?

A

protein digestion

35
Q

Where is HCl (intrinsic factor) secreted from?

A

oxyntic (parietal) cells

36
Q

What is the function of HCl?

A
  • kills bacteria
  • low pH for pepsin (to activate pepsinogen)
  • vitamin B12 absorption
37
Q

Where is mucus + bicarbonate secreted from?

A

mucous neck cells

38
Q

What is the function of mucus and bicarbonate?

A

protects stomach epithelium from acid

39
Q

Where is histamine secreted from?

A

enterochromaffin-like cells (mast-like cells)

40
Q

What is the function of histamine?

A
  • stimulates gastric acid secretion (vasodilation, increased blood flow aids increased acid secretion)
41
Q

Where is somatostatin secreted from?

A

D-cells

42
Q

What is the function of histamine?

A

inhibits gastric acid secretion

43
Q

Where is mucous secreted from?

A

mucous cells

44
Q

What is the function of mucous?

A

protects stomach epithelium from acid

45
Q

Where is gastrin secreted from?

A

G cells (endocrine)

46
Q

What is the function of gastrin?

A
  • stimulates HCl secretion from oxyntic (parietal) cells

- stimulates pepsinogen secretion from peptic (chief) cells

47
Q

List the secretions that are from the Pyloric Glands (antral region)? [3]

A

[1] Mucus

  • secreted from mucous cells
  • protects stomach epithelium from acid

[2] Gastrin

  • secreted from G cells (endocrine)
  • stimulates HCl secretion from oxyntic (parietal) cells and pepsinogen from peptic (chief) cells

[3] Somatostatin

  • secreted from D cells
  • inhibits gastric acid secretion
48
Q

What do the surface epithelial cells secrete?

A
  • secrete thick alkaline mucus containing mucin and bicarbonate
  • functions to lubricate the stomach and protect the mucosa from acid and pepsin
49
Q

What is the function of the thick alkaline mucus containing mucin and bicarbonate?

A

functions to lubricate the stomach and protect the mucosa from acid and pepsi

50
Q

What are the 3 major cells in which gastric secretions are secreted from?

A

[1] Oxyntic Glands

[2] Pyloric Glands

[3] Surface Epithelial Cells

51
Q

How is pepsinogen converted to pepsin?

A

HCl cleaves a small fragment off of pepsinogen molecules to create active pepsin

  • pepsin can then activate other pepsinogen molecules by cleaving off amino acids to form pepsin
52
Q

Is pepsinogen the active or inactive form?

A

inactive form

- it gets changed into pepsin

53
Q

What are the mediators of acid secretion? What increases gastric acid secretion and what decreases gastric acid secretion?

A

INCREASES SECRETION:
[1] ACh
[2] Gastrin
[3] Histamine

DECREASES SECRETION:
[1] Prostaglandins
[2] Somatostatin

54
Q

What receptors are involved with the acid secretion mediator, ACh?

A

M3 receptors

55
Q

What receptors are involved with the acid secretion mediator, Gastrin?

A

CCK-2 receptors

56
Q

What receptors are involved with the acid secretion mediator, Histamine?

A

SSTR2 receptors

57
Q

What is the function of the proton pump (H+/K+ ATPase) - the oxyntic cell?

A
  • driving force is the H+/K+ ATPase
  • – pumps H+ out in exchange for K+
  • Cl- enters the cell in exchange for HCO3- and leaves for lumen through CL- channels down electrochemical gradient
58
Q

What is the final item that all the gastric secretion mediators finally have an effect on?

A

they have an effect on the H+/K+ ATPase pump (proton pump)

59
Q

Does the stomach have a large or small surface area for absorption? Describe what the stomach absorbs (its aborptive abilities).

A

stomach has SMALL surface area for absorption

  • it lacks villus of small intestine
  • it has tight junctions between epithelial cells
  • absorbs VERY FEW substances
  • absorbs SMALL amounts of certain LIPID-SOLUBLE compounds
  • only HIGHLY LIPID SOLUBLE agents absorbed to significant extent
  • – e.g. alcohol, weak acids, non-steroidal anti-inflammatory
60
Q

What are some of the highly lipid-soluble agents taht the stomach can absorb to a significant extent?

A

[1] Alcohol
- lipid soluble

[2] Weak Acids

  • e.g. aspirin
  • largely uncharged at pH of stomach, passes through the lining quickly

[3] Non-Steroidal Anti-Inflammatory Drugs
- e.g ibuprofen

61
Q

What are the 2 components of the gastrointestinal barrier? What are they made up of?

A

[1] Intrinsic Barrier

  • epithelial cell lining
  • tight junctions that tie them together

[2] Extrinsic Barrier

  • consists of secretions and other influences which affect epithelial cells and maintain barrier function
  • – mucous + bicarbonate secretion
  • – hormones and cytokines (affects rates of cell proliferation)
  • – prostaglandins (e.g. prostaglandin E2 - PGE2)
62
Q

What can lead to damage/alteration inthe mucosal defence of the stomach? [4] (just list them)

A

[1] Gastric Acid (Pepsin)
[2] H. Pylori
[3] Drugs (NSAIDs, aspirin, alcohol)
[4] Stress

63
Q

What are some of the causes of Gastritis and Peptic Ulcer Disease?

A

[1] Excess Acid (Pepsin)
- due to reflux, diet, stress, caffeine, smoking…

[2] Decreased Mucus
- irritants to mucosal barrier

[3] Drug Adverse Effects

  • aspirin // NSAIDs
  • weak acids become concentrated into mucosal cells (they can cross the barrier and then build up)
  • inhbition of COX-1 and COX-2 enzymes are important for the maintenance of the integrity of the gastric epithelium + mucus barrier
64
Q

Why are the COX-1 and COX-2 enzymes important for the maintenance of the gastric epithelium and mucus barrier?

A
  • prostaglandins (esp. PGE2) have protective role physiologically
  • they inhibit acid secretion and stimulate mucus secretion
  • they inhibit acid secretion + stimulate mucus secretion
  • reduction in mucosal defence and blood flow will cause gastric ulceration (leading to inhibition of prostaglandin synthesis)
  • neutrophil-endothelial interaction occur as a result of the vascular disturbances and neutrophil activation
  • they mediate the adherence of leukocytes to mucosal endothelial cells
65
Q

What are the 2 main insults that NSAIDs may have?

A

[1] Primary Insult

  • topical irritation
  • leads to direct epithelial acid damage

[2] Secondary Insult

  • due to COX-1 and COX-2 inhibition
  • leads to prostaglanding inhibition, reduced blood flow, leukocyte adherence
66
Q

What does Helicobacter pylori do? What can it lead to?

A
  • helicobacter pylori is a bacterium that causes peptic ulcer disease
  • it infects the antrum of stomach
  • it causes infiltration of leukocytes (inflammation of gastric mucosa)
  • mainly all duodenal + gastric ulcers have H. pylori infection
67
Q

What is the treatment for an ulcer due to H.pylori bacteria?

A

Triple Therapy (first-line therapy, 2 antibiotics and a proton pump inhibitor)

68
Q

What is the Zollinger-Ellison Syndrome? Why does it occur? What does it lead to?

A
  • RARE cause of recurrent peptic ulceration associated with increased gastrin blood concentrations
  • excess acid secretion due to a primary non-beta cell gastrin-secreting tumour in pancreas
  • leads to increased mass of parietal and enterochromaffin-like cells suceptible to overstimulation by gastrin
69
Q

What is the treatment for Zollinger-Ellison syndrome?

A

therapy directed at controlling the gastric acid hypersecretion and removal of the gastrinoma

Gastrointestinal Biology (15 decks)

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