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GI Physiology > G3 - The Oesophagus and Functions of the Stomach > Flashcards

G3 - The Oesophagus and Functions of the Stomach Flashcards

1
Q

what is the function of the oesophagus?

A

carries food and liquid from the mouth to the stomach propelled by peristalsis

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2
Q

what is the muscular tube that begins at the pharynx and ends at the stomach?

A

oesophagus

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3
Q

what are the two sphincters located on the oesophagus?

A

upper and lower oesophageal sphincters

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4
Q

whats lines the oesophagus?

A

stratified squamous epithelium

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5
Q

what innervates the oesophagus?

A

directly - vagus nerve

indirectly - myenteric and submucosus plexus

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6
Q

what does the swallowing centre tigger in the oesophagus?

A

closure of the upper oesophageal sphincter once food has entered the oesophagus and also a primary peristaltic wave

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7
Q

what type of muscles mediates the wave?

A

skeletal muscle proximally and smooth muscle distally

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8
Q

Describe the stations os peristalsis in the oesophagus.

A
  1. Circular fibres behind bolus contract to squeeze it down towards stomach
  2. Longitudinal fibres in front of bolus contract to shorten distance of travel
  3. Lower oesophageal sphincter opens within 2-3 s of the initiation of a swallow this closes after passage of bolus to prevent reflux
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9
Q

when sticky food becomes lodged it stimulates local pressure receptors that cause?

A
  • secondary peristaltic wave

- increased saliva production

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10
Q

What is the maximum capacity of the stomach?

A

1000ml

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11
Q

What nerve determines how relaxed the stomach is?

A

CN X

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12
Q

what is the function of the stomach?

A
  • starting point of digestion
  • continues carbohydrate digestion
  • mixes food with gastric secretions to produce chyme
  • stores food
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13
Q

How much gastric juice is secreted from gastric pits per day?

A

2L

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14
Q

What is chyme pushed through from the antrum to the duodenum?

A

Pyloric Sphincter

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15
Q

What is the structure and segments of the stomach?

A

fundus - next to oesophagus

body - middle section

antrum - next to duodenum

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16
Q

what determines the escape of the chyme through the pyloric sphincter?

A

strength of antral wave

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17
Q

What two factors is stomach emptying governed by?

A
  • gastric factors

- duodenal factors

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18
Q

What are gastric factors of stomach emptying?

A
  • rate of emptying is proportional to volume of chyme in stomach
  • consistency of chyme
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19
Q

what increases distension?

A
  • stretch of smooth muscle
  • stimulation of intrinsic nerve plexuses
  • increased vagus nerve activity and gastrin release
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20
Q

What are duodenal factors of stomach emptying?

A
  • duodenum must be ready to receive chyme and can delay emptying by neuronal response and hormonal response
  • stimuli within the duodenum that drive the neuronal and hormonal responses which include fat, acid, hypertonicity and distension
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21
Q

What does neuronal response involve?

A

It decreases antral peristalic activity through signals from intrinsic nerve plexus and the autonomic nervous system

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22
Q

what does hormonal response involve?

A

the release of enterogastrones from the duodenum which inhibits stomach contraction

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23
Q

what is in the oxyntic mucosa which activates pepsinogen to pepsin? It denatures protein and kills most micro-organisms ingested with food

A

HCL

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24
Q

What is in the oxyntic mucosa which inactivates the precursor of the peptidase, pepsin?

A

pepsinogen

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25
Q

What is in the oxyntic mucosa binds and stabilises vitamin B12 allowing absorption in terminal ileum?

A

Intrinsic factor and Gastroferrin

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26
Q

What is in the oxyntic mucosa which stimulates HCL secretion?

A

histamine

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27
Q

What is the area of cells that lines the antrum called?

A

Pyloric gland area

28
Q

What is in the pyloric gland area which stimulates HCl secretion?

A

Gastrin

29
Q

What is in the pyloric gland area which inhibits HCl secretion?

A

somatostatin

30
Q

What do G cells do?

A
  • secrete gastrin that stimulates parietal, chief and ECL cells
31
Q

What do D cells do?

A
  • secrete somatostatin that inhibit parietal, G and ECL cells?
32
Q

What do mucous cells do?

A

protects the mucosa against mechanical, pepsin and acidic injury?

33
Q

What is the area of cells that lines the fundus and body of the stomach called?

A

Oxyntic Mucosa

34
Q

What do parietal cells do?

A

secrete HCL and intrinsic factor

35
Q

what do chief cells do?

A

secrete pepsinogen, a precursor of pepsin?

36
Q

What do ECL cells do?

A

secrete histamine, that stimulate parietal cells

37
Q

What cells are found in the Oxyntic Mucosa?

A
  • chief cells
  • ECL cells
  • parietal cells
38
Q

What cells are found in the pyloric gland area?

A
  • D cell
  • G cell
  • mucous cells
39
Q

Describe the secretion of HCL by the Gastric Parietal Cells?

A
  1. Carbonic anhydrase combines carbon dioxide with water to produce carbonic acid which is unstable and immediately dissociates into a H+ proton and a HCO3- anion.
  2. The proton is released into the cytoplasm and actively pumped out the parietal cell through the canaliculus via the proton pump into the gastric pit of the lumen then into the stomach.
  3. The bicarbonate anion leaves the cells by the basolateral membrane into the interstitial fluid then into the blood. This leaves the cell via a secondary transport system provided by a Cl/HCO3 antiporter, this couples the outward moment of HCO3 with the inward movement of Cl, this crates a membrane gradient that drives the Cl out of the parietal cells on the apical membrane via a Cl channel.
  4. The H+ and the Cl- combine in the lumen of the gastric pit to produce HCL
40
Q

What increases gastric acid production?

A
  • Acetylcholine
  • Gastrin
  • Histamine
41
Q

How does histamine increase gastric acid production?

A
  1. G cells produce gastrin
  2. these bind to the Gastrin receptor on the ECL cell
  3. this stimulates the production of histamine
  4. histamine binds to the H2 histamine receptor on the parietal
  5. this increases activity of the protein pump
42
Q

How does acetylcholine increase gastric acid production?

A
  1. released by activation of the vagus nerve
    2i) . binds to the M3 receptor of the parietal cell
    3i) . this increases the protein pump
    2ii) binds to the M1 receptor on the ECL cell
    3ii) produces histamine which then acts on H2 receptor on parietal cell to increase proton pump
43
Q

How does prostaglandin decrease gastric acid production?

A
  1. produced locally
  2. activates Prostaglandin (EP2) receptor on the parietal cells
  3. cause inhibition of the proton pump
44
Q

How does somatostatin decrease gastric acid production?

A
  1. produced by D cells
  2. this inhibits the release if gastrin from form G cells
  3. this inhibits histamine production
  4. therefore decreases proton pump activity
45
Q

Where are the majority of the protein pumps located?

A

they are inactive on the anterior of the partial cell

46
Q

What causes the protein pumps to move to the apical surface and insert into membrane?

A
  • Acetylcholine
  • Gastrin
  • Histamine
47
Q

what is the Rate of gastric secretion is controlled by?

A

stimulatory and inhibitory mechanisms

48
Q

what are the stimulatory and inhibitory mechanisms that control rate of gastric secretion?

A
  • cephalic phase
  • gastric phase
  • intestinal phase
49
Q

describe the cephalic phase?

A

Vagus stimulates enteric neurones that:
- release ACh directly activating parietal cells (neurotransmitter action)

  • via release of GRP causes release of gastrin from G cells in to systemic circulation that activates parietal cells (endocrine action)
  • via release of histamine from ECL cells that locally activates parietal cells (paracrine action)
  • via inhibition of D cells decreases the inhibitory effect of ss on G-cells
50
Q

Explain the gastric phase.

A
  • distension of stomach activate reflexes that cause acid secretion at enteric neurones
  • protein digestion stimulates amino acids and enzymes
  • these has an effect on G cells which stimulates secretion
51
Q

what inhibits gastric acid secretion?

A
  • vagal nerve activity decreases upon cessation of eating and following stomach emptying
  • antral pH falls when food exits stomach so release of somatostatin from D cells recommences, decreasing gastrin secretion
  • The factors that reduce gastric motility also reduce gastric secretion
52
Q

how do proton pump inhibitors influence acid secretion?

A

block acid secretion
- block the activity of the proton pump in an irreversible manner by covalently modifying it in the membrane to block its function

53
Q

how doe NSAIDs influence acid secretion?

A

block enzyme cyclooxyrgenase by reducing inhibitory effect of prostaglandin to increase acid secretion

54
Q

how does Muscarinic receptor antagonists influence acid secretion?

A

competitively block the muscarinic receptors on ECL and parietal cells

55
Q

how do H2 histamine receptor antagonists influence acid secretion?

A

act in competitive manner and reversible manner to block the H2 receptors of histamine

56
Q

what on the surface of the the stomach lining continually produce mucous and prostaglandin?

A

surface mucous cells

57
Q

what does the mucous form on the surface of the stomach?

A

forms a gel that has a significant thickness that lives over the epithelium that is reinforces by a hydrophobic monolayer

58
Q

what layer is impermeable to protons?

A

hydrophobic monolayer

59
Q

bicarbonate secreted by the mucous cells does what?

A
  • buffers any protons able to cross the hydrophobic layer creating a strong pH gradient between the lining and the contents of the stomach
60
Q

what do Prostaglandins

do?

A
  • reduce acid secretion
  • increase mucus and bicarbonate secretion
  • increase mucosal
    blood flow
61
Q

what is a Peptic Ulcer?

A

refers to any ulcer in an area where the mucosa is exposed to HCL and pepsin

62
Q

what is a peptic ulcer associated with?

A

with a shift in the balance between mucosal-damaging and mucosal-protecting mechanisms

63
Q

what do NSAIDs do?

A

Reduce prostaglandin formation and

  • trigger gastric ulceration
  • cause bleeding
64
Q

how can a stable prostaglandin analogue can treat gastric damage due to long term NSAID treatment

A
  • inhibits basal and food-stimulating gastric acid formation
  • maintains or increases secretion of mucus and bicarbonate
65
Q

Drug treatment for peptic ulcer aims to promote healing by?

A
  • reducing acid secretion
  • increases mucosal resistance
  • eradicating bacteria
66
Q

what are drugs that reduce acid secretion used to treat?

A
  • peptic ulcer
  • gastro-oesophageal reflux disease
  • acid hypersecretion
67
Q

what are the Mechanism on anti-secretory drugs?

A
  • inhibition of the proton pump
  • competitive antagonism of histamine H2 receptor
  • competitive
    antagonism of M1 and M3 ACh receptors
  • antagonism of gastrin receptors

GI Physiology (5 decks)

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