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Z-GI > The Oesophagus, Stomach and Their Functions > Flashcards

The Oesophagus, Stomach and Their Functions Flashcards

1
Q

what is the oesophagus?

A

is a muscular tube that begins at the pharynx and ends at the stomach

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2
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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3
Q

what is the structure of the oesophagus?

A

has walls with general organisation of that of the intestine and is bounded by the upper and lower oesophageal sphincters

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4
Q

what lines the oesophagus?

A

stratified squamous epithelium

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5
Q

what is the musculature of the oesophagus?

A

striated in the upper third, smooth in the remainder, both organised as outer longitudinal and inner circular layers

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6
Q

what nerve innervates the oesophagus and supplies the muscle directly ?

A

Vagus nerve

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7
Q

what indirectly supplies the oesophagus?

A

the myenteric and submucous plexus

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8
Q

what does the swallowing centre do?

A
  • found in pons and medulla
  • triggers closure of the upper oesophageal sphincter (once food has entered the oesophagus) and also a primary peristaltic wave via vagus
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9
Q

how is the primary peristaltic wave mediated?

A

by skeletal muscle proximally and smooth muscle distally regions

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10
Q

What occurs during peristalsis?

A

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

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11
Q

what happens if sticky food becomes lodged?

A

stimulating local pressure receptors that cause:

  • secondary peristaltic wave - more forceful than primary – locally triggered
  • increased saliva production
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12
Q

what are the functions of the stomach?

A
  • relaxes receptively (driven by vagus) to accommodate food from oesophagus
  • Starting point for digestion of proteins (by pepsin and HCl), continues carbohydrate digestion
  • mixes food with gastric secretions to produce semi-liquid chyme
  • limited amount of absorption
  • stores food before passing it into small intestine as chyme for further digestion and absorption
  • Secretes approximately 2 litre/day of gastric juice from gastric glands in the gastric mucosa
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13
Q

what is the fundus?

A
  • Next to oesophagus
  • Thin smooth muscle layer
  • Receives food but little mixing
  • Little food stored there – usually a pocket of gas
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14
Q

what is the body?

A
  • Middle section
  • Thin smooth muscle layer
  • Little mixing
  • Food stored here
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15
Q

What is the Antrum?

A
  • Next to duodenum
  • Thicker smooth muscle layer
  • Highly contractile
  • Much mixing of c 30mL at a time with gastric secretions
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16
Q

what happens during gastric mixing and emptying?

A
  • Food mixed by the churning action of gastric smooth muscle against a closed pyloric sphincter
  • Peristaltic contraction driven by supra-threshold gastric slow-wave (3 min-1)
  • The pylorus opens only intermittently to allow the movement of chyme into the duodenum
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17
Q

what determines the escape of chyme through pyloric sphincter?

A

The strength of the antral wave

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18
Q

what effects the strength of the astral wave?

A
  • gastric factors

- duodenal factors

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19
Q

Describe the gastric factor.

A

Rate of emptying proportional to volume of chyme in stomach :
Distention increase motility due to stretch of smooth muscle, stimulation of intrinsic nerve plexuses and increased vagus nerve activity and gastrin release

Consistency of chyme - emptying facilitated by thick liquid chyme

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20
Q

Describe the duodenal factor.

A

Duodenum must be ready to receive chyme: delays emptying by:

  • neuronal response -the enterogastric reflex – decreases antral activity by signals from intrinsic nerve plexuses and the ANS
  • Hormonal response – release of enterogastrones [e.g. secretin and cholecystokinin CCK)] from duodenum inhibits stomach contraction
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21
Q

what stimulis within the duodenum drive the neuronal and hormone response?

A
  • Fat -particulary potent-delay in gastric emptying required for digestion and absorption in small intestine
  • Acid – time is required for neutralization of gastric acid by bicarbonate-rich juice secreted from the pancreas (important for optimal function of pancreatic digestive enzymes)
  • Hypertonicity – products of carbohydrate and protein digestion are osmotically active and draw water into the small intestine – danger of reduced plasma volume and circulatory disturbances (e.g. ‘dumping syndrome
  • distension
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22
Q

what cells are responsible for synthesis and release of gastrin?

A

G cells

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23
Q

what helps with secretion of gastrin and what secrets it?

A

Somatostatin released from D cells

24
Q

what do parietal cells do?

A

responsible for synthesis and release of hydrochloric acid and the release of intrinsic factor and gastroferrin which are important in synthesis of vitamin B12 and the movement of iron

25
Q

what do chief cells do?

A

secrete pepsinogen in the pit of the stomach

26
Q

what does enterochromaffin do?

A

releases histamine which acts as a local hormone regulating release of gastric acid

27
Q

what is the function of HCL secretion?

A
  • Activates pepsinogen to pepsin
  • Denatures protein
  • Kills most (not all) micro-organisms ingested with food
28
Q

what is the function of pepsinogen secretion?

A

Inactive precursor of the peptidase, pepsin. Note: pepsin once formed activates pepsinogen (autocatalytic)

29
Q

what is the function of intrinsic factor and gastroferrin secretion?

A

Bind vitamin B12 and Fe2+ respectively, facilitating subsequent absorption

30
Q

what is the function of histamine secretion?

A

Stimulates HCl secretion

31
Q

what is the function of mucus secretion?

A

protective

32
Q

what is the function gastrin secretion?

A

Stimulates HCl secretion

33
Q

what is the function of somatostatin secretion?

A

Inhibits HCl secretion

34
Q

Describe the secretion of HCL by the gastric parietal cell.

A

CA (carbonic anhydrase) responsible for combining carbon dioxide with water to form carbonic acid which is unstable and immediately dissociates into a proton and an anion. The proton is released into the cytoplasm and actively pumped out the parietal cells into the gastric pit, the proton is extruded by a pump through the canaliculi into the lumen and then into the stomach. The secretion of proton releases on primary active transport by the proton pump against a strong concentration gradient.

Bicarbonate ion leaves on the basolateral membrane into the interstitial fluid of the blood. Needs a secondary transport system to leave provided by a CL/HCO3 antiporter, this couples the outward movement of HCO3 with the inward movement of Cl, this creates a membrane gradient that drives the Cl out of the parietal cells on the apical membrane via a Cl channel, The proton pump intakes K this can move back across the membrane by a K channel, or K entering the cell via Na/K ATPase can also exit the cell on the apical membrane via K channels

35
Q

Describe the regulation of hydrochloric acid secretion from the gastric parietal cell.

A
  • 3 major influences that increase gastric acid: acetylcholine, gastrin and histamine
  • Histamine – produced by G cells, acts locally, acts on the H2 reeptors so again increasing activity of proton pump
  • Acetylcholine – released in the activated by vagus nerve and activates muscarinic receptors (M3), increasing activity of proton pump on the parietal cells
  • Indirect pathway is ACH and histamine reacting on the ECL cells which then stimulate parietal cells to increases activity on proton pump
  • Locally produced prostaglandins activate prostaglandin receptors which can cause the inhibition of the stimuli that increase gastric acid production
  • Drugs like aspirin and ibruprofen block the prostaglandin receptors so stop the stomach from digesting itself and result in gastric ulcer formation
  • Somatostatin is released from D cells and inhibits the release of gastrin from the D cells, this happens in between meals and stops the production of acid in the absence of meals
  • pH is lowest in the absence of food
36
Q

where are protein pumps found when there is an absence of acid secretion?

A

found in tubulovesicles and are inactive

37
Q

When do protein pumps move to the surface?

A

In the presence of the 3 factors : ACh, gastrin and histamine

38
Q

what are the 3 phases of gastric acid secretion?

A
  • cephalic phase
  • gastric phase
  • intestinal phase
39
Q

Describe the cephalic phase.

A

“in the head”

  • 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
40
Q

Describe the gastric phase.

A

when food is in stomach

  • distension of stomach activates reflexes that cause acid secretion
  • food buffers pH, D cell inhibition via ss of gastrin release is decreased
  • amino acids (e.g. tryptophan, phenylalanine) stimulate G cells. Other stimulants include: Ca2+, caffeine and alcohol
41
Q

Describe the intestinal phase.

A

after food has left stomach
-chyme entering the upper small intestine causes weak stimulation of gastric section via neuronal and hormonal mechanisms

42
Q

What is the inhibition of the cephalic phase?

A

vagal nerve activity decreases upon cessation of eating and following stomach emptying

43
Q

what is the inhibiton of the gastric phase?

A
  • antral pH falls when food exits stomach (due to decreased buffering of gastric HCl) – release of somatostatin from D cells recommences, decreasing gastrin secretion
  • prostaglandin E2 (PGE2) continually secreted by the gastric mucosa acts locally to reduce histamine- and gastrin-mediated HCl secretion
44
Q

what is the inhibition of the intestinal phase?

A

The factors that reduce gastric motility also reduce gastric secretion (e.g. neuronal reflexes,enterogastrones)

45
Q

what effect does increased pain nausea and negative emotions have?

A

decrease vagal nerve activity (parasympathetic) and increase sympathetic activity that combined reduce gastric acid secretion

46
Q

what drugs can influence acid secretion?

A
  • Proton pump inhibitors are v effective drugs that inhibit acid secretion. They covalently modify the proton pump in the apical membrane and block its function. Therefore for acid secretion to commence new proton pumps would need to be delivered
  • Other drugs block H2 receptors
  • Muscarinic antagonists block the muscarinic receptors on the ECL cells and the parietal cells
47
Q

what is the purpose of the mucous gel layer?

A
  • to protect stomach from acid and pepsin
  • Acid can destroy the mucous too so mucous needs to be continually renewed to keep the gel layer, prostaglandins are important for this
48
Q

what do locally produced prostaglandins do?

A
  • reduce acid secretion
  • increase mucus and bicarbonate secretion
  • increase mucosal blood flow
49
Q

what are peptic ulcer?

A

any ulcer in an area where the mucosa is exposed to HCl and pepsin (stomach, duodenum)

50
Q

how does a peptic ulcer develop?

A

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

51
Q

what do non-steroidal anti-inflammatory drugs do?

A

-reduce prostaglandin formation and may : trigger gastric ulceration or cause bleeding

52
Q

what is an imprtant factor of the development of a peptide ulcer?

A

chronic infection of gastric Antrum with bacterium H. Pylori

53
Q

Describe the formation of a peptide ulcer by H.Pylori.

A
  • H. Pylori, protected in mucus gel, secretes agents causing a persistant inflammation that weakens the mucosal barrier
  • Breakdown of mucosal barrier damages the mucosal cell layer and leaves the submucosa (and deeper layers) subject to attack by HCl and pepsin
54
Q

How does drug treatment of peptide ulcer aim to promote ulcer healing?

A
  • reducing acid secretion
  • increasing mucosal resistance
  • eradicating H. pylori
55
Q

What are drugs that reduce gastric acid secretion used to treat?

A
  • peptide ulcer
  • gastro-oesophageal reflux disease (inappropriate relaxation of lower oesophageal sphincter allowing reflux of acid gastric contents into the oesophagus and subsequent tissue damage
  • acid hypersecretion
56
Q

what mechanism are used to produce this anti-secretatory activity?.

A
  • inhibition of proton pump
  • competitive antagonism of histamine H2 receptors
  • competitive antagonism of muscarinic M1 and M3 Each receptors
  • antagonism of gastrin receptors

Z-GI (5 decks)

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