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ILA > 5. GORD > Flashcards

5. GORD Flashcards

1
Q

what substance is secreted by D cells?

A

Somatostatin

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2
Q

what substance is secreted by Enterochromaffin (ECL) cells?

A

histamine

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3
Q

what substance is secreted by G cells?

A

Gastrin

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4
Q

what substance is secreted by Chief cells?

A

Pepsinogen

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5
Q

what is the function of intrinsic factor produced in the stomach

A

allows absorption of vitamin B12 in the terminal ileum

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6
Q

how do NSAIDs irritate the stomach

A

by inhibition of gastrointestinal mucosal cyclo-oxygenase (COX) activity

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7
Q

how many layers of muscle are present in the stomach wall?

A

3 (longitudinal layer, circular layer, oblique layer)

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8
Q

what is the change in cell type (metaplasia) seen in the lower oesophagus after prolonged reflux of acid?

A

stratified squamous to columnar

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9
Q

describe the function of the vagus nerve and its action on parietal cells

A

Vagus nerve is part of the parasympathetic system and releases acetylcholine onto parietal cells

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10
Q

where does the common bile duct drain into?

A

Duodenum

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11
Q

what vessel supplies arterial blood to the jejunum?

A

superior mesenteric artery

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12
Q

what is the function of the drug ‘Omeprazole’ on the GI tract?

A

inhibition of proton pump to reduce acid secretion

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13
Q

what is the first location that fat is acted upon by lipase enzymes when passing through the GI tract?

A

oral cavity

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14
Q

describe oesophageal motility

A
  • Contractions in oesophagus help propel food bolus towards the stomach
  • A ring of skeletal muscle surrounds the oesophagus just below the pharynx to form the upper oesophageal sphincter
  • Smooth muscle in the last part of the oesophagus forms the lower oesophageal sphincter
  • Food enters the oesophagus when the upper oesophageal sphincter relaxes but it closes once again when food enters
  • Food then moves towards the stomach by peristalsis (progressive wave of muscle contractions moving along oesophagus compressing the lumen and forcing food towards the stomach)
  • Each wave takes about 9 seconds to reach the stomach
  • The lower oesophageal sphincter remains open and relaxed throughout swallowing allowing food to enter the stomach. After all the food passes it closes resealing the junction between the oesophagus and the stomach.
  • When this either stops or is irregular the patient is said to have oesophageal dysmotility.
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15
Q

gastric motility - changing volume for food

A
  • The volume of the stomach increases while eating due to receptive relaxation occurring in the smooth muscle in the body and fundus. This process barely increases luminal pressure.
  • Receptive relaxation is mediated by the PARASYMPATHETIC NERVOUS SYSTEM (via the Vagus nerve) acting on enteric nerve plexuses. These plexuses then release N02 and Serotonin which mediate the relaxation.
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16
Q

gastric motility - peristalsis

A
  • This is the process in which material is propelled from the upper GI tract to the lower GI tract and begins in the stomach
  • It is co-ordinated by a set of pacemaker cells
  • Initially peristaltic waves begin in the gastric body leading to a weak contraction of the body and little mixing
  • There is a more powerful contraction in the gastric antrum and the pylorus closes as the peristaltic wave reaches it.
  • Little chyme enters the duodenum (due to closed pylorus) and antral contents are forced back to the body (mixing). This leads to a churning action.
17
Q

pacemaker cells

A
  • The pacemaker cells are interstitial cells of Cajal and are present in the wall of the stomach
  • These are found in the muscularis propria and depolarise 3x a minute
  • There is a slow depolarisation repolarisation cycle among these cells.
  • The waves are transmitted through gap junctions to adjacent smooth muscle cells
  • The strength of the waves varies (dependent on wide range of factors such as presence of hormones)
  • Action potentials are only generated when the threshold level is reached.
18
Q

how is the strength of peristaltic contractions increased?

A

gastrin and gastric distension (mediated by mechanoreceptors)

19
Q

gastro-oesophageal reflux

A
  • Since the lowest part of the oesophagus is below the diaphragm it is subject to the same abdominal pressures as the stomach so if the pressure in the abdominal cavity increases the pressure above and below the lower oesophageal sphincter simultaneously. This prevents the formation of a pressure gradient between the stomach and the oesophagus forcing food into the oesophagus.
  • However when the lower oesophageal sphincter relaxes small amounts of stomach acid reflux into the oesophagus. This is normal and the acid triggers a second peristaltic wave as well as increasing salivary secretion helping to neutralise the acid.
  • Although this is normal in some people who have less effective lower oesophageal sphincters a condition caused Gastro-oesophageal reflux (acid reflux) arises.
  • In GOR the hydrochloric acid from the stomach irritates the oesophageal walls leading to heartburn (a type of referred pain where the patient feels pain in the chest although the issue is in the upper GI tract)
20
Q

describe the physiology of acid production in the stomach

A
  • HCl produced by parietal cells in the stomach
  • water and CO2 react to produce carbonic acid - catalysed by carbonic anhydrase
  • carbonic acid dissociates to form H+ and HCO3- ion (bicarbonate ion)
  • the H+ ion formed is transported into the lumen of the stomach via the H+/K+ ATPase pump (uses ATP as energy source to exchange 1 K+ ion into the parietal cell for every 1 H+ out into the stomach) - that ensures the polarity of the cell doesn’t change
  • bicarbonate ion transported out of cell into the blood via an anion exchanger transport protein in exchange for a Cl- ion. The chloride ion is transported into the lumen of the stomach via a chloride channel.
  • so both H+ and Cl- ions in the lumen
21
Q

control of acid production

A
  • At rest - not much H+ and K+ ATPases present in parietal cell membrane, the rest are in tubulovesicles in parietal cells
  • more vesicles fuse with cell membrane, leading to an increase of H+ and K+ ATPases into the membrane - so there’s an increased movement of hydrogen ions into stomach, so increase in acid production
22
Q

increasing acid production

A
  • 3 main ways:
  • during CEPHALIC PHASE: activated when seeing or chewing food Acetylcholine (Ach) is released from the vagus nerve
  • leads to direct stimulation of parietal cells
  • produced during gastric phase of digestion when the intrinsic nerves detect stomach distention - also stimulates release of acetylcholine via vagus nerve
23
Q

release of gastrin

A
  • secreted by G cells in the stomach
  • G cells activated by vagus nerve, gastrin related peptide and peptides in stomach lumen produced in protein digestion
  • When G cells are activated, gastrin is produced - released into blood - travels through blood to parietal cells
  • gastrin binds to CCK (cholecystokinin) receptors on parietal cells increases calcium levels
  • causes more fusion of vesicles with the cell membranes which increase the amount of H+ moving into the stomach, causing an increase in acid production.
24
Q

ECL cells

A
  • secrete histamine, histamine binds to H2 receptors on parietal cells
  • cells release histamine in response to presence of gastrin and acetylcholine
  • increased vesicle fusion
  • this happens via secondary messenger - cAMP not via calcium.
25
Q

decreasing acid production

A
  • accumulation of acid in empty stomach within meals
  • increase in acid leads to lower pH within stomach
  • inhibits secretion of gastrin via production of somatostatin from D cells when food is broken down into chyme it passes down the duodenum triggers enterogastric reflex - stimulated by distension of small bowel
  • if excess acid in upper intestine - presence of protein breakdown products and excess irritation to mucosa
  • Inhibitory signals are sent to the stomach via the enteric nervous system, as well as signals to medulla - reduces stimulation of vagus nerve
  • process slows down gastric emptying when intestines are already filled
  • presence of chyme also stimulates entero-endocrine cells to release cholecystokinin and secretin - inhibit gastric acid secretion.
26
Q

mucus-bicarbonate layer

A
  • In both the stomach & duodenum, there is a mucus-bicarbonate layer that sits on top of the mucosa & acts as a first defence against HCl and pepsin
  • This is due to the mucous cells (simple columnar cells) that are present, which secrete a bicarbonate-rich mucus
  • This creates a mucus-bicarbonate gel layer adherent to the epithelium that maintains a pH of around 7 (in contrast to the luminal pH, which is around 1.5-2 due to the presence of H+ ions)
  • The mucus layer provides a pH gradient and an area in which the secreted bicarbonate ions (HCO3-) can neutralise acid that is moving towards the mucosa through diffusion: HCO3- + H+ -> H2CO3 -> H2O + CO2
  • The mucus is also impermeable to pepsin
  • The secretion of bicarbonate is an active process and is activated by vagal stimulation & fundic distension
27
Q

tight epithelial junctions

A

• The tight junctions between the epithelial cells prevent HCl from leaking between them and reaching the submucosa

28
Q

gastric mucosal blood flow

A
  • Sufficient blood flow through the capillary supplies the epithelium with nutrients and oxygen, enabling it to dispose of any H+ ions that enter the mucosa
  • This prevents mucosal hypoxia
29
Q

rapid mucosal repair

A
  • There is a rapid cell turnover at the surface mucous cells, meaning superficial corrosion to the epithelium can be repaired within half an hour to an hour
  • The regenerated epithelial cells are able to migrate to the site of damage and repair the wound
  • This process is called restitution
30
Q

prostaglandins

A
  • Maintain gastric mucosal blood flow

* Enhance the pH gradient in the mucus-bicarbonate layer (by mediating bicarbonate secretion)

31
Q

GORD can be caused or made worst by

A
  • Certain food and drink
  • Being overweight
  • Smoking
  • Pregnancy
  • Stress and anxiety
  • Some medicines, such as anti-inflammatory painkillers (like ibuprofen)
  • A hiatus hernia

ILA (9 decks)

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