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GI Term 4 > 4.1- The Stomach > Flashcards

4.1- The Stomach Flashcards

1
Q

What is the general function of the stomach?

A

stores food, disinfects it and breaks it down to chyme

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2
Q

What is the mechanical function of the stomach?

A

-stores food for 3-4 hours -forms chyme by: peristaltic movement of stomach mixes the bolus with gastric juice and forms chyme

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3
Q

What is the haematopoeitic function of the stomach?

A

-intrinsic factor helps in erythropoiesis and helps absorption of Vit B12 -Deficiency of B12 causes macrocytic anaemia called PERNICIOUS ANAEMIA

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4
Q

What is the secretory function of the stomach?

A

-HCl activates pepsinogen in pepsin -provides acid environment for action of hormones

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5
Q

How does gastric mucosa appear when the stomach is empty?

A

-thrown into longitudinal folds; RUGAE -has openings called gastric pits -gastric glands empty into bottom of pits

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6
Q

What are the 3 types of gastric glands?

A

-Cardia -Fundus and body -Pyloric

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7
Q

What type of glands does the cardia contain?

A

mucus secreting glands

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8
Q

What type of cells do the fungus and body contain?

A

1) PARIETAL CELLS: HCl and intrinsic factor for B12 absorption ie acid secreting cells 2) MUCUS-SECRETING CELLS: gastrin; endocrine cells 3) CHIEF CELLS: secrete pepsinogen and gastric lipase

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9
Q

What cells does the pyloric region contain?

A

-mucus -G cells; secrete gastrin

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10
Q

IMP; Where do gastric ulcers occur usually?

A

-in the Antrum -lesser curvature of the stomach

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11
Q

What are the 4 secretory cells in gastric pits? (CPEN)

A

Chief cells-enzymes Parietal/oxyntic cells-acid Endocrine cells-gastrin Neck cells-mucus

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12
Q

How does a resitng parietal cell get activated into an acid secreting cell?

A

paritetal cells get stimulated by:

ACh

Gastrin

Histamine

therefore secrete acid via canaliculi for exit out of cells

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13
Q

Which cells in the stomach ATTACK?

A

Parietal and chief cells

Hydrochloric acid from parietal cells w a luminal pH below 2

Proteolytic enzymes from chief cells

pepsinogen gets converted ot pepsin

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14
Q

Which cells are responsible for DEFENCE?

A

mucus cells; secrete HCO3- and mucus

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15
Q
A
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16
Q

Describe the mechanism of HCl release from a parietal cell and which cells control its release?

A
  • The enteric galngion (From ANS ie myenteric and submucosal) releases STIMULATORY acetylcholine via postganglionic sympathetic nerves, stimulated by gastric distension as food arrives and acts on muscarinic receptors.
  • HISTAMINE is released by ECL (enterochromaffin like cells) and diffuses locally to parietal cells, where it activates H2 receptors. Histamine release is stimulated by gastrin and ACh
  • G cells secrete GASTRIN into blood and are stimulated by amino acids and peptides in stomach. Gastrin stimulates ECl cells to release histamine AND stimulates parietal cells to release HCl
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17
Q

Describe the interaction between parietal and chief cells

A
  • Parietal cells release HCl upon stimulation
  • This HCl in the gastric lumen catalases the conversion of pepsinogen released by Chief cells to PEPSIN (ACTIVE FORM)
  • Subsequent conversions occur quickly as a result of pepsin’s protease activity
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18
Q

What causes the negative feedback of HCl release ie what inhibits HCl release from parietal cells?

A
  • Somatostatin releasing cells ( D cells) detect high levels of HCl and therefore will release SOMATOSTATIN.
  • Somatostatin has an INHIBITORY EFFECT:
    1) It inhibits parietal cells from releasing HCL
    2) It inhibits ECL cells from releasing histamine ( which stimulates parietal cells)
    3) It inhibits G cells from releasing gastrin ( which stimulates parietal cells and ECL cells)
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19
Q

Describe the mechanism of seceretion of acid (chemical)

A
  • must be made from a slightly alkaline solution
  • 1 is to 1 ratio of alkali to acid
  • cells effectively split water into H+ ion and OH-
  • OH- combines with CO2 to produce HCO3-
  • H+ produced by mitchondria
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20
Q

What does acid production by parietal cells in the stomach depend on?

A

generation of carbonic acid

-subsequent movement of hydrogen aions into gastric lumen results from primary active transport

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21
Q

How is acid produced by parietal cells? Describe in detail

A
  • Hydrogen ions are generated in the parietal cell as carbonic anhydrase converts CO2 and H2O to carbonic acid(H2CO3) , which then dissociates
  • a countertransport mechanism ejects bicarbonate ions into intestinal fluid and imports chloride ions into cell
  • Chloride ions then diffuse across the parietal cell and exit through open chloride channels into the lumen of the gastric gland
  • similarly, the hydrogen ions produced are actively transported also into the lumen of the gastric gland THERFORE HYDROGEN IONS AND CHLORIDE FORM HCL IN GASTRIC GLAND LUMEN
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22
Q

How are parietal cells structurally adapted to acid seceretion?

A
  • Parietal cells have lots of mitochondria needed to produce H+ ions at a high rate BUT cannot accumulate in cells
  • Parietal cells have canaliculi, invaginations of cell wall
  • Canliculi have proton pumps, which expel H+ against HIGH CONC GRADIENT) secreting acid requires lots of energy
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23
Q

What are the 3 stimulatory signals that act on parietal cells for acid secretion?

A

1) Histamine from ECL cells ( entero chromaffin like cells)
2) Gastrin from G cells
3) Acetylcholine from ENS local control

24
Q

Which inhibitory signal acts on parietal cell?

A

Somatostatin from D cells

it inhibits:

G cells

ECL cells

HCl release from parietal cells

25
Q

Describe how gastrin, ACh and histamine stimulate HCl release?

A
  • Gastrin and Ach work by increasing intracellular calcium and activate protein kinases
  • Histamine works via a H2 receptor and by a cAMP mechanism (inhibited at H2 eg cimetidine)
  • all work synergistically
26
Q

What is gastrin?

A
  • polypeptide hormone secreted by G cells in stomach
  • binds to surface receptor on parietal cell
  • stimulates HCl and intrinsic factor secretion via second messenger pathway
27
Q

What is histamine? (GI edition)

A
  • released from ECL cells
  • binds to H2 surface receptor on parietal cell
  • stimulates acid secretion via cAMP
  • ECL cells are stimulated by:
  • gastrin
  • ACh
28
Q

What is ACh?

A
  • released from post ganglionic parasympathetic neurones
  • acts on muscarinic receptor on parietal cell
  • stimulates acid secretion by secondary messenger pathway
29
Q

Why are antagonists good at reducing acid secretion?

A

anatagonists eg cimetidine can do so because H2 receptors are uncommon

30
Q

What are the 3 phases of control?

A
  • Cephalic Phase
  • Gastric phase
  • Intestinal phase
31
Q

What is the Cephalic Phase?

A
  • sight and smell of food, and the act of swallowing activates parasympathetic system, which stimulates ACh release
  • ie detecting and ingesting food via autonomic sitmulation
  • ACh stimultes parietal cells directly and via histamine
32
Q

What is the Gastric Phase?

A

short reflexes via the stomach wall ie ENS

  • Food reaches the stomach, it distends the stomach, further stimulating ACh release
  • buffers stomach acid, so pH rises
  • disinhibits gastrin
  • stomach distends and stimulates intrinsic nerves and further releasing ACh, therefore pH rises to buffer acid in stomach in between meals
  • Initial digestion releases peptides, stimulating gastrin release
  • Histamine release is stimulated by gastrin and ACh
  • Rising pH DISINHIBITS gastrin secretion
  • Acid and enzymes act on proteins to produce peptides, thus further stimulating gastrin release; so pH falls and disinhibitio is removed
33
Q

What happens in the intestinal phase?

A

hormones are secreted by the duodenum

  • stomach begins to empty
  • chyme stimulates release from intestines of hormones which antagonize gastrin
  • accumulation of acid in empty stomach inhibits gastrin secretion
    *
34
Q

What is a result of stomach pH being low between meals?

A
  • can aggravate ulcers
  • night pain
  • once chyme leaves the stomach in significant quantities, it stimulates release of
  • cholecystokinin
  • GIP gastric inhibitory peptide

from intestines

35
Q

What hormones are active in the gastric phase?

A
  • food reaches stomach; buffers stomach, increasing pH therefore disinhibits gastrin
  • stomach disends; stimulates intrinsic nerves; releases ACh

INITIAL DIGESTION RELEASES:

  • Peptides stimulate gastrin release (therefore increased pH will disinhibit gastrin+somatostatin release and inhibitory effects are reduced)
  • Gastrin stimulates histamine release
36
Q

Why does the stomach need defenses?

A
  • luminal pH usually below 2; this would dissolve unprotected mucosa
37
Q

What are the stomach’s defenses?

A
  • surface cells of stomach mucosa secrete a thick layer of alkaline mucus
  • alkaline mucus offers mechanical protection
  • traps H+ ions diffusing into it from stomach lumen, they react with basic groups of mucous and w HCO3- ions produced from surface epithelial cells
  • prevents pH of surface mucosa cells from falling too low
  • production of defences is stimulated by prostaglandins
38
Q

How are the stomach’s defenses breached?

A
  • alcohol dissolves mucus
  • H. pylori
  • NSAIDS
39
Q

How do NSAIDS breach the stomach’s defenses?

A
  • inhibit prostaglandins and therefore reduce defences
  • eg aspirin, if converted into non-ionised form by stomach acid,pass into cells and then re-ionise
  • since defences are overwhelmed, acid attacks cells and produces gastritis and ulceration
40
Q

Name 2 ways in which acid secretion can be reduced?

A

1) Histamine receptor antagonists: H2-cimetidine
2) Proton pump inhibitors: Omeprazole
- also treat ulcers by eliminating H.Pylori with antibiotics

41
Q

What is RECEPTIVE RELAXATION?

A

a neural vagal reflec triggered by swallowing

  • efferent pathway via vagus N
  • Tension in resting stomach wall “actively” relaxed
  • Pressure in stomach does not increase as it fills; limits reflux

THEREFORE you can consume large meals

42
Q

Describe rhythmic contractions of the stomach?

A
  • stomach has longitudinal and circular muscle
  • driven by pacemaker in cardia region (3x/minute)
  • wave of peristalsis spreads towards antrum, accelerating as it goes
  • -*wave of peristalsis initially drives all stomach contents ahead of it
  • overtakes larger lumps as it acclerates; driven back into fundus
43
Q

How is chyme driven ONLY TOWARDS PYLORUS?

A
  • small squirt is ejected
  • then wave reaches pylorus and shuts it
  • rest of the chyme returns to the stomach
44
Q

Name the 4 steps of gastric emptying?

A
  • a peristaltic contraction originates in the upper fundus and sweeps down the pyloric sphincter
  • contaction becoes more vigorous as it reaches thick-muscled antrum
  • strong antral peristaltic contraction propels chyme forward
  • small portion of chyme is pushed through the partially opened sphincter in the duodenum. The stronger the antral contraction, the more chyme is emptied with each contractile wave
45
Q

Give the 2 steps of gastric mixing that happens after gastric emptying?

A
  • when peristaltic contraction reaches pyloric sphincter, the sphincter tightly closed and no further emptying takes place
  • when chyme that was being propelled forward hits the closed sphincter, it it tossed back into the antrum.

Mixing of chyme is accomplished as chyme is propelled forward and tossed back into the antrum w each peristaltic contraction

46
Q

What affects the volume of each squirt in gastric emptying?

A

three squirts a minute

  • rate of acceleration of peristaltic wave
  • affected by hormones from intestine
47
Q

What SLOWS gastric emptying?

A
  • fat in duodenum
  • low pH in duodenum
  • hypertonicity in duodenum

rate of stomach emptying matched to rate of digestion

48
Q

Define gastro-oesophageal reflux disease?

A

GORD

digestive disorder charactersed by an ineffective Lower Oesophageal Sphincter

Result: reflux of stomach contents into oesophagus+ resulting symptoms and pathology

49
Q

What is H. Pylori?

A
  • gram negative bacterium with a helical shape
  • major cause of peptic ulcerations
50
Q

How is H. Pylori adapted to survive the acidic conditions of the stomach?

A

1) Its flagellum and chemotaxis help it maintain its preferred position within the mucous layer of the stomach therefore avoids more acidic lumen
2) Produces enyme UREASE
- urease converts urea to NH3 and CO2
- NH3 utilises a H+ ion to become NH4+ therefore effectively neutralises acidic conditions surrounding the bacteria

51
Q

How do you confirm the presence of H. Pylori in a patient?

A

UREASE BREATH TEST

  • Patient swallows radio-labelled urea
  • 20 minutes later; if you can detect radio-labelled CO2, you can tell that H.Pylori is present
  • because it used urease to convert urea into NH3 and CO2
52
Q

Give an examples of a common H. pylori eradication therapy?

A

1 week of:

  • a proton pump inhibitor eg omeprazole
  • 2 of these antibiotics: metronidazole, clarithromycin, amoxicillin
53
Q

Why are PPI’s more effective than H2 antagonists at reducing stomach acid secretions?

A
  • parietal cells can produce H+ ions other than via H2 receptors
  • muscarinic ACh receptors. gastrin receptors and histamine receptors, with all when stimulated, also result in acid production
  • by blocking H2 receptors, there are still other inputs on parietal cells resulting in acid production
  • if you block the proton pump, then you are effectively blocking all these receptor inputs, as the common path ends at this point
54
Q

Give examples of:

A PPI

A H2 antagonist

A

PPI: omeprazole, lansoprazole

H2 antagonist: cimetidine, ranetidine

55
Q

How do NSAIDs cause peptic ulcers and gastritis?

A
  • NSAIDs are Cox1 inhibitors; Cyclo-oxygenase
  • COX converts arachidonic acid into prostaglandins
  • PgE ( prostaglandin E) is protective of dudodenal mucosa because it increases mucuous productgion and HCO3-
  • prostaglandins also increase mucosal blood flow therefore protective
56
Q

What tests are done to detemine the cause of upper Gi bleeding/ pain?

A

upper GI endoscopy

57
Q

How does high alcohol intake cause gastritis?

A
  • alcohol dissolves mucous
  • therefore acid irritates mucosa, causing gastritis

GI Term 4 (7 decks)

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