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Block 1 > Gastric Motility And Secretion > Flashcards

Gastric Motility And Secretion Flashcards

1
Q

What are the functions of the stomach?

A

Store food

Minimize ingestion of bacteria via acidic pH

Dissolve + partially digest the macromolecules in food (semi-digested = chyme)

Regulate the rate at which the stomach contents empty into SI

Secrete IF

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2
Q

What does gastric motility allow the stomach to do?

A

Serve as a reservoir for a large volume of food

Fragment food into smaller particles + mix it with gastric secretions

Empty gastric contents into duodenum at a controlled rate

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3
Q

What are the 2 divisions of the stomach based on motility variations?

A
  1. Orad (superior body)

2. Caudad (inferior body)

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4
Q

What are the four layers of the GI tract wall from the lower oesophagus, down to the anal canal (from lumen outwards)?

A
  1. Mucosa
  2. Submucosa
  3. Muscularis (circular + longitudinal)
  4. Serosa
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5
Q

How much liquid has the empty stomach got in it?

A

50ml

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6
Q

What state is the stomach in when it is empty?

A

When the stomach is empty, it is contracted + the mucosa/submucosa are highly folded into rugae making it very small

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7
Q

What determines the gastric motility of a piece of GI tract?

A

The movements of the circular + longitudinal muscularis layer of the wall

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8
Q

What is receptive relaxation?

A

When food is swallowed, the SM in the wall of the orad region of the stomach relaxes + the rugae unfold enabling the stomach to increase in volume to as much as 1.5L with little pressure increase

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9
Q

How does the parasympathetic nervous system innervate the GI tract?

A

Vagal nuclei -> vagal nerves

Sacral spinal cord -> pelvic nerves

Innervates the ENS (myenteric + submucosal plexus) -> SM, secretory cells, endocrine cells + blood vessels

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10
Q

How does the sympathetic nervous system innervate the GI tract?

A

CNS preganglionic fibres -> sympathetic ganglia -> postganglionic fibres -> ENS (myenteric + submucosal plexus) -> SM, secretory cells, endocrine cells + blood vessels

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11
Q

What is the Enteric Nervous System (ENS)?

A

The GI tracts intrinsic localised innervation consisting of 2 nerve networks; myenteric plexus + submucosal plexus

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12
Q

How is receptive relaxation mediated?

A

By the vagus nerve which coordinates with the ENS which release NO + 5-HT which relax SM cells in the stomach wall

Also coordination with swallowing centre in brain

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13
Q

How does gastric motility allow the stomach to serve as a reservoir for a large volume of food?

A

Predominant motor activity of the orad region if the accommodation of ingested food (receptive relaxation) because muscle layers are thin so contracts in this region are weak + do not do much -> gastric contents remain in relatively undisturbed layers for an hour or > after eating

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14
Q

How does mixing occur in the stomach?

A
  1. Gastric contractions (peristaltic waves) begin in body of stomach + move towards the antrum
  2. As the wave approaches the antrum they become more powerful contractions
  3. Pyloric sphincter closes
  4. Most of antrum contents forced backwards into body of stomach (retropulsion) mixing food with acid + digestive enzymes whilst food is hitting the back
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15
Q

What is peristalsis?

A

Waves of alternating contractions + relaxations of SM layers that mix + squeeze the contents through hollow tubes to move a bolus along the GI tract

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16
Q

How does peristalsis occur?

A
  1. Contraction of circular muscles behind bolus
  2. Contraction of longitudinal muscles ahead of bolus
  3. Contraction in circular muscle layer forces bolus forward
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17
Q

What is segmentation?

A

Cycles of contraction that mix contents but do not push them in any one direction churning + fragmenting the bolus mixing it with intestinal secretions

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18
Q

How do GI tract contractions come about electrophysiologically?

A

Contractions derive from 2 basic patterns of electrical activity across the SMC membranes: slow waves + APs

SMC undergoes spontaneous cycles of depolarization + repolarization due to Na+ leaking out of cell then coming back in (basic electrical rhythm of GI tract) - this brings about slow waves as not strong enough to make APs

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19
Q

Why do slow waves happen?

A

Result from fluctuations in membrane potential spreading to adjacent sections of SM that are electrically coupled by gap junctions

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20
Q

What frequency do gastric slow waves occur at?

A

~3 per minute

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21
Q

What generates the gastric slow wave rhythm?

A

Pacemaker zone

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22
Q

What do slow waves do?

A

They DO NOT elicit contractions, they co-ordinate contractions by controlling the appearance of APs

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23
Q

How do action potentials come about after slow waves?

A

Excitatory neurotransmitters + hormones further depolarize the membrane increasing the slow wave amplitude

If the peak of a slow wave rises above a certain threshold, the cell fires one or > APs

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24
Q

What do action potentials (APs) do?

A

Elicit muscle contraction - no. + frequency of APs occurring at the slow wave peak determines the strength of muscle contraction

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25
Q

How does gastric emptying occur?

A

Coordinated contractile activity of the stomach, pylorus + proximal SI

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26
Q

Why does the body want to regulate gastric emptying?

A

Allows for optimal digestion + absorption of ingested material

27
Q

What is the pyloric sphincter?

A

Ring of SM + connective tissue between the gastric antrum + the duodenum

28
Q

What are the functions of the pyloric sphincter?

A
  1. Allows regulated emptying of gastric contents at a rate consistent with the ability of duodenum to process chyme
  2. Prevents regurgitation of duodenal contents back into the stomach
29
Q

How is the pyloric sphincter controlled?

A
  1. ANS: SNS fibres increase constriction whilst vagal fibres are excitatory or inhibitory
  2. GI tract hormones: gastrin, CCK, GIP + secretin elicit constriction
30
Q

How is gastric emptying regulated by the nature of the duodenal contents? Why?

A

Receptors on inner mucosa layer of duodenum + jejunum sense acidity, osmotic pressure, certain fats, AAs + peptides -> intestinal hormone release -> antral contraction inhibition/constriction of pyloric sphincter

So substances high in fat, very acidic/hypertonic decrease rate of emptying because products need to be emulsified + absorbed but GI tract cannot cope with too much in one go

31
Q

How much gastric juice does the stomach secrete a day?

A

2-3L

32
Q

What are the main components of gastric juice?

A
  1. HCl
  2. Mucus
  3. Digestive enzymes e.g. pepsinogens, gastric lipase
  4. IF
33
Q

Where is gastric juice secreted from?

A

Secretory epithelial cells in the gastric glands of gastric mucosa (innermost layer of stomach wall) into the lumen

34
Q

What are gastric glands?

A

Gastric pits that extend into mucosa as straight + branched tubules forming gastric glands lined with 4 types of secretory epithelial cells:

  • G cell
  • Chief cell
  • Parietal cell
  • Mucus cell (surface epithelial/neck)
35
Q

What do the secretory epithelial cells in the gastric glands do?

A

G: secrete gastrin

Chief: secrete pepsinogen(inactive precursor of pepsin)

Parietal: secrete HCl + IF

Mucus: secrete mucus

36
Q

Where are parietal cells found?

A

In the proximal 80% of the stomach (“oxyntic gland area”)

37
Q

Where are Gastrin-producing (G) cells found?

A

Antrum (“pyloric gland area”)

38
Q

Where are gastric hormones secreted? What do they do?

A

Gastrin, histamine + somatostatin are secreted by gastric glands

Control secretion of gastric juice

39
Q

Why is histamine not a true hormone?

A

It is a paracrine agent having local affects on neighbouring cells whereas true hormones are secreted into the circulation to affect distant targets in an endocrine fashion

40
Q

What is gastrin?

A

A polypeptide hormone secreted by G cells - principle hormone secreted from the gastric epithelium

41
Q

What effects does gastrin have?

A

Gastric:

  • Stimulate secretion of acid, pepsinogens, mucus + HCO3-
  • Gastric motility stimulation
  • Gastric emptying inhibition

Other:

  • Stimulate pancreatic enzyme + HCO3- secretion
  • Stimulate insulin release
  • Intestinal motility stimulation
42
Q

What is histamine?

A

A paracrine agent that has local effects; secreted by ECL cells scattered throughout the gastric mucosa close to parietal cells

43
Q

What are the effects of histamine?

A

Stimulate acid secretion

Increased local blood flow which supports metabolism increase associated with acid secretion

44
Q

What is somatostatin?

A

A polypeptide hormone synthesized by D cells in the antrum + body of stomach

45
Q

What are the effects of somatostatin?

A

Inhibits gastrin release

Inhibits acid secretion via parietal cell

46
Q

Why are stomach secretions so acidic?

A

[H+] in lumen may reach 150 mM producing a gastric luminal pH of 1-2

47
Q

Describe the specialized structure of parietal cells.

A

Truncated pyramidal shape with apex orientated toward gastric lumen

Extensive invaginations of luminal membrane forming canaliculi whose membranes are lined with ion pumps

High mitochondrial content (supplies energy requirement)

48
Q

How is acid secreted by parietal cells?

A
  1. H+ & HCO3- produced from CO2 + H2O (via CA)
  2. H+ secreted into lumen by H+/K+-ATPase pump (in exchange for K+)
  3. HCO3- moves out of cell, across basolateral membrane via antiport with Cl-
  4. Cl- diffuses passively into lumen via a Cl- channel
49
Q

How is gastric acid secretion regulated?

A

Stimulated by:

  • Gastrin
  • ACh
  • Histamine (release stimulated by gastrin + ACh)

Inhibited by:

  • Somatostatin
  • Prostaglandins E2 + I2
  • Intestinal hormones
50
Q

Where is acetylcholine (ACh) released from in the gut?

A

Near parietal cells from cholinergic parasympathetic nerve terminals

51
Q

How is gastric acid secretion stimulated by hormones?

A
  1. Gastrin (from blood vessels), ACh + histamine bind specific receptors on parietal cells; gastrin, muscarinic + H2 receptors
  2. AC produces cAMP
  3. PLC produces IP3
  4. Both products increase IC Ca2+
  5. Proton pump (H+/K+ exchanger) stimulated to pump H+ out of cell into stomach lumen
52
Q

How does somatostatin inhibit gastric acid secretion?

A

Binds to SSR on ECL + parietal cell having inhibitory effects on histamine production + acid production respectively

Inhibits gastrin

53
Q

How do prostaglandins inhibit gastric acid secretion?

A

PGE2 binds PGE2 receptor on parietal cell inhibiting the effects of ACh, histamine + gastrin via muscarinic, H2 + gastrin receptors

54
Q

What are prostaglandins?

A

A group of lipids derived from arachidonic acid made at sites of tissue damage/infection + can be made in nearly all organs in the body

55
Q

What are the functions of prostaglandins?

A

Involved in healing process

Control processes such as inflammation and blood flow

56
Q

What enzyme catalyses the first step of prostaglandin synthesis?

A

Cyclooxygenase (COX)

57
Q

What is mucus?

A

A mixture of glycoproteins + glycopolysaccharides that forms a gel (up to 200μm thick) on luminal surface of gastric mucosa

58
Q

How is mucus secretion stimulated?

A

By the same stimuli that elicit acid + pepsinogen secretion

59
Q

What is the gastric mucosal barrier?

A

Mucus + alkaline secretions (HCO3- secreted from gastric surface epithelial cells) entrapped within a viscous mucus gel layer which functions to:

  • Viscosity prevents it mixing rapidly with stomach contents keeping the pH near neutral
  • Protects the stomach against acid, proteolytic enzymes + mechanical damage
60
Q

How is the gastric mucosal barrier renewed?

A

Local mucosal irritation stimulates PG production -> increased mucus + HCO3- production, decreased acid secretion + healing of local damage

Stimuli of acid secretion promotes barrier secretions too

61
Q

What side effects do Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in relation to gastric acid secretion?

A

Inhibiting COX + interfering with PG production inhibiting the protective effects of PG

62
Q

How and why is pepsin secreted?

A
  1. Secreted as inactive precursor pepsinogen by chief cells
  2. Low pH in gastric lumen converts pepsinogen to pepsin so acid secretion parallel pepsin secretion
  3. Pepsin becomes active at low pH
  4. Pepsin accelerates protein digestion
63
Q

What is intrinsic factor (IF)? What does it do?

A

Glycoprotein ESSENTIAL for the absorption of vitamin B12 in the intestines; IF production is the ONLY indispensable function of the stomach

64
Q

What does vitamin B12 do? What will a deficiency lead to?

A

Essential for RBCs so deficiency will lead to pernicious anaemia

Block 1 (54 decks)

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