Gastric Motility and Secretion Flashcards

(30 cards)

1
Q

What are the main functions of the stomach?

A
  • stores food
  • mixes and digests food
  • empties contents into the small intestine
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2
Q

What are the 3 main steps of gastric motility?

A
  • Receptive relaxation
  • mixing/peristalsis (contractions)
  • gastric emptying
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3
Q

what are the two areas that the stomach is divided into?

A
  • Orad region: receptive relaxation
  • Caudad region: retropulsion, mixing
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4
Q

What is peristalsis?

A

the rhythmic contraction of smooth muscle in the walls of the GI tract that pushes contents forward, in the esophagus, stomach and intestines

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5
Q

What is receptive relaxation and what controls it?

A

when the upper stomach (orad region) relaxes to receive food bolus, controlled by the vagovagal reflex using VIP and nitric oxide

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6
Q

What are interstitial cells of Cajal (ICCs)?

A

gastric pacemaker cells that set the rhythm for stomach contractions and direct their flow toward the pylorus

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7
Q

What occurs during gastric mixing and Trituration?

A
  • lower stomach contracts to mix and grind the food
  • large particles undergo retropulsion to mix further until they’re small enough to pass
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8
Q

What stimulates gastric contractions during fasting?

A

Motilin stimulates periodic contractions called migrating myoelectric complexes to clear the stomach

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9
Q

What triggers Gastric secretion?

A
  • Vagal stimulation (ACh & GRP)
  • Gastrin from G-cells
  • Histamine from ECL cells
  • Food (especially protein) and stomach distension
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10
Q

What occurs once gastric secretion is triggered?

A
  • parietal cells secrete HCl and intrinsic factor
  • Chief cells release pepsinogen → activated to pepsin by HCl
  • G-cells (in antrum) release gastrin → stimulates HCl via ECL cell → histamine release
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11
Q

What is the “alkaline tide”?

A

After eating, bicarbonate (HCO₃⁻) enters the blood as a result of HCl production, making venous blood temporarily alkaline
* H+/K+-ATPase pumps pump H+ into the lumen to form HCl

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12
Q

What occurs during gastric emptying?

A

well-mixed chyme moves toward the pylorus where particles <1 mm pass; larger ones are pushed back

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13
Q

What is the lower esophageal sphincter and what happens if it isnt functioning?

A

prevents acid from entering the esophagus
** If barrier is compromised, it can lead to esophagitis or possibly esophageal cancers

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14
Q

What inhibits acid secretion in the stomach and what medications block these inhiibitors?

A

Somatostatin and prostaglandins inhibit acid secretion through Gi-protein pathways
- NSAIDs, aspirin, ethanol inhibit PG formation

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15
Q

What two reflex pathways are triggered when stomach stretch receptors are activated?

A
  • Short Reflex (ENS): oxyntic glands secrete HCl and Pepsinogen
  • Long Reflex (Vagovagal Reflex): dorsal vagal complex → signals back down the vagus nerve to release gastrin-releasing peptide (GRP) → G-cells → gastrin into the bloodstream → oxyntic glands → more HCl and pepsinogen
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16
Q

what are the 3 phases of gastric secretion?

A
  • Cephalic: smell, taste, conditioning
  • Gastric: distension, small peptides, amino acids
  • Intestinal: products of protein digestion
17
Q

What slows gastric emptying?

A
  • *fats (via CCK)
  • *acid (via ENS reflexes)
  • nerves (enterogastric reflex)
  • high caloric/dense meal
  • hyperosmolarity
  • food particle size
  • distension of duodenum
    *main
18
Q

What is gastroparesis?

A

abnormally slow gastric emptying, often linked to obesity or diabetes

19
Q

What is amylin?

A

molecule co-secreted with insulin to
- Decreases pancreatic exocrine and bile acid secretions
- stimulate satiety
- Slows gastric emptying and glucagon secretion

20
Q

What is intrinsic factor and where is it made?

A

made by parietal cells in the stomach and is needed to absorb vitamin B12 in the ileum

21
Q

What are the 4 main components of gastric juice?

A
  • HCl
  • pepsinogen
  • intrinsic factor
  • mucus
22
Q

What is Emesis?

A

stimulation of sensory afferent pathways to a higher center or chemoreceptor trigger zone (CTZ) to initiate the vomiting reflex

23
Q

what happens during the expulsion phase of emesis?

A
  • Inhibition of respiration, airway closure and diaphragm descent
  • Increased salivation –> protect dentition
  • Inhibition of gastric motility and inhibition of LES, UES, and pyloric motor activities
    (i.e., opens these sphincters)
24
Q

What is nausea and what are its triggers?

A

a conscious recognition that a food or toxin has been ingested
- GI tract or heart (mechanoreceptors or chemoreceptors) —-> CN IX or X —-> medulla oblongata
- cerebral cortex (food avoidance behaviors)
- change in the vestibular system (motion sickness)

25
what is Bulimia Nervosa
is an eating disorder with significant associated physical complications like - dental enamel and dentin damage - trauma to the oral and esophageal mucosa - salivary capacity reduction - gland enlargement - SEVERE----> electrolyte and fluid imbalances
26
What causes ulcers?
- too much acid (H⁺/pepsin) - weak protective barriers (mucus, HCO₃⁻, blood flow)
27
What causes an increase in peptic ulcer disease?
Gastritis (inflammation) increases ulcer risk, and causes include H. pylori and NSAIDs.
28
How does H. pylori cause ulcers?
makes urease to survive stomach acid, releases toxins, and reduces somatostatin, increasing acid secretion
29
what happens with Duodenal Ulcers?
excess H+ is delivered to the duodenum and can overwhelm the buffering capacity of HCO3- in pancreatic juices
30
What is Zollinger-Ellison syndrome (ZES) and what does it cause?
ZES is caused by a gastrin-secreting tumor (gastrinoma) that leads to: - Very high H⁺ (acid) secretion - No negative feedback, so gastrin keeps rising - Parietal cell growth (trophic effect) - Acid overwhelms HCO₃⁻, inactivates enzymes → poor fat digestion + steatorrhea *Treated with PPIs until tumor removal