Gastrointestinal - Physiology Flashcards
1
Q
GI regulatory substances:
Cholecystokinin
- Source
- Action
- Regulation
A
- Source
- I cells (duodenum, jejunum)
- Action
- Increased pancreatic secretion
- Increased gallbladder contraction
- Decreased gastric emptying
- Increased sphincter of Oddi relaxation
- Acts on neural muscarinic pathways to cause pancreatic secretion
- Regulation
- Increased by fatty acids, amino acids
2
Q
GI regulatory substances:
Gastrin
- Source
- Action
- Regulation
A
- Source
- G cells (antrum of stomach)
- Action
- Increased gastric H+ secretion
- Increased growth of gastric mucosa
- Increased gastric motility
- Regulation
- Increased by stomach distention / alkalinization, amino acids, peptides, vagal stimulation
- Decreased by stomach pH < 1.5
- Really increased in Zollinger-Ellison syndrome.
- Increased by chronic PPI use.
- Phenylalanine and tryptophan are potent stimulators.
3
Q
GI regulatory substances:
Glucose-dependent insulinotropic peptide
- Source
- Action
- Regulation
- AKA
- Oral vs. IV glucose
A
- Source
- K cells (duodenum, jejunum)
- Action
- Exocrine: decreased gastric H+ secretion
- Endocrine: increased insulin release
- Regulation
- Increased by fatty acids, amino acids, oral glucose
- AKA
- Also known as gastric inhibitory peptide (GIP).
- Oral vs. IV glucose
- An oral glucose load is used more rapidly than the equivalent given by IV due to GIP secretion.
4
Q
GI regulatory substances:
Motilin
- Source
- Action
- Regulation
- Motilin receptor agonists
A
- Source
- Small intestine
- Action
- Produces migrating motor complexes (MMCs)
- Motilin receptor agonists (e.g., erythromycin) are used to stimulate intestinal peristalsis
- Regulation
- Increased in fasting state
- Motilin receptor agonists
- e.g., erythromycin
- Used to stimulate intestinal peristalsis.
5
Q
GI regulatory substances:
Secretin
- Source
- Action
- Regulation
A
- Source
- S cells (duodenum)
- Action
- Increased pancreatic HCO3– secretion
- Increased HCO3– neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function.
- Decreased gastric acid secretion
- Increased bile secretion
- Increased pancreatic HCO3– secretion
- Regulation
- Increased by acid, fatty acids in lumen of duodenum
6
Q
GI regulatory substances:
Somatostatin
- Source
- Action
- Regulation
- Notes
A
- Source
- D cells (pancreatic islets, GI mucosa)
- Action
- Inhibitory hormone.
- Decreased gastric acid and pepsinogen secretion
- Decreased pancreatic and small intestine fluid secretion
- Decreased gallbladder contraction
- Decreased insulin and glucagon release
- Antigrowth hormone effects (inhibits digestion and absorption of substances needed for growth).
- Inhibitory hormone.
- Regulation
- Increased by acid
- Decreased by vagal stimulation
7
Q
GI regulatory substances:
Nitric oxide
- Action
- Loss of NO secretion is implicated in…
A
- Action
- Increased smooth muscle relaxation, including lower esophageal sphincter (LES)
- Loss of NO secretion is implicated in…
- Increased LES tone of achalasia.
8
Q
GI regulatory substances:
Vasoactive intestinal polypeptide (VIP)
- Source
- Action
- Regulation
- VIPoma
A
- Source
- Parasympathetic ganglia in sphincters, gallbladder, small intestine
- Action
- Increased intestinal water and electrolyte secretion
- Increased relaxation of intestinal smooth muscle and sphincters
- Regulation
- Increased by distention and vagal stimulation
- Decreased by adrenergic input
-
VIPoma
- Non-α, non-β islet cell pancreatic tumor that secretes VIP.
- Copious Watery Diarrhea, Hypokalemia, and Achlorhydria (WDHA syndrome).
9
Q
GI regulatory substances:
Intrinsic factor
- Source
- Action
A
- Source
- Parietal cells (stomach)
- Action
- Vitamin B12–binding protein (required for B12 uptake in terminal ileum)
- Autoimmune destruction of parietal cells –> chronic gastritis and pernicious anemia.
10
Q
GI regulatory substances:
Gastric acid
- Source
- Action
- Regulation
- Gastrinoma
A
- Source
- Parietal cells (stomach)
- Action
- Decreased stomach pH
- Regulation
- Increased by histamine, ACh, gastrin
- Decreased by somatostatin, GIP, prostaglandin, secretin
-
Gastrinoma
- Gastrin-secreting tumor that causes high levels of acid secretion and ulcers refractory to medical therapy.
11
Q
GI regulatory substances:
Pepsin
- Source
- Action
- Regulation
A
- Source
- Chief cells (stomach)
- Action
- Protein digestion
- Regulation
- Increased by vagal stimulation, local acid
- Inactive pepsinogen –> pepsin by H+
12
Q
GI regulatory substances:
HCO3-
- Source
- Action
- Regulation
A
- Source
- Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum)
- Action
- Neutralizes acid
- Regulation
- Increased by pancreatic and biliary secretion with secretin
- HCO3- is trapped in mucus that covers the gastric epithelium
13
Q
Locations of GI secretory cells
- Gastrin
- Atropine
- Vagal stimulation of G cells
A
- Gastrin
- Increases acid secretion primarily through its effects on enterochromaffin-like (ECL) cells (leading to histamine release) rather than through its direct effect on parietal cells.
- Atropine
- Blocks vagal stimulation of parietal cells.
- Vagal stimulation of G cells
- Unaffected, as a different transmitter (gastrin-releasing peptide or GRP) is used, not ACh.
![](https://s3.amazonaws.com/brainscape-prod/system/cm/125/013/148/a_image_thumb.png?1659443544)
14
Q
Gastric parietal cell
A
![](https://s3.amazonaws.com/brainscape-prod/system/cm/125/014/086/a_image_thumb.png?1659443545)
15
Q
Brunner glands
A
- Located in duodenal submucosa.
- Secrete alkaline mucus.
- Hypertrophy seen in peptic ulcer disease.