PNB 2775 Quiz 2

• What secretes gastrin?

  G cells
• Gastrin secretion is stimulated by:

  1. vagus nerve stimulation (gastrin releasing polypeptide (GRP))
  2. amino acids
• Gastrin secretion is inhibited by:

  1. acid
  2. somatostatin
• What is the function of gastrin secretion?

  acts on parietal CCK-B receptor and ECL cells to stimulate acid release and mucosa growth in stomach and intestines
• The paracrine secretes substances that influence neighboring cells
• What does the paracrine secrete?

  histamine, intrinsic factor, and somatostatin
• Histamine stimulates acid secretion, is secreted by ECL cells in the paracrine, and is stimulated by gastrin and ACh
• Intrinsic factor is secreted by parietal cells in the paracrine, is critical for B12 absorption (RBC production), and without it leads to pernicious anemia
• Somatostatin is secreted by D cells in paracrine, is stimulated by protons, and is the primary feedback signal
• The two enzymes that are secreted in the stomach are pepsin and gastric lipase
• Pepsin is secreted by chief cells as pepsinogen and is stimulated by acid and pepsin and is co-secreted with gastric lipase
• Pepsinogen (chief cell) and HCl (parietal cell) is secreted into the lumen, then histamine (ECL cell) is secreted into the lamina propia, and then gastrin (G cell) is released into the blood
• In the stomach feedback loop, acid in the antrum lumen stimulates somatostatin release to inhibit meal-stimulated gastrin secretion from the G cell into the blood
• Gastric secretion overview:

  1. food/cephalic reflexes initiates gastric secretion
  2. gastrin stimulates acid secretion by direct action on parietal cell or indirectly using histamine
  3. acid stimulates short reflex secretion of pepsinogen
  4. somatostatin released by acid in negative feedback signal that controls acid and pepsin release
• Gastric motility control is caused by neural control (vasovagal reflexes) through mechanical (ex. distention) and chemical (ex. presence of protein digestion products) stimulation, where responses vary between proximal and distal segments
• What are the stomach motor functions?

  storage and mixing
• The proximal stomach region is responsible for storage, while the distal region is responsible for mixing
• Receptive Relaxation is when the stomach relaxes as food moves through the esophagus and enters the stomach
• Adaptive relaxation is the relaxation once stomach is full and the stomach is empty
• Mixing of stomach contents in the distal region is done using peristalsis
• The stomach wall is not specialized for absorption, but is rather specialized for protection
• The stomach only absorbs aspirin, weak acids, and EtOH
• The protective characteristics of the stomach:

  1. thick, alkaline mucus
  2. tight junction between epithelial cells
  3. rapid replacement by GI stem cells
• Gastric ulcers are the destruction (necrosis) of lining of gastric mucosa, where the primary cause is the over-secretion of gastric acid
• The small intestine is composed of the duodenum (common bile duct and pancreatic duct), jejunum, and ileum (Peyer's patches (lymph nodules) and ileocecal valve)
• The supporting structures of the small intestine include plicae (circular folds) and villi
• During gastric emptying the stomach body (reservoir) becomes less relaxed and contracts too push down to prepare for emptying (pump region)
• Gastric emptying characteristics:

  1. strong peristaltic waves in gastric pump
  2. increase in tone (contraction) in gastric reservoir
  3. pyloric sphincter, which relaxes in the presence of VIP and nitric oxide, opens so food could move into the small intestine
  4. duodenum contractions are inhibited (relaxed)
• Gastric emptying is stimulated by:

  1. gastric volume
  2. neural
  3. gastrin
• Gastric emptying is inhibited by:

  1. enterogastric reflex (distention plus acid in duodenum)
  2. GIP
  3. CCK
  4. secretin
• All regulatory hormones for gastric emptying are secreted by the duodenum
• Gastric emptying rate could be increased by:

  1. increased peristaltic wave in gastric pump
  2. increased tonic contraction in gastric reservoir
  3. increased VIP in pyloric sphincter
  4. decreased protons in duodenum
• Dumping syndrome is a condition where the patient has a sudden onset of severe pain in the lower extremities as food (sugary) moves from the stomach into the small bowel too quickly after eating, which is a condition caused by lack of gastric emptying control
• When a gastrectomy is performed to remove dumping syndrome, there is a loss of emptying feedback control and may result in the critical loss of the intrinsic factor
• Symptoms of dumping syndrome are caused by hyperglycemia into hypoglycemia, resulting in sweating, high heart rate, nausea, and diarrhea
• Small intestine motility includes:

  1. segmentation contractions to allow for mixing and slow propulsion by frequency gradient
  2. peristalsis, which is weak in the small intestine
  3. migrating motor complex (MMC), which are migrating peristaltic waves to removes stuck, undigested food
• The migrating motor complex (MMC) is stimulated by motilin and inhibited by feeding
• The upper small intestine secretes cholecystokinin (CCK) from I cells and secretin from S cells
• Functions of cholecystokinin (CCK):

  1. stimulate pancreatic enzyme secretin by augmenting secretin functions
  2. gallbladder contraction
  3. relax sphincter of Oddi
  4. inhibit gastric emptying and secretion
• Cholecystokinin (CCK) is stimulated by:

  1. amino acid
  2. peptides
  3. fatty acids