PHYSIOLOGY: DIGESTIVE SYSTEM Flashcards
(39 cards)
1
Q
- Describe the functions of chewing.
- Describe the swallowing sequence and identify voluntary and involuntary components.
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2
Q
Describe the oral or voluntary phase of swallowing.
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3
Q
Describe the pharyngeal phase of swallowing.
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4
Q
Describe the esophageal phase of swallowing.
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5
Q
Describe the motor patterns of the stomach following ingestion of a meal.
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7
Q
Describe the peristaltic patterns of motility seen in the small intestine.
What does the motility do?
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Segmentation & Peristalsis
8
Q
Describe the segmenting seen in the small intestine.
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9
Q
Describe the basic electrical rhythm (BER) of each region of the GI tract. Explain the role of Interstitial Cells of Cajal in the origin and propagation of the BER.
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The interstitial cell of Cajal (ICC) is a type of interstitial cell found in the gastrointestinal tract. Myenteric Interstitial cells of Cajal serve as a pacemaker which creates the bioelectrical slow wave potential that leads to contraction of the smooth muscle.
10
Q
Describe Peristalsis
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11
Q
Describe Motility in the Fasting State
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12
Q
The type of GI movement primarily responsible for mixing chyme with digestive juices in the intestine is:
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13
Q
What are the small intestinal reflexes
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14
Q
Describe content movement in the large intestines.
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15
Q
Describe Colonic Reflexes
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16
Q
How does the rectum control defecation?
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17
Q
Distension of the rectum results in reflex relaxation of which one of the following?
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18
Q
What are the major components of gastric secretions?
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19
Q
Explain 4 major gastric cells.
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20
Q
Explain pepsinogen and intrinsic factor secretion.
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21
Q
What are Pvloric glands?
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22
Q
What is the role of Parietal Cells and HCl Secretion?
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23
Q
How is HCl secrection controlled?
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24
Q
Which one of the following stimulates H+ secretion from the parietal cell?
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25
Explain how gastric secretion is stimulated during the cephalic phase.
26
Explain how gastric secretion is stimulated during the gastric phase.
27
Explain how gastric secretion is stimulated during the intestinal phase.
28
Explain what is meant by the “gastric mucosal barrier” and indicate the main agents known to disrupt it.
29
What are protective and damaging factors of The Gastric Mucosal Barrier?
30
What inhibits HCl secretion?
* Normal physiological inhibition of gastric acid secretio: Presence of acid; fat; protein digestion products
* Inhibited when HCl no longer needed to convert pepsinogen – pepsin → when chyme moves to small intestine - decreased pH of gastric contents
* Food acts as buffer – when moves to small intestine lose buffering capacity – further H+ secretion reduces pH – inhibits gastrin – decreases H+ secretion
* ** Major inhibitory factor: Somatostatin - a hormone secreted in the pancreas and pituitary gland that inhibits gastric secretion and somatotropin release.**
* Direct: binds to receptors on parietal cells – reduces cAMP levels antagonizes (reducing) histamine effects on H+ secretion
* Indirect: inhibits histamine and gastrin release to reduce stimulatory effects of these peptides
* Prostaglandins: Antagonize histamine’s stimulatory action on H+ secretion- inhibit adenylyl cyclase
31
Tagamet is a drug used to prevent H+ secretion. Which one of the following does Tagamet actively block?
32
What are the endocrine and exocrine functions of gastric inhibitory peptide (glucose-dependent insulinotropic peptide)?
**Gastric Inhibitory Peptide (Glucose-dependent Insulinotropic Peptide, GIP) has an endocrine function to stimulate insulin release and an exocrine function to decrease acid secretion.**
GIP is produced by K cells of the duodenum and jejunum.
GIP secretion is stimulated by the presence of the following substances in the small intestine:
* Fatty acids
* Amino acids
* Orally ingested glucose
Oral glucose is more effective than intravenous glucose in causing insulin release due to GIP secretion.
33
What are the three phases of gastric acid secretion? What are the major stimuli for gastric acid secretion in each?
Regulation of gastric acid secretion is divided into three phases:
1. **Cephalic**
2. **Gastric**
3. **Intestinal**
The cephalic phase occurs before food reaches stomach, and is mediated by **vagus nerve stimulation from chewing and swallowing.**
The gastric phase occurs in the presence of food in **stomach, stimulated by stomach distention and presence of protein and amino acids.** This phase is mediated by cholinergic local and central reflexes, such as the nerves that run through the vagus nerve (vagovagal reflexes).
The intestinal phase occurs in **the presence of chyme in the duodenum**, causing initial stimulation and subsequent inhibition of gastric acid secretion.
34
Waht is chyme exposed to during segementation in the small intestines?
It is exposed to pancreas enzymes while it is mixed.
35
Name the related sphincters in the digestive system.
(1) **Upper esophageal sphincter**
(2) **Cardiac Sphincter**, at the top of the stomach, separating the stomach from the esophagus.
(3) **Iliac Sphincter** , at the bottom of the stomach, separating the stomach from the small intestine.
(4) **Ileocecal Valve** separates the small intestine from the large intestine
(5) **Involuntary Anal Sphincter**, which is responsible for generating the urge to defecate.
(6) **Voluntary Anal Sphincter**, which allows one to control defecation.
36
What are the three phases of gastric acid secretion? What are the major stimuli for gastric acid secretion in each?
Regulation of gastric acid secretion is divided into three phases:
**Cephalic**
**Gastric**
**Intestinal**
The cephalic phase occurs before food reaches stomach, and is mediated by vagus nerve stimulation from chewing and swallowing.
The gastric phase occurs in the presence of food in stomach, stimulated by stomach distention and presence of protein and amino acids. This phase is mediated by cholinergic local and central reflexes, such as the nerves that run through the vagus nerve (vagovagal reflexes).
The intestinal phase occurs in the presence of chyme in the duodenum, causing initial stimulation and subsequent inhibition of gastric acid secretion.
37
Besides directly stimulating parietal cells, histamine also potentiates what two stimulatory pathways to increase gastric acid secretion?
Histamine acts to potentiate **gastrin and vagal stimulation of gastric acid secretion**.
Histamine is produced by mucosal mast cells and enterochromaffin-like cells.
Histamine secretion is stimulated by gastrin and acetylcholine.
38
What are the endocrine and exocrine functions of gastric inhibitory peptide (glucose-dependent insulinotropic peptide)?
Gastric Inhibitory Peptide (Glucose-dependent Insulinotropic Peptide, GIP) has an **endocrine function to stimulate insulin release an an exocrine function to decrease acid secretion.**
## Footnote
GIP is produced by K cells of the duodenum and jejunum.
GIP secretion is stimulated by the presence of the following substances in the small intestine:
Fatty acids
Amino acids
Orally ingested glucose
Oral glucose is more effective than intravenous glucose in causing insulin release due to GIP secretion.
39
What is the transporter responsible for the secretion of gastric acid?
H+ is secreted by parietal cells of the stomach in an active **process mediated by H+/K+-ATPase**. Chloride is secreted through a separate channel to combine with H+ from the H+/K+-ATPase to form HCl.
Stomach acid breaks down proteins and kills microorganisms. Achlorhydria or hypochlorhydria (lack or low levels of stomach acid) can result in poor digestion and increased risk of GI infection.
Carbonic anhydrase in parietal cell cytosol catalyzes the reaction CO2 + H2O → H+ + HCO3-.
HCO3- produced in the parietal cells is transported across the basolateral membranein exchange for Cl-. The rise in blood pH following reabsorption of HCO3- is known as the “alkaline tide."
The H+/K+-ATPase pumps 1 K+ ion into the cell in exchange for 1 H+ ion that goes into the gastric lumen.
Proton pump inhibitors (omeprazole, pantoprazole) target the H+/K+-ATPase.
