Motility II week 1 Flashcards
What are the anatomical divisions of the stomach? What kinds of cells are located in each division? Where is the pacemaker zone located?
Anatomical subdivisions of the stomach:
• fundus
• body (with oxyntic (HCl producing) glandular mucosa, pacemaker zone-interstitial cells of Cajal, where contraction is initiated)
• antrum (pyloric glandular mucosa)
• pylorus (pyloric sphincter, gastroduodenal junction: controls emptying of gastric content and prevents regurgitation of duodenal content)
List 3 functions of stomach motility.
- reservoir for large volumes of food
- fragmentation of food and mixing with gastric secretion-> digestion
- controlled emptying of gastric content into duodenum: important that it is controlled bc of large difference in pH btwn compartments. could develop ulcer if have premature emptying
Where are electrical slow waves initated in the stomach? (be specific) What is the shape of these slow waves?
How are gastric slow waves modulated? (specific molecules)
What is different about slow waves in the antrum and pylorus?
Electrical slow waves initiated in pacemaker zone in gastric wall (greater curvature of gastric body). Gastric slow wave is triphasic: rapid initial depolarization, plateau, repolarization. Note that the shape is similar to a cardiac AP but the magnitude and duration are different (less depolarization and longer duration of slow waves) Contraction occurs when Em reaches threshold potential for contraction. Extent and duration of depolarization correlate with force development.
Modulation of gastric slow waves
• Acetylcholine and gastrin increase amplitude and duration of slow waves and therefore increase contraction.
• Norepinephrine decreases extent of depolarization and duration of plateau and therefore reduces force development.
In antrum and pylorus action potentials are superimposed on slow waves. APs increase force of contraction.
Explain the differences in electrical activity of the stomach as from the fundus to the pyloric sphincter and why this occurs.
Note there are no slow waves or APs in the fundus because this portion of the stomach is a reservoir.
As go down toward pylorus, depolarization is larger and have increased frequency of APs-increased force of contraction-more peristalsis. This increases mixing of gastric juices with chyme. The strongest contractions are at the bottom to push through the pylorus to the small intestine. Note that the cell membranes of smooth muscle cells of the pyloric sphincter are always depolarized and only repolarize during relaxation when chyme exits the stomach.
What are the 4 functions of gastric motility? (just list)
- filling
- storage
- mixing
- emptying
An empty stomach (approx 50 ml) can expand to greater than 1 L. Volume increase is not paralled by a similar increase of intragastric tension. What are 2 reasons for this? Explain the mechanisms behind these principles.
- Plasticity: stomach smooth muscle cells can be stretched (within limits) without a change in tension (developed force).
- Receptive relaxation: Filling (gastric distension) causes reflective relaxation of the fundus and body of the stomach; (filling is sensed by mechanoreceptors) reflex is mediated by vagus nerve (VIP and NO as neurotransmitters). In other parts of the GI tract, distension reflexively causes contraction.
What are the differences btwn the change in intraluminal pressure of a full stomach after a vagotomy and why?
vagotomy: Receptive relaxation does not occur because the vagus nerve has been removed. As a result, an extensive increase in intraluminal pressure of the stomach occurs with eating.
What properties of the fundus make it ideal for gastric storage?
Muscle layers in fundus and body are thin –> only weak peristaltic contractions and motility –> storage of unmixed food.
What is systolic contraction of the antrum? How does the small diameter of the pyloric sphincter aid in gastric mixing?
Gastric mixing: Pacemaker cells initiate autonomous slow waves (approx. 3/min), leading to peristaltic waves of contraction. Propagation with increasing velocity and intensity towards antrum/pylorus. Antrum and pylorus contract almost simultaneously (=systolic contraction of the antrum). The strong antral peristaltic contraction mix food content with gastric secretion to produce chyme (chyme: semifluid mass of partially digested food and digestive secretions formed in the stomach and intestine during digestion). Peristaltic waves squirt a small portion of the antral content into the duodenum. Because of the small diameter of the pyloric ring this sphincter closes early during the systolic contraction and the contractile wave forces antral content back into more proximal parts of the antrum (=retropulsion) resulting in even more effective mixing of the content.
The peristaltic contractions of what region of the stomach are the driving force for gastric emptying? What regulates emptying of the stomach? How is it gastric emptying fine-tuned?
Antral peristaltic contractions are the driving force for gastric emptying. Pylorus (gastroduodenal junction) carefully regulates emptying of stomach. Prevents regurgitation of contents from the duodenum back to the stomach. Neural and hormonal mechanisms in stomach and duodenum/jejunum and outside the GI system fine regulate gastric emptying.
How is pyloric tone (contraction and relaxation) controlled? (NS, hormones, etc.)
Pyloric relaxation: inhibitory vagal fibers (mediated by VIP and NO)
Pyloric constriction: excitatory cholinergic vagal fibers, sympathetic fibers and hormones cholecystokinin, gastrin, gastric inhibitory peptide (GIP), and secretin
What 2 gastric factors influence the rate of gastric empyting?
• Gastric factors
Volume of chyme: increased volume (distension) stimulates motility.
Fluidity: increased fluidity allows more rapid emptying.
What 5 duodenal/jejunal factors effect the rate of gastric emptying?
• Duodenal/jejunal factors
Fat: Fatty acids in duodenum and jejunum stimulate secretion of cholecystokinin (CCK) and gastric inhibitory protein (GIP) –> inhibition of gastric emptying.
Hypertonicity: Chyme entering duodenum is usually hypertonic. Osmoreceptors –> decrease gastric emptying via neural and humoral pathways.
Peptides/amino acids in duodenum: Peptides and amino acids release gastrin from G cells in the antrum and duodenum –> increased constriction of pyloric ring. Peptides and amino acids also promote release of GIP and CCK –> decrease of gastric emptying.
pH: duodenal pH < 3.5 decreases gastric emptying and increases duodenal motility. Acid in duodenum triggers release of secretin. Secretin inhibits antral contraction, stimulates pyloric contraction and stimulates bicarbonate-rich secretion from liver and pancreas (–> neutralization of acidic gastric content).
Distension: Too much chyme in duodenum inhibits gastric emptying.
How may emotions and intense pain influence gastric emptying?
Emotions: influence autonomic balance and therefore may stimulate or inhibit gastric motility
Intense pain: increased sympathetic activity –> inhibition of motility
What are 3 consequences of controlled empyting of the stomach?
- Fat is not emptied into duodenum faster than it can be emulsified by bile components
- Acid is not transported into duodenum more rapidly than it can be neutralized by pancreatic and duodenal secretions
- Other components of chyme do not enter small intestine at a rate faster than can be processed by the small intestine
What is the definition of vomiting? Why does it occur?
Forceful expulsion of gastric and/or intestinal content through the mouth. Protective mechanism against over-distension and/or irritation of stomach and intestines (especially duodenum).
Explain the events that occur during the vomiting reflex. Where is the vomiting center located in the body?
How is aspiration prevented during vomiting?
What often precedes vomiting?
- Vomiting center (medulla oblongata): integration of sensory inputs and coordination of vomiting act.
- Vomiting act: reverse peristalsis of small intestine, relaxation of pyloric sphincter and stomach (to receive intestinal contents). Forced inspiration (against closed glottis) decreases intrathoracic pressure and increases intraabdominal pressure. Forceful contraction of abdominal muscles to sharply increase intraabdominal pressure. Relaxation of esophagus, gastroesophageal and upper esophageal sphincters and contraction of pylorus and antrum facilitate expulsion of intestinal contents
- Approximation of vocal cords, closure of glottis and inhibition of respiration prevents aspiration into respiratory tract
- Retching (gastric content is forced into esophagus but does not enter pharynx; upper esophageal sphincter remains closed) often precedes vomiting
- Autonomic discharge (salivation, dilation of pupils, sweating, pallor, tachypnea, rapid and irregular heart beat)
What are 7 causes of vomiting?
- Tactile: stimulation of back of throat
- Irritation/distension of stomach and duodenum
- Elevated intracranial pressure (e.g. cerebral hemorrhage)
- Rotation/acceleration of the head (e.g. motion sickness)
- Intense pain
- Chemical agents (e.g. emetics): act on upper portions of the GI tract or on specialized chemoreceptors (chemoreceptor trigger zone) in the brain
- Emotional factors
Dumping syndrome can occur after a partial gastrectomy or vagotomy. What is dumping syndrome?
If a portion of the stomach is removed due to cancer, for example, especially a lower portion of the stomach with pyloric valve removal, patients can go into severe shock from eating too much because they no longer have controlled emptying. hypertonic contents–> quickly absorbed into vasculature
What are the subdivisions of the large intestine?
appendix and cecum
colon ascending
-transverse
-descending
-sigmoid
rectum
anal canal
What are teniae coli? Where in the GI tract are they found?
The longitudinal layer of the muscularis externa is concentrated into three bands = teniae coli. Found in the colon.
What is the function of segmentation/haustration in the colon?
Segmentation
• Localized segmental contraction divide colon in neighboring ovoid segments =haustra.
Segmentation of the colon = haustration.
• Function: mixing of content (kneading) –> facilitation of absorption of electrolytes and water.
What is defecation?
What is the defecation reflex? (nerves involved, type of synapses, parts involved)
What voluntary actions are involved in defecation? (parts involved, nerves, etc)
Defecation: Complex behavior involving voluntary actions and reflexes.
Defecation reflex: sacral spinal cord and efferent cholinergic parasympathetic fibers in pelvic nerves. Distension of rectum and relaxation of internal sphincter
Voluntary actions: relaxation of external sphincter (striated muscle, innervated by somatic fibers via pudendal nerves) and increase of intraabdominal pressure
What is an intestinal obstruction?
What are the 2 types of intestinal obstructions and what are the differences btwn them?
Intestinal obstruction: complete arrest or impairment of the passage of intestinal contents
- simple obstruction: no interference with blood supply
- strangulating obstruction: arterial and venous blood flow to bowel segment cut off –> infarction
Air-fluid levels may be observed on an X-ray with an intestinal obstruction. What are they?
X-rays of the abdomen: fluid and gas collect in the intestine –> characteristic pattern called “air-fluid levels”. The air rises above the fluid and there is a flat surface at the “air-fluid” interface (person must be standing upright to get flat surface. otherwise fluid will level out).
