Flashcards
Lecture 16
Flashcards do conjunto (46)
- 1Regulation of Gastric Functions Stomach1.Store food ingested during meal.
2.Regulate release of chyme into duodenum.
3.Secrete HCl and enzymes to begin protein digestion
4.Secrete Ghrelin –control of feeding
5.Churn and Mix food with digestive secretions - 2Stomach Notes-storage place for ingested food.
-regions of the stomach (fundus is the upper third, then the body. Which both act as one unit. Receive food and keep it so that the digestive juices can mix with the food. Can stay for up to 8 hours.)
-Antrum (antral pump) is the lower third. partially digested food is pushed and pulverized. Food molecules are further digested so they pass through the pyloric sphincter (separates content from duodenum and antral). - 3Ghrelin-Ghrelin is secreted by the fundus and body and released into the blood which finds its target (feeding center in the brain). -Hormone that regulates the feeding pattern. Released when fasting and is driven to go and search for me.
- 4Gastrin-Gastrin is in the antrum region. It is secreted there and goes into the blood and reaches the acid secreting cells in the upper portion of the stomach which also secretes digestive juices. When food is mixed, it is broken down further in the antrum. Antral pump, contractions break down food even more and directs it into the duodenum.
-pyloris is tonically contracted by relaxes when there is low viscosity or smoothie like mixture. - 5Gastric Motility
- 6Gastric Motility Cont'd-food can be stored in the region. More volume increases with food digestion but the pressure remains the same, Receptive Relaxation allows for increase in volume with constant pressure up to a certain point.
-as more and more food gets delivered to the antrum, there is more activation of mechanoreceptors so there is more stronger peristaltic activity. Increase in motility is regulated by intrinsic nerves in the autonomic nervous system.
-the motility patterns is due to pacemaker cells which have no movement of food. - 7MMC Migrating Motor Complex-Migrating Motor Complex --> important to move indigested food, Can't get through the pyloric sphincter.
-hormone Motilin (elevated when blood glucose level is low). This is responsible for large peristaltic contraction that is known as the MMC. - 8Extrinsic Branches of the Autonomic Nervous System
- 9Vago-Vagal Reflexes in Receptive Relaxation of Stomach–Vago-vagal reflexes (mechanoreceptors), ACh acts by causing release of inhibitory mediators (NO/VIP).
–Intrinsic reflexes (ascending) within wall of stomach→relax
•Signals triggered by nutrients in duodenal lumen, duodenal or colonic distension, or presence of fat/glucose in ileum (“ileal brake”) cause relaxation of gastric fundus (decreased tone)*
–All retard gastric emptying. - 10CCK-A (receptors on vagal sensory afferents)-CCK A on vagal afferent receptors and therefore when released you stimulate the afferent neurons that causes a decrease in efferent impulses = decreased acid secretion.
-CCK is a enteric NT and triggers release of pancreatic enzymes and contracts the gall bladder directly. - 11More Notes-parietal cells secrete acid.
-mechanoreceptors activate when stretched and they can release ACh or NO/VIP depending on whats needed.
-GI wall to dorsal vagal complex, efferent fibers go back to the muscle wall which decides release of ACh or NO/VIP. Example of a longer neural reflex which regulates gut function.
-ascending signal from lower part to higher which contributes to decrease in motility and acid secretion. Considered shorter neural reflex which regulates acid secretion and motility. - 12Gastric Emptying and Gastric Contents•Receptive relaxation, a vago-vagal reflex, responsible for increased volume with constant pressure.
•Vagotomy decreases receptive relaxation and accomodation, but ENS exerts major control.
•Vagotomy tends to DECREASE or DELAY gastric emptying of solids.
•Emptying depends on nature of gastric contents.
-protein based diet takes longer to empty out because you need the acid secretion from the parietal.
-a solid meal, especially like fried eggs and steak for breakfast, it will stay in your stomach for a long time. Less chance of getting hungry. - 13Vagotomy-vagotomy=operation that transects the vagus nerve.
-as food volume increases, there is an increase in pressure in a vagotomized patient.
-You feel full faster. You feel satiated. Eat smaller meals and liquidy meals. - 14Hormonal Regulation of Gastric Emptying-Secretin= decreases antral contractions and increases pyloric sphincter contractions.
-Gastrin= increases the pyloric sphincter contractions, increase gastric juice secretions, and increases mixing by antral muscle contractions.
-CCK and GIP is important for lipid digestion products which increase pyloric smooth muscle contractility to decrease emptying. Less acid production.
-Four established GI hormones + unidentified enterogastrone inhibit gastric emptying; allows pancreatic
and bile secretions to act on proteins, fats and carbohydrates presented to duodenum. - 15Hormonal Regulation of Gastric Emptying Cont'd
- 16Enterogastrones
- 17Pathophysiology and Clinical Correlation
- 18Gastric Secretions-2L per day.
-Mucus
-HCl
-Intrinsic Factor
-Pepsinogen, Gastric Lipase
-Histamine - 19Oxyntic GlandOxyntic gland:
mucus enzymes
HCL
Ghrelin (Hormone) - 20Pyloric GlandPyloric gland:
gastrin (hormone - 21Mucus-surface epithelial cells which are on the upper part of the gastric pit.
- 22HCl-parietal cells secrete HCl
- 23Intrinsic Factor-prevents pernicious anemia.**= not enough RBC in the body, less O2 delivered in the body so person may appear blue.
-released by parietal cells.
-causes the absorption of Vit. B12 - 24Pepsinogen, Gastric Lipase-released by chief cells.
-pepsinogen is cleaved to pepsin to aid in protein digestion.
-lipase starts the fat digestion. - 25Histamine-comes from ECL cells.
-paracrine factor.
-increases gastric acid secretion. - 26Interdigestive Phase
- 27Interdigestive Notes-mechanoreceptors are responsible for increasing the secretion rate when there is maximum stretching of the stomach.
-proteins are good buffers.
-when we are fasting, there is an interdigestive phase. The nutrients in the small intestine have all been absorbed.
-this is about 8 hours after your last meal.
-the concentration of acid is quite high and the secretion rate of acid is quite low.**
-when stomach is emptying, usually food represents buffers and it represents pH which is quite low and the acid concentration is quite high.
-the secretion rate is low because the high acid concentration in the gastric lumen.*
-somatostatin is released when the gastric lumen has high conc. of acid. *
-somatostatin inhibits gastrin release from the G-cells.* - 28Control of Gastric Acid Secretion ***
- 29At Fasting State-the acid conc. is very high and the secretion rate is low because the luminal H+ ions are acting on the D cells to release somatostatin which inhibits gastrin release in G cells.
These other pathways are NOT activated:
B. vagal stimulation (via ACh) inhibits somatostatin release from D cells
C. Peptides/amino acids directly stimulate G cells to release gastrin
D. Vagus stimulation of G cells via GRP stimulates gastrin release. - 30Control of Gastric Acid Secretion (FED STATE) *
- 31At Fed State-somatostatin release goes down because there is less acid present in the lumen.
So instead there is:
A. -vagal stimulation (via ACh) directly stimulates parietal cells
B. -vagal stimulation directly stimulates histamine release from ECL cells
D. The hormone gastrin stimulates release of histamine from ECL
D. Gastrin directly stimulates parietal cell - 32Morphological Changes in Parietal Cells During Acid Secretion•Resting parietal cell (nonsecreting) with elaborate system of intracellular membranes and abundant mitochondria.
•Actively secreting parietal cell with amplified apical membrane from fusion of tubulovesicles and secretory canaliculi*
•Apical membranes invaginate and interdigitate. - 33Parietal Cell Receptors and Pumps Involved During Acid Secretion•Amplification of apical surface area accompanied by an increased density of H+,K+ATPase molecules.
•Note acetylcholine (via m3muscarinic receptor) and gastrin (via CCK-B receptor) signal via increased cytosolic calcium, whereas histamine signals via increased cAMP (H2receptor).
-CCK-B is the receptor for gastrin.
-the receptor for CCK is CCK-A. -tubular vesicles have the protein pump. - 34Mucosal Barrier1.Apical membrane impermeable to H+ (always allowing K+ to be secreted into the gastric lumen which can cause low K in the blood leading to hypokalemia)
2.Tight junction between cells (no possibility for acid to pass through)
3.Layer of mucus
4.Damaged cells replaced every 3 days - 35Some points on it-carbonic anhydrase has an increased activity which catalyzes CO2 and water to be a weak acid which becomes a bicarbonate and leaves through the basolateral side. -the H+/K ATPase pump.
-This is responsible for moving H+ from low to high concentrations. Million fold gradient. Need a lot of these pumps to generate flux of acid. - 36Important pic to help visualize
- 37Gastrinoma (Zollinger-Ellison Syndrome)–Extragastric endocrine tumor whose cells undergo unregulated secretion of large amounts of gastrin*
–E.g., non-beta cell tumors of pancreas or duodenal tumors*
–High rates of gastric acid secretion at rest and in response to a meal.
–Tumor cells don’t respond to normal negative feedback mechanisms that reduce gastrin release at low luminal pH. - 38Pts with gastrinoma present with what types of symptoms?–Peptic and duodenal ulcers, diarrhea, steatorrhea (fatty stool), hypokalemia**
- 39What pharmacotherapy would be useful to alleviate the symptoms of gastrinomas?- H2antagonists (ranitidine, cimetidine) and PPIs (omeprazole)
- 40Breakdown of the Mucosal Barrier (Peptic Ulcer)-get ulcers or erosion of mucosa.
From:
-Helicobacter pylori
-Chemical exposure (NSAID’s)
-Stressful situations (increase gastric secretions) - 41Combination Therapy for Helicobacter PyloriCombination therapy: antibiotics + proton pump inhibitors reduce H pylori infection
and acid secretion - 42Cephalic Phase•~30% of total acid secretion
•Stimulated vagus nerve→ ACh release stimulates H+ release
-ACh stimulates histamine release
-in antrum parasympathetic & ENS neurons release GRP, which releases gastrin
-Vagus (via ACh) inhibits somatostatin release, which increases acid secretion**
-dorsal vagal complex --> where the vagal nerves originate from. Efferent impulses coming from the dorsal impulses, even before food is present, there is acid being released.
-Happens when there is a conditioned reflexes like smell, taste, thought of food, chewing, swallowing, hypoglycemia. - 43Gastric Phase•Major source of gastric secretion (~50% total).
•Vagal influences + mechanoreceptors and chemoreceptors act with ENS to produce maximal secretion of acid.
•Mucosal distension sends signals to the vagal nucleus. Vagal efferent signals sent back to G cells and parietal cells
•Gastrin release inhibited when antral pH<3, and completely inhibited when pH<2; BUT proteins are pH buffers (so, pH ≤ 5)**
-extension of the stomach causes ACh release and parietal cell secretion.
-vagal afferent fibers, signal is integrated and efferent signals come out and go back to the wall of the stomach and cause more release of GRP and this amplifies more gastrin release. Breaking down polypeptide fragments that are presented to the antral G cells and sense the presence of the small peptides. - 44Gastric Phase•Proteins effective pH buffers, so effective pH may rise up to 5 while acid secretory rates remain high
•Prevents somatostatin release from D cells (promotes acid secretion)* - 45Intestinal Phase-~5 - 10% of gastric acid secretions
•Duodenal G cell and unknown intestinal endocrine cell stimulate parietal acid secretion.
•Luminal absorption of amino acids in intestine stimulates acid secretion (undefined mechanism)*
•In humans, duodenal mucosa hormone named “entero-oxyntin” ↑ acid secretion without increasing serum gastrin
•Lipids & acid, vagovagal inhibits gastrin release** - 46Gastric Digestion and AbsorptionDigestion:
–Proteins from the action of pepsin
–Fat from the action of gastric lipase
–Carbohydrate digestion from salivary amylase (for a time)
-don't even the stomach to digest foods. (causing small digestion of carbohydrates) Removing the entire stomach, obese people do this to reduce the food intake.
-all we need are the pancreatic enzymes. The stomach is there to start protein and lipase digestion.
•Absorption
–Few short chain fatty acids
–Some drugs (weak acids -aspirin) and alcohol
(these are absorbed by the gastric mucosa. Rest absorption happens in the small intestine)
-removing parts of the stomach like the upper part (fundus), we are removing the parietal cells which are important for intrinsic factor secretion. Important for Vit. B12. If we don't have this ability to absorb this, then there is a loss of Vit B12 storage which is important for bone marrow cells like RBC, etc.
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- FlashCards sobre Lecture 16, criado por deepa.chrisilda. em 24-04-2016.
- Criado por
- deepa.chrisilda. · abr 2016
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- 4 fev 2018
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