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Phys4 GI Lect6
Phys4 GI Secretions: Salavary and Gastric
| Question | Answer |
|---|---|
| Parasympathetics role with salivary glands | 1.Parasympathetics leave the Salivary nucleus in the medulla on CN VII & IX. 2.Preganglionics Release ACh on M3 which activates IP3 within the acinar cells. 3.Saliva is secreted. |
| Positive stimuli on the Salivary nucleus of the medulla | 1.Conditioned reflexes. 2.Smell. 3.Taste. 4.Pressure. 5.Nausea. |
| Negative stimuli on the Salivary nucleus of the medulla | 1.Fatigue. 2.Sleep. 3.Fear. 4.Dehydration. |
| Salivary secretion pathway | 1.Acinar cells (squeezed by myoepithelial cells). 2.Intercalated duct. 3.Striated duct. 4.Excretory duct. |
| Ionic composition as saliva moves down the striated duct | HYPOTONIC. Reabsorbed: Na, Cl. Secreted: K, HCO3- |
| Sympathetics role with salivary glands | T1-3 travel to salivary glands after synapsing on Superior cervical ganglia. Release NE on B2 receptors on acinar cells triggering cAMP and secretion. |
| Parasymp and Symp outflow are __________ in the salivary glands | STIMULATORY |
| Main effects seen in response to ACh and NE on salivary glands | 1.Secretion. 2.Vasodilation. 3.Myoepithelial cell contraction. 4.Metabolism. 5.Cell growth. |
| Do GI hormones effect Salivary glands' rate of secretion? | NO |
| Aldosterone's affect on saliva | Increase Na reabsorption & K secretion. |
| ADH's affect on saliva | Inc Na reabsorption |
| Na content in saliva of patient with Hyperaldosteronism | DECREASED (Increased K) |
| Na content in saliva of patient with Addison's disease | INCREASED (Decreased K) |
| PNS affects on Salivary gland BF | 1.Innervation acts on M3 receptors which causes Inc Bradykinin (via Kallikrein) and thus VD. 2.Release VIP which will cause VD. **Metabolites from Inc metabolism will also cause VD. |
| SNS affects on salivary gland BF | NE binds to A1 which will VC. This causes an Inc in metabolites that will then induce VD. **Eventual VD |
| Gastric Secretions: Mucous cells | 1.Mucous. 2.Bicarb. **In pyloric gland area it also secretes pepsinogen |
| Gastric Secretions: Pariteal (Oxyntic) Cells | 1.HCL. 2.IF. |
| Gastric Secretions: Chief (Peptic) Cells | 1.Pepsinogen. 2.Gastric Lipase. |
| Gastric Secretions: ECL cells | Histamine. |
| Gastric Secretions: G-Cells | Gastrin |
| Gastric Secretions: D-Cells | Somatostatin |
| Mechanism Behind parietal cells secreting HCL | 1.HCO/CL exch on basolateral mem pumps Cl- in. 2.Cl- then exits the apical membrane into lumen via channel. 3.H/K ATPase pumps H+ into the lumen where it combines with Cl-. |
| Alkaline tide | Created by the Cl/HCO exchanger during high Parietal cell activity. **HCO3- and H+ are coming from CA reaction. |
| fates of HCO3- and H+ coming from CA reaction | HCO: Blood. H:Lumen. |
| Treatment options for Hypersecretion of Parietal cells | 1.PPI: Omiprozoles (Primary method of treatment). 2.H2 histamine blockers (Zantac, Tagament). 3.Vagotomy. |
| Regulation of Parietal Cell HCL release | 1.Vagus N (ACh M3 receptors). 2.Histamine from ECL cells via H2 receptors (ECL cells activated by Vagus & Gastrin). 3.Gastrin (CCKb receptors) |
| Potentiation in Parietal Cells | The Sum of the 3 regulating factors is much greater than if they worked alone. Also, taking one away will affect ALL 3. **Occurs b/c they are activating Parietal cell via different mechanisms. |
| Gastric acid Secretion phases | 1.Cephalic phase: Cephalic stimuli (senses) 30% of acid secretion. 2.Gastric 50-60% of acid secretion. 3.Intestinal 5-10% of acid secretion. |
| 4 main physiological events in the Cephalic gastric secretion phase | VAGUS: 1.Stim parietal cell (ACh). 2.Stim ECL cell (ACh). 3.Stim G-cell (GRP). 4.Inh D-cell (ACh) which stops somatostatin release. **1,2,&3 occur in Corpus of stomach. 1,3,&4 occur in the antrum |
| Regulation of Somatostatin? what 2 things does it inhibit in terms of gastric secretions? | H+ stimulates it while Vagus Inhibits it. Somatostatin itself inhibits both G-Cell & Parietal cell secretion. |
| What are stimuli for Gastric phase of gastric secretions | 1.Distention of Food: cuases local ENS reflexes and Vagovagal reflex (both trigger G-cell, ECL cell, and direct ACh activation). 2.Digestion of Protein: peptides and aa's target G-cells to release gastrin. |
| What are stimuli for Intestinal phase of gastric secretions | 1.Protein digestion products: Stimulate parietal cell via G-cells, Intestinal endocrine, and absorbed aa's |
| Causes of Inhibition of Gastric Secretion | 1.Somatostatin Inh parietal & G-cell (stim by Gastrin, H+, & secretin in duo). 2.Enterogastrone Inh parietal cell (stim by H+, fat, hyperosmolar). 3.GIP inh parietal and G-cell (stim by FA). 4.CCK inh parietal cell (stim by H+). 5.PGE2: Inh parietal c |
| 2 MAIN hormones that turn off gastric secretion? | 1.Somatostatin. 2.Secretin. |
| Activation and secretion of Chief cell | Activated by ACh from vagus & H+. Releases pepsinogen which is ACTIVATED by the H+ (released from parietal cell) to Pepsin. Pepsin |
| Can Pepsin work in a neutral environment? | NO. |
| Peptic Ulcer Disease (PUD) | Break in the mucosal surface >5mm in size with depth to the mucosa. The acid then attacks the epithelial cells **Includes both Gastric and Duodenal ulcers. |
| 3 layers of protection in the stomach | 1.Pre-epithelial (Mucus, Bicarb that creates a difusion barrier). 2.Epithelial (cellular resistance, restitution, prostaglandins). 3.Subepithelial (Blood Flow & leukocytes). |
| What stimulates the mucus cells to release more mucus? (thus increasing the preepithelial protection) | 1.Vagal Stimulation. 2.Chemical Irritation. |
| Prostaglandins affect on mucosal integrity | 1.Reg the release of muscosal bicarb & mucus. 2.Inh parietal cell. 3.Maintain mucousal BF and epithelial restitution. 4.Reg epithelial cell regeneration. **NSAIDS will dec all these |
| What is Restitution? (seen in the epithelial layer) | Allows nearby healthy cells to migrate to the injured region. **Independent of cell division, requires steady BF. |
| H. Pylori | Gram neg bacteria that colonizes the antral mucosa. Uses UREASE to convert urea to ammonia so it can survive the acidic environment. MAJOR FUNCTIONS: Inh somatostatin release, releases cytotoxins |
| What is 80% responsible for gastric ulcers and 100% responsible for duodenal ulcers? | H. PYLORI. **need to prescribe antibacterial med with ulcer. |
| What is the only essential secretion of the stomach | Intrinsic Factor (IF) released from parietal cells. **Key in B12 absorption. |
| Pathway of B12 absorption | 1.Acid/Pepsin seperate it from food. 2.binds to Heptacorrin. 3.Travels to duo along with IF. 4.Pancreatic proteases cleave heptacorrin. 5.IF binds to free B12. 6.Absorbed in ileum by B12-IF complex |
| Causes of B12 defiecency | 1.Pernicious anemia (destruction of parietal cells and thus IF). 2.Bacterial growth (they use up B12). 3.Chronic pancreatitis (rare). 4.Ileal Resection. |
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WeeG
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