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Phys4 GI Lect6

Phys4 GI Secretions: Salavary and Gastric

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.
Created by: WeeG



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