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Flashcards in Secretions Deck (36):

Mucous vs. Mucus vs. Mucin

o Mucous glands secrete mucus which is bicarbonate rich to buffer and lubricate the GI tract; mucin is glycoprotein that helps form the viscosity of mucus


Thirst - consequences of dehydration and hormonal influences

o Consequences of dehydration – hypovolemia, hypertonicity stimulates thirst and compensation (ADH release)
o Rise in plasma osmolarity (concentration of “stuff”) is detected by receptors in hypothalamus signals thirst to
o Hormonal influences: ADH, Ang II, aldosterone (elevations in these hormones promote sodium and/or water conservation during dehydration)


Hunger and Satiety - hormones that regulate feeding

 Ghrelin secreted into blood during fasting state and stimulates hypothalamic neuropeptide Y to stimulate hunger
 Leptin - produced in adipose cells and suppresses appetite by decreasing neuropeptide Y
 During feeding, peptide YY and glucagon-like peptide-1 (GLP-1) from lower small intestine L cells are secreted into the blood suppressing neuropeptide Y and decreasing appetite


Oral Secretions

 Salivary glands secrete saliva that lubricates food and starts digestion of starches (amylase) and lipids (via lingual lipase secreted by Von Ebner’s glands in tongue)
 R protein secreted to protect vitamin B12 from digestion by proteases


Salivary Glands

 Parotid glands secrete serous saliva
 Submaxillary glands secrete mixed serous/mucous saliva
 Sublingual glands secrete mucous


Saliva Formation

 1.5 L/day is secrete; regulated by parasympathetics (glossopharyngeal and facial nerves – NOT VAGUS)
 Acinar cells responsible for primary secretion of saliva; increase in flow rate increases the osmolarity due to decrease in reabsorption of electrolytes
 Myoepithelial cells – innervated by alpha-adrenergic fibers and can contract
 Striated ducts – secretion and absorption of electrolytes as the primary secretion flow through the ducts changes composition of saliva


Final Tonicity of Saliva

o Final tonicity of saliva is dependent on flow through the ducts; will ALWAYS be HYPOtonic to plasma; HCO3- is primarily absorbed in the ducts
 Increase in flow rate increases osmolality due to decrease in reabsorption of electrolytes


Autonomic Control of Oral Secretions

 Parasympathetics via Ach, VIP (can NOT salivate without) –via glossopharyngeal and facial nerve (NOT VAGUS)
 Sympathetic via beta and alpha adrenergics (causes constriction of myoepithelial cells to release its contents)
 Central nervous system via afferents and efferents to salivary nucleus


Hormone Control of Oral secretions

 ADH increases water absorption, concentrating saliva
 Aldosterone increases K secretion into saliva and Na out of saliva


Factors Increasing Oral Secretion Flow

parasympathetics, CNS (cephalic phase), nausea, esophageal distension, chewy/flavorful food, dry, acidic alkaline foods, meats, sweets, bitter foods


Factors Decreasing Oral Secretion Flow

– sympathetic, ADH/Aldo hormones, sleep, dehydration, drugs, aging


Functions of Saliva

 Coagulation – coagulation factors and platelet-activating factor
 Oral hygiene – buffers, cleansing, importance of flow, antimicrobial activity
 Lubrication – functions of mucin, water
 Digestion – lingual lipase, salivary amylase
 Taste – moistening, dissolves food so taste buds get full experience
 Antimicrobial – physical removal, WVC, opsonins, dimeric IgA, lactoferrins
 Protections – reduce temperature, buffering, protects stomach


Unique Properties of Oral Secretions

Large volume relative to gland size; low osmolality, relatively high K+ concentration compared to plasma


Esophageal Secretions

o Minor serous and mucous glands; primarily in lower segment that helps lubricate the bolus


Gastric Secretions

 HCL – chemical digestion; secreted by parietal cells
 Intrinsic factor – required for B12 absorption by protecting from pancreatic proteases; secreted by parietal cells
• R protein – protects vitamin B12 from degredation; high affinity in acidic environment; cleaved by trypsin in duodenum and intrinsic factor takes over
 Pepsinogen – cleaved to pepsins by acidic environment that digest proteins; secreted by chief cells
 Gastrin – stimulates gastric motility and HCL protection in response to stretch by food; secreted by G cells in antrum of stomach
 Gastric lipase – lipid digestion; secreted by chief cells
 Other -
• Somatostatin – inhibits HCl secretion
• Histamine – stimulates HCl secretion
• Ghrelin – hormone secreted into blood when fasting and acts on hypothalamus to stimulate hunger; opposes satiety effects of leptin, Peptide YY, and GLP-1
 Mucus – lubricates/protects gastric mucosa from low pH


Gastric Secretory Cell Types and their Products

 Surface mucous cells – protection, replace cells in lumen after desquamation
 Mucous neck – protection, progenitors of other cells lower in pit
 Parietal cells – HCl and intrinsic factor
 Chief Cells – pepsinogens, gastric lipase
 Endocrine cells – somatostatin, gastrin


Regulation of Gastric Secretions

 Endocrine – gastrin and GIP act directly on parietal cells; secretin and peptide YY act indirectly by suppressing gastrin
 Paracrine – enterochromaffin-like cells (ECL) secrete histamine and serotonin
• Histamine increases HCl secretion locally by acting on gastric pits
• Serotonin is a vasoactive neuropeptide that causes constriction in intestines associated with peristalsis
 Neural – vagal Ach act on Somatostatin D cells, parietal, and mast cells; can stimulate GRP also


Gastric Secretion Stimulation/Inhibition

 Stimulation – parasympathetics (vagus), gastrin, histamine
• Parasympathetics/Ach – acts directly on parietal cell
• Gastrin – endocrine hormone acting on parietal cell
• Histamine – paracrine hormone acting on parietal cell
 Inhibition – secretin, somatostatin, GIP, peptide YY, prostaglandins
• Secretin – duodenal hormone that decreases gastrin  lowering HCl secretion
• Somatostatin – acts directly on parietal cell
• GIP (gastric inhibitory peptide) – endocrine hormone that decreases secretion of gastrin lowering HCL secretion
• Peptide YY – secreted from small intestine
• Prostaglandins – cytoprotective hormone


HCl and Response to Meal

 Antibactericidal EXCEPT for Helicobacter pylori
 Response to Meal: HCl secretion increases, decreasing the gastric pH  chyme enters duodenum and secretin is secreted  decreases gastrin secretion in stomach and duodenum and stimulates pancreas to release electrolytes  increase in bicarbonate into small intestine increases pH, protecting the mucosa and allowing pancreatic enzymes to work efficiently


Helicobacter Pylori and Chronic NSAID users

- secretes urease that produces ammonia and neutralizes the H+ around H. pylori allowing it to survive; however ammonia (NH4) gets converted to NH3 which is toxic to cells and causes inflammation
• produces mucinase which disrupts the mucus/bicarbonate barrier and causes ulcers
• Critical amount of H. pylori must be reached to cause ulcers
• H. pylori responsible for 90% of non-chronic NSAID associated gastric and duodenal ulcers
• Chronic NSAID use – prostaglandin inhibors which are cytoprotective to the gastric mucosa; therefore when taken on empty stomach acid can enter stomach in absence of food


Phases of Gastric Secretions

 Cephalic (“anticipation”) – chemo and mechanoreceptors on tongue, nasal mucosa; vagal effects, gastrin, acid, enzymes
 Gastric (food in stomach) – local nervous secretory reflexes; vagal reflexes; gastrin stimulation
 Intestinal – acidic chyme enters duodenum; composition of chyme important; feedback to HCl secretion; decrease gastric emptying; nervous mechanisms & hormonal mechanisms


Intestinal Secretions

-made up of intestinal mucosal secretions, pancreas, liver, and gall bladder secretions


Intestinal Cells and Glands (paneth, goblet, endocrine, brunner)

 Cystic fibrosis transmembrane regulator – secrete ions and water
 Paneth cells – host defense, secrete zinc and lysozymes that attack bacteria
 Goblet cells – secrete mucus
 Endocrine cells – secrete gastrin, CCK, secretin, GIP, motilin, serotonin
 Brunner’s glands – located in first part of duodenum; secretes thick mucus and proteases; stimulated by vagus; inhibited by sympathetic
 Enterokinase is from cells in duodenum


Intestinal Neural and Hormonal Regulation

 Chyme contact and distention will increase secretions via local and enteric reflexes
 Parasympathetics will increase secretions; sympathetic will decrease secretions
o Hormonal Regulation – composition of chyme stimulate different hormones


Peptide/amino acid Duodenal Stimulus

Gastrin (G cells)
↑ HCl (at parietal cells), ↑ antral motility, ↑↓ gastric emptying; ↑ intestinal motility


Acid; long chain fatty acid Duodenal Stimulus

Secretin (S cells)
↑ pancreatic, biliary, & intestinal electrolyte buffers (and enzyme) secretions; ↓ HCl by ↓ gastrin; ↓ gastric emptying


Peptide and Fat Duodenal Stimulus

CCK (I cells)
↑ pancreatic enzyme secretions; ↑ gallbladder contraction, relax sphincter of Oddi (↑ motility in small and large intestines, increase mass movements in colon); ↓ gastric emptying


Fatty acids/amino acids & glucose

GIP (K cells)
↑ insulin secretion; ↓ gastric emptying; ↓ gastric motility (mixing)


Ileum Secretions

secretes H+ and bicarbonate
o Carbonic anhydrase in enterocytes of ileum and colon
o H+ acidifies the lumen so bicarbonate is also secreted and acts as buffer in exchange for chloride


Pancreatic Endocrine/Exocrine Secretions

o Endocrine – ductless, secreted into bloodstream
 Insulin, glucagon, and somatostatin which can affect gastric secretion and motility, in addition to their other systemic effects (blood glucose)
o Exocrine – out through ducts and into lumen
 Enzyme secretions and electrolyte secretions
 Pancreatic Acinar cells – capable of making both enzymes and buffers into duct
• Final buffer product can be different from what intitially left the acinar cells to enter ducts depending on the rate of flow (similar to saliva concept)


Other Pancreatic Secretions

o Pancreatic proteases are stored as zymogens and secreted as precursors; once in duodenum, enterokinase (secreted by duodenum) activates these enzymes
 Trypsin (activated by enterokinase) activates all the other zymogens: chymotrypsin, elastase, carboxypeptidases A & B
o Pancreatic amylase – digests carbohydrates; more active than salivary amylase
o Pancreatic lipase, cholesterol esterase, and phospholipase digests fats
 Pre co-lipase – activated by trypsin after entering duodenum; co-factor for pancreatic lipase
o Trypsin inhibitor – in pancreas and duct; keeps trypsin from being activated in pancreatic and bile ducts; lose of inhibitor can cause pancreatitis


Primary Stimuli for enzyme/electrolyte secretion by Pancreas

o Primary stimuli for enzyme secretions are CCK and insulin
o Primary stimuli for electrolyte secretions are secretin and vagovagal reflexes


Colonic Secretions

o Mucus – goblet cells on surface and in crypts; stimulated by contact, parasympathetics, and enteric nervous systems
o Bicarbonate in exchange for Cl-
o Potassium in exchange for Na+ and water
o Colon tends to “house” bacteria; MMC ends at distal ileum and the bacteria collects into colon which is okay because it is dryer and has less nutrients
-feces contents - small amount of K+ and HCO3-


Bulk Absorption Occurs

happens in small intestine; nearly 9L of fluid; large amount occurs with absorption of Na+


Chronic Diarrhea

– lose a lot of bicarbonate (buffer) and therefore become acidotic


Parietal Cells (details)

• Anatomical changes in stimulated parietal cell causes the secretion
• Make H+ from metabolism of CO2
• HCO3 transport OUT of cell via HCO3/Cl antiport
• Use H+/K+ ATPase to send H+ into lumen against a 10^6 gradient; K+ is taken into the cell and then leaks back into lumen
o Number of pumps in membrane dictate amount of acid produced
o Secretions/hormones & drugs (proton pump inhibitors) work by regulating number of pumps in membrane
o Cell contains carbonic anhydrase that converts CO2+H20H2CO3
 H2CO3 rapidly breaks down to H+ and HCO3- as long as H+ inside cell is kept low by transporting H+ ions out of cell
 HCO3 released into blood in exchange of Cl-
 Alkaline tide results as high amounts of HCO3- released into blood but luckily Cl- will travel back into lumen and some will bind to H+
o Canaliculi – increase surface area on lumen side to secrete substances