Term
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Definition
Parotid - high a-amylase, serous
Submandibular - mostly serous, weak a-amylase, lysozyme
Sublingual - mainly mucous
alkaline pH! |
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Definition
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Term
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Definition
Causes - alcoholism (90%), gallstones (blocks common bile duct, secretions back up and overwhelm trypsin inhibitor), tumors, hyperlipidemia, postop, trauma
Sharp, piercing, epigastric pain, nausea, vomiting, fatty diarrhea
Hypotension, shock, respiratory distress, pulmonary edema, abdominal guarding, elevated bilirubin
Defective ductal secretion of HCO3 -> protein plugs -> block ducts -> pain, destruction of pancreatic tissue, inflammation
Chronic -> permanent damage, calcification, diabetes, malnutrition |
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Term
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Definition
Digestive enzymes: acini
- proteases secreted in inactive form; trypsin inhibitor prevents autodigestion of pancreas
- amylases
- lipases, cholesterol esterases
Sphincter of Oddi
Neural
•ACh from vagus, enteric nerves •Enzymes - Hormonal
•Secretin -> serous (HCO3-)
•CCK -> enzymes
o Stimulus for release: fats, peptides, amino acids
•Gastrin -> enzymes |
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Term
| Intestinal secretions (SI) |
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Definition
Brunner’s glands
• Secrete alkaline mucus for protection in response to tactile or irritating stimuli, ACh, GI hormones (secretin, CCK)
Crypts of Liberkuhn
• Mucous goblet cells and epithelial cells secrete an extracellular fluid
• Watery vehicle for absorption of substances
Enzymes
• Not secreted but associated with brush border microvilli
• Peptidases- digestion of proteins
• Sucrose, maltase, isomaltase, lactase digestion of disaccharides
• Intestinal lipase – digestion of lipids
• Enterokinase- activation of pancreatic trypsinogen |
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Definition
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Term
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Definition
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Term
| Modification to secretion by ductal cells |
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Definition
Striated duct cells- modify primary secretions; influenced by aldosterone
Excretory duct- modify secretions; secrete factors (epidermal growth factor, enzymes) |
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Term
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Definition
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Term
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Definition
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Term
| Acute vs. chronic gastritis |
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Definition
Superficial or acute gastritis
- Not very harmful
- Ingested agent (toxin, drug, bacteria) damages tight junctions
- Self-limiting and does not progress to chronic ulceration
- Treat by removing offending agent
•Alcohol, ASA, bacteria, caffine, spices, abx, digitalis, cortisone, NSAIDs
Chronic Atrophic Gastritis
- Role of H. pylori
- Penetrates deeply into gastric mucosa
- Causes progressive, gradual gastric atrophy
- Hypo- or achlohydria, pernicious anemia
- Pepsinogen also not secreted, but digestion almost normal
- Predisposes to malignancy |
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Term
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Definition
Excoriated area of the mucosa because of digestive action of gastric secretions
o Due to imbalance between rate of secretion of acid and pepsin and protection by mucosal barrier and/or acid neutralization
o Location: occur in 1st few cm of duodenum, antrum of stomach, lower esophagus
o Causes:
- Disruption of mucosal barrier
•H. pylori
•Smoking, alcohol, NSAIDs, stress, reflux bile salts, proteases, free radicals, ischemia, heredity, age
•Decreased blood flow
- Excess gastric acid and pepsin secretion
• Zollinger-Ellison: rare; gastrin producing tumor (gastrinoma)
• Psychic stress (parasympathetic stimulation)
• Hyperparathyroidism
Symptoms
• Burning epigastric pain starting 1-3 hours after eating, relieved by antacids or food
• Important to rule out other possible sources of abdominal pain, musculoskeletal pain
Complications: bleeding, perforation, obstruction
Treatment
• Abx for H. pylori
• Reduction of stress
• Antacid drugs
• H+ - K+ proton pump inhibitors
• H2 receptor blockers
Reduce ulcer-inducing factors: smoking, ASA, alcohol
• Surgical removal of 3/5 of stomach
• Vagotomy
• Dietary management |
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Term
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Definition
Osmotic (malabsorptive) – hypertonic fluid
• Fats, cholesterol, lactose, sorbital, laxatives
Secretory (deranged electrolyte transport)
• Cholera toxin, VIP tumor, bile salt malabsorption, neoplasm, bacteria, etc. stimulates excessive secretion of electrolytes and fluid from the crypts of Lieberkuhn in distal ileum and colon
Abnormal GI motility (hypermotility)
• Malabsorption, toxins from colonic bacteria fermenting unabsorbed nutrients, psychogenic (stress)
Exudative (blood, mucus, pus)
• Viral, bacterial |
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Term
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Definition
Formation of saliva
Stage one:
•Formation of primary secretion
o Alpha amylase: active at pH 4-7 (wide range) and in stomach for about 30 minutes until acid inactivates it
o Alpha lipase
o Mucous
o Ions: Na+, Cl-, K+, HCO3-
•Rate of secretion can increase *20x* (parasympathetic stimulation) - not hormones!!
Stage two:
• Modification of primary secretion in the salivary ducts; process affected by rate of secretion
o Na+ actively reabsorbed – influenced by aldosterone
o K+ actively secreted, but at a slower rate (in exchange for H+)
o Cl- passively reabsorbed with Na+
o HCO3- secreted and in exchange for Cl- (thus, pH can = 8.0 at maximal flow rate due to PNS stimulation)
o Ducts low permeability to water -> secondary saliva becomes more hypotonic as it flows down the ducts |
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Term
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Definition
Moisten, lubricate, speech
Excretory: urea, sugar, mercury, lead
Buffer stomach acid (alkaline pH)
Protection: fluid rinses mouth – bacteriostatic
•Thiocyanate, sialoperoxidase, enzymes
•Immune factors: lysozyme, IgA, IgM, IgG,kallicrine
Begin digestion of foods:
•Alpha amylase (ptyalin)
•Lipase
•RNAase, DNAase |
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Term
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Definition
Stim:
Food
Vagal stimulation (ACh)
Gastrin
Other: HCL, pepsin
SoP: mast cells
Stimulate H2 receptors on parietal cells; potentiates secretion produced by ACh and gastrin
Inhibited by: Pepcid, cimetidine, tagamet |
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Term
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Definition
Regulated by same mechanisms that regulate HCl secretion:
•Vagal stimulation -> ACh, GRP
•Enterogastrones
•pH
•Food products (secretagogues)
o Protein digestion products
o Alcohol
o Ca++
o Coffee (caffeinated and decaffeinated – due to amino acids)
Stimulates HCl secretion
Increases gastric and intestinal motility
Increases pancreatic secretions; mild; primarily enzymes
Contraction of GB (mild)
Necessary for the proper growth of GI mucosa (trophic hormone – cell turnover 4-6 days) |
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Term
| Gastrin Releasing Peptide (GRP) – Bombesin |
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Definition
Stim:
Neural reflexes
Dietary protein
Vagus nerve increases release of GRP at G-cell during the cephalic phase
Most likely neurotransmitter responsible for stimulating G cells to secrete gastrin
Action/target organ
•Stomach: stimulates gastrin secretion
•Pancreas: stimulates secretion |
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Term
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Definition
Stim: Released when gastric lumen pH < 2-3
Paracrine agent – released by D cells
Negative feedback inhibition of gastrin release
Inhibits gastrin release by G cell -> reduced acid secretion
*Protective mechanism to keep lumen from becoming too acidic*
Other actions
•Small intestine: inhibits secretion
•Pancreas: inhibits secretion
•GB: inhibits secretion |
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Term
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Definition
Stim:
Activated to pepsin by acid and previously formed pepsin in lumen of stomach
Proteolytic enzyme that begins the process of protein digestion; optimal activity at pH 1.8 – 3.5
•Only protease that can digest meat collagen
Regulation:
Cephalic stage: vagal stimulation; cholinergic nerves within enteric nervous system directly stimulate chief cells to release pepsinogen
Gastric phase: low pH activates local reflexes (ACh) that enhance pepsinogen secretion; vagal stimulation; gastrin
Intestinal phase: secretion, CCK, VIP, enhance pepsinogen release |
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Term
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Definition
Glycoprotein secreted by parietal cells along with acid
Essential for absorption of vitamin B12 in the terminal ileum
Parietal cell destruction (e.g. chronic gastritis, total or parietal gastrectomy)
•Patient will develop hypochlorhydria (reduced acid) or achlorhydria (no acid) and macrocytic/pernicious anemia due to failure of maturation of RBCs
•Liver has large storage capacity for vitamin B12 so it takes several months to 1 year to develop anemia |
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Term
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Definition
Complexes with Fe++ to facilitate iron absorption in small intestine
Gastritis, gastrectomy associated with iron-deficiency anemia
•Decreased Fe++ conversion due to loss of acid
•Decreased gastroferrin-Fe complex formation for absorption
•Body iron and folate stores more limited than those of vitamin B12, so manifests within a few months |
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Term
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Definition
•Pancreatic enzyme secretion
o Effects potentiated by vagal stimulation and secretin
o Contraction of GB and relaxation of sphincter of Oddi
o Decreased gastric emptying |
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Term
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Definition
Stim:
Acid, hyper-, hypo-osmotic chyme
Secreted by S-cells in duodenum and upper jejunum
•Stimulate pancreatic HCO3- water secretion
o Effects potentiated by vagal stimulation and CCK
•Stimulate formation of cAMP in intestine -> increase fluid secretion
•Stimulate bile duct secretion of HCO3 |
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Term
| Large intestine secretion (mucous) |
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Definition
Stimulus for release of secretion:
Distention, tactile, pelvic nerves (PS), submucosal and myenteric plexus
Acute emotional stress -> strong PS stimulation of gut -> lots of mucous, increased motility -> ropy mucous stool every 30 minutes
•Protection against excoriation (scratching of surface lining colon by hard feces)
•Adherent medium for fecal material
•Protection against bacterial activity
•Barrier to acids which are formed by bacteria |
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Term
| Factors that stimulate mucous secretion |
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Definition
•Prostaglandin E2
•ACh
•HCl
•Glucagon
•VIP |
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Term
| Factors that inhibit mucous secretion |
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Definition
•NSAIDs, ASA
•Alcohol
•Bile salts
•Reduced blood supply (stress, hypotension, hypovolemia)
•Alpha- agonists |
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Term
| Regulation of SI secretion |
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Definition
Neural
•ACh, VIP, substance P and serotonin released from submucosal and myenteric plexus neurons
•Parasympathetic
•Sympathetic inhibits (alpha receptors and somatostatin)
Local stimuli
•Distention, tactile, local reflexes
•Irritation (acid, bile, EtOH, toxins)
•Chemical (glucose, acid, bile, ethanol, cholera toxin -> PS reflexes
Hormonal - stimulate epithelial cells directly
•Gastrin
•Secretin
•CCK
•Histamine |
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Term
| Gastric secretions (7 types, plus "other enteroendocrine cells") |
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Definition
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Term
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Definition
Absence of gastric secretion; when acid is not secreted, pepsin is also not secreted
May predispose patient to ulcers and carcinoma
Treatment: removal of cause, H2 blockers, antacids, sucralfate, prostaglandins, vitamin B12 |
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Term
| Is saliva hyper-, hypo-, or isotonic relative to plasma? Why? |
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Definition
ALWAYS hypotonic relative to plasma:
At low flow rates K+ increases a lot, and Na+ and Cl- decrease. HCO3 remains relatively high, even at high rates of secretion. --> saliva becomes hypotonic
- Within the ducts, Na+ is actively absorbed and K+ is actively secreted
Saliva in intercalated ducts has electrolyte conc similar to those of plasma, and is isotonic to plasma.
As fluid moves down the duct, Na+ and Cl- are reabsorbed and K+ and HCO3 are secreted into saliva. The higher the flow of saliva, the less time there is available for modification, and the final saliva more closely resembles plasma in its ionic makeup |
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Term
| How does the rate of salivary secretion affect the pH of saliva? |
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Definition
Slightly acidic (6) at low rates, slightly alkaline (8) at high rates
At high rates of secretion, pH is more alkaline. HCO3 in saliva is higher than that in plasma, except at low flow rates - this makes it more alkaline!
Bottom line: ionic changes in the striated duct (absorption of Na+ and Cl-, release of K+ and bicarb) affect the pH (and osmolarity) of saliva) |
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Term
| Modification of ionic content of primary salivary secretion |
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Definition
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Term
| How can you completely block acid secretion in the stomach? |
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Definition
Proton pump inhibitor!
• Omeprazole
• Prilosec
3 mechanisms i/c acid secretion: ACh, gastrin, histamine - they all stimulate the proton pump to pump H+ out of cell and into gastric lumen
Requires carbonic anhydrase |
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Term
Regulation of gastric secretions
Cephalic phase, gastric phase, intestinal phase
Stimulatory and inhibitory events |
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Definition
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Term
Pancreatic secretions
("acid tide") |
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Definition
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Term
Regulation of secretion of gastric acid
"Alkaline tide" |
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Definition
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