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GI Exam 2 > Secretions of the GI Tract and Pancreas > Flashcards

Secretions of the GI Tract and Pancreas Flashcards

1
Q
  • What are the three types of salivary glands and what do they secrete?
A
  • Parotid (25% daily saliva)
    • Serous
    • Water, ion, enzymes (amylase)
  • Submaxillary and sublingual (75% daily saliva)
    • Serous and mucous cells
    • Aqueous fluid and mucin glycoprotein for lubrication
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2
Q
  • Structure of salivary glands
A
  • Acinus
  • Myoepithelial cells
    • Motile extensions
    • Contract when neurally stimulated to eject saliva
  • Intercalated duct
    • Isotonic saliva
  • Striated duct
    • Contains ductal cells (columnar epithelial cells that produce hypotonic saliva)
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3
Q
  • Saliva is _ compared to plasma and is modified in the _ duct
  • Saliva is high in what electrolytes?
  • Saliva is low in what electrolytes?
A
  • Hypotonic, intercalated
  • K+, HCO3-
  • Na+, Cl-
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4
Q
  • What are the two main steps in the formation of saliva?
A
  1. Formation of isotonic plasma-like solution by acinar cells
  2. Modification of the isotonic solution by ductal cells
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5
Q
  • What transporters are present on the apical and basolateral sides of a salivary ductal cell?
  • Net result of these transporters?
A
  • Apical
    • ​Na+/H+ exchanger
    • Cl-/HCO3- exchanger
    • H+/K+ exchanger
    • CTFR Cl- channel
  • Basolateral
    • ​Na+/K+ ATPase
    • Cl- leak channel
    • Na+/HCO3- symporter (pumping into cell)
  • More NaCl is absorbed than KHCO3 secretion
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6
Q
  • Ductal cells are impermeable to _ making hypotonic saliva
A
  • Water
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7
Q
  • What are the innervations of the salivary glands
  • Of the two, which dominates?
A
  • Parasympathetic
    • Presynaptic nerves in facial and glossopharyngeal nerves
    • Postsynaptic fibers in autonomic ganglia
  • Sympathetic
    • T1-T3
    • Preganglionic nerves in cervical ganglion
    • Postganglionic fibers in glands of periarterial spaces
  • parasympathetics dominate
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8
Q
  • The facial nerve stimulates _ glands
  • The glossopharyngeal nerve stimulates _ glands
A
  • Facial-parotid/serous
  • Glossopharyngeal-sublingual and submaxillary
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9
Q
  • What hormones modify the composition of saliva by decreasing its Na+ concentration and increasing its K+ concentration?
A
  • ADH
  • Aldosterone
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10
Q
  • What conditions will inhibit parasympathetic stimulation of acinar or ductal cells?
  • Which conditions will stimulate?
A
  • Inhibit:
    • Dehydration
    • Fear
    • Sleep
  • Stimulate
    • Conditioning
    • Food
    • Smell
    • Nausea
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11
Q
  • Stimulation of salivary cells results in:
A
  • Increased saliva production
  • Increased HCO3- and enzyme secretions
  • Contraction of myoepithelial cells
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12
Q
  • Parasympathetics activate salivary cells through which receptor and second messenger system?
A
  • ACh on mAChR
  • IP3 and Ca2+
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13
Q
  • Sympathetics activate salivary glands through which receptor and second messenger system?
A
  • NE on beta adrenergic receptor
  • cAMP
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14
Q
  • What is unique about the sympathetic and parasympathetic stimulation of the salivary glands?
A
  • They have the same net effect of increasing saliva secretion
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15
Q
  • Main components of gastric mucosa and their functions
A
  • HCl
    • Necessary for conversion of pepsinogen to pepsin
    • Kills bacteria
  • Pepsinogen
  • Mucus
    • Lines wall of stomach and protects it from damage
    • With HCO3-, neutralizes acid and maintains the surface of the mucosa at neutral pH
  • Intrinsic factor
    • Required for absorption of B12 in the ileum
  • H20
    • Solubilizes ingested material
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16
Q
  • What two glands are the mucosa of the stomach divided into?
A
  • Oxyntic gland
  • Pyloric gland
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17
Q
  • What is the function of the oxyntic gland?
  • Where is this gland located?
A
  • Located in proximal 80% of stomach
  • Secretes acid
  • Contains the following cells:
    • Parietal cells-acid secretion
    • ECL cells-histamine secretion
    • D Cells-somatostatin
    • Chief Cell-pepsinogen
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18
Q
  • Where are pyloric glands located?
  • What is their function?
A
  • Distal 20% of stomach (antrum)
  • Synthesize and release gastrin
  • Contain:
    • G cells-secrete gastrin
    • D cells-secrete somatostatin
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19
Q
  • What do the following cells secrete:
    • Parietal cells
    • Chief cells
    • G cells
    • Mucus cells
A
  • Parietal cells-HCl and intrinsic factor
  • Chief cells-pepsinogen
  • G cells-gastrin
  • Mucus Cells-mucus, HCO3- and pepsinogen
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20
Q
  • What transporters are present on the apical and basolateral sides of parietal cells that function to secrete acid/reabsorb bicarbonate?
A
  • Apical
    • ​K+/H+ exchanger (inhibited with omeprazole)
    • Cl- leak channels (follows H+ entering lumen)
  • Basolateral
    • ​Na+/K+ ATPase
    • HCO3-/Cl- exchanger (responsible for the alkaline tide)
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21
Q
  • What is the two-component model of gastric secretion
A
  • Non-parietal secretions
    • Alkaline secretion of constant and low volume
    • Primary components are Na+,Cl-, K+ (isotonic to plasma)
    • HCO3- secreted at 30 mEq/L
  • Parietal secretions
    • Hyperosmotic
    • 150-160 mEq/L of H+ and 10-20 mEq/L of K+
    • As the secretion rate increases, the concentration of electrolytes begin to approach those of pure parietal cell secretion
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22
Q
  • Which agents stimulate HCl secretion by parietal cells
A
  • ACh (from vagus)
  • Gastrin (from G cells)
  • Histamine (thru ECL cells)
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23
Q
  • Which agents inhibit HCl secretion by Parietal cells
A
  • Somatostatin (from D cells)
  • Prostaglandins (inhibits ECL cells)
  • Both act via Gi to inhibit cAMP pathways
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24
Q
  • Through which receptor does ACh work on parietal cells?
  • What G protein is stimulated and what second messenger pathway is activated?
A
  • M3
  • Gq
  • IP3/Ca2+ to stimulate H+/K+ ATPase on apical surface of parietal cells
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25
* Through which receptor does gastrin work on parietal cells? * Which second messenger system does gastrin use?
* CCKb receptor * Gq * IP3/Ca2+ stimulate the H+/K+ ATPase on the apical surface of the parietal cell
26
* Through which receptor does histamine work on parietal cells? * Which second messenger system does it use?
* H2 receptor * Gs * cAMP stimulates H+/K+ ATPase on apical surface
27
* Through which G protein and second messenger system do prostaglandins and somatostatin act?
* Gi * Inhibit cAMP and inhibit expression of the H+/K+ ATPase on apical surface
28
* What is the passive feedback mechanism regulating HCl secretion
* pH decreases and inhibits gastrin release (which lowers secretion of acid)
29
* ***Which drugs inhibit acid secretion and what receptors do they work on?***
* Atropine-inhibits the M3 ACh receptor * Cimetidine-inhibits H2 histamine receptor
30
* ***Vagus nerve stimulation of HCl secretion:*** * ***​Direct versus Indirect pathway*** * ***Which pathway is blocked by atropine***
* **Direct pathway** * **​**Vagus directly stimulates parietal cells to secrete acid * **Indirect pathway** * **​**Releast of GRP on G cells to stimulate gastrin release * Gastrin will then act on the parietal cells and induce acid secretion * Direct pathway blocked by atropine (remember atropine is blocking the M3 AChR on the basolateral surface of parietal cells)
31
* ***What are some examples of potentiation in the secretion of HCl in the stomach***
* Potentiation-combined response of two stimulants exceeds sum of their individual responses (**requires presence of separate receptors on the targer cell for each stimulant)** * Histamine potentiates ACh and gastrin * ACh potentiates Histamine and gastrin * (AH-potentiation)
32
* ***What are the pharmacological implications of potentiation with regards to acid secretion?***
* Cimetidine (H2 receptor antagonist-inhibits histamine) will block potentiated effects of ACh and gastrin * Atropine (mAChR antagonis that blocks ACh) will block potentiated effects of histamine and gastrin
33
* What are the three phases of gastric HCl secretion? * ***Which phase is absent after a vagotomy?***
* Cephalic phase * Gastric phase * Intestinal phase * Cephalic phase absent after vagotomy
34
* Cephalic phase (30% of acid secretion): * Stimuli * Mechanisms
* Stimuli: * Smelling and tasting * Chewing * Swallowing * Conditioned reflexes * Mechanisms * Vagus nerve (direct and indirect pathways) * Direct-releases ACh on parietal cells * Indirect-releases GRP on G cells to secrete gastrin
35
* Gastric phase (60% of acid secretion): * Stimuli * Mechanisms (4)
* Stimuli * Distension of stomach * Presence of breakdown of proteins * Amino acids and small peptides * Mechanisms * Distension-activates mechanoreceptors in mucosa of oxyntic and pyloric glands * Vagus nerve (direct and indirect pathways) * Distension of antrum-local ENS reflexes release ACh that acts on both parietal and G cells (pyloric-pylorus reflex) * Amino acids and small peptides stimulate gastrin release from G cells
36
* Intestinal phase (5-10% of acid secretion) * Stimuli * Mechanisms
* Stimuli * Meal * Mechanisms * Distension of small intestine-stimulates acid secretion * Digested proteins-stimulate acid secretion via * Direct effect on parietal cells * Gastrin secretion (intestinal G cells)-acts on parietal cells to increase acid production
37
\_ is most important stimulus for pepsinogen secretion This triggers local _ reflexes that stimulate _ cells to secrete pepsinogen
* Vagus nerve stimulation (secretion of acid) * Cholinergic, Chief **Pepsinogen is secreted only when the gastric pH is acidic enough to convert it to pepsin (pH \<5)**
38
\_ is optimal pH for pepsin Pepsin is reversibly inactivated at pH \_ Pepsin is irreversibly inactivated at pH \_
* 1.8-3.5 * 3.5-5.0 * \>7-8
39
* _ is the only secretion that is required by the stomach and essential for the absorption of vitamin B12 in the ileum * It is secreted by _ cells and serves as a mucoprotein * Failure to secrete this is associated with **achlorhydria and absence of parietal cells**
* Intrinsic factor * Parietal cells
40
* **Pernicious anemia**
* Stomach does not produce enough IF * Decreased absorption of Vitamin B12 (important for **RBC development)** * Hard to diagnose because **liver** has B12 stores that can last for months before problem is detected * Common causes: * **Atrophic gastritis**-chronic inflammation of GI mucosa leading to the loss of parietal cells * **Autoimmune metaplastic atrophic gastritis-**immune cells attach IF protein or gastic parietal cells
41
* The mucosal barrier protects the gastric mucosal epithelium against _ and \_
* HCl and pepsin
42
* ***What things protect the gastric mucosa***
* HCO3- * Mucus * Prostaglandins (Misoprostol) * Mucosal blood flow * Gastrin (**growth factor for cells of gastric mucosa)** * Growth factors
43
* ***What things damage the gastric mucosa***
* Acid * Pepsin * **NSAIDs (aspirin)** * **H pylori** * **Alcohol** * **Bile** * **Stress**
44
* ***Zollinger-Ellison Syndrome***
* High H+ secretory rates * **Caused by pancreatic tumor that secretes large amounts of gastrin (gastrinoma)** * **​**Increase in H+ secretion by parietal cells * Increase in parietal cell mass (trophic effect) * **Leads to duodenal ulcer (too much acid for HCO3- to buffer)** * **Low duodenal pH inactivates pancreatic lipases (can't digest fats so you have steatorrhea)** * Sx: * Nausea * Vomiting * Peptic ulcer disease * GERD * Weight Loss * Epigastric pain * Hematemesis * Hematochezia * Melena
45
* What test can be used to diagnose gastrin-secreting tumors? * How does it work? * What is found in testing when patient has a gastrinoma?
* Secreting stimulation * Secreting administered * Normal person-secretin inhibits gastrin release * **Gastrinoma-secretin stimulates gastrin release**
46
* ***Peptic ulcer disease***
* Commonly caused by H. Pylori and overuse of NSAIDs * Result of: * **Loss of protective mucosal barrier** * **Excess H+ and pepsin secretions** * Two types; * Gastric * Usually d/t defects in mucosal barrier * Duodenal * More common * Usually do not become malignant * H+ secretions are higher than normal (could be due to increased activity of parietal cells)
47
***The enzyme _ helps bacteria of H.Pylori to colonize the gastric mucosa*** ***This enzyme is responsible for the conversion of urea to ammonia*** ***Buildup of ammonium (NH4+) causes cytotoxicity*** ***This enzyme will be elevated in gastric and duodenal ulcers caused by H.Pylori***
* Urease
48
* Summary of the disorders of gastric H+ secretion
49
* Pancreatic enzymes are stored in \_ * When released, what contents do they contain?
* Zymogen granules * HCO3- (neutralizes acid) * Lipases (fat digestion) * Amylases (carb digestion) * Proteases (protein digestion)
50
* ***Sympathetic versus parasympathetic innervation of the pancreas***
* **Sympathetic** * **​**Postganglionic nerves from **celiac** and **superior mesenteric plexuses** * **Inhibits pancreatic secretion** * **Parasympathetic** * **​****Vagus nerve** * Preganglionic fibers synapse in ENS * Postganglionic fibers synapse on exocrine pancreas * **Stimulates pancreatic secretions**
51
* ***What are the two components of pancreatic secretions?*** * **What osmolarity is the pancreatic secretion?**
* Enzymatic secretion (**acinar cells**) * Pancreatic amlyases and lipases secreted in ACTIVE form * Pancreatic protease**s secreted in INACTIVE forms and converted to active forms in lumen of the duodenum** * Aqueous secretion (**centroacinar and ductal cells**) * **HCO3- rich fluid that alkalinizes and hydrates protein rich secretions of the acinar cells** * Initial secretion modified by transport processes in ductal epithelial cells * Isoosmotic (300 mOsm)
52
* ***What transporters are present on the apical and basolateral surface of pancreatic ductal cells***
* **APICAL** * **​**HCO3-/Cl- exchanger (with HCO3- going into lumen) * CTFR Cl- Channel (also aids in HCO3- secretion into lumen) * **BASOLATERAL** * **​**Na+/K+ ATPase * Na+/H+ symporter * **PARACELLULAR** * **​**Na+ moves into lumen * Net result of all of these transporters is a secretion of HCO3- and reabsorption of H+
53
* ***Cystic fibrosis*** * ***​****Can lead to recurrent acute and chronic pancreatitis* * *Can lead to loss of _ secretion*
* **Mutation in CTFR channel in apical surface of pancreatic duct cells** * **HCO3-** * Ability to flush active enzymes out of the duct may be lost (can destroy the pancreas and lead to pancreatitis)
54
* What are the three phases of pancreatic secretion?
* Cephalic * Gastric * Intestinal
55
* Cephalic phase of pancreatic secretion * Stimuli * Mechanism
* Stimuli: Smell, Taste, Conditoning * Mechanism: * Vagus nerve * Produces mainly **enzymatic secretion**
56
* Gastric phase of pancreatic secretion * Stimuli * Mechanism
* Stimuli: * Distension of the stomach * Mechanism: * Vagus nerve * **Produces mainly an enzymatic secretion**
57
* Intestinal phase of pancreatic secretion (80%)
* **Enzymatic and aqueous secretions are stimulated**
58
* **Which molecules stimulate the I cells of the pancreas to secrete enzymes? (I cells-enzymatIc; S cells-aqueouS)** * **Through which second messenger do these molecules act?**
* Phenylaline * Methionine * Tryptophan * Small peptides * Fatty Acids * **IP3, Ca2+**
59
* ***Which molecules stimulate the S cells of the pancreas to increase aqueous secretions*** * ***Through which second messenger do these cells act?***
* H+ * Stimulates secretin * cAMP
60
* Summary of GI secretions

GI Exam 2 (14 decks)

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