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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
Q
  • Through which receptor does gastrin work on parietal cells?
  • Which second messenger system does gastrin use?
A
  • CCKb receptor
  • Gq
  • IP3/Ca2+ stimulate the H+/K+ ATPase on the apical surface of the parietal cell
26
Q
  • Through which receptor does histamine work on parietal cells?
  • Which second messenger system does it use?
A
  • H2 receptor
  • Gs
  • cAMP stimulates H+/K+ ATPase on apical surface
27
Q
  • Through which G protein and second messenger system do prostaglandins and somatostatin act?
A
  • Gi
  • Inhibit cAMP and inhibit expression of the H+/K+ ATPase on apical surface
28
Q
  • What is the passive feedback mechanism regulating HCl secretion
A
  • pH decreases and inhibits gastrin release (which lowers secretion of acid)
29
Q
  • Which drugs inhibit acid secretion and what receptors do they work on?
A
  • Atropine-inhibits the M3 ACh receptor
  • Cimetidine-inhibits H2 histamine receptor
30
Q
  • Vagus nerve stimulation of HCl secretion:
    • ​Direct versus Indirect pathway
    • Which pathway is blocked by atropine
A
  • 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
Q
  • What are some examples of potentiation in the secretion of HCl in the stomach
A
  • 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
Q
  • What are the pharmacological implications of potentiation with regards to acid secretion?
A
  • 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
Q
  • What are the three phases of gastric HCl secretion?
  • Which phase is absent after a vagotomy?
A
  • Cephalic phase
  • Gastric phase
  • Intestinal phase
  • Cephalic phase absent after vagotomy
34
Q
  • Cephalic phase (30% of acid secretion):
    • Stimuli
    • Mechanisms
A
  • 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
Q
  • Gastric phase (60% of acid secretion):
    • Stimuli
    • Mechanisms (4)
A
  • 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
Q
  • Intestinal phase (5-10% of acid secretion)
    • Stimuli
    • Mechanisms
A
  • 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
Q

_ is most important stimulus for pepsinogen secretion

This triggers local _ reflexes that stimulate _ cells to secrete pepsinogen

A
  • 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
Q

_ is optimal pH for pepsin

Pepsin is reversibly inactivated at pH _

Pepsin is irreversibly inactivated at pH _

A
  • 1.8-3.5
  • 3.5-5.0
  • >7-8
39
Q
  • _ 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
A
  • Intrinsic factor
  • Parietal cells
40
Q
  • Pernicious anemia
A
  • 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
Q
  • The mucosal barrier protects the gastric mucosal epithelium against _ and _
A
  • HCl and pepsin
42
Q
  • What things protect the gastric mucosa
A
  • HCO3-
  • Mucus
  • Prostaglandins (Misoprostol)
  • Mucosal blood flow
  • Gastrin (growth factor for cells of gastric mucosa)
  • Growth factors
43
Q
  • What things damage the gastric mucosa
A
  • Acid
  • Pepsin
  • NSAIDs (aspirin)
  • H pylori
  • Alcohol
  • Bile
  • Stress
44
Q
  • Zollinger-Ellison Syndrome
A
  • 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
Q
  • What test can be used to diagnose gastrin-secreting tumors?
  • How does it work?
  • What is found in testing when patient has a gastrinoma?
A
  • Secreting stimulation
  • Secreting administered
  • Normal person-secretin inhibits gastrin release
  • Gastrinoma-secretin stimulates gastrin release
46
Q
  • Peptic ulcer disease
A
  • 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
Q

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

A
  • Urease
48
Q
  • Summary of the disorders of gastric H+ secretion
A
49
Q
  • Pancreatic enzymes are stored in _
  • When released, what contents do they contain?
A
  • Zymogen granules
  • HCO3- (neutralizes acid)
  • Lipases (fat digestion)
  • Amylases (carb digestion)
  • Proteases (protein digestion)
50
Q
  • Sympathetic versus parasympathetic innervation of the pancreas
A
  • 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
Q
  • What are the two components of pancreatic secretions?
  • What osmolarity is the pancreatic secretion?
A
  • Enzymatic secretion (acinar cells)
    • Pancreatic amlyases and lipases secreted in ACTIVE form
    • Pancreatic proteases 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
Q
  • What transporters are present on the apical and basolateral surface of pancreatic ductal cells
A
  • 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
Q
  • Cystic fibrosis
    • ​Can lead to recurrent acute and chronic pancreatitis
    • Can lead to loss of _ secretion
A
  • 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
Q
  • What are the three phases of pancreatic secretion?
A
  • Cephalic
  • Gastric
  • Intestinal
55
Q
  • Cephalic phase of pancreatic secretion
  • Stimuli
  • Mechanism
A
  • Stimuli: Smell, Taste, Conditoning
  • Mechanism:
    • Vagus nerve
    • Produces mainly enzymatic secretion
56
Q
  • Gastric phase of pancreatic secretion
    • Stimuli
    • Mechanism
A
  • Stimuli:
    • Distension of the stomach
  • Mechanism:
    • Vagus nerve
    • Produces mainly an enzymatic secretion
57
Q
  • Intestinal phase of pancreatic secretion (80%)
A
  • Enzymatic and aqueous secretions are stimulated
58
Q
  • 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?
A
  • Phenylaline
  • Methionine
  • Tryptophan
  • Small peptides
  • Fatty Acids
  • IP3, Ca2+
59
Q
  • Which molecules stimulate the S cells of the pancreas to increase aqueous secretions
  • Through which second messenger do these cells act?
A
  • H+
  • Stimulates secretin
  • cAMP
60
Q
  • Summary of GI secretions
A

GI Exam 2 (14 decks)

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