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Hannah GI 2 > secretions of the GI tract > Flashcards

secretions of the GI tract Flashcards

1
Q

What are the functions of saliva produced by the salivary glands

A
  1. initial digestion of starches and lipids
  2. buffering and diluting of ingested food
  3. lubricating food with mucus
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2
Q

what are the 3 major salivary glands and what do they secrete

A
  1. parotid gland (serous only)
    - secretes fluid of water, ions, and enzymes (amylase rich)
    - 25% of salvia output
  2. & 3. Sublingual and submaxillary glands
    - mixed serous and mucus gland
    - secretes aqueous fluid and mucin glycoprotein for lubrication
    - 75% of salvia output
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3
Q

Describe the structure of salivary glands

A
  1. acinus (blind end)
    - produce initial isotonic saliva
  2. intercalated duct (middle)
    - contains saliva isotonic to plasma
    * *myoepithelial cells line the acinus and IC duct and contract to eject saliva into mouth by neural stimulation
  3. Striated duct
    - covered by ductal cells (columnar epithelial) that modify initial saliva to final hypotonic saliva
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4
Q

Describe the composition of saliva and how it compares to plasma

A

composition
-water, electrolytes, a-amylase, lingual lipase, mucus, and kallikrein

compared to plasma

  • is hypotonic
  • higher in potassium and bicarbonate
  • lower in sodium and chloride
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5
Q

what is the importance of kallikrein

A

it is needed for bradykinin formation.

bradykinin is a vasodilator that increases the flow of saliva

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6
Q

what is being absorbed and secreted by ductal cells in the salivary glands

A

absorbed to blood
-Na+ and Cl- in larger amount then absorbed ions

secreted to lumen
-K+ and HCO3-

*net absorption (to blood) of solute!

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7
Q

Name the transporters on the basolateral and luminal side of the salivary ductal cell

A

basolateral

  • Na/K ATPase (brings Na to blood and K into cell)
  • Cl- Channels (leaks Cl into blood)
  • HCO3-/Na symporter (brings both into cell)

Luminal (apical)

  • Na/H exchanger ( moves H into lumen, Na into the cell)
  • Cl/ HCO3- exchanger (moves HCO3 into lumen, Cl into cell)
  • H/ K exchanger (moves K into lumen and H into cell)
  • **another way HCO3- can enter lumen is though the cAMP-activated CFTR Cl-channel
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8
Q

T/F Ductal cells are impermeable to water

A

TRUE
-so water can not leave and more solute is being absorbed to blood so it leaves a hypotonic solution inside the salivary gland

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9
Q

The ANS is the main (exclusive) regulator of salivary excretion. what is the PNS and SNS innervation for salivary glands ?

A

PNS

  • presynpatic: glossopharyngeal and facial nerves
    postsynaptic: in autonomic ganglia (submandibular and Otic ganglion) and innervate individual glands

SNS

  • pre: originate at thoracic spinal nerves of T1-T3 and synapse in superior cervical ganglion
  • post: fibers extend to the glands in the periarterial spaces
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10
Q

The facial nerve serves to innervate what gland?

the glossopharyngeal nerve innervates what gland?

A

Facial
-PNS innervation to submandibular and sublingual gland

Glossopharngeal
-PNS innervation of parotid gland

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11
Q

T/F

The PNS and SNS have the same effect on salivary glands to increase secretion of saliva

A

TRUE

-but the PNS effect dominates

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12
Q

What receptors does the PNS pathway for salivary secretion use? and what is its effects to increase saliva excretion?

A

Receptor: mAChR in acinar or ductal cell
-increases IP3 and Ca2+

stimulation of salivary cells: increases saliva production, increases HCO3- and enzyme secretion into the lumen of the striated duct, and contract myoepithelial cells to excrete saliva

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13
Q

What receptors does the SNS pathway for salivary secretion use? and what is its effects to increase saliva excretion?

A

Receptor: Beta-Adrenergic receptor in acing/ductal cells
-increases cAMP

stimulation of salivary cells: increases saliva production, increases HCO3- and enzyme secretion into the lumen of the striated duct, and contract myoepithelial cells to excrete saliva

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14
Q

what effects does ADH and aldosterone have on saliva

A

They change the composition of saliva by decreasing Na and increasing K

ADH
-increases water absorption
Aldosterone
-increases Na/ K exchange

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15
Q

The gastric mucose secretes gastric juice. what are the components of gastric acid?

A 
HCl
Pepsinogen 
Mucus
IF
Water
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16
Q

what is the function of gastric HCl

A
  • secreted by parietal cells
  • kills bacteria that enter the stomach
  • converts pepsinogen to pepsin
  • aids in protein digestion
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17
Q

what is the function of pepsinogen in gastric juice

A
  • secreted by Chief cells
  • inactive precursor to pepsin
  • pepsin breaks down proteases in the stomach
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18
Q

what is the function of gastric mucus?

A
  • from surface/neck mucus cells
  • line and protect walls of the the stomach
  • lubricant
  • with HCO3-it neutralizes acid and maintains neutral pH of the mucosa
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19
Q

What is the function of IF in gastric juice?

A
  • secreted by parietal cells

- helps B12 Absoprtion in the ileum

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20
Q

what is the function of H20 in gastric juice

A
  • medium for the action of HCL and enzymes

- solubilizes much of the ingested material

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21
Q

the gastric mucose is divided into what 2 gland areas? what are the characteristics of each?

A

oxyntic and pyloric gland area
1. oxyntic- in proximal 80% of stomach (body and fundus). secretes acid with parietal cells and pepsinogen with chiefs cells, but has no G cells for gastrin secretion

  1. pyloric- in distal 20% (antrum). synthesizes and releases gastrin to circulation by G cells, but has no parietal cells
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22
Q

what determines the maximal secretory rate of HCl

A

the number of parietal cells which make the gastric pH 1-2 and form HCl in the the villus-like membranes of the canaliculi with lots of mitochondria for energy

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23
Q

what are the transporters on the basolateral and luminal side of gastric parietal cells?

A

basolateral

  • Na/K ATPase pushing Na into the blood and K into the cell
  • HCO3/Cl exchanger pushing HCO3 into the blood and Cl-into the cell

Apical

  • H/K ATPase pushing H+ into the lumen and K into the cell
  • Cl- channel where Cl- can enter the lumen

**net secretion of HCl into the lumen and absorption of HCO3- into the blood

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24
Q

what is the affect of atropine on the regulation of salivary glands

A

atropine inhibits mAChR so it will depress salivary glands

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25
what are the main stimulators and inhibitors of the PNS in the regulation of salivary secretion
stimulators: -conditioning, food, nausea, smell inhibitor: - dehydration, fear, sleep
26
what is the alkaline tide
after a meal the parietal cells secretion of HCL into the lumen and HCO3 absorption in the blood causes an increase of HCO3- in the blood which is called an alkaline tide
27
what is the function of omeprazole in the regulation of parietal cells
it is an proton pump inhibitor that will inhibit the K/H ATPase on the luminal surface of parietal cells so that H+ can not enter the lumen. it will decrease acid secretion and the acidity of the stomach (raise the pH of the stomach) -used to treat peptic ulcers, or Gerd, etc.
28
what are the 3 main stimulators of gastric secretion by parietal cells? and 2 main inhibitors?
stimulators: can potentiate to increase rate of secretion - gastrin - histamine - Ach inhibitors: - somatostatin - prostagladins
29
What controls the Ach release to stimulate parietal cells? what is its receptor? what function does it have that increases H+ secretion?
1. Ach - vagus nerve - M3 muscarinic receptor - Gq - Increases IP3 and Ca2+ - stimulates H/K ATPase to release H ions into the lumen of the cell for secretion
30
What controls the gastrin release to stimulate parietal cells? what is its receptor? what function does it have that increases H+ secretion?
Gastrin - G cells - CCK(beta) receptor - Gq - inreases IP3 and Ca2+ - stimulates H/K ATPase
31
What controls the histamine release to stimulate parietal cells? what is its receptor? what function does it have that increases H+ secretion?
Histamine - ECL cells - H2 receptor - Gs - increases cAMP - stimulates H/K ATPase
32
T/F Ach and gastrin release from Vagus nerve and G cells can stimulate ECL cells to release histamine in parietal cell regulation
true
33
describe the pathway of parietal cell inhibitors
Somatostatin (D cells) and PGEs (protect gastric mucosa) - Gi - inhibit cAMP - inhibit H/K ATPase - both inhibit ECL histamine secretion
34
which parietal cell inhibitor also inhibits G cells to secrete gastrin
somatostatin *secretin also inhibits gastrin
35
describe the passive feedback mechanism that regulates HCL secretion
*negative feedback | as the pH falls, gastrin release is inhibited and HCL secretion is decreased. managed by somatostatin
36
how does atropine, mesoprastole, and cimetidine affect HCL secretion
atropine -it inhibits muscarinic receptors so it will inhibit the M3 receptor used to secrete Ach via vagus nerve stimulation. It will decrease HCL secretion cimetidine - inhibits H2 histamine receptor and the Gs pathway. will decrease HCL secretion - can be used to treat gastric ulcers and GERD Mesoprastole - type of PGE - will activate Gi inhibition pathway - decreases HCL secretion
37
describe the direct and indirect pathway of vagus nerve stimulation of HCL secretion by parietal cells
1. direct - M3 receptor and Ach release to increase the H/K ATPase on parietal cells luminal membrane 2. indirect - it will stimulate GRP secretion which then stimulates G cells to release gastrin into the blood and gastrin will act on parietal cells to increase HCL secretion. also will inhibit D cells and somatostatin release further increasing HCL *atropine will only block the direct pathway due to the mAChR
38
what are the 3 phases of gastric HCL secretion
1. cephalic 2. gastric 3. intestinal
39
describe the cephalic phase of gastric HCL secretion
* *VAGUS and ACH pathway - via vagus nerve from vagal center of medulla - 30% of HCL secreted - stimuli: smelling, tasting, chewing, swallowing, conditioning - vagus causes direct release of ACh to increase HCL - vagus indirectly stimulates gastrin release through GRP **vagotomy will abolish this response
40
describe the gastric phase of gastric HCL secretion
- 60% of HCL secreted - stimuli: stomach distension and presence of breakdown of proteins - distension activates vagus nerve (vagovagal reflex) direct and indirect pathways, and local reflexes (plyopylorus reflex) to secrete ACh direct & indirect pathway - digested proteins stimulate G cells to secrete gastrin * vagatomy will not abolish * gastrin is secreted by stomach and duodenum
41
what drinks also stimulate gastric HCL secretion
coffee (caffeinated and noncaffienated), wine, beer,
42
how does dissension of the stomach activate gastric HCL secretion
through the mechanoreceptors in the mucosa of the oxyntic and pyloric glands
43
describe the intestinal phase of HCL secretion
- 5-10% of HCL secreted - stimuli SI distension or digested proteins - activate intestinal G cells to secrete gastrin from the duodenum to the blood stream which will stimulate parietal cells in the stomach - digested proteins will also stimulate acid secretion via direct effect on parietal cells
44
describe the regulation and release of pepsinogen
Pepsinogen is released from chief cells in the oxyntic glands of gastric mucosa when the pH of the stomach is acidic enough (<5) to convert it to pepsin. * vagus nerve is most important stimulator * local cholinergic reflexes also stimulate chief cells in response to increased H+ concentration
45
what is the optimal pH of pepsin
- Converted at pH of 5 - optimal is 1.8 - 3.5 - reversibly inactive at 3.5 - 5.0 - irreversibly inactivated at > 7 - 8
46
What secretes IF and why is it important
- parietal cells secrete the mucoprotein - is the ONLY essential gastric secretion and is needed for B12 absorption in the ileum - failure to secrete IF is related to achlorhydria and loss of parietal cells - no IF can lead to pernicious anemia
47
what are some common causes of pernicious anemia due to no IF from parietal cells
1. atrophic gastritis - chronic inflammation that causes loss of parietal cells 2. autoimmune metaplastic atrophic gastritus - immune cells attack IF or parietal cells
48
describe the growth of gastric mucosa
- surface mucus cells secrete mucus and epithelial cells secrete HCO3- to create a protective barrier for the gastric mucosa against HCL and pepsin - PGE and gastrin are growth factors to protect - acid, pepsin, NSAIDs, H. Pylori, alcohol, bile, and stress damage the gastric mucosa
49
Name all the protective and damaging factors of gastric mucosa
protective -HCO3, mucus, mucusal blood flow, growth factors Damaging -H+, pepsin, H pylori, stress, NSAIDS, smoking, alcohol,, bile
50
what is Zollinger-Ellison syndrome
- tumor in head of pancreas (gastrinoma) causes high H+ secretion and an increase in parietal cell mass (trophic effect) bc of high gastrin levels - H+ in duodenum causes ulcer and inactivates pancreatic lipases so steatorrhea occurs - used secretion stimulation test as a diagnostic tool
51
what is the secretin stimulation test
- used in dx of gastrinomas - normally secretin inhibits gastrin - in gastrinomas, secretin causes an abnormal increase in gastrin release
52
what is peptic ulcer disease
-normally caused by H. pylori infection and NSAID use which result in loss of protective mucosal barrier or excessive H+ and pepsin secretion -two types : gastric and duodenal ulcers 1. gastric ulcer - formed on lining of stomach usually bc defective mucosal barrier. low H+ secretion and high gastrin levels. 2. duodenal ulcer- on lining of duodenum usually bc H+ secretion is higher than normal. high H+ secretion and gastrin levels. increase in parietal cells mass. more common, and usually not malignant
53
how does H. Pylori break down the mucosal barrier
releases cytotoxins that break down the barrier - urease converts urea to ammonia which alkalinizes the environment. ammonia produces ammonium which is cytotoxic and damages epithelial cells - dx test based on urease activity
54
what is the innervation of the exocrine pancreas
SNS - postganglionic nerves from the celiac and superior mesenteric plexuses (C the X-SMall Pancreas) - inhibits PNS -preganglionic fibers synapse in ENS and postganglionc fibers synapse on exocrine pancreas
55
what are the 2 main components of pancreatic secretions
1. HC03 | 2. enzymatic secretions
56
what is organization of the exocrine pancreatic glands
1. acinus - synthesize major digestive enzymes (pancreatic amylases, lipases, and proteases) 2. centroacinar cells - secrete aqueous soliton with HCO3 3. ductal cells - modification of primary secretion - secrete aqueous soliton with HCO3
57
T/F pancreatic amylases and lipases are secreted in an inactive form and activated in the lumen of duodenum, and pancreatic proteases are secreted in active form
False, it is opposite. proteases are secreted in inactive form
58
what are the transporters located on the luminal and basolateral side of pancreatic ductal cells
basolateral - Na/K ATPase (pushes Na into blood and K into cell) - Na/H+ exchanger ( pushes H+ into blood and Na into cell) Luminal - HCO3/Cl- exchanger ( pushes HCO3 into lumen and Cl- into cell) * cAMP activated CFTR Cl- channel can also move HCO3 into lumen paracellular -Na+ moves into the lumen of ductal cells *Net absorption of H+ into blood and secretion of HCO3 into lumen
59
How does cystic fibrosis affect the pancreas
- in CF the pancreas is one of the 1st organs to fail - it inhibits the CFTR regulated Cl- channel on the luminal surface therefor it stops Cl- movement into cell which can cause a defect in the HCO3/Cl- exchanger which causes HCO3 to move into lumen of ductal cells for secretion - causes loss of HCO3- secretion and pancreatitis
60
what are the 3 phases of pancreatic secretion?
1. cephalic - stimuli::smell, taste, condition - vagus nerve - produces ONLY enzymatic secretion 2. gastric - stimuli: stomach distension - vagus nerve - produces ONLY enzymatic secretion 3. intestinal phase - 80% of pancreatic secretion - causes both enzymatic and aqueous HC03 secretion
61
desrcribe the regulation pathway of HCO3 and enzymatic pancreatic secretion during the intestinal phase
enzymatic - amino acids, peptides, and fatty acids stimulate I cells in duodenum to make CCK (affects potentiated by ACh) - causes increase in IP3 and Ca2+ in acinar cells - causes enzymatic production to increase HCO3 aqueous solution - H+ ions stimulate S cells to secrete secretin (affects potentiated by ACh and CCK - increases cAMP in ductal cells - increases aqueous solution production *ACh comes from vagus nerve therefore vagus (PNS) potentiates both pathways

Hannah GI 2 (11 decks)

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