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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
Q

what are the main stimulators and inhibitors of the PNS in the regulation of salivary secretion

A

stimulators:
-conditioning, food, nausea, smell

inhibitor:
- dehydration, fear, sleep

26
Q

what is the alkaline tide

A

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
Q

what is the function of omeprazole in the regulation of parietal cells

A

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
Q

what are the 3 main stimulators of gastric secretion by parietal cells? and 2 main inhibitors?

A

stimulators: can potentiate to increase rate of secretion
- gastrin
- histamine
- Ach

inhibitors:
- somatostatin
- prostagladins

29
Q

What controls the Ach release to stimulate parietal cells? what is its receptor? what function does it have that increases H+ secretion?

A
  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
Q

What controls the gastrin release to stimulate parietal cells? what is its receptor? what function does it have that increases H+ secretion?

A

Gastrin

  • G cells
  • CCK(beta) receptor
  • Gq
  • inreases IP3 and Ca2+
  • stimulates H/K ATPase
31
Q

What controls the histamine release to stimulate parietal cells? what is its receptor? what function does it have that increases H+ secretion?

A

Histamine

  • ECL cells
  • H2 receptor
  • Gs
  • increases cAMP
  • stimulates H/K ATPase
32
Q

T/F
Ach and gastrin release from Vagus nerve and G cells can stimulate ECL cells to release histamine in parietal cell regulation

A

true

33
Q

describe the pathway of parietal cell inhibitors

A

Somatostatin (D cells) and PGEs (protect gastric mucosa)

  • Gi
  • inhibit cAMP
  • inhibit H/K ATPase
  • both inhibit ECL histamine secretion
34
Q

which parietal cell inhibitor also inhibits G cells to secrete gastrin

A

somatostatin

*secretin also inhibits gastrin

35
Q

describe the passive feedback mechanism that regulates HCL secretion

A

*negative feedback

as the pH falls, gastrin release is inhibited and HCL secretion is decreased. managed by somatostatin

36
Q

how does atropine, mesoprastole, and cimetidine affect HCL secretion

A

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
Q

describe the direct and indirect pathway of vagus nerve stimulation of HCL secretion by parietal cells

A
  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
Q

what are the 3 phases of gastric HCL secretion

A
  1. cephalic
  2. gastric
  3. intestinal
39
Q

describe the cephalic phase of gastric HCL secretion

A
  • *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
Q

describe the gastric phase of gastric HCL secretion

A
  • 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
Q

what drinks also stimulate gastric HCL secretion

A

coffee (caffeinated and noncaffienated), wine, beer,

42
Q

how does dissension of the stomach activate gastric HCL secretion

A

through the mechanoreceptors in the mucosa of the oxyntic and pyloric glands

43
Q

describe the intestinal phase of HCL secretion

A
  • 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
Q

describe the regulation and release of pepsinogen

A

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
Q

what is the optimal pH of pepsin

A
  • Converted at pH of 5
  • optimal is 1.8 - 3.5
  • reversibly inactive at 3.5 - 5.0
  • irreversibly inactivated at > 7 - 8
46
Q

What secretes IF and why is it important

A
  • 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
Q

what are some common causes of pernicious anemia due to no IF from parietal cells

A
  1. atrophic gastritis
    - chronic inflammation that causes loss of parietal cells
  2. autoimmune metaplastic atrophic gastritus
    - immune cells attack IF or parietal cells
48
Q

describe the growth of gastric mucosa

A
  • 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
Q

Name all the protective and damaging factors of gastric mucosa

A

protective
-HCO3, mucus, mucusal blood flow, growth factors

Damaging
-H+, pepsin, H pylori, stress, NSAIDS, smoking, alcohol,, bile

50
Q

what is Zollinger-Ellison syndrome

A
  • 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
Q

what is the secretin stimulation test

A
  • used in dx of gastrinomas
  • normally secretin inhibits gastrin
  • in gastrinomas, secretin causes an abnormal increase in gastrin release
52
Q

what is peptic ulcer disease

A

-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
Q

how does H. Pylori break down the mucosal barrier

A

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
Q

what is the innervation of the exocrine pancreas

A

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
Q

what are the 2 main components of pancreatic secretions

A
  1. HC03

2. enzymatic secretions

56
Q

what is organization of the exocrine pancreatic glands

A
  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
Q

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

A

False, it is opposite. proteases are secreted in inactive form

58
Q

what are the transporters located on the luminal and basolateral side of pancreatic ductal cells

A

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
Q

How does cystic fibrosis affect the pancreas

A
  • 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
Q

what are the 3 phases of pancreatic secretion?

A
  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
Q

desrcribe the regulation pathway of HCO3 and enzymatic pancreatic secretion during the intestinal phase

A

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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