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GIGU test! > Secretions of the Gastrointestinal Tract and the Pancreas > Flashcards

Secretions of the Gastrointestinal Tract and the Pancreas Flashcards

1
Q

What is the Function of Saliva? and what is it composed of?

A
  • Initial digestion of starches and lipids
  • Dilution and buffering of ingested food
  • Lubrication of ingested food with mucus

Saliva is composed of H20, electrolytes, a-amylase, lingual lipase, kallikrein, and mucus

Saliva is hypotonic (compared to plasma)

  • higher K+ and HCO3- concentrations
  • lower Na+ and Cl- concentrations
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2
Q

What are the 3 major salivary glands and what are they composed of and what do they secrete?

A

Parotid Glands:

  • Composed of serous cells
  • secrete fluids composed of water, ions, and enzymes (rich in amylase)
  • secrete 25 percent of the daily output of saliva

Submaxillary and sublingual glands (mixed glands)

  • composed of serous and mucous cells
  • secret aqueous fluid and mucin glycoprotein for lubrication
  • Secrete most of the rest 75% of daily output saliva
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3
Q

4 Structures of the Salivary gland, and each of their functions

A

Acinus (blind end)
-acinar cells secrete initial saliva

Myoepithelial cells

  • have motile extensions
  • when stimulated by neural input, contract to eject saliva into the mouth

Intercalated duct
-Saliva in the intercalated duct is similar in ionic composition to plasma

Striated duct:

  • Lined by columnar epithelial cells (ductal cells)
  • Ductal cells modify the inital saliva to produce the final saliva (hypotonic)
  • Ductal cells alter the concentration of various electrolytes
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4
Q

What is the mechanism of Salivary secretion?

A

Two main steps:

  • Formation of the isotonic plasma like solution by acinar cells
  • Modification of the isotonic solution by the ductal cells

Combined action is absorption of Na+ and Cl- and secretion of K+ and HCO3-
-net absorption of solute, more NaCl is absorbed than KHCO3 is secreted

all this is done via transporters:

  • Na/H exchange
  • Cl/HCO3 exchange
  • H/K exchange

HCO3- leaves the cell to the lumen via cAMP-activated CFTR Cl- channel or via the Cl-/HCO3- exchanger

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5
Q

when saliva first leaves the acinar cells it is isotonic, how does it become hypotonic as it flows through the ducts?

A

Ductal cells are H2O impermeable

-there is a net absorption of solute (more NaCl is avsorbed than KHCO3 secreted)

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6
Q

What are the Innervations of the salivary glands?

A

Parasympathetic:
-presynaptic nerves originate at facial and glossophryngeal nerves, postsynpatic fibers in the autonomic ganglia innervate individual glands

Sympathetic:
-Preganglionic nerves originate at the cervical ganglion, whose postganglionic fibers extend to the glands in the periarterial space

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7
Q

how does parasympathetics and sympathetics affect salivary secretion?

A

Parasympathetics: stimulate salivary cells

  • release of ACh on to the mAChR of the Acinar or ductal cells
  • rlease of IPs and Ca+ leading to increase saliva production and increase in HCO3- and enzyme secretions
  • as well as contraction of myoepithelial cells

Sympathetics: also stimulate the salivary glands

  • release of NE on BAR receptors of acinar or ductal cells
  • release of cAMP leading to increase in salivary production, increase of HCO3- and enzyme secretion
  • contraction of myoepithelial cells
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8
Q

what are some environmental cues for activation and inactivation of the parasympathetic activation of salivary glands?

A

activation:
- conditioning
- food
- Nausea
- smell

inactivation:

  • Dehydration
  • fear
  • sleep
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9
Q

How does ADH and Aldosterone affect saliva?

A

ADH and aldosterone modify the composition of saliva by decreasing its Na+ concentration and increasing its K+ concentration

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10
Q

What are the main components of gastric juice?

A

HCL (H+):

  • Together with pepsin it initiates protein digestion
  • Necessary for the conversion of pepsinogen to pepsin
  • kills a large number of bacteria that enter the stomach

Pepsinogen
-Inactivaate precursor

Mucus

  • Lines the wall of the stomach and protects it rom damage
  • Lubricant
  • Together with HCO3-, it neutralizes acid and maintains the surface of the mucosa at netral pH

Intrinsic factor
-required for the absorption of vitamin B12 in the ileum

H2O

  • medium for the action of HCl and enzymes
  • Solubilizes much of the ingested material
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11
Q

what are the two different gastric mucosa divided into? and where are there locations and what are the main things they secrete?

A

Oxyntic Gland:

  • Located in the proximal 80% of the stomach (body and fundus)
  • Secretes acid

Pyloric Gland:

  • Located in the distal 20% of the somach (antrum)
  • Synthesizes and releases gastrin
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12
Q

What is a major function of parietal cells?

A

Secrete HCL

  • the number of pariteal cells determines the maximal secretory rate
  • the function of the low gastric pH (1-2) is to convert pepsinogen to pepsin
  • HCL is formed at the villus-like membranes of the canaliculi
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13
Q

Cellular mechanism of HCL secretion by gastric parietal cells?

A

Carbonic anhydrase converts CO2 and H20 to H+ and HCO3-

  • HCL is secreted since Cl- will follow H+ , this is done via a K+ and H+ transporter that requires ATP
  • HCO3- is released into the blood and CL- is brought back into the cell

Na+ is sent into the blood and K+ is brought back in, this requires ATP

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14
Q

What is the two component model of gastric secretion?

A

Non-Parietal

  • Basal alkaline secretion of constant and low volume
  • its primary constitutents are Na+ and CL- and K+ is present at the same concentration as plasma
  • HCO3- is secreted at a concentration of 30 mEq/L

Parietal

  • slightly hyperosmotic
  • CL- is the only anion present
  • 150-160 mEq H+/L and 10-20 mEq K+/L

knowledge of composition of gastric juice is required in the treatment of patients suffering from vomitting or patients maintained with IV

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15
Q

what is the feedback mechanism for gastrin as pH levels drop?

A

Gastrin will be inhibited which will decrease HCL secretion

this is done via Somatostatin released from D cells also prostaglandins

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16
Q

what are the 2 pathways for vagus nerve stimuation of HCL secretion by parietal cells

A

Direct pathway:

  • vagus activates parietal cells via ACh
  • Atropine blocks the direct pathway of vagal stimulation

indirect pathway:

  • act on G cells via GRP which then releases gastrin that will circulate to then activate parietal cells to release HCL
  • atropine doesnt affect this pathway because of the use of GRP
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17
Q

How is the regulation of gastrin done?

A
  • Somatostatin acts on G cells to inhibit gastrin release
  • Vagal activation stimulates gastrin release by releasing GRP and inhibiting the release of somatostatin
  • Negative feedback regulation by gastrin (low pH will then increase somatostatin releease
  • H+ in the gastric lumen stimulates release of somatostatin
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18
Q

what is potetiation? and how does it affect the rate of secretion of HCl

A

Combined response to two stimulants exceeds the sum of their individual response
-requires the presence of separate receptors on the target cell for each stimulant

Ex.

  • histamine potentiates the actions of ACh and gastrin
  • ACh potentiatses the actions of histamine and gastrin
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19
Q

WHat are the functions of Cimetidine and Omeprazole?

A

Cimitidine: Antagonist of H2 receptor used to treat duodenal and gastric ulcers, gastroesophageal reflux disease
-helps limit potentiation of ACh and gastrin

Omeprazole: inhibits the H+/K+ ATPase, used in the treatment of ulcers to reduce H+ secretion

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20
Q

What are the three phases of Gastric HCL secretion phase?

A

Cephalic phase via vagus

Gastric phase

  • local nervous secretory reflexes
  • Vagal reflexes
  • Gastrin-histamine stimulation

Intestinal phase:

  • Nervous mechanisms
  • Hormonal mechanisms
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21
Q

What occurs in the Cephalic phase?

A
  • Accounts for 30% of the total HCL secreted in response to a meal
  • Stimuli: smelling and tasting, chewing, swallowing, and conditioned reflexes

Mechanism:

  • Vagus nerve to parietal cell, vagus releases ACh to parietal cells, which causes release of HCl
  • Vagus nerve to gastrin to parietal cell, vaguse releases GRP to G cells, which release gastrin to the circulation and the gastrin is then delivered back to the stomach to stimulate HCL secretion from parietal cells

Vagotomy abolishes this phase!

22
Q

what occurs in the gastric phase?

A
  • Accounts for 60 percent of the total HCL secretion in response to a meal
  • Stimuli: distension of the stomach and presence of breakdown or proteins, amino acids, and small peptides

Mechanism:

1) distension activates the mechanoreceptors in the mucosa of oxyntic and pyloric glands
- vagus nerve to parietal cell
- vagus nerve to gastrin to parietal cell
2) Distension of antrum
- local reflexes release ACh that releases on parietal cell and g cell
3) Amino acids and small peptides
- gastrin release to parietal cell

23
Q

how does coffee affect the HCL secretion?

A

Coffee (caffeinated and decaffinated) also stimulate gastric HCL secretion

24
Q

What happens in the intestine phase?

A

-Accounts for 5-10 percent of the total HCL secreted in response to a meal

Distention of small intestine
-stimulates acid secretion

Digested protein
-stimulates acid secretion via Direct effect on parietal cell and Gastrin via intestinal G cells that then will activate the parietal cells

25
Q

when and what secrets Pepsinogen? what innervates it?

A

Pepsinogen is only secreted when the gastric pH is acidic enough to convert pepsin

Pepsinogen is secreted by chief cells and by mucus cells in the oxyntic glands
-requires H+ secretion from parietal cells to lower pH of gastric contents (pH <5)

Vagus nerve stimulation is the most important stimulus for pepsinogen secretion

H+ triggers local cholinergic reflexes that stimulate chief cells to secrete pepsinogen

26
Q

What does pepsin do?

A

Pepsin converts more pepsinogen to pepsin

  • proteolytic enzyme
  • optimal pH is between 1.8-3.5
  • reversibly inactivated at > pH 3.5-5.0
  • Irreversibly inactivated >pH 7-8
27
Q

What is Intrinsic factor and what is it used for?

A

IF (intrinsic factor is required for absorption of vitamin B12 in the ileum

  • Mucoprotein secreted by parietal cells
  • Binds B12
  • Only secretion by the stomach that is required

Failure to secrete IF is associated with achlorhydria and with absence of parietal cells

28
Q

Mechanism in the absorption of Vitamin B12

A

in the sotmach, B12 will bind R protein and then when they get down to the duodenum the pancreatic proteases will switch R protein with IF where then the B12 IF complex will be absorbed in the distal ileum via IF receptors

29
Q

What leads to Pernicious anemia

A

There is a decrease in B12 due to the fact that the stomach does not produce enough IF

Common causes:

  • Atrophic gastritis: chronic inflammation of the stomach mucosa that leads to loss of parietal cells
  • Autoimmune metaplastic atrophic gastritis, immune system attacks IF protein or gastric parietal cells
30
Q

What are some Disruptions in the absorption of Vitamin B12

A

Gastrectomy: loss of parietal cells (source of IF)

Gastric bypass: Exclusion of the stomach, duodenum, and proximal jejunum alters absorption of vitamin B 12

31
Q

How is the Gastric Mucosa created? and what is its function?

A

Gastric epithelium secretes HCO3- and mucus to form the gel like mucosal barrier

  • mucosa cells secrete mucus
  • surface epithelial cells secrete HCO3-

The mucosal barrier protects the gastric mucosal epithelium against the HCl and pepsin

also the prostoglandins, mucosal blood flow, gastrin, and growth factors protect the gastric mucosa

32
Q

what can damage the gastroduodenal mucosa?

A
  • H+ and pepsin
  • H. pylori
  • NSAIDs
  • Stress-smoking
  • Alcohol
33
Q

What is Zollinger-Ellison syndrome? and how does it affect the body?

A

Large secretion of gastrin by duodenal or pancreatic neuroendocrine tumors

  • increase H+ secretion by parietal cells
  • Increase parietal cell mass
  • H+ secretory rates are the highest
  • inhibit the absorption of sodium and water by the small intestine (secretory diarrhea)

creates ulcer by overwhelming the HCO3- buffer capacity in pancreatic juice

Low pH of intestinal contents

  • inactivates pancreatic digestive enzymes
  • interferes with the emulsification of fat by bile acids
  • damages intestinal epithelial cells and villi
  • leads to maldigestion and malabsorption (both result in steatorrhea
34
Q

what is a Secretin Stimulation test

A

Secretin is used in the diagnosis of gastrin-secreting tumors

Under normal conditions, secretin administration inhibits gastrin release

in gastrinomas, injection of secretin causes a paradoxical increase in gastrin release
-basis for the secretin stimulation test

35
Q

what are the two types of Peptic ulcer disease and what are possible causes?

A

two types:

  • Gastric ulcers
  • Duodenal ulcers

In the US, helicobacter pylori infection and the use of NSAIDS are the predominant causes

  • loss of protective mucosal barrier
  • excessive H+ and pepsin secretions
  • combination of the two above
36
Q

How does Helicobacter pyloru damage the gastric mucosa?

A

H. pylori releases cytotoxins that breakdown the mucosal barrier and underlying cells

THe enzyme urease allows the bacteria to colonize the gastric mucosa

  • urease converts urea to ammonia which alkalinizes the local environment
  • the resulting production of ammonium is believed to be a major cause of cytotoxicity and damages epithelial cells and breaks the mucosal barrier
37
Q

what are the characteristics of Gastric ulcers?

A

Form on the lining of the stomach

Form mainly because gastric mucosal barrier is edfective, opposed to increased acid secretion

38
Q

what are the characteristics of Duodenal ulcers

A

Form on the lining of the duodenum

More common then gastric ulcers

Usually do not become malignant

H+ secretion rates are higher than normal

39
Q

H+ secretion, Gastrin levels, and comments: Gastric ulcer

A

H+ secretions: decreased

Gastrin levels: increased (in response to decreased H+)

Causes damage to protective barrier of gastric mucosa

40
Q

H+ secretion, gastrin levels, comments: Duodenal ulcer

A

H+ secretion: increased

Gastrin levels: increased in response to food ingestion)

increased parietal cell mass due to increased gastrin levels

41
Q

H+ secretion, gastrin levels, and comments: Zollinger-ellison syndrome

A

H+ secretion: major increase

Gastrin levles: major increase

Gastrin is secreted by pancreatic tumor
increase in parietal cell mass due to tropic effect of gastrin levles

42
Q

What is found in Pancreatic Juice?

A

contains HCO3- for the neutralization of H+ from the stomach and enzyme secretions to digest carbohydrates, proteins, and lipids into absorbable molecules

43
Q

What innervates the exocrine pancreas and how does it impact activity

A

Parasympathetic : vagus nerve

  • pregangionic fibers synapse ENS
  • POst ganglionic fibers synapse on the exocrine pancreas
  • will stimulate the pancreatic secretion

Sympathetics

  • Post ganglionic nerves from the celiac and superior mesenteric plexuses
  • inhibits pancreatic secretion
44
Q

What are the two components of the exocrine pancreatic

A

Enzymatic secretion by acinar cells for digestion
‘-pancreatic amylases and lipases are secreted as active enzymes
-pancreatic proteases are secreted in inactive forms and converted to their active forms in the lumen of the duodenum

Aqueous secretion by centroacinar and ductal cells

  • secrete HCO3- rich fluid that alkalinizes and hydrates the protein rich primary secretions of the acinar cell
  • initial secretion is modified by transport processes in the ductal epithelial cells
45
Q

How does HCO3- secrete into the lumen of the pancreatic ductal cell

A

via CL-/HCO3- exchanger or
cAMP activated CFTR Cl- channel

leads to a net result of secretion of HCO3- and a absorption of H+

46
Q

Cystic fibrosis and the pancreas

A

Mutations in the cystic fibrosis transmembrane conductance regulator
-CFTR, regulated Cl- channel in the apical surface of the duct cell

In CF the pancreas is one of the first organs to fail

SOme CFTR mutations can lead to loss of HCO3- secretion

  • abillity to flush active enzymes out of the duct may be loss
  • may lead to recurrent acute and chronic pancreatitis
47
Q

What are the three phases of Pancreatic sectretion?

A

Cephalic phase:

  • Initiated by smell, taste and conditioning
  • mediated by the vagus nerve
  • produces mainly an enzymatic secretion

Gastric phase:

  • initiated by distention of the stomach
  • mediated by vagus nerve
  • produces mainly an enzymatic secretion

Intestinal phase:

  • Accounts for 80 percent of pancreatic secretion
  • enzymatic and aqueous secretions are stimulated
48
Q

Regulation of pancreatic secretions

A

CCK induces the release of pancreatic enzymes into the duodenal lumen

Secretin induces the secretion of HCO3- from pancreatic cells into the duodenum

49
Q

Process of regulation on I cells

A

initiated by Phenylalanine, methionine, tryptophan, small peptides, fatty acids

this acts on I cells to release CCK

this acts on Acinar cells with potentiates ACh to decrease IP3 and Ca+ leading to enzyme release from the acinar cell

50
Q

Process of regulation on S cells

A

H+ will activate S cells to release secretin to act on Ductal cells that causes a decrease in cAMP that then will increase the aqueous secretion of Na+ and HCO3-

GIGU test! (40 decks)

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