W14 - GI system II (5.4, 5.5) Flashcards by LV D

How much saliva is produced daily?

Main functions?

800 - 1500 ml/day

initiates digestion of lipids carbs
lubrication + dilution of food to create bolus

_{further functions on “constituents of saliva” card}

(90% during eating)

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Describe the general structure of the salivary glands.

Differentiate.

tubualveolar structure
= consists of acini + ducts

parotid: purely serous
sublingual gland: mainly mucous
s**ub**m**andibular gland: mixed serom**ucous

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Generally…

How is the secretory function of the GI tract regulated?

enteric NS: direct stimulation or action of ENS cells
autonomic NS:
- parasymp. → ↑ GI activity
- symp. → ↓ or ↑ GI activity (dep. on tissue)
secretogogues: substances that cause secr., either holo-/endocrine

⇒ act on slayer of myoepithelium around acini
→ contraction

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What are the major constituents of saliva?

water
electrolytes (Na⁺, K⁺, HCO₃^-, Cl^-)
proteins
- α-amylase, lipase → digestion
- IgA, lysosyme → antimicrobial effect
- Ca²⁺ binding protein → provides ↑[Ca²⁺] around teeth
- R-protein → vit B₁₂ absorption

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Describe the two-stage model of salivary secretion.

Another name for this mechanism?

= sequential secretion

primary saliva = isotonic
produced/secreted from acinar cells
secondary saliva = hypotonic
modified as it passes through duct cells, reabsorb Na⁺/Cl^-, secrete K⁺, HCO₃^- → alkaline

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Describe the ion transport in acinar cells.

Cl^- diffuses via CFTR into lumen of acinus, causes negative potential
Na⁺/H₂O follow paracellularly
Na/K-ATPase and Na/K/Cl cotransporter maintain balance on basolat. surface
proteins exocytosed

⇒ isotonic primary saliva

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Briefly describe the characteristics of the CFTR channel.

cystic fibrosis transmemb. conductance regulator

Cl^-channel
ABC transporter → needs ATP
if ATP present: passive transport

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Describe the ion transport in duct cells.

Na⁺ reabsorbed via ENaC
HCO₃^- and K⁺ secreted
no aquaporins → impermeable to water

⇒ hypotonic secondary saliva

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How does the flow rate affect the ionic composition of saliva?

the higher the flow rate (eating) the less time for compositional modification by duct cells

⇒ ↑ [Na⁺], ↓[K⁺]
= more similar to that of plasma

ONLY exception:
[HCO₃^-] is HIGHEST at HIGH flow rates
bc secreted selectively upon parasymp. stim.

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Describe the 3 mechanisms of parasymp. regulation of salivary secretion.

via n. VII, IX

ACh binds to m₃-R (G_q) on acinar cells
⇒ ↑ fluid and enzyme secretion
VIP causes vasodilation via G_s
⇒ ↑ secretion due to ↑ blood flow
incr. parasymp. activity (↑ACh) from smelling or seeing food, nausea

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Why does atropin only selectively inhibit the saliva production?

only blocks ACh receptors

→ VIP can still enhance saliva prod.

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Describe the 2 mechanisms of symp. regulation of salivary secretion.

NE binds to acinar/duct cells via

α₁-R (G_q)
→ vasoconstriction + ↓ fluid production
β2-R (G_s)
→ ↑ mucin secretion

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How much gastric juice is secreted daily?

Functions w/ to its constituents.

*1000 - 1500ml/day**
incr. production after meal
mucous/HCO₃^-: protection of mucosa
H⁺: antimicrobial effect, activates pepsinogen to pepsin
lipase, pepsinogen: digestion
intrinsic factor: only essential secretion → necessary for absoprption of vit B₁₂

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As a summary..

Differentiate btw the most important cell types of the stomach, their location and function.

3 functional regions w/ unique functions:

LES + cardia
fundus + body
antrum + pylorus

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Differentiate btw the 2 states of parietal cells.

Function?

resting state - active state
translocation of membranes/transporters to luminal surface for ↑↑ gastric acid secretion

H⁺, Cl^- secretion
intrinsic factor production

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Describe the mechanism of gastric acid secretion.

initiated by translocation of H/K pump

CO₂ + H₂O form H+ + HCO3-
HCO₃^- exported, Cl^- imported by antiporter on basolateral surface
H⁺/K⁺ pump on lum. surface exports H⁺,
Cl^- leaves via CFTR
K⁺ leaves again via channels

_NOTE:_{blood that leaves stomach = alkaline due to ↑[HCO3-]}

Which mechanisms regulate the activity of parietal cell secretion?

stimulated by

neural: ACh by vagus → via m₃-R
hormonal: histamine by ECL cells → via H₂-R (G_s)
paracrine: gastrin by G cells → via CCKB-R, also ECL cells

How is the release of gastrin stimulated?

distension of stomach → ACh
ACh from vagus → GRP
AAs, peptides
enteric reflexes
too high symp. tone → β₂-R

How is the release of gastrin inhibited?

mainly feedback regulation
↑[H⁺] → D cells produce ↑[somatostatin] (G_i) → ↓[gastrin] → ↓[H⁺]
ALSO: inhibited by PGE₂
_{omeprazole for treatment of gastric cancer}

Differentiate btw mucous cells of the stomach.

Function?

surface/neck mucous cells

⇒ secrete Na⁺, Cl^-, HCO₃^-, mucin to buffer HCl
→ cells surface remains near pH 7

Which substances are secreted by chief cells?

What is the necessary stimulus?

ACh, secretin causes

⇒ secretion of pepsinogen, gastric lipase

What can you say about the ionic composition of gastric acid w/r/t its rate of secretion?

ALWAYS isotonic

↑[Cl^-], [K⁺] w/ incr. rate of secretion
↑↑↑[H⁺] w/ incr. rate of secretion
↓↓↓[Na⁺] w/ incr. rate of secretion

Values for peak acid output in male and females.

PAO - male = 25mmol/h
PAO - female = 16mmol/h

> in males due to higher no. of parietal cells

What are the 3 phases of gastric secretion?

cephalic phase
gastric phase
intestinal phase

As a summary.. What happens during the cephalic phase of gastric secretion?

**thought of food, smell, taste, chewing, swallowing** = 40% of total acid secretion vagus → ACh → GRP → G cells → HCl secretion (ACh also directly stimulates parietal cells) __NOTE:__{atropine-resistant pathway bc acting via GRP}

As a summary.. What happens during the gastric phase of gastric acid secretion?

**food reached stomach, hence gastric distension** = 50% of total gastric acid secretion

What happens during the intestinal phase of gastric acid secretion?

_food reaches small intestine_ = 10% of total acid secretion * protein digestion digested in stomach → **free AAs** * distension → signals intestinal endocrine cells to secrete **enterooxyntin** ⇒ stimulus to parietal cells

What are mechanisms other than the pathway using somatostatin to inhibit the release of gastric acid? Where do they happen?

* _antrum:_ **low pH directly** inhibits gastrin release * _duodenum:_ low pH causes release of **secretin/neural reflex** * _duodenum/jejunum:_ hyperosmotic sol. and FAs cause release of **GIP and CCK** ****⇒ inhibited rel. of gastrin/HCl rel. by parietal cells

What happens during the small intestinal phase?

_food reaches small intestine_ → **secretions of pancreas, liver, small intestine**

How much pancreatic juice is secreted daily? Functions? Tonicity.

**700 - 900ml/day** 98% exocrine, 2% endocrine * _exocrine:_ * neutralization of acids * digestive enzymes * _endocrine:_ regulation of blood sugar **_ALWAYS_** **isotonic** _{NOTE: large reserve, even 10% would be enough}

How does the sequential secretion in the pancreas differ from that in salivary glands?

1. acini secrete **_isotonic_ acinar fluid** and lots of **enzymes** 2. **intralobular ductal system:** spontaneous secretion → incr. [HCO₃^-], [K⁺] 3. **extralobular ductal system:** stimulated by secretin to further secrete [HCO₃^-]

List important enzymes that are produced by the pancreas. Where? Examples.

_pancreatic acinar cells_ * zymogen proteases: **chymo-/trypsinogen** * starch-digesting **enzymes: amylase** * lipid-digesting enzymes/precursors: **lipase** * **nucleases** * regulatory factors: **procolipase**

Describe the main features of ion transport in pancreatic duct cells.

* _in apical membr.:_ Cl^-/HCO₃⁻ exchanger * _in basolat. membr.:_ Na/K-ATPase and an Na/H-exchanger 1. **carbonic anhydrase** CO₂ + H₂O → H₂CO₃ → H⁺ and HCO₃⁻ 2. **Cl^-/HCO₃⁻ exchanger** HCO₃⁻ secreted into pancreatic juice 3. **Na/H-exchanger** H⁺ is transported into the blood ⇒ net secretion of HCO₃⁻ into pancreatic ductal juice and net absorption of H⁺ _{(acidification of pancr. venous blood)}

What is cystic fibrosis?

genetic disease, caused by **mutation in CFTR** → impaired Cl- secretion ⇒ clog secretion (since secretion of mucous is not suspended), hence impaired function of a variety of epithelial organs _{if CFTR in pancreas defect, bicarbonate cannot be secr.}

Which substance is the most important stimulant for enzyme secretion in acinar cells?

**CCK** (secreted by I cells of duodenum)

How is the pancreatic secretion regulated? Mechanisms.

neurally and hormonally _activated by:_ * hormonally: **CCK/gastrin, secretin** * neurally: **VIP, GRP, ACh** _inhibited by:_ **somatostatin**

What are the 3 phases of pancreatic secretion? Which one is the most important one?

* **cephalic phase** = sight, smell, taste of food * **gastric phase** = distention of stomach * **intestinal phase** *(cf. own card)* **⇒ 80% of secretion happens in intestinal phase

Which stimuli induce pancreatic secretion in the intestinal phase? Mediator/mechanism.

* **acidic duodenum** (pH → _secretin_ stimulates duct cells * **AAs, FAs, Ca²⁺** → _CCK_ stimulates aff. arm of vagovagal reflexes to acinar and duct cells * **distention of duodenum, hypertonicity** **in duodenum** → _enteropancr. reflexes_ stimulate both cell types

Describe the feedback loop that responds to a fall in luminal pH in the duodenum.