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Physiology I > W14 - GI system II (5.4, 5.5) > Flashcards

W14 - GI system II (5.4, 5.5) Flashcards

1
Q

How much saliva is produced daily?

Main functions?

A

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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2
Q

Describe the general structure of the salivary glands.

Differentiate.

A

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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3
Q

Generally…

How is the secretory function of the GI tract regulated?

A
  • 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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4
Q

What are the major constituents of saliva?

A
  • 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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5
Q

Describe the two-stage model of salivary secretion.

Another name for this mechanism?

A

= sequential secretion

  1. ​primary saliva = isotonic
    produced/secreted from acinar cells
  2. secondary saliva = hypotonic
    modified as it passes through duct cells, reabsorb Na+/Cl-, secrete K+, HCO3- → alkaline
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6
Q

Describe the ion transport in acinar cells.

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

⇒ isotonic primary saliva

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7
Q

Briefly describe the characteristics of the CFTR channel.

A

cystic fibrosis transmemb. conductance regulator

  • Cl- channel
  • ABC transporter → needs ATP
    if ATP present: passive transport
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8
Q

Describe the ion transport in duct cells.

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

⇒ hypotonic secondary saliva

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9
Q

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

A

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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10
Q

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

A

via n. VII, IX

  • ACh binds to m3-R (Gq) on acinar cells
    ⇒ ↑ fluid and enzyme secretion
  • VIP causes vasodilation via Gs
    ⇒ ↑ secretion due to ↑ blood flow
  • incr. parasymp. activity (↑ACh) from smelling or seeing food, nausea
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11
Q

Why does atropin only selectively inhibit the saliva production?

A

only blocks ACh receptors

→ VIP can still enhance saliva prod.

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12
Q

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

A

NE binds to acinar/duct cells via

  • α1-R (Gq)
    → vasoconstriction + ↓ fluid production
  • β2-R (Gs)
    → ↑ mucin secretion
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13
Q

How much gastric juice is secreted daily?

Functions w/ to its constituents.

A
  • *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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14
Q

As a summary..

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

A

3 functional regions w/ unique functions:

  • LES + cardia
  • fundus + body
  • antrum + pylorus
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15
Q

Differentiate btw the 2 states of parietal cells.

Function?

A

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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16
Q

Describe the mechanism of gastric acid secretion.

A

initiated by translocation of H/K pump

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

NOTE: blood that leaves stomach = alkaline due to ↑[HCO3-]

17
Q

Which mechanisms regulate the activity of parietal cell secretion?

A

stimulated by

  • neural: ACh by vagus → via m3-R
  • hormonal: histamine by ECL cells → via H2-R (Gs)
  • paracrine: gastrin by G cells → via CCKB-R, also ECL cells
18
Q

How is the release of gastrin stimulated?

A
  • distension of stomach → ACh
  • ACh from vagus → GRP
  • AAs, peptides
  • enteric reflexes
  • too high symp. tone → β2-R
19
Q

How is the release of gastrin inhibited?

A
  • mainly feedback regulation
    ↑[H+] → D cells produce ↑[somatostatin] (Gi) → ↓[gastrin] → ↓[H+]
  • ALSO: inhibited by PGE2
    omeprazole for treatment of gastric cancer
20
Q

Differentiate btw mucous cells of the stomach.

Function?

A

surface/neck mucous cells

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

21
Q

Which substances are secreted by chief cells?

What is the necessary stimulus?

A

​ACh, secretin causes

⇒ secretion of pepsinogen, gastric lipase

22
Q

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

A

ALWAYS isotonic

  • ↑[Cl-], [K+] w/ incr. rate of secretion
  • ↑↑↑[H+] w/ incr. rate of secretion
  • ↓↓↓[Na+] w/ incr. rate of secretion
23
Q

Values for peak acid output in male and females.

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

> in males due to higher no. of parietal cells

24
Q

What are the 3 phases of gastric secretion?

A
  1. cephalic phase
  2. gastric phase
  3. intestinal phase
25
Q

As a summary..

What happens during the cephalic phase of gastric secretion?

A

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

26
Q

As a summary..

What happens during the gastric phase of gastric acid secretion?

A

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

27
Q

What happens during the intestinal phase of gastric acid secretion?

A

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

28
Q

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

Where do they happen?

A
  • 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

29
Q

What happens during the small intestinal phase?

A

food reaches small intestine
→ secretions of pancreas, liver, small intestine

30
Q

How much pancreatic juice is secreted daily?

Functions?

Tonicity.

A

700 - 900ml/day
98% exocrine, 2% endocrine

  • exocrine:
    • neutralization of acids
    • digestive enzymes
  • endocrine: regulation of blood sugar

ALWAYS isotonic

<u>NOTE:</u> large reserve, even 10% would be enough

31
Q

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

A
  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-]
32
Q

List important enzymes that are produced by the pancreas.

Where?

Examples.

A

pancreatic acinar cells

  • zymogen proteases: chymo-/trypsinogen
  • starch-digesting enzymes: amylase
  • lipid-digesting enzymes/precursors: lipase
  • nucleases
  • regulatory factors: procolipase
33
Q

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

A
  • 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)

34
Q

What is cystic fibrosis?

A

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.

35
Q

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

A

CCK (secreted by I cells of duodenum)

36
Q

How is the pancreatic secretion regulated?

Mechanisms.

A

neurally and hormonally

activated by:

  • hormonally: CCK/gastrin, secretin
  • neurally: VIP, GRP, ACh

​inhibited by: somatostatin

37
Q

What are the 3 phases of pancreatic secretion?

Which one is the most important one?

A
  • cephalic phase = sight, smell, taste of food
  • gastric phase = distention of stomach
  • intestinal phase (cf. own card)

​⇒ 80% of secretion happens in intestinal phase

38
Q

Which stimuli induce pancreatic secretion in the intestinal phase?

Mediator/mechanism.

A
  • 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
39
Q

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

A

Physiology I (10 decks)

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