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GI > Secretion and Swallowing > Flashcards

Secretion and Swallowing Flashcards

1
Q

Three regulatory phases of GI function

A

Cephalic, Gastric (food enters stomach) and Intestinal (

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2
Q

What feedsback to stomach to determine how much ingestor is released into intestinal phase?

A

secretin, CCK, GIP, distension

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3
Q

characteristics of mouth saliva

A

high bicarb
high K
hypotonic
alpha-amylase and lingual lipase

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4
Q

what increases saliva secretion

A

parasympathetic primarily

sympathetic

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5
Q

factors that decrease saliva secretion

A

sleep
dehydration
atropine

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6
Q

functions of saliva

A
  • initial digestion of starches and lipids
  • dilution and buffering of ingested foods
  • protection of teeth and gums (due to high levels of bicarb)
  • lubrication of ingestion foods with mucous
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7
Q

3 glands that secrete saliva

A

sublingual: deep in floor of mouth, mostly mucous cells
- submandibular: under lower edge of mandible, mixed glands containing serous and mucous cells
- parotid: belowear and over masseter, serous cells secreting aqueous fluid composed of water, ions, enzymes

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8
Q

3 stages of salivation

A
  1. acini cells secrete 1st secretion (isotonic) like plasma content (Na. Cl, K, HCO3)
    - this secretion stimulated by neural input -> myoepithelial cells
  2. Modification by duct cells as it travels down, reabsorb Na, Cl and add K. (bicarb are exchanged for Cl - want bicarb to cope with excess acid)
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9
Q

What determines bicarbonate concentration of saliva?

A

flow rate

High flow rates: more bicarbonate ions - higher saliva concentration

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10
Q

2 types of secondary saliva

A

Unstimulated (when asleep)

Stimulated (having lunch)

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11
Q

Two types of salivation reflexes

A

Simple (unconditioned) when something is in your mouth, chemoreceptors in mouth activated in presence of stimulus –>
Impulses sent via afferent nerves –>
salivary centre in medulla
–> impulses via extrinsic autonomic nerves - symp and parasymp stimulation –>
saliva production

Acquired (conditioned) when thinking about/smelling/hearing food –>
cerebral cortex –>
salivary centre in medulla –>
same as above

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12
Q

What effects do sympathetic and parasympathetic stimulation have on saliva secretion?

A

both increase production (but parasympathetic predominates)

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13
Q

Difference between parasympathetic and sympathetic driven saliva?

A

Parasympathetic (sleep, dehydration, food, nausea, smell) via IP3, Ca causes large volume of watery, enzyme rich saliva

Sympathetic (stress) driven via cAMP causes small volume of thick, mucousy saliva.

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14
Q

Deglutition and its 2 stages

A

swallowing: moving food out of mouth and into stomach

  1. oropharyngeal (1 second)
  2. oesophageal (4-10 seconds)
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15
Q

3 stages of Oropharyngeal phase of Deglutition

A
  1. oral phase: bolus held against hard palate by tongue. Requires taste, temp, touch senses for formation of appropriate bolus to be swallowed
  2. oral transit: pushing bolus posteriorly on tongue, to pharynx
  3. pharyngeal: elevation & retraction of velum (soft palate) -> velopharyngeal closure.
    - larynx closes preventing entering airway
    - upper oesophageal sphincter opens, allow bolus to pass into oesophagus
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16
Q

What does oesophageal stage of swallowing depend on?

A

peristaltic waves (there are two)

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17
Q

Describe 1st peristaltic wave:
where?
using which fibres?

A

from beginning to end of oesophagus 4-10s

circular fibres behind bolus squeeze it down. Longitudinal fibres in front shorten distance of travel.

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18
Q

Does water use peristalsis?

A

Not primary wave, it descends quicker than the wave, but it’s blocked out of stomach for 4-5s until the wave reaches the end and triggers the gastroesophageal opening

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19
Q

What is secondary peristalsis?

A

for sticky food that may become lodged, stimulates pressure receptors. More forceful and increased saliva production.

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20
Q

If the oesophagus doesn’t have a digestive role, what is the role of the mucous secretion?

A

protection and lubrication

Simple mucous glands protects against mechanical damage

Gastric end has compound mucous glands which protect against chemical damage

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21
Q

What is receptive relaxation and where does it take place?

A

in the stomach:

makes space downstream for more food to enter without building pressure as we store large volumes of ingesta.

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22
Q

What are hunger pangs caused by?

A

peristaltic waves in stomach when stomach is empty

intense when blood sugar is low

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23
Q

What is secreted in the gastric phase? (4)

A

HCl
Pepsinogen
Intrinsic Factor
Mucous

24
Q

Role of HCl

A

mostly for pepsinogen activation at acid pH. Pepsinogen only activated in acidic and HCl creates pH~2

25
Q

Role of pepsinogen

A

protein digestion

26
Q

Role of intrinsic factor

A

Vitamin B12 absorption (in ileum). Binds with B12, without the Rs in the ileum, we couldn’t form blood cells properly.

27
Q

Factors that increase gastric secretions

A

gastrin
Ach
histamine
parasympathetic

28
Q

Factors that decrease gastric secretion

A

H+ in the stomach
chime in duodenum
somatostatin
atropine

29
Q

Name the gastric cells (4)
Where they are located in the stomach
What they secrete

A

Parietal/body/HCl and Intrinsic Factor
Chief/body/pepsinogen
G cells /antrum/gastrin (to circulation)
Mucous/antrum/mucus

30
Q

Where is the most forceful mixing of the bolus in the stomach?

A

in the antrum. progressively more forceful fundus –> body –> antrum

31
Q

What is retropulsion and why is it important?

A

at very end of antrum, when peristaltic wave reaches the sphincter guarding duodenum, throws the bolus back into the stomach for further mixing.

The sphincter will only allow appropriate chime to pass through in a wave

32
Q

Where do gastric cells originate?

A

in gastric pits

surface epithelium
mucous
parietal cells
peptic chief cells

33
Q

Why doesn’t the HCl denature the parietal cells?

A

because it’s secreted in stages: H and Cl ions secreted separately

34
Q

How do we stop HCl production?

A

Secretion is inhibited when no longer needed to convert pepsinogen to pepsin (after the chime moves into the SI and H+ buffering capacity of food is not longer important)

Done by somatostatin directly (binds itself to Rs on parietal cells) and indirectly (via inhibiting stomach histamine and G cell gastrin release)

35
Q

what stimulates secretion of pepsinogen

A

vagal stimulation to chief cells

- H+ (from HCl) also triggers local reflexes which stimulate chief cells

36
Q

Loss of secretion of intrinsic factor leads to what

A

pernicious anaemia (impaired maturation of RBC)

37
Q

where is absorption of Vitamin B12

A

terminal ileum

38
Q

why is intrinsic factor so important for VitB12 absorption

A

only when bound to each other will the transporter function (receptor mediated endocytosis) and cells recognise B12.

B12 is too big and highly charged to translocate normally

39
Q

Composition of pancreatic secretions

A

aqueous solution
very high in bicarb (main contributor in neutralising the stomach H+)
enzymes

40
Q

What inhibits exocrine pancreatic secretion

A

sympathetic innervation

41
Q

how are pancreatic enzymes stored?

A

in condensed zymogen granules until release (don’t want them to digest the pancreas!)

42
Q

Components of pancreatic secretion

A

aqueous component: from centroacinar cells and ductal cells (isotonic fluid)
modification of ion saliva composition by ductal cells –> increase bicarb conc (in exchange for Cl)

enzymes from acinar cells

43
Q

Which enzymes are released in the enzymatic component of pancreatic secretion? and in what form?

A
  • amylase secreted as active enzymes (polysaccharide -> diasaccharide MORE IMPORTANT than salivary amylase)
  • lipases secreted as active enzymes (triglyceride-> mono + FA)
  • proteolytic secreted in inactive form and activated in duodenum
44
Q

3 major proteolytic enzymes/zymogens

A

trypsinogen
chymotrypsinogen
procarboxypeptidase

45
Q

what is trypsinogen activated by?

A

enteropeptidase (enterokinase) in luminal border of cells lining duodenal mucosa

46
Q

what 3 actions does trypsin have (in enzymatic pathway)?

A
  1. feedback on trypsinogen to make more trypsin
  2. activates chymotrypsinogen
  3. activates procarboxypeptidase
47
Q

What accounts for most of the gastric secretion?

A

60% in gastric phase of digestion

48
Q

What accounts for most of the pancreatic secretion?

A

intestinal phase accounts for 80% of secretion

49
Q

explain the pancreatic response of acinar cells in intestinal phase

A

amino acids, small peptides, FAs in intestinal lumen cause

duodenal I cells to secrete CCK causes

vagal release of Ach to potentiate CCK action triggers

acinar cells to produce enzymes

50
Q

explain the pancreatic response of ductal cells in intestinal phase

A

acidic chyme in duodenum triggers

S cells to release secretin to ductal cells

Ach and CCK to potentiate secretin action

triggers ductal cells to produce Na, K, Cl and BICARB aqueous secretion

this will go back and neutralise the acid

51
Q

3 bile functions of the gallbladder

A
  1. stores bile (continuously produced by hepatocytes and flow to gallbladder via ducts)
  2. concentrates bile: epithelial cells lining gallB absorb ions and water iso-osmotically
  3. ejects bile: begins ~30mins after meal. (stimulus for ejection is release of cholecystokinin from I cells in SI)
52
Q

what is bile? is it enzymatic?

A

essential for digestion and absorption of LIPIDS

prepare lipids for digestion: solubilise products into packets called MICELLES

it’s a mixture of bile salts, bile pigments and cholesterol

not enzymatic

53
Q

Explain bile regulation during cephalic phase of disgestion

A

right before a meal:

neural (parasympathetic) stimulation via vagus nerve to increase bile flow

54
Q

In bile regulation, what is the role of:

  1. chyme in duodenum
  2. CCK release
  3. secretin release
A
  1. stimulates release of CCK and secretin
  2. triggers release of stored bile. Gallbladder contraction. Sphincter of Oddi relaxation.
  3. triggers bile secretions, especially NaHCO3

Cause bile to enter duodenum!!

55
Q

What’s the biggest trigger of mucus secretion by the large intestine?

A

distension of walls

increased secretion triggered by ACh and VIP

decreased secretion triggered by adrenaline and somatostatin

56
Q

Composition of large intestine mucus

A

high L
high bicarb
no digestive enzymes!!

57
Q

Function of large intestine mucus

A

protection
lubrication
neutralisation of H+ produced by gut bacteria

GI (9 decks)

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