Secretion and Swallowing Flashcards
Three regulatory phases of GI function
Cephalic, Gastric (food enters stomach) and Intestinal (
What feedsback to stomach to determine how much ingestor is released into intestinal phase?
secretin, CCK, GIP, distension
characteristics of mouth saliva
high bicarb
high K
hypotonic
alpha-amylase and lingual lipase
what increases saliva secretion
parasympathetic primarily
sympathetic
factors that decrease saliva secretion
sleep
dehydration
atropine
functions of saliva
- 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
3 glands that secrete saliva
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
3 stages of salivation
- acini cells secrete 1st secretion (isotonic) like plasma content (Na. Cl, K, HCO3)
- this secretion stimulated by neural input -> myoepithelial cells - 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)
What determines bicarbonate concentration of saliva?
flow rate
High flow rates: more bicarbonate ions - higher saliva concentration
2 types of secondary saliva
Unstimulated (when asleep)
Stimulated (having lunch)
Two types of salivation reflexes
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
What effects do sympathetic and parasympathetic stimulation have on saliva secretion?
both increase production (but parasympathetic predominates)
Difference between parasympathetic and sympathetic driven saliva?
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.
Deglutition and its 2 stages
swallowing: moving food out of mouth and into stomach
- oropharyngeal (1 second)
- oesophageal (4-10 seconds)
3 stages of Oropharyngeal phase of Deglutition
- oral phase: bolus held against hard palate by tongue. Requires taste, temp, touch senses for formation of appropriate bolus to be swallowed
- oral transit: pushing bolus posteriorly on tongue, to pharynx
- pharyngeal: elevation & retraction of velum (soft palate) -> velopharyngeal closure.
- larynx closes preventing entering airway
- upper oesophageal sphincter opens, allow bolus to pass into oesophagus
What does oesophageal stage of swallowing depend on?
peristaltic waves (there are two)
Describe 1st peristaltic wave:
where?
using which fibres?
from beginning to end of oesophagus 4-10s
circular fibres behind bolus squeeze it down. Longitudinal fibres in front shorten distance of travel.
Does water use peristalsis?
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
What is secondary peristalsis?
for sticky food that may become lodged, stimulates pressure receptors. More forceful and increased saliva production.
If the oesophagus doesn’t have a digestive role, what is the role of the mucous secretion?
protection and lubrication
Simple mucous glands protects against mechanical damage
Gastric end has compound mucous glands which protect against chemical damage
What is receptive relaxation and where does it take place?
in the stomach:
makes space downstream for more food to enter without building pressure as we store large volumes of ingesta.
What are hunger pangs caused by?
peristaltic waves in stomach when stomach is empty
intense when blood sugar is low
What is secreted in the gastric phase? (4)
HCl
Pepsinogen
Intrinsic Factor
Mucous
Role of HCl
mostly for pepsinogen activation at acid pH. Pepsinogen only activated in acidic and HCl creates pH~2
Role of pepsinogen
protein digestion
Role of intrinsic factor
Vitamin B12 absorption (in ileum). Binds with B12, without the Rs in the ileum, we couldn’t form blood cells properly.
Factors that increase gastric secretions
gastrin
Ach
histamine
parasympathetic
Factors that decrease gastric secretion
H+ in the stomach
chime in duodenum
somatostatin
atropine
Name the gastric cells (4)
Where they are located in the stomach
What they secrete
Parietal/body/HCl and Intrinsic Factor
Chief/body/pepsinogen
G cells /antrum/gastrin (to circulation)
Mucous/antrum/mucus
Where is the most forceful mixing of the bolus in the stomach?
in the antrum. progressively more forceful fundus –> body –> antrum
What is retropulsion and why is it important?
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
Where do gastric cells originate?
in gastric pits
surface epithelium
mucous
parietal cells
peptic chief cells
Why doesn’t the HCl denature the parietal cells?
because it’s secreted in stages: H and Cl ions secreted separately
How do we stop HCl production?
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)
what stimulates secretion of pepsinogen
vagal stimulation to chief cells
- H+ (from HCl) also triggers local reflexes which stimulate chief cells
Loss of secretion of intrinsic factor leads to what
pernicious anaemia (impaired maturation of RBC)
where is absorption of Vitamin B12
terminal ileum
why is intrinsic factor so important for VitB12 absorption
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
Composition of pancreatic secretions
aqueous solution
very high in bicarb (main contributor in neutralising the stomach H+)
enzymes
What inhibits exocrine pancreatic secretion
sympathetic innervation
how are pancreatic enzymes stored?
in condensed zymogen granules until release (don’t want them to digest the pancreas!)
Components of pancreatic secretion
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
Which enzymes are released in the enzymatic component of pancreatic secretion? and in what form?
- 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
3 major proteolytic enzymes/zymogens
trypsinogen
chymotrypsinogen
procarboxypeptidase
what is trypsinogen activated by?
enteropeptidase (enterokinase) in luminal border of cells lining duodenal mucosa
what 3 actions does trypsin have (in enzymatic pathway)?
- feedback on trypsinogen to make more trypsin
- activates chymotrypsinogen
- activates procarboxypeptidase
What accounts for most of the gastric secretion?
60% in gastric phase of digestion
What accounts for most of the pancreatic secretion?
intestinal phase accounts for 80% of secretion
explain the pancreatic response of acinar cells in intestinal phase
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
explain the pancreatic response of ductal cells in intestinal phase
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
3 bile functions of the gallbladder
- stores bile (continuously produced by hepatocytes and flow to gallbladder via ducts)
- concentrates bile: epithelial cells lining gallB absorb ions and water iso-osmotically
- ejects bile: begins ~30mins after meal. (stimulus for ejection is release of cholecystokinin from I cells in SI)
what is bile? is it enzymatic?
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
Explain bile regulation during cephalic phase of disgestion
right before a meal:
neural (parasympathetic) stimulation via vagus nerve to increase bile flow
In bile regulation, what is the role of:
- chyme in duodenum
- CCK release
- secretin release
- stimulates release of CCK and secretin
- triggers release of stored bile. Gallbladder contraction. Sphincter of Oddi relaxation.
- triggers bile secretions, especially NaHCO3
Cause bile to enter duodenum!!
What’s the biggest trigger of mucus secretion by the large intestine?
distension of walls
increased secretion triggered by ACh and VIP
decreased secretion triggered by adrenaline and somatostatin
Composition of large intestine mucus
high L
high bicarb
no digestive enzymes!!
Function of large intestine mucus
protection
lubrication
neutralisation of H+ produced by gut bacteria
