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Gastrointestinal > Secretion and Swallowing > Flashcards

Secretion and Swallowing Flashcards

1
Q

Describe the regulation of GI function.

A
  • GI function is co-ordinated by the integration of neural and hormonal signals.
  • Signals can be physical (stretch receptors) or chemical (sight and presence of food).
  • In addition, there is considerable input from higher centres.
  • These signals can be split into three phases:
    • Cephalic
    • Gastric
    • Intestinal
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2
Q

Describe the 3 regulatory phases of GI function.

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
  • Enteric NS feeds back and forth signals in the GI tract.
    • For example, the stomach can feed forward to the intestine to tell it food is coming and the intestine can feed back to the stomach to tell it not to put in any more food.
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3
Q

Describe secretion in the GI tract.

A
  • Addition of substances (fluids, enzymes, ions etc.) into the lumen of the GI tract.
    • Produced by salivary glands (saliva).
    • Cells of the gastric mucosa (gastric secretion).
    • Exocrine cells of the pnacreas (pancreatic secretion).
    • Liver (bile).
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4
Q

Describe the secretion of saliva.

A
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5
Q

What are the functions of salivary secretion?

A
  • Initial digestion of starches and lipids (very little).
  • Dilution and buffering of ingested foods.
  • Protection of teeth and gums.
  • Lubrication of ingested foods with mucous (mucin).
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6
Q

How much saliva is secreted in a day (approximately)?

A

1 litre

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7
Q

Where do salivary secretions come from?

A
  • Sublingual glands
    • ​Deep in floor of mouth, underneath tongue, mostly mucous cells.
  • Submandibular glands
    • ​Under lower edge of mandible, mixed glands containing serous and mucous cells.
  • Parotid glands
    • ​Below ear and over the masseter, serous cells secreting an aqueous fluid composed of water, ions and enzymes.
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8
Q

Describe the 3 stages of salivation.

A
  • Acini cells secrete primary secretion (isotonic).
    • Na+, Cl-, K+, HCO3-.
    • Amylase and mucin production.
  • Myoepithelial cells stimualted by neural input to eject saliva.
  • Duct cells secrete a secondary modification.
    • Reabsorb Na+ and Cl- and add K+.
    • HCO3- concentration is alteres depending on flow rate.
    • At high flow rate, saliva has increased HCO3-.
    • At low flow rate, more HCO3- is extracted.
  • In the mouth saliva is hypotonic - more dilute than plasma.
  • In the
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9
Q

Describe the changes in concentrations of the important ions in saliva.

A
  • When food is in the mouth the bacteria in the mouth and on the teeth feed on the food.
  • The more food in the mouth, potentially the more food supply for the bacteria and the more acid is produced.
  • We need to increase bicarbonate to neutralise the acid so the teeth are not melted by the acid.
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10
Q

Desribe the types of salivation reflexes.

How is saliva secretion increased?

A
  • Simple (unconditioned)
  • Acquired (conditioned)
  • Increase in salivation is the response of both sympathetic and parasympathetic stimuli.
  • Balanced accordingly based on the situation you are in. They both increase saliva secretion.
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11
Q

Describe the regulation of salivary secretion.

A
  • Parasympathetic - dominant in ‘normal’ secretion.
  • Sympathetic - dominant in stressful times.
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12
Q

What is deglutition?

What are the stages of deglutition?

A
  • Swallowing
    • ​Moving food from the mouth into the stomach.
  • Stage 1 - oropharyngeal​
    • ​Mouth → Pharynx → Oesophagus
    • c. 1 second
  • Stage 2 - oesophageal
    • ​Oesophagus → Stomach
    • c.4-10 seconds
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13
Q

Describe the oropharyngeal phase of deglutition.

A
  • Oral phase
    • ​(A) Bolus held against hard palate by tongue. Requires taste, temperature, touch and proprioception senses for formation of a bolus the right size and consistency for being swallowed.
  • Oral transit phase
    • ​(B and C) Lifting bolus on to front of tongue then pushing it posteriorly, towards the pharynx. Pharyngeal phase triggered as bolus moves into the pharynx.
  • Pharyngeal phase
    • ​(D and E) Elevation and retraction of velum (soft palate) → velopharyngeal closure (prevents material entering nasal cavity).
    • Bolus then pushed further into the pharynx by movement of the tongue base and sequential contraction of pharyngeal muscles.
    • Larynx closes preventing material from entering the airway.
    • Upper oesophageal sphincter opens, allowing bolus to pass into the oesophagus.
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14
Q

Describe the oesophageal phase of deglutition.

A
  • Swallowing centre (brain) triggers primary peristaltic wave.
  • Oesophageal peristalsis
    • ​Primary peristaltic wave from beginning to end of oesophagus (c.25cm) takes 4-10 seconds - too quickly for absorption to occur).
    • Peristalsis pushes food to stomach.
      • Circular fibres behind bolus squeeze bolus down.
      • Longitudinal fibres in front of bolus shorten distance of travel.
    • Water will descend quicker than wave but is blocked out of stomach for 4-5 seconds until wave reaches end and triggers gastrooesophageal sphincter opening.
    • Sticky food may become lodged in oesophagus, stimulating pressure receptors, causing:
      • Secondary peristaltic wave - more forceful than primary (no imput from higher centre).
      • Increased saliva production.
    • Food enters the stomach through lower oesophageal sphincter.
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15
Q

Describe the oesophageal secretions.

A
  • Only secretes mucous for lubrication / protection (no real digestive function).
  • Main body lined with simple mucous glands.
    • Protects against mechanical damage.
  • Gastric end (especially) has compound mucous glands.
    • Protects against chemical damage.
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16
Q

Describe the satiety mechanism.

A

Receptive relaxation in the stomach means that we can store large volumes of ingesta (several litres) before feeling uncomfortably ‘full’ after a meal.

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17
Q

Describe why we get hunger pangs.

A
  • Caused by peristaltic waves in the stomach occuring when the stomach is empty.
  • Can be intense and tetanic (fused) for 2-3 minutes.
  • Very intense in young healthy people when blood sugar is low and most intense after fasting for 3 or 4 days.
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18
Q

How is food intake regulated?

A

Interactions of the feeding centre and satiety centre of the hypothalamus play a large role in the regulation of food intake. This is strongly linked with the apetite centre in the amygdala.

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19
Q

What are the components of gastric secretion?

A
  • HCl
    • ​Protein digestion (a little) - mostly for pepsinogen activation at acid pH, creates pH~2.
  • Pepsinogen
    • ​Protein digestion (a little).
  • Intrinsic factor
    • ​Vitamin B12 absorption (in te ileum) - very important.
  • Mucous
    • ​Protection and lubrication.
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20
Q

Which factors increase and decrease the secretion of HCl in the stomach?

A
  • Increased secretion caused by:
    • Gastrin
  • Decreased secretion caused by:
    • H+ in the stomach
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21
Q

Which factors increase and decrease the secretion of pepsinogen in the stomach?

A
  • Increased secretion caused by:
    • Acetylcholine
  • Decreased secretion caused by:
    • Chyme in duodenum
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22
Q

Which factors increase and decrease the secretion of intrinsic factor in the stomach?

A
  • Increased secretion caused by:
    • Histamine
    • Parasympathetic stimulation
  • Decreased secretion caused by:
    • Atropine
    • Cimetidine
    • Omeprazole
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23
Q

What are the secretory products of each type of gastric cell?

Where in the stomach are these cells found?

A
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24
Q

What is pepsinogen?

A

Pepsinogen is an inactive enzyme, which under the action of HCl is converted into pepsin which progresses protein digestion.

25
Q

How is the surface area of the stomach increased?

A
26
Q

Describe the morphology of an oxyntic gland.

What is their function?

A
  • AKA gastric gland / gastric pit.
  • Functions:
    • Secrete mucous
    • Secrete HCl and intrinsic factor
    • Secrete pepsinogen
27
Q

Describe the 3 phases of digestion.

A
  • Cephalic phase (vagal stimulation, gastrin) - 30% of secretion.
    • Smell, taste, chewing, swallowing, conditioned reflex in anticipation of food.
  • Gastric phase (distension, gastrin, enteric nerves) - 60% of secretion.
    • Distension of the stomach and the presence of breakdown products of proteins, amino acids and small peptides in the stomach.
  • Intestinal phase (protein in duo-feedback) - 10% of gastric secretion.
    • Presence of breakdown products of proteins in the duodenum.
28
Q

How is HCl secreted?

A
  • In stages, so parietal cells aren’t denatured.
    • Gastric secretion is secreted as hydrogen and chloride ions separately.
    • Parietal cells cannot be acidic because it would denature the cell so secretes as 2 separate products.
    • There are bicarbonate and chloride exchanges.
29
Q

Describe the conditions for inhibiion of HCl secretion.

A
  • HCl secretion is inhibited when HCl is no longer needed to convert pepsinogen to pepsin.
  • This occurs after the chyme moves into the small intestine and the H+ buffering capacity of the food is no longer a factor.
  • Inhibition by somatostatin
    • ​Direct pathway - binds to receptors on parietal cells (and inhibits HCl-triggering pathway).
    • Indirect pathway - inhibits histamine release from the stomach and gastrin release from G cells.
30
Q

Describe the secretion of pepsinogen.

A
  • Secreted by chief cells in the oxyntic glands in response to vagal stimulation.
  • H+ triggers local reflexes which stimulate chief cells to secrete pepsinogen.
31
Q

When is pepsinogen activated?

A
  • Needs to be inactive until it reaches this pH because otherwise it would be destructive.
32
Q

Describe the secretion of intrinsic factor.

A
  • Secreted by parietal (oxyntic) cells.
  • Important for absorption of vitamin B12 by receptor mediated endocytosis.
  • Loss of secretion of intrinsic factor → pernicious anaemia (impaired maturation of RBC).
    • Most serious consequence of loss of secretory function of the stomach.
    • (Secretions from elsewhere can compensate for other missing stomach secretions).
  • Not absorbed through the normal absorptive processes. It requires presence of receptor-mediated transport.
33
Q

Describe the role of intrinsic factor in vitamin B12 (cyanocobalamin) absorption.

A
  • Vitamin B12 is too large and too highly charged for normal mode of translocation across cell membranes.
  • Uptake occurs by receptor-mediated endocytosis. Cells only recognise B12 when it is bound to intrinsic factor (I.F.).
  • Absorption occurs in the terminal ileum.
34
Q

Where does absorption of B12 occur?

A

Terminal ileum.

35
Q

Describe the secretions of the pancreas.

A
  • Exocrine pancreas secretes ~1L of fluid per day into the duodenum.
  • Composed of an aqueous solution containing enzymes and high HCO3-.
  • The function of the HCO3- is to neutralise stomach H+.
  • Enzymes digest carbohydrates, proteins and lipids.
36
Q

What factors increase high HCO3- (isotonic) pancreatic secretions?

A
  • Secretin
  • Cholecystokinin (CCK) (potentiates secretin)
37
Q

What factors increase pancreatic lipase, amylase and proteases (pancreatic secretions)?

A

Parasympathetic supply

38
Q

What gives innervation to the exocrine pancreas?

A
  • Parasympathetic innercation from the vagus stimulates secretion.
  • Sympathetic innervation inhibits secretion.
39
Q

Describe the enzymes secreted by the pancreas.

A
  • Stored in condensed zymogen granules until release.
  • Zymogen granules - full of pro-enzymes that prevent digestion of the pancreatic tissues.
40
Q

Describe the formation of the aqueous component of pancreatic secretion.

A
  • Aqueous component of secretion is released from centroacinar cells and ductal cells.
    • Pancreatic fluid is an isotonic fluid containing Na+, K+, Cl- and HCO3-.
    • Modification of the (ion) composition by the ductal cells results in a fluid secretion rich in HCO3-.
41
Q

Describe the modification of the ductal fluid of the pancreas.

A
  • It is modified according to flow rate.
42
Q

Describe the formation of the enzymatic component of pancreatic secretion.

A
  • Enzymes are released from acinar cells.
    • Pancreatic amylase and lipases are secreted as active enzymes.
    • Pancreatic proteases are secreted in an inactive form and activated in the duodenum.
43
Q

Describe the 3 types of pancreatic enzymes.

A
  • Pancreatic amylase
    • ​Polysaccharide → disaccharide
    • Much more important than salivary amylase
  • Pancreatic lipase
    • ​Triglycerides → monoglycerides + fatty acids
    • Very important source of lipase
  • Proteolytic
    • ​Cleave proteins at different sites → amino acids and small peptides.
44
Q

What are the 3 major proteolytic enzymes?

A
  • Trrypsinogen
  • Chymotrypsinogen
  • Procarboxypeptidase
  • All inactive (zymogens) to prevent self digestion
45
Q

Describe the activation of pancreatic proteolytic enzymes.

A

They are where they need to be in their active form.

46
Q

Describe the regulation of pancreatic secretion in the 3 phases of digestion.

A
  • Cephalic phase
    • ​Mediated by the vagus nerve (mainly enzymatic secretion).
  • Gastric phase
    • Initiated by distension of the stomach and mediated by the vagus nerve (mainly enzymatic secretion).
  • Intestinal phase
    • ​Accounts for 80% of pancreatic secretion and both enzymatic and aqueous secretions are stimulated.
47
Q

What is the response of the pancreatic acinar cells in the intestinal phase of digestion?

A
  • Duodenal cells secrete CCK in response to the presence of amino acids, small peptides and fatty acids in the intestinal lumen.
  • Vagal release of ACh potentiates CCK action.
  • Triggers acinar cells to produce enzymes.
48
Q

What is the response of the pancreatic ductal cells in the intestinal phase of digestion?

A
  • Secretin released by the S cells of the duodenum is the major stimulus for aqueous rich HCO3- secretion.
  • Secretin release is triggered by the arrival of acidic chyme in the duodenum.
  • ACh and CCK potentiate secretin action.
  • Triggers ductal cells to produce Na+, K+, Cl- and HCO3-.
49
Q

Describe the 3-stage role of the gall bladder.

A
  • Stores bile
    • ​which is continuously produced by the hepatocytes and flows to the gall bladder through the bile duct.
  • Concentrates bile
    • ​Epithelial cells lining the gall bladder absorb ions and water iso-osmotically.
  • Ejects bile
    • ​Begins ~30 minutes after a meal. The major stimulus for ejection is the release of cholecystokinin from the I cells in the duodenum and jejunum.
  • Bile is not enzymatic but has important role in digestion and subsequent absorption of lipids.
50
Q

What are the components of biliary secretion?

What stimulates these secretions?

A
51
Q

What is bile?

What is its function?

A
  • Essential for the digestion and absorption of lipids.
  • Bile salts emulsify lipids to prepare them for digestion and solubilise the products of digestion into ‘packets’ called micelles.
  • Mixture of bile salts, pigments and cholesterol.
  • Bile is not enzymatic.
52
Q

Describe the regulation of bile secretion:

  • In between meals
  • Just before a meal
  • During / after a meal
A
  • In between meals
    • ​Bile salts are recirculated to the liver via the enterohepatic system, therefore more bile is produced.
    • Bile is stored / concentrated in the gall bladder.
  • Cephalic phase (just before a meal)
    • ​Neural (parasympathetic) stimulation via the vagus nerve to increase bile flow.
  • During / after a meal
    • ​Chyme in duodenum stimulated the release of CCK & secretin.
    • Bile enters the duodenum.
53
Q

What is the role of cholecystokinin (CCK)?

A
  • Triggers the release of stored bile
  • Causes gall bladder contraction
  • Causes Sphincter of Oddi relaxation
54
Q

What is the role of secretin?

A

Triggers bile secretion, especially NaHCO3-

55
Q

Give an overview of the regulation of biliary secretions by secretin and CCK.

A
56
Q

What are the secretions of the large intestine?

A
  • Alkaline mucous
    • High [K+] and [HCO3-]
    • No digestive enzymes
57
Q

What are the functions of secretions of the large intestine?

A
  • Protection and lubrication
  • Neutralisation of H+ produced by gut bacteria.
58
Q

How are secretions of the large intestine stimulated?

A
  • Greatest trigger is distension / mechanical stimulation of the walls.
    • Increased secretion triggered by ACh and vasoactive intestinal peptide (VIP).
    • Decreased secretion is trggered by adrenaline and somatostatin.
  • Soma parasympathetic input - extreme parasympathetic stimulation → excess mucous → defecation (e.g. nervousness).

Gastrointestinal (10 decks)

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