salivary and gastric secretions

Question 1

describe the stimulation of salivation?

Answer 1

taste, touch and smell - stimuli which activate higher centres in hypothalamus, sends signals to salivary centres which stimulates sympathetic (noradrenaline) and parasympathetic fibres (ACh) which innervate sublingual, submandibular and parotid glands
- these glands secrete saliva in mouth

parasympathetic activation of submandibular gland produces faster blood flow compared to when the gland secretes saliva at rest

salivary gland requires high blood blood flow - to drive and provide nutrients and electrolytes

Question 2

mechanisms involved in generating hypotonic saliva?

Answer 2

ducts converge into larger ducts which open into main excretory duct draining into mouth

• acinar cells produce isotonic saliva which has a plasma like electrolyte composition
• goes through modifications in duct system - reabsorption of NaCl, secretion of K+ and HCO3-

ends up with an electrolyte conc. less than in plasma - so is now hypotonic

Question 3

histological organisation of the stomach?

Answer 3

mucosa - top layer - secretory phase

submucosa - contains arteries, arterioles, venules and lymphatic vessels - for fat absorption

muscularis - contracts stomach

serosa - blood facing/basolateral membrane

Question 4

Describe physiological functions of gastric juice?

Answer 4

contains HCl - activates pepsinogen into pepsin and kills germs

pepsin - strong proteolytic enzyme digests proteins

mucus - protects epithelia from low pH and acidic environment

Question 5

explain how mucus and bicarbonate secretion create a gastric mucosal barrier?

Answer 5

BVs - fenestrated - highly permeable to water & electrolytes
- endothelial cells in BVs release nitric oxide - causes vasodilation
- vasodilation increases blood flow to drive fluids and electrolytes to protect epithelium
As acid secreted into lumen by parietal cell, serosa releases HCO3- ions into bloodstream to protect upper surface of gastric pit & buffer against the acid

Question 6

what is the gastric pit?

Answer 6

invaginations of stomach epithelium:
- contain many cells

surface epithelial cells - involved in secretion of mucus pepsin and acid
mucous neck cells - secrete mucus
gastric stem cells - regeneration and repair
chief cells - secrete pepsinogen
parietal cells - acid secretion
endocrine cells - secrete gastrin

Question 7

what are the 3 divisions of the gastric mucosa?

Answer 7

oxyntic gland mucosa - where most secretion occurs
cardiac region
antral region - sphincter which controls exit of food from stomach into small intestine

oxyntic glands - gastric HCl secretion
cardiac glands - secretes mucus + some electrolytes
pyloric glands - secretes alkaline mucus juice + electrolytes

Question 8

difference b/w Soll’s 3 receptor model and dimaline model?

Answer 8

Soll’s 3 receptor model
- fact that parietal cells have M3, H2 and CCK2 receptors
- acetylcholine, histamine and gastrin will bind to their respective receptors and cause acid secretion
- all 3 have similar influence on acid secretion

Dimaline model
- gastrin released from G cells will bind to CCK2 receptors on ecl cells, this will cause histamine release which then binds to H2 receptors on parietal cells and causes acid secretion
- histamine - main substance that drives acid secretion
- ACh and gastrin have minor effect on acid secretion

Question 9

briefly describe the 3 phases of gastric acid secretion?

Answer 9

cephalic - involves the brain
- vagal nerve stimulation causes ACh release which acts on M3 receptors on parietal cells
- vagal nerves also stimulate GRP - gastrin releasing peptide - acts on G cells to release gastrin

gastric - G cells release gastrin which binds to CCK2 receptors on ecl cells which causes histamine to be released and it binds to H2 receptors on parietal cells to cause acid secretion
- drives gastrin-histamine acid secretion

intestinal - intestinal endocrine cells release entero-oxyntin causes acid secretion, intestinal G cells release gastrin, fats absorbed in lumen inhibit further acid secretion

Question 10

how is G cell function controlled?

Answer 10

acid secretion and protons will activate the D cells which release somatostatin

somatostatins bind to G cell and inhibit further release of gastrin - neg feedback mechanism

Question 11

compare the 2 drugs used to inhibit acid secretion?

Answer 11

PPIs - irreversibly bind to H/K ATPase pump, so cannot work and secrete protons anymore
- which means D cells wont be stimulated to release somatostatin and won’t cause an inhibitory feedback on the G cells
- so gastrin will continue to cause release of histamine so can lead to histamine build up

H2 antagonists - block histamines actions but are H2 receptors are widespread throughout the body so can lead to many off target effects