overview of the GI tract 1 Flashcards
what lines the oral/buccal cavity?
oral mucosa = thick stratified squamous epithelium that is resistant to abrasion
what does the mouth produce to inhibit bacterial growth?
defensins
what do teeth lie in?
sockets in the mandible and maxilla, covered by gums
what are the 2 types of teeth?
- deciduous teeth (n=20) — appear within the first 6-24 months of life, gradually replaced in childhood as the
- permanent teeth erupt (finished by approx age 12)
what is there lots of in saliva, acting as the first line of defence?
IgA
what are the types of adult teeth, how many are there and what do they do?
- incisors (8) - slice and cut
- canines (4) - tear and rip
- premolars (8) - grind and crush
- molars (12) - grind and crush (mostly grind)
what do cavities or dental caries result from?
from the gradual demineralisation as a result of acid production from bacteria in plaque
what are the 3 main salivary glands?
parotid, submandibular, sublingual
saliva is 99% what?
water
what are the components of saliva?
- water
- lingual lipases and alpha-amylase
- mucoproteins (mucin)
- lysozyme
- immunoglobulins (esp IgA)
- electrolytes
- calcium and phosphate
what is the role of mucoprotiens (mucin) in saliva?
act as lubricants — lubricate passage of food and decrease abrasions of oral mucosa
what is the role of calcium and phosphate in mucous?
dental repair (produced in small quantities)
what is the pH of saliva?
slightly acidic (pH 6.75-7) to provide reasonably optimal conditions for enzyme function
how is salivation controlled?
saliva is secreted continuously but salivation is controlled by salivatory nuclei in the medulla and pons of the brainstem:
- mechanoreceptors and chemoreceptors in the mouth stimulate production of saliva with a HIGH WATER CONTENT
- mechanoreceptors are not just food specific (non food objects induce salivation)
- input from higher brain centres (thinking about food) and lower digestive tract (irritation) can also induce salivation
non-food objects into the mouth stimulate what kind fo saliva production?
saliva with lots of H20 but few enzymes
what are the intrinsic nerve plexuses of the ENS?
myenteric and submucosal nerve plexuses
describe gut innervation
- the submucosal and myenteric plexuses are not simply nerve fibres from the CNS… they have their own neurones, akin to a ‘gut brain’
- the gut is influenced by the rest of the NS, but will FUNCTION WITHOUT ANY INPUT FROM THE BRAIN OR SPINAL CORD — therefore digestion can still occur in people who have severed connections to their CNS
- the transmitter types used by these neurones is very diverse
what does the muscularis externa consist of? exception?
- inner circular and outer longitudinal layer (smooth muscle)
- exception is some parts of the stomach = 3 layers
circular smooth muscle function vs longitudinal function
inner circular — squeezes gut contents
outer longitudinal — shortens that portion of the gut
what are the pacemaker cells of the gut? what modulates this?
interstitial cells of Cajal in smooth muscle — enteric neurones or extrinsic neurons modulate this basic activity
what can loss of the cells of Cajal lead to?
gut motor dysfunction disorders eg. dye to diabetic autonomic neuropathy (affects the enteric NS) —> nausea, vomiting, diarrhoea, constipation
what does the oesophagus connect?
pharynx to stomach
how does the oesophagus normally lie?
closed — highly folded mucosa
what does the submucosa of the oesophagus contain?
blood vessels, lymphatics, nerves, lymphoid tissue and mucus glands
what is the oesophagus lined with and why?
stratified squamous epithelium to resist abrasion
describe the muscularis layer of the oesophagus
- upper 1/3 = skeletal = voluntary
- middle 1/3 = mixed
- lower 1/3 = smooth = involuntary
what is the outer layer mostly in the oesophagus?
adventitia — fixed to adjacent structures by connective tissue
last part beyond the diaphragm covered with serosa
how does the lining change at the gastro-oesophageal junction?
from squamous to columnar epithelium (glandular)
what meta plastic change can occur at the gastro-oesophageal junction?
change of epithelium from stratified squamous to gastric due to repeated damage from gastric reflux = BARRETT’S OESOPHAGUS
—> columnar glandular epithelium move up into lower part of oesophagus
—> can be a precursor to oesophageal cancer
where is peristalsis in the stomach confined to?
the lower part
what does the action of peristalsis and the pyloric valve result in?
vigorous churning of contents and relatively slow gastric emptying
the rate of gastric emptying is controlled to some extent by what?
the caloric value of the contents of the duodenum
thick mucosal and submucosal layers in the stomach form numerous longitudinal folds called what?
rugae
what are there in the small intestine after a meal?
small irregular contractions
what does the small intestine exhibit in the inter digestive state?
the migrating motor complex (MMC) — can take up to 2 hours to pass along the small intestine — thought to have a housekeeping role; sweeps material throguh the gut
what is the signal to stop the inter digestive activity?
ingestion of food
what can the ingestion of food be mimicked by?
gastrin released from stomach and cholecystokinin (CCK) released from intestine
what does cholecystokinin (CCK) do?
it is a potent inhibitor of gastric emptying in response to high caloric value in the duodenum (an example of local integration of activity to meet demand)
what is active almost continuously, although increased activity can be elicited by particular stimuli?
colon
what is transit time in the colon?
2-3 days
what is the major component in terms of transit time, affected by dehydration and storage?
transverse colon
what do contractions of the circular muscle in the colon cause?
HAUSTRA = not like peristalsis
— one haustrum fills and distends this induces contractions that push food into the next
what is the gastrocolic reflex?
powerful propulsive contractions elicited by the introduction of food to the stomach — introduce food at one end, primed to start defaulting at the other end to prevent backlog of material
what type of cells does the cardia of the stomach mostly contain?
mucous cells
what type of cells does the pylorus of the stomach mostly contain?
gastrin-producing cells
what part of the stomach contains all cell types?
body
what does the stomach absorb?
alcohol (although most is absorbed in the small intestine), some water and some vitamin B12
the stomach mixes food and acts as a ________?
reservoir
name some functions of the stomach
- starts digestion (protein, nucleic acids)
- activates some enzymes (pH 1-2)
- destroys some bacteria
- synthesises intrinsic factor (B12 absorption) — the only truly ‘essential’ function of the stomach
list the exocrine gastric secretions
- HCl
- mucus
- pepsinogen (inactive precursor of pepsin)
- intrinsic factor
list the endocrine gastric secretions
- gastrin
- somatostatin
why is the stomach highly folded?
to increase SA
what do goblet cells in the stomach do?
secrete an alkaline mucus (sits on and lines the surface of the stomach to prevent auto digestion)
what do mucous cells in the stomach do?
secrete mucus and pepsinogens
what do parietal cells in the stomach do?
secrete gastric acid and intrinsic factor
what do chief cells in the stomach do?
secrete pepsin and gastric lipase
what do G cells in the stomach do?
secrete gastrin
what do D cells in the stomach do and where are they found?
- found in antrum
- secrete somatostatin
gastric lipases vs proteases production
- lipases produced in their active form
- proteases usually secreted as inactive precursors
HCl function in the stomach
acidifies lumen, produces pepsin from pepsinogen
mucus function in stomach
protects mucosal surface being damaged by HCl
pepsinogen function in stomach
precursor of pepsin (which acts an an endopeptidase — cuts at non-terminal ends of proteins)
intrinsic factor function in stomach
important in the absorption of vitamin B12 (later, in the terminal ileum) and erythropoiesis
gastrin function in stomach
stimulates acid production
somatostatin function in stomach
inhibits release of gastrin (decreases gastric acid production)
what controls pepsinogen secretion?
ACh (vagal input)
what controls HCl secretion?
- ACh (vagal input)
- gastrin (from G cells)
- histamine (from enterochromaffin cells)
- other hormones
what is gastric acid secretion inhibited by?
- somatostatin (via decreased gastrin release)
- secretin (via decreased gastrin secretion)
- gastric inhibitory peptide and other enterogastrones (directly on parietal cells)
what are the 3 phases of gastric secretion?
- cephalic phase
- gastric phase
- intestinal phase
describe the cephalic phase of gastric secretion
thought, smell, sight, taste of food releases ACh, stimulating the parietal cells and also the G cells — vagally mediated, about 40% of gastric acid secretion occurs here
describe the gastric phase of gastric secretion
distension and reflex activation of enteric neurones and vagal outflow stimulate the parietal cells and the G cells. digested proteins in stomach also stimulate the G cells — about 50% of gastric acid secretion occurs here
describe the intestinal phase of gastric secretion
amino acids present in the bloodstream (products of protein digestion) directly stimulate the parietal cells — about 10% of gastric acid secretion occurs here
what is the gastric mechanism of inhibition of gastric secretion?
- if proteins are present in the stomach, they act as buffers to keep luminal pH > 3
- as the stomach empties, therefore, the luminal pH falls below 3 : D cells release somatostatin to inhibit gastrin release and thereby reduce acid secretion
what is the duodenal mechanism of inhibition of gastric secretion?
- acidification of the duodenal lumen releases secretin, which inhibits gastrin secretion
- acidification of the duodenal lumen and the presence of fatty acids and salt in the duodenum release gastric inhibitory peptide, which acts directly on parietal cells to inhibit HCl secretion
