Physiology Flashcards
what three glands is salvia secreted from?
submandibular (70%)
parotid (25%)
sublingual (5%)
what effect does parasympathetic enervation have upon salvia secretion?
increases it
what are the functions of saliva?
lubrication, antibacterial, carb breakdown via amylase
what two factors does the escape of chyme from to stomach depend on?
gastric factors (which are in favour of gastric emptying) and duodenal factors (which are against gastric emptying)
where is hydrochloric acid secreted?
parietal cell via a proton pump - (oxyntic mucosa)
what is the function of HCL in the stomach?
- activate pepsinogen to pepsin
- denatures protein
- kills micro-organisms
what cells is pepsinogen secreted by and what is it function?
Chief cells (oxyntic mucosa)
function:- it is the inactive precursor to pepsin
where is the intrinsic factor secreted from and what is its function?
intrinsic factor is secreted from parietal cells (oxyntic mucosa)
function:- needed for the absorption of B12
where is histamine secreted from and what is its function?
they are secreted by enterochromaffin like cell (oxyntic mucosa)
function:- histamine stimulates HCL production
where is gastrin secreted from and what is its function?
gastrin is secreted from G cells in the pyloric gland area
function:- stimulates HCL production
where is somatostatin secreted and what is its function?
somatostatin is secreted by D cells in the pyloric gland area of the stomach
function:- it inhibits the secretion of HCL
vagal stimulation has what effect on the secretions in the stomach?
vagal stimulation increases the secretion of substances in favour of acid production
what 4 factors help protect the mucosa from HCl/pepsin?
- hydrophobic monolayer
- bicarbonate secretion
- H+ exchanged for sodium
- locally produced prostaglandins (they reduce acid secretion, increase mucous and bicarbonate secretion)
what is the adverse effect of NSAIDs on the stomach?
NSAIDs inhibit the production of prostaglandin by COX 1 inhibition - which can then lead to gastric ulceration and bleeding
how does H. Pylori cause gastric ulceration?
not fully understood,
H. Pylori produces urease which converts urea to ammonia
- this buffers H+, protects the H. pylori itself and caused epithelial damage to the mucosa
- lipases/proteases are secreted degrading the mucosa and damaging the layers underneath
there is also an increased number of G cells, decreased D cells and a increased level of alkaline induced gastrin secretion
what drugs affect gastric acid secretion?
proton pump inhibitors (PPI)
H2 receptor agonists
What is the mode of action of PPIs and give an example.
they decrease acid secretin by inhibiting active (membrane secreted) proton pumps - they only become active in acidic environments
example - omeprazole
what is the mode of action of H2 receptor antagonists and give an example.
they are competitive antagonists and they block histamine mediate acid secretion
example - ranitidine, cimetidine
where is secretin secreted and what is its function?
secretin is secreted from S cells in the duodenal mucosa
it inhibits gastric emptying and secretion ad stimulates secretion by the gall bladder
where is cholecystokinin secreted and what is its function?
it is secreted from Endocrine I cells in the duodenal mucosa
it inhibits gastric emptying and secretion ad stimulates secretion by the gall bladder
where is GIP (glucose dependent insulinotrophic peptide) secreted and what is its function?
endocrine K cells within the duodenal mucosa
it stimulates insulin release by the pancreas
insulin and glucagon are examples of which type of pancreatic secretion?
endocrine secretions, secreted into the bloodstream
give examples of pancreatic exocrine secretions and they functions.
digestive enzymes (from acing cells) and sodium bicarbonate (from duct cells)
they neutralise acidic chyme - protecting the mucosa and providing the optimum pH for pancreatic enzymes
(look at the document diagrams and it is explained really well)
site of bile formation, storage and its function?
bile is secreted by bile duct cells and hepatocytes in response to chyme in the duodenum; this causes gallbladder smooth muscle to contract to release bile for the aid of fat digestion
what is the process of carbohydrate digestion?
mouth salivary alpha amylase and stomach salivary alpha amylase attack 1-4 glycosidic links along with duodenum-pancreatic amylase
glucose and galactose are both absorbed by secondary active transport
fructose is absorbed by facilitated diffusion
what is the process of protein breakdown?
HCl denatures proteins and pepsin clever proteins into peptides
- duodenum-pancraetic enzymes slit peptide binds between amino acids and brush border enzymes cleave amino acids apart
absorption is mostly by active transport, but hydrophobic amino acids are absorbed by passive diffusion
what is the process of lipid digestion?
stomach-gastric lipase and pancreatic lipase
bile salts emulsify large lipid droplets to smaller liid droplets - to provide a larger surface area for the action of pancreatic lipase
absorption of free fatty acids happens through passive diffusion
long fatty acid chains are resynthesises into triglycerides in the ER and incorporated into chylomicrons.
how/where is calcium absorbed in the body and that regulates its absorption?
passively through the small intestine, and active transport in the duodenum/jejunum
it is regulated by D3 and parathyroid hormone
how is B12 absorbed?
B12 binds to intrinsic factor produced in the small intestine and stomach - the B12-intrinsic factor complex is then absorbed in the terminal ileum by endocytosis.
