secretion Flashcards
(22 cards)
salivary secretion by salivary glands &
its function
- saliva contains alpha amylase that helps to hydrolyze starch, glycogen and carbohydrates
- controlled by nervous system innervation
1) sympathetic innervation = saliva is thicker
the release of adrenaline binding to alpha and beta adrenergic receptors stimulates release of thicker saliva
2) parasympathetic innervation = saliva is watery
the release of acetylcholine binds to muscarinic receptors stimulates release of watery saliva
function of saliva
- helps with lubricating the food and mixing the food with the enzymes for chemical digestion
- for oral hygiene
- maintenance of the oral bacteria population
components of the saliva
1) serous secretion = alpha amylase enzyme
2) mucin secretion = glycoprotein
3 key cells that makes up the gastric secretion
protein digestion begins in the stomach (no absorption at all)
parietal cells = produces the components that combines with cl- in the stomach that makes hcl (acidic)
- hcl strong acid helps to kill majority of the microorganism in the stomach except for helicobacter pylori (neutralizes the acid)
- parietal cells also produce intrinsic factors that helps with vitamin B12 absorption
- the higher the rate of secretion the higher the concentration of H+ (vice versa)
- K+ in gastric juice is higher than in the plasma hence during prolong vomiting this can lead to hypokalemia
chief cells = produces pepsinogen that undergoes autocatalysis to become pepsin active enzymes helping with protein denaturation
G cells = gastrin hormone
regulates gastric acid and mucin secretion
purpose of mucus in the gastric secretion
important to protect the gastrin mucosal lining from the acid
rate of gastric secretion
dependent on the amount of parietal cells and varies amongst individuals
basal rate (interdigestive periods) = 1-5 mM/hr
after food = 6-40 mM/hr
gastric ulcer patient < normal
duodenal ulcer patient > normal
pernicious anemia (body’s inability to absorb vitamin B12, due to the lack of intrinsic factors < normal
Major stimulators of HCL secretion + their inhibitors
normal situation:
- acetylcholine
- gastrin
utilizes calcium as their secondary messenger to activate the H+/K+ ATPase pump
inhibit using
- anticholinergic
- gastrin antagonist
stress situation: (intermittent)
- adrenaline
- histamine
utilizes cAMP as their secondary messenger to activate the H+/K+ ATPase
inhibit using
- histamine > H2 antagonist
to inhibit the secondary messengers can use prostaglandins E
to inhibit the H+/K+ ATPase can use omeprazole
function of gastrin
- gastrin secreted by G cells is responsible to control the HCL and mucus secretion
- it also regulates the gastric and intestinal motility
- increase pancreatic secretion
- for proper growth of GI mucosa
pepsinogen secretion by chief cells
- the lower the pH the more rapid the catalytic conversion would occur
- about 10-20% of the proteins get digested in the stomach
- once reaches the duodenum (highly alkaline), the pepsin would be irreversibly inactivated
intrinsic factors secreted by parietal cells
stimulation for the release is by gastrin
- responsible for helping with vitamin B12 absorption
- intrinsic factors will form a complex with vitamin B12 that is highly resistant towards digestion
- IF-B12 complex is absorbed at the terminal ileum
omeprazole can inhibit HCL secretion but this would not affect the release of the intrinsic factors tho they both are produced by the parietal cells.
constituent, function and regulation of mucin
constituent:
it is insoluble in acidic pH but it can be destroyed by pepsin
function:
gastric mucin is secreted to protect the gastric mucosal lining (coat and lubricate)
regulation:
regulated by acetylcholine
mechanical stimulation by food
prostaglandins (inhibitor)
prostaglandins produced by COX1 is used for housekeeping roles
function:
- inhibits parietal cells from secreting HCL
- it helps to mediate mucosal defense by
1) increasing blood flow towards mucosal lining that helps to aid in repair
2) increase mucin, phospholipid and HCO3- secretion
3) increase turnover rate for the mucosal cells
prostaglandin deficiency would lead to gastric mucosal injury (gastric ulcer which is a functional disorder)
- if px takes COX inhibitors (non selective) eg: aspirin or NSAIDS this would have lowered prostaglandin levels because they block the COX1 and 2 pathways so it decreases the by product
purpose of gastric mucosal barrier
- protect the stomach from abrasion and HCL & pepsin
- there is a thick mucous layer that has high concentration of HCO3- and mucin
- the HCO3- ensures that the gastric cells are kept as neutralized as possible and slows down the exit of the molecules
- the mucin helps to slow down the entry of the HCL
- calcium and cholinergic agonist stimulates HCO3- secretion
- adrenergic agonists decreases HCO3- secretion leading to stress ulcer formation
- aspirin and NSAIDS, COX inhibitors inhibits release of HCO3- and mucin leading to also gastric mucosal injury
ulcer therapy
- neutralizing the HCL
- prevent acid release (giving omeprazole)
- give antibiotics if the cause of it is due to helicobacter pylori
- prostaglandins agonist (stimulate the COS to produce PGE)
gastric digestion of carbohydrates, lipids and proteins
- the salivary amylase would continue to breakdown carbohydrates in the stomach
- minimal digestion of lipids, high acidity inhibits fats from forming emulsion
- 10-20% of protein denaturation due to pepsin
gastric absorption
very little absorption takes place and only highly lipid soluble substances like ethanol is rapidly absorbed
the small intestine has a increase in surface area what are the 3 ways?
- micro villi
- villi
- folds especially at the duodenum and upper jejunum
absorption of water & electrolytes
- the absorption of water and electrolytes at the small intestine is 99%, failure to do so will lead to dehydration and circulatory collapse
- water transportation is mainly due to facilitated transportation and electrolytes dependent transportation mechanism (eg: Na+ dependent transport mechanism)
the small intestine secretion consist of what components?
1) mucin
purpose of mucin is to protect the small intestine from the acidic chyme and the pepsin
secretion is stimulated by parasympathetic nerve impulse and 3 major GI hormones
- gastrin
- cholecystokinin (CCK)
- secretin
CCK and secretin is produced from the cells of the small intestine at the duodenum and the upper jejunum
2) enzymes
- there are no cells that produces the enzymes of the small intestine
- enzymes are produced only because of the cells degenerating as the small intestinal cells have a high turnover rate
- the death of the cells produce enzymes like
maltase, sucrase and lactase
3) electrolytes
- the small intestinal juice is high in HCO3- compared to the plasma due to the HCO3-/cl- exchanger, that actively pumps HCO3- from the plasma into the luminal space and in exchange take in the cl- into the cells
stimulation and functions of small intestinal juice
stimulation by mechanical irritation of the mucosa, distention of the gut and
- ach & gastrin (via ca)
- secretin & cck (via cAMP)
function of small intestinal juice
- fluidity of chyme
- maintains slightly alkaline pH
pH and drug absorption
the pH of the GIT varies throughout
- unionised = uncharged = non polar
lipid soluble, water insoluble
able to pass though membrane better absorption at GI tract
- ionised = charged = polar
non lipid soluble, water soluble
- poor absorption
pH affects the % unionised
and disease and drugs may affect pH
large intestine secretion & stimulation
the colon has no villi & microflora present, slow transit and vigorous mixing movement
- mucus (protects large intestines from acidity)
- intestinal juice (high in K+ and HCO3-)
- buffer against H+ produced by bacterial fermentation
stimulation:
parasympathetic nerve impulses would increase secretion
sympathetic nerve impulses decrease secretion
mechanical or chemical irritation of mucosa
pathological alterations of salt and water absorption
failure to absorb an electrolyte normally would lead to
1) congenital cl- diarrhea
- lack of cl-/hco3- exchange, cl- not effectively absorbed
- high cl- in stool and retention of hco3- which results in metabolic alkalosis
2) failure to absorb nutrients normally
- carbohydrates malabsorption
3) hypermotility of intestine > lesser absorption time
4) enhanced secretion of water and electrolytes > secretory diarrhea
the cl- can enter into the intestinal lumen via 2 cl- channels depending on whether isit stressful situation or normal situation
ca+ or CAMP
5) oral rehydration therapy
using glucose or amino acid saline solution helps to bring the sodium back into the cell
