GI secretions Flashcards
Types of saliva secretions
Mucous = contain mucin, more viscous Serous = more watery, contain alpha amylase
Salivary gland structure
Acinus and duct cells
intercalated duct -> intralobular duct -> interlobular duct and then main duct
Functions of saliva
Serous = moistening oral mucosa, lubrication Mucous = lubrication, diffusion barrier for protection
Saliva stage 1 secretion
Acinar cells secrete an isotonic fluid, similar to plasma levels of Na+/Cl- and water
Composition mirrors plasma
Saliva stage 2 secretion
Modification by duct cells Removal of NaCl and replaced by K+/HCO3- Cl-/HCO3- exchanger on apical membrane Saliva always hypotonic to plasma As flow rate increases, there is less time for secondary modifications
Saliva regulation
PNS: ACh increases primary secretions and rate of flow, binds to M3, Gq, phos. protein kinases
SNS: NA binds to alpha receptors, Gq causes more amylase secretion and more viscous saliva, also through beta receptors
Pancreatic secretion components
Similar to saliva, efflux of Cl- from acinar cells through CFTR
Secondary: exchange in lumen of Cl- for HCO3-
Proteins in pancreatic secretions
Precursors to active enzymes
Drain into the descedning duodenum
Proteases, amylases, lipases, nucleases
Phases of digestion
Cephalic: sight, smell, taste of food (increases pancreatic and salivary by ACh)
Gastric: distension of the stomach (increases pancreatic by gastrin and ACh release)
Intestinal: presence of certain products in the duodenum (secretin, CCK), distension of duodenum
Nervous regulation of pancreatic secretion
ACh from vagus, higher command and vasovagal reflex
Pancreatic hormonal regulation
Gastrin: from G cells in antrum of stomach, from distension of stomach
Secretin: from S cells of duodenum, from H+ in duodenum
CCK: from duodenum, stimulated by FA
Somatostatin: inhibits secretions
ACh: higher command and vasovagal reflex triggered by amino acids and FA in duodenum
Gastric secretion components
H+, pepsinogen, mucus, bicarbonate, intrinsic factor
IF function
In small intestine for vitamins B12 absorption
Gastric gland cell types
Chief: pepsinogen secretion
Parietal: acid
Surface epithelial: mucus and bicarbonate
Neuroendocrine: hormones
Acid secretion mechanism
Insertion of vesicles with the H+/K+ ATPase in their membrane into the plasma membrane of parietal cells
Pump H+ into cell in exchange for K+, K+ recycles out
Cl- into lumen from bicarbonate exchanger on the basolateral
water follows to create HCl
H+/K+ ATPase inhibitor
Omeprazole
Regulation of acid secretion
Induced by kinase activity
- ACh from vagus, M3 and IP3
- Gastrin from G cells, from stimulated neurones or protein products in lumen, IP3 and PKC
- Histamine (paracrine), released from enterochromaffin-like cells, activates cAMP, H2 receptors
- Inhibit = somatostatin (Gi)
Histamine antagonist
Ranitidine, blocks H2 receptors
Mucous cells
Produce mucin, glycoprotein with high viscosity
Combines with water, ions and phospholipids to create a mucus gel
Peptic ulcer cause and treatment
Potential cause: Helicobactor pylori bacteria
Antacids: aluminium hydroxide
H2 inhibitor: ranitidine
Proton pump inhibitor: omeprazole
saliva flow rate
basal = 0.5ml/min stimulated = up to 5ml/min
types of salivary gland
parotid = serous, 25% submandibular = both, 75% sublingual = mucus, 5%
serous secretions supplemented by
alpha amylase
mucous secretions mainly contain
mucus
primary saliva secretion
contains amylase
isotonic levels of Na/K/Cl
secondary modifications saliva
occur as they move along duct
remove NaCl, replaced by K + and HCO3- entering the lumen
saliva primary secretion (details)
acinar cells secrete isotonic NaCl
- basolateral NKCC accumulates Cl- in cell which diffuses into lumen
- Na+ pumped out of basolateral by ATPase, diffuse into lumen paracellularly
- K+ diffuses across apical
- water follows by osmosis
secondary saliva modifications (details)
action by duct cells
- Na+ absorbed by ENaC and apical Na-H exchange
- Na+ exits on the Na-K ATPase
- Cl- reabsorbed through transporter with HCO3-, exits on basolateral
- HCO3- secretion into lumen in exchange for Cl-, formed in the cell from CO2 hydration
- K+ accumulated in cells from ATPase, enters lumen through the K/H exchanger
- low water permeability
final composition of saliva
final saliva always hypotonic to plasma
- as flow rate increases, less time for secondary modifications
saliva proteins
alpha amylase and lingual lipase
mucins = glycoproteins
also kallikrein, lysozymes etc,
pancreatic primary secretion
Cl- accumulated in cell from NKCC on basolateral, efflux into lumen by CFTR
Na+ follows paracellularly
pancreatic secondary
exchange of Cl- in the lumen with HCO3- via the same exchanger
Na and K enter lumen from paracellular
how is autodigestion of the pancreas prevented
packaging the enzymes as zymogens lacking enzyme activity
presence of protease inhibitors in secretory vesicles, presence of non-digestive proteases to degrade active enzymes
what hormones/ transmitters act on acinar and duct cells
ACh and CCK
what hormones act only on duct cells
gastrin
secretin
action of mucus and bicarbonate in stomach
combine to prevent acid digestion of the stomach itself
stomach humeral factors release and function
gastrin - stimulates acid secretion
somatostatin inhibits acid secretion
histamine is a paracrine regulatorn
importance of acid secretion
creates an antiseptic ante chamber at the start of the GI tract
denatures preteins
promotes truncation of pepsinogen into pepsin
what is secreted int he body of stomach
acid, pepsinogen and IF
has gastric glands
what is secreted in the antrum of stomach
gastrin, somatostatin and holds food
more of endocrine function
position and function of gastric gland cells
parietal = base and neck, secrete HCl and IF
chief = base and neck, secrete pepsinogen
endocrine = base, secrete regulators like gastrin and somatostatin
mucus neck cells = neck and secrete mucus
superficial epithelium = secrete mucus and bicarbonate
ionic composition of gastric juice
depends on secretory rate
unstimulated - basal secretion from non parietal, so higher Na and Cl
stimulated = more parietal so more HCl
unstimualted parietal cells
lots of tubulovesicels in the sub apical cytoplasm
vesicles contain H+-K+ ATPase proteins
stimulation of acid secretion triggers vesicle insertion into plasma membrane
- ATPase inactive in vesicles
common mediator hypothesis
histamine very effective
both ACh and gastrin also increase histamine release
action of somatostatin from stomach
D cells release Gi reduces acid secretion ACh inhibits and low liumenal pH stimulates release Gastric H.pylori inhibits release
pancreatic/ gastric acid secretion in phases
cephalic = 30%, from vagus gastric = 60%, distension initiates vasovagal reflex, protein products causes gastrin release intestinal = 10%, protein digestion stimulates G cells again
chief cells action
secrete pepsinogens
activated by N terminal truncation, spontaneous activation in acidic lumen
low pH for optimum activity
pepsin ingests 1/5 of protein
protein release from fusion of granules with apical membrane, stimulated by ACh, gastrin, CCK, secretin
mucous cells action
secrete mucin, large glycoprotein with high viscosity
combines with water, ions and phospholipids to create a mucous gel, barrier to H+ ions
stimualted by ACh
