GIT physiology 2 Flashcards
How do molecules move across membranes
paracellular transport
transcellular transport
secreted: body -> lumen
absobed: lumen -> body
What are the normal types of exocrine secretions
Mucus : protection, lubrication, mechanical digestion
Electrolytes + solution: optiomal pH, enzyme function, osmolarity, dilute food
digestive enzymes: Digestion + absobtion
how many L are secreted throughout the GIT
Around 8L meaning reabsoption is very important
~2-3L - gastric
~1.5L - pancreases, salivatory glands, SI
~0.5L - bile
Ions from plasma
What is the secretory rate + secretions from the salivatory glands
0.3->1.5ml/min when stimulated
Secretes: mucus, NaHCO3, NaCl, linugal lipase, salivatory amylase
- optimal pH, irrigation and hydration
What is the difference between gastric secretions before a meal and during a meal
Before meal:
Slow secretion of HCO3- and mucus -> protect the stomach lining
- HCO3- stays in mucus to keep alkaline near epithelium
During meal:
Goblet-cells, cheif cells, parietal cells
- mucus + pepsinogen + intrinsic factor (B12 absoption in ilium) + HCO3- + HCl
What is the function of low pH in the stomach
Activates pepsinogen
Kills microbes
denatures proteins
How do parietal cells secrete acid (HCl)
- carbonic anhydrase combines H2O + CO2 -> H2CO3 -dissociates> H+ + HCO3-
- H+/K+ATPase pumps H+ luminal and K+ into cell - K+ then leave via channel
- anionic counter exchance swaps HCO3- into intersitial space and Cl- into cell
- Cl- diffuses into lumen via channel proteins
H+ + Cl- -> HCl
What occurs during the cephalic phase of gastric acitvity
External stimulus triggers CNS
CNS triggers PS increase -> ENS increase -> submucosal plexus increase
Promotes secretion from G-cells, parietal cells, chief cells,
- G cells secrete gastrin -> further promote parietal + cheif cells
Causes increase in - HCl, pepsinogen, mucus, HCO3-
What are the three phases of gastric activity
Cephalic phase - 20% secteions
gastric phase - 70% secretions
intestinal phase - 10% secretion
What occurs during the gastric phase of gastric activity
Mechano, chemo receptors detect stretch + nutriance change + pH + G-cells detect short peptides -> signals to ENS
Increased myenteric + submucosal plexus
increased gastrin, HCl, mucus, HCO3-, pepsinogen
increased motility - effected by gastrin + myenteric
What occurs during the intestinal phase of gastric activity
Detected by chemo and mechano receptors + enteroendocrine cells in duodenum
EEC secrete - secretin, CCK and GIP
ENS + CNS signaled - PS decrease, sypathetic increase -> decreases acitivty of myenteric plexus + submucosal plexus
Inhibition of parietal cells + g-cells + chief cells
reduces gastric empying
How is the pancreases stimulated and what does it secrete
CCK stimulates acinar cells -> enzymes
Secretin stimulates duct cells -> HCO3-
Acinar secretions:
pancreatic lipase + amylase
trypsinogen, chymotrypsinogen, procarboxypeptidase
How are pancreatic proteases activated in the GIT
Trypsinogen interacts with enterokinase which converts to trypsin
Trypsin -> activates chymotrypsinogen and procarboxypeptidase
released in inactive form to prevent digestion of acinar cells
What stimulates secretions from the gall bladder + how is this secretion regulated (produced)
CCK stimulates gallbladder contractions + hepatopancreatic sphincter relaxation
Production stimulated by bile in blood returning to the liver via enterohepatic circulation + mildly from secretin
95% reabsoped in ileum as it is metabolically expensive to make -> carried back to liver via enterohepatic circulation
What is the composition of the bile secretion
Created by hepocytes
bile duct cells secrete HCO3-
Bile contains waste products
- excess cholestrol
- bilirubin = biproduct from heme breakdown
