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What's the goal of the cephalic and oral phase of GI secretions?
o To prepare the GI tract to receive and digest food
o Via increasing Parasympathetic stimulation
Where is the majority of water/fluid reabsorbed in monogastrics?
Small intestine (except the duodenum)
What's so special about the monogastric's colon and its ability to absorb water?
it can absorb water against a large osmotic gradient
What is the consequence/clinical implication of the gastrointestinal tract not reabsorbing enough fluid/electrolytes?
o Excessive fluid loss - diarrhea
o Decrease in ECF - decrease intravascular volume
o Could create decreased arterial pressure and hypovolemic shock
What are some functions of saliva?
o Lubricates mouth and teeth, aids in swallowing
o Provides antibacterial and digestive enzymes
o Maintains chemical balance of tooth enamel
o Acts as an acid/base buffer
o Provides cooling mechanism
What are the three components of saliva?
o Mucus
o Ptyalin
o Serous component
What is the main function/role of the glandular portion of the salivary glands?
Helps secrete components of saliva: primarily zymogens and mucus
What is the main function/role of the duct portion of the salivary glands?
o Helps direct saliva to mouth
o Contributes the serous portion of saliva - the water and electrolytes
What is the benefit to the salivary glands secreting zymogens rather than active enzymes?
To prevent the enzymes from digesting the salivary gland itself.
What is the osmolarity of the primary secretions from acinar glands relative to plasma?
It is isotonic to plasma
Describe the movement of Na+, K+, Cl-, and HCO3- in the salivary ducts as saliva is being formed
o Na is actively absorbed into duct cells
o K+ is actively secreted into saliva
o Cl- is passively absorbed into duct cells
o HCO3- is secreted into saliva
What is the resulting contents of saliva, ion-wise, and osmolarity relative to plasma?
o Lots of K+ and HCO3-
o Is hypotonic to plasma
o Low in Na+ and Cl-
What would be the effect of a muscarinic antagonist (atropine) on salivary production? What about an acetylcholinesterase inhibitor?
o Muscarinic antagonist: reduce salivary production
o Acetylcholinesterase inhibitor: increased salivary production
Do esophageal secretions, the mucus, help protect the esophagus from gastric reflux?
Not really, nope
What gastric cells did we discuss in class - what are their products?
o Mucous neck cells: mucus, also replaces surface epithelial cells
o Parietal cell: HCl-
o Chief cells: pepsinogens
o ECL cells: histamine
o D cells: somatostatin
o G cells: Gastrin
What do parietal cells secrete?
HCl-
What do chief cells secrete?
pepsinogens
What do ECL cells secrete?
histamine
What do D cells secrete?
somatostatin
What do G cells secrete?
gastrin
What ions are involved in the proton pump? Which cells move against their electrochemical gradients?
o H+ moves against their gradient
o K+ moves against their gradient
o Cl-
o HCO3-
Explain how HCO3-, Cl-, and K+ play a role in the ultimate secretion of H+ and Cl- into lumen of stomach.
o HCO3- is created from CO2 and H2O, the extra H contributes to the H+ pumped into lumen by proton pump
o Cl- passively diffuses across cell into stomach
o K+ is pumped into the parietal cell in exchange for H+ pumping into lumen
What are 3 things that promote the proton pump? One involves the ANS, the other two are gastric cell secretions.
o Vagal input with Acetylcholine (Parasymp. Muscarinic cholinergic receptors)
o G cells secreting Gastrin
o ECL cells secreting Histamine, acting on H2 receptor
What two things act to inhibit the proton pump in parietal cells?
o Somatostatin
o Prostaglandins
What are four pharmacological agents that would act to decrease HCl- production by influencing the proton pump? What is the most effective?
o A muscarinic cholinergic antagonist, e.g. atropine
o H2 receptor blockers, e.g. Pepsid
o Prostaglandin analogue, e.g. misoprostol
o A proton pump inhibitor - the most effective
What are the main ions composing gastric juice?
o H+
o Cl-
o K+
What 3 things stimulate HCl- secretion from the parietal cells?
o Acetylcholine
o Gastrin
o Histamine
What are the neural, hormonal, and paracrine controls of the parietal cell? What is the result on gastric secretion from each?
o Neural: Acetylcholine from Vagal stimulation
o Hormonal: Gastrin from G cells
o Paracrine: Histamine from ECL cells
o They will all act to increase gastric secretion
How are enterochromafin-like cells involved in gastric secretion?
They secrete histamine, which promotes the proton pump and thus gastric acid secretions
What are 3 phases that contribute to gastric acid secretion? What contribute the most? And via what mechanism?
o Cephlic/Oral: via vagal mechanisms
o Gastric phase contributes the most: via vagovagal reflexes, local enteric reflexes, and hormonal gastrin/histamine
o Intestinal phase: via hormonal - release of small amounts of gastrin from duodenum and nervous mechanisms
What are 2 phases that contribute to inhibiting gastric acid secretion?
o Gastric
o Intestinal
In the intestinal phase - how are motility and hormones involved in inhibiting gastric acid secretion?
o Vagovagal and enteric reflexes will inhibit HCl secretion
o Secretin inhibits parietal cells
o Cholecystokinin inhibits parietal cells
In the gastric phase - how does inhibition of gastric acid secretion occur? What signals are involved?
o Somatostain by D cells
o "self-regulatory": Low pH will cause inhibition of parietal and G cells
What is a zymogen?
An inactive proenzyme
Pepsin helps digest what?
PROTEIN
What things activate and inactivate pepsin and pepsinogen?
o Pepsinogen is activated by acidic pH
o Pepsin is inactivated by neutral or alkaline pH
What helps maintain the gastric mucosal barrier? What helps maintain this barrier?
o The viscosity of mucus layer
o HCO3- secretions which is enhanced by prostaglandins
Why would NSAIDs and corticosteroids have a negative impact on the mucosal barrier?
They will block prostaglandin synthesis which will decrease HCO3- secretions and increase HCl secretions, which can lead to ulcers
What category of drugs would decrease gastric secretion from parietal cells?
o H2 receptor antagonists
o Proton pump inhibitors
o Prostaglandin analogues
What's the result of protracted vomiting that causes loss of gastric juices?
the body would be loosing the ions in gastric juices, namely Chloride, and might develop hypochloremia (low calcium) and hypochloremic metabolic alkalosis
How do prostaglandins enhance mucosal protection?
they stimulate mucus and HCO3- secretion while inhibiting HCl- secretion