GI Secretions Flashcards
(88 cards)
1
Q
Point of GI secretions?
A
GI secretions allow for extraction of energy from food. Secretions include water and electrolytes.
2
Q
How much fluid do we ingest daily? How much fluid is handled a day in GI tract? How much fluid is removed through feces? Happens the the rest of the fluid.
A
- 2L
- 109L
- 100mL a day.
- The rest of the fluid not excreted is absorbed or reabsorbed.
3
Q
If we reabsorb the bulk of the fluids that are secreted, why is the body secreting them?
A
- For the stomach, in prehistoric times, food was not sterilized (ingested a lot of microbes). So, acid was secreted to kill the microbes.
- All the digestive enzymes from the pancreas are acid labile (killed by acid). So, basic fluids are secreted from small intestine and pancreas to neutralize acid from the stomach.
- A large portion of fluid secreted into GI tract is passive, mediated by osmotic pressure.
4
Q
Describe result of fluid production upon ingesting carbs and protein.
A
- High production of small particles from large particles, resulting in an increase in osmotic pressure.
- Increase in osmotic pressure results in an increase in fluid into the lumen of upper small intestine.
- As the nutrients go through the small intestine, ad it gets absorbed, the osmotic pressure decreases, and you have an excess amount of water. This excess water simply diffuses back.
5
Q
Name the 6 fluid types that are secreted within the GI tract.
A
- Digestive enzymes
- Water
- Electrolytes
- MUCUS
- Organic substances
- Protective substances
6
Q
What’s the secretion mech of enzymes (proteins)?
A
Exocytosis in response to neuroendocrines. Vesicles carry the enzymes to the plasma membrane and lets them diffuse through.
7
Q
Describe secretion mech of fluids (electrolytes and water)
A
- Ion movement into the lumen comes first. Ultimately energy-dependent.
- Counter ions follow to achieve electroneutrality.
- Water follows to balance osmolarity
8
Q
Amount of salivary secretions released daily
A
1500mL
9
Q
What are the jobs of saliva.
A
- Lubrication (helps with swallowing and speech)…dealing with mucus and fluid.
- Protection…dealing with mucus, HCO3, lysozyme (takes care of gram (+) material), lactoferrin for gram (-) material, secretory IgA (for specific pathogens). Note that without mucus, you would be burnt from hot fluids like coffee.
- Digestion…Amylase (active enzyme upon secretion…the more you chew, the sweeter it becomes. works in oral cavity), lingual lipases (not activated until it enters the stomach by the acid). None so long of these enzyme are necessary so long as pancreas is healthy.
10
Q
When are the enzymes most important?
A
- Newborn would need it if mother is sick and is not producing milk. Mother’s solution is to chew rice extensively, spit it out, and feed the baby. Supplies the baby with the amylase that the baby needs to digest the carbs in the rice.
- Patients with pancreatic insufficiency. Would not be able to digest starch and fat because of lack of amylase and lingual lipases. These two enzymes can digest a lot before they get killed by the gastric acid in the stomach.
11
Q
Characteristics of salivary fluids. Must memorize the.
A
- Contains Na, HCO3, Cl, K.
- The concentration of these electrolytes changes over time with the rate of secretion, but it is ALWAYS hyPOtonic…as in, it’s below the total ion concentration in the plasma.
- Saliva is always low in Na and Cl then in the blood
- K is always HIGHER in the saliva than in the plasma.
- Saliva is rich in HCO3 most of th etime
12
Q
Extensive loss of saliva most likely will cause a decrease in which of the following in the blood?
Na, K, Cl, Ca, Total osmolarity
A
K
13
Q
What is an acinus cell? Describe the process of it’s fluid and electrolyte secretions.
A
Duct for salivary gland. Its cells secrets K, HCO3, Na, and Cl into its lumen. H2o Follows. This primary secretion travels through the duct. Na and Cl are both reabsorbed. Gap junction prevent H20 from following, so H20 is left behind.
14
Q
What happens if secretion rate of acinus is very low? High?
A
- There would be more time for Na and Cl reabsorption, making the saliva ion concentration really low.
- There is not enough time for reabsorption of Na and Cl, so saliva concentration becomes high (increased osmolarity). HOWEVER, total osmolarity is STILL below that of plasma. Note that HCO3 concentration stays low at low acinus secretion rates.
15
Q
What happens to HCO3 and K in the duct area after leaving the acinus?
A
Both HCO3 and K are NOT reabsorbed. In fact, the duct cells secrete even more K and HCO3 into the duct.
16
Q
Describe ion movement in ACINAR cell, aka primary secretion.
A
- Bring Cl into the acinar cell from the serosal side.
- HCO3 and Cl leak together from the acinar cell into the lumen.
- Because HCO3 and Cl are both in the lumen, both with a negative charge, there need to be a balance. SOOO, K is secreted from the serosal side into the acinar cell and then from the acinar cell into the lumen. Electroneutrality is achieved.
- Na comes in to lumen through the same logic, which is to help establish the electroneutrality
- H20 follows Na.
17
Q
What causes primary secretions from the acinar cell to occur?
A
Stimulations by Ach or VIP. increase metabolic rate, which makes more HCO3 available for secretion. The increased metabolism by Ach or VIP also stimulate the HCO3/Cl channel and K channel, both on luminal side, respond due to Ca2+ channels. Needs Na/K ATPase for all of this to work.
18
Q
Describe ion movements in ductal cells as they would modify the saliva concentrations in the lumen.
A
- Na is reabsorbed through dedicated Na channel or Na/H exchanger (H is then thrown into the saliva in this second case)
- Assuming the Na/H exchanger was used, the H is then exchanged back into the ductal cell while spitting out K into the lumen
- HCO3 is spit out into the saliva in exchange for Cl that was in the saliva, which is brought into the ductal cell. Needs Na/K ATPase for all of this to work.
19
Q
What stimulates saliva secretion?
A
Smell, taste, pressure, nausea
20
Q
What pathway does saliva secretion signal follow after entering salivary nucleus of medulla. What do the neurotransmitters generated designed for? What is the end result?
A
Parasymp, which is a major trophic factor (using CN IX, X, VII ), leading to Ach/VIP releases. Ach/VIP lead to vasodilation, acinar cell metabolism, channel activation, glandular growth, and myoepithelium cell contraction. All of this leads to fluid, enzymes, and mucus.
21
Q
What happens if you cut off CN VII?
A
Salivary gland takes L. Very dry mouth results.
22
Q
What inhibits salivary secretion?
A
fatigue, lack of sleep, fear, DEHYDRATION…the strongest factor!
23
Q
Upon inhibition of salivary glands, what pathway is used?
A
Symps of T1-T3. Uses Superiror cervical ganglion, which releases NorEpi and weakens vasodilation, acinar cell metabolism, channel activation, glandular growth, and myoepithelium cell contraction.
24
Q
What is a myoepithelial
A
It is a cell of epithelial origin but but has muscle cell properties. It can contract in order to squeeze the mucus out.
25
How much gastric fluid is released in a day? What are the 2 components of gastric fluid secretions?
1. 2000mL
| 2. Oxyntic and non-oxyntic.
26
What composes the oxyntic component of gastric secretions? What cells secrete them? Describe inducing rate.
HCl (H and Cl), K, and Intrinsic Factor (IF), all of which are secreted from parietal cells. HIGHLY inducible, as it's stimulated during cephalic and gastric phase.
27
What composes the non-oxyntic component of gastric secretions? What cells secrete them? Describe inducing rate.
Mucus, Na, HCO3, all of which are secreted from mucus cells. Then there is pepsinogen, released by chief cells. There is also diffused interstitial fluids consisting of Cl and H2O. Diffusing rate of everything is relatively constant..main component at resting, but is highly diluted by oxyntic component upon induction.
28
Oxyntic or non-oyntic component is dominant at rest. Why does the dominant one AFTER stimulation supersede the non dominant one? What are the isotonic compositions during rest? Stimulation?
1. Non-oxyntic.
2. Oxyntic one is dominant after stimulation because of all the HCl it secretes, making it isotonic HCl. H and Cl are the dominant atoms present at this point. In resting state, composition is isotonic NaCl (more Na and Cl present)
29
What are the major components of gastric fluid? What is significant about Cl concentrations?
Na (not as high), K, Cl, H (last 3 are high...though K doesn't look like it, just take his word for it.)
Note: Cl is always higher than H, when talking about gastric acid,both at lower and higher rate.
30
In a patient with severe vomiting, which plasma ions become too low?
Cl AND H!!!!! ions would become too low, leading to a higher pH in the blood...alkalosis.
31
How does digestion occur through gastric secretions?
Low, acidic pH activates pepsinogen to pepsin, as well as activates lipases. HCl also denatures proteins for optimal digestion by pepsin.
32
How do gastric secretions aid with absorption?
HCl solubilizes minerals such as Ca, PO4, Fe. And INTRINSIC FACTOR is REQUIRED for the absorption of Vit. B12.
33
How do gastric secretions affect general protection?
Mucus is thiccccc in the stomach. CHO3 neutralizes the acids, HCl inactivated the microbes (besides Heliobacter pylori, which colonizes the stomach and leads to stomach cancer.) Note that E. coli, along with other bacteria, can survive pH's less than 2.0
34
Describe the morphology change of HCl secretion from parietal cells at rest and in secreting state.
Resting: Tubulovesicles are plenty. These things are rich in H pumps or H/K atpase in the tubulovesicle membrane. There are also intracellular canaliculi, which is essentially open to the lumen of the stomach. Tubulovesicles and intracellular canuliculi are separate organelles.
Secreting: Upon Ach, Histamine, etc, tubulovessicles link together and become one and actually connect, with the aim of opening to the intracellular canuliculi, leading to the gastric pit.
The acid from the H or K/H pumps is pumped through the tubulivesicles into the intracelllular caniliculi.
35
Describe ion movements of parietal cells during HCl secretion during resting and secreting state
RESTING:
1. Low metabolism causes CO2 and water to form HCO3 and H (bicarbonic acid dissociation product).
2. H stays int he cells. HCO3 leaves the cell the be exchanged by Cl, which enters into the cell.
3. The cell flows through parietal cell and exits on the lumen side, hence Cl secretion into the lumen.
4. K is pumped into the cell and runs all the way through to the lumenal side.
Ovaral very negative voltage on lumenal side...-70 to -80mV
Secreting:
1. Ach, Gastrin, Histamine all cause increase in parietal cell metabolism, INcrease more HCO3, which leaves more nad cause more Cl to be brought it.
2. H pump sitting in tubulovesicle membrane is activated, and it pumps H out into the lumen through the intracellular canuliculi.
3. The H that was secretes neutralizes some of the Cl that was also secreted, and this lower the potential to to -30 to -50mV. Since it's not 0, you can still confirm that there is still always more Cl than H in the lumen at all times.
36
Alkaline tide
Increase of gastric vein pH increase coupled to gastric acid secretion. Remember, H is seceted into the stomach lumen by H atpases, but the increased metabolism also caused and increase in HCO3 to secreted into the portal vein (so that Cl can come into the parietal cell)
37
What is postprandial alkaline tide? What happens in the case of severe vomiting?
Occurs after eating. Situation where after a major meal, tho there is H secreted into the stomach, HCO3 is secreted into the stomach. In the case of severe vomiting, there is a sustained alkaline tide, leading to metabolic alkalosis. Note that the H that is secreted into the stomach lumen is lost in the vomit, leaving nothing but HCO3 in the body, as HCO3 is still being sent to the portal vein.
38
Administration of a proton pump inhibitor (omeprazole) after a major meal will:
No clue...
39
Describe the control of acid secretion in the interdigestive phase.
There is no stimulus, and only 15% of your daily HCl concentration is produced. This is because there is limited Vagal activity (limited PSNS), and limited gastrin and histamine secretion.
40
What stimuli stimulate the cephalic phase of digestion?
1. sight of food
2. smelling
3. chewing
4. tasting
5. swallowing
41
What percentage of daily HCl production comes from the cephalic phase of digestion? What mediates or inhibits this production? What is the significance of the cephalic secretion test?
1. 30%
2. Vagal tone (PSNS), gastrin, and histamine. This is because gastrin and histamine are not that high yet, and the stimuli have stronger effect.
3. Cephalic secretion demonstrated that there is a legitimate presence of acid production based on the presence of that cephalic stimuli alone.
42
Describe the control of acid in the gastric phase.
Gastric phase is stimulated by the food in the stomach. This accounts for 50% of the daily HCl concentration production. PSNS (vagal tone), gastrin, and histamine go HAM with the HCl secretion.
43
Describe the control of acid secretion in the digestive phase.
The digestion product stimulates the produciton of HCl. It only contributes to 5% of the HCl production...HCl production drops 10 fold! Why? A: Once you start gastric emptying, you don't want to inactivate gastric enzymes. So, there's an increased presence of secretin, CK, and GIP. These guys all inhibit HCl secretion.
44
Depict how Ach, Gastrinm and Histamine work together to stimulate HCl production.
Ach stimulates Gastrin production. Both gastrin and Ach stimulate histamine production by calling upon ECL cells...Dr. Corbett fam. They work together to stimulate H pump and Cl channel.
45
Depict how GIP, Secretin, CCK, Somatostatin, and Prostaglandins all work to inhibit HCl secretion.
GIP, CCK, and Secretin all directly inhibit Gastrin secretion. They also all trigger somatostatin production, which also inhibits gastrin secretion. Somatostatin also reduces cAMP activity, reducing HCl production. Prostaglandins also inhibit cAMP, which decreases HCl produciton.
46
How does Gastrin act as a major trophic factor?
Gastrin production leads to parietal cell growth. Increased gastrin presence leads to increased parietal cell growth. Without enough gastrin, you get acid insufficiency.
47
What's the difference between the amount of HCl produced in the inside of the stomach, compared to outside?
The difference is 3 mil fold....more in the stomach. It's so acidic, you could remove rust from iron.
48
How does the body contain HCl without screwin your own body?
1. There is a thiccccc mucosal barrier (thank the mucus cells). Mucus cells also secrete HCO3, which has to diffuse through the mucus.
2. Cytoprotection by prostaglandins. Prostaglandins directly inhibit HCl secretion. They stimulate the production of mucus and CHO3. They also inhibit the synth of non-steroid anti-inflammatory drugs (NSAID) as well as glucocorticoids....this is why you should not be taking these drugs are steroids. These patients have screwed up H secretion, among other stomach problems. Glucocorticoids are a strong inhibitor of the containment mechs.
49
What is the job of the exopancreas secretions?
Takes care of digestion of every kind of food you eat. Starchs, proteins, fats, and nucleic acids are all covered by it. So keep that organ healthy. The hormones they secrete are usually in excess, so it is not the rate limiting factor of digestion.
50
What is the rate limiting step to digestion? What controls the rate of this occurrence? What happens if this rate limiting step disappears?
The rate of gastric emptying, controlled by the pyloric sphincter. If you remove this, you get dumping syndrome.
51
Describe the clinical manifestations of dumping syndrome.
GI: you'll have watery, painless diarrhea, and be gassy. A lot of fluid lost in a very short period of time.
Systemically: you would have weakness, diaphoresis (sweating), and tachycardia
52
Describe the pathophys of rapid gastric emptying.
1. There would be a sudden increase in osmotic pressure because of the fact that all the food ingested would be rapidly broken down into the really tiny pieces (thank pancreas enzymes such as amylase, disaccharideases, and peptidases). The increased osmotic pressure causes water to be pulled into the GI lumen.
2. The increased water presence contributes to increased motility, hence diarrhea.
3. Fermentation of nutrients by the colonic bacteria is the reason for the increased gas. 4. Loss of blood volume to the GI tract results in the weakness and subsequent tachycardia.
5. There's also a sudden increase in blood sugar, which causes insulin to over-secrete, leading to hypoglycemia (reactive hypoglycemia) and consequent diaphoresis and tachycardia.
53
How are enzymes usually produced? What is special about trypsin?
1. Usually produced as zymogens or pro-form, both of which are inactive forms.
2. Trypsin is born from trysinogen. There are trypsin inhibitors present to restrict trypsin production. Once trypsin is activated, all the zymogens get converted to their active forms through it.
54
Where is trypsin activated? How? Why does this exist?
Only after entry into the duodenum (SMALL INTESTIN). The process entails enterokinase in the brush border of the duodenum catalyzing the conversion of trypsinogen to trypsin. Trypsin then the conversion of pancreatic zymogens to active enzymes. This setup is present to prevent the untimely activation of enzymes, which would lead to self-digestion.
55
Which enzymes are produced in active form Why?
Amylase and DNAse and RNAse. Reason for this si that there is no starch in the pancreas. There are only broken cells in the pancreas.
56
What happens if you lose controlled activation of zymogens?
Pancreatitis. This may be caused by
1. a congenital trypsin inhibitor deficiency
2. Abdominal trauma, leading to the activation of trypsin by proteases released from injured pancreatic cells. They can function as trypsin and activate all the other zymogens.
3. Cystic fibrosis, causing enzymes to be stuck in the pancreas. These patients had fluid secreting issues becasues of cystic fibrosis.
57
How much fluid is secreted into the small intestine daily?
1500ml
58
What is goal of fluid secretions from pancreas?
1. Delivers enzymes into the small intestine.
2. It provides fluid optimal for digestive enzymes
3. It protects the small intestine by neutralizing H. Note that digestion in intestine requires a near neutral pH!!!
59
Why can't you feed newborn starchy foods, even if the foods have been liquified?
Their exopancrease has only partially been developed at birth.
60
Describe the ionic properties of pancreatic juice.
1. It is rich in HCO3.
2. Cl secretion is inversely correlated to HCO3 (really low)
3. Concentration is Na is CONSTANTLY high and concentration is K is CONSTANTLY low.
61
Describe ductular fluid secretion in the resting position. Note: H comes from acinar cells. Fluid comes from ductal cells.
1. H pump is facing the SEROSAL side, not the luminal side.
2. the H combines with HCO3 in the blood to make carbonic acid, which breaks into CO2 and H2o.
3. CO2 diffuses into the cell, combines with H2o again to make carbonic acid again, which breaks apart into HCO3 and H again.
4. HCO3 that was just produced is spit out into the lumen and Cl comes in through the same channel.
Note: Cl can be spit back into the lumen through the CFTR channel so that Cl is present for the HCO3 switch.
62
What is CFTR channel?
cystic fibrosis transmembrane conductance regulator (a fancy chloride channel.)
63
What stimulates pancreatic ductular fluid secretion
Secretin. it stimulates CFTR channel, and the translocation of H/K atpase tot he basolateral membrane through cAMP. End result is more H in the serosa and more HCO3 in the lumen.
64
What factors synergize with secretin?
CCK and Ach. They work by enhancing the K channel (aimed towards the serosal side) through Ca. When this happens, K is shuttled into the serosal side, making the pancreatic ductal cell more negative. With this being the case, HCO3 is even more convinced to get out of the cell (since it is also negative.)
65
What is the therapeutic target in the GI tract. What diesease are associated to it?
CFTR channel. Note that it is associated with cystic fibrosis and diarrhea.
66
What is the major inducer of pancreatic secretion? When is it produced? What causes secretin secretion?
1. Secretin, which is produced in the intestinal phase (70% of daily secretin dose).
2. Secretin works in the presence of H+ from the stomach.
67
What controls pancreatic secretions in the intestinal phase?
1. CCK (in the presence of fat, AA, and peptides)
2. Vagal tone (Ach)
3. Secretin (in the presence of H from the stomach.)
68
How much fluid is secreted in the intestines? What are the major functions components? Functions?
1. 1500ml/day. These secretions are highly inducible, bumping up to more than 10000ml/day in cases of diarrhea.
2. Fluids and mucus.
3. Goal is to protect the intestine, maintain luminal isotonicity (passive diffusion), and aiding in digestion/absorption.
69
What is the major secretion from duodenum? Jejunum-ileum? What channel is presen in both of them?
Duodenum: HCO3. Combines with pancreatic secretions to neutralize acid.
Jejunum-ileum: neutral pH secretions since the acid has already been neutralized. CFTR channel is present in both of them. Works to put Cl into the lumen, causing positive ion and water to both follow.
70
What channel is present in duodenum and not int he jejunum-ileum?
HCO3/Cl exchanger is present in duodenum, and not in the jejunum-ileum.
71
What activates the CFTR channel?
Presence of H activates Secretin. Secretin turns on cAMP, which activates PKA. This PKA phosphoylates CFTR, turning it on. Note, CFTR channel has multiple transmembrane domains, which forms a pore, which leads from the cytoplasm to the lumen. The very pore, however is regulated by the phosphorylation pathway depicted. When not phosphorylated, the pore is closed.
72
What happens if a toxin constituitively binds with ATP increase cAMP production?
Cl would be constantly shuttled into the lumen. Fluid will follow. End result is diarrhea.
73
How do you minimize dehydration from infection induced-secretory diarrhea?
Note that in diarrhea, there is a lot of CFTR-mediated Cl secretion into the lumen. So a lot of Na and water follow. Currently, there is not much that can be done to turn off the channel secretions until the toxin or bacteria dies/is inactivated. HOWEVER, we can turn off absorptions from the peak villi. Apparently, some of the enterocytes at the tip of the
74
Describe the external fluid circuit.
1. It shows that epithelial cells at the base of the billi are different from the villi peaks.
2. The epithelial cells at the base of the villi secrete Na, and Cl (due to CFTR), and water follows, all of which goes into the lumen
3. At the peaks of the villi are receptors or transporters which bring Na and Cl (and thus water) back into the blood.
75
How do you remedy CFTR overstimualtion?
You exploit the SGLT channels at the peaks of the villi. the sglt CHannels pump in Na, and this Na attracts Cl and water (because of charge and osmolarity). So, your goal is to overstimulate the SGLT channel, ramping up Na reabsorption into the blood. You overstimualte SGLT by giving glucose and table salt!!! That simple. This drastically reduces diarreah associated death.
76
How much fluid is involved in hepatic secretions and excretions? What substances are secreted by hepatocytes? WHat's secreted by ductular cells?
1. 500ml.
2. Organic stuff and water + electrolytes (bile acid-independent.)
3. Ductular cells secrete alkaline fluid rich in HCO3. This goes into the small intestine to neutralize the acid.
77
What organic substances are released from the hepatocytes?
2/3 is bile salts, 1/4 is phospholipids.
78
What are the functions of hepatocytes?
1. Emulsify lipids and digestion products of lipids.
2. Maintaining cholesterol in solution (by bile salts and phospholipids)
3. Excreting (cholesterol, bile pigment, sterols, heavy metals, etc)
It is impossible to dissolve cholesterol.
79
How do you obtain bile salts?
Note: Bile acids are converted to bile salts BEFORE secretion, after which the bile salt can go directly into the intestine or go to gallbladder for storage. Bile acids or salts are either synthesized by hepatocytes (primary bile acid, less than 10% of daily total) or recycled from the intestine and modified by gut bacteria (secondary bile acid, more than 90% of daily total)
80
Difference between bile acid and bile salt?
Baseline pK is 6 for a bile acid. When bound by AA, the pKa drops, and it is now a build salt. Bile salts are amphipathic, which allow them to form micelles that solubilize (emulsify) lipids in water. Bile acids can't do this.
81
How do we secrete bile salts? How do you use recycled bile salts?
Secreted by active transporters. these transporters cannot transport bile acid without conjugation by the amino acid first. Bile acids can only be recycled by being re-conjugated
82
How does the liver secrete positive/negative charged phospholipids?
Specific molecules in the liver, some of which deal with resistance to chemotherapy (therpeutic treatments for ).
83
Where does bile go after the liver secretes it?
1. Gall bladder. note that at night time, the opening of the bile duct into the intestine is closed off, so all the bile produced by the liver is shuttled to the gallbladder. It can store 30ml. We are constantly secreting it. The gallbladder concentrates it.
84
How much bile do you secrete? Relationship between the fat we ingest and the bile salts secreted?
10 to 30 grams of bile salts daily. The more fat you eat, the more bile salts you secrete. Since the body only has 3g of bile, it means that the bile salt is reused 10 times. Bile salts get reabsorbes by the jejunum (most), ileum.
85
Why can't you reabsorb salts in the colon? How do you overcome this?
It is not reabsorbed in the colon because the colon lacks the transporters. Overcome this through the bacteria in the colon, which removes bile salt conjugation, converting it back to a bile acid. The bacteria can also convert it chemically (secondary bile acid)
86
Describe the physical property of bile salts/acids. How much bile salt is lost daily?
They are hydrophobic, passing by freely so long as there is a concentration gradient. This is how bile acids are reclaimed in the colon, even tho 10% of bile acid is lost daily.
87
Describe destination influences during digestive period (after eating)
When you eat, and the food reaches small intestine, CCK relaxes sphincter of Oddi (opening of bile duct into duodenum) and increases the tension of the gallbladder. This allows for bile salt to enter duodenum directly. This continues so long as there are lipids in the duodenum. Secreting also secretes a ton of HCO3 to go with the bile to protect the duodenum lumen.
88
What leads to primary bile acid synth?
A high concentration of bile salts (bile acids being converted to BA in the liver), primary synth is reduced. This is normally the case during digestive period (normally throughout the day.) When the lipids are fully absorbed, CCK is removed (sphincter of Oddi is now closed), secretin is removed, and gallbladder is relaxed. This is intergestive period. The bile is forced to stay in the gall bladder and be concentrated there. Note also during this interdigestive period, there is no recirculating of the bile acids/salt, so primary bile acid production is high since bile salts are low.
