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60 Cards in this Set
- Front
- Back
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Describe the structure and function of a villus. What can it be used to identify?
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-The VILLOUS – can be used to identify the small intestine
The villous lining of the small intestinal allows for avid absorption. |
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What forms the large surface area of the small intestine?
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The large surface area of the SI is formed by folding of the lining, the villi (which sit on folds) and the microvilli (Which are on the villi). The epithelial cells surround these "fingers" that enclose a LYMPH LACETAL covered by a CAPILLARY NET. These specialized structures provide an outlet for the absorbed nutrients.
-Note that the lining is made of these single cell epithelial cells between the lumen of the small intestine and the vasculature and the lymph in the projection -There is not a lot of obstruction to be able to absorb into these cells and get the nutrients into the blood or lymph The villi line the small intestine from the bile duct in the duodenum through the ileum, although they are less dense in the distal areas. The microvilli on the villi make up the brush border of the lumen. -->BRUSH BORDER ENZYMES on top of the epithelial cells/associated with the brush border facilitate the final digestion of carbohydrates and protein. You need the brush border not only for absorption but also for final digestion of these nutrient. If you have disruption of this border you have malabsorption of nutrients. -->-At top of villous have MICROVILLI – this is the absorptive area – huge amount of SURFACE AREA for absorption -Within this fingerlike projection next to it are crypt of Lieberkuhn (mucus, endocrine cells, etc) **Villi can be used to identify the small intestine!!! |
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What is the lifespan of a enterocyte?
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~3-5 days
-Cells are replaces by progenitor cells from the Crypts of Lieberkuhn |
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What can cause atrophy of the brush border?
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-Protein deprivation
-Celiac disease |
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Sucrose =
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Sucrose = glucose + fructose
*Table sugar * This disaccharide (in addition to lactose) stays in system and isnt digested until the small intestine’s brush border enzymes *Broken down by SUCRASE |
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Lactose=
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Lactose = Glucose + Galactose
*Milk sugar * This disaccharide (in addition to sucrose) stays in system and isnt digested until the small intestine’s brush border enzymes *broken down by LACTASE |
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What types of molecules might we ingest that are considered carbs?
What enzymes break them down? What types of carbohydrates can be absorbed? |
1. Starch
Majority of carbs ingested are starch and disaccharide -starch are main carbs we take in – mainly plant starches -all starch is polymers of glucose with ALPHA LINKAGES -all we need to do is break alpha linkage to break down to smaller polymers of glucose and those are going to be maltooligosaccharids 2. sucrose 3. lactose 4. cellulose – plant fiber – this is an undigestable carbohydrate. - Although it’s glucose, it’s linked by beta (not alpha) linkages, and we don’t have cellulase that can digest beta linkages. -Other animals (like horses and cows) do have that enzyme. -The cellulose that we ingest is going to contribute to what we call a healthy gut. Because we don’t digest it it keeps on going down the tract and gets secreted in the feces. NOTE: Only MONOSACCHARIDES (glucose, galactose, and fructose) can be absorbed into the enterocytes. |
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Where is starch broken down? What breaks it down? How long does this digestion take? What are the breakdown products?
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**About 25-30% of digestion is preduodenal, the rest is duodenal via pancreatic and brush border enzymes**
1. The breakdown of starch begins in the MOUTH by SALIVARY ALPHA-AMYLASE -->This comes out of salivary acinus and is secreted with saliva into mouth. -->It easily digests glycogen linages to make malose-oligosaccharids. Main form is maltose (9+glucose molecules in length). Minor form = isomaltose. --> At this point have maltose and isomaltose being made already as we start salivating and chewing food. As it goes into stomach we have smaller glucose polymers. *Note: no enzymes for starch digestion are present in the stomach, only bulk digestion via HCl. Only have corrosive action of the acid. 2. The majority of digestion occurs in the SMALL INTESTINE by PANCREATIC AMYLASE -Essentially all polysaccharides are digested within 10-20 minutes -- by the time the chyme reaches the upper jejunum -Pancreatic amylase It’s activated by chloride and it comes out. Is there Cl- in duodenum? YES we’re secreting all these buffers (na, bicarb, etc). Thus we make more and more maltose and a little isomaltose. We digest down to smaller glucose polymers but they are still bigger than can be absorbed. -Breakdown products: 1. Maltose 2. Small glucose polymers A. alpha-limit dextrins B. Maltotriose **THESE PRODUCTS ARE NOT ABSORBED 3. Intestinal membrane BRUSH BORDER ENZYMES (SACCHARIDASES) allow the final digestion to monosacchrides (glucose galactose or fructose): **NOTE: To break down MALTOSE and 3-9 GLUCOSE POLYMERS, the brush border enzymes MALTASE and ISOMALTASE (alpha-limit dextrinase) break down the polymers to GLUCOSE, MALTOSE, and OLIGOSACCHARIDES |
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Why do we need plant fiber in our diet?
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**carbohydrates are osmotic agents **
-normally we absorb all these carbohydrates that we can digest into the body, works well, nutrients and fluids come in with it -carbs that stay in the tract (ie. indigestable carbs aka cellulose) keep water with it because it’s osmotic, so we have more fluid in the feces! -We only secrete ~200 mL in the feces This is associated with fiber and bile - If you eat more fiber you will have more water in your feces, more stretch in the colon so when you get these mass movements going there is more stretch and strong contractions and more moves faster. - Fiber helps us have more regular bowel movements because there is more water there. This is the importance of cellulose and plant fiber in our diet. |
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What happens with lactose intolerance?
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Lactose intolerance
-Membrane disaccharidase deficiency -Leads to increase in lumenal osmolarity and lactic acid |
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Review the brush border enzymes for:
-maltose and 3-9 glucose polymers -lactose -sucrose How do the breakdown products of these molecules enter cells? |
Lactose --Lactase--> Glucose and Galactose
Sucrose --Sucrase--> Glucose and fructose Starch glycogen --maltase and isomaltase (alpha-limit dextrinase-->glucose, maltose, and oligosaccharides Note: Sucrase and isomaltase are synthesized as a single polypeptide chain: at the brush border, proteases cleave the protein into the two enzymes (as seen in figure). How do monosaccharides get in? Glucose and galactose come in via Na+ dependent COTRANSPORT**** It is 2’ active transport with sodium! Fructose is facilitated transport via its own protein Note: What would happen if you have a low sodium diet? Would you have problems absorbing the glucose and galactose? Remember that we are secreting into the digestive tract but because there is so much sodium in the tract there is a driving force to get it back in using all these transporters. The majority of the sodium here came from ECF, not from diet. |
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One more time: how are the monosaccharides absorbed into enterocytes? What factors influence transport? How do they leave enterocytes? What happens then???? Is the body prepared to handle this?
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First, remember that carbs are hydrophilic and can easily move through the unstirred water layer
Next, once they've been digested by the brush border enzymes: GLUCOSE is TRANSPORTED into the enterocyte using the GLUCOSE-SODIUM TRANSPORTER (SGLT1), which also carries GALACTOSE. It is SODIUM DEPENDENT SECONDARY ACTIVE TRANPORT. It uses Na/K ATPase on the basolateral side of the cell FRUCTOSE is transported through specific GLUT5 CARRIER PROTEINS They LEAVE the cells through GLUT-2 TRANSPORTERS. Goes to blood and then to the liver. Liver is like a blood glucose monitor, stores glycogen, releases glucose to systemic circulation. Systemic circulation is already prepared for glucose because we started secreting duodenal hormones GIP that goes to pancreas to stimulate insulin production to ready the system. As soon as we can get glucose and monosaccharides to liver for processing through portal system the blood is already prepared for it. |
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What is Olestra?
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-Olestra is a sucrose polyester that is not digested or absorbed, and is used as a fat substitute (especially for fried foods).
-It has no caloric content because it remains in the GI tract and is excreted… however, the carbohydrate part (sucrose) is great food for colonic bacteria in addition to being an osmotic agent… this produces gases, increased motility and reduced absorption, resulting in cramps, flatulence, and diarrhea. |
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What is sucralose?
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sucralose aka splenda
-Sucarlose is a chlorinated sugar compound (chlorocarbon) that (for the most part) is not digested or absorbed. -Can have same type of problems as olestra (bloating, gas, diarrhea), because of the presence of sugar moiety. -Usually not consumed in high enough quantities to be problematic (unless you eat like a whole pie made from it) |
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Where is protein broken down? What breaks it down? What are the final products?
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1. IN THE STOMACH
-HCl digests proteins -HCl and gastric and intestinal hormones stimulate secretion of PEPSINOGENS from the chief cells in the gastric pit. -PEPSINOGENS are cleaved to PEPSINS by the acidic environment. -PEPSINS aid specific protein digestion and are effectively inactivated in higher pH (aka in the duodenum) -The PANCREAS What stimulates pancreatic acinar cells to secrete enzymes? CCK! CCK stimuates pancreatic enzymes. Proteases are a big part of that. They come into the lumen of the small intestine and 2. IN THE SMALL INTESTINE/AT THE BRUSH BORDER: Activation of PANCREATIC PROTEASES by INTESTINAL ENTEROKINASE ****enterokinase only in the lumen! -Trypsinogen is activated to trypsin, which then activates chymotrypsinogen and proelastase which then break down protein into di, tri, and amino acids which can then get into the cell. -Proteins are digested into smaller peptides ***need to keep trypsinogen in zymogen form in pancreas and ducts so they don’t get eaten up. To keep in zymogen form, we have trypsin inhibitor, which is present in the intralobular and main ducts. 3. INSIDE THE ENTEROCYTE: -While di and tri peptides and amino acids can be absorbed into the enterocytes, CYTOPLASMIC PEPTIDASES break any di- and tri-peptides into amino acids. THE FINAL PRODUCTS ARE AMINO ACIDS |
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So wait, how do these mono, di- and tri-peptides get into the enterocytes in the first place? How do they get out? Where do they go then?
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-They come in via facilitate transport via special PROTEINS that help transport **
-the majority of aa’s come in in a variety of different ways. WE don’t need to know the dif ways, just know that some are Na dependent other independent other facilitated transport eg. SODIUM LINKED COTRANSPORTERS CARRY: neutral aa; phenylalanine and methionine; dicarboxylic amino acids, proline and hydroxyproline eg. DI AND TRI-PEPTIDES ENTER CELL BY A SPECIFIC PEPTIDE TRANSPORT PROTEIN Remember, inside the cell the only thing that can get out are AMINO ACIDS. This is the only substance where we have this issue! Thus, we have CYTOPLASMIC PEPTIDASES to break down di’s and tri’s so it can get out to the blood ** Now were in the portal blood which goes to the liver . We need to detoxify. These are proteins, they contribute to the acid pool . We need to deaminate the proteins and make ammonia and combine with Co2 to make urea . Urea is excreted by kidneys . WE are protecting the acid/base status of the body while we get rid of the extra acid Key aspect: liver takes proteins and makes albumin fibrinogen immunoglobulis as well |
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What prevents pepsins from tearing up the small intestine?
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-Pepsins are effectively inactivated in higher pH
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Where are lipids digested? What is responsible for lipid digestion?
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1. IN THE MOUTH -- LINGUAL LIPASE cleaves triglycerides to fatty acids and diglycerides
2. IN THE STOMACH -- GASTRIC LIPASE cleaves triglycerides to fatty acids and diglycerides Note: gastric lipase comes out of chief cells (pepsin and gastric lipase both out of chief cells) 3. IN THE SMALL INTESTINE -- a. Entry of peptides and fats into the duodenum stimulates CCK release which causes gallbladder constriction and release of bile, sphincter of Oddi relaxation, and release of pancreatic enzymes like PANCREATIC LIPASE (aka glycerol ester lipase) which cleaves triglycerides to fatty acids and monoglycerides b. Cholesterol esterase cleaves cholesterol esters into cholesterol and water soluble acid **these products can diffuse through the enterocytes while cholesterol esters can't **This enzyme also cleaves ESTER-TYPE SUBSTANCES LIKE FAT SOLUBLE VITAMINS E and D c. PHOSPHOLIPASE A2 is activated by trypsin and cleaves phospholipids (like lecithin) into lysolecithin. Remember, pancreatic lipase is different from lingual and gastric lipases in that it requires a COLIPASE to work. The pancreatic lipase is secreted in active form but is inactive in the presence of bile salts and acids because the bile binds to the surface of triglyceride oil drops to form an emulsion. COLIPASE secreted from the pancreas is activated in the duodenum by TRYPSIN, and binds to bile salts by the oil drops. Then, one lipase molecule forms a complex with one co-lipase molecule. This process "opens a door" for the pancreatic lipase to access the lipids. This is CRITICAL to the formation of MICELLES. |
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What is glycerol ester lipase? Where is it from? What does it do? Is it secreted in active or inactive form?
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Glycerol ester lipase aka pancreatic lipase is a pancreatic enzyme that cleaves triglycerides to fatty acids and monoglycerides in the small intestine.
**Remember, pancreatic lipase is different from lingual and gastric lipases in that it requires a COLIPASE to work. The pancreatic lipase is secreted in active form but is inactive in the presence of bile salts and acids because the bile binds to the surface of triglyceride oil drops to form an emulsion. COLIPASE secreted from the pancreas is activated in the duodenum by TRYPSIN, and binds to bile salts by the oil drops. Then, one lipase molecule forms a complex with one co-lipase molecule. This process "opens a door" for the pancreatic lipase to access the lipids. This is CRITICAL to the formation of MICELLES. |
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What accounts for the majority (70-80%) of fat digestion?
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PANCREATIC LIPASE/COLIPASE
accounts for the majority of fat digestion BUT lingual and gastric lipases become important if there is a problem with the pancreatic lipase working. |
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Where is 1' bile made? How does it get to the duodenum -- ie. via what signal? What is the environment that fat sees when it enters the small intestine?
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1’ bile is made in liver and is secreted into the early duodenum It is stored in the gall bladder
CCK is secreted in response to chyme in the bile, and this helps to squish the gall bladder and open sphincter. CCK also starts the enzyme secretion into the duodenum. It also stimulates the bile production in the liver. Dehydrated bile rehydrates with secretions from stomach and pancreas. We need this because of the hydrophobic nature of lipids – we need to get the bile secreted in for the proper absorption of lipids! We get droplets of bile of chyme into the tract and most of the fat is going to be at the top. We do get some fats through early but most comes out late. Even early we get dribs of bile coming into the tract. This is important because it means that the BILE IS ALREADY IN THE LUMEN of the small intestine as chyme is coming in. Remember the environment that bile comes into and sees. Think of micelle like a taxi – have hydrophilic on outside and the lipophilic on the inside. The taxi is able to get you through the unstirred water layer, which is pretty much IMPERMEABLE TO THE HYDROPHOBIC LIPIDS. This nice micelle taxi carries the lipids through the unstirred water layer and like a taxi it lets the lipids off and the lipids diffuse in but the bile stays in the lumen and goes down the digestive tract. It delivers the lipids to the enterocytes and then drives on down the road. |
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What is present in micelles?
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-free fatty acid
-monoglycerides -cholesterol esters in bile if you have enough it makes the micelle! |
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How does bile help you absorb lipids?
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-Bile is emulsifier
-It acts as an amphipathic emulsifier, and, in conjunction with pancreatic lipase/co-lipase, it breaks the fat into constituent lipids. -When these lipids are inserted into the bile salts, the whole shebang is able to move through the unstirred water layer. Remember, pancreatic lipase is different from lingual and gastric lipases in that it requires a COLIPASE to work. The pancreatic lipase is secreted in active form but is inactive in the presence of bile salts and acids because the bile binds to the surface of triglyceride oil drops to form an emulsion. COLIPASE secreted from the pancreas is activated in the duodenum by TRYPSIN, and binds to bile salts by the oil drops. Then, one lipase molecule forms a complex with one co-lipase molecule. This process "opens a door" for the pancreatic lipase to access the lipids. This is CRITICAL to the formation of MICELLES. NOTE: critical micellar concentraion (1-2 mmol / L) |
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What cleaves Vitamin D and E?
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CHOLESTEROL ESTERASE cleaves ESTER-TYPE SUBSTANCES LIKE FAT SOLUBLE VITAMINS E and D
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What happens to the bile salts after lipids are absorbed?
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BILE RECYCLING
-They are released into the lumen after lipids are absorbed -Bile is absorbed at binding sites on the terminal ileum -Stored in gall bladder |
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What happens to bile recycling after ileal resection?
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-Loss of bile salts
-Increased liver synthesis of bile -Loss of vitamin B12 |
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What is the rate limiting step for lipid absorption?
How do lipids enter the cell? What lipids are able to cross? What happens to the bile salts? |
The UNSTIRRED WATER LAYER PROTECTS the enterocytes and is the RATE LIMITING STEP for lipid absorption.
Lipids enter the cell by DIFFUSION -Fatty acids -2 monoglycerides -Cholesterol -Lysolecithin -Fat soluble vitamins (ADEK) Most of the bile salts remain in the lumen of the intestine |
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Chylomicron
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-Lipids in the enterocytes are re-esterified with free fatty acids in the SMOOTH ENDOPLASMIC RETICULUM to form triglycerides, cholesterol esters, and phospholipids
-These lipids then get a BETA-LIPOPROTEIN COAT (APO B), which helps them EXOCYTOSE. ** THESE ARE NOW CALLED CHYLOMICRONS -CHYLOMICRONS ARE PRIMARILY MADE OF: -95% triglyceride -4% phospholipids -1% Cholesterol |
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What happens once lipids are inside the enterocytes?
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REPROCESSING: Lipids diffuse through the enterocyte membrane, enter the SMOOTH ENDOPLASMIC RETICULUM, and are re-esterified with free fatty acids into triglycerides, phospholipids, and cholesterol esters.
-These lipids then get a BETA-LIPOPROTEIN COAT (APO B), which helps them EXOCYTOSE. ** THESE ARE NOW CALLED CHYLOMICRONS Chylomicrons are TOO BIG to get directly into capillaries, so they diffuse into the lacteals, circulate through the lymph and into the larger vessels in the venous circularion Goes into the lacteals then gets dumped into the blood in the thoracic cavity. This goes into lymph, so we bypass the liver on the first round. Lipid metabolism in liver comes through systemic circulation through normal cardiac output. The newly absorbed fats are coming through systemic circulation! There is a lag time. Usually when you get your blood drawn they ask you to have an overnight fast and they don’t want to be seeing big blobby coat of fat in your blood. If you take blood after eating a meal with fat in it, you see big coat of fat floating up. |
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What part of the gut is most active in fat absorption?
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The duodenum and jejunum are most active in fat absorption!
Most ingested fat is absorbed by MIDJEJUNUM, although some small chain fatty acids can diffuse into the portal blood. |
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How do the fat soluble vitamins get to the enterocytes?
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Fat soluble vitamins – ADEK
A and D are a little less hydrophobic and can diffuse in independently or ride in on micelles E and K have to come in on micelles and be made into chylomicrons |
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What happens if you don't have beta-lipoprotein?
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Now, if you don’t have beta-lipoprotein, then have abeta-lipoproteinemia and the fat builds up in these cells and the cells get sloughed off and we lose them!!!
We need chylomicrons to get fats into the body !!! |
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Steatorrhea
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-Fat in stool from malabsoption
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What causes fat in stools?
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-colonic bacteria
-desquamated intestinal cells -malabsorption |
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Describe the structure of this micelle!
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-taurine and glycine with hydrophilic ends on outside where water is
*Conjugated bile acids are conjugated with glycine or taurine and are polar. - lipophilic ends are attached that’s where lipids will be. - this shows you lipids in water w bile |
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Conjugated bile acids
v. Unconjugated bile acids v. Primary bile acids v. Secondary bile acids? Where are they recovered? |
Primary recovery is through active and passive absorption in the TERMINAL ILEUM. Once they are absorbed into the cell, they diffuse into the portal blood and return to the liver. The liver extracts the bile acids in one pass, and reconjugates the 2' bile acids.
CONJUGATED BILE ACIDS -conjugated with glycine or taurine -are POLAR -are COTRANSPORTED W SODIUM down the sodium gradient. They naturally form salts with sodium -majority of bile is conjugated UNCONJUGATED BILE ACIDS -Less polar -Absorbed by simple diffusion -Small % of reclaimed bile PRIMARY BILE ACIDS -Conjugated and hydroxylated in the liver SECONDARY BILE ACIDS -Have been deconjugated and dehydroxylated by intestinal bacteria and are less polar as a result |
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How much bile does the liver make per day v. how much is recycled?
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Liver makes about 10% a day – we lose about 10% of each cycle in feces. It was unconjugated and unable to be reabsorbed through cells to portal system
When we lose this we also lose things associated with bile – cholesterol & bilirubin ** the only way we can lose cholesterol in body is through bile loss **Bilirubin is also coming out with the bile We lose 10% w each cycle but RECYCLE 90%. |
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What determines how many bile cycles you have in a meal?
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In each meal depending on how much you eat and how much fat determines how many bile cycles you have
Not too much fat? 2 cycles If you have a high fat meal, it can recycle 6 times before all the fat is out |
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Where does water absorption occur primarily?
What do water intake and secretions into the GI tract total? How does water move? |
We put a lot of secretions into tract (9L/DAY!!!!) to facilitate digestion and absorption of nutrients and now we need to get it back. It came from the blood but now we need to make it up.
The majority of this water is going to come in with bulk absorption of nutrients and electrolytes in the small intestine. The intestines absorb all the 200 ml -- net transport of water out of the lumen. The colon can absorb ½ L a day. This is what happens when you dehydrate chyme to make feces. There are bidirectional ion and water fluxes in order to preserve OSMOLALITY and ELECTRONEUTRALITY. **ACTIVE TRANSPORT OF NUTRIENTS CREATES AN OSMOTIC GRADIENT AND WATER FOLLOWS** |
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What happens if you drank an extra 3L of water over what you normally required?
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Reabsorption can upregulate. If you drink more water without exercising more, will absorb more water. Normally water takes about 90 minutes to leave the stomach, and it is rapidly absorbed by osmosis in the small intestine (15-20 minutes). Colon can absorb up to a liter if it needs to.
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How does sodium get absorbed?
Be sure to talk about ALL the different types of transporters and where you'd find them! |
The SODIUM PUMP (Na/K ATPase) on the basolateral side of the enterocytes sets up a concentration gradient!
There are DIFFERENT LUMINAL TRANSPORTERS: -3 Na+ are exchanged for 2 K+: this makes the interstitial fluid hypertonic and positively charged, so water and anions (like Cl-) follow to preserve ELECTRONUTRALITY -In the jejunum Na+ and BICARBONATE are absorbed: carbonic acid is made by carbonic anhydrase and H+ ions enter the lumen through an Na/H antiporter -In the small intestine, there is a specific Na+ co-transport with amino acids and monosaccharides (glucose, galactose) -In the colon, enterocytes produce carbonic anhydrase, and H+ enters the lumen through the Na/H antiporter. ---- Conceptually: Sodium is a key extracellular ion, so you need to get it back. It comes back with absorption of lots of nutrients – sodium dependent transport. If you run out of nutrients then you have exchangers - sodium hydrogen exchangers. Remember that water follows salt (na) and Cl follows Na as well. |
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How and where is chloride reabsorbed?
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-Passive diffusion following sodium in the duodenum and jejunum to preserve electroneutrality (can follow transport of amino acids and monosaccharides that are co-transported with sodium)
-Chloride/bicarbonate exchanger in ileum and proximal colon: lots of bicarbonate is secreted into the ileum and colon to neutralize the H+ products secreted by bacteria Remember that water follows salt (na) and Cl follows Na as well. Also, when H ion goes out, it gets put into the carbonic anhydrase cycle and we can make co2 and h2o and those can diffuse in. we can reform hydrogen ions to pump more. |
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How and where is potassium absorbed?
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-Potassium is PASSIVELY absorbed in the jejunum and ileum: the concentration gradient increases as water is absorbed -- it has to have a high concentration in the lumen to move since intracellular K+ is high!
-Primarily secreted in the colon, but it can be absorbed if lumenal concentration is high (over 25 mM) |
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What reduces K+ absorption?
What increases K+ secretion? |
DIARRHEA reduces K+ absorption since the rapid flow disperses concentration gradient for movement into the cells. This can contribute to the development of metabolic acidosis during prolonged diarrhea.
ALDOSTERONE increases K+ secretion in the colon in exchange for sodium |
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How and where is iron absorbed?
What do we need iron for? How much iron do we absorb and lose per day? Where do we get iron loses from? |
-KNOW TRANSFERRIN (other transporters not important for exam)
-Need iron for RBC production -Iron is toxic to the body so it always has to be bound -We usually lose 3 mg and absorb 3 mg per day (but menstruating women and actively growing children need more because they're making more RBCs. have a + balance for iron. Women lose iron from bleeding and need more iron at times as well). Absorptive ability increases when needed. -Store iron in FERRITIN STORES IN LIVER -Under normal circumstances we absorb a small amount and lose a small amount -Iron comes in organic and inorganic forms. We can absorb both. The REDUCED STATE is easiest to absorb. The oxidized state can form more insoluble salts and compounds that can't be absorbed. -We can also get Hemin in (heme iron) via facilitated transport, it's lipophilic and can go right into the cell. there's heme oxidase and xanthin oxidase here that splits it from heme and takes it to the Fe2+ state. This is immediately bound. -Any other that comes in through DMT1 transporter these are regulatory sites that we may need to know in future -Fe2+ that comes in is immediately bound ** FREE IRON IS TOCIC TO THE CELLS -Free iron is toxic to the cells, so to get it into the enterocyte (from duodenum and jejunum), iron needs a CARRIER PROTEIN (DMT1) to cross the membrane and enter the cell. The brush border membrane receptors bind the complex and it enters the cell (probably by endocytosis). Iron is stored bound to intracellular ferritin, or released at the basolateral membrane (through hephestin/IREG1 complex) and bound to plasma TRANSFERRIN -The transferrin is resecreted into the lumen -Iron is ALWAYS BOUND. We can get it into the cell efficiently but we also have xanthine oxidase and heme oxidase to reduce it when necessary. Also have ferritin storage. Can get iron in as long as we have it in our diet, and if we dont get from diet the liver has storage to make up for those days we don't get it. -Where do loses come from? Desquamation of intestinal cells. Lose cells? Lose iron. How do we fix? Can take in more, but the normal daily where is the iron going is being lost here (Iron ingested = ~20 mg, ~1mg absorbed; exfolliation results in loss of the ferritin stores (~1mg) so we stay in balance) |
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How and where is calcium absorbed?
How can we increase the amount of calcium absorbed? Where is the main site of regulation? |
-need calcium for bones
-have PTH and other calcium regulatory hormones -regulate calcium by hormones (PTH, calcitonin) which can be regulated once we get calcium into blood, but how do we get it in? -divalent cation that favors reduced state. If it's not reduced can form insoluble salts, esp with phosphate, and at that point it's lost. -Bile salts FACILITATE calcium absorption -Major site of absorption in the JEJUNUM -Have calcium binding protein as well as transporters that sense the need (can put more transporters and calbindin -- calcium binding proteins associated with the transporters) .. upregulate these via vitamin D. and then we can get more calcium in. PTH increases membrane calcium binding protein (CaBP) -Need to take vitamin D and calcium at the same time, but not necessarily working at the exact same time. High levels of vitamin D in the blood help upregulate calcium transporters at the luminal site so you can get more calcium in as well as calcium ATPase pump. Once we get calcium in it always has to be bound -Why does calcium have to be bound intracellularly? 10^-10 normally inside cell because it's a signaling molecule so you want to bind it intracellularly and get it out of there. Get it out via antiporter with Na+ as well as Ca/Atpase (upreg by vit d) -40% of calcium in blood is bound 60% is free. Doesn't need to be bound in blood -Intestinal absorption is the major site of regulation (not the kidney): responds to changes in PLASMA CALCIUM concentration |
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How is B12 absorbed? Where is it absorbed?
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1. Mouth: in the saliva, we have R binders secreted. That R binder bound B12 and protected from stomach pepsins and proteases in stomach. B12 is necessary for RBC maturation will cause pernicious anemia if you don’t have it. Need to protect it.
2. In the stomach, we have another factor, intrinsic factor, that is secreted from parietal cells (also secrete HCl) and that comes and also binds to B12. A lot of it binds in the stomach but by the time were in the duodenum we have this R protein R binder B12 Intrinsic Factor complex. 3. And theeen once in the duodenum the trypsin cleaves the R protein and we have B12 intrinsic factor complexes once we’re in the small intestine because the trypsin got rid of the R protein. When the intrinsic factor is there we can get rid of the R protein in the small intestine because intrinsic factor protects against pancreatic proteases. Now we have b12/intrinsic factor complex that dimerizes with another dimer . This dimer comes down but there aren’t transporters for this until no transporters this for TERMINAL ILEUM (functions = bile recycling and b12 absorption). 4. In the TERMINAL ILEUM, the dimer spies its recognition site, the dimer is intercalated, IF leaves, B12 goes out into cell and in the blood its bound to binding protein, TRANSCOBALAMIN II. This binds it, protects it, and shuttles it to the bone marrow or the liver. In the liver it’s put into vitamin storage so that as needed it can be elaborated. |
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Where does dehydration of chyme to make feces occur?
What type of motility makes this happen? What signals mass movements? |
-Now were in the colon
-bulk absorption is the absorption of all the nutrients which happens in the small intestine - there are not transporters or anything like this in the colon because its made for storage and final reclamation of sodium and water in the chyme. Thus, there is no big nutrient transport Motility majority of the time? Have taniae coli coming in slow movement haustrations!!! This facilitates absorption in the absence of villi and gives plenty of time for sodium and water to come out via segmental propulsion!!!! Going to get sodium and water reclaimed and we get drier and drier mush and semi- mush … several times a day we get out of segmental propulsion and haustra that relax and get peristaltic mass movements. This happens mostly when we eat -- get signals that start mass movement. What signals? Depends on when we eat.. Facilitated by VAGUS and gastrin!!! A little cck. What is signaling? Something is coming in upper GI tract that says you’ve eaten. Lets get the chyme out of the system so we push feces lower in the tract. The vagus works up to left colic flex and then pelvic nerves after that. After rectal stretch, get rectosphincteric reflex. With rectal stretch have urge to deficate and relaxation of internal anal sphincter and we constrict external anal sphincter. What do we need intact to have this neural impulse to be translated? Enteric nerves needed to make defecation work properly. main thing is storage and dehydration of chyme to make the feces |
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What can cause diarrhea?
What happens in the intestines that results in diarrhea? |
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Where do bacteria live in the GI tract?
What are the “good” bacteria called? What do they do? |
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What are bacteroides?
Are they good, bad, or both? |
Bacteroides is a genus of Gram-negative, bacillus bacteria. Bacteroides are normally mutualistic, making up the most substantial portion of the mammalian gastrointestinal flora, where they play a fundamental role in processing of complex molecules to simpler ones in the host intestine.
Bacteroides (are not E. coli!) can cause infection if abscesses occur and have been implicated in initiation of colon cancer and possibly colitis. These also are very good at becoming resistant to antibiotics. |
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What is the main source of gas that will be expelled as flatus?
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Bacterial digestion of starches/sugars/fiber is the main source of gas that will be expelled as flatus.
**bacterial metabolism of carbohydrates **stomach (O2, N2) **duodenum (CO2) **Ileum and colon (CO2, H2, CH3, H2S, NH3), polyamines (putrscine, spermine) flatulence. |
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Is there E. coli present in the intestines normally? If so, is this harmful?
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Not much E. coli is normally present in intestines and it is not harmful-- except some strains that can be present in contaminated food, and then it can cause big problems in the small intestine.
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Are ferrous or ferric forms of iron more likely to form insoluble salts? Which is more easily absorbed?
Which form does low pH favor? What else can aid in absorption? |
Ferrous (Fe2+) forms are LESS LIKELY to form insoluble salt forms, and thus, is more easily absorbed than ferric (Fe3+) forms.
pH is important: low pH favors the FERROUS form, so ACIDIC pH of the stomach and duodenum helps iron absorption. Vitamin C (and other REDUCING AGENTS) also produce the ferrous form. |
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How do we absorb phosphate?
How is absorption enhanced? |
-Na-Pi cotransporter (just like the kidney!)
-The intestines will readily absorb Pi, except if there is surplus of calcium, which can form insoluble Ca-Pi compounds -Absorption is enhanced by increased plasma vitamin d3 or PTH (indirectly) |
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How do we absorb magnesium?
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Passive diffusion through entire small intestine, although higher rates proximally due to acidic environment.
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How do we absorb fat soluble v. water soluble vitamins?
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-Fat soluble are incorporated into micelles and diffuse into the enterocytes
-Water soluble vitamins like niacin, thiamine, folic acid, and vitamin C are absorbed by secondary active transport with sodium -Pyridoxine is absorbed by diffusion -Riboflavin is absorbed by facilitated transport |
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Colonic salvage
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The final absorption of sodium and water -- aldosterone effect
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Whee does fecal production begin?
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In the late transverse colon
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What are the main electrolytes in feces?
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Potassium and bicarb
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