Exam 4 - Digestive System

protein digestion - what are 2 other peptidases on the enterocytes of the small intestine brush border? what are endopeptidases? what are the 4 endopeptidases? what are exopeptidases? what are the 2 exopeptidases?

-2 other peptidases on enterocytes of the small intestine brush border are: -->aminopeptidases -->carboxypeptidases -Endopeptidases: peptidases that cleave internal peptide bonds (only bonds btw amino acids) -->includes pepsin, trypsin, chymotrypsin, and enteropeptidase -Exopeptidases: peptidases that cleave outside peptide bonds (only terminal amino bonds) -->includes carboxypeptidase and aminopeptidase

stomach at rest - where do the H+ ions come from (what reaction)? how are H+ ions pumped out into lumen? how is bicarbonate pumped out? where are most K+/H+ ATPases located and why is this beneficial? how does Cl exit into lumen? why is it important for K+ to leak out of cells also?

-H+ ions come from reaction of carbonic anhydrase (takes CO2 + H2O -->H+ and bicarbonate) -->H+ ions pumped out through K/H+ ATPase; pushes H+ out and K+ in -bicarbonate moved out through Cl/HCO3 exchanger; Cl moved in -most K/H+ ATPases are not on PM but stored intracellularly to prevent further acidification of lumen (keeps acid production low) -Cl exits through Cl channels on apical membrane to acidify stomach with hydrochloric acid (HCl) -K also leaks out through channels to keep K/H ATPase functioning

salivary glands ductal cells - where do Na and Cl go after it is reclaimed? how does parasympathetic NS regulate ductal cells?

-Na and Cl can then move into blood so that we reclaim important salts -parasympathetic also regulates ductal cells; releases Ach which acts on muscarinic receptors to get more Cl uptake and more bicarbonate and K secretion

PYY signals to the brain - what is PYY? what happens when the duodenum receives chyme from the stomach and what does it release? what happens if the duodenum is empty? what happens after PYY enters the blood, what neurons does it inhibit? this leads to less output of what? and less suppression of?

-Peptide YY (PYY): released from enterocytes in the duodenum, in the presence of nutrients in the small intestine -->when duodenum receives chyme from the stomach, it becomes distended and chemoreceptors are activated to release a lot of PYY into the blood -->in an empty duodenum then there is no activation of chemoreceptors or stretch receptors so very little PYY is released -PYY enters the blood and will activate receptors on the orexigenic neurons and will inhibit them -->less NPY output, so less feeding stimulus -->less suppression of anorexigenic neurons

what protects the stomach (digestive epithelium) from acids, enzymes and pathogens? what are two key components of mucus? the acidic layer (HCl) of the stomach lumen accumulates where? what happens if the mucus layer is damaged?

-acid and protealytic enzymes are dangerous to stomach cells -key protection of the epithelial cells comes from mucus -->mucins: secreted from vesicles and swell and expand to gel like matrix to separate acidic lumen of stomach from surface of the epithelial cells of stomach -->bicarbonate: mucus layer maintains neutral pH with bicarbonate in the gel-like matrix -HCl will accumulate above the alkaline mucus layer -damaged mucus lining can expose cells underneath and lead to ulceration of the gastric epithelium of the stomach

salivary glands ductal cells - is all about modifying what? reclaims what two ions? since water cannot follow back through the ductal cells, saliva is more what? what type of pH does saliva have and why? to reclaim Na+, what channel is used? to reclaim Cl-, what channel is used? what is another way to reclaim Cl-? what channel does Cl- use to get back into interstitial fluid? where does bicarbonate come from in cells? how does bicarbonate and H+ ions leave from inside the cell? how does H+ get into the cell? in the ductal cells what are the 2 major ions going into saliva ?

-all about modifying composition of saliva to try and reclaim important stuff before it exits the salivary glands and saliva leaves body -reclaim NaCl but water cannot follow so saliva is more water than salt (hypotonic) and has a slightly neutral or alkaline pH since bicarbonate is secreted into it as well -to reclaim Na: use epithelial sodium channels (ENaC); Na follows concentration gradient into cell then transported across basolateral membrane -to reclaim Cl: transported in in exchange for bicarbonate (Cl/HCO3 exchanger); antiport transporter bring Cl in and HCO3 out -Cl brought back in can leak through Cl channels in apical membrane or go back into interstitial fluid through basolateral Cl channels -->Cl- can also have paracellular transport by following Na back to the basolateral/serous side of cells -bicarbonate comes from carbonic anhydrase enzyme in cells converting CO2 waste to bicarbonate; bicarbonate leaves through Cl/HCO3 exchanger, H+ leave through Na/H exchanger in apical and basolateral membranes -H+ can come into cells through K/H exchanger -now the major ions in saliva are bicarbonate and potassium

gastric acidification - all enzymes that function in the stomach have to undergo what? why is it important to maintain acid secretion for these enzymes in the stomach? what is pepsin and why is it dangerous? what is pepsinogen? how is pepsinogen activated? many gastric enzymes are most active what pH?

-all enzymes that function in the stomach have undergone selection to function in acidic environments -important to maintain acid secretion so that these enzymes can continue to function -pepsin (protease) is dangerous enzyme since it may break down proteins on the surface of digestive cells and damage them -->to avoid this, chief cells secrete pepsinogen which is the inactive form of pepsin at neutral/alkaline pH -->only becomes active in the lumen of the stomach (acidic pH < 2), not in the gastric glands -->pepsinogen is activated since acidic environment allows the zymogen to unfold slightly which allows catalytic part of enzyme to cleave masking sequence that blocks the catalytic area (self catalytic) -many gastric enzymes are most active at acidic pH

endocrine roles of the pancreas - what 3 endocrine cells (Islets of Langerhans) are important in secretions? what 3 things does insulin do? is insulin released under high or low blood glucose levels? what 2 things does glucagon do? is glucagon released under high or low blood glucose levels? what 2 things does somatostatin do?

-alpha, beta and delta cells are the ones that play a key role 1. Beta cells: secrete insulin; has inhibitory effect on glucagon secretion -->activates insulin receptors on alpha cells (inhibit glucagon secretion) -->lowers blood glucose levels by getting it into cells; released under high blood glucose levels -->signals body into energy (glucose) storage mode 2. Alpha cells: secrete glucagon -->stimulate both secretion of insulin and somatostatin -->glucagon in blood raises blood glucose levels (tissues release it); released under low blood glucose levels 3. Delta cells: secrete somatostatin -->somatostatin is an inhibitory signal on digestive function -->inhibits insulin and glucagon secretion

PYY signals to the brain - anorexigenic neurons release what neurotransmitter? this signal stimulates what after binding effector neurons? what does this do to feeding and metabolism? this is also _____ feedback.

-anorexigenic neurons release the neurotransmitter, alpha-melanocyte stimulating hormone (aMSH): influences feeding pathways to suppress feeding -->aMSH is released from anorexigenic neurons onto effector neurons leading to a signals that says to stop eating and burn more calories (inc metabolism) -->since there is already a lot of chyme in the intestine, then it makes you feel full to not bring in anymore food; and need to inc metabolism since there is nutrients available already -also a negative feedback loop: drop in presence of food then you get hungry again

serous cells of the salivary gland - the basolateral membrane contains many of what important ATPase? what is the difference btw primary and secondary active transporters? the sodium gradient created by the Na/K pump allows Na to flow into cell coupled to what other ions? how does Cl- leave the cell to enter the lumen (what receptor)? what happens to Cl- transport in cystic fibrosis? what 2 things follow the flow of Cl- into lumen?

-basolateral membrane is where many of the Na/K ATPases are found; hydrolyze ATP to force Na out and K into cell against conc gradients (direct/primary active transport) -indirect/secondary active transport is when transporter uses a gradient that another pump established by hydrolyzing ATP -Na gradient allows Na to flow from high outside cell to low inside cell; coupled to influx of K and 2 Cl -Cl leaves through apical membrane through chloride channel called CFTR; to get it into the interstitial lumen for water to follow -in Cystic Fibrosis, there is a mutation in CFTR so Cl can't move into interstitial fluid and neither can water making the mucus thicker -Na follows Cl flowing across apical membrane into lumen and water also follows (paracellular or through aquaporin channels)

protein digestion - where does protein digestion begin? what enzyme in the stomach breaks down proteins? how does HCl in the stomach also help with digestion?

-begins in the stomach with pepsinogen (secreted from chief cells); pepsinogen is activated into pepsin in the acidic lumen of the stomach -pepsin is the main protease in stomach starting breakdown of proteins -HCl is also denaturing proteins allowing pepsin to get access to peptide bonds to cleave them

liver and gallbladder - what is bile and what is its pH? what is the main component of bile? what structure do bile salts have? bile salts are _____pathic, meaning? what are 5 other components of bile?

-bile is a alkaline solution (7-8) which helps in pancreatic juice to neutralize gastric acid from stomach 1. bile is largely composed of bile salts (modified steroid molecules) -->steroids have ring like structure that is a hydrophobic molecular scaffold -->bile salts are amphipathic (has both hydrophobic and hydrophilic components); allows them to react readily through hydrophobic side with lipids and fats and with water through hydrophilic sides 2. phospholipids 3. cholesterol 4. pigments: bilirubin (from heme breakdown in blood) uptaken by liver then it is dumped into bile duct to remove from body; in intestines it is modified to stercobilin 5. H2O 6. bicarbonate: makes it an alkaline solution

iron absorption - does the body have a way to get rid of excess iron? what is one of the only ways to get rid of iron inside enterocytes? if there is too much iron in the blood what does the liver produce and what does it do to iron leaving enterocytes? what happens when iron in blood is low?

-body does not have a good way of getting rid of excess iron; by holding ferrous iron bound to ferritin in the enterocytes, it is stored and prevented from causing too much iron in body tissues -->only way to get rid of iron bound in enterocytes is to have the cells die and be removed -->body can slow down import of iron from enterocyte into blood through hepcidin (made by liver) which is a protein that inhibit the ferroportin transporter (iron can't come into blood) -->when iron levels in blood drop, liver stops producing hepcidin so iron can be transported into blood

carbohydrate digestion - what polysaccharide is undigestible by humans? since plants have cell walls made of this, plant eaters have what enzyme? what is fiber?

-certain polysaccharides are undigestible by humans -->cellulose: polymer of many glucose molecules; we do not have cellulase enzymes that can break down bond (present in bacteria and fungi) -->all plants have cells walls made of cellulose so herbivores main source of glucose is cellulose -->for humans, cellulose is considered fiber (adds bulk to substances moving through digestive system but something we can't digest and absorb) so its excreted in feces

iron absorption - what two ways can iron enter the body? what 2 different forms can iron exist as? how does iron bound to heme enter the enterocyte apical membrane? how does it exit the cell? how is heme bound to iron transported in the blood?

-comes into body through diet and may be conjugated to heme or as free iron -iron can exist in different states; ferrous iron (Fe2+) or ferric iron (Fe3+) -->ferrous form can be bound to heme's porforin ring -iron absorption: -->heme transporter: absorbs heme groups with ferrous iron bound on the apical membrane -->can then exit across basolateral membrane through heme transporter -->heme can then be absorbed by blood to bind transport proteins in blood like transferrin or hemopexin

what 3 digestive enzymes need to be kept out of the gastric epithelium? chief cells have ____ stimulation to release digestive enzymes. G cells can release gastrin what two ways to activate chief cells? what is the barrier to protect the digestive epithelium from digestive enzymes?

-digestive enzymes also need to be kept out of gastric epithelium -pepsinogen: becomes pepsin when activated -gastric lipase: enzymes that breaks down lipids; breaks bonds connecting fatty acids to glycerol -acidic mammalian chitinase: enzyme that breaks down chitin (cell wall of fungi) and is a main component of arthropods -chief cells have parasympathetic stimulation to release digestive enzymes -G cells release gastrin either locally or into blood as hormone can then activate chief cells -mucus barrier keeps all these enzymes away from the epithelial cells and only releases them into the lumen of the stomach

pancreas in digestion - all ductal cells of the pancreas lead to what? all ducts of the gallbladder, liver, and pancreas lead to what? what is this structure regulated/controlled by?

-ductal cells all lead to a common pancreatic duct; which releases substances, in common with secretions from liver and gallbladder, through the common bile duct -->regulated by the Sphincter of Oddi; which keeps the secretions of pancreas and gallbladder from entering intestine when closed; when it relaxes and opens it allows secretions to enter small intestine to aid in digestion

pancreas in digestion - ductal cells have what ATPase? what does carbonic anhydrase make? how does bicarbonate exit? how does Cl exit? how are H+ ions removed? how does Na flow into cell? Na is attracted to flow of bicarbonate out meaning that what follows?

-ductal cells have Na/K ATPase creating sodium gradient -also have carbonic anhydrase to make bicarbonate and H+ ions -->bicarbonate pumped across apical membrane into lumen of the pancreatic duct by HCO3/Cl exchanger -->Cl leaks out through CFTR channels; cycled -->H+ ions removed through a Na/H exchanger; Na flows back into cell -->Na allows flow out attracted to flow of bicarbonate; get a sodium bicarbonate soln and water flowing (paracelluar or trancellularly/aquaporins)

pancreas in digestion - what is the role of ductal cells in the pancreas? why do we need a lot of bicarbonate (to neutralize what)? while stomach enzymes function in acidic pH, the rest of the digestive enzymes need?

-ductal cells modify pancreatic juices by making it bicarbonate rich -important for lots of bicarbonate since chyme coming from stomach, has very acidic pH, so it must be neutralized -->the rest of the digestive enzymes need more neutral pH to function

What is emulsification? what component of bile allows it to do this? what happens to the surface area of fats being digested? why is this beneficial for digestive enzymes ?

-emulsification: process in which large lipid globules are broken down into several small lipid globules -->biles salts breaks them apart into smaller droplets of lipids -->increases surface area of fat being digested; enzymes can then more efficiently digest fatty acids/lipids

gastric phase of digestion - in endocrine response, G cells can sense what 3 things to activate calcium sensitive receptors? this activates G cells to release what into what two places? what 3 other cells do G cell secretions activate?

-endocrine response: -->G cells sense Ca2+, AAs, polyamines to activates calcium sensitive receptors which cause G cells to release gastrin locally and into blood -->gastrin in blood can travel and activate gastric cells at a distance -->gastrin stimulates all other cells; ECL to release histamine, parietal cells, and chief cells

intestinal phase of digestion - endocrine response is about intestinal cells releasing what into the blood? what does CKK do in the liver, gallbladder, and pancreas? what does secretin inhibit? what does secretin stimulate to neutralize acids in chyme? what is GIP and what does it stimulate?

-endocrine response: intestinal cells releasing hormones into the blood to influence distance targets; key hormones being released are: -->CKK enters blood and targets liver and gallbladder cells to release more bile, targets pancreas to release digestive enzymes -->secretin inhibits parietal and chief cells to slow down gastric activity; also stimulates pancreas to increase bicarbonate secretion to let intestines neutralize acids in chyme delivered to it -->GIP (glucose dependent insulinotropic peptide); role is to stimulate insulin secretion by stimulating endocrine beta cells

fatty acid and cholesterol absorption - enterocyte cells are also making proteins in the ER, so what 4 things are present in the ER? what do these 4 things create? where do chylomicrons move to and how do they exit the cell? what happens once chylomicrons exit the cell? how do they get into the blood circulation? do lipids go to the liver?

-enterocytes are making proteins so in the ER you have monglycerides, fatty acids, cholesterol, and specific proteins -then form a chylomicron; large complexes of phospholipids containing fatty acids, mono/triglycerides, cholesterol, and proteins -moves to golgi and eventually gets into excretory vesicles which release chylomicrons through basolateral membrane into interstitial fluid -only way that chylomicrons can get into blood is by entering into the lacteal (the lymphatic vessels of the small intestine which absorb digested fats); permeable when it receives signals to expand to allow entrance of chylomicrons -->lacteal then transports chylomicrons into lymphatic system and then eventually into blood -->lipids bypass the liver

coordination of digestion - what are some external stimuli? how can external stimuli impact the digestive system function? what are some internal stimuli and they do what to the function of digestive system? what 3 receptors can be affected by the local enteric NS sensing the presence of food? what are short reflexes and what do they do? what are long reflexes and what do they do?

-external stimuli: sight, smell, taste, thought of food -->can impact digestive system function through outputs of CNS -internal stimuli: when food or other components are in the GI tract -->sensed and influence the function of the digestive system -local enteric NS sensing presence of food and nutrients; releasing info to affect digestive processes -->chemoreceptors, osmoreceptors, mechanoreceptors -->short reflexes; local (intrinsic) nerve plexus (gut brain) affects smooth muscle or glands -->result is a change in contractile or secretory activity -->long reflexes; sent to CNS and cause autonomic input

fatty acid and cholesterol absorption - what 2 ways do individual fatty acids and monoglycerides pass through the apical membrane? what 2 ways does cholesterol pass through the apical membrane? where do fatty acids, glycerides, and cholesterol accumulate in the cell?

-fatty acids, cholesterol, and monoacylglycerol must not be absorbed across the apical membrane 1. individual fatty acids and monoacylglycerides: -->protein dependent path: relies on transmembrane protein transporters; fatty acid translocase moves monoglycerides and fatty acid across PM through protein transporter -->protein independent path: fatty acids are very hydrophobic so they can readily pass through hydrophobic PM -->then end up in ER 2. cholesterol: -->protein dependent: diffuses into cell in protein dependent way through protein transporters; mostly protein mediated -->protein independent: also has hydrophobic areas so can diffuse across PM -->cholesterol also accumulates in ER

the epithelial barrier is made up of apical and basolateral membranes, where is each located? what are epithelial cells separated by? this prevents what? what 2 ways can molecules and water move past the epithelial barrier?

-form an epithelial barrier that has an apical membrane on top with basolateral membrane on the sides and bottom -the cells are separated by tight junction proteins that prevent movement of molecules and water in btw cells from interstitial fluid from basolateral side to apical side; instead water must go through cells -transcellular transport: movement of molecule/water through cells -paracellular transport: movement of molecules/water btw the cells

iron absorption - ferric iron is converted to what before entering the apical membrane? what enzyme is this mediated by? how does free ferrous iron enter the apical membrane? incoming ferrous iron is sequestered by what inside the cell? how does ferrous iron leave the cell? what happens to ferrous iron when it enters the interstitial fluid? what happens when iron enters blood?

-free iron in diet absorption: -->ferric iron is reduced (gain of electrons) to ferrous iron (Fe2+) -->reduction of ferric iron is mediated by cytochrome B enzyme -->ferrous iron is transported across apical membrane by Divalent Metal transporter; transports a variety of divalent metals -->or incoming ferrous iron can be sequestered with ferritin, which will eventually release it to be transported through basolateral membrane -->Ferrous iron can then move across basolateral membrane through ferroportin transporter -->once in interstitial fluid, ferrous iron will then be transformed into ferric iron which will then bind to transferrin and be transported in blood

gastric acidification - why is HCl secretion important in dealing with pathogens? most pathogens require what pH environment to survive? most fungi are acidic and will still not survive in stomach, why?

-gastric acid (HCl) is important for creating a chemical barrier for pathogens -->food could be contaminated with microbes that can cause disease -->most organisms are neutrophils so they cannot grow and die in acidic environment; especially pathogens that want to get into our neutral pH environment (acidophiles or alkalophiles will die in the rest of our body) -most fungi do well in acidic environment (4-6) but cannot survive in 1-3 pH in stomach

gastric acidification - acidity helps initiate break down of what? protons in the lumen do what to H bonds of food particles/proteins? enzymes then can do what to the structure?

-gastric acid helps initiate break down of food molecules coming into stomach -->H bonds keep them in intact structure but protons in lumen of stomach weaken bonds causing proteins to denature, opening them up to allow enzymes to cleave bonds

the stomach - describe all of the 6 types of cells of the gastric pit and gastric gland: -goblet cells -parietal cells -chief cells -D cells -G cells -ECL cells

-gastric gland composed of a variety of cells: 1. goblet cells: main cells at the top of the gastric pit; mucus cells secreting mucus -->mucus creates physical barrier to protect cells of the digestive system from cytotoxic or protease chemicals 2. parietal cells: acid secreting cells; secrete HCl to acidify the stomach 3. chief cells: relase digestive enzymes; pepsin, gastric lipase, mammalian chitanase 4. D cells: regulatory cells; release somatostatin (inhibit acid and enzyme secretion) 5. G cells: secrete gastrin; a stimulating signal (ramp up acid and enzyme secretion) 6. ECL cells: enterochromaffin-like cells; secrete histamine (main signals for acid secretion)

ghrelin signals to the brain - what is ghrelin? what happens when ghrelin enters the blood? orexigenic neurons release what signal onto the effector neurons? what is the result of this in hunger and metabolism? this released substance also inhibits what neurons?

-ghrelin is a hormone signal that is released from cells in an empty stomach; when stomach is satiated/full then less ghrelin is released -->ghrelin enters the blood and activates receptors found on orexigenic neurons which releases NPY -->Neuropeptide Y (NPY): is released onto the effector neurons and drives feeling of hunger so you want to eat more, also reduces metabolism -->NPY also inhibits anorexigenic neurons

endocrine roles of the pancreas - what happens to insulin and somatostatin levels when glucagon secretion increases? somatostatin inhibits what? what happens to both insulin and somatostatin when glucagon decreases? the rhythmic rise and fall of glucagon, insulin and somatostatin are due to what?

-glucagon INC (both in blood and released in pancreas), then both somatostatin and insulin INC -somatostatin (INC) then inhibits both glucagon and insulin (DEC) -as glucagon DEC, then both insulin and somatostatin DEC -->rhythmic rise and fall of glucagon, insulin, and somatostatin since they are all locally influencing each others release in the pancreas -->LOW glucagon and insulin when HIGH somatostatin (since it inhibits both) -->glucagon stimulates both insulin and somatostatin so shortly after rise in glucagon, then INC in both (ins. & som.) -->after rise in insulin and somatostatin, then you get a fast DEC in glucagon

salivary glands mucus cells - goblet cell primary function is to release what? what is mucus? what is mucin? mucin is highly glycosylated meaning what (how does it make mucus thick)? mucins are tightly bundled in endosomes but do what when released? what is mucin release activated by?

-goblet cells primary function is to release mucins -mucus: slimy material that coats epithelial surfaces to provide a physical trap; fluid water filled with viscous gel-like proteins, mucins -mucin: actual proteins that is highly glycosylated, meaning it has many sugar molecules attached to it; good at absorbing ions and water to it to create large gel like matrix to make mucus so thick -mucins are tightly bundled in endosomes but when released they expand to create mucus matrix -mucin secretion into saliva stimulated by epinephrine from adrenal medulla binding to beta adrenergic receptors

the gut microbiome - what are good bacteria? what are 6 things that good bacteria do for us? where can bad bacteria enter the gut through? what are 4 things that bad bacteria can cause?

-good bacteria: members of our microbiome that benefit us and benefit from living inside us -->take up space so they prevent colonization by bad bacteria and pathogens -->release chemical signals that regulate the function and identity of other microorganisms living in the digestive tract -->production of vitamin K (important for blood clotting) -->break down a lot of nutrients that we cannot break down ourselves (ex. cellulose) -->can also conduct fermentation -->bring in energy and resources from things we could not otherwise use -bad bacteria: organisms that do not benefit us and instead take resources and disrupt cell function -->can enter through contaminated food -->can cause infection after surgery -->can cause diarrhea, inflammation of colon, or even death

gut microbiome - what is the gut microbiome? it is estimated that there are about ___X as many other cells than humans cells in the body. what are symbiotic organisms? what are commensal organisms? what are mutualistic organisms? what are pathogenic organisms?

-gut microbiome: the collection of all other living organisms (microbes) that occupy the body and influence digestive function -estimated that there are about 10X as many other cells than just human cells (ex. bacteria, fungi, archaea, protozoa, viruses) -symbiotic: means living with; organisms living in or on the body -->can be good or bad for us -commensal: organisms that live in or on bodies who do not affect us positively or negatively -mutualistic: organisms that are benefited from living in/on us and we are also benefited from them -pathogenic: organisms that are harmful/detrimental to us; take away resources and impair functions of our cells

large intestine - what are the 3 main components of the large intestine and what does each do? why are the microorganisms in our microbiome important?

-has 3 main components: 1. Cecum: houses many of the gut microbiome; bacteria and other microorganisms live in digestive tract 2. Appendix 3. Colon: site of finishing up absorption of water and electrolytes; reclaims water and salts so we don't lose them -microorganisms in microbiome can help digest, breakdown, and absorb a lot of nutrients; responsible for making important vitamins and cofactors

liver and gallbladder - what artery brings oxygenated blood to liver? what is the hepatic portal vein? why would blood be carried to the liver before going back to the heart? how does all blood leave the liver to go back to the heart?

-hepatic artery brings oxygenated blood to liver -hepatic portal vein is where blood leaves capillary beds in the GI tract and travels to the liver through the hepatic portal vein -->another series of capillaries allow nutrient rich blood to reach liver first before going back to heart to filter out any pathogens -then all blood leaves liver through hepatic vein and goes back to the heart

structure of the liver - why is it important that hepatocytes are in close contact with sinusoidal capillaries? the outflow of blood from the liver occurs through what what vein? what vein lets blood exit the liver? incoming oxygen rich blood enter the liver through? where does the hepatic portal vein bring blood from?

-hepatocytes are in close contact with sinusoidal capillaries; allows hepatocytes to secrete things into blood -outflow of blood is through central vein so sinusoidal capillaries collect protein secretions and funnel it into the vein to exit liver through hepatic vein -incoming oxygen rich blood through hepatic artery to supply oxygen to hepatocytes -hepatic portal vein brings in blood from portal system; mixes together blood from sinusoidal capillaries then leaves through central vein, and leaves liver through hepatic vein

calcium absorption - there are ___ levels of Ca in the lumen. what are 2 transporters used to get Ca into apical membrane? what is the paracellular path to get Ca into the interstitial fluid? what is Calbindin? why must Ca be tightly regulated in the cell? what are 2 ways (transporters) to get Ca out of the cell?

-high levels of Ca in the lumen -Ca absorption: -->can be transported through the paracellular path but most Ca is transported through transcellular path -->TRP channels: transient receptor potential Ca channels; Ca flows through with its Ca gradient, creating a change in the membrane potential -->voltage gated Ca channels: bring in calcium with its Ca gradient -incoming Ca must be tightly bound up by a protein called Calbindin inside the cell -->since if Ca is just free it may interact with other signaling proteins inside cell to activate kinases, phosphatases, etc. to alter function of the cell -->Calbinidin then transports it to basolateral membrane where it releases it -->Na/Ca exchanger: uses Na gradient to bring Na into cell and efflux Ca from cell -->Ca ATPase: is a plasma membrane ATPase in the SR; pumps Ca out of cell into interstitial fluid by hydrolyzing ATP

ghrelin signals to the brain - in the hypothalamus what are 2 neurons which are involved in feeding? the outputs of these neurons converge on a common set of? this determines whether you feel ___ or ____. these neurons also affect metabolism, how does each work? through these signals the stomach can tell the brain what?

-hypothalamus: in clusters of neurons within the brain there are some neurons that are orexigenic (stimulate feeding) and other are anorexigenic (inhibit feeding) -->the outputs of these neurons converge on common set of effector neurons that determine whether you feel hungry or full -->also effect metabolism so if you feel full, there are signals that ramp up metabolism (have lots of energy that needs to be digested); if there is a sense of hunger, then you want to bring in food and you reduce metabolism (reserves low so need to preserve them) -stomach tells the brain fill me or don't fill me

active stomach - what do D cells do in case parietal cells secrete too much acid? what happens to the acidity of the stomach when food enters and why?

-if parietal cells secrete too much acid, D cells have receptors that sense H+ ions; then activate D cells to release somatostatin to inhibit parietal and G cells (feedback mechanism to not get stomach too acidic) -when food hits stomach then pH can rise to 4-5 since H+ being used to denature bonds in food to break down proteins

pancreas - supplies most of what to the small intestine to break things down? secretes what to make intestine more neutral? secretes what two hormones into the blood? secretes somatostatin which is an indicator of what?

-important in digestion; supplies most of digestive enzymes for breaking down proteins, lipids, nucleic acids, and carbohydrates in small intestine -secretes bicarbonate; acid from stomach needs to be neutralized in the intestine -secretes hormones into the blood; insulin and glucagon -secretes somatostatin, indicator of gastric function and GI motility to coordinate movement of food through digestive system and activity of secretory cells in tract

protein digestion - what is the tertiary structure of proteins degraded by? what structures can polypeptide chains be broken down into?

-in an acidic environment many of the H bonds holding together the tertiary structures of proteins will be broken allowing peptidases to come in and cleave the peptide bonds -polypeptide broken down as the bonds are hydrolyzed and can create: -->tripeptides -->dipeptides -->individual amino acids

insulin from pancreas tells brain about glucose - what does the brain use insulin to indirectly measure? what happens when insulin enters the blood (what receptors can it bind)? what is insulin effect on orexigenic neurons? what is insulin effect on anorexigenic neurons? what happens to feeding and metabolism? after not eating then what happens to the balance?

-insulin is indirectly used by the brain to measure blood glucose levels -when insulin enters the blood, it can bind to receptors on either orexigenic or anorexigenic neurons -->insulin inhibits orexigenic pathways and stimulates anorexigenic pathways -->net balance shifting toward more aMSH signaling on effector neurons to eat less and burn more -->since insulin tells the brain there is lots of sugar available so no need to bring in more food and ramp up metabolism to break down glucose -after not eating then there is lower blood glucose and less insulin; shift toward orexigenic pathways

iron absorption - if iron dissociates from heme inside the enterocyte what happens to heme? what happens to ferrous iron inside the cell? how does iron exit the cell? what is ferrous iron converted into in the interstitial fluid? what is this mediated by? what happens when iron enters the blood?

-iron can also dissociate from heme inside enterocyte cell and heme is metabolized and excrete as bilirubin while the ferrous iron is stored inside the cell conjugated to ferritin -->ferrous iron can then be released by ferritin and transported across basolateral membrane through ferroportin transporter (ferrous iron transporter) -->ferrous iron is then oxidized (loss of electron) converting it into ferric iron (Fe3+); oxidation is mediated by protein hephaestin -->ferric iron then enters blood and binds to transferrin

pancreas in digestion - what is the main key regulation of bicarbonate (what NS)? what is secretin? can we eat without the pancreas? why?

-key regulation of bicarbonate secretion is through parasympathetic stimulation (Ach activating muscarinic receptors) stimulates bicarbonate secretion by altering activity and expression of key transporters/channels -secretin: released by intestinal cells and activates secretin receptor; intestine signals to pancreas to release more bicarbonate and digestive enzymes -we cannot eat without the pancreas since digestion is dependent on bicarbonate and all digestive enzymes from it

leptin from adipose to brain - what happens when leptin enters the blood (what does it do to orexigenic and anorexigenic neurons)? which pathway is inhibited? what happens to feeding and metabolism? what happens to leptin signal after a period of not eating? what does this lead to (which pathway is activated more)?

-leptin enters the blood as a hormone; there are leptin receptors on both the orexigenic and anorexigenic neurons -->leptin inhibits orexigenic neurons and stimulates the anorexigenic neurons -->more aMHS on effectors and less NPY -->inhibiting the orexigenic pathway leading to a net signal of eat less and burn more (have plenty of fat so stop bringing in food and crank up metabolism to burn the reserves) -after a period of not eating then majority of storage will be used so the leptin signal is depleted -->reduced leptin then causes orexigenic pathway increase activity and anorexigenic pathways becoming suppressed

leptin from adipose to brain - what is leptin? depending on BMI and how many fat cells you have what is true of the energy/lipid reserves you have? if you have more fat cells then you produce how much leptin? if you have less fat cells then you produce how much leptin?

-leptin: is a signal released from peripheral adipose tissues (white fat cells) -->depending on BMI then you can have few/small fat cells (not a lot of energy/lipid reserves), or many/large fat cells (a lot of energy/lipid reserves) -->brain can see how stocked body is with energy reserves/fat and can help determine if it should bring food in or can not need to bring food in, or if it should lower metabolism or ramp it up -more fat cells = more leptin produced -fewer fat cells = less leptin produced

endocrine/exocrine functions of liver - what are 4 substances secreted by the liver into the blood (endocrine)? what 2 things does the liver excrete into the intestine (exocrine)? how is bile secreted into the GI tract? what happens to excess bile? one component of bile, bile salts, are synthesized where and do what? they are taken back up by the portal system to do what?

-liver has many endocrine functions; secretes many substances into the blood passing through it (ex. compliment proteins, plasma proteins, hormones, angiotensinogen) -liver exocrine function include hepatocytes secreting bile and bilirubin -->bile passes out through series of ducts; secreted through common bile duct into GI tract; excess bile stored in gallbladder -components of bile: -->bile salts: synthesized by liver and help in lipids to be chemically digested; bile salts taken back up by portal system and brought back to liver to reuse them

liver and gall bladder - the liver produces what to break apart surface area of lipids? what does the gallbladder store?

-liver produces and secrete bile, to help break apart and increase overall surface area of lipids allowing lipases to have more area to attack -gallbladder stores bile being produced by liver and release it when needed

gut microbiome - are different environments of the GI tract all the same? what is the environment of the stomach and what is the CFU like? what is the environment of the intestines and what is the CFU like? what is the environment of the colon and what is the CFU like? where is vitamin K produced and by what? what is CFU?

-local environments throughout GI tract are very different -part of the role of the microbiome is not only to do useful chemical reactions but also take up space in the body that other bacteria might adhere to (don't let harmful bacteria adhere) -->stomach: very acidic environment (pH: 1-3), with relatively little amount of bacteria present, very aerobic environment -->small intestine: pH is around 6-7, anaerobic environment. duodenum: large shifts in pH, not many bacteria present. jejunum and ileum: more bacteria present, more stable pH/environment -->colon: neutral pH (6-7), largest amount of bacteria present in the entire digestive tract, anaerobic environment, mainly where vitamin K is produced -CFU: colony forming units; measure of how many bacteria living in a certain area

intestinal phase of digestion - in long neural reflex local stretch and chemoreceptors activate ___ NS and send signals to? what does the medulla oblongata inhibit and what does it increase response of? what does more sympathetic input to the stomach do?

-long neural reflex (enterogastric reflex): -->local stretch and chemoreceptors activate enteric NS and send signals to CNS -->medulla oblongata: inhibits the parasympethatic divisions and stimulates the sympathetic nuclei -->more sympathetic input to stomach; telling stomach to stop digesting and sending chyme to intestine

gastric phase of digestion - in long neural reflex, stretch and chemoreceptors send afferents where? parasympathetic response descends via what nerve? this releases Ach to activate what receptors? this activation leads to what 3 things?

-long neural reflex: beyond local enteric NS; stretch receptors and chemoreceptors send afferents up to CNS -->results in descending information through the dorsal vagus nerve that targets the GI tract -->means more Ach, more muscarinic receptor activation -->more gastric acid, mucus secretion and motility to ramp up digestion

small intestine - is the main area for what 2 functions? what are the 3 segments and what is each responsible for?

-main area for digestion and absorption -has 3 segments: 1. duodenum: where most of the pancreatic enzymes are delivered for breaking down carbohydrates, proteins, and lipids; major site for nutrient breakdown and chemical digestion -->some absorption 2. Jejunum: mainly about absorbing nutrients; some digestion 3. Ileum: finishing off area for absorbing important things (ex. vitamin B12 and bile salts)

pancreas in digestion - what is the main stimulation for serous release? where is CKK released from? what is cholecystokinin and what does it do to pancreatic secretions? why is it good that CKK comes from different sources in the digestive tract?

-main stimulation for serous release is by the parasympathetic NS (Ach activating muscarinic receptors) -cholecystokinin (CKK) is released from neurons in the enteric NS (local brain of digestion) to ramp up pancreatic secretions -->comes from different sources (ex. cells of small intestine) to allow different components of digestive system to communicate with each other

stomach - is a major area for what types of digestion? is a good area to do what with food? what is pepsin and what does it do? what is HCl or gastric acid and what do they do?

-major area for mechanical digestion and chemical digestion -stores and holds food; most digestion and absorption happens in small intestines -key area for starting protein digestion; HCl or gastric acid also causes proteins to denature -pepsin secreted to cleave peptide bonds to begin protein digestion

carbohydrate digestion - maltase breaks down maltose into? lactase breaks down lactose into? sucrase breaks down sucrose into?

-maltase breaks down disacc. maltose into: -->2 glucose monomers -lactase breaks down disacc. lactose into: -->1 glucose -->1 galactose -sucrase breaks down disacc. sucrose into: -->1 glucose -->1 fructose

fat digestion - many fatty acids are what? what bonds does lipase cleave from glycerols? what components are left after cleavage? what are cholesterol esterases and what do they do?

-many fatty acids are triglycerides or triacylglycerides (3 hydrocarbon chains attached to a glycerol) -lipase cleaves/hydrolyzes ester bond connecting fatty acid to glycerol; leaving a free glycerol and 3 individual fatty acids -->sometimes monoacylglycerol is released so break down of lipids produces individual fatty acids, glycerol and a single fatty acid chain still attached to the glycerol -cholesterol esterases: cleave ester bond conjugating cholesterol molecule and free it from lipid droplets to get free cholesterol

carbohydrate absorption - monsaccharides are what type of sugars? how do glucose and galactose enter the epithelial cell? they are Na _____. once inside the cell, glucose and galactose exit how? once in interstitial fluid, where do glucose and galactose go? how does fructose enter the epithelial cell? it is Na _____. once inside the cell, fructose exits how? once in interstitial fluid, where does fructose go?

-monosaccharides are hexosugars 1. glucose and galactose enter through apical membrane through a Na/glucose cotransporter (same direction) using the Na gradient from ATPase in basolateral membrane -->once inside glucose and galactose exit through basolateral membrane through GLUT2 (facilitated diffusion; high inside low outside) -->in interstitial fluid then glucose and galactose can enter blood through fenestrated capillaries in GI tract and move through hepatic portal vein to the liver 2. fructose enters apical membrane through the GLUT5 transporter -->once inside, fructose will exit through the basolateral membrane through the GLUT2 glucose transporter (facilitated diffusion; high inside low outside) -->Na independent travel through cell -->in interstitial fluid then fructose can enter blood through fenestrated capillaries in GI tract and move through hepatic portal vein to the liver

key structures of the digestive system (9)

-mouth -salivary glands -esophagus -stomach -small intestines -large intestines -liver -gall bladder -pancreas

pathogen defense (bacteria and fungi) - mouth and salivary glands secrete mucins, lysozyme, defensins, and IgA, describe what each does.

-mouth and salivary glands secrete: -->mucins (mucus): secreted by salivary glands; mucus provides a physical barrier that traps pathogens and debris; have ciliated epithelial cells to move mucus up and out; can spit out mucus or swallow it to destroy it in the stomach; also spatially segregates things; mucus is also a nutrient source for the good bacteria -->lysozyme: enzyme secreted by salivary glands to break down bacterial cell walls; allows bacteria to lyse and rupture; many of its AAs are positively charged so it an insert into PM -->defensins: pore forming proteins that insert into PM of pathogens to disrupt ion gradients (bacteria can't make energy/ATP), and also lose vital nutrients through pores so it dies -->IgA: dimer secreted by plasma cells that can be secreted through apical membrane into gut lumen, saliva, sweat, tears, etc.; clumps/agglutinates pathogens; can occur outside cells, inside cells or when pathogens have moved past cells

stomach at rest - when there is no food in stomach, is there active digestion? there is ____ levels of acid secretion. is the lumen acidic? why would it be helpful for the stomach to be acidic? which cells which release somatostatin are most active during this time? what are parietal cells releasing?

-no food in stomach; no active digestion -low rates of acid secretion (HCl) -lumen still acidic (pH btw 1-3) to help keep barrier for pathogens; mucus coming up from respiratory tract with debris trapped are either spit out or swallowed to decontaminate debris -somatostatin released from D cells; most active ! -parietal cells are the acid secreting cells

what is normal blood glucose levels? what is hypoglycemia? what is hyperglycemia? what is the brain's main source of energy ?

-normal blood glucose levels are maintained very tightly (80-100 mg/dL) -hypoglycemia: low blood glucose levels -hyperglycemia: high blood glucose levels -brain relies mostly on glucose for energy production

water absorption - on average we should drink how much water a day (mL or L)? how many mL of fluid output is excreted in feces? how much fluid does each compartment of the digestive system secrete (salivary, gastric, intestinal, bile, pancreatic)? how much water in total mL does the digestive system absorb a day?

-on average we are supposed to drink 2 L of water a day (2000 mL) -2000 mL of water are added into the digestive system in the stomach -output of the digestive system contains feces with about 100 mL of fluid in it; we end up absorbing 1900 mL of the original fluid we intake plus way more since most components of digestive system are secreting fluids -->salivary glands secrete 1500 mL of fluid a day (saliva) -->stomach gastric secretions are about 2000 mL a day -->liver produces bile which is about another 500 mL -->intestinal secretions are 1500 mL -->pancreas pancreatic secretions are about 1500 mL -sum of all secretions/fluids entering the digestive system is 9000 mL of fluid on average; only about 100 mL is coming out so our digestive system is absorbing 8000 mL of fluid a day

amino acid and peptide absorption - what happens to any of the peptides or AAs when they enter interstitial fluid? how do they get to the liver?

-once any of the AAs or peptides are in the interstitial fluid then they can get into the blood through the fenestrated capillaries -then will be transported to the liver through the hepatic portal vein and eventually back to the heart

insulin from pancreas tells brain about glucose - how do pancreatic beta cells monitor glucose levels? how is glucose absorbed by beta cells (what receptor)? what happens to glucose after being absorbed (what is made)? shutting of K channels, depolarizes the cell leading to release of what? more blood glucose, then ___ insulin. less blood glucose, then ___ insulin.

-pancreatic beta cells release insulin and are monitoring glucose levels; if more glucose is in the blood (after eating) then theres absorption of glucose which enter beta cells through GLUT2 transporters -->allow glucose in and beta cells will metabolize it to make ATP -->more ATP causes shutting of K channels, this causes cell to depolarize and stimulate exocytosis of insulin from vesicles -->insulin will then enter the blood -more blood glucose = more insulin release -less blood glucose = less insulin release

fat digestion - where do pancreatic lipase and procolipase come from ? what does trypsin activated? how does colipase activate pancreatic lipase? what does pancreatic lipase do to fat globules?

-pancreatic lipase and procolipase come from pancreas and entering small intestine -->trypsin converts inactive procolipase into colipase -->colipase activates pancreatic lipase by recruiting it to the bile salts that are emulsifying the fat globules (separate it into multiple smaller fat droplets) -->pancreatic lipase can then break down the bonds and liberate fatty acids

active stomach - parasympathetic stimulation happens _____ food is in stomach. what can stimulate the parasympathetic outflow? what 3 components found in food activate calcium receptors on G cells? what does this lead to release of? histamine ramps up what?

-parasympathetic stimulation happens before food in stomach; smells can stimulate parasympathetic outflow but also food itself -->Ca2+, amino acids, and polyamines activate calcium sensing receptors on G cells to release gastrin; gastrin ramps up histamine release which both ramp up acid secretion more -parasympathetic stimulation gets process going but presence of food ramps it up even more

active stomach - receive signals that food is? acid production is _____. the parasympathetic NS releases Ach to bind G cells, parietal cells, and D cells, what is the effect on each of these cells? gastrin from G cells binds to ECL cells to do what? histamine can bind to and activate what cells?

-receive signals that food is on the way or in the stomach -acid production is increased -parasympathetic NS ramps up acid production; release Ach to bind muscarinic receptors on G cells, parietal cells, and D cells -->inhibits D cells; shuts down somatostatin release -->activates parietal cells -->activates G cells; release gastrin which binds receptors on ECL (release histamine) cells and parietal cells to stimulate them -->histamine activates parietal cells; results in insertion of vesicles containing K+H+ ATPases into PM (more secretion of HCl)

calcium absorption - regulation of Ca absorption is tightly coupled to what? what type of receptor does vitamin D have? what are 3 things that vitamin D receptor activation does?

-regulation of Ca absorption is tightly coupled to vitamin D; vitamin D activates receptor (a transcription factor) to: -->drive expression of transient receptor channel (TRP channels) -->inc expression of calbindin -->inc expression and activity of Ca ATPase and Na/Ca exchanger

rectum and anus - plays role in removal of what from the digestive tract?

-release the undigested material (feces) from digestive tract through deification; things that couldn't be broken down or absorbed -contains a lot of fiber, bilirubin, etc.

how are pancreatic juices similar or different from saliva?

-saliva is all about reclaiming NaCl in the ducts; don't want to be losing too much salt -saliva also uses NaCl to move water to make up bulk of saliva -pancreatic juice also use NaCl to drive water flow but do not reclaim most of it since they dump pancreatic juices into the intestines -->need to maintain normal osmolarity in the intestines so enzymes can function; we are not losing the salt since intestines can reclaim it

protein digestion - where does the final step in protein digestion take place? what are the 3 enzymes from the pancreas that the small intestine relies on? how do these enzymes get into the small intestine? how is trypsinogen activated? what does trypsin activate?

-second step in protein digestion is when chyme moves into the small intestine (finishes in small intestines) -->rely on digestive enzymes from pancreas (trypsinogen, chymotrypsinogen, procarboxypeptidase) into pancreatic duct which then flows to small intestine through sphincter of oddi -->these zymogens enter small intestine where chyme is waiting -trypsinogen is key zymogen for activating all others -->trypsinogen cleaved by enteropeptidases (peptidases bound to PM of enterocytes in small intestine in brush border) to active trypsin protease -->trypsin then cleaves chymotrypsinogen and procarboxypeptidase into active proteases, chymotrypsin and carboxypeptidase

salivary glands - what is saliva? is it continuously flowing? saliva does what to food and helps make what? how are chemoreceptors in the mouth activated? secretion of enzymes like amylase does what? how does saliva maintain pH of the mouth?

-secrete saliva; a fluid filled with enzymes and electrolytes that will cleanse the mouth (continuously flowing) -saliva will moisten and lubricate food in mouth to compact it into a bolus -saliva helps dissolve and break apart molecules in food; activates chemoreceptors for taste in mouth -secretion of enzymes (amylase) to initiate breakdown of starches and sugars -saliva maintains fairly neutral or alkaline pH, through secretion of bicarbonate

secretory cells are arranged in clusters called what? what are three types of cells that make up the salivary glands and what does each do?

-secretory cells are arranged in clusters; each cluster is called an acinus (acini) -cells in acinus can be: 1. mucous cells: secrete mucin proteins to create mucus; physically trap bacteria and debris 2. serous cells: secrete proteins, bicarbonate, electrolytes and salts -->pump salts from blood into lumen of salivary gland so that water follows 3. ductal cells: line the duct and modify composition of saliva; reclaim many important salts so that it is a hypotonic solution

pancreas in digestion - serous cells of the acinar secrete fluids to creat an isotonic solution, which is ____ to plasma. what is the isotonic solution made up of (3)? what are the 5 inactive (zymogen) enzymes that are released from serous cells? is pancreatic lipase active?

-serous cells (of the acinar cells) secrete various fluids, to create an enzyme solution -->is isotonic (similar salt and water osmolarity to blood) -->has enzymes in it; all are zymogens (inactive precursors) -isotonic enzyme solution created by serous cells releasing vesicles containing inactive enzymes: -->trypsinogen: forms active trypsin when cleaved in intestine -->chymotrypsinogen: -->procarboxypeptidase: -->pancreatic lipase: active but has low activity, requires colipase to become fully active which is secreted as prolipase (inactive) -->pancreatic amylase: for starch breakdown in small intestine

what is the main regulation from the autonomic NS? where does Ach bind and how does it affect the activity of epithelial cells? does parasympathetic regulation produce more or less saliva? where does norepinephrine bind and how does it affect the activity of epithelial cells? does sympathetic regulation through norepinephrine produce more or less saliva? where does epinephrine bind and how does it affect the activity of epithelial cells? does sympathetic regulation through epinephrine increase or decrease release of digestive enzymes?

-serous cells also secrete digestive enzymes like amylase -main regulation from autonomic NS is from parasympathetic NS which has vesicles releasing acetylcholine (Ach) -->Ach binds muscarinic receptors (GPCR) on epithelial cells that will increase activity of these cells (rest and digest); increase flux of Cl, Na and water out of these cells (inc fluid flow to make more and faster flowing saliva going into the mouth) -sympathetic NS regulates salivary glands; releases norepinephrine -->norep. activates alpha 1 adrenergic receptors in blood vessels; leads to Ca2+ influx to get smooth muscle contraction, vasoconstriction (reduces blood flow to salivary gland and water / NaCl coming into salivary gland to reduce saliva flow/production) -->epinephrine (from adrenal medulla) binds to serous cells which have beta 1 adrenergic receptors; stimulates release of digestive enzymes

pancreas in digestion - serous cells create a sodium gradient through how? how do K and Cl get into cell? How does Na get pumped out of cell? how does Cl exit the cell? in CF there is also problems with digestion, why? flow of Cl out of cell is followed by flow of what 2 things? enzyme solution is isotonic meaning?

-serous cells and pancreas create a sodium gradient using Na/K ATPase; allows uptake of K and 2 Cl ions through the Na/K/Cl transporter -->Na gets pumped back out through Na/K ATPase -->Cl exits through apical membrane into lumen of pancreatic duct through CFTRs (in CF there is digestive problems as well with pancreatic juices not as voluminous) -->Cl allows Na to follow, which makes water follow (paracellular or transcellular/aquaporins) -->same salt water balance as in the plasma

serous cells of the salivary gland - serous cells make an isotonic enzyme solution meaning it is what in relation to the composition of blood? the osmolarity of interstitial fluid and saliva are what? water can move across epithelial barriers through what channels? there are no water channels in what region? why doesn't water flow back into interstitial fluid when salts are get reuptaken? what enzyme does the isotonic enzyme solution contain?

-serous cells make an isotonic enzyme solution; has the same electrolyte salt composition as the blood so its moving salts and Cl- and water follows -osmolarity of interstitial fluid and saliva are equal since water can move across epithelial barriers through aquaporins; there are no aquaporins in the ductal region -when salts are reuptaked, water can't follow since there is no aquaporins for it so what is left behind is a hypotonic solution (less salt than in blood) -the isotonic enzyme solution also contains the enzyme amylase; to help break down starches

salt (NaCl) absorption large intestine - why are there not any Na/glucose or Na/AA transporters in the large intestine? what are 2 ways (transporters) that Na is brought into the cell? how does Na exit the cell? where does NaCl go after it is in the interstitial fluid?

-since most of the AAs and glucose has already been absorbed by the time things get to the large intestine 1. Na absorption: -->ENaC (IN LARGE INTESTINE): epithelial Na channel; brings Na in using Na gradient -->Na/H exchanger (IN LARGE/SMALL INTESTINE): use Na gradient to bring Na in -->Na can then exit at the basolateral membrane through Na/K ATPase -NaCl then passes through fenestrated capillaries into the blood

pathogen defense (bacteria and fungi) - small and large intestines secrete mucins, IgA, and house a lot of the good bacteria of our microbiome, describe what each does.

-small and large intestines secrete: -->mucins (mucus): creating physical barrier; protect gastric cells from the HCl; can also trap bacteria; spatial segregation -->IgA: dimer secreted by plasma cells that can be secreted through apical membrane into gut lumen, saliva, sweat, tears, etc.; clumps/agglutinates pathogens; can occur outside cells, inside cells or when pathogens have moved past cells -->good bacteria of our microbiome: good bacteria take up space so pathogens can't adhere and colonize; also break down nutrients we can't breakdown; release chemicals to control growth and proliferation of other bacteria; can produce vitamin K

pancreas in digestion - small intestine digestion is dependent on what from the pancreas? the pancreas is an _____ organ, meaning it releases secretions where? what are the 2 type of exocrine (acinar) cells?

-small intestines digestion is dependent on digestive enzymes coming from the pancreas -pancreas is an exocrine organ (release their chemicals into a duct to go to outside body; aka lumen is outside of the body) that has secretory acinar cells into a duct system -exocrine (acinar) cells are: 1. serous cells: secrete fluid 2. ductal cells: modify fluid from serous cells; and form ducts for secretions to go into small intestine

esophagus - what is the main role in food transport? what can be reversed?

-smooth muscle contractions propel food in a bolus from mouth to stomach -peristalsic waves can be reversed to bring things back up (vomiting)

liver and gallbladder - where does bile from bile secreting hepatocytes go to (common)? what does the common bile duct do? where is excess bile stored? smooth muscle contractions of the bile duct do what? what does the Sphincter of Oddi do? what happens when the sphincter relaxes? CKK stimulates production/section of what? CKK also relaxes what?

-special hepatocytes secreting exocrine solution into duct system (ex. bile salts and fluid) that goes into a common bile duct; takes all bile from liver to small intestine and excess is stored in gallbladder -smooth muscle contractions of the bile duct help deliver bile form liver and gallbladder into the small intestine -Sphincter of Oddi is a smooth muscle sphincter that remains contracted to prevent pancreatic juice outflow from pancreatic duct and bile from leaving the gallbladder or liver -->relaxes then opens up and allows digestive juices to enter first segment of small intestine (duodenum) -CKK stimulates bile production and secretion -->stimulates production of bile in the liver and peristalsis (contractions) of the common bile duct to propel bile from gallbladder and liver -->relaxes the sphincter of oddi so bile can enter into the duodenum

carbohydrate digestion - where does digestion of carbohydrates start? what enzyme in saliva breaks down starches? do salivary glands and pancreas each have their own amylase? what happens after amylase breaks down polysaccharides? what 3 enzymes are disaccharides broken down by? what is the smallest form of carbohydrate that can be absorbed by the small intestine?

-starts in the mouth with salivary amylase secreted in saliva; breaks down starch molecules into smaller pieces for other digestive enzymes -salivary glands and pancreas both secrete their own amylase to break down starch into smaller carbohydrates -individuals enzymes (maltase, lactase, sucrase) break down polysaccharides -->amylases break down polysaccharides into disaccharides -->individual enzymes (maltase, lactase, sucrase) break down disaccharides into monosaccharides -->monosaccharides are smallest form of carbohydrate absorbed by small intestine

fat digestion - where does fat digestion start? what salivary gland enzyme breaks down fats? what enzyme in the stomach continues fat digestion? where does majority of digestion take place and with what enzyme? what is pancreatic lipase activated by? what is procolipase activated by? what is fat digestion enhanced by?

-starts in the oral cavity with salivary glands secreting lingual lipase which breaks down fats and lipids can be released from food so we can taste flavors (activates taste receptors) -gastric lipase is released from stomach chief cells to continue fat digestion -most digestion of fats takes place in small intestine through pancreatic lipase (from pancreatic duct through sphincter to intestine) -->activated by colipase from pancreas (starts as procolipase and activated in small intestine) -fat digestion enhanced by bile salts from liver and gallbladder

pathogen defense (bacteria and fungi) - the stomach secretes mucins, gastric acid (HCl), and acidic mammalian chitinase (AMCase), describe what each does.

-stomach secretes: -->mucins (mucus): goblet cells produce mucins with a mucus physical barrier to protect gastric cells from the HCl; can also trap bacteria; spatial segregation -->gastric acid (HCl): secreted by parietal cells which acts as a chemical barrier; can denature proteins and molecules that pathogens need to survive or get into cells; neutralizes any contaminants in food -->acidic mammalian chitinase (AMCase): degrades chitin (major cell wall component of fungi and parasites with a chitin exoskeleton) rendering pathogens more susceptible to other components of immune system; cannot be broken down by pepsin in stomach; can also work in the intestine and not be broken down by trypsin and chymotrypsin

the stomach - the stomach tissue is highly _____ with many gastric pits. What do gastric pits descend down into? what do these invaginations of gastric pits allows for? in the first layer, the mucosa, what is it largely made up of? the thin layer of smooth muscle under the mucosa does what? what is the submucosa largely made up of? what does the muscularis externa do and what 3 types of muscle does it have? what is the outermost layer, the serosa, largely made up of? what is the enteric nervous system?

-stomach tissue is highly folded with many gastric pits; descent down into gastric glands (infolded invaginations of mucosa) that create much larger surface area -mucosa is largely made up of the invaginations of the glandular epithelium (secretory cells) -thin layer of smooth muscle beneath mucosa; can reposition overlying mucosa -submucosa: largely just connective tissue that contains blood and lymphatic vessels (bring in water and salts) -->also has nerves -muscularis externa: three different sheets of smooth muscle; circular, longitudinal, oblique; which contract to mechanically mix/digest and peristalsis to pass food -serosa: outermost layer; connective tissues with lymphatic / blood vessels that supply signals to the smooth muscle; also lots of nerves -enteric nervous system: is the guts NS that is locally in charge and can coordinate many basic digestive system functions; autonomic NS regulates digestion through CNS signals

stomach at rest - how does somatostatin regulate other types of cells?

-there are receptors for somatostatin on parietal cells, G cells, and ECL cells -->inhibits the cells from releasing gastrin (G cells) or histamine (ECL cells), and keep parietal cell in low activity state

carbohydrate absorption - intestine has highly folded epithelium called what and how does it look? how does highly folded epithelial lining benefit absorption? in the center of a villus what 2 components are present and what does each absorb? what are intestine enterocytes?

-there is a highly folded epithelium (no pits) which form finger-like folded structures called a villus -->the villi are finger-like projection folds of intestinal epithelial lining that creates a large expanded surface area; chyme moving over and around them can readily be broken down and absorbed -in center of each villus there is capillary blood supply to helps absorb incoming nutrients -in center of each villus there is also an expansion of a lymphatic duct (lacteal); absorption of fats -intestine enterocytes: individuals epithelial cells; each has a highly folded apical membrane increasing surface area for absorption further

pancreas in digestion - trypsinogen is only activated where? what is the epithelial lining of the duodenum called? how is trypsinogen activated? what happens if trypsinogen is prematurely activated (can cause what disease)? what are 2 ways that pancreatic cells prevent damage by prematurely activated trypsinogen?

-trypsinogen is only activated in small intestine -the brush border (intestinal epithelium lining) in the duodenum; since there is many villi that creates fuzzy border -->enzymes on the villi will cleave trypsinogen and activate it (cut off inhibitory peptide); creates active trypsin (protease) -some diseases where trypsin becomes prematurely activated; damages cells in exocrine pancreas and can cause pancreatitis -pancreatic cells have 2 ways to prevent trypsin activation: 1. secrete a blocking peptide to bind catalytic domain of trypsin to prevent it from cleaving any peptide bonds (inactivates it) 2. secretes enzymes that can degrade active trypsin

water absorption - the vast majority of fluid reabsorption occurs where? the rest of the water absorption occurs where? how much fluid is lost through the respiratory system? how much fluid is lost through the urinary system? how much fluid is lost through the lacrimal fluid of the eyes? how much fluid is lost through sweat?

-vast majority of fluids are being reabsorbed in the small intestine (8000 mL) and the rest is being reabsorbed in the large intestine (900 mL) -losing a lot of fluids through other systems: -->respiratory tract: have to humidify air; lose about 300-400 mL of water a day by breathing -->urinary system: we lose 800-2000 mL of urine a day -->eyes: uses 150-300 mL of lacrimal (tear) fluid (keeps eye surfaced moist) a day and we lose about 30% through evaporation -->sweat: at rest we can lose about 500-700 mL of fluid through sweat and 15000 mL max

water absorption - what does water follow? what does this create (___ gradient)? is most water transport transcellular or paracellular? what determines which direction water moves? if there is more salt in the lumen what happens? if there is more salt in the interstitial fluid what happens? all body compartments maintain the same what?

-water follows salts (Na); by moving Na from one side of the endothelium to the other then it creates an osmotic potential/gradient -most water transport is transcellular through aquaporins; allow water to flow bidirectionally but osmotic gradient determines which way it moves -->more salt in lumen, then water flow from cells/blood to lumen -->more salts in interstitial fluid, then water flows into body -once water is pulled in, it will enter the blood -all body compartments maintain same osmolarity

ghrelin signals to the brain - what happens when food is brought into the stomach? this is _____ feedback. what happens to the ghrelin signal after food is brought in? what happens to metabolism?

-when food is brought in after feeling hungry, then this will distend the stomach; this leads to decrease in ghrelin released -->negative feedback: the stimulus (an empty stomach) signals to brain through ghrelin, then we bring food into stomach and distention reduces ghrelin signal -->then we feel full and switch to anorexigenic pathway; we digest and move food into intestines

what are the 3 phases of coordination of digestion?

1. Cephalic phase 2. Gastric phase 3. Intestinal phase

Cephalic phase of digestion - occurs when? what stimuli cause this? the output of the CNS, the parasympathetic response innervates which two parts of the digestive tract? in the salivary glands serous cells are activated to secrete more what? serous cells also secrete more ___ enzymes. sympathetic outflow from adrenal medulla means more epinephrine enters the blood and causes increased secretion of what from mucus cells? parasympathetic response in the stomach promotes secretion of what from parietal cells? increased release of what from G cells and ECL cells? what happens to D cells? what do chief cells secrete?

1. Cephalic phase: head phase; occurs before food enter digestive system (sight, smell, taste) -sensory stimuli are received by CNS and output of CNS, the parasympathetic response, will: -innervate salivary glands -->activate secretion of serous cells (more NaCl with water following) to inc saliva production -->inc serous secretion of digestive enzymes -->inc sympathetic outflow through adrenal medulla; epinephrine enters blood to activate beta receptors on mucus cells to stimulate mucus secretion and bicarbonate (inc salivation) -innervation of stomach -->promotes secretion of acid (HCl); G cells inc release of gastrin which will activate ECL cells to release histamine to promote acid secretion by parietal cells -->inhibits D cell to release somatostatin locally -->chief cells secrete digestive enzymes

salt (NaCl) absorption small intestine - what are 3 ways (transporters) that Na can be brought into the enterocyte cell? how does Na exit the cell? what are 2 ways that Cl can be brought into the cell (transporter)? what is the paracellular way that Cl can be taken into the interstitial fluid?

1. Na absorption: -->Na/glucose cotransporter (IN SMALL INTESTINE): use Na gradient to bring Na in -->Na/AA cotransporters (IN SMALL INTESTINE): use Na gradient to bring Na in -->Na/H exchanger (IN LARGE/SMALL INTESTINE): use Na gradient to bring Na in -->Na can then exit at the basolateral membrane through Na/K ATPase 2. Cl absorption: -->Cl/bicarbonate exchanger (IN LARGE/SMALL INTESTINE); brings in Cl and releases bicarbonate (from CA converted into HCO3 and H+) -->Cl can then exit through basolateral membrane through a K/Cl cotransporter (both same direction out) -->Na+ taken into blood is going to draw Cl through the paracellular pathway also

what are the 3 major salivary glands? how many salivary glands are there?

1. Parotid 2. Submandibular (below mandible) 3. Sublingual (below tongue) -three paired salivary glands on both sides of the head so 6 total -main function of the salivary glands is to secrete things

Key functions of digestive system (4) and briefly describe. what are the 2 types of digestion? what is peristalsis? what is chyme?

1. Secretion: movement/transport/diffusion of substances from inside body across epithelial barrier to outside world -->lumen is the gut cavity so secretion is movement of molecules form inside to outside world of the lumen 2. Absorption: taking up molecule from outside world (lumen) passing epithelial barriers into body 3. Digestion: -->mechanical: (contractions of smooth muscle) physical forces break apart substances -->chemical: chemical reactions breaking down molecules (ex. enzymes) 4. Motility: smooth muscle layers allow exertion of forces on food to propagate it through digestive tract (peristalsis); allows chyme (thick semifluid mass of partially digested food and digestive secretions) through digestive tract for removal as waste

what are 4 things that can be obtained from the digestive system?

1. carbohydrates (polysaccharides, monosaccharides) 2. proteins (peptides, amino acids) 3. lipids (fatty acids, cholesterol) 4. water and electrolytes (Na, Cl, Ca, Fe)

what are 3 key mechanisms of the digestive system?

1. coordination of digestion -->cephalic phase -->gastric phase -->intestinal phase 2. pathogen defense (pathogen and fungi) 3. energy balance (hunger vs satiety)

glucose homeostasis (low blood glucose) - what 3 things does glucagon do in the liver? what does glucagon do in the adipose tissue (fat)?

1. glucagon to liver: -->alpha cells release glucagon in response to low blood glucose -->glucagon signals to liver to start breaking down glycogen to release glucose into blood -->stimulates gluconeogenesis; new synthesis of glucose through metabolism of amino acids 2. glucagon to adipose tissue (fat): -->stimulates glycolysis (breakdown of lipids) to release fatty acids to enter blood and be used by different tissues for energy production (to spare glucose)

amino acid and peptide absorption - individuals AAs are transported across the apical surface how? is dependent on a ____ gradient created by? how do individuals AAs exit the cell? how are di/tripeptides transported through apical membrane? is dependent on a ____ gradient created by? how do di/tripeptides exit the cell? how can intracellular peptidases create another path for di and tripeptides to exit the cell? how do small peptides enter and exit the cell?

1. individual AAs: are transported across the apical surface using Na/AA cotransporter (same direction) which uses the Na gradient from ATPase -->once absorbed they are transported across the basolateral membrane by AA transporters (facilitated diffusion; independent of Na gradient) 2. dipeptides and tripeptides: transport is coupled to a H/peptide cotransporter (PepT1) which uses a H+ gradient from Na/H exchanger (Na in and H out) -->H+ flows back into cell using gradient and also influx of peptide -->di or tri peptide then transported across basolateral membrane through a peptide transporter -->transport can also be through intracellular peptidases that can cleave the peptide bonds in di or tri peptide and convert them into AAs to be transported across basolateral membrane through AA transporters 3. small peptides: too big to be directly moved through transport protein in membrane; instead there are receptors that bind peptides to trigger endocytosis into and endosome -->endosome trafficked across cell then fuse at basolateral side releasing small peptides (transcytosis)

glucose homeostasis (high blood glucose) - what 4 things does insulin secretion do in the liver? what 4 things does insulin do in skeletal muscle ? what 2 things does insulin do in adipose tissue (fat)?

1. insulin to liver: -->stimulates beta cells (pancreas) to release insulin -->insulin in blood goes to liver; hepatocytes inc glycogen synthesis -->glycogen is a polymer of glucose molecules that traps glucose (remove from blood) to store it in glycogen chains in liver -->insulin also stimulates liver to inc fatty acid synthesis; releases them to blood so other tissues can use it for metabolism 2. insulin to skeletal muscle: -->muscle and fat cells have special glucose transporters (GLUT 4); located inside vesicles inside the cell but insulin causes them to be inserted into PM to bring glucose in (clear it from blood) -->GLUT 4 transporters internalized when there is low levels of glucose -->insulin promotes retention of glucose (glycogen synthesis) -->insulin stimulates amino acid intake for protein synthesis 3. insulin to adipose tissue (fat): -->insulin also has GLUT 4 transporters to insert into PM to uptake glucose -->insulin promotes lipid storage; turns it into fat to store it

saliva is made up of mostly what? of the ions in saliva, what are the two high and low ones? what 3 types of proteins/enzymes are in saliva?

1. mostly water -->serous cells pump salts to get water to follow 2. ions: in saliva that leave the salivary gland are -->highest: K+ and bicarbonate -->lowest: Na+ and Cl- (initially) 3. proteins -->mucins -->digestive enzymes; salivary amylase which breaks down starches and large polysaccharides into smaller polysacs -->immune factors; lysozyme, IgA, defensins

feeding behavior - what are 3 general feeding behaviors that influence bringing food in?

1. simple behavior in which the hypothalamus monitors peripheral indicators of stomach full or empty, nutrient balance, energy storage, and blood glucose 2. conditioned feeding responses: ex. feel the need to eat when you watch TV overrides nutrient signals 3. emotional/health: emotional triggers can lead to activation of feeding circuits to also override nutrient signals; sickness starves pathogens of nutrients

gastric phase of digestion - occurs when? what two receptors detect that food has entered the stomach? activation of local enteric or gut NS is associated with ____ neural reflexes. short neural reflexes will, ramp up what two things to increase chemical and mechanical digestion ?

2. gastric phase: when food actually hits the stomach -enteric gut NS: food has entered stomach and sensory afferents will detect stretch (mechanoreceptors), nutrients/chemicals in food and rise in stomach pH (chemoreceptors) -->short neural reflexes: activated first; involves activation of local enteric or gut NS -->stimulation of short neural NS will ramp up acid/enzyme secretion (chemical digestion) and ramp up smooth muscle contraction (mechanical digestion)

intestinal phase of digestion - occurs when? in short neural reflex local stretch and chemoreceptors detect what? short neural reflex activates enteric NS both locally in intestine and in stomach to inhibit what?

3. intestinal phase: when broken down food / chyme entering the duodenum -short neural reflex: -->stretch receptors detecting expansion due to presence of chyme -->chemoreceptors detect a drop in pH (since chyme comes with a lot of gastric acid) -->activates the enteric NS, both locally in intestine and in upper regions of stomach; intestines can then inhibit gastric motility so stomach stops sending them more chyme until intestine can process present chyme

What is a zymogen?

An inactive enzyme precursor

pancreas in digestion - what are the endocrine cells of the pancreas called (islets of?) what are the 4 types of endocrine cells and what does each do? which type is the most common? where do glucagon and insulin go? where does somatostatin go? what does pancreatic polypeptide do?

endocrine cells are called the Islets of Langerhans: 1. alpha cells (20%): secrete glucagon 2. beta cells (65%): secrete insulin -->alpha and beta cells release into the interstitial fluid to be picked up in blood (hormones) 3. delta cells 10%): secrete somatostatin -->goes into blood travels throughout body to inhibit digestive cells 4. gamma cells (rare): secrete pancreatic polypeptide -->regulates function of other pancreatic endocrine cells