PATHOPHYSIOLOGY EXAM 5—DIGESTION

PART I: GENERAL ANATOMY AND PHYSIOLOGY OF CEPHALIC AND GASTRIC

DIGESTION

1-What are the general effects of sympathetic and parasympathetic on digestion and
sphincters?
-sympathetic: slows digestion and constricts sphincters
-parasympathetic: speeds digestion and relaxes sphincters
2-Explain the difference between mechanical and chemical digestion.
-mechanical: increased surface area
-chemical: break chemical bonds (enzymatic)
3-What kinds of sugars can we absorb and how does it get transported?
-mono and disaccharides using 2ndary active transport
4-How do fats get absorbed?
-diffuse
5-How do peptides get absorbed?
-peptides as long as 3 amino acids get across
6-Define the following: ingestion, mastication, propulsion, deglutition, peristalsis, peristaltic
waves, mass movement, mixing (segmental contractions), secretions, digestion, absorption,
elimination, defecation, regulation.
-ingestion: introduction of solid or liquid food to the stomach (mouth & NG tube)
-mastication: chewing (mechanical digestion increases surface area)
-propulsion: move from one end to the other
-deglutition: swallowing
-peristalsis: moves material through most of the GI tract
-peristaltic waves: relaxed smooth muscle in front of the bolus and strong contraction behind
to drive along
-mass movement: large segments in large intestine stimulated by eating with a 30 minute
delay
-mixing-segmental contractions of the small intestine-mix with digestive enzymes
-secretions-mucus (lubrication), water, enzymes
-digestion-breakdown organic molecules into their component parts
-absorption: movement from the digestive tract to the circulation
-elimination: removal of waste from the body
-defacation: pooping
-regulation: locally and generally (vagus)
7-What are tunics and names the them.
-tunics are the layers of the digestive tube from esophagus to anus
-from lumen to edge: mucosa, submucosa, muscularis externa, serosa
8-What is the function of the mucosa?
-inner layer containing the mucous epithelium; mostly composed of stratified squamous
because of mixing and friction, some is columnar so only limited secretion
-lamina propria which is loose connective tissue which is mainly collagen and elastin
-muscularis mucosae is a thin smooth muscle layer, contractions causes folds and ridges
9-What is the function of the submucosa?
-thick connective tissue with nerves and blood vessels and skeletal muscle
-contains the submucosal plexus which is the parasympathetic nerve network
10-What is the function of the muscularis externa?
-contains circular and longitudinal smooth muscle except in stomach where there are 3 layers
of muscles—this is what makes peristaltic contractions
-contains myenteric plexus has nerve fibers and parasympathetic cell bodies between the
longitudinal and circular muscles layers
11-What is the function of the serosa?
-it is the outermost layer known as the adventitia which is a connective tissue layer known as
the visceral peritoneum in the peritoneal cavity which is covered by squamous epithelium
12-What is the mesentery?
-all blood vessels and lymph and nerves enter and exit the GIT like a sheet of connective
tissue
13-Why is lymphatic drainage important in the GIT?
-because Kf is so big the oncotic pressure is high so lymphatic drainage is important
14-What tunic is when a bleeding ulcer occurs?
-it must get to the submucosa
15-What is special about the enteric nervous system?
-it is the nerves for the GIT and it is known as the little brain because there are so many
neurons there
16-What are the 2 major levels of control that are the neuronal regulation?
-extrinsic regulation: autonomic nervous system (symp and para)
-intrinsic regulation: the enteric nervous system/intramural plexus within the wall of the
GIT
17-What is the role of the sympathetic nervous system on the GIT?
-innervates the intramural plexus, not the GIT directly-decreases motility and secretory
activities, inhibits muscularis externa via the intramural plexus and stimulates the muscularis
mucosae and certain sphincters
18-What is the role of the parasympathetic nervous system on the GIT?
-increases motility and secretory activities, the vagus nerve stimulates all but the colon,
rectum and anus, the nerves terminates on the intramural plexus
19-What are some characteristics of the enteric nervous system?
-the combination of the myenteric an submcosal plexuses
-has many neurons, innervate all area of motility and secretion
-all sorts of receptors send afferent activity to the CNS and the enteric nervous system
which then in the medulla integrates the info and through efferent activity of the symp and
parasymp alters activity of the enteric nervous system
20-Overall, how is the GIT controlled?
-the autonomic indirectly controls the GIT but in the absence of it motility and secretions
continue due to the enteric nervous system
21-What would happen if we had a spinal cord injury?
-we would lose more symp than parasym
22-What are the types of saliva?
-serous (1-1.5 L/day)-watery; has amylase that breaks covalent bonds b/w glucose molecules
and complex carbos, also has lysozymes that is antibacterial
-mucus viscous fluid that lubricates
23-What are the salivary glands?
-parotid-largest, serous
-submandibular-serous & mucosal (gleak gland)
-sublingual-1st mucosal, 2nd serous
-all cells surrounding the gland ducts are cuboidal for secretion
24-Describe how the saliva make up is formed?
-the acinar cells secrete amylase in the bulb and as it moves down the duct it is modified with
water, K, HCO3 and Na and Cl gets absorbed
25-What are the three phases of swallowing?
-voluntary phase: form bolus and push it back using somatic muscles
-pharyngeal phase: reflex initiated by tactile receptors in pharynx (nose and glottis seal off-
no muscle movement, moves due to food moving)
-esophogeal phase: constriction of the smooth muscle of the pharyngeal constrictor muscle
and relaxation of upper esophageal sphincter (autonomic)
26-Why does milk come out our nose when we laugh?
-the soft pallet relaxes and the milk goes into our nasopharnyx
27-What are the roles of the upper and lower esophageal sphincter?
-upper is to keep food out and air out and lower is to keep food in the stomach
28-What is a hiatal hernia?
-moving of stomach out of the diaphragm (peritoneal) into thoracic cavity
29-What are two things that cause hiatal hernias?
-relaxation of the lower esophageal sphincter
-GERD
30-What is another name for lower esophageal sphincter?
-the cardiac sphincter
31-What relaxes the cardiac sphincter?
-increased parasympathetic activation
32-What is achalasia?
-over contraction of the cardiac sphincter, resulting in decreased entrance of food to the
stomach with swallowing (kid spit up)
33-What does sympathetic activity do to the sphincters?
-it increases constriction of the sphincters
34-What is the sphincter at the bottom of the stomach?
-the pyloric sphincter
35-What happens if the pyloric sphincter doesn’t open enough?
-it can cause GERD
36-What are the parts of the stomach?
-fundus is upper portion; body is the largest portion; greater and lesser curvature are the
curved parts; antrum is the pyloric region where the stomach begins to narrow and is the
thickest portion of the stomach because of all of the smooth muscle
37-What is rugae?
-large wrinkles of the stomach
38-What lines the stomach?
-simple columnar epithelial cells with gastric pits and gastric glands that produce fluids
39-What are sphincters essentially?
-the highest concentration of smooth muscle
40-What is chyme?
-it is mixture of secretions and food
41-Where do ulcers occur and where most frequently?
-esophagus, antrum and DUODENUM
42-Explain the steps that regulated stomach secretions?
-cephalic phase: regulated by the medulla in response to smells, thoughts, chewing (increase
secretion results)
-gastric phase: with presence of food in stomach much is secreted due to stretching and
mechanoreceptors
-intestinal phase: regulates HCl production, chyme enters duodenum through hormonal and
neuronal control
43-What are some things secreted during the gastric phase?
-pepsinogen, HCl, intrinsic factor and gastrin
44-What are some things that control gastric secretions?
-pH below 2 inhibits gastric secretions and pH above 3 stimulates gastric secretion
45-What are the cells responsible for gastric secretions and explain?
-lining cells: surface mucosal cells & mucus neck cells that produce mucus to protect the lining
of the stomach
-secretary cells: parietal & chief cells
-parietal: produce HCl that kills bacteria and create an environment that is necessary
for our stomach enzymes to work, also makes intrinsic factor that helps us absorb B12 for
absorption in the ileum
-chief: produce pepsinogen that is cleaved to pepsin at an acid pH that breaks covalent
bonds in proteins to make smaller peptides (doesn’t work in duodenum b/c of pH—likes 3)
-endocrine cells: regulatory hormones are secreted-regulated secretions, alter composition
of secretions, alter the level of motility of the GIT by altering smooth muscle contractions
46-How is the rate of emptying through the pyloric sphincter regulated? Based on what?
-content size, is duodenum ready for the acid to be neutralized by bile salts, contents of the
food (fatty or not-does emulsification need to occur)
47-What emulsifies fat?
-bile enzymes
48-What are the major transporters involved in H+ secretions to regulated pH?
-ATPase on luminal side that pumps out H+, pumps in K+, pumps out Cl-,
-on the basolateral side there is a countertransporter pumping HCO3 out and Cl in, and K out
and a Na/K exchanger pumping K in the cell
49-What are the things in the GIT that will respond to sym and parasymp stimulation?
-muscularis externa, muscularis mucosae, endocrine cells, secretory cells, blood vessels
50-What things do we detect to regulated gastric emptying?
-acid, fats, hypertonicity, amino acids detected into duodenum
51-List the three phases of gastric secretions and explain each one.
-cephalic, gastric and intestinal
-cephalic: taste, smell or chewing stimulates the vagal nuclei in the medulla, this releases
parasympathetic sensations via the vagal nerve goes to the stomach to the myenteric plexus
of the stomach, this stimulates secretions of parietal and chief cells and stimulates gasrin
secretion by endocrine cells, the gastrin goes through the circulation and back to the
stomach where it further stimulates chief and parietal cells
-gastric: efferent vagal stimulation will stimulate parietal, chief and mucus cells. The low pH
will inhibit these secretions; stomach distension will also locally stimulates secretions
-intestinal: the presence in the duodenum of chyme with a pH > 3 or amino acids and peptides
stimulates gastric secretions through the vagus nerve pathway and secretions of gasrin. If
in the duodenum there is hypotonic chyme or a pH of lower than 2, or chyme with fat
digestion products, this will inhibit gastric secretions by three ways.
52-What are the three ways that gastric secretions will be inhibited?
-afferent vagal impulses inhibit efferent impulses from the medulla
-secretin inhibits gastrin secretion in the duodenum
-secretin, gastric inhibitory polypeptide and CCK produced by the duodenum will inhibit
gastric secretions in the stomach
53-Gastrin: what is it, where does it come from, what does it do, how is it regulated, what
does it regulate, what is the pathway it follows?
-comes from G-cells in the stomach walls
-production and release are stimulated by stomach distension and peptides in the chyme and
vagal stimulation
-it serves to stimulate the chief and parietal cells (pepsinogen and acid) of the stomach lining
to increase gastric secretions
-causes constriction of the pyloric sphincter to decrease emptying and increased
contractions of the stomach
-gastrin from the G cells goes into the stomach, into portal circulation, liver, heart, arterial
circulation and effects chief and parietal cells to make HCl
54-What is special about G-cells and gastrin?
-it is the only one that secretes directly into the stomach
55-Why does it need to go into the blood too?
-because that is the only way that it will effect gastric emptying rate
56-Secretin: what is it, where does it come from, what does it do, how is it regulated, what
does it regulate, what is the pathway it follows?
-comes from S-cells in the duodenum
-production and release are stimulated by the low pH in the duodenum
-it inhibits the secretion of the parietal cells and chief cells in the stomach
-it stimulates the pancreatic ductal cells to increase bicarbonate production and bile
secretions by the gall bladder
-released in the blood stream of the duodenum and goes into portal circulation to liver where
bile is stored and now released, to the heart to arterial circulation, to the pancrease where it
stimulates ductal cells to release bicarbonate
57-What is the most important part of the digestive tract and why?
-the duodenum because most solute and water is reabsorbed here
58-Cholecystokinin (CCK): what is it, where does it come from, what does it do, how is it
regulated, what does it regulate, what is the pathway that it follows?
-from the I-cells in the duodenum
-production and release are stimulated by fats primarily but also proteins
-stimulates the production (hepatocytes) and the release (gall bladder) of bile into the
duodenum and secretions of pancreatic enzymes
-in the presence of fat it inhibits gastric emptying and it plays a role in being satisfied
-inhibits gastric secretions because it is trying to slow down things
-the I-cell produce it into the blood where it goes into portal circulation and stimulates the
gall bladder and liver to produce and release and then on to the heart and arterial circulation
where it stimulates the acinar cells of the pancreas to release pancreatic enzymes to be
dumped into the duodenum
59-How does it get to the duodenum?
-the bile and the enzymes go in via the sphincter of Oddi also known as the common bile duct
60-What would sympathetic stimulation do to the Sphincter of Oddi?
-it would contract and then there would be less enzyme dumped in and that would slow
digestion
61-Gastric Inhibitor Protein (GIP): what is it, where does it come from, what does it do, how
is it regulated, what does it regulate, what is the pathway that it follows?
-comes from K-cells in the duodenum
-fats and carbohydrates (low protein) in the duodenum stimulate both production and release
-inhibits motor and secretory activity of the stomach, inhibits gastrin production and
stimulates the release of insulin from the beta cells of the pancreas, also stimulates the
production of pancreatic enzymes from acinar cells
-released by K cells in duodenum and goes into portal circulation to liver, heart and arterial
circulation and to stomach where it stops the acid secretion, stomach mvmt etc, and to the
pancreas where it stimulates insulin release, and enzyme release
62-What is another name for GIP?
-glucose dependent insulinotropic peptide
63-How does GIP get a jump on things for our bodies?
-it stimulates insulin release before our blood glucose levels get too high
64-What is the fastest moving meal and what is the slowest moving meal?
-fastest is carbos, soups
-slowest is fat, protein
65-What are a few random things that will stimulate motility?
-alcohol and caffeine

PART II: MOVING FROM GASTRIC TO THE INTESTINAL PHASE OF DIGESTION

--DUODENUM—

1-To this point we have regulated the content of the chyme that enters the small intestine
why regulating what?
-size, pH, specific content
2-Which of the above is the most important overall factor?
-fat
3-How much water is absorbed in the small and large intestine and what segments of the
small intestine do the most absorption?
-92% water in the small intestine, 8% in large intestine and duodenum and jejunum is where
most absorption occurs
4-What is the difference between mechanical digestion and emulsification of fats?
-emulsification doesn’t break chemical bonds, it is a mechanical process whereas lipases are
enzymatic and break chemical bonds
5-Give some characteristics about the duodenum that are important.
-it is the first 5% of the small intestine, most nutrients are absorbed here, has a bump
known as the major duodenal papilla, location of the sphincter of Oddi (hepatopancreatic
ampulla), the lesser duodenal papilla is there that is the exocrine part of the pancreas
secretion where the ductal and acinar cells that produce lipases, water and bicarbonate
secrete into
-has a brush border (increase SA x600)
6-What comes out of the sphincter of Oddi?
-bile duct and pancreatic duct meet and come out there
7-What’s important about the brush border other than it increases surface area?
-it has enzymes bound to it such as nucleases, disaccharidases, peptidases
8-What are the two kinds of contractions that occur here?
-segmental: mix contents
-peristalitic: unidirectional movement of content
9-What kind of stimulation would contract the sphincter of Oddi?
-sympathetic (decrease digestion)
10-What kind of stimulation would contract the gall bladder?
-parasympthetic (increase digestion)
11-How many ways can pancreatic secretions enter the duodenum and how many ways can the
bile enter the duodenum?
-pancreatic secretions can enter 2 ways: Sphincter of Oddi and the lesser duodenal papilla;
bile can only come in via the Oddi
12-What else is secretes with the gall bladder?
-the liver secretions
13-What happens if someone blocks the bile duct? (stones)
-jaundice will ensue and bilirubin will accumulate and you get yellow and the fat in your skin
will get emulsified and itch
14-What are the three major layers of the duodenum?
-the mucosa (brush border), submucosa, muscle layer
15-Explain why people who are immune suppressed get sepsis?
-not from outside bacteria but from portal blood because that normally has bacteria in it but
it goes into the liver where the Kuppfer cells clean the blood up
16-Why do we get bacteria in our blood here?
-Kf is very high so there is a lot of absorption and drainage, as a result we have lots of
lymphatics there
17-What is the name of the lymphatic that goes into each villus?
-central lacteal
18-What else is in a villus?
-the central lacteal, artery and vein

--JEJUNUM--
19-What are the major difference between the duodenum and the jejunum?
-it 45% of the small intestine and it is narrower and has less brush border
20-What is the junction with the large intestine called?
-the ileocecal sphincter
21-Name all the sources and the amounts of fluid that enter the GIT every day?
-2000 mL ingested, 1500 mL of saliva, 2000 mL of gastric secretions, 500 mL of bile, 1500
mL of pancreatic juices
22-Where does all that get absorbed?
-8500 mL by small intestine
-400 mL colone
23-So we ingest _______ Liter and we reabsorbe _______ liters?
-9 liters and 8.9 liters
24-What proportion of the small intestine is made up of the ileum?
-50%
25-Where do you find the appendix?
-in the lower right quadrant

--LARGE INTESTINE—
26-What are the components of the large intestine?
-cecum, colon, rectum and anal canal
27-What percent of the chyme becomes feces?
-90%
28-What is mass movement?
-peristaltic contractions that occur 15-30 minutes after eating that pushes the poop along
29-What is the cecum?
-it is the first portion of the large intestine where there can be infections because of lack of
lymph drainage, can lead to appendicitis and peritonitis
30-What is the colon?
-it has four parts the ascending, transverse, descending, sigmoid
31-What is the rectum?
-straight section between the sigmoidal colon and the anal canal
32-What is the anal canal?
-internal anal sphincter (autonomic) and external anal sphincter (somatic)
33-What are most of the contractions of the large intestine?
-segmental not peristaltic
34-What are haustra contractions?
-back and forth moving segments of the large intestine
35-Where does gas get trapped?
-in the right hand corner where the ascending meets the transverse

--LIVER--
36-Speak generally about the liver?
-largest organ in the body, located under the right diaphragm, processes nutrients,
synthesizes new molecules and detoxifies chemical, organized in lobules, blood flow from the
hepatic artery and the portal vein to the central vein and through the sinusoids
37-Where does the hepatic artery originate?
-the abdominal aorta
38-Where does the portal vein?
-all portions of the GIT
39-Explain in detail the blood flow to, within, and out of the liver?
-blood comes in via the hepatic artery and is oxygenated, blood also comes from the portal
vein with lots of nutrients bacteria and other things from the GIT and they mix in sinusoid.
The sinusoid is lined with fenestrated cells and Kupffer cells that are macrophages that
clean shit up and then there are the prankable cells known as hepatocytes and they absorb
blood and produce bile and secrete it into the bile duct for enterohepatic circulation. The
remaining blood goes into the central vein and back into circulation
40-What are the two drainage points for the liver?
-bile ducts and central vein
41-Where do heme degradation products go?
-into the bile duct
42-Explain enterohepatic cycling?
-eat drug and gets absorbed into the mesenteric vein, to the portal vein, to the liver, into a
bile duct to be excreted into the stomach and return to central circulation
43-What are the components of bile?
-bile acids, cholesterol, bile pigments
44-Where do bile pigments come from?
-heme degradation
45-Where do gall stones form from?
-bile salts that fall out of solution
46-What is the function of bile?
-neutralize acids in chyme because it contain bicarbonate-works like a surfactant, not a
lipase: mainly emulsifies fat, aid in excretion of bilirubin, stored in the gall bladder and is
secreted when gall bladder is contracted which is caused by CCK or secretin
47-What are the two main functions of bile?
-emulsifies and neutralizes
48-Is the sphincter of Oddi usually open or closed?
-closed
49-What does the sphincter of oddi do?
-regulates the release of bile, opens up with parasympathetic stimulation, CCK and gastrin
stimulate the opening of sphincter of oddi
50-Where does bicarbonate come from?
-bile and ductal cells
51-What is the relationship between bile and enterohepatic cycling?
-bile acids are released with a meal and emulsify fats and are absorbed with the fat and
enter the portal circulation, are then actively taken up by the hepatocytes and re-secreted
into the bile duct (only 20% is loss in feces)
52-What is glycogen and what is it all about?
-it is the storage form of sugar in the liver, its formation is stimulated by insulin and
inhibited by glucagon
53-Where is all the iron in the body?
-67% is bound in heme, 30% is bound to ferritin, 3% is bound by transferring
54-How many binding sites for iron does heme have?
-4
55-How much iron is found in the blood?
-only 3%
56-What are the steps that explain the process by which iron is transferred from the
intestine to the bone marrow for more heme to be made?
-iron in intestine is bound to tranferrin when absorbed
-it gets delivered to the erythroblasts in the bone marrow
-it gets incorporated into heme
-the RBC live for 120 days and are then degraded when they can’t deform to go through the
spleen
-splenic macrophages and kupfer cells in the liver degrade the old ones
-hemoglobin is degraded and the globin is catabolized to its amino acids and the iron is
recycled
-the porphyrin ring is degraded to biliverdin by heme oxygenase which is then comverted to
bilirubin by biliverdin reductase
-bilirubin is then transferred to the liver bound by albumin and conjugated with a sugar
molecule by glucuronyl transferase and now it is water soluble
-bilirubin glucuronide is then secreted into the bile in the gall bladder for secretion into the
small intestine
-in the intestine some of the bilirubin is converted into urobilinogen and some is lost in the
feces and some of which is reabsorbed and excreted by the kidneys
57-What happens to half-life of RBC if spleen is removed?
-it increases
58-Where does heme get broken down to release the iron for recycling?
-in the macrophage
59-Explain this step again.
-heme is reduced by heme oxygenase to biliverdin, water and iron3+ and gets bound to
ferritin immediately
-the biliverdin then gets reduced by biliverdin reductase to bilirubin (all occurs in phage)
60-What happens if you are immunocompromised?
-you have less macrophages so heme accumulates
61-What happens next?
-you have bilirubin that goes to the liver where the hepatocytes conjugate the bilirubin
62-What happens if you have hepatitis?
-you accumulate unconjugated bilirubin
63-What happens next?
-the conjugated bilirubin travels to the gall bladder and down the bile duct to duodenum
where some of it gets converted into urobilinogen
64-What happens if there is a blockage in the bile duct?
-conjugated bilirubin accumulates
65-What happens once it become urobilinogen?
-some of it gets pooped out and some gets reabsorbed after getting unconjugated by the
bacteria in the gut and peed out because it is freely filtered
66-What are the overall percentages that tell what happens to bile salts?
-15-35% are lost in the feces and 65-85% are reabsorbed and are unconjugated by bacteria
in the gut
67-What are the two different kind of iron?
-there is element that is in veggies and vitamins and then there is that which is in red meat
68-Overall, what is important to know about iron?
-it is stringently controlled because of the oxidative damage that can be caused, heme iron is
fat soluble and transported with proteins so it is not easily controlled, eating too much red
meat can give cardiovascular disease because of oxidative damage
69-What is hemochromatosis?
-liver impairment that leads to too much iron falling out of solution and causing problems and
people get heart disease at a young age and die early in life
70-Again explain the heme degradation process and where the steps occur?
-the RBC get old and they go through the spleen and don’t fit so that means they need to get
broken down so the macrophages take them up either in the spleen or the liver by heme
oxidase and biliverdin reductase to bilirubin that is bound to albumin in the blood and then in
the liver it gets conjugated by hepatocytes and put in bile duct and make their way to the
small intestine via the bile duct, where it can get broken down by bacteria in the intestine
into urobiligen and shit out or can get reabsorbed and peed out, or urobiligen can get into the
enterohepatic circulation
71-What happens to the iron?
-when the phage breaks it down it gets recycled to transferring in the plasma and then back
to new hemoglobin molecules in RBC
72-When the RBC gets broken down, what happens to the globin?
-it gets broken down into the amino acid pool
73-This is the last time, go over the cycle again.
-RBC destruction in the macrophage, the hemoglobin is broken, the globin goes to the aa pool
and the iron goes into the iron pool, the biliverdin that results from heme oxygenase is
unconjugated at first at gets reduced by biliverdin reductase, from there it binds with
albumin in the blood and gets conjugated by the hepatocytes in the liver and then is excreted
in the bile where it gets turned into urobilinogen and can be peed out if reabsorbed into
central vein or pooped out if not
74-What is different about conjugate vs unconjugated?
-conjucgated is much more water soluble
75-What are the things that CCK stimulates?
-gallbladder contraction and relaxation of sphincter of Oddi
76-What does gastrin do again?!*!*!*!*!*!*!*!*!*!*
-it increases gastric emptying rate, increased in motility and increase parasympathetic
activity yet it still causes increase contraction of pyloric sphincter (only one to do this, all
the other slow up the process)

--PANCREAS—
77-What does the pancreas secrete that is exocrine?
-ions and bicarbonate from the ductal cells as well as protein degrading enzymes, increases
osmolarity and water follow it
78-What is important about this pancreatic secretion?
-it neutralizes acids that are in duodenum
79-What stimulates it?
-CCK
80-What kind of protein degrading enzymes does it produce?
-trypsin, chymotrypsin, carboxypeptidase
81-Where does the water and the bicarbonate come from again?
-ductal cells not the acinar cells
82-What kind of cells produce the enzymes?
-acinar cell
83-What is the most abundant enzyme produced?
-trypsin
84-What is the deal with trypsin?
-it is secreted in the inactive form but is active when it is cleaved, it is inactivated by trypsin
inhibitor
85-How does trypsin inhibitor inhibit trypsin?
-it binds to it and forms typsinogen which is what is originally secreted by the acinar cells
86-How are chymotrypsin and carboxypeptidase secreted?
-they are secreted in the inactive form that are activated by cleavage from trypsin and all
other proteases are activated by trypsin
87-What does this say about the trypsin inhibitor?
-that it will inhibit the production of the other proteases too
88-What is the main carbohydrate digesting enzyme?
-amylase
89-What is the main lipid degrading enzyme?
-pancreatic lipases and phospholipases that chemically breakdown lipids into fatty acids and
monoglycerides
90-What stimulates the secretion of acinar fluid from the acinar cells as well as the other
and why?
-CCK stimulates the acinar cells to produce acinar fluid with all the Na, K, HCO3, Cl
91-What is the deal with secretin and acinar cells?
-secretin stimulates the secretion of these acinar cells to but to release more bicarbonate to
bring up the pH
92-Where are these acinar cells located?
-in the pancrease to do their secretions
93-Explain the control of pancreatic secretions when food enters the duodenum?
-parasympathetic will stimulate it, CCK will stimulate it, food entering the duodenum, secretin
will be secreted by the presence of low pH in the duodenum
94-Where is secretin come from?
-ductal cells
95-What comes from acinar cells and what comes from ductal cells?
-enzymes come from acinar cells and bicarbonate comes from ductal cells
96-ACH and CCK stimulate what the most?
-stimulate the production of enzymes from the acinar cells more than the production of
alkaline fluid from the ductal cells
97-What effect does secretin have on the ductal and acinar cells?
-it has no effect on the acinar cells but stimulates the production of large amount of alkaline
fluid from the ductal cells
98-What stops the pancreas from secreting?
-sympathetic activity
99-What is the overall effect of these ducts and how do they work together?
-ACH and CCK cause large quantities of enzymes to be produced and stored in the acinar cells
or the ducts and when secretin stimulates the ductal cells to produce fluid it adds to the
concentrated enzyme and washes them down the duct to the duodenum by the major
duodenal papilla
100-How do these bicarbonate ions effect water movment?
-water follows where the bicarb, Na and K go
101-Explain the cycle of pancreatic secretion.
-acid and food from the stomach cause the release of secretin and CCK. Both get absorbed
into the blood stream and causes ductal cells to release water, bicarbonate (secretin) and
acinar cells secreted enzymes (CCK stimulated)
102-How is HCl buffered in the duodenum? What is the optimum pH for the pancreatic
secretions?
-HCl + NaHCO3  NaCl + H2CO3  CO2 + H20, the carbon dioxide diffuses into the blood
and we blow it off; optimum secretion pH is 8
103-Explain the peritoneum.
-serous membrane surrounds the cavity, visceral peritoneum covers the organs and the
parietal peritoneum covers the abdominal walls
104-What are mesenteries?
-connective tissue carrying blood vessels and nerves to hold the organs of the abdominal
cavity in place
105-What do the mesenteric veins converge to produce?
-the portal vein
106-Name some exocrine things and some endocrine things?
-exocrine-enzymes
-endocrine-CCK, secretin etch
107-Why doesn’t pepsin work in the duodenum?
-because it needs an acidic environment
108-Explain the absorption of water?
-8L/day: it is all by diffusion—as nutrients are being reabsorbed the water follows it through
the pores with a high Kf
109-Expain the absorption of ions?
-Na is the main one: 30 g are secreted into the GIT each day and 8 g are eaten everyday
-it is actively transported into the basement membrane side and then the luminal side
absorbs sodium from the lumen passively by concentration gradient
-Cl moves with Na
-Ca is actively transported in the presence of vitamin D
-iron is absorbed by direct transfer from the intestinal epithelial cell to transferring
-Mg, K, PO4 are all actively transported
110-What is the carbonic anhydrase reaction?
-H + HCO3  H2CO3  carbon dioxide and water
111-Where does this ion absorption occur?
-in the jejunum
112-What happens in the ileum?
-sugars and amino acids are absorbed thanks to a cotransporter with sodium, H, HCO3 is
pumped out
113-Explain how proteins are absorbed?
-absorbed as small peptides (di, tri or single AA—mainly)—via a cotransporter with sodium
114-Explain absorption of carbohydrates.
-must be broken down into simple sugars such as glucose, galactose and fructose and they are
absorbed thanks to secondary active transport on a cotransporter with sodium
115-What are the steps that starches take?
-starchsmaltoseglucose
116-Where do the enzymes come from that break down lactose, galactose?
-brush border to ultimately make glucose for absorption
117-Explain the breakdown of the sugars further from lumen to blood stream?
-sucrose, maltose, lactose are carried from the lumen into the brush border where they are
broken down further and move into the intracellular region where they become the
monosaccharides such as glucose, galactose and fructose
118-Explain absorption of fats.
-broken down into monoglycerides and fatty acids which are absorbed in micelles with bile
salts
119-How do the bile salts contribute?
-they ferry products of fat digestion into the epithelial cells and then reenter the chyme to
transport more
120-Explain this process in more detail.
-micelles of bile salts and lipids diffuse into unstirred layer and the lipids partition out of the
micelles
121-Where are LDL and HDL formed?
-in the liver
122-Chemically, how does a bile acid work?
-a bile acid is amphipathic and it mixes in with lipids, cholesterol into mixed micelles and it is
easier to be absorbed, doesn’t break bonds only insertes in a polar-non-polar manner

--PATHOLOGY--
123-What are some causes of vomiting? Explain the process.
-defect in lower esophageal sphincter (cardiac) prevents contents of stomach from entering
duodenum, ingestion of ipecac, rancid substances, activation of chemoreceptors in the
medulla (alcohol)—these stimuli effect the vomiting center in the brain
-deep inspiration and closing of glottis which causes pressure in the thoracic cavity to
decrease and extension of esophagus, abdominal muscle contraction, relaxation of lower
esophageal sphincter, contraction of duodenum and pylorus of the stomach
124-What is the overall effect of vomiting?
-pressure in lower stomach gets bigger than the esophagus so the contents of the stomach
and duodenum are expelled
125-What is retching?
-when you are trying to vomit and your upper esophageal sphincter
126-What is the main thing that happens with vomiting?
-you lose H+ ions
127-What is the deal with diarrhea?
-the loss of greater than 200 mL of water a day
128-What are the two types of diarrhea and describe them each.
-osmotic diarrhea: due to too much solute in the GIT (salt water or non-absorbable things);
this happens with lactose intolerance
-secretory diarrhea: excessive secretion of fluid by mucosal cells or the inhibition to absorbe
salts; E.coli and cholera can make us secret water and ions, or tumors
129-What happens if we eat a bunch of cellulose?
-nothing because it is not in solution
130-What happens in cholera?
-fecal to oral transmission, ingest enough viable bacteria that produce toxins that prevent
the deactivation of adenylate cyclase, so cAMO levels in the cell rise to 10x their normal
values, this activates kinases which phosphorylate a bunch of membrane proteins that
increase the secretion of ions and therefore water into the gut, this causes severe
dehydration
131-What is the treatment for this?
-oral rehydration wither sterile sodium and KCl, NaCHO3 and glucose in clean water given
frequently until recovery—need high glucose or AA solution with sodium—juice is not good to
do this because there isn ‘t enough sodium in it
132-Why does the above method work so well?
-you want solute so that it gets absorbed and water follows it to replenish lost electrolytes
133-What are the three rehydration methods and which is the best?
-give iso-osmotic fluid-the co-transport of glucose and sodium induces a water to flow to
blood with ions but does not reduce extent or duration of diarrhea
-give hyperosmotic fluid-pulls water from body—BAD!
-give food-based substance-each polymer acts like a glucose as far as osmolarity goes but it
can get broken down and absorbed quickly so no osmotic penalty, water and ions are returned
to the blood quickly and less of both are lost in stool-the extent and duration of diarrhea are
reduced
134-What is giardia?
-a eukaryotic organism that is fecal to mouth in origin.-common in hikers, daycares,
-ingest, attaches to intestine, can’t reabsorb sodium so decrease water reabsorption,
damages epithelial cells, has a cyst stage that makes it hard to kill with chlorine or iodine,
can use Flagyl or metronidazole, furaxolidone which will kill the thing in 3-7 days but will take
weeks to fix the intestine (effects 20% of world pop)
135-What is the deal with constipation?
-2% of population, normal poop range is 3x a day to 1x a week
136-What are some causes of constipation?
-abnormality of the myenteric plexus of the colon to make megacolon so we get no mass
movement, spinal cord injury, MS, stroke, post-abdominal surgery, low diet, anti-depressents
(anti-cholinegics), opiates
137-What are some treatment options for constipation?
-improve diet, exercise, enemas, laxitives
138-What are the three kinds of ulcers? What are ulcers? Which is most prevalent?
-esophageal, gastric, duodenal; degradation of the mucosal layer and exposure and damage of
the underlying muscle layers, duodenal
139-Explain esophageal ulcers.
-GERD can cause it when chyme from the stomach enters the esophagus, either because the
sphincter is kicked or weakened,
-hiatal hernia
-treatment with antiacids, gastric secretion inhibitors, surgical tightening of the sphincter
140-Explain gastric ulcers.
-male and females get them equally and are only ¼ as common as duodenal ulcers
-caused by decreased mucus production, duodenal reflux at pyloric sphincter, ulcerogenic
drugs, pylori obstruction, head-trauma could cause increase parasympathetic activity and
increases gastric and intestinal secretions
141-Explain duodenal ulcers?
-most popular (15%) population, caused by H.Pylori, can be treated with antibiotics, can be
result of high gastrin levels, death of mucosal epithelium, release of toxins that stimulate
inflammation and ulceration
142-What is jaundice?
-yellowing of skin and eyes caused by too much bilirubin in blood either conjugated or
unconjugated, caused by high rate of hemolysis, disorders of the bile duct or liver cells
143-What are the two kinds and explain them?
-obstructive jaundice: blockage of common bile duct by a tumor or gallstone, feces will be
clay color, or disturbance of hepatocytes ro canaliculi (high conjugated)
-hemolytic jaundice: higher production of bilirubin than that which the liver can conjugate
and excrete into the bile do to too much loss of RBC (leads to high unconjugated)
144-What is hepatitis?
-inflammation of the liver; blood-blood, fecal to oral, get necrosis of hepatocytes so
unconjugated bilirubin will accumulate as a result, immune based cell mediated damage, death
of hepatocytes results
145-What is cirrhosis of the liver?
-one of the leading causes of death, slow developing fibrosis of the liver, gets hard,
increased shunt in liver so increased chance of infection in the body, caniculi can get blocked
and jaundice can form, can result from drinking due to oxidation reactions, or can be caused
by hepatitis