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75 Cards in this Set

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What are the parts of the stomach?
fundus - up top
body - middle part
antrum - end (near duodenum)
What does gastrin come from? Where are the cells located? What does gastrin do? What stimulates and inhibits gastrin release
comes from G cells in the antrum of the stomach
Gastrin: increases gastric H+ secretion, increases growth of gastric mucosa, and increases gastric motility
Stimulated by: distention of the stomach, peptides, amino acids, vagal stimulation (from gastrin releasing peptide)
inhibited by pH<1.5
What are the most potent stimulators of gastrin secretion?
Phenylalaine and tryptophan
In what condition is gastrin elevated?
Zollinger-Ellison (gastrinoma)
occurs when gastrin is secreted by the non-B cells of the pancreas
What does CCK come from? Where are the cells located? What does CCK do? What simulates and inhibits CCK?
CCK comes from I cells in the duodenum and jejunum
CCK: increases pancreatic enzyme secretion, increases contraction of the gallbladdder (relaxes sphincter of Oddi), inhibits gastric emptying
stimulated by increased fatty acids, and amino acids
In choelithiasis why does pain occur after eating?
because of release of CCK - which causes contraction of the gall bladder
What does secretin come from? Where are the cells located What does secretin do? What stimulates and inhibits secretin?
From S cells which are located in the duodenum
secretin: increases pancreatic HCO3- secretion, decreases gastric acid secretion, increases bile secretion
stimulated by increase in acid, fatty acids in lumen of duodenum

*the HCO3- neutralizes gastric acid in the duodenum, allowing pancreatic enzymes to function
What does HCO3- do in the duodenum? what releases it?
it neutralizes gastric acid in the duodenum - allowing the pancreatic enzymes to work
released by secretin - from S cells in the duodenum
What does somatostatin come from? Where are the cells located? What does somatostatin do? What sitmulates and inhibits release of it?
Somatostatin is from D cells (in pancreatic islets, and GI mucosa)
it decreases gastric acid and pepsinogen secretion, decreases pancreatic and small intestine fluid secretion, decreases gallbladder contraction, and decreases insulin and glucagon release
stimulated by increased acid
decrease production by vagal stimulation
What is an inhibitor hormone?
somatostatin- antigrowth hormone effects (digestion and absorption of substances needed for growth)
What is used to treat VIPomas and carcinoid tumors?
somatostatin
Where is glucose dependent insulinotrophic peptide (GIP) released from? Where are they located. What is GIPs function? What simulates and inhibits it?
from K cells in the duodenum and jejunum
GIP - exocrine: decrease gastric H+ secretion
endocrine: increase insulin release
stimulated by increase in fatty acids, amino acids and oral glucose
VIPoma
non-a, non-B islet cell pancreatic tumor that secretes VIP. Copious diarrhea
Vasoactive intestinal polypeptide (VIP) what secretes it? WHere is it located? What does it do? What inhibits and stimulates it?
From parasympathetic ganglia in sphincters, gallbladder and small intestine
it increases water and electrolyte absorption, increased relaxation of intestinal smooth muscle sphincters
stimulated by increased distention and vagal stimulation
inhibited by adrenergic input
What is the action of NO? If you loose it what happens in the GI tract?
it increases smooth muscle relaxation, including lower esophageal sphincter
*If you loose NO - cannot relax lower esophageal sphincter - get achlasia (bird beak sign)
Motilin where is it released from? What does it do? WHat inhibits and stimulates it?
From the small intestine
it produeces migrating motor complexes (MMCs)
it is increased in fasting state
Ghrelin where is it released? Where are they located? What is its function? What stimulates and inhibits it?
released from P/D1 cells in the stomach
causes increase growth hormone, ACTH, cortisol and prolactin secretion
increased before meals
decreased after meals
what regulates hunger?
ghrelin - lost following gastric bypass surgery
associated with hyperphagia in prader-willi syndrome
Where does HCO3- come from? What is its action? What regulates it?
made in mucosal cells (stomach, duodenum, salivary glands, pancreas) and brunner's glands (duodenum)
it neutralizes acid
it stimulated with increased pancreatic and biliary secretion with secretin
HCO3- is trapped in mucus that covers the gastric epithelium
What makes parietal cells? Where? what is its action?
made in parietal cells in the stomach - needed for the absorption of vitamin B12 in the terminal ileum
*autoimmune disease against parietal cells = pernicious anemia and chronic gastritis
what makes gastric acid (HCl) ? What does it do? How is it regulated?
made by parietal cells in the stomach - causes a decreased pH in the stomach
it is increased by histamine, Ach and gastrin
decreased by somatostatin, GIP, prostaglandin and secretin secretion
What makes pepsin? What does it do? What regulates it?
made by chief cells in the stomach
it digests proteins
it is increased by vagal stimulation, local acid

inactive pepsinogen - pepsin by H+
what do parietal cells make?
HCl and intrinsic factor
what does atropine do in the GI tract?
inhibits Ach - thus inhibiting the production of HCl from the parietal cells

it does not block the production of gastrin from G cells - b/c that is stimulated by GRP (not Ach)
what do chief cells make?
pepsinogen - converted to pepsin in the presence of H+ (low pH)
What stimulates parietal cells to make HCl?
vagus nerve - Ach - blocked by atropine
What do ECL cells do?
release histamine which activates parietal cells
the ECL cells are stimulated by gastrin
What does gastrin do to ECL cells?
stimulates the release of histamine - which stimulates parietal cells (cause release of intrinsic factor and HCl)
gastrinoma
gastrin secreting tumor that causes continuous high levels of acid secretion and ulcers
What are the 2 ways that G cells increase gastric acid?
G cells produce gastrin - which directly stimulates parietal cells to make HCl - also gastrin stimulates ECL cells to make histamine which stimulates parietal cells to make HCl
What produces saliva? Which one is most serous? Which one is most mucinous?
Parotid, sublingual, submandibular, submaxillary glands.
Parotid is most serous (sides are serous)
Sublingual is most mucinous (mucinous in the middle)
What is the functions of saliva?
- a-amylase (ptyalin) begins starch digestion; inactivated by low pH on reaching stomach
- HCO3- neutralizes oral bacterial acids, maintains dental health
- mucins (glycoproteins) lubricate food
- antibacterial secretory products
- growth factors that promote epithelail renewal
What stimulates saliva secretion?
sympathetic (T1-T3 superior cervical ganglion) and parasympathetic (facial (VII) and glossopharyngeal (IX) nerve activity
What is the saliva like in low flow and high flow rates?
low flow rate - hypotonic (more time to reabsorb Na and Cl)
high flow rate - closer to isotonic (less time to reabsorb Na and Cl)
What can be damaged during surgery on the parotid gland?
facial nerve (CN VII) - it runs through the parotid gland
What receptors does Ach work through on the parietal cell?
M3 receptor - Gq - IP3/Ca2+ = stimulates H+/K+ ATPase - secretes H+ into the gastric lumen (K+ goes into the parietal cell) - causes HCO3 - release into the lumen - alkaline tide
How does GRP affect a parietal cell?
The Vagus nerve - stimulates the G cell via GRP which stimulates a parietal cell - via CCKb receptor - stimulates Gq - IP3/Ca2+ - stimulates K+/H+ ATPase - H goes into the gastric lumen - while K+ goes into parietal cell (HCO3- goes into gastric lumen too - alkaline tide)
What does omeprazole do?
inhibits the action of the H+/K+ ATPase on the gastric lumen side of parietal cells - prevents the release of acid into the gastric lumen
What does carbonic anhydrase do?
converts H2CO3 into H2O + CO2 and vice versa - works in kidneys (proximal tubules) and gastric parietal cells (causes alkaline tide)
What are the 2 functions of gastrin?
they stimulate parietal cells to make HCl and intrinisc factor - they also stimulate ECL cells to release histamine that acts on parietal cells to make HCl and intrinsic factor (works on H2 receptor - stimulates cAMP - which stimulates H+/K+ ATPase - releasing H+ into the gastric lumen - and K+ goes into parietal cell
What inhibits the action of histamine on the gastric parietal cell?
Cimetidine - reversibly blocks the interaction between histamine and H2 receptor (so can't signal parietal cell to to release HCl and intrinsic factor)
What does prostaglandins/misoprostol do to parietal cells?
inhibits cAMP (inhibiting - H+/K+ ATPase - inhibiting release of H+)
What does somatostatin do to parietal cells?
inhibits cAMP - thus inhibiting H+/K+ ATPase activity (preventing H+ release into gastric lumen)
H2 blockers - what are they? What do they do?
end in -dine
cimetidine, ranitidine, famotidine, nizatidine
they reversibly inhibit histamine from binding to H2 receptors on parietal cells (thus inhibiting cAMP - and H+/K+ ATPase activity - inhibiting H+ release into the gastric lumen)
used: peptic ulcers, gastritis, mild esophageal reflux
Toxicities of cimetidine
potent inhibitor of P-450; has antiandrogenic effects (prolactin release, gynecomastia, impotentence, decrease libido in men); can cross blood brain barrier (confusion, dizziness, headaches) and placenta.

Both cimetidine and ranitidine decrease renal excretion of creatinine

Other H2 blockers don't have this effect.
Proton pump inhibitors - what are they? What do they do? What are they used for?
end in -prazole
omeprazole, lansoprazole
they irreversibly inhibit the H+/K+ ATPase on the gastric lumen side of parietal cells - inhibit the release of H+ into the gastric lumen

used for: peptic ulcer disease, gastritis, esophageal reflux, Zollinger-Ellison syndrome
what do brunner's glands do?
secrete alkaline mucus to neutralize acid contents entering the duodenum from the stomach. Located in duodenal submucosa (only GI submucosal glands). Hypertrophy of brunner's glands seen in peptic ulcer disease
What is located in the submucosa of the duodenum?
brunner's glands - release alkaline mucus - to neutralize the acid released from the stomach - hypertrophy of the glands seen in peptic ulcer disease
What condition do you see hypertrophy of brunners glands?
peptic ulcer disease
What are some different pancreatic enzymes?
a-amylase, lipase, phospholipase A, colipase, proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)
Function of a-amylase
starch digestion - hydrolyzes 1,4 glycosidic bonds
Function of lipase, phospholipase A, colipase
fat digestion
lipids to fatty acids
Function of proteases? What are examples of some?
trypsin, chymotrypsin, elastase, carboxypeptidases

peptide digestion secreted as proenzymes "zymogens" that are inactive
Function of trypsinogen
activated into trypsin via enterokinase/enteropeptidase an enzyme from the duodenal mucosa (brush border) - then trypsin activates the other proteases and activates more trypsin production
Salivary amylase
starts digestion, hydrolyzes a-1,4 linkages to yield disaccharides (maltose, maltotriose, and a-limit dextrans)
what enzyme starts digestion/
salivary amylase
pancreatic amylase
highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and disaccharides
oligosaccharide hydrolases
at brush border of intestine - rate limiting step in carbohydrate digestion, produce monosaccharides from oligo- and disaccharides
Where is the concentration of pancreatic amylase the highest?
duodenal lumen
How are carbohydrates absorbed?
only MONOSACCHARIDES can be absorbed (fructose, glucose, galactose)
glucose and galactose are absorbed by sodium dependent SGLT-1 transporter
fructose - absorbed via facilitated diffusion via GLUT-5 transporter
all of the monosaccharides go from the enterocyte to the blood via GLUT-2 transporter
GLUT-2 transporter what does it do?
transports monosacchardies (fructose, glucose, galactose) from enterocyte into the blood
GLUT-5 transporter what does it do?
facilitated diffusion of fructose from the lumen of the intestine into the enterocyte
SGLT-1 transporter what does it do?
reabsorbtion of glucose and galactose into the enterocyte
it is Na+ dependent!
Where is Iron, Folate, vit B12 absorbed?
Iron - absorbed as Fe2+ in the duodenum
Folate - absorbed in the jejunum
vit B12 - absorbed in the ileum with bile acids
What are peyers patches? Where are they located?
unencapsulated lymphoid tissue found in lamina propria and submucosa of small intestine - contain specalized M cells that take up antigen

B cells that are stimulated in germinal centers of peyers patches differentiate into IgA-secreting plasma cells, which ultimately reside in lamina propria. IgA recieves protective secretory component and is then transported across epithelium to gut to deal with intraluminal antigen
What is the antibody present in the gut?
IgA - made from peyers patches in the lamina propria and submucosa of the small intestint
What cells take up antigen in then small intestine?
M cells - specalized cells of peyers patches - role is to take up antigen
What composes bile?
bile salts (bile acids conjugated to glycine or taurine, making them water soluable), cholestrol, phospholipids, water, bilirubin and ions
What is the only significant mechanism for cholestrol excretion?
through bile!
What is needed for digestion of triglycerides and micelle formation in the small intestine?
bile
products of lipid digestion are solubilized into micelles by bile salts - the micelles allow fatty acids, monosaccharides, cholesterol to diffuse across the lumenal membrane - on the outside of micelles - there is bile salts
Where are bile acids reabsorbed?
in the terminal ileum - if have resection of the terminal ileum - cannot reabsorb fat and will get steatorrhea
what is bilirubin?
breakdown product of heme metabolism (from hemoglobin in RBC's)
What is the path of bilirubin?
heme (from hemoglobin in RBC) break down produces unconjugated bilirubin (indirect - non water soluble)- in the blood pairs with albumin - and have a albumin-unconjugated bilirubin complex - goes to the liver - UGT pairs unconjugated bilirubin with glucuronyic acid - forms conjugated bilirubin (direct - water soluble) - is excreted from the liver in bile - dumps into duodneum - bacteria in the gut change it to urobilinogen - 80% is excreted in feces as sterocobilin - gives feces its color
20% of urobilinogen is reabsorbed (10% excreted in kidneys as urobillin - gives urine its color, 90% is reabsorbed into enterohepatic circulation
sterocobilin
bilirubin excreted in the feces - gives feces its color
urobilin
bilirubin in the urine - gives urine its color