GI System (Wayne--Week 1, 2)

Question 1

Mouth

Answer 1

Chewing and some amylase begin digestion

Swallowing

Question 2

Esophagus

Answer 2

Propels food to stomach

Secretes mucus

Question 3

Stomach

Answer 3

Stores, mixes, dissolves, continues digestion of food

Regulates gastric emptying

Kills some microbes

Secretes: HCl, pepsinogen, intrinsic factor, mucus

pH 2 or below after eating food??

Question 4

Small intestine

Answer 4

Digestion and absorption, mixing luminal contents, propel contents toward large intestine

Secretes: CCK, ??, water, salt, mucus

Question 5

Large intestine

Answer 5

Store and concentrate undigested material

Absorb salt and water

Mix and propel contents

Defecation

Secretes: mucus

Question 6

Salivary glands

Answer 6

Parotid (CN IX), submandibular (CN VII), sublingual (CN VII)

Secrete hypotonic solution to moisten food

Secrete mucus to lubricate food

Secrete amylase to digest polysaccharides

Xerostomia = dry mouth; sialorrhea = excessive salivation

Question 7

Pancreas

Answer 7

Secretes many enzymes into small intestine to digest carbohydrates, proteins, fats, nucleic acid

Secretes bicarbonate to neutralize HCl entering small intestine from stomach

(Exocrine pancreas)

Question 8

Liver

Answer 8

Secretes bile into gallbladder

Secretes bicarbonate to neutralize HCl entering small intestine from stomach

Detoxifies and allows organic waste products and materials to be eliminated in feces

Question 9

Gallbladder

Answer 9

Stores and concentrates bile between meals (releases bile into small intestine in response to fatty meal)

Question 10

Regulation of GI functions

Answer 10

1) Neural regulation (extrinsic and enteric nervous systems)
2) Hormone and paracrine regulation

Question 11

Hormones of GI system

Answer 11

Gastrin

CCK

Secretin

GIP

Motilin

Ghrelin

Question 12

Paracrine factors of GI system

Answer 12

Somatostatin

Histamine

Question 13

Cholecystokinin (CCK)

Answer 13

Secreted by I cells of small intestine

Stimulated by chyme coming into small intestine from stomach containing fat/triglycerides (most important) and proteins

Inhibits gastric emptying

Stimulates small intestine motility

Stimulates pancreas to secrete enzymes

Stimulates gallbladder contraction and relaxation of Sphincter of Oddi

Negative feedback because as fat is digested, there is less of it in the small intestine to stimulate CCK secretion

Question 14

Ghrelin

Answer 14

Secreted by P/D1 cells in the stomach (and some in small intestine)

Stimulated by fasting (ie between meals or overnight)

Stimulates HCl secretion from parietal cells, gastric emptying, motility

Stimulates appetite center in hypothalamus

Stimulates growth hormone secretion from pituitary

Question 15

Histamine

Answer 15

Paracrine factor

Stimulated by gastrin

Secreted from ECL cells in body of stomach

Stimulates parietal cell HCl secretion (directly and by potentiating actions of gastrin and ACh)

Question 16

Cephalic phase

Answer 16

Happens before any food reaches stomach (seeing, smelling, tasting, chewing, emotions)
by stimulation of receptors in the head

Parasympathetic efferent pathway activated (vagus efferent)–> enteric nerves activated (ACh) –> G cells secrete gastrin and parietal cells secrete HCl –> HCl and stomach motility prepare stomach in advance for food

Question 17

Gastric phase

Answer 17

Happens when food enters the stomach

AAs and peptides stimulate: G cells to secrete gastrin (which stimulates parietal cells to secrete HCl and activates stomach motility)

Stomach distention stimulates: (1) Vagus nerve to stimulate enteric nervous system (ACh) and (2) mechnoreceptors to stimulate enteric nerves, which both stimulate parietal cells to secrete HCl and G cells to secrete gastrin

Note: caffeine directly stimulates parietal cells to secrete HCl

Question 18

Intestinal phase

Answer 18

Happens when food bolus enters small intestine

Distention of small intestine, acidity, hyperosmolarity, fat/AAs stimulate extrinsic and enteric neural reflexes and cause secretion of secretin, CCK, GIP

Note: different response from cephalic phase and gastric phase!

Question 19

Secretion of saliva

Answer 19

Stimulated by food in mouth, act of chewing, smell/thought of food (CN VII = submandibular and sublingual, CN IX = parotid, use ACh; sympathetic T1-T3 use NE)

Inhibited by dehydration, fear, sleep

Rate of secretion increased with larger bites of food or acidic foods

Both sympathetic and parasympathetic stimulate secretion (and there is no hormonal regulation)

Question 20

Swallowing

Answer 20

Afferent from pharynx activate swallowing center in brainstem, then efferent from swallowing center stimulate pharyngeal muscles to contract proximal to distal–peristaltic contractions

1) Food into pharynx by tongue
2) Soft palate elevates
3) Epiglottis covers glottis and UES relaxes
4) Food enters esophagus, UES closes, glottis opens and breathing resumes

Question 21

Anatomical and functional divisions of stomach

Answer 21

Anatomical: fundus is top, body is middle, antrum is bottom

Functional: top is orad (relaxes to accommodate food), bottom is caudad (peristalsis)

Question 22

What is the only essential function of the stomach?

Answer 22

Only necessary function is secretion of intrinsic factor

Question 23

Basal electric rhythm (slow waves)

Answer 23

Rhythmic fluctuations in membrane potential in caudad region of stomach that occur 3 times per minute (always)

Interstitial cells of Cajal (ICC) are what drive this pacemaker rhythm

If magnitude of plateau is low (sympathetic activation hyperpolarizes Vm) then lower frequency of AP firing during plateau and weaker contractions of caudad stomach

If magnitude of plateau is high (parasympathetic activation, gastrin and motilin all depolarize Vm) then higher frequency of AP firing during plateau and stronger contractions of caudad stomach

Question 24

HCl in the stomach

Answer 24

Converts pepsinogen to pepsin

Kills ingested microbes

Causes high acidity which inhibits gastric emptying if chyme entering small intestine is very acidic

Question 25

Mechanism of HCl secretion by parietal cells

Answer 25

Inside parietal cell, CO2 and H2O converted to H+ and HCO3- --\> H+ active transport out into lumen via H/K ATPase --\> Cl- enters (via active transport, against electrochemical gradient) into cell as HCO3- leaves --\> Cl- channels on luminal side let Cl out also More H/K ATPase means more H+ pumped out Note: Don't get buildup of H+ in cell when you block pumps because just don't have driving force for reaction to create H+ anymore

Question 26

What stimulates HCl secretion from parietal cells, and how?

Answer 26

Cephalic and gastric phases cause release of gastrin (from G cells) and ACh (from enteric nerves) --\> gastrin acts directly on parietal cells and stimulates histamine secretion --\> gastrin, histamine and ACh increase number of H/K ATPase inserted nto luminal membrane of parietal cells --\> increased HCl secretion 1) Vagus/enteric nerves to parietal cells directly 2) Gastrin onto parietal cells directly 3) Gastrin to ECL cells to histamine to parietal cells 4) ACh onto parietal cells directly

Question 27

Pepsin secretion

Answer 27

Pepsinogen is secreted from chief cells of stomach --\> HCl (secreted from parietal cells) turns pepsinogen into pepsin --\> pepsin also turns pepsinogen into pepsin (positive feedback) --\> pepsin cleaves protein into peptides

Question 28

How is vitamin B12 absorbed?

Answer 28

Different from other water soluble vitamins because it is not absorbed by diffusion or mediated transport Vitamin B12 (VB) is bound to food --\> pepsin optimizes release of VB, but is not necessary --\> intrinsic factor (IF) forms a complex with VB in duodenum --\> IF-VB complex binds receptor in ileum and is endocytosed into epithelial cells Note: VB (aka cobalamin) necessary for RBC maturation, get pernicious anemia without VB

Question 29

Causes of vomiting

Answer 29

Distention of stomach or small intestine (eat too much too fast) Chemoreceptors in intestine wall and brain Increased pressure in skull Rotation of head (motion sickness) Pain Emotion Tactile sensation at back of throat

Question 30

Steps in vomiting

Answer 30

1) Autonomic discharge causes salivation, sweating, increased HR, skin pallor, nausea 2) Retching (deep breath, closure of glottis, elevation of soft palate, abdominal muscles contract, LES and body of stomach relax, stomach contents enter esophagus but UES closed so stomach contents do not go into mouth) 3) Vomiting (further increase in abdominal muscle contractions, large increase in intrathoracic pressure, stomach contents forced through UES and out mouth; can also have reverse peristalsis in upper small intestine so intestinal contents forced into stomach

Question 31

What determines rate of gastric emptying into duodenum?

Answer 31

Quality of chyme: 1) High acidity --\> enteric neural reflex --\> contraction of pyloric sphincter 2) High fat content --\> CCK secretion --\> contraction of pyloric sphincter 3) Hyperosmotic chyme --\> contraction of pyloric sphincter

Question 32

Why is it important to slow gastric emptying?

Answer 32

1) Limit amount of acid in duodenum 2) Fatty/hyperosmotic chyme has enough time to be optimally digested

Question 33

Sementation contractions in small intestine

Answer 33

Shortly after eating meal, when chyme enters small intestine Rhythmic contractions that mix up luminal contents by dividing it up (NOT peristalsis) Higher frequency of contractions at more proximal end and slower at distal end of small intestine

Question 34

Peristaltic contractions in small intestine

Answer 34

Shortly after eating meal, when chyme enters small intestine Wave of contractions that push bolus of chyme along (relaxation in front of bolus)

Question 35

Migrating myoelectric complex (MMC) in small intestine

Answer 35

Happens during fasting, 1x every 90 minutes Periods of brief intense contractions once every 90 minutes during otherwise period of quiescence Sweeps undigested luminal contents from stomach through small intestine, and maintains low bacterial count in upper intestine Note: if no MMC, then bacterial buildup in upper intestine and would get uncomfortable gas in places it shouldn't be

Question 36

What stimulates small intestine motility?

Answer 36

**Motilin** secreted during fasting stimulates MMC **CCK** secreted during eating (fat) stimulates segmentation and peristalsis **Gastrin** from stomach stimulates segmentation and peristalsis **Insulin** from endocrine pancreas stimulates segmentation and peristalsis **Serotonin** from EC cells after eating stimulates motility

Question 37

What inhibits small intestine motility?

Answer 37

Epinephrine (due to stress --\> sympathetic --\> adrenal medulla) inhibits motility To divert energy away from intestine and toward heart/lungs/etc that need it; if chronic stress, can get indigestion

Question 38

How does the exocrine pancreas secrete HCO3-?

Answer 38

CO2 diffuses from blood into pancreatic duct cell --\> H+ is pumped back into blood across serosal membrane via Na/H exchanger (due to Na gradient) --\> HCO3-/Cl exchanged across luminal membrane to get HCO3- secreted into lumen Open Cl- channels let Cl- out into lumen, which is key!

Question 39

How is pancreatic HCO3- secretion hormonally controlled?

Answer 39

Secretin Acid from stomach --\> stimulates small intestine to secrete secretin (from S cells of duodenum) into bloodstream --\> stimulates pancreas to secrete HCO3- (by increasing expression of Cl- channels and increasing open probability of Cl- channels) --\> neutralization of intestinal acid Negative feedback

Question 40

How does the pancreas secrete enzymes into duodenum?

Answer 40

Enzymes secreted as zymogens to ensure that the pancreas doesn't digest itself Trypsinogen converted to trypsin by membrane bound **enterokinase** on **intestinal epithelial cells** Trypsin converts other zymogens into active enzymes

Question 41

Active pancreatic enzymes that digest proteins into peptides

Answer 41

Trypsin Chymotrypsin Elastase Carboxypeptidase

Question 42

Active pancreatic enzymes that digest emulsified fats into free fatty acids and monoglycerides

Answer 42

Lipase Cholesterol ester hydrolase Phospholipase A2

Question 43

Active pancreatic enzymes that digest starch into disaccharides (converted to monosaccharides later by intestinal brush border enzymes)

Answer 43

Amylase

Question 44

Active pancreatic enzymes that digest DNA and RNA into free nucleotides

Answer 44

Deoxyribonuclease Ribonuclease

Question 45

How is zymogen secretion by the pancreas hormonally controlled?

Answer 45

CCK Intestinal fatty acids, AAs --\> CCK secretion in small intestine --\> increased secretion of zymogens Negative feedback

Question 46

What is bile for?

Answer 46

Solubilizes fat in small intestine (required for lipid absorption)

Question 47

Bile composition

Answer 47

**Bile salts** (functionally most impt) Phospholipids Cholesterol Bile pigments Inorganic ions (Na, K, Ca, Cl, HCO3)

Question 48

Bile salts (synthesis, secretion, recycling)

Answer 48

Synthesized in liver (only 5% needs to be synthesized) Secreted from liver --\> common bile duct --\> gallbldder --\> duodenum 95% of bile salts recycled (reabsorbed in ileum, returned to liver via enterohepatic circulation)

Question 49

What stimulates bile release from gallbladder to duodenum?

Answer 49

CCK Fatty acid in duodenum --\> secretion of CCK --\> gallbladder contraction, relaxation of Sphincter of Oddi

Question 50

Between meals, is bile still secreted?

Answer 50

Bile is **not** secreted **into the duodenum** between meals because the Sphincter of Oddi is closed However, bile **is** secreted from **the liver into the gallbladder** to be stored

Question 51

How and when does chyme move from small to large intestine?

Answer 51

After a meal, there is reflex contraction of ileum --\> ileocecal sphincter relaxes --\> chyme enters cecum and distends cecum --\> distention of cecum activates neural reflex that causes ilealcecal sphincter to contract (prevents fecal material from moving backward)

Question 52

Why would it be bad for chyme to move backward from large to small intestine?

Answer 52

Lots of bacteria in large intestine, and don't want that getting into small intestine (If bacteria in small intestine, it would metabolize/ferment all the nutrients that we need to absorb!)

Question 53

Segmentation contractions in large intestine

Answer 53

1x every 30 min to slowly propel fecal material through large intestine (takes 18-24 hours to go all the way through) Note: segmentation contractions in large intestine do (slowly) move material, but segmentation contractions in small intestine do not move material, just mix

Question 54

Mass movement contractions in the large intestine

Answer 54

Happens when you eat a meal (gastrocolic reflex) Spreads rapidly across transverse segment of large intestine toward rectum (makes you feel like you hav to go?)

Question 55

Internal vs. external anal sphincter

Answer 55

Internal: smooth muscle; autonomic control External: skeletal muscle; voluntary control

Question 56

Defecation reflex

Answer 56

Mass movement of fecal material into rectum --\> distention of rectum --\> mechanoreceptor-mediated reflex --\> contraction of rectum and relaxation of internal anal sphincter --\> voluntary relaxation of external anal sphincter --\> defecation

Question 57

How does the small intestine have such a large surface area?

Answer 57

Villi Microvilli-glycocalyx complex (brush border)

Question 58

Carbohydrate digestion

Answer 58

Amylase in mouth, then intestine --\> disaccharides Enzymes on brush border: glucoamylase, sucrase, isomaltase, trehalase, lactase End products are monosaccharides: glucose, galactose, fructose

Question 59

How are monosaccharides absorbed?

Answer 59

Glucose: SGLT1 (Na/glucose cotransport into cell) --\> GLUT2 (into blood) Galactose: SGLT1 (Na/glucose cotransport into cell) --\> GLUT2 (into blood) Fructose: GLUT5 (facilitated diffusion down gradient) --\> GLUT2 (into blood)

Question 60

What is our body's limit for glucose absorption?

Answer 60

22lbs of monosaccharides in 24 hours! HUUUGE! We never reach our limit Na+ is the limiting factor and we always have enough luminal Na+

Question 61

Lactase deficiency

Answer 61

Cannot digest lactose --\> lactose remains in gut --\> osmotic diarrhea, gas (abdominal distention and pain), fermentation of lactose by bacteria in gut (so breathe out more hydrogen) Most people (other than from Northern Europe) lose activity or amount of lactase bound to brush border (glycocalyx) Cure: avoid dairy or take lactase pills so you can digest lactose

Question 62

How are proteins digested and absorbed?

Answer 62

Digestion in stomach by **pepsin** (not necessary) and in small intestine by **trypsin, chymotrypsin, elastase, carboxypeptidase** --\> large peptides, di/tri-peptides, free AAs --\> large peptides further digested by peptidases into di/tri-peptides and free AAs --\> **secondary active transport** to get di/tri-peptides and free AAs into cell --\> some di/tri-peptides further digested by **cytoplasmic peptidases** --\> di/tri-peptides and free AAs into blood by **facilitated diffusion** Some proteins/large peptides are endocytosed/exocytosed to get into blood (mostly in infants)

Question 63

Cystic Fibrosis effect on GI

Answer 63

Problem with Cl channel in pancreatic duct cells --\> pancreatic insufficiency so can't secrete pancreatic "juice" --\> deficit in trypsin --\> insufficient activation of zymogens --\> deficit in protein, fat, carbohydrate digestion/absorption

Question 64

Fat digestion

Answer 64

In small intestine, **bile salts** and **phospholipids** emulsify large fat globules into smaller pieces and prevent reaggregation --\> **lipase** splits triglyceride into fatty acids and monoglyceride --\> loosely held **micelles** are aggregates of fatty acids and monoglycerides (micelles easily break down though) --\> fatty acid and monoglyceride enter epithelial cells by diffusion --\> once inside cell, **re-form triglyceride** in smooth ER, enclosed in membrane --\> exocytosed, combine with phospholipids, cholesterol, fat-soluble vitamins to form **chylomicrons** --\> chylomicrons enter **lacteals**, go into lymphatic system to thoracic duct to veins --\> circulating chylomicrons are source of triglycerides for fuel for cells of body

Question 65

What are the deficits you get from insufficient lipase?

Answer 65

1) Deficit in fat digestion 2) Steatorrhea (fatty stool) 3) Malabsorption of fat soluble vitamins (need process of fat absorption to absorb these Note: you get lipase insufficiency if you have **chronic pancreatitis**

Question 66

Two barriers to pathogen invasion via the GI tract

Answer 66

1) Non-immune mechanisms 2) Intestinal immune system

Question 67

Non-immune mechanisms of GI protection

Answer 67

1) Acidic stomach 2) Digestive enzymes, bile acids, antimicrobial peptides (??) 3) Mucus in GI lumen 4) Peristaltic contractions 5) Commensal bacteria in colon

Question 68

Immune mechanisms of GI protection

Answer 68

Both innate and adaptive immunity in the gut GALT: Peyer's patches, tonsils/adenoids, salivary glands, appendix; intraepithelial lymphocytes in intestinal epithelium; lymphoid cells (mononuclear cells) in lamina propria

Question 69

Peyer's Patches

Answer 69

Afferent (sense invaders) component of GI immune system Located in small intestine, highest density in terminal ileum \>/= 5 lymphoid follicles of T and B cells Above Peyer's patch is follicle associated epithelium with M cells (APC!) and dendritic cells (APC, obvi!) M cells present to underlying follicles!

Question 70

Intestinal epithelium

Answer 70

Made up of epithelial cells and intraepithelial lymphocytes (IELs) Regular epithelial cells are APCs! IELs between lumen and lamina propria (soooo, in epithelium..?), and are **CD8+ T cells** (secrete cytokines); first line of defense against pathogens

Question 71

Lamina propria

Answer 71

Contains T cells, B cells, plasma cells (secrete IgA), macrophages, mast cells, eosinophils, neutrophils

Question 72

What does IgA secreted by plasma cells of the lamina propria do?

Answer 72

Luminal IgA binds microbial/food antigens, viruses, and **prevents intestinal absorption** Intracellular IgA in vesicles binds antigens and transports them to apical surface to be expelled from the cell into the lumen where there is luminal IgA waiting for them Does NOT activate inflammation

Question 73

How do infants have immunity?

Answer 73

IgA not produced until 5-6 months of age, and before this, baby gets **IgA from mother's milk** Mother ingests something with pathogen --\> Peyer's patch sends out lymphoid cells to lead immune response --\> lymphoid cells get to all mucosal tissues including mammary glands and mount immune response, including IgA secretion --\> secrete IgA into breast milk --\> baby ingests IgA and has protection against that same antigen

Question 74

Does the GI immune system protect other immune systems and vice versa?

Answer 74

Yes, GALT is connected to other MALTs GALT --\> lymphoid cell --\> lymph vessel --\> regional lymph nodes --\> peripheral blood --\> mucosal tissues' MALT (nasal passages, airways, urogenital tract, mammary glantds)

Question 75

Innate immune system of GI tract

Answer 75

Pattern recognition receptors on IELs, macrophages and DCs Remember, GI tract in a constant state of low level inflammation because constantly innundated with foreign molecules (food, microbes)

Question 76

Oral tolerance

Answer 76

Absence of peripheral immune response in presence of antigen-activated mucosal immune response and production of IgA Oral tolerance to food antigens and commensal bacteria Dependent on type of antigen, frequency, dose, and host factors (genetics, age) Potential therapeutic use to treat auto-immune diseases Oral tolerance mechanism not understood

Question 77

Food allergy

Answer 77

Breakdown of normal mechanism of oral tolerance Ingest food you see as foreign --\> **antigen binds to IgE** on surface of mast cells in lamina propria, **sensitization** --\> more antigen transported across epithelium into lamina propria --\> **next time** food eaten, binding to IgE on mast cells causes secretion of **chemicals** that increase intestinal Cl- secretion and alter motility --\> **diarrhea** Allergic response to food **triggers visceral hypersensitization** (esp colorectal distention, which causes pain in colorectal compartment), so if distend colorectal compartment with balloon, they're in a ton of pain compared to controls Syetemic response to allergen --\> anaphylaxis

Question 78

Food sensitivity

Answer 78

Get abdominal pain and diarrhea, but this is not an allergy Only way to know diff between food allergy and food sensitivity is to do immune test Mechanism not understood

Question 79

Intestinal "commensal" bacteria

Answer 79

400 different species in intestine Highest concentration in colon, lowest in stomach GI tract sterile at birth, but at 1 month, fully colonized intestines Acquired from what we eat and drink

Question 80

What are the benefits of commensal bacteria in the large intestine?

Answer 80

1) Important for development of mucosal immune system and mucosal epithelium proliferation and differentiation 2) Aid in metabolism of endogenous (bilirubin --\> urobilogen; bile acids) and exogenous (dietary fiber, carbs, peptides) substances 3) Inhibit colonization of intestinal mucosa by pathogenic microbes by outcompeting for food

Question 81

Antibiotics can cause diarrhea in humans, but what treatment can reduce this?

Answer 81

Probiotics (good bacteria found in yogurt)

Question 82

Somatostatin

Answer 82

Secreted from **D cells** in antrum of **stomach** (paracrine) and pancreas and enteric nervous system interneurons (neurocrine) Low pH in stomach stimulates secretion Paracrine functions: **inhibits G cells** from secreting gastrin; **inhibits parietal cells** from secreting HCl; **inhibits pepsinogen** secretion; i**nhibits gastric emptying**; **inhibits histamine secretion** from ECL cells (?) Neurocrine: **inhibits small intestine motility**; **inhibits zymogen secretion** from pancreas; **inhibits contraction of gall bladder** Released at highest rate during interdigestive phase (between meals) ANTI-GROWTH HORMONE (inhibits digestion/absorption and these are needed for growth! Also directly causes GH not to be released...)

Question 83

What is special about the ileum?

Answer 83

Where **intrinsic factor/B12** are absorbed into bloodstream Where **bile salts** are reabsorbed into bloodstream (to be recycled) Also has highest density of **peyer's patches**

Question 84

Why does aspirin give you ulcers?

Answer 84

Aspirin is a COX2 inhibitor which means you won't be able to produce prostaglandins Prostaglandins are needed to **decrease acid** secretion by parietal cells Prostaglandins are needed to **increase mucus** production by mucous cells

Question 85

What are examples of parasympathetic postganglionic nerves that do NOT release ACh?

Answer 85

Para post neurons release **NO** and **VIP** to relax **LES** (smooth muscle) Para post neurons release **NO** to relax blood vessels of **corpus cavernosum** (for erection) Para post neurons release **GRP** onto **G cells in the stomach** to release gastrin Note: these are called non-adrenergic non-cholinergic (NANC)

Question 86

Glucose-dependent Insulinotropic Peptide/Gastric Inhibitory Peptide (GIP)

Answer 86

Hormone that is secreted by K cells in duodenum and jejunum of small intestine Stimulated by protein, fat, carbohydrates (FOOD) in the duodenum and jejunum Inhibits parietal cell HCl secretion Stimulates insulin secretion

Question 87

Acetylcholine as GI neurocrine

Answer 87

Secreted by sympathetic and parasympathetic preganglionic fibers and **parasympathetic postganglionic fibers** Stimulates **contraction** of smooth muscle in wall of **digestive tube** **Inhibits** contraction of digestive **sphincters** Stimulates **salivary gland** acinar cell secretion Stimulates parietal cell secretion of **HCl** in body of stomach Stimulates ECL cells in body of stomach to secrete **histamine** Stimulates pancreatic acinar cell secretion of **zymogens** and **pancreatic** ductal cell secretion of bicarbonate

Question 88

NE as GI neurocrine

Answer 88

Secreted by **sympathetic postganglionic** fibers and small amount from **adrenal medulla** Inhibits contraction of smooth muscle wall in intestine, resulting in **wall relaxation** and **decreased motility** Stimulates **contraction** of digestive sphincters Stimulates **salivary gland** acinar cell secretion

Question 89

5HT as GI neurocrine

Answer 89

Secreted by **enteric nervous system interneurons** and **EC cells** in GI mucosa, and from brain Stimulates intestinal **wall motility** Activates **vagal afferents** (vomiting)

Question 90

Vasoactive intestinal peptide (VIP) as GI neurocrine

Answer 90

Secreted by **enteric nervous system interneurons** Inhibits contraction of smooth muscle in wall of small intestine, resulting in relaxation of wall and **decreased motility** Inhibits smooth muscle contraction in splanchnic blood vessels, resulting in **vasodilation** Stimulates intestinal **Cl- and water secretion**

Question 91

Enkephalins as GI neurocrine

Answer 91

Secreted by enteric nervous system interneurons; brain Stimulates **contraction** of LES, pyloric sphincter, ileocecal sphincter **Inhibits** peristalsis in small intestine **Inhibits** intestinal secretion Contributes to **contraction** of Sphincter of Oddi and gallbladder Note: enkephalins are a family of **opioids** (constipation)

Question 92

Nitric oxide (NO) as GI neurocrine

Answer 92

Secreted by **enteric nervous system interneurons** LES **relaxation** Inhibits contraction of smooth muscle in wall of small intestine, resulting in relaxation of wall and **decreased motility** Inhibits smooth muscle contraction in splanchnic blood vessels, resulting in **vasodilation**