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Block 3: GI, Endocrine, Reproductive > GI System (Wayne--Week 1, 2) > Flashcards

GI System (Wayne--Week 1, 2) Flashcards

1
Q

Mouth

A

Chewing and some amylase begin digestion

Swallowing

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2
Q

Esophagus

A

Propels food to stomach

Secretes mucus

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3
Q

Stomach

A

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??

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4
Q

Small intestine

A

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

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

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5
Q

Large intestine

A

Store and concentrate undigested material

Absorb salt and water

Mix and propel contents

Defecation

Secretes: mucus

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6
Q

Salivary glands

A

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

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7
Q

Pancreas

A

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)

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8
Q

Liver

A

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

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9
Q

Gallbladder

A

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

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10
Q

Regulation of GI functions

A

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

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11
Q

Hormones of GI system

A

Gastrin

CCK

Secretin

GIP

Motilin

Ghrelin

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12
Q

Paracrine factors of GI system

A

Somatostatin

Histamine

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13
Q

Cholecystokinin (CCK)

A

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

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14
Q

Ghrelin

A

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

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15
Q

Histamine

A

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)

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16
Q

Cephalic phase

A

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

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17
Q

Gastric phase

A

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

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18
Q

Intestinal phase

A

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!

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19
Q

Secretion of saliva

A

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)

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20
Q

Swallowing

A

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

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21
Q

Anatomical and functional divisions of stomach

A

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

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

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22
Q

What is the only essential function of the stomach?

A

Only necessary function is secretion of intrinsic factor

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23
Q

Basal electric rhythm (slow waves)

A

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

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24
Q

HCl in the stomach

A

Converts pepsinogen to pepsin

Kills ingested microbes

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

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25
Q

Mechanism of HCl secretion by parietal cells

A

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

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26
Q

What stimulates HCl secretion from parietal cells, and how?

A

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

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27
Q

Pepsin secretion

A

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

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28
Q

How is vitamin B12 absorbed?

A

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

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29
Q

Causes of vomiting

A

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

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30
Q

Steps in vomiting

A

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

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31
Q

What determines rate of gastric emptying into duodenum?

A

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

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32
Q

Why is it important to slow gastric emptying?

A

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

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33
Q

Sementation contractions in small intestine

A

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

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34
Q

Peristaltic contractions in small intestine

A

Shortly after eating meal, when chyme enters small intestine

Wave of contractions that push bolus of chyme along (relaxation in front of bolus)

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35
Q

Migrating myoelectric complex (MMC) in small intestine

A

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

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36
Q

What stimulates small intestine motility?

A

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

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37
Q

What inhibits small intestine motility?

A

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

38
Q

How does the exocrine pancreas secrete HCO3-?

A

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!

39
Q

How is pancreatic HCO3- secretion hormonally controlled?

A

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

40
Q

How does the pancreas secrete enzymes into duodenum?

A

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

41
Q

Active pancreatic enzymes that digest proteins into peptides

A

Trypsin

Chymotrypsin

Elastase

Carboxypeptidase

42
Q

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

A

Lipase

Cholesterol ester hydrolase

Phospholipase A2

43
Q

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

A

Amylase

44
Q

Active pancreatic enzymes that digest DNA and RNA into free nucleotides

A

Deoxyribonuclease

Ribonuclease

45
Q

How is zymogen secretion by the pancreas hormonally controlled?

A

CCK

Intestinal fatty acids, AAs –> CCK secretion in small intestine –> increased secretion of zymogens

Negative feedback

46
Q

What is bile for?

A

Solubilizes fat in small intestine (required for lipid absorption)

47
Q

Bile composition

A

Bile salts (functionally most impt)

Phospholipids

Cholesterol

Bile pigments

Inorganic ions (Na, K, Ca, Cl, HCO3)

48
Q

Bile salts (synthesis, secretion, recycling)

A

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)

49
Q

What stimulates bile release from gallbladder to duodenum?

A

CCK

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

50
Q

Between meals, is bile still secreted?

A

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

51
Q

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

A

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)

52
Q

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

A

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!)

53
Q

Segmentation contractions in large intestine

A

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

54
Q

Mass movement contractions in the large intestine

A

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?)

55
Q

Internal vs. external anal sphincter

A

Internal: smooth muscle; autonomic control

External: skeletal muscle; voluntary control

56
Q

Defecation reflex

A

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

57
Q

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

A

Villi

Microvilli-glycocalyx complex (brush border)

58
Q

Carbohydrate digestion

A

Amylase in mouth, then intestine –> disaccharides

Enzymes on brush border: glucoamylase, sucrase, isomaltase, trehalase, lactase

End products are monosaccharides: glucose, galactose, fructose

59
Q

How are monosaccharides absorbed?

A

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)

60
Q

What is our body’s limit for glucose absorption?

A

22lbs of monosaccharides in 24 hours! HUUUGE!

We never reach our limit

Na+ is the limiting factor and we always have enough luminal Na+

61
Q

Lactase deficiency

A

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

62
Q

How are proteins digested and absorbed?

A

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)

63
Q

Cystic Fibrosis effect on GI

A

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

64
Q

Fat digestion

A

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

65
Q

What are the deficits you get from insufficient lipase?

A

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

66
Q

Two barriers to pathogen invasion via the GI tract

A

1) Non-immune mechanisms
2) Intestinal immune system

67
Q

Non-immune mechanisms of GI protection

A

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

68
Q

Immune mechanisms of GI protection

A

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

69
Q

Peyer’s Patches

A

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!

70
Q

Intestinal epithelium

A

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

71
Q

Lamina propria

A

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

72
Q

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

A

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

73
Q

How do infants have immunity?

A

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

74
Q

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

A

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)

75
Q

Innate immune system of GI tract

A

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)

76
Q

Oral tolerance

A

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

77
Q

Food allergy

A

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

78
Q

Food sensitivity

A

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

79
Q

Intestinal “commensal” bacteria

A

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

80
Q

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

A

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

81
Q

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

A

Probiotics (good bacteria found in yogurt)

82
Q

Somatostatin

A

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; inhibits 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…)

83
Q

What is special about the ileum?

A

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

84
Q

Why does aspirin give you ulcers?

A

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

85
Q

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

A

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)

86
Q

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

A

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

87
Q

Acetylcholine as GI neurocrine

A

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

88
Q

NE as GI neurocrine

A

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

89
Q

5HT as GI neurocrine

A

Secreted by enteric nervous system interneurons and EC cells in GI mucosa, and from brain

Stimulates intestinal wall motility

Activates vagal afferents (vomiting)

90
Q

Vasoactive intestinal peptide (VIP) as GI neurocrine

A

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

91
Q

Enkephalins as GI neurocrine

A

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)

92
Q

Nitric oxide (NO) as GI neurocrine

A

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

Block 3: GI, Endocrine, Reproductive (30 decks)

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