GI Physiology

Question 1

Saliva

Answer 1

-parotid, sublingual, submaxillary glands
-HCO3- and K+
-alpha amylase and lingual lipase
-saliva has NO hormonal stimulation
-parasympathetic (dominant) and sympathetic BOTH activate it -> facial and glossopharyngeal
-stimulated by conditioning, food, nausea, smell
-sleep, dehydration, and atropine inhibit secretion
-lubricates, dilutes, buffers
-initial digestion of starches and lipids
-acinar cells secrete
-from high to low: Na, HCO3-, Cl, K

Question 2

bile juice

Answer 2

-bile salts, bilirubin, phospholipids, cholesterol
-stimulated by CCK (contraction of gallbladder and relaxation of sphincter of oddi) and parasympathetic
-inhibited by ileal resection

Question 3

pancreatic juice

Answer 3

-exocrine
-HCO3-, pancreatic lipase, amylase, proteases
-stimulated by secretin, CCK, parasympathetic
-digestive protects stimulates pancreatic enzymes
-H+ in duodenum stimulates buffer for pancreatic juice

Question 4

Gastric Juice

Answer 4

-HCl, intrinsic factor, and pepsinogen -> all in the body of stomach
-parietal cells secrete HCl and INTRINSIC FACTOR
-chief cells secrete PEPSINOGEN
-mucus- lubricates and protects
-HCl and pepsinogen -> protein digestion (NON-ESSENTIAL)
-intrinsic factor -> B12 absorption (ESSENTIAL)
-stimulated by parasympathetic, gastrin, ACh, histamine
-inhibited by H+ in stomach, chyme in duodenum, somatostatin, atropine, cimetidine, omeprazole

Question 5

pepsinogen

Answer 5

-secreted by chief cells
-converted to active form, pepsin, if there is low pH (HCl)
-pepsin digests proteins
-HCO3- inhibits

Question 6

cholecystokinin (CCK)

Answer 6

-promotes fat absorption and digestion (and proteins and carbs)
-HORMONE
-secreted by I cells of duodenum and jejunum
-stimulated by peptides, amino acids, fatty acids, monoglycerides
-warns that fat and protein is coming to be absorbed and digested
-1. increase pancreatic enzyme and HCO3- secretion
-2. stimulates contraction of gallbladder and relaxes sphincter of oddi
-3. stimulates growth of exocrine pancrease and gallbladder
-4. inhibits gastric emptying
-inhibited by somatostatin
-lipids in stomach -> delay gastric emptying -> allows for slower rate for lipid digestion

Question 7

secretin

Answer 7

-HORMONE
-secreted by S cells of duodenum
-stimulated by H+ and fatty acids in duodenum -> pH <4.5
-1. increases pancreatic and biliary HCO3- secretion -> neutralizes for pancreatic lipase to digest fats
-2. decrease gastric H+ secretion
-3. inhibits trophic effect of gastrin on gastric mucosa
-inhibited by high pH (> 4.5)

Question 8

gastrin

Answer 8

-HORMONE
-secreted by G cells in antrum
-stimulated by small peptides, amino acids, distention of stomach, vagal stimulation (GRP)
-1. increases gastric H+ secretion by parietal cells
-2. stimulates growth of gastric mucosa -> trophy
-inhibited by low pH and somatostatin
-if gastrin is too high it causes very low pH -> pancreatic lipase cant function -> no fat absorption -> steatorrhea

Question 9

glucose-dependent insulinotropic peptide (GIP)

Answer 9

-secreted by K cells in duodenum and jejunum
-ONLY HORMONE STIMULATED BY ALL 3 NUTRIENTS (fatty acids, amino acids, oral glucose)
-1. increase insulin secretion from pancreatic beta cells (this makes GIP an incretin- promotes insulin)
-2. decrease gastric H+ secretion
-3. inhibits gastric emptying
-inhibited by starvation?

Question 10

somatostatin

Answer 10

-inhibitory PARACRINE peptide -only acts locally via diffusion
-secreted by D cells
-stimulated by decreased pH
-somatostatin INHIBITS other GI hormones and gastric H+ secretion

Question 11

motilin

Answer 11

-secreted from upper duodenum during fasting states
-increase motility
-initiate interdigestive myoelectric complexes that occur at 90 min intervals
-inhibited by glucose

Question 12

pancreatic polypeptide

Answer 12

-secreted by pancreas
-stimulated by carbs, proteins, lipids
-inhibits pancreatic secretion of HCO3- and enzymes

Question 13

glucagon like peptide (GLP-1)

Answer 13

-secreted by L cells of small intestine
-incretin- stimulates insulin secretion
-inhibits glucagon secretion
-increases sensitivity of pancreatic beta cells to glucose
-decreases gastric emptying
-inhibits appetite
-possible tx for diabetes mellitus 2

Question 14

enteroglucagon

Answer 14

-secreted by intestinal cells
-stimulated by decrease blood glucose
-causes liver to increase glycogenolysis and gluconeogenesis

Question 15

histamine

Answer 15

-paracrine but not a peptide
-stimulates H+ secretion by gastric parietal cells (like gastrin and ACh)

Question 16

leptin

Answer 16

-secreted by fat cells
-secreted in proportion to fat stored in adipose
-decreases appetite and increases energy expenditure
-long term effects
-“Satiety hormone”
-crosses BBB and acts on hypothalamus

Question 17

insulin

Answer 17

-decreases appetite
-increase energy use
-fluctuate during the day (different than leptin which is long term)
-short term effects to decrease appetite
-stimulated in response to glucose
-secreted by pancreatic beta cells
-stimulated by glucagon

Question 18

appetite suppression

Answer 18

-GLP-1
-insulin
-leptin

Question 19

ghrelin

Answer 19

-secreted by gastric cells just before a meal
-increases appetite
-periods of starvation and weight loss stimulate ghrelin

Question 20

peptide YY (PYY)

Answer 20

-secreted by intestinal L cells after a meal
-decreases appetite
-inhibits ghrelin
-inhibits pancreatic secretion
-signals that digestion is complete
-stimulated by food/digestion inhibited by fasting

Question 21

pepsinogen

Answer 21

-secreted by chief cells
-pepsinogen becomes pepsin in the presence of low HCl pH
-stimulated by H+ (low pH)
-digests proteins
-inhibited by HCO3- and PPI, H2 blockers

Question 22

extrinsic systemic: sympathetic input

Answer 22

-INHIBIT
-4 ganglia: celiac, superior mesenteric, inferior mesenteric, hypogastric
-ganglia are located outside the organ
-norepinephrine (NE) -> relax smooth muscle in wall, contraction of sphincters, increase salivary secretion

Question 23

extrinsic systemic: parasympathetic input

Answer 23

-ACTIVATE
-vagus- upper GI
-pelvic- lower GI
-synapse directly on the walls of myenteric and submucosal plexuses

VASOVAGAL REFLEX
-afferent vagus (75%) picks up signals from mecho and chemo receptors -> effect vagus (25%) stimulates smooth muscles, endocrine, and secretory processes
-ex. ACh -> contract smooth muscles in wall, relax sphincters, increase salivary secretion, increase gastric secretion, increase pancreatic secretion
-ex. gastrin releasing peptide (GRP), or bombesin -> increase gastrin

Question 24

intrinsic system aka enteric

Answer 24

-submucosal and myenteric plexuses
-intrinsic system does not require extrinsic input (sympathetic and parasympathetic
-intrinsic system picks up signals from mucosal receptors and stimulates smooth muscle, endocrines, and secretion via interneurons
-the extrinsic input is just a modulator

-vasoactive intestinal peptide (VIP) -> relax smooth muscle, increase intestinal secretion, increase pancreatic secretion
-nitric oxide (NO) -> relax smooth muscle wall
-ekephalins (opiates) -> contraction of smooth muscle, decrease intestinal secretion
-neuropeptide Y -> relax smooth muscles, decrease intestinal secretion
-Substance P -> contraction of smooth muscle, increase salivary secretion

Question 25

which increases salivary secretion -> sympathetic or parasympathetic?

Answer 25

BOTH!!!!

Question 26

neurocrines

Answer 26

-action potentials
-ACh- contraction smooth muscle in wall, relax sphincters, increase salivary secretion, increase gastric secretion, increase pancreatic secretion
-Vasoactive intestinal peptide (VIP)- relaxation of smooth muscle, increase intestinal secretion, increase pancreatic secretion
-nitric oxide (NO)- relaxation of smooth muscle
-gastrin releasing peptide (GRP)- increase gastrin
-substance P- contraction of smooth muscle, increase salivary secretion
-ENKEPHALINS (opiates)- contraction of smooth muscle, decrease intestinal secretion
-norepinephrine- relax smooth muscle in wall, contraction of sphincters, increase salivary secretion

Question 27

ZE syndrome

Answer 27

-hypertrophy and increase H+
-high H+ and gastrin
-gastrin secreted by pancreatic tumor
-high gastrin -> increase parietal cell
-duodenal ulcers
-1) inactivates pancreatic lipase -> steatorrhea
-2) duodenum is acidic (HCO3- cant neutralize) -> no absorption of lipids in duodenum -> steatorrhea
-decrease fat absorption and digestion
-diarrhea- LARGE volume passed stimulated by gastrin
-tx- PPI

Question 28

GI smooth muscle: which are not smooth, circular vs long, electrical activity

Answer 28

-all of GI tract is smooth muscle except:
-1.pharynx
-2.upper 1/3 esophagus
-3. anal sphincter
-these muscles are striated

-circular muscle contraction -> decrease diameter
-longitudinal muscle -> decrease length
-when one contracts the other relaxes -> peristalsis

-gap junctions
-burst of action potential -> oscillating depolarization and repolarization
-twitches summate -> one long contraction -> tension

Question 29

swallowing

Answer 29

-3 phases:
-1. UES- voluntary
-2. pharyngeal- reflex
-3. esophageal- reflex
-involuntary swallowing- medulla
-gravity helps
-primary peristaltic contraction- contracts behind the food to increase pressure
-vasovagal reflex- stomach relaxes to decrease pressure and allow food to come through
-while LES contracted -> esophagus pressure > stomach pressure
-secondary peristaltic contraction- only stimulated by enteric if primary fails

Question 30

achalasia

Answer 30

-LES cant relax
-impaired peristalsis lower 2/3
-dilation of esophagus above LES

Question 31

acid reflux: obesity and pregnancy

Answer 31

-stomach pressure is increased
-causes reflux

Question 32

vomiting

Answer 32

-relaxation of stomach, pylorus, and LES
-forced inspiration increase the pressure of the stomach
-reverse peristalsis
-retching- LES remains closed

Question 33

physical vs chemical barrier in stomach

Answer 33

-mucus- physical -> secreted in antrum
-chemical - chemical (HCO3-)

Question 34

inhibition of H+ secretion

Answer 34

-atropine- blocks ACh
-H2 blockers- cimedtidine/famotidine- blocks histamine -> ulcers
-PPI- omeprazole- blocks H+-K+ ATPase -> essential blocks everything
-POTENTIATION- when you block one thing it has a greater effect of just inhibiting that signal
-ex. when you block histamine it affects gastrin and ACh -> having a larger effect

Question 35

PUD

Answer 35

-increase H+ or pepsin
-decreased mucus barrier
-things that make it worse -> NSAIDs, h. pylori, stress, smoking, alcohol
-make better -> prostaglandins, mucosal blood flow, growth factors

Question 36

gastric vs duodenal ulcer

Answer 36

-gastric ulcer - decrease H+ secretion, increased gastrin (bc low H+) -> damages protective barrier of gastric mucosa
-duodenal ulcer - increase H+ secretion, increase gastrin (in response to food) -> increase partietal cell mass due to increased gastrin

Question 37

digestion of carbs

Answer 37

-amylase in saliva and pancreas/duodenum
-absorbed in small intestine
-products of digestion- glucose, galactose, fructose
-starch -> disaccharides -> monosaccharides (glucose, galactose, fructose)
-facilitated diffusion and secondary active transport
-lactose -> glucose and galactose

Question 38

protein digestion

Answer 38

-pepsin in stomach (NON ESSENTIAL)
-pancreatic + brush border proteases in small intestine
-absorbed in small intestine- cotransport
-products of digestion- AA, dipeptides, tripeptides
-trypsin, chymotrypsin, carboxypeptidase, elastase -> pancreas/duodenum
-amino-oligopeptidase, dipeptidase, enterokinase -> intestinal mucosa

Question 39

digestion of lipids

Answer 39

-lingual lipase- saliva
-absorbed in small intestine
-products of digestion- fatty acid, monoglycerides, cholesterol
-lipase colipase, phospholipase A2, cholesterol ester, hydrolase - pancreas/duodenum

Question 40

process of bile

Answer 40

-bile- bile salts, cholesterol, bile pigment (bilirubin) -> make up pee and poop color
-liver produces the bile
-gallbladder stores the bile
-bile emulsifies the lipids -> micelles
-bile salts are absorbed via the portal vein in the ileum to be recirculated
-liver cant keep up with production of new bile
-CCK stimulates slow gastric emptying to allow time for lipids to be digested (complicated process)
-CCK stimulates contraction of gallbladder to release bile
-CCK stimulates relaxation of sphincter of oddi

Question 41

ileal resection

Answer 41

-without the ileum there is no bile salt absorption and recirculation to the liver
-liver cant keep up with the synthesis of new bile salts
-decreases bile salts overall
-decrease lipid absorption
-steatorrhea (lipids are being excreted)
-diarrhea can also occur bc increased Cl -> Na and water follow -> secretory diarrhea
-ALSO, pernicious anemia bc no B12 absorption (also caused by gastrectomy)

Question 43

abnormal protein digestion

Answer 43

-chronic pancreatitis and cystic fibrosis (thick secretions block pancreatic ducts) -> decrease pancreatic enzymes (proteases) -> no protein absorption
-cystinuria (genetic disorder of protein transporters) -> no protein absorption

Question 44

abnormal lipid digestion

Answer 44

-pancreatic disease and hypersecretion of gastrin (decrease pH) -> decrease/inactivate pancreatic lipase -> malabsorption of lipids -> steatorrhea
-ileal resection and bacterial overgrowth (bile acids absorbed early) -> decrease bile acids -> malabsorption of lipids -> steatorrhea

Question 45

calcium malabsorption

Answer 45

-vitamin D deficiency or chronic renal failure (kidneys absorb Ca)
-causes inadequate calcium absorption
-children- rickets
-adults- osteomalacia

Question 46

jaundice

Answer 46

-increase RBC destruction
-increase unconjugated bilirubin
-bile duct obstruction
-liver disease cfa

Question 47

fluids ingested and secreted vs absorbed

Answer 47

-ingested and secreted- 9L
-absorbed - almost all the 9L

Question 48

small vs large intestine

Answer 48

-small- leaky, paracellular transport
-large intestine- tight

Question 49

aldosterone

Answer 49

-stimulates Na absorption and K secretion

Question 50

diarrhea

Answer 50

-decrease Na and water -> dehydration -> decrease arterial pressure
-decrease K -> hypokalemia, metabolic acidosis
-decrease HCO3- -> hyperchoremic metabolic acidosis with normal anion gap
-secretory diarrhea ex. cholera caused by bacterial overgrowth (e.coli or vibrio cholerae)

Question 51

bile acid sequestrants

Answer 51

-cholestyramine
-bind to bile acids -> inhibiting their absorption -> liver tries to make more bile acids due to excessive excretion -> cholesterol is needed to make bile -> decreases cholesterol and increases bile!!!
-Used for patients with high LDLs (hyperlipidemia)
-Also antidiarrheal affect for bile acid diarrhea - bile acid diarrhea - drug binds to negatively charged bile acids → bile acids can’t trigger diarrhea in colon mucosa

Question 52

statin

Answer 52

-inhibits the release of all GI hormones
-inhibits gastric H+ secretion
-Inhibits cholesterol synthesis → decrease LDLs
-steatorrhea and diarrhea?

Question 53

antacids

Answer 53

-inhibits pepsin

Question 54

5-ASA

Answer 54

-Inhibits production of inflammatory chemicals and modulates immune response = anti-inflammatory
-In the same family as aspirin
-allows for healing of the brush border → proper absorption of nutrients and digestion
-Helps reduce symptoms of pain, diarrhea, rectal bleeding

Question 55

antispasmodics SE

Answer 55

S/E: urinary retention, tachycardia, dry mouth, constipation
Basically lowered parasympathetic NS, increased sympathetic NS