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GI Physiology Flashcards

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1
Q

Saliva

A

-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

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2
Q

bile juice

A

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

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3
Q

pancreatic juice

A

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

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4
Q

Gastric Juice

A

-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

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5
Q

pepsinogen

A

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

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6
Q

cholecystokinin (CCK)

A

-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

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7
Q

secretin

A

-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)

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8
Q

gastrin

A

-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

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9
Q

glucose-dependent insulinotropic peptide (GIP)

A

-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?

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10
Q

somatostatin

A

-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

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11
Q

motilin

A

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

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12
Q

pancreatic polypeptide

A

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

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13
Q

glucagon like peptide (GLP-1)

A

-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

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14
Q

enteroglucagon

A

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

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15
Q

histamine

A

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

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16
Q

leptin

A

-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

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17
Q

insulin

A

-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

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18
Q

appetite suppression

A

-GLP-1
-insulin
-leptin

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19
Q

ghrelin

A

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

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20
Q

peptide YY (PYY)

A

-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

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21
Q

pepsinogen

A

-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

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22
Q

extrinsic systemic: sympathetic input

A

-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

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23
Q

extrinsic systemic: parasympathetic input

Study These Flashcards
A

-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

24
Q

intrinsic system aka enteric

Study These Flashcards
A

-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

25
which increases salivary secretion -> sympathetic or parasympathetic?
BOTH!!!!
26
neurocrines
-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
27
ZE syndrome
-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
28
GI smooth muscle: which are not smooth, circular vs long, electrical activity
-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
29
swallowing
-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
30
achalasia
-LES cant relax -impaired peristalsis lower 2/3 -dilation of esophagus above LES
31
acid reflux: obesity and pregnancy
-stomach pressure is increased -causes reflux
32
vomiting
-relaxation of stomach, pylorus, and LES -forced inspiration increase the pressure of the stomach -reverse peristalsis -retching- LES remains closed
33
physical vs chemical barrier in stomach
-mucus- physical -> secreted in antrum -chemical - chemical (HCO3-)
34
inhibition of H+ secretion
-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
35
PUD
-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
36
gastric vs duodenal ulcer
-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
37
digestion of carbs
-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
38
protein digestion
-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
39
digestion of lipids
-lingual lipase- saliva -absorbed in small intestine -products of digestion- fatty acid, monoglycerides, cholesterol -lipase colipase, phospholipase A2, cholesterol ester, hydrolase - pancreas/duodenum
40
process of bile
-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
41
ileal resection
-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)
42
43
abnormal protein digestion
-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
44
abnormal lipid digestion
-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
45
calcium malabsorption
-vitamin D deficiency or chronic renal failure (kidneys absorb Ca) -causes inadequate calcium absorption -children- rickets -adults- osteomalacia
46
jaundice
-increase RBC destruction -increase unconjugated bilirubin -bile duct obstruction -liver disease cfa
47
fluids ingested and secreted vs absorbed
-ingested and secreted- 9L -absorbed - almost all the 9L
48
small vs large intestine
-small- leaky, paracellular transport -large intestine- tight
49
aldosterone
-stimulates Na absorption and K secretion
50
diarrhea
-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)
51
bile acid sequestrants
-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
52
statin
-inhibits the release of all GI hormones -inhibits gastric H+ secretion -Inhibits cholesterol synthesis → decrease LDLs -steatorrhea and diarrhea?
53
antacids
-inhibits pepsin
54
5-ASA
-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
55
antispasmodics SE
S/E: urinary retention, tachycardia, dry mouth, constipation Basically lowered parasympathetic NS, increased sympathetic NS

Physiology (24 decks)

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