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M:1 year > deck_636935 > Flashcards

deck_636935 Flashcards

2
Q

GI Functions

A

Digestion and absorptionEliminationProtection of epithelium

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3
Q

Myenteric plexus

A

Part of enteric nervous systemlocated b/w circular and longitudinal muscle layersRegulates motility, peristalic and segmental contractions

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4
Q

Submucosal Plexus

A

Part of enteric nervous systemlocated b/w submucosa and circular muscularisregulates: glandular, endocrine and epithelial cell secretion; also circular muscle layer

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5
Q

Parasymp on GI

A

synapse in enteric nervous ganglionsexcitatory and release of ACH–> increase ENS activityIncrease motilityvasodilation (indirect)Increase secretionDecrease sphincter tone

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6
Q

Sympathetic on GI

A

Inhibitory and release norepinephrine –> decrease ENS activityDecrease motilityvasoconstrict (direct)Decrease secretionincrease sphincter tone

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7
Q

Blood drainage through GI

A

Drains into hepatic portal vein –> liver –> general circulation

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8
Q

GALT roles

A
  1. Protection from pathogens2. immunogenic tolerance to food and “good” bacteria
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9
Q

Gastrin

A

Released by G cells of antral stomach Stim by: small peptides and aa’s distention of the stomach vagal stimulation by GRP Gastrin stimulates: parietal cells to secrete HCl ECL cells to secrete histamine –> stimulates acid secretion growth of mucosaAcid (low pH) in the stomach inhibits gastrin release.

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10
Q

CCK

A

Released by I cells in duodenumStim by: proteins, fat CCK stimulates: gallbladder contraction –> bile release secretion of pancreatic enzymes (lipase and proteases) inhibits gastric emptying increases secretin action growth of exocrine pancreas

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11
Q

Secretin

A

Released by S cells in duodenumStim by: H+ and FA’sSecretin Stimulates: HCO3 release from pancreas pancreatic secretion exocrine pancreas growth inhibits parietal cell H+ release

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12
Q

GIP

A

Released by: cells of the duodenum and jejunumStim by: oral glucose, FAs, AAsGIP stimulates: insulin release by pancreatic ß-cells (sensitizes beta cells) may inhibit gastric acid secretion

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13
Q

Motilin

A

Released by: duodenal mucosa during fastingincreases contraction and motility–> prepare GI for next meal

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14
Q

Ghrelin

A

Produced by stomachincreases b/w mealscauses: GH release, hunger, weight gain, fat massdecreases: fat utilization

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15
Q

Vasoactive Intestinal Peptide

A

relaxes GI SM (particularly around sphincters)stim’s local mesenteric blood flowstim’s pancreatic and intestinal fluid secretion

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16
Q

Somatostatin

A

GI paracrine that puts stops GI activityinhibits GI hormones and gastric acidinhibited by vagal parasympathetic

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17
Q

Interstitial Cells of Cajal

A

Pacemaker cells of SM in the GIDrives the frequency of slow waves –> determines rate of action potential and contraction

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18
Q

Hormones and Nerves effect on GI SM

A

set slow wave frequency by ICC not changed by hormone or nervesamplitude/contraction strength (via increased action potential frequency) can be modified Norepinephrine –> decrease contractile activityACH –> increases contractile activity both modulate Ca efflux and influx

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19
Q

GI SM excitatory agents

A

ACH, substance P, Opeoids, CCK, Bombesin, serotonin

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20
Q

GI SM inhibitory agents

A

VIP, glucagon, NO, somatostatin, norepinephrine

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21
Q

Bile functions

A

emulsify fat for digestion by lipasessolubilize FA’s into micellesvehicle for toxins and waste

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22
Q

describe flow of bile

A

bile salts and acids secreted from liver continuouslysecretion draws water and electrolytes into bileadditional fluid and electrolytes added by ductsclose sphincter of odi and hydrostatic pressure causes filling of gallbladdergallbladder concentrates bile CCK and ACh stimulate release of bilebile acts in small intestines -> reabsorbed in ileum to portal vein -> back to liver

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23
Q

Primary Bile acids

A

synthesized in hepatocytes from cholesterolcholic acidchendodeoxycholic acid

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24
Q

secondary bile acids

A

synthesized by gut bacteria from primary bile acids

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25
Q

bile salts

A

form by liver from conjugating bile acids with glycine or taurinedecreases pKa -> more soluble in intestinal pH

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26
Q

components of bile

A

bile acids and salts 50%cholesterol 4%lecithin (phospholipid) 30-40%bile pigment (bilirubin) 2%

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27
Q

bile and blood flow through liver

A

counter current flow ->allows exchange of bile and blood and minimizes concentration gradient b/w the bile and bloodbile caniculi carry bile peripherally while hepatic artery and portal artery carry blood centrallyCanicular fluid similar to plasma… ducts modify

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28
Q

blood and bile transport

A

bile acids: secondary active transport into hepatocyte from blood, facilitated diffusion into bilewater and electrolytes: paracellularlly down [] gradient

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29
Q

regulation of bile flow

A

Feedback regulation: B.A.’s in hepatic portal blood -> stim. bile acid secretion and inhibit bile acid synthesissecretin - stim. duct cell secretionCCK and ACh - stim gallbladder contraction

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30
Q

reabsorption of bile

A

95% reabsorbedIleum: active absorption of ionized conjugated bile salts (Na dependent)passive of unconjugated and unionized conjugated throughout entire SI and colon

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31
Q

total body bile pool

A

2-3 grams -> cycles through liver multiple times per day -> total liver bile output 15-30 g/day

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32
Q

colon cancer

A

associated with high fat dietsLithocholic Acid is also linked to colon cancerVitamin D is associated with less colon cancer

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33
Q

Formation of gallstones

A

organ substances of bile precipitate out of solutionCholesterol gallstone: increased cholesterol and decreased bile acids = gallstones Pigment stone: formed by precipitation of unconjugated bilirubin and Ca

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34
Q

risk factors for gallstones

A

ObesityGenderEthnicityAge Rapid weight lossFastingEstrogendiabetescholesterol lowering drugs

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35
Q

Carb digestion

A

begins in mouth with alpha amylasecontinues in duodenum w/ lumenal break down of polysaccharidescontact membrane digestion of disaccharides by brush border (alpha dextranase)absorption of monosaccharides

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36
Q

Carb absorption

A

Must be monosaccharideslumen -> enterocyte: SGLT1 (fructose via GLUT 5)enterocyte -> blood: GLUT 2

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37
Q

exocrine pancreas produces

A

enzymes to digest carbohydrates, fats, and proteins and HCO3 to neutralize gastric acid.

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38
Q

acinar cells and stimuli

A

produce enzymesstimuli: CCK, ACh

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39
Q

ductal cells and stimuli

A

produce HCO3- (aqueous secretion)stimuli: secretin (CCK and ACh potentiate)

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40
Q

secretin 2ndary messenger

A

cAMP

41
Q

CCK and ACh 2ndary messenger

A

increased [Ca] via IP3

42
Q

Most Carb abnormality

A

deficiency in digestion increased osmotic pressure in lumen -> osmotic diarrhea ex) lactose intolerance

43
Q

acinar cells and stimuli

A

produce enzymesstimuli: CCK, ACh

44
Q

ductal cells and stimuli

A

produce HCO3- (aqueous secretion)stimuli: secretin (CCK and ACh potentiate)

45
Q

secretin 2ndary messenger

A

cAMP

46
Q

CCK and ACh 2ndary messenger

A

increased [Ca] via IP3

47
Q

Most Carb abnormality

A

deficiency in digestion increased osmotic pressure in lumen -> osmotic diarrhea ex) lactose intolerance

48
Q

Protein digestion

A

All proteins assimilatedbegins in stomach with pepsinThen proteases in SI take over and cleave proteins into AA’s, di, and tri peptides

49
Q

Pancreatic proteases

A

trypsin, elastase, chymotrypsin, carboxypeptidase A and BTrypsin is activated by enterokinase, then activates all the restDigest themselves after

50
Q

Protein absorption

A

Absorbed across 7 different AA specific channelsAA absorption is Na coupledPeptide absorption is proton coupleddi and tri peptides absorb faster (70% of absorbed protein)

51
Q

Lipid digestion:

A

begins in mouth and stomach via lingual and gastric amylases -> release FA’smajority digested in SI: bile eulsifies fats -> increased exposure of fats to amylases -> TG’s -> FA’s and MonoglyceridesPL’S -> lysolecithin, FA’s, monolipidsCHO -> free cholesterol, FA’s, Glycerol

52
Q

Lipid absorption

A

bile salts aid in micelle formation of lypolitic products -> transports to acid microclimate outside of enterocytes -> lipids are protonated by acid aid in solubility and diffusion into enterocytes with help of FA binding proteinsglycerol = soluble -> free diffusion short and medium chain -> free diffusionCholesterol absorbed slowest

53
Q

Chylomicron structure

A

core: FA’s and cholesterolsurface: phospholipids and apoproteins

54
Q

Chylomicron synthesis

A

Lipids are converted back to TG’s, PL’s and cholesterols are re-esterified in SERchylomicron form by GolgiChylomicron is exocytized and enters lacteal -> enters blood at thoracic duct

55
Q

3 types of lipid absorption abnormalities

A
  1. decreased bile salts ex) resected ileum2. increased acid in duodenum -> from hypersecretion in stomach ex) zollinger-elison syndrome3. Pancreatic insufficiency -> decreased enzymes ex) cystic fibrosis, pancreatitislipid absorption abnormalities are more common than carb and protein
56
Q

ß-lipoproteinemia

A

Failure of enterocytes to synthesize apoprotein B results in the inability to export chylomicrons

57
Q

Fat soluble vitamins

A

D. E. A. K

58
Q

Ca absorption

A
  1. passive paracellular2. active transcellular - vit. D stim taken up in Ca channel extruded by Na-Ca pump
59
Q

Iron reabsorption

A

reabsorbed as Fe2+enters: DCT1 channel or binds transferrin

60
Q

B12 reabsorption

A

binds heptacurrin in mouthbinds IF in duodenumtaken up in ileum by IF receptor mediated transport

61
Q

pernicious anemia

A

autoimmune destruction of Parietal cells in stomach -> decrease IF -> decreased B12 reabsorption

62
Q

fluid in intestines and how much aborbed

A

9L in (2 ingested, 7 secreted)8.8 absorbed (majority in SI)

63
Q

Small intestines absorption

A

leaky epithelium -> isotonic absorption

64
Q

Colon aborption

A

tight epithelium -> hyperosmotic absorption

65
Q

How is feces alkalinized

A

by the colon Cl-HCO3 exchangernet secretion of H2CO3 and absorption of NaCl in these cells

66
Q

K+ in intestines

A

absorbed in small intestines -> passively paracellularlysecreted actively by K+ channels (aldosterone stimulated) and passively paracellularly

67
Q

Intestines reabsorption site

A

villi

68
Q

intestines secretion site and substance

A

cryptsCl is main secretion (through CFTR regulated by cAMP)Na (paracellularly) and water follows

69
Q

4 causes of diarrhea

A
  1. secretory - increased Cl secretion (cAMP mediated)2. Osmotic diarrhea3. mucosal destruction - leaky epithelium and decreased absorption and increased secretion4. increased motility - decrease absorption time
70
Q

GI secretegogues

A

Mucosa: serotonin, neurotensin, guanylinLamin propria: prostaglandins, NO, histamineEnteric nerves: ACh, VIP

71
Q

Stress Activation (LES)

A

pressure on LES –> contracts

72
Q

Active relaxation (LES)

A

swallow causes vagal relaxation of LES (VIF action potentials) and Orad stomach –> remains relaxed till peristalsis ends

73
Q

swallowing phases

A

oral: voluntarily initated, becomes involuntarypharyngeal: pressure drops -> food passes -> pressure increases againesophageal: slower peristalsis

74
Q

Gastric SM function

A

1) relax -> accomodate food (fundus)2) contraction -> mix and digest food3) peristalsis -> propel into duodenum (body and antrum)

75
Q

Receptive relaxation

A

relaxation of orad region of stomach as food enters -> allows for increased digestion (particularly by alpha amylase) mediated by vagus (vagovagal) VIP important in relaxationCCK, secretin, GIP increase orad distensibility too

76
Q

Gastric emptying stimulators

A

filling of stomach -> local enteric -> antral contractionproteins in stomach -> gastrin -> antral contraction

77
Q

gastric emptying inhibitors

A

acid in duodenum -> secretin -> slows antral contraction, + pyloric contractionfats in duodenum -> CCK -> antral and pyloric contractionpeptides and AA’s in duodenumhyperosmolarity in duodenum

78
Q

Migratory Motor Complex

A

sweeps undigestible, cell debris, mucus etc into colonduring fasting state3 phases: no spike potential -> irreg spike potentials -> regular spike potentialsMotilin stimulates

79
Q

slow waves in stomach vs SI

A

stomach: slow waves trigger contractions, even if smallSI: only slow waves reaching threshold and causing AP’s or SP’s cause contraction

80
Q

SI muscle contraction stimulators

A

Opiates, Parasympathetic, serotonin, opiates, gastrin, cck, insulin

81
Q

SI muscle contraction inhibitors

A

Sympathetics, VIP, Glucagon, NO

82
Q

Law of intestines

A

distension -> contraction above and relaxation below

83
Q

Vomiting

A

ANS -> controled by vomiting center in medullaprotective (prolonged -> dehydration, alkalosis, hypokalemia)reverse peristalsis in distal SILES relaxesinspiration and abdominal contractionstrong abdominal contraction moves material through UES

84
Q

motility of cecum and prox colon

A

high tone and enteric inhibits to relax -> mixing contractions -> 1-3 mass movements per day

85
Q

saliva osmotic state

A

ALWAYS hypotonic to plasmaleaving acini it is isotonic to plasm -> ducts remove NaCl

86
Q

rate of secretion and saliva

A

increased secretion rate -> less ductal modificationdecreased secretion rate -> more hypotonic

87
Q

Salivary gland secretion stim

A

parasymp (ACh) and symp (norepinephrine)parasymp = stronger - increases ion transport, increases myoepithelial cell contraction, direct, metabolic and kallikrein stimulated vasodilation

88
Q

components of gastric juice

A

HCl -> parietal cellsPepsinogen -> chief cellsMucin -> surface epithelial and mucous neck cellsIF -> parietal cells (essential)ALWAYS isotonic to plasma

89
Q

Parietal HCl secretion mechanism

A

H2CO3 -> H+ to lumen via H-K exchange and HCO3 to blood via HCO3-Cl exchangeCl- to lumen via Cl channel

90
Q

stimulators of gastric HCl secretion

A

AChGastrinHistamineTogether they potentiate each others response

91
Q

Cephalic Phase

A

MOUTH: parasympathetic -> saliva secretionSTOMACH: vegas -> gastrin -> parietal cells and ECL cells -> HCl and histamine -> parietal cells -> HCl- vegas -> pepsinogenINTESTINE: vegas -> pancreatic enzyme secretion (acini)

92
Q

Gastric phase

A

MOUTH: noneSTOMACH: - vegas -> gastrin -> parietal and ECL -> HCl and Histamine- distention -> parietal -> HCl- vegas -> parietal -> HCl- vegas -> chief cells -> pepsinogen- AA’s and fat -> gastrin -> parietal -> HCl- H+ -> chief -> pepsinogen and parietal -> decrease HClINTESTINE: vegas -> Pancreatic acinar -> enzymes

93
Q

intestinal phase

A

MOUTH: nothingSTOMACH: CCK -> decreased gastric emptying and decreased HCl production- Secretin -> decreased HClINTESTINES: - AA’s, Fat, CHO -> CCK -> gallbladder contraction and Oddi relax and acinar secretion- H+ -> Secretin -> HCO3- Vegas -> ACh -> gallbladder contraction and acinar secretion- CHO -> GIP -> B-cell sensitization

94
Q

inhibition of Gastric acid

A

secretin, CCK, GIP and Hypertonicity

95
Q

Pepsinogen secretion stim

A

Vegas stim, Gastrin, Acid, Secretin, CCK

96
Q

Pancreatic Acinar cells

A

secrete digestive enzymesACh and CCK mediated

97
Q

Pancreatic Duct cells

A

secrete aqueous secretion -> HCO3 and fluidSecretin (potentiated by CCK and ACh)

98
Q

pancreatic secretion

A

parasympathetic stimulatesSympathetic inhibits at all rates secretion is IsotonicCl and HCO3 are reciprocal

M:1 year (19 decks)

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