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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
components of bile
bile acids and salts 50%cholesterol 4%lecithin (phospholipid) 30-40%bile pigment (bilirubin) 2%
27
bile and blood flow through liver
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
28
blood and bile transport
bile acids: secondary active transport into hepatocyte from blood, facilitated diffusion into bilewater and electrolytes: paracellularlly down [] gradient
29
regulation of bile flow
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
30
reabsorption of bile
95% reabsorbedIleum: active absorption of ionized conjugated bile salts (Na dependent)passive of unconjugated and unionized conjugated throughout entire SI and colon
31
total body bile pool
2-3 grams -> cycles through liver multiple times per day -> total liver bile output 15-30 g/day
32
colon cancer
associated with high fat dietsLithocholic Acid is also linked to colon cancerVitamin D is associated with less colon cancer
33
Formation of gallstones
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
34
risk factors for gallstones
ObesityGenderEthnicityAge Rapid weight lossFastingEstrogendiabetescholesterol lowering drugs
35
Carb digestion
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
36
Carb absorption
Must be monosaccharideslumen -> enterocyte: SGLT1 (fructose via GLUT 5)enterocyte -> blood: GLUT 2
37
exocrine pancreas produces
enzymes to digest carbohydrates, fats, and proteins and HCO3 to neutralize gastric acid.
38
acinar cells and stimuli
produce enzymesstimuli: CCK, ACh
39
ductal cells and stimuli
produce HCO3- (aqueous secretion)stimuli: secretin (CCK and ACh potentiate)
40
secretin 2ndary messenger
cAMP
41
CCK and ACh 2ndary messenger
increased [Ca] via IP3
42
Most Carb abnormality
deficiency in digestion increased osmotic pressure in lumen -> osmotic diarrhea ex) lactose intolerance
43
acinar cells and stimuli
produce enzymesstimuli: CCK, ACh
44
ductal cells and stimuli
produce HCO3- (aqueous secretion)stimuli: secretin (CCK and ACh potentiate)
45
secretin 2ndary messenger
cAMP
46
CCK and ACh 2ndary messenger
increased [Ca] via IP3
47
Most Carb abnormality
deficiency in digestion increased osmotic pressure in lumen -> osmotic diarrhea ex) lactose intolerance
48
Protein digestion
All proteins assimilatedbegins in stomach with pepsinThen proteases in SI take over and cleave proteins into AA's, di, and tri peptides
49
Pancreatic proteases
trypsin, elastase, chymotrypsin, carboxypeptidase A and BTrypsin is activated by enterokinase, then activates all the restDigest themselves after
50
Protein absorption
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
Lipid digestion:
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
Lipid absorption
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
Chylomicron structure
core: FA's and cholesterolsurface: phospholipids and apoproteins
54
Chylomicron synthesis
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
3 types of lipid absorption abnormalities
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
ß-lipoproteinemia
Failure of enterocytes to synthesize apoprotein B results in the inability to export chylomicrons
57
Fat soluble vitamins
D. E. A. K
58
Ca absorption
1. passive paracellular2. active transcellular - vit. D stim taken up in Ca channel extruded by Na-Ca pump
59
Iron reabsorption
reabsorbed as Fe2+enters: DCT1 channel or binds transferrin
60
B12 reabsorption
binds heptacurrin in mouthbinds IF in duodenumtaken up in ileum by IF receptor mediated transport
61
pernicious anemia
autoimmune destruction of Parietal cells in stomach -> decrease IF -> decreased B12 reabsorption
62
fluid in intestines and how much aborbed
9L in (2 ingested, 7 secreted)8.8 absorbed (majority in SI)
63
Small intestines absorption
leaky epithelium -> isotonic absorption
64
Colon aborption
tight epithelium -> hyperosmotic absorption
65
How is feces alkalinized
by the colon Cl-HCO3 exchangernet secretion of H2CO3 and absorption of NaCl in these cells
66
K+ in intestines
absorbed in small intestines -> passively paracellularlysecreted actively by K+ channels (aldosterone stimulated) and passively paracellularly
67
Intestines reabsorption site
villi
68
intestines secretion site and substance
cryptsCl is main secretion (through CFTR regulated by cAMP)Na (paracellularly) and water follows
69
4 causes of diarrhea
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
GI secretegogues
Mucosa: serotonin, neurotensin, guanylinLamin propria: prostaglandins, NO, histamineEnteric nerves: ACh, VIP
71
Stress Activation (LES)
pressure on LES --> contracts
72
Active relaxation (LES)
swallow causes vagal relaxation of LES (VIF action potentials) and Orad stomach --> remains relaxed till peristalsis ends
73
swallowing phases
oral: voluntarily initated, becomes involuntarypharyngeal: pressure drops -> food passes -> pressure increases againesophageal: slower peristalsis
74
Gastric SM function
1) relax -> accomodate food (fundus)2) contraction -> mix and digest food3) peristalsis -> propel into duodenum (body and antrum)
75
Receptive relaxation
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
Gastric emptying stimulators
filling of stomach -> local enteric -> antral contractionproteins in stomach -> gastrin -> antral contraction
77
gastric emptying inhibitors
acid in duodenum -> secretin -> slows antral contraction, + pyloric contractionfats in duodenum -> CCK -> antral and pyloric contractionpeptides and AA's in duodenumhyperosmolarity in duodenum
78
Migratory Motor Complex
sweeps undigestible, cell debris, mucus etc into colonduring fasting state3 phases: no spike potential -> irreg spike potentials -> regular spike potentialsMotilin stimulates
79
slow waves in stomach vs SI
stomach: slow waves trigger contractions, even if smallSI: only slow waves reaching threshold and causing AP's or SP's cause contraction
80
SI muscle contraction stimulators
Opiates, Parasympathetic, serotonin, opiates, gastrin, cck, insulin
81
SI muscle contraction inhibitors
Sympathetics, VIP, Glucagon, NO
82
Law of intestines
distension -> contraction above and relaxation below
83
Vomiting
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
motility of cecum and prox colon
high tone and enteric inhibits to relax -> mixing contractions -> 1-3 mass movements per day
85
saliva osmotic state
ALWAYS hypotonic to plasmaleaving acini it is isotonic to plasm -> ducts remove NaCl
86
rate of secretion and saliva
increased secretion rate -> less ductal modificationdecreased secretion rate -> more hypotonic
87
Salivary gland secretion stim
parasymp (ACh) and symp (norepinephrine)parasymp = stronger - increases ion transport, increases myoepithelial cell contraction, direct, metabolic and kallikrein stimulated vasodilation
88
components of gastric juice
HCl -> parietal cellsPepsinogen -> chief cellsMucin -> surface epithelial and mucous neck cellsIF -> parietal cells (essential)ALWAYS isotonic to plasma
89
Parietal HCl secretion mechanism
H2CO3 -> H+ to lumen via H-K exchange and HCO3 to blood via HCO3-Cl exchangeCl- to lumen via Cl channel
90
stimulators of gastric HCl secretion
AChGastrinHistamineTogether they potentiate each others response
91
Cephalic Phase
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
Gastric phase
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
intestinal phase
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
inhibition of Gastric acid
secretin, CCK, GIP and Hypertonicity
95
Pepsinogen secretion stim
Vegas stim, Gastrin, Acid, Secretin, CCK
96
Pancreatic Acinar cells
secrete digestive enzymesACh and CCK mediated
97
Pancreatic Duct cells
secrete aqueous secretion -> HCO3 and fluidSecretin (potentiated by CCK and ACh)
98
pancreatic secretion
parasympathetic stimulatesSympathetic inhibits at all rates secretion is IsotonicCl and HCO3 are reciprocal

M:1 year (19 decks)

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