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Peds GI RC > Physiology > Flashcards

Physiology Flashcards

1
Q

Gastric factors that control gastric emptying?

A
  • Rate of emptying proportion to volume of chyme
  • gastric distention triggers motility - direct effects on gastric stretch receptor
  • vagal nerve and intrinsic nerves of stomach wall
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2
Q

Duodenal factors controlling gastric emptying

A

-particle size/consistency - pylorus retains particles > 2 mm
-pH = acid pH of antral content decrease emptying
-osmolarity - hypertonic gastric contents increase osmoreceptors and chemoreceptors in duodenum and decrease gastric emptying
increase fat content = decrease emptying
-duodenal mucosal receptors for FA, AA and CHO - triggered by increase size or energy density = increased emptying
-ileal break = unabsorbed nutrients in the ileum and colon = increase PYY, GLP-1, GLP-2 which decrease gastric emptying

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3
Q

Where does CCK come from

A

Source: I cells in SI
Receptor: CCK receptor in CNS
Action: suppresses appetite by decreasing gastric emptying and secretion, promotes gallbladder contraction and pancreatic enzyme, water and ion secretion

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4
Q

Where does Gastrin-Releasing Peptide come from

A

Source: G cells in antrum in response to vagus stimulation
Receptor: G cells
Action: induces satiety by increasing gastric acid secretion and decreasing gastric emptying

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5
Q

What does Apolipoprotein a-IV do

A

Source: intestinal mucosa
Receptor: CNS
Action: centrally mediated appetite suppression in response to fat absorption

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6
Q

What does Leptin do?

A

Source: adipocytes
Receptor: hypothalamus
Action: decrease appetite

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7
Q

What does Peptide Tyrosine-tyrosine (PYY) do

A

Source: L cells in ileum and colon
Receptor: neuropeptide Y receptors in the CNS and ANS
Action: decrease appetite by slowing gastric emptying and decreasing pancreatic secretion

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8
Q

What does Pancreatic polypeptide (PP) do?

A

Source: F cells - Pancreatic endocrine cells
Receptor: PP receptors in pancreas, GI and CNS
Action: decrease pancreatic exocrine secretion, gallbladder contractions and gut motility

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9
Q

What does Glucagon-like peptide (GLP) do?

A

Source: ileal L cells
Receptors: GLP-1 receptors in the pancreas
Action: decrease gastric motility; contributes to satiety by decrease absorption of CHOs

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10
Q

What does Ghrelin do

A

Source: Produced by D cells in stomach and epsilon cells in pancreas
Receptor: Ghrelin receptor in hypothalamus and pituitary gland
Action: increase hunger and GH

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11
Q

Where is Serotonin from

A
  • Released by intestinal enterochromaffin cells and nerve terminals of the enteric nervous system
  • mediates CCK and secretin secretion into portal circ
  • bind to receptors on gallbladder and pancreas
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12
Q

What does secretin do

A

-increases pancreatic enzymes and HCO3- secretion

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13
Q

How is pancreatic secretion controlled

A

-Coordination cephalic (vagus), gastric (acid, pepsin and gastric emptying) and intestinal (CCK/secretin)

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14
Q

Where does enterokinase come from?

A
  • Duodenal crypts of Lieberkuhn
  • secreted in response to chyme
  • activates pancreatic trypsinogen to trypsin
  • trypsin activates other enzymes
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15
Q

How are LCFA transferred across the BBM

A
  • Extracellular: LCFA bind to FA transport protein complex on the enterocyte
  • Intracellular: LCFAs are coupled to CoA by LCFA acyl CoA synthetase to prevent efflux from the enterocyte
  • Fatty-acid-binding protein acts as a cytoplasmic buffer for incoporation of LCFA into the cell
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16
Q

What is the intracellular processing of lipids

A
  • Absorbed intracellular FAs bind to fatty-acid-binding proteins for transport into the ER
  • in ER triglyceride is resynthesizes in 2 days
    a) Monoglyceride pathway in which triglycerides are resynthesizes from absorbed FA and monoglycerides
    b) Microsomal triglyceride transfer protein (MTP) transfers resynthesizes triglycerol (TG), phospholipids and cholesterol to apolipoproteins A1, A4 and B48
  • deficiency of MTP = abetalipoproteinemia
  • Triglycerides and phospholipids synthesized via the alpha-glycerophopsphate pathway in which alpha-glycerophsophate is acylated with formation of phsophatidic acid and triglyceride
  • absorbed cholesterol transported as esterified cholesterol almost exclusively by lymphatics
  • After resynthesis, TG, cholesterol, cholesterol esters and phospholipids are exported as chylomicrons and VLDLs
17
Q

BBM hydrolases

A

Lactase: lactose–> glucose and galactose
Maltase: alpha4-linked oligosaccharides –> glucose
Sucrase: Sucrose–>glucose and fructose
Isomaltase: alpha limit dextrin and alpha 1,6 and 1,4–> glucose
Trehalase: trehalose (alpha-linked glucose-glucose) –> glucose

18
Q

Defects in stages of fat digestion/absorption

A

1) Emulsification/formation of micelles: defect in FA ionization due to hyperacidity
2) Hydrolysis: deficiency of pancreatic lipase, colipase or HCO3 ion: pancreatic insufficiency
3) Solubilization: deficiency of bile salts- bile obstruction, impaired synthesis, TI disease/loss, SIBO
4) Mucosal cell: enteropathy, deficiency of lipoproteins celiac disease, giardia (abetalipoproteinemia, anderson disease)
5) Chylomicron transport: lymphatics obstruction or malformation- Hennekan syndrome, PLE, post small bowel treatment

19
Q

Enterocyte Monosacchardie transport

A

Monosaccharides transported by saturable carrier systems in the enterocyte BBMI in proximal and mid SI

20
Q

How are glucose and galactose transported across BBM

A
  • Na+-glucose cotransporter (SGLT1)
  • Each glucose brings 2 Na+ ions with it plus 2 accompanying anions
  • drives water molecules across the BBM to maintain cellular iso-osmolarity

Congenital glucose-galactose malabsorption caused by mutation in SGLT1= severe neonatal diarrhea with CHO-containing feedings

21
Q

How is fructose absorbed

A
  • Facilitated diffusion using carrier protein GLUT5
  • fructose minimally metabolized in enterocyte
  • transported across BLM by GLUT5 and rapidly metabolized by liver
22
Q

How do monosaccharides excit epithelial cell by BLM

A 
Glucose= GLUT2
Fructose = GLUT5
23
Q

How much of starch is undigested

A
  • 20%

- metabolized by colonic bacteria into SCFA

24
Q

Which proteins are resistant to proteolysis in the gut lumen

A
  • secretory IgA
  • Intrinsic Factor
  • Alph1 Antitrypsin

Good markers for PLE

25
Q

Outline intraluminal digestion of protein

A

1) pepsinogen released from chief cells stimulated by gastrin, histamine and cholinergic nerves
2) pepsin released from pepsinogen but autoactivation in acidic environemnt
3) Enterokinase liberated from epithelial membranes by bile acids - activates trypsinogen to trypsin
4) Trypsin activates other proenzymes and trypsinogen
5) Pancreatic proteases
a) Endopeptidase (trypsin, chymotrypsin and elastase) cleave peptide bonds
b) Exopeptidase (carboxy peptidase A and B) remove single AA from C terminus
6) Final products of intraluminal protein digestion are 30% neutral and basic AA and 70% short peptides (2-6 AA long)

26
Q

How does protein digestion occur at the brush border

A

Peptidases present in gut lumen and epithelium

-peptidases -> free AA and di and tripeptides

27
Q

How does absorption of proteins occur?

A
  • Di and tripeptides utilize a separate transport system from single AAs
  • Active absorption of di- or tripeptides at BBM is faster than for active absorption of AA
  • peptide absorption occurs via:
    a) Na+-H+ exchanger in BBM maintains intracellular alkaline pH
    b) Na+-K+ ATPase in BLM maintains inside negative membrane potential
    c) cytoplasmic peptidases prevent intracellular accumulation of absorbed peptides
28
Q

How do proteins exit from epithelium

A
  • major mechanism are active transport and passive diffusion across BLM
  • BLM has different transport proteins for AAs and peptides
  • Oligopeptides and AAs are released to portal circulation
  • majority of absorbed proteins reaching portal vein is in form of AA
29
Q

Which form of iron is absorbed better

A
  • F2+ (ferrous) form is absorbed better that F3+ (ferric) form which is highly insoluble and predominant dietary form
  • At the BBM ferric iron reduced to ferrous form before cell entry
  • absorbed in duodenum
  • Intracellular iron-binding proteins transfer iron to BLM for delivery across cell membrane and subsequent binding to transferrin
30
Q

Why despite immaturity of protein digestion can infants cope with as much as 3-4 g/protein/kg a day

A
  • breast milk protease assists in protein digestion
  • trypsin and elastase in breast milk
  • infant intestine can absorb intake macromolecules
  • whole proteins, such as Ig can be absorbed via pinocytosis and endocytosis
31
Q

What are the 3 routes and mechanisms of electrolyte absorption

A

A. Active ion-coupled mechanism
B. NHEs: involve absorption of electrolytes in absence of nutrients via brush border proteins known as NHEs
C. Paracellular pathways: dominant route for passive solute transport

32
Q

What are the different kinds of Active Ion-coupled mechanism

A
  1. Na+ gradient
    a. Organic solutes like glucose, galactose, AA and oligopeptides absorbed/transported as below:
    1) at apical epithelial mucosa: Na+ coupling provided the electrochemical gradient aganst Na+’s conc gradient
    2) At BLM: transported independent of ion movement, down their conc gradient into intestinal capillaries
  2. Protein-coupled transport
    a. some oligopeptides are absorbed intact, unhydrolyzed across the apical membrane via H+ couple transport
    b. Indirectly coupled to Na+ ion: needed H+ is provided by Na+/H+ exchange
  3. Salt and water absorption
    a. Salt is absorbed along with organic solutes
    b. Salt absorption creates an osmotic gradient for water absorption
33
Q

What is the function of intracellular tight junctions/zonula occludens

A
  • barrier btw apical and basolateral compartments
  • restricts the flow of luminal contents into blood stream
  • counterregulates the gradient generally by transcellular pathways
  • selectively allows passive diffusion of small hydrophilic molecules and ions from lumen to blood and lymphatics

Peds GI RC (12 decks)

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