Physiology Flashcards
Gastric factors that control gastric emptying?
- 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
Duodenal factors controlling gastric emptying
-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
Where does CCK come from
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
Where does Gastrin-Releasing Peptide come from
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
What does Apolipoprotein a-IV do
Source: intestinal mucosa
Receptor: CNS
Action: centrally mediated appetite suppression in response to fat absorption
What does Leptin do?
Source: adipocytes
Receptor: hypothalamus
Action: decrease appetite
What does Peptide Tyrosine-tyrosine (PYY) do
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
What does Pancreatic polypeptide (PP) do?
Source: F cells - Pancreatic endocrine cells
Receptor: PP receptors in pancreas, GI and CNS
Action: decrease pancreatic exocrine secretion, gallbladder contractions and gut motility
What does Glucagon-like peptide (GLP) do?
Source: ileal L cells
Receptors: GLP-1 receptors in the pancreas
Action: decrease gastric motility; contributes to satiety by decrease absorption of CHOs
What does Ghrelin do
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
Where is Serotonin from
- 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
What does secretin do
-increases pancreatic enzymes and HCO3- secretion
How is pancreatic secretion controlled
-Coordination cephalic (vagus), gastric (acid, pepsin and gastric emptying) and intestinal (CCK/secretin)
Where does enterokinase come from?
- Duodenal crypts of Lieberkuhn
- secreted in response to chyme
- activates pancreatic trypsinogen to trypsin
- trypsin activates other enzymes
How are LCFA transferred across the BBM
- 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
What is the intracellular processing of lipids
- 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
BBM hydrolases
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
Defects in stages of fat digestion/absorption
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
Enterocyte Monosacchardie transport
Monosaccharides transported by saturable carrier systems in the enterocyte BBMI in proximal and mid SI
How are glucose and galactose transported across BBM
- 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
How is fructose absorbed
- Facilitated diffusion using carrier protein GLUT5
- fructose minimally metabolized in enterocyte
- transported across BLM by GLUT5 and rapidly metabolized by liver
How do monosaccharides excit epithelial cell by BLM
Glucose= GLUT2 Fructose = GLUT5
How much of starch is undigested
- 20%
- metabolized by colonic bacteria into SCFA
Which proteins are resistant to proteolysis in the gut lumen
- secretory IgA
- Intrinsic Factor
- Alph1 Antitrypsin
Good markers for PLE
