Digestion & Absorption Processes in the GI Tract Flashcards
Small Intestine Structure is ideal for absorption
Folds of Kerckring that are arranged longitudinal folds with villi & microvilli to INCREASE the surface area of the small intestine
**Villi are longest in the DUODENUM + shorter in the Terminal Ileum
Where is the site of membrane (contact) site of activity?
Microvillar surface where there is a # of digestive enzymes (called the Brushborder)
What are the 3 different types of cells in the intestinal epithelium?
1.) Enterocytes:
+normal epithelial cells that are there for digestion,
absorption, & secretion
2.) Goblet Cells:
+ mucus secreting cells
+ give physical barrier from pathogens, chemical
barrier (mucosal barrier), immunologic protection
(macrophages)
3.) Paneth Cells:
+ part of the mucosal defenses against infection
-secrete agents that destroy bacteria or
produce inflammatory responses
How does the Enterocyte membrane regulate the control the flux of solutes between the lumen and the blood?
Pinocytosis- at the base of the microvilli, major mechanism in the uptake of protein
Passive Diffusion- particles move through pores in the cell membrane or through intercellular spaces
Facilitated Diffusion
Active Transport
Transmural Movement during absorption in small intestine
Unstirred Layer of Fluid Glycocalyx Apical Membrane Cytoplasm of the cell Basolateral Membrane Basement Membrane Wall of the Blood Capillary/ Wall of the Lymphatic Vessels
The GI System is good at adaptation. Why?
- Adaptations alter the function to maintain homeostasis
- Capacity of the intestine to adapt is key in many scenarios like:
a. ) small bowel resection
b. ) bypass of the stomach (duodenal switch)
Limitations to Adaptations:
a.) Resection of the distal ileum- abolishes bile and
vitamin B12 absorption
b.) Certain genetic abnormalities lead to a loss of adaptation (lactase deficiency)
+ dysfunctional lactase enzyme that causes major
problem with the breakdown of lactose
Only monocytes are absorbed by enterocytes. What are they?
Glucose, Galactose, & Fructose
What are the key absorption sites from the lumen of the duodenum?
Apical Lumen Side:
SGLT 1- Na+/Glucose symporter
SGLT1- Na+/Galactose symporter
GLUT5- Fructose
Basolateral Side:
GLUT 2 Transporter- Glucose, Galactose, Fructose
Na+/K+ ATPASE- Na+ ion into the blood and K+ out into the enterocyte
What is lactose intolerance? Where does the usual breakdown occur and with what carbohydrate breakdown?
Lactose Intolerance- due to deficiency in the lactase enzyme in the brush border of microvilli
Undigested Lactose-> OSMOTIC DIARRHEA-
**Lactose-> glucose + galactose
Sx of Lactose intolerance: bacteria-produced methane gas, osmotic diarrhea (to equalize the concentrated lactose product on luminal side)
How are proteins digested?
Proteins are digested into digestable forms in the stomach and the small intestine.
Stomach: Pepsinogen-> Pepsin
Small Intestine:
Trypsinogen-> Trypsin (enterokinase)
a.) trypsinogen-> trypsin (activated trypsin)
b.) chymotrypsinogen-> chymotrypsin (activated
trypsin)
c.) Proelastase-> elastase (activated trypsin)
d.) Procarboxypeptidase A-> carboxypeptidase A
(activated trypsin)
e.) Procarboxypeptidase B -> carboxypeptidase b
(activated trypsin)
***All of these enzymes create oligopeptides
Which proteases create building block AAs, Dipeptides, and tripeptides?
Peptidase enzymes along the brush border
The type of transport mechanisms of the AAs are the same as the carbohydrate transporters
4 separate cotransporting symporters (APICAL SIDE):
Na+/Neutral
Na+/Basic AA
Na+/Acidic AA
Na+/Imino AA
4 Separate single transporters on the BASOLATERAL SIDE: Neutral AA transporter Acidic AA transporter Basic AA transporter Imino AA transporter
Disorders of Protein Assimilation
a.) Deficiency of Pancreatic Enzymes
b.) Congenital Trypsin Absence (causes the lack of the trypsin protein)
c.) Cystinuria- defect in or absence of dibasic a.a. transporter (cystine, lysine, arginine, ornithine)
+ Cystinuria is a problem with dibasic transporter
(cystine(C), lysine (K), arginine (R), ornithine)
- Absent transporter so it is urinated OUT
Hartnup Disease
*inability to absorb neutral AAs; TRYPTOPHAN ESPECIALLY
+ Sx include: diarrhea, mood changes, neurological
problems, skin rash, photosensitivity, short stature,
uncoordinated movements
Cystic Fibrosis
- CFTR Mutation causes inability to secrete Cl- into the lumen and causes the absorption of H20 into the ductal cells of the pancreas
Digestion of the lipids in the stomach and small intestine
Triglycerides-> Monoglycerides + FAs (lingual lipases, gastric lipases, pancreatic lipases)
Cholesterol Ester–> Cholesterol + FAs (cholesterol ester hydrolase)
Phospholipids–> Lysolecithin + FAs (phospholipase A2)
How is the problem with pancreatic lipase solved when there is exposure to bile?
Pancreatic lipase-Bile Attachment is removed by the activation of Colipase via TRYPSIN
Describe the activity of pancreatic lipase
Pancreatic Lipase breaks down the TAG–> DAG + 1 FA
What is the optimum pH of pancreatic lipase?
pH=6
What is the process for the processing of lipids?
- ) Cholesterol, Monoacylglyceral, LysoPL, and FFA are created via Bile Salts
- ) Cholesterol Esters, Phospholipids, TAG are all formed back into creating a micelle that is secreted into the bloodstream into the lymph
What is the importance of ApoB protein during Fat absorption?
ApoB causes the ability of the formed chylomicron to move across the basolateral side of the enterocyte membrane.
NO APO-B PROTEIN LEADS TO ABETALIPOPROTEINEMIA*
sx: steatorrhea
What causes steatorrhea?
Problem with pancreatic enzyme secretion, bile acid secretion, emulsification, micelle formation, diffusion of lipids into intestinal epithelial cells, chylomicron formation, transfer of chylomicrons into the lymph
What are factors that cause deficits in bile salt secretions?
Ileal resection
small intestinal bacterial overgrowth (SIBO)
What are the main causes of small intestine bacterial overgrowth?
Decreased Gastric Acid Secretion (gives more ability for the bacteria to grow into the intestinal mucosa and the overgrowing bacteria causes deconjugated bile salts, impaired micelle formation, and fat malabsorption
***the decreased H+ secretion-> bacterial overgrowth-> deconjugation of the bile salts-> impaired micelle formation-> fat malabsorption because of impaired micelle formations
What is Tropical Sprue?
decreases the number of intestinal epithelial cells, reduces the microvillar surface area; lipid absorption is impaired because the surface area for absorption is decreased!
sx: cramps, nausea, weight loss, gas, indigestion
tx: tetracycline + folate for 6 months
What is Celiac Sprue?
Autoimmune Disorder that leads to the destruction of small intestine villi as well as hyperplasia of the intestinal crypts
What is the importance of Cobalamin (Vitamin B12)?
* important in creating DNA as it reduces ribonucleotides to deoxyribonucleotides (needed for DNA synthesis)
- Especially important in the synthesis of Red Blood Cells
-Leads to Pernicious Anemia (due to failure of Red
Blood Cell Maturation)
What causes the disruption of the absorption of Vitamin B12?
Gastrectomy- loss of parietal cells (source of IF deficiency that binds to Vitamin B12/Cobalamin)
Gastric Bypass- exclusion of the stomach, duodenum, proximal jejunum can lead to alterations in absorption vitamin B12
Atrophic Gastritis- chronic inflammation of the stomach mucosa that leads to loss of parietal cells
Autoimmune Metaplastic Atrophic Gastritis- immune system attacks IF protein or gastric parietal cells
How does intestinal iron absorption work?
1.) DCYTB receptor reduces non-heme Fe3+-> Fe2+
2.) DMT transports Fe2+ into the cell
3.) Fe2+ in transferred onto Mobilferrin
4.) Fe2+ leaves through Ferroportion Channel on the
basolateral side
5.) Fe2+ gets transferred by the plasma transferrin from
the blood
