Digestion and Absorption in GI Tract Flashcards
Where does digestion begin and end?
begin in stomach and mouth
complete in SI
Where does absorption take place?
Function?
SI
movement of nutrients, H2O, electrolytes from lumen of the intestine into the blood
Cellular pathway
lumen-> apical membrane-> intestinal epithelial cell-> basolateral membrane -> blood
- transporter in membrane
Paracellular pathway
across a epithelium
intestinal epithelial cell-> lateral intercellular space-> intestinal epithelial cell
-tight junctions
Types of digestive activity
- cavital (luminal)
2. membrane (contact)
Cavital digestive activty
digestion resulting from the action of enzymes secreted by the salivary glands, stomach, and pancreas
Membrane digestive activity
hydrolysis by enzymes synthesized by epithelial cells
Folds of Kerckrin
longitudinal folds in SI
villi and microvilli increase surface area of the SI
Where are villis the longest and shortest?
long: duodenum
short: terminal ileum
Microvillar surface, Brush border
site of activity for a # of digestive enzymes
barrier that must be traversed by nutrients, water, and electrolytes
cell types in intestinal epithelium (3)
- Enterocytes
- goblet cells
- paneth cells
enterocytes
epithelial cells
digestion, absorption, secretion
turnover rate: cells are replaced 3-6 days
suspectible to irradiation and chemotherapy
Goblet cells
mucus-secreting cells
physical, chemical and immunological protection
paneth cells
part of mucosal defenses against infection
secrete agents that destruct bacteria or produce inflammatory responses
How does enterocyte membrane control flux of solute and fluid btw the blood and lumen?
-4
- Pinocytosis
- at base of microvilli
- major mechanism in uptake of protein - passive diffusion
- particles move through pores in cell membrane or through intercellular spaces - Facilitated diffusion
- Active diffusion
What barriers does the solution have to move across the enterocytes - from lumen to blood? (7)
- unstirred layer of fluid
- glycocalyx
- apical membrane
- cytoplasm of cell
- basolateral membrane
- basement membrane
- wall of blood capillary or wall of capillary of lymphatic vessel
Adaptations in digestion in absorption
- key factors
- exceptions
alteration in fxn to maintain homeostasis
depends on capacity of intestine
exm. small bowel resection or bypass
- if ileum is resection, b12 and bile absorption is abolished
-genetic abnormalities can lead to loss of adaption
End products of carbohydrate digestion
- glucose
- galactose
- fructose
**only MONOsaccharides are absorbeed by enterocytes
Key transporters in absorption of carbohydrates
- Lumen side (2)
- basolateral side (2)
Lumen
- SGLT1 (x2) - Na/glucose or galactose symporter (in)
- GLUT 5- frutose in
Basolateral
1. Na/K atpase (k in)
2. Glut 2 (x3)
glucose or galactose or fructose out
Lactose intolerance
failure to digest carbohydrates
brush border lactose is deficient or absent
undigested lactose remains in lumen and holds H2O and causes osmotic diarrhea
-> fermented into methane and H gas -> excess gas
Protein absorption location
stomach and SI
Lactose
- enzyme breakdown
lactase to breakdown into glucose and galactose
Sucrose
- enzyme breakdown
sucrase to breakdown into glucose and fructose
Starch
-ezyme breakdown
amylase, maltose (maltase), maltotriose (sucrase) breakdown into glucose
Enzymes for protein digestion (3)
- Endopeptidases
- trypsin
- chymotrypsin
- elastase - Exopeptidases
- carboxypeptidases A and B - Pancreatic protease
- all in SI
stomach is pepsinogen
Trypsin
catalyzes hydrolysis of trypsinogen (autocatalysis)
Pancreatic proteases
digest themselves and each other
Proteins-> AA, oligopeptides, dipeptides, tripeptides
Tranporters for protein digestions
- lumen side (3)
- basolateral side ( 2)
Lumen
- Na/H+ antiporter (Na out of lumen)
- Na+/ AA cotransporter (in cell)
- 4 separate cotransporter for neutral, acidic, basic, and imino aa - H+/ di/tripeptide cotransporter (in cell)
Basolateral
- Na/K atpase (k in cell)
- facilitated diffusion for AA
- 4 separate diffusion for neutral, acidic, basic, and imino aa
Main cause of disorder of protein assimilation
deficiency of pancreatic enzymes or defects in transporters of intestinal epithelial cells
Chronic pancreatitis and cystic fibrosis
deficiency of pancreatic enzymes
Congenital Trypsin absence
no pancreatic enzymes
Cystinuria
defect/absence in Na/AA cotransporter
- transporter for dibasic AA absent in SI and kidney
-genetic disorder
- AA secreted in urine
- cystine buildup in urine and form crystals and stones
Hartnup Disease
- describe
- symptoms
- no neutral AA absorption
- genetic disorder (SLC6A19 gene)
- pellagra (defiency of niacin)
symptoms: diarrhea, mood change - red scaly skin rash -photosensitivy - short stature - uncoordinated movement -urine secretion of neutral AA
Cystic fibrosis
- describe
- target organ
CFTR: Cl- channel in apical surface of duct cell
-pancreas first organ to fail
- loss of HCO3 secretion
- lead to acute or chronic pancreatitis
Lipid digestion location
stomach and SI
Types of lipid digested
triglyceride, cholesterol ester, phospholipids
- will breakdown into monoglyceride, FA, cholesterol, or lysolecithin
Complication of lipid digestion
insolubility of lipid
- need MICELLES to transport to apical membrane of intestinal epithelial cell for absorption
Enzymes for stomach and lipid digestion
- Lingual and gastric lipases
- lipid breakdown to glycerol and FA (small droplets)
- > emulsify in stomach - CCK
- secreted when dietary lipids appear in SI
- slows rate of gastric emptying
Enzymes for small intestine and lipid digestion
** most lipid digestion occurs in SI
- Bile salts emulsify lipds
- pancreatic lipase (colipase)
- inactive bile salt - Colipase
- inactive form (procolipase)
- activated by trypsin
- works w pancreatic lipase - cholesterol ester hydrolase
- catalyze cholesterol production
- hydrolyze triglyceride to produce glycerol - Phospholipase A2
- proenzyme activated by trypsin
pancreatic lipase optimum ph
6
Mechanism for lipid processing/assimilation (8)
- pancreatic enzyme secretion
- bile acid secretion
- emulsification
- solubilization by micelles
5 . diffusion of micellular content into intestinal epithelial cells
6.. reesterification - chylomicron formation
- exocytosis of chylomicrons into lymphs
What happens in for APoB in epithelial cells of SI
abetalipoproteinemia
- no absorption of dietary lipids
Any abnormalities in lipid assimilation
STEATORRHEA
Abnormalities of pancreatic enzyme secretion
-diseases(3)
damages regulation of acidity in duodenum (bc responsible for HCO3- secretion)
- pancreatic insufficiency
- failture to secrete enough pancreatic enzymes - Zollinger Ellison Syndrome
- gastrin-secreting tumor of pancrease
- increase H secretion by gastric parietal cells
- overload of acid in duodenum - Pancreatitis
- impaired HCO3 and enzyme secretion
Defiency of bile salts
- causes (2)
-interferes with micelles formation
Causes
- ileal resection
- interrupt enterohepatic circulation of bile salts
- bile salt pool is reduced - small intestin bacterial overgrowth
- bacteria deconjugate bile salts
- impair micelle formation and fat malabsorption
- damage intestinal mucosa
- increase gastric acid secrtion and SI motility
Tropical Sprue
- causes
- symptoms
- treatment
decrease # of intestinal epithelial cells-> less microvillar surface area= impaired lipid absorption
- due to infection
Steatorrhea
- B12 and folate deficiency
diarrhea, cramps, nausea, weight loss, gas
TX: tetracycline, folate
Celiac sprue
- describe
- prevalence
- symptoms
- tx
autoimmune disorder
antibodies against gluten (Gliadin)
- lead to destruction of SI villi (atrophy) as well as hyperplasia of intestinal crypts
malabsorption related to deficiencies in folate, iron, calcium, vitA/B/D
mostly in causasian and europeans, women>men
symptoms:
abdominal pain, constipation, diarrhea, weight loss, vomit, nausea, steatorrhea, numbness, rash, fatigue, easy bruising
tX: gluten free diet
defects in digestion and absorption
- causes malabsorption
- less acid secretion and churning in stomach
- decrease enzyme secretion in duodenum
- less SA and transport in SI
- lymphatic obstruction
Vitamins in GI tract
- Fat-soluble vitamins (DEKA)
- same mechanism of absorption as lipids - Water soluble vitamins(B1/2/3/12, C, biotin, folic acid, nicotinic acid, pantothenic acid)
- absorbed via Na dependent cotransport mechanism
- Vit B 12 (cobalamin) form complexes with other proteins to be absorbed (R proteins, **IF, transcobalamin)
Vitamin B12
Cobalamin
- metabolic fxn with H acceptor coenzyme
- reducing ribonucleotide to deoxy a step necessary in gene replication
- important in DNA synthesis in RBC cells and folate
disease
- pernicious anemia caused by RBC maturation when B12 is defiency
- > macrocytic and megablastic anemia
Disruption in absorption of Vitamin B12
- Gastrectomy: loss of parietal cells (source of IF)
2. Gastric bypass: exclusion of the stomach, duodenum, and proximal jejenum after absorption of Vitamin B12
Pernicious anemia
stomach does not produce enough IF
- lowers vitamin B12
1. atrophic gastritis
2. Autoimmune metaplastic atropic gastritis
Atrophic gastritis
chronic inflammation of the stomach mucosa that leads to loss of parietal cells
Autoimmune metaplastic atrophic gastritis
immune system attacks IF protein and gastric parietal cells
Vitamin D/Calcium absorption
calcium absorption depends on the presence of Vitamin D
- absorbed into enterocytes, but also reabsorbed
- SI: binding protein calbindin
calcitrol and PTH govern
Vitamin D defiency
- disease
RIckets (child)
results from inadequate calcium reabsorption
Iron Absorption
secrets apotranferrin into bile, enters duodenum
Apotransferrin binds with free iron and hemoglobin => form transferrin
-> transferin binds to membrane receptors of intestinal epithelial cells -> absorbed via pinocytosis and later release
What is absorbed in duodenum?
fat sugar AA iron folate calcium water electrolytes
What is absorbed in jejunum?
sugar aa calcium water sodium
What is absorbed in ileum
b12
bile salt
water
electrolytes
What is absorbed in colon
water electrolytes calcium AA medium triglycerides
