Digestion/Absorption Flashcards
Folds of Kercking
Longitudinal folds on luminal surface of small intestine
Brush border
Increases surface area and is site of activity for numerous digestive enzymes
Enterocytes
- Epithelial cells
- Focusing on digestion, absorption, secretion
Goblet cells
Mucus-secreting cells for protection
Paneth cells
Part of mucosal defenses against infection that secrete agents to destroy bacteria or produce inflammation
Effect of terminal ileal resection?
- Abolished bile salt and Vitamin B12 absorption
Carb Digestion (mouth)
- Some starch broken down
- Salivary amylase
- Starch broken into maltose and polymers of glucose
Carb digestion (SI)
- Most starch breakdown occurs here
- Pancreatic amylase *
- Starch – maltose and polymers of glucose
Maltose becomes
Glucose + Glucose
Trehalose becomes
Glucose + Glucose
Lactose becomes
Galactose + Glucose
Sucrose becomes
Glucose + Fructose
Monosaccharide transporters from lumen to duodenal epithelial cell?
SGLT1 + GLUT5
SGLT 1
secondary active transporter for glucose and galactose (from lumen to epithelial cell)
GLUT 5
facilitated diffusion for fructose (from lumen to epithelial cell)
GLUT 2
facilitated diffusion into blood (from epithelial cell to blood)
Transporters from epithelial cell to blood
- Na/K ATPase
- GLUT 2
What results from lactose intolerance?
Lactose stays in lumen, holds H2O in lumen and osmotic diarrhea results
D-xylose test
- Pt ingests 25 g D-xylose and urine collected for 5 hrs
- 4g+ in urine = absorbed properly
- < 4 g in urine = not properly absorbed (some absorption disorder present)
Endopeptidases
hydrolyze interior bonds
pepsin, trypsin, chymotrypsin, elastase
Exopeptidases
hydrolyze one amino acid at a time from carboxyl end
carboxypeptidase A/B
Protein digestion (stomach)
- 10-20% breakdown occurs here (not essential)
- Pepsin (pepsinogen activated at pH 2,3)
Protein digestion (pancreas)
- Proteins broken down into di/tri peptides
- Trypsin, chymotrypsin, carboxypeptidase, elastase
Role of trypsin and chymotrypsin in protein digestion
Cleaves into small polypeptides
Role of carboxypeptidase in protein digestion
Cleaves AA into carboxyl ends
Protein digestion (SI)
- Aminopolypeptidase, dipeptidases
- AA/peptides absorbed into enterocytes
What enzyme(s) activate zymogens?
Trypsin or enterokinase (trypsinogen)
Co-transport of AAs in SI
Travel with Na+ in co-transporters
Peptides travel w/ H+
Chronic pancreatitis
Deficiency of pancreatic enzymes (ie. lack of proteases)
Congenital trypsin absence
No trypsin… no functional pancreatic enzymes
Cystinuria
- Defect in/absence of Na+/AA cotransporters
- Dibasic AA (Cys, Lys, Arg, Orn) transporters specifically
Hartnup disease
- SI cannot absorb neutral AAs
- Sx resemble pellagra (dementia, diarrhea, dermatitis)
Cystic Fibrosis
- CFTR-regulated Cl- channel on apical membrane w/ mutation
- Mutation causes loss of HCO3- secretion (enzymes cannot move from ducts – pancreatitis)
- Autodigestion of pancreas possible
Biggest issue with lipid digestion
Insolubility of lipids
Lipid digestion (stomach)
- Lingual/gastric lipase act on TAGs (10% TAG absorption)
- Time required for CCK to act… so CCK inhibits gastric emptying to allow time for more mixing and GB emptying
Lipid digestion (SI)
- Majority of digestion here
- Bile salts emulsify fats
- Variety of enzymes secreted into SI to facilitate digestion
Pancreatic lipase
- Secreted as active
- Inactivated by bile salts w/o colipase (which is activated by trypsin to displace bile salts)
Cholesterol ester hydrolase
- Secreted as active
- catalyzes production of free cholesterol
- TAG – glycerol
Phospholipase A2
- Secreted as proenzyme
- Breaks down phospholipids
Steps in fat absorption
- Solubilization by micelles (apical side)
- Diffusion of micellar content across apical membrane
- Reesterification
- Chylomicron formation
- Exocytosis of chylomicrons into lymphatics (through BL)
Component needed for lipid absorption
ApoB (w/o it you get abetalipoproteinemia)
Key indication of lipid absorption issue
Steatorrhea
Key theme of lipid absorption issue
Improper acidity of duodenal contents (too much acid/not enough HCO3-)
Factors causing bile salt deficits
- Ileal resection
- Small intestinal bacterial overgrowth (bacteria deconjugate bile salts, which impairs micelle formation)
Problems with tropical sprue
- Loss/decreased number of intestinal epithelial cells
- Reduced microvilli surface area
- Fat soluble vitamins also afected
- Diarrhea main indication
Small intestine bacterial overgrowth
- Inappropriate growth of bacteria
- Malabsorption
- Breath test can indicate methane or hydrogen
Common causes of pernicious anemia
- Atrophic gastritis (chronic inflammation – loss of parietal cells)
- Autoimmune metaplastic atrophic gastritis (immune systems attacks IF)
Significance of gastric bypass/gastrotomy
- Loss of parietal cells – loss of IF – Pernicious anemia
Iron Absorption
- Liver secretes apotransferrin into bile
- Apotransferrin binds with Fe/Hb to form transferrin
- Vitamin C aids in process
- Fe3+ to Fe2+
Main site of absorption for most nutrients/vitamins
Small intestine
