Maldigestion and Malabsorption Flashcards
absorbable form of dietary carbohydrates.
only monosaccharides - glucose, galactose, fructose
how do dietary carbs become monosaccharides?
steps of carbohydrate digestion
- physical denaturation: mastication and antral grinding
- amylase: starch –> oligosaccharides (pancreatic more important than salivary
- brush border digestion: oligosaccharides –> monosaccharides
- carbohydrate absorption
how are carbohydrates absorbed?
@ apical membrane
- Fructose: GLUT 5, facilitated diffusion
- Glucose and galactose: active transport (Na/glucose transport w/ SGLT1)
@basolateral membrane - facilitated diffusion w/ GLUT2
where does most of the carb digestion occur
proximal jejunum = most important
colonic salvage
2-20% of ingested starch escapes SI absorption
metabolized by colonic flora to SCFAs (propionate, acetate, butyrate) –> increases osmostic load –> diarrhea
SCFAs absorbed by colonic enterocytes
side effect - gas b/t this is fermentation
Steps in protein digestion
- mechanical breakdown
- gastric hydrolysis
- trypsin and luminal digestion
- absorption to the enterocyte
mechanisms for protein absorption to the enterocyte
- apical membrane AA transporters:
- Na-K pump
- specific for similar AAs
- di-, tri-, tetra- absorbed intact via carrier molecules
- broken down to AAs by cytosolic peptidase
- paracellular route for intact peptides
most intraluminal hydrolysis in protein digestion is done via…
trypsin-activated peptidasees and brush border enzymes
steps in fat digestion
- emulsification
- gastric hydrolysis (15% of digestion): TAGs –> DAGs
- completion of lipolysis: TAG –> MAG + 2 FAs
- micelle formation
- absorption into enterocyte, chylomicron formation
- post-processing of dietary fat
what does gastric hydrolysis?
gastric and lingual lipase stimulated by gastrin (from chief cells)
what happens in step 3 - completion of lipolysis?
- CCK aand GIP are stimulated by FAs in duodenum –> increase biliary and pancreatic secretions
- Pancreatic lipases hydrolyze TAG –> MAG + 2FAs
- req pancreatic co-lipase, alkaline pH, bile salt
what do micelles do?
- MAGs and FAs assoc w/ bile salts and phospholipids
- transport poorly soluble MAG and FAs to surface of enterocyte
how are chylomicrons formed?
causes of vit B12 malabsorption
- decreased intrinsic factor: pernicious anemia, gastrectomy
- increased R factor B12 binding: pancreatic insufficiency
- increased bacterial B12 uptake: bacterial overgrowth
- decreased ileal B12 absorption: Crohn’s, ileal resection
steps of vitamin B12 absorption
- dietary intake - B12 bound to food protein
- Cleaved by acid, pepsin in stomach
- pancreatic proteases (trypsin) frees B12 from salivary R protein in stomach
- B12 binds to intrinsic factor for absorption
three types of lactase deficiency
- acquired or primary - common
- congenital (rare)
- reversible: due to diffuse inflammation of the brush border
why don’t we get sucrose or maltose intolerance?
multiple enzymes to break down these monosaccharides
Hartnup disease
defect in Na linked neutral AA transporter in gut and kidneys (tryptophan, histidine, phenylalanine)
clinical manifestations: usually none B/C THEY GET THE NUTRIENTS THROUGH PARACELLULAR AND DI-, TRI-, TETRA-PEPTIDE ABSORPTION
cystinuria
defect in transporter for dibasic AA uptake in small intestions (cystine, ornithine, arginine, lysine)
cystine not very soluble, precipitates in kidney tubule
clinical manifestation: cystine kidney stones
pt lost her distal ileum. what vitamins are we worried about?
Vit B12
Fat soluble vitamins: ADEK (95% of bile absorbed in terminal ileum– these are essential to uptake of these vits in fat)
predisposing causes of bacterial overgrowth
- anatomic derangements: ileoceccal resection, fistula
- achlorhydria: gastric H+ is an antibiotic that decreases bacterial flora
- stasis: impaired motility, aging
genotypes assoc w/ celiac disease
HLA-DQ2 or HLA-DQ8 required
celiac disease - what is it, where does it effect the GI tract?
immune response to gliadin
primarily upper intestine - lymphocytic infiltration of lamina propria and epithelium and villous atrophy
how does celiac disease cause destruction of enterocytes?
- gliadins formed during intraluminal digestion of gluten by brush border enzymes
- gliadin causes damage to epithelial cells
- ttG deaminates gliadin -
- deaminated gliadin binds HLA-DQ2/8 on APC
- inflammtory cascade - w/ T cells and B cells –> antibodies produced
mechanisms of diarrhea in celiac
- destruction of neuroendocrine cells –> less CCK/secretin release –> pancreatic insufficiency –> steatorrhea
- decreased brush border enzymes –> carb and protein malabsorption
- loss of villous structure –> decreased surface area
- inflammation –> intestinal secretion
5 mechs of pancreatic insufficiency that cause malabsorption and/or vitamin deficiency
Carbs: amylase production, bicarb and Cl- for amylase
Protein: pancreatic proteases (zymogens and active)
Fats: Bicarb, lipase + colipase
why are oxalate stones a complication of pancreatic insufficiency?
- malabsorbed fat binds Ca and Mg ions
- Ca and Mg can’t precipitate w/ free oxalate
- lots of free oxalate diffuses into blood –> stones in kidneys
how does abetaliproteinemia cause fat malabsorption?
chylomicron formation
Whipple’s disease
exposure to dust borne soil
bacteria grow in “foamy” macrophages –> lymphangiectasia –> fat malabsorption, steatorrhea, loss of protein
tx: long term abx
