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SBM IV GI > Maldigestion and Malabsorption > Flashcards

Maldigestion and Malabsorption Flashcards

1
Q

absorbable form of dietary carbohydrates.

A

only monosaccharides - glucose, galactose, fructose

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2
Q

how do dietary carbs become monosaccharides?

A
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3
Q

steps of carbohydrate digestion

A
  1. physical denaturation: mastication and antral grinding
  2. amylase: starch –> oligosaccharides (pancreatic more important than salivary
  3. brush border digestion: oligosaccharides –> monosaccharides
  4. carbohydrate absorption
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4
Q

how are carbohydrates absorbed?

A

@ apical membrane

  • Fructose: GLUT 5, facilitated diffusion
  • Glucose and galactose: active transport (Na/glucose transport w/ SGLT1)

@basolateral membrane - facilitated diffusion w/ GLUT2

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5
Q

where does most of the carb digestion occur

A

proximal jejunum = most important

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6
Q

colonic salvage

A

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

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7
Q

Steps in protein digestion

A
  1. mechanical breakdown
  2. gastric hydrolysis
  3. trypsin and luminal digestion
  4. absorption to the enterocyte
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8
Q

mechanisms for protein absorption to the enterocyte

A
  • 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
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9
Q

most intraluminal hydrolysis in protein digestion is done via…

A

trypsin-activated peptidasees and brush border enzymes

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10
Q

steps in fat digestion

A
  1. emulsification
  2. gastric hydrolysis (15% of digestion): TAGs –> DAGs
  3. completion of lipolysis: TAG –> MAG + 2 FAs
  4. micelle formation
  5. absorption into enterocyte, chylomicron formation
  6. post-processing of dietary fat
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11
Q

what does gastric hydrolysis?

A

gastric and lingual lipase stimulated by gastrin (from chief cells)

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12
Q

what happens in step 3 - completion of lipolysis?

A
  • 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
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13
Q

what do micelles do?

A
  • MAGs and FAs assoc w/ bile salts and phospholipids
  • transport poorly soluble MAG and FAs to surface of enterocyte
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14
Q

how are chylomicrons formed?

A
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15
Q

causes of vit B12 malabsorption

A
  • 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
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16
Q

steps of vitamin B12 absorption

A
  1. dietary intake - B12 bound to food protein
  2. Cleaved by acid, pepsin in stomach
  3. pancreatic proteases (trypsin) frees B12 from salivary R protein in stomach
  4. B12 binds to intrinsic factor for absorption
17
Q

three types of lactase deficiency

A
  • acquired or primary - common
  • congenital (rare)
  • reversible: due to diffuse inflammation of the brush border
18
Q

why don’t we get sucrose or maltose intolerance?

A

multiple enzymes to break down these monosaccharides

19
Q

Hartnup disease

A

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

20
Q

cystinuria

A

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

21
Q

pt lost her distal ileum. what vitamins are we worried about?

A

Vit B12

Fat soluble vitamins: ADEK (95% of bile absorbed in terminal ileum– these are essential to uptake of these vits in fat)

22
Q

predisposing causes of bacterial overgrowth

A
  1. anatomic derangements: ileoceccal resection, fistula
  2. achlorhydria: gastric H+ is an antibiotic that decreases bacterial flora
  3. stasis: impaired motility, aging
23
Q

genotypes assoc w/ celiac disease

A

HLA-DQ2 or HLA-DQ8 required

24
Q

celiac disease - what is it, where does it effect the GI tract?

A

immune response to gliadin

primarily upper intestine - lymphocytic infiltration of lamina propria and epithelium and villous atrophy

25
Q

how does celiac disease cause destruction of enterocytes?

A
  • 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
26
Q

mechanisms of diarrhea in celiac

A
  • 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
27
Q

5 mechs of pancreatic insufficiency that cause malabsorption and/or vitamin deficiency

A

Carbs: amylase production, bicarb and Cl- for amylase

Protein: pancreatic proteases (zymogens and active)

Fats: Bicarb, lipase + colipase

28
Q

why are oxalate stones a complication of pancreatic insufficiency?

A
  • 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
29
Q

how does abetaliproteinemia cause fat malabsorption?

A

chylomicron formation

30
Q

Whipple’s disease

A

exposure to dust borne soil

bacteria grow in “foamy” macrophages –> lymphangiectasia –> fat malabsorption, steatorrhea, loss of protein

tx: long term abx

SBM IV GI (26 decks)

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