Lecture 21: Digestion and Absorption in the GI tract Flashcards
(41 cards)
Lactose intolerance:
Classic presentation and findings
AP, bloating, diarrhea after eating dairy.
Positive Hydrogen breath test
What is the pathophysiology of lactose intolerance
lack of brush border enzyme lactase that metabolizes lactose > unabsorbed lactose becomes SCFAs & H2 > acetate, butyrate and proprionate ferments to methane and H2 > effect is to keep water in lumen of intestine (not reabsorbed) > osmotic diarrhea
What are the major sugars in the human diet?
Primary sugars include sucrose, lactose, starch
Everything else is secondary sugars
Cellulose is indigestible
Where are carbs digested and what are the main players?
What are the major products of carbohydrate breakdown in these locations?
Mouth: starch breakdown begins, main enzyme is salivary amylase
Small intestine:
most starch broken down here, main enzyme is pancreatic amylase
Major product:
Starch > maltose + 3-9 polymers of glucose
How do these disaccharides break down (include enzymes) Maltose Trehalose Lactose Sucrose
- glucose + glucose (maltase)
- glucose + glucose (trehalase)
- glucose + galactose (lactase)
- glucose + fructose (sucrase)
How are the monosaccharides transported from the SI lumen to the blood (include type of transport)?
From lumen to SI cell:
- SGLT carries glucose and galactose with Na+ in (secondary active transport)
- GLUT5 carries fructose in (facilitated diffusion)
From SI cell to blood:
- Na/K ATPase maintains Na/K balance (primary active)
- GLUT2 carries glucose, galactose and fructose into bloodstream (facilitated diffusion)
How would you clinically test for carb absorption issues?
-D-xylose test, methane, 13CO2, sucrose breath tests
How do you perform a D-xylose test?
- Patient ingests 25 g of D-xylose which is absorbed but not utilized by human body
- if <4g of D-xylose is excreted by urine = CHO malabsorption is present
What are the major causes of protein assimilation disorders?
-pancreatic enzyme or SI transporter deficiency
Chronic pancreatitis
Congenital trypsin absence
- lack of proteases (e.g. trypsinogen)
- lack of trypsin, no pancreatic enzymes (since trypsin activates a lot of other pancreatic enzymes)
Cystinuria
Cause
Clinical
- SLC3A1/SLC7A49 defect causes deficient COAL AA transporter > not reabsorbed by kidney
- COAL AAs form stones or are excreted in feces
Hartnup disease
Cause
Clinical
- can’t absorb neutral AAs due to SLC6A19/B(0)AT1 mutation
- pellegra like (diarrhea, dermatitis, dementia), increased neutral AAs in urine
Cystic fibrosis (GI manifestation)
Cause
Clinical
- CTFR mutation, HCO3- can’t be released into duct = acidic duct = digestive enzymes digest the pancreas
- pancreatitis
Where are proteins digested and what are the main players?
What are the major products?
Stomach:
Pepsin activated at pH 2-3, breaks down a small amount of protein
Pancreas releases these enzymes:
Trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase (all these activated by trypsin)
- turns protein to small polypeptides
Small intestine enterocytes release these enzymes:
aminopolypeptidase, dipeptidases - broken down into AAs
Explain the activation cascade of gastric pancreatic enzymes
Gastric:
Pepsinogen > pepsin (activated by low pH)
Pancreatic:
pancreas releases enzymes to duodenum > enterokinase/trypsin activates trypsinogen > more trypsin > activates the other pancreatic enzymes
How are the peptides transported from the SI lumen to the blood?
Lumen to SI:
- different types of AAs (basic, acidic, neutral, imino) have their specific transporters into the enterocyte
- carried with H-dipeptides and H-tripeptides
SI to blood:
- Na/K ATPase maintains balance
- different types of AAs have their specific transporters into the blood stream (facilitated diffusion)
- dipeptides and tripeptides also diffuse
Celiac Sprue/Celiac Disease
classic presentation and findings
-greasy, pale and foul smelling diarrhea/steatorrhea, AP, weight loss
Positive for anti-transgluatminase (tTG-IgA) antibodies
What is the pathophysiology of Celiac Disease?
-presence of Abs against gliadin (found in gluten) > small intestinal villi atrophy and crypt hyperplasia > malabsorption of lipids (e.g. Vit. A, B9, B12, D, Fe and Ca2+)
Be sure to look at the histo images of damaged villi on the slides
Tropical Sprue
Cause
Clinical
- possible intestinal infection causes decreased number of intestinal epithelial cells decreasing microvilli surface area > lipid malabsorption
- diarrhea (major sign), treat with abx
What characteristics of the intestinal mucosa make it ideal for absorption?
-intestinal mucosa brush border made of folds of Kerckring with lots of villi and microvilli > increased surface area for absorption
What types of cells are in the intestinal mucosa that aid with digestion?
Enterocytes
Goblet cells - secrete mucus
Paneth cells - immune defense
What mechanisms are used to transport molecules into enterocytes?
-Pinocytosis, passive and facilitated diffusion, active transport
What is an important step in lipid absorption?
emulsification by bile salts and lecithin > induces micelle formation
What are the major players of lipid digestion in the stomach?
- lingual and gastric lipase break down TAGs
- CCK - inhibits gastric emptying and increases gallbladder secretion (mixes the bolus)
