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Phys4 GI Lect8

Phys4 Digestion and Absorption of Carbs & Proteins

3 ways surface area is amplified for Increased absorption 1.Folds of Kerkring. 2.Microscopic villi and Crypts of Lieberkuhn. 3.Submicroscopic microvilli. **Enterocytes absorb, digest, and secrete while Goblet cells secrete mucus.
What is the primary site for absorption? DUODENUM
When is carbohydrate digestion completed? Proximal Jejunum
When are protein & fat digestion completed? Distal Jejunum.
3 part process to digestion 1.Luminal or cavity digestion. 2.Membrane digestion. 3.Intracellular digestion.
Where does carb digestion start? In the mouth, Amylase in saliva b/c it favors neutral pH (although does still work in Orad stomach).
Action and Products of Amylase 1.ACTION: Luminal digestion (and some membrane digestion) Cleaves 1-4 linkage (can NOT cleave 1-6 linkages or 1-4 linkages close to 1-6). 2.PRODUCTS: Maltose and Maltotriose.
Is Amylase secreted in the active form? YES
What are the ONLY types of carbs that get absorbed? List them and their polysaccarides MONOSACCARIDES (hexoses): 1.Glucose & galactose from lactose (via lactase). 2.Glucose from maltose & maltotriose (via glucoamylase). 3.Glucose & fructose from sucrose & Alpha 1-6 dextrins (via Sucrase-isomaltase).
What are the 3 main enzymes involved in carb digestion at the brush border? 1.Lactase. 2.Glucoamylase. 3.Sucrase-isomaltase.
What is the RATE-LIMITING step in carb digestion? UPTAKE across enterocyte. **Enzymes are plentiful and not limiting.
How do glucose and galactose cross the apical membrane? frutcose? How do all 3 cross the basolateral membrane? 1.Glucose & galactose enter via SGLT1 transporter (symporter with Na). 2.Fructose enters via GLUT5 facilitated diffusion. 3.ALL 3 leave via GLUT2 facilitated diffusion.
If you have a patient with glucose intolerance due to absorption problems, could you supplement with galactose? NO, they used the same transporter... ya dumbass
What could be the cuase of poor carb nutrient assimilation? MALDIGESTION: 1.Lactase deficiency. 2.Chronic alcoholism. 3.Celiac disesae (sprue). 4.Bacterial infections. 5.Protozoan/Helminthes infection. MALABSORPTION: 1.Congenital glu/gal transporter defect. 2.Celiac Sprue. **4&5 cause cell structura
What is a symptomatic result of Malabsorption or maldigestion (poor nutrient assimilation) Osmotic Diarrhea. **B/c of all the food products in the lumen
Where does protein digestion begin? Stomach via pepsin (H+ activates chief cell pepsinogen to pepsin)
Classification of Pancreatic Proteases that digest proteins in the small intestine (and their precursors ENDOPEPTIDASES: 1.Trypsin (trypsinogen). 2.Chymotrypsin (chymotrypsinogen). 3.Elastase (Proelastase). EXOPEPTIDASES: 1&2.Carboxypeptidase A & B (Pro-). **yield aa's & oligopeptides from proteins
What does Enterokinase (a brush boarder enzyme triggered by bile salts) activate? What is the chain reaction resulting? Activates trypsinogen to trypsin. **Trypsin then activates ALL of pancreatic proteases
What activates Enterokinase? Trypsinogen. **Bile salts only trigger its release from brush boarder cells.
What is the role of trypsinogen in Pancreatitis? It becomes prematurly activated w/in the pancreas which leads to a proteolytic activation cascade and thus destruction.
Absorption of Proteins 1.40% as free aa's. 2.60% as di,tri, & large peptides via PepT1 transporter (H+/oligopeptide symporter). **PepT1 symporter is faster and more efficient so di/tri peptides are absorbed faster.
Created by: WeeG



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