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Phys4 GI Lect8
Phys4 Digestion and Absorption of Carbs & Proteins
| Question | Answer |
|---|---|
| 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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