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100 Cards in this Set
- Front
- Back
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glycogenesis
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synthesis of glycogen...after a meal with insulin to store glucose
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glycogenolysis
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break down of glycogen to glucose stimulated by glucagon and epinephrine
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glycolysis
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breakdown of glucose to pyruvate
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gluconeogenesis
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making glucose from non-CHO sources like pyruvate, lactate and glycerol
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what happens in RER
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protein synthesis
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what happens in SER
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lipid synthesis
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eicosanoids
-made from? and ex |
arachidonic acid
ex: prostaglandins, leukotrienes (pro-inflammatory), LTB4 and thromboxines |
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explains how FA's like PUFA's can reflect diet with example
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diet can reflect membrane FA's
Ex: fish oil (omega 3s) change the membrane and reduce inflammation by displacing arachidonic acid -EPA and DHA |
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describe plasma membrane and hydrophobic and philic parts
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hydrophobic tails inside
hydrophilic polar heads on outside |
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describe plasma membrane as barrier, what its made of and its permeability
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phospholipid bilayer
-fluidity depends on many things -barrier against outsider materials and entrance requires a special mechanism |
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what happens when fish oil dispalces arachidonic acid
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it makes different prostaglandins LTB5 and it's less pro-inflammatory
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describe mitochondrial DNA and why its only from the mother
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usually circular
only from mom because the mitochondria of sperm is in the tail which is lost after fertilization |
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where does some protein syntehsis occur in the mito
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ribosomes and DNA
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what happens in inner mitochondrial membrane
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where metabolic rxns occur like TCA and Krebs
-enzymes for oxidative phosphorylation embedded here |
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compare the inner and outer membrane of the mitochondria
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inner is selectively permeable
outer is porous |
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what happens to substrates made in mito matrix near enzymes
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get converted to ATP
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describe cytochrome p450s...where are they, and what are they
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enzyme systems in different parts of the cell
-mainly in SER |
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principle fxn of cytochrome p450 and mechanism
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metabolize wastes and drugs
detoxification system oxidases= o2 to substrate conjugated to a polar side chain and makes it more hydrophilic so it can be eliminated |
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microsomes
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centrifugation after homogenization where nuclear material is on bottom, then mito and then ER leftover that's not strands anymore is microsomes
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where golgi apparatus processes from and what it does
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from RER
packages proteins that are completely elongated and releases them at the surface of the plasma membrane |
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clathrin triskelion protein
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3 heavy and 3 light chains
very strong, reinforced structure -forms sphere with others |
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what do clathrin proteins do
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reinforce and coat outside of vesicle and allow it to move in
-proteins fall off and it loses structure -in cell membrane before ligand |
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cell signaling 3 broad types of receptors
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1. ion channels
2. internalize ligand intact 3. those that initiate an internal chemical signal |
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describe ion channels and give an example
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acetylcholine receptor
-binding opens channel for Na+ to enter |
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describe and example of internalizing a lignad intact**
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insulin is internalized in clathrin-coated pit
-stimulates protein synthesis of GLUT4 receptors |
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receptors that initiate an internal chemical signal**describe and give an example
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hormones, events, 2nd messenger
chemical rxns like protein kinases |
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3 major mechanisms of enzyme regulation
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1. covalent modification by hormones
2. allosteric modification 3. enzyme induction |
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explain covalent modification by hormones and give examples
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chemical, protein kinases (phosphorylate)
and phosphatase(dephosphorylates enzymes) |
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explain allosteric modification and give an example
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enzymes behave sigmoidally because of the presence of an activator
-positive or negatively modulated by regulators ex: cAMP |
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positive allosteric modulators effect on Km and enzyme affinity
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they decrease Km(hemoglobin) and increase the affinity of the enzyme for the substrate-can increase vmax and rxn speed
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explain enzyme induction and give an example
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regulate by producing more enzyme (protein synthesis)
-says nothing about activity -enzyme inducer stimulates protein synthesis (chemical) ex: cytochrome p450 levels in liver increase when shot of chemical is given |
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which is the slowest mechanism of enzyme regulation? positive side?
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enzyme induction
-it can persist for a long period of time |
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enzyme induction puts enzyme activity in terms of
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rate
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endothermic means energy is...
exothermic |
endo=added
exo=gives up energy |
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explain ATP's free energy significance
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good source of energy and acceptor because it's in the middle of hydrolysis of phosphorylated cmpds
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for every NADH down ETC how many ATP are made
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3
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2 ways energy is made in the body
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1. directly linking to a substrated(phosphocreatine to creatine)
2. ETC that uses electron flow to generate free energy by phosphorylated ADP to ATP |
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what drives electron flow down ETC from NADH to react with oxygen and generate ATP
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1. depends on std redox potential and tendency to donate or accept electrons
2. must flow from most negative to most positive |
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standard reduction potential measures? - means? + means?
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tendency to donate or accept electonrs.
negative = greater tendency to lose/donate electrons + : more likely to accept electrons |
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electron acceptors get oxidized or reduced?q
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reduced
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2 mechanisms for ATP production in the cell
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1. substrate level phosphorylation: ATP during glycolysis
2. Oxidative phosphorylation: generation of ATP liked to substrate redox as electrons pass down ETC -starts with substrates in the Krebs cycle, -Dehydrogenase enzyems catalyze removal of hydrogens and electrons from Krebs cycle substrates -removal of H's and e- is coupled with reduction of NAD or FAD |
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how much saliva is made a day and what does it contain?
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-1L/day
-electrolytes, mucus, enzymes, IgA |
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enzymes in the oral cavity
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alpha amylase: can hydrolyze some alpha 1,4 linkages and simple starches
lingual lipase: infants for milk, decreases with age |
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fxn of mucus in the oral cavity
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coats food and protects lining of mouth and esophagus
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passage through esophagus takes how long
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about 10 seconds
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what happens in esophagus upon swallowing
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pressure on LES drops
-LES relaxes and opens |
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closure of LES fxn
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prevents acid or chyme from entering esophagus once in stomach
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GERD is? may cause?
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when acid or chyme enters the esophagus
-may cause esophagitis or esophageal cancer |
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what happens in the pyloric portion of the stomach
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-significant contractions to grind and make chyme
-responds to many stimuli -releases food into duodenum in small amts 1 tsp |
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impt part of stomach body
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gastric glands
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what secretes HCl
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gastric parietal cells
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two systems for secreting HCl and their net effect
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1. K/Cl transport system
2. H+/K ATPase system -Cl and protons secreted to bring K in |
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K/Cl transport system
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Cl is secreted into lumen of stomach and K ions secreted passively from parietal so K goes in
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H/K ATPase system
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proton pump that requires ATP
-K goes into cell in exchange for 2 protons |
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Functions of HCl
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1. activation of pepsinogen
2. denature proteins 3. release nutrients from organic complexes (iron) 4. kill bacteria in food |
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how HCl activates pepsinogen
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in presence of acid it's released from stomach glands and becomes pepsin to digest some proteins
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how HCl denatures proteins
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it makes the active site more available and it unfrods quat and tert structure for enzymes to access to peptide bonds
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how does HCl help release nutrients from organic complexes
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acid makes iron release
-heme and non-heme iron (veggies, HCl increases Fe availability in this form) |
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what is the intrinsic factor responsible for
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vitamin b12 absorption
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neck/mucus cells secrete
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mucus and bicarbonate
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peptic or chief cells secrete
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pepsinogen
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oxyntic or parietal cells secrete
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HCl and intrinsic factor
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enteroendocrine or g cells secrete
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gastrin to regulate digestion
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serosa or adventitia contains
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CT, major blood vessels
-on outside |
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submucosa contains
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blood vessels to pick up nutrients
-nerve and lympatic tissue for immune response |
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which muscle is responsible for peristalsis contractions
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longitudainal and circular?
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mucosa fxn
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absorption and digestions, lamina propria, muscularis mucosa, epithelial lining
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villi/explain
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increases SA of intestines
-intestinal absorption cells (epithelial) form at the bottom (crypts) and migrate to tips as mature cells -rapid turnover of 3-5days |
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what happens at tip of intestinal cell with villi
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digestion and absorption
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H2 receptor examples
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zantac and pepsid AC
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proton pump inhibitor examples
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nexium and prilosec
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obesity treatments
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1. adjustable laproscopic band
2. roux en y gastric bypass: past of intestines removed |
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dumping syndrome
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contents of the stomach are dumped undigested into the small intestine
-severege digestive stress = acute, right after a meal or many hours later (headache,dizzy) -metabolites move rapidly into blood |
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glycocalyx
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water layer above glycoprotein
-digestion for CHO |
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microvilli brush border are on what side of cell>
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lumen
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basal lateral side means it moves to
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leave the epithelial cell into blood stream
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why are micelles formed
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to interact with pancreatic lipase for digestion
-phospholipids -orient around triglycerides in diet and then emulsify for digestion |
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how are micelles arranged
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hydrophobic fatty acids inside and intestinal juices on out. bile salts and phospholipids are both amphoteric
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GERD caused by hiatal hernia
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-stomach gets through hole in diaphragm
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what foods spur GERD
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alcohol
acidic foods (citrus) spicy foods peppermint/spearmint chocolate smoking coffee |
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how long does it take the stomach to empty
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2-5 hours
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what does pancreatic lipase normally do?
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hydrolyzes triacylglycerol to 2 FA's and 2 monoacylglycerols
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micelles help to what with transport
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get through apical side of mucosal layer intact
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chylomicrons fxn and what they are
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formed in small intestinal mucosal cells and ends up in lymphatic system if long chain fatty acids
-some SCFA's go into blood from lymph at thoracic duct in neck |
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pancreatic amylase breaks CHO down to and where
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oligosaccs and disaccs
-luminal digestion |
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where does the final breakdown to monosaccharides occur
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membrane digestion at brush border by enzymes** secreted by mucosal cells
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products of final starch breakdown, which ones
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galactose, glucose, fructose
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how do galactose and glucose move after digestion and fructose?
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galac and gluc do active transport
-fructose does facilitated diffusion |
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what are pancreatic proteases for?
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specific peptides, normally zymogens that then convert and make AA's or dipeptides that get absorbed into mucosal cells and cross the basal lateral side
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how is protein digestion diff than CHO
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a significant amount occurs in stomach and lumen of small intestine because of pancreatic proteases that make AA's or dipeptides and then get absorbed by mucosal cells
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explain lactose intolerance...and how to measure
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-deficient in lactase so lactose doesn't go to galac and gluc
-lactose in the large intestine gets into contact with bacteria where H2 is given off and can be measured in the breath |
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side effects of lactose intolerance
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bloating
diarrhea dehydration |
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free aldehyde content of aldoses tells
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how much of the sugar exists in open chain form
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intestinal proteases fxn
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hydrolyze peptide bonds and then tri, dipeptides and AAs can be absorbed by the enterocyte
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name some intestinal proteases
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trypsinogen
chymotrypsinogen elastase/collagenase colipase cholestrol estease procarboxypeptidases pancreatic lipase |
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what can happen to oligopeptides and some tripeptides after initially broken down
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may be further hydrolyzed by brush border aminiopeptidases before absorption
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intestinal bacteria fxn
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help metabolize compounds in large intestine
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colon fxn
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fermentation
-dehydrates undigested material and electrolytes |
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deoxycholic acid from cholic acid has...describe, why
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can have AA derivatives
-can be reabsorbed from large intestine |
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chenodeoxycholic acid goes to? and what happens to that
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lithocholic acid that normally gets excreted in the feces
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