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43 Cards in this Set
- Front
- Back
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How is insulin release triggered?
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glucose enters the B-islet cells and causes an increase in the ATP. The high ATP inhibits K+ leak channels and this provokes a depolarization of the cell and influx of Ca+, leading to the exocytosis of insulin vesicles.
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How is insulin made? (2 steps in synthesis)
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preproinsulin ----> has the N' signal sequence cleaved off and 3 s--s bonds added to become ----> proinsulin
Proinsulin ---> *c-peptide portion is removed* ----> insulin (2 chains joined by S--S bonds) |
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When insulin binds to it's receptors what happens? (short-term not long term)
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Insulin binds to the alpha-subunit and activates the tyrosine kinase portion of the beta-subunits. The TK autophosphorylates triggering a cascade of intracellular events.
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What are the 4 major (longer-term) effects of insulin on metabolism?
1. increases...... 2. stimulates _____ (how?) 3. stimulates _____ & inhibits ___ 4. stimulates ______ but blocks ____ |
1. increases the # of glucose transporters at the cell surface (= more glucose uptake)
2. stimulates glycolysis by activating PFK2 which produces a PFK1 activator 3. Stimulates glycogen synthesis and inhibits glycogen Bdown (activates protein phosphatase to de-Plate Glycogen P-lase and P-lase Kinase) 4. Stimulates fat, protein & glycogen synthesis but blocks GNG! |
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why should you avoid excess carbs before a running?
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B/c the insulin will push the body into an anabolic state and will prevent lipolysis. Instead of insulin, you want glucagon and andrenalin as the principal hormones b/c they will give you access to you fat fuels.
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What is the function of the following cells:
1. M secreting cells 2. M Neck cells 3. Enterochromaffin cells |
1. M secreting cells: make protective pH ~ 7 mucous
2. M Neck cells: can diff up or down into different cells types (make mucous of unknown function) 3. Enterochromaffin cells: paracrine secretions to regulate/coordinate tissues |
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What is the function of the following cells:
1. D-cells: 2. Chief cells: 3. Parietal cells: |
1. D-cells: secretes somatostatin (inhibits gastrin)
2. Chief cells: secretes pepsinogen (activated to pepsin by low pH) 3. Parietal cells: pink, they are the principal cell type, make HCl |
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What 3 things stimulate the parietal cells to secrete HCl?
1. G - 2 options 2. H - stimulated by? 3. A - what other 2 things does it stim? |
1. Gastrin: binds to either the parietal cell itself (CCK-B receptor) or to the ECL cell (to cause the release of histamine)
2. Histamin: released from ECL cell (see above) in response to gastrin/ACtH (H2 receptor) 3. Acetylcholine: neuroT, stimulates parietal directly and also stims the G and ECL cells |
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What stimulates the secretion of pepsinogen and from what cell?
How is it activated/inactivated and what does it do? What are (2) functions of pepsin? |
Pepsinogen is secreted from chief-cells in response to ACth.
Activated by a low pH <4 (optimal = 1.8-3.5), irreversibly inactivated by pH 7-8. Function: - digests proteins - mucolytic (when combined with HCl it causes much more ulceration than the acid alone!) |
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In addition to activating pepsin and other gastric lipases, what are 4 other functions of gastric HCl?
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1. Assists duodenal inorganic Fe absorption
2. -ve F-back (inhibition) of gastrin 3. ---+---> HCO3 secretion from the pancrease 4. suppression of ingested microorganisms |
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What is the function of:
Mucin/HCO3 Pepsins Intrinsic Factor Gastric Lipase |
Mucin/HCO3 = protection against HCl and pepsins
Pepsins = early hydrolysis of proteins, liberation of B12 from dietary proteins Intrinsic Factor = binds vit B12 for subsequent ileal absorption Gastric Lipase = early hydrolysis of dietary triglycerides |
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What are the 3 mechanisms of NSAID-mediated GI injury?
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1. sits on mucous and causes local irritation
2. active metabolites that get reflexed back (do damage?) 3. Inhibit COX1, which is responsible for maintaining baseline levels of p-glandins (secreted by surface gastric epithelium cells) |
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The major function of prostaglandins is epithelial defense and repair. What are 3 other functions?
1. regulate 2. inhibit 3. maintain |
1. regulates release of mucosal HCO3-/mucous
2. inhibits parietal HCl secretion 3. Maintain mucosal blood flow and epithelial cells restitiution |
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What is the difference between H.pylori infection in the antrum vs. the body (corpus) of the stomach?
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H.pylori in the antrum has a lower risk of cancer than do ulcers of the corpus.
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After managing the ABC's and stopping the offending agent, what are 3 other principles of treatment for peptic ulcers?
1. ↑ pH (3 reasons why) 2. cytoprotection 3. eradicated the H.pylori |
1. ↑ pH: minimizes direct injury; improves platelet aggregation and impairs clot lysis
2. cytoprotection: give prostaglandins analogues 3. eradicated the H.pylori: after this is done, maintenance acid suppression not routinely necessary |
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What enzyme is found in each of the following intestinal locations:
1. Intraluminal 2. Brush border 3. Intracellular |
1. Intraluminal: amylase
2. Brush border: oligosaccharidases and peptidases 3. Intracellular: dipeptidases |
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Which of the tips or the crypts of the SI villi, are responsible for absorption and which do secretion?
What happens if you gastroenteritis? (acute = bacterial, chronic = coeliac) |
Absorption = tips
Secretion = crypts Gastroenteritis will detroy the tips of the villi and this will leave unapposed crypt function = ↓ food absorption; lactose intolerance and diarrhea. If chronic will get crypt hyperplasia and secretory diarrhea. |
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What are the 2 main components of the mucosal barrier in the small intestine?
How does a fatty acid get through? |
1. Unstirred water layer - fats can't dissolve in this
2. Lipid bilayer of the cell - hydrophobic molecules can't get through this A bile acid gets the fatty acid through the water layer and then a fatty-acid transporter gets it into the cell. |
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What are the 3 main mechanisms of transport in the Small Intest?
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1. Passive diffusion:
- rate p~ to [gradient] but cannot go against [gradients], - no saturation kinetics - affected by water layer 2. Facillitated diffusion (carriers) - rate faster than for diffusion - saturation kinetics observed - cannot move against [gradient] 3. Active transport: - use carrier proteins and consumes ATP - e.g. Na+ & glucose/galactose; Na+ pumped-out by Na/K ATPase, sugar is facilitated or diffused |
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People can't be intolerate of α-Dextrins, Maltotiose and Maltose, because they are all digested by several enzymes. What 3 sugars can you be intolerant to?
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1. Lactose
2. Sucrose 3. Trehalose |
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What 4 factors will influence the occurrence of symptoms in lactase deficiency?
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1. Load from stomach - fat will ↓ gastric emptying
2. Lactase activity - mucosal mass? 3. Transit time - if slow will have less intolerance 4. Fermentation - if undigested lactose makes it to the colon it will be converted to gas; if excessive will generate an osmotic reaction |
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After being exposed to the jaws of pancreatic enzymes, what happens to ingested proteins? (ie what happens to bigger peptides, di/tripeptides and aa?)
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1. If they are a large peptide, then carboxypeptidases will cleave aa off the ends, or Elastase/Trypsin/Chymotrypsin will cleave them into smaller peptides.
2. Free aa will be T-ported into the cell with carriers and from there they can diffuse into capillaries 3. di and tri peptides will enter the mucosa cells via carrier proteins and will be ---> aa by cytoplasmic peptidases |
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When fat arrives in the duodenum, what 2 hormones are triggered?
How are the fats digested/absorbed? |
CCK - signals GB contraction = bile acid release; pancreatic enzyme secretion
Secretin - ductal HCO3 secretion from pancrease The bile salts will emulsify fat blobs into small droplets that can be ----> fatty acids & monoglycerides by lipase forming mixed micelles. When micelles contact the epithelium - the lipids diffuse accross the cell membrane and enter the cell. |
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What are 3 requirement for optimal lipase activity?
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1. High pH (gracias pancreatic HCO3!)
2. Co-lipase - stabilizes lipase to adhere onto the fat droplets 3. bile acids to help form micelles - solubizes fatty acids to cross the unstirred water layer |
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What are the functions of the fat-soluble vitamins?
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A - night vision
D - Ca absorption K - Blood clotting E - protects RBC's (esp. membranes); antioxidant |
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Describe the following mechanisms of fat malabsorption:
1. Intraluminal 2. Mucosal 3. Lymphatic |
1. Intraluminal:
- impaired hydrolysis d/t lipase or co-lipase deficiencies - impaired micelle fomation b/c of bile salt deficiency d/t prob with synthesis (cirrhosis), delivery (CBD obstruction) or enterohepatic circulation (crohn's) - problems with pH regulation 2. Mucosal - impaired uptake d/t ↓ # of, or defective enterocytes -impaired chylomicron formation & release (a-betalipoproteinemia = fat stuck in cells) 3. Lymphatic (blocked) - congenital defects - cancer infiltration |
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For each of the following nutrients list the major areas of absorption:
1. Iron & Ca 2. Carbohydrates 3. Protein, lipids Na+ and water 4. Cobalamin 5. Bile acids |
1. Iron & Ca = DUODENUM
2. Carbohydrates = D, J & I 3. Protein, lipids Na+ and water = D, J, & I 4. Cobalamin = ILEUM 5. Bile acids= all over but mostly the ILEUM |
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Where in the digestive tract would you expect to find passive transport of water and lytes? What about active?
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The proximal portion of the GI tract uses mostly passive diffusion and the distal portion uses mostly active.
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If a person has 1L of diarrhea, what type of diarrhea is it? Why?
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If diarrhea is > 1L, this is secretory. It is a problem with the SB such that the water entering the colon exceeded it's capacity of 5L. Etiology = gastro that destroyed villi tips ---> active secretion with ↓ absorption.
If diarrhea is < 0.5L it is a non-secretory diarrhea . Problem with colon. Etiology = ↓ absorptive capacity (colitis) or rapid motility (IBS) ** frequency of diarrhea is not as important as volume of stool |
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What is the difference (in terms of shape) between villus and crypt cells?
What is the difference (in terms of tight junctions) between villus and crypt cells? |
The villus cells are bigger/taller b/c they have lots of golgi and ER's to make all the digestive enzymes.
The tight junctions of the villus cells are very tight and NOT permeable to water. The TJ's of the crypt cells are the opposite and this allows for back diffusion of inflamatory exudates into the GI lumen (back diffusion ↑ in cases of crypt hyperplasia!) |
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Describe the movement of sodium in the GI tract:
- fed state - fasting - other? |
- Fed state: Na+ absorbed in the proximal bowel via Na/glucose co-Tport
- Fasting: Na+ absorbed from distal bowel only - Scavenger Na+ channels in the rectum that can be up-regulated by steroids and inhibited in inflamation |
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Describe the movement of Cl- in the GI tract:
-fed -fasting -other |
- Fed = absorbed via nutrient co-transport along the whole tract
- Fasting = absorbed via Na/Cl in distal bowl only - HCO3-dependant channels = when dehydrated the body will absorb Cl- (b/c water follows) BUT for each Cl- gained you loose a HCO3 = M.acidosis! |
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Where is K actively absobed and secreted? Where does it move passively?
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POTASSIUM
Active: absorption in rectum ONLY secreted in colon Passive: absorbed proximally, secreted distally Thus if you get chronic diarrhea will loose lots of K+ b/c body can only actively absorb it from the rectum and this is not enough = HoK, M.acidosis!! |
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What are 4 major causes of diarrhea? (give an example for each)
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1. Inhibited or impaired electrolyte/fluid absorption (E.Coli)
2. Osmotically active substances in GI lumen (lactose in ppl with intolerance) 3. Increase in propulsive contractions (IBS, caffeine) 4. Increase in electrolyte secretion (cholera) |
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What are 2 major causes of increased anion secretion in the GI tract?
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1. Bacteria/cholera can bind a G-protein and cause the activation of Adenylate Cyclase = cascade --> net increase in Cl- secretion = secretory diarrhea
2. Hyperplastic crypt cells (d/t loss of tips) will cause unapposed Cl- secretion and back diffusion |
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Increasing intestinal absorption is an obvious mechanism of anti-diarrheal medications. What are 3 ways of doing this? (give drug examples for each)
What is another mechanism? (drug that does this?) |
Increase intestinal absorption:
1. ↑ transit time by changing propulsive --> segmental contractions (opiates!) 2. Na& glucose in lumen will be absorbed in co-Tporter and water will follow (pedialyte) 3. ↑-regulate the Na channels in the rectum (steroids) Block anion secretion and secondary water movement (opiates) |
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What substances act on each of the following 2nd messangers:
1. cAMP 2. Cai 3. cGMP What is the net affect of these 2nd messangers? (2 things) |
1. cAMP: Histamine (allergic gastroent), VIP(can come from a tumor) & PGE2
2. Cai: Acetylcholine, Serotonin, Bradykinnin 3. cGMP: Heat-stable enterotoxins like E.coli ** these will increase anion secretion and block Na/Cl absorption |
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What is an RQ and is it higher for fats or suger?
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RQ = CO2 produced / O2 used
RQ = 1.0 for glucose and 0.7 for fats, therefore B-oxidation uses more O2 than glycolysis |
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What are the 4 steps that the body must go through to access fats? ie. to go from adipose to the carnitine shuttle?
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1. EP binds it's receptor: +Adenylate cyclase --> +PKA*
2. PKA will P-late HSL which can then attack TG's and hydrolyze ester bonds 3. Albumin brings the released FFA to muscle cells where they are joined to large, Hphillic Acetyl CoA 4. FA - CoA enters the mitochondria via carnitine shuttle * caffeine will inhibit the enzyme that B↓ PKA! |
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How does the carnitine shuttle work?
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FFA -- CoA + L-carnitine go into CAT 1
FFA - carnitine + CoA-SH come out! A translocase carries the FFA - carnitine through the inner-membrane where CAT 2 takes FFA-carnitine + CoA-SH and releases: FFA - Acetly CoA + L-Carnitine (moves back out) |
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If you eat sugar when your body is doing B-oxidation, what will happen?
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It will = disaster b/c insulin will lead to the production of malonyl CoA and this will shut down the whole B-oxidation party!
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During B-oxidation of FFA, what happens to the glycerol back-bone?
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The glycerol is used for glucose production/glycolysis to sustain BS, via GNG:
muscle --> lactate --> Liver ---> pyruvate --> Bwards thru glycolysis p-way |
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Why does the body need the carnitine shuttle system?
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To regulate B-oxidation! Once FFA cross the inner-membrane there is no holding them back! It's fiery free-for all in there.
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