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Molecular - Block 3 > Block 3 Questions > Flashcards

Block 3 Questions Flashcards

1
Q

Cell type that synthesizes and releases NO

A

Endothelial Cells

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2
Q

<p class=”large” style=”text-align:center”;>Yield of Phase 2 Glycolysis per Glucose</p>

A

<p class=”large” style=”text-align:center”;>2 NADH, 4 ATP, 2 Pyruvate</p>

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3
Q

<p class=”large” style=”text-align:center”;>Which steps in metabolic pathway are enzyme catalyzed?</p>

A

<p class=”large” style=”text-align:center”;>All</p>

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4
Q

<p class=”large” style=”text-align:center”;>Which G-Protein activates PLC-beta</p>

A

<p class=”large” style=”text-align:center”;>Gq</p>

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5
Q

<p class=”large” style=”text-align:center”;>Which G proteins activate Adenylyl Cyclase?</p>

A

<p class=”large” style=”text-align:center”;>Gs and Golf</p>

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6
Q

<p>Where does regulation of Pyruvate Kinase occur?</p>

A

<p>Liver, not muscle; Responds to ATP (inhibit) and F-1,6-BisP (Activate)</p>

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7
Q

<p class=”large” style=”text-align:center”;>Where are undigested sugars metabolized?</p>

A

<p class=”large” style=”text-align:center”;>By bacteria in the large intestine</p>

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8
Q

<p class=”large” style=”text-align:center”;>When does post-prandial state end?</p>

A

<p class=”large” style=”text-align:center”;>When last meal is digested</p>

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9
Q

<p class=”large” style=”text-align:center”;>What type of hormone is Insulin?</p>

A

<p class=”large” style=”text-align:center”;>Anabolic</p>

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10
Q

<p class=”large” style=”text-align:center”;>What type of hormone is Glucagon?</p>

A

<p class=”large” style=”text-align:center”;>Catabolic (breaks down)</p>

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11
Q

<p class=”large” style=”text-align:center”;>What to Jak-Stat receptors need?</p>

A

<p class=”large” style=”text-align:center”;>Must recruit a kinase, unlike RTK’s; Jak is the kinase</p>

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12
Q

<p class=”large” style=”text-align:center”;>What steps do allosteric enzymes usually catalyze?</p>

A

<p class=”large” style=”text-align:center”;>Irreversible Steps</p>

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13
Q

<p class=”large” style=”text-align:center”;>What serves as an alternate fuel for muscle during the basal state?</p>

A

<p class=”large” style=”text-align:center”;>Ketone Bodies (formed in liver)</p>

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14
Q

<p>What storage molecule is used to make Lactate when O2 is limiting?</p>

A

<p>Glycogen during exercise</p>

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15
Q

<p class=”large” style=”text-align:center”;>What is the committed step in a metabolic pathway?</p>

A

<p class=”large” style=”text-align:center”;>First ir-reversible step unique to a pathway</p>

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16
Q

<p class=”large” style=”text-align:center”;>What is RXR</p>

A

<p class=”large” style=”text-align:center”;>Nuclear receptor that forms heterodimer with some steroid receptors</p>

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17
Q

<p class=”large” style=”text-align:center”;>What is Jak?</p>

A

<p class=”large” style=”text-align:center”;>Janus Kinase; Binds Jak-Stat receptor and phosphorylates receptor on tyrosine residues.</p>

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18
Q

<p class=”large” style=”text-align:center”;>What is a common reactant in the Oxidation of foods?</p>

A

<p class=”large” style=”text-align:center”;>O2</p>

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19
Q

<p class=”large” style=”text-align:center”;>What enzyme has 80% of total intestinal maltase activity?</p>

A

<p class=”large” style=”text-align:center”;>Sucrase-Isomaltase compound</p>

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20
Q

<p class=”large” style=”text-align:center”;>What can turn Glygolysis on regardless of energy state of cell?</p>

A

<p class=”large” style=”text-align:center”;>Fructose-2,6-BisPhosphate binding to PFK-1</p>

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21
Q

<p class=”large” style=”text-align:center”;>What can increase exposure of drug to CYP3A4</p>

A

<p class=”large” style=”text-align:center”;>P-gp/MDR1 cyclicly pumpin drug back out into lumen</p>

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22
Q

<p class=”large” style=”text-align:center”;>What alternative fuel does the brain use in the starved state?</p>

A

<p class=”large” style=”text-align:center”;>Ketone Bodies</p>

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23
Q

<p class=”large” style=”text-align:center”;>What activates PKA?</p>

A

<p class=”large” style=”text-align:center”;>cAMP</p>

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24
Q

<p class=”large” style=”text-align:center”;>What activates alpha subunit of G protein</p>

A

<p class=”large” style=”text-align:center”;>Ligand binding causes exchange for GTP, which activates</p>

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25
Q

<p class=”large” style=”text-align:center”;>Vitamin C (Ascorbic Acid)</p>

A

<p class=”large” style=”text-align:center”;>Carb, required for hydroxylation of proline and lysin in collagen</p>

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26
Q

<p class=”large” style=”text-align:center”;>Viagra</p>

A

<p class=”large” style=”text-align:center”;>Blocks cGMP phosphodiesterase, prolonging vasodilation</p>

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27
Q

<p class=”large” style=”text-align:center”;>Variation in plasma glucagon</p>

A

<p class=”large” style=”text-align:center”;>Minimal</p>

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28
Q

<p class=”large” style=”text-align:center”;>Types of ABC’s</p>

A

<p class=”large” style=”text-align:center”;>P-Glycoprotein, MDR protein, BRCP</p>

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29
Q

<p class=”large” style=”text-align:center”;>Two basic tests for Glycosuria</p>

A

<p class=”large” style=”text-align:center”;>Glucose Oxidase method, Copper Reduction Tests</p>

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30
Q

<p class=”large” style=”text-align:center”;>Trehalase Activity</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyze alpha-1,1-linkage found in trehalose (2 glucoses linked alpha-1,1-)</p>

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31
Q

<p class=”large” style=”text-align:center”;>Transporter of Fatty Acids</p>

A

<p class=”large” style=”text-align:center”;>FABP2 or SLC27A4</p>

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32
Q

<p class=”large” style=”text-align:center”;>Tissues that use Cori Cycle?</p>

A

<p class=”large” style=”text-align:center”;>RBC’s and Muscle</p>

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33
Q

<p class=”large” style=”text-align:center”;>Third Step of Metabolism</p>

A

<p class=”large” style=”text-align:center”;>Complete oxidation of AcCoA to H20 and CO2, Mitochondria, Lots of ATP</p>

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34
Q

<p class=”large” style=”text-align:center”;>The rate of ionized v un-ionized fraction of drug depends on what?</p>

A

<p class=”large” style=”text-align:center”;>pKa of drug and pH of surroundings</p>

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35
Q

<p class=”large” style=”text-align:center”;>Sucrase Activity</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyzes alpha-1,2-linkaged of Sucrose to Glucose and Fructose</p>

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36
Q

<p class=”large” style=”text-align:center”;>Substrates of PFK-1</p>

A

<p class=”large” style=”text-align:center”;>Fructose-6-Phosphate, Mg-ATP</p>

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37
Q

<p class=”large” style=”text-align:center”;>Substrates for Lipogenesis</p>

A

<p class=”large” style=”text-align:center”;>Glucose, Glycerol, AcCoA</p>

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38
Q

<p class=”large” style=”text-align:center”;>Substrates for Glycogenesis</p>

A

<p class=”large” style=”text-align:center”;>Glucose-1-Phosphate, Glucose</p>

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39
Q

<p class=”large” style=”text-align:center”;>Substrates for Gluconeogenesis</p>

A

<p class=”large” style=”text-align:center”;>Lactate, Alanine, Glycerol</p>

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40
Q

<p class=”large” style=”text-align:center”;>Structure of Amylose</p>

A

<p class=”large” style=”text-align:center”;>Unbranched chains of Glucose linked alpha-1,4</p>

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41
Q

<p class=”large” style=”text-align:center”;>Structure of Amylopectin</p>

A

<p class=”large” style=”text-align:center”;>Alpha-1,4-linked chains w/ alpha-1,6-linked branches</p>

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42
Q

<p class=”large” style=”text-align:center”;>Steroid receptors found in nucleus</p>

A

<p class=”large” style=”text-align:center”;>RA, Vit D, TH; Heterodimers with RXR; Co-repressor released upon ligand binding</p>

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43
Q

<p class=”large” style=”text-align:center”;>Steroid receptors found in Cytosol</p>

A

<p class=”large” style=”text-align:center”;>Glucocorticoid, Estrogen, Progesteone; Trapped in cytosol bound to inhibitor proteins; Upon ligand binding, translocate to nucleus</p>

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44
Q

<p class=”large” style=”text-align:center”;>STAT’s</p>

A

<p class=”large” style=”text-align:center”;>After phosphorylated by Jaks, dissociate and dimerize; Migrates to nucleus; Has SH2 and SH3 domains that help dimerize</p>

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45
Q

<p class=”large” style=”text-align:center”;>Specific Binding</p>

A

<p class=”large” style=”text-align:center”;>Total Binding minus Non-specific Binding</p>

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46
Q

<p class=”large” style=”text-align:center”;>Sorbitol (Aldose Reductase) Pathway</p>

A

<p class=”large” style=”text-align:center”;>Converts Glucose to Fructose or Sorbitol</p>

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47
Q

<p class=”large” style=”text-align:center”;>Small G-Proteins</p>

A

<p class=”large” style=”text-align:center”;>Ras, Raf; Require aux proteins to work</p>

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48
Q

<p class=”large” style=”text-align:center”;>SLC2A5 (GLUT5)</p>

A

<p class=”large” style=”text-align:center”;>Faciliated transport of fructose from lumen into epithelial cell</p>

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49
Q

<p class=”large” style=”text-align:center”;>SLC2A2 (GLUT2)</p>

A

<p class=”large” style=”text-align:center”;>Basolateral membrane faciliated transport of sugar into interstitium</p>

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50
Q

<p class=”large” style=”text-align:center”;>Site of Disaccharidase action</p>

A

<p class=”large” style=”text-align:center”;>Intestinal lumen</p>

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51
Q

<p class=”large” style=”text-align:center”;>SH3 Binding</p>

A

<p class=”large” style=”text-align:center”;>Poly proline sequences</p>

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52
Q

<p class=”large” style=”text-align:center”;>SH2 Binding</p>

A

<p class=”large” style=”text-align:center”;>5-AA stretch with Tyr-PO4 at N-terminal</p>

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53
Q

<p class=”large” style=”text-align:center”;>Second Step of Metabolism</p>

A

<p class=”large” style=”text-align:center”;>Breakdown of simple subunits to AcCoA, cytosolic, limited ATP and NADH formed</p>

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54
Q

<p class=”large” style=”text-align:center”;>Second largest energy reserve in humans</p>

A

<p class=”large” style=”text-align:center”;>Protein in Muscle</p>

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55
Q

<p class=”large” style=”text-align:center”;>RTK’s control what:</p>

A

<p class=”large” style=”text-align:center”;>(1) MAPK (proliferation); (2) PI3K/AKT Signaling (survival)</p>

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56
Q

<p class=”large” style=”text-align:center”;>Role of NAD+ in Anaerobic Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>E-acceptor for Glyceraldehyde-3-Phospate-Dehydrogenase</p>

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57
Q

<p class=”large” style=”text-align:center”;>Role of Emuslification in intestine</p>

A

<p class=”large” style=”text-align:center”;>Disperse TG’s in the aqueous chyme; Makes TG’s more accessible for hydrolysis</p>

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58
Q

<p class=”large” style=”text-align:center”;>Renal Threshold for Blood Glucose</p>

A

<p class=”large” style=”text-align:center”;>160-180; at this level, glucose appears in urine</p>

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59
Q

<p class=”large” style=”text-align:center”;>Reasons for reduced bioavailability when oral</p>

A

<p class=”large” style=”text-align:center”;>Incomplete absoprtion; First-pass elimination</p>

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60
Q

<p class=”large” style=”text-align:center”;>Reactants of Phase 2 Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>Glyceraldehyde-3-Phosphate</p>

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61
Q

<p class=”large” style=”text-align:center”;>Reactants of Phase 1 Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>Glucose</p>

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62
Q

<p class=”large” style=”text-align:center”;>Rate Limiting Step in Metabolic Pathway</p>

A

<p class=”large” style=”text-align:center”;>Slowest step, Often a regulatory enzyme, Irreversible</p>

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63
Q

<p class=”large” style=”text-align:center”;>Rate Limiting Enzyme of Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>PFK-1 (F-6-P converted to F-1,6-BiP)</p>

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64
Q

<p class=”large” style=”text-align:center”;>Purpose of HCO3-</p>

A

<p class=”large” style=”text-align:center”;>Increase pH to higher so amylase can work in intestine</p>

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65
Q

<p class=”large” style=”text-align:center”;>Purpose of Comp. Binding Assays</p>

A

<p class=”large” style=”text-align:center”;>Determine potency of ligands in competition for binding to receptor, then determine affinity of ligands for receptor</p>

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66
Q

<p class=”large” style=”text-align:center”;>PTEN</p>

A

<p class=”large” style=”text-align:center”;>Tumor Suppressor, counteracts PI3K, promoting apoptosis; Deletion results in rescue from Apoptosis</p>

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67
Q

<p class=”large” style=”text-align:center”;>Protein kinase activated by cGMP</p>

A

<p class=”large” style=”text-align:center”;>PKG</p>

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68
Q

<p class=”large” style=”text-align:center”;>Products of Phase 1 Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>2 moles Glyceraldehyde-3-Phosphate, 2 ADP (2 ATP used)</p>

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69
Q

<p class=”large” style=”text-align:center”;>Primary energy reserve in humans</p>

A

<p class=”large” style=”text-align:center”;>TAG’s in Adipose</p>

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70
Q

<p class=”large” style=”text-align:center”;>Presence of excess hydrogen upon exhalation</p>

A

<p class=”large” style=”text-align:center”;>Indicates inability to metabolize various sugars</p>

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71
Q

<p class=”large” style=”text-align:center”;>PKA</p>

A

<p class=”large” style=”text-align:center”;>cAMP dependent protein kinase; Serine/Threonine</p>

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72
Q

<p>Phosphofructosekinase-1 in Glycolysis</p>

A

<p>Requires ATP; Irreversible; Commits glucose; Fructose-6-Phosphate to Fructose-1,6-BisPhosphate</p>

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73
Q

<p class=”large” style=”text-align:center”;>Pharmaceutical Equivalents</p>

A

<p class=”large” style=”text-align:center”;>Same active ingredient and are identical in strength of conc., dosage form, and route of administration</p>

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74
Q

<p>Pentose Phosphate Pathway</p>

A

<p>Generates 5 carbon sugars for ribonucleotide biosynthesis; Source of NADPH</p>

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75
Q

<p class=”large” style=”text-align:center”;>Order of MAPK proteins</p>

A

<p class=”large” style=”text-align:center”;>Raf -> Mek -> Erk</p>

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76
Q

<p>Primary location of Glucose-6-Phosphatase</p>

A

<p>Liver, Some in Kidney and Pancreas</p>

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77
Q

<p class=”large” style=”text-align:center”;>OATP</p>

A

<p class=”large” style=”text-align:center”;>Carry materials INTO enterocyte</p>

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78
Q

<p class=”large” style=”text-align:center”;>NT that activates NO synthesis</p>

A

<p class=”large” style=”text-align:center”;>ACh binds to receptor on enodthelial cell</p>

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79
Q

<p class=”large” style=”text-align:center”;>Nitroglycerin</p>

A

<p class=”large” style=”text-align:center”;>Breaks down in blood slowly to NO</p>

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80
Q

<p class=”large” style=”text-align:center”;>Net Yield of Anaerobic Glycolysis (after LDH)</p>

A

<p class=”large” style=”text-align:center”;>2 ATP, 2 Lactate, 2 NAD+</p>

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81
Q

<p class=”large” style=”text-align:center”;>Net Yield from Glycolytic Pathway</p>

A

<p class=”large” style=”text-align:center”;>2 ATP, 2 NADH, 2 Pyruvate per Glucose</p>

82
Q

<p class=”large” style=”text-align:center”;>N Terminus of Intracellular Receptors</p>

A

<p class=”large” style=”text-align:center”;>Variable, Not required for function</p>

83
Q

<p class=”large” style=”text-align:center”;>mTOR and AKT</p>

A

<p class=”large” style=”text-align:center”;>mTOR helps activate AKT</p>

84
Q

<p class=”large” style=”text-align:center”;>Most potent activator of PFK-1</p>

A

<p class=”large” style=”text-align:center”;>Fructose-2,6-BisP; Levels of this result from high F-6-P, overcome inhibitory effect of ATP</p>

85
Q

<p class=”large” style=”text-align:center”;>Most important regulator for Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>Fructose-2,6-BisP</p>

86
Q

<p class=”large” style=”text-align:center”;>Most abundant CYP in intestinal wall</p>

A

<p class=”large” style=”text-align:center”;>CYP3A4</p>

87
Q

<p class=”large” style=”text-align:center”;>More negative Standard Free energy of hydrolysis means what?</p>

A

<p class=”large” style=”text-align:center”;>More reaction will go to completion (toward products)</p>

88
Q

<p class=”large” style=”text-align:center”;>Maltase activity</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyze alpha-1,4-glycosidic linkages (most abundant linkages); Cleave Maltose</p>

89
Q

<p class=”large” style=”text-align:center”;>Malate-Aspartate Shuttle</p>

A

<p class=”large” style=”text-align:center”;>NADH, Amino group from Glutamate transferred to Aspartate</p>

90
Q

<p class=”large” style=”text-align:center”;>Major storage form of glucose in plants?</p>

A

<p class=”large” style=”text-align:center”;>Starch</p>

91
Q

<p class=”large” style=”text-align:center”;>Major source of carb in human diet?</p>

A

<p class=”large” style=”text-align:center”;>Starch</p>

92
Q

<p class=”large” style=”text-align:center”;>Major Sites of Glycolysis Regulation</p>

A

<p class=”large” style=”text-align:center”;>Hexokinases, Pyruvate Kinase, PFK-1 (ATP Feedback), Pyruvate Dehydrogenase (ATP Feedback)</p>

93
Q

<p class=”large” style=”text-align:center”;>Major effect of NO</p>

A

<p class=”large” style=”text-align:center”;>Smooth muscle relaxation</p>

94
Q

<p class=”large” style=”text-align:center”;>Main product of Glycogen breakdown</p>

A

<p class=”large” style=”text-align:center”;>Glucose-1-Phosphate</p>

95
Q

<p>Cellular Location of G-6-Phosphatase</p>

A

<p>ER membrane of Liver, Kidney</p>

96
Q

<p class=”large” style=”text-align:center”;>Lactase Actvity</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyzes beta-1,4-glycosidic linkages; Hydrolyzes Lactose to Glucose and Galactose</p>

97
Q

<p class=”large” style=”text-align:center”;>Lactase Activity</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyze beta-1,4-linkages found in lactose (disaccharidase)</p>

98
Q

<p class=”large” style=”text-align:center”;>Kd</p>

A

<p class=”large” style=”text-align:center”;>Ligand concentration which results in 50% occupancy</p>

99
Q

<p class=”large” style=”text-align:center”;>Isomaltase Activity</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyze alpha-1,6-glycosidic linkages; Cleaves isomaltase</p>

100
Q

<p class=”large” style=”text-align:center”;>Insulin-stimulated GLUT</p>

A

<p class=”large” style=”text-align:center”;>GLUT4</p>

101
Q

<p class=”large” style=”text-align:center”;>Inhibitors of PFK-1</p>

A

<p class=”large” style=”text-align:center”;>ATP, Citrate</p>

102
Q

<p class=”large” style=”text-align:center”;>In Comp Binding Assay, what is radiolabeled?</p>

A

<p class=”large” style=”text-align:center”;>Ligand with known affinity maintained at same concentration</p>

103
Q

<p class=”large” style=”text-align:center”;>Impaired Glucose Tolerance</p>

A

<p class=”large” style=”text-align:center”;>Asymptomatic condition, Dx on basis of OGTT</p>

104
Q

<p class=”large” style=”text-align:center”;>How to determine Bioequivalence</p>

A

<p class=”large” style=”text-align:center”;>Same blood concentration-time curve</p>

105
Q

<p class=”large” style=”text-align:center”;>How much glucose is usually present in urine?</p>

A

<p class=”large” style=”text-align:center”;>Little, if any</p>

106
Q

<p class=”large” style=”text-align:center”;>How is Water absorbed into intestines?</p>

A

<p class=”large” style=”text-align:center”;>Passive diffusion paracellularly; Faciliated transport via Aquaporins</p>

107
Q

<p class=”large” style=”text-align:center”;>How is Na+ absorbed in intestines?</p>

A

<p class=”large” style=”text-align:center”;>Gradient into cell is favorable: Na-channels, Cotransport w/ another molecule</p>

108
Q

<p class=”large” style=”text-align:center”;>How is Fructose imported into instestinal epithelium?</p>

A

<p class=”large” style=”text-align:center”;>SLC2A5 (GLUT5) Faciliated transport</p>

109
Q

<p class=”large” style=”text-align:center”;>How does most water enter intestinal lumen?</p>

A

<p class=”large” style=”text-align:center”;>Paracellular pathway</p>

110
Q

<p class=”large” style=”text-align:center”;>How does glucose move out of epithelial basolateral membrane?</p>

A

<p class=”large” style=”text-align:center”;>Faciliated transport through SLC2A2 (GLUT2)</p>

111
Q

<p class=”large” style=”text-align:center”;>How does cytosolic NADH enter mitochondria?</p>

A

<p class=”large” style=”text-align:center”;>Glycerol-3-Phosphate Shuttle and Malate-Aspartate Shuttle</p>

112
Q

<p class=”large” style=”text-align:center”;>How do Glucocorticoids prime Gluconeogenesis</p>

A

<p class=”large” style=”text-align:center”;>Induce expression of necessary enzymes</p>

113
Q

<p class=”large” style=”text-align:center”;>How are Ketone Bodies formed?</p>

A

<p class=”large” style=”text-align:center”;>Two AcCoA’s are linked in the liver</p>

114
Q

<p class=”large” style=”text-align:center”;>How are individual AA’s absorbed into instestine?</p>

A

<p class=”large” style=”text-align:center”;>Na-dependent secondary active transport</p>

115
Q

<p class=”large” style=”text-align:center”;>How are Di- and Tri-Peptides abosrobed into intestine?</p>

A

<p class=”large” style=”text-align:center”;>H+-dependent cotransport (SLC15A1)</p>

116
Q

<p class=”large” style=”text-align:center”;>HK 4 (Glucokinase)</p>

A

<p class=”large” style=”text-align:center”;>Liver, Pancreas; High Km (low affinity); Induced by insulin</p>

117
Q

<p class=”large” style=”text-align:center”;>HK 1-3</p>

A

<p class=”large” style=”text-align:center”;>Found in all cells, Low Km; Inhibited by G-6-P (their product)</p>

118
Q

<p class=”large” style=”text-align:center”;>High ATP and PFK-1</p>

A

<p class=”large” style=”text-align:center”;>Inhibits if high ATP in cell, therefore inhibiting Glycolysis</p>

119
Q

<p class=”large” style=”text-align:center”;>GRB2</p>

A

<p class=”large” style=”text-align:center”;>Two SH3, One SH2, Multi-functional adapter</p>

120
Q

<p class=”large” style=”text-align:center”;>GPCR’s</p>

A

<p class=”large” style=”text-align:center”;>7 TM segments; Carbs on extracellular N-terminus</p>

121
Q

<p class=”large” style=”text-align:center”;>Gold Standard Blood Glucose test</p>

A

<p class=”large” style=”text-align:center”;>Hexokinase Assay (HK catalyzes phosphorylation to G-6-P)</p>

122
Q

<p class=”large” style=”text-align:center”;>Glycerol-3-Phosphate Shuttle</p>

A

<p class=”large” style=”text-align:center”;>Antiporter, IMM, Reducing equivalents of NADH exchanged to FAD(2H) inside</p>

123
Q

<p class=”large” style=”text-align:center”;>GLUT4</p>

A

<p class=”large” style=”text-align:center”;>Insulin-stimulated; Recruited to membrane of adipose cells</p>

124
Q

<p class=”large” style=”text-align:center”;>GLUT3</p>

A

<p class=”large” style=”text-align:center”;>Surface of neuronal cells</p>

125
Q

<p class=”large” style=”text-align:center”;>GLUT2 in Pancreas</p>

A

<p class=”large” style=”text-align:center”;>Glucose uptake in beta cells; ATP produced, increasing Ca2+; Insulin vesicles released</p>

126
Q

<p class=”large” style=”text-align:center”;>GLUT2 in Liver</p>

A

<p class=”large” style=”text-align:center”;>High Km; High glucose levels; Stimulated to lower levels</p>

127
Q

<p class=”large” style=”text-align:center”;>GLUT1</p>

A

<p class=”large” style=”text-align:center”;>RBC’s; Km of 1-7; Blood-brain barrier</p>

128
Q

<p class=”large” style=”text-align:center”;>GLUT with highest Km</p>

A

<p class=”large” style=”text-align:center”;>GLUT2</p>

129
Q

<p class=”large” style=”text-align:center”;>GLUT on surface of neuronal cells</p>

A

<p class=”large” style=”text-align:center”;>GLUT3</p>

130
Q

<p class=”large” style=”text-align:center”;>GLUT on RBC’s</p>

A

<p class=”large” style=”text-align:center”;>GLUT1</p>

131
Q

<p class=”large” style=”text-align:center”;>GLUT necessary for insulin release</p>

A

<p class=”large” style=”text-align:center”;>GLUT2</p>

132
Q

<p class=”large” style=”text-align:center”;>GLUT in Blood-brain barrier</p>

A

<p class=”large” style=”text-align:center”;>GLUT1</p>

133
Q

<p class=”large” style=”text-align:center”;>Glucose Oxidase Assay</p>

A

<p class=”large” style=”text-align:center”;>Highly specific for glucose. Used for home glucose testing.</p>

134
Q

<p class=”large” style=”text-align:center”;>Glucose absorption in intestine</p>

A

<p class=”large” style=”text-align:center”;>SLC5A1; One molecule of sugar cotransported w/ 2 Na+ into cell</p>

135
Q

<p class=”large” style=”text-align:center”;>G protein subunit with intrinsic GTPase activity</p>

A

<p class=”large” style=”text-align:center”;>Alpha</p>

136
Q

<p class=”large” style=”text-align:center”;>Function of SLC5A1</p>

A

<p class=”large” style=”text-align:center”;>Glucose and Galactose cotransport into cell w/ 2 Na+</p>

137
Q

<p class=”large” style=”text-align:center”;>Function of Precose</p>

A

<p class=”large” style=”text-align:center”;>(Diabetes) Inhibits alpha-glucosidase activity in small intestine, which breaks down starches into monosaccharides</p>

138
Q

<p class=”large” style=”text-align:center”;>Function of CYP3A4</p>

A

<p class=”large” style=”text-align:center”;>In small intestine, breaks down/inactivates drugs before they can have effect</p>

139
Q

<p class=”large” style=”text-align:center”;>Function of Beano</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyzes carbs found in beans, not normally hydrolyzed</p>

140
Q

<p class=”large” style=”text-align:center”;>Function of ABC’s</p>

A

<p class=”large” style=”text-align:center”;>Pump substrates out into lumen</p>

141
Q

<p class=”large” style=”text-align:center”;>Formation of what is a key central reaction in the utilization of Glucose</p>

A

<p class=”large” style=”text-align:center”;>Gluc-6-Phosphate</p>

142
Q

<p class=”large” style=”text-align:center”;>Formation of NO</p>

A

<p class=”large” style=”text-align:center”;>Deaminatino of Arginine by NO Synthetase (NOS)</p>

143
Q

<p class=”large” style=”text-align:center”;>First Step of Metabolism</p>

A

<p class=”large” style=”text-align:center”;>Breakdown of Large Macromolecules, typically extracellular</p>

144
Q

<p class=”large” style=”text-align:center”;>First commited step of Glycolysis pathway</p>

A

<p class=”large” style=”text-align:center”;>PFK-1: F-6-P converted to F-1,6-BiP</p>

145
Q

<p class=”large” style=”text-align:center”;>Features of GLUT proteins</p>

A

<p class=”large” style=”text-align:center”;>12 TM segments, Both terminal residues are cytoplasmic, No energy used</p>

146
Q

<p class=”large” style=”text-align:center”;>Fate of NADH after Anaerobic Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>NADH re-oxidized to NAD+ in cytosol by LDH, converting Pyruvate to Lactate</p>

147
Q

<p class=”large” style=”text-align:center”;>Fate of NADH after Aerobic Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>Oxidized in mitochondria via ETC</p>

148
Q

<p class=”large” style=”text-align:center”;>Fate of Lactate released in blood?</p>

A

<p class=”large” style=”text-align:center”;>Oxidized back to Pyruvate, which is in Gluconeogenesis</p>

149
Q

<p class=”large” style=”text-align:center”;>FABP2</p>

A

<p class=”large” style=”text-align:center”;>Transports FA’s into intestinal epithelium</p>

150
Q

<p class=”large” style=”text-align:center”;>Exposure of RBC’s to Hyperglycemia</p>

A

<p class=”large” style=”text-align:center”;>Nonenzymatic glycosylation of Hb, forming Hb A1c</p>

151
Q

<p class=”large” style=”text-align:center”;>Examples of Intracellular Receptors</p>

A

<p class=”large” style=”text-align:center”;>Steroid, RA, Thyroid Hormone, Vit D</p>

152
Q

<p class=”large” style=”text-align:center”;>Energy use of Phase 1 Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>2 ATPs</p>

153
Q

<p class=”large” style=”text-align:center”;>Energy released by oxidative catabolism is used to synthesize what?</p>

A

<p class=”large” style=”text-align:center”;>ATP and other high energy compounds</p>

154
Q

<p class=”large” style=”text-align:center”;>End Products of Proteolysis</p>

A

<p class=”large” style=”text-align:center”;>Glucose, Ketones</p>

155
Q

<p class=”large” style=”text-align:center”;>End Products of Lipolysis</p>

A

<p class=”large” style=”text-align:center”;>AcCoA, Glycerol</p>

156
Q

<p class=”large” style=”text-align:center”;>End Products of Lipogenesis</p>

A

<p class=”large” style=”text-align:center”;>FA’s, TAG’s</p>

157
Q

<p class=”large” style=”text-align:center”;>End Products of Glycolysis</p>

A

<p class=”large” style=”text-align:center”;>Pyruvate, ATP</p>

158
Q

<p class=”large” style=”text-align:center”;>Effect of Vasodilators on GI Perfusion</p>

A

<p class=”large” style=”text-align:center”;>Increase rate of absorption</p>

159
Q

<p class=”large” style=”text-align:center”;>Effect of Insulin on Ketogenesis?</p>

A

<p class=”large” style=”text-align:center”;>Decrease</p>

160
Q

<p class=”large” style=”text-align:center”;>Effect of Glucagon on Ketogenesis?</p>

A

<p class=”large” style=”text-align:center”;>Increase</p>

161
Q

<p class=”large” style=”text-align:center”;>EC_50</p>

A

<p class=”large” style=”text-align:center”;>Effective concentration of competitor required for 50% effect; Conc. required to displace 50% of labeled ligand</p>

162
Q

<p class=”large” style=”text-align:center”;>Disadvantages of Reduction Methods</p>

A

<p class=”large” style=”text-align:center”;>Lack of specificity and sensitivity (still sold OTC)</p>

163
Q

<p class=”large” style=”text-align:center”;>Disadvantages of Oral Drug Delivery</p>

A

<p class=”large” style=”text-align:center”;>Limited Absorption; Emesis; Destruction; Food; Cooperation; Flora first</p>

164
Q

<p class=”large” style=”text-align:center”;>Digestion of Maltotriose</p>

A

<p class=”large” style=”text-align:center”;>Glucoamylase Complex (alpha-1,4); Product is 3 Glucose</p>

165
Q

<p class=”large” style=”text-align:center”;>Digestion of Maltose</p>

A

<p class=”large” style=”text-align:center”;>alpha-Glucoamylase (alpha-1,4) and Sucrase-Isomaltase (alpha-1,4); Product is 2 Glucose</p>

166
Q

<p class=”large” style=”text-align:center”;>Degree of Ionization</p>

A

<p class=”large” style=”text-align:center”;>Concentration gradient of the un-ionized form across the membrane</p>

167
Q

<p class=”large” style=”text-align:center”;>Degradation of cGMP</p>

A

<p class=”large” style=”text-align:center”;>cGMP Phosphodiesterase</p>

168
Q

<p class=”large” style=”text-align:center”;>Definition of Bioavailability</p>

A

<p class=”large” style=”text-align:center”;>Fraction of unchanged drug reaching the systemic circulation following administration</p>

169
Q

<p class=”large” style=”text-align:center”;>Criteria for a Physiological Receptor</p>

A

<p class=”large” style=”text-align:center”;>Saturable, Specific, Kinetics</p>

170
Q

<p class=”large” style=”text-align:center”;>Composition of Sucrose</p>

A

<p class=”large” style=”text-align:center”;>Disacchardie of Glucose and Fructose</p>

171
Q

<p class=”large” style=”text-align:center”;>Composition of Starch</p>

A

<p class=”large” style=”text-align:center”;>Amylose and Amylopectin</p>

172
Q

<p class=”large” style=”text-align:center”;>Composition of Lactose</p>

A

<p class=”large” style=”text-align:center”;>Disaccharide of Galactose and Glucose (beta-1,4-linkage)</p>

173
Q

<p class=”large” style=”text-align:center”;>Citrate and PFK-1</p>

A

<p class=”large” style=”text-align:center”;>Inhibits, sign that CAC is saturated, glycolysis not needed</p>

174
Q

<p class=”large” style=”text-align:center”;>Chelators</p>

A

<p class=”large” style=”text-align:center”;>Bind up endogenous substrates like fat or bile acids</p>

175
Q

<p class=”large” style=”text-align:center”;>Cellular Location of Pyruvate Dehydrogenase activity</p>

A

<p class=”large” style=”text-align:center”;>Mitochondrial Matrix</p>

177
Q

<p class=”large” style=”text-align:center”;>Calmodulin</p>

A

<p class=”large” style=”text-align:center”;>(1) Conformation change upon Ca binding; (2) Activates other enzymes</p>

178
Q

<p class=”large” style=”text-align:center”;>C Terminal of Intracellular Receptors</p>

A

<p class=”large” style=”text-align:center”;>Ligand-binding domain</p>

179
Q

<p class=”large” style=”text-align:center”;>Breakdown of fuel stores in an oxidative method?</p>

A

<p class=”large” style=”text-align:center”;>Catabolic Metabolism</p>

180
Q

<p class=”large” style=”text-align:center”;>Bioequivalence</p>

A

<p class=”large” style=”text-align:center”;>Rates and extents of bioavailability of the active ingredient are not significantly diff</p>

181
Q

<p class=”large” style=”text-align:center”;>Area under blood concentration-time curve</p>

A

<p class=”large” style=”text-align:center”;>Proportional to extent of bioavailability of a drug</p>

182
Q

<p class=”large” style=”text-align:center”;>Are metabolic pathways reversible?</p>

A

<p class=”large” style=”text-align:center”;>No, deltaG is negative; individual steps may be reversible though</p>

183
Q

<p class=”large” style=”text-align:center”;>AMP and PFK-1</p>

A

<p class=”large” style=”text-align:center”;>Increases affinity of PFK-1 for F-6-P, increased activity</p>

184
Q

<p class=”large” style=”text-align:center”;>Alpha-Limit Dextrin Digestion</p>

A

<p class=”large” style=”text-align:center”;>Isomaltase; Products are Maltose, Maltotriose, Glucose</p>

185
Q

<p class=”large” style=”text-align:center”;>Alpha subunit of G protein</p>

A

<p class=”large” style=”text-align:center”;>Intrinsic GTPase activity</p>

186
Q

<p class=”large” style=”text-align:center”;>Alcohol and Hypoglycemia</p>

A

<p class=”large” style=”text-align:center”;>Metabolism of alcohol increases NADH in liver, which inhibits Gluconeogenesis</p>

187
Q

<p class=”large” style=”text-align:center”;>Advantages of Drugs taken Rectally</p>

A

<p class=”large” style=”text-align:center”;>Faster Onset, Higher Bioavailability, Shorter Peak, Short Duration</p>

188
Q

<p class=”large” style=”text-align:center”;>Activators of PFK-1</p>

A

<p class=”large” style=”text-align:center”;>AMP; F-2,6-BiP (it’s product)</p>

189
Q

<p class=”large” style=”text-align:center”;>Actions of Insulin</p>

A

<p class=”large” style=”text-align:center”;>Increase Glc uptake by muscle and adipose, Increase hepatic Glycogenesis and Lipogenesis</p>

190
Q

<p class=”large” style=”text-align:center”;>Actions of Growth Hormone</p>

A

<p class=”large” style=”text-align:center”;>Secreted in Hypoglycemia, Increases hepatic glc production, Reduces glc use by some tissues</p>

191
Q

<p class=”large” style=”text-align:center”;>Actions of Glucagon</p>

A

<p class=”large” style=”text-align:center”;>Stimulate Glycogenolysis, Gluconeogenesis; AA to Glc; TG’s to FA’s</p>

192
Q

<p class=”large” style=”text-align:center”;>Actions of Epi</p>

A

<p class=”large” style=”text-align:center”;>Stimulate Glycogenolysis, Adipose tissue Lipolysis, Inhibit insulin secretion</p>

193
Q

<p class=”large” style=”text-align:center”;>Actions of Cortisol</p>

A

<p class=”large” style=”text-align:center”;>Stimulate Glucagon release, Gluconeogenesis</p>

194
Q

<p class=”large” style=”text-align:center”;>Action of Pyrophosphatase</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyze Pyrophosphate into 2 additional Pi</p>

195
Q

<p class=”large” style=”text-align:center”;>Action of PLC-beta</p>

A

<p class=”large” style=”text-align:center”;>(1) Cleave Inositol Phospholipid into Diaglycerol and IP3; (2) IP3 opens Ca channels in ER; (3) Diaglyercol and Ca activate PKC</p>

196
Q

<p class=”large” style=”text-align:center”;>Action of NO</p>

A

<p class=”large” style=”text-align:center”;>Activates soluble Guanylyl Cyclase, which synthesizes cGMP from GTP</p>

197
Q

<p class=”large” style=”text-align:center”;>Action of Gq</p>

A

<p class=”large” style=”text-align:center”;>Activate PLC-beta</p>

198
Q

<p class=”large” style=”text-align:center”;>Action of Glucoamylase</p>

A

<p class=”large” style=”text-align:center”;>Hydrolyzes alpha-1,4-glycosidic linkages of Maltose and Maltotriose; Cleaves glucose from nonreducing end of oligosaccharides; Cleaves maltose and isomaltose</p>

199
Q

<p class=”large” style=”text-align:center”;>Action of CFTR Channel?</p>

A

<p class=”large” style=”text-align:center”;>Pumps Cl- into intestinal lumen; Osmotically active ion and negative charge in lumen; Na+ follows through tight junctions, water follows through tight junctions</p>

200
Q

<p class=”large” style=”text-align:center”;>Action of Beta Gamma subunits</p>

A

<p class=”large” style=”text-align:center”;>Open K+ channels</p>

201
Q

<p class=”large” style=”text-align:center”;>Action of Amylase</p>

A

<p class=”large” style=”text-align:center”;>Starch and Glycogen; Hydrolyzes alpha-1,4-glycosidic linkages, forming maltose, maltrotriose, glucose, and limit dextrins</p>

202
Q

<p class=”large” style=”text-align:center”;>Action of AKT (PKB)</p>

A

<p class=”large” style=”text-align:center”;>Phosphorylates “Bad”, which inhibits Apoptosis</p>

203
Q

<p class=”large” style=”text-align:center”;>2,3-BPG</p>

A

<p class=”large” style=”text-align:center”;>Reduces affinity of Hb for Oxygen when binds</p>

Molecular - Block 3 (1 decks)

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