Missed Things MCT Midterm PDF

Missed Things MCT Midterm 1. Ferroportin: Brings Fe2+ into erythrocytes 2. Transferrin: (TIBC) Transporter of Fe in blood to bone marrow and macrophages 3. Ferritin: stored iron Fe3+ 4. Hereditary Spherocytosis: A genetic defect in the RBC cell membrane 5. Erythromycin: deactivates 50S ribosom...

Missed Things MCT Midterm 1. Ferroportin: Brings Fe2+ into erythrocytes 2. Transferrin: (TIBC) Transporter of Fe in blood to bone marrow and macrophages 3. Ferritin: stored iron Fe3+ 4. Hereditary Spherocytosis: A genetic defect in the RBC cell membrane 5. Erythromycin: deactivates 50S ribosomal subunit 6. RNA pol 1: rRNA 7. RNA pol 2: mRNA 8. RNA pol 3: tRNA 9. Metformin: C1 inhibitor so ATP production reduced what leads to stoppage of gluconeogenesis as cAMP pathways activated 10. Glycogen stores last 12-18 hrs 11. Oral glucose test for DM 12. Substrates for gluconeogenesis: glycerol, lactate, pyruvate, AA, propionyl coA 13. Glucokinase has a high Km which leads to uptake of glucose after meal but a lag bc the uptake happens after hexokinase has saturated 14. Muscles and adipocytes have GLUT4; liver has GLUT2 15. CN poisoning can lead to acidosis 16. Transaminase is in the cytoplasm 17. Phenytoin can cause normocytic anemia 18. G6PD deficiency: lack of G6P dehydrogenase → no reduced glutathione which makes RBC more susceptible to oxidative stress. Intolerance of fava beans and sulfa drugs. May present with back pain and bloody urine. 19. PK Deficiency: decreases glycolysis so decreases ATP; affects RBC membrane; NADH:NAD+ ratio is increased 20. Cl = (.7*Vd)/t1/2 21. Cl = Vd*Ke 22. Vd = (LD*F)/Cp 23. LD = Cp*Vd/F 24. MD = Cp*cl*t/F 25. Sickle cell anemia is due to a point mutation in the B globin gene: Glutamic acid→ Valine 26. I Cell disease: Mutation in the N-acetylglucosamine-1-phosphotransferase; similar to hurlers; skeletal abnormalities and intellectual disability; inability of cell to create mannose-6-phosphate so enzymes are secreted extracellularly instead of to lysosomes 27. Mannose 6 phosphate directs enzymes to lysosome 28. MUD: Blocked degradation of branched amino acids 29. (isoleucine, leucine, valine) due to lack of branched chain α-ketoacid dehydrogenase (B1). Causes increased α-ketoacids in the blood, especially those of leucine 30. Inulin: tyrosine kinase 31. Glucagon: GPCR: adenylyl cyclase 32. MSUD: no alpha ketoglutarate dehydrogenase complex; branched AA affected and accumulated. Most common AA to accumulate is Leucine Typically manifests within a few days of birth and urine is sweet smelling. 33. Sulfonylureas may cause hypoglycemia 34. Citrate: inhibits PFK1 and glycolysis; activated FA synthesis 35. Alkaptonuria: no homogentisic acid oxidase which results in buildup of homogenistic acid. Therapy include limiting intake of tyrosine or phenylalanine. This condition results in the buildup of brownish or black pigment in skin, sclera, bone marrow, connective tissue, and dark urine. 36. Homocystinuria: no cystathionine B synthase or methionine synthetase leads to accumulation of homocysteine 37. To stop lactic acidosis in DKA, STOP SUPPLYING INSULIN 38. PKU: no conversion of F to tyrosine bc F carboxylase lacking 39. Atypical PKU: no dihydropteridine reductase causes no F to tyr and lowers dopamine 40. Kusmal Breathing: decreased pH 41. Glycogenolysis: glycogen phosphorylase first; glycogen6P Phosphatase last step 42. Branching enzyme: alpha 1,4-glucosidase; alpha 1,6-glucosidase 43. Debranching enzymes: 4:6 transferase 44. Xeroderma Pigmentosum: due to nucleotide excision repair defect 45. Lynch syndrome due to defect in DNA mismatch repair 46. NT Excision Repair: happens in G1 47. Alpha amanitin affects DNA polymerase 2 48. Ataxia telangiectasia: due to inability to do NHEJ in dsDNA breaks. Presents with ataxia, spider adenomas, and Ig A,G,E deficiency 49. Aplastic anemia due to defect in dsDNA repair function 50. Taut form of Hb found in peripheral tissues where O2 content is low. 51. Chronic blood loss common in liver cirrhosis secondary to alcoholism. Blood loss results in anemia 52. Base Excision Repair: step 1: dna glycosylase to remove base, step 2: endonuclease at 5’ and lyase at 3’ end to cut step 4: DNA polymerase fills in step 5: dna ligase closes 53. Enzymes for glycogen storage are in cytosol 54. TZD cause water retention 55. Hereditary spherocytosis is hereditary 56. Phosphotidylcholine makes up surfactant 57. Use a fucking calculator 58. Sensitivity reduces false negatives 59. Specificity reduces false positives 60. Trypsin is a pancreatic enzyme. Over release leads to pancreatitis. Pepsinogen is a gastric enzyme 61. Methemoglobinemia causes change from Fe2+ to Fe3+. May manifest with chocolate colored blood and cyanosis 62. In gluconeogenesis, pyruvate and oxaloacetate are found in the mitochondria 63. PFK-1 is activated by insulin, AMP, ADP, F26BP 64. PFK-1 inhibited by ATP, citrate, glucagon 65. Lysosomal proteins moved out of cell in hurlers syndrome 66. Glycogen phosphorylase is the first step of glycogenolysis 67. In the TCA, pyruvate to acetyl coA to citrate 68. DKA leads to hyperkalemia 69. Cortisol increases blood sugar levels by increasing emtabolism of sugars, carbs, and proteins 70. Steroid hormones bind receptors to make intracellular receptor complexes 71. GLP-1 agonists decrease glucagon and increase insulin 72. Deficiency in LPL causes inability to use chylomicrons and leads to high TGL in blood. This causes milky plasma on blood test.