USMLE 15

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rere_girl4ever
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293410
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USMLE 15
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2015-01-20 16:42:02
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USMLE 15
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  1. What causes this? What can be used to control it?
    • Exophthalmos- Graves disease
    • Infiltration of lymphocytes into the extraocular muscles and connective tissue.
    • Retro-orbital fibroblasts are then stmulated by TH1 cells to produce excessive amounts of glycosaminoglycans.
    • Tx: CORTICOSTEROIDS e.g Prednisone
  2. What mediates iodide uptake by the thyroid?
    • Sodium-iodide symporter
    • This uptake of iodide occurs against its concentration gradient.
  3. What is the function of the sodium-iodide symporter?
    Mediates iodide uptake by the thyroid against its concentration gradient.
  4. What is the MOA of Perchlorate?
    Inhibits the sodium-iodide symporter which mediates thyroid uptake of iodide.
  5. What is the MOA of Pertechnetate?
    Inhibits Sodium-iodide symporter which mediates the uptake of iodide by the thyroid.
  6. What is the MOA of Thiocyanate?
    Inhibits the sodium-iodide symporter which mediates thyroid uptake of iodide
  7. These anions can competitively inhibit the basolateral sodium-iodide symporter.
    • Perchlorate
    • Pertechnetate
    • Thiocyanate
  8. What is the function of thyroid peroxidase?
    • 1. Oxidation and organification of iodide
    • 2. Coupling of monoiodotyrosine and di-iodotyrosine
  9. This enzyme is used in the oxidation and organification of iodide.
    Thyroid peroxidase
  10. This enzyme couples iodide with tyrosine residues on thyroglobulin.
    Thyroid peroxidase
  11. Why is there such a high RBC chloride content in venous blood?
    • 1. Carbonic anhydrase activity forms bicarbonate from CO2 and water.
    • 2. Many of the bicarbonate diffuse out of the RBC into plasma.
    • 3. To maintain electrical neutrality, chloride ions diffuse into the RBC to take their place. ⇦CHLORIDE SHIFT
  12. Urethritis which cannot be cured by ceftriaxone indicates?
    • Nongonococcal urethritis-
    • Caused by Chlamydia trachomatis or Ureaplasma urealyticum
  13. Coagulase negative staphyloccus?
    • Staphyloccus epidermidis- Novobiocin sensitive
    • Staphyloccus aureus- Novobiocin resistant
  14. Coagulase positive staphyloccus?
    Staphyloccus aureus
  15. How does infection with Staphyloccus epidermidis occur?
    • Prosthetic devices (eg. hip implant, shunt, heart valve) and intravenous catheters.
    • Produce extracellular polysaccharide matrix
  16. This organism produces extracellular polysaccharide matrix.
    Staphyloccus epidermidis (biofilms)
  17. What enzyme is deficient in Xeroderma pigmentosum?
    ENDONUCLEASE
  18. How does DNA polymerase I takes out the RNA primer?
    5'→3' exonuclease
  19. How does DNA polymerase III proofread?
    3'→5' exonuclease
  20. This enzyme has 3'→5' exonuclease activity.
    DNA polymerase III- Proofreading
  21. This enzyme has 5'→3' exonuclease activity.
    DNA polymerase I - degrades RNA primer
  22. Defective repair of mismatched bases is associated with which disease?
    Hereditary nonpolyposis colorectal cancer
  23. Hereditary nonpolyposis colorectal cancer is due to a defect in?
    Defect in repair of mismatched bases.
  24. Birbeck granules are characteristic of this disease.
    Langerhans cell histiocytosis
  25. What are langerhans cells?
    Dendritic cells found in the skin that act as APCs.
  26. Where do langerhans cells come from and describe its characteristics.
    Derived from myeloid cell line and posess characteristic raquet-shaped intracytoplasmic granules known as Birbecks granules.
  27. Where are langerhans cells found?
    Skin and mucous membranes
  28. This cell has a characteristic tennis-raquet shaped intracytoplasmic granule.
    Langerhans cells
  29. Where are Kupffer cells found and what role do they play?
    • Macrophage-derived cell in LIVER.
    • Lie within hepatic sinusoids.
  30. What are osteoclasts? Where are they derived from?
    • Multinucleated cells that dissolve bone by secreting acid and collagenases.
    • Differentiate from monocytes, macrophages.
  31. What are mesangial cells? Where are they derived from?
    • Specialized  smooth muscle cells around blood vessels in the kidney, which function to regulate blood flow through the capillaries.
    • Are derived from MONOCYTES.
  32. What are the causes of Mirtal stenosis?
    Rheumatic fever
  33. What are the Mitral and Tricuspid valves derived from?
    Fused endocardial cushions of the AV canal
  34. Which murmurs can be caused by rheumatic fever?
    • Mitral Regurgitation/ Tricuspid regurgitation
    • Mitral stenosis
    • Mitral valve prolapse
    • Aortic Regurgitation
  35. What is the MOA of Cilostazol?
    • Phosphodiesterase III inhibitor;  Increases cAMP in platelets, resulting in inhibition of platelet aggregation.
    • Arteriolar VASODILATOR
  36. What is the MOA and use of Dipyridamole?
    • Phosphodiesterase III inhibitor;  Increases cAMP in platelets, resulting in inhibition of platelet aggregation.
    • Arteriolar VASODILATOR
  37. What is the MOA of Heparin?
    Activates antithrombin, which decreases thrombin and factor 10a
  38. What is the MOA and use of Agatroban?
    • Inhibit thrombin directly
    • tx: Heparin induced thrombocytopenia
  39. What is the MOA of Warfarin?
    Inhibitor of epoxide reductase (which converts Vitamin K from the oxidized to the reduced form) needed to produce factors 2, 7, 9, 10, Protein C and S.
  40. What is the MOA and use of tPA?
    • tPA/ Alteplase
    • Converts plasminogen to plasmin which cleaves thrombin and fibrin clots.
    • Tx: ST elevation MI, Pulmonary embolism
  41. What is the MOA and use of Alteplase?
    • tPA/ Alteplase
    • Converts plasminogen to plasmin which cleaves thrombin and fibrin clots.
    • Tx: ST elevation MI, Pulmonary embolism
  42. What are the effects of thromboxane A2?
    Platelet aggregation and vasoconstriction
  43. What is the MOA of Ticlopidine?
    • Inhibit platelet aggregation by irreversibly  blocking ADP receptors.
    • Prevent expression of GPIIb/IIIa on platelet surface
  44. What is the MOA of Clopidogrel?
    • Inhibit platelet aggregation by irreversibly  blocking ADP receptors.
    • Prevent expression of GPIIb/IIIa on platelet surface
  45. What is the MOA of Abciximab?
    • Bind to GPIIb/IIIa on platelets, preventing aggregaton.
    • Made from monoclonal antibody Fab fragments.

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