med chem test 4

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med chem test 4
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med chem test 4
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  1. 3 phases of HIV infections
    • acute infection
    • clinical latency
    • chronic infection
  2. phase of HIV infection with fever, rash, swollen lymph nodes (poor diagnosis)
    acute infection
  3. phase of HIV infection with no outward signs and symptoms but virus can be replicating at a rate of >106 particles/day. could be up to 10 years out
    clinical latency
  4. phase of HIV infection with progressive deterioration, fever, night sweats, feeling of intense tiredness, weight loss, chronic diarrhea
    chronic infection
  5. what determines HIV+ to AIDS
    first opportunistic infection
  6. strategy for monitoring progression of HIV
    CD4 cell count
  7. what effect does the virus have on the CD4 cells
    due to the high number of CD4 receptors on T-lymphocytes the viruses bind and invade these cells causing a drop in the numbers
  8. what happens to the CD4 count in acute infection
    a small drop will occur then rebound back to normal
  9. following the CD4 count, when do you initiate medication
    when a steady decline begins
  10. following an acute illness (cold, flu, etc.) when do you measure CD4 counts
    1 month later otherwise you get a false impression
  11. besides CD4 count what else do you monitor for HIV
    viral load- particles/mL of serum
  12. following viral load, when do you start medication
    showing a big increase
  13. common opportunistic infection seen in HIV
    pneumocystisis pneumonia
  14. what medication is usually prescribed for pneumocystisis pneumonia, and the potential problem
    TMP/SMZ - increases levels of most drugs and can cause toxicities
  15. 3 steps of the HIV testing flow diagram
    • 1 - elisa
    • 2 - western blot
    • 3 - viral RNA (northern immuno blot)
  16. which test HIV test detects a specific protein in a mix with size information obtained
    western blot
  17. describe the RNA genome of HIV
    nine genes flanked by long terminal repeats (LTRs)
  18. what 3 genes are common to all retroviruses
    • gag
    • pol
    • env
  19. what has happened to the CD4 T-lymphocyte levels in the seroconversion
    the body has built antibodies
  20. what proteins make up the envelope (env) of the HIV RNA
    • gp120 - tip
    • gp141 - shaft
  21. 5 steps of HIV infection
    • virus particle bind to CD4 and co-receptor on T-cell or macrophage
    • viral envelope fuses with cell membrane allowing viral genome to enter the cell
    • reverse transcriptase copies viral RNA genome into double-stranded DNA which is integrated into host DNA
    • T-cell activation induces transcription of provirus and translation of viral proteins
    • virus particles are assembled and bud from the cell
  22. DHHS recommendation - any symptomatic patient (OI) regardless of CD4/VL status
    start medication
  23. DHHS recommendation - CD4 < 500 or VL < 10,000-20,000 and asymptomatic
    offer medication but is reasonable to just monitor CD4/VL
  24. DHHS recommendation - CD4 > 500 or VL < 10,000-20,000 and asymptomatic
    would delay medication and monitor patient carefully due to long term risks of medication (vascular necrosis)
  25. DHHS recommendation - VL > 20,000
    offer therapy sonce viral load of > 20,000 is associated with poor overall outcome
  26. most serious issue with HIV therapy
    patient compliance - treatment is complex so patient must become educated
  27. biggest problem with MD dosing
    underdosing/overdosing
  28. 6 classes of HIV drugs
    • NRTI - nucleoside reverse transcriptase inhibitors
    • NNRTI - non-nucleoside reverse transcriptase inhibitors
    • nucleoside analogue reverse transcriptase inhibitors
    • PI - HIV protease inhibitors
    • cell fusion inhibitors
    • INSTI - integrase strand transfer inhibitors
  29. MOA of HIV protease inhibitors
    inhibit the aspartate protease needed for viral assemble from viral polyproteins (azapeptide class)
  30. MOA of cell fusion inhibitors
    • inhibitor of the action of the GP41 protein
    • chemokine (C-C motif) receptor 5 (CCR5) co-receptor antagonist
  31. MOA of INSTI
    blocks the integrase enzyme required for viral insertion into human DNA
  32. excess abdominal fat and hyperlipidemia
    common side effect of taking HIV drugs
    lipodystrophy
  33. drug for lipodystrophy
    injection once daily
    egrifta - tesamorelin
  34. what must you watch out for because of the serious drug interactions with HIV drugs
    herbals
  35. what are 2 problems with combination regimens
    • 1. overlapping side effects profiles make taking drug unbearable
    • 2. due to resistance regimens are no longer effective
  36. what is a HAART regimen
    • high activity anti-retroviral therapy
    • minimum of 3 drugs
  37. RNA virus - who attacks who
    T-cells attack CD4 cells
  38. 8 objectives in treating HIV
    • 1. suppress viral load to < 20-50
    • 2. preserve immune function
    • 3. maintain anti-retroviral efficiency
    • 4. maintain max. # of treatment options
    • 5. reduce incidence and severity of OI
    • 6. minimize drug side effects
    • 7. ENSURE patient compliance
    • 8 survival and quality of life
  39. 6 factors considered to start therapy
    • 1. clinical presentation
    • 2. disease progression
    • 3. treatment history
    • 4. patients desire to start therapy
    • 5. patients understanding of compliance and commitment
    • 6. individualize therapy for each patient
  40. 9 factors to picking an effective drug regimen
    • 1. potentcy
    • 2. efficacy
    • 3. toxicity
    • 4. tolerability
    • 5. convenience
    • 6. viral resistance profile
    • 7. minimize # of pills
    • 8. food-drug interactions
    • 9. drug-drug interactions
  41. elisa negative
    retest in 3 months
  42. elisa positive
    western blot test
  43. elisa equivocal
    retest
  44. western blot positive
    HIV positive
  45. western blot negative
    retest in 3 months
  46. western blot equivocal
    retest via western blot
  47. western blot retest negative
    HIV negative
  48. retest via western blot equivocal
    viral RNA
  49. viral RNA positive
    HIV positive
  50. viral RNA negative
    HIV negative
  51. if a patient suspects they may be infected with the HIV virus what should they do and why
    • test at county/state public health
    • if (-) they remain a number and avoid insurance companies labeling them as high risk
    • if (+) then it is the same as Dr's office, reported to the state health department
  52. 3 stages of herpes infection
    • 1. infects epithelial cells and spread to sensory neurons
    • 2. CD8 T-cells immune response, clears epithelium and the virus does dormant in the trigeminal ganglion
    • 3. stressors reactivate the virus which travels down axons and reinfects.
  53. 4 stressors that reactivate herpes virus
    • sunlight
    • bacterial infection
    • hormones
    • heavy physical exercise
  54. the administration of a medication for the purpose of preventing disease or infection
    chemoprophylaxis
  55. 7 steps of viral infection
    • 1. adsorption
    • 2. entry
    • 3. uncoating
    • 4. transcription
    • 5. translation
    • 6. assembly
    • 7. release
  56. viral - attachment to host surface receptors
    adsorption
  57. viral - penetration into the cell
    entry
  58. viral - release of viral nucleic acid from the protein coat
    uncoating
  59. viral - production of viral mRNA
    transcription
  60. viral - synthesis of viral proteins and viral nucleic acid
    translation
  61. viral - all parts put together to give active virus
    assembly
  62. viral - exocytosis or rupture of the host cell
    release
  63. 6 causes of hepatitis
    • immune cells
    • infections
    • chemicals
    • cystic fibrosis
    • hemochromatosis
    • wilson's disease (genetic/copper excess disease)
  64. hepatitis from fecal/oral infection route
    A
  65. hepatitis from
    blood stuff
    B & C
  66. hepatitis from
    abusing IV or injection drugs
    being infected while pregnant
    man on man
    D

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