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3 phases of HIV infections
- acute infection
- clinical latency
- chronic infection
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phase of HIV infection with fever, rash, swollen lymph nodes (poor diagnosis)
acute infection
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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
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phase of HIV infection with progressive deterioration, fever, night sweats, feeling of intense tiredness, weight loss, chronic diarrhea
chronic infection
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what determines HIV+ to AIDS
first opportunistic infection
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strategy for monitoring progression of HIV
CD4 cell count
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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
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what happens to the CD4 count in acute infection
a small drop will occur then rebound back to normal
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following the CD4 count, when do you initiate medication
when a steady decline begins
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following an acute illness (cold, flu, etc.) when do you measure CD4 counts
1 month later otherwise you get a false impression
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besides CD4 count what else do you monitor for HIV
viral load- particles/mL of serum
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following viral load, when do you start medication
showing a big increase
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common opportunistic infection seen in HIV
pneumocystisis pneumonia
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what medication is usually prescribed for pneumocystisis pneumonia, and the potential problem
TMP/SMZ - increases levels of most drugs and can cause toxicities
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3 steps of the HIV testing flow diagram
- 1 - elisa
- 2 - western blot
- 3 - viral RNA (northern immuno blot)
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which test HIV test detects a specific protein in a mix with size information obtained
western blot
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describe the RNA genome of HIV
nine genes flanked by long terminal repeats (LTRs)
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what 3 genes are common to all retroviruses
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what has happened to the CD4 T-lymphocyte levels in the seroconversion
the body has built antibodies
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what proteins make up the envelope (env) of the HIV RNA
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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
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DHHS recommendation - any symptomatic patient (OI) regardless of CD4/VL status
start medication
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DHHS recommendation - CD4 < 500 or VL < 10,000-20,000 and asymptomatic
offer medication but is reasonable to just monitor CD4/VL
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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)
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DHHS recommendation - VL > 20,000
offer therapy sonce viral load of > 20,000 is associated with poor overall outcome
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most serious issue with HIV therapy
patient compliance - treatment is complex so patient must become educated
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biggest problem with MD dosing
underdosing/overdosing
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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
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MOA of HIV protease inhibitors
inhibit the aspartate protease needed for viral assemble from viral polyproteins (azapeptide class)
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MOA of cell fusion inhibitors
- inhibitor of the action of the GP41 protein
- chemokine (C-C motif) receptor 5 (CCR5) co-receptor antagonist
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MOA of INSTI
blocks the integrase enzyme required for viral insertion into human DNA
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excess abdominal fat and hyperlipidemia
common side effect of taking HIV drugs
lipodystrophy
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drug for lipodystrophy
injection once daily
egrifta - tesamorelin
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what must you watch out for because of the serious drug interactions with HIV drugs
herbals
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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
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what is a HAART regimen
- high activity anti-retroviral therapy
- minimum of 3 drugs
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RNA virus - who attacks who
T-cells attack CD4 cells
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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
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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
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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
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elisa negative
retest in 3 months
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elisa positive
western blot test
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western blot positive
HIV positive
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western blot negative
retest in 3 months
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western blot equivocal
retest via western blot
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western blot retest negative
HIV negative
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retest via western blot equivocal
viral RNA
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viral RNA positive
HIV positive
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viral RNA negative
HIV negative
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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
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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.
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4 stressors that reactivate herpes virus
- sunlight
- bacterial infection
- hormones
- heavy physical exercise
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the administration of a medication for the purpose of preventing disease or infection
chemoprophylaxis
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7 steps of viral infection
- 1. adsorption
- 2. entry
- 3. uncoating
- 4. transcription
- 5. translation
- 6. assembly
- 7. release
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viral - attachment to host surface receptors
adsorption
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viral - penetration into the cell
entry
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viral - release of viral nucleic acid from the protein coat
uncoating
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viral - production of viral mRNA
transcription
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viral - synthesis of viral proteins and viral nucleic acid
translation
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viral - all parts put together to give active virus
assembly
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viral - exocytosis or rupture of the host cell
release
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6 causes of hepatitis
- immune cells
- infections
- chemicals
- cystic fibrosis
- hemochromatosis
- wilson's disease (genetic/copper excess disease)
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hepatitis from fecal/oral infection route
A
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hepatitis from
blood stuff
B & C
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hepatitis from
abusing IV or injection drugs
being infected while pregnant
man on man
D
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