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64 Cards in this Set
- Front
- Back
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the way HIV works
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finds and destroys CD4 (helper T cells that are the backbone of the immune system) cells that the immune system must have to fight disease
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AIDS
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final stage of HIV infection
when someone has 1 or more opportunistic infections and a low number of T-cells |
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what most people with AIDS die from
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opportunistic infections because the immune system is so weak that the body can't fight infections
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first known case of HIV
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Congo in 1959
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HIV in the U.S.
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since the mid-70's
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formal tracking of AIDS in the U.S.
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1982
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HIV virus discovered
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1983
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original source of HIV virus
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chimpanzees- discovered in 1999
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how HIV was introduced to the human population
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when hunters became exposed to the infected blood of the chimps
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region of the world with the most HIV cases
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sub-sahara africa
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stages of HIV infection
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viral transmission- high CD4 count, low viral RNA
primary HIV infection (acute syndrome)- lower CD4 count, peak of viral RNA seroconversion asymptomatic chronic infection- balance between CD4 count and viral RNA symptomatic HIV infection- low CD4 count, viral RNA slowly rising AIDS- extremely low CD4 count, extremely high viral RNA advanced HIV/AIDS- CD4 < 50 |
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where is HIV found
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blood, semen, or vaginal fluid of infected person
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how is HIV transmitted
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having sex with someone infected with HIV
sharing needles/syringes with someone infected with HIV being exposed to HIV before or during birth or through breast-feeding |
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HIV via blood transfusions
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not common anymore bc all donated blood in the U.S. gets tested for HIV (starting in 1985)
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how HIV is NOT transmitted
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shaking hands, hugging, casual kissing
toilet seats, drinking fountains, doorknobs, dishes, drinking glasses, food, pets mosquitoes |
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primary HIV infection (acute retroviral syndrome)
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symptomatic in 80-90%
occurs 2-4 weeks after exposure lasts 1-2 weeks increased likelihood of infecting others due to peak of viral load |
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acute retroviral syndrome signs and symptoms
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fever
lymphadenopathy pharyngitis rash (red maculopapular lesions mostly on face and trunk) myalgia/arthralgia |
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rate of HIV progression
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low viral load and high CD4 count- highly predictive of improved survival
symptomatic primary infection- poor prognosis; rapid progression to AIDS |
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interventions that prolong survival
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antiretroviral therapy
PCP prophylaxis MAC prophylaxis care |
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seroconversion
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the time it takes for antibodies to form to HIV- detectable within 3 weeks
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testing strategies to determine if HIV is present or not
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*best done during seroconversion stage- 3 weeks*
plasma HIV RNA HIV Ab formation- ELISA assay -can get samples from blood (most common), saliva, or urine |
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measurement of how bad the HIV infection is
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CD4 count
viral load |
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CD4 count
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measure of damage ALREADY DONE
declines by about 30-90/yr indicates progression of HIV and risk of opportunistic infections |
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viral load
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measure of POTENTIAL FOR DAMAGE
shows velocity of viral reproduction ONLY monitors HIV in blood lower viral load- slower progression |
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classification system
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CD4 > 500- 1
CD4 between 200-499- 2 CD4 < 200- 3 A- asymptomatic primary B- symptomatic C- opportunistic infections |
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goals of antiretroviral therapy
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suppress viral load
preserve and strengthen the immune system limit adverse effects, improve quality of life prevent morbidity and mortality |
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suppressing viral load
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HAART- highly active antiretroviral therapy
complete eradication is not possible RNA < 50 copies within 12-24 weeks of HAART |
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preserving and strengthening the immune system
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increased CD4 count
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examples of opportunistic infections
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candidiasis
coccidioidomycosis cryptococcosis CMV MAC PCP histoplasmosis kaposi's sarcoma toxoplasmosis lymphoma |
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initiating antiretroviral therapy
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history of an AIDS-defining illness OR with CD4 < 350
regardless of CD4 count in: -pregnancy -hep. B -nephropathy |
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clinical controversies about when to start antiretroviral therapy
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panels divided in half when trying to decide if therapy should be started when CD4 counts are:
-between 350-500 -> 500 |
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tools of therapy
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maximize adherence
use correct doses and schedules rational sequencing of drugs- first is best preservation of future treatment options |
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resistance testing
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recommended before beginning treatment (due to resistance) and even when entering into care
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preferred resistance testing
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genotypic testing
-first time patients -patients who failed during first or second regimens |
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NRTI'S
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end in -ine and -vir
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NRTI'S MOA
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look like nucleotides that are used by reverse transcriptase to form the DNA (base analogs)
once these base analogs are placed in the growing chain, growth stops |
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NRTI warnings- absolute
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ABSOLUTELY DON'T GO TOGETHER because similar MOA/reduced phosphorylation
-AZT and d4T -3TC and FTC |
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NRTI warnings- caution
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because of increased toxicities and drug interactions
-ddl and d4T -ddl and TDF |
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NRTI adverse effects
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peripheral neuropathy
lactic acidosis (rare) lipoatrophy pancreatitis (ddl or d4T) GI headaches TREATMENT SHOULD BE SUSPENDED IF RISING AST LEVELS, HEPATOMEGALY, OR METABOLIC ACIDOSIS |
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abacavir (ABC)
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5% hypersensitivity- screen for HLA-B to reduce risk
multi-organ system involvement common side effects- fever, rash, GI, respiratory symptoms resolve if discontinued but can come back and be fatal if re-given |
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NNRTI'S
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-vir- in the middle
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NNRTI MOA
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bind directly to reverse transcriptase; reverse transcriptase can't add new bases to the growing chain
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NNRTI side effects
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rash- steven johnson's syndrome
elevated transaminase SEVERE hepatotoxicity with nevirapine (black box) GI CNS with efavirenz |
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NNRTI resistance and drug interactions
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cross-resistance across entire class
CYP3A4 drug interactions (inducers AND inhibitors) |
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PI'S
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end in -navir
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PI MOA
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blocks the breakup of the proteins by protease so that new viruses can't be assembled
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PI side effects
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fat redistribution (EXCEPT atazanavir)
GI headaches |
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PI drug interactions
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CYP3A4 inhibitors (increase drug concentrations)
ritonavir- STRONGEST inhibitor saquinavir- WEAKEST inhibitor |
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ritonavir (suicide inhibitor)
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boost half-life of other PI'S
-allows for extended dosing intervals -decrease pill burden -decrease side effects |
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boosted PI'S
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ritonavir + lopinavir
ritonavir + tipranavir ritonavir + darunavir |
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fusion inhibitor
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fuzeon
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fuzeon MOA
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binds to gp41 subunit and prevents conformational changes for fusion
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fuzeon dosing
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SQ injectons BID
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fuzeon side effects
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very little!
-injection site reactions |
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fuzeon advantages
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effective against resistant HIV
low potential for drug interactions low potential for systemic toxicity |
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CCR5 inhibitor
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selzentry
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selzentry MOA
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inhibit binding of the virus to the CCR5 receptor on the T-cell
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selzentry facts
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trophile assay (genetic testing) must be done to determine if the patient carries the specific R5 virus that binds to the CCR5 receptor
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selzentry dosing
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adjustments required when PI'S or NNRTI'S are co-administered
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selzentry side effects
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liver toxicity
CV events |
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integrase inhibitor
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isentress
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isentress MOA
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blocks integrase; stops integration of viral DNA into host chromosome
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isentress facts
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does not require ritonavir boosting
isentress + tenofovir + emtricitabine preferred for FIRST TIME PATIENTS |
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isentress side effects
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GI
CPK elevation |
