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Random infectious dz (inpt) > HIV > Flashcards

HIV Flashcards

1
Q

how does hiv retorvirus work?

A

infects all cells containing the T4 antigen, primarily the CD4 helper inducer lympocytes

-attaches to the T4 antigen, replicates, and causes cell fusion or death

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2
Q

what cells serve as a reservoir of viurs and promotes its dissemination to other organs?

A

macrophages

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3
Q

how is HIV transmitted?

A

through bodily fluids: risks include sexual contact, parenteral exposure and perinatal exposure

  • sex, IDU, vertical transmission
  • artifical insemination, organ transplantation
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4
Q

what is the acute HIV syndrome?

A

-occurs 2-6 weeks post exposure

infrequently identified, cluster of nonspecific findings similar to EBV infxn; need high index of suspicion

  • sx hit w/in days of initally acquiring virus
  • after this, virus goes into lysogenic cycle, only shedding occasionally for several years

-some pts may develp persistent generalized lymphdenopathy w/o symptomatic HIV dz

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5
Q

what is the average time of infection to presentation of symptoms?

A

about 10 years

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6
Q

what are systemic manifestations of HIV?

A

fever, night sweats, weight loss

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7
Q

what is the wasting syndrome?

A

result of increased metabolic weight and decreased protein synthesis w/ a disproportionate loss of muscle mass

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8
Q

what are common sights that are common for infxn and malignancies in HIV pts?

A

lungs, URI, lymph, CNS, PNS, mouth, GI tract, eyes and skin

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9
Q

what is AIDs defined by?

A

a CD4 count below 200 cells or the development of an AIDs indicator

-can be made with or w/o lab evidence of an HIV infextn

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10
Q

what is the current HIV/AIDs classification sx?

A

stage I: ASX
stage II: minor sx
stage III: moderate sx
stage IV: AIDS

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11
Q

describe an acute phast reaction

A
  1. infxn
  2. cytokines, chemokines, and prostaglandines into circulation
  3. cytokines reach brain, cause behaviors associated with infxn
  4. prostaglandins reach brains fever centers, causing fever
  5. cytokines reach bone marrow, causing increased monocytee/ neutrophil release
    IL1 and TNF reach leiver, causing production of opsonins (ike complement) + protease inhibitors (antivirals) and their relaease into the bloodstream
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12
Q

what are dendritic cells?

A

antigen resenting cells of epithelial tissues

-types of macrophages

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13
Q

what does is the primary immune response?

A
  • the first exposure
  • generally takes 10-17 days to occu after exposure
  • sx of illness occurs during these days
  • antigen-selected B and T cells proliferate and differentiate into effector cells
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14
Q

what is a secondary immune response?

A

all other exposures after

  • 2-7 days
  • greater response bc due to memory cells
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15
Q

What is active immunity?

A

immune response to a vaccine or pahtogen in a indiviudal

-memory cells

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16
Q

passive immunity?

A

comes from the administration of antibodies NOT made by the host.

  • This results in no memory cell production, because it does not stimulate the action of Helper T cells. There is no long-term immunity.
  • Passive immunity can also come from mother to fetus or baby, because antibodies pass in the placenta (IgG) and breast milk (IgA).
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17
Q

what type of virus is HIV?

A
  • membrane coating
  • two copes o RNA genome
  • reverse transcriptase
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18
Q

how does a retrovirus replicate?

A
  • reverse transcripase uses RNA to produce one DNA strand
  • reverse transcriptase produces the complementary DNA strand
  • viral DNA enter the nucles and integrates into the chromosome becoming a proviurs
  • a provirus DNA is used to produce mRNA
  • mRNA is translated to produce viral proteins
  • viral particls are assembled and leave the host cell
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19
Q

what does the serology of a chronic HIV infection look like?

A
  • viral load in blood stream is low
  • anitbodis to various viral antigens are high
  • CD4 counts are gradually going down
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20
Q

how is late stage HIV infxn defined?

A

-HIV kills more and more helper T cells, the immune response is impaired-including the ability to generate antibodies, even to HIV itself

  • this decrease in HIV anbx may be the trigger for the virus returning tinot a lytic phase
  • virus will eventually emerge and “go lytic” killing most of the remaining helper T cells in a realiatively short peroid of time
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21
Q

How do emerging viruses cause human diseases?

A

1) mutation= RNA viruses mutate rapidly bc RNA polymerase has no “prrofreader” fxn
2) contact btw species: viruses can spread, particularly when mutated

3) spread from isolated populations

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22
Q

what are HIV diagnostic studes?

A
  • detect antibodies bia ELISA and Western blot
  • need two ELISAs followed by a Western to confirm HIV infx
  • western blot confirsm the true postive
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23
Q

when do most pts develop antibodies?

A

within 6 mnths of expuse

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24
Q

who all should be screend for HIV?

A
  • pts at high risk of infx,
  • pts in all health care settting
  • all prego women
  • written consent is no longer recommended by the CDC

-HIV screening for pts aged 13-64 in all health care settings

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25
Q

what are other laboratory finding one may see in hIV?

A

anemia, leukopenis, thrombocytopenia, polyclonal hyper gammaglobulinemia,

hypercholesterolemaia

cutaneous anergy

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26
Q

what is cutanious anergy?

A

inability to react to skin test bc of a weakened immune system

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27
Q

what is the predominant type of HIV found in US?

A

HIV -1

HIV-2 is found in afrtic

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28
Q

when is the HIV window period?

A

when antibody tests will not show evidence of disease

-avg of 25 days until antibody tests are positive, make take up to 3 mnths

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29
Q

what comes after the actute phase of HIV?

A

asymptomatic infx

  • few mnths to median of 11 years before AIDs
  • HIV replication is present during all stages of infx, and progressively depletes CD4 lymphocytes

-fever, weight loss, D, cough, SOB and oral candidiases as dz progresses

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30
Q

what are some opporunistic infxns seen with AIDs?

A

pneumocystis pna, toxoplasma gonddii encephalitis

disseminated mycobacterium avium complex dz

cryptococcosis, coccidioidomycosis
Karposi
TB,

bacteral pna

Lymphoma

isosporiasis, chronic intestinal > 1 mnth

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31
Q

what are some quick HIV tests?

A

Orasure: oral fluid, if positive, western blot

oraquck advance (1/2): oral or blood

p24 antigen: good if you think pt is in window period

PCR for viral load: RNA or nucleic acid- 2 wksamplicfication test (NAAT)- can detect after 11 days

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32
Q

what is the best wat to monitor the illness progression?

A

CD4 count- measure a the tsame time of day by the same laboratory

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33
Q

how often do CD4 counts need to be measured?

A
  • if > 350, every 6 mnths
  • or every 3 mnths or with a change in pt status
  • risk of dz progressio increasd with a CD4 count of less than 200 or a CD4lymhpocytes percentage of less than 20
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34
Q

what is the viral load?

A

measure of hte actively replicating virus, which correlaes with dz progressio: changing viral loads also may support tx response

35
Q

tx of HIV: primary prevention efforts:

A

safer sex (latex only), harm reduction programs, drug rehab, screen of all blood products, and universal precautions in health care delivery

36
Q

secondary prevention methosds

A

antiretrovirals, chemophohylaxis

  • screen for dz such as TB
  • counsel on ways to maintin health and prevent spread of dz
37
Q

when should PEP be started?

A

w/in 72 hours of exposrue

-the chance of contracting HIV from a needelstick inury involving a pt with knonwn HIV is 0.3%

38
Q

how often should a health care worker that has been stuck be tested?

A

6 wks, 3 mnths, 6 mnths

39
Q

what is an option fo PEP?

A

antiretroviral therapy: decision to begin therapy based on pt

combo therapy w/ drugs from different calsses should be continued for up to 4 weeks

-full course PEP reduces the chance of HIV transmssion up to 70%

40
Q

what is the goal of HIV tx?

A

suppression of the viral load; a rising or persistenly high viral load, clinical progression, or continued immunologic detrioration signals tx failure

41
Q

what is tx based on?

A

CD4 count, viral load, and overall pt status

42
Q

HIV -related illness w/ CD4 count < 500

A 
salmonella
Cdiff
kaposi sarcoma
Mycobateriam TB
HSV, HZV
43
Q

HIV-related illness with CD4< 200

A

candida (esophagus, bronchi, trachea, lungs

HIV encephalopathy
AIDS dementia syndomre
Pneumocystis jiroveci pna

44
Q

HIV related illness < 100

A 
B-cell lymphoma (nonhodgkin)
toxoplasmosis
Isospora
Microsporidia
Histoplasmosis
cryptococcosiss
coccidioidomcosis
cryptosporidia
45
Q

hIV related illness < 50 P

A

PML
MAC
CMV
CNS lymphoma

46
Q

what are some ex of nucleoside reverse transcriptase inhibitors (NRtI)?

A 
Abacavir
Emtricitabine
lamivudine
stavudine
zalcitabine
didanosine
zidovudine
47
Q

how to NRTIs work?

A

competitive inhibitors of HIV reverse transcripase:
leads to termination of viral DNA growth
-blocks viral replicaion

48
Q

what is zidovudine (AZT) used for?

A

prevention of materna-fetal transmission

49
Q

what are some common NRTI combo meds?

A

Truvada: Emtricitabine/tenofovir

Combivir: zidovudine/lamivudine

Trizivir

50
Q

NRTI Adverse effects?

A

lactic acidosis

hepatic steatosis

lipodystrophy: liphypertropy, lipoatropy

51
Q

Abacavir adr?

A
  • hypersentisitivity rx: screen for HLA B 5701
  • rash
  • MI
52
Q

tenofovier adr?

A

renal impairment, decrease in bone mineral density
HA
GI intolerance

53
Q

emtricitabine adr?

A

minimal toxicity

hyperpigmentaion

54
Q

didanosine and zalcitabine and stavudine adr?

A

pancreatitis, peripheral neruopathy, hepatitis

55
Q

non-nucleoside reverse transcriptase inhibitors?

A 
nevirapine
delavirdine
efavirenz
etravirine
edurant
56
Q

NNRTI ADR

A

hepatoxicity

rash (SJS)

57
Q

edurant adr

A

mood changes, depression, hepatitis

58
Q

Integrase inhibitors?

A

raltegravir
elvitegravir
dolutegravie
cabotegravir

59
Q

II MOA

A

The HIV DNA is then carried to the cell’s nucleus (center), where the cell’s DNA is kept. Then, another viral enzyme called integrase hides the proviral DNA into the cell’s DNA. Then, when the cell tries to make new proteins, it can accidentally make new HIVs.
Integration can be blocked byintegrase inhibitors.

60
Q

raltegravie adr?

A 
Nausea
Headache
Diarrhea
CPK elevation, myopathy, rhabdomyolysis
Ras
61
Q

dolutegravir ADR

A

HA
insomnia
rash

62
Q

proteinse inhibitors

A

not really used as first line anymore

63
Q

protease inhibitors to konw?

A

crixivan: indinavir
kaletra: lopinavir/ritonavir
norvir: ritonavir

64
Q

PI adr?

A 
Hyperlipidemia 
Lipodystrophy 
Hepatotoxicity
GI intolerance
Possibility of increased bleeding riskfor hemophiliacs
Drug-drug interactions
65
Q

kaletra adr:

A

GI intolerance
Diabetes/insulin resistance
Possible increased risk of MI
PR and QT prolongation

66
Q

indinavir adr?

A

Nephrolithiasis
GI intolerance
Diabetes/insulin resistance

67
Q

Fusion inhibitor?

A

Enfuvirtide
binds HIV envelope glycoprotein
prevents viral fusion w/ target membrne

68
Q

Enfuvirtide ADR

A

Injection-site reactions
Hypersensitivity reaction
Increased risk of bacterial pneumonia

69
Q

entry inhibitors?

A

maraviroc

binds CCR5 protein on human cell membrane, blocking HIV from cell entry

70
Q

maraviroc adr?

A

hepatitis, rash

71
Q

what are some ex pof pharmacokinetic boosters?

A

ritonavir, cobicistat

boost blood levels of other ARV meds: inhibit P450 3A4 enzymers

72
Q

what are teh 3 As of HIV tx?

A

appropriate ARV regimen
adherence
activity testing

73
Q

what to test and when to test it?

A

baselline: CD4 X 2, HIV RNA

74
Q

what do you tst rifth before starting ART?

A

DC4 and HIV RNA

75
Q

what to test whil on ART?

A 
CD4
Q 3 – 6 months x 2 yrs
If CD4 < 300 cells/mcL
After 2 yrs of ART
Annually if CD4 > 300
HIV RNA
2 – 4 wks after starting ART
Q 4 – 8 wks until < 200 copies/ml
Every 3 – 4 months in stable patients
Virologic failure: > 200 copies/ml
76
Q

when do you start treatment?

A 
Pregnancy
low CD4 counts (< 200 cells/mcl)
high viral load (>100K copies/ml)
concomitant hepatitis
AIDS-related symptoms
77
Q

what about drug resistance testing?

A

Before starting ART
Resistance in 10 - 17% of HIV-infected patients
Recommended for all at initiation
Recommended for all pregnant women
Virologic failure
During ART
< 4 weeks after discontinuation of treatme

78
Q

what must you screen for before using abacavire?

A

HLAB5701

79
Q

what must you check before using maraviroc?

A

whether or no the pts viral strain uses CCR5

80
Q

what are the 3 main categories of combo tx for HIV?

A

1 INSTI + 2 NRTIs

1 PK-boosted PI (actully 2 drugs) + 2 NRTIs

1 NNRTI + 2 NRTIs
NRTI pair should include 3TC or FTC

81
Q

what are 3 first line combos?

A

trvada

atripla

stribild

82
Q

what not to prescribe?

A 
NRTI monotherapy
PI monotherapy
2 NRTIs alone 
2 NNRTIs
3 NRTIs
ABC/3TC/ZDV or TDF/3TC/ZDV may be ok
83
Q

why does treatment fail?

A 
High pretreatment HIV RNA
Low pretreatment CD4 counts
Comorbidities
Substance abuse
Psychiatric or neurocognitive issues
Drug resistance
Poor adherence (this is the biggest)
Accessibility (cost, getting to medical care
84
Q

what can be prescribed for PrEP?

A

truvada
-same efficacy as PEP

ADr: N

Random infectious dz (inpt) (8 decks)

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