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FA17 Infectious Disease > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

1
Q

most predominant type of HIV in US

A

HIV-1

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2
Q

most predominant type of HIV in developing world

A

HIV-2

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3
Q

what does it mean to say HIV is retrovirus?

A

RNA virus that uses our own molecular biochemistry to produce copies

constantly mutating so vaccine development is difficult

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4
Q

how is HIV transmitted?

A
  1. Sexual contact
  2. Needle sticks
  3. Vertically (mother to baby)
  4. Blood transfusion
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5
Q

risk of sexual transmission of HIV is increased if

A

presence of inflammatory/ulcerative lesions of mucosa

trauma

uncircumcised partner

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6
Q

dominant mode of HIV transmission worldwide?

A

heterosexual intercourse

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7
Q

risk of vertical transmission is increased with

A

vaginal delivery
mothers with high viral load
mothers who breast fed

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8
Q

how is risk of vertical transmission decreased?

A

antiretroviral treatment to mother during pregnancy and immediately after birth

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9
Q

how is risk of IV drug use decreased

A

post exposure prophylaxis

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10
Q

HIV race in US

A

disproportionally affects African Americans and to lesser extent Hispanics

this is a socioeconomic issue

latino MSM are only grp increasing

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11
Q

HIV in US - age

A

mc acquired by young adult (20-24)

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12
Q

other HIV stats (just review)

A

1 in 8 are unaware of their positive status

south has greatest numbers in US

numbers of people w/HIV decreases with antiretroviral therapy - only 41% of people have access

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13
Q

HIV pathophysiology

A
  1. entry into cells mediated primary by viral binding to CD4
  2. inside, reverse transcriptase converts RNA genome into DNA
  3. viral genome is inserted into our genome (CD4= virus factory)
  4. cell lysis releases millions of HIV visions into blood stream
  5. Macrophages disseminate virus to other organs
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14
Q

Depleting CD4 cells therefore affects immunity: (humoral and cellular)

A
  1. Cellular - CD4 T cell destruction, disorganized NK and CD8 activity
  2. Humoral - B lymphocyte dysfunction
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15
Q

natural progression of HIV (5 steps)

A
  1. 4-11 days of exposure, rapid viral replication
  2. 2-6 weeks = flu like illness
  3. brisk immune response ensues and T lymphocyte population rebounds, high viral load decreases rapidly
  4. 6-12 months later, viral load stabilizes (viral set point) and is latent
    - infectious but not symptomatic
  5. eventually CD4 levels decline and viral load rises, causing immune dysfunction
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16
Q

Acute Retroviral Syndrome

A

2-6 wks following exposure

lasts 7-21 days

marks process of seroconversion (decreasing CD4 and increasing HIV)

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17
Q

acute retroviral syndrome symptoms

A

HA, fatigue, myalgia, acute/aseptic meningitis

pts have low glucose and high protein

missed opportunity to start therapy and change behavior

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18
Q

asymptomatic phase

A

pt feels fine but suffers from persistent lymphadenopathy

early, transient thrombocytopenia

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19
Q

early symptomatic phase

A

pts have increased susceptiability to pulmonary infection and bacteremia (H. flu, tb, pneumo pneumonia) AND mucocutanous disease

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20
Q

common mucocutaneous lesions in early HIV states

A

shingles/zoster
thrust
HSV
oral hairy leukoplakia

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21
Q

late symptomatic phase

A

high risk of developing opportunistic infection at CD4 counts < 200

its are started on prophylaxis

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22
Q

testing for HIV - who gets tested?

A

everyone should be tested at least once in life

high risk and persons in healthcare be tested annually

pregnant women (1st and 3rd trimester)

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23
Q

false negative HIV tests

A

possible for any test between when there exposure and Ab detection (home tests)

ABs take 3-12 weeks to develop

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24
Q

office tests used in HIV

A

ELISA confirmed by Western blot

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25
ELISA HIV abs tests
HIV ab in saliva and p24 hg
26
initial management of HIV
excellent history with ROS complete physical exam
27
lab testing of initial management HIV (8)
1. CBC + Dif, chem, LFT, TSH, lipid, b12 2. PPD (5+ m positive) 3. . toxoplasmosis 4. RPR (syphilis) 5. CMV serology 6. Gonococcal/Chlamydia NAAT 7. viral hep screen 8. baseline HIV genotype
28
category A
asymptomatic HIV infection w/o history of symptoms or AIDS defining conditions
29
category B
HIV infection w/symptoms directly attributed to HIV infection or complicated by HIV infection
30
category C
HIV infection with AIDS defining opportunistic infection
31
principals of ART (3)
1. suppressive (not curative) so it is lifelong 2. ALL ART is associated with significant toxicity 3. risk of developing resistance increases if you don't adhere exactly to treatment
32
ART should only be initiated in patients:
1. when benefit is > risk | 2. pt will adhere to regemine
33
when is ART started? why?
advocated for patient at time of diagnosis (regardless of CD4 count) this is to aid in CD4 recovery (stopping viral replication) and decrease transmission viral load can go to less than detectible levels
34
goal of ART
make virus undetectable in blood
35
individuals with HIV are monitored..... (w. and how often)
viral loads and CD4 counts every 3-4 months
36
classes of ART meds
1. Reverse transcriptase inhibitor (NRTIs and NNRTIs) 2. Protease Inhibitors 3. Fusion inhibitors 4. Entry inhibitors 5. Integrase Inhibitors (INSTIs)
37
NRTIs and NNRTIs
stop virus from converting itself to DNA usually use 2 NRTIs plus third active drug from different class
38
patients with ART will eventually experience
viral escape viral loads will increase then you test for resistance and switch meds
39
Prevention of HIV
1. abstinence or reduction in number of sexual partners 2. avoidance of high risk sex acts (receiving anal sex) 3. using barrier contraception 4. testing and treatment of other STDs in pt/ and partner 5. maternal testing and dz control 6. c-section and avoidance of breast feeding 7. avoidance of shared/refused needles
40
PrEP
pre exposure medication given to people at risk of HIV ex. HIV discordant couples, sex workers, IVDAs
41
PrEP drugs
Truvada (daily) testing q3 months for HIV, q6 months for renal function
42
PEP
post exposure prophylaxis given to persons following exposure and at risk must be starting w/in 72 hrs and 2-3 drugs for 28 days ELISA testing at 6 weeks
43
criteria for progression to AIDS
CD4 counts <200 Development of specific neoplasms (Kaposi's sarcoma, invasive cervical CA, CNS lymphoma) HIV wasting syndrome development of opportunist infection
44
classic OIs of HIV CD4 200-500 (4)
polydermatomal zoster TB recurrent bacterial pneumonia thrush
45
classic OIs of HIV CD4 100-200 (3)
PCP disseminated histoplasmosis PML
46
classic OIs of HIV CD4 <100 (7) ** pretty much anything
``` Candidia esophagitiis CMV retinitis /esophagitits/colitis disseminated MAC toxoplasmosis crypto meningitis crypto enters HSV ```
47
classic opportunistic neoplasm's of HIV CD4 200-500 (3)
mucocutaneous kaposis sarcoma oral hairy leukoplakia cervical cancer
48
classic opportunistic neoplasm's of HIV CD4 100-200 (2)
visceral Kaposi's NHL
49
prevention of OIs CD4 <200
PCP prophylaxiss TMP-SMZ daily (pneumocystis pneumonia)
50
prevention of OIs CD4 <100
TMP-SMZ DS daily for seropositive patient
51
prevention of OIs CD4 <50
Azithromycin 1200 mg fear of MAC
52
TB positive (and prophylaxis)
PPD > 5 mm isoniazid or rifampin
53
MOST frequent presenting OI of AIDS in US
pneumocystis jirovecci
54
pneumocystis jirovecci
fungi found in soil, homes, environment and is non pathogenic in healthy individuals usually when CD4 <200
55
pneumocystis jirovecci s/s
``` gradual onset of DOE fevers weight lost catch in inspiratory effort cough ``` Hypoxemia (common and severe)
56
CXR pneumocystis jirovecci
subtle bilateral interstitial pattern but likely will be completely normal pleural effusions are unusual pt is sicker than CXR indicates
57
CXR of pneumocystis jirovecci v. bacterial CAP
pleural effusions are unusual in pneumocystis jirovecci CAP typically shows pleural effusion
58
diagnosis of pneumocystis jirovecci is confirmed by
induced sputum or washings from BAL
59
pneumocystis jirovecci tremens
high dose Bactrim (TMP/SMX) IV x 3 weeks
60
MC presenting OI in developing world
Tuberculosis
61
when should Tuberculosis always be considered
in HIV patients with pulmonary or systemic complaints of illness (esp if <200)
62
early HIV TB
TYPICAL reactivation pattern night sweats, weight loss, productive cough, fever infiltrate and cavitation
63
late TB
atypical CXR pattern Miliary pattern, lower lung field disease, few-no cavitation and possible PE
64
TB dx
finding of AFB in-sputum or QuantiFERON Tb assay
65
CAP incidence in HIV
3-4x higher in HIV than in general population present with quicker and more severe Productive cough, high fever, plurtici chest pain, chills, non specific symptoms
66
CAP HIV v. normal
focal infiltrates are more common in high HIV diffuse infiltrates with more advance disease cavitation is unsual
67
opportunist infection that usually occurs in late AIDS ( CD4 <50)
disseminated MAC
68
disseminated MAC
persistent fevers, night sweats, fatigue, weight loss and anorexia
69
disseminated MAC prophylaxis and treatment
prophylaxis: azithromycin treatment: clarithromycin, rifampin, ethambutol
70
potential causes of diarrhea in AIDS (4)
1. infection (crypto, MAC< salmonella, campylobacter, CMV) 2. idiopathic 3. ART drug S.E. 4. C. Diff
71
dx of diarrhea
examine stool for pathogens evaluate for parasites scope it if these are negative
72
problems with which body symptoms are common in almost all HIV pts
CNS disorders ranges, bit found in all mental changes and meningitis
73
AIDS dementia complex
HIV gets into CNS and its display motor dysfunction, ataxia, poor concentration and memory, slow thought process, and apathy/social withdrawal often confused with depression
74
MC cause of intracerebral mass lesions in HIV patients
toxoplasmosis causes multifocal cerebrates and S/s both diffuse and local
75
toxoplasmosis s.s
fever HA focal neurological deficits multiple too masses w/ diffuse symptoms
76
diagnostic toxoplasmosis workup
serological testing for T. gondii Abs
77
what will be shown in toxoplasmosis
ring enhancing lesions on MRI CSF non diagnostic
78
CNS lymphoma
CD4 <100 associated with EBV AIDS defining cancer
79
CNS lymphoma s/s
``` afebrile HA AMS focal neuro findings personality/behavioral changes seizures ```
80
PML
demyelinating disease caused by JC virus deep white matter lesions NOT RING ENHANCING
81
PML s/s
progressive dementia, vision changes, seizures, hemiparesis
82
meningitis HIV (types) (4)
1. Aseptic 2. Chronic 3. Meningoencepholitis 4. acute bacterial meningitis
83
aseptic meningitis
usually caused by a virus can be an aspect of acute retroviral syndrome acute onset of fever, HA, photophobia, meningismus
84
chronic meningitis
typically due to fungal infection (cryptococcus, histoplasmosis, coccidiomycosis) Its present with difficulty concentrating, HA, fever, or altered mental status Diagnosed by usual tests
85
meningoencephalitits
fever and AMS progressing into coma CT shows diffuse disease (EEG helpful) caused by viral pathogens
86
Acute bacterial meningitis
less common than other types presents in characteristic way increased neutrophils, proteins low glucose

FA17 Infectious Disease (9 decks)

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