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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
Q

ELISA HIV abs tests

A

HIV ab in saliva and p24 hg

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26
Q

initial management of HIV

A

excellent history with ROS

complete physical exam

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27
Q

lab testing of initial management HIV (8)

A
  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
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28
Q

category A

A

asymptomatic HIV infection w/o history of symptoms or AIDS defining conditions

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29
Q

category B

A

HIV infection w/symptoms directly attributed to HIV infection or complicated by HIV infection

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30
Q

category C

A

HIV infection with AIDS defining opportunistic infection

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31
Q

principals of ART (3)

A
  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
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32
Q

ART should only be initiated in patients:

A
  1. when benefit is > risk

2. pt will adhere to regemine

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33
Q

when is ART started? why?

A

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

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34
Q

goal of ART

A

make virus undetectable in blood

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35
Q

individuals with HIV are monitored….. (w. and how often)

A

viral loads and CD4 counts every 3-4 months

36
Q

classes of ART meds

A
  1. Reverse transcriptase inhibitor (NRTIs and NNRTIs)
  2. Protease Inhibitors
  3. Fusion inhibitors
  4. Entry inhibitors
  5. Integrase Inhibitors (INSTIs)
37
Q

NRTIs and NNRTIs

A

stop virus from converting itself to DNA

usually use 2 NRTIs plus third active drug from different class

38
Q

patients with ART will eventually experience

A

viral escape

viral loads will increase

then you test for resistance and switch meds

39
Q

Prevention of HIV

A
  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
Q

PrEP

A

pre exposure medication given to people at risk of HIV

ex. HIV discordant couples, sex workers, IVDAs

41
Q

PrEP drugs

A

Truvada (daily)

testing q3 months for HIV, q6 months for renal function

42
Q

PEP

A

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
Q

criteria for progression to AIDS

A

CD4 counts <200

Development of specific neoplasms (Kaposi’s sarcoma, invasive cervical CA, CNS lymphoma)

HIV wasting syndrome

development of opportunist infection

44
Q

classic OIs of HIV

CD4 200-500

(4)

A

polydermatomal zoster

TB

recurrent bacterial pneumonia

thrush

45
Q

classic OIs of HIV

CD4 100-200 (3)

A

PCP

disseminated histoplasmosis

PML

46
Q

classic OIs of HIV

CD4 <100 (7)

** pretty much anything

A 
Candidia esophagitiis
CMV retinitis /esophagitits/colitis 
disseminated MAC 
toxoplasmosis 
crypto meningitis 
crypto enters 
HSV
47
Q

classic opportunistic neoplasm’s of HIV

CD4 200-500 (3)

A

mucocutaneous kaposis sarcoma

oral hairy leukoplakia

cervical cancer

48
Q

classic opportunistic neoplasm’s of HIV

CD4 100-200 (2)

A

visceral Kaposi’s

NHL

49
Q

prevention of OIs CD4 <200

A

PCP prophylaxiss

TMP-SMZ daily (pneumocystis pneumonia)

50
Q

prevention of OIs CD4 <100

A

TMP-SMZ DS daily for seropositive patient

51
Q

prevention of OIs CD4 <50

A

Azithromycin 1200 mg

fear of MAC

52
Q

TB positive (and prophylaxis)

A

PPD > 5 mm

isoniazid or rifampin

53
Q

MOST frequent presenting OI of AIDS in US

A

pneumocystis jirovecci

54
Q

pneumocystis jirovecci

A

fungi found in soil, homes, environment and is non pathogenic in healthy individuals

usually when CD4 <200

55
Q

pneumocystis jirovecci s/s

A 
gradual onset of DOE 
fevers 
weight lost 
catch in inspiratory effort 
cough

Hypoxemia (common and severe)

56
Q

CXR pneumocystis jirovecci

A

subtle bilateral interstitial pattern but likely will be completely normal

pleural effusions are unusual

pt is sicker than CXR indicates

57
Q

CXR of pneumocystis jirovecci v. bacterial CAP

A

pleural effusions are unusual in pneumocystis jirovecci

CAP typically shows pleural effusion

58
Q

diagnosis of pneumocystis jirovecci is confirmed by

A

induced sputum or washings from BAL

59
Q

pneumocystis jirovecci tremens

A

high dose Bactrim (TMP/SMX) IV x 3 weeks

60
Q

MC presenting OI in developing world

A

Tuberculosis

61
Q

when should Tuberculosis always be considered

A

in HIV patients with pulmonary or systemic complaints of illness

(esp if <200)

62
Q

early HIV TB

A

TYPICAL reactivation pattern

night sweats, weight loss, productive cough, fever

infiltrate and cavitation

63
Q

late TB

A

atypical CXR pattern

Miliary pattern, lower lung field disease, few-no cavitation and possible PE

64
Q

TB dx

A

finding of AFB in-sputum or QuantiFERON Tb assay

65
Q

CAP incidence in HIV

A

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
Q

CAP HIV v. normal

A

focal infiltrates are more common in high HIV

diffuse infiltrates with more advance disease

cavitation is unsual

67
Q

opportunist infection that usually occurs in late AIDS ( CD4 <50)

A

disseminated MAC

68
Q

disseminated MAC

A

persistent fevers, night sweats, fatigue, weight loss and anorexia

69
Q

disseminated MAC prophylaxis and treatment

A

prophylaxis: azithromycin
treatment: clarithromycin, rifampin, ethambutol

70
Q

potential causes of diarrhea in AIDS (4)

A
  1. infection (crypto, MAC< salmonella, campylobacter, CMV)
  2. idiopathic
  3. ART drug S.E.
  4. C. Diff
71
Q

dx of diarrhea

A

examine stool for pathogens

evaluate for parasites

scope it if these are negative

72
Q

problems with which body symptoms are common in almost all HIV pts

A

CNS disorders

ranges, bit found in all

mental changes and meningitis

73
Q

AIDS dementia complex

A

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
Q

MC cause of intracerebral mass lesions in HIV patients

A

toxoplasmosis

causes multifocal cerebrates and S/s both diffuse and local

75
Q

toxoplasmosis s.s

A

fever
HA
focal neurological deficits

multiple too masses w/ diffuse symptoms

76
Q

diagnostic toxoplasmosis workup

A

serological testing for T. gondii Abs

77
Q

what will be shown in toxoplasmosis

A

ring enhancing lesions on MRI

CSF non diagnostic

78
Q

CNS lymphoma

A

CD4 <100 associated with EBV

AIDS defining cancer

79
Q

CNS lymphoma s/s

A 
afebrile 
HA 
AMS 
focal neuro findings 
personality/behavioral changes 
seizures
80
Q

PML

A

demyelinating disease caused by JC virus

deep white matter lesions

NOT RING ENHANCING

81
Q

PML s/s

A

progressive dementia, vision changes, seizures, hemiparesis

82
Q

meningitis HIV (types) (4)

A
  1. Aseptic
  2. Chronic
  3. Meningoencepholitis
  4. acute bacterial meningitis
83
Q

aseptic meningitis

A

usually caused by a virus

can be an aspect of acute retroviral syndrome

acute onset of fever, HA, photophobia, meningismus

84
Q

chronic meningitis

A

typically due to fungal infection (cryptococcus, histoplasmosis, coccidiomycosis)

Its present with difficulty concentrating, HA, fever, or altered mental status

Diagnosed by usual tests

85
Q

meningoencephalitits

A

fever and AMS progressing into coma

CT shows diffuse disease (EEG helpful)

caused by viral pathogens

86
Q

Acute bacterial meningitis

A

less common than other types

presents in characteristic way

increased neutrophils, proteins
low glucose

FA17 Infectious Disease (9 decks)

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