Lecture 6: HIV Flashcards

1
Q

What kind of cells does HIV invade?

A

CD4 T helper cells
Dendritic cells
Monocytes

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2
Q

When does a person have AIDS?

A

CD4 count < 200 cells/mL
OR
Presence of any AIDS defining condition

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3
Q

What is the origin virus of HIV?

A

SIV (Simian)

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4
Q

Where did HIV originate?

A

Kinshasa (Northernish africa)

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5
Q

Where did HIV first hit the US?

A

NYC 1970s

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6
Q

When was AIDS defined?

A

1981/1982.

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7
Q

What was the first US case of AIDS?

A

Female partner of a known HIV infected in 1983.

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8
Q

When was HIV actually discovered?

A

1984
AKA it came after AIDS was defined.

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9
Q

When did we start having HIV blood tests?

A

1985, a year after HIV was identified and 4 years after AIDS was identified.

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10
Q

When did HIV start declining?

A

1995, as we developed an oral HIV test.

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11
Q

Where was AIDS the leading cause of death in 1999?

A

Africa.
4th in the World.

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12
Q

When did generic HIV drugs start rolling out?

A

2001

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13
Q

When was PrEP made?

A

2012

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14
Q

When did blood donation rules finally change in regards to HIV?

A

2015

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15
Q

Where in the US is HIV most prevalent?

A

The south

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16
Q

Who does the WHO define as the greatest populations at risk for HIV?

A

Men who have sex with men
Transgender
IVDU
Sex workers
Heterosexuals

Healthcare workers (needlestick transmission is 3 in 1000)

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17
Q

What is HIV’s mode of transmission?

A

Blood
Semen
Pre-seminal fluid
Rectal fluid
Vaginal fluid
Breast milk
Contact with mucous membranes/damaged tissue
Direct injection

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18
Q

What is the most common entryway for HIV transmission?

A

Anogenital mucosa
second is receptive anal intercourse.

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19
Q

How is HIV NOT transmitted?

A

Saliva
Sweat
Tears
Vomit
Urine
Nasal secretions

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20
Q

What is the rarest HIV transmission rate?

A

Blood transfusions in the US. 1 in 1million.

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21
Q

What is the highest HIV transmission rate?

A

Mother to child. 13-40%

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22
Q

How does HIV work? (7)

A
  1. Fuses to host cell
  2. Forces entry, injecting HIV RNA, reverse transcriptase, integrase, and viral proteins.
  3. Viral DNA is made by reverse transcriptase.
  4. Viral DNA transports across the cell nucleus to integrate with the Host DNA.
  5. New Viral RNA is made as part of the cell’s genomic RNA.
  6. New viral RNA and proteins move to cell surface, forming an immature HIV.
  7. Virus is released and protease cleaves to create a new mature virus.
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23
Q

What exactly does HIV interact with on a cell surface?

A

gp120 on virion envelope + T-cell coreceptor (CXCR4) via a CCR5 co-receptor

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24
Q

What is transinfection?

A

A dendritic cell with HIV bound to it transfers it to CD4 T cells.

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25
Q

What are the stages of HIV infection?

A

Viral transmission/HIV acquisition
Acute HIV infection/Acute retroviral syndrome (Symptomatic stage)
Chronic HIV infection (AIDS! Not always symptomatic)
Advanced HIV infection (CD4 <50)

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26
Q

What are the 4 stages of an acute HIV infection?

A
  1. Viral penetration of mucosal epithelium
  2. Infection of submucosal CD4 T cells, dendritic cells, and monocytes.
  3. Spreads to lymph nodes
  4. HIV viremia
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27
Q

What is an acute retroviral syndrome?

A

A nonspecific viral syndrome with symptoms identical to the flu.

Spontaneous resolutions.

Asymptomatic post syndrome for a while.

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28
Q

When does acute retroviral syndrome occur?

A

Usually during acute HIV infection.

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29
Q

What are the key systems to review in your PE for HIV suspicion?

A

HEENT
Lymphatics
Abd exam (HSM)
Skin

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30
Q

What people should be tested for HIV?

A

Known or suspected sexual or hematologic exposure
Promiscuous sexual history
IVDU
Accidental needlesticks
Pregnancy
Recent STI

Note:
CDC recommends routine screening from 13-64 at least once in your lifetime.

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31
Q

What are the tests available for HIV?

A

ELISA test
HIV Rapid antibody test
Serum Western Blot
Serum, p24 antigen
Serum PCR
CD4 Count
Serum Viral load

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32
Q

What lab test is primarily indicated for infants?

A

Serum HIV DNA PCR

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33
Q

What is the primary lab test for HIV?

A

ELISA

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34
Q

What is the next step after an ELISA test?

A

Western blot to confirm

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35
Q

When do you order Serum viral load tests?

A

Either prior to HIV tx or very late.

Viral load is not as indicative because it drops in the latent period.

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36
Q

When is a p24 antigen test indicated?

A

ASAP post infection

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37
Q

What positive lab test indicates a provider to NOT RX abacavir?

A

Human leukocyte antigen-B*5701

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38
Q

What should all positive HIV patients be offered?

A

ART!!!!

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39
Q

What is the CDCs recommendation on safe sex?

A

Counsel all patients not to exchange bodily fluids unless they are in a long-term mutually monogamous relationship with someone who has tested HIV antibody negative and has not engaged in unsafe sex, injection drug use, or other HIV risk behaviors for at least 6 months prior to or at any time since the negative test.

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40
Q

What is used to reduce the risk of HIV transmission to uninfected partners?

A

Early ART

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41
Q

What is used to reduce an HIV negative person at risk for infection?

A

Pre-exposure ART Prophylaxis

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42
Q

What is used to reduce HIV infections once exposed?

A

Post-exposure prophylaxis

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43
Q

What is something people undergoing elective surgeries can do to reduce HIV transmission?

A

Donate their own blood prior to surgery.

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44
Q

What is PrEP? What does it consist of?

A

It is PRE-exposure prophylaxis.

It is targeted to high-risk patients and uses Tenofovir/Truvada, which is an NRTI.

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45
Q

How can an HIV+ pregnant women transmit HIV to her baby?

A

Via pregnancy
Via vaginal birth
Via breastfeeding

46
Q

How is perinatal transmission of HIV prevented?

A

Routine HIV testing of all preggos.
ART + C section depending on viral load.
NO BREASTFEEDING if HIV+

47
Q

What uncommon respiratory disease in the US is found in HIV positive patients more frequently?

A

TB

48
Q

How do we screen and treat for TB in an HIV+ patient?

A

Annual PPD testing.
CXR
If infiltrates are present, acid fast staining and 4 drug regimen via ID specialist.

49
Q

How does TB commonly present?

A

UL consolidation/cavitary lesions.

+/- mediastinal or hilar adenopathy

50
Q

What is a common STD associated with HIV+ patients?

A

Syphilis.

51
Q

Who is syphilis most prevalent among?

A

MSM

52
Q

How is syphilis screened for and confirmed?

A

RPR or VRDL every 6m

Confirmed with a treponemal antibody test

TX is still penicillin

53
Q

What is the most common finding of primary syphilis?

A

Chancres

54
Q

What is the most common finding of secondary syphilis?

A

Nonpruritic, maculopapular or pustular rashes, usually on the palms and soles.

55
Q

What should I be wary when vaccinating someone with HIV?

A

Live vaccines.

Depending on their status, live vaccines may need to be avoided.

56
Q

What are lifestyle changes to prevent HIV/AIDS associated diseases?

A

Safe sex
Avoid raw meat, eggs, shellfish
Avoid cleaning cat litter
Avoid cat scratches/bites
Consider consumption of bottled water

57
Q

What is the ART for HIV+ preggo?

A

Zidovudine/Retrovir

58
Q

What is the PEP for a healthcare worker?

A

ART for 4 weeks of 3 drug combination.
Tenofovir + emtricitabine (Truvada) PLUS dolutegravir or raltegravir

59
Q

What qualifies as HAART?

A

3 meds from at least 2 different classes.

60
Q

What should you test all patients for prior to starting ART?

A

Resistance testing.

Antiretrovirals are very potent meds, need to make sure it actually has a benefit.

61
Q

What are the drug classes that are part of ART?

A

NRTI (nucleoside reverse transcriptase inhibitor)
NRTI (nucleotide reverse transcriptase inhibitor)
NNRTI (non-nucleoside reverse transcriptase inhibitor)
Protease inhibitors
Entry inhibitors/Fusion inhibitors
Integrase inhibitors

62
Q

What ART works on the virion envelope?

A

Fusion/entry inhibitors

63
Q

What ART drugs work in the cytoplasm?

A

NRTIs and NNRTIs and protease inhibitors

64
Q

What ART drug works on DNA?

A

Integrase inhibitors

65
Q

What is the main complication of an NRTI (nucleoside)?

A

Peripheral neuropathy

66
Q

What is the main complication of an NRTI (nucleotide)?

A

Renal failure. Requires creatinine monitoring.

67
Q

What is the main complication of an NNRTI?

A

None.
Generally well-tolerated with no monitoring.

68
Q

What is the main indication and concern regarding protease inhibitors?

A

Mainly used to boost regimens and suppress the replication of HIV.

It is metabolized by CYP450, so it has a high potential for drug interactions.

69
Q

When are entry/fusion inhibitors used for HIV?

A

Add-on therapy for MDR patients.

70
Q

What are integrase inhibitors mainly indicated for?

A

Rapid decreases in viral load.
Slows HIV replication.

71
Q

What are the key points in ART monitoring?

A

Resistance testing prior to any therapy.

Adherence!!

Monitor for toxicity
Monitor for CD4 and viral loads.

72
Q

What is a huge concern at very low CD4 counts?

A

Cancer can become prevalent.

73
Q

What is a common oral infection in AIDS? (First)

A

Mucocutaneous candidiasis aka oral candidiasis

74
Q

How does oral candidiasis prsent?

A

Complaint of unpleasant taste or mouth dryness.
Pseudomembranous (removable white plaques) or erythematous (red friable plaques)

75
Q

What is a common rash in AIDS?

A

Mucocutaneous candidiasis (fungal rash)
Tinea cruris = inguinal rash, which is the most common.

76
Q

What is oral hairy leukoplakia?

A

EBV etiology.

White lesion on LATERAL aspect of tongue that cannot be rubbed off.

Corrugated appearance with fine or thick “hairy” projections.

77
Q

How do I tell oral candidiasis and oral hairy leukoplakia apart?

A

Appearance.

Oral C is on the top of the tongue and can be rubbed off.

Oral hairy is on the SIDES of the tongue and CANNOT be rubbed off.

78
Q

What are the symptoms of genital herpes?

A

Small, grouped vesicles on penile shaft, labia, perianal skin, or buttocks.

79
Q

What are the symptoms of herpes zoster?

A

Painful, vesicular lesions occurring along dermatome. (VERY PAINFUL)

80
Q

What is molluscum contagiosum caused by?

A

Pox virus etiology.

81
Q

What demographic is usually susceptible to molluscum contagiosum?

A

Children, but in HIV infected adults, it also appears.

82
Q

How does molluscum contagiosum present?

A

Umbilicated fleshy papules.

83
Q

What is the most common cause of pulmonary disease in HIV infected patients?

A

CAP

Pneumococcal penumonia
H flu
P aeruginosa

84
Q

What is the most common opportunistic infection in AIDS?

A

PCP/Pneumocystis jiroveci pneumonia

85
Q

What are the characteristics of PCP?

A

Fungal in origin.
Fever, cough, dyspnea, hypoxemia
CXR with diffuse/perihilar infiltrates

AIDS-DEFINING CONDITION!!!

86
Q

How is PCP diagnosed?

A

Sputum stain
Fluorescence antibody testing of sputum
Serum LDH is elevated in 95% of pts.
Beta-glucan test

87
Q

What is a common AIDS complication in the throat?

A

Esophageal candidiasis by C. albicans.

AIDS-DEFINING CONDITION

88
Q

How does Esophageal candidiasis present?

A

Dysphagia or difficulty swallowing.

Diagnosed via EGD.

89
Q

What is Kaposi’s sarcoma?

A

A cancer that forms in the lining of blood and lymph vessels.
Etiology is HHV8. (herpesvirus)

AIDS-DEFINING CONDITION

90
Q

How does Kaposi’s sarcoma present?

A

Purplish, NON-BLANCHING lesions, either papular or nodular.

Can appear ANYWHERE.

91
Q

What is wasting syndrome?

A

Anxorexia/N/V leading to decreased caloric intake
Malabsorption
Increased metabolic rate
Disproportionate loss of muscle mass

92
Q

What infection is common in late-stage HIV?

A

Mycobacterium Avium

93
Q

How does mycobacterium avium present and get diagnosed?

A

Presents as persistent fevers and weight loss.

Bacteremia in 98% with multi organ involvement.

94
Q

What kind of meningitis is common in AIDS?

A

Cryptococcal meningitis.

95
Q

How does cryptococcal meningitis spread?

A

C. neoformans, which is an encapsulated budding yeast found in soil and PIGEON DUNG.
Spread via inhalation, spreading from the lungs to the CNS.

96
Q

How is cryptococcal meningitis diagnosed?

A

Gram stain of CSF.
Serum cryptococcal antigen.

97
Q

What is the most common retinal infection in AIDS?

A

CMV retinitis

98
Q

How does CMV retinitis present?

A

Retinal perivascular hemorrhages with white fluffy exudate/cotton wool spots.

Rapid progressive visual loss with optic nerve involvement or retinal detachment.

99
Q

What is the most common space-occupying lesion in HIV patients?

A

Toxoplasmosis

100
Q

What causes toxoplasmosis?

A

Toxoplasmosis parasite, often found in CAT LITTER.

101
Q

How does toxoplasmosis present?

A

HA, focal neurologic deficits, AMS, seizures.

CT scans w/ contrast will show the lesions.

102
Q

How is toxoplasmosis diagnosed?

A

Multiple head CTs with contrast.
Positive toxoplasma serologic testing

103
Q

When does toxoplasmosis prophylaxis begin?

A

<100 CD4

104
Q

What is the most common infection at any CD4 count and its tx/screening?

A

TB.

Annual testing + prophylaxis.

105
Q

What is the most common infection at CD4 <250 and its tx/screening?

A

Coccidiomycosis

Annual IgG and IgM serologic screening.

Prophylaxis if at CD4 > 250.

106
Q

What is the most common infection at CD4 <200 and its tx/screening?

A

Pneumocystis

Bactrim for prophylaxis until CD4 is above > 200.

107
Q

What is the most common infection at CD4 <150 and its tx/screening?

A

Histoplasmosis.
Itraconazole only considered in hyperendemic areas.

DC when CD4 >150 for 6 months.

108
Q

What are the 2 most common infections at CD4 < 100 and tx/screening?

A

Toxoplasmosis:
Bactrim if < 100 + positive IgG serology.
DC if CD4 > 200 for >3 months.

Cryptococcosis:
Prophylaxis not advised.

109
Q

What is the most common infection at CD4 < 50 and tx/screening?

A

MAC (mycobacterium avium complex)
Blood cultures first!

Negative = zithromax prophylaxis.

DC when CD4 > 100 for >3 mo

110
Q

When is AIDS day?

A

12/1

111
Q

What are the specific diseases mentioned in lecture that fall under AIDS-defining?

A

Esophageal candidiasis
PCP
CMV retinitis
Kaposi’s sarcoma
MAC
Toxoplasmosis
Wasting syndrome attributed to HIV
Cryptococcosis? (Says extrapulmonary)