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Infectious Disease > Week 6: HIV testing and treatment > Flashcards

Week 6: HIV testing and treatment Flashcards

1
Q
A
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2
Q

Question: What is differential diagnosis and what tests to be performed?

A
  • HIV
  • allergic dermatitis
  • secondary syphilis
  • coxsackie
  • scarlet fever (throat swab rapid antigen test or culture
    *
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3
Q

Great start at Prevention & Treatment of HIV

A
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4
Q

HIV screening guidelines

A
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5
Q

Case

A
  • so not strep
  • has secondary syphilis
  • could have HIV depending on generation of test
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6
Q

Clinical course of HIV and CD4 count and viral load

A
  • viral load goes from nothing to very high around 10 million copies and very contagious but too soon to have antibody test
  • viral load could be high but Ab test could be negative
  • sero-conversion is Ab negative to Ab positive
  • CD4 cells are located everywhere in the body (test the blood)
  • HIV only infects via CD4 receptor and only activated CD4 cells
  • HIV is enveloped so when it replicates it takes a piece of the cell membrane with it
  • so CD4 goes down then back up as they are recruited and then slow decline around 100 cells per year
  • Immune system is constantly stimulated because HIV viral replication is very prone to mutation which keeps changing
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7
Q

HIV testing

A
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8
Q

Forms of HIV testing

A
  • HIV Ab Elisa screen
  • Western blot
  • HIV Ab Elisa followed by automatic WB confirmation
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9
Q

Rapid HIV Testing

A

HIV Ab Elisa screen

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10
Q

HIV Confirmatory testing

A

Western blot

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11
Q

3rd generation HIV screening

A
  • HIV Ab Elisa followed by automatic WB confirmation
  • Antigens bind HIV antibodies from patient sample
  • Allows detection in early seroconversion
  • 6-8 week window period
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12
Q

Features of HIV Ab Elisa screen

A
  • High sensitivity
  • false-positive possible
  • 6-8 week window period
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13
Q

Features of Western blot HIV testing

A
  • High specificity
  • Confirmatory testing
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14
Q

Features of 4th generation HIV testing

A
  • Antigens bind HIV Abs from patient sample & monoclonal Abs detect p24 antigen
  • Allows detection prior to seroconversion
  • Detect between 12-26 days from exposure
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15
Q

What is Acute Retroviral Syndrome?

A

Symptomatic acute HIV infection that occurs 2-4 weeks after infection which presents like nonspecific flu-like illness for 3-14 days

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16
Q

Diagnosis of Acute Retroviral Syndrome

A

3rd or 4th generation HIV screening test negative or indeterminate with HIV RNA high

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17
Q

Are you contagious in Acute Retroviral Syndrome?

A

Highly infectious at this time

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18
Q

Presentation of Acute Retroviral Syndrome

A

Symptomatic acute HIV infection presenting as non-specific flu-like illness for 3-14 days 2-4 weeks post HIV infection

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19
Q

HIV screening algorithm

A
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20
Q

Continued case presentation

A
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21
Q

Potentially infectious agents of HIV

A
  • Blood
  • Breast milk
  • Tissue
  • Semen
  • Vaginal secretions
  • Anal secretions
  • Visibly bloody fluids
  • Other bodily fluids
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22
Q

NOT infectious agents of HIV

A
  • Urine
  • Saliva
  • Sweat
  • Tears
  • Nasal secretions
  • Sputum
  • Vomitus
  • Stool
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23
Q

Forms of higher risk HIV transmission risk

A
  • Receptive anal sex 0.3% - 3%
  • Needle sharing 0.67%
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24
Q

Forms of lower risk HIV transmission risk

A
  • oral sex 0.06%
  • Insertive sex 0.03 - 0.14%
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25
Q

CD4 count of HIV clinical Assessment

A
  • Used to stage disease
  • Stage 1: asymptomatic CD4>500
  • Stage 2: CD4 200-500
  • Stage 3: CD4 <200, <14%, or opportunistic disease or malignancy
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26
Q

HIV Viral load of HIV clinical Assessment

A
  • Used to monitor ARV therapy
  • Well controlled: viral load undetectable
  • Suboptimally or uncontrolled viral load detectable
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27
Q

Stage 1 HIV

A
  • asymptomatic
  • CD4>500
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28
Q

Stage 2 HIV

A

CD4 200-500

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29
Q

Stage 3 HIV

A
  • CD4<200, <14%
  • opportunistic disease or malignancy
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30
Q

Well controled HIV

A

viral load is undetectable

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31
Q

Suboptimally or uncontrolled HIV

A
  • Viral load is detectable
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32
Q

How is HIV viral load determined

A

HIV RNA Quantitative PCR

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33
Q

Describe the natural history of HIV infection

A
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34
Q

What stage are most new diagnosis of HIV?

A
  • 38% of new HIV diagnosis in the U.S. already have advanced disease
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35
Q

Why is it important to diagnose HIV early?

A

People who know they have HIV can begin treatment

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36
Q

HIV treatment

A
  • HAART/ART
  • results in viral suppression and markedly reduced transmission
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37
Q

What is the best treatment for HIV?

A

Prevention but also treating those with HIV reduces risk of transmission with HAART/ART treatment

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38
Q

When to start HIV treatment

A

ASAP in all HIV-infected adults as long as the patient is ready (A1 recommendation)

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39
Q

HIV Treatment must start conditions

A
  • opportunistic infections
  • Tuberculosis
  • HIV-AN, Co-infection with HBV or HCV
  • Pregnant women
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40
Q

ARV agents mechanism of action

A
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41
Q

ARV Mechanism of action cont.

A
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42
Q

NRTI Antiretroviral Medications

NRTI means?

A

nucleoside reverse transcriptase inhibitors

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43
Q

NNRTI Antiretroviral Medications

NNRTI means?

A

non-nucleoside reverse transcriptase inhibitors

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44
Q

PI Antiretroviral Medications

PI means?

A

Protease Inhibitor

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45
Q

Types of antiretroviral medications

6 listed

A
  • NRTIs
  • NNRTIs
  • PIs
  • Integrase Inhibitors
  • Entry inhibitors
  • Phamokinetic boosters
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46
Q

Current NRTI Antiretroviral Medications

A
  • Abacavir
  • didanosine
  • Emtricitabine
  • Lamivudine
  • Stavudine
  • Tenofovir AF or DF
  • Zidovudine
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47
Q
A
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48
Q

Current NNRTI Antiretroviral Medications

5 listed

A
  • Doravirine
  • Efavirenz
  • Etravirine
  • Nevirapine
  • Rilpivirine
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49
Q

Current PI Antiretroviral Medications

A

*Include booster*

  • Atazanavir
  • Darunavir
  • Fosamprenavir
  • Indinavir
  • Lopinavir
  • Nelfinavir
  • Saquinavir
  • Tipranavir
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50
Q

Current Integrase Inhibitors Antiretroviral Medications

4 listed

A
  • Bictegravir
  • Dolutegravir
  • Elvitegravir (with cobicistat)
  • Raltegravir
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51
Q

Current Entry Inhibitiors Antiretroviral Medications

3 listed

A
  • Enfuvirtide
  • Ibalizumab
  • Maraviroc
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52
Q

Current Pharmacokinetic Boosters Antiretroviral Medications

2 listed

A
  • Ritonavir
  • Cobicistat
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53
Q

HAART guidelines: Initial Regiment

A
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54
Q

Describe prevention of HIV Resistance

A
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55
Q

Explain steps of HIV infection & replication

10 listed

A

FBIRITAABM

  1. Free virus
  2. Binding and fusion: to a CD4 molecule and one of two coreceptors (either CCR5 or CXCR4) Receptor molecules are common on the cell surface. Then the virus fuses with the cell
  3. Infection: Virus penetrates cell and contents are emptied into cell
  4. Reverse Transcription: Single strans of viral RNA are converted into double-stranded DNA by the reverse transcriptase enzyme
  5. Integration: Viral DNA is combined with the cell’s own DNA by the integrase enzyme
  6. Transcription: When the infected cell divides the viral DNA is “read” and long chains of proteins are made
  7. Assembly: Sets of viral protein chains come together
  8. Budding: Immature virus pushes out of the cell taking some of the cell membrane with it. The protease enzume starts processing the proteins in the newly forming virus
  9. Immature virus breaks free of the infected cell
  10. Maturation: The protease enzyme finishes cutting HIV protein chains into infividual proteins that combine to make a new working virus
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56
Q

How drug resistance arises in HIV Treatment

A
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57
Q

Causes of HIV Resistance to Antiretrovirals (ARVs)

A
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58
Q

ARVs AKA

A

Antiretrovirals

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59
Q

CD4 coreceptors for HIV

A

CCR5 and CXCR4

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60
Q

HIV Fusion Inhibitors

A
  • Enfuvitide
  • Maraviroc
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61
Q

Maraviroc MOA

A

CCR5 inhibitor to prevent binding and fusion of HIV

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62
Q

Enfuvitide MOA

A

prevent HIV fusion with CD4 cells

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63
Q

Contents of HIV virus capsid

A
  • Single-stranded RNA
  • Three enzymes
    • Reverse Transcriptase
    • Integrase
    • Protease
64
Q

Drugs that target retroviral (HIV) reverse transcriptase

A
  • NRTIs
  • NNRTIs
65
Q

Antiretroviral medications molecular targets

5 listed

A
  • Fusion inhibitors
  • CCR5 inhibitor
  • Reverse transcriptase
  • Integrase inhibitors
  • Protease inhibitors
66
Q

Old guidelines of HAART

A

2 NRTIs + (II or boosted-PI or NNRTI)

67
Q

Most recent HAART guidelines

A

2 NRTIs + Integrase inhibitor

68
Q

How to prevent HIV Drug Resistance?

A

3 agents of at least 2 different classes

69
Q

If a person is taking adequate antiretroviral therapy, can they develop drug resistance?

A

No, if the virus is not replicating, no new mutations can occur!

70
Q

How does HIV resistance arise?

A
  • Basically the drugs stop the virus from replicating but if something happens where drug resistance is formed than drug resistant virus will predominate
71
Q

Causes of HIV Resistance to ARVs

A
  • Inadequate drug therapy
  • Poor adherence causing subtherapeutic drug levels
  • Poor absorption causing subtherapeutic drug levels
  • Drug-drug interactions
  • Infected with resistant virus during initial infection
  • Superinfection with resistant virus
72
Q

How to determine if a patient is infected with a drug resistant strain of HIV?

A

Genotype testing

  • Compares the genetic makeup of the patient’s HIV versus the wild-type strain
  • Identifies known mutations which are associated with resistance to specific genes
73
Q

When to order HIV genotype?

A
  • At acute infection/entry into care
  • Suboptimal suppression of viral load after starting HAART
  • Virologic failure during ART
  • USed to assist in selecting active drugs for a new regimen
74
Q

Case

A
75
Q

ARV drug-interactions

A
  • HIV medications are metabolized by the cytochrome P450 mechanism in the liver
  • These antiretroviral medications have many potential drug-interactions with other medications that are also metabolized by this system
    • Inducers: can decrease levels of other drugs
    • Inhibitors: can increase levels of other drugs
  • Check for drug-drug interactions prior to starting any new medication or if someone has side-effects
76
Q

Drug interactions of “Boosters”

A
  • Ritonavir or Cobicistat
  • Drug induced Cushing’s
    • Intranasal, inhaled, intra-articular, IM steroid in patients on ritonavir or cobicistat
    • Beclomethasone appears safe
  • Statins, SSRIs, others
77
Q

Antiretrovirals that require acidic stomach

A
  • Atazanavir
  • Rilpivirine
78
Q

Drug interactions of Integrase Inhibitors

A
  • Avoid cations
  • DTG increases metformin
79
Q

Case

A
80
Q

Why screen ALL pregnant women for HIV?

A
81
Q

What is the effect of HAART on the risk of vertical HIV transmission

A
82
Q

Case

A
83
Q

Question

A
84
Q

Methods of reducing acquisition of HIV

11 listed

A
85
Q

Explain HIV virus distribution after infection

A
86
Q

PEP vs PrEP

A
87
Q

What is HIV PEP?

A

Post-exposure prophylaxis

88
Q

When is HIV PEP indicated?

A
  • Given after high-risk exposure to reduce risk of HIV infection
  • Start within 72 hours of exposure
89
Q

HIV PEP dosing

A

28 day course of daily 3-drug regimen

90
Q

What is HIV PrEP?

A

Pre-exposure prophylaxis

91
Q

When is HIV PrEP indicated?

A
  • Daily regimen given before exposure to reduce risk of HIV infection
  • Start at least 7 days prior to exposure
92
Q

HIV PrEP dosing

A

Daily 2-drug regimen

93
Q

HIV PEP drugs

A

Start 3 drug regimen <= 72 hours from exposure

2 NRTIs (Tenofovir/emtricitabine) + II (Raltegravir)

94
Q

HIV PEP

A
95
Q

HIV PEP Side effects

A
  • Mild nausea
  • Diarrhea
  • Headache
96
Q

HIV PrEP contrainidications

3 listed

A
  • Active HIV
  • Renal dysfunction
  • Caution with HBV
97
Q

PrEP drugs

A

Currently only one FDA-approved formulation

  • Tenofovir disoproxil fumarate (TDF)/Emtricitabine (FTC) 1 tab qday
  • Approved for adolescents & adults >= 35 kg (77 lbs)
98
Q

Question

A
99
Q

Case

A
100
Q

Case CXR

A
101
Q

What are the general clinical clues of HIV infection?

11 listed

A
102
Q

What are the lab clinical clues of HIV infection?

5 listed

A
  • Leukopenia
  • Anemia
  • Thrombocytopenia
  • Polyclonal hypergammaglobulinemia
  • Endocrinopathies
103
Q

Common Bacterial Pulmonary syndromes associated with HIV

A
104
Q

Common mycobacterial pulmonary syndromes associated with HIV

A
  • M. tuberculosis
  • M. avium complex
105
Q

Common viral pulmonary syndromes associated with HIV

A
  • Influenza
  • RSV
  • CMV
106
Q

Common parasitic pulmonary syndromes associated with HIV

A
  • Toxoplasmosis
  • Strongyloides
107
Q

Common Fungi pulmonary syndromes associated with HIV

A
  • Pneumoncystis jirovecii
  • Cryptococcus
  • Histoplasmosis
  • Coccidiodomycosis
  • Blastomycosis
  • Aspergillus
108
Q

Common non-infectious pulmonary syndromes associated with HIV

6 listed

A
  • Kaposi’s Sarcoma
  • Non-Hodgkin’s Lymphoma
  • Bronchogenic carcinoma
  • Lymphocutic interstitial pneumonitis (LIP)
  • Crack lung
  • Primary pulmonary hypertension
109
Q

Case

A
110
Q

What is Pneumocystic jirovecii and where is it found?

A

Ubiquitous yeast in the environment

111
Q

Pneumocystic jirovecii infections caused by?

A

Disease from reactivation or new infection

112
Q

Who is most commonly infected with Pneumocystic jirovecii

A

Majority of cases of Pneumocystis pneumonia are in patients who are unaware of their HIV status or CD4 <200

113
Q

A common co-infection of Pneumocystic jirovecii

A

Oral Candidiasis (thrush) is a common co-infection of Pneumocystic jirovecii

114
Q

Clinical presentation of Pneumocystic jirovecii

A
  • Subacute, progressive dyspnea, non-productive cough, pleuritic chest pain
  • Hypoxemia, especially with activity (LDH>500)
115
Q

Pneumocystic jirovecii CXR findings

A

Variable

  • Classic: diffuse, bilateral interstitial infiltrates
  • May be normal in early disease
116
Q

Chest CT of Pneumocystic jirovecii

A

Patchy-ground glass attenuation

117
Q

Treatment of Pneumocystic jirovecii

A
  • TMP/SMX high dose x 21 days
  • Add prednisone if pO2 < 70 mmHg or A-a gradient > 35 mmHg
118
Q

PCP Prophylaxis When and What

A
119
Q

Case

A
120
Q

Opportunistic infections with CNS involvment classes of disease

A
  • Meningitis
  • Encephalitis
  • Neurosyphilis
  • CNS Lymphoma
121
Q

Opportunistic infections with CNS involvment: Meningitis

5 listed

A
  • Cryptococcus
  • M. tuberculosis
  • Listeria monocytogenes
  • Typical bacterial
  • Typical viral
122
Q

Opportunistic infections with CNS involvment: Encephalitis

A
  • Reactivation of latent infections
  • CMV, HSV, VZV
  • JV virus: PML (Progressive Multifocal Leukoencephalopathy)
  • Toxoplasma gondii
123
Q

Opportunistic infections with CNS involvment: Neurosyphilis

A

syphilis

124
Q

Opportunistic infections with CNS involvment: CNS lymphoma

A

CNS lymphoma

125
Q

How is Toxoplasma gondii encephalitis caused?

A
  • Reactivation of latent tissue cysts
  • Primary infection is from undercooked meat or shed in cat feces
126
Q

Toxoplasma gondii encephalitis clinical presentation

A
  • Focal encephalitis with headache, confusion, seizure or motor weakness & fever
127
Q

Toxoplasma gondii encephalitis CT/MRI

A

Single or multiple contrast-enhancing lesion with edema

128
Q

Toxoplasma gondii encephalitis Treatment

A
  • Pyrimethamine + Sulfadiazine + Leukovorin for 6 weeks
  • Long-term secondary prophylaxis
129
Q

Toxoplasma gondii encephalitis reactivation prophylaxis When and What

A
130
Q

Case

A
131
Q

Case cont

A
132
Q

Classes of Causes of pancytopenia

A
  • Bacterial
  • Mycobacterial
  • Viral
  • Malignancy
  • Fungal
  • Malnutrition
  • Drug/toxin
133
Q

Bacterial Causes of pancytopenia

A

Sepsis

134
Q

Mycobacterial Causes of pancytopenia

A
  • M. Tuberculosis
  • M. avium complex
135
Q

Viral Causes of pancytopenia

A
  • CMV
  • Parvovirus B-19
136
Q

Malignancy causes of pancytopenia

A

Lymphoma

137
Q

Fungal Causes of pancytopenia

A
  • Cryptococcosis
  • Blastomycosis
  • Coccidiodomycosis
  • Histoplasmosis
138
Q

Drug/toxin Causes of pancytopenia

A
  • Fapsone
  • Alcohol
  • Additive to cocaine
139
Q

Case cont cont.

A
140
Q

What is Mycobacterium avium Complex and where is it found?

A

AFB (Acid-Fast Bacteria) that is ubiquitous in the environment

141
Q

How is infection with Mycobacterium avium Complex transmitted?

A
  • Inhalation
  • Ingestion
142
Q

Risk factors for Mycobacterium avium Complex infection

A
  • CD4 < 100; Most are < 50
  • HIV RNA > 100,000 copies/mL
143
Q

Mycobacterium avium Complex Clinical presentations

A

Can present as Disseminated multi-organ infection or local infection

144
Q

Clinical presentation of disseminated multi-organ infection of Mycobacterium avium Complex

A
  • Fever
  • Night sweats
  • Weight loss
  • diarrhea
  • Abdominal pain
  • Anemia
  • Elevated Alk Phos
  • Lymadenopathy
  • Hepatosplenmegaly
145
Q

Clinical presentation of local Mycobacterium avium Complex infection

A
  • Pneumonia
  • Colitis
146
Q

Treatment of Mycobacterium avium Complex infection

A

Clarithromycin + Ethambutol + Rifabutin

147
Q

The challenges of Treating Mycobacterium avium Complex infections

A
  • Drug-interactions with HAART
  • Medication toxicity
148
Q

MAC AKA

A

Mycobacterium avium Complex

149
Q

Mycobacterium avium Complex prophylaxis What and When?

A
150
Q

Opportunistic infections at any CD4 level

A

PPD or IGRA reactive

151
Q

Opportunistic infections at CD4 < 200 cells/uL

A

PJP Prophylaxis

152
Q

Opportunistic infections at CD4 < 100 cells/uL

A

Toxoplasma prophylaxis

153
Q

Opportunistic infections at CD4 < 50 cells/uL

A

MAC Prophylaxis

154
Q

Case

A
155
Q

Assesing need for prophylaxis

A

Infectious Disease (82 decks)

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