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Block G -- Infection > Dr. Karatzios -- HIV > Flashcards

Dr. Karatzios -- HIV Flashcards

1
Q

Predominant mode of adult acquisition of HIV

A

Heterosexual intercourse

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2
Q

Predominent mode of childhood acquisition of HIV

A

Perinatal exposure

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3
Q

6 highly endemic areas for HIV

A
  • Sub-Saharan Africa
  • Southeast Asia (Thailand)
  • India
  • Haiti
  • China
  • Russia
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4
Q

How HIV enters cells (3 points)

A
  • HIV viral envelope protein (gp120)
  • Human T cell receptor
  • Human co-receptors (CCR5 or CXCR4 or both)
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5
Q

6 cells that HIV infects

A
  • CD4+ T lymphocytes
  • Dendritic cells (skin, lymph nodes, brain)
  • Macrophages
  • CD8+ T lymphocytes
  • NKC
  • Natural killer T cells (viral reservoir)
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6
Q

3 systems in which HIV lives

A
  • Lymphoid organs
  • CNS
  • Genitourinary system
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7
Q

3 lymphoid organs in which HIV can live

A
  • Peripheral lymph nodes
  • GI lymph nodes
  • Bone marrow
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8
Q

Method of transmission of HIV living in GI lymph nodes

A

Neonatal

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9
Q

How does HIV enter the CNS?

A

HIV Tat protein disrupts the BBB –> Microglial and dendritic cells

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10
Q

2 reservoirs of HIV replication

A
  • CNS
  • Genitourinary system
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11
Q

3 parts of the genitourinary system in which HIV can live

A
  • Semen
  • Renal epithelium
  • Marcophages and lymphocytes in cervix
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12
Q

How does HIV infect semen?

A

HIV crosses the blood-testis barrier

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13
Q

Why is there a high rate of genomic mutation in HIV?

A

Reverse transcriptase is extremely error-prone

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14
Q

2 types of genomic mutations that HIV may undergo?

A
  • Spontaneous mutations over time
  • Drug-driven mutations
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15
Q

2 potential outcomes of spontaneous HIV mutations

A
  • Many are silent/no-effect
  • Some confer resistance to medications
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16
Q

Compare wild type HIV to mutated HIV

A
  • Highly mutated = “less fit”
  • Wild type = easily transmissible and replicates more efficiently
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17
Q

When do mutants overtake wild type HIV?

A
  • If medications are failing –> mutants accumulate
  • Held in reserve and overtake wild type once medications restarted
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18
Q

When does wild type HIV overtake mutants?

A

Once medications are stopped

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19
Q

Effect of initial viremia from HIV

A

Infection of lymph nodes

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20
Q

Effect of secondary viremia from HIV

A

Mononucleosis-like illness

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21
Q

2 events occurring during the window period between initial and secondary viremia

A
  • Silent viral replication in lymph nodes
  • Little or no HIV antibodies
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22
Q

Length of window period between initial and secondary viremia

A

Up to 3 months

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23
Q

7 symptoms of acute HIV syndrome

A

Mononucleosis-like illness

  • Fever
  • Malaise
  • Non-exudative pharyngitis
  • Maculpapular rash (50%)
  • Myalgias
  • Headache
  • GI distress
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24
Q

5 signs of acute HIV syndrome

A

Mononucleosis-like illness

  • Generalized lymphadenopathy
  • Hepatosplenomegaly
  • Oral or vaginal thrush
  • Lymphopenia THEN acute lymphocytosis
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25
Q

Lab findings of acute HIV syndrome

A
  • HIV antibody negative
  • PCR and antigen positive
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26
Q

Timeline of acute HIV syndrome

A
  • 1 - 6 weeks after infection
  • Lasts up to 3 weeks
  • Spontaneous resolution
  • –> Window period
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27
Q

Main cell type destroyed by HIV

A

CD4+ T cells

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28
Q

3 ways CD4+ T cells are destroyed

A
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29
Q

Severe immune suppression by age (in No/mm3)

A
  • <12 months = <750
  • 1 - 5 years = <500
  • >6 years = <200
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30
Q

Describe the natural history of HIV disease

A
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31
Q

Use of HIV serology

A

Screening and confirmatory test in humans >18 months age

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32
Q

Use of HIV PCR

A

Screening and confirmatory test in humans < 18 months age

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33
Q

How to determine viral copy number

A
  • Viral RNA numbers expressed as number of copies/mL blood or log:
    • log 2 = 100 copies/mL
    • log 3 = 1000 copies/mL
    • < log 1.6 = <40 copies/mL = undetectable
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34
Q

4 infections associated with HIV disease

A
  • Sinopulmonary infections
  • Salmonellosis
  • Meningitis
  • Candidiasis
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35
Q

Cardiac problem associated with HIV

A

Cardiomyopathy

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36
Q

3 growth and sexual development issues related to HIV

A
  • Delayed
  • Decrease in testosterone/libido
  • Osteoporosis
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37
Q

3 neurological issues related to HIV

A
  • Cognitive delay
  • Encephalopathy
  • Dementia
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38
Q

Renal problem associated with HIV

A

HIV nephropathy

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39
Q

2 psychiatric issues related to HIV

A
  • Depression
  • ADHD
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40
Q

Proportion of AIDS patients with esophageal disease

A

1/3

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41
Q

6 typical symptoms of esophageal disease in HIV patients

A
  • Dysphagia
  • Odynophagia
  • Retrosternal pain
  • Nausea
  • Anorexia
  • Weight loss

NOTE: Usually indolent onset

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42
Q

2 causes of dysphagia and odynophagia in AIDS patient

A
  • Esophageal inflammation
  • Ulceration
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43
Q

Likely cause of HIV-associated idiopathic esophageal ulcers

A

HIV seen in lymphocytes and lamina propria

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44
Q

Biopsy findings of herpes virus esophagitis

A

Multinucleated giant cells

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45
Q

Which other kind of esophagitis does HIV-associated idiopathic esophageal ulcers resemble?

A

CMV esophagitis

  • Shallow ulcers
  • Inclusion bodies on biopsy
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46
Q

3 infectious oral lesions associated with AIDS

A
  • Herpes simplex
  • Oral hairy leukoplakia
    • EBV-related
    • Non-painful
  • Oral candidiasis (usually painful)
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47
Q

Oral neoplastic lesion associated with HIV/AIDS

A

Kaposi’s sarcoma

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48
Q

Effect of HBV in HIV/AIDS (3)

A
  • Spontaneous reactivation seen in AIDS
  • 19x more likely to die if HIV/HBV co-infected
  • HBV does not influence HIV progression, however
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49
Q

3 causes of death in HIV/HBV co-infection

A
  • Cirrhosis
  • Live failure
  • Carcinoma
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50
Q

Effect of HCV in HIV/AIDS

A
  • 94x higher risk of mortality
  • HCV may affect progression of HIV

NOTE: All HIV+ patients should be screened for HCV

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51
Q

3 pharmacological causes of hepatitis in HIV/AIDS patients

A
  • Protease inhibitors
  • NNRTI
  • Antimycobacterial drugs
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52
Q

Protease inhibitor that can cause hepatitis and steatosis in HIV patients

A

Ritonavir

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53
Q

NNRTI that can cause hepatitis in HIV patients

A

Nevirapine

54
Q

3 antimycobacterial drugs that can cause hepatitis in HIV patients

A
  • Rifampin
  • Rifabutin
  • INH
55
Q

3 pharmacological causes of jaundice in HIV patient

A
  • Protease inhibitors (atazanavir)
  • Septra
  • Macrolides
56
Q

2 pharmacological causes of steatosis in HIV patients

A
  • Mitochondrial toxicity and lactic acidosis (i.e. NRTI such as ZDV, d4T, ddI)
  • Protease inhibitors (ritonavir)
57
Q

2 common general causes of diarrhea in HIV/AIDS patients

A
  • Colitis
  • Malabsorption

NOTE: There are many causes and this affects 95% of patients in 3rd world with a 72% 10-mo mortality (chronic diarrhea)

58
Q

5 bacterial causes of diarrhea in HIV patients

A
  • SSCYE, Listeria monocytogenes
  • *Mycobacterium avium *complex
    • Obstructive as well
  • Mycobacterium tuberculosis
    • Obstructive as well
  • Toxin-mediated (i.e. C. difficile)
  • Bacterial overgrowth
59
Q

5 viral causes of diarrhea in HIV patients

A
  • CMV
  • Adenovirus
  • Rotavirus
  • HIV
  • Other causes of viral gastroenteritis
60
Q

6 parasitic causes of diarrhea in HIV patients

A
  • Giardia lamblia
  • Cryptosporidium parvum
  • Microsporida
  • Isospora belli
  • Cyclospora cayetanensis
  • Entamoeba histolytica
61
Q

Fungal cause of diarrhea in HIV patients

A

Histoplasma capsulatum

62
Q

4 risk factors for diarrhea in HIV patients

A
  • Severe immunosuppression
  • Environmental conditions
  • Travel-related exposures
  • MSM
63
Q

2 pharmacological causes of diarrhea in HIV patients

A
  • Most all antiretrovirals
  • Antibiotics
64
Q

3 immune-mediated causes of diarrhea in HIV patients

A
  • IBD
  • Immune Reconstitution Syndrome
  • Celiac disease
65
Q

2 neoplastic causes of diarrhea in HIV patients

A
  • Intestinal lymphoma
  • Kaposi’s sarcoma
66
Q

3 reasons why HIV-associated enteropathy may be due to HIV itself

A
  • Direct alteration of enterochromaffin cell function
  • Enterocyte degeneration
  • Microtubular depolymerization
67
Q

2 results of HPV disease in setting of HIV

A
  • Anal condillomatosis
  • Cervical/Anal cancer
68
Q

3 bacteria involved in sexually transmitted proctitis

A
  • Chlamydia trachomatis
  • Neisseria gonorrhea
  • Treponema pallidum
69
Q

7 opporunistic infections in the setting of AIDS

A
  • Pneumocystosis jiroveci
  • Toxoplasma gondii
  • Candida esophagitis/moniliasis
  • CMV
  • Disseminated vericella zoster
  • Mycobacterium avium intercellulare
  • JC virus/Progressive multifocal leukoencephalopathy
70
Q

4 non-opportunistic infections associated with AIDS

A
  • Salmonellosis
  • Crypto/microsporidiosis
  • Isospora belli
  • Giardia lamblia
71
Q

3 neoplastic transformations in the setting of AIDS

A
  • HHV-8: Kaposi sarcoma
  • Castleman disease
  • CNS lymphoma
72
Q

Median duration of disease prior to HAART

73
Q

Median duration of disease after HAART

74
Q

Most frequent opportunistic pathogen in AIDS patients

A

Pneumocystis jiroveci

75
Q

4 symptoms and signs of pneumocystis jiroveci in AIDS patients

A
  • Fever
  • Cough
  • SOB
  • Hypoxia

NOTE: Can involve extra-pulmonary areas as well (liver)

76
Q

4 primary prophylaxis options for pneumocystic jiroveci

A
  • Septra po
  • Dapsone
  • Atovaquone
  • Pentamidine
77
Q

Patients to administer *pneumocystic jiroveci *prophylaxis (2)

A
  • All HIV+ children <1 year regardless of CD4 count
  • Older children and adults when CD4 <200 (or <15% of total lymphocytic count)
78
Q

3 treatments of pneumocystic jiroveci

A
  • Septra (IV or po)
  • Systemic corticosteroids
  • Supplemental oxygen
79
Q

Secondary prophylaxis for pneumocystic jiroveci

A

Septra until CD4 > 200 for 3 months

80
Q

Define *mycobacterium avium *complex

A

Disseminated disease based in the GIT and reticuloendothelial system

81
Q

3 symptoms of *mycobacterium avium *complex infection

A
  • Pulmonary disease
  • Fever
  • Weight loss
82
Q

2 primary prophylaxis drugs for mycobacterium avium complex

A
  • Azithromycin
  • Clarithromycin
83
Q

Patients to give primary prophylaxis for *mycobacterium avium *complex

A
  • Childen < 5 yo that are severely immunosuppressed
  • People >6 yo with CD4 < 50 cells
84
Q

Treatment for *mycobacterium avium *complex

A
  • Macrolide + rifabutin
  • Other second-line drugs
85
Q

Secondary prophylaxis for *mycobacterium avium *complex

A

Macrolide + rifabutin until CD4 >75 for 3 months

86
Q

Effect of HIV on mycobacterium tuberculosis transmission

A

HIV patients can transmit this to other much more easily than non-HIV patients

87
Q

5 effects of *cryptococcus neoformans *in setting of HIV/AIDS

A
  • Meningitis
  • Raised intracranial pressure
  • Necrotizing intracranial pressure
  • Necrotizing lymphadenitis (mediastinal, cervical)
  • Necrotizing pneumonitis
  • Skin abscesses
88
Q

Treatment for cryptococcus neoformans

A
  • Amphotericin B + Fluconazole IV
  • Followed by fluconazole po for weeks to months
89
Q

Length of secondary prophylaxis for cryptococcus neoformans

A

Usually lifelong

90
Q

6 manifestations of CMV in setting of HIV/AIDS

A
  • Retinitis
  • Uveitis
  • Retinal detachment
  • Visual loss
  • Pneumonitis
  • Disseminated
91
Q

7 opportunistic viruses in setting of AIDS

A
  • CMV
  • HSV
  • VZV
  • HHV-8
  • HBC
  • HCV
  • JCV
92
Q

3 manifestations of toxoplasma gondii in setting of HIV/AIDS

A
  • Encephalitis
  • Seizures
  • Disseminated CNS lesions (ring enhancing)
93
Q

Treatment for toxoplasmia gondii

A

Sulfadiazine + pyrimethamine + folinic acid (leucovorin)

94
Q

Secondary prophylaxis for toxoplasma gondii

A

Sulfadiazine + clindamycin until CD4 > 200 for 3 - 6 months

95
Q

4 drugs involved in Highly Active AntiRetroviral Therapy (HAART)

A

Combination therapy with

  • NRTI
  • NNRTI
  • PI (protease inhibitors)
  • FI (fusion inhibitors)
96
Q

2 aims of HAART

A
  • Reduction of HIV viral load to undetectable levels
  • Elevation of CD4 Th lymphcyte counts
97
Q

8 NRTIs

A
  • ZDV
  • 3TC
  • d4T
  • ddI
  • ddC
  • Abacavir
  • Emtricitabine
  • Tenofovir
98
Q

4 combinations of NRTIs

A
  • COmbivir
  • Trizivir
  • Kivexa
  • Truvada
99
Q

5 NNRTIs

A
  • Delaviridine
  • Efavirenz
  • Nevirpine
  • Etravirine
  • Rilpivirine
100
Q

2 NNRTI combinations

A

Atripla

Complera

101
Q

Fusion inhibitor drug

A

Efurvitide

102
Q

FI mechanism

A

Inhibition of fusion of HIV with human cells (a salvage mechanism)

103
Q

FI administration

A

Subcutaneous injection

104
Q

2 newer classes of HAART drugs

A
  • Integrase inhibitors
  • Coreceptor antagonists
105
Q

Integrase inhibitor mechanism

A

Prevent integration of pro-viral DNA into human chromosomal DNA

106
Q

2 integrase inhibitors

A

Raltegravir (Isentress)

Elvitegravir

107
Q

Coreceptor antagonist mechanism

A

Prevent binding of HIV onto human cells

108
Q

Coreceptor antagonist drug

109
Q

How to boost antiretrovirals

A

Inhibition of liver cytochrome p450 enzymes that metabolize some antiretrovirals (PIs, elvitegravir)

110
Q

Aim of cytochrome p450 inhibition in antiretroviral therapy

A

Increase levels of antiretrovirals in the blood and tissues for max efficiency

111
Q

2 boosting agents for antiretrovirals

A

Low doses of ritonavir

Newer = cobicistat

112
Q

2 problems with ritonavir (a PI)

A

GI side fx and hyperlipidemia

May drug-drug interaction because of p450 inhibition

113
Q

Advantage of using cobicistat

A

Less side fx than ritonavir

114
Q

CD4 count when HIV treatment is mandatory

A

<300 cells/mL

115
Q

Viral load log when HIV treatment is mandatory

116
Q

4 obstacles to HIV treatment

A
  • Adherence to medication
  • Intolreance and toxicity due to medications
  • Metabolic complications due to medications
  • HIV resistance to antiretrovirals
117
Q

Compare the viral load of neonates to adults

A

Initial higher viral load –> may take longer to become undetectable

118
Q

Describe the progression of rapidly progressing HIV in children

A
  • Rapid destruction of immune system
  • AIDS before 5 years of age (<5 months)
  • 50% 5 year survival
119
Q

5 manifestations of AIDS in children

A
  • Opportunistic infections
  • Failure to thrive
  • Hepatitis
  • Diarrhea
  • Neurocognitive deterioration
120
Q

Describe the disease progression of slowly progressing HIV in children

A
  • Effective immune activity and viral suppression
  • Asymptomatic or lymphadenopathy/parotitis
  • 68% 5-y survival; 71% 6.5-y survival
121
Q

3 main aspects of disease presentation of HIV in children

A
  • Growth failure
    • Decline in weight-growth velocity despite adequate nutrition
  • Progressive neurodevelopmental deterioration
  • LIP (lymphoid interstitial pneumonitis)
122
Q

3 manifestations of LIP in children with HIV

A
  • Immune0mediated lymphocytic infiltration of lungs
  • Respiratory distress; hypoxia
  • Reticulonodular infiltrates
123
Q

Treatment for LIP in HIV children

A

Corticosteroids

124
Q

Opportunistic infection for children with HIV

A

*Pneumocystis jiroveci *pneumonia

125
Q

6 live vaccines

A
  • MMR
  • Varivax
  • Yellow fever
  • Oral typhoid
  • Oral polio
  • Intranasal influenza
126
Q

Vaccine recommendations for children with HIV (3)

A

In severely immunosuppressed:

  • Vaccines not effective (defer or re-immunize once reconstituted)
  • Live vaccines contraindicated until CD4 rises to normal levels
  • BCG absolute contraindication
127
Q

5 methods of acquisition of HIV in children

A
  • Perinatal exposure
  • Blood product transfusion
  • Sexual abuse

Adolescent years:

  • Sexual intercourse
  • IV drugs
128
Q

3 perinatal exposures that may cause children to contract HIV

A
  • Intrapartum especially
  • Postpartum (i.e. breastmilk)
  • Rarely in utero
129
Q

4 measures to reduce mother-child transmission of HIV

A
  • Implementation of universal prenatal HIV counseling and testing
  • Antiretroviral treatment and prophylaxis
  • Scheduled C-section (in some cases)
  • Avoidance of breastfeeding
130
Q

Main tool for reducing perinatal exposure HIV transmission

A

Universal informed opt-out screening for HIV infection in all pregnant women

131
Q

3 highest risk infectious materials for HIV transmission

A
  • Concentrated lab HIV
  • Blood
  • Any fluid contaminated with blood
132
Q

6 infectious materials of intermediate risk for HIV transmission

A
  • Semen
  • Vaginal secretions
  • CSF
  • Amniotic fluid
  • Pleural/pericardial/peritonial/synovial fluids
  • Human milk

Block G -- Infection (23 decks)

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