Exam 5: Opportunistic Infections Flashcards

1
Q

Normal CD4 count

A

500-1200 cells/mm

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2
Q

Average decline of cd4 cells per year without ART

A

50-100 cells/year

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3
Q

CD4 cell counts ___ and especially ____ are associated with the development of OI

A

<500

<200

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4
Q

What three infections may occur at any CD4 cell count but are more common at lower CD4 cell counts

A
  1. mycobacterium tuberculosis
  2. pneumococcal disease
  3. dermatomal zoster
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5
Q

OIs developing at CD4 counts <500

A

vulvovaginal candidiasis
thrush
oral leukoplakia

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6
Q

OIs developing at CD4 counts between 0 and 200

A
  1. PJP
  2. CMV
  3. Toxoplasma gondii encephalitis
  4. MAC
  5. cryptococcus neoforms meningitis
  6. cryptosporidum diarrhea
  7. CNS lymphoma
  8. Kaposi’s Sarcoma
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7
Q

what infections can increase plasma HIV viral load which accelerates HIV progression and increases risk of HIV transmission

A

TB

Syphilis

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8
Q

Initial ART therapy in the setting of an acute OI

A

Initiation of ART during an acute OI is very useful in the management of OIs for which effective therapy is not available, such as PML, cryptosporidiosis, and Kaposi’s sarcoma

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9
Q

Disadvantage of immediately starting ARTs in the setting of acute OI

A
  1. IRIS
  2. Overlapping or additive drug toxicities
  3. DIs b/w ART and OI therapy
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10
Q

What is IRIS

A

immune reconstitution inflammatory syndrome: when immune system begins to recover, it begins to respond to already acquired OI

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11
Q

IRIS characterization

A

fever and worsening clinical manifestations of the OI

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12
Q

What OIs can IRIS be seen in

A
  1. MAC
  2. TB
  3. PJP
  4. toxoplasma
  5. HBV and HCV
  6. Histoplasma
  7. Varicella
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13
Q

What patients are at risk for IRIS

A
  1. Low CD4 counts (<50)

2. High HIV viral load (>100,00)

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14
Q

Treatment of IRIS

A
  1. NSAIDs if Mild

2. Corticosteroid: Prednisone 1-2 mg/kg qd x1-2 weeks with taper if severe

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15
Q

Most common OIs

A

oropharyngeal and esophageal candidiasis

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16
Q

CD4 cell count when candida occurs

A

<200

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17
Q

Which has lower CD4 counts: oral or esophageal candidiasis

A

esophageal

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18
Q

Candida pathogenesis

A

Alterations in the host immune system, such as defects in cell-mediated immunity, can alter the commensal status of candida species so that invasion of host tissue and infection occurs

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19
Q

How can non-albicans candida species occur

A

develop in patients who have received repeated or long-term exposure to fluconazole

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20
Q

thrush clinical exam

A

painless, creamy white, plaque-like lesions on the buccal mucosa, hard or soft palate, oropharyngeal mucosa or tongue sulface

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21
Q

topical vs systemic therapy for thrush

A

systemic therapy is preferred and superior to topical therapy, especially in patients with multiple epidoses

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22
Q

topical treatment options for thrush

A
  1. nystatin suspension
  2. clotrimazole troches
  3. miconazole buccal tab
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23
Q

nystatin suspension thrush dosing

A

5ml swish and swallow qid x10-14 days

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24
Q

clotrimazole troches thrush dosing

A

10mg oral lozenge five times a day for 14 days

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25
miconaole buccal tab thrush dosing
50mg tablet applied to mucosal surface qd x14
26
systemic DOC for thrush with dosing
fluconazole 100mg PO QD x7-14 days
27
esophageal candidiasis DOC with dosing
fluconazole 200mg (up to 400mg) IV or PO QD x14-21 days
28
can you use topical therapy for esophageal candidiasis
NO
29
-Azoles AE
GI upset and hepatotoxicity
30
-Azoles monitoring
Liver enzymes should be monitored periodically during prolonged therapy (>21 days)
31
use of primary prophylaxis for candidiasis
Not routinely recommended because of the effectiveness of therapy for acute infection, the low attributable mortality associated with mucosal candidiasis
32
Primary treatment for vulvovaginal candidiasis
1. topical azoles for 3 to 7 days 2. single dose fluconazole 3. itraconazole solution
33
when to give oral fluconazole for vulvovaginal candidiasis
severe or recurrent episodes
34
Common CD4 count in cryptococcus neoformans
<100
35
Cryptococcal meningitis symptoms
mild and non-specific | fever, malaise, headache, nausea, dizziness, lethargy, irritability, impaired memory, behavioral changes
36
Cryptococcal meningitis diagnostics
1. CSF analysis: increases opening and intracranial pressure 2. few white blood cells 3. encapsulated yeast forms 4. positive serum cryptococcal antigen titer
37
What can dissemintated cryptococcal infections causes
pneumonia
38
treatment phases for Cryptococcal meningitis
induction, consolidation, and maintenance
39
induction therapy for Cryptococcal meningitis
liposomal amphotericin B 3-4 mg/kg IV qd + oral flucytosine 25 mg/kg q 6 h PO >2 weeks
40
consolidation therapy for Cryptococcal meningitis
fluconazole 400-800mg PO QD
41
maintenance therapy for Cryptococcal meningitis
fluconazole 200mg qd for a year or longer
42
ART therapy initiation while treating cryptococcal meningitis
initiation should be delayed until induction and possibly induction/consolidation to avoid IRIS
43
use of primary prophylaxis for Cryptococcal meningitis
not routinely recommended because of relative infrequency of infection
44
use of secondary prophylaxis for Cryptococcal meningitis
chronic maintenance or suppression therapy with oral fluconazole for at least one year is necessary due to high rate of relapse
45
when can secondary prophylaxis for Cryptococcal meningitis be stopped
1. pt completes one year of maintenance therapy 2. pt is asymptomatic 3. pt has sustained immune reconstitution with ART with CD4 >100 for more than three months
46
flucytosine monitoring
flucytosine can cause decreased WBC or platelets: obtain CBC at least once or twice weekly
47
amphotericin AE
nephrotoxicity, hypokalemia, hypomagnesemia, infusion related reactions
48
CD4 count with PJP
<200
49
PJP symptoms
subacute onset of progressive, exertional dyspnea, fever, non-productive cough, and chest discomfort that worsens over a period of days to weeks
50
How are ABGs affected in PJP
hypoxemia may occur in pts: pO2<70
51
chest xray in PJP
diffuse, bilateral, symmetrical ground glass interstitial infiltrates
52
DOC for moderate to severe PJP
trimethoprim-sulfamethoxazole 15-20 mg/kg/day of the TMP component IV divided q6-8h for 21 days (may switch to PO after clinical improvement)
53
____ should be given to patients with moderate to severe PJP when ______
adjunctive corticosteroids PaO2 <75
54
adjunctive corticosteroid DOC and dosing for PJP
Prednisone 40mg BID x5 40mg QD x5 20mg QD x11
55
ART therapy initiation while treating PJP
ART should be initiated within 2 weeks of diagnosis of PJP
56
use of primary prophylaxis for PJP
1. CD4 <200 2. CD4 percentage <14% of total lymphocute count 3. CH4 >200 but <250 if initiation of ART is delayed
57
primary prophylaxis for PJP
Bactrim DS or SS PO QD | or Dapsone 100mg QD
58
use of secondary prophylaxis for PJP
must be given after completion of treatment for all patients
59
When can primary or secondary prophylaxis for PJP stop
Both can be stopped when: | 1. CD4 >200 for at least 3 months in response to ART therapy
60
TMP-SMX AE
``` rash fever leukopenia thrombocytopenia hyperkalemia ```
61
TMP-SMX monitoring
CBC, Scr, and K at least 2-3
62
Greatest risk of developing toxoplasma gondii
AIDS and CD4 <100
63
toxoplasma manifestations
focal encephalitis with headache, confusion, motor weakness, and fever
64
toxoplasma diagnostics
1. serum toxoplasma gondii IgG antibody positive | 2. Detection of T. gondii by PCR in CSF analysis
65
Expensive treatment of choice for toxoplasma
pyrimethamine: 200mg X1 then 50-75 mg PO QD +leucovorin: 10-25mg PO QD + sulfadiazine 1000-1500 mg PO q6h all for 6 weeks
66
Cheap treatment of choice for toxoplasmosis
TMP/SMX 10 mg/kg/day based on TMP component
67
Treatment duration for toxoplasmosis
at least 6 weeks
68
_____ should be given to patients with mass effect associated with focal lesions or associated edema and d/c as soon as feasible
adjunctive corticosteroids (dexamethasone)
69
ART therapy initiation while treating toxoplasmosis
should be started within 2 to 3 weeks of the diagnosis/treatment of toxoplasmosis
70
use of primary prophylaxis for toxoplasmosis and treatment
CD4 <100; treat with bactrim ds qd
71
can primary prophylaxis for toxoplasmosis be d/c
Yes when: 1. CD4 >200 for >3 months in response to ART 2. CD4 is 100-200 and HIV RNA is below detection limit for at least 3-6 months
72
use of secondary prophylaxis for toxoplasmosis
should be given to all patients after completion of treatment; treat with bactrim ds qd
73
can secondary prophylaxis for toxoplasmosis be d/c
Yes when: | Cd4 >200 for >6 months
74
pyrimethamine AE
rash, nausea, and bone marrow suppression (anemia, neutropenia, thrombocytopenia) than can be decreased or reversed by the concomitant administration of leucovorin
75
MAC is the _____________ infection in patients with AIDS and can contribute substantially to their morbidity
most common systemic, bacterial
76
When does MAC occur
late in HIV infection when CD4 <50
77
MAC clinical presentation
gradual onset of systemic symptoms, including fever, dairrhea, night sweats, weight loss
78
How to detect presence of MAC
AFB cultures of blood, bone marrow, lymph node, and stool
79
MAC treatment guideline
2 or more antimycobacterial drugs to delay or prevent the emergency of resistance
80
MAC treatment
1. Clarithomycin 500mg BID 2 Ethambutol 15mg/kg qD 3. Rfiabutin 300mg QD
81
Treatment duration for MAC
>12 months
82
ART therapy initiation while treating MAC
Should have ART initiated ASAP (preferably within initiation of MAC therapy
83
use of primary prophylaxis for MAC
not recommended for adults who immediately initiate ART regardless of CD4 count Azithromycin 1200mg weekly for pts not on ART and have CD4<50
84
can primary prophylaxis for MAC be d/c
Yes when patients initiate effective ART
85
use of secondary prophylaxis for MAC
secondary prophylaxis should be administered to ALL patients with MAC after one year of treatment: azithromycin 1200mg qw
86
can secondary prophylaxis for MAC be d/c
Yes when CD4 increases to >100 for >6 months
87
Azithromycin and clarithomycin AE
nausea, vomiting, adbominal pain
88
ethambutol Ae
optic neuritis and hepatotoxicity
89
rifabutin AE
hepatotoxicity, uveitis, red-orange discoloration of body fluids