Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Clinical 2 (Sam) > Opportunistic Infections > Flashcards

Opportunistic Infections Flashcards

1
Q

HAART

A

highly active antiretroviral

therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IRIS

A

immune reconstitution syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define Opportunistic Infections

A

Defined as “infections that are more frequent or more severe because of immunosuppression in HIV-infected persons”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Prior to _____, OI’s were the principal cause of morbidity and mortality in the HIV infected population

A

HAART

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What had the most profound illness on reducing OI-related mortality in HIV-infected persons?

A

HAART

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 major OI’s

A

PCP
MAC
CMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

However, many patients, for whatever reason do not take HAART optimally, leading to ?

A

treatment failure and HIV progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

OI’s are directly related to overall immune function (______)

A

CD4+ and T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HAART reduces OI’s and improves survival, independent of __________ ________

A

antimicrobial prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

HAART does not replace the need for antimicrobial prophylaxis in _____ ______ _______

A

severe immune suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Although hospitalizations and deaths have decreased dramatically due to ART, OI’s remain a leading cause of ?

A

morbidity and mortality in HIV-infected persons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some AIDS indicator conditions? (AIDS-defining illnesses)

A
  • Cervical cancer, invasive
  • Encephalopathy, HIV-related
  • Lymphoma, Burkitt
  • Lymphoma, immunoblastic
  • Lumphoma, primary or brain
  • Wasting syndrome due to HIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List and describe some bacterial opportunistic infections

A
  • Mycobacterium avid complex (MAC) infection - lungs

- Recurrent bacterial infections can also occur such as repeated episodes of bacterial pneumonia or salmonella sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List and describe some fungal opportunistic infections

A
  • Pneumocystis carny (PCP) pneumonia - lungs
  • Candid - in the mouth, esophagus, trachea, bronchi, lungs or gut
  • Histoplasmosis
  • Coccidiomycosis
  • Aspergillosis
  • Cryptococcosis - outside the lungs particularly cryptococcal meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List and describe some protozoal opportunistic infections

A
  • Toxoplasmosis of the brain

- Cryptosporidium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List and describe some viral opportunistic infections

A
  • Cytomegalovirus (CMV) disease outside the liver, spleen or lymph nodes and CMV retinitis
  • Herpes simplex virus (HSV) - systemic, encephalitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

The lower your immune system is, the _____ the incidence of OI

A

higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the presenting symptom of HIV and leads for testing for HIV?

A

opportunistic infections

*basically a person with normal immune function would not get these infections, so if you present with one, they will test for HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the management of an acute OI

A

1) Start treatment for the OI (if treatment exists)
2) Start HAART
- During treatment of acute OI
- Timing of start of HAART dependent on the particular OI (ex.. TB and cryptococcus)

Rationale:

  • decrease mortality from OI with earlier HAART start vs morbidity/mortality from IRIS
  • medications to treat both, side effects/toxicity - difficult to differentiate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is IRIS?

A

immune reconstitution inflammatory syndrome (IRIS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe IRIS (immune reconstitution inflammatory syndrome)

A
  • Characterized by fever, worsening clinical signs of the OI or symptoms of new OI
  • Occur in the first weeks after starting ART
  • May occur with a number of conditions (slide 12)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the management of acute OIs in the setting of ART

A

1) OI occurs shortly after initiation (within 12 weeks) of ART
- Subclinical infection unmasked by early immune reconstitution (not failure of ART)
- Start treatment for the OI, continue ART

2) OI occurs > 12 weeks after initiation of aRT in patients with CD4 count > 200 cells/mm3 and suppressed HIV RNA
- May be difficult to determine whether IRIS or new OI due to incomplete immunity
- Start treatment for OI, continue ART, consider modifying Art if CD4 response to ART is suboptimal

3) OI in patient with immunologic and virology failure on ART - Clinical failure of ART
- Start treatment for OI, modify ART for better virologic control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

All are examples of ____ infections:

  • Mucocutaneous candidiasis
  • Pneumocystis carnii pneumonia (PCP)
  • Cryptococcosis
  • Histoplasmosis
  • Coccidiomycosis
  • Aspergillosis
A

fungal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Mucocutaneous candidiasis:

Usually caused by ______ _______, other species seen in advanced immunosuppresion

A

Candida albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Mucocutaneous candidiasis: | ______ and ______ candidiasis are common
Oropharyngeal and esophageal
26
Mucocutaneous candidiasis: | Most common in patients which what CD4 count?
<200 (but can occur at higher CD4 counts)
27
Vulvovaginal candidiasis (yeast infections) occur in who?
non-HIV infected women
28
Vulvovaginal candidiasis (yeast infections) may be more severe or recur more frequently in advanced ________
immunosuppresion
29
Mucocutaneous candidiasis: | Oropharyngeal = _____
thrush
30
Mucocutaneous candidiasis: | Describe pseudomembranous oropharyngeal (thrush)
-painless, creamy white plaques on buccal, oropharyngeal mucosa and/or tongue; can be scarped off eailsy
31
Mucocutaneous candidiasis: | Describe erythematous oropharyngeal (thrush)
patches on anterior and posterior palate or tongue
32
Mucocutaneous candidiasis: | What is another type of oropharyngeal (thrush)
angular cheilosis
33
Mucocutaneous candidiasis: | Describe esophageal
- Retrosternal burning or discomfort, odynophagia, fever | - Endoscopy - whitish plaques +/- mucosal ulceration
34
Mucocutaneous candidiasis: | Describe vaginal
creamy discharge, mucosal burning and itching
35
What is the drug of choice for treatment for mucocutaneous candidiasis?
Oral fluconazole for 7-14 days - effective and in some studies superior to topical therapy - more convenient and generally better tolerated compared to topical
36
List some other options for the treatment of mucocutaneous candidiasis ?
- Topical (Nystatin suspension, clotrimazole troches) - Itraconazole oral solution - Posaconazole oral solution
37
Mucocutaneous candidiasis: | Is routine primary prophylaxis recommended? Why/why not?
NO - very low attributable mortality - acute therapy is highly effective - can lead to disease caused by drug-resistant species - drug interactions - expensive
38
What is primary prophylaxis?
prevention BEFORE development of disease
39
What is secondary prophylaxis?
prevention of RE-OCCURRENCE (after treatment of OI)
40
What is PCP Pneumonia caused by?
Pneumocystis jiroveci | also called PCP - pneumocystis carinii
41
PCP Pneumonia: | _______ in the environment
Ubiquitous (present, appearing and found everywhere)
42
PCP Pneumonia: | Who is the initial infection caused in?
- Initial infection usually in early childhood | - 2/3 of healthy children have antibodies by age 2-4 years old
43
PCP Pneumonia: | May result from ?
reactivation or new exposure
44
PCP Pneumonia: | In immunosuppressed patients, possible ________ spread
airborne
45
What is the most common life threatening OI?
PCP Pneumonia
46
In advanced immunosuppression, treated PCP associated with ____% mortality
20-40
47
Who do the majority of PCP infections occur in?
The majority of PCP cases occur among patients who are unaware of their HIV infection or are not receiving ongoing HIV care or among those with advanced immunosuppression (CD4+ counts < 200)
48
Incidence of PCP has declined substantially with widespread use of _______ and ___.
prophylaxis and ART
49
Describe the clinical manifestation of PCP?
- Progressive exertion dyspnea, fever, nonproductive cough, chest discomfort - Hypoxemia: characteristic, may be mild or severe - Subacute onset, worsens over days-weeks (fulminant pneumonia is uncommon) Fulminant = sever/sudden onset - Chest exam may be normal, or diffuse dry rales, tachypnea, tachycardia (especially with exertion) - CXR - bilateral infiltrates - Definitive diagnosis requires demonstrating organism in sputum
50
PCP: | Untreated = ___% mortality
100%
51
Describe the treatment of PCP
- Treatment started before definitive diagnosis - 21 day treatment - DOC = TMP/SMX
52
What is the dose of TMP/SMX
15-20 mg/kg/day IV
53
Adjust dose of TMP/SMX for ?
Renal insufficiency
54
Adverse reactions with TMP/SMX
Adverse reactions (seen in 20-85% of patients with AIDS): rash, SJS, fever, leukopenia, thrombocytopenia, azotemia (nitrogen in blood), hepatitis, hyperkalemia
55
PCP treatment: | Who gets corticosteroids?
For moderate-severe disease (hypoxia) within 72 hours improved mortality
56
PCP treatment: | What corticosteroids and what dose?
Prednisone 40mg Bid days 1-5 then taper
57
PCP treatment: | What are some alternative therapeutic regimens for moderate-severe disease?
- Clindamycin-primaquine | - IV pentamidine
58
PCP treatment: | What are some alternative therapeutic regimens for mild-moderate disease?
- Oral TMP/SMX - Dapsone and TMP - Primaquine plus clindamycin - Atovaquone suspension
59
When do you start ART (antiretroviral therapy) after PCP treatment?
If not on ART then initiate, when possible, within 2 weeks of diagnosed PCP, if signs of clinical improvement
60
PCP primary prophylaxis: | Who should we initiate this in?
- patients with CD4 count < 200 - patients with history of oropharyngeal candidiasis - consider for those with CD4 <14% or AIDS defining illness
61
How long is PCP primary/secondary prophylaxis for?
For life (unless immune reconstitution on ART)
62
What is the preferred treatment for PCP primary/secondary prophylaxis?
TMP/SMX 1 DS tab daily or 1 SS tab daily
63
What is the alternate treatment for PCP primary/secondary prophylaxis?
TMP/SMX 1 DS tab three times/week
64
When should we discontinue PCP prophylaxis?
in patients on ART with sustained increase in CD4 count > 200 for > 3 months
65
When should you restart maintenance therapy for PCP prophylaxis?
-If CD4 count decreases to < 200 or -If PCP recurs at CD4 count > 200
66
All are examples of ______ infections: - Toxoplasma gondii encephalitis (TE) - Cryptosporidiosis - Microsporidiosis
parasitic
67
Toxoplasma gondii Encephalitis: | What is it caused by?
T gondii (a protozoa)
68
Toxoplasma gondii Encephalitis: | What is disease usually caused by?
reactivation of latent tissue cysts
69
Toxoplasma gondii Encephalitis: | Primary infection may be associated with ??
acute cerebral or disseminated disease
70
Toxoplasma gondii Encephalitis: | What is the primary infection acquired from?
tissue cysts in raw or undercooked meat or ingestion of sporulated oocysts (from cat faces) in soil, water or food
71
Toxoplasma gondii Encephalitis: | Is it transmitted from person-person?
No
72
Toxoplasma gondii Encephalitis: | Rarely occurs in patients with CD4 > ____
200
73
Toxoplasma gondii Encephalitis: | Primarily occurs in patients with CD4 < ____
50
74
Toxoplasma gondii Encephalitis: symptoms?
CNS: | -fever, headache, seizures (10%), focal neurological abnormalities (60-90%), mental status change, coma
75
Toxoplasma gondii Encephalitis: Dissemination may occur and cause ?
- retinochoroiditis (eye) - pneumonia (lung) - other organ involvement
76
Toxoplasma gondii Encephalitis: What imaging is involved?
CR, MRI of brain: multiple contrast-enhancing lesions, often with edema
77
Toxoplasma gondii Encephalitis: Detection of organism using ____ _____
brain biopsy (invasive)
78
Toxoplasma gondii Encephalitis: Almost all HIV+ patients with TE toxoplasmosis are positive for what antibody
IgG
79
Toxoplasma gondii Encephalitis: Preferred treatment regimen?
Pyrimethamine + Sulfadiazine + Leucovorin this is very expensive, why we don't use it in NA
80
Toxoplasma gondii Encephalitis: Alternate treatment regimen?
Pyrimethamine + Clindamycin + Leucovorin | does not protect against PCP so will need additional PCP prophylaxis
81
Toxoplasma gondii Encephalitis: Potential treatment regimen?
TMP/SMX can be considered an option if there is a valid reason not to use the preferred regimen
82
Toxoplasma gondii Encephalitis: Duration of treatment?
> 6 weeks, longer if extensive disease or incomplete response
83
Toxoplasma gondii Encephalitis: When should adjunctive corticosteroids be administered and what do you need to monitor?
Only if clinically indicated for treatment of cerebral swelling; monitor closely and discontinue ASAP. Monitor for development of other OIs
84
Toxoplasma gondii Encephalitis: When should anticonvulsants be administered?
to patients who have a history of seizures, but should not be administered as prophylactics to all patients
85
Toxoplasma gondii Encephalitis: Monitor for?
- Clinical improvement - Radiological improvement - Adverse effects
86
Toxoplasma gondii Encephalitis: Time of starting ART ?
No set recommendation but many will start within 2-3 weeks of toxoplasmosis diagnosis
87
Toxoplasma gondii Encephalitis: Who should get primary prophylaxis?
CD4 count < 100 and positive IgG T. Gondii serology
88
Toxoplasma gondii Encephalitis: What is the primary prophylaxis treatment?
TMP/SMX - 1 DS tab daily (also covers PCP)
89
Toxoplasma gondii Encephalitis: Alternative prophylactic treatment?
- TMP/SMX 1 DS tab three times/week - dapsone-pyrimethamine plus leucovorin (also covers PCP) - Atovaquone (with or without pyrimethamine/leucovorin also can be considered)
90
Toxoplasma gondii Encephalitis: Discontinue primary prophylaxis if?
- If CD4 count > 200 for > 3 months on ART | - Reintroduced if the CD4+ count decreases to <100-200
91
Toxoplasma gondii Encephalitis: What is the preferred treatment for secondary prophylaxis?
Pyrimethamine + Sulfadiazine + Leucovorin
92
Toxoplasma gondii Encephalitis: What is the alternative treatment for secondary prophylaxis?
Atovaquone +/- Pyrimethamine or sulfadiazine
93
Toxoplasma gondii Encephalitis: When should you discontinue secondary prophylaxis?
If completed initial therapy for TE and remained asymptomatic with regard to signs and symptoms of TE and have a sustained increase in their CD4+ counts of > 200 after ART (> 6 months)
94
Mycobacterium tuberculosis: | Co-infection as initial presentation or presents after starting _____ (IRIS)
HAART
95
Mycobacterium tuberculosis: | What is the treatment?
concomitant but staggered start of HAART in patient not already of HAART due to adverse due to adverse effects from medications and risk of severe IRIS - start of HAART based on CD4 count
96
Significant drug interactions between TB meds and ________
antiretrovirals
97
Where are MAC organisms?
everywhere in the environment - water, soil
98
How is MAC transmitted?
inhalation, ingestion or inoculation via the respiratory or GI tract
99
Who does MAC generally occur in?
among persons with CD4+ counts < 50
100
Without ART or chemoprophylaxis in AIDS patients incidence of disseminated MAC disease = ___%
20-40
101
What is the major risk factor for disseminated MAC
CD4 count < 50
102
Symptoms of MAC?
- Usually a disseminated multi organ infection - Localized manifestations: lymphadenitis (cervical or mesenteric), pneumonitis, pericarditis, osteomyelitis, skin or soft tissue abscesses, genital ulcers, CNS infection - Fever, night sweats, weight loss, fatigue, diarrhea, abdominal pain, anemia, neutropenia
103
How is MAC diagnosed?
culture of organism from blood, bone marrow, lymph node or other normally sterile tissue or fluid
104
Disseminated MAC: | Strategy for treatment
initial treatment followed by chronic maintenance therapy
105
Disseminated MAC: | What is the initial treatment?
>12 months | -At least 2 effective drugs, to prevent resistance
106
Disseminated MAC: | What is the preferred treatment?
Clarithromycin 500mg PO BID + Ethambutol 15 mg/kg PO daily (+/- Rifabutin)
107
Disseminated MAC: | What is the alternative treatment ?
Azithromycin 500-600mg PO daily + Ethambutol PO (+/- Rifabutin)
108
Disseminated MAC: | When do you start ART?
If not on ART then initiate ASAP after effective treatment
109
Disseminated MAC: | How long is maintenance therapy after completion of initial therapy ?
Lifelong (unless immune reconstitution on ART)
110
Disseminated MAC: | When should you consider discontinuation of secondary prophylaxis?
Consider discontinuation of secondary prophylaxis if treated > 12 months, no signs or symptoms of MAC, and sustained (>6 months) increase in CD4 count to > 100 cells on ART
111
Disseminated MAC: | When should you restart secondary prophylaxis ?
if CD4 count decreases to < 100
112
Disseminated MAC: | Indication ?
CD4 count < 50
113
Disseminated MAC: | Drugs ?
- Azithromycin 1200-1250 mg PO once weekly - Clarithromycin 500 mg po BID - Alternative: Rifabutin 300 mg PO daily
114
Disseminated MAC: | Discontinue primary prophylaxis in patient on ART when ?
CD4 count > 100 for > 3 months
115
GO OVER CASES
PROB WON'T BUT OKAY

Clinical 2 (Sam) (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions