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infectious disease > HIV related infections and complications > Flashcards

HIV related infections and complications Flashcards

1
Q

cryptococcal meningoencephalitis

A

invasive fungal infection caused by Cryptococcus neoformans seen in HIV pts
originates from lungs but can get to CNS and present with traditional meningitis symptoms

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2
Q

Treatment of cryptococcal meningoencephalitis in HIV pts

A

Needs yeast eradication and given in several phases: induction, consolidation and maintenance

Induction therapy: consists of 2 weeks of amphotericin B +/- flucytosine.

Consolidation: After CSF is clear can be switched to 8 weeks of fluconazole

Maintenance: Then 1 year of fluconazole therapy

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3
Q

When do you discontinue fluconazole or maintenance therapy in HIV pts who had cryptococcal meningoencephalitis?

A

after consolidation therapy are on fluconazole for 1 yr post infection. However can be discontinued once CD4 >100 with antiretroviral therapy

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4
Q

When to do serial LP in HIV pts w/ cryptococcal menigoencephalitis ?

A

when there is increased ICP (CSF>200 mmHg) and (seen in 50% of pts) AND headache, AMS, visual hearing loss and cranial nerve deficits

Goal to reduce ICP <200 or by 50% and decreases mortality

If do not respond, need to get ventriculostomy drain.

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5
Q

Is there any role for acetazolamide to lower ICP in cryptococcal

A

No.

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6
Q

If newly diagnosis HIV pt without ART who has cryptococcal meningoencephalitis, when do you start antiviral therapy?

A

wait 2-10 weeks after starting antifungal therapy to treat HIV because thought is that if started right away the ART can cause IRIS (immune reconstitution inflammation syndrome)

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7
Q

Drugs that interfere with folic acid metabolism

A

methotrexate
phenytoin
pyrimethamine
trimethoprim

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8
Q

treatment of systemic CNS toxoplasmosis

A

sulfadiazine and pyrimethamine

if unable to tolerate sulfadiazine can take clindamycin (preferred) over atovaquone or azithromycin.

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9
Q

longterm side effect of pyrimethamine

A

inhibits dihydrofolate reductase (similar to methotrexate and trimethoprim)

Blocks dividing cells and can first manifest as bone marrow suppression.

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10
Q

How to treat folic acid deficiency while on pyrimethamine

A

leucovorin - reduced folic acid that bypasses the blocked enzyme and has equivalent activity to folic acid.

Should be given concurrently with pyrimethamine to prevent leukopenia, megaloblastic anemia, and thrombocytopenia

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11
Q

do we give anti seizure medications to pts who have toxoplasmosis of CNS?

A

no unless they have seizure history.

Also try to avoid phenytoin with pts who are on pyrimethamine

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12
Q

PCP prophylaxis

A

bactrim or TMP SMX but if already treated with sulfadiazine and pyrimethamine for CNS toxoplasmosis - no need for additional coverage

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13
Q

toxoplasma encephalitis clinical presentation

A

fever, headache, confusion, focal neurological deficits/seizures

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14
Q

primary CNS lymphoma presentation

A

fever, night sweats, weight loss (80% of pts) , confusion, memory deficits, aphasia, and motor deficits, and focal neurological deficits, seizures

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15
Q

progressive multifocal leukoencephalopathy PML presentation

A

rapidly progressive neurological deficits (confusion, motor deficits, ataxia, aphasia, visual symptoms, and cognitive impairment)

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16
Q

lab findings with toxoplasma encephalitis

A

CD4 count<100

toxoplasma IgG antibodies

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17
Q

lab findings with primary CNS lymphoma

A

CD4 count<50

positive CSF cytology or Epstein Barr virus polymerase chain reaction positivity

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18
Q

lab findings for PML (progressive multifocal leukoencephalopathy)

A

CD 4 count <200

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19
Q

imaging studies for toxoplasma encephalitis

A

multiple ring enhancing lesions with mass effect and edema

commonly seen involving the basal ganglia

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20
Q

imaging studies for primary CNS lymphoma

A

solitary enhancing lesions with mass effect and edema
larger lesions >4cm compared to toxoplasma encephalitis. generally can involve the corpus callosum, periventricular or periependymal areas.

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21
Q

PML imaging findings:

A

bilateral usually asymmetrical white matter lesions

no mass effect, enhancement or edema

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22
Q

brain abscess etiology

A

direct extension of a dental sinus or ear infection and hematolgenous dissemination tends to be drom IVDA and endocarditis that leads tomultiple findings.

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23
Q

bacteria that can cause a brain abscess are:

A

streptocuccus and staph aureas but HIV pts can have listeria, nocardia, fungal and parasitic (toxoplasmosis)

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24
Q

unilateral headache, focal neurological deficits, seizures, papilledema and see single or multiple ring enhancing lesions at the grey white matter junction and significant vasogenic edema and mass effect

A

brain abscess- may not see systemic fever or sepsis in brain abscess

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25
Q

treatment of brain abscess

A

antibiotics and surgical drainage.

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26
Q

HIV associated encephalopathy

A

affects whole brain and see progressive dementia and brain atrophy on CT. No ring enhancing lesions

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27
Q

what causes PML?

A

JC virus reactivation and this happens with CD4 counts <200 and we see multifocal areas of white matter demyelination without mass effect, edema or enhancement.

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28
Q

Prophylaxis for PCP in HIV

A

bactrim

alternate therapies:
dapsone
atovaquone
pentamidine

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29
Q

when is HIV pt at risk for PCP infection

A

CD4 count <200
OR oropharyngeal candidasis is present
or history of PCP infection

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30
Q

when is HIV pt at risk for toxoplasma gondii infection?

A

CD4 count <100 and positive IgG antibody

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31
Q

prophylaxis against toxoplasma gondii in HIV pt

A

bactrim

alternate therapies:
dapsone + pyrimethamine + leucovorin (folinic acid)

atorvaquone + pyrimethamine + leucovorin

remember need leucovorin to prevent toxic effects of methotrexate or pyrimethamine.

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32
Q

when is a HIV pt at risk for histoplasma capsulatum

A

CD4 count <150 and in endemic area

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33
Q

prophylaxis against histoplasma capsulatum in HIV pt

A

itraconazole

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34
Q

when is a HIV pt at risk for varicella zoster virus infection?

A

close contact with person with chicken pox or shingles and no history of prior dx or negative antibody to VSV

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35
Q

prophylaxis against VZV in HIV pt?

A

variZIG (varicellar immunoglobulin) or IVIG administered within 4 days of exposure.

36
Q

when do we do prophylaxis against PCP

A

CD4 <200 or if pt has oropharyngeal candidasis.

37
Q

when can HIV prophylaxis be stopped

A

when ART improves CD4 count >200 for 3 months

reduces risk for drug toxicity and interactions or developing drug resistant organisms.

38
Q

Do we provide MAC prophylaxis still for HIV pts CD4<50?

A

no we do not given low risk for MAC.

among pts taking ART and lack of differences in MAC dx outcomes in ppl who took prophylaxis and those who didn’t

previously azithromycin was used.

39
Q

prophylaxis for coccidiomycosis

A

generally not recommended except in those that live or travel to endemic regions - can be screened twice annually with serological testing.

If seropositive and CD4<250 can give fluconazole prophylaxis if there is no dx manifestations

40
Q

most common lymphomas related to HIV

A

See Hodgkin lymphoma and diffuse large B cell (non hodgkin lymphoma)

Seen with CD4 count is <100

41
Q

poorly controlled HIV, marked body cavity lymphadenopathy and bone lucency

A

non hodgkin lymphoma

4% of HIV pts have lymphoma at time of diagnosis ..

42
Q

risk factors for lymphoma with HIV

A

direct effects of HIV, immunosuppressive state, co infection with EBV virus

43
Q

what helps to decrease incidence of lymphoma in HIV

A

HAART prevents severe immunosuppression.

44
Q

CMV encephalitis happens when CD4 count is …?

A

CD4 count is <50 cells.

45
Q

CMV encephalitis presentation

A

see dementia, delirium and focal neurological deficits

46
Q

MRI of CMV encephalitis shows

A

see diffuse micronodular encephalitis or periventricular inflammation (ventriculoencephalitis)

47
Q

skin concerns that can be 1st manifestation of a HIV infection?

A

sudden onset severe psoriasis

recurrent herpes zoster

disseminated molluscum contagiosum

severe seborrheic dermatitis.

48
Q

AIDS nephropathy (kidney dx) also is associated with

A

associated with significant proteinuria

49
Q

common causes of esophagitis in HIV pts?

A

candida lesions
CMV lesions
HSV lesions

50
Q

clinical features of candida species causing esophagitis in an HIV pt

EGD findings are:

Biopsy results are :

A 
involves the entire esophagus
pain with solids more than liquids
often associated with oral thrush
EGD: white exudate (cottage cheese esophagus)
Biopsy: pseudohyphae in mucosa
51
Q

clinical features of CMV causing esophagitis in an HIV pt

EGD findings are:

Biopsy results are :

A

odynophagia and substernal chest pain

EGD: sharply demarcated, LINEAR UCLERS in distal 1/3 of esophagus

Biopsy: intranuclear inclusions (OWL eyes)

52
Q

clinical features of HSV causing esophagitis in an HIV pt

EGD findings are:

Biopsy results are :

A

usually has oral lesions with abrupt onset
odynophagia and substernal chest pain

EGD: well circumscribed SHALLOW ulcers
can see other HSV infections elsewhere (herpes labialis)

Biopsy: stains positive for HSV and viral culture

53
Q

Treatment of candida esophagitis in an HIV pt?

A

antifungal therapy (fluconazole)

54
Q

Treatment of CMV esophagitis in an HIV pt?

A

IV ganciclovir

55
Q

Treatment of HSV esophagitis in a HIV pt?

A

acyclovir

56
Q

ulcerative esophagitis in HIV pt is seen with these pathogens

Typical presentation

Next step of management.

A

Seen due to viral infections like: CMV and HSV

retrosternal pain and fevers can occur, severe odynophagia, no typical findings of candida - oral thrush

needs endoscopy with culture and biopsy instead of empiric tx for candida

57
Q

Complications of HSV ulcerative esophagitis

A

can lead to bleeding and tracheoesophageal fistula formation

58
Q

CMV esophagitis often happens with (this other presentation)

A

concurrent retinitis which can lead to blindness.

59
Q

PCP pneumonia presentation

A

subacute course of dyspnea, dry cough and fever is classic.
Can have chest pain, malaise, weight loss, headache, night sweats, chills and fatigue

advanced HIV/AIDS pts 6-7% can be asymptomatic

60
Q

Does lack of fever exclude PCP pneumonia?

A

No. It just means it’s less likely a bacterial or mycobacterial source

61
Q

what is seen on labs with 90% of HIV pts who have PCP pneumonia?

A

LDH levels >50 above baseline.

LDH>450 is predictive of PCP rather than a pulmonary process.

62
Q

what is seen on the arterial blood gas of PCP pneumonia pt?

A

hypoxemia and increased alveolar arterial oxygen gradient and respiratory alkalosis

63
Q

what is seen on CXR with PCP pneumonia?

A

see thinned walled cavitary lesions. Spontaneous pneumothorax develops in 5% of pts.

Pneumothorax likely due to rupture of cystic lesions that may present in active dx

64
Q

what are side effects of bactrim?

A

skin - Steven Johnson syndrome, TEN (toxic epidermal necrolysis) exfoliative dermatitis

Hematological: megaloblastic pancytopenia (folate deficiency), can see G6PD deficiency - getting hemolytic episode.

Renal: hyperkalemia, impairs tubular secretion of Cr without affecting GFR
see crystalluria
interstitial nephritis

65
Q

who is more sensitive to side effects of bactrim?

A

HIV positive pts 15% of pts with HIV can see SJS, TENs, and exfoliative dermatitis.

66
Q

candida esophagitis in HIV pts will have these symptoms:

A

involves entire esophagus, pain with solids more than liquids
often seen with oral thrush
EGD: white exudate or cottage cheese esophagus
biopsy:pseudohyphae in mucosa

67
Q

Treatment of candida esophagitis?

How long is treatment?

Do we use nystatin for treatment?

A

antifungal with fluconazole for 14-21 days

Systemic therapy is required.

Topical treatment with nystatin swish and swallow is only meant for people who don’t have HIV and there are high rates of failure.

68
Q

CMV esophagitis will have these symptoms:

A

odynophagia and substernal chest pain

EGD: shows sharply demarcated linear lesions in distal 1/3 of esophagus

biopsy: see cells with intranuclear OWL eye inclusions

69
Q

Herpes simplex HIV esophagitis will have these symptoms:

A

usually oral lesions with abrupt onset
odynophagia and substernal pain

EGD: well circumscribed shallow ulcers
Biopsy: stains positive for HSV and viral culture

70
Q

treatment of HSV esophagitis:

A

acyclovir

71
Q

Treatment of CMV esophagitis:

A

IV ganciclovir

72
Q

if HIV pt with white plaques and angular cheillitis has signs of oral thrush you should also think that:

A

he has candidal esophagitis and treat with fluconazole

73
Q

if there’s no oral thrush on exam, does that mean that HIV pt with odynophagia doesn’t have candidal esophagitis?

A

no. 18% don’t have oral thrush and still have candidal esophagitis.

74
Q

if empiric treatment for candidal esophagitis fail to improve symptoms what must be done next?

A

get EGD and biopsy.

75
Q

pt has new diagnosis of HIV and CD4 level is 730. He is a RN and from Ecuador. He has three birds and one cat. What is he at greatest risk for in terms of disease? histoplasmosis, Crytpococcus, PCP, toxoplasma gondi or TB

A

TB- because his CD4 count is 730 so not at risk for cryptococcus neoformans, histoplasmosis, PCP, or Toxoplasma gondii

He is a RN and from Ecuador.

TB co infection with HIV can happen at ANY CD4 level and hsould be considered. Needs testing for latent TB

76
Q

How do HIV pts get cryptococcus neoformans infection?

when are they susceptible to infection?

What kind of infection do they get?

A

yeast transmitted from inhalation of bird feces. (remember the pigeons and doves ceremony for HIV pts)

Only susceptible when CD4 count is <200 and typically see disseminated cryptococcal dx or meningoencephalitis

77
Q

Where do HIV pts get histoplasma capsulatum?

At what CD4 count are they susceptible to infection?

A

dimorphic fungus that can develop into disseminated dx in AIDS. Seen with bird or bat feces. endemic to ohio river valley

Seen when CD4<150

78
Q

How do HIV pts get PCP or pneumocystis carinii (jirovecii)?

At what CD4 count are they susceptible to infection?

A

environmental fungus that is inhaled. Can get primary infection as a child but remain asymptomatic.

Seen when CD4<200

79
Q

how to HIV pts get toxoplasma gondii?

At what CD4 count are they susceptible to infection?

A

parasite found in cat stools

oocytes remain dormant but can reactivate and cause neurological dx

seen when CD4 <100

80
Q

what must be checked prior to starting dapsone as second line prophylaxis for PCP?

A

CD4< 200 need PCP prophylaxis

if using 2nd line dapsone need to check for G6PD deficiency prior to starting.

81
Q

poorly controlled HIV
hypoxemic and CXR with bilateral infiltrates
normal ventricular function and valvular function

A

Think PCP or PJP

82
Q

diagnosis of PCP

A

bronchoscopy

83
Q

if pt has PCP and has hypoxemia <70 mmHg what do you give him?

A

steroids

bactrim, clindamycin and primaquine or dapsone for 21 days

84
Q

Bacillary angiomatosis

A

cat scratch dx

seen in untreated HIV pts

fever, weight loss, classic exophytic papules that bleed when traumatized

see hemorrhagic angiomas of liver.

cats are vector and transmission happens with scratches, bites, infected feces.

diagnosis is with biopsies.

85
Q

what virus causes Kaposi’s sarcoma in HIV pts?

A

HHV 8

infectious disease (52 decks)

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