HIV-Cutaneous Manifestations Flashcards

1
Q

Cutaneous manifestations CD4>500

A

Oral hairy leukoplakia

Acute retroviral syndrome

Vaginal candidiasis

Seb derm

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2
Q

Cutaneous manifestations CD4 250-500

A

Thrush

Herpes zoster

Severe psoriasis

Eruptive atypical melanocytic nevi and melanoma

Kaposis

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3
Q

Cutaneous manifestations CD4 50-250

A

Severe seb derm

eosinophilic folliculitis

Mollusca (extensive)

Disseminated cryptococcus, NTM, histo, cocci, HSV, Mollusca

Non-hodgkins lymphoma

Bacillary angiomatosis

Botryomycosis

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4
Q

Cutaneous manifestation CD4 <50

A
  • Erosive HSV (large, non-healing)
  • papular pruritic eruption
  • Giant mollusca
  • Perianal CMV ulcers
  • Major apthae
  • MAC
  • Acquired icthyosis
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5
Q

Diseases at CD4<200 (non derm) and prophylaxis

A

PJP

Prophylaxis: Septra (1 DS tab)

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6
Q

Diseases at CD4<100 and prophylaxis

A

Toxo

Ppx: Septra (2x dose)

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7
Q

Diseases at CD4<50

A

MAC (Abdominal syndrome!)

Ppx: Azithromycin

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8
Q

Bacterial pneumonias in HIV with CD<200

A

Legionella and staph <100

Psuedomonas and aspergillosis <50

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9
Q

Pathophys HIV infections and associated drug targets

A
  1. Binding to CD4+ cell via a few receptors including CCR5 or CXCR4 (CCR5 inhibitor)
  2. Fusion with plasma membrane (fusion inhibitor)
  3. RNA-→ DNA via reverse trasncriptase (Nucleoside RTI)
  4. DNa incorporated into host DNA via integrase (integrate inhibitor)
  5. Then can replicate and produce more virus, proteases further process the proteins for virus replication (protease inhibitors)
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10
Q

When does acute retroviral syndrome occur after inoculation?

A

4-6 weeks after

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11
Q

How long doses it take ofor CD4 counts to drop?

A

Initial infection results in a reduction in circulating CD4 + T cells, which is followed by a recovery to nearly normal levels and a subsequent slow fall of about 50 to 100 cells/mm 3 per year.

-In contrast, the CD4 + T cells residing within the gastrointestinal tract are rapidly depleted early on.

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12
Q

chronic inflammation in HIV patients due to?

A
  • low grade HIV replication
  • recurrent infections and re-activations
  • immune response to HIV
  • impaired mucosal integrity and bacterial translocation
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13
Q

Clinical features of acute retroviral syndrome

A

fever, headache, myalgia, arthralgia, pharyngitis, night sweats, x 14 days ash

  • morbilliform eruption that is generalized, face and trunk predominantly, 4-5 days
  • occasionally can get oral and anal ulcers
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14
Q

Infectious complications HIV (list)

A
  1. Viral
    1. HSV
    2. VZV
    3. Molluscum
  2. Bacterial
  3. Fungal
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15
Q

How is HSV different in HIV?

A
  • more persistent, frequent, larger/deeper/more extensive, non-healing
  • can occur in mobile, unattached oropharynx and esophagus
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16
Q

How to test for HSV

A
  • Scrape ulcer edge for PCR, DFA (direct fluorescent ab) or culture
  • Skin bx for Tzank smear
17
Q

Treatment HSV

A

higher rates (5%) resistance due to low thymidine kinase activity in HSV.

May need to treat longer, until all lesions healed

18
Q

Alternatives to acyclovir if resistant? and why do they work?

A

Foscarnet, cidofovir, imiquimod

*don’t rely on thymidine kinase activity

19
Q

How is VZV in HIV?

A
  • much higher risk getting and reactivation of zoster
  • Tend to get multiple lesions over longer period time
  • more lesions, longer to heal
  • lesions tend to be multiple dermatomes, disseminated lesions, hyperkeratotic verrucous plaques or chronic non healing ulcers
  • more likely to develop systemic involvement (pneumonitis, hepatitis, encephalitis)
20
Q

Treatment VZV

A

Acyclovir until lesions resolve

VZV immunoglobulin within 10 days exposure if non immune

21
Q

Molluscum in HIV

A

LARGE molluscum, widespread, persistent, on the face

22
Q

Treatment molluscum

A

Destructive

With ART (or can re-appear with IRIS)

Cidofovir

23
Q

What do you need to r/o with molluscum in HIV?

A

Disseminated fungal

Cryptococcus

24
Q

How does HPV presenting in HIV-infected individuals?

A

Multiple, coalescent and extensive: Common warts, condyloma acuminata, squamous intra-epithelial neoplasia and carcinoma.

Higher incidence high risk anogenital HPV and CIN (cervical) and higher risk progression to carcinoma

25
Q

AEDV?

A

Acquired epidermodysplasia verruciformis

hypopigmented to pink tinea versicolor-like lesions and numerous flat-topped papules that are due to HPV-5, -8, and other β HPV types

26
Q

Effect of ART on HPV?

A

Does not tend to clear them or prevent occurrence (can also represent IRIS)

MAY prevent progression to AIN or CIN

27
Q

What is oral hairy leukoplakia caused by?

A

EBV