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oral pathology > HIV oral manifestations > Flashcards

HIV oral manifestations Flashcards

1
Q

HIV virus type

A
  • ss-RNA virus
  • 2 types (HIV-1 worldwide, HIV-2 west Africa)
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2
Q

Eastern/Southern Africa how many people living with HIV

A

> 50% of people

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3
Q

where is the virus within the body

A

in most body fluids

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4
Q

how is HIV transmitted

A

male-to-male sexual contact > heterosexual contact > injection drug use

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5
Q

incidence rates of infection

A

blacks > hispanics > whites

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6
Q

occupational risk:

A

percutaneous (0.3%), mucous membrane (0.09%)

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7
Q

HIV target cells

A

CD4+ helper T cell mainly (also infects MACs)

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8
Q

how does HIV bind

A

through gp41 and gp120 with CD4 and CCR4 or CCR5 interaction

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9
Q

how does DNA get integrated into host genome

A

RNA is reverse transcribed into DNA which integrates into the host genome

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10
Q

what occurs with decrease in CD4+ T cells

A

cell lysis or latency occurs

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11
Q

cell lysis or latency leads to what

A

decreased response to viruses, fungi, encapsulated bacteria

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12
Q

HIV clinical presentation:

A
  • 1-6 weeks post exposure: acute retroviral syndrome (flu-like) followed by latency. *latency can be established with/in first few days of infection
  • months to ~10 yrs later: increased viremia, decreased CD4+ T cells leading to AIDS-related complex (ARC) and opportunistic infections
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13
Q

describe ARC

A

chronic fever, weight loss, diarrhea, oral candidiasis, herpes zoster and/or oral hairy leukoplakia (EBV)

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14
Q

what are the opportunistic infections

A
  • bacterial: mycobacteria
  • viral: CMV, HSV
  • fungal: penumocystis jiroveci (fungal pneumonia), cryptococcus meningitis
  • protozoal: CNS toxoplasmosis
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15
Q

what are the neurologic dysfunctions

A

seizures, dementia

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16
Q

how is AIDS diagnosed

A
  • screening test (enzyme immunoassay or rapid ab test) followed by Western blot
    —–> seroconversion 3-12 weeks post-expousre (p24 antigen capture used in this early window)
  • AIDS defined (serology + one or more of the following)
    1. CD4+ T cell count < 200/mL
    2. CD4+ T cell < 14% of total lymphocytes
    3. AIDS-defining condition
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17
Q

AIDS tx

A

combination antiretroviral therapy (cART) - target RT, protease, fusion, integrase, CCR5

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18
Q

why do we need to know H/N lesions

A
  1. oral lesions may be first sign of infection
  2. in HIV+ patients not receiving medication - indicates need for tx
  3. recognition in a HIV+ patient receiving tx may signal viral resistance to tx
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19
Q

what is the most common oral manifestation of HIV infection

A

oral candidiasis

20
Q

what are the oral candidiasis subtypes that have been seen

A

pseudomembranous-thrush, erythematous, chronic hyperplastic, angular cheilitis

21
Q

oral candidiasis tx

A

clotrimazole, fluconazole

22
Q

what do you do if you see recurrent oral candidiasis infections in undiagnosed patient

A

refer for testing

23
Q

describe Linear Gingival Erythema

A
  • red, linear band at the marginal gingiva that extends 2-3mm apically
  • spontaneous bleeding, petechiae may be noted
  • lack of response to improved oral hygiene
24
Q

cause of linear gingival erythema

A

reaction to subging. bacteria of unusual pattern of candidiasis has been suggested (most cases respond to antifungals)

25
Q

describe necrotizing ulvcerative gingivitis

A
  • similar to that seen in non-immunocompromised patients: loss of interdental papillae without bone loss, bleeding, pain, halitosis
  • may be seen in a setting of relatively few apparent local factors
26
Q

describe necrotizing ulcerative periodontitis

A
  • similar to NUG (pain, bleeding, edema) but with extensive bone loss
  • may be multifocal or generalized
  • may be seen in a setting of relatively few apparent local factors
  • don’t see deep pocketing due to gingival necrosis as bone is lost
27
Q

describe necrotizing stomatitis

A
  • extensive destruction of gingiva, periodontal bone, adjacent soft tissue and deeper osseous structures
28
Q

necrotizing stomatitis tx

A

extensive debridement, systemic antibiotics, close f/up - possible additional debridement

29
Q

describe hariy leukoplakia

A
  • most are HIV-infected (or other immunocompromised; rare in healthy patients)
  • non-removeable white plaques of the lateral tongue
30
Q

what is hairy leukoplakia caused by

A

EBV; often there is superimposed candidiasis

31
Q

hairy leukoplakia tx

A

no tx necessary; resolves if pt. is on effective cART

32
Q

describe Kaposi sarcoma

A
  • in US primarily associated with HIV infection with decreasing incidence
  • skin or visceral involvement, with 70% of AIDS-related KS having oral involvement (usually palate, gingiva or tongue)
  • reddish-purple, flat or nodular. usually multiple lesions noted
33
Q

what is kaposi sarcoma caused by

A

human herpes virus 8, high titers in saliva and oral/oropharyngeal tropic

34
Q

kaposi sarcoma tx

A

often regresses with cART. non-responsive lesions: topical therapy, excision, intralesional chemotx. 70% 5 yr survival

35
Q

describe persistent lymphadeopathy

A
  • generalized non-tender lymphadenopath
  • cervical lymph nodes are frequently affected, including posterior cervical nodes
  • other causes of lymphadenopathy (other infections: lymphoma) may have to be ruled out
36
Q

what is the most common malignancy in AIDS population

A

AIDS-related lymphoma

37
Q

describe AIDS-related lymphoma

A
  • usually extra-nodal (CNS or GI tract)
  • oral examples may resemble KS. also can involve bone (appears as diffuse bone loss)
  • many cases are associated with EBV
  • usually very aggressive with a poor prognosis (median survival of 3-4 months)
38
Q

describe salivary gland involvement

A
  • bilateral parotid enlargement is typically seen
  • due to lymphocytic infiltration of glandular tissue
  • accompanied by formation of lymphoepithelial cyst-like changes
  • xerostomia may be present
39
Q

what are the HIV-related viral infections

A
  • herpes simplex
  • varicella-zoster
  • EBV
  • human papillomavirus
40
Q

describe recurrent herpes simplex

A
  • represents reactivation of virus in most cases
  • lesions are more widespread, have an atypical pattern (persistent, painful, diffuse, shallow ulcerations)
  • must be txed with acyclovir or one of the acyclovir analogues
41
Q

describe herpes zoster

A
  • may see in younger than normal patients (< 40 yrs)
  • typical unilateral vesicles and ulcers following trigeminal nerve branches; may show cutaneous spread beyond the expected dermatome
  • intense pain, may see bone loss
42
Q

describe papillomavirus

A
  • seen with increased frequency intraorally in HIV+ patients
  • exophytic lesions, solitary or (more commonly) multiple, that may resemble routine squamous papilloma, condyloma or focal epithelial hyperplasia
43
Q

describe histoplasmosis

A
  • AIDS-defining illness
  • generally pulmonary, but dissemination to oral mucosa may occur
  • presents as non-healing, usually painful, ulcers
  • tx: may require IV amphotericin B
44
Q

describe aphthous-like ulcers

A
  • probable immune-mediated etiology
  • painful, persistent, may be solitary or multiple
  • may need to rule out infectious causes (HSV, EBV, CMV)
  • respond to topical corticosteroids
45
Q

describe mulluscum contagiosum

A
  • caused by pox virus
  • many more lesions develop compared to non-immunocompromised patient
  • facial skin is usually affected
  • lesions tend not to regress, unlike their normal course in immune competent person
46
Q

describe oral squamous cell carcinoma

A
  • HIV-infected patient have ~2x increased risk with greater risk with increasing immune suppression
  • same clinical appearance and tx
47
Q
A

oral pathology (7 decks)

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