CH7 - Viral Infections - HIV / AIDS Flashcards

(31 cards)

1
Q

What is the difference between HIV-1 and HIV-2?

A

HIV-1: worldwide distrubution, responsible for majority of cases

HIV-2: Western Africa, lower risk of transmission, slower disease progression

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2
Q

What was the first HIV publication about in 1981?

When was cART therapy introduced?

A

Pneumocystis jiroveci pneumonia in 5 men from LA (it took a few years to then see HIV as the cause) (It is today still one of the most common presentations leading to an AIDS diagnosis)

cART = 1996

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3
Q

Where are 70% of the worlds HIV infections?

A

Sub-Saharan Africa

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4
Q

What are the three main ways of transmission of HIV in the US? What body fluids can it be found in?

A

Male-to-male sexual contact (2/3 of annual infections)

heterosexual contact

IV drug use

most bodily fluids: serum, blood, saliva, semen, tears,
urine, breast milk, ear secretions, and vaginal secretions

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5
Q

Which cell is the primary target of HIV? Which glycoproteins are critical to this process?

A

Helper T4 cells…gp120, gp41

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6
Q

What other infection does acute HIV infection present like?

What are two oral signs of acute HIV infection?

A

infectious mononucleosis (LAD, sore throat, fever, maculopapular rash, etc)

  1. mucosal erythema
  2. focal ulcerations
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7
Q

What is the term for lymphadenopathy during latency in HIV patients?

A

Persistent Generalized Lymphadenopathy (PGL)

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8
Q

Oral candidiasis is not itself diagnostic of AIDS in an HIV patient, but if left untreated, how long does it usually take to reach AIDS after seeing oral candidiasis?

A

within 2 years

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9
Q

HIV patients: Erythematous candidiasis typically appears when the CD4+ lymphocyte count drops below ___ cells per mm3, whereas the pseudomembranous pattern usually develops when the count drops below ____ cells per mm3.

A

erythematous = 400

pseudomembranous = 200

Interesting! So the weaker the immune system the more pesudomemranous candidiasis. I guess this is also why erythematous candidiasis is so much more common in the general population?

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10
Q

What is the treatment of choice for HIV candidiasis patients without esophageal involvement and a CD4 count above 50?

What about with esophageal involvment and CD4 below 50, high viral load?

A

without esophageal involvement and a CD4 count above 50: Clotrimazole..nystatin is ineffective

with esophageal involvment and CD4 below 50, high viral load: fluconazole

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11
Q

What are the two cytologic buzzwords for OHL?

A
  1. “balloon cells” in the upper spinous layer

2. nuclear beading (margination of chromatin) in superficial epithelial cells

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12
Q

Where are cutaneous KS cases most often found? (2)

A
  1. face

2. lower extremities

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13
Q

What are the two clinical differentials for KS?

A
  1. bacilliary angiomatosis (cat-scratch bacillus)

2. lymphoma

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14
Q

Persistent generalized lymphadenopathy (PGL) is not itself diagnostic of AIDS in an HIV patient, but if left untreated, how long does it usually take to reach AIDS after seeing PGL?

A

5 years

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15
Q

What two viruses are the suspected culprits for both plasmablastic lymphoma and primary effusion lymphoma in HIV patients?

A

EBV and HHV8

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16
Q

Where does lymphoma in AIDS patients typically present?

A

extra nodal locations (4% oral presentation gingiva, palate, tongue)

17
Q

What are the three types of periodontal disease strongly associated with HIV?

A
  1. Linear gingival erythema
  2. NUG
  3. NUP
18
Q

What are common pathogens associated with necrotizing stomatitis? (extention of NUG onto the palate or alveolus)

19
Q

TB detection in HIV patients is difficult, what is the best way?

A

Liquid culture or PCR

20
Q

Which age group has a higher prevalence of HIV-associated salivary gland disease?

21
Q

Another one to add to the bilateral parotid swelling differential: HIV-associated salivary gland disease. What does it show on histology?

A

lymphocytic infiltration, hyperplasia of intraparotid

lymph nodes, and, in long-standing cases, lymphoepithelial cyst formation.

22
Q

HIV-associated salivary gland disease is considered a localized manifestation of what syndrome?

What is the triad of signs?

What is the treatment?

A

DILS: diffuse infiltrative lymphocytosis syndrome

  1. salivary gland enlargment
  2. LAD
  3. intersitial pneumonia

Oral prednisone and cART therapy

23
Q

What % of HIV patients have thrombocytopenia?

Not in Neville, but good to know: What is the threshold?

A

40%

Thrombocytopenia: normal range platelets 150K-450K. Emergency treatment <50K

24
Q

Persistence of active HSV infection for more than HOW LONG in a patient infected with HIV is one accepted definition of AIDS

25
HIV patients can present with unusual strains of HPV...what are 3 examples?
besides the usual's (6,11 for sqam paps and cond acuminata, 2 for VV's) HPV 7 (butchers warts) HPV 13,32 (Heck dz)
26
What is the most common deep fungal infection in AIDS patients?
Histoplasmosis How do Crypto and Candida fit into this?
27
What is the risk for HIV patients to develop oral or pharyngeal SCC compared to the general population?
2x
28
What is the most common method for HIV testing? How are positive and false positives verified?
antibody: enzymoe immunoassay (EIA) on blood, oral fluid (saliva? lol), and urine verifiy with Western blot
29
What is the AIDS diagnostic criteria? What are the 9 AIDS defining conditions that an Oral Pathologist may see or diagnose (there are 27 of them total)?
1. laboratory evidence of HIV plus any one of the following 2. CD4+ T lymphocyte count less than 200 per mL 3. CD4+ T lymphocyte percentage less than 14% of total lymphocytes 4. Documentation of an AIDS defining condition AIDS defining conditions: 1. Esophageal Candidiasis 2. Coccidiomycosis (Dissemniated/extrapulm) 3. Histoplasmosis 4. Cryptococcus 5. CMV 6. HSV chronic ulcer(s) more than 1 month duration 7. KS 8. Lymphoma (Burkitt, Immunoblastic) 9. TB
30
What is the term for paradoxical worsening of HIV patients after initiating cART during advanced stages of disease?
immune reconstitution syndrome (IRS)
31
What is the theory for why cART therapy is unable to cure HIV infection?
persistence of the virus in the peripheral blood and lymphoid tissues