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MED COMP PTS > HIV/AIDS pts > Flashcards

HIV/AIDS pts Flashcards

1
Q

discovery of HIV

A

The human immunodeficiency virus (HIV) was first
isolated in 1983 and was retrospectively identified as
the cause of acquired immunodeficiency syndrome
(AIDS; reported 1981)

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2
Q

HIV family

A

HIV is a non-transforming retrovirus of the lentivirus subfamily.
* Two main subtypes, HIV-1 and HIV-2, based on
genetic and antigenic differences, and many strains of
each

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3
Q

more common form of HIV

A

HIV-1 being more common (overall) particularly in
sub-Saharan Africa, while HIV-2 is more prevalent in
West Africa and associated with slower disease course

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4
Q

Since the onset of the worldwide pandemic, more than ___________-people have been infected with HIV, of whom approximately _________ have died because of
AIDS.

A

Since the onset of the worldwide pandemic, more than 70,000,000 people have
been infected with HIV, of whom approximately 35,000,000 have died because of
AIDS.

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5
Q

how many new HIV infections per year

A

2.7mil

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6
Q

what region has the highest % of the total HIV infected individuals

A

eastern/south africa (54%)

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7
Q
  • Approximately _________ people in the U.S. are living with HIV today.
A
  • Approximately 1.2 million people in the U.S. are living with HIV today.
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8
Q

CDC estimate for new HIV infections per year in US

A

38,000

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9
Q

male vs female rate of infection in the US

A

the rate for males (22.1) was 5 times the rate for females (4.8)

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10
Q

HIV infection by age groups

A

By age group, in 2018, the number of new HIV diagnoses was highest among people aged 25-44

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11
Q

single greatest risk factor of HIV

A

male-to-male sexual contact remains the
largest single risk facto

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12
Q

rise in HIV infection in what demographic

A

greater proportion of cases arising in blacks/African Americans, Hispanics/Latinos, females, and heterosexuals.
* Although blacks/African Americans represented
only about 14% of the United States population,
they accounted for 44% of new HIV infections.

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13
Q

what region is HIV most prevalent in the US

A

south

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14
Q

body fluids for HIV transmission

A
  • Blood, semen, breast milk, and vaginal secretions are the main fluids that have been shown to be associated with transmission of the virus. HIV can also be found in tears, saliva, cerebrospinal fluid, amniotic fluid, and urine
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15
Q

How are body fluids used to transmit HIV

A

Transmission of HIV is by exchange of infected bodily fluids predominantly through intimate sexual contact and by parenteral means. (Sharing needles and blood transfusions, organ transplants etc.)

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16
Q

where can HIV infection occur? what can aid in this?

A
  • HIV infection can occur through oropharyngeal, cervical, vaginal, and gastrointestinal mucosal surfaces, even in the absence of mucosal disruption.
  • Infection is particularly aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation.
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17
Q

The most common method of sexual transmission in the United States is:

A

The most common method of sexual transmission in the United States is anal intercourse in men who have sex with men (MSM), in whom the risk of HIV infection is 40 times higher than in other men and in women

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18
Q

heterosexual transmission

A

Heterosexual transmission (male to female or female to male) is the second most common form of transmission in the United States but accounts for 80% of the world’s HIV infections.

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19
Q

transmission thru needles

A

third most common route

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20
Q

The risk of transmission from a blood transfusion is estimated to be less than:

A

less than 1 in 1 million because of current screening measures

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21
Q

children/casual contact transmission

A

Children (< 13 yr) usually through perinatal exposure (mother to infant).
Casual contact has not been demonstrated as a means of transmission.

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22
Q

HIV oral transmission

A
  • Transmission by oral fluids is somewhat controversial and rarely documented.
  • Saliva contains a number of HIV inhibitory factors, which appear to reduce the ability of the virus to infect its target cells.
  • The presence of erosions, ulcerations, and hemorrhagic inflammatory pathoses (e.g., gingivitis, periodontitis) may predispose an individual to oral transmission.
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23
Q

HIV structure

A

enveloped single stranded RNA virus

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24
Q

HIV key antigenic components

A

gag, pol, env

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25
Q

Gag

(HIV ag)

A

processed to matrix and other core proteins to determine core
p17, p24 (capsid), p7

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26
Q

Pol

(HIV)

A

reverse transcriptase, RNase H and integrase functions
p66/51 (RT), p32 (IN), p11 (PR)

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27
Q

other HIV antigens

A

two regulatory proteins (Tat and Rev) that are essential for viral replication, and four accessory proteins (Nef, Vif, Vpu, Vpr).

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28
Q

HIV cell cycle stages

A

Entry>Replication> Release

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29
Q

HIV entry

A
  • HIV primarily infects cells with CD4 cell-surface
    receptor molecules (CD4+ T helper lymphocytes
    mainly) at the site of HIV entry.
  • Infection is aided by Langerhans cells in mucosal
    epithelial surfaces which can become infected
    delivering HIV to underlying T cells, ultimately
    resulting in dissemination to lymphoid organs
  • The virus uses CD4+ cells to gain entry by fusion
    with a susceptible cell membrane or by
    endocytosis (with the help of co-receptors
    CXCR4 and CCR5)
  • The probability of infection depends on both the
    number of infective HIV virions in the body fluid
    which contacts the host and the number of cells
    with appropriate CD4 receptors available at the
    site of contact.
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30
Q

HIV entry picture

A
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31
Q

CD4+ cells capable of being infected

A

T-helper lymphocytes, Langerhans,
macrophages, and some dendritic cells

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32
Q

HIV replication

A
  • Once within the cell, the viral particle uncoats from its spherical envelope to release its RNA.
  • The enzyme product of the pol gene, a reverse transcriptase that is bound to the HIV RNA, synthesizes linear double-stranded cDNA that is the template for HIV integrase.
  • It is this HIV proviral DNA which is then inserted into the host cell genomic DNA by the integrase enzyme of the HIV.
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33
Q

HIV replication diagram

A
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34
Q

HIV release

A
  • Just before the budding process, HIV protease cleaves Gag proteins into their functional form which get assembled at the inner part of the host cell membrane, and virions then begin to bud off.
  • Nucleocapsid (NC) protein interacts with the RNA within the capsid
  • Capsid (CA) protein surrounds the RNA of HIV
  • Matrix (MA) protein surrounds the capsid and lies just beneath the viral envelope.
  • Release of HIV from the host cell occurs in several steps.
  • The cells HIV selects for replication are soon “swell and burst” by caspase-3-mediated apoptosis (~5%), the remaining >95% of quiescent lymphoid CD4 T- cells die by caspase-1-mediated pyroptosis triggered by abortive viral infection.
  • The spectrum of HIV disease changes as CD4+ cell count declines.
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35
Q

Seroconversion

A

transition from the point of viral infection to when antibodies of the virus become present in the blood (circulating antibodies).

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36
Q

The CDC Staging of HIV Infection in Adults and Adolescents

A

stage 1, 2, 3 (full blown AIDS)

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37
Q

stage 1

timeframe and symptoms

A
  • During the first 2 to 6 weeks after initial infection with HIV, ~70% of patients develop an acute flulike syndrome marked by viremia (acute seroconversion syndrome) that may last 10 to 14 days (sometimes up to 4 weeks). Others may not manifest this symptom complex
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38
Q

stage 1 symptoms

how many actually seek care?

A

Symptomatic persons often develop mononucleosis-like symptoms: lymphadenopathy, fever, pharyngitis, weakness, diarrhea, nausea, vomiting, myalgia, headache, weight loss, and a skin rash (roseola-like or urticarial). Only an estimated 20% of symptomatic persons seek medical attention

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39
Q

CD4 count in stage 1

A

A concomitant transient fall in CD4+ cells occurs along with high titers of plasma HIV, but patients do not develop evidence of immunosuppression (>500 cell/ml; CD4+ cell count tend to return toward normal levels after acute symptoms

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40
Q

Ab development in HIV stage 1

A

CD4 drop is usually followed by developing antibodies (anti-gag, anti-gp120, anti-p24) between weeks 6
and 12. A few may take 6 months or longer to achieve seroconversion particularly in patients without acute symptoms. (6 weeks – 6 months, 97% within the first 3 months of infection)

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41
Q

The severity of the initial acute infection with HIV (i.e., level of viremia) is predictive of:

A

The severity of the initial acute infection with HIV (i.e., level of viremia) is predictive of the course the infection will follow. Generally, the longer the acute infection lasts the earlier patients develop AIDS

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42
Q

Latent asymptomatic period

how long can it last

A

continuum of stage 1; asymoptomatic stage 2
Can last up to 8–10 years.

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43
Q

latent asym period viral activity

A
  • The virus disseminates throughout lymphoid tissue, incubates, replicates (several thousand copies), and alters many physiologic processes, resulting in hyperimmune activation, persistent inflammation, and impaired gut function and flora.
  • Evolution of the virus within its host to generate closely related yet distinct mutant viruses that serve to evade the surveying immune response and circulating
    antibodies
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44
Q

latent asym CD4 count and IS ability

A

There is a progressive decline in immune function evident as progressive depletion of CD4+ cell count (CD4+ lymphocytes >500 cells/μL) & slow but usually progressive increase in viral load

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45
Q

non-progressors of the latent asym period

A

<1% are non-progressors and maintain a low viral load.
* Silent clinically except for persistent generalized lymphadenopathy (Up to 70% of patients).

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46
Q

stage 2 can last:

A

1-3 yrs

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47
Q

stage 2
s/s progression?
CD4?
viral load?
plattets?

A
  • Signs and symptoms increase as the CD4+ count drops below 500 cells/μL and approaches 200 cells/μL (often between 200 and 300/μL)
  • Viral load continues to increase.
  • Platelet count may decrease in about 10% of patients
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48
Q

stage 2 s/s?

A

Any or a combination of the following:
* Persistent generalized lymphadenopathy
* Fungal infections
* Vaginal yeast and trichomonal infections
* Oral hairy leukoplakia (OHL)
* Herpes Simplex Viruses (HSV-1 & HSV-2)
* Herpes Zoster (VZV)
* HIV-related retinopathy
* Constitutional symptoms: fever, night sweats, fatigue, diarrhea, weight loss, weaknes

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49
Q

stage 3

susceptiable to?

A

AIDS
* When the CD4+ count drops to below 200 cells/μL (also high viral load) or documentation of an AIDS-defining condition, the person has AIDS and is susceptible to opportunistic infections and maliganacies

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50
Q
  • Opportunistic infection(s) of AIDS
A

Pneumocystis jiroveci pneumonia, cryptococcosis, tuberculosis, toxoplasmosis, histoplasmosis, etc

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51
Q

plattets and PMN with AIDs

A

may be low

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52
Q
  • CD4+ cell count <50/μL at high risk for:
A

lymphoma and death

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53
Q

malignancies associated with AIDS

A

Kaposi sarcoma, Burkitt lymphoma, non-
Hodgkin lymphoma, primary CNS lymphoma, invasive
cervical cancer, carcinoma of rectum, slim (wasting)
disease

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54
Q

AIDS death usually due to

A

wasting, opportunistic infection, or malignancies.

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55
Q

CD4/8 ratio

A

CD4/CD8 ratio reflects immune system health. A normal ratio is between 1 & 4.

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56
Q

CD4/8 counts with HIV infection

when are these done?

A

CD4+ and CD8+ cell counts should be performed at the time of HIV diagnosis and then every 3 to 4 months

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57
Q

types of HIV testing

A
  • Nucleic acid tests (NATs)
  • Antigen/antibody tests
  • Antibody tests
  • HIV tests are typically performed on blood or oral
    fluid. They may also be performed on urine
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58
Q

NA HIV tests:
* Detect?
* Polymerase chain reaction (PCR)–based assays of the viral RNA is performed to determine if?
*** Detect HIV when?
* routinely used?
* *The greatest viral load is found when?

A
  • Detect the actual virus in the blood.
  • Polymerase chain reaction (PCR)–based assays of the viral RNA is performed to determine if a person has HIV or the viral load in the blood (i.e., degree of viremia)
    and monitor response to therapy.
    * Detect HIV sooner (superior) than other types of tests.
  • More expensive and not routinely used.
  • Detection ranges are from 40 copies/mL to more than 750,000 copies/mL. The greatest viral load is found during the first 3 months after initial infection and during late stages of the disease
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59
Q

Ag/Ab tests for HIV

A
  • Detect both HIV antibodies and antigens in blood
    samples.
  • In HIV-infected individuals, p24 is produced even before antibodies develop.
  • Antigen/antibody tests are recommended for testing
    done in labs and are now common in the United
    States.
  • This lab test involves** drawing blood from a vein.
    There is also a rapid antigen/antibody test available
    that is done with a finger prick.**
  • E.g., Abbott has developed a combination assay, the ARCHITECT HIV Ag/Ab Combo assay (Abbott Laboratories, Abbott Park, IL), that can simultaneously detect the combined presence of HIV antigens (p24 antigen) and antibodies to HIV. This test is important for diagnosing HIV infection in the acute phase of the disease when antibodies are not yet present and for ongoing monitoring of patients.
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60
Q

Antibody tests for HIV

A
  • Only detect antibodies to HIV in blood or oral fluid.
  • In general, antibody tests that use blood from a vein can detect HIV sooner after infection than tests done with blood from a finger prick or with oral fluid.
  • Most rapid tests and the only currently approved HIV self- test (OraQuick) are antibody tests.
  • Enzyme-linked immunosorbent assay (ELISA) testing for HIV in saliva is 98% sensitive in detecting antibodies to **HIV
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61
Q

OraQuick

A
  • Upper and lower gums are swabbed with the test stick.
  • Test stick is inserted into the kit’s test tube (vial) which
    contains a developer solution.
  • 20-40 minutes wait time before reading the test result.
  • 92% sensitivity.
    *** Additional testing should be done in a medical setting toconfirm the test result:
  • Positive.
  • Negative and exposure may have been within the
    previous three months.**
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62
Q

current practice for HIV exposure in medical setting

A

Current practice in medical setting is to screen first ELISA. If the results are positive, a second ELISA is performed (due to high rate of false positive). All positive results are then confirmed with Western blot analysis. This combination of tests is accurate more than 99% of the time and the patients are considered
potentially infectious

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63
Q

what do positive ELISA and western blot indicate

A

exposure to HIV

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64
Q

dental use of HIV screening

A

National surveys conducted on American general dentists predicted their willingness in implementing oral HIV rapid testing during dental visits.
* Although opposed by challenges of cost, licensing, and patient acceptance, potential models for integrating HIV screening into routine dental practice have been proposed representing a step forward towards early detection of the disease.

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65
Q

The natural history of human immunodeficiency virus infection diagram

A
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66
Q

Antiretroviral Medications (ARVs)

A

Highly active antiretroviral therapy, now known as combined antiretroviral therapy (cART) or ART, refers to the antiretroviral medications (ARVs) prescribed as an HIV drug regimen for the prevention and treatment of HIV/AIDS.

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67
Q

Guidelines developed for effective drug therapy to treat HIV/AIDS in most patients living
with HIV/AIDS incorporate:

A

a three-drug regimen as a standard for long-term therapeutic effectiveness against the virus

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68
Q

ARVs selected as part of a regimen are tailored to?

A

pt specific needs,taking into consideration the patient’s comorbidities or previous ART for example

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69
Q

life expectency with ART tx

A

The life expectancy of an HIV-infected individual appropriately treated with ART is now estimated to be nearly that of the general population, both in developed and developing countries, although it also is estimated to be about 1.7-fold higher than in healthy people with no comorbid conditions.

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70
Q

current guidelines for when ART tx started

A

Current guidelines from around the world now recommend starting ART in all HIV-
infected patients, regardless of CD4 cell count because of both clinical benefits to the
patient and reduction in HIV transmission to others.

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71
Q

Patients who respond to therapy generally show:

A

increase in CD4+ count in the range of 50 to 150 cells/μL per year and viral loads of less than 5 copies/mL.

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72
Q

Virologic suppression and virologic failure

A

Virologic suppression is defined as less than 48 copies/mL, and virologic failure is defined as a
confirmed viral load of greater than 200 copies/mL in the presence of ART

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73
Q

ART monitoring

A
  • Patients who are taking ART medications must be closely monitored for drug effectiveness (which often wanes over time), development of antiviral resistance, drug toxicity, and/or drug interactions.
  • Antiviral resistance testing is recommended when treatment is failing.
  • Some important toxicities include hyperlactemia, mitochondrial dysfunction, peripheral neuropathy, hepatotoxicity, and lipodystrophy.
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74
Q

Pre-exposure prophylaxis

A
  • A way for people who do not have HIV but who are at very high risk of getting HIV to prevent HIV infection by taking a pill every day.
  • The pill (brand name Truvada) contains two medicines (tenofovir and emtricitabine) that are used in combination with other medicines to treat HIV.

When someone is exposed to HIV through sex or injection drug use, these medicines can work to keep the virus from establishing a permanent infection

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75
Q

Management of Infants Born to Women with
HIV Infection

A
  • All newborns who were exposed perinatally to HIV should receive postpartum ARVs to reduce the risk of perinatal transmission of HIV.
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76
Q

The average dental practice is predicted to encounter _
____ patients infected with HIV per year

A

at least 2

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77
Q

In the United States, ____% of individuals who have
acquired HIV are unaware of their status,
contributing to as high as ___% of continuous HIV
spread.

A

In the United States, 15% of individuals who have
acquired HIV are unaware of their status,
contributing to as high as 40% of continuous HIV
spread.

78
Q

HIV from needle stick vs HepB/C

A

The risk of HIV transmission from infected patients to
health care workers is very low, reportedly about 3 of
every 1000 cases (0.3%) through a needlestick or other
sharp instrument contaminated with the virus.
* In comparison, the risk of infection from a needlestick is 30% for hepatitis B and is 3% for hepatitis C.

79
Q

CDC recomendation following exposure to HIV blood

tx based on?

A

recommends postexposure prophylaxis (PEP) as soon as possible after exposure to HIV-infected blood, regimen recommended is based on the severity
of the exposure and the HIV status of the source patient (two- vs three- drug regimen of antiretroviral medication)
* A less severe exposure (i.e., superficial), an
asymptomatic source patient or has a low viral load
(<1500 viral copies/mL) use a two-drug PEP.
* A more severe exposure (i.e., deep), or when the
patient is symptomatic, has AIDS, or a high viral load
use of at least a three-drug PEP.

80
Q

tests for serconversion timeframe following HIV exposure

A

performed at 3, 6, and 12 months

81
Q

The risk of transmission from healthcare
personnel to patients is also minimized by:

A

The risk of transmission from healthcare
personnel to patients is also minimized by adherence
to standard infection control procedures

82
Q
  • Standard precautions are a set of:
A
  • Standard precautions are a set of infection control practices used to prevent transmission of diseases that can be acquired by contact with blood, body fluids, non-intact skin (including rashes), and mucous membranes.
83
Q

Standard precautions must be used for:

A

Standard precautions must be used for all patients

84
Q

o Several guidelines have emerged regarding the rights of dentists and patients with AIDS, including the following:
* Dental treatment may not be withheld if the patient refuses to undergo?
* A patient with AIDS who needs emergency dental treatment may not be refused care simply
because?
* is there a medical or scientific reason exists to justify why patients with AIDS who seek routine dental
care may be declined treatment by the dentist?
* If the dentist and the patient agree, the dentist may do what?
* A patient who has been under the care of a dentist and then develops AIDS or a related condition
must be? or?
* The CDC and the American Dental Association recommend that infected dentists do what?

A

o Several guidelines have emerged regarding the rights of dentists and patients with AIDS,
including the following:
* Dental treatment may not be withheld if the patient refuses to undergo testing for HIV exposure.
* A patient with AIDS who needs emergency dental treatment may not be refused care simply
because the dentist does not want to treat patients with AIDS.
* No medical or scientific reason exists to justify why patients with AIDS who seek routine dental
care may be declined treatment by the dentist, regardless of the practitioner’s personal reason.
* If the dentist and the patient agree, the dentist may refer the patient to another provider who is
more willing or better suited (in keeping with the patient’s oral health status) to provide
treatment.
* A patient who has been under the care of a dentist and then develops AIDS or a related condition
must be treated by that dentist or receive a referral that is satisfactory for and agreed to by the
patient.
* The CDC and the American Dental Association recommend that infected dentists inform their
patients of their HIV serostatus and should receive consent or refrain from performing invasive
procedures

85
Q

o Two major consideration in dental treatment for patients living with HIV/AIDS
and additonal considerations

A
  1. Current CD4+ lymphocyte count.
  2. Level of viral load.
    Other: neutrophils, platelets
86
Q
  • Dental treatment of HIV-infected patients without symptoms
A

no different from that provided for any other patient in the practice. Generally, this is true for patients with a
CD4+ cell count of more than 350/μ

87
Q

symptomatic pts and prophylaxis

A
  • Patients who are symptomatic for the early stages of AIDS (i.e., CD4+ cell count <200/μL) have increased susceptibility to opportunistic infections and may be medicated with prophylactic drugs
88
Q
  • Patients with AIDS can recieve what care after the
    possibility of significant immunosuppression, neutropenia, or thrombocytopenia has been ruled out
A
  • Patients with AIDS can receive almost any dental care needed and desired after the
    possibility of significant immunosuppression, neutropenia, or thrombocytopenia has
    been ruled out
89
Q

HIV pts req invasive procedures

A

Medical consultation (adverse reactions with ART and/or current blood dyscrasias)
* Patients with CD4+ cell counts below 200/μL or severe neutropenia (neutrophil count <500/μL): use prophylactic antibiotics; in patients with severe thrombocytopenia special measures my be indicated (platelet replacement

90
Q

In HIV patients with periodontal disease whose general health status is not clear, what can be done?

A

In patients with periodontal disease whose general health status is not clear, periodontal scaling for several teeth can be provided to allow assessment of tissue
response and bleeding. If no problems are noted, the rest of the mouth can be treated.
Adjunctive antibacterial measures may be required if the patient’s CD4+ cell count is below 200/μL or if tissues remain unresponsive to routine therapy

91
Q

RCT in HIV pts

A

Root canal therapy has good success in patients with HIV infection, and no modifications are required

92
Q

analgesics with HIV pts

A
93
Q

Abx with HIV pts

A
94
Q

anesthesia, anx and allergies with HIV pts

A

none

95
Q

bleeding issues with HIV

A

poorly controlled dx can cause thrombocytopenia

96
Q

breathing issues with HIV

A

potential for pul infections

97
Q

BP issues with HIV?

A

none

98
Q

chair position for HIV pts

A

doesnt matter

99
Q

CV health for HIV pts

A

some ART may have CV ADR

100
Q

issues with drugs in HIV pts

A

many interactions with ARTs, check lists for interactions

101
Q

follow ups with HIV pts

A

stage 1 pts req routine follow up, stages 2 and 3 may be more frequent and req prophylaxis

102
Q

Since the late 1980s to date, oral manifestations have been acknowledged to represent a _____ component of HIV infection that can correlate with?

A

Since the late 1980s to date, oral manifestations have been acknowledged to represent a major component of HIV infection that can correlate with treatment responses and disease progression

103
Q

oral lesion can represent?

A

early clinical sign of HIV disease soon after
seroconversion alerting clinicians for further investigation in the appropriate
clinical scenario.

104
Q

Although it is unlikely to encounter many of the oral lesions associated with HIV in general dental practice, oral healthcare providers should be?

A

Although it is unlikely to encounter many of the oral lesions associated with HIV
in general dental practice, oral healthcare providers should be familiar with HIV-
related oral manifestations and comfortable in managing and referring patients
with HIV/AIDS.

105
Q

most common oral manifestation of HIV

A

candidasis

106
Q

most common malignancy associated with HIV worldwide

A

karposi sarcoma

107
Q

what has decreased the incidence of oral HIV signs

A

ARTs

108
Q
  • After seroconversion, HIV disease often
    remains silent except for:
A

Persistent generalized lymphadenopathy (PGL)

109
Q

PGL prevalence

A

The prevalence of this early clinical sign
varies; however, in several studies it
approaches 70%

110
Q

PGL consists of:

A

PGL consists of lymphadenopathy that
has been present for > 3 months and
involves two or more extrainguinal sites.

111
Q

most frequent PGL sites

A

posterior and anterior cervical, submandibular, occipital, and axillary nodes

112
Q

PGL node size

A

usually is larger than 1 cm, and varies from 0.5 to 5.0 cm

113
Q

what is indicated with PGL and why?

A
  • Because lymphoma is known to occur in this population, a lymph node biopsy may be indicated
    for localized or bulky adenopathy, when cytopenia or an elevated ESR is present, or when requested for patient reassurance
114
Q

PGL does warn of?

A

PGL does warn of progression to AIDS; almost one-third of affected and untreated patients will have diagnostic features of AIDS within 5 years.

115
Q

Persistent generalized lymphadenopathy (PGL)
* Histopathologic examination

A
  • Histopathologic examination reveals florid follicular hyperplasia.
  • P24 in germinal centers
116
Q
  • The most common organism identified in oral candidiasis is:
A

Candida albicans

117
Q

Approximately ____ of HIV-infected individuals and more than _____% of patients with AIDS
develop oral candidiasis at some time during their disease course.

A

Approximately one-third of HIV-infected individuals and more than 90% of patients with AIDS
develop oral candidiasis at some time during their disease course.

118
Q

forms of candidasis and associated CD4 count

A
  1. Pseudomembranous candidiasis (appears when the CD4+ lymphocyte count <200 cells/mm3)
  2. Erythematous candidiasis (appears when the CD4+ lymphocyte count <400 cells/mm3)
  3. Hyperplastic candidiasis
  4. Angular cheilitis
119
Q

chronic multifocal candidasis

A

Chronic multifocal oral involvement is common in HIV-infected patients

120
Q

Some studies have shown that development of candidiasis correlates more closely with:

A

Some studies have shown that development of candidiasis correlates more closely with viral load
than CD4+ cell count.

121
Q

can candidasis be painful

A

Oral candidiasis can be painful and associated with a reduction in taste and smell, which may lead to decreased food intake and further wasting.

122
Q

names

A
123
Q

stian for candidasis

A

PSA

124
Q

tx of candidasis
* Nystatin?
* Topical clotrimazole?
* Systemic fluconazole and itraconazole?
* If azoles fail, then?

A
  • Nystatin often is ineffective.
  • Topical clotrimazole is effective but has high rate of recurrence.
  • Systemic fluconazole and itraconazole are effective but have a number of drug interactions and
    may result in drug-resistant candidiasis.
  • If azoles fail, then IV amphotericin B can be administered. (nephrotoxicity)
125
Q

Oral hairy leukoplakia

A

The most common EBV-related lesion in patients with
AIDS. (EBV is associated with several forms of lymphoma in HIV-infected patients

126
Q
  • The presence of OHL in HIV-infected patients is a sign of:
A
  • The presence of OHL in HIV-infected patients is a sign of severe immunosuppression and advanced disease.
127
Q

what other situation has OHL been reported

A

OHL also has been reported in transplant recipients, but its presence in the absence of a known cause of
immunosuppression strongly suggests HIV infection

128
Q

OHL clinically presents as:

A

OHL clinically presents as a white mucosal plaque that does not rub off. Most cases occur on the lateral border of the tongue and range in appearance from faint, white vertical streaks to thickened, furrowed areas of leukoplakia with a shaggy surface

The lesions infrequently may extend to cover the entire dorsal and lateral surfaces of the tongue. Rarely, the buccal mucosa, soft palate, pharynx, or esophagus may be involved.

129
Q

OHL tx

A

usually none

130
Q

OHL histo
Thickened?
* Epithelium?
* Characteristic pattern of?
* Dysplasia?
* In a patient with known HIV infection, the clinical features of OHL typically are sufficient for?
* When definitive diagnosis is necessary, demonstration of EBV can be achieved by?

A

Thickened parakeratin (corrugated or thin projections)
* Epithelium is acanthotic and exhibits a bandlike zone of lightly stained cells with abundant cytoplasm (“balloon cells”) in the upper spinous layer.
* Characteristic pattern of peripheral margination of
chromatin termed nuclear beading caused by extensive EBV replication that displaces the chromatin to the nuclear margin.
* Dysplasia is not noted.
* In a patient with known HIV infection, the clinical features of OHL typically are sufficient for a presumptive diagnosis.
* When definitive diagnosis is necessary, demonstration of EBV can be achieved by in situ hybridization, PCR,
immunohistochemistry (IHC), Southern blotting, or electron microscopy.

131
Q

HIV related Mucosal, cutaneous, and/or nail(s) hyperpigmentation may be induced by:

A
  1. drugs taken by HIV/AIDS patients such as zidovudine and emtricitabine-based HIV regimens.
  2. Drugs used to control microbial infections in these patients such as ketoconazole (fungal-
    infections), clofazimine (leprosy and some TB), and pyrimethamine (toxoplasmosis/anti- parasitic).
  3. Destruction of the adrenal cortex by disseminated infections (e.g. deep fungal infections)
  4. Pigmentation with no apparent cause has arisen in HIV-infected patients, and some investigators
    have theorized that this may be a direct result of HIV infection.
132
Q

tx for hyperpigmentation
usually?
rule out?
adrenal insuff?

A
  • Usually, no treatment is indicated.
  • Single lesions may have to be biopsied so that melanoma can be ruled out.
  • Patients with adrenal insufficiency may require
    corticosteroids.
133
Q

perio and gingival dxs associated with HIV?

A

linear gingivits
NUG
NUP
Necrotizing stomatitis

134
Q

Linear gingivitis
* Linear gingivitis appears as?
* The alveolar mucosa and gingiva?
* This diagnosis should be reserved for?
* Results from?

A

Linear gingivitis

  • Linear gingivitis appears with a distinctive linear band of erythema that involves the free gingival margin and
    extends 2 to 3 mm apically.
  • The alveolar mucosa and gingiva may demonstrate punctate or diffuse erythema in a significant percentage of cases.
  • This diagnosis should be reserved for gingivitis that does not respond to improved plaque control and exhibits a greater degree of erythema than would be expected for the amount of plaque present
  • Results from an abnormal host immune response to subgingival bacteria or may represent an unusual pattern of candidiasis.
135
Q
  • Necrotizing ulcerative gingivitis (NUG) appears as?
  • Patients with NUG have:
A
  • Necrotizing ulcerative gingivitis (NUG) appears as ulceration and necrosis of one or more interdental papillae with no periodontal attachment loss.
  • Patients with NUG have interproximal gingival necrosis, bleeding, pain, and halitosis.
136
Q
  • Necrotizing ulcerative periodontitis (NUP) is characterized by :
  • how many teeth can be affected? usually?
  • common signs and symptoms
  • Deep pocketing?
A
  • Necrotizing ulcerative periodontitis (NUP) is characterized by gingival ulceration and necrosis associated with rapidly progressing loss of periodontal attachment. (Attachment loss of more than 6 mm within a 6-month period is not unusual)
  • Although severe cases can affect all teeth, multiple isolated defects often are seen and contrast with the diffuse pattern associated with typical chronic periodontitis.
  • Edema, severe pain, and spontaneous hemorrhage are common.
  • Deep pocketing usually is not seen because extensive gingival necrosis typically coincides with loss of the adjacent alveolar bone.
137
Q
  • Necrotizing stomatitis may be seen as?
  • Involves what tissues?
A
  • Necrotizing stomatitis may be seen as an extension of NUP or may involve oral mucosa separate from the
    gingiva. (biopsy in this case is indicated)
  • Involves predominantly soft tissue or extend into the underlying bone, resulting in extensive sequestratio
138
Q

linear ging tx

A

may be treated with débridement, povidone-iodine irrigation, chlorhexidine
mouth rinse, and/or antifungal medicatio

139
Q

NUG/NUP tx
* The treatment of NUG and NUP revolves around:
* The initial removal of necrotic tissue typically is combined with?
* The use of systemic antibiotics? but?
* All patients should use what initally and for long term maintenence?
* After initial débridement, removal of additional diseased tissue should be performed within? and again every? for_____ appointments, depending on? At this point, _____recalls are necessary until the process stabilizes; evaluations then are performed every ____ months

A
  • The treatment of NUG and NUP revolves around débridement, antimicrobial therapy, pain
    management, immediate follow-up care, and long-term maintenance.
  • The initial removal of necrotic tissue typically is combined with povidone-iodine irrigation.
  • The use of systemic antibiotics usually is not necessary, but metronidazole (narrow spectrum to
    suppress periodontal pathogens without strongly promoting candidal overgrowth) has been
    administered to patients with extensive involvement and severe acute pain.
  • All patients should use chlorhexidine mouth rinses initially and for long-term maintenance.
  • After initial débridement, removal of additional diseased tissue should be performed within 24
    hours and again every 7 to 10 days for two to three appointments, depending on the patient’s
    response. At this point, monthly recalls are necessary until the process stabilizes; evaluations then
    are performed every 3 months
140
Q

HIV Patients may demonstrate conventional gingivitis, chronic periodontitis, and progressive non-
necrotizing periodontitis, how is this tx?

A
  • In these cases, periodontal attachment loss can be combated successfully with regular professional
    scaling and root planing, plus optimization of oral hygiene. Patients should be encouraged to
    discontinue their tobacco habit.
141
Q

The prevalence of oral recurrent HSV infection among HIV-infected individuals increases significantly
once the CD4+ cell count is?

A

under 50

142
Q

Within the setting of HIV infection, recurrent herpetic lesions may be?

A

Within the setting of HIV infection, recurrent herpetic lesions may be widespread, occur in an atypical
pattern, and persist for months.

143
Q

Herpes labialis may extend to?

A

Herpes labialis may extend to the facial skin and exhibit extensive lateral spread.

144
Q

Persistence of active HSV infection for more than 1 month in a patient infected with HIV is?

A

Persistence of active HSV infection for more than 1 month in a patient infected with HIV is one
accepted definition of AIDS.

145
Q

what shuld be performed on all persistent oral ulcerations of HIV pts

A

Evaluation for HSV should be performed on all persistent oral ulcerations in HIV-infected individuals

146
Q

Tx of HSV with HIV pts

A
  • Systemic acyclovir, valacyclovir, or famciclovir for at least 5 days can be effective. Higher doses may be needed during severe immunosuppression.
  • An elixir or syrup of diphenhydramine (Benadryl) of 12.5 mg/5 mL can be used for pain control.
147
Q

Among patients with HIV infection, herpes zoster is often?, with increased rates of?

A

Among patients with HIV infection, herpes zoster is often severe, with increased morbidity and mortality
rates

148
Q

shignles in HIV pts compared to healthy

A

Many of these patients are younger than 40 years, in contrast to immunocompetent patients who typically
develop herpes zoster later in life

149
Q

well controlled HIV vs AIDS zoster presentation

A
  • In patients with well-controlled HIV disease, herpes zoster usually is confined to a single dermatome but persists longer than usual.
  • In full-blown AIDS, dissemination to multiple dermatomes is not unusual
150
Q

Severe intraoral involvement of zoster may lead to:

A

Severe intraoral involvement may lead to bone
sequestration and loss of teeth; these sequelae may be
delayed a month or more after the initial onset of herpes zoster

151
Q

pain with zoster?

A

intense

152
Q

tx/prevention of zoster in hiv pts

A
  • Valacyclovir 1 g PO tid; famciclovir 500 mg PO tid; acyclovir 800 mg PO 5 times per day.
  • IV acyclovir may be needed for severe herpes zoster in patients with immunosuppression.
  • Routine zoster vaccination for HIV-infected patients is not recommended currently; however, according
    to some experts, zoster vaccination may be considered for those with well-controlled HIV disease and
    CD4+ cell counts > 200/ mm 3
153
Q

HIV related salivary gland dx

A
  • HIV-associated salivary gland disease can arise anytime during HIV infection and is considered a
    localized manifestation of diffuse infiltrative lymphocytosis syndrome (DILS)
154
Q

DILS is characterized by:

A

DILS is characterized by CD8+ lymphocytosis with diffuse lymphocytic infiltration of various sites, such
as the major or minor salivary glands, lacrimal glands, lungs, kidneys, muscle, nerve, and liv

155
Q

The main clinical sign of DILS

A

The main clinical sign is salivary gland enlargement, particularly affecting the parotid.
Bilateral involvement is seen in about 60% of cases and often is associated with cervical lymphadenopath

156
Q

variable finding of DILS

A

xero

157
Q

DILS Microscopic changes within the affected
glands may include:

A

Microscopic changes within the affected
glands may include lymphocytic infiltration,
hyperplasia of intraparotid lymph nodes, and,
in long-standing cases, lymphoepithelial cyst
formation

158
Q
  • The most widely accepted treatments for DILS:
A
  • The most widely accepted treatments for DILS
    are oral prednisone and antiretroviral therapy,
    although some patients have been treated with
    surgery or radiation therapy
159
Q

Recurrent aphthous stomatitis (RAS)
Most lesions are what forms?
* With more severe reduction of CD4+ cell count, which form becomes more prevalent?
* Lesions that are chronic or atypical or that do not
respond to treatment should be?
* Treatment of persistent lesions involves?

A

Most lesions are of the more uncommon forms—major
and herpetiform.
* With more severe reduction of CD4+ cell count, major
lesions become more prevalent.
* Lesions that are chronic or atypical or that do not
respond to treatment should be biopsied.
* Treatment of persistent lesions involves potent topical or intralesional corticosteroids. Systemic steroids generally are avoided to prevent further immunosuppression

160
Q

HIV-related (non-specific) oral ulceration

A
  • The EC-Clearinghouse-WHO cohorts (1993) defined oral ulceration in the context of HIV as a distinct entity not corresponding to any pattern (minor, major, or
    herpetiform) of recurrent aphthous stomatitis (RAS) nor
    caused by fungal, bacterial, or viral organisms
161
Q

ART and oral ulcerations

A

ART may cause these

162
Q

Among HIV-infected individuals, most HPV lesions arise in?

A

the anogenital region, although oral involvement also is
possible.

163
Q

Benign HPV lesions:

A

Oral squamous papilloma, verruca vulgaris, condyloma acuminatum, and multifocal epithelial hyperplasia

164
Q

The prevalence of these oral HPV lesions in HIV-infected patients is greater than?

A

that observed among immunocompetent individuals.

165
Q

unusual HPV types and HIV

A

Unusual HPV types (such as, HPV-7 [associated with butcher’s warts], HPV-13, and HPV-32 [associated with multifocal epithelial hyperplasia]) frequently are identified in oral HPV lesions arising in HIV-infected patient

166
Q

most common HPV lesion locations

A

The labial mucosa, tongue, buccal mucosa, and gingiva are most frequently involved.

167
Q

HPV lesion app

A
  • The lesions may exhibit a cluster of white, spikelike
    projections, pink cauliflower-like growths, or slightly elevated sessile papules.
168
Q

HPV histology

A
  • Lesions may be sessile or papillary and covered by acanthotic or hyperplastic stratified squamous epithelium
  • The affected epithelium often demonstrates vacuolization of numerous epithelial cells (i.e., koilocytosis) and occasionally may exhibit mild variation in nuclear size
169
Q

why should we monitor HPV lesions

A

Dysplasia has been noted within HPV-
related lesions in patients with AIDS
and mandates close observation for
development of squamous cell
carcinoma.

170
Q

HPV lesion tx

A

Surgical excision is the most commonly used treatment for oral HPV lesions; additional surgical options include cryosurgery, electrocautery, and laser ablation.
* All of these surgical methods are associated with frequent recurrence.
* Electrocautery and laser ablation may expose the surgical team and patient to a plume containing infectious HPV.

171
Q

decreased CD4 and malignancies

A
  • The marked reduction in CD4+ T-helper lymphocytes, to a great degree, explains the lack of an effective
    immune response seen in patients with AIDS and contributes to the increase in malignant disease that has been found to be associated with AIDS, including Kaposi sarcoma, lymphoma, and carcinomas
172
Q

most common malignancy among the AIDS population in the United States.

A

Non-Hodgkin lymphoma (NHL) currently represents the most common malignancy among the AIDS
population in the United States.

173
Q

most HIV NHL cases represent? and are associated with?

A

Most cases represent high-grade, aggressive B-cell neoplasms.
May be associated with EBV and/or HHV8

174
Q

Lymphoma in patients with AIDS usually occurs in?

A

Lymphoma in patients with AIDS usually occurs in extranodal
locations

175
Q

AIDS NHL oral lesions

A

Oral lesions are seen in approximately 4% of patients with AIDS-related NHL and most frequently involve the gingiva, palate, and tongue.

176
Q

AIDS NHL radiogrpahic signs?

A

Intraosseous involvement also has been documented and may resemble diffuse progressive periodontitis with loss of periodontal attachment and loosening of teeth.
In these cases, widening of the periodontal ligament and loss of lamina dura may represent radiographic clues to the diagnosis

177
Q

With the inclusion of ART, lymphoma survival for the HIV- infected population often approaches that for?

A

general population

178
Q

karposi sarcoma most likely arises from?

A
  • The lesion most likely arises from endothelial cells, which may express markers for both lymphatic and
    blood vessel differentiation and is caused by human herpesvirus 8 (HHV-8)
179
Q

4 clinical presentations of karposi sarcoma

A
  1. Classic
  2. Endemic (African)
  3. Iatrogenic (transplant-associated)
  4. Epidemic (AIDS-related)
180
Q

Kaposi sarcoma in US AIDS

A

Kaposi sarcoma currently represents the
second most common malignancy
among people with AIDS in the United
State

181
Q

In Western countries, Kaposi sarcoma has been reported primarily in?

A

In Western countries, Kaposi sarcoma has been reported primarily in HIV-infected, adult, male
homosexuals and is thought to be related to sexual transmission of HHV-8

182
Q

Karposi sarcoma In Africa

A

in Africa both AIDS-related and
endemic types of Kaposi sarcoma
frequently are seen, with no gender
predilection and a significant number
of children affected

183
Q

karposi sarcoma infections without sex?

A

Infection before sexual activity
suggests alternate transmission
pathways.

184
Q

what can be found in saliva titers in karposi

A

Relatively high titers of HHV-8 have
been found in saliva, and HHV-8
exhibits tropism for oral and
oropharyngeal epithelial cells.

185
Q

what is req for karposi diagnosis

A

A biopsy is required for definitive
diagnosis, although a presumptive
clinical diagnosis sometimes is made

186
Q

lesions app similarly to karposi

A

bacillary angiomatosis and lymphoma

187
Q

Relative to the general population, HIV-infected individuals have an estimated _________risk of
developing oral cavity and pharyngeal cancer.

A

twofold increase

188
Q

HIV/AIDS pts risk factors for oral/pharyngeal cancers

A

Studies of various HIV/AIDS cohorts have demonstrated a high prevalence of known risk factors for
oral and pharyngeal cancers (e.g., tobacco use and HPV infection)

189
Q

Oral squamous cell carcinoma tends to occur at a _____ age among HIV-infected individuals than
non-HIV-infected individuals

A

Oral squamous cell carcinoma tends to occur at a younger age among HIV-infected individuals than
non-HIV-infected individuals

190
Q

tx of oral SCCa in HIV/AIDS

A

Treatment also is not significantly different for HIV-infected patients and consists of surgical resection,
radiation therapy, and/or chemotherapy

191
Q

Most HIV-infected patients with a diagnosis of oral squamous cell carcinoma have ______ disease
and an __________ prognosis

A

Most HIV-infected patients with a diagnosis of oral squamous cell carcinoma have advanced disease
and an unfavorable prognosis

MED COMP PTS (9 decks)

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