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NURS361 - Pathophysiology II > Module 5-2 - HIV > Flashcards

Module 5-2 - HIV Flashcards

1
Q

How big is the HIV issue?

A

1 in 7 do not know they have it and over 1 million in the US have it alone

Globally 37.9 million have it and 32 million have died

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2
Q

In what groups has the highest Incidence of HIV?

A

African American gay and bisexual men, but Latino gay and bisexual men have increased in incidence over time

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3
Q

What area of the US has the largest incidence of HIV?

A

The South (52%)

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4
Q

What does HIV stand for?

A

Human Immunodeficiency Virus

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5
Q

What does AIDS Stand for?

A

Acquired Immunodeficiency Syndrome

It is the late stage of HIV and is the disease caused by it

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6
Q

What is the structure of an HIV viral particle?

A

Oval Shaped Protein Coat

Capside with RNA, enzymes, P24 Protein, and P17

Envelope with the lipid layer, GP120 and GP41 - Glycoproteins sticking out of the lipid membrane

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7
Q

What is special about the HIV P24 protein?

A

This protein serves as an antigen that we can test for antibodies and for the the virus presence/antigen

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8
Q

GP120 and GP 41

A

Glycoproteins that are like spikes sticking out of the lipid membrane and aids HIV in getting into cells

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9
Q

What is one of the components of HIV that makes it unique?

A

It contains reverse transcriptase enzyme

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10
Q

Most viruses cannot…

A

replicate on their own, they need to be in a cell to reproduce

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11
Q

Retrovirus

A

HIV

it inserts itself as vRNA and makes DNA from the vRNA, and then splices the vDNA into the genetic material of healthy cells

So, it enters the hosts genetic material causing a permanently infected cell

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12
Q

What does a new virus take from an infected cell when leaving?

A

It takes the phospholipid bilayer for itself

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13
Q

Capsid

A

The protein shell of a virus containing its genetic material

It has 2 strands of RNA, Reverse Transcriptase, and P17 and P24 proteins in it (in HIV)

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14
Q

Envelope

A

Lipid bilayer containing the virus and capsid that has GP120 and GP41 sticking out of it (in HIV) allowing access to cells

Made from the host cells membrane as it left the cell

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15
Q

How exactly does a retrovirus infect cells?

A

The GP120 and 41 on the surface allow it to bind to CD4 receptors on T4 cells and then inject its contents into the cytoplasm

The contents (2 RNA strands and reverse transcriptase) can then be used to make DNA

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16
Q

What aspect of HIV causes the immune deficiency disorder?

A

The fact that it infects and hurts T4 cells (thus hindering the immune response)

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17
Q

What occurs once reverse transcriptase uses the viral RNA to make DNA?

A

The DNA then goes from the cytoplasm into the nucleus, and along with other viral enzymes, inserts itself into the host cell genome

Once vDNA is inserted, its there permanently and the cell is infected and no longer your own

RNA can then be made using the DNA to make virions using the cells machinery

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18
Q

What can occur after the vDNA has entered the genome?

A

It can either go latent or activate and begin making viral particles (RNA and RTranscriptase)

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19
Q

Latent

A

A virus that inserts itself and remains dormant, not producing new viral particles

It can do this if there is not the right kind of GP on the surface or if the formation of a capsid hasn’t progressed to maturity yet for example

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20
Q

What happens once vDNA activates to make new Virions?

A

Proteases will cleave proteins made by viral mRNA and package them into a protein coat

The viral particles can then be put into the protein coat to make the immature capsid

The capsid can eventually make an envelope using the phospholipid bilayer of the cell and bud off the membrane to go make more infected cells and copies

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21
Q

Thera re classes of HIV meds addressing…

A

every step of HIV reproduction

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22
Q

What happens since the new virion takes a chunk of the membrane with it?

A

It will have GP120 and GP41 on its surface of the envelope

Can then connect to CD4 on other T4 cells and invade as a result

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23
Q

Where do the names of GP120 and GP41 come from?

A

their molecular weight

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24
Q

Why can T8 cells have difficulty killing virus infected cells?

A

If the virus DNA is already in the nucleus, the T8 cell cannot identify that the cell is infected unless the virus is actively replicating already

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25
Q

HAART

A

Highly Active Antiretroviral Treatment

HIV treatment method

It involves hitting the disease fast and hard as soon as you learn of infection with drugs that will eradicate it ASAP - its trying to prevent viral particles from seeding and allowing reproduction later

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26
Q

Seeding

A

When the viral DNA goes dormant and remains undetected and safe until it can widely disseminate and activate

Because of seeding, it is important to destroy all viral particles before seeding occurs to allow greater survival probability

Wanna stop this fast and early

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27
Q

Summation: Stages of Viral Replication

A
  1. HIV binds to the CD4 cell on T4 cells and RNA, proteins, and enzymes released into cytoplasm
  2. HIV Reverse Transcriptase converts vRNA into vDNA
  3. HIV vDNA then moves to the host nucleus and is spliced into the host genome/DNA
  4. HIV vRNA moves out of the nucleus to the cytoplasm and makes long chains of viral proteins and enzymes
  5. Immature viral particle forms containing cellular and HIV protein. Chains cut into smaller pieces by protease
  6. Infectious viral particle is now ready to be released containing HIV RNA, viral proteins and enzymes
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28
Q

The function of the immune system?

A

Function = Prevent/Fight Disease

It controls of eliminates viruses and other microbes that threaten the body with infection and disease

It eliminates damaged cells that are or may be cancerous

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29
Q

The immune system is divided into two branches…

A
  1. Antibody Mediated –> Copes with disease causing microbes in the blood
  2. Cell Mediated –> Copes with microbes located within cells
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30
Q

When does Cell Mediated Response v Humoral Response get to the viral particles compared to each other?

A

Humoral response get to the virus before it even enters the cell and cell mediated gets there after

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31
Q

What is so important about CD4 cells and HIV?

A

CD4 cells (Helper T Cells) coordinate and activate both B lymphocytes (antibody mediated) and cell killing cytotoxic (CD8) lymphocytes (cell mediated) - the cell mediated response copes with microbes located inside cells like viruses

However, HIV can infect and destroy CD4 cells (gets your body to attack the Helper cells since they are infected) –> loss of CD4 means the immune system will collapse with HIV disease

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32
Q

What is used as a marker of the progression of HIV?

A

Decline in (Absolute) CD4 cells

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33
Q

When are CD8 cells important for HIV infection?

A

In the initial immune response to HIV and the latent stage

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34
Q

What do CD8 cells do?

A

They kill infected cells that are producing virus

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35
Q

What can CD8 cells do to prevent HIV replication?

A
  1. They can kill the cell
  2. They can secrete soluble factors that suppress HIV replication by blocking and occupying receptors needed for the entry of certain strains of HIV into the target cell
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36
Q

What are the two issues that exist with HIV and CD8 cells ?

A
  1. If the CD8 cannot get the job done early enough, the HIV virus can seed, and once latent the CD8 cells cannot detect them until its too late
  2. New info shows 2 new strains of the HIV virus that target CD8 cells as well as CD4
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37
Q

If CD4 cells are infected with HIV, what occurs with CD4 cells to lead to increased susceptibility to opportunistic and other infections?

A

CD4 can not make interleukins to stimulate an immune response –> loss of stimulus for T and B cell activation occurs –> lymphopenia, decreased CD4/Cd8 ratio, and decreased delayed hypersensitivity –> increased risk

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38
Q

If CD4 cells are infected with HIV, what occurs with CD8 cells to lead to increased susceptibility to opportunistic and other infections?

A

CD8 cells have impaired feedback and cytotoxic activity since they cannot get orders from CD4 –> lymphopenia, decreased CD4/Cd8 ratio, and decreased delayed hypersensitivity –> increased risk

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39
Q

If CD4 cells are infected with HIV, what occurs with Macrophage cells to lead to increased susceptibility to opportunistic and other infections?

A

Macrophages have decreased chemotaxis, phagocytosis, IL-1 production, and ability to present antigens to cells (d/t no T4 response) –> Increased risk

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40
Q

If CD4 cells are infected with HIV, what occurs with B cells to lead to increased susceptibility to opportunistic and other infections?

A

B cells have diminished antibody production in response to antigens and decreased production of immunoglobulins –> decreased nonspecific serum immunoglobulin –> increased risk

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41
Q

Why does a drop in ratio between CD4 and CD8 cells cause delayed hypersensitivity?

A

It is referring to Type IV hypersens. (no antibodies)

There is no T4 stimulation leading to not enough T8 cells reacting to something to have an immune response happen

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42
Q

Absence of an immune response may mean…

A

either you do not have an infection or you could have no immune system

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43
Q

Anergy

A

No immune system and cannot mount an immune response

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44
Q

Why may we want to give an HIV patient a Tb test?

A

It is a common comorbidity

If we give the test and wait for the response and there is none, then they may not have enough T8 cells rather than not have Tb

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45
Q

What is a way to check if you have no immune system (anergy) or no exposure?

A

Expose them to yeast / yeast mold antigen which almost everyone has been exposed to

If they react to the yeast injection, they have no been exposed to Tb and have an immune system, but if they are Anergic they will not react to the yeast either

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46
Q

Which Interleukin is important for Chemotaxis?

A

IL-1

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47
Q

Why does macrophage presenting ability decrease with HIV?

A

T4 cells are not producing the needed cytokines that are supposed to amplify and stimulate and immune response

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48
Q

Those with HIV end up with strange rates of…

A

cancer and infection

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49
Q

What is HIV replication rate like?

A

Crazy fast early on - billions per day with a high mutation rate (3300 mutants made per day)

99% of HIV in the blood is from newly infected cells

30% of HIV in plasma is replenished daily

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50
Q

How many days does it take for HIV entire population turnover?

A

14 days

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51
Q

What is the mutation rate of HIV?

A

1 in 3 replication cycles - 3300 mutant viruses per day

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52
Q

When does extensive HIV seeding occur?

A

early in the disease process

CD4 only has a lifespan of 1-2 days so if HIV is not taken care of early then the extensive seeing will occur

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53
Q

Sanctuary Sites

A

Body has a difficult time detecting HIV in these areas

HIV gets to these areas by going inside macrophages and crossing into the CNS to cause dementia (like a macrophage trojan horse)

These are the dendritic cells of the lymph nodes and glial cells of the CNS

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54
Q

Lifespan of a CD4 Cell

A

1.2 days (billions made, infected, and destroyed daily in HIV)

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55
Q

What happens to T4 cell levels over time with HIV?

A

The T4 infected cells will eventually be attacked by CD8 cells killing them and infected macrophages

Eventually you run out of T4 cells to keep up with viral replication rate

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56
Q

Transmissible Body Fluids for HIV

A

Blood

Semen

Vaginal Secretions

Breast Milk (so this is contraindicated in HIV+ women)

Cerebral Spinal Fluid

Synovial Fluid

Pleural and Amniotic Fluid

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57
Q

Non Transmissible Body Fluids for HIV

A

Urine

Sweat

Saliva

Tears

Vomit

Mucus

Feces

The virus can be found here but not transmitted here

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58
Q

How can vertical transmission of HIV be very low?

A

IF the mother is compliant with medication regimen

2-8% rather than 15% without (or 29% to 2% with AZT treatment)

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59
Q

Methods of Transmission for HIV

A
  1. Unprotected sex - oral, anal, vaginal
  2. Blood to blood contact - sharing needles, occupational exposure, fighting, tattooing, body piercing, transfusions
  3. Mother to newborn - in utero, childbirth, breast feeding
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60
Q

Risk Factors for HIV Infection

A

Sexual Activity

Injection Drug Use

Recipients of Blood Products (1975- March 1985)

Hemophiliacs who received Pooled Plasma

Children of HIV Infected Women

Needlestick accidents

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61
Q

How many children of HIV infected women will be infected without treatment?

A

30%

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62
Q

What is used to immediately treat post exposure needlestick accidents?

A

Retrovir (Zidovudine) - given ASAP within 24 hours!

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63
Q

What is the greatest HIV transmission risk?

A

Receptive Anal Intercourse (receptive meaning semen stays inside, and the membranes tear in this case)

there is a 95% chance of getting it from HIV infected blood donors but this rarely occurs nowadays

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64
Q

What is the least HIV transmission risk?

A

Insertive Vaginal intercourse is 1/10,000 chance (insertive meaning penis goes in but ejaculate was not)

There is a 1/1,000,000 chance to get HIV from screened blood though

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65
Q

Other Factors that increase HIV Risk?

A
  1. Acute infection about 12 weeks after HIV contraction makes transmission likelihood 26x more likely
  2. Other STIs can amplify risk x8
  3. Exposure to gender inequality and intimate partner violence can raise a womans HIV risk x1.5
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66
Q

Why is it that your HIV transmission risk is 26x more 12 weeks after contraction (during acute infection)?

A

the viral load has skyrocketed during the acute phase is why

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67
Q

Other factors that decrease HIV risk?

A

Circumcision (60%) lower in hetero males

Treatment as prevention

Pre exposure prophylaxis

Condoms (80% lower)

Only having intercourse with someone of the same sero status (HIV-HIV, Negative-Negative)

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68
Q

Tests for HIV

A

ELISA

Western Blot

p24 Antigen

Absolute CD4+ Lymphocyte count and CD4 Lymphocyte Percentage

HIV Viral Load Tests

CBC

DNA - Viral nucleic acid tests

Viral Culture

Immunofluorescence Antibody Testing

Urine and Saliva Serologic Testing

Home Testing

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69
Q

ELISA Testing

A

Enzyme Linked Immunosorbent Assay

Determines response of antibodies to HIV Virus

Used in children older than 18 mo

High sensitivity with low specificity - so lots of false positives

There is a plate of viral particles mixed and if there is antibodies they will bind to the antigens on the bottom of the plate, then if more antibodies that change color are added then it is a positive case

If blood washes off and no color change occurs it is negative

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70
Q

What is ELISA good as?

A

A Screening Test

High sensitivity means it can rule out those without HIV but low specificity means you can have a lot of false positives

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71
Q

Western Blot Testing

A

Confirms the presence of HIV Antibodies and is more specific for HIV

Useful children 18 mo and up

Positive HIV antibody test in children younger than 18 mo only indicates the mother is infected

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72
Q

What are the most common HIV tests?

A

ELISA and Western Blot

73
Q

How are ELISA and Western Blot used together

A

You can be confident in a negative ELISA test, but if there is uncertainty with a positive you can confirm it with a western blot (which sorts out the false positives)

74
Q

P24 Antigen Test

A

Used to detect HIV Antigen in children <18 mo

Test can be useful at any age

Only a positive result is significant!

2 or more positive results are diagnostic for HIV Infection

It looks for the p24 protein on HIV - so this test looks for the actual virus rather than antibodies like in ELISA and W Blot

75
Q

Why may a p24 Antigen Test be used immediately upon suspicion?

A

Since ELISA and W Blot take 3-6 months since thats how long it takes to make antibodies, this can be positive for looking the virus itself while the the other two can come out false negative if done too early

76
Q

In what situation is a p24 Antigen test very helpful?

A

For immediate use after finding out your partner is HIV+

77
Q

CD4+ Testing

A

Used to assess immune status, risk for disease progression and need for PCP Prophylaxis

This checks for the CD4+ (T4/Helper Cells) and can be used to see how the immune system is working and how far an already known case has progressed

78
Q

DNA HIV - Viral Nucleic Acid Tests

A

ex: PCR - Polymerase Chain Reaction, Nucleic acid sequence based amplification, Branched chain DNA tests

These kinds of tests look for minute amounts of HIV and use special replication processes to make things larger and large until we can get a viral load that is detectable and countable

79
Q

What is a massive advantage to DNA HIV - Viral Nucleic Acid Tests?

A

They can shorten the window period allowing detection of HIV in as little as 12 days

80
Q

HIV Viral Culture

A

Highly specific test

Negative results are meaningless since it can be very difficult to grow

Not frequently used to diagnose HIV

81
Q

IAT (Immunofluorescence Antibody Testing)

A

Alternative to the western blot in order to confirm HIV infection

A positive ELISA can be followed by a W Blot or IAT

82
Q

Urine and Saliva Serologic Testing (EIA)

A

Ex: Urine EIA, Saliva EIA, Rapid Enzyme EIA

This tests for HIV Antibodies

83
Q

Home Testing

A

Fingerstick specimen is sent to a laboratory to detect HIV

84
Q

Significance of an ELISA HIV Test

A

It is a screening test for HIV Antibodies

85
Q

Significance of Western Blot and IAT for HIV?

A

Confirmatory Tests for HIV Antibodies

86
Q

CBC for HIV Significance

A

Anemia, Neutropenia, and Thrombocytopenia indicate infection

Shows blood manifestations that may occur as a result of the disease

87
Q

Absolute CD4 Lymphocyte Count Significane

A

Predictor for HIV Progression and immune function

88
Q

What level of CD4 indicates an increased risk for infection and malignancy (count and percentage)?

A

CD4 <200 cells/mcL

CD4 <20%

89
Q

CD4 Lymphocyte Percentage Significane

A

Predictor for HIV Progression and monitors immune function

90
Q

HIV Viral Load Test Significance

A

Measures the amount of actively replicating HIV and correlates levels with disease progression

Can also monitor disease activity

91
Q

P24 Antigen Test Significance

A

Indicates active HIV replication is occurring

Cannot give a definite negative, but a positive can be detected through finding HIV viral particles quickly

92
Q

What are the Laboratory Criteria for a positive case of HIV?

A
  1. Positive result from an HIV antibody screening test, i.e. ELISA, confirmed by a positive result from a supplemental HIV antibody test, i.e. W blot.

OR

  1. Positive result or report of a detectable quantity from any of the following HIV virologic (NON ANTIBODY) Tests: HIV Nucleic Acid Detection Test (i.e. PCR), HIV pp24 Antigen Test with Neutralization Assay, or HIV Isolation (Viral Culture)
93
Q

What is the overall takeaway about HIV Diagnosis?

A

Results are rarely determined by just one test, need multiple

94
Q

HIV Disease Process Definition

A

A chronic infection (no longer a death sentence) with a very variable course (may take a while, but extensive seeding worsens prognosis)

It infects cells with CD4 receptors (T4 / Helper T Lymphocytes)

Leads to cell death and decline in immune function

95
Q

S/S of HIV (Pre Symptomatic Phase)

A

Acute Infection

Self Limited Syndrome lasting 6-8 weeks post infection

Associations with development of HIV Antibody

Asymptomatic Infection/Period

Persistent Generalized Lymphadenopathy

96
Q

Acute HIV Infection

A

Initial symptoms in the window period / up to 6-8 weeks post infection associated with antibody development

Not often equated to HIV

S/S: - Flu Like:
Mononucleosis Like Syndrome
Fever
Rash
Myalgia
Malaise
97
Q

Asymptomatic HIV Infection

A

Period following initial infection

Variable duration (depends on treatment)

No S/S except potential persistent generalized lymphadenopathy

During this time ELISA can show you have antibodies indicating exposure

98
Q

Persistent Generalized Lymphadenopathy (PGL)

A

Lymph node enlargement 1 cm or greater in two or more extra-inguinal sites (generalized in the body and they are persistent and stay large in the neck, arm, etc)

It is assoc with inflammation and infection in the nodes

Adenopathy is if they are 1 cm in 2 or more extra inguinal sites for longer than 3 months!

99
Q

HIV Disease Spectrum

A
  1. 1-3 mo: HIV infection / Window Period- Flu like symptoms
  2. 1-10+ Years: Asymptomatic Period - no symptoms, except potential PGL
  3. Post-Asymp.: Symptomatic Period - after the immune system is worn down
  4. Post Symptomatic and Meets Criteria: AIDS
100
Q

Window Period

A

Time 1-3 months post infection when antibodies are formed and the initial HIV infection occurred

It is a window since we generally cannot diagnose the disease during this time

101
Q

What are some S/S that begin to occur once the immune system is worn down by HIV and the symptomatic period begins?

A

Fatigue

Diarrhea

Fever

Thrush

Skin Rash

Weight Loss

Swollen Glands

102
Q

Thrush

A

Yeast infection in the mouth

Commonly seen in symptomatic HIV Patients

103
Q

Is infection and symptoms occurring indicative of HIV becoming AIDS?

A

NO

Infections will occur more without an immune system, but there are defining conditions for AIDS

These infections are opportunistic and could occur to anyone, but AIDS defined conditions are highly unusual

104
Q

AIDS Stage

A

Final stage of HIV Infection

The conditions defining AIDS are significant opportunistic conditions such as oral candidiasis in the mouth down to the throat and esophagus

105
Q

Who determined what conditions are defining conditions of AIDS?

A

WHO

106
Q

Course and general time periods for the Clinical Presentation of HIV Infection

A
  1. Window Period/Acute Infection - no antibodies, flu like symptoms - within 2-4 months post infection
  2. Asymptomatic/Subclinical Phase - virus and antibodies are present with no symptoms except lymph enlargement, and can be tested for during this period - 4 months to about 8+ years
  3. HIV Related Disease/Symptomatic Period - Infections begin to occur as the immune system weakens, but not the massive once indicative of AIDS - Whenever subclinical phase ends until onset of AIDS
  4. AIDS - about 10 years out if they follow treatment - severe opportunistic conditions that can cause death
107
Q

How does Viral Load for HIV change over the course of infection?

A

Initially there is a large spike from reverse transcriptase and new replication, but they are killed off quickly

But once the immune system cannot keep up, the seeded HIV will rise again and win over the body

108
Q

How do HIV Antibody levels change over the course of infection?

A

Initially upon infection there will be none with some initial IgM followed by IgG response typical of immune response

Overtime IgG will rise over several months and then plateau

As HIV destroys T4 cells, B cells will not activate and this means there is less IgG, so overtime the levels will drop

At the end of life they are anergic with no antibodies left - so there wouldn’t even be a Tb reaction upon testing!

109
Q

How does CD4 Cell Count change over the course of HIV infection?

A

T4 will initially go up during the first few months and drop during the acute infection, but during the asymptomatic period it will gradually decline (while viral load increases)

Once low enough major opportunistic infections occur resulting in AIDS

110
Q

What level of CD4 is indicative of major opportunistic infections and an AIDS diagnosis?

A

Below 200 cells/mcL

Below 600 indicates the non normal range

111
Q

Infection Staging of HIV

A

Stage 1
Stage 2
Stage 3 (AIDS)
HIV Infection, Stage Unknown

112
Q

Stage 1 HIV

A

No AIDS Defining condition AND EITHER:

  1. CD4+ T Lymphocyte count of >500 cells/mcL
    OR
  2. CD4+ T Lymphocyte percentage of total lymphocytes of > 29%

*No s/s occur during this time

113
Q

Stage 2 HIV

A

No AIDS Defining Conditions AND EITHER

  1. CD4+ T Lymphocyte count of 200-499 cells/mcL
    OR
  2. CD4+ T Lymphocyte percentage of total lymphocytes of 14-28%
114
Q

Stage 3 HIV

A

Full Blown AIDS:

CD4+ T Lymphocyte of <200 cells/mcL

OR

CD4+ T Lymphocyte percentage of <14%

OR

Documentation of AIDS defining condition

115
Q

What supersedes CD4+ count and percentage for an AIDS diagnosis?

A

An AIDS defining condition

If you have an AIDS condition, you have AIDS, regardless of the count

116
Q

HIV Infection, Stage Unknown

A

No information available on CD4+ T Lymphocyte count or percentage, and no information available on AIDS defining conditions

117
Q

What is a major cause of death and comorbidity during Stage 3 HIV?

A

Tuberculosis (Tb)

118
Q

HIV has __ Effects

A

Systemic

*It spreads through the whole body and effects all systems and organs of the body - just having systemic symptoms may not cause you to think of HIV immediately though until you get an AIDS defining condition

119
Q

Areas of the Body that may have HIV Systemic Effects occurring?

A

Systemic

Sinopulmonary

CNS Diseases

Peripheral Nervous System Disease\

Rheumatologic Manifestations

Myopathy

Oral Lesions

Retinitis

GI Manifestations

Endocrine Manifestations

Skin Manifestations

Inflammatory Reactions

HIV Related Malignancies

Gynecologic Manifestations

IT IMPACTS EVERYTHING!!!!!

120
Q

What are some examples of the systemic effects of HIV?

A

Fever

Night Sweats

Weight Loss

Nausea

(These things compounded with other system effects can lead to poor body image and also increased incidence of cancer)

121
Q

Informational Card:

What are some Sinopulmonary systemic effects of HIV?

A

Pneumocystis Carinii PNeumonia (AIDS defining)

Non infectious Pneumonia

Sinusitis

122
Q

Informational Card:

What are some CNS Disease systemic effects of HIV?

A

toxoplasmosis

CNS lymphoma

AIDS DEMENTIA!!! Complex

Cryptococcal meningitis

HIV Myelopathy

Progressive multifocal leukoencephalopathy

123
Q

Informational Card:

What are some PNS disease systemic effects of HIV?

A

Peripheral Neuropathy

124
Q

Informational Card:

What are some rheumatologic manifestation systemic effects of HIV?

A

arthritis

SLE

125
Q

Informational Card:

What are some myopathy systemic effects of HIV?

A

Proximal muscle weakness

126
Q

Informational Card:

What are some oral systemic effects of HIV?

A

oral candidiasis

hairy leukoplakia

angular cheilitis

gingivitis

aphthous ulcers

127
Q

Informational Card:

What are some retinitis systemic effects of HIV?

A

CMV (cytomegalovirus)

blindness

128
Q

Informational Card:

What are some GI manifestation systemic effects of HIV?

A 
Candidial esophagitis
Hepatic disease
Biliary disease
Enterocolitis
Gastropathy
Malabsorption syndrome
129
Q

Informational Card:

What are some endocrine manifestation systemic effects of HIV?

A

Adrenal insufficiency

Thyroid function

130
Q

Informational Card:

What are some skin manifestation systemic effects of HIV?

A 
Herpes simplex infections
Herpes zoster
Molluscum contagiosum
Folliculitis
Superficial abscesses
Bullous impetigo
Bacillary angiomatosis
Fungal rashes
Kaposi’s sarcoma
Seborrheic dermatitis
Xerosis
Psoriasis
131
Q

Informational Card:

What are some inflammatory systemic effects of HIV?

A

Unusual presentations of opportunistic infections

132
Q

Informational Card:

What are some HIV related malignancy systemic effects of HIV?

A 
Kaposi’s sarcoma
Non-Hodgkin's lymphoma
Hodgkin’s Disease
Anal dysplasia & squamous cell carcinoma
Cervical dysplasia & neoplasia
133
Q

Informational Card:

What are some gynecologic manifestation systemic effects of HIV?

A

Vaginal candidiasis
Cervical dysplasia & neoplasia
Pelvic inflammatory disease

134
Q

What are the treatment guidelines like for HIV?

A

Treatment guidelines have changed many times

Many views on this subject –> ultimately decision to begin treatment rests with the patient and the doctor

There are HIV treatment guideline portals for use as well

135
Q

Drug Resistance Testing

A

Testing recommended when entering care (regardless of therapy or treatment and whether it begins immediately) to check for HIV resistance to drugs

Should be used to determine what drugs should be selected when changing antiretroviral regimens

136
Q

Types of Drug Resistance Testing for HIV

A

Genotypic Assays

Phenotypic Assays

137
Q

Genotypic Assays

A

Detects drug resistance mutations present in relevant viral genes

this one is generally preferred for antiretroviral (drug) naive persons

usually done first to identify the strain, and then if treatment fails a phenotypic assay is done

138
Q

Phenotypic Assay

A

Like a sensitivity test

measures the ability of a virus to grow in different concentrations of antiretroviral drugs

139
Q

Is Genotypic Resistance Testing recommended for pregnant women?

A

Yes

It should be done prior to initiation of therapy and for those entering pregnancy with detectable HIV RNA levels while on therapy

140
Q

What are the HIV Treatment Goals

A
  1. Reduce HIV Related Morbidity and prolong survival (it is no longer death sentence, its a chronic condition)
  2. Improve quality of life
  3. Restore and preserve immunologic function (keep T4 high)
  4. Maximally and durably suppress viral load (use antiretroviral drugs)
  5. Prevent vertical HIV transmission
141
Q

HAART

A

Highly Active Antiretroviral Treatment

It is a treatment to keep the HIV viral load to undetectable levels and minimize seeding of the lymphatic system with HIV by hitting it fast, hard, and early

Its a multi drug approach though to strike at various points of the viral life cycle

142
Q

What things do the multiple drugs in HAART do?

A
  1. Decrease development of resistance to medications

2. Minimize medication toxicities (by having many drugs at low doses)

143
Q

What can make HIV treatment difficult?

A

If there is extensive seeding and the virus is latent

144
Q

The drugs that treat cancer and HIV vary enough so that they …

A

can prevent steps at all phases of viral/cancer replication

145
Q

What can be difficult about HAART?

A

While we give low doses of multiple drugs to decrease toxicity and SE, the side effects are sometimes too much for people and they stop taking them (which can lead to viral resistance)

The older treatment drugs used to be far hasher as well on people

146
Q

What is a common drug used in HAART?

A

AZT

147
Q

What has HAART done for the HIV epidemic?

A

It has boosted treatment as prevention and greatly reduced progression to AIDS

This keeps T4 higher and keeps the viral load down to stay asymptomatic longer

148
Q

What viral load amount of HIV makes transmission almost nil?

A

50 copies per mililiters

149
Q

What categories of pharmacotherapeutics are important for treating HIV

A
  1. Antiretrovirals

2. Treatment Regimens

150
Q

What are the major categories of Antiretrovirals

A
  1. Nucleoside Revers Transcriptase Inhibitors
  2. Non-nucleoside Reverse Transcriptase Inhibitors
  3. Protease Inhibitors
  4. Fusion Inhibitors
151
Q

What are important considerations for treatment regimens for HIV?

A
  1. Combination therapy with demonstrated clinical benefit (helps reduce toxicity)
  2. Do Treatment with agents no previously exposed to
  3. Non-overlapping toxicities & avoid negative synergism (drugs inhibit each other’s activity - avoid these)
152
Q

Reverse Transcriptase Inhibitors

A

Antiretroviral

Acts early in the HIV life cycle

Prevents the HIV enzyme from making vDNA from vRNA –> prevents new viruses from being produced since it cannot make DNA to get into the genome

2 forms: nucleoside and nonnucleoside

Breaks the “teeth off the DNA zipper”

153
Q

What is the difference between Nucleoside and Non-nucleoside Reverse Transcriptase Inhibitors?

A

Nucleoside - work by chain termination and competitive inhibition of nucleoside triphosphates - this affects the building blocks of vDNA

Nonnucleoside - Do NOT need intracellular phosphorylation for activation; Directly bind to and disrupt catalytic sites of revers transcriptase –> chain termination — so this one works on the enzyme to cause chain termination at the catalytic site

154
Q

You can salvage an attacked cell if..

A

you get to it before vDNA is produced

155
Q

Protease Inhibitors

A

Antiretrovirals

Act late in the life cycle of the HIV

Block HIV enzyme proteases –> prevents creation or cleavage of HIV polyproteins needed for production of new virions

It prevents proteins produced from ribosomes from making the capsid, thus preventing virion babies

156
Q

Fusion Inhibitors

A

Antiretrovirals

Act very early in the cycle by preventing viral contents from even getting in!

Attach to proteins on the surface of T cells or HIV

Prevent the binding of proteins on HIVs outer coat (GP120 and GP41) with surface receptors of T cells (CCR5 and CXCR4 = CD4 receptors)

Newest kind of med but one of the best to prevent seeding

157
Q

Enfuvirtide

A

Fusion inhibitor that binds to GP41 to prevent HIV from binding to cells

158
Q

Pre-Exposure Prophylaxis (PrEP)

A

Prevention medication - ex: truvada

Given to HIV(-) people who engage in risky behaviors in order to prevent HIV infection

Blocks HIV Reverse Transcriptase

MUST BE TAKEN DAILY TO PREVENT

Requires quaterly testing for HIV, STDs, and SEs

159
Q

Who else can take PrEP?

A

No just negative HIV prevention cases, but also positive individuals can take it as a reverse transcriptase inhibitor

160
Q

Side Effects of PrEP

A

Nausea

Mild Bone Density Loss

Kidney Problems

(all stop once meds are done)

161
Q

Downfall of PrEP prevention

A
  1. no protection against other STDs
  2. needs to be taken daily
  3. needs quarterly testing for HIV, STDs, and SE
162
Q

Common HIV Drug Side Effects

A

Diarrhea

Pancytopenia

Dyslipidemias

Lipodystrophy

Lactic Acidemia

Hypertriglyceridemia

Nephrolithiasis

Insulin Resistance

163
Q

What is the key issue for HIV drug treatment?

A

ADHERENCE

They must adhere to get maximal and durable suppression of HIV activity and immune preservation or prevent the infection

It can be tough because of the SE (like potential type II diabetes)

164
Q

Why is Adherence to HIV drugs such a big issue?

A
  1. Optimum therapeutic response needs adherence
  2. Treatment failure leads to increased seeding in lymphoid reservoirs
  3. Adherence is the only thing preventing drug resistance
165
Q

Lipodystrophy

A

fat redistribution

The fat goes to become central fat or a buffalo hump - but this is moreso the case in older meds we rarely use now

166
Q

What is the prognosis for untreated HIV–>AIDS?

A

life expectancy of 2-3 years

167
Q

When does AIDS usually develop?

A

When CD4 < 200

168
Q

What is CD4 decline like in untreated HIV?

A

declines at about 50-80 per year and gets more rapid as it drops below 200

169
Q

What is the important takeaway about treatment of HIV presently?

A

Potent antiretroviral regimens may delay or even reverse immune dysfunction - now people can live long and relatively healthy lives

170
Q

Who is the major group of Pediatric HIV patients?

A

Newborns that contracted it from their mother either through placenta, blood exchange during vaginal delivery, or milk during breastfeeding

171
Q

When do pediatric HIV symptoms usually develop?

A

Within 6 months

172
Q

What is the life expectancy of a pediatric HIV patient?

A

<3 years old

173
Q

What is the transplacental infection rate for giving HIV to a newborn?

A

30% (chance to give via placenta)

174
Q

Treatment of an HIV+ mother can reduce perinatal transmission by how much?

A

66%!

This brings vertical transmission chance from 30% down to 2%

175
Q

Post Exposure Prophylaxis

A

Universal precautions and prophylaxis used in order to treat accidental exposure to HIV for a healthcare worker like a needlestick accident

176
Q

Post Exposure Prophylaxis, so long as its caught within 24 hours, have a __% chance of effective prevention of the virus?

A

100%

177
Q

Effectiveness of Post exposure prophylaxis drops __% in those treated within 72 hours rather than 24

A

52%!

178
Q

At what point is someone not a candidate for post exposure prophylaxis?

A

if not treated within 72 hours of exposure

179
Q

What is the key to maintaining and preventing the HIV virus?

A

Early Detection and Treatment (to decrease transmission and maintain health)

NURS361 - Pathophysiology II (20 decks)

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