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Human Immunodeficiency Virus (HIV) Infection and Acquired Immunodeficiency Syndrome (AIDS)
Human Immunodeficiency Virus (HIV) Infection and Acquired Immunodeficiency Syndrome (AIDS)
AIDS
NOTE:
● Strategic goals:
2. Epidemiology:
Note: In the 1984, the first case of AIDS was identified then the
following year the Department of Health began serological
surveillance for HIV. In 1986, HIV was declared a notifiable Predictions for the leading causes of disabilityand mortality in
disease and thefollowing year the National AIDS Prevention and 2030
Control Committee was created. In the year 1991, National
Sentinel Surveillance initiative to monitor trends of HIV/AIDS in
high-risk groups and determine its spread in low-risk groups. In
the year 1992, National AIDS prevention and Control Programs
Surveillance and Education Activities were created.
2. Many older adults do not consider themselves at risk for HIV HIV – is a retrovirus
infection.
❖ Cannot replicate outside of living host cells.
● Because they say that they are so strong. SaPilipinas
usually sinasabi na malakas pa ako sa kalabaw ❖ Contain only RNA; no DNA
unknowingly hindi talaga nila alam ang maidudulot ng
❖ Differs from other viruses because of anenzyme called
HIV
reverse transcriptase which help the virus replicate and
3. Older gay men, who grew up and lived in an era when place its genetic material in the deoxyribonucleic acid
disclosure of their sexual orientation was not acceptable and (DNA) of the host cell.
who have lost long-time partners, may begin new relationships
RESULT = replication of as many 2 billion viralparticles/day
with younger men. released from the host cell into thecirculatory system, infecting
4. Older adults may be intravenous (IV)/injection drug users. other cells in the body.
2 HIV subtypes
Seventh is cleavage. The HIV enzyme protease cuts now the Stage 0 - Primary Infection (Acute/Recent HIV Infection, Acute
polyprotein chains into the individual proteins that make up the HIV Syndrome)
new viruses.
• The period from infection with HIV to the development of
And number 8, we have budding. This time new proteins and HIV-specific antibodies (within 2to 4 weeks after infection
viral rna migrate to the membrane of the infected CD4 T-Cell, with HIV).
exit from the cell and start the process all over. When the buds
rupture they release many copies of the virus which will infect • Window period – is the time it takes for the bodyto produce
other T-Cells. HIV antibodies after being exposed to HIV.
STAGES OF HIV DISEASE • During this stage an HIV-positive person tests negative on
the HIV antibody blood test,although he or she is infected
and highly infectious, because his or her viral load is very
high.
During this time the immune system reacts tothe virus by Note: In stage 0, when the body’s immune system puts up a fight,
developing antibodies – this is referred to as it is called ARS, yung akala flu lang. So eto yung time na
seroconversion. sasabihin ng infected client na parang trinatrangkaso ako
because he got the infection at the time. So early symptoms of
infection disappear on their own within weeks, ay ok na ko
minsan sasabihin niya. Going back we have theearly symptoms,
this would include most common ofall we have fever, nilalagnat
po ang ating patient. Then makakaramdam po siya ng
headache, lymphadenopathy, pharyngitis, skin rash, body
aches, we have your myalgias, arthralgias, then we have your
diarrhea and night sweats.
Refer to the pic above: “Within 4-8 weeks, yung viralset point
Stage 1 - HIV Asymptomatic /Chronic HIV infection (More natin is represented by red lines after that, bumagsak or kumonti
Than 500 CD4 T Lymphocytes/mm3) ung viral set point which is pagdating ng 2-12 years”
● Stage is free from symptoms, person may lookand feel
well but HIV is continuing to weaken his immune system.
Stage 2 - HIV Symptomatic ( 200 to 499 CD4 T
● Level of HIV in the blood drops to very low levels. Lymphocytes/mm3)
● HIV neutralizing antibodies are detectable in the blood The immune system becomes damaged and weakened
by HIV and symptoms develop.
● May have : Persistent generalized lymphadenopathy
The symptoms are caused by the emergence of
(PGL) - painless, non- tender enlarged lymph nodes
opportunistic infections (illness caused by various
(lymphadenopathy) in at least two areas of thebody for
organisms, some of which USUALLY do not cause disease
at least 3 months,
in people with normal immune system. (but because of the
trap in theimmune system of patient with HIV, this time
they can’t protect themselves so opportunistic infection
emerges.)
Examples of conditions
• It is a white lesion on the lateral border of thetongue This condition is more commonly referred to as
and associated with AIDS. immune thrombocytopenia
We can see in the picture the time where infection set in and the
time of years in horizontal lines. May decline sa CD4 cell from
1st year to 2nd year to 3rd year and 4th year makikita natin
na may bacteria infection then varicella zoster, these are early
opportunistic infection then later on may late opportunistic
infections as CD4 cells continue todecline
Stage unknown refers to a person with laboratory confirmation
of HIV infection, but no information about CD4 cell count or
percentage (and no information about the presence of AIDS-
defining clinical conditions).
3. Tuberculosis – s/s
Night sweats
Integumentary Manifestations
• Generalized folliculitis
HOW HIV SPREADS
• Seborrheic dermatitis
• Molluscum contagiosum is a viral infection ● Unprotected penetrative sex - have vaginal, anal or oral
characterized by deforming plaque formation. sex with an infected partner whose blood, semen or
vaginal secretions, enter the body. The virus can enter the
body through mouth sores or small tears that sometimes
develop in the rectum or vagina during sexual activity.
In this picture, we have a patient with this disease ● By sharing needles - Sharing contaminated IV drug
paraphernalia (needles and syringes) putsyou at high risk
Lesions in the groin and thigh areas on presentationof a 25- of HIV and other infectious
year-old, HIV-seropositive man with molluscum contagiosum virus
infection. Extensive, ulcerating lesions were accompanied by
perinodularscarring.
4. Environmental control: Develop procedures forroutine care, • Means taking HIV medicines within 72 hours after a
cleaning, and disinfection of environmental surfaces, especially possible exposure to HIV to prevent HIVinfection
frequently touched surfaces in patient care areas.
• After an unintended exposure to the blood or body fluids
5. Textiles and laundry: Handle in a manner that prevents of a person who either is HIV positiveor whose HIV status IS
transfer of microorganisms to others and tothe environment. UNKNOWN, the need for post-exposure prophylaxis (PEP)
6. Needles and other sharps: Do not recap, bend, break, or must be assessed within 2 hours.
hand-manipulate used needles. • Exposure can be – large bore needle stick, significant
mucosal contact with body fluids, contact with body fluids
7. Patient resuscitation: Use mouthpiece, resuscitation bag, via break in the skin.
and other ventilation devices to prevent contact with mouth and
oral secretions. Post Exposure Prophylaxis for Health CareProviders
8. Patient placement: Prioritize for single-patient room if ● It includes taking antiretroviral medicines ASAP, but no
patient is at increased risk of transmission, islikely to contaminate more than 72 hours(3 days) afterpossible HIV exposure;
the environment, does not maintain appropriate hygiene, or is at 2 or 3 drugs are usually prescribed which must be taken
increased risk of acquiring infection or developing adverse for 28days.
outcome following infection
● Retrovir (zidovudine) and Epivir (lamivudine) for 28
9. Respiratory hygiene/cough etiquette days
Instruct symptomatic people to cover mouth andnose when ● Occupational exposures – needle stick injury
sneezing or coughing
• Wear a surgical mask if tolerated. 1. Nucleic Acid Tests (NAT) a.k.a.RNA test
2. Antigen/Antibody Tests
3. Antibody Tests
• Abacavir (Ziagen)
• Tenofovir (Viread)
• Emtricitabine (Emtriva)
• Lamivudine (Epivir)
• Zidovudine (Retrovir).
Examples
- Bictegravir Sodium/
Emtricitabine/Tenofovir Alafenamide Fumar
(Biktarvy)
- Raltegravir (Isentress)
• As we see in the picture yung pinag-aralan natin yung
- Dolutegravir (Tivicay).
HIV cycle life, what will the drug do? It will now stop,
so NNRTIs and NRTIs now block the conversion of HIV 5. Entry or fusion inhibitors block HIV's entry intoCD4 T cells.
RNA to HIVDNA.
Examples
2. Non-nucleoside reverse transcriptaseinhibitors (NNRTIs)
turn off a protein needed by HIV to make copies of itself. - Maraviroc (Selzentry).
- Enfuvirtide (Fuzeon)
Examples
Examples:
- Atazanavir (Reyataz)
- Darunavir (Prezista)
- Lopinavir/ritonavir (Kaletra)
1. Hepatotoxicity
2. Nephrotoxicity
3. Osteopenia
4. Increase risk of CVD and MI
TREATMENT OF OPPORTUNISTICINFECTIONS
5. Fat redistribution syndrome
Pneumocystis Pneumonia
6. Metabolic alterations – dyslipidemia, insulin resistance
7. Fat redistribution syndrome • Trimethrophim – sulfamethoxazole (TMP- SMZ) is the
(LIPODYSTROPHY) treatment of choice.
• Adjunctive corticosteroids should be started as early as
• Lipoatrophy – localized subcutaneousfat loss in possible and certainly within 72 hours after starting
the face, arms, legs andbuttocks. specific PCP therapy.