Week 3 Flashcards

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1
Q

clinical presentation of Pneumocystis jirovecii pneumonia

A
• progressive dyspnea on exertion 
• nonproductive cough 
• fever 
• chest discomfort 
• subacute onset 
- tachnypnea, hypoxia
-tachycardia
- end-inspiratory crackles
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2
Q

AIDS

A
  • Acquired Immunodeficiency Syndrome.
  • AIDS is the most advanced stage of HIV infection characterized by abnormally low CD4 lymphocyte count (less than 200 cells/µL) or occurrence of opportunistic infections associated with HIV-induced immunosuppression
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3
Q

effect of HIV on CD4 T-cells

A
  • HIV attacks and kills/deactivates CD4 cells

- the longer HIV is uncontrolled the lower the CD4 count goes

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4
Q

significance of CD4 lymphopenia in HIV infection

A
  • As the CD4+ T cell count continues to drop, risk for an opportunistic infection increases due to the inability of the immune system to fight off these infections like it normally would.
  • Once the CD4+ T cell count drops below 200, a person is diagnosed with AIDS.
  • There are HIV associated infections based on CD4+ T Cell Count
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5
Q

laboratory methods used to evaluate HIV/AIDS

A
  • Rapid testing : second-generation HIV immunoassays that measure immunoglobulin (Ig) G antibody to HIV-1 and HIV-2 in blood or oral fluids, used for at risk patients
  • use 3 diff amino assays; 1st: screening for HIV1-2 antigen/antibody; 2nd: HIV 1 and 2 differentiation immunoassay; 3rd: HIV1 nucleic acid testing, HIV RNA testing on pooled HIV antibody-negative specimens from individuals in high-prevalence populations
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6
Q

Epidemiology Pneumocystis jirovecii

A
  • causes infection almost exclusively in debilitated and immunosuppressed patients, especially those with HIV infection.
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7
Q

HLA B5701 testing

A

A test that detects the presence of HLA-B5701. HLA-B5701 is a genetic variation that is linked to hypersensitivity to the antiretroviral (ARV) drug abacavir. A person who tests positive for HLA-B*5701 should not use abacavir or any other abacavir-containing medicine.

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8
Q

HIV resistance tests

A

used to help select a drug regimen that will likely be effective in treating a person with an HIV infection. The test is used to determine whether the HIV strain infecting an individual is resistant or has developed resistance to one or more drugs used to treat HIV. Testing analyzes the genes of the virus to detect the presence of one or more mutations that are associated with antiretroviral drug (ART) resistance.

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9
Q

ART

A
  • Antiretroviral Therapy.
  • six major classes
  • usually includes a combination of two nucleoside analogue reverse transcriptase inhibitors (NRTIs) plus a third medication from a different class.
  • should be offered to all patients with HIV infection, regardless of CD4 count
  • achieve an undetectable HIV viral load
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10
Q

initial presentation (signs/symptoms) of acute HIV infection

A
  • often mistaken for infectious mononucleosis
  • fever, malaise, fatigue, several types of dermatitis, sore throat, arthralgias, generalized lymphadenopathy, and septic meningitis.
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11
Q

modes of transmission of HIV

A
  • requires contact with body fluids
  • Sexual: Direct transfer of genital, rectal or oral fluids through sexual intercourse
  • Needle- or instrument-related: Sharing of blood-contaminated needles or exposure to contaminated instruments
  • Maternal: Childbirth or breastfeeding
  • Transfusion- or transplant-related
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12
Q

risk factors associated with HIV infection

A
  • Unprotected sexual intercourse, especially receptive anal intercourse (8-fold higher risk of transmission)
  • A large number of sexual partners
  • Prior or current sexually transmitted diseases (STDs): Gonorrhea and chlamydia infections increase the HIV transmission risk 3-fold, syphilis raises the transmission risk 7-fold, and herpes genitalis raises the transmission risk up to 25-fold during an outbreak
  • Sharing of intravenous drug paraphernalia
  • Receipt of blood products (before 1985 in the United States)
  • Maternal HIV infection (for newborns, infants, and children): Steps taken to reduce the risk of transmission at birth include cesarean delivery and prenatal antiretroviral therapy in the mother and antiretroviral therapy in the newborn immediately after birth.
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13
Q

Pathophysiology of HIV

A
  • HIV attaches to and penetrates host T cells via CD4+ molecules and chemokine receptors.
  • After attachment, HIV RNA and several HIV-encoded enzymes are released into the host cell.
  • Viral replication requires that reverse transcriptase (an RNA-dependent DNA polymerase) copy HIV RNA, producing proviral DNA;
  • Proviral DNA enters the host cell’s nucleus and is integrated into the host DNA in a process that involves integrase,
  • With each cell division, the integrated proviral DNA is duplicated along with the host DNA.
  • proviral HIV DNA can be transcribed to HIV RNA and translated to HIV proteins
  • envelope glycoproteins 41 and 120 are assembled into HIV virions at the host cell inner membrane and budded from the cell surface within an envelop of modified human cell membrane.
  • Each host cell may produce thousands of virions.
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14
Q

How does HIV gain resistance

A
  • copying mechanism is prone to errors, resulting in frequent mutations and thus new HIV genotypes.
  • These mutations facilitate the generation of HIV that can resist control by the host’s immune system and by antiretroviral drugs.
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15
Q

Two main consequences of HIV infection are

A
  • Damage to the immune system, specifically depletion of CD4+ lymphocytes
  • Immune activation
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16
Q

opportunistic disease screening in patients newly diagnosed with HIV

A

a. PPD for TB
b. RPR for syphilis
c. Immunoassay for hepatitis
d. NAAT for Neisseria gonorrhea and Chlamydia trachomatis

17
Q

virologic failure

A

occurs when antiretroviral therapy (ART) fails to suppress and sustain a person’s viral load to less than 200 copies/mL.

18
Q

CCR5 co-receptor tropism

A
  • gp120 is able to attachto either CCR5 or CXCR4.
  • Mixed tropism results when an individual has two virus populations; one usingCCR5 and the otherCXCR4 to bind to the CD4 T-cell.
19
Q

signs/symptoms of acute Cryptococcus neoformans meningitis

A

• Headache, Confusion, Lethargy, Nausea and vomiting (with increased intracranial pressure), Fever and stiff neck (with an aggressive inflammatory response; less common)

20
Q

Pathophysiology of C neoformans

A

inhalation, the yeast spores are deposited into the pulmonary alveoli, where they must survive the neutral-to-alkaline pH and physiologic concentrations of carbon dioxide before they are phagocytized by alveolar macrophages