HIV Flashcards by Gabriel Faget

HIV genome characteristics?

-ss + RNA enveloped DIPLOID Genome.

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Mechanism transmission?

-Fluid (mayorly sexuxally>IV drugs>blood transfusion)

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What genes and products are ass.?

1.Envp.–>gp160= gp140 (attaches CD4+ Tcells) + gp41 (fusion)
2.Gag–> p24 (antigen that diagnosig test detects + p17
3.Pol.–> Revrse Transcriptase, Integrase, Protease.

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What are the steps of HIV infections?

1.gp binding to CD4+ recep (Tcells, machrophages, dendtitic cells)
2.Co-stimulation–> CCR5(Early–>present in macrophages)
and CRX4 (Late—>present more T cells).
3.Infusion occures (due to co-stimulation promotes gp41 expression–>fusion).Then reverse transcriptase,integrase, and protease do there thing.

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Why some people get HIV but don’t get sick?

Homogenous mutations–>Immunity
Heterogenous mutations—>Resistance

-All towards CCR5.

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What the normal T cell count?

500-1K

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Why on latency phase you don’t have sympt?

-Due to CD8 T cells finding the infecton–> CD4 T cells are being killed (reducing).

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What are the HIV stages and there association on what hapening and CD4+ T cell count?

-Flu-like: virus reaches lymph nodes–>promotes viral replicat and drop CD4+ count–>immune system activation–>incr CD8+ and CD4+–>stop of sympt.** 300-1K T cell count**

Feeling Fine (latent)–>virus spiking slowly (2-10yrs.) T cell count normal

Falling Count–> <300 T cell count

Final Crisis–>AIDS <200 T cell count–><100 or even <50. Due to CD8+ Exhaustion

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What cell do you see in Hodgkins Lymphoma
Subtypes?

-Reedsternebrg cells (Owl Eye)–>CD15+ and CD30+

-Lymphoyte rich (Best prognosis)
Lymphoyte poor (WORST PROGNOSIS, immunocompromised)
Mixed (Eosinphilia, immunocompromised)
Nodular (most comm)

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NON- Hodgkin Lymphoma subtypes?

-Burkits
Diffuse
Follicular
Mantle
Marginal
CNS (consideres a AIDS defininig illnes ass with EBV)->confusion, memmory loss,seizures)

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How to differentiate NON-Hodgkyn Lymphoma with Toxoplasmosis?

-Do CSF analysis

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How do differentiated lesion between Kaposi and Bartonella lesion?

-Biopsy
Neutrophils–>zoonotic bact
Lymphocytes–>Virus

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What superimposed organism are asscociated with HIV ?

<500 (Candida,EBV,HPV,Mycobacterium TB, HHV-8 “Kaposi Sarcoma”)
<200 (Pneumocystitis Jirovecci, HIV related Nephropathy and cerebral atrophy, JC virus, Histoplasma)
<100 (EBV,Candida,Cryptococcus Neoformnas, CMV,Bartonella spp,Toxoplasma Gonddi).
<50 (M.Avium)

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Candida
Presentation
Treat

-<500–>Oral Trush (scrapable)
-<100->Esophagitis

-Treat -azole or Nystatin (topical)
-Pseudohyphae that at 20*C form Budding Yeast.

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EBV
Presentation
Treat
Cells it infects

-<500–>Oral Hairy Leukoplakia (NOT scrappable)
-<100–>CNS Lymphoma (single ring enhancing lesions on MRI)

-Diag:+Monospot test, atypical lymphocytes on smear
-Atacks CD21 cells (B cells)

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Mycobacterium TB
Presentation
Stain

-Recativation of latent TB–> Hemoptysis and lesion in upper lobes (more O2)

-Ziehl Neelsen stain (acid fast organism)–>have mycolic acid.

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Kaposi Sarcoma
-Presentation

-Endothelial tumor
-Red/Purple varocous plaque like lesions.
-HHV-8

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JC Virus

-What drug incr risk of getting complication of JC virus?

-Recativated and damages oligodendrocytes–>De-mylination–> Progressive Multifocal Leukoenchephalopathy–>Rapid progrosive disorder that is usually fatal, but iniatially present with vission,speech,coordination and memory problems.
-Can aslo present withn.
-MRI–> NON-Enhancing lesions in occipetal and parietal UMN lesion–.Hypertonia ans Hyperreflexia with +Babinski siglobes.

The disease progresses to blindness, dementia, coma, and death, typically within 6 months.

Natalizumab–> targets 4 alpha integrins–> PML

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Histoplasma
Presentation
Morphology

-Opportunisctic fungus, found in Bats and Bird poop and OHIO and Missipi valley (rivers).
-Present with generic symptoms (weight loos, fever….)
-Dimorphic fungi.

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Pneumocystis Jirovveci
-Presentation
-Specific finfing on test
-Culture
Treeat

-Cholesterol made fungus–>Silver stain to identify (beitifull blue sky).
-Causes Atypical pneumoniea (Ground Glass app on chest X-ray).
-SMX-TMP and Dapsone (same SMX), atovaquone (inhib mitocondrial activity),pentamidine

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Cryptoccocus Neoformans
Presentation
Special stain

-Ass with INHALING bird droppings.
Cryptococossis–>Enchephalitis (soap buble app),Meningitis and pneumonia.
-Indian Ink

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CMV
Presentation
3 special things you see.

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-CREEP (Colitis,Retinitis,Esophagitis,Enchephalitis,Pneumonia
-On biopsy you see intracytoplasmatic inclusion (Single OWL EYE)
Monospot test -
Endoscopy shows linear ulcers
Funduscopy–>cotton wool spots
HHV-5

Bartonella spp

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-Ass cat scratch
-Baciallry Angiomatosis–>Neutrophil infiltration

Toxoplasmosis Gondii

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-PROTOZOA. **
-Ass cat feces (oocytes) and eating cyst in meat.
Crosses placenta.
- Recativated on AIDS–>Brain abcess (multiple enhancing lesions)
- Biopsy–>Tachyzoits**

M.Avium

-<50 CD4+ -NON TB sympt with focal lymphadenotis,night sweats,weight loss, diarr.

HIV ass Dementhia is ??

-People with** low CD4+ count and High Viral Loads**. -Non being treated for HIV.

Bridinzki sign?

-Meningitis

Drug of choice for Pneumocystis Jirovecci?

-TMP-SMX

Where does your CD4+ drop the most

Acute phase

What time you start developing anti-gp120 antibodies against HIV?

1 month after initial infection and remains elevated for ever.

What we use to diag HIV?

HIV-1/2Ag/Ab immuno-assays (Highly specific and sensative -Misses acute phase-->you may proceed to VIRAL LOAD TEST (also used to monitor treat,) -If immunoassay is positive you must do NAAT. If immunoassay is negative,nothing else.

What are the diff clasdifications of HIV drugs?

NRTI'S NNRTI'S Integrase inhib. Protease inhib Entry inhib.

Abacavir,Tenofovir,Zidovudine?? AE

**NRTI's** -Competitive inhib. that block reverse transcriptase and need to be phosphorylated. **-TENOFOVIR** is the only nucleoTide (has sugar,phosphatea and base).All of the other are nucleoside **-Zidovudine**-->may be used for prophylaxis and PREGNANCY. AE: **Myelossupresion (Zidovudine),Nephrotoxicity(Tenofovir) and Abacavir prevented in HLA-B57 mutations-->causes hypersensitivity reaction. **

How to prevent myelosupression of NRTI"s?

-EPO, G-CSF (Granulocyte Colony Stimulating Growth Factor)

Intergrase inhib all end in... AE

---tegravir -AE: **incr CK (myopathy)** and weight gain

NNRTI's -AE

**Nevirapine** **Efavirenz** (AE: vivid dreams and CNS sympt) -Bind to other side in RT,therefore don't requiere phosphorylation. AE-->rash and hepatotoxicity

Why exactly do NRTI's requiere phosphorylation?

-The are nucleosides

Protease inhb. end in .....

---NAVIR -They inhibit maturation of virus. AE: Hyperglycemia

Ryfacymins characteristics (4)

-RNA polymerase inhib Red/orange fluif secretions Rapid resistance if used alone Ramps up Cyt P450

What relation does your Rifacymins have with Protease inhib?

Rimfampin will reduce action of Protease inhib. (by incr meatbolism) Rifabuitin-->dosen't have this effect.

What HIV drug is Cyt P450 inhibitor?

**-Rito**navir**

Enfuviritide Maraviroc

-Inhibits gp41-->dosent permit viral fusion. -Inhibits CCR5-->prevent initial interaction)

Why HIV virus mutates a lot?

-Rverse Transcriptase dosen't have ability to coorect mistakes.

What a good entry point of HIV virus?

-GI tract-->lot's of T cells.

Why is more common for males to transmit it tha female?

-More HIV in semen.

How does HIV cause neurological symptoms?

-Crosses BBB after acute phase and resides in macrophages, microglia and astrocytes-->dosent kill them. The gene are toxic to neurons.

What is the pre-exposure prophylaxis medications?

-Tenofovir + Emtricitabine (Both NRTI's)

What drug causes Mitocondrial toxicity??

-NRTI's -Loss mitoconcondria -**Peripheral neuropathy, **myopathy,**pancreatitis** and** lactic acidosis**

tat gene rev gene

activates transcription of genes transport mRNA from cytoplasm to nucleus **Both requires for viral replication-->NO drugs++ -Auxilliary genes-->NOT needed for replication (not import)

Which of the following factors is the most important determinant of the rate of disease progression from initial HIV infection to clinical diagnosis of AIDS?

-Initial HIV viral load-->if your start with high loads-->most rapidly to get a +HIV test. -If you start with low CD4+ count-->your virus will take mote time to replicate-->diagnosis time will take more.

Confirmatory test for HIV?

-NAAT

Why do we use for PLASMA VIRAL LOAD and HIV PCR in stages of HIV?

**-Load-**-> to monitor treat of viral drugs **-PCR HIV**--> acute stage (first stage)--> LOW viral load.

Diff esophagitis of CMV and EBV?

CMV-->whipple lines EBV-->line ulcerations

HIV Flashcards

(54 cards)