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ENDO/REPRO > HIV > Flashcards

HIV Flashcards

1
Q

HIV genome characteristics?

A

-ss + RNA enveloped DIPLOID Genome.

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2
Q

Mechanism transmission?

A

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

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3
Q

What genes and products are ass.?

A

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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4
Q

What are the steps of HIV infections?

A

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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5
Q

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

A

Homogenous mutations–>Immunity
Heterogenous mutations—>Resistance

-All towards CCR5.

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6
Q

What the normal T cell count?

A

500-1K

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7
Q

Why on latency phase you don’t have sympt?

A

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

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8
Q

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

A

-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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9
Q

What cell do you see in Hodgkins Lymphoma
Subtypes?

A

-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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10
Q

NON- Hodgkin Lymphoma subtypes?

A

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

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11
Q

How to differentiate NON-Hodgkyn Lymphoma with Toxoplasmosis?

A

-Do CSF analysis

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12
Q

How do differentiated lesion between Kaposi and Bartonella lesion?

A

-Biopsy
Neutrophils–>zoonotic bact
Lymphocytes–>Virus

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13
Q

What superimposed organism are asscociated with HIV ?

A
  • <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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14
Q

Candida
Presentation
Treat

A

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

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

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15
Q

EBV
Presentation
Treat
Cells it infects

A

-<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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16
Q

Mycobacterium TB
Presentation
Stain

A

-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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17
Q

Kaposi Sarcoma
-Presentation

A

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

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18
Q

JC Virus

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

A

-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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19
Q

Histoplasma
Presentation
Morphology

A

-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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20
Q

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

A

-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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21
Q

Cryptoccocus Neoformans
Presentation
Special stain

A

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

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22
Q

CMV
Presentation
3 special things you see.

A

-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

23
Q

Bartonella spp

A

-Ass cat scratch
-Baciallry Angiomatosis–>Neutrophil infiltration

24
Q

Toxoplasmosis Gondii

A

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

25
Q

M.Avium

A

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

26
Q

HIV ass Dementhia is ??

A

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

27
Q

Bridinzki sign?

A

-Meningitis

28
Q

Drug of choice for Pneumocystis Jirovecci?

A

-TMP-SMX

29
Q

Where does your CD4+ drop the most

A

Acute phase

30
Q

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

A

1 month after initial infection and remains elevated for ever.

31
Q

What we use to diag HIV?

A

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.

32
Q

What are the diff clasdifications of HIV drugs?

A

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

33
Q

Abacavir,Tenofovir,Zidovudine??
AE

A

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. **

34
Q

How to prevent myelosupression of NRTI”s?

A

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

35
Q

Intergrase inhib all end in…
AE

A

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

36
Q

NNRTI’s
-AE

A

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

37
Q

Why exactly do NRTI’s requiere phosphorylation?

A

-The are nucleosides

38
Q

Protease inhb. end in …..

A

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

39
Q

Ryfacymins characteristics (4)

A

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

40
Q

What relation does your Rifacymins have with Protease inhib?

A

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

41
Q

What HIV drug is Cyt P450 inhibitor?

A

-Ritonavir**

42
Q

Enfuviritide
Maraviroc

A

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

43
Q

Why HIV virus mutates a lot?

A

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

44
Q

What a good entry point of HIV virus?

A

-GI tract–>lot’s of T cells.

45
Q

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

A

-More HIV in semen.

46
Q

How does HIV cause neurological symptoms?

A

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

47
Q

What is the pre-exposure prophylaxis medications?

A

-Tenofovir + Emtricitabine (Both NRTI’s)

48
Q

What drug causes Mitocondrial toxicity??

A

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

49
Q
A
50
Q

tat gene
rev gene

A

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)

51
Q

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?

A

-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.

52
Q

Confirmatory test for HIV?

A

-NAAT

53
Q

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

A

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

54
Q

Diff esophagitis of CMV and EBV?

A

CMV–>whipple lines
EBV–>line ulcerations

ENDO/REPRO (10 decks)

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