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MID II > HIV Epi/OI's > Flashcards

HIV Epi/OI's Flashcards

1
Q

What is the average length of the latent period in HIV infection?

A

10-11 yeras

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2
Q

Does the virus replicate during the latent period?

A

Yes, even though the individual is asymptomatic

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3
Q

Which strains of HIV are common in US and Western Europe?

Africa/Asia?

A

It’s always HIV-1

Europe/US = Clade (subtype) B

Africa/Asia = A, C, E

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4
Q

When does viral load reach set point?

A

by 6 months of infection

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5
Q

What is acute retroviral symptoms?

What is the clinical presentation?

A

It’s what you get 5-30 days after infection

Mild, self-limited, flu-like symptoms: fever, fatigue, sore throat, lymphadenopathy, macular erythematous rash

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6
Q

Why is it important to identify acutely infected HIV patients? 2 reasons

A
  1. they are extremely infectious, so reducing their transmission-prone behavior is vital
  2. there are important pathogenesis and treatment studies directed at this stage of infection (i.e. does treatment during acute infection induce better long term immunologic control of HIV?)
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7
Q

What happens during the asymptomatic phase of HIV infection?

A

Ongoing viral replication

CD4 depletion (lose 50 cells/year)

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8
Q

What’s the average viral load set point in HIV infection?

A

30,000 copies of HIV-1 RNA/mL

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9
Q

Why is it important to identify asymptomatic HIV patients? 3 reasons

A
  1. Behavioral changes to minimize the spread
  2. Prophylactic regiments for OI’s based on CD4 staging
  3. If antiretroviral treatment is initiated before the late stages of HIV disease, you can reverse or halt immune deterioration before complications develop
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10
Q

Which OI’s present >300 T CD4 cells?

A

TB

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11
Q

Which OI’s present at 200 CD4 cells?

A

PCP

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12
Q

Which OI’s present at 100 CD4 cells?

A

Toxoplasma encephalitis

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13
Q

Which OI’s present at 50 CD4 cells?

A

CMV

dMAC

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14
Q

What are the top 10 AIDS complications?

A

 Pneumocystis Pneumonia
 Toxoplasmosis
 Cryptococcal meningitis
 Disseminated Mycobacterium Avium Complex
 Cytomegalovirus
 Kaposis sarcoma
 Non Hodgkin Lymphoma
 Muscosal candidiasis
 Herpes Zoster
 Herpes Simplex

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15
Q

How to distingush oral thrush and oral hairy leukopenia?

A

Oral thrush (candidiasis) = cheese-like, scrapes off (also seein in patients taking steroids, so not specific for AIDS patients)

OHL (EBV): shiny, straited pattern, doesn’t scrape off; it’s patho-indicative of HIV, doesn’t progress but common & useful clinically

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16
Q

What are early indicators of HIV infection?

A

Oral thrush

Oral hairy leukopenia

Bacterial pneumonia (Strep pneumo)

Psoriasis, sebhorreic dermatitis

Frequent/severe recurrences of Herpes simplex genito anal lesions

*Herpes Zoster (Shingles): dermatomal distribution, common prodrome in HIV, most patients will have a scar

*TB

Kaposis sarcoma: cancer caused by a herpes virus (can show up at higher CD4 count than others)

* indicates it can precede AIDS by years!

If you see any of these in an otherwise healthy young adult or those who have a history of HIV risk behavior, suspect HIV

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17
Q

Which types of OI’s are associated wtih AIDS? (i.e. why do you find a predictable set of OI’s in AID?)

A

It’s a predictable set of pathogens bc it’s just T cells that are infected in AIDS, not the whole immune system

It’s intracellular pathogens because T cells deal with these– thats why you get a reactivation of latent infections

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18
Q

What might be an uncomfortable side effect of reconstitution of T cells with antiretriviral therapy?

A

It reverses OI susceptibility, but may trigger an antiinflammatory response to active OI’s

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19
Q

What is PCP?

How is it transmitted?

A

Pneumocystis pneumonia

Fungus P. jirovecii

Most people are exposed during childhood, possibly transmitted patient to patient but it’s unclear!

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20
Q

What other patients (besides HIV patients) can you see PCP?

A

Severe immunosuppression: bone marrow transplant, organ transplat, hematologic malignancy, chronic steroid therapy, cytotoxic chemo

21
Q

What CD4 count do you find PCP?

A

<200

22
Q

What is the pathogenesis & clinical features of PCP?

A

Proliferation of PCP in alveoli –> exudative response, rarely extrapulmonary involvement

Fever, dry cough, dyspnea

Diffuse interstitial infiltrate on Xray “bat wing” pattern

Ground glass opacity on CT

Severe disease is A-a gradient >35 or pO2<70

23
Q

How do you diagnose PCP?

A

Lung biopsy (bronchoscopy) & histology: silver stains

If you don’t see ground glass opacities on CT, hold off on PCP treatment & treat for bacterial pneumonia to see if pt gets better

24
Q

How do you treat PCP?

A

Trimethoprim-sulfamethoxasole

Pentamidine isethionate = comparable efficacy but more toxic

Use systemic corticosteroids in patients with severe disease (as defined by blood gas)

Prevent with oral TS

25
Q

What is weird about PCP and steroids?

A

Steroid use can lead to PCP, but if a patient is on steroids, and you taper the steroids off, they develop PCP (due to unmasking of inflammatory response –> disease manifests)

This showed clinicians that steroid use can help treat PCP!!

More effective in patients who haven’t progressed to respiratory failure

Use when pO2<70 or Aa gradient >35

26
Q

When would you give TS to prevent PCP?

A

CD4<200

prior PCP

Unexplained fever, weight loss or diarrhea

TS also prevents toxoplasmosis, pneumococcal disease, salmonella, others

27
Q

What is toxoplasmosis? How do you get it? How does it present in HIV? Who’s at risk? How to ID those at risk?

A

Toxoplasma gondii = parasite, you get it from eating eggs from cat poop

Reactivation of dormant cyst, mostly CNS lesions

Serum IgG indicates past infection

Common in Caribean, C. America

28
Q

What CD4 count is threshhold of toxo?

A

<100

29
Q

What is the clinical presentation of CNS toxo?

A

Diagnose with focal presentation, CNS imaging, seropositivity (IgG)

Mass lesion in brain (MRI)

Stroke, seizure

30
Q

How do you treat CNS toxo?

A

Combo of Pyrimethamine and **sulfadiazine **(or clindamycin)

31
Q

What’s used to prevent toxo?

A

Prophylaxis in seropositive patients who have CD4<100

Give pyrimethamine

32
Q

How do you distinguish toxoplasmosis v lymphoma? What makes them difficult to distinguish?

A

Both have mass effect, contrast enhancement, and occur at low CD4

Toxo more likely to have multiple lesions

Treat for toxo & see if it responds OR exclude toxo with a negative antibody test + biopsy

33
Q

What is the only OI that is curable & doesn’t require lifelong suppression?

What’s typical treatment?

A

TB

Treat with standard therapy for 6-9 months

34
Q

What is the clinical presentation for cryptococcal disease?

A

Meningitis

Headache, fever

Can include widespread dissemination

35
Q

What CD4 count is crytococcal disease found?

A

<100

36
Q

How do you diagnose cryptococcal meningitis?

A

CSF cryptococcal antigen + culture

37
Q

What’s the treatment for cryptococcal disease?

A

Amphotericin B

Fluconazole suppression in the long term

38
Q

What is MAC?

A

Mycobacterium avium complex disease

39
Q

What CD4 count do you get MAC?

A

<50

You get a reactivation or posisble reinfection from GI route

40
Q

What is the clinical manifestation of MAC?

A

Nonspecific: fever, weight loss, anemia, diarrhea, hepatosplenomegaly

41
Q

How do you diagnose MAC?

A

Biopsy with acid fast staining of affected organs

Blood culture if they have high level of mycobacteremia

42
Q

How do you treat MAC?

A

Azithromycin + ethambutol (lifelong)

43
Q

What is CMV?

A

Herpes group DNA virus, sexually transmitted

In AIDS, you get viral infection reactivation

44
Q

What is the clinical presentation of CMV in HIV patients?

A

Reactivation can occur anywhere

In HIV– retinitis (leading to blindness), GI tract involvement (ulcers anywhere from oral to colon)

(In organ transplant patneints - pneumonia is more common or hepatitis in liver transplant patients)

Diagnose retinitis with ocular fundus exam: hemorrhage and exudate will be seen

Diagnose GI with biopsy

45
Q

What CD4 count do you get CMV?

A

<50

46
Q

How do you treat CMV?

A

Ganciclovir (antiviral agent- GI, oral, or intraocular implant)

47
Q

What is IRIS?

A

Immune reconstitution inflammatory syndrome

Patient with mild or no symptoms becomes ill after ART due to improving immune system (i.e. TB - HIV patients can’t progress to severe symptoms because their immune sys couldnt form granulomas. treatment with ARV–> stronger immune sys & respond to TB & symptoms get worse)

Sometimes, if pt has intracranial process i.e. toxo or crypto, you should delay anti-HIV treatment for weeks until the OI has been well controlled to avoid this paradoxical worsening

48
Q

What malignancies are common in HIV patients?

A

Kaposis sarcoma - HHV8

Non Hodgkins lymphoma

Cerical cancer- HPV related

Restoring immune system with ARV helps control these

MID II (22 decks)

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