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clin med > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

1
Q

when does HIV become “AIDs”?

A

CD4 count below 200/ mm3 : when Opportunistic infections come about is “AIDS-defining illness”

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2
Q

what are two ways that we Dx HIV?

A

HIV infection by ELISA (enzyme assay for antibodies) and then confirmatory Western blot
Viral load calculated by PCR, in copies/ mm3 (mm3 = microliter, or ul)

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3
Q

3 stages of HIV/AIDs

A

Acute retroviral syndrome
Asymptomatic stage
Symptomatic stage (AIDS): Opportunistic infections (primary and reactivation)

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4
Q

what is the median duration of the asymptomatic stage?

A

10 years

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5
Q

what is going on with the virus during the asymptomatic stage? What about symptomatic? (weeds)

A

asymp: undergoing replication
symptoms: enough insult to the immune system to see an effect

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6
Q

when are the peak levels for viral load?

A

peak: around 2-4 wks after HIV exposure (acute syndrome)
drops down: for 8-10 years (latency)
peak: 12 -13 years post-exposure (overt AIDS)

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7
Q

when are the drops for CD4 counts?

A

drop: around 2-4wks after HIV exposure (acute syndrome)
rise: 8-10 years (latency)
drop: 12-13 years post-exposure (overt AIDS)

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8
Q

transmission of HIV

A

via infected body fluids

excludes tears, aerosoles, saliva, GI contents

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9
Q

Studies of vertical HIV transmission:
~__% with no treatment (untreated HIV mom to baby), but
___ % with ____ monotherapy

A

30% no treatment

<10% with AZT (zidovudine) monotherapy

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10
Q

current therapy for vertical treatment of HIV? no breastfeeding reduces risk to < __%.

A

Current therapy: “triple therapy” (multidrug therapy)

no breastfeeding reduces risk to <1%

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11
Q

HIV is a ___ virus. with a ___ envelope and _____ on the surface

A

RNA, lipid envelope, glycoproteins (gps)

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12
Q

____ binds to T-helper cell CD4 receptor for attack

_______ are required for successful infection (weeds)

A 
gp 120 (glycoprotien)
coreceptors.
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13
Q

what are the coreceptors required for successful transmission of HIV ? What about those individuals who lack these?

A

CCR5 and CXCR4 (CCR5 for initial infection);

rare individuals who lack CCR5 can be exposed but are not infected

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14
Q

4 parts of HIV replication cycle

A
  1. Receptor binding
  2. Reverse transcriptase (RNA  DNA) by incorporating nucleosides
  3. Integrase incorporates into host DNA
  4. Protease is necessary to cleave viral proteins into structural peptides to produce new viral particles
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15
Q

if infected with HIV, one of three things can happen to CD4+ T cell. what are they?

A
  1. Replicate and fuse with cellular DNA or
  2. Cell death (apoptosis) or
  3. Virus sits in cell in latent state
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16
Q

what is a significant “other” type of cell that HIV virus can directly infect (other than T cells) and what can it cause?

A

Brain –> encephalitis

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17
Q

Always check for all the ___ you can think of for a person who has a single STI

A

STIs

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18
Q

Coinfection with Hep B, C, syphilis or other STI appears to make HIV infection more _______and ________

A

Coinfection appears to make HIV infection more efficient and progression more severe

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19
Q

much more aggressive course of TB infection if the patient has ___ as well.

A

HIV

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20
Q

Pearl: if a patient has current complaints of more than one distinct kind of ______ _____ or _______, be suspicious of HIV
Also be suspicious with _______ or ________

A

skin complaint or infection

widespread MRSA furuncles or boils

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21
Q

CDC recommends routine HIV screening for all persons ___ to ____ years of age in the United States. what is the “philosophy” for this testing.

A

13- 64
“Opt out”, rather than “opt in” philosophy for testing
- Minimally, if you test for any STD, include HIV in the test

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22
Q

Lab testing for HIV:

  1. order HIV test, will include _____ and if this is positive, will do confirmatory _____.
  2. Also if positive, Then need to do _____ and _____.
  3. _____ ______ (also helpful)
  4. if all positive…. what do you do?
A
  1. Order HIV test, will include a preliminary ELISA, and if positive, lab will do confirmatory Western blot
    - May be indeterminate on WB
  2. If positive, will need to do genotyping and phenotyping as a guide to retroviral therapy (some mutations confer resistance to specific drugs)
  3. viral load
  4. Time to call in the experts if positive– REFER!
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23
Q

acute HIV illness presentation

A

presents like any other acute viral illness

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24
Q

Clinical presentation for more advanced HIV: what three things should you note?

A

dementia, wasting, NOTICE opportunistic infections!

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25
Q

AIDS = HIV infection plus..

A

CD4+ count <200
or
Presence of an opportunistic infection

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26
Q

two major opportunistic infection types to note

A

candidiasis and lung infections (like pnuemocystic pneumonia (PCP) and toxoplasmosis)

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27
Q

what is the most common presentation of lung infection in AIDS Symptoms?

A

Pneumocystis jiroveci (PCP): 
 (dyspnea, cyanosis, rales etc)

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28
Q

how do you Dx PCP?

A

induced sputum or bronchial lavage

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29
Q

txt for pcp

A

Treatment (21 days): Trimethoprim-Sulfamethoxazole (Bactrim)

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30
Q

how does one get toxoplasmosis?

A

Exposed through consumption of undercooked meat, ingestion of oocysts from cat feces

31
Q

toxoplasmosis: how does one present if normal immune system and infection vs immunocompromised w/ infection?

A

normal: asymptomatic

Immunosupressed (AIDS) get symptomatic, progressive lethal infection

32
Q

someone is at risk of symptomatic, lethal toxoplasmosis if T-cell count is < ____ . What does this lead to?

A

At risk if T-cell count < 100

-encephalopathy

33
Q

Dx of toxoplasmosis in immunocompromised pt? two types

A

Dx. Serology will tell if previously exposed

Dx. CT or MRI of brain for characteristic lesions

34
Q

txt for toxoplasmosis in immunocompromised pts? (weeds)

A

Start empiric therapy based on clinical picture and imaging

Should dramatically improve

If not improving – brain biopsy

35
Q

Cryptococcal meningitis: where does this come from?

A

encapsulated fungus in soil and bird droppings

36
Q

chronic meningitis in AIDs is likely what?

A

cryptococcal meningitis

37
Q

Dx of crytococcal meningitis

A

lumbar puncture

38
Q

Txt for cryptococcal meningitis

A

antifungals

maybe weeds: (Treatment: Amphotericin then Fluconazole maintenance until CD4 > 200 for 6 months and no symptoms)

39
Q

mycobacterium avium (MAC) usually presents when in the course of AIDS?

A

Usually late in the course of AIDS (CD4 < 50)

40
Q

MAC presentation (weeds)

A

Persistent fevers, night sweats, fatigue, weight loss, and anorexia

Hepatosplenomegaly, lymphadenopathy, and occasionally jaundice

41
Q

txt for MAC

weeds maybe

A

Use 2 or 3 drugs
Clarithromycin
Ethambutol
Rifabutin

(similar to TB txt)

42
Q

CMV- cytomegalovirus

A

Ubiquitous herpes virus: Congenital infection can be serious in immunocompetent

43
Q

HIV pts with CMV get ____ and _____ (weeds)

A

HIV patients – retinitis (optho- white exudates with hemorrhage), colitis/esophagitis (diarrhea, bleeding)

44
Q

overall for immunocompromised txts… what is the goal?

A

increase CD4 counts, get immune system working again!

45
Q

CMV txt (weeds)

A

ganiclovir

46
Q

Progressive Multifocal Leukoencephalopathy: is what? key features? MRI shows what?

A

opportunistic infection
(associated with JC virus- dont need to know what this virus is)
- cognitive impairment
-MRI: dense white matter lesions without edema

47
Q

Persons with AIDS have a high incidence of certain malignancies, especially _____, _____ and _______

A

Kaposi sarcoma (KS), non-Hodgkin lymphoma, and noninvasive cervical carcinoma

48
Q

Kaposi purple skin lesion but ALSO likes the ____

A

lungs

49
Q

“looks like toxoplasmosis, no fever, doesnt respond to toxo therapy” … what is this?

A

CNS lymphoma

50
Q

cervical cancer: what is the schedule for pap smears for those with HIV? Women with HIV have ___ fold increase in the chance of getting cervical cancer

A

Pap smear at baseline, at 6 months, then annually
(after initial Dx)
1.7 fold increase if HIV positive.

51
Q

what are the “sites of anti-retroviral drug action”?

A

many places where we can interfere in the replication cycle of the virus: different classes of HIV drugs

52
Q

what is the “triple therapy” for HIV txt?

A

HAART “triple therapy” or more, now often called simply “ART”
3+ classes of antivirals
-usually NRTI plus NNRTI plus PI

NRTI (nucleoside reverse transcriptase inhibitor)
NNRTI (non-nucleoside RTI)
PI (protease inhibitor)

53
Q

why can’t you start HIV drugs in primary care practice?

A

NEED to know CD4 counts, genotype and viral load. Send to an expert!

54
Q

what is the most important thing about HIV txt? why?

A

Adherence, adherence, adherence!!!

High mutation rate of virus speeds resistance

55
Q

how do you change drug therapies for HIV pts?

A

VERY carefully

56
Q

do you delay therapy for HIV?

A

NO!

57
Q

what are the 4 major opportunistic infections for HIV?

A

TB
pneumocystitis jiroveci (PCP)
toxoplasmosis
Mycobacterium avium complex(MAC)

58
Q

prophylaxis for some conditions will be _____. It is better to remember what _____ need prophylaxis than to remember all the infections and prophylactic agents.

what are the triggers?!

A

The important point is to remember that prophylaxis for some conditions will be necessary!!
It is better to remember what triggers the need for prophylaxis than to remember all the infections and all the prophylactic agents

trigger: Low CD4 counts!!!

59
Q

what is the goal of ART (acute retroviral therapy)?

A

Undetectable viral load by PCR

60
Q

monitoring for ART: continual monitoring for ____. monitor ____ and _____ . surveillance for _____ _______

A

Continual monitoring for adherence
Monitor CD4, viral load
Surveillance for opportunistic infections

61
Q

what are the monitoring complications for ART?

A 
Metabolic complications (i.e. metabolic syndrome, insulin resistance, lipodystrophy, etc) 
* lipid and glucose metabolism are effected
62
Q

3 key signs of metabolic complications with ART?

A 
lipoatrophy (thinning in fat areas like cheeks)
protease paunch (looks like "beer gut"),
buffalo hump (hunchback)
63
Q

two major aspects of prevention

A

“Routine” HIV testing (CDC recommendation)

PrEP (pre-exposure prophylaxis)

64
Q

PrEP has up to __% risk reduction

A

90

65
Q

who have the highest rates of transmission ?

A

teens and elderly (nursing homes)

66
Q

what does “treatment as prevention” mean?

A

achieve undetectable viral loads through ART = risk of transmitting infection is low

67
Q

what is “U=U”?

A

“undetectable=untransmittable”

Late 2017 international consensus

68
Q

U=U: Data from multiple large studies have shown negligible risk of transmission in people with HIV, with _____ ______ _____

A

undetectable viral loads (< 200 copies/ml)

69
Q

post-exposure prophylaxis: chance of contracting the virus from a needle stick (without treatment) is __:____ . while needle sharing is a __:____

A

needle stick 1:300

needle sharing 1:150

70
Q

which needle is more dangerous than others?

A

hollow bore: holds more blood in it

71
Q

is there practicality behind the “cure” for HIV?

A

unsure… given the need for both HLA matching, and CCR5 mutation, and the need for a stem cell transplant

72
Q

what is the “cure” for HIV that was discovered? (maybe weeds)

A

2 case reports of people with HIV who received stem cell transplants for lymphoma Tx, one in Germany, one in England
Bone marrow donors had CCR5 mutation, which was conferred to recipients
HIV undetectable on no ART

73
Q

what are the only 2 non-HIV retroviruses with clear pathologies?

A

HTLV-1 and HTLV-2 (Human T-cell Lymphotrophic Viruses)

74
Q

what is a non-HIV retrovirus?

A

RNA viruses that use reverse transcriptase and infect T-cells. but unlike HIV, not devastating effect on immune system like HIV/AIDS does

clin med (88 decks)

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