Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med I > HIV and opportunistic infections > Flashcards

HIV and opportunistic infections Flashcards

1
Q

who gets opportunistic infections

A
  • immunodeficient
  • chemo pts
  • chronic steroid use
  • elderly
  • transplant pts
  • generally associated with T cell immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the common fungal opportunistic infections

A
  • cryptococcus
  • histoplasma
  • candida
  • pneumocystis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the common viral opportunistic infections

A
  • CMV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the common parasitic opportunistic infections

A
  • toxoplasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

risk factors for fungal opportunistic infections

A
  • severity of T cell mediated immunity
  • recent or current use of antifungals
  • risk of exposure
  • neutropenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how is cryptococcus transmitted

A
  • air droplets and bird droppings
  • spores inhaled -> lodged into lung alveoli -> dissemination -> infection
  • is a fungus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

clinical manifestations of cryptococcus

A
  • meningitis*
  • insidious onset
  • altered mental status* - usually irritable
  • papilledema*
  • malaise, fever
  • n/v
  • fullness in ears
  • CT will be normal
  • opening pressure during LP will be very high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

diagnosis of cryptococcus

A
  • test for antigen in CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

treatment of cryptococcus

A
  • amphotericin B

- fluconazole*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how is histoplasmosis transmitted

A
  • inhalation
  • exposure to chicken coops
  • endemic to certain parts of US
  • is a fungus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical manifestations of histoplasmosis

A
  • 1-3 mo after exposure
  • fever
  • weight loss*
  • dyspnea on exertion
  • skin ulcers*
  • hepatosplenomegaly
  • lymphadenopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

diagnosis of histoplasmosis

A
  • urine test

- h. capsulatium antigen sensitivity in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

treatment of histoplasmosis

A
  • amphotericin b

- itraconazole*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the CD4 counts where candidiasis infections occur

A
  • < 300

- esophagitis may also occur when <100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the most common cause of dysphagia and odynophagia in AIDS pts

A
  • candidiasis

- is a fungus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

treatment for candidiasis

A
  • fluconazole*

- avoid topical treatments d/t low cure rate and high relapse rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

diagnosis

A
  • gold standard= EGD endoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

clinical manifestations of candidiasis

A
  • burning/ stabbing in mouth and/or throat
  • white markings with surrounding erythema
  • raised tissue
  • not uncommon to have candidiasis, herpes, and CMV co-infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is pneumocystis jirovecii transmitted

A
  • attach to alveolar epithelium -> inflammation, interstitial edema, diffuse alveolar damage
  • enviornmental exposure is main cause
  • fungus with tropism for lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

clinical presentation of pneumocystis jirovecii

A
  • gradual onset
  • fever
  • dry cough
  • dyspnea
  • average 1 month before medical consut
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

diagnosis of pneumocystis jirovecii

A
  • imaging- HRCT chest

- lab- BAL immunoflorescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

treatment of pneumocystis jirovecii

A
  • bactrim
  • either IV or PO X 21 days
  • steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

at what CD4 level does CMV infection occur?

A
  • <50
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CMV clinical manifestations

A
  • mainly affects retina
  • no pain
  • floaters, blurred vision, decreased peripheral vision
  • light flashes
  • sudden vision loss
  • starts in 1 eye but usually involves both
  • blindness d/t retinal detachment
  • *** any acute vision loss, young, and immunosuppressed is CMV until proven otherwise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

diagnosis of CMV

A
  • perivascular fluffy yellow-white retinal infiltrate +/- hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

treatment of CMV

A
  • IV ganciclovir
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

at what CD4 count does toxoplasmosis infection occur?

A
  • CD4 <100 has 30% risk without ppx

- CD4 < 50 has 75% annual risk without ppx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what causes toxoplasmosis

A
  • t. gondii

- 30% of people in US are seropositive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

clinical manifestations of toxoplasmosis

A
  • HA
  • confusion
  • fever
  • lethargy
  • seizures
  • altered mental status
  • psychomotor retardation
  • may mimic lymphoma
30
Q

diagnosis of toxoplasmosis

A
  • IgG serology for t. gondii
  • order MRI
  • LP for malignant cells and EBV, order PCR for t. gondii
  • brain biopsy if no clinical or radiological improvement after 2 weeks tx
31
Q

treatment of toxoplasmosis

A
  • pyrimethamine + sulfadiazine + leucovorin
32
Q

how the HIV virus works

A

1. attaches to host cell via CD4 cells and coreceptors
2. fusion, RNA virus sends out genetic material
3. reverse transcriptase makes RNA into DNA
4. DNA is integrated into host DNA via integrase
5. DNA -> RNA -> viral proteins
6. new virus formed, protease assembles mature proteins
*= target of drug therapy

33
Q

stages of HIV infection

A
  • early infection
  • clinical latency
  • AIDS
34
Q

when do you diagnose someone with AIDS

A
  • CD4 <200

- dx with AIDS defining condition

35
Q

general course of infection in untreated pt

A
  • first few weeks VL is detectable (once it hits 50)
  • weeks 3-6 VL peaks then spontaneously drops
  • VERY contagious during peak
  • CD4 dips down during acute infections
  • over years CD4 drops and VL increases
  • 7-10 years in untreated pt until AIDS dx or death
36
Q

what labs do you order when HIV is suspected

A
  • VL
  • CD4 count
  • Hep B and C
  • Toxicology
  • STD tests
  • PPD
  • CMV
  • make sure vaccines are up to date
37
Q

what are the parameters for positive PPD test

A
  • health care worker- 10 mm
  • general population- 15 mm
  • HIV- 5 mm
38
Q

who is at the highest risk for HIV infection

A
  • MSM
  • heterosexual women
  • IVDU
  • minorities
  • ages 25-35 highest risk new dx
  • ages 35-44 second highest risk new dx
39
Q

what are HIV transmission risk factors

A
  • VL
  • lack of circumcision
  • sexual partners
  • sexual practice
  • STD- ulcers increase risk by 4X
  • genetics
40
Q

what is the most risky sexual practice for HIV transmission

A

receptive anal intercourse

41
Q

common sx of acute HIV infection

A
  • fever
  • lymphadenopaty
  • pharyngitis
  • rash
  • myalgia/ arthralgia
  • HA
  • less commonly oral or genital ulcers, N/V/D
42
Q

how do you screen for HIV?

A
  • 4th gen Ag/Ab testing
  • pushes back theoretical time to pos to days 16 or 17
  • MUST f/u with VL testing
  • VL ALWAYS high during acute infections
43
Q

differential dx for primary HIV infection

A
  • EBV (mono)
  • CMV
  • toxoplasmosis
  • rubella
  • syphilis
  • hepatitis
  • other viral infections
44
Q

common conditions in early symptomatic HIV

A
  • persistant vaginal candidiasis
  • oral hairy leukoplakia
  • shingles on more than one dermatome
  • cervical dysplasia or carcinoma
45
Q

AIDS defining conditions

A
  • candidiasis of bronich, trachea, lungs, esophagus
  • invasive cervical cancer
  • coccidiomycosis
  • cryptosporidiosis
  • CMV retinitis
  • encephalopathy
  • chronic herpes ulcers > 1 mo
  • histoplasmosis
  • kaposi sarcoma
  • lymphoma
  • mycobacterium
  • pneumocystis jirovecii
  • toxoplasmosis
46
Q

HIV medication categories

A
  • nRTIs (nucleoside reverse transcriptase inhibitors)
  • nnRIT
  • PI (protease inhibitor)
  • entry inhibitors
  • INSTIs (integrase strand transfer inhibitors)
47
Q

HIV treatment considerations

A
  • must be ready to start
  • tx everyone who is infected
  • consider dosing sched/ how many pills/ food
  • must include 3 active drugs to start
  • genotyping before start
48
Q

nRTIs

A
  • backbone of tx
  • all regimens have at least 2 of theses
  • all can cause metabolic acidosis- monitor bmp if someone is very sick after initiation
  • tenofovir
  • lamivudine
  • emtricitabine
  • abacavir
  • zidovudine
49
Q

tenofovir

A
  • new form= TALA
  • less toxicities
  • commonly used
  • nRTI
50
Q

lamivudine

A
  • low threshold to resistance

- nRTI

51
Q

emtricitabine

A
  • low threshold to resistance

- nRTI

52
Q

abacavir

A
  • HLA 5701 testing
  • if pos for HLA can cause cardiotoxicity
  • nRTI
53
Q

zidovudine

A
  • rarely used d/t metabolic ADRs
  • used during delivery
  • nRTI
54
Q

efavirenz

A
  • very effective
  • rash- will go away
  • vivid dreams
  • nnRTI
55
Q

etravirine

A
  • “salvage treatment”
  • effective vs. efavirenz resistant strains
  • nnRTI
56
Q

rilpivirine

A

new nnRTI

57
Q

doravarine

A

newest nnRTI

58
Q

protease inhibitors

A
  • not used bc very metabolically toxic

- usually need metabolic booster- ritonavir or cobicistat (DDI risk)

59
Q

atazanavir

A
  • can cause jaundice

- PI

60
Q

darunavir

A
  • resistant to many mutations

- PI

61
Q

INSTIs

A
  • very save, effective and well tolerated
62
Q

raltegravir

A
  • INSTI
63
Q

elvitegravir

A
  • only coformulated with cobicistat

- INSTI

64
Q

dolutegravir

A
  • most effective
  • high resistance barrier
  • BBW for use in pregnancy - neural tube defects
  • INSTI
65
Q

pictegravir

A
  • coformulated with metabolic booster

- INSTI

66
Q

entry inhibitors

A
  • maraviroc
  • blocks CCR5a receptor
  • test for tropism
67
Q

recommended starting HIV regimens

A
  • 2 nRTIs and INSTI
  • twho have boosted INSTI
  • preferred nRTI is TALA
68
Q

alternative starting HIV regimens

A
  • two NRTIs and one nnRTI
  • boosted PI plus two NRTI
  • two drug regimen if cannot use other drugs
69
Q

what should happen to the VL after initiation of HIV tx?

A
  • decrease 10 fold in first 2-4 weeks
70
Q

what do you do if a pt is failing HIV regimen?

A
  • check adherence- usually the cause

- persistent failure then should check genotype and phenotype while still on regimen

Clin Med I (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions