Brainscape's Knowledge GenomeTM

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


See full index

Reproduction > Human Immunodeficiency Virus > Flashcards

Human Immunodeficiency Virus Flashcards

1
Q

what type of virus is HIV?

A

retrovirus

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

what syndrome does HIV cause?

A

AIDS by opportunistic infections and aids related cancers

*AIDS related conditions are the single highest predictor of mortality in HIV

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

how is AIDS preventable?

A

by early HIV diagnosis and treatment

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

what is the life expectancy of those with HIV?

A

near normal

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

what are the two main types of HIV?

A

HIV2 = originated in west african sootey mangabey, very rare

HIV1 = originated in central/west african chimps, HIV1 group M is responsible for the pandemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is CD4?

A

glycoprotein found on surface of a range of cells including CD4+ cells, dendritic cells, macrophages and microglial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what receptors are the target site for HIV?

A

CD4+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the role of CD4+ Th lymphocytes?

A

recognition of MHC2 antigen-presenting cell
activation of B cells
activation of cytotoxic T cells (CD8+)
cytokine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what effect does HIV infection have on immune response?

A

sequestration of cells in lymphoid tissue (reduced circulating CD4+ cells)
reduced proliferation of CD4+
reduction of CD8+ activation
reduction in antibody class switching
chronic immune activation (microbial translocation)

*this causes susceptibility to viral infections, fungal infections, mycobacterial infections and infection induced cancer

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

at which CD4 count do opportunistic infections present?

A

<200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HIV viral replication is rapid or slow?

A

rapid (new generation every 6-12 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does infection come about in HIV?

A

infection of mucosal CD4 cell (langerhans and dendritic cells)
transport to regional lymph nodes
infection established within 3 days (window of opportunity)
dissemination of virus

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

if HIV is untreated, what is the average time until death?

A

9-11

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

what % of those with primary HIV present with symptoms and what are these symptoms?

A

80%

fever
rash (maculopapular)
myalgia 
pharyngitis 
headache / aseptic meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

on average, how long after infection will those with primary HIV infection get symptoms?

A

2-4 weeks

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

primary HIV has a very low risk of transmission - true or false?

A

false - very high risk

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

what is asymptomatic HIV infection?

A

ongoing viral replication
ongoing CD4 count
ongoing immune activation
risk of onward transmission

*but, symptoms have stopped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is an opportunistic infection?

A

infection caused by pathogen that does not normally produce disease in a healthy individual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the most common opportunistic infection in HIV?

A

pneumocystis pneumonia (PCP)

*caused by pneumocystis jivroveci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how does PCP present?

A

insidious onset - SOB and dry cough

sensitive sign - exercise desaturation (treat based on this, not xray)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how is PCP diagnosed?

A

CXR - may be normal, interstitial infiltrates, reticulonodular markings

BAL and immunofluorescence +/- PCR

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

how is PCP treated?

A

high dose co-trimoxazole (+/- steroid)

prophylaxis - low dose co-trimoxazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

with tuberculosis, what types are more common in those with HIV+ than HIV- individuals?

A 
symptomatic primary infection
reactivation of latent TB
lymphadenopathies
miliary TB
extrapulmonary TB
multi-drug resistant TB
immune reconstitution syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what organisms causes cerebral toxoplasmosis?

A

toxoplasma gondii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the symptoms of cerebral toxoplasmosis?

A

reactivation of latent infection causing multiple cerebral abscess (chorioretinitis) so it causes:

headache 
fever
focal neurology 
seizures
reduced consciousness
raised ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what causes cytomegalovirus

A

reactivation of latent infection caused by retinitis, colitis and oesophagitis

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

how does CMV present?

A

reduced visual acuity
floaters
abdo pain, diarrhoea, PR bleeding

*ophthalmic screening for all individuals CD4<50

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

what skin infections can be opportunistic infections in HIV?

A

herpes zoster - multidermatomal, recurrent

herpes simplex - extensive, hypertrophic, aciclovir resistant

HPV - extensive, recalcitrant, dysplastic (women have annual smears when they have HIV)

other - penicilliosis and histoplasmosis

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

what organism causes HIV associated neurocognitive impairment?

A

HIV-1 (can be at any CD4 count)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how does HIV associated neurocognitive impairment present?

A

reduced short term memory

+/- motor dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what causes progressive multifocal leukoencephalopathy?

A

JC virus causing reactivation of latent infection

*CD4 threshold <100

32
Q

what are the symptoms of PML?

A

rapidly progressing
focal neurology
confusion
personality change

33
Q

other than HIV associated neurocognitive impairment and PML, what are other neurological presentations of HIV?

A 
distal sensory polyneuropathy 
mononeuritis multiplex
vacuolar myelopathy 
aseptic meningitis 
gullian-barre syndrome 
viral meningitis (CMV, HSV)
cryptococcal meningitis 
neurosyphilis
34
Q

what causes HIV-associated wasting (slims disease)?

A

metabolic (chronic immune activation)
anorexia (multifactorial)
malabsorption / diarrhoea
hypogonadism (low testosterone)

35
Q

what causes kaposi’s sarcoma (vascular tumour)?

A

HHV8

*affected up to 40% pre-ART era

36
Q

how does kaposi’s sarcoma present?

A

cutaneous
mucosal
visceral - pulmonary GI

37
Q

what is the treatment of kaposi’s sarcoma?

A

HAART (for cutaneous)

systemic chemotherapy (if visceral)

38
Q

what causes non-hodgkins lymphoma?

A

EBV (everyone diagnosed with this screened for HIV)

39
Q

how does non-hodgkins lymphoma present?

A 
more advanced
B symptoms 
bone marrow involvement 
extranodal disease 
increased CNV involvement
40
Q

how is non-hodgkins lymphoma diagnosed and treated?

A

diagnosed - same for HIV-

treatment - as for HIV- but add HAART

41
Q

what AIDS related cancer can be caused by HPV?

A

cervical cancer

*HIV testing should be offered to all complicated HPV disease

42
Q

what other conditions can occur in HIV which are not opportunistic infections?

A 
mucosal candidiasis 
seborrhoeic dermatitis 
diarrhoea
fatigue 
worsening psoriasis 
lymphadenopathy 
parotitis 
epidemiology linked conditions - STIs, Hep B and C
43
Q

what haematologic manifestations can be present in HIV?

A

anaemia (up to 90%
thrombocytopenia (ITP)

*caused by HIV, opportunistic infection, AIDS malignancies and HIV drugs

44
Q

what factors increase the risk of sexual transmission of HIV?

A

anoreceptive sex
trauma
genital ulceration
concurrent STI

*between men (53%), men and women (42%)

45
Q

other than sexual, what are other modes of transmission?

A

injection drug use
infected blood products
iatrogenic
mother to child (in utero, delivery and breast-feeding)

46
Q

what proportion of HIV+ infants will die before first birthday if untreated?

A

1 in 3

47
Q

what is the total number of people living with HIV in the UK?

A

104,000

*7% undiagnosed

48
Q

in order, what are the common risk groups of HIV?

A

MSM
heterosexuals (age 15-44, particularly black africans)
people who inject drugs (age 15-44)

49
Q

what group are most likely to be undiagnosed?

A

heterosexual men (most likely to present late)

*heterosexual women earlier as screened as part of antenatal process

50
Q

who is HIV testing recommended to in high prevalence areas in UK (only lothian just now)?

A

all general medical admissions

all new patients registering at general practice

51
Q

those attending what clinics are offered HIV testing due to higher prevalence in these groups?

A

termination of pregnancy services
GUM clinics
drug dependency services

52
Q

those attending what clinics are offered HIV testing due to risks of it being undiagnosed?

A

antenatal services

assisted conception services

53
Q

when HIV falls within the differential diagnoses, the patient should get a HIV test without a risk assessment - true or false?

A

true

*eg worsening psoriasis

54
Q

what should you do in terms of HIV testing if patient is incapacitated?

A

only test if in patients best interest
consent from relative not required
if safe, wait until patient regains capacity
obtain support from HIV team if required

55
Q

what markers of HIV are used by labs to detect infection?

A 
antibody (takes 3 months)
antigen (p24 = 14-28 days)
viral RNA (viral genome, quick but expensive)
56
Q

what is the window period for 4th generation HIV testing (antigen testing)?

A

4 weeks

*negative at 4 weeks = highly likely to exclude HIV infection

57
Q

what is the rapid HIV tests (POCT)?

A 
fingerprick blood specimen or saliva, results in 20-30 mins
3rd gen (Ab only) or 4th (Ab/Ag)

*but, expensive and poor positive predictive value

58
Q

what is the treatment for HIV?

A

anti-retroviral therapy

59
Q

what are the different targets for anti-retroviral drugs?

A 
reverse transcriptase 
integrase 
protease
entry (fusion and CCR5 receptor)
maturation
60
Q

what was the first anti-HIV drug to be introduced?

A

zidovudine (nucleoside analogues reverse transcriptae inhibitors)

*was found that dual NRTI therapy reduced mortality by 33%

61
Q

what is highly active anti-retroviral therapy and what is its purpose?

A

a combination of 3 drugs from at least 2 drug classes to which the virus is susceptible

purpose - reduce viral load to undetectable, restore immunocompetence, reduce morbidity and mortality

62
Q

give an example of a single tablet co-formulation which can be used in HIV treatment?

A

tenofovir (NtRTI)
emtricitabine (NRTI)
efavirenz (NNTRI)

63
Q

which ART drugs can cause GI side effects?

A

protease inhibitors

64
Q

what ART drugs can cause dermatological side effects (rash, hypersensitivity, stevens-johnsons)?

A

abacavir

nevirapine

65
Q

what ART drugs can cause CNS side effects (mood, psychosis)?

A

efavirenz

66
Q

what ART drugs can cause renal toxicity (proximal renal tubulopathies)?

A

tenofovir

atazanavir

67
Q

what ART drugs can cause bone side effects (osteomalacia)?

A

tenofovir

68
Q

what ART drugs can cause CVS side effects (increased MI risk)?

A

abacavir
lopinavir
maraviroc

69
Q

what ART drugs can cause anaemia?

A

zidovudine

70
Q

what ART drugs can cause GI effects such as transaminitis and fulminant hepatitis?

A

nevirapine

most others

71
Q

why do some drugs require pharmacological boosting (with potent liver enzyme inhibitors)?

A

because protease inhibitors are generally potent liver enzyme inhibitors but NNRTIs are generally potent liver enzyme inducers

72
Q

what are the conception options for HIV+ male with HIV- female?

A

treatment as prevention
+/- timed condomless sex
?HIV PrEP for female partner

73
Q

what are the conception options for HIV+ female with HIV- male?

A

treatment as prevention
+/- timed condomless sex
? self insemination
? HIV PrEP for male partner

74
Q

how do you prevent mother to child transmission?

A 
HAART during pregnancy 
vaginal delivery if undetected viral load 
caesarean if detected viral load 
4/52 PEP for neonate 
exclusive formula feeding

*<1% risk of MTCT in UK, <0.1% if VL undetected at delivery

75
Q

what is the reduction in HIV risk in countries with PrEP (pre exposure prophylaxis)?

A

close to 100% if taken daily

*those with no PrEP (england, wales) have 6000 new HIV diagnoses every year for 10 years

Reproduction (45 decks)

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