Brainscape's Knowledge GenomeTM

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


See full index

Reproduction > HIV > Flashcards

HIV Flashcards

1
Q

what type of virus is HIV

A

retrovirus (When it makes DNA it uses reverse transcriptase rather than dna transcriptase enzyme)

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

what are the two groups of things AIDs causes

A

oppurtunistic infections

AIDs related cancers

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

what does AIDs stand for

A

acquired immunodeficiency syndrome

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

what are the two types of HIV

A

HIV-1 responsible for global pandemic

HIV-2 less virulent, usually limited to west africa

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

what does HIV target

A

CD4+ receptoes

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

what is CD4

A 
glycoprotein found on the surface of a range of cells:
T helper lymphocytes 
dendritic cells 
macrophages 
microglial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what do CD4+T helper cells do

A 
involved in inducing adaptive immune response
recognise MGC2 antigen presenting cell
activate B cells 
activate CD8+ cells 
cytokine release

(transmit message from antigen presenting cells to effector cells- B and T cells, marcophages)

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

how does HIV affect the immune response

A

sequesters cells in lymphoid tissue and reduced proliferation of CD4+= reduced CD4+ cells

reduction of CD8+ (cytotoxic) T cell activation = dysregulates cytokine expression, increased susceptibility to viral infections

reduction in antibody class switching= reduces affinity of antibodies produced

chronic immune activation (microbial translocation)

combined makes patient more susceptible to viral, fungal, mycobacterial infections and infection induced cancers

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

what is a normal CD4+Th cell count

A

500-1600 cells/mm3

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

what CD4+T count poses a risk for opportunistic infections

A

<200

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

when is there rapid HIV viral replication

A

in early and very late infection

new generation every 6-12 hours

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

what happens to viral load as antibodies start to form

A

goes down

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

CD4 count rises in asymptomatic infection, does it ever go back to normal

A

no, gets lower as disease progresses

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

what is the path of HIV infection

A

mucosal CD4 cells (langerhans and dendritics cells) usually rectal, vaginal or cervical

transport to regional lymph nodes

infection established within 3 days of entry

dissemination of virus

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

when are the onset of symptoms in primary infection

A

2-4 weeks after infection

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

what are the symptoms of primary infection

A 
combo of 
fever
rash (maculopapular) 
myalgia 
pharyngitis 
headache/ aseptic meningitis (can infect microglial cells as primary infection)

flu/ glandular like illness

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

is there risk of transmission during primary infection

A

yes- very high

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

what is happening during asymptomatic HIV infection

A

ongoing:
- viral replication
- CD4 count depletion
- immune activation

risk of transmission

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

does HIV become latent

A

no, as not sleeping during asymptomatic infection and immune system not back to normal

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

what type of lesions on MRI in toxoplasmosa

A

ring enhanced lesions in brain

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

what causes penumocystis pneumonia

IN EXAM

A

pneumocystis jiroveci

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

what CD4 threshold predisposes you to pneumocystis pneumonia
(IN EXAM)

A

<200

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

what are the symptoms of pneumocystis pneumonia

IN EXAM

A

insidious onset
SOB
dry cough
may have low grade fever

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

what are the signs of pneumocystis pneumonia

IN EXAM

A 
exercise desaturation
CXR:
-may be normal
-interstitial infiltrates 
-reticulonodular markings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how do you diagnose pneumocystis pneumonia

IN EXAM

A

BAL (bronchoalveolar lavage - bronchoscopeis passed through the mouth or nose into thelungsand fluid is squirted into a small part of the lung and then collected for examination)
and immunofluorescence +/- PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the treatment for pneumocystis pneumonia

IN EXAM

A

high dose co-trimoxazole +/- steroid

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

what is the prophylaxis for pneumocystis pneumonia

IN EXAM

A

low dose co-trimoxazole

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

what should you be aware of in TB and HIV

A

drug- drug interactions

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

what forms of TB infection are more common in HIV+ve patients

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
30
Q

what causes cerebral toxoplasmosis

A

toxoplasma gondii

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

what is the pathology of cerebral toxoplasmosis

A

reactivation of latent infection- causes multiple cerebral abscess (chorioretinitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the symptoms/ signs of cerebral toxoplasmosis

A 
heachache 
fever
focal neurology (as focal abscesses) 
seizures 
reduced consciousness 
raised ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what CD4 threshold puts you at risk for cerebral toxoplasmosis

A

<150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what screen (not HIV) does everyone with a CD4 count <50 get

A

ophthalmic (looking for CMV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what CD4 threshold puts you at risk for cytomegalovirus

A

<50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the pathology of CMV

A

reactivation of latent virus causes retinitis, colitis and oesophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the presentation of CMV

A 
reduced visual acuity- can cause blindness
floaters
abdo pain 
diarrhoea 
PR bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what skin infections are seen in HIV

A

herpes zoster:

  • multidermatomal
  • recurrent

herpes simplex:

  • extensive
  • hypertrophic (can form wart/ tumour like mass)
  • aciclovir resistant

HPV:

  • extensive
  • recalcitrant
  • dysplastic
  • women with HIV have annual cervical screening

penicilliosis
histoplasmosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what organisms causes HIV associated neurocognitive impairment

A

HIV-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what CD4 count purs you at risk of HIV associated neurocognitive impairment

A

any

increased incidence with increased immunosuppression though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the presentation of HIV associated neurocognitive impairment

A

reduced short term memory +/- motor dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what organisms causes progressive multifocal leukoencephalopathy

A

JC virus (reactivation of latent virus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what CD4 count puts you at risk of progressive multifocal leukoencephalopathy

A

<100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the presentation of progressive multifocal leukoencephalopathy

A

rapidly progressing
focal neurology
confusion
personality change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the pathology of progressive multifocal leukoencephalopathy

A

progressive white matter change, multifocal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are neurological presentation of HIV

A 
HIV associated neurocognitive impairment 
progressive multifocal leukoencephalopathy 
distal sensory polyneuropathy
mononeuritis mulitplex 
vacuolar myelopathy
aseptic meningitis 
guillan barre syndrome 
viral meningitis (CMV, HSV)
cryptococcal meningitis 
neurosyphilis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what causes HIV associated wasting

A

metabolic (chronic immune activation)
anorexia (multifactoral inc psychological)
malabsorption/ diarrhoea
hypogonadism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are the AIDs related cancers

A

kaposi’s sarcoma
non hodgkins lymphoma
cervical cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what organism causes karposis sarcoma

A

human herpes virus 8

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

what type of tumour is karposis sarcoma

A

vascular tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what CD4 count puts you at risk of karposis sarcoma

A

any

increased incidence with increase immunosuppression though

52
Q

where can you get karposis sarcoma

A

cutaneous
mucosal
visceral (pulmonary, GI)

53
Q

what is the treatment for karposis sarcoma

A

HAART
local therapies
systemic chemotherapy

54
Q

what organism causes non hodgkins lymphoma in AIDs

A

EBV (burkitts lymphoma, primary CNS lymphoma)

55
Q

what is the presentation of non hodgkins lymphoma in AIDs

A 
more advanced 
B symptoms (systemic symptoms in both hodgkins and non hodgkins lymphoma- fever, night sweats, weight loss)
bone marrow involvement 
extranodal disease 
increased CNS involvement
56
Q

is the diagnosis and treatment any different for non hodgkins lymphoma in AIDs

A

diagnosis same

treatment add HAART

57
Q

what organism causes cervical cancer

A

HPV

58
Q

why is HPV more likely to cause cervical cancer in AIDs

A

persistence of HPV infection

rapid progression to severe dysplasias and invasive disease

59
Q

what can HPV in AIDs cause

A

recalcitrant warts

high grade cervical, vulval, anal, penil intraepithelial neoplasia

60
Q

what are the non opportunistic infection symptoms of HIV

A 
mucosal candidiasis 
seborrhoeic dermatitis (eczema and fungal infection)
diarrhoea 
fatigue
worsening psoriasis
lymphadenopathy
parotitis 
epidemiologically linked conditions: STIs, hep B and C
61
Q

is mucosal candidiasis an OI

A

no

62
Q

is seborrhoeic dermatitis an OI

A

no

63
Q

why does psoriasis get worse in HIV

A

as is CD8 mediated- when CD4 goes down these go up

both go down in AIDs

64
Q

what are the possible haematological manifestations of HIV

A

anaemia (up to 90% affected)

thrombocytopenia (ITP) (CD4 300-600)

65
Q

what causes the haematological manifestations of HIV

A

HIV itself
opportunistic infections
AIDs malignancies
(HIV drugs)

66
Q

what CD4 can you get haematological manifestations

A

any

higher incidence with higher immunosuppression

67
Q

what is the most common mode of HIV transmission

A

sexual transmission (95%)

  • sex between men (53%)
  • sex between men and women (42%)
68
Q

what increases the risk of sexual transmission of HIV

A

anoreceptive sex (lots of CD4, only 1 cell thick- more susceptible to trauma)
trauma
genital ulceration
concurrent STI

69
Q

what are the ways in which HIV is transmitted parenterally

A

injection drug use (2%)
infected blood products
iatrogenic

70
Q

via what ways can a mother transmit HIV to her child

A

in utero/ trans-placental
delivery
breast feeding

71
Q

how many at risk babies get infected

A

1 in 4

72
Q

what is the risk of mother to child transmission when viral load undetected at delivery

A

0.1%

73
Q

what percentage of people living with HIV in UK are undiagnosed

A

7%

~7500

74
Q

who are the high risk groups for HIV

A

highest risk= MSM (1 in 17/ 1 in 7 in london)

heterosexuals (aged 15-44, 1:1000. black african men 1:25, black african women 1:23)

PWID (aged 15-44, 1:263)

75
Q

what group of people are most likely to be diagnosed late

A

heterosexual men

76
Q

who should be tested for HIV

A

universal testing in high prevalence areas (>0,2%) (all general medical admissions, all new patients registering at general practice)
some places have opt out testing (TOP services, GUM clinics, drug dependency services - higher prevalence in these populations. antenatal services and assisted conception services- risk of undiagnosed HIV in these settings unacceptable)
screening of high risk groups
when clinical indicators

77
Q

what high risk groups are screened for HIV

A 
MSM
female partners of bisexual men 
people who inject drugs 
partners of people living with HIV
adults/children from endemic areas 
children born to HIV+ or untested mothers from endemic areas
sexual partners from endemic areas 
history of iatrogenic exposure in an endemic area
78
Q

what are the endemic areas for HIV

A

sub saharan africa
caribbean
thailand (south east asia)

rising epidemics in russia and eastern europe

79
Q

what do you need to do to gain consent for a HIV test

A

Explain to patient they are being offered an HIV test and why
- normalise

What the benefits of testing are

  • Improve long term health
  • Protect partner(s)

How and when they can expect to receive results

Reassure re: confidentiality

Written information can be made available (different languages)

80
Q

is it venous or arterial blood for serology in HIV test

A

venous

81
Q

what do you do for HIV testing if patient incapacitated

A

only test if in their best interest
consent from relative not required
if safe wait till patient regains capacity
get support from HIV team if required

82
Q

what markers of HIV are used to detect infection

A 
viral RNA (viral genome)
capsule protein (P24) (antigen)
antibodies
83
Q

how long till seroconversion (formation of antibodies)

A

3 months

84
Q

what does seroconversion mark

A

the end of primary infection, start of chronic infection

85
Q

what happens to P24 (antigen) as HIV progresses

A

high in primary infection, goes down during chronic infection, rises again in late disease

86
Q

what happens to viral load as HIV progresses

A

high initial infection

87
Q

what do 3rd gen HIV tests look for

A

HIV 1 and 2 antibody
detect IgM and IgG
very sensitive/ sepcific in established infection
window period of 20-25 days

88
Q

what do 4th gen HIV tests look for

A

combines antibody and antigen

shortens window period to 14-28 days

89
Q

what does a negative 4th gen HIV test mean

A

highly likely to exclude HIV infection

90
Q

how do rapid HIV tests work

A

finger prick blood or saliva
results in 20-30 mins
can be 3rd or 4th gen

91
Q

what are the downsides of rapid HIV tests

A

Expensive ~£10
Poor positive predictive value in low prevalence settings
Not suitable for high volume

92
Q

what does undiagnosed HIV cause

A

Late diagnosis
Morbidity/mortality
Onward transmission

93
Q

what CD4 count do you give PCP prophylaxis

A

<200

94
Q

do you always do RNA sequencing in HIV infection

A

yes always to find out which type it is

type B most common in MSM and PWID

95
Q

what else do you screen for in HIV infection depending on where a patient has traveled

A

TD and schistosomiasis

96
Q

what else should you test for in MSM

A

LGV

97
Q

describe the life cycle of HIV

A

binding to CD4 molecules and coreceptors (CCR5 and CXCR4)
virus fuses with the cell
virus penetrates and empties its contents into cell
reverse transcriptase converts single stranded viral RNA into double stranded DNA
intergrase combines viral DNA with cells own
transcription of viral DNA when host cell divides
sets of viral protein chains come together
budding- immature virus pushes out of the cell taking some of the membrane with it
protease starts processing the proteins in newly forming virus
immature virus breaks free from infected cell protease enzyme finishes cutting HIV protein chains into individual proteins that combine to make a new working virus

98
Q

what can anti retoviral drugs target

A 
reverse transcriptase (NRTI and NNRTI)
integrase 
protease
entry into cell: fusion and CCR5 receptors
99
Q

what is highly active anti

THIS IS IN EXAM

A

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

100
Q

what is the purpose of HAART

A

reduce viral load to undetectable
restore immunocompetence (allows immune system to recover)
reduce morbidity and mortality

101
Q

how do you prevent HIV drug resistance

A 
ADHERENCE 
lifestyle 
tolerability 
pharmacokinetics 
drug-drug interactions 
treatment interuptions (virus becomes restistence when in monotherapy, when break in treatment drug with longest half life will become monotherapy)
102
Q

what do you do if a patient isnt going to be able to take medication for a while

A

stop therapy before break and give protease therapy- hard to get resistance to
allowing some viral breakthroughs is better than resistance

103
Q

what is an ARV

A

anti retro viral

104
Q

what are the common HAART toxicities

A

gi side effects: protease inhibitors, (transaminitis, fulminant hepatitis- nevirapine)

skin:rash, hypersensitivity, SJS (abacavir, nevirapine)

CNS: mood, psychosis (efavirenz)

renal toxicity: proximal renal tubulopathies (tenofovir, atazanavir)

bone: osteomalacia (tenofovir)

CVS: increased MI risk (abacavir, lopinavir, maraviroc)

haematology: anaemia (zidovudine)

105
Q

how do protease inhibitors affect liver enzymes

A

protease inhibitors are potent liver enzyme inhibitors= they may increase the bioavailability of other drugs which are metabolised by those enzymes
they may decrease the bioavailability of drugs which require metabolism for their activation

106
Q

how do NNRTIs affect liver enzymes

A

are potent liver enzyme inducers:
they may decrease the bioavailability of other drugs which are metabolised by those enzymes
they may increase the bioavailability of drugs which require metabolism for their activation

107
Q

what are common co infections with HIV that affect treatment options

A

hep C and TB

hep B and HIV have same treatment

108
Q

what do a lot of women with HIV get

A

early menopause- osteoporosis

109
Q

what preventative medicine can be done in HIV treatment

A 
exercise 
smoking cessation (CVS risk)
STI screening 
hep A/B vaccine 
flu vaccine 
HPV vaccine 
harm reduction- needle exchange, condoms etc
110
Q

how can HIV affect psychosocial well being

A

Adjustment to diagnosis

Confusion, guilt (+ survivor guilt), blame

Impact of HIV on health

Concerns about future

Feelings of isolation

Relationships

Spiritual

111
Q

is partner notification and disclosure mandatory

A

no, is a voluntary process

112
Q

what are the different strategies to partner notification and disclosure

A 
partner referral (partner tells them)
provider referral (HCP contacts partners, is anonymous)
conditional referral (if HPC doesnt hear from partner by a certain time will contact them)
113
Q

when does a doctor have a duty of care to a patients partner

A

when they are a known third party

114
Q

what are the barrier to partner notification and disclosure

A

fear:
-rejection
-isolation
-violence
confidentiality
stigma

115
Q

what is stigma

A

the shame/ disgrace attached to something regarded as socially unacceptable

116
Q

how does stigma in HIV manifest

A

discrimination and ostracisim

117
Q

how is the sexual transmission of HIV prevented

A

condom use
HIV treatment
STI screening and treatment
sero-adaptive sexual behaviours (more likely to pass it on in MSM if insertive partner)
disclosure (more accepting of condoms)
post exposure prophylaxis (up to 72 hours after, taken for 4 weeks)
pre exposure prophylaxis (taken every day/ event based dosing)

118
Q

can you pass on HIV when viral load is <200

A

no

119
Q

what are the conception options for sero-discordant couples

A

for all:

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

HIV + female, -male:
-?self insemination

120
Q

does adding PrEP when undetectable reduce risk of transmission

A

no as risk already 0

121
Q

how can you prevent mother to child transmission

A

HAART during pregnancy - SVD if undetectable, caearean if detectable

  • 4/52 PEP for neonate (give AVR to baby for up to 4 weeks after birth)
  • exclusive formula feeding
122
Q

how does having other STIs affect risk of HIV

A

increases risk of both getting it and passing it on

123
Q

what prevention strategies have helped reduce HIV transmission

A 
needle exchange
STI testing and treatment 
condom programmes
PEP and PrEP
circumcision (epithelium on glans becomes keratinised, reduced chance of acquiring HIV)
treatment as prevention 
behavioural change interventions
124
Q

where in UK is PrEP licensed

A

just scotland

125
Q

what is the PrEP eligibility criteria

A

is patient high risk?:

  • HIV + partner with detectable viral load (>50)
  • MSM/ transwoman (unprotected anal intercourse in 12/12 and likely to do so again in next 3/12 or confirmes bacterial rectal STI in last 12/12)
  • other high risk factor

is patient eligible?:

  • age >/= 16
  • HIV negative
  • can commit to 3/12ly follow up
  • willing to stop if eligibility criteria no longer apply
  • resident in scotland
126
Q

does PrEP work

A

reduces incidence by 86%

Reproduction (51 decks)

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