HIV + OI Flashcards

1
Q

Through what TWO mechanism does HIV cause disease of the central nervous system (CNS)?

A

1) DIRECT impact from HIV

2) indirect due to CD4 DEPLETION

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2
Q

Space occupying lesion + HIV - differential diagnosis - INFECTIVE causes?

A
Toxoplasmosis
TB
Cryptococcus
Syphilitic gummae
PML
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3
Q

Space occupying lesion + HIV - differential diagnosis - NEOPLASTIC causes?

A

Primary CNS lymphoma

Metastatic non-Hodgkin lymphoma

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4
Q

Encephalitis + HIV - differential diagnosis?

A

HIV (directly)
VZV
HSV
syphilis

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5
Q

Meningitis + HIV - differential diagnosis?

A
HIV seroconversion
Cryptococcus
TB
Syphilis
Streptococcus pneumonia
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6
Q

Spastic paraparesis + HIV - differential diagnosis?

A
HIV-vacuolar myelopathy
Transverse myelitis
HSV
HTLV-1
Toxoplasmosis
Syphilis
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7
Q

Polyradiculitis + HIV - differential diagnosis?

A

CMV

Non-Hodgkin lymphoma

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8
Q

What is the most common systemic FUNGAL infection associated with immunosuppression from HIV?

A

CRYPTOCOCCUS

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9
Q

What type of organism is CRYPTOCOCCUS?

A

encapsulated YEAST

in environment

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10
Q

What is the most common STRAIN of cryptococcus?

A

CRYPTOCOCCUS neoformans GRUBII

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11
Q

In addition to grubii, which other strains of cryptococcus are common in HIV?

A

neoformans NEOFORMANS
or
neoformans GATTII

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12
Q

What has CRYPTOCOCCUS neoformans GATTII been found in?

A

EUCALYPTUS trees

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13
Q

What has CRYPTOCOCCUS neoformans NEOFORMANS been found in?

A

BIRD (Pigeon) droppings

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14
Q

In what region is CRYPTOCOCCUS neoformans GATTII most common?

A

TROPICAL or SUBTROPICAL region

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15
Q

How does CRYPTOCOCCUS enter the body?

A

INHALATION

rapidly spreads from LUNG to CNS

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16
Q

What common dermatological manifestation in HIV does cryptococcal skin disease resemble?

A

MOLLUSCUM

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17
Q

What is the most common symptoms of cryptococcus meningitis?

A

HEADACHE

FEVER

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18
Q

In addition to cryptococcus meningitis what other systems may be affected by cryptococcus?

A

RESPIRATORY
SKIN papule/molluscum-like
BLOOD

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19
Q

In cryptococcus disease what is the clinical presentation of haematological disease?

A

FEVER
NIGHT SWEATS
RIGORS

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20
Q

Which system does CRYPTOCOCCUS most commonly affect?

A

CNS

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21
Q

What is the most sensitive test for cryptococcus disease?

A

CSF for cryptococcal antigen

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22
Q

What is a useful initial investigation for cryptococcus disease to guide further management?

A
serumccryptococcal antigen (CRAG)
(if positive, do LP)
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23
Q

If serum cryptococcal antigen (CRAG) is positive what investigation is indicated?

A

LP for CSF and manometry

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24
Q

Prior to lumbar puncture for neurology associated with HIV and low CD4 what investigation should be performed?

A

CT or MRI of brain

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25
Q

What are poor prognostic indicators for cryptococcal disease?

A
Blood CULTURE positive
low white cell count on CSF
high CSF cryptococcal ANTIGEN
CONFUSED 
raised intracranial PRESSURE
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26
Q

What is INDUCTION therapy for cryptococcal meningitis?

A
LIPOSOMAL AMPHOTERICIN B
4mg/kg/day
\+
5-FLUCYTOSINE
100mg/kg/day
TWO (2) weeks
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27
Q

What is MAINTENANCE therapy for cryptococcal meningitis?

A

FLUCONAZOLE 400mg daily

EIGHT (8) weeks

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28
Q

Is prophylaxis recommended for cryptococcal disease?

A

SECONDARY only

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29
Q

What is SECONDARY prophylaxis for cryptococcal meningitis?

A

FLUCONAZOLE 200mg daily

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30
Q

What is the BENEFIT of adding FLUCYTOSINE to induction treatment for cryptococcal disease?

A

quicker STERILISATION of CSF

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31
Q

What is the DISADVANTAGE of adding FLUCYTOSINE to induction treatment for cryptococcal disease?

A

haematological TOXICITY

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32
Q

What toxicity is amphotericin B associated with?

A

RENAL

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33
Q

Which preparation of amphotericin B is associated with less RENAL toxicity?

A

LIPOSOMAL

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34
Q

How is raised intracranial pressure managed in cryptococcal meningitis?

A

repeated lumbar puncture

reduce pressure to <200mmH20 or 50% opening

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35
Q

If repeat lumbar puncture does not improve ICP in cryptococcal meningitis what is recommended?

A

NEUROSURGICAL input

VP shunt

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36
Q

Cryptococcal meningitis + corticosteroid - is it useful?

A

NO

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37
Q

If cryptococcal disease is not involving CNS what is the treatment?

A

FLUCONAZOLE 400mg daily
then
secondary prophylaxis

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38
Q

When should ART be started following treatment for cryptococcal disease?

A

TWO weeks

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39
Q

What are common manifestations of cryptococcal IRIS?

A
aseptic meningitis
raised ICP
space occupying lesion
pulmonary infiltrates/cavities
lymphadenopathy
hypercalcaemia
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40
Q

When can SECONDARY prophylaxis for CRYPTOCOCCAL disease be STOPPED?

A

CD4 >100
&
undetectable VL 3 months

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41
Q

What is the most common cause of CNS mass lesions in immunocompromised people with HIV?

A

Toxoplasma abscess

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42
Q

What type of organism is TOXOPLASMA GONDII?

A

obligate intracellular protozoan

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43
Q

Which site of which animal is toxoplasma gondii reliant on to complete its life cycle?

A

Feline (CAT) INTESTINAL tract

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44
Q

How do humans acquire toxoplasma gondii?

A

Eating dead animal
or
ingesting oocytes from contaminated soil, water, food

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45
Q

What is the mechanism of TOXOPLASMOSIS disease in immunocompromised people?

A

REACTIVATION of infection acquired in early life

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46
Q

What is the risk of developing toxoplasma encephalitis if IgG T gondii positive and HIV positive, not on ART?

A

25%

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47
Q

What is the typical presentation of toxoplasma abscess?

A

FOCAL neurology
headache
vomiting
seizures

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48
Q

What is the preferred imaging modality for toxoplasma abscess?

A

MRI

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49
Q

In addition to brain imaging, what other investigation is useful to help diagnose toxoplasma abscess?

A

LP for CSF PCR for T gondii

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50
Q

What is the main differential diagnosis for toxoplasma abscess?

A

Primary CNS Lymphoma
Tuberculoma
PML

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51
Q

What is the typical and appearance of toxoplasma abscess on brain imaging?

A

MULTIPLE
RING enhancing
Grey-White interface
DEEP GREY matter of basal ganglia or thalamus

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52
Q

What patient factor may result in a lack of ring enhancement of toxoplasma abscess?

A

Low CD4 cell count

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53
Q

What features of a CNS mass suggest LYMPHOMA more likely than toxoplasma abscess?

A

SINGLE

Periventricular

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54
Q

What features of a CNS mass suggest PML more likely than toxoplasma abscess?

A

WHITE matter
rarely enhancing
no mass effect

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55
Q

What imaging modality is useful to help distinguish between lymphoma and toxoplasma abscess?

A

SPECT - high uptake in lymphoma

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56
Q

What is first line treatment for toxoplasma encephalitis/abscess?

A
PYRIMETHAMINE
loading 200mg then 50-75mg/day
\+
FOLINIC acid 15mg/day
\+
SULPHADIAZINE 
1-2gram 4x/day
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57
Q

If a person cannot tolerate SULPHADIAZINE for toxoplasma abscess, what is the alternative?

A

CLINDAMYCIN

600mg 4x/day

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58
Q

Why is folinic acid given as part of treatment for toxoplasma abscess?

A

to counteract MYELOSUPPRESSIVE effect of PYRIMETHAMINE

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59
Q

How long is induction therapy for toxoplasma abscess?

A

SIX (6) weeks

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60
Q

What is the MAINTENANCE regimen for toxoplasma abscess?

A
same drugs as induction, LOWER dose
PYRIMETHAMINE
25mg/day
\+
FOLINIC acid 15mg/day
\+
SULPHADIAZINE 
500mg 4x/day or 1-2gram 2x/day
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61
Q

When are steroids indicated for toxoplasma encephalitis?

A

symptoms or signs of raised intracranial pressure

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62
Q

What is the dosing regimen for steroids in the event of raised intracranial pressure due to toxoplasma abscess?

A

DEXAMETHASONE 4mg 4x/day

wean gradually

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63
Q

Within what time frame is a response to antimicrobials expected when treating toxoplasma abscess?

A

TWO weeks

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64
Q

When should brain biopsy be considered in the context of treatment for toxoplasma abscess?

A

No response to treatment at 2 weeks
or
clinical deterioration on treatment

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65
Q

When do PLW HIV need PRIMARY prophylaxis for toxoplasmosis?

A

CD4 cell count <200

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66
Q

What is the first line primary PROPHYLAXIS for toxoplasma abscess?

A

Co-trimoxazole

480-960mg daily

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67
Q

How long should PROPHYLAXIS for toxoplasma abscess be continued?

A

until CD4 >200
&
on ART THREE (3) months

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68
Q

How long should MAINTENANCE for toxoplasma abscess/encephalitis be continued?

A

until CD4 >200
&
on ART SIX (6) months

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69
Q

When should ART be started in the context of toxoplasma abscess?

A

2 weeks after toxoplasma treatment started

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70
Q

What organism causes progressive multifocal leukoencephalopathy (PML)?

A

Virus JC

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71
Q

What proportion of the population are seropositive for JC virus?

A

70%

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72
Q

Where does JC virus remain latent in immunocompetent people?

A

spleen
bone marrow
kidneys
Blymphocytes

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73
Q

What happens to JC virus in IMMUNOSUPPRESSED people?

A
REPLICATES
transported to BRAIN
by B-LYMPHOCYTES
infects OLIGODENDROCYTES
via SEROTONIN receptor
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74
Q

What proportion of people with AIDS develop PML from JC virus?

A

5%

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75
Q

What is the pathological process of PML?

A

IRREVERSIBLE

DEMYELINATION

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76
Q

What is the typical presentation of PML?

A

SUBACUTE
PROGRESSIVE
FOCAL neurology

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77
Q

What investigations are required to make a diagnosis of PML?

A

MRI brain

CSF for JC PCR

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78
Q

What are the poor prognostic factors in PML?

A
OLDER age
BRAINSTEM involvement
LOW GCS
HIGH JC viral load in CSF
CD4 <100
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79
Q

What is the treatment for PML?

A

ART

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80
Q

What is the one year survival for PML on ART?

A

50%

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81
Q

What is the one year survival for PML not on ART?

A

10%

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82
Q

What type of virus is cytomegalovirus (CMV)?

A

Human B-Herpes virus (type 5)

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83
Q

Which population group at risk of HIV is most likely to be seropositive for CMV?

A

MSM (nearly all)

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84
Q

Through what mechanism is does CMV develop in PLW HIV?

A

REACTIVATION leads to
VIRAEMIA
+
END-ORGAN disease

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85
Q

At what CD4 count does risk of end organ disease from CMV increase?

A

<50

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86
Q

Which is the main site of CMV disease?

A

RETINA (3/4 of CMV disease)

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87
Q

Other than the retina, what other sites can have CMV disease?

A
GI tract
LUNG
LIVER
HEART
ADRENAL
CNS
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88
Q

What proportion of CMV disease affects the RETINA?

A

3/4

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89
Q

What proportion of CMV disease affects the CNS?

A

<1%

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90
Q

What is the typical presentation of CMV ENCEPHALITIS?

A
progressive DISORIENTATION
WITHDRAWAL
APATHY
Cranial nerve PALSY
NYSTAGMUS
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91
Q

What is the typical presentation of CMV lumbosacral POLYRADICULITIS?

A
PAINFUL
rapidly PROGRESSIVE
BILATERAL
ASCENDING flaccid paralysis
saddle anaesthesia, areflexia, spincter dysfunction, urinary retention
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92
Q

What are the investigations for CMV CNS disease?

A

MRI brain
+
LP for CMV PCR on CSF

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93
Q

What are the CT findings in CMV encephalitis?

A

diffuse WHITE matter hypodensities
ventricular ENLARGEMENT
MENINGEAL enhancement
Ring-enhancing

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94
Q

What is the finding in CSF in CMV CNS disease?

A

polymorphonuclear cell PLEOCYTOSIS (wcc)

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95
Q

Which antivirals have efficacy against CMV retinitis?

A

GANCICLOVIR
FOSCARNET
valganciclovir
cidofovir

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96
Q

What is the preferred FIRST line treatment for CMV CNS disease?

A
Ganciclovir 5mg/kg 
TWICE daily
THREE (3) weeks
then 
maintenance
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97
Q

Is prophylaxis required for CMV CNS disease?

A

No

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98
Q

What is the maintenance therapy for CMV CNS disease?

A

IV Ganciclovir 5mg/kg DAILY
or
oral VALGANCICLOVIR 900mg daily

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99
Q

What are causes of NON-INFECTIOUS HIV-related lung disease?

A
KS
Lymphoma
Lung CANCER
EMPHYSEMA
Lymphoid interstitial pneumonitis (LIP)
Non-specific interstitial pneumonitis (NSIP)
IRIS
SARCOID
Pulmonary hypertension
Pulmonary thromboembolic disease
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100
Q

What type of organism is pneumocystis jirovecii?

A

FUNGUS

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101
Q

What proportion of PCP occurs in PLW HIV with CD4 count <200?

A

90%

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102
Q

What is the typical presentation of PCP?

A

EXERTIONAL dyspnoea
PROGRESSES over weeks
MALAISE
dry COUGH

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103
Q

What should presentation of pneumothorax in a PLW HIV prompt investigation for?

A

PCP

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104
Q

What proportion of PCP have a normal CXR?

A

40%

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105
Q

What observation is useful to perform in suspected PCP with a normal CXR?

A

oxygen saturation on exercise

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106
Q

Through what TWO processes should respiratory sample be got for investigation of PCP?

A

INDUCED sputum
or
Broncho-alveolar lavage (BAL)

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107
Q

What is more specific, direct visualisation or NAAT for pneumocystis jirovecii?

A

direct visualisation

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108
Q

For how long can adequate respiratory samples be obtained for investigating PCP after starting treatment?

A

7-10 days (ie don’t delay Rx)

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109
Q

PCP - moderate/severe disease (for treatment purposes) - define?

A

PaO2 <9.3kPa (70mmHg)
or
SpO2 <92%

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110
Q

What is the FIRST line treatment of moderate/severe PCP?

A

IV co-trimoxazole
+
CORTICOSTEROIDS
TWENTY ONE (21 ) days

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111
Q

What is the dose of CO-TRIMOXAZOLE for moderate/severe PCP?

A
IV co-trimoxazole
120mg/kg/day (split 3x or 4x daily)
THREE (3) days
then
90mg/kg/day
EIGHTEEN (18) days
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112
Q

Why is there a dose reduction of co-trimoxazole for PCP treatment?

A

Similar efficacy
less toxicity
than continuous high dose

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113
Q

What is the CORTICOSTEROID regimen for moderate/severe PCP?

A
PREDNISOLONE
40mg TWICE daily days 1-5
40mg ONCE daily days 6-10
20mg ONCE daily days 11-21
then stop
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114
Q

What is the appropriate conversion to methylprednisolone for PCP treatment if oral route is not available?

A

75% of oral regimen

30 BD/30 OD/15 OD

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115
Q

How long may treatment for PCP take to show improvement?

A

7 days or more

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116
Q

What are suitable alternative agents for treatment of PCP?

A

Clindamycin
Primaquine
Pentamidine

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117
Q

What is the definition of MILD PCP disease - presentation, O2, CXR?

A
  • SOB on exertion +/- cough/sweats
  • PaO2 >11kPa (83mmHg), SaO2 >96
  • normal CXR
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118
Q

What is the definition of MODERATE PCP disease - presentation, O2, CXR?

A
  • SOB on minimal exertion, cough + fever
  • PaO2 8.1-11kPa (61-83), SaO2 91-96
  • Diffuse interstitial changes
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119
Q

What is the definition of SEVERE PCP disease - presentation, O2, CXR?

A
  • SOB at rest
  • PaO2 <8.0kPa (<60), SaO2 <91
  • Extensive interstitial changes
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120
Q

G6PD deficiency should be checked prior to which drugs used for PCP treatment?

A

Co-trimoxazole
Dapsone
Primaquine

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121
Q

Which groups of people are most likely to have G6PD deficiency?

A

African
Mediterranean
Sephardic Jews
Chinese

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122
Q

What is the risk in a person with G6PD?

A

Haemolysis with certain drugs

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123
Q

What non-invasive ventilation is useful for hypoxia related to PCP?

A

CPAP

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124
Q

At what CD4 count is PCP prophylaxis recommended in PLW HIV?

A

CD4 <200
or
<14%

125
Q

What is the preferred regimen for PCP prophylaxis?

A

480mg daily
(less side effects)
can use 960mg daily or 960mg 3x/week)

126
Q

What cross protection does co-trimoxazole offer in terms of OI prophylaxis in PLW HIV?

A

PCP
toxoplasmosis
other bacterial infection

127
Q

Other than co-trimoxazole which agents provide cross protection for both PCP + toxoplasmosis?

A

Dapsone + pyrimethamine
or
Atovaquone

128
Q

When should ART be started following PCP treatment start?

A

within 2 weeks

129
Q

When can PCP prophylaxis stop?

A

CD4 >200
+
3 months on ART

130
Q

In what situation may PCP prophylaxis be required lifelong?

A

PCP infection at CD4 count>200

131
Q

Which organisms are most likely cause of bacterial pneumonia in PLW HIV?

A

Streptococcus pneumoniae

Haemophilus influenzae

132
Q

What is the association between bacteraemia and pneumonia in PLW HIV?

A

higher rates bacteraemia in PLW HIV compared to HIV negative people

133
Q

What investigation is indicated in for work up for pneumonia in PLW HIV?

A
Sputum culture (if purulent)
CXR
Blood culture (if inpatient)
134
Q

What preventative measure can be used to reduce risk of bacterial pneumonia in PLW HIV?

A

Polysaccharide vaccine 23 (PCV-23)

- protects against 23 serotypes of pneumococcus

135
Q

What is the treatment regimens for community acquired pneumonia in PLW HIV - mild, moderate, severe disease?

A

same as HIV negative

  • amoxicillin oral
  • amoxicillin + macrolide or doxycycline
  • IV co-amoxiclav + macrolide
136
Q

How does pulmonary CRYPTOCOCCOSIS present?

A

similar to PCP

SOB, fever, cough

137
Q

What feature on CXR may be present in pulmonary CRYPTOCOCCOSIS?

A

solitary nodules

cavities

138
Q

If pulmonary CRYPTOCOCCOSIS is suspected what additional investigation is required other than respiratory sample?

A

CSF for CNS disease
&
serum CRAG is helpful

139
Q

If pulmonary CRYPTOCOCCOSIS is present in isolation what is the treatment?

A

Fluconazole 400mg DAILY
TEN (10) weeks
then
200mg daily

140
Q

What fungus commonly colonises the lung of people with lung disease?

A

Aspergillus

141
Q

When does invasive aspergillosis occur?

A

Aspergillus INVADES parenchyma

DISSEMINATION to other organs

142
Q

What factors increase the risk of invasive aspergillosis in PLW HIV?

A
RARE
but
NEUTROPENIA
TRANSPLANTATION
STEROID use
143
Q

What investigations are required to diagnose aspergillosis in PLW HIV?

A

Fungal culture of sample
CT chest
Broncho-alveolar lavage (BAL)
Bronchoscopy +/- biopsy

144
Q

What does the galactomannan test check for in aspergillosis?

A

detects presence of a cell wall constituent of aspergillus

145
Q

What is the FIRST line regimen for invasive ASPERGILLOSIS?

A
Loading:
VORICONAZOLE 
6mg/kg TWICE daily
24 hours
then
4mg/kg TWICE daily
SEVEN (7) days
then
200mg TWICE daily
TWELVE (12) weeks total
146
Q

What is required to improve absorption of voriconazole?

A

Take with FULL meal

147
Q

Is prophylaxis required in PLW HIV for pulmonary aspergillosis?

A

NO

Maintenance may be required in chronic aspergillosis syndromes

148
Q

What does the detection of CMV in urine,l blood or BAL without evidence of end organ disease mean?

A

CMV INFECTION

but not DISEASE

149
Q

How is PULMONARY CMV diagnosed?

A

BAL or respiratory biopsy CMV positive
+
Clinical syndrome

150
Q

What is the limitation of respiratory sampling in diagnosing pulmonary CMV?

A

CMV commonly sheds in respiratory tract but does not mean end-organ disease

151
Q

When should anti-CMV treatment be given in the setting of respiratory disease?

A

NO alternative diagnosis
+
CMV in BAL or biopsy

152
Q

If it is likely they is co-infection with CMV and another pathogen causing respiratory disease, what is the management?

A

Treat co-pathogen first

153
Q

What is the treatment for pulmonary CMV?

A

Ganciclovir 5mg/kg
TWICE daily
21 days

154
Q

What is the association between PLW HIV and Influenza A virus?

A

more SEVERE disease

155
Q

What is the investigation of choice for influenza A?

A

nasal swab for viral swab

156
Q

What treatment option can be considered for PLW HIV and influenza A?

A

OSELTAMIVIR

157
Q

When is oseltamivir indicated for influenza A treatment?

A

Fever
<48 hours
or significant immunosuppression

158
Q

What is the regimen for OSELTAMIVIR to treat influenza A?

A

Oseltamivir
75mg TWICE daily
5 days

159
Q

What is the potential benefit of ZANAMIVIR for the treatment of Influenza A in PLW HIV?

A

improved EFFICACY in those with significant IMMUNOSUPPRESSION due to oseltamivir RESISTANCE

160
Q

In addition to treatment for influenza A. what else should people with immunocompromise be treated with?

A

antibiotics

DOXCYCLINE or CO-AMOXICLAV

161
Q

What 3 specific criteria might should be met to consider influenza A prophylaxis?

A

1) CD4 <200
2) not vaccinated against flu
3) exposure < 48 hours

162
Q

Why is primary or secondary prophylaxis not recommended for oesophageal candidiasis?

A

rapid emergence of RESISTANCE

163
Q

In what specific situation might continuous treatment with FLUCONAZOLE be recommended for people with recurrent oesophageal candidiasis?

A

4 or more episodes per year

continuous = less resistance

164
Q

What investigations are indicated in acute diarrhoea in PLW HIV?

A

Stool culture
+
Blood culture (especially if sepsis)

165
Q

How often is retinal screening recommended in PLW HIV and CD4 count <50?

A

3 monthly

166
Q

How is diagnosis of CMV retinitis made?

A

on visualisation of retina
+/-
symptoms

167
Q

Is oral or IV therapy preferred in CMV retinitis?

A

ORAL

valganciclovir

168
Q

What is the preferred regimen for CMV retinitis?

A
VALGANCICLOVIR oral
900mg TWICE daily
TWO weeks
then 
maintenance
169
Q

When is ganciclovir implant or intravitreal injection recommended for CMV retinitis?

A

Lesions affecting zone 1 ie near OPTIC DISC
or
unable to tolerate systemic therapy

170
Q

What needs to be monitored whilst on anti–CMV treatment?

A
RENAL function
ELECTROLYTES
BONE MARROW (ie FBC)
171
Q

When can anti-CMV treatment be stopped?

A
CD4 >100
and
undetectable VL
\+
agreement with ophthalmologist
172
Q

Why might anti-CMV treatment fail?

A

DOSE related
or
RESISTANCE

173
Q

If a woman of reproductive age is treated with CIDOFOVIR for CMV what should she be advised?

A

No pregnancy ONE month

174
Q

If a man of reproductive potential/desire is treated with CIDOFOVIR for CMV what should he be advised?

A

No conception THREE month

175
Q

What group of PLW HIV are at greatest risk of immune recovery uveitis in CMV retinal disease?

A

25% of retina affected

176
Q

If a PLW HIV has CMV IRIS what is the recommendation for eye follow up?

A

LIFELONG

177
Q

In addition to antiviral treatment of CMV what is recommended for CMV IRIS?

A

STEROIDs

178
Q

What other pathogens may cause eye disease in PLW HIV?

A

SYPHILIS
TOXOPLASMOSIS
VZV

179
Q

How may syphilis present in the eye?

A
IRITIS
VITRITIS
OPTIC NEURITIS
PAPILLITIS
NEURORETINITIS
RETINAL VASCULITIS
NECROTISING RETINITIS
180
Q

How should ocular syphilis be treated?

A

the same as NEUROSYPHILIS

181
Q

What is the most common cause of POSTERIOR UVEITIS in immunoCOMPETENT people?

A

TOXOPLASMOSIS

182
Q

What TWO aggressive eye syndromes are associated with VARICELLA ZOSTER virus?

A

PROGRESSIVE outer retinal necrosis (PORN)
&
ACUTE retinal necrosis (ARN)

183
Q

Why is visual prognosis poor in patients with VZV associated retinal necrosis?

A

risk of:
retinal DETACHMENT
ISCHAEMIC optic neuropathy
OPTIC NERVE involvement

184
Q

What is the treatment of choice for VZV eye disease in PLW HIV?

A

CIDOFOVIR

185
Q

Pyrexia of unknown origin - define?

A
FEVER >38.3
several occasions
>FOUR weeks
or
> 3 days in hospital, after negative initial investigation
186
Q

What is the overall most common cause of PUO in PLW HIV?

A

INFECTION

187
Q

Why is a LIFETIME travel history essential in PUO in PLW HIV?

A

REACTIVATION of tropical infection frequent

188
Q

In PLW HIV on ART what are the common causes of PUO?

A

LYMPHOMA

TB

189
Q

What other broad causes should be considered in PUO in PLW HIV?

A
Non-infective:
RHEUMATOLOGICAL
CONNECTIVE TISSUE disease
VASCULITIS including temporal arteritis
Polymyalgia rheumatica
SARCOID
190
Q

On starting ART what might PUO be a sign of?

A

IRIS to underlying pathogen

191
Q

BARTONELLOSIS (Bartnella sp.) can be a cause of PUO in PLW HIV - how is this diagnosed?

A

Culture and PCR of BLOOD or BIOPSY

192
Q

How is bartonellosis treated?

A

ERYTHROMYCIN
500mg 4x/day
THREE months

193
Q

What cutaneous manifestation is bartonellosis associated with in PLW HIV?

A

BACILLARY ANGIOMATOSIS

194
Q

What is BACILLARY ANGIOMATOSIS?

A
FRIABLE
red
vascular
EXOPHYTIC lesions
papules or nodules
195
Q

What initial blood tests are recommended in PLW HIV and PUO?

A
FBC
U&E, LFT
CRP
LDH
serum CRAG
Blood cultures
SYPHILIS serology
HEPATITIS serology
CMV serology
196
Q

When are ANA and rheumatoid factor recommended in the investigation of PUO in PLW HIV?

A

if CONNECTIVE tissue disease suspected

197
Q

What initial imaging is recommended in PLW HIV and PUO?

A

CXR

Echo

198
Q

Culture of what sample is recommended in PLW HIV and PUO?

A

URINE
SPUTUM inc for Mycobacterium
BLOOD

199
Q

What additional system specific investigation is recommended in PLW HIV and PUO and CARDIO-RESPIRATORY symptoms?

A

ECHO
VTE screen
Bronchoscopy +/- BAL

200
Q

What additional system specific investigation is recommended in PLW HIV and PUO and GASTROINTESTINAL symptoms?

A
STOOL culture for culture, OVA, CYSTS, PARASITES
ENDOSCOPY - upper &/or lower GI
\+/- BIOPSY
US abdomen
\+/- CT abdomen
201
Q

What additional system specific investigation is recommended in PLW HIV and PUO and NEUROLOGICAL symptoms?

A
CRAG
CT brain with CONTRAST
\+/- MRI brain
CSF
EEG
202
Q

What additional system specific investigation is recommended in PLW HIV and PUO and MUCOCUTANEOUS symptoms?

A

BIOPSY
Drug review
STI screen

203
Q

What additional system specific investigation is recommended in PLW HIV and PUO and LYMPHADENOPATHY?

A

FNA
excision biopsy
CT chest/abdomen/pelvis

204
Q

What additional system specific investigation is recommended in PLW HIV and PUO with ABNORMAL LFTS?

A
HEPATITIS serology
CMV PCR
US liver +/- CT
Toxicology
BIOPSY
PARASITE serology
205
Q

When is bone marrow aspirate indicated in PLW HIV and PUO?

A

When a diagnosis for PUO has not been made through other investigation or haematological malignancy or disseminated infection likely (ie TB/leishmaniasis)

206
Q

What are the THREE phases of herpes viruses infection?

A

PRIMARY
LATENT
REACTIVATION

207
Q

What are the THREE broad groups within the herpes virus family?

A

ALPHA (HSV 1,2 and VZV)
BETA (CMV, HHV6 & 7)
GAMMA (EBV & HHV8)

208
Q

What virus causes varicella infection (chickenpox) and zoster (shingles)?

A

VARICELLA ZOSTER virus

209
Q

How is VZV acquired?

A

Through respiratory route

210
Q

Which site of the body does VZV establish latency?

A

DORSAL ROOT GANGLIA

211
Q

What is the impact of immunosuppression on VZV latency?

A

REACTIVATION more likely
more SEVERE disease
DISSEMINATED more likely

212
Q

If PRIMARY VZV occurs in PLW HIV what is the potential clinical sequelae?

A

DISSEMINATED disease

PNEUMONITIS

213
Q

What is the risk of VZV reactivation on starting ART?

A

2-4 fold increase risk of disease in first few months due to IRIS

214
Q

What is the definition of HERPES ZOSTER OPHTHALMICUS?

A

VZV disease involves the ophthalmic division of trigeminal nerve

215
Q

What are the potential complications of herpes zoster ophthalmicus?

A
Loss of vision
Keratitis
anterior uveitis
severe neuralgia
necrotising retinopathy
216
Q

What CNS complications can occur from VZV infection in PLW HIV?

A
leukoencephalitis
vasculitis with infarct
myelitis
meningitis
optic neuritis
217
Q

What is the recommended treatment for VZV varicella infection?

A

IV ACICLOVIR 10mg/kg 3x/day

7-10 days

218
Q

What is the recommended treatment for VZV zoster infection?

A

oral ACICLOVIR 800mg 5x/day

7 days

219
Q

Which site of the body does herpes simplex virus establish latency?

A

LOCAL SENSORY GANGLIA

220
Q

Which HSV is more common in PLW HIV than HIV negative people?

A

HSV2

221
Q

What is the risk of HIV transmission in a person with genital HSV2 compared to no HSV?

A

2x higher

222
Q

Which sites of the body may be affected by systemic HSV disease?

A
EYE
LUNG
LIVER 
OESOPHAGUS
CNS
223
Q

What is the definitive investigation for HSV encephalitis?

A

CSF for HSV DNA PCR

224
Q

What is the treatment for oral or genital HSV in PLW HIV?

A

oral ACICLOVIR
400mg 5x/day
7-10 days

225
Q

What agent can be used in aciclovir resistant HSV?

A

FOSCARNET

226
Q

What is the most common non-TB mycobacterium that causes infection in PLW HIV?

A

Mycobacterium avium

227
Q

In which group of PLW HIV does disseminated mycobacterium avian occur?

A

CD4 <50

228
Q

What are common symptoms or signs of MAI?

A
Fever
Night sweats
Fatigue
Weight loss
Anorexia
Diarrhoea
Hepatomegaly
Lymphadenopathy
229
Q

What are common blood abnormalities of MAI?

A

Anaemia
Leukopenia
raised ALP
low albumin

230
Q

What a unusual clinical syndromes may be suggestive of MAI?

A

Oral ulceration
Septic arthritis/osteomyelitis
Enophthalmitis
Pericarditis

231
Q

What is the definitive investigation for MAI?

A

Culture of blood, bone marrow or sterile site (ie not sputum or stool)

232
Q

What is the preferred regimen for MAI?

A
macrolide:
CLARITHROMYCIN 500mg TWICE daily
or
AZITHROMYCIN 500mg daily
\+
ETHAMBUTOL 15mg/kg/DAY
\+/- 
RIFABUTIN 300mg/DAY
233
Q

When should RIFABUTIN be added to treatment for MAI?

A

High risk of short term MORTALITY

  • CD4 <25
  • very symptomatic of MAI
  • inability for ART
234
Q

What is the benefit of adding RIFABUTIN to treatment regimen for MAI?

A
  • improved SURVIVAL

- less RESISTANCE

235
Q

When should ART be started in the context of MAI?

A

Immediately or within 2 weeks of MAI Rx

236
Q

What is the criteria to STOP treatment for MAI in PLW HIV?

A
THREE months treatment
\+
VL undetectable
\+
CD4 >100 for 3 MONTHS
237
Q

In the event that an alternative treatment regimen is required for MAI, what is the benefit of continuing ETHAMBUTOL?

A

facilitates PENETRATION of other agents into MYCOBACTERIUM

238
Q

In the event of focal MAI (ie pulmonary disease) what is the recommended length of treatment?

A

12 months

3 drug regimen

239
Q

In which instances should PRIMARY prophylaxis for MAI be considered?

A
CD4 <50
\+
not on ART
or 
ART failure
240
Q

If PRIMARY prophylaxis for MAI is given what is the recommended regimen?

A

AZITHROMYCIN 1250mg WEEKLY

241
Q

What useful ADJUNCTS to usual therapy may be considered in MAI IRIS?

A
  • PREDNISOLONE 20-40mg 4-8 weeks
  • IL-2 or GCSF
  • Leukotriene inhibitors
  • Fine needle aspiration of pus due to lymphadenitis
242
Q

What is the SECOND most common non-TB mycobacterium that causes infection in PLW HIV?

A

Mycobacterium kansasii

243
Q

What is the recommended regimen for M. kansasii?

A
RIFAMPICIN/RIFABUTIN
\+
ETHAMBUTOL
\+
ISONIAZID + PYRIDOXINE

for TWELVE (12) months

244
Q

For how long should the recommended regimen for M. kansasii be given?

A

12 months

245
Q

What is the most common presentation fo Mycobacterium KANSASII?

A

PULMONARY

246
Q

What type of organism is malaria?

A

protozoal parasite

247
Q

How is malaria transmitted?

A

BITE by FEMALE ANOPHELES mosquito

248
Q

What is the most serious malaria species?

A

plasmodium FALCIPARUM

249
Q

What is the association between CD4 count and severity of malaria?

A

CD4 <200 more likely SEVERE malaria

250
Q

What is the clinical presentation of MALARIA?

A
FEVER
HEADACHE
ARTHRALGIA
MYALGIA
DIARRHOEA
251
Q

What are the potential complications of malaria?

A
HYPERPARASITAEMIA
AKI
DIC
HYPGLYCAEMIA
LACTIC ACIDOSIS
FULMINANT HEPATIC FAILURE
CEREBRAL MALARIA
252
Q

Within what time frame does plasmodium FALCIPARUM present?

A

THREE (3) months

253
Q

How is MALARIA diagnosed?

A

THICK and THIN blood film

254
Q

What does the THICK blood film look for in MALARIA?

A

diagnose malaria

percentage of parasitaemia

255
Q

What does the THIN blood film look for in MALARIA?

A

speciation

256
Q

If a blood film is NEGATIVE but MALARIA is suspected, what other test can be done?

A

RAPID antigen test

257
Q

What is the definition of SEVERE FALCIPARUM malaria?

A

> 2% parasitaemia
+/-
organ dysfunction

258
Q

What is the treatment for SEVERE FALCIPARUM?

A

IV artesunate

259
Q

What is the treatment for non-severe FALCIPARUM?

A

ORAL artemether-lumefantrine

260
Q

What is the potential CARDIAC complication of IV quinine?

A

prolonged QRS and QT interval

261
Q

What is the treatment for NON-FALCIPARUM malaria?

A

oral CHLOROQUINE THREE days
then
oral PRIMAQUINE FOURTEEN days

262
Q

Which agent used in treatment of non-falciparum malaria can cause haemolysis in people with G6PD deficiency?

A

PRIMAQUINE

263
Q

Why are there TWO phases to treatment for non-falciparum malaria?

A

2nd phase to ERADICATE liver parasite stages

264
Q

What does the ABCD of malaria PREVENTION stand for?

A

Awareness of risk
BIte prevention
Chemoprophylaxis
Diagnosis and treatment

265
Q

What are the main options for MALARIA PROPHYLAXIS?

A

MALARONE
DOXYCYCLINE
CHLOROQUINE + PROGUANIL

266
Q

What type of organism is leishmania?

A

Protozoa

267
Q

How are leishmania sp. transmitted?

A

SANDFLY

268
Q

What are the THREE types of leishmania disease?

A

VISCERAL
MUCOCUTANEOUS
CUTANEOUS

269
Q

What is the most common type of LEISHMANIA in PLW HIV?

A

VISCERAL

270
Q

What organomegaly is most likely in visceral leishmaniasis?

A

SPLENOMEGALY

271
Q

How does a cutaneous leishmania lesion present?

A

PAPULE to a chronic, DESTRUCTIVE ulcer

272
Q

What are the preferred specimens for diagnosis of visceral leishmaniasis?

A

SPLENIC
BONE MARROW
BIOPSY of lymph node or skin lesion

273
Q

What is the treatment regimen for VISCERAL leishmaniasis?

A

Liposomal AMPHOTERICIN B
4mg/kg 10 doses, 6 week course
day 1-5, 10, 17, 24, 31, 38

274
Q

What is the relapse rate of treated leishmaniasis in PLW HIV?

A

HIGH

275
Q

What prophylaxis is recommended for leishmaniasis in PLW HIV?

A

SECONDARY only (pre-ART)

276
Q

When can SECONDARY prophylaxis be stopped in visceral leishmania?

A

CD4 >200 for 3-6 months

on ART

277
Q

What is the organism that causes CHAGAS disease?

A

PARASITE

TRYPAHNOSOMA CRUZI

278
Q

Where in the world is TRYPANOSOMA CRUZI limited to?

A

CENTRAL & SOUTH AMERICA

279
Q

How is TRYPANOSOMA CRUZI transmitted to humans?

A

BITE of TRIATOMINE insect

280
Q

What is the impact of immunosuppression on trypanosome cruzi?

A

REACTIVATION of infection

281
Q

What are the TWO main presentations of trypanosoma CRUZI in PLW HIV?

A
CNS:
Space occupying lesion
Meningoencephalitis
CARDIAC:
Myocarditis
282
Q

How is CHAGAS (trypanosoma cruzi) disease diagnosed?

A

Brain imaging
CSF for PCR
Biopsy

283
Q

What is the treatment for HAGAS (trpanosoma cruzi) disease?

A

BENZNIDAZOLE
5mg/kg split TWO doses
60-90 days

284
Q

Which DIMORPHIC fungi are of importance in PLW HIV?

A

HISTOPLASMA CAPSULATUM
BLASTOMYCES DERMATITIDIS
COCCIDIOIDES IMMITIS
PENICILLIUM MARNEFFEI

285
Q

How does DISSEMINATED disease of DIMORPHIC FUNGI present in PLW HIV?

A
Fever
weight loss
rash
lymphadenopathy
lung consolidation or cavitation
CNS features
Sepsis
286
Q

How is DISSEMINATED disease of DIMORPHIC FUNGI diagnosed in PLW HIV?

A
CULTURE of
sputum or BAL
Bone marrow
or
BIOPSY
287
Q

What is the treatment summary for DIMORPHIC FUNGI in PLW HIV?

A
ITRACONAZOLE
histoplasma & blastomyces
FLUCONAZOLE
coccidioidomycosis
AMPHOTERICIN B
penicilliosis
288
Q

What disease is caused by PENICILLIUM MARNEFFEI?

A

PENICILLIOSIS

289
Q

What type of organism is PENICILLIUM MARNEFFEI?

A

DIMORPHIC FUNGI

290
Q

What type of organism is HISTOPLASMA CAPSULATUM?

A

DIMORPHIC FUNGI

291
Q

What type of organism is BLASTOMYCES DERMATITIDIS?

A

DIMORPHIC FUNGI

292
Q

What type of organism is COCCIDIOIDES IMMITIS?

A

DIMORPHIC FUNGI

293
Q

Which area of the World doesPENICILLIUM MARNEFFEI come from ?

A

Southeast Asia

294
Q

Is PRIMARY prophylaxis recommended for PENICILLIOSIS in PLW HIV?

A

consider
CD4 <100
travel to endemic area

295
Q

What is the regimen for PRIMARY prophylaxis of PENICILLIOSIS in PLW HIV?

A

ITRACONAZOLE 200mg daily

296
Q

In pregnancy, what are the recommendations for CXR?

A

little or no risk to foetus
with
ABDOMINAL shield

297
Q

In pregnancy, when can MRI be performed?

A

avoid FIRST trimester

298
Q

In pregnancy, what parts of the body can be CT scanned?

A

BRAIN
CHEST
LIMBS

299
Q

Why is it relatively safe to perform CT in pregnancy (not abdominal)?

A

little radiation scatter

300
Q

In pregnancy, Can contrast for CT be used?

A

YES

301
Q

Which opportunistic infections can be transmitted vertically?

A
TB
CRYPTOCOCCAL
CMV
PCP
TOXOPLASMOSIS
302
Q

In pregnancy, treatment for PCP?

A

CO-TRIMOXAZOLE

same as non-pregnant

303
Q

In pregnancy, treatment for CRYPTOCOCCUS?

A

liposomal AMPHOTERICIN B

same as non-pregnant

304
Q

In pregnancy, treatment for CANDIDIASIS?

A
VAGINAL - topical preparation
ORAL - NYSTATIN
OESOPHAGEAL
- first trimester AMPHOTERICIN
- 2nd and 3rd trimerst - FLUCONAZOLE
305
Q

In pregnancy, treatment for TOXOPLASMOSIS?

A
SULPHADIAZINE
\+
PYRIMETHAMINE
\+ 
FOLINIC ACID
306
Q

In pregnancy, treatment for CMV?

A

GANCICLOVIR or VALGANCICLOVIR

however all associated with congenital abnormality in animal studies

307
Q

In pregnancy, what is the potential impact from active TB on birth outcomes?

A

Low birth weight
preterm birth
intra-uterine growth restriction

308
Q

In pregnancy, treatment for TB?

A
RIFAMPICIN
\+
ISONIAZID (with pyridoxine)
\+
PYRAZINAMIDE
\+
ETHAMBUTOL
ie RIPE
same as non-pregnant
309
Q

pregnancy, treatment for MAI?

A

AZITHROMYCIN