HIV Flashcards

1
Q

What are 8 HIV symptoms?

A
Fever
Headache
Muscle aches and joint pain
Rash
Sore throat and painful mouth sores
Swollen lymph nodes
Diarrhoea
Weight loss
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2
Q

What 5 things can cause diarrhoea in HIV?

A

Effects of the virus itself eg. HIV enteritis or opportunistic infections:
Possible causes:
- cryptosporidium + other protozoa (most common)
- cytomegalovirus
- mycobacterium avium intracellulare
- giardia

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3
Q

What is the most common infective cause of diarrhoea in HIV pts?

What stain can be used to reveal what characteristics?

What is the treatment for it?

A

Cryptosporidium, which is an intracellular protozoa and has an incubation period of 7 days. Presentation is v variable, ranging from mild to severe diarrhoea.

Modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium.

Treatment is difficult, with the mainstay of management being supportive therapy* = nitazoxanide is licensed in the US for immunocompetent patients

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4
Q

What is Mycobacterium avium intracellulare?

A

An atypical mycobacterium seen with the CD4 count is below 50.

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5
Q

What are the 6 typical features of Mycobacterium avium intracellulare?

A

Typical features include fever, sweats, abdominal pain and diarrhoea. There may be hepatomegaly and deranged LFTs.

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6
Q

How is Mycobacterium avium intracellulare diagnosed?

A

Diagnosis is made by blood cultures and bone marrow examination.

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7
Q

How can Mycobacterium avium intracellulare be managed?

A

Management is with rifabutin, ethambutol and clarithromycin

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8
Q

What is the incubation period of cryptosporidium?

A

7 days

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9
Q

How can Cryptosporidium be diagnosed?

A

A modified Ziehl-Neelsen stain (Acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium.

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10
Q

What is the treatment of Cryptosporidium?

A

Treatment is difficult, with the mainstay of management being supportive therapy* = nitazoxanide is licensed in the US for immunocompetent patients

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11
Q

What is Kaposi’s sarcoma caused by?

A

Human Herpes Virus 8 (HHV-8)

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12
Q

How does Kaposi’s sarcoma present?

A

As purple papules or plaques on the skin or mucosa eg. GI and Resp tract
Skin lesions may later ulcerate.

Respiratory involvement may cause massive haemoptysis and pleural effusion

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13
Q

What is the management for Kaposi’s sarcoma?

A

Radiotherapy and Resection

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14
Q

What is ART?

A

Anti-retroviral therapy (ART) involves a combination of at least 3 drugs, typically 2 nucleoside reverse transcriptase inhibitors (NRTI) and either a protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI). This combination both decreases viral replication but also reduces the risk of viral resistance emerging.

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15
Q

What are the 2015 BHIVA guidelines in regards to starting ART with HIV?

A

It is now recommended that patients start ART as soon as they have been diagnosed with HIV, rather than waiting until a particular CD4 count, as was previously advocated.

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16
Q

What are 2 entry inhibitors and what do they do?

A

Maraviroc - binds to CCR5, preventing an interaction with gp41

Enfuvirtide - binds to gp41, also known as ‘fusion inhibitor’

They prevent HIV-1 from entering and infecting immune cells

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17
Q

What are 8 examples of NRTI?

A

Nucleoside analogue reverse transcriptase inhibitors (NRTI):

  1. Zidovudine (AZT)
  2. Abacavir
  3. Emtricitabine
  4. Didanosine
  5. Lamivudine
  6. Stavudine
  7. Zalcitabine
  8. Tenofovir
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18
Q

What is a general NRTI side effect?

A

Peripheral neuropathy

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19
Q

What is tenofovir? And 2 adverse effects?

A

Used in BHIVAs 2 recommended regime NRTI. Adverse effects include renal impairment and osteoporosis

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20
Q

What are 3 side effects of Zidovudine?

A

Anaemia, myopathy, black nails

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21
Q

What is a side effect of Didanosine?

A

Pancreatitis

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22
Q

What are 2 examples of Non-nucleoside reverse transcriptase inhibitors (NNRTIs)?

A

Nevirapine

Efavirenz

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23
Q

What are 2 side effects of NNRTIs?

A

P450 enzyme interaction (nevirapine induces), rashes

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24
Q

What are 4 examples of Protease Inhibitors? (PIs)

A
  1. Indinavir
  2. Nelfinavir
  3. Ritonavir
  4. Saquinavir
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25
Q

What are 5 common side effects of PIs?

A
  1. Diabetes
  2. Hyperlipidaemia
  3. Buffalo hump
  4. Central obesity
  5. P450 enzyme inhibition
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26
Q

What are 2 side effects of Indinavir?

A

Renal stones

Asymptomatic hyperbilirubinaemia

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27
Q

What is a side effect of ritonavir?

A

A potent inhibitor of P450 system

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28
Q

What are 3 examples of Integrase inhibitors?

A

Raltegravir, Elvitegravir, Dolutegravir

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29
Q

What do integrase inhibitors do?

A

Block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell.

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30
Q

What are 3 neurological lesions of HIV?

A

Toxoplasmosis
Primary CNS lymphoma
Tuberculosis

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31
Q

How much does toxoplasmosis account for cerebral lesions in HIV pts?

A

50% - Toxoplasmosis accounts for around 50% of cerebral lesions in patients with HIV

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32
Q

What are 3 symptoms of toxoplasmosis?

A

headache
confusion
drowsiness

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33
Q

How would toxoplasmosis present on a CT scan?

A

Usually a single or multiple ring enhancing lesions, mass effect may be seen

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34
Q

What is the 2 management for toxoplasmosis?

A

Sulfadiazine

Pyrimethamine

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35
Q

How many cerebral lesions do Primary CNS lymphoma account for?

A

30% - Primary CNS lymphoma accounts for around 30% of cerebral lesions

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36
Q

Which virus is primary CNS lymphoma associated with?

A

Epstein-Barr virus

37
Q

How does Primary CNS lymphoma present on CT scan?

A

Single or multiple homogenous enhancing lesions

38
Q

What is the treatment for Primary CNS lymphoma?

A

Generally involves steroids (may significantly reduce tumor size), chemotherapy eg. methotrexate + with or w/o whole brain irradiation.
Surgical may be considered for lower grade tumors

39
Q

Differentiating between toxoplasmosis and lymphoma is a common clinical scenario in HIV patients. How are toxoplasmosis and Primary CNS lymphoma different? (3)

A

Toxo.. = multiple lesions; Lymphoma = single lesion

Toxo = ring or nodular enhancement; lymphoma = solid (homogenous) enhancement

Toxo = Thallium SPECT negative; Lymphoma = Thallium SPECT positive

40
Q

Is tuberculosis more or less common than other focal neurological lesions in terms of HIV complications?

A

Tuberculosis is much less common than toxoplasmosis or primary CNS lymphoma

41
Q

What will a CT scan show in tuberculosis?

A

Single enhancing lesion

42
Q

What will a CT scan show in tuberculosis?

A

Single enhancing lesion

43
Q

What are 4 generalised neurological disease in terms of HIV?

A
  1. Encephalitis
  2. Cryptococcus
  3. Progressive Multifocal Leukoencephalopathy (PML)
  4. AIDS dementia complex
44
Q

What can encephalitis be caused by?

A

CMV or HIV itself

45
Q

How common is HSV encephalitis?

A

HSV encephalitis but is relatively rare in the context of HIV

46
Q

How does encephalitis look on the CT?

A

Oedematous brain

47
Q

What is the most common fungal infection of CNS?

A

Cryptococcus

48
Q

What 6 things does cryptococcus cause in relation to HIV?

A
Headache
Fever
malaise
nausea/ vomiting
seizures
focal neurological deficit
49
Q

What would be the CSF opening pressure in cryptococcus

A

high opening pressure

50
Q

What would be the india ink test for CSF in cryptococcus?

A

Positive

51
Q

What would CT scan of cryptococcus show?

A

Meningeal enhancement, cerebral oedema

52
Q

What is the typical presentation of Cryptococcus?

A

Meningitis, but may occasionally cause a space occupying lesion

53
Q

What is progressive multifocal leukoencephalopathy (PML)?

A

Widespread demyelination, due to infection of oligodendrocytes by JC virus (a polyoma DNA virus)

54
Q

What are 4 symptoms of Progressive Multifocal Leukoencephalopathy (PML)?

A

Subacute onset of behavioural changes, speech, motor, visual impairment

55
Q

What would a CT scan of Progressive Multifocal Leukoencephalopathy (PML) show?

A

Single or multiple lesions, no mass effect, don’t usually enhance. MRI is better - high-signal demyelinating white matter lesions are seen.

56
Q

What is AIDS dementia complex caused by?

A

HIV virus itself

57
Q

What are 2 symptoms of AIDS dementia complex?

A

Behavioural changes, motor impairment

58
Q

What does CT scan of AIDS dementia complex show?

A

Cortical and subcortical atrophy

59
Q

What is the most common cause of oesophagitis in pts with HIV?

A

Oesophageal candidiasis

60
Q

In which HIV pts is oesophageal candidiasis usually seen?

A

Pts with a CD4 count of less than 100.

61
Q

What are 2 symptoms of oesophageal candidiasis?

A

Dysphagia, odynophagia

62
Q

What are the first-line treatments for oesophageal candidiasis?

A

Fluconazole and itraconazole

63
Q

What are 5 opportunistic infections that may be encountered by HIV pts with CD4 count between 200-500 cells/mm³

A

Oral thrush - secondary to Candida albicans
Shingles - secondary to herpes zoster
Hairy leukoplasia - secondary to EBV
Kaposi sarcoma - secondary to HHV-8

64
Q

What are 5 opportunistic infections that may be encountered by HIV pts with CD4 count between 100-200 cells/mm³

A

Cryptosporidiosis - pts with CD4 count of 200-500 may also develop cryptosporidiosis, but the disease is usually self-limiting and similar to that in immunocompetent hosts

Cerebral toxoplasmosis

Progressive multifocal leukoencephalopathy - secondary to JC virus

Pneumocystis jirovecii pneumonia

HIV dementia

65
Q

What are 4 opportunistic infections that may be encountered by HIV pts with CD4 count between 50-100 cells/mm³

A

Aspergillosis - secondary to Aspergillus fumigatus
Oesophageal candidiasis - secondary to Candida albicans
Cryptococcal meningitis
Primary CNS lymphoma - secondary to EBV

66
Q

What are 2 opportunistic infections that may be encountered by HIV pts with CD4 count <50 cells/mm³

A

Cytomegalovirus retinitis - affects around 30-40% pts with CD4 < 50 cells/mm³

Mycobacterium avium - intracellulare infection

67
Q

What is pneumocystis jiroveci also known as?

A

Pneumocystis carinii pneuomonia (PCP)

68
Q

What is pneumocystis jiroveci?

A

It is an unicellular eukaryote, generally classified as a fungus but some authorities consider it a protozoa

69
Q

What is the most common opportunistic infection in AIDS?

A

Pneumocystis jiroveci pneumonia (PCP)

70
Q

What should all pts with a CD4 count <200/mm³ receive?

A

PCP prophylaxis

71
Q

What are 4 features of penumocystis jiroveci pneumonia?

A

SOB
dry cough
fever
v. few chest signs

72
Q

Pneumothorax is a common complication of what?

A

PCP

73
Q

What is a common complication of PCP?

A

Pneumothorax

74
Q

How common are extrapulmonary manifestations of PCP?

A

They are rare 1-2% of cases

75
Q

What are 3 extrapulmonary manifestations of PCP?

A

hepatosplenomegaly
lymphadenopathy
choroid lesions

76
Q

What are 3 investigations for PCP?

A
  1. CXR - typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray findings eg. lobar consolidation. May be normal
  2. exercise-induced desaturation
  3. sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate PCP (silver stain shows characteristic cysts)
77
Q

What are 4 management options for PCP?

A
  1. Co-trimoxazole
  2. IV pentamide in severe cases
  3. aerosolized pentamide is an alternative treatment for PCP but is less effected with a risk of pneumothorax
  4. steroids if hypoxic (if pO2 < 9.3kPa then steroids reduce risk of resp failure by 50% and death by a third)
78
Q

In what percentage is HIV seroconversion symptomatic?

A

60-80%

79
Q

When does HIV seroconversion occur?

A

3-12wks after infection

80
Q

How does HIV seroconversion typically present?

A

as glandular fever type illness

81
Q

What are 9 features of HIV seroconversion?

A
sore throat
lymphadenopathy
malaise
myalgia
arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis
82
Q

How is HIV diagnosed? What are the 2 tests to confirm diagnosis?

A

HIV antibodies may not be present

HIV PCR and p24 antigen tests can confirm diagnosis

83
Q

What 7 steps are involved in the HIV replication cycle?

A
  1. fusion of HIV to the host cell surface
  2. HIV RNA, reverse transcriptase, integrase, and other viral proteins enter the host cell
  3. Viral DNA is formed by reverse transcription
  4. Viral DNA is transported across the nucleus and integrates into the host DNA
  5. New viral RNA is used as genomic RNA and to make viral proteins.
  6. New viral RNA and proteins move to the cell surface and new, immature, HIV forms
  7. The virus matures by protease releasing individual HIV proteins
84
Q

What is the standard for diagnosis and screening of HIV?

A

Combination tests (HIV p24 antigen and HIV antibody)

The combined test should be repeated if the first test was positive to confirm the diagnosis.

Some centres may also test the viral load (HIV RNA levels) if HIV is suspected at the same time

85
Q

When are HIV antibodies present?

A

They may not be present in early infection, but most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months

86
Q

What does HIV antibodies testing consist of?

A

It usually consists of both a screening ELISA (Enzyme Linked Immuno-Sorbent Assay) test and a confirmatory Western Blot Assay

87
Q

What is p24 antigen? When is it positive?

A

It is a viral core protein that appears early in the blood as the viral RNA levels rise. It is usually positive from about 1wk to 3-4wks after infection with HIV

88
Q

When should asymptomatic HIV pts be tested?

A

at least 4wks after possible exposure

89
Q

What should you do with an initial negative HIV test?

A

after an initial negative result when testing for HIV in an asymptomatic patient, offer a repeat test at 12 weeks