HIV Pathology & Presentation Flashcards

(59 cards)

1
Q

What type of virus is HIV?

A

RNA Retrovirus - means it uses reverse transcriptase to transcribe copies of itself

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2
Q

What type & group of HIV was responsible for global epidemic?

A

HIV-1 Group M

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3
Q

HIV 2 is mostly localised to ____ and is ____ virulent than HIV-1.

A

West Africa, less virulent than HIV-1

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4
Q

At what stages of infection is there rapid replication and how often is there new generation?

A

Very early and very late stage

every 6-12 hours

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5
Q

Through what types of surface does HIV usually transfer?

A

Across mucosal surfaces e.g. vaginal, cervix or rectum

or percutaneous, or can be break in integrity of mucosa

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6
Q

How does infection occur?

A

infection of mucosal CD4+ (Langerhans & dendritic) cells that bring it across mucosa to regional lymph nodes after which it is disseminated e.g. to GALT, brain and spleen

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7
Q

After how long is infection established after entry into the body?

A

Within 3 days of entry

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8
Q

What is the target site for HIV?

A

CD4+ receptors

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9
Q

What is CD4 and on list 4 cells it is found on.

A

Cluster of Differentiation - a glycoprotein found on the surface of cells e.g. T helper lymphocytes, dendritic cells, macrophages, microglial cells
HIV can affect them but mostly t helper

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10
Q

Which type of cell has the specific CD4+ receptor?

A

T helper lymphocytes

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11
Q

What are 4 main roles of CD4+ T Helper lymphocytes in the induction of adaptive immune response?

A

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

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12
Q

List the effects of HIV infection on CD4+ cells, CD8+ cells, antibodies and the immune system overall.

A

reduced numbers and quality of CD4+ cells, increased number but reduced activation of CD8+ cells, reduced affinity of antibodies produced (not quite right) and chronic immune activation - overall some parts of immune system in overdrive and some depleted

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13
Q

What can cause Chronic Immune Activation in HIV?

A

Response to infection or microbial translocation from depleted GALT (bugs getting across gut barrier)

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14
Q

What are HIV +ve patients susceptible to?

A

viral, fungal, parasitic & mycobacterial infection , infection-induced cancers

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15
Q

What is normal parameter for CD4 Th cells?

A

500-1600 cells/mm3

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16
Q

What is parameter for highest risk of opportunistic infections in HIV?

A

<200 cells/mm3

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17
Q

Outline the overview of CD4+ cell levels in untreated HIV infection.

A

Initially in first 6 weeks CD4+ cells steeply decline, gradually increase a small bit in 6-12 weeks then very gradually decline over the next 11 years.

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18
Q

What is the average time to death without HIV treatment?

A

9-11 years

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19
Q

Approx. 80% of patients present with symptoms at their primary infective stage. What is the average time between infection and onset of symptoms?

A

2-4 weeks

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20
Q

List 5 symptoms that patients may experience in primary HIV infective stage?

A
  • fever
  • rash (maculopapular)
  • myalgia
  • pharyngitis
  • headache/aseptic meningitis
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21
Q

During the asymptomatic HIV infective stage there is ongoing viral replication, ongoing CD4 count depletion and ongoing immune activation. However, there is no risk of onward transmission. True/false?

A

False- first part all true but there is risk of onward transmission

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22
Q

An opportunistic infection is caused by a pathogen that does not normally produce in a healthy individual. List some AIDS-defining conditions. (6)

A
Pneumocystic pneumonia,
TB, 
cerebral toxoplasmosis, 
cytomegalovirus, 
HIV-associated neurocognitive impairment, 
PML
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23
Q

What is the organism of PCP and at what CD4 threshold does it tend to occur?

A

pneumocystis jiroveci, <200

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24
Q

What are the signs and symptoms of pneumocystis pneumonia?

A

symptoms: insidious onset, SOB, dry cough
Signs: chest may sound normal, exercise oxygen desaturation

25
What are CXR findings in PCP?
May be normal early on, signs will e interstitial infiltrates, reticulonodular markings
26
How is PCP diagnosed?
BAL (broncho alveolar lavage) and immunofluorescence +/- PCR
27
What is the treatment for PCP and what is the prophylaxis for people with CD4+ count <200?
high dose co-trimoxazole (+/- steroid) | prophylaxis is low dose co-trimoxazole
28
List 7 TB related illnesses people with HIV are more likely to have compared with HIV-ve individuals.
``` symptomatic primary infection, reactivation of latent TB, lymphadenopathies, miliary TB, extrapulmonary TB, multi-drug resistant TB, immune reconstitution syndrome ```
29
What is the organism that causes cerebral toxoplasmosis?
Toxoplasma gondii
30
What is the CD4 threshold for cerebral toxoplasmosis?
<150
31
Cerebral toxoplasmosis is a disease most people (especially with cats) have been exposed to. However in HIV+ patients it can cause reactivation of latent T.gondii in the CNS. What does this cause and how can it present?
Causes multiple cerebral abscesses & sometimes chorioretinitis. Presents as headache, fever, focal neurology, seizures, reduced consciousness, raised ICP
32
How do the cerebral abscesses of cerebral toxoplasmosis present on CT?
multiple ring enhanced lesions +/- oedema surrounding them
33
Patients with a CD4 count <200 on low dose trimoxazole for PCP are also partially protected against what with this?
Cerebral toxoplasmosis
34
At what CD4 count does cytomegalovirus tend to occur in HIV+ patients?
<50
35
Most people (90%) have been infected with cytomegalovirus before. However latent infection can be reactivated in HIV+ patients. What can this cause?
ROC - retinitis, oesophagitis, colitis
36
A patient with HIV+ presents with reduced visual acuity, floaters, abdo pain, diarrhoea and PR bleeding. What could be the cause?
Cytomegalovirus reactivation
37
All patients with CD4<50 get ophthalmic screening. True/false?
True
38
What is the name for the HIV "dementia" caused by HIV-1 attacking microglial cells?
HIV-associated neurocognitive impairment
39
At what cell count does HIV-associated neurocognitive impairment tend to occur and how can it present?
All CD4 levels but tends to be when CD4 is lower. Presents as reduced short term memory +/- motor dysfunction
40
What organism causes Progressive Multifocal Leukoencephalopathy (PML)?
reactivation of JC virus
41
At what CD4 threshold does PML tend to occur?
<100
42
What are the signs & symptoms of PML?
rapidly progressing symptoms, focal neurology, confusion, personality change
43
How does PML appear on MRI scan?
Similar to MS - white matter changes -> demyelination
44
Herpes zoster, herpes simplex and human papilloma virus are common skin infections in HIV+ patients. How might these present in HIV+?
Herpes zoster: multidermatomal, recurrent. Herpes simplex: extensive (ulveration), hypertrophic, aciclovir resistant. HPV: extensive, recalcitrant, dysplastic
45
What is "Slim's Disease" and what are 4 potential aetiologies?
HIV-related cachexia. Aetiologies include metabolic (chronic immune activation), anorexia (multifactorial), malabsorption/diarrhoea, hypogonadism
46
Kaposi's sarcoma incidence increases with increased immunosuppression. What organism causes Kaposi's sarcoma?
Human herpes virus 8
47
What type of tumour is Kaposi's sarcoma?
Vascular tumour
48
How can Kaposi's sarcoma present?
cutaneous lesions (plaque/papule), mucosal lesion (mouth, genital mucosa, conjunctiva), visceral (pulmonary, GI)
49
What is the treatment for Kaposi's sarcoma?
Anti-retrovirals (usually enough for cutaneous and mucosal lesions), local therapies e.g. liquid nitrogen, systemic chemotherapy
50
List 3 AIDS-related cancers.
Kaposi's sarcoma, Non-Hodgkins Lymphoma, Cervical cancer
51
Non-Hodgkins lymphoma incidence increases with increased immunosuppression. What is the causative organism and what other 2 lymphomas can this also cause?
EBV - can also cause Burkitt's lymphoma and primary CNS lymphoma
52
HIV+ patients present with more advanced lymphoma in comparison to HIV- patients with non-hodgkins. How else does non-hodgkin's lymphoma present in HIV+?
B symptoms (fever, sweats, weight loss), bone marrow involvement, extranodal disease, increased CNS involvement (can look like abscess)
53
What is treatment for non-hodgkin's lymphoma?
Variable - chemo, radio, maybe surgical. For HIV+ add retrovirals
54
What is treatment for non-hodgkin's lymphoma?
Variable - chemo, radio, maybe surgical. For HIV+ add retrovirals
55
What is the causative organism of cervical cancer and how does it differ in HIV+ patients?
HPV - persistence of infection and rapid progression to dysplasias and invasive disease in HIV+
56
List 8 common symptoms/signs of non-AIDS symptomatic HIV stage.
mucosal candidiasis, seborrheic dermatitis, diarrhoea, fatigue, worsening psoriasis, lymphadenopathy, parotitis, epidemiologically linked conditions e.g. STIs, Hep B and Hep C
57
List 8 non-AIDS neurological presentations of HIV.
distal sensory polyneuropathy, mononeuritis multiplex, vacuolar myelopathy, aseptic meningitis, guillan-barre syndrome, viral meningitis (CMV, HSV), cryptococcal meningitis, neurosyphillis
58
What can cause haematological manifestations in the non-AIDS symptomatic stage of HIV?
HIV, opportunistic infections, AIDS malignancies e.g. lymphomas
59
What are two haematologic manifestations of non-AIDS symptomatic HIV and what causes them?
1. leuko/lymphopenias due to decreased CD4 | 2. thrombocytopenia due to HIV infecting megakaryocytes