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Repro > HIV Pathology & Presentation > Flashcards

HIV Pathology & Presentation Flashcards

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
Q

What are CXR findings in PCP?

A

May be normal early on, signs will e interstitial infiltrates, reticulonodular markings

26
Q

How is PCP diagnosed?

A

BAL (broncho alveolar lavage) and immunofluorescence +/- PCR

27
Q

What is the treatment for PCP and what is the prophylaxis for people with CD4+ count <200?

A

high dose co-trimoxazole (+/- steroid)

prophylaxis is low dose co-trimoxazole

28
Q

List 7 TB related illnesses people with HIV are more likely to have compared with HIV-ve individuals.

A 
symptomatic primary infection, 
reactivation of latent TB, 
lymphadenopathies, 
miliary TB, 
extrapulmonary TB, 
multi-drug resistant TB, 
immune reconstitution syndrome
29
Q

What is the organism that causes cerebral toxoplasmosis?

A

Toxoplasma gondii

30
Q

What is the CD4 threshold for cerebral toxoplasmosis?

31
Q

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?

A

Causes multiple cerebral abscesses & sometimes chorioretinitis.
Presents as headache, fever, focal neurology, seizures, reduced consciousness, raised ICP

32
Q

How do the cerebral abscesses of cerebral toxoplasmosis present on CT?

A

multiple ring enhanced lesions +/- oedema surrounding them

33
Q

Patients with a CD4 count <200 on low dose trimoxazole for PCP are also partially protected against what with this?

A

Cerebral toxoplasmosis

34
Q

At what CD4 count does cytomegalovirus tend to occur in HIV+ patients?

35
Q

Most people (90%) have been infected with cytomegalovirus before. However latent infection can be reactivated in HIV+ patients. What can this cause?

A

ROC - retinitis, oesophagitis, colitis

36
Q

A patient with HIV+ presents with reduced visual acuity, floaters, abdo pain, diarrhoea and PR bleeding. What could be the cause?

A

Cytomegalovirus reactivation

37
Q

All patients with CD4<50 get ophthalmic screening. True/false?

38
Q

What is the name for the HIV “dementia” caused by HIV-1 attacking microglial cells?

A

HIV-associated neurocognitive impairment

39
Q

At what cell count does HIV-associated neurocognitive impairment tend to occur and how can it present?

A

All CD4 levels but tends to be when CD4 is lower. Presents as reduced short term memory +/- motor dysfunction

40
Q

What organism causes Progressive Multifocal Leukoencephalopathy (PML)?

A

reactivation of JC virus

41
Q

At what CD4 threshold does PML tend to occur?

42
Q

What are the signs & symptoms of PML?

A

rapidly progressing symptoms, focal neurology, confusion, personality change

43
Q

How does PML appear on MRI scan?

A

Similar to MS - white matter changes -> demyelination

44
Q

Herpes zoster, herpes simplex and human papilloma virus are common skin infections in HIV+ patients. How might these present in HIV+?

A

Herpes zoster: multidermatomal, recurrent. Herpes simplex: extensive (ulveration), hypertrophic, aciclovir resistant. HPV: extensive, recalcitrant, dysplastic

45
Q

What is “Slim’s Disease” and what are 4 potential aetiologies?

A

HIV-related cachexia. Aetiologies include metabolic (chronic immune activation), anorexia (multifactorial), malabsorption/diarrhoea, hypogonadism

46
Q

Kaposi’s sarcoma incidence increases with increased immunosuppression. What organism causes Kaposi’s sarcoma?

A

Human herpes virus 8

47
Q

What type of tumour is Kaposi’s sarcoma?

A

Vascular tumour

48
Q

How can Kaposi’s sarcoma present?

A

cutaneous lesions (plaque/papule), mucosal lesion (mouth, genital mucosa, conjunctiva), visceral (pulmonary, GI)

49
Q

What is the treatment for Kaposi’s sarcoma?

A

Anti-retrovirals (usually enough for cutaneous and mucosal lesions), local therapies e.g. liquid nitrogen, systemic chemotherapy

50
Q

List 3 AIDS-related cancers.

A

Kaposi’s sarcoma, Non-Hodgkins Lymphoma, Cervical cancer

51
Q

Non-Hodgkins lymphoma incidence increases with increased immunosuppression. What is the causative organism and what other 2 lymphomas can this also cause?

A

EBV - can also cause Burkitt’s lymphoma and primary CNS lymphoma

52
Q

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+?

A

B symptoms (fever, sweats, weight loss), bone marrow involvement, extranodal disease, increased CNS involvement (can look like abscess)

53
Q

What is treatment for non-hodgkin’s lymphoma?

A

Variable - chemo, radio, maybe surgical. For HIV+ add retrovirals

54
Q

What is treatment for non-hodgkin’s lymphoma?

A

Variable - chemo, radio, maybe surgical. For HIV+ add retrovirals

55
Q

What is the causative organism of cervical cancer and how does it differ in HIV+ patients?

A

HPV - persistence of infection and rapid progression to dysplasias and invasive disease in HIV+

56
Q

List 8 common symptoms/signs of non-AIDS symptomatic HIV stage.

A

mucosal candidiasis, seborrheic dermatitis, diarrhoea, fatigue, worsening psoriasis, lymphadenopathy, parotitis, epidemiologically linked conditions e.g. STIs, Hep B and Hep C

57
Q

List 8 non-AIDS neurological presentations of HIV.

A

distal sensory polyneuropathy, mononeuritis multiplex, vacuolar myelopathy, aseptic meningitis, guillan-barre syndrome, viral meningitis (CMV, HSV), cryptococcal meningitis, neurosyphillis

58
Q

What can cause haematological manifestations in the non-AIDS symptomatic stage of HIV?

A

HIV, opportunistic infections, AIDS malignancies e.g. lymphomas

59
Q

What are two haematologic manifestations of non-AIDS symptomatic HIV and what causes them?

A
  1. leuko/lymphopenias due to decreased CD4

2. thrombocytopenia due to HIV infecting megakaryocytes

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