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Multisystem Clinical/Poorly Defined > AIDS Related Malignancies > Flashcards

AIDS Related Malignancies Flashcards

1
Q

What cancers, if present in someone who has HIV lead immediately to the diagnosis of AIDS, regardless of any other findings, good or bad?

A
  • Kaposi sarcoma
  • Lymphoma
  • Squamos Cell carcinoma of the cervix

***Squamos cell carcinoma of the anus is not AIDS defining, bit is AIDS Associated

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2
Q

Signs of Kaposci sarcoma in AIDS patients

A

Lots of skin lesions, could also see lesions under endoscopy and in the lungs under bronchoscopy

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3
Q

What are the subsets of etiologies for Kaposi Sarcoma?

A
  • Sporadic - Aging men of mediterranean descent
  • Endemic - sub Saharan African unrelated to HIV (further broken down into lymphadenopathic and cutaneous)
  • Epidemic - associated with HIV
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4
Q

Who gets Kaposi Sarcoma?

A

Immune deficiency

  • Aged individuals
  • Transplant patients
  • Immunosupressed agents

Caused by Kaposi Herpes virus, and this is present in all KS lesions regardless of risk group

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5
Q

Where do we detect KSHV?

A

Shed in the saliva, which is the primary route of transmission

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6
Q

Discuss where KSHV goes and what it does in the body

A

Likes lymphatic and vascular endothelium, mesenchymal stem cells, B cells, macrophages, and hops around via various receptors.

It does not integrate, rather it stays episomal.

During the latent infection it is not producing new progeny and has limited expression of virus genes.

During the lytic phase, it has many viral genes expressed and makes a lot of progeny

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7
Q

Discuss histology for Kaposi Sarcoma

A

In the dermis we see extravasated RBCs, abnormal vessels dissecting through dermal collagen, and most importantly, spindle shaped KS tumor cells, thought to be lymphatic endothelial cells.

Confirm these spindle cells with IHC, positive for LANA (latent associated nuclear antigen) which is something KSHV makes but not human cells

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8
Q

What genes are active in someone who has Kaposi Sarcoma

A
  • LANA-1 - Inhibits p53, induces angiogenesis
  • vCyclin - induces entry to cell cycle by blocking cyclin D Kinase inhibitors
  • vFLIP - Inhibits apoptosis
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9
Q

Treating HIV is the best way to stop KSHV from progressing. Why?

A

Restoration of virus KSHV-specific CD4+ T cells improves CD8+ T cell antiviral response.

So start up those ARTs!

We also see

  • Improved B Cell function which results in more neutralizing antibody
  • Restoration of NK cell function
  • Suppression of HIV replication decreases level of HIV tat (oncogenic) and inflammatory proteins
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10
Q

How do we treat advanced KS that is lytic = many more genes active and is replicating like crazy (without disrupting the cell of course)?

A

Liposomal adriamycin is the favored agent for advanced KS in combination with modern cART.

  • Better tolerated than paclitaxel (causes peripheral neuropathy)
  • Better response rates and better tolerated than combination bleomycin+vinblastine)
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11
Q

What do we think of when we see/hear the term “Starry Sky”

A

“Stars” are the macrophages, “Sky” is bunched up lymphocytes

Burkitt Lymphoma

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12
Q

Discuss the three lymphomas that are AIDS defining

A
  • Peripheral lymphoma - This is what we think of when we say lymphoma, this is in your lymph nodes (axilla, groin, neck, etc., really ANYWHERE)
  • Primary CNS Lymphoma - In the brain as a big mass of lymphoma. Do not mistake with peripheral lymphoma of the CNS which is just lymphoma floating around your CSF attaching to nerves and stuff
  • Primary Effusion Lymphoma (PEL) - No solid tumor, just this effuse thing
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13
Q

Centroblastic vs immunoblastic diffuse large B Cell peripheral lymphoma histology

A

Diffuse large B cell centroblastic lymphoma is in immune intact HIV patients and is only associated 30% of the time with EBV. This is the favorable histology for prognosis.

Diffuse large B Cell immunoblastic is seen in immature B cells in immune suppressed HIV patients and is due 100% of the time to EBV

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14
Q

How do we treat B Cell lymphoma in HIV patients?

A

EPOCH or CHOP multi agent chemotherapies

Etoposide
Prednisone
Vincristine (Oncovin)
Cyclophosphamide
Doxorubicin

Also, all patients receive CNS prophylaxis with intrathecal (subarachnoid) methotrexate or cytosine arabinoside

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15
Q

Primary CNS lymphoma histology and lab work

A

Most common histology is diffuse large B cell, immunoblastic type, and remember, it’s a big ol mass of cells.

Always EBV +

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16
Q

Who gets primary CNS lymphoma?

A

Severe immune suppression (long standing HIV infection and very low CD4+ T cell counts)

17
Q

How do we treat primary CNS lymphoma?

A
  • Start by optimizing the ARTs the patient is on to enhance or restore EBV immunity
  • Radiation to the brain
  • Multi-agent chemotherapy with high dose methotrexate with a leucovorin rescue along with temozolomide and rituximab

Turns survival from 4 to 15 months.

Basically, a lot of chemotherapies to try and keep this thing at bay as long as possible. ART therapy ahead of time is what prevents this from even happening.

18
Q

What weird findings do we see with Primary Effusion lymphoma?

A

You get LANA-1, like with KSHV but instead of endothelial infection, you get infection of B cells, causing a loss of CD20 markers.

Super rare,

19
Q

How does Primary Effusion lymphoma present?

A
  • Young homosexual men with advanced HIV
  • Usually restricted to pericardium, pleura, and peritoneal cavity without any tumor mass

Less than 6 month survival, tumor is refractory to chemo

20
Q

HPV is linked to what non-AIDS defining cancers?

A
  • Squamos cell of the anus

- Oropharyngeal carcinoma

21
Q

Alcohol is linked to what non-AIDS defining cancers?

A
  • Oropharyngeal carcinoma

- Hepatocellular carcinoma

22
Q

EBV is linked to what non-AIDS defining cancer?

A

Hodgkin Lymphoma

23
Q

Carcinogens/immune suppression are linked to what non-AIDS defining cancers?

A
  • Lung Cancer

- Colorectal cancer

24
Q

Polyoma virus is linked to what non-AIDS defining cancer?

A

Non-melanoma skin cancer

  • Merkel Cell
  • Sebaceous cell
25
Q

Age is linked to what non-AIDS defining cancers?

A
  • Squamos cell of the anus
  • Oropharyngeal carcinoma
  • Hepatocellular carcinoma
26
Q

So in summary, why the hell do we get cancer from AIDS?

A

Loss of CD4+ T cell loss compromises the host’s ability to control oncogenic viral infections

27
Q

When is ART therapy not enough for AIDS-caused malignancies?

A

Once transformed, particularly CINIII and KS, you will need more than ART to prevent/control malignancy

Multisystem Clinical/Poorly Defined (8 decks)

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