HIV and Opportunistic - THE REST Flashcards

1
Q

Most common cause of CNS space occupying lesion in AIDS pts

A

Toxoplasmosis gondii

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2
Q

Discuss the course of Toxoplasmosis

A

Cause: reactivation of latent cysts in tissues, infected meat/water, animal feces, cat litter boxes, transplacental transmission (if first time infection for mom)

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3
Q

Discuss MRI findings for Toxoplasmosis

A

MRI: brain has multiple ring enhancing lesions

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4
Q

Histology and Lab reports for Toxoplasmosis

A

Histo: necrotizing granulomas with thin capsule, cysts in muscles.

Labs: serology= (+) IgG toxoplasma antibody
Brain biopsy to differentiate from CNS lymphoma.

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5
Q

Symptoms of Toxo

A

Sx: Sz, lethargy, AMS, localized weakness, encephalitis, Chorioretinitis.

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6
Q

How do we treat Toxo

A

Tx: Sulfadiazene and pyrimethamine with a luecovorin rescue. Prophylacitc when IgG positive and CD4+

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7
Q

Discuss the morphological and histological findings of Kaposi Sarcoma

A

KSHV virus causes (Herpes 8)

Gross: - Red-purple patches, macules, papules, plaques or nodules

Morph: - nodular, Sheets of plump, proliferating spindle cells

Dilated irregular endothelial cell-lined vascular spaces with interspersed lymphocytes, plasma cells, and macrophages

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8
Q

Discuss the course of Kaposi Sarcoma

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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9
Q

Labs for Kaposi Sarcoma

A

Lab:Confirm these spindle cells with IHC, positive for LANA (latent associated nuclear antigen)

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10
Q

What genetic findings do we associate with Kaposi

A

1) LANA-1 - Inhibits p53, induces angiogenesis
2) vCyclin - induces entry to cell cycle by blocking cyclin D Kinase inhibitors
3) vFLIP - Inhibits apoptosis

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11
Q

Treatment for Kaposi Sarcoma

A

Tx: excision,radiation,chemo Rx (good prognosis). Begin with ARTs (inhibit HIV to restore CD4 and CD8 counts). Advanced cases = Liposomal adriamycin is the favored agent for advanced KS in combination with modern cART

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12
Q

Discuss the gross view and the histology we see with Bacillary Angiomatosis

A

Gross: non-blanching, Red papules or nodules in skin; similar to Kaposi’s

Histo: PMN inflammation & capillary proliferation
- Bacilli clusters (+) Warthin-Starry stain

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13
Q

Discuss the signs of burkitt lymphoma

A

sx: extranodal masses
- Africa: endemic, jaw
- USA: sporadic, intestinal

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14
Q

Treatment for Burkitt Lymphoma

A

tx: chemo, very responsive

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15
Q

What is Hodgkin Lymphoma and what does it look like

A

neoplasms of large B cells: Reed-Sternberg cells (CD15 and CD30)

secretes cytokines

histo: multi-lobed “owl eyed” nuclei, inflamm and fibrosis

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16
Q

Symptoms of Hodgkin Lymphoma

A

sx: fever, chills, weight loss, night sweats

localized to a single axial group of nodes (cervical, mediastinal, para-aortic)

17
Q

What is the worst type of Hodgkin Lymphoma that we see in HIV patients and how does it present

A

Lymphocyte depletion
worst prognosis; most aggressive

presents with advanced disease

Reticular variant:paucity of background reactive cells
most EBV+

18
Q

General review of Chorioretinitis and what can cause it

A

inflammation of the choroid (thin pigmented vascular coat of the eye) and retina (“posterior uveitis”)

sx: floating black spots, blurred vision, pain or redness in the eye, sensitivity to light, or excessive tearing

cause in Adults (*immunocompromised):

  • viruses: HSV, VZV, CMV
  • fungi: Candida, Aspergillus, Histoplasmosis, Fusarium
  • protozoa: Toxoplasmosis (picture above)
  • helminths: Toxocara canis
  • bacteria: Mycobacteria tuberculosis
19
Q

What causes HIV thrombocytopenia

A

Impaired platelet production + increased destruction = thrombocytopenia, secondary to megakaryocytes (make platelets) having CD4 and CXCR4 receptors for HIV to find.

HIV also hyperproliferates B cells and dysregulates them leading to production of autoantibodies, many of which target platelets (glycoprotein IIb and II complexes on platelets) and Megakaryocytes (which are ALSO more prone to self-apoptosing = further destruction)