Brain - inflammatory Flashcards

1
Q

In MUO, focal signs are associated with an increased survival compared to dogs with multifocal signs: true or false?​

A

False​

(a study from 1998 found this association, but 3 more recent studies didn’t found this result)​

Cornelis, 2019​

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2
Q

Give molecules with following action:​
- Regulation of gene expression​
- DNA Alkylation (antiproliferatives)​
- Antimetabolites: purine & pyrimidine​
- Kinase and Phosphorylase Inhibitors​
- Inhibition of microtubule formation​

A

Regulation of Gene Expression​
Enter nucleus to interfere directly with transcription of gene products.​
Glucocorticoids, vitamin D analogues​

DNA Alkylation (antiproliferatives)​
Interfere directly with the structure of DNA in order to block subsequent replication, which is required for cell proliferation.​
Cyclophosphamide, lomustine, procarbazine, chlorambucile​

Antimetabolites​
Interfere with pathways responsible for the synthesis of the purine (adenine, guanine) or pyrimidine (thymine, cytosine) molecules necessary for DNA synthesis and cell proliferation, or with enzymes involved in other processes critical to cell survival or proliferation.​

Inhibits purine synthesis: 6-mercaptopurine, azathioprine, mycophenolate mofetil​

Inhibits pyrimidine synthesis: Cytosine arabinoside, leflunomide​

Kinase and Phosphorylase Inhibitors​
The most common enzyme inhibited is calcineurin, which belongs to the serine/threonine phosphatase superfamily and acts to dephosphorylate nuclear factor of activated T cells (NFAT). This interferes with the translocation of NFAT into the nucleus of activated T cells, impairing a number of important functions, such as the production of IL-2 and other proinflammatory cytokines.​
Cyclosporine A​

Inhibition of microtubule formation in mitotic spindle​
Arrest of dividing cells at the metaphase stage​
Vincristine​

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3
Q

Which autoantibodies can be found in Pugs with MUO?​

A

GFAP in CSF​

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4
Q

Which factors are associated with the short-term prognosis in MUO?​
1. Decreased mentation at presentation​
2. Presence of seizures​
3. Increased percentage of neutrophils on CSF analysis​
4. Bodyweight​
5. Duration of clinical signs and treatment prior to diagnosis

A

1,2,3

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5
Q

Which one is a risk factor for the development of postencephalitic epilepsy in dogs with MUO?​

  1. MRI abnormalities in the hippocampus​
  2. Lesions in occipital lobes​
  3. Hydrocephaly​
  4. Young age
A

1

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6
Q

What are the 2 risk factors for post encephalitis epilepsy development?​

A

23% develop PEE​

Acute symptomatic seizures = seizures at the early stage of the disease​
MRI lesions in the hippocampus​

They were younger when compared with those without PEE and had shorter MST.​

Among PEE, 21% develop drug-resistant epilepsy​

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7
Q

What are the risk factors for dying with MUO?​

A

During first week:​

Decreased mentation​
Seizures​
Increased neutrophils in CSF​

After: obtundation​

Note: large breed dogs present more commonly decreased mentation than small and medium breed dogs, but no overall difference in MST​

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8
Q

Gene associated with risk for NME

A

dog leucocyte antigen MHC class II (chromosome 12)
polymorphism in chromosome 15 Pug, 4 Maltese

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9
Q

how many Pug carry at-risk gene for NME

A

2/3 of pug carry at least 1 DLA at-risk haplotype, 6-18% carry the high risk homozygous DLA haplotype

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10
Q

most common sign of early NME/clinical NME

A

early NME: multifocal spinal hyperesthesia, paw placement deficit, reduced menace response (90%), mild lethargy (75%), proprioceptive ataxia (65%)

clinical NME: seizure, circling, visual deficits, behavior change , lethargy

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11
Q

MRI change in early/clinical NME

A

MRI change in 90% of ealry form: meningeal enhancement, focal contrast-enhancing lesion within parenchyma, T2 hyperintense lesion (early necrosis)
abnormal CSF in 50%

clinical: loss W/G matter distinction, parenchymal inflam/necrotic lesion, leptomeningeal enhancement. Maj in parietal/occipital lobe
abnormal CSF 90-80% (lymphocytic pleocytosis)

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12
Q
A
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