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Neurologia > Neuroimunologia > Flashcards

Neuroimunologia Flashcards

1
Q

Amiloidose gera dano axonal ou desmielinizante

A

Axonal

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2
Q

Quando STC deve pensar em amiloidose

A

Bilateral, progressiva, resistente a tratamento, com sintomas em outros órgãos

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3
Q

Manifestações oculares da amiloidose

A

Floaters, flashes, glaucoma, catarata, olho seco

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4
Q

Manifestações de SNC de amiloidose

A

Sangramentos, AIT, aura, epilepsia

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5
Q

Como detectar amiloidose

A

Biópsia de músculo e nervo, PET scan do coração

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6
Q

Amiloidose é acometimento sensitivo, motor ou misto?

A

Misto

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7
Q

Clínica neuropatia amiloidose

A

Comprimento dependente, simétrica, progressiva, disautonomia

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8
Q

É comum restrição a difusão e captação de contraste em encefalite autoimune?

A

Não, melhor pensar em infecção e neoplasia

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9
Q

Hérpes vírus pode ser trigger para encefalite autoimune?

A

Sim

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10
Q

Devemos testar anti-mog em casos típicos de EM?

A

Não, muitos podem vir positivos em baixos títulos

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11
Q

Precisa retestar paciente que veio anti-mog negativo na fase aguda sem tratamento?

A

Não

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12
Q

Quantos meses depois do tratamento poderia tentar testar anti-mog?

A

3 meses

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13
Q

Precisa tratar MOGAD monofásico?

A

Não

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14
Q

Principal fator de risco para recorrência de MOGAD?

A

Ter recorrido uma vez

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15
Q

Tratamento MOGAD

A

Pulso, IGG, plasmaférese, desmame lento de corticoide em um ano

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16
Q

Manifestações Sjrögen no SNC

A

Vasculite, AVC, AIT

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17
Q

Achados laboratoriais de Neuro Sjrögen

A

Eosinofilia e diminuição do nível de IGG

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18
Q

O que pensar quando temos vários anticorpos positivos em baixos títulos?

A

Reação cruzada

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19
Q

Exame padrão ouro já vasculite

A

Angiografia

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20
Q

Exames de imagem na vasculite

A

Vessel wall e angiografia

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21
Q

Limitação exames de imagem na vasculite

A

Não vê bem pequenos vasos

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22
Q

Anticorpo na Sd de Miller Fisher

A

Anti gq1b

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23
Q

Alvo inebilizumab

A

Anti CD 19

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24
Q

Significado CAR-T cell

A

Chimeric Antigen Receptor T-cell

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25
Q

Tempo de aparecimento médio de complicação autoimune de inibidor de check point

A

5-15 semanas

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26
Q

Cânceres mais associados a síndromes paraneoplásicas

A

Mama, linfoma, ginecológico, medular tireoideano, pulmão

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27
Q

Sintomas de cerebelite

A

Cefaleia, febre, confusão, náusea e ataxia cerebelar

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28
Q

DD cerebelite

A

Infarto de cerebelo, câncer cerebelar, meningoencefalite infecciosa, ADEM, PRES

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29
Q

Se inchaço de cerebelo na imagem, o que fazer e por que?

A

Corticoide para evitar inchaço e hérniação

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30
Q

Imagem de cerebelite

A

Acometimento bilateral e difuso de cerebelo

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31
Q

Mielite na NMO - características

A

3 ou mais segmentos contíguos intramedulares com lesão ou atrofia

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32
Q

Onde é a lesão da síndrome de área postrema

A

Dorso da medula

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33
Q

Lesões de tronco da NMO - características

A

Periependimarias

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34
Q

Lesão do nervo óptico da NMO - características

A

Mais de 1/2 nervo óptico ou envolvendo quiasma

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35
Q

Definição síndrome da área postrema

A

Nausea, vômitos e soluços

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36
Q

Red flag do tempo de progressão do surto de NMO

A

Menos de 4 horas ou mais de 4 semanas para o ápice

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37
Q

Presença de BOC é red flag para NMO?

A

Sim

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38
Q

Porcentagem de casos monofásicos de NMO

A

5-10%

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39
Q

O que aumenta o risco de recorrência na NMO?

A

Soropositividade

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40
Q

Diagnóstico NMO com anticorpo

A

1 core clinical + excluir outras causas

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41
Q

Diagnóstico de NMO sem anticorpo

A

2 core clinical, sendo um neurite ou LETM ou síndrome de área postrema

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42
Q

Core clinical da NMO

A

Neurite óptica, LETM, síndrome de área postrema, síndrome diencefálica ou narcolepsia, síndrome de tronco aguda, síndrome cerebral com lesões típicas

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43
Q

Relação câncer urotelial e síndromes paraneoplasicas

A

Pouca relação, mas possível em carcinoma urotelial

44
Q

Qual doença desmielinizante pode ter lesões que desaparecem?

45
Q

O que significa PLAID?

A

PLCG2 associated antibody deficiency and immune dysregulation

46
Q

Característica PLAID

A

Reação alérgica a temperaturas frias

47
Q

Tolebrutinib class

A

Oral BTK inhibitor

48
Q

Autoimmune diseases associated with vasculitis

A

Lupus and rheumatoid arthritis

49
Q

Infectious diseases associated with vasculitis

A

Hepatites B and C

50
Q

Cancers that can trigger vasculitis

A

Lymphoma and leukemia

51
Q

Sneddon Syndrome

A

Slowly progressive neurocutaneous syndrome with livedo racemosa and recurrent cerebrovascular events

52
Q

Divry Van Bogaert Syndrome

A

Familial juvenile-onset disorder with livedo racemosa, white matter disease, dementia, epilepsy and cerebral angiomatosis in angiography (leptomeningial and transdural anastomoses)

53
Q

Clinical findings in vasculitis

A

Headache that does not go away
Confusion and forgetfulness (dementia)
Sensibility complaints
Weakness (usually arms and legs)
Pain
Vision problems
Seizures
Problems speaking or understanding
Fever, sick feeling, weight loss, rashes or skin discoloration
Multiple organ damage

54
Q

Findings in image of vasculitis in Brain

A

Aneurysms
Thrombosis
Swelling of the brain

55
Q

Vasculitis investigation

A

RCP, segmentation rate, auto-antibodies, CSF, biopsy, image, angiogram, USG

56
Q

Vasculitis treatment

A

Steroids, azathioprine, cyclophosphamide, rituximab, aneurysms treatment

57
Q

Giant cell arteitis affects what arteries?

A

Aorta and its primary branches (temporal artery and ophthalmic artery)

58
Q

Giant cell arteitis epidemiology?

A

Age 50 and older

59
Q

Giant cell arteitis symptoms?

A

New, severe headache. Blurred, double vision or sudden vision loss. Pain in jaw or tongue. Tendernes in temporal arteries. Fever, weight loss, neck, muscle and joint pain. Fatigue.

60
Q

Primary angiitis of CNS symptons

A

slowly progression of headache, dementia, behavioral changes, pain, sensory abnormalities and tremor. Seisures. Multiple AVC, AIT

61
Q

Primary angiitis of CNS epidemiology

A

any age, peak at 50, mostly males

62
Q

Takayasu’s arteritis arteries affected

63
Q

Takayasu’s arteritis epidemiology

A

women age of 40

64
Q

Takayasu’s arteritis symptoms

A

headache, dizziness, cold and numbness in the limbs, visual disturbances, problems with memory . Strokes, heart attacts, intestine damage

65
Q

Takayasu’s arteritis image

A

narrowing, blockage or swelling

66
Q

Polyarteritis nodosa epidemiology

A

40-60 year, more man

67
Q

Polyarteritis nodosa symptoms

A

fever, abdominal pain, numbness or pain in legs and limbs, muscle aches, weakness, weight loss. Kidney failure, HPT. PNS neuropathy is more comom than CNS

68
Q

Deficiency of adenosine deaminase 2 (DADA2) is a mutation in what gene?

A

CECR1 gene

69
Q

Deficiency of adenosine deaminase 2 (DADA2) causes what disease?

A

Vasculitis

70
Q

Deficiency of adenosine deaminase 2 (DADA2) symptons

A

fever, skin nodules, livedo reticularis, joint pain. Strokes in chielhood

72
Q

Meaning ICANS?

A

Immune Effector Cell-Associated Neurotoxicity Syndrome

73
Q

% patients with ICANS

A

20-60% patients

74
Q

ICANs pathology

A

release of inflammatory cytokines secreted by macrophages and monocytes, increasing vascular permeability and endothelial activation and leading to blood–brain barrier breakdown

75
Q

Risk factor for ICANS

A

high disease burden, older age, and the specific CAR-T product

76
Q

When does ICAN appear?

A

5 days, but some in 3 weeks

77
Q

Symptoms of ICANS

A

Tremor, confusion, agitation, seizures, cerebral oedema, hesitancy of speach, aphasia, status epilepticus, hemorrhagic

78
Q

Score for ICANS

A

Immune Effector Cell Encephalopathy Score (ICE)

79
Q

ICANS treatment

A

10-20mg dexamethasone 6/6hrs ou metilprednisolone 1g for at least 4 days

80
Q

What to do in severe responses of CAR-T cell?

A

Anakira (IL 1 receptor antagonist) or chemotherapy to kill car t cell

81
Q

Treatment intracranial hipertension in ICANS

A

Acetazolamide 1000mg IV + 250-1000 every 12 hours, elevate head bed, hyperventilation, hyperosmolar therapy with manitol

82
Q

Anti-γ-aminobutyric acid B (GABAB)-receptor encephalitis presentation

A

Seizures, cognitive impairment, confusion, and personality changes

83
Q

Anti-γ-aminobutyric acid B (GABAB)-receptor encephalitis is usually associated with what disease?

A

Small-cell lung cancer

84
Q

Anti-IgLON5 autoimmune encephalitis presentation

A

Sleep disorder (parasomnia, insomnia, excessive daytime sleepiness, and sleep-disordered breathing), bulbar symptoms, gait abnormalities, recurrent visual and acoustic hallucinations

85
Q

Gene ALSP

A

CSF1R (colony-stimulating factor-1 receptor)

86
Q

Meaning ALSP

A

Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia

87
Q

Percentage of ALSP in leukodystrophys

88
Q

ALSP inheritance pattern

A

Autosomal dominant

89
Q

Brain CT in ALSP

A

Multifocal calcifications in white matter

90
Q

ALSP clinical presentation

A

Behavioral changes, executive dysfunction, depression, anxiety, psychosis, progressive cognitive decline, gait disturbances, parkinsonism and epilepsy

91
Q

ALSP typical MR imaging findings

A

Bilateral patchy, diffuse, or confluent T2 hyperintensities in the white matter. Frontal and parietal lobe predominance, Without enhancement. Subcortical U-fibers are generally spared. DWI persistent hyperintensities are punctate with restricted diffusion or normal intensity on ADC maps.

92
Q

ALSP MR imaging in pre symptomatic

A

Asymmetric small-sized nodular hyperintensities

93
Q

Difference between ALSP and MS

A

There is no white matter lesion in callososeptal interface in ALSP and no brain calcification in MS

94
Q

Corpus callosum morphology in ALSP

95
Q

DD of ALSP besides MS

A

Adult-onset leukoencephalopathy due to autosomal recessive mutations in the mitochondrial alanyl-transfer RNA synthetase 2 gene (AARS2-L)

96
Q

Difference in MRI between ALSP and AARS-L

A

Marked restricted diffusion on ADC map in AARS2-L; in ALSP, ADC values are similar to or slightly lower than normal white matter
calcifications in the frontal periventricular white matter in ALSP but not in AARS-L

97
Q

Marchiafava-Bignami disease epidemiology

A

Chronic alcoholics (with middle-aged to elderly male patients 40-60 years of age

98
Q

Marchiafava-Bignami disease clinical presentation

A

Motor or cognitive disturbances, a hemispheric disconnection syndrome (apraxia, hemialexia, dementia) and/or seizures.

99
Q

Marchiafava-Bignami disease pathology

A

Deficiency of the vitamin B group results in necrosis and demyelination of the corpus callosum. Some reports present cases of extension into the hemispheric white matter, internal capsule and middle cerebellar peduncle. Although rare, Morel laminar sclerosis can also be seen

100
Q

Marchiafava-Bignami disease CT changes

A

Hypoattenuating regions in the corpus callosum
in exceptional situations of hemorrhage, these regions may turn iso- or hyperattenuating

101
Q

Marchiafava-Bignami disease MRI

A

Corpus callosum may appear edematous in the acute phase and atrophic in the chronic phase.
T1: hypointense foci in the corpus callosum in the acute phase
T2:
- acute phase: hyperintensities in the corpus callosum
- subacute phase: may show hypointense focal lesions (likely as a result of hemosiderin)
ears of the lynx sign may be seen.

102
Q

Marchiafava-Bignami disease DD

A

MS
Diffuse axonal injury if preceding trauma
Callosal infarction: rare due to its rich blood supply
Transient lesions of the splenium of the corpus callosum

103
Q

Cause of progressive multifocal leukoencephalopathy (PML)

A

Polyomavirus JC (JC virus)

104
Q

Risk factors for PML

A

Chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkin’s disease or lymphoma). Autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus. HIV-1 infection.

105
Q

Treatment of PML

A

Withdraw the medications causing, can use plasmapheresis to accelerate

Neurologia (14 decks)

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