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Neuro II (b) Flashcards

1
Q

Autoimmune demyelinating disorder

A

Multiple Sclerosis

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2
Q

Epi of Multiple Sclerosis

A

Most common demyelinating disorder
F>M

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3
Q

Patho of Multiple Sclerosis:
* ————– -> Increased risk for MS
* Polymorphisms in the genes encoding receptors for ———-
* Increased Th17 and Th1 CD4+ cells
* Contribution from CD8+ T cells and B cells

A
  • HLA-DR2 Variants–> Increased risk for MS
  • Polymorphisms in the genes encoding receptors for IL-1 & IL-7
  • Increased Th17 and Th1 CD4+ cells
  • Contribution from CD8+ T cells and B cells
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4
Q

Macroscopic Features:
Characteristic lesions (“plaques”): Multiple, well circumscribed, slightly depressed, glassy-appearing, gray-tan, irregular shaped

features of?

A

Multiple Sclerosis

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5
Q

Multiple sclerosis

Macroscopic Features:
Characteristic lesions (“———-”): Multiple, well circumscribed, slightly depressed, ———– -appearing, gray-tan, irregular shaped

A

Macroscopic Features:
Characteristic lesions (“plaques”): Multiple, well circumscribed, slightly depressed, glassy-appearing, gray-tan, irregular shaped

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6
Q

location of “Plaques” in Multiple sclerosis

A
  • Paraventricular regions (most common)
  • Optic nerves and chiasm
  • Brain stem
  • Cerebellum
  • Spinal cord
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7
Q

Microscopically in Multiple Sclerosis Active plaques are identified, which type of Active plaque is this?
———–: Sharp margins, macrophage infiltrates

A

Type I

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8
Q

Microscopically in Multiple Sclerosis Active plaques are identified, which type of Active plaque is this?
———-: Sharp margins, macrophages + complement deposition

A

Type II

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9
Q

Microscopically in Multiple Sclerosis Active plaques are identified, which type of Active plaque is this?
———-: Less well-defined borders, oligodendrocyte apoptosis

A

Type III

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10
Q

Microscopically in Multiple Sclerosis Active plaques are identified, which type of Active plaque is this?
———–: Non-apoptotic oligodendrocyte loss

A

Type IV

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11
Q

CM of Multiple Sclerosis

A

1) Mild changes in Cognitive function (thinking and learning)
2) Gradual, neurologic Deficits (Abnormal reflexes, inability to speak)

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12
Q

Inherited dysmyelinating diseases

A

Leukodystrophies

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13
Q

cause of Leukodystrophies

A

Abnormal myelin synthesis or turnover
(Dysmyelinating disease)

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14
Q

Macroscopic Features:
* Diffuse gray and translucent colour of the white matter
* Decrease in the volume of the white matter –> Brain atrophy, Ventricular enlargement, Secondary changes in the gray matter

Microscopic Findings:
* Myelin loss
* Lipid stuffed macrophages

features of?

A

Leukodystrophies

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15
Q

Clinical presentation of Leukodystrophies

A
  • Affected children –> Normal at birth, but developmental abnormalities manifested during infancy and childhood
  • Deterioration in motor skills
  • Spasticity
  • Hypotonia
  • Ataxia
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16
Q

Examples of Leukodystrophies

A

1) Alexander disease
2) Canavan disease
3) Krabbe disease
etc

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17
Q

CM of Acute Disseminated Encephalo-Myelitis

A
  • Development of symptoms, 1-2 weeks after an antecedent infection

Non-localising Symptoms:
* Headache
* Lethargy
* Coma

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18
Q

Macroscopic features:
* Swollen and softened Pons and Medulla

Microscopic features:
* perivascular cellular infiltrate, composed of Macropahges and mononuclear cells
* Myelin loss associated w/ a perivascular macrophage infiltrate (Heidenhain stain)

features of?

A

Acute Disseminated Encephalo-Myelitis

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19
Q

Epi of Acute Haemorrhagic Leukoencephalitis

A
  • More devastating related disorder
  • Affects children and young adults

More devastating compared to acute disseminated encephalomyelitis

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20
Q

Macroscopic features:
* Multiple scatterd petechial haemorrhages

Microscopic features:
* Multiple foci of inflammatory demyelination,
with diffuse oedema in the adjacent white matter
* Perivascular neutrophil infiltrates in cerebral white matter

features of?

A

Acute Haemorrhagic Leukoencephalitis

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21
Q

——– :Inflammatory demyelinating disease; Ab-mediated autoimmune disorder

A

Neuro-myelitis Optica (NMO)

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22
Q

Loc of Neuro-Myelitis Optica

A

optic nerves and spinal cord

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23
Q

Microscopic features:
* Spinal Cord lesion with extensive destruction of the parenchyma
* Perivascular infiltrates of eosinophils and neutrophils

features of?

A

Neuro-Myelitis Optica (NMO)

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24
Q

Cause of Central Pontine Myelinolysis

A
  • Alcoholism
  • Severe electrolyte or osmolar imbalance
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25
CM of Central Pontine Myelinolysis
Rapidly evolving **quadriplegia** (paralysis of the 4 limbs)
26
Central Pontine Myelinolysis is characterised by the development of **----------**, induced by changes in osmotic pressure --> loss of **-------** in the **-------** of the **--------**
Central Pontine Myelinolysis is characterised by the development of **Oedema**, induced by changes in osmotic pressure --> loss of **Mylein** in the **center** of the **pons**
27
cause of Thiamine Deficiency (vitamine B1)
* Chronic alcoholism * Gastric disorders (Carcinoma, Chronic Gastritis)
28
Thiamine Deficiency --> **---------**
**Wernicke Encephalopathy**
29
CM of Wernicke Encephalopathy
* Abrupt onset of confusion * Abnormalities in eye movement * Ataxia
30
CM of Thiamine Deficiency
1) Systemic effects (beri-beri) 2) Abrupt onset of confusion, Abnormalities in eye movement, Ataxia - **Wernicke Encepahlopathy** 3) Irreversible memory disturbance (Korsakoff syndrome)
31
Macroscopic Features: * Foci of **haemorrhage and necrosis**, in the **mamillary bodies and para-ventricular (3rd & 4th ventricles)** Microscopic Findings: * **Early lesions: Dilated capillaries** with prominent endothelial cells **Haemorrhages** * **Late lesions:** Cystic spaces with **haemosiderin-laden macrophages** * Lesions in the medial dorsal nucleus of thalamus --> Association with Korsakoff syndrome features of?
Wernick Encephalopathy Thaimine Deficiency
32
Microscopic features of Acute/Chronic Wernike's Encephalopathy
33
cause of Hepatic Encephalopathy
Elevated levels of urea together with inflammation and hyponatriaemia
34
patho of Hepatic Encephalopathy: **----------** metabolism within **----------** through glutamine synthetase
**Ammonia** metabolism within **astrocytes** through glutamine synthetase
35
Microscopic Findings: * **Astrocytes (Alzheimer type II cells)** with swollen, pale nuclei in the cortex and basal ganglia featurse of?
Hepatic Encephalopathy
36
Toxic Disorder caused by Lead?
Diffuse Encephalopathy
37
Toxicity from Aresnic causes?
Encephalopathy and peripheral Neuropathy (SensoryMotor Axonopathy)
38
Mercury Toxicity --> **------**
Tremors, emotional changes, insomnia, muscle atrophy, disturbances in sensations, changes in nerve responses, cognitive dysfunction
39
Organophosphates (in pesticides) Toxicity ---> **--------**
Memory, cognitive, mental, emotional, motor and sensory deficits
40
Methanol Toxicity --> **-------**
Blindness
41
# ** Carbon Monoxide Toxicity --> **-------**
Hypoxic injury to the Globus pallidus
42
Ethanol Toxicity --> **------**
Chronic alcoholism --> **Atrophy in the anterior cerebellar vermis** --> Truncal ataxia, unsteady gait and nystagmu
43
Ionising radiation toxicity --> **------**
Headaches, nausea, vomiting and papilloedema
44
Microscopic features: * Large areas of coagulative necrosis, * oedema and * thick-walled vessels with **intramural fibrin-like material** * Haemosiderin accumulation * Extensive vascular hyalinisation * Neurofibrillary tangles features of?
Toxicity due Ionising radiation
45
Most common cause of dementia in the elderly population
Alzehimer disease
46
Epi of Alzheimer disease?
3% --> 65-74 years old; 19% -> 75-84 years old; 47% -->84 years old | * **Elderly**
47
Increased risk for AD in Patients with ?
**Down Syndrome**
48
CM of Alzheimer disease
* **Insidious onset of impaired higher intellectual function** * **Altered mood and behaviour** * Disorientation, memory loss, aphasia (later in the disease) * Disabled, mute and immobile patient (after 5-10 years)
49
Pathogenesis of Alzheimer Disease: * Progressive accumulation of **------------** in the brain * **-----** leads to hyper-phosphorylation of **-----** --> Redistribution of tau from axons into dendrites and cell bodies --> Formation of **-----------**
* Progressive accumulation of **beta Amyloid (Αβ)** in the brain * **Αβ** leads to hyper-phosphorylation of **Tau** --> Redistribution of tau from axons into dendrites and cell bodies --> Formation of **tangles**
50
Macroscopic Features: * Variable degree of **cortical atrophy** --> Widening of the cerebral sulci and thinning of the gyri * **Hydrocephalus ex vacuo** * **Neuritic and Diffuse Plaques** (extra-cellular lesion) * **Neurofibrillary tangles** (intra-cellular lesion) features of?
Alzheimer Disease
51
Microscopically in AD there are plaque formation extracellualry, **Diffuse and Neuritic** plaques. which one is this? * Focal, sphaerical, collections of tortuous**(dystrophic plaques) around a central Αβ-amyloid core** * loc. **Hippocampus, amygdala and neocortex**
Neuritic Plaque
52
Microscopically in AD there are plaque formation extracellualry, **Diffuse and Neuritic** plaques. which one is this? * **Αβ-deposits lacking the surrounding neuritic reaction** * Localisation: Cerebral cortex, basal ganglia, cerebellar cortex
Diffuse Plaques
53
# Alzeheimer Disease Microscopic Findings: **-------------------**: * **Paired helical filaments** --> Basophilic fibrillary structures in the cytoplasm of the neurons * Abnormally **hyper-phosphorylated tau protein** --> Major component of paired helical filaments * Localisation: **Entorhinal cortex**, hippocampus, amygdala, basal forebrain
**Neuro-Fibrillary Tangles (NFTs)**
54
CM of Fronto-Temporal Lobar Degeneration
1) **Behavioural changes** (cases that frontal lobes more affected) 2) **Language problems** (cases that temporal lobes more affected) 3) **Memory disturbances** (later in the course of the disease)
55
Subtype of Fronto-Temporal Degeneration-tau ?
**Pick disease** (characteristic smooth, globular, pale basophilic inclusions, **[Pick bodies])**
56
Pick disease (FTLD-tau) is characterised by the presence of?
characteristic smooth, globular, pale basophilic inclusions, **[Pick bodies])**
57
Macroscopic features: * **"Knife-like"** thinning of the gyri Microscopic features: * **Pick bodies** features of?
Pick disease
58
**----------**: Movement disorder in the absence of a toxic exposure or other underlying known aetiology (dopamine antagonists or toxins)
Parkinson Disease
59
cause of Parkinson disease
Damage to the dopaminergic neurons
60
Macroscopic Features: * Pallor of the **substantia nigra** and locus coeruleus Microscopic Findings: * Loss of the **pigmented Neurons and gliosis** in the above regions * Presence of Lewy Bodies in the remaining neurons * **Lewy Bodies:** - Intra-cytoplasmic, eosinophilic, **round inclusions** with a dense core and a peripheral pale halo - **Composed of α-Synuclein**, Neurofilaments and Ubiquitin * **Lewy Neurites**: Dystrophic neurites containing **abnormally aggregated α-Synuclein** features of?
Parkinson Disease
61
CF of Parkinson Disease
* Tremor * Rigidity * **Bradykinesia** * Instability
62
Tx for Parkinson Disease
L-DOPA
63
Autosomal dominant movement disorder Caused by CAG trinucleotide expansion ?
Huntington Disease
64
CM of Huntington Disease
* **Choreiform** (dance-like) movement disorder --> Increased and involuntary **jerky movements** of all body parts * Twisting movements of the extremities * **Forgetfulness** * Affective disorders * Severe dementia (possible)
65
Macroscopic Features: * **Small brain** * Prominent atrophy of the **Caudate Nucleus**, and less severe the Putamen * Atrophy of the Globus Pallidus, secondarily * **Dilatation of the lateral and third ventricles** Microscopic Findings: * Severe **loss of neurons from Striatum** * **Fibrillary gliosis** * **Intra-nuclear inclusions (aggregates of ubiquition)** features of?
Huntington Disease
66
cause of Freidreich Ataxia
AR disorder, GAA trinucleotide repeat expansion in the gene encoding Frataxin
67
CM of Friedreich Ataxia
68
cause of Amyotrophic Lateral Sclerosis
Loss of motor neurons in the: * Spinal cord and Brain stem (lower motor neurons) * Motor cortex (upper motor neurons --> Betz cells)
69
Amyotrophic Lateral Sclerosis is caused by mutations in the genes **-----** and **FUS**
**TDP-43**
70
CM of Amyotrophic Lateral Sclerosis based on loss of lower motor neurons
* Denervation of muscles * Muscular atrophy * Weakness * Fasciculations
71
CM of Amyotrophic Lateral Sclerosis based on Loss of Upper motor Neurons
* Paresis * Hyper-reflexia * Spasticity
72
Macroscopic Features: * Thin and gray anterior roots of the spinal cord * Mildly **atrophic pre-central gyrus** (severe cases) Microscopic Findings: * **Lwey body-like inclusions** * **Degeneration of the lateral cortico-spinal tracts** * Reactive gliosis * Loss of anterior root myelinated fibers * **Cytoplasmic inclusions (TDP-43 [+])**, with exception the SOD-1 cases * **Hyaline inclusions** * **Bunina bodies** features of?
Amyotrophic Lateral Sclerosis
73
progression and prognosis of Amyotrophic Lateral Sclerosis : Involvement of the respiratory muscles --> Recurrent bouts of pulmonary infections -> **------**
**Death**

patho II (29 decks)

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