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patho II > Neuro II (b) > Flashcards

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
Q

CM of Central Pontine Myelinolysis

A

Rapidly evolving quadriplegia
(paralysis of the 4 limbs)

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26
Q

Central Pontine Myelinolysis is characterised by the development of ———-, induced by changes in osmotic pressure –> loss of ——- in the ——- of the ——–

A

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

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27
Q

cause of Thiamine Deficiency (vitamine B1)

A
  • Chronic alcoholism
  • Gastric disorders (Carcinoma, Chronic Gastritis)
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28
Q

Thiamine Deficiency –> ———

A

Wernicke Encephalopathy

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29
Q

CM of Wernicke Encephalopathy

A
  • Abrupt onset of confusion
  • Abnormalities in eye movement
  • Ataxia
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30
Q

CM of Thiamine Deficiency

A

1) Systemic effects (beri-beri)
2) Abrupt onset of confusion, Abnormalities in eye movement, Ataxia - Wernicke Encepahlopathy
3) Irreversible memory disturbance (Korsakoff syndrome)

31
Q

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?

A

Wernick Encephalopathy Thaimine Deficiency

32
Q

Microscopic features of Acute/Chronic Wernike’s Encephalopathy

A
33
Q

cause of Hepatic Encephalopathy

A

Elevated levels of urea together with inflammation and hyponatriaemia

34
Q

patho of Hepatic Encephalopathy:
———- metabolism within ———- through glutamine synthetase

A

Ammonia metabolism within astrocytes through glutamine synthetase

35
Q

Microscopic Findings:
* Astrocytes (Alzheimer type II cells) with swollen, pale nuclei in the cortex and basal ganglia

featurse of?

A

Hepatic Encephalopathy

36
Q

Toxic Disorder caused by Lead?

A

Diffuse Encephalopathy

37
Q

Toxicity from Aresnic causes?

A

Encephalopathy and peripheral Neuropathy (SensoryMotor Axonopathy)

38
Q

Mercury Toxicity –> ——

A

Tremors, emotional changes, insomnia, muscle
atrophy, disturbances in sensations, changes in nerve responses, cognitive dysfunction

39
Q

Organophosphates (in pesticides) Toxicity —> ——–

A

Memory, cognitive, mental,
emotional, motor and sensory deficits

40
Q

Methanol Toxicity –> ——-

A

Blindness

41
Q

**

Carbon Monoxide Toxicity –> ——-

A

Hypoxic injury to the Globus pallidus

42
Q

Ethanol Toxicity –> ——

A

Chronic alcoholism –> Atrophy in the anterior
cerebellar vermis –> Truncal ataxia, unsteady gait
and nystagmu

43
Q

Ionising radiation toxicity –> ——

A

Headaches, nausea,
vomiting and papilloedema

44
Q

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?

A

Toxicity due Ionising radiation

45
Q

Most common cause of dementia in the elderly population

A

Alzehimer disease

46
Q

Epi of Alzheimer disease?

A

3% –> 65-74 years old; 19% -> 75-84
years old; 47% –>84 years old

* Elderly

47
Q

Increased risk for AD in Patients with ?

A

Down Syndrome

48
Q

CM of Alzheimer disease

A
  • 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
Q

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 ———–

A
  • 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
Q

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?

A

Alzheimer Disease

51
Q

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

A

Neuritic Plaque

52
Q

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

A

Diffuse Plaques

53
Q

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

A

Neuro-Fibrillary Tangles (NFTs)

54
Q

CM of Fronto-Temporal Lobar Degeneration

A

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
Q

Subtype of Fronto-Temporal Degeneration-tau ?

A

Pick disease
(characteristic smooth, globular, pale basophilic inclusions, [Pick bodies])

56
Q

Pick disease (FTLD-tau) is characterised by the presence of?

A

characteristic smooth, globular, pale basophilic inclusions, [Pick bodies])

57
Q

Macroscopic features:
* “Knife-like” thinning of the gyri

Microscopic features:
* Pick bodies

features of?

A

Pick disease

58
Q

———-: Movement disorder in the absence of a toxic exposure or other underlying known aetiology (dopamine antagonists or toxins)

A

Parkinson Disease

59
Q

cause of Parkinson disease

A

Damage to the dopaminergic neurons

60
Q

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?

A

Parkinson Disease

61
Q

CF of Parkinson Disease

A
  • Tremor
  • Rigidity
  • Bradykinesia
  • Instability
62
Q

Tx for Parkinson Disease

A

L-DOPA

63
Q

Autosomal dominant movement disorder
Caused by CAG trinucleotide expansion ?

A

Huntington Disease

64
Q

CM of Huntington Disease

A
  • 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
Q

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?

A

Huntington Disease

66
Q

cause of Freidreich Ataxia

A

AR disorder, GAA trinucleotide repeat expansion in the gene encoding Frataxin

67
Q

CM of Friedreich Ataxia

A
68
Q

cause of Amyotrophic Lateral Sclerosis

A

Loss of motor neurons in the:
* Spinal cord and Brain stem (lower motor neurons)
* Motor cortex (upper motor neurons –> Betz cells)

69
Q

Amyotrophic Lateral Sclerosis is caused by mutations in the genes —– and FUS

A

TDP-43

70
Q

CM of Amyotrophic Lateral Sclerosis based on loss of lower motor neurons

A
  • Denervation of muscles
  • Muscular atrophy
  • Weakness
  • Fasciculations
71
Q

CM of Amyotrophic Lateral Sclerosis based on Loss of Upper motor Neurons

A
  • Paresis
  • Hyper-reflexia
  • Spasticity
72
Q

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?

A

Amyotrophic Lateral Sclerosis

73
Q

progression and prognosis of Amyotrophic Lateral Sclerosis :
Involvement of the respiratory muscles –> Recurrent bouts of pulmonary infections -> ——

A

Death

patho II (29 decks)

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