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D&T2 Exam 1 > CNS Diseases > Flashcards

CNS Diseases Flashcards

1
Q

Alzheimer disease

A

Progressive loss of neurons in cerebral cortex

Decreased choline acetyltransferase and ACh in cerebral cortex

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2
Q

Alzheimer disease pathogens is

A

Amyloid precursor protein (APP) may be cleaves to form AB peptide- forms beta pleated sheets of amyloid that can’t be broken down

Tau is critical in AD

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3
Q

Alzheimer disease genetics

A

Abnormalities of chromosomes 1, 14, 19, and 21

Mutations promote the gen of increased amounts of AB peptide (especially AB42 via gamma secretase complex)

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4
Q

Chromosome 21

A

APP

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5
Q

Chromosome 14

A

Presenilin 1

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6
Q

Chromosome 1

A

Presenilin 2

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7
Q

Chromosome 19

A

ApoE

E4 is seen more frequently with AD

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8
Q

Morphology of AD

A

Thinned gyri and widened sulci in frontal, parietal, and medial temporal lobes

Cortical gray matter thinned

Dilation of lateral ventricles

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9
Q

Neurotic plaques of AD

A

Central amyloid core (AB42) with clear halo

Microglia and reactive astrocytes at periphery

Hippocampus, amygdala, neocortex-spares motor and sensory cortices

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10
Q

Cerebral amyloid angiopathy

A

Deposition of amyloid in walls of small meningeal and cortical arteries (amyloid is predominantly AB40)

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11
Q

Frontotemporal lobar degenerations

A

Heterogeneous set of disorders associated with focal degeneration of frontal and/or temporal lobes

Alterations in personality, behavior and language preceding dementia

Associated with cellular inclusions of tau or TDP43

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12
Q

Pick disease

FTLD-tau

A

40-65 years

Selective lobar atrophy of anterior frontal and temporal lobes- knife edge atrophy
Posterior 2/3rd of superior temporal gyrus, parietal and occipital lobes are usually preserved

Most severe neuronal loss in outer 3 layers of the cortex

Surviving neurons may contain pick bodies

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13
Q

Pick bodies

A

Intracytoplasmic accumulations of silver positive material

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14
Q

Basal ganglia degenerations

A

Parkinson disease
Parkinsonism
Huntington disease

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15
Q

Idiopathic parkinson disease

A

Depigmentation, neuronal loss, gliosis of pigmented nuclei

Damages neuronal pathway from substantia nigra to corpus striatum
Decrease DA in corpus striatum

Mutations in gene for alpha synuclein on chromosome 4q have been implicated- affect its folding/alter its structure

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16
Q

Parkinson’s disease

A

Depigmented substantia nigra and locus ceruleus

Loss of DA neurons
Gliosis of substantia nigra and locus ceruleus
Lewy bodies

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17
Q

Lewy bodies

A

Eosinophilic cytoplasmic inclusions in damaged cells

In cortex cause dementia

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18
Q

Parkinson’s disease clinical

A 
Slowly progressive; extrapyramidal dysfunction
Cog-wheel rigidity
Resting tremor
Bradykinesia
Gait, festinating

Slow difficult speech

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19
Q

Pallidotomy

A

Decrease symptoms of rigidity

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20
Q

MPTP Parkinsonism side effect

A

Irreversible

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21
Q

Huntington disease

A

Rare; AD; complete penetrance; delayed appearance

Abnormality of HD gene on short arm of chromosome 4
CAG trinucleotide repeat (more repeats=earlier onset)

22
Q

Huntington disease morphology

A

Loss of neurons and atrophy
Caudate nucleus
Putamen
Can be atrophy of cerebral cortex

Severe loss of striatal neurons

23
Q

Huntington disease symptoms

A

Presents 20-50 yo
Dementia and psychotic sx (cerebrum)
Choreiform movements (basal ganglia)

24
Q

Spinocerebellar degenerations

A

Affect cerebellum, brain stem, spinal cord, peripheral nerves

25
Friedreich ataxia
Spinocerebellar degenerations Trinucleotide repeat disorder (GAA) Results in frataxin protein deficiency Degenerations of spinocerebellar tracts, posterior columns, pyramidal tract, peripheral nerves Late childhood Pes cavus, kyphoscoliosis, cardiac disease, DM
26
ALS
Thinned ventral roots of spinal cord UMN destruction leads to degeneration of myelin in lateral corticospinal tracts Decrease neurons in anterior horn throughout length of spinal cord, loss of anterior root myelinated fibers Skeletal muscles show neurogenic atrophy SOD1 gene, chromosome 21
27
ALS symptoms
Upper motor paralysis of extremities Hypertonia of muscles Exaggerated deep tendon reflexes Lower motor neuron signs Muscle weakness Eventual paralysis of respiratory muscles
28
ALS UMN
``` Weakness Increased reflexes Spasticity Pseudobulbar Babinski sign ```
29
ALS LMN
``` Weakness Decreased reflexes Atrophy Fasciculations Muscle denervation ```
30
ALS treatment
Riluzole (glutamate antagonist)
31
Spinal muscular atrophy
SMA type 1- Werdnig Hoffman disease Deletions of SMN on chromosome 5 Loss of motor neurons in ant horn of spinal cord- atrophy of ant spinal roots and peripheral motor nerves- denervation and atrophy of skeletal muscle groups Floppy baby
32
MS
Episodes of neurologic deficits separated in time, attributable to white matter lesions separated in space Most common autoimmune, inflammatory, Demyelinating disorder Age 20-40 females more than males
33
MS pathogenesis
Initiated by TH1 and TH16 which react against myelin Ag Risk associated with HLA DRB1
34
MS morphology
Plaques in the white matter Adjacent to lateral ventricles, optic nerves and chains, brain stem, cerebellum and spinal cord Active plaques=myelin breakdown
35
MS clinical
Unilateral vision impairment from optic nerve involvement Ataxia, nystagmus, internuclear opthalmoplegia Motor and sensory impairment, spasticity, bladder dysfunction
36
MS CSF
Gamma globulin increased Oligoclonal bands Due to proliferation of B cells in NS
37
Neuromyelitis optica
Abs to aquaporin-4, major H2O channel of atrocytes Areas of demyelination also show loss of aquaporin 4 Bilateral optic neuritis Spinal cord demyelination
38
Central pontine myelinolysis Osmotic demyelination syndrome
Caused by rapid correction of hyponatremia Acute hyponatremia can cause cerebral edema If hyponatremia occurs slowly, brain adapts without edema
39
Osmotic demyelination syndrome pathogenesis
Adaptation involves loss of electrolytes and water which protects from cerebral edema After rapid correction of hyponatremia, brain shrinks and cannot rapidly replace lost electrolytes
40
Osmotic demyelination syndrome clinical
Dysarthria, dysphagia, lethargy, confusion, paraparesis, quadriparesis, disorientation, locked in
41
Osmotic demyelination syndrome morphology
Symmetrical loss of myelin- diffuse or in brain stem, pontine tegmentum Periventricular and subpial regions preserved
42
Osmotic demyelination syndrome at risk
Alcoholism Liver transplant Electrolyte or osmolar imbalance
43
Thiamine B1 deficiency
Korsakoff- memory disturbances | Largely irreversible
44
Thiamine deficiency morphology
Mammillary bodies Focal hemorrhage and necrosis Also 3rd and 4th ventricles Memory disturbances caused by lesions in medial dorsal nucleus of the thalamus
45
B12 deficiency
``` Ataxia Parathesias of lower extremities Spastic weakness to paraplegia Degeneration of axons -ascending tracts -descending pyramidal tracts ```
46
Hypoglycemia
Resembles hypoxia Large pyramidal neurons of cortex Sommer sector of hippocampus Purkinje cells of cerebellum
47
Hyperglycemia
Ketoacidosis (DM1) Hyperosmolar coma (DM2) Dehydration
48
Hepatic encephalopathy
Alzheimer type II astrocytes in hyperammonemia No abnormalities in neurons
49
Carbon monoxide
Affects pyramidal neurons of cortex, purkinje cells of cerebellum, sommer sector of hippocampus Bilateral necrosis of globes pallidus Demyelination
50
Methanol
Degeneration of retinal ganglion cells Selective bilateral putamenal necrosis Focal white matter necrosis Anion gap metabolic acidosis Treat with fomepizole- blocks alcohol DH
51
Ethanol
Atrophy and loss of granule cells in anterior vermis Advanced cases: loss of purkinje cells with proliferation of adjacent astrocytes
52
Radiation
Coagulative necrosis affecting all elements of white matter: astrocytes, axons, oligodendrocytes, blood vessels; with adjacent edema

D&T2 Exam 1 (11 decks)

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