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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
Q

Friedreich ataxia

A

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
Q

ALS

A

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
Q

ALS symptoms

A

Upper motor paralysis of extremities
Hypertonia of muscles
Exaggerated deep tendon reflexes

Lower motor neuron signs
Muscle weakness
Eventual paralysis of respiratory muscles

28
Q

ALS UMN

A 
Weakness
Increased reflexes
Spasticity
Pseudobulbar
Babinski sign
29
Q

ALS LMN

A 
Weakness
Decreased reflexes
Atrophy
Fasciculations 
Muscle denervation
30
Q

ALS treatment

A

Riluzole (glutamate antagonist)

31
Q

Spinal muscular atrophy

A

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
Q

MS

A

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
Q

MS pathogenesis

A

Initiated by TH1 and TH16 which react against myelin Ag

Risk associated with HLA DRB1

34
Q

MS morphology

A

Plaques in the white matter
Adjacent to lateral ventricles, optic nerves and chains, brain stem, cerebellum and spinal cord

Active plaques=myelin breakdown

35
Q

MS clinical

A

Unilateral vision impairment from optic nerve involvement

Ataxia, nystagmus, internuclear opthalmoplegia

Motor and sensory impairment, spasticity, bladder dysfunction

36
Q

MS CSF

A

Gamma globulin increased
Oligoclonal bands
Due to proliferation of B cells in NS

37
Q

Neuromyelitis optica

A

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
Q

Central pontine myelinolysis

Osmotic demyelination syndrome

A

Caused by rapid correction of hyponatremia

Acute hyponatremia can cause cerebral edema

If hyponatremia occurs slowly, brain adapts without edema

39
Q

Osmotic demyelination syndrome pathogenesis

A

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
Q

Osmotic demyelination syndrome clinical

A

Dysarthria, dysphagia, lethargy, confusion, paraparesis, quadriparesis, disorientation, locked in

41
Q

Osmotic demyelination syndrome morphology

A

Symmetrical loss of myelin- diffuse or in brain stem, pontine tegmentum

Periventricular and subpial regions preserved

42
Q

Osmotic demyelination syndrome at risk

A

Alcoholism
Liver transplant
Electrolyte or osmolar imbalance

43
Q

Thiamine B1 deficiency

A

Korsakoff- memory disturbances

Largely irreversible

44
Q

Thiamine deficiency morphology

A

Mammillary bodies
Focal hemorrhage and necrosis
Also 3rd and 4th ventricles

Memory disturbances caused by lesions in medial dorsal nucleus of the thalamus

45
Q

B12 deficiency

A 
Ataxia
Parathesias of lower extremities
Spastic weakness to paraplegia
Degeneration of axons
-ascending tracts
-descending pyramidal tracts
46
Q

Hypoglycemia

A

Resembles hypoxia

Large pyramidal neurons of cortex
Sommer sector of hippocampus
Purkinje cells of cerebellum

47
Q

Hyperglycemia

A

Ketoacidosis (DM1)

Hyperosmolar coma (DM2)

Dehydration

48
Q

Hepatic encephalopathy

A

Alzheimer type II astrocytes in hyperammonemia

No abnormalities in neurons

49
Q

Carbon monoxide

A

Affects pyramidal neurons of cortex, purkinje cells of cerebellum, sommer sector of hippocampus

Bilateral necrosis of globes pallidus
Demyelination

50
Q

Methanol

A

Degeneration of retinal ganglion cells

Selective bilateral putamenal necrosis

Focal white matter necrosis

Anion gap metabolic acidosis

Treat with fomepizole- blocks alcohol DH

51
Q

Ethanol

A

Atrophy and loss of granule cells in anterior vermis

Advanced cases: loss of purkinje cells with proliferation of adjacent astrocytes

52
Q

Radiation

A

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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