Chronic disorder of neurologic function Flashcards by Kari Gitlewski

characterized by excessive cortical electrical discharges and spontaneous positive potentials r/t Na+

Seizure disorder

How well did you know this?

Not at all

Perfectly

neurons are hyperactive and hypersensitive to their environment

seizure disorder pathogenesis

How well did you know this?

Not at all

Perfectly

decreased distance between membrane and threshold potential

neurons hypersensitive

How well did you know this?

Not at all

Perfectly

Anticonvulsants target

Positive ions, Na+ and Ca++ (depolarization of the cell)

2. Enhance GABA- inhibitory (hyper polarize cell- Cl-)

How well did you know this?

Not at all

Perfectly

PROGRESSIVE deterioration and CONTINUING decline of memory and cognitive changes

Dementia

How well did you know this?

Not at all

Perfectly

two types of dementia

Alzheimers and Vascular

How well did you know this?

Not at all

Perfectly

degeneration of CORTICAL neurons in temporal and frontal lobes

dementia

How well did you know this?

Not at all

Perfectly

brain atrophy around TEMPORAL

amyloid plaques

neurofibulary tangles

Alzheimers

How well did you know this?

Not at all

Perfectly

Characterized by a LOSS of function

Alzheimers disease

How well did you know this?

Not at all

Perfectly

mild cognitive impairment

NOT Alzheimers

How well did you know this?

Not at all

Perfectly

plaques and tangles

proteinopathies

How well did you know this?

Not at all

Perfectly

extracellular space

plaques

How well did you know this?

Not at all

Perfectly

intracellular space

tanagles

How well did you know this?

Not at all

Perfectly

B- amyloid deposits

Plaques

How well did you know this?

Not at all

Perfectly

Tau Protein

Tangles

How well did you know this?

Not at all

Perfectly

dense central AB core with inflammatory cells and DYSTROPHIC neurites in periphery

plaques

How well did you know this?

Not at all

Perfectly

high potential for aggregation and accumulation

plaques

How well did you know this?

Not at all

Perfectly

paired helical filament configuration

tangles

How well did you know this?

Not at all

Perfectly

disassociates from microtubule and begins to fold

tangles

How well did you know this?

Not at all

Perfectly

AB peptide gets clever into

AB42

How well did you know this?

Not at all

Perfectly

B-amaeyloid is a byproduct that exists EXTRACELLULARLY and gets cleared in 3 ways normally

Uptake by another neuron
Macrophages
enzymes

How well did you know this?

Not at all

Perfectly

INCREASED in alzheimers

CSF Tou

normally stays in neuron membrane, if it has increased in CSF it has LEAKED out of the neuron and their is an accumulation.

How well did you know this?

Not at all

Perfectly

DECREASED in alzheimers

AB42 normally in CSF, if it is decreased it has accumulated somewhere else (extracellular space)
FDG PET - glucose metabolism ahs decreased indicating decreased neuronal function (neurodegerative disease)

How well did you know this?

Not at all

Perfectly

most common byproduct of alzheimers

AB42

How well did you know this?

Not at all

Perfectly

risk factor for alzheimerw

E4 allele of APOE has a higher affinity for B-Amyloid

INCREASES metabolism, INCREASES aggregation and DECREASES clearance of AB peptide

E4 allele of APOE

how do we increase or cognitive reserve

exercise your brain and start with a higher baseline

syndrome with evidence of CLINICAL STROKE or VASCULAR BRAIN INJURY

dementia; vascular cognitive impairment

cognitive impairment r/t cerebrovascular injuries

vascular dementia

communication with WHITE MATTER degrades

vascular dementia

vascular dementia from ______________ more so than ____________.

cumulative tissue damage large cerebral infarcts

atherosclerosis is often associated

hyaline substance in vessel wall- yellow lipid deposits

acute state of brain dysfunction, abrupt onset

delerium

Leukoaraiosis

confluent white matter lesions

Lacunar Infarcts

small, white mater infarcts

CAA

Cerebral amyloid angiopathy

micro infarcts

leading cause of vascular dimentia

progressive failure of cerebral functions, onset is gradual

dementia

hyperkinetic confusional state

delirium with sympathetic NS overactivity

hypokinetic confusional state

delirium with parasympathetic NS Confusional states

degeneration of dopaminergic neurons in basal ganglia and development of LEWY bodies

Parkinsons

TRAP

tremor rigidity akinesia/bradykinesia postural instability

treated with LEVADOPA

Parkinsons Levadopa = precursor to dopamine

breakdown the precursor to Dopamine

MAO - Parkinsons treated with MAOI

Autoimmune, inflammatory, progressive demyelination of the CNS

Multiple Sclerosis

demyelination often occurs at optic, oculomotor and spinal tracts

Multiple sclerosis

exacerbated by heat, infection, trauma and stress

Multiple sclerosis

MS: immune cells attacking meylin

Autoreactive T cells

MS: activated to chew up myelin sheath

macrophages

MS: these cells DIE, normally function to deposit myelin to cover axons

oligodendorcytes

macrophage alone attacks myelin sheath

macrophage mediated

macrophage works with helper t and b to create antibodies that destroy myelin

Antibody mediated

attacking NERVE ENDING of ODC that is responsible for melioration causing demylination

Distal Oligodendropathy

Macrophage is attacking Oligodendrocyte in General

Primary ODC damage with peripheral Secondary demyelination

double vision, weakness, poor coordination, sensory deficits, bowel and bladder control may be lost memory impairment

Multiple sclerosis symptoms

progressive, UPPER and LOWER motor neurons

ALS

Pathogenesis of ALS

1. Excitotoxicity (Glutamate, Ca++) 2. Oxidative Stress 3. Mitochondrial Dysfunction 4. Neuorinflammation

hyperrelexia in weak atrophied extremity

ALS

neurons die in retrograde and anterograde fashin

ALS

secondary injury from spinal cord injury from

swelling hemorrhage ischemia inflammation

temporary loss of reflexes below the spinal cord injury

Spinal Shock

muscles flacid/skeletal and autonomic reflexes lost

spinal shock

Cervical or upper thoracic injury

neurogenic shock

loss of brainstem and higher control of SNS

neurogenic Shock

hypotension, bradycardia, circulatory collapse

Neurogenic shock

secondary complication due to injury of ANS at or above T6

Autonomic Dysreflexia

visceral stimulus or activation of pain receptors BELOW the injury are common stimuli

Autonomic Dysreflexia

manifests as: hypotension, headace, bradycardia, flushing ABOVE the level of injury and clammy BELOW level of injury

Autonomic Dysreflexia

IN Autonomic Dysreflexia a stimulus generates ______________ which will cause widespread ______________ in splanchinc vasculature and an increase in peripheral resistance, where blood is then shunted to _____________ circulation. _______________ sense increased blood pressure and activate the __________________ to lower the blood pressure. with this activation theirs a loss of ____________ tone and increased peripheral ______________.

sympathetic response vasoconstriction general circulation Baroreceptors PSNS sympathetic tone vasodilation

stablilization of vertebrae

treament for Autonomic Dysreflexia

in neurogenic shock we want to

Maintain oxygenation and blood pressure

neuropathic condition with progressive weakness and diminished or absent MYOTATIC reflexes

Guillian- Barre Syndrome

inflammatory, demyelinating disease of the PERIPHERAL nervous system

Guillian- Barre Syndrome

A lower motor neuron disorder

Guillian- Barre Syndrome

AIDP

Guillian- Barre Syndrome acute inflammatory demyelinating polyneuropathy

muscle weakness that begins in lower extremities and speeds to proximal spinal neurons

Guillian- Barre Syndrome

Treatment include plasmapheresis and immunoglobulin

Guillian- Barre Syndrome