Diseases Flashcards

1
Q

Seizure Definition

A

Transient neurologic event of sudden or excessive cortical electrical discharges.

Manifested by disturbance of skeletal muscle function, sensation, autonomic visceral function, behavior or consciousness.

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2
Q

What is a seizure disorder refers to recurrent seizures?

A

Epilepsy

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3
Q

Seizure causes: _____ injury, ______, metabolic/nutritional disorders, ________ (no know cause)

A

cerebral
lesions
idiopathic

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4
Q

Pathogenesis of Seizure. Due to alteration in _______ ______ that makes certain neurons abnormally _________ and _________ to changes in their environment (epileptogenic focus)

A

membrane potential
hyperactive
hypersensitive

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5
Q

Treatment for seizures:

A

Anticonvulsants: can target Na+ and Ca2+ channels or enhance GABA

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6
Q

What is dementia?

A

Syndrome associated with many pathologies; characterized by progressive deterioration and continuing decline of memory and other cognitive changes.

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7
Q

Age-related dementia: _______ condition resulting in progressive cognitive decline
Name Types: _______ and ________

A

irreversible
Alzheimer
Vascular

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8
Q

Dementia - Alzheimer Disease.

Where are degeneration of neurons?

A

temporal and frontal lobes
brain atrophy
amyloid plaques
neurofibrillary tangles

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9
Q

What are pathologic features of Alzheimer Disease?

A

Proteinopathies - plaques and tangles

Periplaque inflammatory reaction and neurodegeneration: synapse loss, neuron loss gross cerebral

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10
Q

Neuritic plaque and neurofibrilary tangle.

Where are they located?

A

Neuritic plaque: forms in extracellular space

Neurofibrillary tangle: intracellular aggregates

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11
Q

What are some pathologic properties of Alzhemier?

A

Beta amyloid protein (AB peptide)

Neuritic plaque: dense central AB core with inflammatory cells and dystrophic neurities in periphery

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12
Q

What are Tau proteins?

What does an MRI imaging show?

Amyloid accumulation has what biomarker?

Neurodegeneration or neuronal injury has what biomarker?

A

Dissociates, assumes paired helical filament configuration and forms insoluble tangles

FDG PET –> glucose metabolism (synaptic activity); cerebral atrophy (hippocampus) which reflects microscopic neurodegeneration (loss of synpases)

Amyloid: Decrease CSF AB 42

Neurodegeneration: Increase CSF tau and decrease FDG PET

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13
Q

What is a major risk factor for Alzheimer?

_______ reserve: different mechanisms including numbers of neurons and synapses, sensitivity of neurons and glia to pathologic process

A

Epislon 4 allele of APOE gene (cholesterol metabolism)

Cognitive

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14
Q

What is Vascular Cognitive Impairment?

Syndrome with evidence of ______ ________ or subclinical vascular ____ _______ and cognitive impairment affect at least one ______ domain.

A

Clinical stroke
Brain injury
cognitive

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15
Q

Vascular Cognitive Impairments:

_____ impairment due to ______ pathologies
cumulative _____ damage more so than large ______ _______
white matter

A

Cognitive
tissue damage
cerebral infarcts

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16
Q

What are the 4 pathogenesis of vascular cognitive impairment?

A

1) cerebral amyloid angiography
2) atherosclerosis
3) confluent white matter lesions; small white matter infarcts
4) hyaline substance in vessel wall

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17
Q

What is is the biggest cause of vascular cognitive impairment?

A

Endothelial dysfunction

18
Q

What are clinical manifestations of vascular cognitive impairment?

A

Early: memory loss - especially short term memory, long term memory may be perserved; thinking ability declines, decreasing ability to function at work and in social settings; anxiety, agitation

19
Q

What treatment is there for vascular cognitive impairment?

What can we do?

A

No FDA approved treatment for VCI or vascular dementia

Preventive measure = control risk factors

20
Q

Delirium:

Hyperkinetic _________ state: autonomic nervous system over activity

_______ state of brain __________

Excited delirium syndrome:

Hypokinetic delirium:

A

confusional

acute; dysfunction

agitated delirium

hypokinetic confusional state

21
Q

Delirium:

A

Is an acute state of brain dysfunction
onset is usually abrupt
ANS is over active
Common in critical care units, post surgically or during withdrawal from CNS depressants

22
Q

Dementia:

A

Is the progressive failure of many cerebral function
Onset is usually gradual
Progressive dementia produce nerve cell degeneration and brain atrophy
Age is the greatest risk factor

23
Q

Parkinson Disease:

________ neurologic disorder associated with ________ impairment.

Degeneration of what type of neurons? Location?

A

Progressive; motor

Dopaminergic neurons in the substantia nigra (basal ganglia)

24
Q

What are signs and symptoms of Parkinson Disease?

A

Difficulty initiating and controlling movements
Bradykinesia, tremors, rigidity, postural instability coupled with gradual symptom progression and sustained response to therapy

25
Q

What are clinical Manifestations of Parkinson Disease?

A
Tremor
Masklike face
Arms flexed at elbows and wrists
Stooped posture
Rigidity
Hips and knees slightly flexed
Short shuffling steps
26
Q

There are 4 types of Spinal cord and peripheral nerve disease

1) __________ ____________
2) ___________ lateral _________
3) Spinal ________ __________
4) Guillain - _______ Syndrome

A

1) Multiple Sclerosis
2) Amyotrophic Lateral Sclerosis
3) Cord Injury
4) Barre

27
Q

Is there a cure for Parkinson Disease?

What drugs can be given?

What surgical intervention?

A

No cure

Can give restoring dopamine levels or activity by administering dopamine precursors, dopamine agonists, monoamine oxidase inhibitors and anticholinergics, antidepressants therapy

Ablative surgical procedures may be helpful for motor symptoms

28
Q

Multiple Sclerosis:

Inflammatory _________ disease of the CNS that primarily affect what population?

Why is it an autoimmune disease? What does it destroy?

Where does demyelination occur?

What causes this disease?

A

Demyelinating

Young adults

Autoimmune results in inflammation and scarring (sclerosis) of myelin sheath covering nerves

CNS and often affects the optic and oculomotor nerves and spinal cord

Unknown, but immunological abnormalities genetics and environmental factors suspected.

29
Q

What type of cells are involved in MS?

A

Demyelinate: dendritic cells, monocyte/macrophages
Autoreactive T cells: helper T and cytotoxic T lymphocytes, Natural Killer cells
ODC: oligodendrocyte and endothelial cells and pericyte and neurons

30
Q

MS is characterized by what? What are some trigger factors for these symptoms?

What are some manifestations?

Treatments? What kind of medications can be given and when is it given?

A

Exacerbation and remissions; exacerbated by heat, infection, trauma and stress

Double/blurred vision, weakness, poor coordination, and sensory deficits; bowel and bladder control may be lost; memory impairment common

No cure; short term steroid therapy may be helpful during acute exacerbations and immune-modifying drugs may slow progression of symptoms

31
Q

What is Amyotrophic Lateral Sclerosis: progressive disease affecting both the _______ and ______ motor neurons

Pathogenesis: ___________

Signs and symptoms of ALS?

A

Upper and lower

Unknown; genetic associations and CSF analysis

Weakness and wasting of the upper extremities usually occur, followed by impaired speech, swallowing and breathing

32
Q

ALS Pathogenesis:

1) Excitotoxicity caused by what substances? 2 Things
2) Oxidative Stress
3) __________ dysfunction
4) What type of inflammation?

A

1) Glutamate and calcium influx
3) Mitochondrial
4) Neuroinflammation

33
Q

Whats are some clinical manifestations of ALS?

How do you diagnose this disease?

A

Clinical: weakness, atrophy, cramps, stiffness, irregular twitching of muscles, hyper reflexia in weak, atrophied extremity (highly suggestive)

Diagnosis: clinical signs and symptoms, EMG, nerve conduction studies (transcranial magnetic stimulation, UMN), MRI and serum laboratory testing

34
Q

What happens to the spinal cord in spinal cord injury?

Mechanisms of injury include?

Secondary injury may result from _________, ________, ________ and inflammation.

A

Cord can be compressed, transected or contused (bruised)

Hyperflexion, Hyperextension, compression

Hemorrhage, swelling, ischemia

35
Q

Spinal shock occurs __________ and characterized by temporary loss of reflexes ________ the level of injury.

What do the muscles look like and what is lost?

When do the reflexes return?

A

immediately; below

Muscles are flaccid; autonomic reflexes

End of spinal shock and reflexes return and flaccidity replaced by spasticity

36
Q

What type of injury occurs to cause neurogenic shock?

What part of the ANS is affected?

Symptoms of neurogenic shock include?

A

cervical or upper thoracic injury

SNS; loss of brainstem and higher center control

hypotension, bradycardia, circulatory collapse

37
Q

What is autonomic dysreflexia which occurs during spinal cord injury? Its usually what type of complication due to injury of __________?

Injury occurs where?

What can trigger this reflex or common stimulus?

What are some signs and symptoms of this?

A

Acute (hyper) reflexive response to sympathetic activation below the level of injury. Usually a secondary complication due to injury of ANS.

Injury at or above T6

Visceral stimulation (full bladder or bowel) and activation of pain receptors below the injury are common stimuli?

Signs: hypertension, headache, bradycardia, flushing above the level of injury, and clammy skin below the skin of injury

38
Q

What is the pathophysiology of autonomic dysreflexia?

Brain detects hypertension by what receptors? Which then leads to what?

A

Stimulus generates sympathetic response –> widespread vasoconstriction most significantly in sphanchic vasculature –> increase peripheral resistance –> shunt blood to general circulation –> increases BP

Baroreceptors. It activates PSNS to lower BP –> PSNS over activity + Lack of sympathetic tone –> peripheral VASODILATION!

39
Q

Treatment for autonomic dysreflexia include:?

Appropriate stabilization of ________ ______

Neurogenic shock: Intensive care unit to maintain _______ and ______ __________

A

Spinal vertebrae
May be accomplished surgically with internal fixation or with external fixation and bracing

oxygenation and blood pressure

40
Q

Guillain Barre Syndrome:

Neuropathic condition characterized by _______ ______ and diminished or absent _________ reflexes.

Inflammatory demyelinating disease of the ________ nervous system or an _________ disorder.

AIDP?

A

progressive weakness; mytotatic

peripheral; Lower motor neuron (LMN)

Acute inflammatory demyelinating polynueropathy

41
Q

Guillian Barre Syndrome

What are signs and symptoms? Is the weakness ascending or descending? How does this differ from MS?

Diagnosis?

Treatment?

A

Muscle weakness that begins in LOWER extremities and spreads to the proximal spinal neurons. Progressive ascending weakness or paralysis and affect respiratory muscles. MS is descending –> weakness starts from top to bottom

Diagnosis: history, physical examination and nerve conduction studies and lumbar puncture

Treatment: supportive, plasmapheresis, immunoglobulin