Unit 3 CNS Flashcards

1
Q

Descrive CVA (cerebrovascular accidents)/stroke.

A
  • a clinical syndrome characterized by a focal neurological deficit, due to an abnormality of the cerebral circulation
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2
Q

Describe the blood supply to the brain.

A
  • Two internal carotid arteries anteriorly
    • Ophthalmic, posterior communicating, anterior choroidal, anterior cerebral, and middle cerebral
  • Vertebral arteries posteriorly
  • Internal carotid and vertebral arteries communicate at the base of the brain through the circle of Willis.

http://postimg.org/image/8gfcmdt0b/

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3
Q

Describe the cerebral vascular arteries.

A

Lateral View

http://en.wikipedia.org/wiki/File:Cerebral_vascular_territories.jpg

Medial View

http://en.wikipedia.org/wiki/File:Cerebral_vascular_territories_midline.jpg

Middle cerebral artery (upper body)

Anterior cerebral artery (lower body)

Occiptial (visual, etc.)

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4
Q

What are the etiologies (risk factors) of a stroke?

A
  • Age
  • Gender
  • Race
  • High cholesterol levels
  • Cigarette smoking
  • Diabetes mellitus
  • Other risk factors
    • Heart diseases
    • Blood diseases
    • Alcohol, cocaine and illicit drug use (Chlamydia pneumoniae)
    • Sedentary life style
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5
Q

What are the two types of stroke?

A

Ischemic strokes

  • Caused by an interruption of blood flow in a cerebral vessel and are the most common type of stroke, accounting for 70–80% of all strokes.

Hemorrhagic strokes

  • Caused by bleeding into brain tissue, usually from a blood vessel rupture caused by hypertension, aneurysms, arteriovenous malformations, head injury, or blood dyscrasias
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6
Q

What is a thrombosis?

A
  • a solid mass of blood constituents (blood clot) formed within the vascular system in a living being

Predisposing Factors

  • Changes in the intimal surface of the blood vessel
  • Changes in the pattern of blood flow
  • Changes in the blood constituents
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7
Q

What is an emobolism?

A
  • is a mass of material in the vascular system able to become dislodged within a vessel and block its lumen
    • a piece of thrombus
    • foreign bodies
    • fat tissue
    • bacterial organism
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8
Q

What are the risk factors for a hemorrhagic stroke?

A

Hemorrhage

  • severe hypertension
  • aneurysm
  • congenital berry aneurysm
  • arteriovenous malformation
  • bleeding disorders
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9
Q

What are signs and symptoms of a Cerebral Aneurysm?

A
  • Most small aneurysms are asymptomatic.
  • Large aneurysms may cause chronic headache, neurologic deficits, or both.
  • Other manifestations include signs of meningeal irritation, cranial nerve deficits,
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10
Q

What are arterious malformations?

A
  • blood is shunted from the high-pressure arterial system to the low-pressure venous system without the buffering advantage of the capillary network.
  • The draining venous channels are exposed to high levels of pressure, predisposing them to rupture and hemorrhage
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11
Q

What are the classes of stroke?

A
  • TIA
    • presents with neurological deficit but will full recover within 24hr, warning sign of higher risk stroke in the future
    • embolism most likely
  • Evolving stroke (stroke in evolution)
    • progressing, begins with warm then moves to legs, most likely a thrombus (ischemia or small hemorrhage)
  • Completed stroke
    • paralysis of R or L side
    • R side stoke = language difficulties
    • hemorrhagic or big thrmobus
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12
Q

Descrive the pathophysiology of a stroke.

A
  • destruction of brain substance
  • edema of surrounding brain tissue
  • increased intracranial pressure

Ischemic

  • Cerebrovascular obstructions by an embolism or thrombus
  • central core of dead or dying cells surrounded by a penumbra (halo of cells recieving marginal bloodflow)
  • Cell in penumbra have marginal bloodflow and their metabolic activities are impaired. although areas undergoes an electrical failure, the structural integrity of the cells is maintained
  • Function of cells in penumbra depends on return of circulation, volume of toxic products produced by dying cells, degree of cerebral edema, and alterations in local blood flow.

Hemorrhagic

  • rupture of blood vessel
  • hemorrhage into brain tissue
  • focal hematoma
  • infarction
  • increased ICP by hematoma
  • edema
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13
Q

What are the clinical manifestations of a stroke?

A

Clinical Manifestations are Determined:

  • by the cerebral artery that is affected
  • Size of the vessel – Lacunar infarct
  • by the area of brain tissue that is supplied by that vessel
  • By the adequacy of the collateral circulation
  • Presence or absence of cerebral edema and increased ICP
  • Ischemic (more focal) and hemorrhagic (more global)

See figure below for arteries (effects listed according to list below) (see page 1266 for more details), http://postimg.org/image/9mg9g3k8d/

  • anterior cerebral artery
  • middle cerebral artery
  • posterior cerebral artery
  • basilar and vertebral artery
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14
Q

What is brain herniation?

A

There are four main types of brain herniation syndromes. These include the cingulate, central, uncal, and cerebellar tonsillar herniations described below:

Subfalcine (or cingulate) herniation:

  • A section of brain herniates under the falx cerebri. This can cause compression of the anterior cerebral artery.

Downward Transtentorial (or central) herniation:

  • The thalamic area herniates down over the tentorial notch. This can lead to decorticate posturing during which the individual’s body is in an extended position but the arms and wrists flex in response to pain.

Temporal Transtentorial (or uncal) herniation:

  • The medial part of the temporal lobe herniates down over the tentorial notch. This can lead to pressure on the brainstem and decerebrate posturing, often beginning unilaterally and progressing to involve both sides. Decerebrate posturing is full extension of the arms, legs, and back.
  • The paramedian arteries that branch off of the basilar artery may rupture due to excessive stretching. This will cause a characteristic brain bleed known as Duret hemorrhages. The result is usually fatal.
  • Uncal herniation can also create dilated pupils on the same side as the lesion. This is due to stretching of cranial nerve III.
  • Paresis (slight or partial paralysis) may also be present on the ipsilateral side (same side as the lesion). However, this is known as a false localizing sign because it is actually due to compression damage on the side opposite the lesion to an area known as the crux cerebri. This area is where the bulbar and corticospinal tracts run on their way to the spinal cord.

Cerebellar Tonsillar herniation:

  • Part of the cerebellum herniates through the foramen magnum. Neck stiffness, known as nuchal rigidity, is a common finding. Irregular respiration can quickly lead to cessation of breathing due to direct pressure on the medulla.
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15
Q

What is conciousness and how is it measured (TQ)?

A
  • is a state of awareness of self and the environment and of being able to become oriented to new stimuli
  • rely on RAS (ascending fibers) for being alert
  • the content and cognitive aspects of consciousness are determined by a functioning cerebral cortex

Levels of Conciousness

  • Confusion – conscious but disorientated
  • Delirium - restless, delusions
  • Obtundation – decreased alertness with psychomotor retardation
  • Stupor – not unconscious, but no spontaneous activity
  • Coma - unarousable, unresponsive

http://www.smartdraw.com/examples/view/traumatic+brain+injury+-+glasgow+coma+scale/

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16
Q

What tests can be used to investigation a brain head injury?

A

General

Specific

  • Chest X ray
  • CT
  • ?MRI
  • ?arteriogram

Nursing interventions

  • Neurologic monitoring
  • Cerebral edema management
  • Seizure control
  • Medication administration
17
Q

What are signs and symptoms of increased cranial pressure (TQ)?

A
  • headache,
  • vomiting without nausea,
  • ocular palsies,
  • altered level of consciousness,
  • back pain and
  • papilledema.
  • pupillary dilatation,
  • abducens palsies,
  • and the Cushing’s triad.
    • increased systolic blood pressure,
    • a widened pulse pressure,
    • bradycardia,
    • and an abnormal respiratory pattern.
18
Q

What are disorders of cognition?

A

The term “dementia” refers to a syndrome of cognitive impairment

Caused by any disorder that damages large association areas of the cerebral cortex (cortical) or subcortical areas subserving memory and learning

19
Q

What is dementia?

A

Impairment of short- and long-term memory, associated with abstract thinking, impaired judgment, other higher cortical functions, or personality change

Caused by any disorder that permanently damages large association areas serving memory and learning

Progressive failure of cerebral functions that is not caused by an impaired level of consciousness

Classifications

  • Cortical
    • Alzheimer and Pick diseases
  • Subcortical
    • Parkinson and Huntington diseases
  • Cortical and subcortical
    • Infectious and Creutzfeldt-Jakob diseases
20
Q

Describe Alzhemier’s

A

Etiology

  • Aging, genetic linkage – mutations in chromosome 21, 14 and 1

Pathophysiology

  • Cortical atrophy, loss of neurons
  • Particularly in the parietal and temporal lobes, hippocampus, basal forebrain
  • Associated ventricular enlargement

Pathological features

  • Senile plaques and neurofibrillary tangles
  • Amyloid beta derived from APP
21
Q

What are the stages of alzheimer’s disease (TQ)?

A

Initial change is subtle

  • Short-term memory loss
  • Mild changes in personality
  • Randomly forget important and unimportant details

Stage 1

  • Last for 2 – 4 years

Stage 2

  • Very mild

Stages 3 and 4 (Mild to moderate cognitive decline)

  • Performance issues in social or work
  • Decline in the ability to plan and organize
  • Seem subdued and withdrawn

Stage 5 – moderately severe

  • Assistance required for day to day activities

Stages 6 and 7 (Terminal stage)

  • Have to be institutionalized
  • the last stage of the disease.
  • Loss of ability to respond to the environment
  • Require total care
  • Bedridden
  • Death can occur as a result of complications related to chronic debilitation.
22
Q

Why is weight loss an issue in Alzeimers?

A
  • include loss of appetite secondary to deterioration of brain regions associated with feeding behavior and
  • functional and behavioral problems
    • unable to chew
    • forget to eat
    • eat bad or expired food
    • unable to feed themselves (skill loss)
23
Q

What is Huntington’s Disease?

A
  • Autosomal dominant inherited disorder
  • Progressive degeneration of the cerebral cortex and basal ganglia
  • Decreased neurotransmitter – GABA and GABA receptors
  • Occurs in younger age group (35-44)

Clinical Manifestations

  • progressive dysfunction of intellectual and thought process
  • loss of working memory
  • slow thinking
  • restlessness and irritability
  • Chorea – progressive rigidity
  • depression
24
Q

Alzheimer and Huntington are diseases under the group ‘dementia” – a progressive degeneration of cognitive function due to organic causes.

What are the similarities and differences between this 2 (TQ)?

A
25
Q

What are other types of dementia?

A

Pick’s disease - frontotemporal dementia, very rare and poor prognosis http://en.wikipedia.org/wiki/Pick’s_disease

Creutzfeldt-Jakob Disease http://en.wikipedia.org/wiki/Creutzfeldt%E2%80%93Jakob_disease

Wernicke-Korsakoff Syndrome

https://en.wikipedia.org/wiki/Wernicke%E2%80%93Korsakoff_syndrome

26
Q

What are the Primary functions of the:
Frontal lobe
Parietal lobe
Temporal lobe
Occipital lobe

Higher order functions
Supplementary areas, association cortex
Limbic System
Basal ganglion

A

What are the Primary functions of the:

  • Frontal lobe (motor, speech and language)
  • Parietal lobe (sensory)
  • Temporal lobe (part of limbic system)
  • Occipital lobe (vision

Higher order functions

  • Supplementary areas, association cortex (motor and sensory integration)
  • Limbic System (emotions)
  • Basal ganglion (voluntary motor control)
27
Q

What are the higher order functions of the frontal lobe?

A
  • Abstract vs. concrete reasoning
  • Motivation/volition
  • Concentration
  • Decision making
  • Purposeful behavior
  • Memory, sequencing, making meaning of language
  • Speech organization and production
  • Aspects of emotional response
28
Q

What are the higher order functions of the partiel lobe?

A
  • Sensory integration and spatial relations
  • Bodily awareness
  • Filtration of background stimuli
  • Personality factors and symptom denial
  • Memory and nonverbal memory
  • Concept formation
29
Q

What are the higher order functions of the temporal lobe?

A
  • Visual-spatial recognition
  • Attention
  • Motivation
  • Emotional modulation and interpretation
  • Impulse and aggression control
  • Interpretation and meaning of social contact
  • Aspects of sexual action and meaning
30
Q

What are the higher order functions of the occipital lobe?

A
  • Meaningfulness of visual experience
  • Depth perception
  • Pattern, form and location in space
31
Q

What are the functions of these areas of the brain?

  • Supplementary motor area
  • Premotor cortex
  • Posterior parietal cortex
A

Supplementary motor area – preparatory role in programming of complex sequences
Premotor cortex – assists primary motor cortex
Posterior parietal cortex – guides premotor cortex

32
Q

Review this diagram to identify the primary and higher order functions of areas of the brain (TQ!).

http://postimg.org/image/hus496iil/

A
33
Q

What are the primary functions of Werneke area and Brocca’s area? If a patient’s R side was paralyzed would they also have difficulties speaking?

A
  • Werneck - understand language
  • Brocca’s - speaking
  • 90% L side dominant
  • R side paralysis = difficulties speaking
  • L side paralysis = no difficulties
34
Q

What types of aphasia are there?

A
  • sensory (parietal/temporal)
    • can speak but it won’t make sense
  • motor (frontal)
    • understand but cannot talk (prone to depression)
35
Q

What parts of the brain make up the limbic system?

36
Q

Describe how memory is acquired (TQ).

A
  • Storage of acquired knowledge for later recall
  • Memory trace
    • Neural change responsible for retention or storage of knowledge
  • Short-term memory
    • Lasts for seconds to hours
  • Long-term memory
    • Retained for days to years
  • Consolidation
    • Process of transferring and fixing short-term memory traces into long-term memory stores
  • Two stages: 1) short term (consolidation), 2) long term

http://postimg.org/image/cw2mwco91/

37
Q

What are the functions of the following neurotransmitters?

A
  • acetylcholine
  • amines
    • dopamine, E, NE, and serotonin
  • aminoacids
    • GABA
    • Glutamate
    • Aspartate
    • Glycine

http://postimg.org/image/dewdi2iwt/