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NURS 320 > Exam 1: Alterations of Neurologic Function > Flashcards

Exam 1: Alterations of Neurologic Function Flashcards

1
Q

Cerebrovascular Accident

A

impairment of one or more vessels in the cerebral circulation -> interrupts blood supply -> ischemia of brain tissue

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2
Q

CVA is caused by

A

thrombosis
embolus
stenosis
hemorrhage

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3
Q

CVA: Risk Factors

A

Age (mostly > 65 yrs; 28% occur in < 65 yrs)
Atherosclerotic risk factors
Associated with HTN & diabetes (↑ in stroke incidence)
Smoking (50% ↑)
Atrial fibrillation: 6-fold risk for stroke
Use of medications such as sympathomimetics and oral contraceptives

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4
Q

Acute Manifestations of CVA

A
  • focal neurologic changes
  • may rapidly change
  • depends greatly on area of brain damage
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5
Q

Chronic Manifestations of CVA

A 
Paralysis
Ptosis
Homonymous hemianopsia (visual field loss)
Aphasia (impairment of language ability)
Loss of bowel and bladder control
Emotional instability
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6
Q

CVA: Pathophysiology

A

Involves occlusion of a cerebral vessel → ischemia of brain tissue supplied by that vessel

If obstruction not removed → tissue infarcts and dies → permanent neurological deficit or death

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7
Q

Severity of CVA is dependent on

A

location and extent of obstruction
degree of collateral circulation
promptness of diagnosis and treatment

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8
Q

Types of Stroke

A
  1. Thrombotic Stroke (Cerebral Thromboses)
  2. Embolic Stroke
  3. Hemorrhagic Stroke
  4. Lacunar Stroke
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9
Q

Thrombotic Stroke develops most often from

A

Atherosclerosis with thrombus formation

Inflammatory disease processes damage arterial walls (arteritis)

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10
Q

Conditions causing inadequate cerebral perfusion include

A

dehydration
hypotension
prolonged vasoconstriction from malignant hypertension

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11
Q

Transient ischemic attacks precedes in about 80% of cases:

A
  • temporary decrease blood flow; all neurologic deficits clear w/in 24 hours
  • changes in vision, speech, motor function, dizziness or LOC
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12
Q

Embolic Stroke

A

involves fragments that break from a thrombus formed outside the brain or in the heart, aorta or common carotid

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13
Q

Embolic Stroke: Risk Factors

A 
Myocardial infarction
Atrial fibrillation
Valvular disease
Endocarditis
Hypercoagulability
Air or fat emboli
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14
Q

Hemorrhagic Stroke (intracranial hemorrhage)

A

Accounts for 10% of all strokes and is most catastrophic type.
Onset is sudden.
Acute hypertension is a risk factor.

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15
Q

Hemorrhagic Stroke: Common Causes

A

HTN
Ruptured aneurysms or vascular malformation
Bleeding into a tumor
Hemorrhage associated with bleeding disorders
Anticoagulation
Head trauma
Illicit drug use

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16
Q

What is the most important preventative measure of hemorrhagic stroke?

A

BP control

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17
Q

Lacunar Stroke

A
  • occurs where small perforating arterioles branch off large cerebral vessels in the basal ganglia, internal capsule and brainstem
  • small arterioles exposed to constant high pressure flow of large arteries -> thickened, thrombosed, eventual obstructed small arterioles.
  • motor and sensory deficits
18
Q

Lacunar strokes account for what percent of all CVAs

A

20%

19
Q

Lacunar Strokes are associated with

A

smoking
HTN
diabetes

20
Q

Complications of CVA

A

Coma or death
Permanent neurological deficits (paralysis, impaired intellectual capability, speech defects, loss of short-term memory, impaired judgment)

21
Q

Treatment of Strokes are directed at

A

prevention of ischemic injury

control of cerebral edema and increased ICP

22
Q

What is the goal for treatment of the acute phase of a stroke?

A

stabilization of respiratory and cardiovascular function

23
Q

Ischemic Stroke Treatment

A

Thrombolytic (fibrinolytic) drugs: tissue plasminogen activator (TPA)

- Reestablishes blood flow to the brain by dissolving clots.    - Should be given w/in 3 hours to be effective.
24
Q

Hemorrhagic Stroke Treatment

A

Focuses on stopping or reducing the bleed.

Neurosurgical consult.

25
Q

Secondary Prevention: What medications could you use to prevent another stroke?

A

Statins (greatly reduces risk of stroke with prior TIA)
Antihypertensives
Antiplatelets (keeps platelets from sticking together)
Anticoagulants (prevents clots from forming and keep existing clots from getting bigger)

26
Q

Circle of Willis

A

provides an alternative route for blood flow when one of the communicating arteries is obstructed.

27
Q

Intracranial aneurysm may result from

A 
arteriosclerosis
congenital abnormality
trauma
inflammation
cocaine
28
Q

Intracranial Aneurysm

A

most occur in or near the circle of willis

20-25% of cases…. more than one

29
Q

Intracranial Aneurysm: Pathophysiology

A

no pathologic mechanism exists

30
Q

Intracranial Aneurysms can be classified on shape and form:

A
  1. saccular aneurysms

2. fusiform aneurysms

31
Q

Saccular aneurysms

A

result from congenital abnormalities

highest incidence of rupturing or bleeding 20-50 y.o.

32
Q

Fusiform aneurysms

A

giant aneurysms

result of diffuses arteriosclerotic changes.. mostly found terminal portion of internal carotid arteries

33
Q

Clinical Manifestations of Intracranial Aneurysms

A
  • often asymptomatic
  • first indication is an acute subarachnoid hemorrhage, intracerebral hemorrhage or both.
  • CN III, IV, V, and VI are most often affected
34
Q

Treatment of intracranial aneurysm

A

surgical management

35
Q

Subarachnoid Hemorrhage

A

blood escapes from defect or injured vessel into the subarachnoid space

36
Q

Risk for Subarachnoid Hemorrhages include:

A

Existing intracranial aneurysm
Existing intracranial arteriovenous malformation
Prior head injury
HTN

37
Q

Pathophysiology of Subarachnoid Hemorrhages

A
  • Vessel leaks…blood enters subarachnoid space
  • Vessel tears..blood under pressure pumped into subarachnoid space
  • Blood increases intracranial volume.. produces inflammatory reaction.
  • Cerebral blood flow and perfusion decrease.
  • Autoregulation of blood flow impaired -> leads to increased systolic blood pressure.
38
Q

Clinical Manifestations of Subarachnoid Hemorrhages: Leaking Vessel

A

Headache
Changes in mental status or LOC
N/V
Focal neurologic effects

39
Q

Clinical Manifestations of Subarachnoid Hemorrhages: Ruptured Vessel

A 
Sudden, throbbing “explosive” headache
N/V
Visual disturbances
Motor deficits
LOC due to increased ICP
Meningeal irritation/inflammation occurs (neck stiffness “nuchal rigidity”, photophobia, blurred vision, irritability, restlessness, low-grade fever)
40
Q

Treatment of Subarachnoid Hemorrhages are directed at

A

Controlling ICP
Preventing ischemia and hypoxia of neural tissues
Preventing rebleeding episodes

41
Q

Subarachnoid Hemorrhages Treatment

A

Address patient’s airway, breathing, and circulatory status (ABCs).

Avoid excessive sedation.

May encounter osmotic agents (Mannitol), loop diuretics (Furosemide) to reduce ICP; IV steroid therapy to control brain edema.

NURS 320 (28 decks)

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