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

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
Secondary Prevention: What medications could you use to prevent another stroke?
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
Circle of Willis
provides an alternative route for blood flow when one of the communicating arteries is obstructed.
27
Intracranial aneurysm may result from
``` arteriosclerosis congenital abnormality trauma inflammation cocaine ```
28
Intracranial Aneurysm
most occur in or near the circle of willis | 20-25% of cases.... more than one
29
Intracranial Aneurysm: Pathophysiology
no pathologic mechanism exists
30
Intracranial Aneurysms can be classified on shape and form:
1. saccular aneurysms | 2. fusiform aneurysms
31
Saccular aneurysms
result from congenital abnormalities | highest incidence of rupturing or bleeding 20-50 y.o.
32
Fusiform aneurysms
giant aneurysms | result of diffuses arteriosclerotic changes.. mostly found terminal portion of internal carotid arteries
33
Clinical Manifestations of Intracranial Aneurysms
- often asymptomatic - first indication is an acute subarachnoid hemorrhage, intracerebral hemorrhage or both. - CN III, IV, V, and VI are most often affected
34
Treatment of intracranial aneurysm
surgical management
35
Subarachnoid Hemorrhage
blood escapes from defect or injured vessel into the subarachnoid space
36
Risk for Subarachnoid Hemorrhages include:
Existing intracranial aneurysm Existing intracranial arteriovenous malformation Prior head injury HTN
37
Pathophysiology of Subarachnoid Hemorrhages
- 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
Clinical Manifestations of Subarachnoid Hemorrhages: Leaking Vessel
Headache Changes in mental status or LOC N/V Focal neurologic effects
39
Clinical Manifestations of Subarachnoid Hemorrhages: Ruptured Vessel
``` 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
Treatment of Subarachnoid Hemorrhages are directed at
Controlling ICP Preventing ischemia and hypoxia of neural tissues Preventing rebleeding episodes
41
Subarachnoid Hemorrhages Treatment
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.