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NUR 370 Pathophysiology > Neurological Disorders > Flashcards

Neurological Disorders Flashcards

1
Q

What are the three essential components of the brain? What is the volume of the brain?

A

78% Brain tissue
12% Blood
10% Cerebro-spinal fluid (CSF)

1700 mL

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2
Q

What is regular ICP? What is considered increased ICP?

A
  • Usually this ranges from 3-15mmHg
  • Pressures greater than 20mmHg represent increased ICP *
  • In adults, prolonged ICP between 25 and 30mmHg are usually fatal
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3
Q

Cerebral Perfusion Pressure

A

Amount of blood flow from the systemic circulation to provide adequate perfusion to brain tissue

Approx. 50-70mmHg

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4
Q

Mean arterial pressure (MAP), include formula and range

A

The average pressure during the cardiac cycle

MAP = (SBP + 2(DBP))/3
Range of 10-110mmHg

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5
Q

What is needed for effective perfusion?

A

To maintain effective perfusion to the brain we need to manipulate MAP and ICP *
CPP= MAP - ICP

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6
Q

What are the risk factors for increased ICP?

A
  • Space occupying lesion
  • Tumour, blood, abscess
  • Cerebral infarction (ischemic stroke)
  • Obstruction to the outflow of CSF (hydrocephalus)
  • Ingested or accumulated toxins (medications)
  • Edema from cranial surgery or injury
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7
Q

How does the brain compensate for changes in ICP?

A
  • Displacement of CSF into the spinal canal
  • Reduction of blood volume
  • This alters brain metabolism and eventually leads to - hypoxia and ischemia
  • The last stage (and most lethal) is displacement of brain tissue.
  • This process is called herniation
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8
Q

What is brain herniation?

A
  • Occurs when the brain shifts across structures within the skull such as the falx cerebri, the tentorium cerebelli and the foraman magnum
  • Occurs late in the course of increased ICP
  • Always constitutes an emergency
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9
Q

Describe the autoregulation of cerebral blood flow in relation to systemic blood pressure

A
  • The automatic alteration in the diameter of the cerebral blood vessels maintains a constant blood flow to the brain
  • Under normal circumstances the body is able to regulate cerebral blood flow.
  • Systemic blood pressure decreases, cerebral vessels constrict to maintain constant flow
  • Systemic blood pressure increases, Cerebral vessels dilate to buffer the amount of blood entering the brain
  • With increases in ICP, autoregulation is lost
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10
Q

What is cerebral edema and what can it cause?

A
  • An increase in the fluid content of brain tissue
  • Causes an increase in extracellular or intracellular tissue volume after brain insult (trauma, tumour, ischemia, etc)
  • Its harmful effects are caused by distortion of the blood vessels, displacement of brain tissues, and eventual brain herniation
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11
Q

What is the blood-brain barrier? What molecules can pass through it? What processes disrupt it?

A
  • Endothelial cells line the blood vessels in the brain creating a semipermeable membrane
  • O2, CO2, H20 and glucose can simply pass
  • Electrolytes, dyes and organic substances pass more slowly
  • Toxic substances, plasma proteins, and other large substances cannot permeate through the BBB
  • Trauma, cranial surgery, or some tumours can disrupt the BBB; as a result, fluids can travel from the intravascular space to the extravascular space causing cerebral edema.
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12
Q

What are some early clinical manifestations of increased ICP? What are some late signs?

A

Early
Decreasing levels of consciousness (confusion, restlessness, lethargy)
Headache
Sensory deficits (changes in speech, sight)
Cranial nerve palsies
Motor weakness
Seizure
Dilated pupil (ipsilateral side of the lesion)

Late
Papilledema – swelling and hyperemia of the optic disc
Bilateral pupillary dilation and fixation
Hyperthermia followed by hypothermia
Impaired brain stem reflexes
Hemiplegia, posturing
Vomiting (projectile)

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13
Q

What components make up Cushing’s triad?

A
  • Increased SBP with widening pulse pressure
  • Bradycardia
  • Abnormal respiratory patterns
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14
Q

what are the three components of the Glasgow coma scale?

A
  • Eye opening
  • Verbal response
  • Motor response
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15
Q

What are the ABCs of management in nursing care for ICP?

A

Airway: Preventing hypoventilation, managing secretions
Blood pressure: Fluid management and medications
Calm
Decreasing stimulation and decreasing stress, Dim the lights
Elevate the head: 30 degrees facilitates venous outflow from the brain via gravity and CSF to drain into spinal canal
Eyes: Oculomotor nerve is first compromised with cerebral edema. When compressed, pupil dilates and becomes less reactive to light
Fluids and electrolytes: Close monitoring of fluid balance, Osmotic diuretics (hypertonic saline and mannitol) pulling fluid from swollen brain cells
Food: Increased caloric needs to fuel injured brain
Family: Providing informational support and involvement in care
Glasgow coma scale: Routine and accurate assessment
Hyperthermia: Managing fever
Hip flexion - Avoid
ICP Monitoring: Observation and assessment, identifying changes, and treating as appropriate

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16
Q

What are the most common causes of head injuries?

A

Falls
Motor vehicle crashes (MVC)
Sports related injuries
Gun shot wounds

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17
Q

What are scalp injuries?

A

Just referring to the skin injury, the scalp is extremely vascular and will bleed a lot when lacerated

Highly vascular
Complications include blood loss and infection

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18
Q

What are penetrating head injuries?

A
  • Caused by a break of the dura mater in the brain exposing cranial contents
  • Most penetrating injuries are life-threatening .
19
Q

What is a coup-contrecoup injury?

A

Injury at the point of primary impact against the skull and injury on side of the brain opposite from the movement of the brain within the skull

20
Q

What is a skull fracture?

A
  • Break in one of the bones forming the cranial portion of the skull
  • May damage brain tissue, vessels and/or membrane underneath the site of impact
21
Q

What are the different types of skull fractures?

A

Linear: Thin line, without splintering, depression, or distortion of bone
Depressed: Depression of the bone toward the brain; can injure the brain by crushing or bruising it
Basilar skull fractures: Fracture of the base of the skull
Manifestations include raccoon eyes, Battle’s sign (bruising behind ear), leaking of CSF (rhinorrhea – the nose or otorrhea – the ear)

22
Q

What is a concussion? Signs and Symptoms? Treatment?

A
  • Jarring injury of the brain which results in a disturbance of cerebral function
  • Also referred to as mild traumatic brain injury (mTBI)
  • Cannot be detected by x-rays, CT scans or MRI
  • Signs and symptoms include:headache, dizziness, vomiting, nausea, lack of coordination, difficulty balancing
  • Loss of consciousness is not a requirement of diagnosis – anything that causes jarring of the brain can cause a concussion
  • Treatment is bed rest followed by a slow transition to light activity
23
Q

What is 2nd injury syndrome?

A

Second impact syndrome – a 2nd concussion occurs before the first has healed
Rapid and severe brain swelling

24
Q

What are the different types of intracranial hemorrhage?

A

Types of bleeds

  • Epidural
  • Subdural
  • Subarachnoid
  • Intracerebral
  • Intraventricular
25
Q

What is a epidural hematoma?

A
  • Bleeding between dura and the inner surface of the skull
  • Compresses dura mater
  • Most commonly the result of torn arteries – MMA (mini meningeal artery)
  • Often patient may be unconscious at the scene, followed by a brief lucid interval, then a subsequent LOC
  • Medical emergency - least common, but most significant
26
Q

What is a subdural hematoma?

A
  • Blood in the subdural space
  • A result of tearing of veins
  • Onset of symptoms may be slower as a result of venous source
    Classified as:
  • Acute – within 48 hours of injury
  • Subacute – within 2 to 14 days after injury
  • Chronic – weeks or months after minor head injury (very slow bleeding)
27
Q

What is a subarachnoid hemorrhage?

A 
Bleeding in the subarachnoid space
May be a result of: 
a traumatic force
a ruptured cerebral aneurysm
an arteriovenous malformation (AVM)
28
Q

What is an intracerebral hemorrhage?

A

Bleeding within the brain tissue itself

Can be a result of traumatic injury, aneurysm AVM, hypertensive injury to blood vessel walls

29
Q

What is an intraventricular hemorrhage?

A

Bleeding into the ventricles
May result from trauma or stroke
More common in infants

30
Q

What are the different types of stroke?

A

Ischemic (83%)
Caused by thrombotic or embolic blockage of cerebral vessels that stop blood from flowing to cerebral tissue
Sudden impairment of cerebral circulation in one or more blood vessels supplying the brain
Can affect large or small vessels

Hemorrhagic (17%)
Caused by ruptured vessel and bleeding into the brain tissue or subarachnoid space

31
Q

What are the different types of ischemic strokes, explain? What are the risk factors?

A

Thrombotic strokes
Atherosclerosis causes fatty deposits and plaque formation this leading to arterial stenosis, platelet adhesion and ultimately vessel lumen obstruction
Common site of thrombus formation is at the bifurcation of the common carotid artery int eh the internal and external carotid arteries

Embolic strokes
Common embolus is plaque
Embolus forms outside of brain, then detaches and travels through the cerebral circulation where it lodges in and occludes a cerebral artery

Risk factors include:
Chronic atrial fibrillation, prosthetic heart valves and endocarditis

32
Q

What is the pathophysiology of ischemic stroke?

A

Brain is extremely sensitive to blood supply and is perfused at the expense of less vital organs
Hypoxia leads to cerebral ischemia and temporary neurologic deficits or irreversible damage depends on how long the blood was restricted
- The extent of infarction depends on
- The location of the occluded artery
- The size of the occluded artery
- The adequacy of collateral circulation

Cell death and permanent changes can occur within 3 to 10 minutes

33
Q

What is a primary neuronal injury?

A

Cells in the centre of stroke area (core ischemic zone) die almost immediately

34
Q

What is a penumbra?

A

Zone of hypoperfusion around the infarcted area

Depends on the amount of collateral circulation present

35
Q

What is hemorrhagic stroke?

A

Rupture of a cerebral vessel causing bleeding into brain tissue
Often secondary to hypertension
Most common after age 50
Hemorrhage volume is the most important predictor of outcomes
Effects depend on the site and extent of bleeding

36
Q

What is the pathophysiology of hemorrhagic stroke?

A
  • Sites where blood vessels have weakened may lead to rupture and bleeding into the surrounding tissue
  • Brain tissue can become compressed producing ischemia, increased ICP and necrosis of tissue
  • Cerebral edema develops and can take up to 2 weeks to resolve.
  • Leading causes of weakened blood vessels are aneurysms and AVMs
37
Q

What are the risk factors for stroke?

A 
Hypertension!
Cardiovascular disease and atrial fibrillation
Diabetes mellitus
Immobility
Prior stroke, carotid stenosis, history of TIAs
Stress
Hyperlipidemia
Cigarette smoking
Heavy alcohol consumption
Cocaine use
High-estrogen contraceptive combined with hypertension
Advancing age
Family history of stroke
38
Q

What are the general clinical manifestations of stroke?

A 
Headache
Vomiting
Seizures
Changes in mental status
Motor changes
Communication
39
Q

What are the clinical manifestations of ischemic stroke?

A

Transient hemiparesis, loss of speech, and hemisensory loss

Develops over minutes to hours or days

40
Q

What are the clinical manifestations of hemorrhagic stroke?

A

Occurs rapidly, typically whilst awak
Severe occipital and nuchal headaches
Vertigo or syncope
Paresthesias and transient paralysis

41
Q

What are the effects after stroke?

A

Hemiparesis (weakness) or hemiplegia (paralysis on one side of the body)
Aphasia – deficit in the ability to communicate
Wernicke’s: speech comprehension
Broca’s: speech production
Dysarthria – imperfect articulation
Dysphagia – difficulty swallowing
Apraxia – difficulty making skilled movements
Visual changes – depth and visual perception, homonymous hemianopia (visual loss in the same half of the visual field of each eye)
Horner’s syndrome – paralysis of the sympathetic nerves to the eye
Agnosia – inability to recognize familiar objects
Unilateral neglect – inability to respond to stimulus on the contralateral side
Sensory deficits
Behavioural changes
incontinence

42
Q

What are the management strategies of a stroke?

A

Identify stroke early
Maintain cerebral oxygenation – patent airway, elevate head, oxygen
Restore cerebral blood flow (ischemic stroke) – thrombolytic therapy
Prevent and manage complication – bleeding, cerebral edema, stroke recurrence, aspiration
Rehabilitation (look at functional deficits and find ways to improve their quality of life)

43
Q

What is a transient ischemic attack?

A

Sudden, brief episodes of neurologic dysfunction caused by temporary, focal cerebral ischemia
Recovery is complete – most TIAs last 5-20 minutes
OFTEN SERVES AS A WARNING SIGN OF AN IMPENDING STROKE
1/3 of all people with untreated TIAs experience a stroke within 5 years

44
Q

Describe the pathophysiology, manifestation and management of TIAs

A

Pathophysiology
Similar to ischemic stroke, only transient

Manifestations
Develop based on the area of the brain affected

Management
Prevent progression of the TIA into a stroke
Determine the cause
Identify and decrease modifiable risk factors

NUR 370 Pathophysiology (3 decks)

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