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Med Surge 3 > Final Exam- Neuro > Flashcards

Final Exam- Neuro Flashcards

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1
Q

Nervous systems two major parts

A
  1. Central nervous system - brain and spinal cord
  2. Peripheral nervous system - cranial nerves, spinal nerves, autonomic nervous system
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2
Q

In the brain you have…

A

The cerebrum: divided into frontal, temporal, parietal, and occipital lobe
The brain stem: Midbrain, ponds, medulla
The cerebellum

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3
Q

Brain stem is responsible for

A

respirations, heart rate, BP, sleep/wakefulness, reflex, balance, consciousness. (Basically everything that allows you to function)

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4
Q

Functions of each of the lobes in the brain

A

Frontal: concentration, abstract thought, information storage or memory, and motor function. It contains Broca area, which is in the left hemisphere and is critical for motor control of speech

Temporal: auditory receptive areas and plays a role in memory of sound and understanding of language and music.

Parietal: analyzes sensory information, is essential to a person’s awareness of body position in space, size and shape discrimination, and right–left orientation

Occipital: visual interpretation and memory

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5
Q

Structures protections the brain

A

The meninges
1. Dura mater - thick fibrous protective layer
2. Arachnoid mater - thin (looks like spider web) CSF in this space
3. Pia mater - covers entire brain surface for extra protection

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6
Q

Cerebral Spinal fluid…
Cerebral circulation…
Blood-Brain barrier
The spinal cord…

A

Cerebral spinal fluid Should always be clear, fluid is very important in maintaining immune and metabolic function in the brain, it protects brain and spinal cord

Cerebral circulation gives constant supply of O2 that the brain needs

Blood brain barrier: acts as a gate keeper keeping harmful substances from entering the brain

The spinal cord is the connection between the brain the the periphery, it is about 18in long and as thick as a finger

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7
Q

How many pairs of spinal nerves are there

A

31 pairs

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8
Q

Autonomic nervous system

A

Regulates the activities of internal organs (acts independently of the bodies consciousness)
Sympathetic: wide spread, fight or flight response
Parasympathetic: specific localized response, rest and digest response

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9
Q

Akinetic Mutism:

A

pt lacks ability to move or speak, unresponsive to the environment around them but may open their eyes

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10
Q

Persistent vegetative state:

A

devoid of cognitive function

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11
Q

Minimally conscious state

A

Occasional signs of awareness

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12
Q

Locked-in syndrome:

A

Inability to move or respond except for eye movements due to a lesion effecting the pons (pt is aware)

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13
Q

Diagnostics: ALC

A

Glasgow coma scale
CT
MRI
EEG (number one indicator of brain death)

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14
Q

Glasgow coma scale

A

Mild: 13-15
Moderate: 9-12
Severe: 3-8
“Less than 8 we intubate”

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15
Q

Medical Management: ALC

A

Airway, circulatory status, ensure adequate perfusion to the brain, IV fluids, meds, nutritional support, reverse the cause

The primary nursing dx is ineffective airway clearance

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16
Q

Decorticate vs Decerebrate

A

Positioning due to painful stimulus such as needle stick due to injury to the spinal cord. Decerebrate is much worse.
Decorticate is arms to chest
Decerebrate is arms to side

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17
Q

Potential complications of ALC

A
  • Respiratory distress
  • Pneumonia
  • Aspiration
  • Pressure Ulcer
  • Venous Thromboembolism
  • Contractures (ROM exercises, Q2 turns, and splints help with that)
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18
Q

Normal ICP is…

A

0-15

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19
Q

Monroe Kellie hypothesis

A

There are three components; brain, blood, and CSF
If there is an increase in volume in one area, then there needs to be a decrease in volume in a different area to compensate for
This can happen in small ways too ie when you cough or sneeze

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20
Q

Cerebral edema causes there to be…

A

Decreased CSF production and flow

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21
Q

Cerebral profusion pressure must be between

A

70-100 or cell death will occur

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22
Q

Causes of increased ICP

A

TBI
Stroke
Brain tumor

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23
Q

Signs of increased ICP (Cushings triad)

A

Opposite of shock
1. Bradycardia
2. Hypertension (systolic)
3. Decreased RR

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24
Q

Other signs of increased ICP

A

• Changes in LOC
• Slowing of speech
• Decreased motor function
• Headache
• Seizures
• Vomiting
• Coma
• Babinski reflex
• Irregular RR
• Pupils fixed and dilated
• Nuchal rigidity

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25
Assessments for increased ICP
Neuro exam - pupils - GCS - Reflexes - VS - ICP
26
Nursing diagnostics/interventions: increased ICP
- Ineffective airway clearance – suction for no more than 15 seconds – we do not want them to cough - Ineffective breathing pattern o Hyperventilation causes increased CO2 and increases vasoconstriction - Inadequate cerebral tissue perfusion o Avoid hip flexion o Avoid rotation of the neck (may cause blockage of blood flow) o Have HOB 35-40 degrees
27
Complications/Priority problems: increased ICP
- Brain Stem Herniation- due to swelling of the brain - Diabetes Insipidus (if urine output is >200 ml/hr) o Major fluid and electrolyte replacement o Give desmopressin (synthetic vasopressin) - Syndrome of inappropriate antidiuretic hormone (SIADH) (decreased urine output) o Fluid restriction o Sodium becomes very diluted - Dehydration and Electrolyte imbalance
28
Assessments and Dx tools: increased ICP
- CT - MRI - Neuro assessment - Invasive ICP monitoring - Lumbar puncture to check for fluid in the spine
29
Pharmacological Tx: increased ICP
- Mannitol – diuretic to pull fluid off brain - Barbiturates (phenobarbital) - Anti seizure meds (Phenytoin) - Corticosteroids – helps with inflammation
30
Medical management: increased ICP
- Monitor ICP and cerebral O2 - Raise HOB - Low stimulus environment - Monitor Is and Os - Decrease cerebral edema - Maintaining Cerebral perfusion - Reducing CSF and intracranial blood volume
31
How to decrease cerebral edema
o by giving mannitol (osmotic diuretic) it dehydrates brain tissue and reduces cerebral edema. o If it is due to a brain tumor you may see decahedron given a corticosteroid. o Put on fluid restriction o Sedatives decrease brain activity which also helps decrease ICP
32
How to maintain cerebral perfusion
o Increased Cardiac Output from fluid or pressors o Keep above cerebral perfusion above 70
33
How to reduce CSF and intracranial blood volume
o Put drains in o Keep CO2 levels 30-35 to try and cause vasoconstriction o Barbiturates reduce O2 needed from the brain o Bring body temp down to decrease the O2 demand on the brain
34
Intracranial surgeries
- Craniotomy - Ventriculostomy drain - Burr holes
35
Types of ischemic strokes
- Large artery thrombosis - Small penetrating artery thrombosis (lacunar) - Cardiogenic embolism o Caused by AFIB pts - Cryptogenic - Other o Cocaine use o Vasospasms from migraine
36
Tx for ischemic stroke
- Thrombolytic therapy 3-4 hours from when someone is having symptoms to TPA (clot buster) o 10% of dosage IV bonus over 1 min and then the remaining dose is given over an hour - Aspirin/plavix - Anti coagulants o IV heparin o Sub Q lovenox - Thrombectomy - Angioplasty and stenting - Endovascular therapy - Elevate HOB to reduce ICP
37
Acute phase of recovery: ischemic stroke
- Ongoing frequent monitoring of all systems - Monitor for potential complications; swallowing problems, respiratory problems, signs and symptoms of decreased ICP, and meningeal irritation
38
TIA
Neurological deficits last less than one hr- Tx them like a stoke pt
39
Dx for stoke
- Ct scan within 25 min of presenting to the ER - MRI - Echo - EKG
40
Preventative Tx/Secondary prevention of TIA
- Health maintenance measures including a healthy diet, exercise, and the prevention and treatment of periodontal disease - Anticoagulants - Carotid endarterectomy - Antiplatelet therapy: aspirin, dipyridamole plus aspirin (Aggrenox), clopidogrel (Plavix) - "Statins" - Antihypertensive medications
41
Carotid Endarterectomy
- Main surgical procedure for TIA’s or mild stokes - Removal of arthrosclerotic plaque or thrombus from the carotid artery - Carotid artery stenting to keep artery open and maintain blood flow to the brain
42
Complications of carotid endarterectomy
- Monitor for hematoma at the site - Monitor BP high BP can lead to hematoma - Monitor for hyper profusion syndrome
43
Types of hemorrhagic strokes
- Intracerebral hemorrhage - monitored in ICU - Intracranial aneurysm - Arteriovenous Malformations - Subarachnoid hemorrhage - monitored in the ICU
44
Epidural Hemorrhage
 Tear of artery after skull fracture  Acute very rapid mental changes  Brief loss of consciousness  Crotralateral Hemiparesis or ipsilater pupil dilation
45
Subdural Hemorrhage
 Chronic: 2-14 days after head injury, subtle symptoms over time that cause confusion and ataxia  Acute: within 48hrs headache and focal deficits
46
Intracerebral Hemorrhage
 Rapid deterioration and focal deficits  Blood pools in tissue of brain there are many causes  Tx elevated BP and limit expansion of bleed
47
Subarachnoid Hemorrhage
 Cause by aneurysms or AV malformations  “Worst headache of my life”  ALC  Nausea, vomiting, nuchal rigidity
48
Clinical Manifestations of Hemorrhagic stroke Right sided vs left sided stroke
- Exploding headache - Early and sudden change in LOC - Vomiting - Right sided stoke o Weakness on the left side of the body o Left visual field deficit o Poor judgement, impulsive behavior, lack of awareness - Left sided stroke o Weakness on the right side of the body o Right visual field deficit o More slow and cautious behavior o Aphasia
49
Collaborative problems/Potential Complications of hemorrhagic stroke
- Vasospasm - Seizures - Hydrocephalus - Rebleeding - Hyponatremia
50
51
Tx of hemorrhagic stroke
- Decrease ICP - Slowly decrease BP (we need to keep perfusion to the brain) - Vi K (if they are on blood thinners) - Mannitol (to get fluid off) - Evacuate blood from the skull - Do not want a lot of visitors, pts need to rest May put in a ventricular ostomy
52
Contusion
brain is bruised and damaged in a specific area o Effects of injury peak at 18-36 hours o characterized by a loss of consciousness, stupor and confusion o Due to blunt trauma
53
Diffuse axonal injury
o Can occur from acceleration/deceleration injuries or shaken baby syndrome o Results from widespread shearing and rotational forces that produce damage throughout the brain to axons in the corpus callosum, cerebral hemisphere, and brain stem o Pt enters immediate coma o Pt will have Decorticate or Decerebrate positioning with global cerebral edema
54
Types of TBI
Primary: direct contact to the head/brain causing extra cranial injuries as well and Intercranial injuries Secondary: injury evolves over several days after the initial injury and results in inadequate delivery of nutrients and o2 to the cell
55
Basilar Skull fractures produce…
- bleeding from the nose, pharynx, or ears - blood may appear under the conjunctiva - Ecchymosis may be seen over the mastoid (battle sign) - Drainage of CSF from ears (otorrhea) and nose (rhinorrhea) suggest basal skull fracture
56
General Clinical manifestations of TBI
- ALC - Pupillary abnormalities - Altered or absent gag reflex - Neuro deficits - Change in VS (Cushings triad) - Hyper or hypothermia - Sensory, vision, or hearing impairment
57
Signs of post contusion syndrome
o Headache o Dizziness o Anxiety o Irritability o Lethargy
58
Acute/Subacute subdural hematoma
o Signs of increased ICP o Hemiparesis o Coma
59
Chronic subdural hematoma
o Severe headache o Personality changes o Mental deterioration o Focal seizures
60
Dx of TBIs
X-ray, CT, MRI, cerebral angiography
61
C4 spinal injury
C4- quadriplegic/tetraplegic, complete paralysis below the neck
62
C6 spinal injury
C6- partial paralysis of hands and arms as well as lower body
63
T6 spinal injury
T6- paraplegic paralysis below the chest
64
L6 spinal injury
L6- paraplegia paralysis below the waist
65
Clinical Manifestations of SCI
- Sensory and motor paralysis below the level of injury - Loss of bowl and bladder control - Loss of sweating and vasomotor tone - Reduction of BP - Pain in back or neck if pt is conscious - Decreased reflexes - Loss of sensation
66
Complications of SCI
- Bladder/bowel dysfunction - Respiratory (failure, PNA) - DVT - Pressure injuries - Orthostatic hypotension - Autonomic Dysreflexia
67
Neurogenic shock
Loss of sympathetic tone, causing relative hypovolemia. Occurs 30 min after a cord injury to T5 or above and lasts up to 6 weeks
68
Risk factors of Neurogenic shock
- SCI - Spinal anesthesia - Nervous system damage - Depressant action of medication - Hypoglycemia
69
Clinical manifestations of neurogenic shock
- Poikilothermia: Dry, warm skin - Bradycardia - Hypotension
70
Medical management of neurogenic shock
- Airway support - Fluids - Atropine (for bradycardia) - Vasopressors
71
Autonomic dysreflexia
a life-threatening emergency in pts with a spinal cord injury that causes a hypertensive emergency (harmless to ppl with out a SCI) Occurs after spinal shock has resolved A spinal cord injury at the T-6 or higher
72
Clinical manifestations of autonomic dysreflexia
- Pounding headache w paroxysmal hypertension - Profuse diaphoresis above the level of lesion - Nausea - Nasal congestion - Bradycardia
73
Causes of autonomic dysreflexia
- Distended bladder - Distention or contraction of visceral organs - Stimulation of the skin
74
Tx of autonomic dysreflexia
- Remove triggering stimuli - Place pt in sitting positing - Empty bladder with urinary cath - Mass in bowel is removed - Skin is examined for signs of irritation - Antihypertensives are given Can occur years after initial injury
75
Disaster Mitigation, Preparedness, Response, and Recovery
Mitigation Prevention and reduction of consequences of a disaster. Risks assessment, inspection, education. Preparedness Planning, training, and education for unavoidable disasters. Develop disaster action plan, identify evacuation route, developed a communication plan, disaster drill, supply kits Response Implement evacuations, search and rescue, triage Recovery Restoration, decreasing vulnerability to future disasters

Med Surge 3 (11 decks)

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