Neuro week 2 Flashcards
(152 cards)
1
Q
Coma
A
Unarousable unresponsiveness, no purposeful responses to internal or external stimuli
2
Q
Akinetic mutism
A
state of unresponsiveness to the environment in which the patient makes no voluntary movement
3
Q
persistent vegitative state
A
unresponsive patient resumes sleep-wake cycles after coma but is devoid of cognitive or affective mental function
4
Q
minimally conscious state
A
inconsistent but reproducible signs of awareness
5
Q
Locked-in syndrome
A
lesion affecting the pons and results in paralysis and the inability to speak, but vertical eye movements and lid evaluation remain intact and are used to indicate responsiveness
6
Q
Clinical manifestations for altered level of consciousness
A
Occur along a continuum, and the clinical manifestations depend on where the patient is on the continuum.
Initial alterations = subtle behavioral changes, such as restlessness or increased anxiety. The pupils, normally round and quickly reactive to light, become sluggish (response is slower)
As the patient’s state of alertness and consciousness decreases, changes occur in the pupillary response, eye opening response, verbal response, and motor response.
As the patient becomes comatose, the pupils become fixed (no response to light). The patient in a coma does not open the eyes to voice or command, respond verbally, or move the extremities in response to a request to do so
7
Q
Altered level of consciousness: assessment
A
evaluation of mental status, cranial nerve function, cerebellar function (balance, coordination), reflexes, and motor/sensory function
8
Q
Altered level of consciousness: diagnostics
A
GCS CT Perfusion CT MRI MRS EEG PET SPECT
9
Q
Altered level of consciousness: labs
A
BG electrolytes serum ammonia Liver function tests BUN serum osmolality prothrombin partial thromboplastin etc
10
Q
Altered level of consciousness: medical management
A
nutritional support, adequate O2 and perfusion, circulation
11
Q
Go review and take notes on slide 4 “protecting the patient”
A
you may already know a lot of these things that is why i am not putting it in here
12
Q
Head injury: focus
A
prevention (seatbelt, helmet, etc.)
13
Q
Primary head injury
A
Initial damage (concussion, contusion, laceration, torn blood vessel)
14
Q
Secondary head injury
A
Ensuing hours or days after the injury, resulting in cerebral edema, ischemia, seizures, infection, hyperthermia, hypovolemia, hypoxia
15
Q
Skull fractures: simple, comminuted, depressed, basilar
A
simple: break in continuity
Comminuted: more than 2 pieces
Depressed: compressed onto brain tissue
Basilar: back of head area
16
Q
What does a patient with a skull fracture generally look like?
A
Depends on severity. Confused, forgetful, not as sharp as they used to be.
17
Q
What do skull fractures frequently produce?
A
Hemorrhage from the nose, pharynx, or ears, and blood may appear under the conjunctiva. You may also note an area of ecchymosis that may be seen over the mastoid (Battle sign) develop 12-24 hours after injury.
18
Q
When might a basilar skull fracture be suspected?
A
suspected when cerebrospinal fluid (CSF) escapes from the ears (CSF otorrhea) and the nose (CSF rhinorrhea). A halo sign (a blood stain surrounded by a yellowish stain) may be seen on bed linens or on the headdressing and is highly suggestive of a CSF leak
19
Q
Why is drainage of CSF a serious issue
A
meningeal infection, abscess formation, and osteomyelitis can occur if organisms gain access to the cranial contents via the nose, ear, or sinus through a tear in the dura
20
Q
Skull fracture: assessment
A
close observation, do not blow nose
21
Q
Skull fracture: something the nurse should remember to do
A
keep HOB at 30 or above to reduce ICP and promote spontaneous close of the leak
22
Q
Concussion
A
(also referred to as a mild TBI) involves an alteration in mental status that results from trauma and may or may not involve loss of consciousness.
23
Q
Concussion: how long does it last and what are the s/s
A
no longer than 24 hours and may include symptoms such asheadache, nausea, vomiting, photophobia (sensitivity to light), amnesia, and blurry vision
24
Q
Concussion: treatment
A
observing the patient for symptoms, including headache, dizziness, lethargy, irritability, anxiety, photophobia, phonophobia (fear of sound or of speaking aloud), difficulty concentrating, and memory difficulties.
The occurrence of these symptoms after the injury is referred to aspostconcussive syndrome
25
Contussion
more severe than concussion; bruising of brain with possible surface hemorrhage
26
Contussion: s/s
patient unconscious for more than few seconds or minutes
-- may lie motionless, faint pulse, shallow respirations, cool, pale skin
-- may be aroused with effort but soon slips back into unconsciousness
27
Diffuse axonal injury
widespread damage to axons in the cerebral hemispheres, corpus callosum, and brainstem. It can be seen with mild, moderate, or severe head trauma.
28
Diffuse axonal injury: s/s
- The patient experiences immediate coma, global cerebral edema, decorticate and decerebrate rigidity, or posturing
29
Decoricate
posturing involves abnormal flexion of the upper extremities and extension of the lower extremities and indicates damage to the upper midbrain;
30
Decerebrate
posturing involves extreme extension of the upper and lower extremities and indicates severe damage to the brain at the lower midbrain and upper pons
31
Intracranial hemorrhage: Epidural hematoma
symptoms are caused by expanding hematoma
Momentary loss of consciousness then will become lucid – CSF trying to compensate and regain hemostatsis.
If not – sudden signs of compression appear – deteriorates rapidly. EXTREME emergency – burr holes to decrease pressure
32
Intracranial hemorrhage: Subdural hematoma
Collection of blood between dura and brain
a. acute (24-48)
b. subacute (48 hours-2 weeks after injury)
change in LOC, pupils reaction, hemiparesis, gait disturbances, headache, aphasia, AMS, agitation
33
Intracerebral hemorrhage: solution
decompressed caniotomies
34
Brain injury management
A patient with a head injury is presumed to have a cervical spine injury until such injury is ruled out; therefore, immobilization of the spine via cervical collar, spinal backboard, and the avoidance of movement is essential.
35
TBI focused assessment
a. ALOC
b. Pupillary abnormalities
c. Sudden onset neuro deficits
d. changes in vitals
e. changes in vision, hearing and sensory functions
f. headaches
g. seizures
36
Treatments to prevent secondary brain injury
stabilization of CV and respiratory function to maintain adequate cerebral perfusion, control of hemorrhage and hypovolemia, and maintenance of optimal ABG
37
ICP: Monro-Kellie hypothesis
because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others. Due to this limited space, the brain compensates by moving around CFS, increase the absorption or decreasing its production, or decreasing blood volume. If these compensations were not made, ICP would rise
38
Normal ICP
5 - 15
39
When does treatment to correct ICP begin
treatment begins at 20
40
Early signs of increased ICP
HA, N/V, behavior change (restless, disorientation)
Change in LOC.
Agitation
Slowing of speech
Delay in response to verbal orders
Any sudden condition such as restlessness, confusion, increased drowsiness has neurological significance.
41
How might you assess someone if you were worried about increased ICP?
GCS, sternal rub, nail bed stimulation
42
increased ICP: priority intervention
airway, restoring neuro function, HOB 30 or more, fluid restriction
43
increased ICP: medications used/not used
Used: Mannitol, hypertonic solutions
NO: hypotonic solutions (0.45% NS)
44
increased ICP: assessment
Lumbar puncture is avoided in patients with increased ICP, because the sudden release of pressure in the lumbar area can cause the brain to herniate
45
Late signs of increased ICP
Comatose
Decreased rr and pulse
Increased temp., BP, and pulse pressure
Fluctuating pulse
46
Management of ICP
```
Osmotic diuretics
Fluid restriction
Draining CSF
Control fever
Maintain systemic BP and oxygenation
Reduce metabolic demands
HOB 30+
Neck stays aligned
```
47
How can a nurse reduce metabolic demands?
dim lights, decrease stimulation, bed rest, anxiolytics, cluster cares
48
What is the primary hormone with the posterior pituitary gland?
ADH (vasopressin) --> think fluid balance with this hormone
49
HYPO-ADH =
diabetes insipidus (HIGH AND DRY)
50
Hypo-AHD (diabetes insipidus): manifestations
```
peeing
weak, thready pulse
decrease skin turgor
dizzy, low BP
hemoconcentration - hypernatremia
```
51
Hypo-ADH (diabetes insipidus): treatment
Need to replace vasopressin using desmopressin
Thiazide diuretic to help stimulate vasopressin
DO NOT RESTRICT FLUID
52
Hyper-ADH =
SIADH (too much ADH)
53
Hyper-ADH (SIADH): manifestations
```
Reabsorbing more water
Bounding pulse
Increase BP
HA
Edema
USG - 1.030 (dark, concentrated)
Hemodilution - severe hyponatremia
```
54
Hyper-ADH (SIADH): tx
```
I&O
Daily weight
cognition
HOB flat to promote venous return
Fl. restriction
Furosemide only is Na is > 125
```
55
What is an indication that lasix should NOT be given
Na+ less than 125
56
Intracranial surgery: craniotomy
involves opening the skull surgically to gain access to intracranial structures
57
Bone flat
– remove portion of skull; allows brain to swell
58
Burr hole
drill into brain to relieve presssure
59
Types of intracranial surgery
Supratentorial
Infratentorial
Transsphenoidal
60
Nursing interventions: Supratentorial
Maintain head of bed elevated at 30 degrees, with neck in neutral alignment
61
Nursing interventions: Infratentorial
Maintain neck in straight alignment
Avoid flexion of the neck to prevent possible tearing of the suture line.
62
Nursing interventions: Transsphenoidal
Maintain nasal packing in place and reinforce as needed.
Instruct patient to avoid blowing the nose.
Provide oral care according to institutional procedure.
Keep HOB elevated to promote venous drainage
63
What are possible complications of manipulation of the pituitary gland that you might see with a transsphenoidal intracranial surgery
CSF leak, visual disturbances, post op meningitis, SIADH
64
Intracranial surgery: postop nursing management
Reducing cerebral edema (dexamethasone)
Pain relief
Prevent sz. (phenytoin, levetiracetam)
Monitor ICP
65
Complete spinal cord lesion
total loss of sensation and voluntary muscle control below the lesion
66
What are the most common spinal cord injuries?
C5 & 6
T12
L1
67
Primary vs secondary spinal cord injuries
Primary: result of initial trauma
Secondary: can be reverses during 4-6 hours after. Results from nerve fibers swell and disintegrate leading to hypoxia, ischemia, edema, hemorrhage
68
What are we concerned about the higher the spinal cord injury?
respirations
69
Acute complications SCI: spinal shock
Depression of reflex activity in spinal cord below the level of injury
70
What may be affected with spinal shock, and how is this treated?
bowel and bladder reflexes may be impacted, which can cause bowel distention and paralytic ileus. This is treated with NG tube to decompress the intestine.
71
Acute complication of SCI: neurogenic shock
Loss of ANS below level of lesion
72
Neurogenic shock manifestations
Vital organs are impacted, leading to hypotension, bradycardia, decreased cardiac output, venous pooling in extremities, peripheral vasodilation, warm skin.
Patient does not perspire on the paralyzed portions of the body (close observation for early detection of fever)
73
Acute complication of SPI: DVT
Related to immobility
- measure thigh and calf daily
- anticoagulation when brain injury and other bleeding have been ruled out
74
Acute complication of SCI: orthostatic hypotension
First 2 weeks following SCI - unstable and low BP due to loss of reflex vasoconstriction
- lesions above T7
- slow position changes
- compression stockings and abdominal binders all times
75
SCI Emergency Management: ASIA Impairment scale
go look at this slide 22
76
Autonomic Dysreflexia
Medical emergency -- exaggerated autonomic response to stimuli that are harmless in normal people.
77
When might autonomic dysreflexia manifest, and how does it manifest?
```
Occurs after spinal shock has resolved with injuries above T6.
HA
Paroxysmal hypertension
Profuse diaphoresis
Nausea
Nasal congestion
Bradycardia
```
78
What can trigger autonomic dysreflexia?
distended bladder
constipation
stimulation of the skin
79
Autonomic dysreflexia: interventions
```
HOB raised
Bladder mt
Constipation assessed
Skin assessed
Hydralazine IV
```
80
What is a seizure
episodes of abnormal motor, sensory, autonomic, or psychic activity (or a combination of these) that result from sudden excessive discharge from cerebral neurons
81
What is the active phase of a seizure called
Ictal
82
Status epilepticus
Someone who can not stop seizing
83
What are 3 things needed for a seizure?
1. Excitable neurons
2. increase in excitatory glutaminergic activity through recurrent connections to spread the discharge
3. Reduction in activity of normal inhibitory GABA projection
84
Causes of seizures
```
Cerebrovascular disease
Hypoxemia of any cause, including vascular insufficiency
Fever (childhood)
Head injury
Hypertension
CNS infections
Metabolic and toxic conditions (e.g., kidney injury, hyponatremia, hypocalcemia, hypoglycemia, pesticide exposure)
Brain tumor
Drug and alcohol withdrawal
Allergies
```
85
Focal seizure
Partial seizure
With or without consciousness
In one spot of brain
May not even notice them
86
Generalized seizure: Tonic-clonic
Generalized seizures that affect the entire brain; they begin with rigidity (tonic phase), followed by repetitive clonic activity of all extremities characterized by stiffening or jerking of the body.
87
tonic seizures
characterized by muscle stiffening, dilation of the pupils, and altered respiratory patterns; the body becomes stiff and the person may fall backward. The seizure usually lasts less than 1 minute, and recovery is rapid.
88
Clonic seizure
Characterized by jerking movements, which involve muscles on both sides of the body
89
Absence seizures
Short episodes of staring and loss of awareness
90
Atonic seizures
Sudden loss of muscle tone, resulting in falls or a “drop” to the ground, with rapid recovery
91
Myoclonic seizures
Characterized by jerking (myoclonic) movements of a muscle or muscle group, without loss of consciousness
92
What are the types of epilepsy?
Focal and generalized
93
Focal seizure - retains awareness
There is no impairment of consciousness, similar to simple partial seizures, may have movement of body parts, may experience an aura.
94
Focal seizures - altered awareness
There is impairment of consciousness, similar to complex partial seizures, this can spread to both hemispheres of brain.
95
Where in the brain is a generalized seizure happening
both hemispheres
96
What are the types of generalized seizures
```
Tonic-clonic
Tonic
Clonic
Absence
Atonic
Myoclonic
```
97
What is important to keep in mind with someone who has received long-term anticonvulsant therapy
These patients are at increased risk for fractures resulting from bone disease (osteoporosis, osteomalacia, and hyperparathyroidism), which is a side effect of therapy.
so...
During seizure, the patient is protected from injury with sz. precautions and monitored closely.
98
What test will be performed of someone having sz or someone suspected of having sz?
EEG - electrodes on head
99
What is important information to gather of someone who is experiencing sz?
Hx. clot, stroke, medication, stress, alcohol use, withdrawal, last alcoholic drink, blood thinners, etc.
100
If you know someone is being admitted for sz., how will you prepare the room?
```
Privacy provided as soon as possible
Loose clothing
2 or 3 side rails up
Bed lowest position
Bed rails padded
Pillow under head
O2 tubing
O2 and suction available
```
101
Keppra (Levetiracetam): what?
anticonvulsant
102
Keppra (Levetiracetam): dose-related sfx
Somnolence, dizzy, fatigue
103
Keppra (Levetiracetam): toxic effects
unknown
104
Seizures: gero considerations
Increased incidence
Treat underlying cause
Absorption, distribution, metabolism and excretion of medications are altered in the older adult as a result of age-related changes in renal and liver function
105
Why might there be an increased incidence of seizures among the gero population
medication, head injury, dementia, infection, alcoholism, and aging
106
Triggers for migraine
Foods that contain tyramine, such as chocolate, cheese, coffee, dairy products
Dietary habits that result in long periods between meals
Menstruation and ovulation (caused by hormone fluctuation)
Alcohol (causes vasodilation of blood vessels)
Fatigue and fluctuations in sleep patterns
107
Migraine headaches: teaching
Headache diary
Stress management and lifestyle changes
Correct pharm management
--> acute therapy and prophylaxis to include medication regiment and sfx
comfort measures (dark place, quiet)
108
Surgical management of seizures
Lobectomy
Resection surgery
Stimulator
109
Bacterial meningitis infectious agents
Streptococcus pneumoniae and Neisseria Meningitidis
110
Bacterial meningitis risk factors
```
Tobacco use
Mastoiditis
Immunosuppressed
Young or Old
Low GCS
```
111
Bacterial meningitis: treatment
Antibacterial (penicillin, IV dextramethasone), anticonvulsants
112
Bacterial meningitis: clinical manifestations
```
HA
Fever
Stiff neck (nuchal rigidity)
ALOC
Positive Kernig sign
Positive Brudzinski sign
```
113
What does the nurse recognize as expected findings in a client with bacterial meningitis
The nurse recognizes that with fever, tachycardia and tachypnea are expected.
If bradycardia and decreased RR are seen, the nurse should consider ICP as an etiology for the decreased HR and RR.
114
What is a positive Kernig sign
When the patient is lying supine with the hip flexed to a 90-degree angle, resistance to passive extension of the knee is a positive Kernig sign
This pain is caused by inflammation of the meninges and spinal roots.
115
What is a positive Brudzinski sign
When the patient’s neck is flexed (after ruling out cervical trauma or injury), flexion of the knees and hips is produced; when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity
116
What meningitis is more common and what one is more deadly
common - viral
| deadly - bacterial
117
What is common with viral meningitis?
HIV and children
118
Clinical manifestations of viral meningitis
```
HA
low grade fever
stiff nech
photophobia
malaise
URI
NO ALOC or sz.
```
119
What is the biggest difference between viral and bacterial meningitis
with viral, you will see no sz. and no AMS but you will see that with bacterial
120
Viral meningitis treatment
HOB 30
dark quiet room
isolation (both types)
121
Encephalitis
acute inflammation of brain tissue
122
Herpes Simplex Encephalitis impacts what
olfactory and trigeminal nerves - common pathways
123
Herpes Simplex Encephalitis: s/s
HA, Fever, Stiff neck & confusion
124
Herpes Simplex Encephalitis: tx
Acyclovir
125
Arboviral encephalitis - cause
misquito
126
Arboviral encephalitis: s/s
Flu-like, can have HA and nuchal rigidity, SIADH, rash
127
What is Bell's palsy
facial paralysis
128
Bell's Palsy: s/s
```
increased lacrimation
Painful sensations in the face
Ear pain
Speech difficulties
Smiling
– absence of wrinkling on the forehead
Mask-like face
```
129
Bell's palsy: treatment
Corticosteroid therapy
Heat to help blood flow
Eye ointment --> lid can not close because they can not blink
130
Multiple Sclerosis
Destruction of the myelin that surrounds certain nerve fibers about brain and spinal cord – therefore impairing impulse
131
Multiple Sclerosis: primary symptoms
```
Unilateral visual loss
Fatigue
Depression
Weakness
Limb numbness
Difficulty with coordination
Loss of balance
Pain (nerve fibers open)
```
Think fatigue and loss of coordination d/t destruction of myelin --> impairs impulses
132
MS: treatment
Interferon beta-1a and interferon beta-1b
Promote physical mobility (rest right before they become too fatigued, no strenuous)
Bowel/bladder training
Coping
133
Myasthenia Gravis: what
Autoimmune disorder -- muscle weakness of voluntary muscles
134
Myasthenia Gravis: s/s
Diplopia
Weakness with muscles in the face/throat
Dysphonia
Motor Dysfunction only – no effect on sensation or coordination
Muscle weakness, intensifies with activity, improves with rest
135
Myasthenia Gravis: Treatment
```
Acetylcholinesterase test – diagnose
Ice pack over eyes for 2 minutes
Pyridostigmine bromide
Corticosteroids
Caution at dentist office with Novocain
```
136
What is the neurotransmitter that plays a big role in myasthenia gravis
acetacholine
137
Nursing management: MG
Meals coincide with the peak anticholinesterase medications
Patient must sit up right during meals
Soft foods
Suction available
Supplemental feedings
Impaired vision – tape/patch eye closed
Avoid stress factors – emotional stress, infections (respiratory), vigorous exercise, high environmental temperatures
Rest throughout the day
138
Myastenic crisis
Temporary exacerbation of s/s
| Respiratory weakness
139
Cholinergic crisis
Muscle weakness
Respiratory impairment
Excessive pulmonary secretions
140
Guillain-Barre Syndrome
Autoimmune attack on peripheral nerve myelin
Rapid, acute, segmental demyelination of peripheral nerves
Typically happens about 2 weeks after an infection
141
What are big characteristics of Guillain-Barre Syndrome?
Dyskinesia, Hyporeflexia, and paresthesia
142
Guillain-barre syndrome s/s
Muscle Weakness
Sensory impairment
Depending on how far up the symptoms go – complications
Does not affect cognitive function or LOC
143
Guillain-Barre Syndrome: tx
IVIG
| Plasmapheresis
144
Guillain-Barre Syndrome: nursing considerations
```
medication ER
Monitor respiratory function
Physical Mobility
Adequate Nutrition
Improving Communication
Fear and Anxiety – include Family
```
145
Parkinson's disease
Slowly progressing neurological Movement
Decreased levels of dopamine – leaves more excitatory neurotransmitters
Symptoms appear after 60% neurons are lost
146
Parkinson's s/s
```
Tremor
Rigidity
Akinesia/Bradykinesia
Postural disturbances
Uncontrolled sweating, orthostatic hypotension, urinary retention, constipation
Cognitive changes
Sleep disturbances
```
147
Parkinson's treatment
Levodopa with Carbidopa
148
Nursing management for parkinson's disease
```
Improve mobility
Self-care
Bowel Elimination
Nutrition & Swallowing
Communication
Coping
```
149
Alzheimers disease
most common type of dementia. This disease is a progressive, irreversible, degenerative neurologic disease that begins insidiously and is characterized by gradual losses of cognitive function and disturbances in behavior and affect
150
Alzheimers disease s/s
Forgetfulness
Subtle memory loss
Personality changes
151
Alzheimers: tx
Cholinesterase inhibitors - donepezil hydrochloride (Aricept), rivastigmine tartrate (Exelon), and galantamine hydrobromide (Reminyl), enhance acetylcholine uptake in the brain, thus maintaining memory skills for a period of time.
Memantine (Namenda) is an N-methyl-D-aspartate receptor antagonist that is thought to interfere with glutaminergic overstimulation.
152
Alzheimers: nursing management
Safety
Support
Self-care
Reducing Anxiety/Agitation
