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NCLEX Preparation > The Nervous System > Flashcards

The Nervous System Flashcards

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1
Q

function of the occipital lobe

A

vision

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2
Q

function of the parietal lobe

A

perception, math, spelling, logic

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3
Q

function of temporal lobe

A

memory, language

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4
Q

Frontal Lobe

A

thinking, planning, organizing, problem-solving, emotions, behavioural control, personality.

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5
Q

function of the cerebellum

A

balance

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6
Q

Broca’s area function

A

expressive language

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7
Q

Wrenicke’s Area function

A

language, understanding spoken language.

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8
Q

components of the peripheral nervous system

A

cranial nerves, spinal nerves, and peripheral nerves.

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9
Q

function of the CSF

A

protects the brain and spinal cord from injury
provides nourishment to the brain
normal ICP of CSF is 5-15mmHg

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10
Q

Monroe-Kellie Hypothesis

A

The skull is riigid container filled with blood, brain, and CSF; if one increases, the other increases.

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11
Q

Causes of increased ICP

A

tumours, bleeding, hydranencephaly, and edema

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12
Q

Signs and Symptoms of increased ICP

A

headache; vomiting; changes in consciousness and orientation; drowsiness; thirst; decreased GCS; hypertonic; decerebrate; decorticate; hypotonic; flaccid; deceased reflexes; pupillary changes; nystagmus; papilledema; change in speech; shivering; confusion

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13
Q

Decorticate Positioning

A

damage to the mid-brain; flexion of arms towards the spinal cord; clenching fist; rigid muscles.

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14
Q

Decerebrate Positioning

A

damage to the deep brain and Pons. Involves extension of arms with flexion of the wrists and clenched fists; legs straight; rigid; head and neck arched back.

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15
Q

Functions of the Sympathetic Nervous System

A
  • dilates pupils
  • inhibits salvation
  • increases HR
  • dilates bronchi
  • inhibits peristalsis
  • glucose release
  • adrenaline and noradrenaline release
  • inhibits bladder
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16
Q

Functions of the Parasympathetic Nervous System

A
  • constricts pupils
  • stimulates salivation
  • decreases HR
  • constricts bronchi
  • stimulates peristalsis
  • bile release
  • stimulates intestines
  • constricts the bladder
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17
Q

Cranial nerve 1

A

Olfactory - sense of smell

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18
Q

Cranial nerve II

A

Optic - vision

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19
Q

Cranial nerve III

A

Oculomotor - eye movement

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20
Q

Cranial nerve IV

A

Trochlear - hearing

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21
Q

Cranial nerve V

A

Trigeminal - mastoid control; chewing

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22
Q

Cranial Nerve VI

A

Abducens - extra-ocular motor function of the eye

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23
Q

Cranial nerve VII

A

Facial (face and tongue control)

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24
Q

Cranial Nerve VIII

A

Vestibulocochlear - hearing and balance

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25
Q

Cranial IX

A

Glossopharyngeal – motor, parasympathetic, and sensory information from nose, mouth, and throat; enables swallowing.

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26
Q

Cranial Nerve X

A

vagus nerve – swallowing and speaking

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27
Q

Cranial Nerve XI

A

accessory nerve – supplies sternocleidomastoid and trapezius muscles

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28
Q

Cranial Nerve XII

A

hypoglossal – efferent nerve for tongue musculature.

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29
Q

Midazolam

A

Pharm. Class: Benzodiazepine; Anti-Anxiety Agent
Indications: anxiety
Onset: Rapid
Duration: 1-2 hrs

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30
Q

Alprazolam

A

Pharm. Class: Benzodiazepine
Indication: Anxiety
Onset: Intermediate
Duration: 6-12 hrs

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31
Q

Clonazepam

A

Pharm. Class: Benzodiazepine
Onset: Intermediate
Duration: 18-50 hrs

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32
Q

Lorazepam

A

Pharm. Class: Benzodiazepines
Indication: Anxiety; seizure
Onset: Intermediate
Duration: 2-6 hrs

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33
Q

Diazepam

A

Pharm. Class: Long-Acting Benzodiazepine
Indication: anxiety; MHSU
Duration: 20-50hrs

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34
Q

Phenytoin (Dilantin)

A

Pharm. Class: Anticonvulsant
Action: treats seizures; provides prophylaxis through blocking sustained high-frequency repetitive firing action potentials in the brain.
Therapeutic Level: 10-20mg/L
Considerations: May cause gingival hyperplasia; antacids can reduce effects on the body.

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35
Q

Acetaminophen

A

Pharm Class: NSAID; #1 fever control
Therapeutic Indication: antipyretic; non-opioid analgesia
Action: inhibits the synthesis of prostaglandins which leads to decrease in transmission of pain signals and fever response.
Considerations: 4g max daily dose; long-term 3g per day recommended; monitor liver function
Antidote: Acetylcysteine.

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36
Q

ASA

A

Pharm. Class: antipyretic; non-opioid analgesic
Indication: pain, arthritis, stroke, MI prophylaxis
Action: inhibits the production of prostaglandins which decreases ischemic symptoms of heart disease.
Considerations: Risk of bleeding (D/C within 5 days of surgery); caution with paediatric patients; may cause peptic ulcers; give with food.

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37
Q

Morphine

A

Pharm. Class: CNS depressant; opioid analgesia
Action: binds to opioid receptors in the brain to alter perception of pain while producing CNS depression.
Considerations: constipation; CNS depression; monitor HR, RR
Antidote: Naloxone.
Other Opioids: fentanyl, hydromorphone, morphine, oxycodone, oxycontin.

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38
Q

Signs and Symptoms of Basilar Skull Fracture

A
  • battle sign
  • raccoon eyes
  • cerebrospinal rhinnorhea
  • torn/non-torn dura
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39
Q

Battle Sign

A

Bruising over the mastoid process

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40
Q

Why wouldn’t you insert an NG tube on a patient with a basilar skull fracture?

A

you could insert the NG tube directly into the brain

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41
Q

Halo Test

A

testing rhinnorhea for presence of CSF halo around droplet on paper. Additionally, the presence of glucose would indicate CSF fluid.

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42
Q

Epidural Hematoma

A

dura pulled off the skull; rapid expansion of arterial blood between duramatter and skull.

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43
Q

Subdural Hematoma

A

dura attached; slow expansion of venous blood between arachnoid and dura.

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44
Q

Hydrocephalus

A

accumulation of CSF causes increase in ICP
Causes: tumour; hemorrhage; infection; congenital
Treatment:
- VP shunt (tube inserted to redirect csf to the urinary tract)
- External Ventricular Drain (drains CSF directly)

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45
Q

Optimal CSF pressure

A

5-15mmHg

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46
Q

Meningitis

A

inflammation of the spinal cord or brain, caused by virus or bacteria

47
Q

Signs and Symptoms of meningitis

A

Nucchal rigidity; photophobia; Kernig’s sign

48
Q

Kernig’s Sign

A

Involuntary flexion of legs

49
Q

Treatment of Meningitis

A

steroids
analgesia
Antibiotics if bacterial
Bacterial/Viral should be on contact precautions
Prevention with HiB Vaccine (Health Promotion)

50
Q

Spinal Cord Injury

A

damage to the spinal cord causes permanent damage to the strength, sensation, and other bodily functions below the site of injury.
- signs and symptoms depend on the site of injury
- higher the injury, more function lost
- Injuries above T-6 cause autonomic dysreflexia

51
Q

Autonomic Dysreflexia

A

medical emergency!
Characterized by sudden, severe hypotension, bradycardia, headache, stuffiness, flushed skin, diaphoresis, blurred vision, and anxiety.
Patho: irritation below the SCI sends nerve signals to the spine. Nerve signals are blocked at the SCI, causing increasing BP. Brain sends signals to lower BP, but it is blocked off by SCI, causing diaphoresis and headache and increased ICP.

52
Q

Treatment for SCI

A

Sit up to lower the BP
Antihypertensives (hydralazine)
find stimulus and remove it
urinary rentention – catheterize
constipation – remove impaction

53
Q

Stroke

A

occurs when blood vessels that carry oxygen and nutrients to the brain is blocked by a clot or bursts.

54
Q

Hemorrhagic Stroke

A

bleeding; bessel ruptures and bleeds into the brain; blood accumulates, increasing ICP; may be caused by aneurysm; characterized by severe headaches.

55
Q

Ischemic Stroke

A

lack of oxygen to the brain caused by clot; may be embolic or thrombotic; sudden in onset.

56
Q

Warning Signs of Ischemic Stroke

A

dizziness, loss of balance, blurry vision, abnormal pupil response, and hemianopia.

57
Q

Acute signs of Ischemic Stroke

A

unilateral facial droop; unilateral Arm/leg weakness; aphasia, aphasia, altered level of consciousness.

58
Q

Treatment for Hemorrhagic Stroke

A

CT to determine brain perfusion
- get bleeding under control
- if caused by aneurysm, coiling or clipping
- craniotomy
- EVD

59
Q

Treatment for Ischemic Stroke

A

CT to determine brain perfusion
- permissive hypertension
- antibthrombolytics (TPA breaks up clot to restore blood flow; must be done within 60 min)
- percutaneous thrombectomy (surgery to remove the clot)

60
Q

define partial seizure

A

involves specific area of the brain

61
Q

define generalized seizure

A

involving the entire brain

62
Q

define simple seizure

A

no loss of consciousness

63
Q

define complex seizure

A

impaired consciousness from confusion to loss of consciousness

64
Q

Define Tonic Clonic Seizure

A

seizure characterized by muscle stiffening and jerking motions.

65
Q

Myoclonic

A

sudden, brief contractions of a muscle or group of muscles.

66
Q

Atonic Seizure

A

no movement at all.

67
Q

Acute treatment of sudden onset seizure

A

Stay with patient
note time, duration, and characteristics
remove harmful objects in the environment
cushion head
loosen restrictive clothing
assist to side-lying
maintain airways and protect from injury.
Medications: Lorazepam (short term); Phenytoin (long-term)
Considerations: monitor therapeutic levels; do not stop meds abruptly.

68
Q

Seizure Precautions

A
  • O2 and suction ready
  • side rails up and padded
  • pillow under head
  • bed in lowest position
  • side-lying
69
Q

Parkinson’s

A

Progressive nervous system disease caused by degeneration of dopamine neuron’s; starts with tremors.

70
Q

Signs and Symptoms of Parkinson’s

A

Tremors (usually starts on one side)
rigidity
hypophonia
mask-like face
akinesia
stooped posture
difficulty balancing
OH

71
Q

Treatment for Parkinson’s

A

Fall precautions
Comfort care
PT/OT/SW
Medications: Carbidopa/Levidopa to increase dopamine in the brain.

72
Q

MS

A

autoimmune; CNS inflammation; damage to myelin sheaths, damaging nerve transmission

73
Q

Signs and Symptoms of MS

A
  • tingling/numbness
  • weakness
  • optic neuritis
  • ataxia
  • nystagmus
  • tremor
  • slowed speech
  • hypotonia
  • epilepsy seizures
  • msk spasticity
74
Q

Treatment for MS

A

No cure
Comfort care
Corticosteroids for exacerbations to reduce inflammation
plasmapheresis – plasma exchange

75
Q

Myasthenia Gravis

A

autoimmune disease that destroys the communication between muscles; diagnosed with tension test.

76
Q

Signs and Symptoms of Myasthenia Gravis

A

weak muscles and ptosis

77
Q

Treatment for myasthenia gravis

A

cholinesterase inhibitors, corticosteroids, immunosuppressants.

78
Q

Sepsis:

A

a systemic inflammatory reaction to infection that the body cannot tolerate; may be viral, fungal, or bacterial.

79
Q

Sign and Symptoms of Sepsis

A

decreased urine output, change in LOC, hypotension, hypoperfusion of tissues; edema, tachycardia, increased lactase*; decreased spo2; tachypnea; warm, flushed skin.

80
Q

Delirium

A

Abrupt onset
Favorable prognosis if the underlying cause is treated
May be caused by infection, medications, F&E imbalance, or sensory impairment
Impairments with attention that fluctuate in intensity
Difficulty with judgment and executive functioning
Memory impairments
Altered level of consciousness
Emotional lability

81
Q

natural substance for insomnia

A

valerian root
melatonin

82
Q

Phenytoin

A

Phenytoin is indicated in the prevention of seizures. Phenytoin’s most common adverse effects include gingival hyperplasia, excessive body hair growth, and folic acid deficiency. The normal phenytoin level is 10-20 mcg/mL, and toxicity is any level greater than 40 mcg/mL. Features of phenytoin toxicity include nystagmus, unsteady gait, and a worsening mental status as the levels rise.

83
Q

Zolpidem

A

Also known as Ambien. Sleeping agent; treats insomnia

84
Q

Acamprosate

A

Medication prescribed to help alcoholics quit drinking

85
Q

Etanercept

A

medication used to manage and treat autoimmune conditions such as plaque psoriasis, rheumatoid arthritis, psoriatic arthritis, AS, etc.

86
Q

Status Epilepticus

A

Medical Emergency
prolonged seizure that lasts longer than 5 minutes
or
repeated seizures over 30 mins
- a potential complication of all seizures
- notify PHCP and TEAM immediately
- Priorities: airway, supplemental O2, IV access

87
Q

Which medication should a patient with peptic ulcer disease avoid?

A

Aspirin and NSAIDs
Aspirin disrupts the normal mucosal defense and repair, making the mucosa more susceptible to acid. The nurse should instruct this client on the importance of avoiding aspirin and all other nonsteroidal anti-inflammatories (NSAIDs) now and in the future.

88
Q

Huntington’s Disease

A

The cardinal features of Huntington’s disease include chorea (brief, involuntary movements involving the trunk, limbs, and face). This disease has common psychiatric symptoms such as depression, paranoia, delusions, and hallucinations. Weight loss is also a common finding caused by the excessive energy expended in abnormal movements.
Huntington’s disease is a neurodegenerative disease that is not well understood. This disease causes neuropsychiatric symptoms such as chorea, dystonia, abnormal eye movements, hallucinations, and weight loss. Treatments include VMAT2 inhibitors such as tetrabenazine. Adjunctive treatments such as benzodiazepines may be utilized for symptoms such as uncontrolled chorea.

89
Q

Autonomic Dysreflexia

A

Autonomic dysreflexia (AD) is a condition in which the involuntary nervous system overreacts to external or bodily stimuli. It’s also known as autonomic hyperreflexia. This reaction causes:

A dangerous spike in blood pressure
Bradycardia
Constriction of your peripheral blood vessels
Other changes in your body’s autonomic functions
The condition is most commonly seen in people with spinal cord injuries above the sixth thoracic vertebra, or T6. It may also affect people who have multiple sclerosis, Guillain-Barre Syndrome, and some head or brain injuries. AD can also be a side effect of medication or drug use.

AD is a severe condition that’s considered a medical emergency. It can be life-threatening and result in:

Stroke
Retinal hemorrhage
Cardiac arrest
Pulmonary edema
The symptoms of AD may include:

Anxiety and apprehension
Nasal congestion
High blood pressure with systolic readings often over 200 mmHg
A pounding headache
Flushing of the skin
Profuse sweating, particularly on the forehead
Lightheadedness
Dizziness
Confusion
Dilated pupils
Sweating above the level of injury. In individuals with spinal cord injury at or above the T6 level, there is a loss of normal autonomic nervous system control, leading to a lack of sympathetic regulation of the sweat glands. As a result, when a noxious stimulus or irritation occurs below the level of injury, it can trigger a reflex sympathetic response, leading to sweating above the level of injury.

90
Q

Spinal Shock

A

Absent bowel sounds, gastric distention, bradycardia, hypotension, and flaccid paralysis are concerning findings for spinal shock. When caring for a client following a spinal cord injury, spinal shock is one of the many complications which may occur within 48 hours following the injury.
Spinal shock may occur immediately following a spinal cord injury or within 48 hours of the insult.

The cause is thought to be the excessive amount of potassium in the extracellular space that reduces neural transmission.
Manifestations associated with spinal shock include flaccid paralysis, absent bowel and bladder control, and loss of reflex activity.
Males may develop priapism.
Treatment involves frequent assessment of vital signs, correcting any fluid or electrolyte abnormalities, and prompt administering corticosteroids.

91
Q

parameters to monitor for ECT

A

Standard American Society of Anesthesiologists (ASA) recommends monitoring the client’s heart rate, blood pressure, ECG, capnography, and temperature during any electroconvulsive therapy (ECT) procedure, as clients undergoing an ECT procedure often experience a temporary rise in blood pressure during treatment.
While preparing a client scheduled to undergo electroconvulsive therapy (ECT), the nurse should understand that applying a blood pressure cuff to the client must be performed before the client’s ECT procedure.
Electroconvulsive therapy (ECT) is indicated for the treatment of severe or treatment-resistant depression, psychosis, bipolar disorder, and catatonia.
Modern electroconvulsive therapy (ECT), delivered under heavy sedation/general anesthesia, is typically well tolerated, although confusion and memory impairment may occur acutely.
Response to six to ten electroconvulsive therapy (ECT) treatments is usually dramatic and, at times, life-saving.

92
Q

dysfunction of cranial nerve III

A

Ptosis, or eye drooping, occurs with cranial nerve III (oculomotor) lesions, myasthenia gravis, and Horner syndrome. Dysfunction of cranial nerve III is also associated with dilated pupil, absent light reflex, and impaired extraocular muscle movement.

93
Q

12 cranial nerves

A

The twelve cranial nerves include -

CN I: Olfactory

CN II: Optic

CN III: Oculomotor

CN IV: Trochlear

CN V: Trigeminal

CN VI: Abducens

CN VII: Facial

CN VIII: Vestibulocochlear

CN IX: Glossopharyngeal

CN X: Vagus

CN XI: Accessory

CN XII: Hypoglossal

94
Q

plasmapheresis

A

In clients with multiple sclerosis, an autoimmune reaction occurs. This autoimmune reaction causes immune cells and antibodies to attack and destroy the myelin sheath (a coating made of fat and proteins that protects nerves and helps transmit electrical signals) and the underlying nerve fibers in the brain, optic nerves, and spinal cord. During plasmapheresis, these antibodies are removed from the client’s plasma, removing the cause of myelin sheath demyelination.

95
Q

MS

A

The cause of multiple sclerosis (MS) is unknown but likely involves an attack by the immune system against the body’s own tissues (i.e., an autoimmune reaction).
In most multiple sclerosis clients, periods of relatively good health alternate with episodes of worsening symptoms.
MS is a progressive disease, as symptoms gradually worsen over time.
Clients may experience visual problems, abnormal sensations, and weak or clumsy movements.
Diagnosis is based on clinical symptoms, physical examination, and magnetic resonance imaging.
Treatment includes corticosteroids, immunomodulators to prevent exacerbations and delay eventual disability, antidepressants, and/or supportive care.
Life span is typically unaffected unless the disorder is very severe.

96
Q

Bells Palsy

A

Bell’s palsy is an unexplained episode of facial muscle weakness or paralysis. It begins suddenly and worsens over 48 hours. This condition results from damage to the facial nerve (the 7th cranial nerve). Pain and discomfort usually occur on one side of the face or head.
Bell’s palsy can strike anyone at any age. It occurs most often in pregnant women, and people who have diabetes, influenza, a cold, or another upper respiratory ailment. Bell’s palsy affects men and woman equally. It is less common before age 15 or after age 60.
Bell’s palsy is not considered permanent, but in rare cases, it does not disappear. Currently, there is no known cure for Bell’s palsy; however, recovery usually begins 2 weeks to 6 months from the onset of the symptoms. Most people with Bell’s palsy recover full facial strength and expression.

97
Q

Bells Palsy Causes

A

It is thought that it may be due to inflammation that is directed by the body’s immune system against the nerve controlling movement of the face. Bell’s palsy is sometimes associated with the following:

Diabetes
High blood pressure
Injury
Toxins
Lyme disease
Guillain-Barré syndrome
Sarcoidosis
Myasthenia gravis
Multiple sclerosis
Infection, especially following a viral infection with Herpes simplex virus (a virus that is related to the cause of the common “cold sores” of the mouth)

98
Q

Bells Palsy Signs and Symptoms

A

These are the most common symptoms of Bell’s palsy:

Disordered movement of the muscles that control facial expressions, such as smiling, squinting, blinking, or closing the eyelid
Loss of feeling in the face
Headache
Tearing
Drooling
Loss of the sense of taste on the front two-thirds of the tongue
Hypersensitivity to sound in the affected ear (hyperacusis)
Inability to close the eye on the affected side of the face
The symptoms of Bell’s palsy may look like other conditions or medical problems. Always see your healthcare provider for a diagnosis.

99
Q

Bells Palsy Diagnosis

A

Your healthcare provider can usually diagnose Bell’s palsy by looking at your symptoms. There are no specific tests used to diagnose Bell’s palsy. However, your healthcare provider may order tests to rule out other conditions that can cause similar symptoms and to determine the extent of nerve involvement or damage. These tests may include:

Electromyography (EMG) to determine the extent of the nerve involvement
Blood tests to determine if another condition such as diabetes or Lyme disease is present
Magnetic resonance imaging (MRI) or computed tomography (CT) to determine if there is a structural cause for your symptoms.

100
Q

Bells Palsy treatment

A

Steroids to reduce inflammation
Antiviral medicine, such as acyclovir
Analgesics or moist heat to relieve pain
Physical therapy to stimulate the facial nerve
Some people may choose to use alternative therapies in the treatment of Bell’s palsy, but there is no proof they make a difference in recovery. Such treatment may include:

Relaxation
Acupuncture
Electrical stimulation
Biofeedback training
Vitamin therapy, including B12, B6, and the mineral zinc

101
Q

Medications for Migraine Headache

A

reatment for an acute migraine headache (MH) involves abortive medications such as ketorolac (NSAID), dexamethasone (corticosteroid), and acetaminophen-caffeine. Depending on the severity of the MH, the provider takes a stepwise or aggressive approach to treatment.
The treatment for an acute migraine headache aims to abort the headache and the associative symptoms such as nausea and vomiting. Commonly, a client may be prescribed an anti-emetic such as metoclopramide to assist with abating the symptoms. The below table reviews the treatment options for a migraine headache.
* Verapamil
* Propranolol
Topiramate
* Onabotulinumtoxin-A
* Valproic Acid
Nortriptyline
* Galcanezumab
Abortive Treatment
Ketorolac
Acetaminophen
Caffeine
Magnesium sulfate
* Dexamethasone
Sumatriptan

102
Q

why is increased urine output after neurological surgery concerning?

A

an excessive amount of urine output for 1 hour and is concerning for diabetes insipidus given the procedure the patient recently underwent. Any urine output greater than 300 mL is alarming and the healthcare provider should be notified immediately. Diabetes insipidus is a severe complication from neurosurgery that occurs around the pituitary. This amount of urinary output can lead to shock if not treated promptly.

103
Q

Reynaud’s Phenomenon

A

Raynaud’s phenomenon (RP) results from vascular spasms in the fingers that are triggered by cold temperatures and emotional stress.
P may be a finding associated with other autoimmune conditions such as scleroderma. Clinical features of RP include cutaneous vasospasms that are painful. During the vasospasms, the affected area will change colors (cyanosis to flushing). These vasospasms may impact the fingers, ear, nose, and face. Triggers for these vasospasms include stress and exposure to cold temperatures.

➢ Mainstay medical management includes calcium channel blockers such as nifedipine or amlodipine. These medications help prevent these painful vasospasms.

➢ Nursing care focuses on having the client wear gloves in cold environments and avoid injuries to the affected area. Smoking cessation should also be stressed, as it may worsen the condition.

104
Q

Which previous conditions directly correlate with the development of Guillian-Barre Syndrome

A

Upper respiratory infections or stomach infections correlate with the development of Guillain-Barre syndrome. Guillain-Barre syndrome is a disorder that involves the peripheral and cranial nerves causing ascending paralysis.

105
Q

Epilepsy

A

Epilepsy is an idiopathic condition that requires management with anticonvulsants such as topiramate, valproic acid, or phenytoin. Acute seizures are managed with benzodiazepines such as lorazepam or diazepam. These medications work to terminate a seizure. During an acute seizure, the nurse should place the patient on their side, loosen restrictive clothing, and anticipate a prescription for a parenteral benzodiazepine such as diazepam.

106
Q

Migraine Headache

A

An array of symptoms may be reported for a client experiencing a migraine headache (MH).

The most common manifestations associated with an acute migraine headache include

Unilateral frontotemporal pain that may be described as throbbing or dull
Sensitivity to light (photophobia) and sound (phonophobia)
Nausea and/or vomiting
Altered mentation (drowsiness)
Dizziness, numbness, and tingling sensations

107
Q

Side Effects of Opioids

A

miosis; mood changes; change in LOC; respiratory depression reduced salivation; pruritis; pneumonia (aspiration); hypotension; headache; infrequent elimination (constipation/urinary retention); nausea; restlessness; emesis

108
Q

Fentanyl

A

Fentanyl is an opioid medication that may be given in a variety of routes, including intravenous, intramuscular, transdermal, intranasal, and buccal. Prior to the administration of an opioid, the nurse should assess the client’s pain level, blood pressure, and respiration. The fentanyl patch should be applied no greater than 72 hours.

109
Q

The most common side effects of rivastigmine

A

The most common side effects of rivastigmine are flu-like symptoms, dizziness, and weight loss. The FDA has approved limited drugs for Alzheimer’s Disease. The most effective medications act by intensifying the effect of acetylcholine at the cholinergic receptor. Acetylcholine is naturally degraded in the synapse by the enzyme acetylcholinesterase. When acetylcholinesterase is inhibited, acetylcholine levels increase and significantly affect the receptors.

110
Q

Mirtazepine

A

Mirtazapine is an agent used to treat depressive and anxiety disorders. This medication causes sedation and is dosed at night. This may be helpful for those with depressive disorders and who suffer from concomitant insomnia. Mirtazapine has the following side effects –

Increased appetite
Weight gain
Sedation
Dizziness
Confusion

111
Q

Delirium

A

Delirium is an altered sensorium. It is characterized by acute changes in the patient’s level of consciousness. Many causes of delirium include medications (dexamethasone, opioid toxicity), nicotine withdrawal, dehydration, uncontrolled pain, constipation, urinary retention, infection, hypoxia, renal failure, hyponatremia, hypercalcemia, hyperglycemia, and emotional distress. Initially, non-pharmacological interventions should be attempted to identify and address reversible etiology and relieve terminal agitation/delirium. For example, address the reversible causes such as treating constipation or discontinuing medications such as dexamethasone, modifying precipitating factors such as sensory deprivation or uncontrolled pain, etc. If no rapidly reversible factors are identified or if the patient is terminal, dopamine antagonists must be used.

112
Q

Hyperactive Delirium

A

Hyperactive delirium is characterized by agitation, restlessness, and emotional lability. Hypoactive delirium is characterized by flat affect, apathy, lethargy, or decreased responsiveness.

113
Q

Dementia VS Delirium

A

Alzheimer’s disease is a form of dementia, not delirium. Vascular disease (tiny cerebral infarcts) is a direct contributor to dementia. A preventative measure for vascular dementia is mitigation of hypertension and diabetes as these two conditions directly cause vascular dementia.

114
Q

Delirium Tremens

A

DTs can be fatal if untreated. DTs result from florid alcohol withdrawal causing the client to experience hallucinations, hypertension, agitation, nystagmus, and potential seizure activity. Clonidine is an alpha-agonist and is primarily used in the treatment of hypertension. Clonidine is helpful during DTs because it lowers the client’s blood pressure and gives the client some drowsiness which is useful if they are agitated.\
✓ Delirium Tremens (DTs) are a medical emergency and may cause autonomic hyperactivity, resulting in tachycardia, diaphoresis, fever, anxiety, insomnia, and hypertension.

✓ Delusions and visual and tactile hallucinations are common in alcohol withdrawal delirium.

✓ This may occur within 72 hours following the last alcoholic beverage consumed.

✓ Withdrawal seizures may occur within 12 to 24 hours after alcohol cessation.

✓ These seizures are generalized and tonic-clonic. Additional seizures may occur within hours of the first seizure.

✓ Diazepam is given intravenously as a common treatment for withdrawal seizures.
Nursing care for DTs includes -

Rapid assessment of the client’s vital signs
Initiate seizure precautions and establish patent intravenous access
Obtain a prescription for benzodiazepines, such as lorazepam or diazepam
Administer intravenous fluids and electrolytes to replete the lost fluids
Assess the client using the CiWa-Ar scale to trend the severity of the symptoms

NCLEX Preparation (18 decks)

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