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NURSING 220 > TEST 4 > Flashcards

TEST 4 Flashcards

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1
Q

What is central cord syndrome?

A

Incomplete Lesion (injury)-
Motor problems (fine motor)
Upper extremities more affected
Spastic paralysis of upper extremities
Lower extremities less affected
Bowel & Bladder dysfunction variable

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2
Q

cause of central cord syndrome?

A

Trauma
Traumatic lesions tend to improve in 1-2 weeks
Tumors
Infections

Surgical decompression may be indicated if r/t spinal stenosis

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3
Q

what is anterior cord syndrome?

A

Incomplete Lesion (injury)
Loss below the level of lesion:
Pain
Temperature
Motor function below level of lesion

Retain below level of lesion: (gross sensation)
Light touch
Position
Vibration sensation

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4
Q

cause of anterior cord syndrome?

A

Trauma (anterior cord compression)
Association fracture-dislocation of vertebrae
Acute disk herniation
Hyperflexion
Artery infarct

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5
Q

what is brown-sequard syndrome?

A

Incomplete cord lesion (Injury)
Lateral cord syndrome
Ipsilateral paralysis/ Ipsilateral paresis
Loss or weakness with movement
Contralateral loss of pain and temperature

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6
Q

cause of brown-sequard syndrome?

A

Infection
Inflammation
-MS
-TB
Tumor
Trauma
-Penetrating
-Fracture or dislocation
-Acute disc rupture

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7
Q

what is cauda equina syndrome?

A

Progressive compression of nerve roots at base of spinal cord
-Lumbar pain
-Weakness or paralysis of lower extremities
-Saddle anesthesia
-Bowel & bladder incontinence

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8
Q

causes of cauda equina syndrome?

A

Usually from herniated disc

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9
Q

what is Sciwora?

A

Spinal cord injury without radiographic abnormality

Condition affecting pediatric patients 8 and younger
Objective signs of spinal cord injury from trauma without bony abnormalities or changes on X-ray or CT
Incidence 20-32%
Younger patients may have more severe neuro symptoms
Symptoms may be delayed
Risk related to large blood supply to cord & elasticity of vertebral column
Injuries are usually considered “stable”
Immobilization for 3 months standard treatment
MRI (gold standard)
-Demonstrate: Ligamental injury, disk injury, cord lesions, or hemorrhage

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10
Q

T4 is located where?

A

nipple line

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11
Q

T10 is located where?

A

base of ribs, roughly point of umbilicus

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12
Q

C6, 7, & 8 are located where?

A

hands and fingers

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13
Q

T1 is located where?

A

terminate triceps (shrug shoulders)

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14
Q

L5-S1 is located where?

A

feet (felx/extend)

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15
Q

A in ASIA scale?

A

A = Complete. No sensory or motor function is preserved in the sacral segments S4-S5.

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16
Q

B in ASIA scale?

A

B = Sensory Incomplete. Sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-S5 (light touch, pin prick at S4-S5: or deep anal pressure (DAP), AND no motor function is preserved more than three levels below the motor level on either side of the body.

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17
Q

C in ASIA Scale?

A

C = Motor Incomplete. Motor function is preserved below the neurological level, and more than half of key muscle functions below neurological level of injury (NLI) have a muscle grade less than 3

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18
Q

D in ASIA scale?

A

D = Motor Incomplete. Motor function is preserved below the neurological level, and at least half of key muscle functions below the NLI have a muscle grade of 3 or > 3.

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19
Q

E in ASIA scale?

A

normal

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20
Q

emergency management of SCI

A

Immobilization!
-Cervical collar
Resuscitation as needed
Move as a unit- avoid additional or worsening injury
Testing
-X-Ray- bony abnormalities
-CT- 3 dimensional view of bone
-MRI- ligament and tissue
Interventions/ Actions
-Initial and continuous assessment
-Frequent vital signs
-Avoid hyperoxia
-Maintain MAP >85mmHg
Pharmacologic treatments

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21
Q

respiratory clinical manifestations of SCI

A

C1 – C3: Absence of ability to breathe independently.
C4: poor cough, diaphragmatic breathing, hypoventilation
C5 – T6: decreased respiratory reserve
T6 or T7 – L4: functional respiratory system with adequate reserve
ASSESSMENT q2H AT LEAST
Ascending edema of the spinal cord in the acute phase -Can cause respiratory difficulties requiring immediate intervention

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22
Q

non-physical restraints

A

talk down, listen, minimizing stimulation

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23
Q

what is STAMP?

A

Staring
Tone (or volume of voice)
Anxiety
Mumbling
Pacing

used for IDing potentially violent pts

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24
Q

Restraints

A

reminder to look at restraint doc on canvas

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25
Q

what is EMTALA?

A

emergency medical and active labor act-
duty to treat regardless of inability to pay or insurance coverage

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26
Q

EMTALA treatment guidelines

A

EDs must provide medical screening exam and look for emergency medical conditions, then stabilize if EMC present AND care for pregnant patients with contractions if emergency exists or inadequate time for safe transfer before delivery

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27
Q

EMTALA reasons for transfer?

A

specialized care not available at facility
continuity of care
lack of resources
patient request

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28
Q

triage: emergent

A

life threatening, seen immediately, assess q15min

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29
Q

triage: urgent

A

serious health problem, seen within 1hr, assess q30min

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30
Q

triage: non-urgent

A

episodic illness, seen within 24hrs, assess q1-2h

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31
Q

what is ABCDEFGHI assessment?

A

Primary Assessment
A- Airway/ C-spine precautions
B- Breathing
C- Circulation- obvious hemorrhage
D- Deficit- LOC, AVPU, GCS
Secondary Assessment
E- Environmental/ Expose
F- Full set of vital signs/ Family
G- Give comfort
H- History/ Head to toe
I- Inspect Posterior/ Interventions

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32
Q

what is blunt trauma?

A

Physical trauma (closed) body as a result of:
Impact
Injury
Physical Attack

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33
Q

biomechanical forces that cause blunt trauma?

A

compression, stretch, sheer

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34
Q

what is compression force?

A

Impact stops part of the body
Inertia keeps remaining anatomy in motion

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35
Q

what is stretch force?

A

Protein fibers pulled, injured or torn

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36
Q

what is sheer force?

A

Structures under opposing forces are damaged

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37
Q

types of blunt trauma?

A

MVC, falls, assault

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38
Q

what are fragile solid organs that damage easily in blunt trauma?

A

brain, spleen

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39
Q

turner sign is where

A

flank

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40
Q

cullen sign is where

A

umbilical

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41
Q

what do turner and cullen signs indicate

A

retroperitoneal hemorrhage

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42
Q

what are hollow organs

A

Heart
Stomach
Lungs
Bowel
Bladder

Tolerate trauma well
If full of air or fluid may rupture

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43
Q

what are solid organs

A

Kidneys
Liver
Pancreas

Held together with strong tissue
Fracture with injury

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44
Q

presentation for blunt trauma to abdomen

A

Pain
Tenderness
Hemorrhage (no obvious source)
Hypovolemia
turner sign
cullen sign

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45
Q

presentation of chest blunt trauma

A

Pain
Tenderness
Shortness of breath

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46
Q

what do you palpate on chest assessment for blunt trauma

A

sternum, ribs

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47
Q

where do you immobilize for a fracture

A

above and below the joint

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48
Q

what do you have to think about every time you splint, wrap, cast, or immobilize

A

compartment syndrome

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49
Q

what are considered major fractures

A

pelvis, femur

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50
Q

what are the types of penetrating trauma?

A

hgih velocity
low velocity

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51
Q

high velocity trauma types

A

GSW, blast injuries

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52
Q

low velocity trauma types

A

stabbing, impalement

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53
Q

penetrating trauma assessment

A

MOI very important
Never remove an object
-Diagnostic imaging to determine extent of injury
-Removed in OR
-Cheek- exception
–Direct pressure can be applied to both sides of injury
Extent of injury depend on
-Velocity
-Number of projectiles

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54
Q

what is crushing trauma?

A

Body Part caught between 2 objects
-Industrial between machine parts
-Runover by a car between tire and road

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55
Q

crushing trauma can cause what complications

A

Intracellular fluid is released when cells are crushed (think electrolytes)
Myoglobin release due to muscle damage
-Rhabdomyolysis
-Myoglobin causes renal failure
-Clog kidneys
Compartment swelling leads to increased muscle damage
-Compartment syndrome
-Fasciotomy treatment

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56
Q

6 P’s of compartment syndrome

A

Pain:
-Earliest
-Progressive
-Disproportionate to injury
Pressure
Pallor (decreased O2)
Paresthesia
Paresis- muscle weakness related to nerve damage
Pulseless
-Late and ominous sign

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57
Q

causes of compartment syndrome

A

Bleeding
Edema
Constricting cast
Constricting dressing
Splinting
Prolonged positioning
Burns
Infections

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58
Q

how is compartment syndrome diagnosed?

A

Presenting symptoms
MOI
Pressure measurement

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59
Q

treatment for compartment syndrome?

A

Identify increased pressure
Release pressure with a fasciotomy

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60
Q

treatment priorities for compartment syndrome

A

Maintain hemodynamic status
-1 Liter crystalloid fluid
-Additional needs- give blood
Keep patient warm
Stop any active bleeding
-Direct pressure
-Tourniquet
Permissive hypotension resuscitation
Stabilize fractures
-Splinting
Disposition
-Admit
-OR
-Transfer
-Discharge

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61
Q

what is the trauma triad of death?

A

hypothermia, coagulopathy, acidosis (and hypocalcemia to make diamond of death)

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62
Q

what to do for acidosis in triad of death?

A

NS or LR

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63
Q

what to do for coagulopathy in triad of death

A

blood products- 1 U PRC to 1 U plasma to 1 U platelets

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64
Q

triad of death treatment

A

Stop the bleeding
Assume your patient’s temp is dropping
Limit patient exposure to environment
Turn up the heat!
Measure lactate levels
Measure end-tidal CO2
Treat hypoventilation
Track & treat coagulation labs

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65
Q

frost nip is ___ and ____.

A

mild and reversible

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66
Q

affected locations of frost nip

A

Earlobes
Cheeks
Nose
Fingers
Toes

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67
Q

frost nip presentation

A

Reddened or blanched skin
Cool/cold to the touch

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68
Q

frost nip tx

A

rewarming

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69
Q

frost bite causes …

A

Severe tissue & cell damage
Intracellular water turns to ice
Cold cause decreased blood flow

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70
Q

frost bite presentation

A

Damage depends on depth of freezing
Swelling
Blistering
Pain
Gangrene
Muscle necrosis

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71
Q

frost bite tx

A

External and internal warming
Tepid water emersion
Warm blankets
Warm O2

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72
Q

DO NOT what with frost bite

A

massage areas- causes more damage

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73
Q

who is at risk for frost bite

A

old, young, homeless, beta blockers, alcoholics, malnourished, diabetics, smokers, PVD

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74
Q

hypothermia causes

A

Core temp is 95◦ or less
Result of exposure to cold
Inability to maintain temperature in absence of low ambient temps.

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75
Q

what happens when temp <90

A

-Shivering suppressed
-B/P & P non-palpable
-Vfib
*Defib is ineffective on a cold heart
*Internal and external warming initial treatment

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76
Q

causes of heat exhaustion

A

Excessive heat exposure & dehydration
Very hot environment
Heavy activity
Not enough fluid and salt intake

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77
Q

presentation of heat exhaustion

A

Muscle cramps
Shoulders
Abdomen
Lower extremities
Profound diaphoresis
Thirst
Syncope
Headache
Dizziness
Pale moist skin
Nausea & Vomiting
Temperature 101-102 degrees
Tachycardia

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78
Q

tx for heat exhaustion

A

Move to cool, shady area
PO fluids
Electrolyte containing
IV fluids if necessary
Encourage rest

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79
Q

causes of heat stroke

A

Non-exertional prolonged exposure to high temperatures
Exertional heat stroke: strenuous activity in high temperatures

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80
Q

heat stroke presentation

A

May not have sweat
Weakness
Hot dry skin
Tachypnea
Tachycardia
Hypotension
Temperature 105 or higher
CNS dysfunction:
-Delirious
-Unconscious
-Seizures
-Coma

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81
Q

heat stroke tx

A

Removing clothing
Moving to a cool, shady area; shelters
Active cooling
IV fluids
Medication
-Seizures
-Uncontrollable shivering
Frequent vital signs
Labs

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82
Q

meds that alter physiologic response to heat

A

Phenothiazines
Anticholinergics
Antihistamines
Beta-blockers
Benzodiazepines
Amphetamines
Neuroleptics
Tricyclic antidepressants
Cocaine
Alcohol

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83
Q

risk factors for near drowning

A

Alcohol
Inability to swim
Diving injuries
Hypothermia
Exhaustion
No life jacket

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84
Q

what is mammalian dive reflex

A

Reflex occurs when mammals are submerged in water <70 degrees
Protective mechanism to maintain cardiac and cerebral blood flow
When face submerged:
-Laryngeal spasm starts
-Heart rate slows
-Vasoconstriction

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85
Q

near drowning complications

A

Respiratory
-ARDS
-Hypoxia
-Hypercarbia
-Loss of surfactant (fresh water)
-Pulmonary edema (salt water)
Acidosis
-Respiratory
-Metabolic
Hypothermia

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86
Q

drowning morbidity and mortality primarily due to what

A

anoxic brain injury caused by airway obstruction from laryngospasm or aspirated water

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87
Q

chemical ingestion poisoning can be __ or ___.

A

alkaline or acidic

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88
Q

chemical ingestion tx

A

Identification of substance
Removing toxin
-Gastric lavage
Decrease absorption
-Activated Charcoal
-Dilution

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89
Q

symptoms of ingestion poisoning

A

Early symptoms of may include an intoxicated feeling.
Headache
Fatigue,
Lack of coordination
Grogginess
Slurred speech
Nausea
Vomiting
Continued breakdown causes damage to:
-Kidney
-Lung
-Brain
-Nervous system function.
-Organ damage can occur 24 to 72 hours after
ingestion.

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90
Q

button battery ingestion complications

A

Tracheoesophageal fistula
Esophageal perforation
Vocal cord paralysis
Mediastinitis
Pneumothorax
Pneumoperitoneum
Tracheal Stenosis
Tracheomalacia
Aspiration pneumonia
Empyema
Lung abscess

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91
Q

button battery ingestion tx

A

Endoscopic or surgical removal if lodged
Allow to pass
Honey may help neutralize pH

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92
Q

carbon monoxide poisoning

A

CNS symptoms
Skin color
-Cyanotic
-Pale to pink
-Unreliable sign

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93
Q

carbon monoxide poisoning tx

A

Fresh air
100% O2
Hyperbaric chamber

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94
Q

C1, 2, 3, 4, _________; C5 _______

A

breathe no more; stay alive

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95
Q

primary spinal cord injury

A

Initial insult
Irreversible
Microscopic hemorrhage in gray matter
Edema to white matter

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96
Q

secondary spinal cord injury

A

Contusions
Tears cause nerve fibers swelling & disintegration
Ischemia
Hypoxia
Edema
Hemorrhagic lesions
*Destruction of myelin & axons -potentially reversible if treatment within 4-6 hours

97
Q

SCI MOI: hyperflexion

A

bending forward

98
Q

SCI MOI: hyperextension

A

backward

99
Q

SCI MOI: excessive rotation

A

either flexion- or extension-rotation

100
Q

SCI MOI: compression

A

downward motion

101
Q

types of spinal fractures

A

compression, wedge, burst

102
Q

what is a compression spinal fracture

A

collapsing as a result of pressure or degeneration of the spinal bones

103
Q

what is a wedge spinal fracture?

A

result from degeneration of the spine or trauma

104
Q

what is a burst spinal fracture?

A

when a disc/bone in your spine is externally compressed, becoming crushed, spreading fragments throughout your spine

105
Q

what are chance spine fractures?

A

pediatric seatbelt syndrome- flexion distraction injury of L-spine

106
Q

-plegia

A

complete lesion

107
Q

paresis

A

some muscle strength is preserved

108
Q

tetraplegia

A

Injury of the cervical spinal cord.
Usually still move arms using the segments above the injury
Ex. C7 injury, can still flex forearms, using the C5 segment

109
Q

paraplegia

A

Injury of the thoracic /lumbo-sacral cord ( T1 to S5)

110
Q

hemiplegia

A

Paralysis of one half of the body usually in brain injuries (e.g., stroke)

111
Q

C1-C4 motor complete injury -tetraplegia

A

Chronically Ventilator dependent
Require assistance to cough
Dependent on others for self-care
Problems with pressure
Variety of power wheelchairs controlled by the head, chin or mouth for mobility

112
Q

C5 motor complete injury -tetraplegia

A

Not chronically ventilator dependent
Require assistance to cough
Diaphragmatic breathing only
Dependent on others for self-care
Problems with pressure relief
Variety of power wheelchairs controlled by the head, chin or mouth

113
Q

whats included in post-injury assessment for SCI

A

Sustain life: ABCs
Prevent further cord damage
-Stabilize fractures
Assessment: Motor status
-Against gravity
-Against resistance
-Both sides of the body
-Ask to move
–Legs
–Hands
–Fingers
–Wrists
–Shrug shoulders
Assessment: Sensory and Vibration
Pinprick starting at toes and working upward
Always have patient close eyes or look away for accurate results
Assess for head injury and increased ICP

114
Q

maintain map of __ for emergency SCI mgmt

A

> 85mmHg

115
Q

C1-C3 SCI respiratory clinical manifestations

A

Absence of ability to breathe independently

116
Q

C4 SCI resp clinical manifestations

A

poor cough, diaphragmatic breathing, hypoventilation

117
Q

C5-C6 SCI resp clinical manifestations

A

decreased respiratory reserve

118
Q

T6 or T7-L4 SCI resp clinical manifestations

A

functional respiratory system with adequate reserve

119
Q

C1-T5 SCI cardiac clinical manifestations

A

decreased or absent SNS influence.
Injury above T6 may develop neurogenic shock

120
Q

cardiac interventions for SCI

A

Perfusion-
Vasopressors to maintain perfusing MAP (85 mmHg)
Neosynephrine/Phenylephrine (IV, Acute treatment)
Midodrine/ProAmatine (PO, chronic treatment)
DVT prophylaxis-
Apply pneumatic compression boots or stockings
Perform ROM at least q8h
Helps prevent muscle contraction
Increases venous return
Thigh and calf measurements daily
Compression stockings

121
Q

urinary clinical manifestations for SCI

A

Acute
-Atonic bladder with RETENTION in spinal shock
Chronic problems
-Post acute phase
–Irritability causing dribbling
–Frequent urination.
-Neurogenic bladder
–Spastic or flaccid
-Retention and distention
–Urinary infection
–Calculi
Interventions/ Actions
INTERMITTENT CATHETERIZATION!
Sexual function

122
Q

what is crede’s crude

A

maneuver applying pressure over the symphysis pubis to expel the urine when cathing; used to initiate voiding in bladder retention with neurogenic bladder

123
Q

what is poikilothermic?

A

the adjustment of body temp to room temperature

124
Q

SCI complication: hypercalcemia sx

A

Dehydration
Fatigue
“lethargy”
Apathy
Abdominal pain
Anorexia
Nausea
Vomiting
Polydipsia
Polyuria
Behavioral changes
Kidney stone- develop over time

125
Q

hypercalcemia tx

A

Acute Treatment
Hydration first
Monitor for volume overload
Medications to increase Calcium excretion
Pamidronate- slows release of calcium from bones (Biphosphonate) 2-3 days to work
Calcitonin- synthetic hormone that causes decrease blood calcium and increase bone calcium
Loop diuretics can help excrete calcium
Prednisone- (temporary) increases excretion of calcium
Long term
Reduce amount of Vitamin C intake
> 500mg of Ascorbic acid increases oxalate concentration and risk of stones

126
Q

spinal shock presentation

A

Loss of reflex function below level of injury
A sudden depression of reflex activity in the spinal cord (areflexia)

127
Q

occurence of spinal shock

A

Immediately after complete cord transection
May begin within 1 hour with incomplete lesions
Lasts upto 6 weeks
Regaining reflexes slowly

128
Q

complications of spinal shock

A

Blood flow to cord may be compromised
Hypotension can increase cord damage

129
Q

spinal shock assessment findings

A

Motor/ Sensation
Loss of all spinal reflexes below injury,
Loss of sensation
Absence of visceral and somatic sensations below level of injury
Cardiac
Blood pressure normal to hypotensive
Heart rate normal to bradycardia
Urinary
Decreased bladder function
Abdomen
Bowel distension
Paralytic ileus- begins 2-3 days post injury, resolves by day 7

130
Q

spinal shock interventions

A

Maintain MAP to perfuse spinal cord
NG tube PRN paralytic ileus
Urinary bladder interventions
Maintain skin integrity
Frequent position changes
Passive ROM to avoid contractures

131
Q

neurogenic shock presentation

A

Hallmark: Hypotension
due to vasodilation, due to loss of sympathetic tonic input
Bradycardia
Not tachycardia, the usual shock response
Inability to convey the information to the vasomotor centers in spinal cord

132
Q

neurogenic shock occurence

A

Spinal cord injuries T6 or above
Symptoms begin within 24 hours of injury
Lasts days to weeks

133
Q

neurogenic shock complications

A

DVT due to blood pooling
Orthostatic hypotension due to loss of vascular muscle tone
Unable to regulate temperature, observe close for fever
Fluid resuscitation alone can cause volume overload and pulmonary edema

134
Q

neurogenic shock assessment findings

A

Cardio/Vascular
Loss of tone: muscle tone in blood vessel walls = pooling of blood
Decrease in: BP, heart rate, cardiac output
Peripheral vasodilation = venous pooling
Postural hypotension
Motor
Loss of ANS function below level of injury
Integumentary
Pt does not perspire in affected areas
Loss of temperature regulation
Venous pooling in extremities

135
Q

neurogenic shock interventions

A

Transfer or change positions slowly
Monitor for DVT
Monitor vital signs
Vasopressors for hypotension- fluid will not improve
Atropine for severe bradycardia
* A drop in cardiac output and blood pressure can be life threatening*

136
Q

causes of autonomic dysreflexia

A

Noxious stimuli causes overactivation of ANS
Causes vasospasm
Potentially life threatening medical emergency
Abrupt onset of excessively high blood pressure 200-300

137
Q

occurrence of autonomic dysreflexia

A

Spinal cord injuries above T6
After recovery from spinal shock
Usually at least 6 months after initial injury

138
Q

complications of autonomic dysreflexia if left untreated

A

Seizure
Stroke
MI
Death

139
Q

stages of autonomic dysreflexia

A

Noxious Stimuli
Message sent from affected area to spinal cord
Sympathetic response initiated
Vasoconstriction below injury level
Systemic hypertension
Baroreceptors detect hypertension
Reflex Bradycardia & vasodilation
Signal blocked at injury site

140
Q

autonomic dysreflexia presentation

A

Cardiovascular
Hypertension > 200/100
Bradycardia
Integumentary
Above injury level
Flushed face
Red blotches on skin
Profuse sweating
Below injury level
Goose Pimples Cold, clammy skin
GI
Nausea
Neuro
Headache
Restlessness

141
Q

autonomic dysreflexia interventions

A

Immediately place in sitting position
Reduce or eliminate noxious stimuli
-Impaction- digital exam
-Constipation
-Urine retention- straight cath, check foley patency
-Renal stones
-Ejaculation
-Tactile stimulation
-Skin lesions/pressure ulcers- change position
-Ingrown toenail
-Pain
Loosen or remove constricting clothing (TEDS)
Administer antihypertensives as ordered
Educate patient and family about prevention and treatment

142
Q

SCI acute pharmacological tx

A

vasopressors and high dose solumedrol

143
Q

SCI long term pharmacological tx

A

GI symptoms- Histamine 2 blockers
Bradycardia- Atropine
Bladder spasticity- anticholinergics
Autonomic dysreflexia- antihypertensives
Hypotension- vasopressors
DVT/ PE prevention- Lovenox, heparin (consider risks)
Spasms- antispasmodics

144
Q

SCI surgical tx

A

Reduces injury & Stabilizes the spinal cord
Indications
-Cord compression
-Bony fragments or unstable vertebral body
-Bone fragments in the spinal canal
-Compound fracture
-Penetrating trauma to the cord

145
Q

gardner wells tongs are contraindicated for …

A

unstable hyperextension injuries

146
Q

what is bipolar I

A

manic episode with at least one depressive episode

147
Q

what is bipolar II

A

Recurrent depressive episodes with at least one hypomanic episode

148
Q

what is bipolar mixed

A

Cycles periods of mania, normal mood, depression

149
Q

what is cyclothymic

A

Chronic mood disturbance (at least 2 yrs)
No loss of societal/occupational functioning
Exhibits hypomania/depression but never meets above criteria
Never without depression/hypomania for more than two months

150
Q

symptoms of dysthymic disorder

A

chronic mood disturbance
Insomnia
Loss of appetite
Decreased energy
Decreased self-esteem
Trouble concentrating
Sadness
Helplessness
Less severe than major depression

151
Q

what are the 2 types of seasonal affective disorder

A

winter/fall onset and spring onset

152
Q

winter/fall SAD sx

A

Increased sleep
Increased appetite – especially carbs
Weight gain
Interpersonal conflicts
Irritability
Heaviness in extremities

153
Q

spring SAD sx

A

Insomnia
Weight loss
Decreased appetite

154
Q

sx of premenstrual dysphoric disorder

A

Labile mood
Irritability
Increased interpersonal conflict
Trouble concentrating
Feeling overwhelmed or unable to cope
Anxiety
Tension
Hopelessness

155
Q

what is mania

A

A distinct period during which mood is abnormally and persistently elevated, expansive, or irritable lasting at least 1 week

156
Q

mania sx

A

Inflated self-esteem/grandiosity
Decreased need for sleep
Excessive/pressured speech (unrelenting, rapid, often loud without pause)
Flight of ideas -racing, often unconnected thoughts
Distractibility
Increased activity/psychomotor agitation
Excessive pleasure-seeking/risk taking behaviors
Spending money, sexual behaviors
Mood- excessively cheerful, enthusiastic, expansive, irritable
Deny problems, blame others for issues
Can experience delusions & hallucinations when in manic episode
Length of mania varies

157
Q

what is hypomania

A

Period of abnormal and persistent elevated, expansive, or irritable mood.
Difference hypomania do not impair ability to function
No psychotic features
Over time may lead to mania

158
Q

what is mixed episode (mania)

A

Experiencing both mania and depression nearly every day for at least 1 week
Also called rapid cycling

159
Q

interventions for bipolar

A

Provide for safety
Must set boundaries and limits for the patient
Meeting physiologic needs (Maslow)
Decrease stimuli
Establish routines
Ringer foods (high protein/high calorie)
Monitor fluids/sleep
Providing therapeutic communication
Use positive communication to avoid perception of judgement or frustration
Use clear, direct, simple sentences
Ask them to repeat brief messages
Accept responsibility for not understanding their speech
Promoting acceptable behaviors
Treat patient with dignity and respect
Remain matter-of-fact and non-judgmental
Use distraction

160
Q

psychopharmacology for bipolar

A

Lifetime regimen of medication
Antimanic
Lithium
Anticonvulsants
Mood stabilizers
Only psych disorder in which meds can prevent acute exacerbations
Antipsychotic
During acute manic stage (if disordered thinking seen)
Some patients stay on long-term

161
Q

lithium blood levels

A

0.5 – 1.0 mEq/L Normal
0.8 – 1.5 mEq/L Therapeutic
>1.5 mEq/L Toxicity

162
Q

lithium toxicity sx

A

N/V/D, drowsiness, muscle weakness, slurred speech

163
Q

challenging side effects of lithium

A

Tremors
Thirst
Vomiting &/or Diarrhea
Weight gain
Concentration issues
Rebound symptoms if stopped suddenly
Thyroid Issues

164
Q

what is lithium

A

Salt naturally found in the body
Response rate approx. 70-80%
Stabilizes mood
Avoid extremes of mania/depression
Binds to salt receptor sites
Cleared in kidneys
Need regular bloodwork checks levels

165
Q

alternative meds for bipolar

A

valproic acid (depakote)
carbamezapine (tegretol)

166
Q

depakote therapeutic level

A

50-125

167
Q

therapeutic level of carbamezapine

A

4-12

168
Q

what speeds conduction on a neuron

A

myelin sheath

169
Q

neurons are unable to ________.

A

unable to create or store glucose

get glucose by perfusion, adequate blood flow to brain

170
Q

normal glucose level of CSF

A

40-80 mg/DL

171
Q

what are causes of altered LOC

A

increased ICP sustained pressure 15 mmHg or more
cerebral infarction
hematoma
intracranial hemorrhage
tumors
infections
demyelinating disorders
hydrocephalus

172
Q

normal adult intracranial pressure

A

5-15 mmHg

173
Q

why is increased intracranial pressure a life threatening emergency?

A

Increased ICP causes ↓ cerebral blood flow
-Hypoxemia and hypoxia
-Hypercapnia and ↓pH
-Cerebral vasodilation (↑ blood flow),
-Edema
-Continued Increasing ICP
-Irreversible brain damage, brain herniation, & death

174
Q

clinical manifestations of increased ICP

A

Changes in cortical function
Irritability, agitation
Behavior, personality changes
Memory,
Impaired judgment
Changes in speech pattern
LOC decreases

175
Q

what is a big difference with pediatric clinical manifestations of increased ICP?

A

downward deviation of eyes

176
Q

increased ICP interventions

A

Elevate head of bed to 30-45 degrees
Tight glycemic control (keep in 80-180 range)
Prevent shivering
Avoid hyperthermia
Optimize blood pressure-
Avoid hypo/hypertension
Careful fluid resuscitation-
may need pt to keep PaO2 of 60 and sat of 90

177
Q

increased ICP pharmacological interventions

A

Vasopressors- maintain MAP and CPP
Antihypertensive medications as needed
Pain medications
Anxiety medications
Seizure- preventions and acute treatment
Barbiturates- Cerebral protection, decrease cerebral metabolic needs
Osmotic diuretics- Shift fluids into intravascular (Mannitol, Hypertonic saline)

178
Q

TBI primary injury

A

initial direct damage to tissues and blood vessels-permanent damage

179
Q

TBI secondary injury

A

cascade of complex biochemical responses damaging neurons not involved in initial injury.
Impaired cerebral blood flow regulation
Hypoxia
Hypotension
Ischemia
Seizures
Fever
HYPOPERFUSION
Mortality rate can be higher than Primary Injury

180
Q

red flags for TBIs

A

Sudden acute headache
Nausea & vomiting
Increased restlessness
Agitation
Nuchal rigidity
Motor weakness
Pupil changes
Changes in VS
Decrease in GCS

181
Q

types of TBIs

A

Concussion
-Chronic Traumatic Encephalopathy
Epidural Hematoma
Subdural Hematoma
Intracerebral Hematoma
Basilar Skull Fracture

182
Q

cause and result of concussion

A

Direct blow to head, neck, face or torso
Results
Rapid onset of short-lived impaired neuro function with spontaneous resolution
May or may not involve LOC
Normal Neuroimaging (no structural damage)

183
Q

mild concussion

A

GCS score from 14-15 and less than 30 min

184
Q

moderate concussion

A

GCS score from 9-13 and 30 min to 6 hours

185
Q

severe concussion

A

GCS score below 9 and over 6 hours

186
Q

concussion sx

A

physical- headache, N/V, balance or vision problems, fatigue, photosensitivity, noise sensitivity, being dazed
cognitive- feeling foggy, difficulty w concentrating, forgetting recent info, confusion
emotional- irritability, sadness, over emotional, nervousness
sleep- drowsiness, sleeping more, difficulty falling asleep

187
Q

what is cushings triad?

A

increased systolic BP, decreased pulse, decreased respirations

188
Q

what is post concussive syndrome

A

Can last weeks to months
Risk not necessarily associated w/ severity of injury
Normally within the first 7-10 days
H/A described as tension, dizziness, fatigue, irritability, anxiety, insomnia, decreased concentration/ memory, sensitivity to noise and light
Cumulative threat

189
Q

what is concussion secondary impact syndrome

A

After initial concussion additional trauma to brain (before fully healed) can lead to short and long-term neurologic problems
Additional Brain trauma
May only be minor
Causes neurologic disturbance
Typically with catastrophic results
Signs & Symptoms
Cerebral edema
Cerebral blood flow compromised
Decrease in tissue pH
Hypoxemia and Hypotension

190
Q

what is chronic traumatic encephalopathy

A

Repeated brain trauma cause increased tau release in the brain
Younger (12 & under) athletes sustain more damage with repeated injury
Symptoms can be delayed 8-10 years
Progression is predictable through 4 identified stages
End stage develops into Parkinson’s disease or Alzheimer’s like presentation
Postmortem currently only definitive diagnosis

191
Q

CTE stage 1

A

Attentional deficits, headaches, and dizziness

192
Q

CTE stage 2

A

Increased prominence of mood swings or emotional changes, impulsive behavior, or poor judgement. (may include explosive, pathological, intoxicated and morbid paranoia or jealousy)

193
Q

CTE stage 3

A

Memory and cognitive impairment including trouble with executive functioning

194
Q

CTE stage 4

A

Progressive Alzheimer like dementia with motor symptoms, Parkinson’s like or lack of coordination, hypomimia (speech abnormalities)

195
Q

what is epidural hematoma

A

Rupture or laceration of artery
Usually by Skull fracture
Arterial bleeding
Blood accumulates between skull & dura mater
Extreme emergency: Rapid Progression

196
Q

epidural hematoma sx

A

Transient LOC then
Lucid intervals
Then rapid deterioration in neuro status
Neurologic deficits
Resulting in coma
Respiratory arrest

197
Q

epidural hematoma tx

A

craniotomy to relieve pressure

198
Q

acute subdural hematoma sx

A

Symptoms within 48 hours
Signs & Symptoms
Altered LOC
S/S of IICP
Hemiparesis
Hemiplegia opposite side from hematoma
Unilateral fixed and dilated pupils on same side

199
Q

subacute subdural hematoma sx

A

Symptoms between 48 hours and 2 weeks
Signs & Symptoms
Altered LOC
S/S of IICP
Hemiparesis
Hemiplegia opposite side from hematoma
unilateral fixed and dilated pupils on same side

200
Q

chronic subdural hematoma sx

A

2 weeks after injury
Seen with alcoholism, anticoagulants
Signs & symptoms
Headache
Progressive personality changes
Decrease in LOC
Ataxia
Incontinence
Seizures

201
Q

common causes of intracerebral hematoma

A

Occurs deep within brain tissue
Common causes
Contusions
Untreated hypertension

202
Q

locations of intracerebral hematoma

A

frontal lobes, temporal lobes

203
Q

s/s of intracerebral hematoma

A

Progressive rapid decline in LOC
Headache
S/S of IICP
Pupil changes
Contralateral hemiplegia
Systemic hypertension,
CVA presentation

204
Q

what is basilar skull fracture

A

Fracture to floor of skull
Laceration to vasculature
Often leads to CSF leakage
High risk for infection

205
Q

signs of brain herniation

A

2 or more of the following:
Movement
Extensor posturing
Lack of motor response to noxious stimuli
Pupils
Asymmetric
Dilated
Non-reactive pupils
Level of Consciousness
Drop in GCS >2 in patient with initial GCS of <9

206
Q

pharmacology for increased ICP

A

Diuretics
Sedation
Paralytics are chemical restraints
Antipyretics
Anticonvulsants
GI prophylaxis
TPN if enteral feeding not possible
IV fluids

207
Q

diuretics for increased ICP

A

Hypertonic Saline
Mannitol (Osmotic) Used for ICP over 15-20mmHg
Draws water out of edematous brain tissue into vasculature
Always use lowest dose possible
Loop Diuretics
Furosemide .
Inhibit Na and Cl reabsorption
Reduce rate of CSF production

208
Q

what is persistent vegetativ state

A

Complete unawareness of self or environment
Loss of all cognitive functions
Death of cerebral hemispheres
Continued function of the brainstem and cerebellum
May have eye opening to external stimuli
Unable to follow commands
Bowel and bladder incontinence
Variable cranial nerve preservation
May retain cough, gag, and swallow reflex
But unable to coordinate actions
Dx 1 month after injury

209
Q

what is locked-in-syndrome?

A

Lesion in pons of the brain
Complete paralysis
Inability to speak
Tetraplegia
Alert & fully aware of environment
Pervasive awareness and cognitive function
Some eye movements
Blinking is the only form of communication
Normal hearing and seeing
No chew, swallow, gag reflexes, or breathing on their own

210
Q

prognosis of locked in syndrome varies according to ____.

A

cause
pathological process
age
condition

211
Q

what is brain death

A

Irreversible loss of function of the entire brain
Absence of brain stem reflexes

212
Q

what is a seizure?

A

Abnormal discharge of energy & subsequent spread through cerebral cortex.
Disrupts neurologic functioning.
Result in generalized or localized motor activity
*key piece of information is the patient’s hx or not of seizures

213
Q

causes of seizures

A

TOXINS/POISONING
DRUGS
METABOLIC DISTURBANCES/ ELECTROLYETS
HYPOGLYCEMIA
KIDNEY FAILURE
INFECTION
SHOCK
Bleeding in the brain
TRAUMATIC BRAIN INJURY
STROKE
TUMORS/ CANCERS
FEVER
ALCOHOL
HYPOXIA
ECLAMPSIA
MEDICATION NON-COMPLIANCE

214
Q

generalized seizures

A

occurs in both hemispheres
may begin with an aura
tonic clonic and absence

215
Q

what is tonic-clonic seizure

A

muscle hypertonic state to clonic or ridged contractions
rhythmic
recurrent jerking
possible airway compromise
followed by post-ictal state

216
Q

what is petite mal seizure

A

absence
loss of awareness
no change in muscle tone
common in children

217
Q

what is a partial seizure

A

limited to a discrete part of brain
rare post ictal state because only one area
sx dependent on location

218
Q

what is a simple seizure

A

remain conscious
sudden unexplained feelings
sense something aren’t real
may have language impairment
may have muscle involvement

219
Q

what is a complex seizure

A

may have an aura
amnesia before and after
impairment of awareness with typical movements (lip smacking, picking at clothing)

220
Q

what is status epilepticus

A

prolonged continuous seizure activity or multiple seizures in a short period of time without full recovery

221
Q

precipitating seizure events

A

AURAS
-LIGHTS
-SOUNDS
-SMELLS
SPECIFIC COMPLAINTS
-WEAKNESS
-PAIN
UNUSUAL BEHAVIORS
RECENT INFECTION
HEADACHE/RECENT TRAUMA TO THE HEAD
HISTORY OF SUBSTANCE ABUSE
MEDICATION CHANGES

222
Q

DO for seizure interventions

A

Keep them safe
Monitor Airway
Place in side-lying position
Move objects away
Time the seizure
Observe characteristics
Have suction ready
Pad siderails
Ask family about precipitating factors
-Medication compliance
-Trauma
-Toxic ingestion
-Infection
-Hypoglycemia

223
Q

DONT for seizure interventions

A

Restrain the patient
Put anything in their mouth
Leave the patient

224
Q

brief seizure

A

less than 5 minutes

225
Q

prolonged seizure

A

over 30 minutes

226
Q

goal of therapy for status epilepticus

A

rapid termination of both clinical and electrical seizure activity
Airway control
Midazolam (Versed) IV/IN if IV not established
Diazepam (Valium) & Lorazepam (Ativan) given IV

227
Q

acute complications for status epilepticus

A

Hyperthermia
Pulmonary Edema
Cardiac Arrhythmias
Cardiovascular Collapse
Death

228
Q

long term complications for status epilepticus

A

Epilepsy
Encephalopathy
Local Neurologic deficits

229
Q

clinical presentation of New Onset Refractory Status Epilepticus

A

Patients suddenly develop a prolonged seizure or a flurry of seizures that do not respond to at least two standard anti-convulsant medications and for which cause for the seizures remains unidentifiable beyond 72 hours.

230
Q

What is NORSE?

A

defined as refractory status epilepticus without an obvious cause after initial investigations

231
Q

seizure medications

A

anticonvulsants- levetiracetam (keppra), carbamezapine (tegretol), phenytoin (dilantin)
barbiturates- phenobarbital
benzodiazepines- diazepam (valium), lorazepam (ativan)

232
Q

what is tegretol first choice for?

A

partial, generalized tonic clonic and mixed seizures

233
Q

common adverse effects of tegretol

A

fatigue, vision changes, nausea, dizziness, rash, serious blood disorders

234
Q

risk factors for dilantin toxicity

A

Advanced age
Concurrent use of medications
-Other seizure medications
-Antibiotics
-Antiarrhythmics
-Alcohol
-Tuberculosis medications

235
Q

symptoms of dilantin toxicity

A

Fast, uncontrollable eye movements or double vision
Dizziness, drowsiness, or confusion
Lack of coordination of fingers, hands, arms, legs, or body
Slurred speech
Nausea or vomiting, Decreased appetite
Decreased activity
Abdominal bloating
Irregular jerky movements in children or the elderly

236
Q

public health

A

reminder to look at public health pictures- lyme

237
Q

required documentation for non-behavioral restraints

A
  • Verification of restraint order
  • Modification in plan of care
  • Alternatives tried prior to restraints
  • Individual assessment and reassessment related to restraints
  • Clinical justification for restraints
  • Type of restraint used
  • Education provided to patient or family about restraints
  • Monitoring results
  • Care provided while in restraints
  • Staff concerns related to safety that led to restraints
  • Any injuries sustained by patient (if applicable)
238
Q

required documentation for behavioral restraints

A
  • Verification of restraint order
  • Modification in plan of care
  • Alternatives used or considered prior to restraints
  • Individual assessment and reassessment related to restraints
  • Clinical justification for restraints
  • Type of restraint used
  • Education provided to patient or family about restraints
  • Monitoring results
  • Care provided while in restraints
  • Staff concerns related to safety that led to restraints
  • Any injuries sustained by patient (if applicable)
  • Participants in restraint application

NURSING 220 (4 decks)

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