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Patho 3 (Path 312) > CNS disorders (Mod 2) > Flashcards

CNS disorders (Mod 2) Flashcards

1
Q

What are 6 types of brain/spinal cord injuries?

A
  • Traumatic Brain Injury (TBI)
  • Stroke
  • Infection (Meningitis, Encephalitis)
  • Seizures
  • Tumors
  • Spinal Cord Injury (Covered in Mod )
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2
Q

What kind of ventilation would you most likely use for a patient with a brain/spinal cord injury?

A

Pressure support ventilation for spinal cord injury.

  • If TBI is suspected, follow TBI protocol
  • TBI goals are CO2 35-40 w/O2 goals 80-120
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3
Q

When would you expect Central neurogenic hyperventilation?

A

Coning

  • loss of respiratory drive
  • response to reduced CO2 levels in the blood from brain lesions or injury
  • Destruction of the brain stem
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4
Q

When would you expect central neurogenic hyperventilation?

  • aka causes
A

CNS lymphoma

  • caused by compression of midbrain via edema or trauma
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5
Q

When would you expect Biots breathing?

A

Episodes of deep inspirations w/periods of apnea

  • Damage to the medulla
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6
Q

When would you expect Apneustic breathing?

A
  • Prolonged, gasping inspiration but not effective respirations. Need to bag
  • Damage to upper pons
  • Poor prognosis
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7
Q

When would you expect Cheyne Stokes Respiration

A

Associated w/decreased cardiac output (heart failure), central sleep apnea, and damage to respiratory centres

  • cycles of gradual increase in rate and volume followed by gradual decrease, then period of apnea
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8
Q

What is the relationship between cerebral blood flow (CBF) and CO2

(slide 6)

A

Decreased CO2 vasoconstriction brain vessels causing decreased CBF

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9
Q

What is a sign of coning?

A

Cushings triad

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10
Q

What are ventialtor strategies for brain/spinal injuries?

A
  1. Low-normal PaCO2 to decrease CBF and ICP
  2. Hyperventilation if coning is suspected, can decrease O2 delivery
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11
Q

CPP is compromised of?

A

MAP and ICP

  • CPP = MAP - ICP
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12
Q

Normal ICP?

A

10-15 mmHg

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13
Q

What happens if ICP is between 15-20?

A

microcirculation compromised (capillary compression)

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14
Q

What happens if ICP is between 30-35?

A

Venous drainage impeded

  • edema develops in uninjuried tissue
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15
Q

Why do you want to hyperventilate a pt suspected of coning?

A

Reduce metabolic demand of the heart

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16
Q

is primary or secondary brian injury more likely to cause the diffuse cascade that leads to brain death?

A

Secondary; continuation of damage following the TBI

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17
Q

what is TBI defined as?

A

Damage caused to the brain by external mech forces

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18
Q

Mild TBI characteristics?

A

Glasgow Coma Scale 13-15

  • loss of consciousness up to 15 minutes
  • Usually recover
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19
Q

Moderate TBI injury characteristics

A

GCS 9-12

  • LOC up to 6 hours, may deteriorate because of rising ICP
  • CT scan useful but may not need hemodynamic or respiratory support
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20
Q

Severe TBI characteristics

A

GCS 3-8,

  • LOC over 6 hours, CT scan to identify extent of damage
  • Respiratory and circulatory support typically needed
  • Combative patients may need to be heavily sedated to acquire a CT scan, necessitating intubation.
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21
Q

Signs and symptoms of Mild TBI injury?

A

Headache, nausea, vomitting, dizziness, lack of motor coordination, clumsiness, visual disturbances, changes in sleep patterns

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22
Q

signs and symptoms of severe injury?

A

Loss of consciousness, Dilated pupils (one or both), “blown pupils,” Apnea, Paralysis/Weakness

  • Cushion’s Triad (Bradycardia, Hypertension, Irregular respiration)
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23
Q

Decorticate vs Decerebrate

A
  1. Decerebrate is more severe; damage to brainstem. hyperextended body.
  2. Decorticate; damage to cerebrum; arms adducted inward.
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24
Q

What does shifting of the ventricles mean?

A

shifting of the ventricles; means we’ll see the midline of the brain shift

  • treated w/burr hole (cerebral drainage)
  • usually occurs when blood is between the layers of the brain
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25
Q

What is a epidural hematoma?

A

Blood between skull and dura

  • Trauma etiology
  • Conditino detiorates rapidly as fluid acclimates
  • Treated w/burr hole (cerebral drainage)
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26
Q

Treatment for epidural hematomas?

A

Treated w/Burr hole

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27
Q

What is a subdural hematoma?

A

Accumulation of blood between dura and arachnoid layers

  • Accelration/deceleration injury -> rupture cerebral veins
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28
Q

What is the onset of subdural hematomas (3)

  • acute
  • subacute
  • chronic
A
  • Acute = within 48 hours
  • subacute = 3-20days
  • Chronic = 20+ days
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29
Q

TBI penetrating head injury characteristics

A

obvious and lifethreaning

  • weapons
  • vascualr tearing from object entering skull
  • route for infection
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30
Q

TBI diagnostics

A
  • DI (CT and MRI)
  • Angiography
  • ICU (ICP monitoring, SjvO2, Licox, EEG)
  • CT = quick and accurate…MRI = more detailed = better prediction of outcome.
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31
Q

What does SjvO2 reflect?

A

How much brain tissue is extracting oxygen

  • remember, it is measured by the blood leaving the brain
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32
Q

why does seizure activity increase…? (2)

A
  1. Increases cerebral metabolic demand
  2. Increases ICP
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33
Q

What is TBI acute management for a primary injury?

A
  • Transport to neuro treatment center
  • Supportive Management-ABC’s
  • Surgical Care (craniotomy, burr hole, hematoma evacuation
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34
Q

Surgical care for primary TBI injuries?

A
  • Burr hole -> done emergency ​

​
- Craniotomy: planed out, remove a portion of the skull to allow room for edema to happen in the brain ​ grafted under the patient skin to preserve

  • Hematoma evacuation-burr hole and a taking catheter and exoculating blood  
  • Mass excision - removal of foreign objects
  • Tissue debridement, getting rid of dead tissue
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35
Q

TBI Acute management for a secondary injury?

A
  • Therapeutic hypothermia
  • ICP control
  • Maintain MAP to maintain CPP
  • Manage cerebral edema
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36
Q

What drugs can be given to maintain MAP or CPP?

A

FLuids and vasopressors

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37
Q

How is cerebral edema managed?

A

Mannitol, lasix, hypertonic saline

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38
Q

For Chronic brain injury management, what are some expected complications?

A

Depends on severity of injury, For higher brain death:

  • Tracheostomy and infection management
  • DVT and Pressure sores
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39
Q

Rehab for chronic brain injury?

A

Months to years

  • PT
  • SLP (speech language pathology)
  • Cognitive rehabilitaiton therapy
  • Occupational therapy
  • Mental health support
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40
Q

How can ICP control be managed?

A
  • Position
  • Sedation, anelgesia, paralytics
  • Therapeutc hyperventilation (Vent strategy and ABG goals)
  • Extra-ventricular drain (EVD)
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41
Q

Define Stroke

A

Rupture of block of blood vessel in brain

  • Deprives brain of blood supply
  • Areas of ischemia can be permanently damaged (infarction)
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42
Q

Stroke risk factors

A
  • Age
  • Genetics
  • Hypertension
  • Diabetes
  • High cholesterol
  • Tobacco use
  • Cardiac disease
  • Oral contraceptives
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43
Q

How does diabetes increase the risk of stroke

A

High glucose (hyperglycemia) damages blood vessels

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44
Q

FAST acronym?

A

S and S for Stroke

  • Facial drop
  • Arms weakness
  • Speech difficulty
  • Time to call 911
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45
Q

Signs and symptoms of stroke

A

Arm weakness (if they can’t keep it up)

  • numbers, confusion, vision problems, dizziness, severe headache w/no known cause
  • weakness, memory problems, fatigue, nausea, vomiting (more common in women)
  • speech difficulty and face drooping
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46
Q

Classification of strokes (6)

  • break these up later into separate cards
A

Ischemic strokes (majority of strokes)

  • Thrombotic
  • Embolic
  • Lacunar
  • TIA
  • Hemorrhagic
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47
Q

What are Hemorrhagic strokes caused by?

A

Aneurysms (bulging of vessels that burst)

  • weakened area in blood vessel (ballooning)
  • If bursts or leaks, bleeds into the brain
  • Precipated often by stress/HTN
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48
Q

What are the subdivisions of hemorrhagic strokes?

A

Intracerebral hemorrhage and Intracranial Hemorrhage

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49
Q

Prehospital phase ischemic stroke treatment

A

Speedy Transport to centre (that is EVT capable)

  • Eligible pts IV thrombosis is (tPA aka Alteplase aka clot buster)
  • Thrombolysis (within 4.5 hours of signs)
  • EVT (up to 24 hours of signs)
50
Q

Hospital phase treatment for ischemic stroke

A
  • Supportive care aka airway management
  • Medical management via clot buster
  • mechanical thrombectomy (stent device used to remove clot)
51
Q

Hemorrhagic stroke treatment

A
  • Burr hole
  • Craniotomy
  • Endovascular coiling/stent -> remove clot in patients with large vessel occlusion (LVO) stroke
  • Artery bypass and occlusion
  • Clipping
52
Q

What are seizures indicative of?

A

Indicative of other underlying problems (usually brain issues)

  • problem w/brain converting chemical to electrical impulses in the brain
  • imbalance of excitatory and inhibitor (which is why you see rapid movement)
  • can be acute or chronic
53
Q

How are seizures identified?

A

EEG (electroencephalogram)

54
Q

Are seizures acute or chronic?

A

Both

  • Acute = febrile
  • Chronic = epilepsy (2 or more seizures)
55
Q

How long do Seizures last?

A

Typically few secs to mins w/quick cognitive recovery (quick onset)

  • > 5 mins or multiple concurrent seizures Status epilepticus —> medical emergency
56
Q

What is Status epilepticus

A

Medical emergency when a seizure last > 5 mins or there are multiple concurrent seizures for classification

  • can cause damage to the brain and death
57
Q

What are early signs that a person is experiencing a seizure?

A

Prodromes/aura; they can tell you when its happening

  • Fear/anxiety
  • Nausea
  • vertigo
  • visual impairment (brain spots/wavy lines)
58
Q

What is the etiology of chronic seizure conditions?

A

No precipitating event

59
Q

Structural origin of seizures?

A

Trauma, stroke, tumor, malformation of the brain, meningitis

60
Q

Metabolic syndrome that could cause seizures?

A

Diabetes

61
Q

What are the common causes of seizures that have no genetic, chronic, genetic, or structural baring?

A
  • Febrile
  • Electrolyte Imbalances
  • Withdrawl (alcohol and illicit drugs)
  • Kidney/Liver failure
  • Electrolyte imbalances (Na)
  • Unknown
  • Diabetes
62
Q

What is Epilepsy?

A

When 2 seizures occur greater than 24hrs apart or EEG shows high risk of future seizures

  • No precipitating event
  • Pts may not be responsive to treatment (30%)
  • Mostly chronic condition
63
Q

How are Seizures classified?

A

By location rather than cause

64
Q

What is a Focal seizure?

A

Occurs in one area of the brain

  • person may be aware
  • Can become generalized
  • one part of the brain is firing
65
Q

What is a generalized seizure?

A

Awareness not intact

  • occurs in both hemispheres of the brain
  • loss of consciousness
66
Q

2 types of seizures?

A
  1. Focal
  2. Generalized (clonic/grand mal)
67
Q

What is a Clonic Tonic Seizure

(old term was Grand Mal)

A
  • Rythmic jerking of large muscle groups with
    periods of stiffness
  • Typically have a postictal period/phase-confused,drowsy
  • Person most at risk during this type of seizure
68
Q

What are Myoclonic seizures

A

Sporadic, isolated jerking movement

  • more common in kids
69
Q

Treatment for Seizures?

A

Dependant on level of impairment

  • Tonic/clonic most impairment
  • Supportive treatment
  • Acute: benzos, barbituates, propofol
  • Chronic: antiepileptic aka gabapentin
70
Q

Supportive treatment for seizures?

A
  • Positioning
  • Airway managment
  • intubation
  • Bite block/screw thingy -> Crank their teeth open to secure airway
71
Q

What is Cheyne stokes respirations commonly associated with?

A

Decreased Cardiac output and Heart failure.

  • Central sleep apnea
  • Damage to resp centers
72
Q

Therapy goals for abnormal breathing patterns if brain injury is suspected?

A

Keep metabolic demand low, and wake them to evaluate LOC

  • Keep ICP down
  • breathing above the vent
73
Q

What does low cerebral CO2 cause?

A

Decreases ICP

  • Decreased CO2 = vasoconstriction
74
Q

Goal for managing secondary brain injury complications?

A
  1. Maintain CPP 50-70
  2. Avoid ischemia
  3. Prevent systemic and neurological complications
75
Q

Contributors to secondary brain injury aka how does a injury lead to neuron cell death? (5)

A

TLDR: following primary injury, the body uses up energy by compensating via aerobic compensation. The body will shift fluids into places where they aren’t supposed to be and lactic acid will buildup

  1. Primary injury -> depolarization -> aerobic metabolism -> decreased energy stores
  2. K+ out of cells, Na+, Ca++, H2O into cells -> damage and edema
  3. Aerobic metabolism = lactic acid buildup
  4. Release of excitatory neurotransmitters = ion shift
  5. Free O2 radicals = nitric oxide = cell damage
76
Q

What ICP goals should be targeted if secondary brain injury is at risk of occuring?

A

Maintain ICP < 20

77
Q

Why does ICP increase?

A

When vasodilation and fluids flood the brain.

  • When the brain fails to compensate, ICP increases
  • Blood flow depends on perfusion pressure, so… MAP-ICP = CPP
78
Q

Normal CPP?

A

50-70

79
Q

What neurological factors contribute to secondary brain injury?

A
  1. Increased ICP
  2. Seizures
  3. Cerebral vasospasm, loss of autoregulation, ischemia
80
Q

What does cerebral blood flow vary according to?

A

CBF varies based on CPP

  • cerebrovascular vessels will constrict or dilate based on blood flow needs
  • autoregulation of CBF is a compensation mech
81
Q

What systemic factors (extracerebral) would contribute to secondary brain injury?

A

TLDR: whenever blood pressure drops, there will be risk of anerboic compensation and ischemia. It results in less blood flow to the brain and O2 as a result

  • note that hypotension affects CBF when systolic BP < 90
82
Q

On physical assessment, how can you identify cerebellum injury

A

If pupils are fixed and dilated, and hands are drawn into chest and feet pointed towards each other its a cerebellum injury

83
Q

Brain layer order (meningis) from outer to inner?

A

Skull, Dura, arachnoid, Pia, Brain

83
Q

What is the outermost layer of hte meninges

A

Dura

84
Q

What are subarachnoid bleeds and intracerebral hemorrhages known as?

A

Stroke, they’re defined by the location of brain

85
Q

Etiology of Epidural Hematomas?

A

Can either be arterial or venous in orgin; but usually caused by blunt trauma to the head, in the temporal region

  • Injuries in the middle meningeal artery bleed to the epidural space…
  • any meningeal artery can lead to arterial epidural hematoma
86
Q

When does a venous epidural hematoma occur?

A

When skull fractures fill the epidural space, more common in kids

86
Q

What could cause midline shift of the brain?

A

Pressure from the bleed. if pressure accumulates we see shifting in the ventricles.

  • treated with bur hole to drain blood from area to stop bleeding
87
Q

Etiology of subdural hematomas?

A

When blood enters the subdural space (arachnoid space) because of a tear in a blood vessel.

  • Most commonly a vein is leaking blood out of the torn vessel into the space below the dura matter
  • Bleed is scary because it is not noticed right away
  • Acceleration deceleration injury, when you brain is accelerating and than decelerates.
88
Q

What is the purpose of therapeutic hypothermia?

A

Decrease metabolic demand

88
Q

ICP control strategies? (4)

A
  • Raise HOB 30 degrees
  • Sedation, analgesia, paralytics ->mannitol as well
  • Therapeutic hyperventilation (aim for low normal PaCO2 and O2 80-120mmhg)
  • Extra ventricular drain (EVD)
89
Q

Which drugs would likely be used to maintain MAP and in turn CPP?

A

Fluid of vasopressins or norepi

  • mannitol and lasix could also be used to wash out fluid overload from hypertonic saline
90
Q

Licox monitoring levels

  • hint, twitches
A
91
Q

Quick diagnosis for strokes?

A

Lift arms, does one arm drop (push on arms to test for weakness)​

  • 911-every second counts!!!​
  • Left-sided stroke, right sided stroke and brain stem stroke
92
Q

What usually causes deaths with seizures?

A

Position obstruction, consistent seizures is cognitive and causes edema and swelling.

  • Clear the area around seizure events
  • Tell them to get into the recovery position
93
Q

What is charlottes web?

A

A CBD that is used to treat seizures in peds

94
Q

Is Epilepsy genetic?

A

Yep, usually found with kids under 5, under 2 most commonly ,

  • Febrile​: happens once with kids and they dont seize again
95
Q

Management of delirium tremors

A

To control DT and Seizures; patient has to be sedated intubated and ventilated until the withdrawal is over.

  • ppl dependent on alcohol or inebriated most of the time, bc they’re so severe when they suddenly stop.
96
Q

What is the Posttical Period?

A

30 mins after seizure event.

  • Pt is usually confused and don’t know what happened
97
Q

Acute treatment for seizures

A

Benzos, barbituates, propofol if they’re in a state where the seizure is prolonged

98
Q

Thrombotic stroke?

A

Blood clot forms in artery leading to brain

99
Q

Embolic stroke?

A

Clot develops elsewhere in body and travels to brain

100
Q

Lacunar stroke

A

Atherosclerosis causes obstruction (gradual progression to this event)

101
Q

Transient Ischemic attack (TIA)?

A

Temporary interruption of blood flow to brain. Symptoms resolve.

  • people go into surgery to have their arteries scrapped out to prevent a stroke from happening 
  • some lead to stroke
102
Q

What drugs are usually given if a blood clot is found?

A

Clot busters baby: Alteplase a fibrinolytic agent often referred to as a tissue plasminogen activator (tPa)

103
Q

Meningitis​

A

Infection of the membranes (meninges) surrounding the brain

  • Characterized by cytokine damage leaking in CSF
  • Diagnosed by lumbar puncture
104
Q

Encephalitis

A

Inflammation of the brain parenchyma.

  • swelling = cerebral edema = Increased ICP
  • Causes destruction of nerve cells and brain damage
  • Destruction of nerve cells, intracerebral hemorrhage​
105
Q

Myelitis

A

Infection of the spine

106
Q

Encephalomyelitis

A

Both brain and spinal cord involved with infection/inflammation

107
Q

Most common cause of CNS infection?

A

Herpes Simplex virus

  • super dangerous in infants, cautious and treated with anti virals
108
Q

Etiology of CNS infection/inflammation causing pathologies like meningitis

A

Pathogen (bacteria/virus/fungus) invade brain and cause inflammation​

  • usually herpes
  • Bacterial meningitis is rare, but deadly
109
Q

Treatments for Bacterial meningitis?

A

Antibiotics asap, person gets sick fast but can be okay for a while.

  • vaccine uptake is decreasing though
110
Q

Usual causes of bacterial meningitis

A

Streptococcal, Pneumococcal, and meningococcal most common.

  • vaccines are available, but uptake is decreasing.
111
Q

How are encephalitis and meningitis diagnosed?

A
  • Encephalitis by CT or MRI
  • meningitis by lumbar puncture; Serology tests to detect virus; Leukocytosis is a marker of infection in the cerebral spinal fluid.
112
Q

Cardinal sign of meningitis?

A

Severe stiff neck/back + headache

113
Q

Prevention of CNS infection/inflammation?

A

Immunization (MMR, Chickenpox): Rate of vaccine are declining and outbreaks are coming back.

  • Supportive care: intubation and ventilation if they can’t manage their airways
  • Antivirals (acyclovir for HSV virus)
  • antibiotics if bacterial
  • corticosteroids (limited support)
114
Q

Etiology of Cerebral Abscess

A

Caused by bacteria/fungus from location in the head from sinuses, dental procedures, or any open head injury)

  • opportunistic (IV drug use, HIV)
  • high mortality rate
115
Q

sign and symptoms for Cerebral Abscess?

A

Headache, confusion, stiffness, confusion, weakness, nausea, and vomitting.

116
Q

Treatment for Cerebral Abscess

A

Antibiotics, antifungals, steroids. Aspiration of puss via CT guided aspiration or craniotomy

117
Q

Brain tumor diagnosis?

A

Tested with tissue biopsy

118
Q
A

Patho 3 (Path 312) (10 decks)

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