Neurological Diseases Flashcards

Test 3

1
Q

CBF is modulated by ____ (5)

A

Cerebral metabolic rate
CPP
PACO2
PAO2
Various drugs and intracranial pathology

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2
Q

CPP =

A

Cerebral perfusion pressure

CPP = MAP - ICP

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3
Q

Cerebral blood flow is ____

A

Autoregulated

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4
Q

What is the value of CBF?

A

50 ml/100g brain tissue per min –>
750ml/min

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5
Q

CBF is about ___% of CO

A

15%

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6
Q

What does the intracranial & spinal vault contain?

A

Neural tissue (brain/spinal cord)
Blood
CSF

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7
Q

The spinal vault is enclosed by the ______ & ______

A

Dura mater

Bone

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8
Q

What is the combined volume of brain tissue, CSF, and intracranial blood? What is the ICP at this volume?

A

1200 - 1500 ml

ICP = 5 - 15 mmHg

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9
Q

What is the Monro-Kellie hypothesis?

A

Any increase in one component of intracranial volume must be offset by a decrease in another component to prevent in elevated ICP

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10
Q

T/F: eventually, a point is reached with a small increase in intracranial content results in a large increase in ICP –> cerebral ischemia

A

T

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11
Q

The _______ separates the two cerebral hemispheres

A

Falx cerebri

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12
Q

Describe the Tentorium cerebelli

A

Rostral to the cerebellum

Separates the supratentorial & intratentoiral spaces

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13
Q

Increases in contents in 1 may cause ______ increases in ICP

A

regional

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14
Q

Describe a subfalcine herniation

A

Against the falx cerebri –> compress branches of anterior cerebral art. –> midline shift

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15
Q

Describe Transtentorial Herniation

A

Supratentorial contents against tentorium cerebelli –>compress brainstem (in a rostral to caudal direction)

S/S: AMS
Defects and ocular reflexes
Hemodynamic/respiratory compromise
Death

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16
Q

Describe Uncal herniation

A

Uncus (medial portion of temporal lobe) herniate over the tentorium cerebelli

S/S: ipsilateral oculomotor nerve dysfunction
Pupil dilation
ptosis
Lateral deviation of the affected eye
Brainstem compression
Death

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17
Q

describe herniation of the cerebellar tonsils

A

Caused by elevated infratentorial pressure –> cerebellar structures herniate thru foramen magnum

S/S: medullary dysfunction
Cardiorespiratory instability
Death

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18
Q

What causes an increase in ICP? (4) How?

A
  1. Tumors: size; causes edema in surrounding brain tissue; tumors in 3rd ventricle obstruct CSF flow
  2. Intracranial hematomas
  3. Blood in CSF: obstructs CSF absorption; granulations further IICP
  4. Infections (Meningitis/encephalitis): edema; obstruction of CSF reabsorption
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19
Q

List methods to decrease ICP (8)

A
  1. Elevate head
  2. Hyperventilation: lowers PaCO2
  3. EVD: drains CSF
  4. Hyperosmotic drugs: increase serum osmo –> drawing fluid across BBB
  5. Diuretics
  6. Corticosteroids
  7. Propofol (Cerebral vasoconstricting anesthetics): decreases CMRO2/CBF
  8. Sx decompression
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20
Q

What is MS? Rx; S/S; Triggers; Tx

A

Multiple Sclerosis

Genetic Neurological disorder
Progressive, autoimmune
Demyelination of central nerve fibers

Rx: Female; smoking; other autoimmune disorders; EBV (Ebstein-barr virus), 1st degree relative that has it

S/S: motor weakness, sensory disorders, visual impairment, autonomic instability

Triggers: Stress, elevated temps; post partum

Tx: No cure
Managed w/ steroids, immune modulators, targeted antibodies (IVIG)

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21
Q

MS is more common in ______ and the onset is ______yo

A

females

20-40 yo

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22
Q

What my considerations with MS?

A
  1. Respiratory compromise –> pulm function tests
  2. Liver function tests lab if on dantrolene & azathioprine (bone marrow suppression & liver function impairment)
  3. Preop steriods
  4. temp management –> can trigger an exacerbation
  5. Avoid succs –> induce hyperkalemia
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23
Q

T/F: With MS, you cant do GA

A

F

All anestheia options are acceptable

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24
Q

What is MG? Rx; S/S; Triggers; Tx

A

Myasthenia Gravis
Genetic Neurological disorder
Autoimmune antibodies generated against N-ACh-r at skeletal motor endplate

S/S: muscle weakness, diplopia, ptosis

tiggers: pain, insomnia, infection, Sx

Tx: Ach-E inhibitors (pyridostigmine), immunosuppressants, steroids, plasmapheresis, IVIG, thymectomy

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25
Q

MG affects _______ muscle and is exacerbated with ________

A

skeletal muscle (ONLY)

exercise

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26
Q

MS has _____ & ______ involvement. What symptoms will you see?

A

ocular

bulbar

ocular: diplopia, ptosis
Bulbar: laryngeal/pharyngeal weakness –> resp/aspiration!!!!

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27
Q

MG has _______hyperplasia and 90% of pts improves with ________

A

thymic

thymectomy

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28
Q

What are MG considerations?

A

-Reduce paralytic dose – prolong muscle weakness

-Caution w/ opioids – resp compromise

Pyridostigmine may prolong Succs & Ester LA –> this is bc this med is used in the treat tx of this.

-Liver function test if on Azathioprine

-Preop steroids

Counsel pt on risk of needing to be on vent longer post Sx

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29
Q

Eaton-Lambert has S/S similar to _____

A

MG

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30
Q

What is Eaton-Lambert syndrome? Rx; S/S; Tx

A

Genetic Neurological disorder
Autoimmune antibodies against VG Ca++ channels

Reduces Ca influx into presynaps –> decrease Ach release at NMJ

Sx: progressive limb-girdle weakness, dysautonomia, oculobulbar palsy (similar to MG)

Tx: 3-4 diaminopyridine (K channel blocker), Azathioprine, Ach-E inhibitors, steroids, plasmapheresis, IVIG

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31
Q

Eaton-Lambert syndrome is ________ sensitive than MG to muscle relaxants

A

More

ELS is very very sensitive to them!!!

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32
Q

What are Eaton-Lambert syndrome considerations?

A

Optimize resp. function
Very sensitive to muscle relaxants
Use EXTREME caution with opioids as well
Counsel on needing vent post Sx

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33
Q

What is Muscular Dystrophy (MD)?

A

Hereditary disorder of muscle fiber degeneration –> dystrophin-glycoprotein breakdown –> skeletal muscle permeability; myonecrosis, fibrosis

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34
Q

There are ___ types of MD

A

6

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35
Q

What is the most common type of MD?

A

Duchenne MD
Most severe form

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36
Q

Duchenne MD occurs in _____ and has an onset of ____

A

boys

2-5yo

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37
Q

Duchenne MD will be wheelchair bound by _______ and has a lifespan of _____. What is this caused by?

A

Wheelchair bound: 8-10 yrs

Lifespan: 20-25yrs
Death caused by: cardiopulmonary complications

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38
Q

What are the S/S of MD?

A

Progressive muscle wasting w/o muscle/sensory abnormalities; long bone fragility; resp weakness; frequently PNA; EKG changes

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39
Q

In MD, your _______ lab will be elevated. Why is this?

A

Creatine kinase

dt muscle wasting

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40
Q

What is hypermetabolic syndrome? What patholgy is this seen in?

A

Seen in MD

Similar to MH –> triggered by Succs & VA

Can lead to rhabdo, hyperK+, vfib, cardiac arrest

Keep MH cart close w/ Dantrolene!!

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41
Q

What medications do you avoid in MD? Why? What can you use instead?

A

Succs & VA

exacerbate instability of muscle membrane –> hypermetabolic syndrome

You can use Roc and TIVA for GA

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42
Q

What considerations should we have with MD?

A

EKG, Echo
Hypermetabolic syndrome (no succs/VA)
Have MH cart close

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43
Q

Why do we need an EKG and Echo for MD?

A

Evaluate for cardiomyopathy

EKG changes can occur

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44
Q

What is the prefered type of anesthesia for MD? Why?

A

RA over GA to avoid triggers and cardiopulmonary complications

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45
Q

What are the 3 different types of Myotonic Dystrophies?

A

Myotonic Dystrophy
Myotonia Congenita
Central Core Disease

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46
Q

Define Myotonia (Myotonic)

A

Prolonged contraction after muscle stimulation

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47
Q

Describe Myotonic Dystrophy: Onset; s/s

A

Onset: 20-30yo

S/S: muscle wasting in face, masseter, hands, pretibial
-Can affect pharyngeal, laryngeal, diaphragm
-Cardiac Conduction may be affected 20% MVP

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48
Q

Describe Myotonia Congenita

A

Involves skeletal muscles only

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49
Q

Describe Central Core Disease: s/s

A

Core muscle cells lack mitochondrial enzymes

s/s: proximal muscle weakness, scoliosis

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50
Q

______ is seen in several muscle disorders

A

Myotonia

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51
Q

Which Myotonic dystrophy is the most common type?

A

Myotonic dystrophy

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52
Q

Which Myotonic dystrophy is the milder form?

A

Mytonia Congenita

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53
Q

Which Myotonic dystrophy is very rare?

A

Central core disease

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54
Q

What are all Myotonic dystrophies triggered by?

A

Stress
Cold

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55
Q

What is the Tx for Myotonic dystrophies?

A

No cure

Manage: Quinine, Procainamide (anti arrhythmic), steroids

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56
Q

What are the considerations for Myotonic dystrophies?

A

-Assess cardiac/pulmonary abnormalites
-GI hypomotility –> aspiration risk
-High risk endocrine abnormalities –> check thyroid/glucose
-Keep pts warm
-optimize preop resp status
-Avoid Succs –> trigger
-Caution w/ opioids
-postop resp weakness

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57
Q

What are the 3 Dementia Syndromes?

A

Alzheimer’s (70%)
Vascular dementia (25%)
Parkinsons (5%)

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58
Q

What considerations should we have when Dementia?

A

-May not be able to give informed consent
-advanced directive
-potential aspiration (may have full stomach - cant remember/tell when last ate)
-Review preop meds – AChE-I, MAOI, psych meds
-risk of postop delirium – consider TIVA
-RA > GA

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59
Q

What type of anesthesia is prefered in Dementia? Why?

A

RA or TIVA

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60
Q

Parkinsons disease has an _______ cause

A

unknown

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61
Q

T/F: You can give a Dementia pt versed

A

F

Increased risk of postop delirium

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62
Q

What is the biggest risk factor for Parkinson’s?

A

Advanced age

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63
Q

What is Parkinson’s disease?

A

Degeneration of dopaminergic fibers of basal ganglia –> decreased dopamine release –>motor neurons overstimulated –> increased extrapyramidal motor system

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64
Q

What does dopamine suppress?

A

Overstimulation of the extrapyramidal motor system

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65
Q

What are the triad s/s of Parkinson’s?

A

Skeletal muscle tremor
Rigidity
Akinesia

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66
Q

What are the s/s of Parkinson’s? Tx?

A

s/s: Rhythmic “pill rolling”
facial rigidity
Slurred speech
Difficulty swallowing
Respiratory difficulty
Depression
Dementia
Akinesia

Tx: Levodopa; anticholinergics; MAOIs, deep brain stimulators

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67
Q

What are considerations for Parkinson’s?

A

-assess severity – degree of pulmonary compromise
-Home meds – MAOIs interact with demerol
-Pulm function test
-EKG/Echo
-aspirational risk –> most have dysphagia at baseline

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68
Q

In Parkinson, PO Levodopa must be ________. Why?

A

Continued

Avoid unstable, extreme extrapyramidal effects –> chest wall rigidity

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69
Q

What medications do you avoid in Parkinsons?

A

Reglan
Phenothiazine
Butyrophenones

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70
Q

If pt is taking an MAOI, you want to avoid giving ________

A

Demerol

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71
Q

In Parkinsons, what consideration should we have with deep brain stimulators?

A

Bipolar is recommended –> If not, discontinue.

Need to avoid interaction with cautery

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72
Q

The main AE of brain tumurs are _______

A

Neuro deficits

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73
Q

What are the s/s of brain tumors:

A

-IICP
-Papilledema
-HA
-AMS
-Mobility impairment
-N/V
-Autonomic dysfunction
-Seizures

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74
Q

What is the frontal lobe responsible for?

A

Personality
Movement
Sense of smell

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75
Q

What is the temporal lobe responsible for?

A

Memory
Speech
Musical Rhythm

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76
Q

What is the partietal lobe responsible for?

A

Identification of objects
Sense of pain & touch
Body navigation
Spatial position

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77
Q

What part of the brain is responsible for identification of pain and touch?

A

Parietal Lobe

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78
Q

What is the occipital lobe responsible for?

A

Vision

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79
Q

What is the medulla responsible for?

A

Control of heart and lungs

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80
Q

What are the pons responsible for?

A

Control of eye and face movement

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81
Q

What is the most common CNS glial cells?

A

Astrocytes

82
Q

What are the tumors originating from the astrocytes called? What are the different types?

A

Astrocytomas

Types: Gliomas
Pilocyctic astrocytomas
Anaplastic astrocytoma
Glioblastoma Multiforme

83
Q

Describe Gliomas

A

Primary tumor
found in yound adults
s/s: new onset seizures

84
Q

Describe Pilocyctic Astrocytomas

A

Benign
Found in children & young adults
Good outcomes w/ resection

85
Q

Describe Anaplastic Astrocytoma

A

Poorly differentiated
Can evolve into a Glioblastoma Multiforme

86
Q

Describe Glioblastoma Multiforme

A

High mortality
requires sx debulking & chemo

Life expectancy usually weeks even w/ Tx

87
Q

What is the least aggressive astrocytoma?

88
Q

What astrocytomas usually evolves into a Glioblastoma Multiforme?

A

Anaplastic Astrocytoma

89
Q

Describe Meningiomas

A

Benign
Arise from Dura or arachnoid tissue
Good prognosis w resection

90
Q

Describe Pituitary Adenomas

A

Non-cancerous
Varying sub types

tx: Transsphenoidal or open crani for removal –> curative

91
Q

Describe Acoustic Neuromas

A

Benign Schawannomas
vestibular component of CN VIII within auditory canal
Good prognosis w/ resction/radiation

92
Q

Which cranial nerve is within the auditory canal? Which tumor has involvement with this?

A

CN VIII (8)

Acoustic Neuromas

93
Q

Describe Metastatic Carcinomas

A

Vary widely in origin & s/s

Outcomes less favorable

94
Q

What are considerations w/ brain tumors?

A

-inquire about previous therapies
-CT/MRI
-Autonomic dysfunction – EKG

95
Q

Radiation damage can cause ______ and Chemotherapy can cause ______ effects

A

lethargy/AMS

neuro

96
Q

What meds are pts usually on that have/has had a brain tumor? What do we need to consider?

A

Steroids – continue to& monitor glucose

Anticonvulants

97
Q

Why are supratentorial lesions at increased risk for seizures?

A

Closer to motor cortex

98
Q

________ is often used to reduce intracranial volume/pressure

99
Q

What are the 2 types of strokes? Which is more common? More deadly?

A

Ischemic – more common

Hemorrhagic – more deadly

100
Q

What is the leading cause of death and disability worldwide?

101
Q

Strokes are characterized by sudden _______ deficits

102
Q

____% of strokes are ischemic and _____% of strokes are hemorrhagic

103
Q

What arteries supply blood to the brain?

A

Internal carotid arteries
Vertebral arteries

104
Q

The Internal carotid arteries & Vertebral arteries join on the _______ surface of the brain. What do they form?

A

Inferior

Circle of Willis

105
Q

What is the circle of Willis?

A

Vessel joint on the inferior surface of the brain

Provides collateral circulation to multiple areas of the brain

106
Q

The circle of Willis provides _______ circulation

A

Collateral

107
Q

Artery occlusion presentation: Anterior cerebral

A

Contralateral leg weakness

108
Q

Artery occlusion presentation: Middle cerebral

A

-Contralateral hemiparesis & hemisensory deficit
-Aphasia
-Contralateral visual field deficit

109
Q

Artery occlusion presentation: Posterior cerebral

A

-Contralateral visual field deficit
-Contralateral hemiparesis

110
Q

Artery occlusion presentation: Penetrating arteries

A

-Contralateral hemiparesis
-Contralateral hemisensory deficits

111
Q

Artery occlusion presentation: Basilar artery

A

Oculomotor deficits
ataxia
crossed sensory deficit
motor deficits

112
Q

Artery occlusion presentation: Vertebral Artery

A

Lower cranial nere deficits
ataxia
crossed sensory deficit

113
Q

Ischemic strokes are caused by an _______ and cause _______

A

Occlusion

Brain cell necrosis

114
Q

What is a TIA?

A

Transient ischemic attack

Sudden focal vascular neuro deficit

115
Q

TIAs normally resolve within _____hrs

116
Q

T/F: Pts who experience TIAs normally dont have strokes

A

F

1/3 of pts who have a TIA will experience a stroke

117
Q

If a stroke is suspected, a STAT ___________ is needed

A

NONCONTRAST CT

118
Q

Thrombolytic therapy should be initiated within ______ of hospital arrival

119
Q

What is the TOAST classification?

A

Categorizes ischemic strokes into 5 groups/classes based on cause

120
Q

Describe TOAST classification: class 1

A

Large artery artherosclerosis

ex) carotid stenosis

121
Q

Describe TOAST classification: class 2

A

Small vessel occlusion

Ex) Lacunar stroke

122
Q

Describe TOAST classification: class 3

A

Cardioaortic embolic

Ex. emboli from afib

123
Q

Describe TOAST classification: class 4

A

Other etiology

Ex. hypercoag/vasculopathies

124
Q

Describe TOAST classification: class 5

A

Undetermined etiology

125
Q

What is the initial Tx in Ischemic CVA?

126
Q

What is the time frame for TPA post onset of s/s?

A

3 - 4.5 hrs

127
Q

What is the best option for an Ischemic stroke? Describe this

A

Revascularization

Done in the IR
Angiographic fluoroscopy is used

Direct administration of thrombolytics or thrombectomy to the clot

128
Q

What considerations should we have w revascularization?

A

Be concise/efficient – not use alot of time/avoid delay

Focus: baseline neuro
Ability to lay flat
CV function

Can procedure be done under sedation
Secure airway? (Aspiration)

Consider other CV risk factors that may effect hemodynamics (HTN, DM, CAD, Afib, Valve)

129
Q

Hemorrhagic stroke is _____x more likely to cause death than ischemic

130
Q

What are the 2 most reliable predictors of outcome in hemorrhagic stroke?

A

Blood volume

Change in LOC

131
Q

Subtypes of hemorrhagic stroke are based on ________. What are they?

A

Location

  1. Intraparenchymal hemorrhage: blood w/i brain
  2. epidural hematoma
  3. subdural hematoma
  4. subarachnoid hemorrhage
  5. Intraventricular hemorrhage: blood w/i ventricle
132
Q

Which subtype of hemorhagic stroke usually occurs in conjuction w another?

A

Intraventricular hemorrhage:

133
Q

What is the Tx for hemorrhagic stroke? What type of unit do they go to?

A

Conservative: Reduce ICP, BP control, Seizure precautions, monitoring

Sx: Evac –> Neuro ICU required

134
Q

With new anticoagulants for thrombus, when is the soonest you can do an elective Sx?

A

No elective Sx within 3 months

135
Q

If you need to pause warfarin (LA anticoagulants), what can you bridge it with?

136
Q

T/F: If you’ve had a stroke, you have to continue your anticoags with RA

A

F

Need to d/c for sufficient time to safely before RA/LA

137
Q

What are cerebrovascular/stroke consideration we should have?

A

Neuro assessment

Ask about HA, tinnitus, vision/memory, bathroom issues

Imaging
EKG
Labs

Aline, 2 IVs, CVC

138
Q

T/F: Majority of cerebral aneuryms are Dx before ruputure

A

F

Only 1/3 of pts Dx/Sx before ruputure

139
Q

What are s/s & risk factors of cerebral aneurysms? Tx?

A

s/s: HA
Photophobia
confusion
hemiparesis
coma

rx: HTN
smoking
female
PO contraceptives
cocaine

Tx: coiling, stenting, trapping/bypass

140
Q

T/F: Males are more at risk of cerebral aneurysms

141
Q

Interventions for cerebral aneurysms should be performed w/i ______ for best outcomes

142
Q

The risk of a vasospasm happens in _______ post Subarachnoid hemorrhage (SAH)

A

3 - 15 days

143
Q

What triggers a Subarachnoid hemorrhage (SAH) vasospasm? What is the patho of this?

A

Free hgb triggers inflmmatory mediators –> decrease NO –> increase endothelin 1 –> vasconstriction

144
Q

What is the Tx for Subarachnoid hemorrhage (SAH) vasospasm? What is the initial Tx? Why?

A

Triple H: HTN (initial)
Hypervolemia
Hemodilution

HTN is initial to avoid complications of hypervolemia

145
Q

What are the interventional Tx for Subarachnoid hemorrhage (SAH) vasospasm?

A

Balloon dilation & direct injection of vasodilators

146
Q

What is AV malformation?

A

Arteriovenous malformation

Congenital
Arterial to venous connection WITHOUT capillaries

147
Q

Majority of AV malformations are _________

A

Supratentorial

148
Q

What is the Dx for AV malformation? Tx?

A

Dx: Angiogram
MRI

Tx: radiation
angio-guided embolization
surgical-resect (higher mortality)

149
Q

Which AV malformation Tx has the highest mortality?

A

Surgical Resection

150
Q

What is a congenital brain abnormalities?

A

Hereditary defect in development or structure of the CNS

151
Q

T/F: Congenital brain abnormalities can be diffuse or confined

152
Q

What are the common Congenital brain abnormalities? (4)

A
  1. Chiari Malformation
  2. Tuberous Sclerosis
  3. Von Hippel-Lindau Disease
  4. Neurofibromatosis
153
Q

What is Chiari Malformation? S/s; Tx.

A

Congenital displacement of the cerebellum

s/s: HA extending to shoulder/arm
visual disturbances
ataxia

Tx: Sx decompression

154
Q

Chiari malformation had ____ different types

155
Q

Describe Type 1 Chiari Malformation

A

Downward displacement of cerebellum

156
Q

Describe Type 2 Chiari Malformation

A

“Arnold Chiari”

Downward displacement of cerebellar vermis

Associated w myelomeningocele

157
Q

Describe Type 3 Chiari Malformation

A

rare

occipital encephalocele w/ downward cerebellar displacement

158
Q

Describe Type 4 Chiari Malformation

A

Cerebellar hypoplasia w/o pisplacement of posterior fossa contents

Not compatible w life

159
Q

Which Chiari Malformation is associated with myelomeningocele?

160
Q

Which Chiari Malformation is not compatible with life?

161
Q

With Chiari Malformation, you can __________ to decrease ICP

A

hyperventilate

162
Q

What is Tuberous Sclerosis?

A

Genertic disease causing benign hematomas, angiofibromas, and other malformations ANYWHERE IN THE BODY

163
Q

Tuberous Sclerosis is also called _______

A

Bournevile disease

164
Q

In Tuberous Sclerosis, lesions of the brain include _____ tumors & giant cell _________

A

cortical tumors

giant cell astrocytomas

165
Q

In Tuberous Sclerosis, often involves co-existing tumors in which places?

A

Face
Oropharnyx
Heart
Lungs
Liver
Kidney

166
Q

How will Tuberous Sclerosis present?

A

Mental retardation
Seizures

167
Q

What are considerations w Tuberous Sclerosis?

A

Airway compromise
Cardiac & kidney involvement

168
Q

What is Von Hippel-Lindau Disease?

A

Genetic

formations of benign tumors of CNS
Location:Eyes
Adrenals
Pancreas
Kidneys

May present w pheochromocytoma
May have co-existing spinal tumor

169
Q

What congenital disorder may present with pheochromocytoma? What considerations should we have?

A

Von Hippel-Lindau Disease

Increased catecholamines –> increased BP!!!

170
Q

What type of anesthesia may be limited in Von Hippel-Lindau Disease. Why?

A

Neuraxial anesthesia

May have co-existing spinal tumor

171
Q

What is Neurofribromatosis? Tx

A

Genetic disorder of CNS that causes tumors to form on the nerves in the body anywhere at anytime

Tx: No cure

172
Q

What are the 3 types of Neurofribromatosis? Which chromosomes are affected?

A

Type 1: chromosome-17

Type 2: Chromosome-22

Schwannomatosis: Chromosome-22

173
Q

Which type of Neurofribromatosis is most common?

174
Q

Which type of Neurofribromatosis is most rare?

A

Schwannomatosis

175
Q

What are the considerations w Neurofribromatosis?

A

IICP
Airway
Scoliosis
possibility of pheochromocytoma

176
Q

What type of anesthesia should we avoid with Neurofribromatosis? Why?

A

Neuraxial anesthesia

High likelihood of spinal tumors

177
Q

T/F: No 2 cases of Neurofribromatosis are the same

A

T

They are HIGHLY varied and unpredictable

178
Q

Neurofribromatosis affects almost ___% of organs in the body

179
Q

What is the patho for hydrocephalus?

A

Imbalance between CSF production/absorption –>
CSF accumulation–> IICP –> ventricular dilation

180
Q

T/F: Hydrocephalus can be congenital or acquired

181
Q

what is the Tx for hydrocephalus?

A

Diuretics: Furosemide
-acetazolamide

Serial lumbar punctures as temporizing measure

Majority require Sx: Ventriculoperitoneal (VP) shunt
-endoscopic third ventriculostomy (ETV)

182
Q

what is a VP shunt? What is it a treatment for?

A

“Ventriculoperitoneal shunt”

Drain place in brain ventricle –> empties into peritoneum

Tx for Hydrocephalus

183
Q

What is an ETV? What is it treatment for?

A

“endoscopic third ventriculostomy”

Catheter placed into the lateral ventricle of brain –> drains into the peritoneal space, R atrium, or pleural space (rare)

184
Q

The _______ is rarely used to drain with ETV

A

pleural space

185
Q

VP shunt malfuntion is mostly likely to occur within ______ of placement

186
Q

How are TBIs categorized?

A

By breech of dura as either

“Penetrating” or “Nonpenetrating”

187
Q

Severity of a TBI is based on the ______

A

GCS (Glasgow-Coma Scale)

188
Q

What is the difference between a primary and secondary injury in a TBI? What are examples.

A

Primary occurs at time of injury

Secondary is what happens after, as a result of the primary injury
Ex: neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte, and balances, neurogenic shock

189
Q

Intubation is usually required in a TBI if GCS is less than ____

190
Q

With a TBI we need a stat ______

A

CT of head/neck

191
Q

What is the main consideration with a TBI?

A

Do not delay surgery!!!!!!!

-C-spine stabilization
-uncrossmatched blood if no time for type&screen
-NO NGT/OGT!!!!!! – basal skill fx risk
-ISTAT, pressors, bicarb, Ca, blood

192
Q

T/F: You can put a NGT/OGT in a pt with a TBI

A

F

You should refrain from doing this – risk of basal skull fx

193
Q

What is a seizure? What is epilepsy?

A

Seizure: transient, paroxysmal, synchronous discharge of neurons in the brain

Epilepsy: recurrent seizures d/t congenital or acquired factors

194
Q

What causes seizures?

A

Could be congenital

Transient abnormalities: hypoglycemia
-hyponatremia
-hyperthermia
-intoxication

195
Q

Anti-epileptic drugs decrease ________ & enhance ________

A

Neuronal excitability

Neuron inhibition

196
Q

What are anesthesia considerations with seizures?

A

-Determine source of seizure
-Figure how well the seizures are controlled
-give anti-seizure meds BEFORE incision
-review home meds

197
Q

What anti-seizure medications are CYP450 inducer? What does this mean?

A

Phenytoin
Tegretol
Barbiturates

These drugs will increase the metabolism of other drugs that are metabolized in the liver –> ** drugs metabolized by the liver will require higher dosages**

198
Q

what procedure do you use to intubate post seizure?

A

RSI w/ cricoid pressure

199
Q

What is the grading system for the prognosis/mortality w aneurysm?

A

Hunt & Hess classification: Scores 1-5; higher score = increased mortality

World Federation of neurologic surgeons grading system –> Glasgow-Coma Scale

200
Q

What is the AV Malformation (AVM) grading system called?

A

Spetzler-Martin AVM grading system: Points assigned; the more points totaled = the higher risk of neuro deficit.