Neuro Flashcards
(153 cards)
1
Q
Multiple Sclerosis pathophys
A
progressive, autoimmune demylelination of central nerve fibers
2
Q
onset of MS
A
20-40
3
Q
risk factors for MS
A
female
1st degree relative
Epstein Barr Virus
other autoimmune disorders
smoking
4
Q
triggers for MS
A
stress
elevated temps
postpartum period
5
Q
s/s of MS
A
motor weakness, sensory disorders, visual impairment, autonomic instability
varies based on site of demyleination
6
Q
treatment for MS
A
no cure
managed by corticosteroids, immune modulators, targeted antibodies
7
Q
pre-anesthetic considerations for MS
A
assess existing deficits
if respiratory compromise - consider PFTs
Labs: CBC with platelets, BMP w/wo LFT
consider preop steroids
temperature management is crucial
avoid succinycholine
8
Q
why might you draw a BMP with LFT on a MS patient
A
on dantrolene and azathioprine - causes bone marrow suppression, liver function impairment
*close attention to glucose and electrolyes as steroids may impact levels
9
Q
what anesthetic plan might you have for a MS patient
A
General, regional, peripheral nerve block are acceptable options
10
Q
what RSI agent would you avoid in MS
A
succinycholine - may induce HyperK+
upregulation of nACh receptors
11
Q
what might hyperthemia do to an MS patient
A
preciptate an exacerbation of MS symptoms
12
Q
Myasthenia Gravis Pathophysiology
A
autoimmune: antibodies generated against N-ACh-receptors at skeletal motor endplate
*no effect on smooth or cardiac muscle
12
Q
which cranial nerves are commonly affected by myasthenia gravis? what effects do they have?
A
ocular (common) - diplopia, ptosis
bulbar - laryngeal/pharyngeal weakness leading to respiratory insuffiency, aspiration risk
12
Q
when is maysthenia gravis (MG) muscle weakness exacerbated
A
w/ exercise
13
Q
thymic hyperplasia in myasthenia gravis is common at _____% with _____% of patients improving with thymectomy
A
thymic hyperplasia in myasthenia gravis is common at 10% with 90% of patients improving with thymectomy
14
Q
what can cause symptom exacerbation with myasthenia gravis
A
pain, insomnia, infection, surgery
stress
15
Q
treatment of myasthenia gravis
A
ACh-E inhibitors (pyridostigmine), immunosuppressive agents, steroids, plasmapharesis, IVIG
16
Q
MG preanesthetic considerations
A
assess existing deficits
if respiratory compromise, consider PFTs
optimize respiratory function
Labs: CBC, BMP +/- LFT
counsel pt on increased risk of postop vent support until fully recovered from anesthesia
17
Q
4 medication considerations with MG
A
- reduce NMB dose to avoid prolonged muscle weakness
- caution with opioid to avoid respiratory compromise
- ACh-E inhibitors prolong succinycholine and ester LAs (X-caine)
- preop steroid with anyone on long term steroids
18
Q
when would you add an LFT to MG chem panel
A
if the patient is on azathiporine
19
Q
eaton-lambert syndrome pathophysiology
A
autoantibodies against VG Ca++Channels
-reduce Ca++ influx decreasing ACh release at the NMJ
20
Q
> 60% of eaton lambert syndrome cases are associated with what
A
small cell lung carcinoma
21
Q
s/s of Eaton Lambert Syndrome
A
progressive limb-girdle weakness, dysautonomia, oculbulbar palsy
22
Q
treatment for eaton lambert syndrome
A
Selective K+ channel blocker
“3-4 diaminopyridine”
ACh-E inhibitors
Aziathioprine (immunologics)
Steroids
Plasmapheresis, IVIG
23
preanesthetic considerations for ELS (Eaton Lambert Syndrome)
assess exsisting deficits
if respiratory compromise - PFTs
optimize respiratory functoin
*extreme caution with NMB and opioid dosing
*may need post-op respiratory support until fully recovered from anesthesia*
| consider regional
24
ELS and neuromuscular blockers
VERY SENSITIVE to ND-NMB and D-NMB
*significantly more sensitive to ND-NMB than MG patients
25
muscular dystophy pathophysiology
hereditary disorder of msucle fiber degerneration caused by breakdown of the **dystophin-glycoprotein complex**
- leading to myonecrosis, fibrosis, and skeletal membrane permeability
26
what is the most common and severe form of muscular dysrophy
who does it affect- onset & lifespan
Duchenne (DMD)
occurs only on boys, onset 2-5y
Wheelchair bound by 8-10 y
lifespan ~20-25 d/t cardiopulm complications
27
s/s of muscular dystrophy
progressive skeletal muscle wasting without motor/sensory abnormalities, kyphoscolosis, long bone fragility, respiratory weakness, frequent PNE, EKG changes
28
what lab is elevated in muscular dystrophy and why?
creatine kinase due to muscle wasting
29
what is myotonia
prolonged contractions after muscle stimulation, seen in several muscle disorders
30
most common myotonia
myotonic dystrophy
onset: 20-30 years
**muscle wasting in face, masseter, hand, pre-tibial muscles & may effect pharyngeal, laryngeal, diaphragmatic muscles**
cardiac conduction may be effected
31
what valvular disorder is seen in myotonic dystrophy
20% have mitral valve prolapse
32
myotnia congenita involves what muscles
involves skeletal (smooth/ cardiac muscles are spared)
| (milder form)
33
what is central core disease
rare. core muscles cells lack mitochondrial enzymes
- proximal muscle weakness & scoliosis
34
what triggers myotonias
stress and cold temps
35
treatment for myotonias
no cure
managed with quinine, procainamide, steroids
36
preanesthetic condiserations for muscular dystrophies
CBC, BMP, PFTs, consider CK
preop EKG, ECHO - elvaluate for cardiomyopathy
37
drug condiserations for muscular dystrophies
caution with Non-depolarizing NMB (careful montiroing throughout)
hypermetabolic syndrome - similar to MH seen with sux and volatile anesthetics
can lead to rhabdo, HyperK+, vfib & cardiac arrest
Sux and VA may exacerbate instability of muscle membrane
## Footnote
consider lose dose Roc and TIVA for GA, Have MH cart with dantrolene available
38
pre anesthetic considerations for myotonic dystrophy (9)
* assess extent of CV and pulmonary abnormalities
* assess breath and heart sounds
* GI hypomotility (aspiration risk)
* high reaction of endocrine abnormalities (check thyroid and glucose levels)
* keep warm to avoid flares
* avoid Depolarizing NMB b/c fasiculations trigger myotonia
* caution with opioids
* optimize respiratory status
* incerased risk of postop respitatory weakness
39
3 major dementia syndromes
alzheimers (70%)
Vascular dementia (25%)
parkinsons (5%)
40
basic preop consierations with dementia patients
assess baseline level of cognitive dysfunction
- if patient unable to give informed consent look to medical POA
- investigate any advanced directives for medical decision making
- review basic labs and pertinent test/imaging
- potential aspiration risk (may be full stomach)
- increased risk for postop delirium (consider TIVA)
41
which preop meds need to be reviewed prior to anesthetic with dementia patients
ACh-I, MAOIs, psych meds
42
preferred anesthetic plan on dementia patietns
regional - decreased opioid requirement
*balance opioids to meet analgesic requirement without exacerbating delirium*
43
parkinson's disease pathophysiology
degeneration of dopaminergic fibers of basal ganglia
unknown case. advanced age is the biggest risk factor
44
dopamine regulates the _________ by ____ _____ stimulation, which is stimulated by _______
dopamine regulates the **extrapyramidal motor system** by **inhibiting exess** stimulation, which is stimulated by **ACh**
45
T/F in parkinsons the motor neurons are under stimulated
false, in parkinon's motor neurons are over stiumulated
46
triad of symptoms with parkinsons
skeletal muscle **t**remor, **r**igitidity, **a**kinesia, **p**osture
TRAP
47
other symptoms of parkinsons
pill roll tremor, facial rigidity, slurred speech, difficulty swallowing, respiratory difficutlty, depression, and dementia
48
treatment for parkinsons
Levadopa (cross BBB), anticholinergics, MAOIs (inhibit dopamine degredation), deep brain stimulator
49
preanesthetic considerations for parkinsons
assess severity with special attetention to respiratory compromise
review home meds (MAOIs)
basic labs along with PFT if respiratory symptoms
EKG, ECHO if indicated
increased aspiration risk (dysphagia, or possible dementia)
50
mediations to avoid in parkinsons patients
avoid reglan, phenothiazines, butyrophenones
avoid demerol if on MAOI
51
parkinsons home med to continue prior to surgery
PO levadopa **must** be continued to avoid unstable extrapyramidal effects such as chest wall rigidity
52
parkinsons patient with Deep brain stimulator considerations
* DBS may need to be disabled to avoid interaction with cautery
* if cautery used, biopolar recommended
53
in regards to brain tumors what can cause neurologic deficits
the mass effects!
increases ICP, papilledema, headache, mental impairment, mobility impairment, vomiting, autonomic dysfunction, seizures
54
brain tumors - pre anesthesia considerations
history, previous therapies, presenting symptoms & neurological deficits
radiation damage may lead to lethargy and AMS
chemoteraphy may also have neuro effects
CBC, BMP (glucose), EKG
CT/MRI
preop steroids and antiseizure per surgeon
55
why are patients w brain tumors on steroids
minimize cerebral edema
*continue steroids and monitor glucose
56
what diuretic is used to reduce ICP and pressure
mannitol
57
autonomic dysfunction from brain tumor may manifest on
EKG
labile HR and BP
58
anticonvulsants are common with which lesions
supratentorial lesions closer to motor cortex
59
cerebrovascular disease preop considerations
* review history, deficits, imaging, treatments, and co-existing disease
* assess orientation, pupils, bilateral grip stregnth, LE strength
* ask about headache, tinnitus, vision/memory loss, bathroom issues
* assess cause of CVA - vascular, embolic
* Imaging- carotid U/S, CT/MRI head and neck and ECHO
* preop EKG
* CBC, BMP (including glucose)
* cerebral oximetry
* Aline, 2 IV and/or CVC
60
causes of embolic CVA
afib, prostethic valve, right to left shunt, PFO
61
new anticoagulant use for cardiac thrombus means what
no elective cases within 3 months
62
if pt is on anticoagulant for CVA prophylaxis
consult prescriber to establish protocol
63
high risk patients on long acting anticoags need what to bridge the gap
short acting anticoagulants (LMWH, IV unfractionated heparin)
*close monitoring of coagulation status is required
64
can you do regional anesthesia on a pt with CVA history and anticoags
if anticoags have been D/Cd for sufficient time to perform block
65
clincal manifestations of regional strokes - anterior cerebral artery
contralateral leg weakness
66
# 1.
clincal manifestations of regional strokes - middle cerebral artery
contralateral hemiparesis and hemisensory deficits (face and arm more than legs)
aphasia (dominant hemisphere)
contralaterral visual defect
67
clincal manifestations of regional strokes - posterior cerebral artery
contralateral visual vield defect
contralateral hemiparesis
68
clincal manifestations of regional strokes - penetrating arteries
contralateral hemiparesis
contralateral hemisensory deficits
69
clincal manifestations of regional strokes - basilar artery
oculomotor deficits and or ataxia with crossed sensory and motor deficits
70
clincal manifestations of regional strokes - veterbal artery
lower cranial nerve deficits and or ataxia with crossed senory deficits
71
majority of aneurysms not diagnosed before _____
rupture
* only 1/3 aneursyms pts have sx before rupture
72
s/s of cerebral aneursym
headache, photophobia, confusion, hemiparesis, coma
73
risk factors for cerebral aneursym
HTN
smoking
female
oral contraceptive
cocaine use
74
diagnosis of cerebral aneursym
CT/angio
MRI
lumbar puncture with CSF analysis (if rupture suspected)
75
intervention for cerebal aneurysm should be preformed within how many hours of rupture for best outcome
72 hours
76
pre-anesthesia considerations for cerebral aneursyms
CT/MRI, EKG, ECHO, CBC, BMP, T&C with blood available
*BP control, mannitol (avoid rupture)
*seizure prophylaxis
*CVC
77
surgical treatment of cerebral aneursyms
coiling, stenting, trapping, bypass (very large aneursyms)
*Neurosurgery on standby incase of intraop rupture/SAH
78
T/F pts with cerebral aneurysms may be on steroids
True, monitor glucose
79
when are vasospasms likely to occur post Sub archonid hemorrage (SAH)
3-15 days post SAH
80
triple H therapy for SAH vasospasm
hypertension
hypervolume
hemodilution
*to avoid complications of hypervolemia, **HTN** is the initial main treatment
81
interventional treatment for post SAH vasospasm
balloon dilation
direct injection of vasodilators to relieve the vasospasm
82
aneursym grading for prognosis
Hunt & Hess
0- unruptured
1- reputrued with minimal headdache and no neuro deficits
2- moderate to sever headache, no deficit other than cranial nerve palsy
3- drowsiness, confusion, mild focal motor deficit
4- stupor, significant hemiparesis, early decebration
5 - deep coma, decebrate rigidity
83
what is an AVM
aterial to venous connection without intervening capillaries
*high flow, low resistance shunting
*believed to be congetinal
84
symtpoms of AVM
range from mass-effects to hemorrhage
85
where are majority of AVM located
supratentorial
86
diagnosis of AVM
angio, MRI
87
treatment of AVM
radiation, angio-guided embolization
surgical resection (higher mortality)
88
pre anesthesia considerations for AVM
H&P, review meds, imaging, CBC, BMP, T&C, EKG, ECHO
*BP control, seizure prophalyxsis (supratentorial)
*large bore IV access x2 or CVC, Aline
89
traumatic brain injury "TBI" severity is categorized by
GCS - glascow-coma scale
90
secondary injuries- TBI (6)
| TBI (traumatic brain injury)
neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, neurogenic shock
90
primary injury -TBI
| TBI (traumatic brain injury)
occurs at time of insult
91
intubation is required in severe TBI
GCS <9
Airway trauma
respiratory distress
92
mild hyperventilation to control
ICP
93
pre anesthesia considerations for TBI
**do not delay emergent surgery**
review co-morbidities, degree of injury, imaging, labs, gross neuro exam
*C-Spine stabilization, IV access, CVC, ALine, possible uncrossmatched blood if no time for T&C
*intraop ISTAT, pressors, bicarb, Calcium, blood products
94
why to refrain from NGT/OGT in TBI
potential basal skull fracture
95
chari malformation
congential displacement of cerellum
C/o Headache, extending to shoulders/arm, visual disturbances, ataxia
Tx= surgical decompression
96
pre-anesthesia considerations for Chari malformation
Review H&P, deficits, imaging, CBC, BMP, T&C
May hyperventilate to ↓ICP, Lg bore IV x 2 or CVC, Aline
97
classifications of Chiari Malformation
Type I - downward displacement of cerebellum
Type 2 - downward displacement of cerebellar vermis, often assoiated with myelomeningocele
Type 3 - rare
Type 4 - not compatible with life
98
Pre-anesthesia considerations for seizures
Determine source of seizures (if known) and how well they are controlled.
**Want anti-seizure drugs on board before incision.**
Review drugs and pharmacokinetic/pharmacodynamic actions
99
May be called to intubate post-seizure
RSI w/cricoid pressure
100
seizure
& causes
transient, paroxysmal, and synchronous discharge of neurons in the brain
caused by transient abnormalities: hypoglycemia, hyponatremia, hyperthermia, intoxication
-In these cases, treating the underlying cause is curative
101
Epilepsy
recurrent seizures d/t congenital or acquired factors
102
Antiepileptic drugs decrease ____ excitability/enhance _____
Antiepileptic drugs decrease **neuronal** excitability/enhance **inhibition**
103
which seizure drugs cause drug-drug interactions
Phenytoin, Tegretol, Barbiturates are enzyme-inducers
| may need a larger dose
104
Cerebral Blood Flow is modulated by
cerebral metabolic rate
cerebral perufsion pressure (CPP = MAP - ICP)
PaCO2
PaO2
various drugs and intracranial pathologies
105
with autoregulation CBF is approximately _____ mL/100g brain tissue per minute
50 mL/100g brain tissue per minute
750 mL/min
15% cardiac output
106
the intracranial and spinal vault is enclosed by what? what are the contents in the vault
neural tissue (brain + spinal cord), blood, and CSF
enclosed by dura mater and bone
107
under normal conditions what is the volume of brain tissue, intracranial CSF, and intracranial blood and ICP
1200-1500 mL
at this volume ICP = 5-15 mmHg
108
what is the monroe kellie hypothesis
any increase in one component of intracranial volume must be offset by a decrease in another component to prevent elevated ICP
109
what happens if the compensation for decreasing ICP fail
cerebral ischemia
110
falx cerebri seperates what
the 2 cerebral hemispheres
111
the tentorium cerebelli is a reflection of dura that lies rostral to the cerebellum and marks the border between the
supratentorial and infratentorial spaces
112
increases in contents of one region may cause regional increases in ICP and in extreme instance the contents can
herniate into a different compartment
113
subfalcine herniation
herniation of hemispheric contents under the flax cerebri
typically compressing branches of the anterior cerebral artery, creating a MLS
| midline shift (MLS)
## Footnote
1
114
transtentorial herniation
herniation of the supratentorial contents past the tentorium cerebelli causing brainstem compression in a rostral to caudal direction
## Footnote
2
115
uncal herniation
subtype of transtentorial herniation
uncus (medial portion of temporal lobe) herniates over the tentorium cerebelli
## Footnote
4
116
signs of uncal herniation
ipsilateral oculomotor nerve dysfunction
*pupillary dilation, ptosis, lateral deviation of the affected eye, brainstem compression, death
117
herniation of cerebellar tonsils
occur due to elevated infratentorial pressure causing the cerebellar structure to herniate through the foramen magnunm
## Footnote
3
118
symptoms of herniation of cerebellar tonsils
medullary dysfunction, cardiorespiratory instability death
119
causes of increased ICP
tumors
intracranial hematomas
infections - meningitis or encephalitis
120
how do tumors contribute to increased ICP
directly bc of their size (space-occupying lesions)
inderectly by causing edema in surrounding tissue
obstructing CSF flow, as seen with tumors involving the 3rd ventricle
121
how to do intracranial hematomas increase ICP
obstruction of CSF reabsorption
and granulations
122
methods to decrease ICP
* elevate HOB to encoruage jugular venous outflow
* hyperventilation
* CSF drainage (EVD)
* hyperosmotic drugs
* diuretics - induce. systemic hypovolemia
* corticosteroids - decrease swelling and the integrity of BBB
* cerebral vascocontricting agents(prop- decreases CMRO2 and CBF)
* surgical decompression
123
neuro assessment
preop and postop neuro assessment
review imaging, current meds/treatment
124
which anesthetic plan is preferred with muscular dystrophies
RA > GA to avoid trigers and cardiopulmonary complications
125
astrocytomas
most common CNS glial cells
*gliomas
pilocytic astrocytomas
anaplastic astrocytomas
glioblastoma multiforme
126
gliomas
primary tumors, least aggresive astrocytomas - found in young adults with new onset seizure
127
pilocytic astrocytomas
children and young adults
mostly benign, good outcomes if resected
128
anaplastic astrocytomas
poorly differentiated
ususally eveolve into glioblastoma multiforme
129
glioblastoma multiforme
carry a high mortality rate
usualy require surgical debulking and chemo
life expectancy is usually within weeks even with treatment
130
menigiomas
usually benign, arise from dura or arachnoid tissue
*good prognosis with surgical resection
131
pituitary adenomas
noncancerous, varying subtypes
transphenodial or open cranitomy for removal is usually curative
132
acoustic neuromas
usually benign schawnnomas involving vestiular component of CN VIII within auditory canal
good prog with resection +/- radiation
133
metastatic carcinomas
vary widely in orgin and symptoms
outcomes generally less favorable
134
blood is supplied to the brain from
internal carotids and vetebral arteries
## Footnote
these vessels join on the inferior surface of the brain to form the circle of willis, which during ideal circumstances provides collateral circualtion to multiple areas of the brain
135
TIA
| transiet ischemic attack
sudden focal vascular, neurologic deficit that resolves within 24 hour
1/3 patients who experience a TIA will subsequently suffer a stroke
stoke prognosis depend on time from onset thrombolytic intervention (<90min)
136
suspected stroke requires
stat non-contrast CT due r/o intracerebral hemorrhage
137
causes of ischmemic stroke are categorized according to the TOAST classifications
Large artery atherosclerosis (carotid stenosis)
Small vessel occlusion (lacunar stroke)
Cardioaortic embolic (afib emboli)
other eitology (hypercoaguable or vasculopathy)
undetermined etiology
138
recommended treatment for acute ischemic stroke
PO aspirin - initial
IV or intra-arterial tPA when criteria are met within a limite time window
thrombectomy
revascularization
139
pre-anesthetic considerations for ischemic CVA
avoid delay in treatment
baseline neuro assessment, CV function, ability to lie flat
airway needed?
**patients with ischemic stroke frequently have CV risk factors (HTN, DM, CAD, AFib, valvular disease) and can impact vasoactive drug choices and hemodynamic goals**
140
hemorrhagic CVA treatment
depends on severity
*conservative treatment is centered around reducing ICP, BP control, seizure precautions and vigilant monitoring*
surgical treatment for evacuation of hematoma
intubation depending on cardiopulm status
ICU monitoring
141
2 reliable predictors of outcomes for hemorrhagic CVA
estimated blood volume and change in LOC
142
subtypes of hemorrhagic strokes
IPH - intraparychemal - blood within the brain
epidural - epidural space
subdural - subdural space
SAH - subaracnoid space
IVH - intraventricular - within the ventricular system
## Footnote
IVH usually occur in conjunction with other types of hemorrhagic stroke
143
cause of vasospasm with SAH
free Hgb tiggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1 leading to vasoconstriction
144
hydrocephalus
disorder of CSF accumulation causing increased ICP resulting in ventricualr dilation
| imbalance between production and absorption
145
causes of hydrocephalus
congenital or acquired due to meningitis, tumors, head injury, stroke
146
treatment for hydrocephalus
diuretics (furesomide and acetazolamide decrease CSF production)
serial lumbar punctures (temporzing measure)
VP shunt - drain placed in ventricle and empties in peritoneum
Endoscopic Thrid Ventriculostomy - catheter placed into lateral ventricle and drains into peritoneal space, Right atrium, or pleural space
147
neurofibromatosis
autosomal dominant
3 types (type I most common)
numerous disease presentations
Anesthesia considerations account for increased ICP, airway issues, scolisis, and the possibility of pheochromocytoma
| avoid neuraxial due to high likelihood of spinal tumors
148
von hippel-lindau disease
autosomal dominant
benign tumors of the CNS, eye, adrenals, pancreas and kidneys
**may present with pheochromocytoma**
anesthesia considerations take into account exaggerated HTN
| Neuraxial may be limited if there is co-existing spinal cord tumor
149
tuberous sclerosis
| AKA Bourneville Disease
autosomal dominant disease causing beingn hemartomas,, angiofibromas and other malformations occuring in the body
lesions of the brain include cortical tumors and giant-cell astrocytomas
150
presentation of tuberous sclerosis and anesthesia considerations
mental retardation and seizure disorders
anesthesia make take into account airway compromise, kidney or cardiac involvement
