NEURO Flashcards
1
Q
What disease is a mutation of the FMR1 gene?
A
Fragile X syndrome
2
Q
Impaired pruning of neuronal synapses occurs in which genetic disorder?
A
Fragile X syndrome
3
Q
Disruption of normal myelination in the CNS (especially lateral ventricles) causes what disease?
A
Periventricular leukomalacia
4
Q
Disruption of normal neuronal migration during fetal development causes what disesase?
A
Lissencephaly (“smooth brain”)
5
Q
What are the myelin cells of the CNS called?
A
oligodendrocytes
6
Q
What are the myelin cells of the PNS called?
A
Schwann cells
7
Q
What cell assists in maintaining the homeostatic milieu of the brain parenchyma?
A
astrocytes
8
Q
What cell is the predominant phagocytic cell in the CNS?
A
microglia
9
Q
What cell surrounds endothelial cells in the CNS, helping to regulate blood vessel reactivity?
A
pericytes
10
Q
The diencephalon is what two major parts of the brain?
A
hypothalamus and thalamus
11
Q
The spinal cord ends where in a neonate?
A
L3
12
Q
Where should you go for an LP in a neonate?
A
L4-L5
13
Q
CN1?
A
olfactory
14
Q
CN2?
A
optic
15
Q
CN3?
A
oculomotor
16
Q
CN4?
A
trochlear
17
Q
CN5?
A
trigeminal
18
Q
CN6?
A
abducens
19
Q
CN7?
A
facial
20
Q
CN8?
A
vestibulochoclear
21
Q
CN9?
A
glossopharyngeal
22
Q
CN10?
A
vagus
23
Q
CN11?
A
accessory
24
Q
CN12?
A
hypoglossal
25
Which cranial nerves emerge from the medulla?
9, 10, 11, 12
26
Which cranial nerves emerge from the pons?
5, 6, 7, 8
27
Osmotic demyelination syndrome results in profound demyelination of which area of the brain?
pons, basal ganglia, thalamus
28
Locked in syndrome occurs from injury to which area of the brain?
pons
29
Insult or injury to the cerebellum results in: ipsilateral or contralateral motor deficits?
ipsilateral
30
Which cranial nerves emerge from the midbrain?
3, 4
31
Bell's palsy (facial nerve injury, lower nerve): complete loss of face function or sparing of forehead?
complete loss
32
Stroke (upper nerve): complete loss of face function or sparing of forehead?
sparing of forehead
33
Paroxysmal sympathetic hypersensitivity (dysautonomia) is severe when injury occurs to what area of the brain?
midbrain
34
Occlusion of which major brain artery results in leg, trunk and shoulder weakness?
anterior cerebral artery
35
Occlusion of which major brain artery results in contralateral sensory or vision loss?
posterior cerebral artery
36
Which artery is the sole supply to the lumbar spine during aortic cross clamp?
great radicular artery
37
Cerebral blood flow is highest in: neonates, infants, children, or adolescents?
children
38
CePP (cerebral perfusion pressure) =
CePP = MAP - ICP
39
PaO2 <60 causes what to happen to cerebral vasculature?
vasodilation
40
What space is between the lateral ventricles and the third ventricle?
foramen of Monroe
41
What space is between the third ventricle and the fourth ventricle?
aqueduct of Sylvius
42
What is the preganglionic neurotransmitter for the sympathetic nervous system?
ACh
43
What is the postganglionic neurotransmitter for the sympathetic nervous system?
NE
44
Injury above what spinal level causes spinal shock?
T1 (loss of sympathetic tone)
45
What is the preganglionic neurotransmitter for the autonomic nervous system?
ACh
46
What is the neurotransmitter of the neuromuscular junction?
ACh
47
What type of acetylcholine receptors are at the motor end plate in the neuromuscular junction?
nicotinic
48
What enzyme hydrolyzes ACh in the neuromuscular junction?
acetylcholinesterase
49
Patients who develop malignant hyperthermia may have a mutation in what receptor?
ryanodine receptor (receptor on NMJ sarcoplasmic reticulum that releases Ca+)
50
Which is the thin filament: actin or myosin?
actin
51
Which is the thick filament: actin or myosin?
myosin (think myosin heads are thick)
52
Ca+ binds to what molecule to initiate muscle contraction?
troponin C (which then releases tropomyosin)
53
Which is energy-dependent: muscle contraction or relaxation?
both
54
After free ATP is used, what is the second source of ATP in muscle?
creatine phosphate
55
Creatine phosphate is converted to ATP by what enzyme?
creatine kinase
55
Neostigmine mechanism of action?
inhibits acetylcholinesterase (increases ACh)
56
Neostigmine is used for what?
reversal of neuromuscular blockade (indirect)
57
What medication should be given with Neostigmine and why?
glycopyrrolate or atropine (muscarinic ACh receptor antagonist) to prevent unwanted parasympathetic activity
58
Sugammadex mechanism of action?
selectively binds (inactivates) aminosteroid NMBs
59
Sugammadex only works to reverse the neuromuscular blockade of which agents?
aminosteroids (rocuronium > vecuronium > pancuronium)
60
How is succinylcholine metabolized?
by PLASMA cholinesterase (not acetylcholinesterase in the NMJ)
61
Which disease involves autoantibodies to the post-synaptic ACh receptor of the NMJ?
Myasthenia gravis
62
Which disease involves autoantibodies to the pre-synaptic Ca+ channel of the NMJ?
Eaton-Lambert syndrome (weakness that improves with activity)
63
What are the GCS values for E (eye)?
4 open, 3 to voice, 2 to pain, 1 no response
64
What are the GCS values for V (verbal)?
5 oriented, 4 disoriented (or consolable cry), 3 nonsensical (or inconsable cry), 2 moans, 1 no response
65
What are the GCS values for M (motor)?
6 normal, 5 localizes pain (withdraws to touch), 4 withdraws to pain, 3 decorticate (flexion), 2 decerebrate (extension), 1 no response
66
Which involves arm flexion: decerebrate or decorticate posturing?
decorticate
67
Which involves arm extension: decorticate or decerebrate posturing?
decerebrate
68
Which is the order of progression for decorticate vs decerebrate posturing?
first decorticate (flexion), then decerebrate (extension)
69
In an intubated patient, how is GCS score adjusted?
V score is replaced with T1 (1 point)
70
CN3 causes what eye movement?
up and down, eyelids, efferent pupil response
71
CN4 causes what eye movements?
down and in
72
CN6 causes what eye movements?
out
73
Which CN controls pupil dilation?
CN3
74
Which CNs are involved in the corneal reflex?
CN5 and CN7
75
Which CNs are involved in eye movements?
CNs 3, 4, 6
76
In which patient is the doll's eye reflex contraindicated?
those with cervical spine injury
77
What does a positive/present doll's eye reflex mean?
eyes move in opposite direction of head to stay midline (intact brain function)
78
What does a negative/absent doll's eye reflex mean?
eyes are fixed during turning (compromised brain function)
79
During cold caloric testing, what constitute a normal resopnse?
FAST nystagmus after COLD water OPPOSITE the side of stimulation ("fast COWS"; cold opposite, warm same)
80
During cold caloric testing, if both eyes move slowly to cold stimulus and stop, what does this indicate?
cortical compromise, intact brainstem
81
During cold caloric testing, if dysconjugate deviation occurs, what does this indicate?
impending herniation
82
What CNs are involved in the gag reflex?
CN9 and CN10
83
What are the 4 stages of motor response progression in brain injury?
1 hyperreflexia, 2 decorticate, 3 decerebrate, 4 flaccid paralysis
84
Decerebrate posturing indicates injury to what level of the brain?
lower midbrain and upper pons
85
The dorsal respiratory group is located where in the brain?
medulla
86
The dorsal respiratory group is responsible for what?
rhythmic breathing
87
When the ventral respiratory group is stimulated, what occurs?
active exhalation
88
The pneumotaxic center is located where in the brain?
pons
89
The pneumotaxic center is responsible for what?
ending inspiration
90
What are Cheyne-Stokes respirations?
crescendo decrescendo pattern (fast shallow breathing, then slow deep breathing)
91
Cheyne-Stokes respirations indicate injury at what level of the brain?
midbrain
92
Sustained hyperventilation indicates injury at what level of the brain?
lower midbrain and upper pons
93
What is apneustic breathing?
prolonged inhalation with expiratory pause
94
Apneustic breathing indicates injury at what level of the brain?
pons
95
What is ataxic breathing?
irregular, ineffective breathing
96
Ataxic breathing indicates injury at what level of the brain?
medulla
97
What is the progression of abnormal breathing that occurs in rostral-caudal brain injury?
1 Cheyne-Stokes (midbrain), 2 hyperventilation (midbrain), 3 apneustic breathing (pons), 4 ataxic breathing (medulla), 5 apnea
98
Pinpoint pupils are indicative of injury to what level of the brainstem?
pons
99
Midline pupils with irregular light response is indicative of injury to what level of the brainstem?
midbrain
100
Midline pupils fixed and dilated are indicative of injury to what level of the brainstem?
medulla
101
What is Cushing's triad?
hypertension, bradycardia, irregular respirations
102
Injury to what area of the brain leads to Cushing's triad?
medulla
103
What is the most common herniation syndrome?
central (rostral-caudal herniation)
104
Rapid development of a unilateral fixed and dilated pupil (CN3) indicates what type of herniation?
uncal herniation
105
Uncal herniation involves what part of the brain?
medial temporal lobe herniating across tentorium
106
Equal paralysis (contralateral) of the face, arms, and legs indicates injury to what area of the brain?
internal capsule
107
Hemiplegia with contralateral CN3 palsy indicates injury to what area of the brain?
midbrain
108
Hemiplegia with contralateral CN4 or CN6 palsy indicates injury to what area of the brain?
pons
109
Difficulty swallowing or phonating indicates injury to what area of the brain?
medulla
110
Spinal nerve root: loss of deltoid?
C5
111
Spinal nerve root: loss of biceps and forearm pronators?
C6
112
Spinal nerve root: loss of triceps and wrist extensors?
C7
113
Spinal nerve root: loss of finger flexors?
C8
114
Spinal nerve root: loss of finger adductors?
T1
115
Posterior cord syndrome is caused by injury to what area of the spinal cord?
dorsal columns
116
Loss of proprioception and vibration occurs in what injury?
posterior cord (dorsal column)
117
Loss of pain and temperature sensation occurs in what injury?
anterior cord
118
Vascular insufficiency (disc herniation or aortic cross clamp) causes what type of spinal cord injury?
anterior cord syndrome (pain and temperature) and motor impairment
119
Upper extremity > lower extremity weakness and loss of pain in cape-like distribution occurs in what type of spinal cord injury?
central cord
120
What is Brown-Sequard syndrome?
hemisection of the spinal cord
121
Ipsilateral motor and proprioception and contralateral sensory loss occurs in what spinal cord injury?
hemisection (Brown-Sequard)
122
The potential for autonomic dysfunction occurs in spinal cord injuries above what level?
T6
123
What are the 3 components of the ICP waveform?
P1 - percussion wave (systolic blood pressure), P2 - tidal wave (rebound pulsations), P3 - dicrotic wave (venous pulsations)
124
Which component of the ICP waveform is normally highest?
P1 (systolic blood pressure)
125
Which component of the ICP waveform is a proxy for compliance?
P2
126
Extremely high amplitude ICP plateau waves lasting for 5-20 min?
Lundberg A waves
127
High amplitude ICP waves lasting for 1-2 min?
Lundberg B waves
128
After a Lundberg A wave, what happens to ICP?
reset at higher baseline
129
Lundberg A waves are thought to be related to what?
inappropriately high cerebral blood volume (impaired autoregulation)
130
In an intact brain, a rise in systolic pressure should do what to ICP?
decrease (intact cerebrovascular reactivity)
131
In an injured brain, a rise in systolic pressure will do what to ICP?
increase (loss of cerebrovascular reactivity)
132
Newborn CSF volume?
50 mL
133
Adult CSF volume?
150-200 mL
134
Beta-2 transferrin is specific to what (a marker of what)?
CSF (detects CSF leakage)
135
Albuminocytologic dissociation (raised protein, normal WBCs) is associated with what disease?
GBS
136
Normal newborn opening pressure?
4-5 cmH2O
137
Normal adult opening pressure?
10 cmH2O
138
Intracranial hypertension is diagnosed with what opening pressure?
>20-25 cmH2O
139
Lateralized periodic discharges (LPDs) on EEG are indicative of what diagnosis?
herpes encephalitis
140
TOF: 0 twitches indicates how much paralysis?
100%
141
TOF: 1 twitch indicates how much paralysis?
90%
142
TOF: 2 twitches indicates how much paralysis?
80%
143
TOF: 3 twitches indicates how much paralysis?
75%
144
TOF: 4 twitches indicates how much paralysis?
0-75%
145
What muscle is used for TOF monitoring?
adductor pollicis (thumb)
146
What is the goal TOF for adequate NMB?
1-2/4 twitches (80%)
147
On T1 weighted MRI, what color is CSF?
dark
148
On T2 weighted MRI, what color is CSF?
bright
149
On T2-FLAIR MRI, what color is CSF?
dark (FLAIR nulls CSF bright)
150
On CT, what color is acute blood?
bright
151
On CT, what color is infarction?
dark
152
On T2 MRI, what color is hyperacute bleed (<24H)?
bright
153
On T2 MRI, what color is acute-subacute bleed (1-7 days)?
dark
154
On T2 MRI, what color is infarction?
bright
155
Bright spot on DWI MRI indicates what?
restricted diffusion (eg, ischemia)
156
If worried about a patient having stroke, what 2 sequences should you check on MRI?
T2, DWI
157
What is the underlying mechanism of cell death in primary brain injury?
necrosis
158
What is the underlying mechanism of cell death in secondary brain injury?
apoptosis
159
What is the ischemic threshold of cerebral blood flow?
20 mL/100 g/min
160
Brain excitotoxicity invovles supraphysiologic amounts of what?
glutamate
161
Elevated glutamate leads to neuronal damage through opening of what channels?
NMDA and AMPA (Ca+ release)
162
A key step in the generation of free radicals is oxidation of what?
cardiolipin (phospholipid)
163
The generation of free radicals involves oxidation of phospholipids by what enzyme?
cytochrome c
164
Cytotoxic edema mechanism?
upregulation of ion channels, allowing water influx (into cells)
165
Vasogenic edema mechanism?
disruption of BBB, allowing water influx (interstitial)
166
When does CBF peak?
4 years (to 10 years)
167
TCD measures blood flow velocity of what?
middle cerebral artery
168
TCD measurement is a surrogate for what?
CBF
169
Critical threshold for SjvO2 in brain injury?
<50%
170
Compared with CT, brain MRI is more sensitive for all brain lesions except what?
skull fractures, SAH
171
Goal dBP during CPR (infants and children)?
>25 infants, >30 children
172
Post-CPR for normothermic TTM, how many days of normothermia are indicated?
5 days
173
What is the "normothermia" temperature goal post-CPR?
36-37.5
174
What is the "hypothermia" temperature goal post-CPR?
32-34C
175
Post-CPR for hypothermia TTM, how many days of hypothermia/normothermia?
2 days hypothermia, 3 days normothermia
176
Order these: Obtundation, lethargy, stupor
Lethargy (minimal), obtundation (moderate), stupor (severe)
177
ADEM involves immune-related damage to what area?
white matter (brain and spinal cord)
178
What serum antibody may be elevated in ADEM?
anti-MOG IgG (myelin oligodendrocyte glycoprotein; nonspecific)
179
What antibody is elevated in neuromyelitis optica?
anti-AQP4 (aquaporin-4)
180
What is the treatment for ADEM?
IVMP, IVIG, PLEX
181
What are 4 common autoimmune encephalitis anatibodies?
anti-NMDAR, anti-VGKC (voltage gated K channel), anti-GAD65, anti-MOG (myelin oligodendrocyte glycoprotein)
182
PANDAS is thought to be an autoimmune response to what infection?
group A strep
183
Treatment of autoimmune encephalitis?
IVMP, IVIG, PLEX
184
Refractory autoimmune encephalitis may require treatment with what?
rituximab (CD20) or cyclophosphamide
185
What immunomodulators are associated with PRES?
calcineurin inhibitors (tacrolimus, cyclosporine)
186
What antineoplastic drugs are associated with PRES?
cytarabine, cisplatin
187
What is the difference between phenytoin and fosphenytoin?
phenytoin is lipophilic and requires propylene glycol; fosphenytoin (prodrug) is water soluble and does not need propylene glycol
188
Phenytoin and hypoalbuminemia concern?
phenytoin is highly protein bound; if hypoalbuminemia, free concentration may be toxic
189
Phenytoin mechanism of action?
Na+ channel blockade causes increase in threshold for depolarization
190
Phenytoin major adverse effect?
dysrhythmia
191
Rapid infusion of propylene glycol (phenytoin) can cause what?
bradycardia and hypotension
192
Which antiepileptic may be particularly useful in terminating SE of neonates?
phenobarbital
193
Phenobarbital effect on hepatic enzymes?
induces CYP metabolism (lowers other drug levels)
194
What's the other name for valproic acid?
depakote
195
Which antiepileptic can cause platelet dysfunction or thrombocytopenia, pancreatitis, and hyperammonemia?
VPA
196
VPA effect on hepatic enzymes?
inhibitor of CYP metabolism (raises other drug levels)
197
Keppra mechanism of action?
binds to presynaptic vesicles, inhibiting neurotransmitter release
198
What is the most common reason for keppra discontinuation?
aggression/behavioral problems
199
Proximal weakness (hip) with muscle biopsy showing round areas devoid of oxidative enzymes is suggestive of what disease?
central core disease
200
Central core disease involves a mutation in what?
ryanodine receptor (RYR1)
201
Patients with central core or multi-minicore diseases are at risk of what?
malignant hyperthermia
202
Nemaline myopathy is characterized by rods that are reactive against what?
alpha-actinin
203
Generalized weakness, high arched palate, skeletal anomalies and cardiac anomalies are suggestive of what disease?
Nemaline myopathy
204
Myotubular myopathy is inherited how?
X-linked
205
What is the most severe congenital myopathy?
myotubular myopathy
206
SMA inheritance pattern?
autosomal recessive
207
SMA pathophysiology?
apoptosis of the anterior motor horn neurons (spinal cord; LMNs)
208
Werdnig-Hoffman disease is a type of what disease?
SMA (type 1)
209
What is Spinraza?
antisense oligonucleotide that alters splicing of SMN2 gene to increase normal SMN1 protein (for SMA)
210
What is Zolgensma?
adeno-viral vector that delivers SMN1 gene (SMA)
211
Botulinum toxin mechanism of action?
prevents presynaptic ACh release
212
Descending paralysis (including cranial nerves) is suggestive of what disease?
botulinum
213
Treatment of botulinum?
IV-BIG (IV botulism Ig)
214
What medication should be avoided in patients with botulinum?
aminoglycosides (gentamicin, amikacin, tobramycin) due to intrinsic neuromuscular blocking effects
215
Transverse myelitis involves inflammation of what areas?
both gray and white matter of the spinal cord
216
A patient presenting with weakness, autonomic dysfunction and a sensory level is suggestive of what disorder?
transverse myelitis
217
Transverse myelitis treatment?
IVMP, IVIG, PLEX
218
Tick paralysis neurotoxin mechanism of action?
prevents ACh release into NMJ
219
Symmetrical ascending paralysis that mimics GBS is suggestive of what disorder?
tick paralysis
220
Acute flacid myelitis involves destruction of what areas?
gray matter of spinal cord
221
GBS involves immune-mediated injury to what area?
myelin sheath of peripheral nerve
222
Rapidly ascending paralysis with areflexia is suggestive of what disease?
GBS
223
GBS treatment?
IVIG, PLEX (not IVMP)
224
What are common infectious triggers of GBS?
campylobacter, CMV, EBV, myocplasma pneumoniae, influenza
225
Miller-Fisher syndrome is a distinct form of what disease?
GBS (involves opthalmoplegia)
226
What is the "20/30/40" rule of PFTs?
respiratory failure impending if vital capacity <20 mL/kg, max inspiratory pressure <-30 mmHg, or max expiratory pressure <40 mmHg
227
Myasthenia gravis mechanism of action?
autoantibody to post synaptic ACh receptor
228
What are the 4 levels of sedation?
minimal, moderate, deep, general anesthesia
229
Level of sedation: airway may require intervention but normal breathing?
moderate
230
Level of sedation: airway occasionally requires intervention with possibly impaired breathing?
deep
231
What type of drug affects memory incorporation (unable to recall events)?
amnestic
232
What type of drug produces drowsiness and aids in onset of sleep?
hypnotic
233
In which age is the narrowest part of the airway the subglottic region?
<8-10 years
234
A child with a modified Mallampati score of 3-4 is at risk for what?
difficult intubation
235
Mallampati class: full tonsillar pillars seen?
class 1
236
Mallampati class: uvula but not full tonsillar pillars?
class 2
237
Mallampati class: base of uvula only?
class 3
238
Mallampati class: no uvula?
class 4
239
ASA class: mild systemic disease?
ASA II
240
ASA class: severe systemic disease?
ASA III
241
ASA class: disease is constant threat to life?
ASA IV
242
ASA class: moribund (not expected to live 24h)?
ASA V
243
The GABA receptor is what type of receptor?
chloride ion channel
244
Benzodiazepine mechanism of action?
enhance GABA activity
245
GABA binding to GABA receptor causes what?
chloride flux, hyperpolarization, decreased neurotransmission
246
Major inhibitory neurotransmitter in the spinal cord and brain stem?
glycine
247
What common medications use propylene glycol as solvent?
phenytoin, diazepam and lorazepam
248
Diazepam, lorazepam and midazolam all use what as a preservative?
benzyl alcohol
249
Which benzodiazepine is best in liver insufficiency?
lorazepam (phase II metabolism)
250
Propofol mechanism of action?
decreases the rate of dissociation of GABA from its receptor
251
Propofol vasodilation mechanism of action?
NO release and calcium channel blockade
252
What is the major hemodynamic side effect of propofol?
bradycardia
253
Ketamine mechanism of action?
NMDA inhibition (inhibits glutamate neurotransmission)
254
Ketamine inotropy effect?
direct negative inotrope (usually counteracted by indirect sympathomimetic activity)
255
Barbiturate mechanism of action?
GABA agonist (low dose), direct cell hyperpolarization independent of GABA (high doses)
256
Immunosuppression is a side effect of which class of sedative?
barbiturates
257
Mechanism of barbiturate-induced immunosuppression?
lymphocyte apoptosis, T cell dysregulation
258
Opiate receptor stimulation causes inhibition of neurotransmitters, including what excitatory neurotransmitter of pain?
substance P
259
Remifentanil metabolism mechanism?
tissue and plasma esterases (safe in renal and liver dysfunction)
260
Accumulation of Dilaudid metabolite in renal injury can cause what?
seizures or myoclonus
261
Methadone mechanism of action?
u receptor agonist, NMDA antagonist
262
Maximum daily dose of acetaminophen?
3000 mg
263
The ED95 in NMB indicates what?
the dose that produces complete flaccidity in 95% of population
264
Presynaptic nicotinic ACRs in the NMJ do what when stimulated?
increase ACh release (positive feedback mechanism)
265
What % of ACRs must be blocked by NMBs before an effect is measurable?
>50%
266
Succinylcholine metabolism?
degraded by plasma cholinesterase (not acetylcholinesterase in NMJ)
267
Fastest onset of NMB is by what medication?
succinylcholine
268
If a you give a patient who received succinylcholine the drug neostigmine or pyridostigmine, what happens?
prolongs succinylcholine-induced paralysis (inhibit plasma cholinesterase and acetylcholinesterase)
269
Succinylcholine must be avoided in which patients?
burn injury, crush injury, severe systemic disease, immobilization, muscular dystrophy
270
Giving a patient with burn injury succinylcholine puts them at risk for what?
hyperkalemia
271
Hyperkalemic effect of succinylcholine occurs why?
activation of extrajunctional ACRs
272
A patient with central core or multiminicore disease must not receive what medication?
succinylcholine (risk of MH)
273
Treatment of malignant hyperthermia?
Dantrolene
274
Dantrolene mechanism of action?
decreases calcium release from sarcoplasmic reticulum
275
To avoid fasciculations by succinylcholine, give what before?
small dose of non-depolarizing NMB
276
Prolonged succinylcholine infusions lead to "phase 2 block," which is what?
the post-junctional membrane potential moves toward resting state so that the ACR does not respond to ACh; similar to non-depolarizing NMB
277
Cisatricurium metabolism?
Hoffman degradation (safer in renal and hepatic dysfunction)
278
Which NMB are aminosteroids?
rocuronium, pancuronium, vecuronium
279
Which NMB are benzylisoquinolines?
atracurium, cisatricurium
280
Disuse atrophy or acute myopathy: CK levels?
elevated
281
Disuse atrophy or acute myopathy: muscle biopsy?
necrosis
282
Critical illness polyneuropathy: CK levels?
normal
283
Critical illness polyneuropathy: DTRs?
markedly diminished or absent
284
Critical illness myopathy: CK levels?
mildly increased or normal
285
Critical illness myopathy: muscle biopsy?
atrophy to necrosis
286
TOF response to succinylcholine vs rocuronium?
succinylcholine decreases all twitches equally; rocuronium decreases subsequent twitches
287
What can be used to assess intense NMB before a response to TOF has reappeared?
tetanic stimulation (post-tetanic count)
288
What is typically the goal number of TOF twitches during surgery?
1-2 out of 4 (less in ICU, maybe 3 out of 4)
289
What nerve is most commonly used for TOF monitoring?
ulnar nerve
290
Does hypothermia make NMB last longer or shorter?
longer
291
Neostigmine mechanism of action?
inactives acetylcholinesterase (increases ACh)
292
Reversal agent for succinylcholine?
none exist
293
When giving neostigmine, must also give what?
anticholinergic (atropine or glycopyrrolate)
294
Sugammadex mechanism of action?
forms a complex with rocuronium and/or vecuronium, inactivating them
295
Sugammadex common cardiovascular complication?
bradycardia
296
Sugammadex interferes with what common medicine?
progesterone hormonal contraceptives (binds in vitro)
297
Which muscle is most resistant to neuromuscular blockade?
diaphragm
298
What muscle recovers fastest from NMB?
diaphragm
299
What muscles recover slowest/are first to weaken with NMB?
upper airway
300
What type of ACh receptors do NMBs bind to?
nicotonic
301
What happens when you give a neostigmine to a patient who got succinylcholine?
prolongs NMB
302
Succinylcholine effect on ICP?
increases
303
What is the only inhalational anesthetic that doesn't cause malignant hyperthermia?
nitrous oxide
304
Is propofol safe in patients with malignant hyperthermia?
yes
305
A diagnosis of pseudocholinesterase deficiency can be made when a dibucaine number is what?
<80%
306
What blood product can be administered to a patient with pseudocholinesterase deficiency?
FFP (has some enzyme)
307
Which NMB agent causes histamine release?
atracurium
308
Major side effect of atracurium?
histamine release
309
Atracurium and Cisatracurium breakdown into what potentially toxic agent?
Laudanosine
310
Laudanosine toxicity can cause what?
seizures (Laudanosine is a cis/atracurium byproduct)
311
What NMB is ideal in renal failure?
cisatracurium
312
Major side effect of pancuronium?
tachycardia
313
Which NMB agent should be avoided in liver failure?
Vecuronium (hepatic metabolism of active metabolites)
314
Associated use of what drug can cause prolonged paralysis with NMB use?
aminoglycosides
315
Prolonged NMB: hypothermia or hyperthermia?
hypothermia
316
Prolonged NMB: hyperkalemia or hypokalemia?
hypokalemia
317
Prolonged NMB: hypomag or hypermag?
hypomagnesemic
318
When using TOF monitoring, how many Hz is applied for how many seconds?
2 Hz for 2 seconds
319
What are the two main classes of local anesthetics?
aminoesters and aminoamides
320
Metabolism of aminoester local anesthetics?
plasma esterases
321
Metabolism of aminoamide local anesthetics?
liver
322
Chloroprocaine, procaine, and benzocaine are what type of local anesthetic?
aminoesters (plasma esterase metabolism)
323
Bupivacine, lidocaine, mepivacaine, and ropivacaine are what type of local anesthetic?
aminoamides (liver metabolism)
324
Risk of systemic absorption of local anesthetics is greatest at what site of block?
intercostal nerve block
325
Maximum cumulative dose of licodaine WITH epi?
7 mg/kg
326
Maximum cumulative dose of lidocaine WITHOUT epi?
3 mg/kg
327
What is the most common epidural medication in children?
bupivacaine
328
Cardiac arrest from what local anesthetic is particularly difficult to reverse?
bupivacaine
329
What can you give in bupivacaine toxicity?
lipids (20%)
