Unit 7 - Neuro - Brain Flashcards
1
Q
list 4 types of cells in CNS
A
astrocytes
ependymal cells
oligodendrocytes
microglia
2
Q
what type of CNS cell is most prone to brain tumors
A
glial
3
Q
function of dendrites
A
receive & process signal
4
Q
function of soma
A
integrates signal
5
Q
function of axon
A
send signal
6
Q
function of presynaptic terminal
A
releases NTs
7
Q
what is the “nerve glue” that supports neural function
A
glial cells
8
Q
4 functions of glial cells
A
- Create a healthy ionic environment
- Modulate nerve conduction
- Control reuptake of neurotransmitters
- Repair neurons following neuronal
9
Q
3 types of neurons in CNS
A
- Multipolar
- Pseudounipolar
- Bipolar
10
Q
what type of neurons are most CNS neurons
A
multipolar
11
Q
where are pseudounipolar CNS neurons found
A
dorsal root ganglion & cranial ganglion
12
Q
where are bipolar CNS neurons found
A
retina
ear
13
Q
most abundant type of glial cell
A
astrocytes
14
Q
where are ependymal cells concentrated
A
in 3rd & 4th ventricles + spinal canal
15
Q
cells from choroid plexus, which produces CSF
A
ependymal cells
16
Q
glial cells that form myelin sheath in CNS
A
Oligodendrocytes
17
Q
CNS cells that act as macrophages and phagocytize neuronal debris
A
microglia
18
Q
type of glial cell that regulates metabolic environment
A
astrocytes
19
Q
type of glial cell that repairs neuron after neuronal injury
A
astrocytes
20
Q
2 major structures of diencephalon
A
thalamus
hypothalamus
21
Q
3 anatomic structures of brainstem
A
midbrain
pons
medulla oblongata
22
Q
where is the RAS located
A
brainstem
23
Q
4 brain areas
A
cerebral hemispheres, diencephalon, brainstem, cerebellum
24
Q
connects 2 cerebral hemispheres
A
Corpus callosum
25
where is corpus collosum located
deep in longitudinal fissure
26
lobe that contains motor cortex
frontal
27
lobe that contains somatic sensory cortex
parietal
28
lobe that contains vision cortex
occipital
29
lobe that contains auditory cortex & speech centers
temporal
30
Wernicke’s area
understanding speech
31
Wernicke’s area
understanding speech
32
Broca’s area
motor control of speech
33
where is broca's area
in frontal lobe, connected to Wernicke’s via neural pathways
34
functions of cerebral cortex
* cognition, movement (precentral gyrus of frontal lobe)
* sensation (postcentral gyrus of parietal lobe)
35
functions of hippocampus
memory and learning
36
functions of hippocampus
memory and learning
37
responsible for emotion, appetite, responds to pain and stressors
amygdala
38
responsible for fine control of movement
Basal ganglia
39
acts as a relay station that directs information to various cortical structures
thalamus
40
primary neurohumoral organ
hypothalamus
41
part of brainstem responsible for autonomic integration
medulla
42
3 parts of cerebellum
* Archicerebellum
* Paleocerebellum
* Neocerebellum
43
part of cerebellum that maintains equilibrium
Archicerebellum
44
part of cerebellum that regulates muscle tone
Paleocerebellum
45
part of cerebellum that coordinates voluntary muscle movement
Neocerebellum
46
function of CN 3
oculomotor
eye movement, pupil constriction
47
CN innvervation of eye muscles
CN 3:
* inferior oblique (extorsion-elevation)
* superior rectus (supraduction)
* medial rectus (adduction)
* inferior rectus (infraduction)
CN 4:
* superior oblique (intorsion-depressioN)
CN 6:
* lateral rectus (abduction)
48
branches & functions of CN 5
V1 = opthalamic (somatic sensation to face)
V2 = maxillary (somatic sensation to anterior 2/3 tongue)
V3 = mandibular (muscles of mastication)
49
branches of facial n.
temporal
zygomatic
buccal
mandibular
cervical
| Two Zebras Bit My Carrot
50
functions of facial nerve
* facial movement (except mastication)
* eyelid closing
* taste to anterior 2/3 tongue
51
sensory function of CN 9
somatic sensation to posterior 1/3 tongue
52
CN responsible for swallowing
vagus
53
CN responsible for 70% of all PNS activity
CN 10
54
all CN are part of peripheral nervous system except:
CN 2
55
only CN surrounded by dura
CN 2
| optic n.
56
what is Tic douloreaux
trigeminal neuralgia
generates excruciating neuropathic facial pain
57
s/s injury to facial n.
bell’s palsy = unilateral facial paralysis
58
locations of CSF
* ventricles (L lateral, R lateral, 3rd, 4th)
* cisterns around brain
* subarachnoid space in brain and spinal cord
59
CSF volume
~150 mL
60
produces CSF
ependymal cells of choroid plexus in cerebral ventricles (30 mL/hr)
61
normal CSF pressure
5-15 mmHg
62
reabsorbs CSF
arachnoid villi in superior sagittal sinus
63
what is CSF absorption via arachnoid villi dependent on
pressure gradient between CSF and venous circulation
64
separates CSF from plasma
Blood brain barrier
65
causes BBB to become dysfunctional
sites of tumor, injury, infection, or ischemia
66
places BBB is not present
* CTZ
* posterior pituitary gland
* pineal gland
* choroid plexus
* parts of hypothalamus
67
how can some drugs that can't pass BBB cause N/V?
absence of BBB at CTZ
68
normal CSF flow
lateral ventricles - foramen of Monro - 3rd ventricle - Aqueduct of Sylvius - 4th ventricle - Foramen of Luschka - Foramen of Magendie - subarachnoid space - superior sagittal sinus (site of reabsorption)
69
composition of CSF
* Isotonic with plasma, but not an ultrafiltrate of plasma
* Osmolarity = 295 mOsm/L
70
similarities & differences in composition of CSF vs. plasma
* Similarities: Na+ level, HCO3, PaCO2
* Differences: K+, pH, glucose, protein
71
most common type of hydrocephalus
Obstructive
72
cause of communicating hydrocephalus
decreased CSF absorption by arachnoid villi (ex. intracranial hemorrhage)
or overproduction of CSF (very rare)
73
what is cerebral autoregulation
brain’s ability to maintain a constant cerebral blood flow over a wide range of mean arterial blood pressures
74
cerebral blood flow =
cerebral perfusion pressure / cerebral vascular resistance
75
normal global CBF
45-55 mL/100g tissue/min
or 15% CO
76
normal cortical CBF
75-80 mL/100g tissue/min
77
normal subcortical CBF
20 mL/100g tissue/min
78
CBF assoc. with evidence of ischemia
CBF ~ 20 mL/100g tissue/min
79
CBF assoc. with complete cortical suppression
CBF ~ 15 mL/100g tissue/min
80
CBF assoc. with membrane failure & cell death
CBF < 15 mL/100g tissue/min
81
normal CMRO2
3.0 – 3.8 mL/O2/100g brain tissue/min
82
5 Determinants of Cerebral Blood Flow
1. Cerebral metabolic rate for oxygen
2. Cerebral perfusion pressure
3. PaCO2
4. PaO2
5. Venous pressure
83
O2 utilization by the brain
60% for electrical activity
40% for cellular integrity
84
decreasing CMRO2
Hypothermia
Halogenated anesthetics
Propofol
Etomidate
Barbiturates
85
increasing CMRO2
Hyperthermia
Seizures
Ketamine
N2O
86
why do volatiles increase CBF but decrease CMRO2
Volatiles uncouple CBF from CRMRO2
87
improves outcomes after out-of-hospital V-fib and resuscitation
Mild hypothermia (32-34°C) for 12-24 hours
88
CPP =
MAP - ICP (or CVP, whicever is higher)
89
Brain autoregulates CBF between :
CPP of 50-150 mmHg or MAP 60-160 mmHg
90
Brain autoregulates CBF between :
CPP of 50-150 mmHg or MAP 60-160 mmHg
91
O2 utilization by the brain
60% for electrical activity
40% for cellular integrity
92
CMRO2 decrease with hypothermia
↓ by 7% for every 1°C decrease in temp
93
temp assoc with EEG suppression
18-20°C
94
negative effects assoc with temp > 42°C
* denatures protein
* destroys neurons
* ↓ CBF
95
why does CPP become dependent on MAP when above upper or lower limit of autoregulation
veins either maximally dilated (below lower limit) or maximally constricted (above upper limit)
96
MAP to ensure CPP 50
MAP 55-65 mmHg if ICP is normal (5-15)
## Footnote
higher ICP requires higher MAP to maintain CPP
97
normal controls of cerebral autoregulation
* products of local metabolism
* myogenic mechanics
* autonomic innervation
98
3 things that decrease effectiveness of cerebral autoregulation
1. brain tumor
2. head trauma
3. volatiles
99
contemporary model of chronic HTN and cerebral autoregulation
* Suggests plateau of curve narrows and CBF becomes more closely dependent on CPP
* Likely a high degree of patient-to-patient variability
100
traditional model of chronic HTN and cerebral autoregulation
* Chronic HTN shifts entire curve to the right
* Brain becomes more tolerant of HTN and less tolerant of hypotension
101
at a PaCO2 of 40, global CBF is:
50 mL/100g brain tissue/min
102
For every 1 mmHg increase in PaCO2, CBF will increase by:
1-2 mL/100g brain tissue/min
103
For every 1 mmHg decrease in PaCO2, CBF will decrease by
1-2 mL/100g brain tissue/min
104
maximal vasodilation occurs at PaO2 of:
80-100 mmHg
105
Maximal vasoconstriction occurs at PaCO2 of:
~ 25 mmHg
106
how is cerebral vascular resistance controlled
The pH of the CSF & arterioles controls
107
how does respiratory acidosis affect CBF
**increases CBF**
↓ CSF pH (↑ PaCO2) = ↓ CVR = ↑ CBF
108
how does respiratory alkalosis affect CBF
**decreases CBF**
↑ CSF (↓ PaCO2) = ↑ CVR = ↓ CBF
109
how does metabolic acidosis affect CBF
doesn’t directly affect CBF (H+ in blood doesn’t pass BBB)
110
what causes the "steal" phenomena
cerebral vessels that supply ischemic/atherosclerotic vessels are maximally dilated
situations causing vasodilation dilate vessels that supply healthy brain tissue and "steal" flow from ischemic areas
111
what is the Robinhood effect
* Concept of using hyperventilation to constrict cerebral vessels that supply healthy brain tissue
* Idea is that flow will be redistributed to ischemic regions, which are maximally dilated
112
how can the Robinhood effect cause harm
from cerebral ischemia (not enough CBF) and shifting oxyhgb dissociation curve to the left
113
how does PaO2 < 50-60 affect CBF
causes cerebral vasodilation, increases CBF
114
when PaO2 > _ , CBF is unaffected
60
115
Conditions that impair venous drainage:
* Jugular compression due to improper head positioning (ex. head flexion when sitting)
* Increased intrathoracic pressure 2/2 coughing or PEEP
* Vena cava thrombosis
* Vena cava syndrome
116
cerebral HTN
ICP > 20 mmHg
117
S/S intracranial HTN
* headache
* N/V
* papilledema
* pupil dilation and non-reactivity to light
* focal neurological deficit
* seizure
* coma
118
Monroe-Kellie hypothesis
describes pressure-volume equilibrium between brain, blood, & CSF within the confines of the cranium
| Increase in one component must be countered with a decrease in one or bo
119
Monroe-Kellie hypothesis
describes pressure-volume equilibrium between brain, blood, & CSF within the confines of the cranium
| Increase in one component must be countered with a decrease in one or bo
120
brain causes of increased CBV
* cerebral swelling
* tumor
121
blood causes of increased CBV
* increased CBF
* bleeding
122
CSF causes of increased CBV
* increased CSF produciton by choroid plexus
* reduced CSF removal by arachnoid villi
* obstruction to reabsorption
* passage of fluid across BBB
123
Cushing's triad
HTN, bradycardia, irregular respirations
124
what causes irregular respirations with inc ICP
Compression of medulla
125
most common site of herniation
temporal uncus
126
what causes fixed/dilated pupils with temporal uncus herniation
CN 3 originates from midbrain, crosses near tentorium
herniation applies pressure to the nerve, making it ischemic
127
what is Pseudotumor Cerebri
idiopathic intracranial HTN
condition where ICP increases for no apparent reason (“false tumor”)
128
what is papilledema
swelling of optic n./
129
2 methods to decrease CBV
1. decrease CBF
2. increase venous outflow
130
2 methods to decrease CSF
1. CSF drainage
2. drugs
131
2 methods to decrease cerebellar mass
1. tumor debulking
2. diuretics
132
2 methods to decrease cerebral edema
1. diuretics
2. corticosteroids
133
how does hyperventilation decrease CBF
Mild hyperventilation (30-35) constricts vessels = ↑ CVR = ↓ CBF= ↓ ICP
134
PaO2 < ____ increases risk of cerebral ischemia
30
135
how long do the decreased CBF effects of mild hyperventilation last
6-20 hours
| (pH of CSF equilibrates with PaCO2)
136
how long do the decreased CBF effects of mild hyperventilation last
6-20 hours
| (pH of CSF equilibrates with PaCO2)
137
PaO2 < ____ greatly increases CBF and ICP
50-60
138
drugs to avoid when trying to decrease CBF
vasodilators - NTG, Nipride
139
positioning that facilitates venous drainage from brain
Head elevation > 30 °
140
positioning that can increase ICP
* Neck flexion or extension (can compress jugular veins)
* Trendelenburg
141
how can PEEP affect ICP
PEEP = ↑ intrathoracic pressure = ↓ venous drainage from brain (can ↑ ICP)
142
when is CSF drainage the most useful treatment of increased ICP
obstruction to CSF flow (hydrocephalus)
143
drugs that decrease CSF production
Acetazolamide & furosemide
144
where does arterial bleeding in the brain most commonly occur
subarachnoid space
(between arachnoid and pia mater)
145
where does venous bleeding in the brain usually occur
subdural space
between dura and arachnoid mater
146
what forms myelin sheath in PNS
Schwann cells
147
3 meningeal layers covering brain and spinal cord
1. dura mater
2. arachnoid mater
3. pia mater
148
3 meningeal layers covering brain and spinal cord
1. dura mater
2. arachnoid mater
3. pia mater
149
glial cells that increase neuronal conduction velocity
oligodendrocytes
150
CN most likely to be compressed by pituitary tumor
CN 2
151
where is CSF produced
choroid plexus
152
153
fixed/dilated pupil suggests herniation of:
temporal uncus
154
main blood supply to brain's posterior circulation
basilar artery (only 1)
155
gives rise to paired posterior communicating arteries
basilar artery
156
gives rise to paired vertebral arteries
subclavian arteries
157
gives rise to paired middle cerebral arteries
internal carotids
158
anticonvulsant that is excreted unchanged by kidneys
gabapentin
159
methods to decrease cerebral mass with increased ICP
tumor debulking
evacuation of hematoma
mannitol
160
how do loop diuretics decrease cerebral edema
inducing diuresis and increasing rate of CSF production
161
how do osmotic diuretics reduce cerebral edema
by increasing serum osmolarity and "pulling" water across BBB
| 0.25-1 g/kg mannitol
162
dose of mannitol to decrease cerebral edema
0.25-1 g/kg
163
how does 3% NaCl affect cerebral edema
high tonicity decreases cerebral edema by "pulling" water across BBB
164
downside of using mannitol for decreasing cerebral edema
transiently increases blood volume
can increase ICP and stress failing heart
165
use of steroids in cerebral edema
decadron & methylpred decrease cerebral edema from mass lesions & spinal cord injuries
should NOT be used with TBI or funcitonal pituitary adenoma
166
methods to decrease CBV
* propofol
* hyperventilation
* maintain neck neutrality
* HOB elevated
167
methods to derease CSF
VP shunt
acetelazomide
interventricular drain
168
decreased cerebral mass/edema
corticosteroids
debulking
mannitol
169
what med should be used to support CPP with increased ICP
phenylephrine
170
why should dextrose solutions be avoidd
171
why should dextrose solutions be avoided in cases of increased ICP/head injury
in the setting of cerebral ischemia, excess glucose in brain is converted to lactic acid & worsens outcomes
172
173
supplies anterior circulation to the brain
internal carotids
174
where do internal carotids enter skull
foramen lacerum
175
anterior cerebral circulation flow
Aorta - carotid - internal carotid - circle of Willis - cerebral hemispheres
176
what supplies posterior cerebral circulation
vertebral arteries
177
main supply of posterior cerebral circulation
basilar artery (only 1)
178
posterior cerebral circulation flow
aorta - subclavian a. - vertebral a. - basilar a - posterior fossa structures and cervical spinal cord
179
primary function of circle of Willis
provide redundancy of blood flow in the brain
180
how does venous blood from cerebral cortex & cerebellum drain
via superior sagittal sinus & dural sinuses
181
how does venous blood from basal brain structures drain
via inferior sagittal sinus, the vein of Galen, and straight sinuses
182
where do venous cerebral pathways converge
confluence of sinuses
183
how does venous blood exit the brain
all exits via paired jugular veins
184
Most common type of CVA
ischemic
185
most likely cause of ischemic CVA
cardio-embolic event like A-fib
186
A person who exhibits a sudden change in neurologic function or progressive change in neuro status is most likely experiencing a ?
CVA
187
what is a TIA
focal neuro deficit that spontaneously resolves within 24 hours
| warning sign of cerebrovascular disease, impending stroke
188
what is a TIA
focal neuro deficit that spontaneously resolves within 24 hours
| warning sign of cerebrovascular disease, impending stroke
189
ischemic stroke risk factors
* HTN (most important)
* smoking
* DM
* HLD
* excessive ETOH
* ↑ homocysteine level
190
treatment for stroke symptoms after hemorrhage ruled out
* 1st line: aspirin
* IV thrombolytic within 4.5 hours of stmprom onset
191
when should patients undergo embolectomy
pts with large vessel occlusion should undergo within 6 hours
192
target BP after ischemic CVA
under 185/110
193
purpose of fluid replacement with CVA
supports BP, CO, CPP, & improves CBF by ↓ viscosity
194
why is blood sugar control important in CVA pts
during cerebral hypoxia, glucose is converted to lactic acid
cerebral acidosis destroys brain tisue
195
most common cause of subarachnoid bleeding
aneurysm rupture
| most from circle of Willis
196
most common cause of subarachnoid bleeding
aneurysm rupture
| most from circle of Willis
197
transmural pressure =
MAP - ICP
198
Most common sign of SAH
intense headache often described as “worst headache of my life”
## Footnote
Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time
199
Most common sign of SAH
intense headache often described as “worst headache of my life”
## Footnote
Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time
200
Most common sign of SAH
intense headache often described as “worst headache of my life”
## Footnote
Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time
201
what causes meningismus in hemorrhagic stroke patients
blood spreads and irritates meninges
202
Morbidity of hemorrhagic stroke results from:
* obstructive hydrocephalus
* rebleeding
* vasospasm
203
surgical options for hemorrhagic stroke
aneurysm clipping or endovascular coiling
204
general intraop SBP goal in aneurysm clipping or endovascular coiling
120-150 mmHg
205
when should surgical repair of hemorrhagic stroke take place
24-48 hours following initial bleed
## Footnote
Intervention at this time makes triple H therapy safer
206
what should you do if aneurysm ruptures during coiling procedure and heparin has been given
immediately reverse with 1mg protamine for every 100 u heparin
207
why is controlled hypotension not needed when clamp is used for hemorrhagic stroke
↓ transmural pressure and risk of rupture & eliminates need
## Footnote
High/normal BP required to perfuse collateral circulation
208
why is controlled hypotension not needed when clamp is used for hemorrhagic stroke
↓ transmural pressure and risk of rupture & eliminates need
## Footnote
High/normal BP required to perfuse collateral circulation
209
why is controlled hypotension not needed when clamp is used for hemorrhagic stroke
↓ transmural pressure and risk of rupture & eliminates need
## Footnote
High/normal BP required to perfuse collateral circulation
210
Most significant drawback of controlled hypotension for cerebral aneurysm clipping
decreased CPP
211
major cause of M&M in pts who have suffered SAH
Cerebral vasospasm
212
what causes cerebral vasospasm after SAH
delayed contraction of cerebral arteries
## Footnote
Positive correlation between amount of blood on CT & incidence of spasm
213
when is cerebral vasospasm most likely to occur with SAH
4-9 days after bleed
214
methods to monitor for cerebral vasospasm after SAH
Frequent neuro checks and daily transcranial Dopplers
215
Most common presentation of cerebral vasospasm
new neuro deficit, AMS
216
Gold standard for cerebral vasospasm diagnosis
cerebral angiography
217
BP goal for cerebral vasospasm treatment
increase MAP 20-30 mmHg above baseline
218
Triple H Therapy
* hypervolemia
* HTN
* hemodilution to Hct 27-32%
219
only CCB to ↓ M&M from vasospasm
nimodipine
## Footnote
↑ collateral blood flow
220
only CCB to ↓ M&M from vasospasm
nimodipine
## Footnote
↑ collateral blood flow
221
treatment of medically-refractory cerebral vasospasm
* intra-arterial vasodilators (verapamil, nicardipine), papaverine, milrinone
* balloon angioplasty
222
most common cause of hyponatremia with SAH
Cerebral Salt Wasting Syndrome
## Footnote
not SIADH
223
most common cause of hyponatremia with SAH
Cerebral Salt Wasting Syndrome
## Footnote
not SIADH
224
treatment for Cerebral Salt Wasting Syndrome
isotonic crystalloids
225
Head CT probably not required if minor trauma +
* No physical evidence of trauma above clavicles
* No headache
* No N/V
* No neuro deficit
* No impaired short-term memory
* No intoxication
* No seizures
* Age < 60 years
226
GCS: motor response
1 = no motor response
2 = abnormal extension to pain
3 = abnormal flexion to pain
4 = withdrawal to pain
5 = localizes pain
6 = obeys commands
227
GCS: verbal Response
1 = no verbal response
2 = incomprehensible sounds
3 = inappropriate words
4 = confused
5 = oriented
228
GCS: eye opening
1 = no eye opening
2 = eye opening to pain/pressure
3 = eye opening to sound
4 = opens spontaneously
229
GCS: pupil reactivity
-2 = both NR to light
-1 = one NR to light
0 =PERRL
230
how can warfarin be reversed
* FFP
* prothrombin complex concentrate
* recombinant factor 7a
231
how can Clopidogrel/aspirin be reversed
* platelet transfusion
* recombinant factor 7a
232
CPP goal for TBI
> 70
233
fluids to avoid in TBI
* dextrose fluids
* hypotonic solutions
* albumin
234
inhaled anesthetic to avoid with TBI
N2O
235
sz activity localized to particular cortical region
Partial seizure
236
Generalized seizure
activity affects both hemispheres
237
Jacksonian march
partial seizure progresses to generalized seizure
238
phases of grand mal sz
Tonic phase = whole body rigidity
Clonic phase = repetitive jerking motions
239
types of seizures assoc with respiratory arrest
grand mal
status epilepticus
240
Acute treatment of grand mal sz
propofol, diazepam, thiopental
241
Surgical treatment of grand mal sz
vagal nerve stim, foci resection
242
sz linked to particular cortical region
focal cortical
## Footnote
usually no LOC
243
sz linked to particular cortical region
focal cortical
## Footnote
usually no LOC
244
sz with temporary loss of awareness (remains awake)
Absence (Petit Mal)
245
sz assoc. with temporary loss of consciousness & postural tone
Akinetic
246
Status Epilepticus
Seizure activity > 30 min or 2 grand mal seizures without regaining consciousness in between
247
treatment of Status Epilepticus
phenobarbital, thiopental, phenytoin, benzos, propofol, GA
248
in adults, epilepsy usually results from 1 of what 2 things
1) structural brain lesion: tumor, head trauma, cerebrovascular event
2) metabolic cause: hypoglycemia, drug toxicity, withdrawal, infection
249
how do inhaled anesthetics affect EEG activity
tend to ↓ EEG activity (dose-dependent) but all have been implicated in producing seizures (very rare)
250
S/S seizures under GA
↑ HR, HTN, ↑ EtCO2
251
IV anesthetic that can induce sz
ketamine
252
EEG effects. of etomidate
commonly causes myoclonus - not assoc. with ↑ EEG activity in pts without epilepsy
253
meds useful for cortical mapping in pts with sz disorders (increase EEG activity)
1. methohexital
2. etomidate
3. alfentanil
254
first-line agent for control of sz activity
propofol
255
anticonvulsants assoc with NDNMB resistance
* phenytoin
* Carbamazepine
256
anticonvulsant that undergoes zero order kinetics
Phenytoin
257
SEs of phenytoin
* dysrhythmias/hypotension (if IV rate > 50 mcg/min)
* gingival hyperplasia
* aplastic anemia, cerebellar-vestibular dysfunction (nystagmus, ataxia)
* SJS
* birth defects
258
anticonvulsant assoc with purple glove syndrome
phenytoin
259
anticonvulsant that slows phenytoin metabolism
valproic acid
260
SEs of Valproic Acid
* hepatotoxicity
* thrombocytopenia
* displaces phenytoin from plasma proteins
261
SEs of Valproic Acid
* hepatotoxicity
* thrombocytopenia
* displaces phenytoin from plasma proteins
262
MOA of carbamazepine, phenytoin, and valproic acid
block voltage-gated Na+ channels
membrane stabilizer
263
anticonvulsant useful for trigeminal neuralgia
Carbamazepine
264
SEs of Carbamazepine
* aplastic anemia
* thrombocytopenia
* liver dysfunction
* leukopenia
* hyponatremia (ADH-like effect)
265
MOA of gabapentin
inhibition of alpha-2 delta subunit of voltage-gated Ca2+ channels in CNS
decreased excitatory NT release
## Footnote
Chemical analogue of GABA, NOT GABA agonist
266
SEs of gabapentinoids
dizziness, somnolence
267
why should gabapentin be tapered off
Abrupt withdrawal can produce sz if patient has hx sz
## Footnote
taper for at least 1 week
268
why should gabapentin be tapered off
Abrupt withdrawal can produce sz if patient has hx sz
## Footnote
taper for at least 1 week
269
why should gabapentin be tapered off
Abrupt withdrawal can produce sz if patient has hx sz
## Footnote
taper for at least 1 week
270
most common cause of dementia in pts > 65
Alzheimer’s Disease
271
key findings in alzheimers
beta amyloid rich plaques & neurofibrillary tangles in the brain
272
consequences of amyloid plaque formation in Alzheimers
* dysfunctional synaptic transmission (most noticeable with ACh)
* apoptosis
273
class of drugs used to treat Alzheimer's & AIs of use
cholinesterase inhibitors
increase duration of succs (questionable significance)
274
patho of Parkinson's
dopaminergic neurons in basal ganglia destroyed
| decreased dopamine + normal ACh = relative ACh increase
275
what is suppressed vs overactive in parkinsons
corticospinal motor system suppressed
extrapyramidal motor system overactive
276
what drugs increase extrapyramidal s/s in pt with parkinsons
dopamine antagonists
* Reglan
* haldol
* droperidol
* promethazine
277
most common cause of POVL
ION
278
patho of ION
optic nerve ischemia
| likely r/t venous congestion
279
procedural risk factors for ION
* prone
* wilson frame
* long duration
* large blood loss
* low ratio colloid:crystalloid
* hypotension
280
pt risk factors for ION
* male
* obese
* DM
* HTN
* smoking
* old age
* atherosclerosis
