Unit 7 - Neuro - Brain Flashcards
list 4 types of cells in CNS
astrocytes
ependymal cells
oligodendrocytes
microglia
what type of CNS cell is most prone to brain tumors
glial
function of dendrites
receive & process signal
function of soma
integrates signal
function of axon
send signal
function of presynaptic terminal
releases NTs
what is the “nerve glue” that supports neural function
glial cells
4 functions of glial cells
- Create a healthy ionic environment
- Modulate nerve conduction
- Control reuptake of neurotransmitters
- Repair neurons following neuronal
3 types of neurons in CNS
- Multipolar
- Pseudounipolar
- Bipolar
what type of neurons are most CNS neurons
multipolar
where are pseudounipolar CNS neurons found
dorsal root ganglion & cranial ganglion
where are bipolar CNS neurons found
retina
ear
most abundant type of glial cell
astrocytes
where are ependymal cells concentrated
in 3rd & 4th ventricles + spinal canal
cells from choroid plexus, which produces CSF
ependymal cells
glial cells that form myelin sheath in CNS
Oligodendrocytes
CNS cells that act as macrophages and phagocytize neuronal debris
microglia
type of glial cell that regulates metabolic environment
astrocytes
type of glial cell that repairs neuron after neuronal injury
astrocytes
2 major structures of diencephalon
thalamus
hypothalamus
3 anatomic structures of brainstem
midbrain
pons
medulla oblongata
where is the RAS located
brainstem
4 brain areas
cerebral hemispheres, diencephalon, brainstem, cerebellum
connects 2 cerebral hemispheres
Corpus callosum
where is corpus collosum located
deep in longitudinal fissure
lobe that contains motor cortex
frontal
lobe that contains somatic sensory cortex
parietal
lobe that contains vision cortex
occipital
lobe that contains auditory cortex & speech centers
temporal
Wernicke’s area
understanding speech
Wernicke’s area
understanding speech
Broca’s area
motor control of speech
where is broca’s area
in frontal lobe, connected to Wernicke’s via neural pathways
functions of cerebral cortex
- cognition, movement (precentral gyrus of frontal lobe)
- sensation (postcentral gyrus of parietal lobe)
functions of hippocampus
memory and learning
functions of hippocampus
memory and learning
responsible for emotion, appetite, responds to pain and stressors
amygdala
responsible for fine control of movement
Basal ganglia
acts as a relay station that directs information to various cortical structures
thalamus
primary neurohumoral organ
hypothalamus
part of brainstem responsible for autonomic integration
medulla
3 parts of cerebellum
- Archicerebellum
- Paleocerebellum
- Neocerebellum
part of cerebellum that maintains equilibrium
Archicerebellum
part of cerebellum that regulates muscle tone
Paleocerebellum
part of cerebellum that coordinates voluntary muscle movement
Neocerebellum
function of CN 3
oculomotor
eye movement, pupil constriction
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)
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)
branches of facial n.
temporal
zygomatic
buccal
mandibular
cervical
Two Zebras Bit My Carrot
functions of facial nerve
- facial movement (except mastication)
- eyelid closing
- taste to anterior 2/3 tongue
sensory function of CN 9
somatic sensation to posterior 1/3 tongue
CN responsible for swallowing
vagus
CN responsible for 70% of all PNS activity
CN 10
all CN are part of peripheral nervous system except:
CN 2
only CN surrounded by dura
CN 2
optic n.
what is Tic douloreaux
trigeminal neuralgia
generates excruciating neuropathic facial pain
s/s injury to facial n.
bell’s palsy = unilateral facial paralysis
locations of CSF
- ventricles (L lateral, R lateral, 3rd, 4th)
- cisterns around brain
- subarachnoid space in brain and spinal cord
CSF volume
~150 mL
produces CSF
ependymal cells of choroid plexus in cerebral ventricles (30 mL/hr)
normal CSF pressure
5-15 mmHg
reabsorbs CSF
arachnoid villi in superior sagittal sinus
what is CSF absorption via arachnoid villi dependent on
pressure gradient between CSF and venous circulation
separates CSF from plasma
Blood brain barrier
causes BBB to become dysfunctional
sites of tumor, injury, infection, or ischemia
places BBB is not present
- CTZ
- posterior pituitary gland
- pineal gland
- choroid plexus
- parts of hypothalamus
how can some drugs that can’t pass BBB cause N/V?
absence of BBB at CTZ
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)
composition of CSF
- Isotonic with plasma, but not an ultrafiltrate of plasma
- Osmolarity = 295 mOsm/L
similarities & differences in composition of CSF vs. plasma
- Similarities: Na+ level, HCO3, PaCO2
- Differences: K+, pH, glucose, protein
most common type of hydrocephalus
Obstructive
cause of communicating hydrocephalus
decreased CSF absorption by arachnoid villi (ex. intracranial hemorrhage)
or overproduction of CSF (very rare)
what is cerebral autoregulation
brain’s ability to maintain a constant cerebral blood flow over a wide range of mean arterial blood pressures
cerebral blood flow =
cerebral perfusion pressure / cerebral vascular resistance
normal global CBF
45-55 mL/100g tissue/min
or 15% CO
normal cortical CBF
75-80 mL/100g tissue/min
normal subcortical CBF
20 mL/100g tissue/min
CBF assoc. with evidence of ischemia
CBF ~ 20 mL/100g tissue/min
CBF assoc. with complete cortical suppression
CBF ~ 15 mL/100g tissue/min
CBF assoc. with membrane failure & cell death
CBF < 15 mL/100g tissue/min
normal CMRO2
3.0 – 3.8 mL/O2/100g brain tissue/min
5 Determinants of Cerebral Blood Flow
- Cerebral metabolic rate for oxygen
- Cerebral perfusion pressure
- PaCO2
- PaO2
- Venous pressure
O2 utilization by the brain
60% for electrical activity
40% for cellular integrity
decreasing CMRO2
Hypothermia
Halogenated anesthetics
Propofol
Etomidate
Barbiturates
increasing CMRO2
Hyperthermia
Seizures
Ketamine
N2O
why do volatiles increase CBF but decrease CMRO2
Volatiles uncouple CBF from CRMRO2
improves outcomes after out-of-hospital V-fib and resuscitation
Mild hypothermia (32-34°C) for 12-24 hours
CPP =
MAP - ICP (or CVP, whicever is higher)
Brain autoregulates CBF between :
CPP of 50-150 mmHg or MAP 60-160 mmHg
Brain autoregulates CBF between :
CPP of 50-150 mmHg or MAP 60-160 mmHg
O2 utilization by the brain
60% for electrical activity
40% for cellular integrity
CMRO2 decrease with hypothermia
↓ by 7% for every 1°C decrease in temp
temp assoc with EEG suppression
18-20°C
negative effects assoc with temp > 42°C
- denatures protein
- destroys neurons
- ↓ CBF
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)
MAP to ensure CPP 50
MAP 55-65 mmHg if ICP is normal (5-15)
higher ICP requires higher MAP to maintain CPP
normal controls of cerebral autoregulation
- products of local metabolism
- myogenic mechanics
- autonomic innervation
3 things that decrease effectiveness of cerebral autoregulation
- brain tumor
- head trauma
- volatiles
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
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
at a PaCO2 of 40, global CBF is:
50 mL/100g brain tissue/min
For every 1 mmHg increase in PaCO2, CBF will increase by:
1-2 mL/100g brain tissue/min
For every 1 mmHg decrease in PaCO2, CBF will decrease by
1-2 mL/100g brain tissue/min
maximal vasodilation occurs at PaO2 of:
80-100 mmHg
Maximal vasoconstriction occurs at PaCO2 of:
~ 25 mmHg
how is cerebral vascular resistance controlled
The pH of the CSF & arterioles controls
how does respiratory acidosis affect CBF
increases CBF
↓ CSF pH (↑ PaCO2) = ↓ CVR = ↑ CBF
how does respiratory alkalosis affect CBF
decreases CBF
↑ CSF (↓ PaCO2) = ↑ CVR = ↓ CBF
how does metabolic acidosis affect CBF
doesn’t directly affect CBF (H+ in blood doesn’t pass BBB)
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
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
how can the Robinhood effect cause harm
from cerebral ischemia (not enough CBF) and shifting oxyhgb dissociation curve to the left
how does PaO2 < 50-60 affect CBF
causes cerebral vasodilation, increases CBF
when PaO2 > _ , CBF is unaffected
60
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
cerebral HTN
ICP > 20 mmHg
S/S intracranial HTN
- headache
- N/V
- papilledema
- pupil dilation and non-reactivity to light
- focal neurological deficit
- seizure
- coma
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
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
brain causes of increased CBV
- cerebral swelling
- tumor
blood causes of increased CBV
- increased CBF
- bleeding
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
Cushing’s triad
HTN, bradycardia, irregular respirations
what causes irregular respirations with inc ICP
Compression of medulla
most common site of herniation
temporal uncus
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
what is Pseudotumor Cerebri
idiopathic intracranial HTN
condition where ICP increases for no apparent reason (“false tumor”)
what is papilledema
swelling of optic n./
2 methods to decrease CBV
- decrease CBF
- increase venous outflow
2 methods to decrease CSF
- CSF drainage
- drugs
2 methods to decrease cerebellar mass
- tumor debulking
- diuretics
2 methods to decrease cerebral edema
- diuretics
- corticosteroids
how does hyperventilation decrease CBF
Mild hyperventilation (30-35) constricts vessels = ↑ CVR = ↓ CBF= ↓ ICP
PaO2 < ____ increases risk of cerebral ischemia
30
how long do the decreased CBF effects of mild hyperventilation last
6-20 hours
(pH of CSF equilibrates with PaCO2)
how long do the decreased CBF effects of mild hyperventilation last
6-20 hours
(pH of CSF equilibrates with PaCO2)
PaO2 < ____ greatly increases CBF and ICP
50-60
drugs to avoid when trying to decrease CBF
vasodilators - NTG, Nipride
positioning that facilitates venous drainage from brain
Head elevation > 30 °
positioning that can increase ICP
- Neck flexion or extension (can compress jugular veins)
- Trendelenburg
how can PEEP affect ICP
PEEP = ↑ intrathoracic pressure = ↓ venous drainage from brain (can ↑ ICP)
when is CSF drainage the most useful treatment of increased ICP
obstruction to CSF flow (hydrocephalus)
drugs that decrease CSF production
Acetazolamide & furosemide
where does arterial bleeding in the brain most commonly occur
subarachnoid space
(between arachnoid and pia mater)
where does venous bleeding in the brain usually occur
subdural space
between dura and arachnoid mater
what forms myelin sheath in PNS
Schwann cells
3 meningeal layers covering brain and spinal cord
- dura mater
- arachnoid mater
- pia mater
3 meningeal layers covering brain and spinal cord
- dura mater
- arachnoid mater
- pia mater
glial cells that increase neuronal conduction velocity
oligodendrocytes
CN most likely to be compressed by pituitary tumor
CN 2
where is CSF produced
choroid plexus
fixed/dilated pupil suggests herniation of:
temporal uncus
main blood supply to brain’s posterior circulation
basilar artery (only 1)
gives rise to paired posterior communicating arteries
basilar artery
gives rise to paired vertebral arteries
subclavian arteries
gives rise to paired middle cerebral arteries
internal carotids
anticonvulsant that is excreted unchanged by kidneys
gabapentin
methods to decrease cerebral mass with increased ICP
tumor debulking
evacuation of hematoma
mannitol
how do loop diuretics decrease cerebral edema
inducing diuresis and increasing rate of CSF production
how do osmotic diuretics reduce cerebral edema
by increasing serum osmolarity and “pulling” water across BBB
0.25-1 g/kg mannitol
dose of mannitol to decrease cerebral edema
0.25-1 g/kg
how does 3% NaCl affect cerebral edema
high tonicity decreases cerebral edema by “pulling” water across BBB
downside of using mannitol for decreasing cerebral edema
transiently increases blood volume
can increase ICP and stress failing heart
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
methods to decrease CBV
- propofol
- hyperventilation
- maintain neck neutrality
- HOB elevated
methods to derease CSF
VP shunt
acetelazomide
interventricular drain
decreased cerebral mass/edema
corticosteroids
debulking
mannitol
what med should be used to support CPP with increased ICP
phenylephrine
why should dextrose solutions be avoidd
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
supplies anterior circulation to the brain
internal carotids
where do internal carotids enter skull
foramen lacerum
anterior cerebral circulation flow
Aorta - carotid - internal carotid - circle of Willis - cerebral hemispheres
what supplies posterior cerebral circulation
vertebral arteries
main supply of posterior cerebral circulation
basilar artery (only 1)
posterior cerebral circulation flow
aorta - subclavian a. - vertebral a. - basilar a - posterior fossa structures and cervical spinal cord
primary function of circle of Willis
provide redundancy of blood flow in the brain
how does venous blood from cerebral cortex & cerebellum drain
via superior sagittal sinus & dural sinuses
how does venous blood from basal brain structures drain
via inferior sagittal sinus, the vein of Galen, and straight sinuses
where do venous cerebral pathways converge
confluence of sinuses
how does venous blood exit the brain
all exits via paired jugular veins
Most common type of CVA
ischemic
most likely cause of ischemic CVA
cardio-embolic event like A-fib
A person who exhibits a sudden change in neurologic function or progressive change in neuro status is most likely experiencing a ?
CVA
what is a TIA
focal neuro deficit that spontaneously resolves within 24 hours
warning sign of cerebrovascular disease, impending stroke
what is a TIA
focal neuro deficit that spontaneously resolves within 24 hours
warning sign of cerebrovascular disease, impending stroke
ischemic stroke risk factors
- HTN (most important)
- smoking
- DM
- HLD
- excessive ETOH
- ↑ homocysteine level
treatment for stroke symptoms after hemorrhage ruled out
- 1st line: aspirin
- IV thrombolytic within 4.5 hours of stmprom onset
when should patients undergo embolectomy
pts with large vessel occlusion should undergo within 6 hours
target BP after ischemic CVA
under 185/110
purpose of fluid replacement with CVA
supports BP, CO, CPP, & improves CBF by ↓ viscosity
why is blood sugar control important in CVA pts
during cerebral hypoxia, glucose is converted to lactic acid
cerebral acidosis destroys brain tisue
most common cause of subarachnoid bleeding
aneurysm rupture
most from circle of Willis
most common cause of subarachnoid bleeding
aneurysm rupture
most from circle of Willis
transmural pressure =
MAP - ICP
Most common sign of SAH
intense headache often described as “worst headache of my life”
Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time
Most common sign of SAH
intense headache often described as “worst headache of my life”
Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time
Most common sign of SAH
intense headache often described as “worst headache of my life”
Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time
what causes meningismus in hemorrhagic stroke patients
blood spreads and irritates meninges
Morbidity of hemorrhagic stroke results from:
- obstructive hydrocephalus
- rebleeding
- vasospasm
surgical options for hemorrhagic stroke
aneurysm clipping or endovascular coiling
general intraop SBP goal in aneurysm clipping or endovascular coiling
120-150 mmHg
when should surgical repair of hemorrhagic stroke take place
24-48 hours following initial bleed
Intervention at this time makes triple H therapy safer
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
why is controlled hypotension not needed when clamp is used for hemorrhagic stroke
↓ transmural pressure and risk of rupture & eliminates need
High/normal BP required to perfuse collateral circulation
why is controlled hypotension not needed when clamp is used for hemorrhagic stroke
↓ transmural pressure and risk of rupture & eliminates need
High/normal BP required to perfuse collateral circulation
why is controlled hypotension not needed when clamp is used for hemorrhagic stroke
↓ transmural pressure and risk of rupture & eliminates need
High/normal BP required to perfuse collateral circulation
Most significant drawback of controlled hypotension for cerebral aneurysm clipping
decreased CPP
major cause of M&M in pts who have suffered SAH
Cerebral vasospasm
what causes cerebral vasospasm after SAH
delayed contraction of cerebral arteries
Positive correlation between amount of blood on CT & incidence of spasm
when is cerebral vasospasm most likely to occur with SAH
4-9 days after bleed
methods to monitor for cerebral vasospasm after SAH
Frequent neuro checks and daily transcranial Dopplers
Most common presentation of cerebral vasospasm
new neuro deficit, AMS
Gold standard for cerebral vasospasm diagnosis
cerebral angiography
BP goal for cerebral vasospasm treatment
increase MAP 20-30 mmHg above baseline
Triple H Therapy
- hypervolemia
- HTN
- hemodilution to Hct 27-32%
only CCB to ↓ M&M from vasospasm
nimodipine
↑ collateral blood flow
only CCB to ↓ M&M from vasospasm
nimodipine
↑ collateral blood flow
treatment of medically-refractory cerebral vasospasm
- intra-arterial vasodilators (verapamil, nicardipine), papaverine, milrinone
- balloon angioplasty
most common cause of hyponatremia with SAH
Cerebral Salt Wasting Syndrome
not SIADH
most common cause of hyponatremia with SAH
Cerebral Salt Wasting Syndrome
not SIADH
treatment for Cerebral Salt Wasting Syndrome
isotonic crystalloids
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
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
GCS: verbal Response
1 = no verbal response
2 = incomprehensible sounds
3 = inappropriate words
4 = confused
5 = oriented
GCS: eye opening
1 = no eye opening
2 = eye opening to pain/pressure
3 = eye opening to sound
4 = opens spontaneously
GCS: pupil reactivity
-2 = both NR to light
-1 = one NR to light
0 =PERRL
how can warfarin be reversed
- FFP
- prothrombin complex concentrate
- recombinant factor 7a
how can Clopidogrel/aspirin be reversed
- platelet transfusion
- recombinant factor 7a
CPP goal for TBI
> 70
fluids to avoid in TBI
- dextrose fluids
- hypotonic solutions
- albumin
inhaled anesthetic to avoid with TBI
N2O
sz activity localized to particular cortical region
Partial seizure
Generalized seizure
activity affects both hemispheres
Jacksonian march
partial seizure progresses to generalized seizure
phases of grand mal sz
Tonic phase = whole body rigidity
Clonic phase = repetitive jerking motions
types of seizures assoc with respiratory arrest
grand mal
status epilepticus
Acute treatment of grand mal sz
propofol, diazepam, thiopental
Surgical treatment of grand mal sz
vagal nerve stim, foci resection
sz linked to particular cortical region
focal cortical
usually no LOC
sz linked to particular cortical region
focal cortical
usually no LOC
sz with temporary loss of awareness (remains awake)
Absence (Petit Mal)
sz assoc. with temporary loss of consciousness & postural tone
Akinetic
Status Epilepticus
Seizure activity > 30 min or 2 grand mal seizures without regaining consciousness in between
treatment of Status Epilepticus
phenobarbital, thiopental, phenytoin, benzos, propofol, GA
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
how do inhaled anesthetics affect EEG activity
tend to ↓ EEG activity (dose-dependent) but all have been implicated in producing seizures (very rare)
S/S seizures under GA
↑ HR, HTN, ↑ EtCO2
IV anesthetic that can induce sz
ketamine
EEG effects. of etomidate
commonly causes myoclonus - not assoc. with ↑ EEG activity in pts without epilepsy
meds useful for cortical mapping in pts with sz disorders (increase EEG activity)
- methohexital
- etomidate
- alfentanil
first-line agent for control of sz activity
propofol
anticonvulsants assoc with NDNMB resistance
- phenytoin
- Carbamazepine
anticonvulsant that undergoes zero order kinetics
Phenytoin
SEs of phenytoin
- dysrhythmias/hypotension (if IV rate > 50 mcg/min)
- gingival hyperplasia
- aplastic anemia, cerebellar-vestibular dysfunction (nystagmus, ataxia)
- SJS
- birth defects
anticonvulsant assoc with purple glove syndrome
phenytoin
anticonvulsant that slows phenytoin metabolism
valproic acid
SEs of Valproic Acid
- hepatotoxicity
- thrombocytopenia
- displaces phenytoin from plasma proteins
SEs of Valproic Acid
- hepatotoxicity
- thrombocytopenia
- displaces phenytoin from plasma proteins
MOA of carbamazepine, phenytoin, and valproic acid
block voltage-gated Na+ channels
membrane stabilizer
anticonvulsant useful for trigeminal neuralgia
Carbamazepine
SEs of Carbamazepine
- aplastic anemia
- thrombocytopenia
- liver dysfunction
- leukopenia
- hyponatremia (ADH-like effect)
MOA of gabapentin
inhibition of alpha-2 delta subunit of voltage-gated Ca2+ channels in CNS
decreased excitatory NT release
Chemical analogue of GABA, NOT GABA agonist
SEs of gabapentinoids
dizziness, somnolence
why should gabapentin be tapered off
Abrupt withdrawal can produce sz if patient has hx sz
taper for at least 1 week
why should gabapentin be tapered off
Abrupt withdrawal can produce sz if patient has hx sz
taper for at least 1 week
why should gabapentin be tapered off
Abrupt withdrawal can produce sz if patient has hx sz
taper for at least 1 week
most common cause of dementia in pts > 65
Alzheimer’s Disease
key findings in alzheimers
beta amyloid rich plaques & neurofibrillary tangles in the brain
consequences of amyloid plaque formation in Alzheimers
- dysfunctional synaptic transmission (most noticeable with ACh)
- apoptosis
class of drugs used to treat Alzheimer’s & AIs of use
cholinesterase inhibitors
increase duration of succs (questionable significance)
patho of Parkinson’s
dopaminergic neurons in basal ganglia destroyed
decreased dopamine + normal ACh = relative ACh increase
what is suppressed vs overactive in parkinsons
corticospinal motor system suppressed
extrapyramidal motor system overactive
what drugs increase extrapyramidal s/s in pt with parkinsons
dopamine antagonists
* Reglan
* haldol
* droperidol
* promethazine
most common cause of POVL
ION
patho of ION
optic nerve ischemia
likely r/t venous congestion
procedural risk factors for ION
- prone
- wilson frame
- long duration
- large blood loss
- low ratio colloid:crystalloid
- hypotension
pt risk factors for ION
- male
- obese
- DM
- HTN
- smoking
- old age
- atherosclerosis
