Pathophys - Test Iii - Cranial Nerves And Sns, Psns

Front 1

cranial nerve I

Back 1

olfactory

Front 2

cranial nerve II

Back 2

optic

Front 3

cranial nerve III

Back 3

Oculomotor

Front 4

cranial nerve IV

Back 4

Trochlear

Front 5

cranial nerve V

Back 5

Trigeminal

Front 6

cranial nerve VI

Back 6

Abducens

Front 7

cranial nerve VII

Back 7

Facial

Front 8

cranial nerve VIII

Back 8

vestibulocochlear

Front 9

cranial nerve IX

Back 9

glossopharyngeal

Front 10

cranial nerve X

Back 10

Vagus

Front 11

cranial nerve XI

Back 11

spinal accessory

Front 12

cranial nerve XII

Back 12

hypoglossal

Front 13

pneumonic for cranial nerves

Back 13

Ooo, to touch and feel a girls vagina, so hot!

Front 14

anatomy of cranial nerves on page 14 of cranial nerve pack

Back 14

anatomy of cranial nerves on page 14

Front 15

pg 29 of cranial nerve pack has good table of comparison between nervous systems

Back 15

pg 29 of cranial nerve pack has good table of comparison between nervous systems

Front 16

parasympathetic nervous systems effect on mental activity

Back 16

no innervation

Front 17

parasympathetic nervous systems effect on blood vessels

Back 17

little effect

Front 18

parasympathetic nervous systems effect on uterus

Back 18

dependent stage of cycle

Front 19

parasympathetic nervous systems effect on endocrine/pancreas

Back 19

stimulates insulin secretion

Front 20

parasympathetic nervous systems effect on cardiac muscle

Back 20

decreases HR, small decrease in contractility through muscarinic receptors

Front 21

parasympathetic nervous systems effect on coronary blood vessels

Back 21

constricts

Front 22

parasympathetic nervous systems effect on bladder and urethra

Back 22

contracts bladder smooth muscle, relaxes urethral sphincter

Front 23

parasympathetic nervous systems effect on lungs

Back 23

contracts bronchiole smooth muscle

Front 24

parasympathetic nervous systems effect on digestive organs

Back 24

increases peristalsis and enzyme/mucus secretion

Front 25

parasympathetic nervous systems effect on liver

Back 25

no innervation

Front 26

parasympathetic nervous systems effect on kidney

Back 26

no innervation

Front 27

parasympathetic nervous systems effect on penis

Back 27

vasodilates penile arteries - erection

Front 28

parasympathetic nervous systems effect on vagina, clitoris

Back 28

vasodilation and erection

Front 29

parasympathetic nervous systems effect on blood coagulation

Back 29

no effect

Front 30

parasympathetic nervous systems effect on cellular metabolism

Back 30

no effect

Front 31

parasympathetic nervous systems effect on adipose tissue

Back 31

no effect

Front 32

sympathetic nervous systems effect on mental activity

Back 32

increases alertness

Front 33

sympathetic nervous systems effect on blood vessels

Back 33

constricts most blood vessels and increases BP (alpha 1 receptors)
but dilates blood vessels serving skeletal muscles fibers (beta 2 receptors)

Front 34

sympathetic nervous systems effect on uterus

Back 34

depends on the stage of the cycle

Front 35

sympathetic nervous systems effect on endocrine/pancreas

Back 35

inhibits insulin secretion

Front 36

sympathetic nervous systems effect on cardiac muscle

Back 36

increases HR and inotrope (beta 1 receptors in atria)

Front 37

sympathetic nervous systems effect on coronary blood vessels

Back 37

dilates

Front 38

sympathetic nervous systems effect on bladder and urethra

Back 38

relaxes bladder smooth muscle and contracts urethral sphincter

Front 39

sympathetic nervous systems effect on lungs

Back 39

dilates bronchioles (beta 2 receptors)

Front 40

sympathetic nervous systems effect on digestive organs

Back 40

decreases glandular and muscular activity

Front 41

sympathetic nervous systems effect on liver

Back 41

no innervation (indirectly affected)

Front 42

sympathetic nervous systems effect on kidney

Back 42

releases enzyme renin which increases BP

Front 43

sympathetic nervous systems effect on penis

Back 43

smooth muscle contraction and ejaculation (P to point, S to shoot)

Front 44

sympathetic nervous systems effect on vagina, clitoris

Back 44

vaginal reverse peristalsis

Front 45

sympathetic nervous systems effect on blood coagulation

Back 45

increases coagulation rate

Front 46

sympathetic nervous systems effect on cellular metabolism

Back 46

increases metabolic rate

Front 47

sympathetic nervous systems effect on adipose tissue

Back 47

stimulates fat breakdown

Front 48

Huntington's Chorea is caused by a destruction or dysfunction of

Back 48

the caudate nucleus of the basal ganglia

Front 49

Huntington's Chorea is caused by not enough

Back 49

acetylcholine and GABA

Front 50

Huntington's Chorea is caused by too much

Back 50

dopamine

Front 51

Dopamine is moderated by

Back 51

GABA which inhibits dopamine's effects

Front 52

Huntington's Chorea presents in what age group

Back 52

30 - 40's

Front 53

Huntington's Chorea gene is

Back 53

autosomal dominant

Front 54

GABA inhibits what function

Back 54

consciousness

Front 55

Huntington's Chorea is characterized by

Back 55

mood swings, dementia, jerky uncontrolled random movements pharyngeal muscle control is lost
death in 15 to 20 years after diagnosis

Front 56

Huntington's Chorea mood swings exhibit

Back 56

violent tendencies, rage, egocentric behavior, compulsive disorders like gambling, hypersexuality, alcoholism

Front 57

how would you intubate someone with Huntington's Chorea

Back 57

rapid sequence due to loss of pharyngeal muscle tone

Front 58

good drug to use for patient with Huntington's Chorea

Back 58

haldol

Front 59

drugs people with Huntington's Chorea are sensitive to

Back 59

drugs that require cholinesterase to break them down (succs, NDMRs) - so will have longer effect

Front 60

sedate people with Huntington's Chorea with

Back 60

butryphenone or phenothiazines

Front 61

dystonia is

Back 61

a category of conditions in which sustained muscle contractions cause twisting and repetitive movements and abnormal postures for a variety of causes - typically deficiencies in GABA

Front 62

GABA stands for

Back 62

gamma amino butyric acid

Front 63

intense contractions of the neck and facial muscles is known as

Back 63

spasmodic torticollis

Front 64

treatment for extrapyramidal side effects like toricollis from antidopaminergic drugs is

Back 64

benadryl

Front 65

considerations for patients with sapsmodic torticollis

Back 65

awake fiberoptic intubation due to distorted anatomy
positioning issues
sometimes get dystonic drug reactions - so give benadryl
NDMRs will relax the muscles

Front 66

how much benadryl do you give for spasmodic torticollis reaction

Back 66

25 - 50 mg IV

Front 67

treatment for spasmodic torticollis other than benadryl

Back 67

rhizotomy at C1 - C3

Front 68

Hallervorden-Spatz disease is genetic

Back 68

autosomal recessive (rare)

Front 69

Hallervorden-Spatz disease is a disorder of

Back 69

the basal ganglia

Front 70

Hallervorden-Spatz disease onsets at what age

Back 70

late childhood

Front 71

Hallervorden-Spatz disease progresses to death after how many years

Back 71

10

Front 72

people with Hallervorden-Spatz disease will present as

Back 72

some muscle wasting but also some body builder muscles

Front 73

Hallervorden-Spatz disease characteristics

Back 73

dementia, dystonia, torticollis, scoliosis,

Front 74

anesthetic concerns for Hallervorden-Spatz disease

Back 74

positioning is challenging due to contractures and bone deformities and intubation is difficult because of poor positioning

Front 75

what worsens Hallervorden-Spatz disease

Back 75

noxious stimuli

Front 76

what drug may you want to avoid with Hallervorden-Spatz disease

Back 76

succs because of so many wasted muscle groups may have upregulation of receptors leading to hyperkalemia

Front 77

Alzheimer's disease is caused by

Back 77

a neurodegeneration of the grey matter

Front 78

Alzheimer's disease risk increases with

Back 78

age

Front 79

Alzheimer's disease typically affects patients over

Back 79

70

Front 80

Alzheimer's disease accounts for how much of the dementia in the US

Back 80

40 - 80%

Front 81

symptoms of Alzheimer's disease

Back 81

progressive impairment of memory, judgement, decision making and emotional lability

Front 82

treatments for Alzheimer's disease

Back 82

slow the disease progression but can not cure it or fix it indefinitely

Front 83

anesthetic challenges in patients with Alzheimer's disease

Back 83

consent issues
uncooperative behaviors
central acting drugs can produce prolonged effects in Alzheimer's disease

Front 84

patients with Alzheimer's disease should consent to surgery if

Back 84

they demonstrate a cognitive understanding of the procedure and its implications - allow them to have as much involvement as possible - they often feel very frustrated with forgetting

Front 85

uncooperative patients with Alzheimer's disease limit

Back 85

use of regional techniques

Front 86

side effect of anesthetic drugs on patients with Alzheimer's disease

Back 86

prolonged and unpredictable effects
often have post op confusion and delirium - may be associated with anticholinergics that cross the BBB (atropine, scopolamine)

Front 87

if you need to use an anticholinergic in a patient with Alzheimer's disease try

Back 87

robinul (glycopyrrolate) because it does not cross the BBB

Front 88

good antisaligog drugs

Back 88

robinul, scopolamine

Front 89

multiple sclerosis is caused by

Back 89

reversible demyelination at random sites in the brain and spinal cord but chronic inflammation and scarring eventually produces permanent effects

Front 90

multiple sclerosis is possible initiated by

Back 90

a viral infection triggering an autoimmune reaction

Front 91

age group of primary affect of multiple sclerosis

Back 91

20 - 40 years of age

Front 92

people more likely to get multiple sclerosis

Back 92

women

Front 93

multiple sclerosis is characterized by

Back 93

periods of attacks and remissions with the remissions becoming less and less frequent
symptoms completely depend on what group of neurons are being affected (sensory, motor, visual)

Front 94

multiple sclerosis symptoms are exacerbated by

Back 94

increased temperature

Front 95

why does increased temperature exacerbate multiple sclerosis

Back 95

increased temperature decreases transmission and conduction across demyelinated neurons - as little as 0.5 degree increase can cause complete block in conduction

Front 96

anesthetic concerns for patients with multiple sclerosis

Back 96

do not overheat with bair hugger
anesthesia and surgery may worsen patients conditions triggering attacks that can last for weeks
unpredictable effects of drugs
spinals will exacerbate but epidurals and regional blocks will not
avoid succs
labile cardiovascular system

Front 97

poliomyelitis is caused by

Back 97

enterovirus that initially infects the reticuloendothelial system - it enters the CNS and targets motor neurons in the brainstem and anterior horn of the spinal cord

Front 98

incidence of poliomyelitis is still high in

Back 98

india, pakistan, and nigeria

Front 99

post polio sequelae include

Back 99

fatigue, skeletal muscle weakness, joint pain, cold intolerance, dysphagia, sleep and breathing problems, RAS affected

Front 100

anesthetic concerns for patients with post polio sequelae

Back 100

very sensitive to sedative meds and anesthetics
delayed wakening
sensitivity to NDMRs
profound shivering post op
increased post op pain
probably should not be outpatient

Front 101

post polio sequelae leaves patients sensitive to

Back 101

cold and pain

Front 102

why are people with post polio sequelae sensitive to pain

Back 102

the poliovirus damaged endogenous opiod secreting cells in the brain and spinal cord

Front 103

explain what happens to the neurons (picture on pg 20) in post polio sequelae

Back 103

polio virus destroys innervation to some parts of some muscle, body tries to regenerate it but it is not as strong and will burn out with overwork and eventually loses entire nerve innervation of that muscle

Front 104

Amyotrophic Lateral Sclerosis affects only

Back 104

motor neurons

Front 105

describe course of Amyotrophic Lateral Sclerosis

Back 105

rapidly progressive disease that affects one side of body first but eventually affects entire body with respiratory muscle eventually being paralyzed, leading to death

Front 106

anesthetic considerations for a patient with Amyotrophic Lateral Sclerosis

Back 106

may be very difficult to wean, let patient know they may need to be intubated for a while post op, may not be wise to do spinal because of risk of confusion between disease and nerve injury
avoid succs, awake extubation, sensitive to NDMRs

Front 107

Guillain Barre syndrome is

Back 107

a common immune reaction against the myelin following a viral or GI infection

Front 108

Guillain Barre syndrome is associated with

Back 108

HIV and neoplastic diseases

Front 109

some people with Guillain Barre syndrome respond to

Back 109

plasmaphoresis

Front 110

Guillain Barre syndrome is characterized by

Back 110

progressive rise in loss of motor function and autonomic instability

Front 111

what % of patient die with Guillain Barre syndrome

Back 111

10% die of complications from Guillain Barre syndrome

Front 112

autonomic dysfunction is

Back 112

a set of symptoms that may be included in many other disease processes or conditions

Front 113

autonomic dysfunction can be related to

Back 113

congenital abnormalities, acquired, familial

Front 114

autonomic dysfunction symptoms depend on

Back 114

what nerves are involved

Front 115

most common concern for us associated with autonomic dysfunction

Back 115

hypo or hypertension

Front 116

anesthetic considerations for patient with autonomic dysfunction

Back 116

patients may be on several different types of drugs
hypo or hyper tension
use direct acting drugs to treat bp
very sensitive to vasopressors
blood loss is poorly tolerated

Front 117

what patients may develop autonomic dysfunction

Back 117

diabetics

Front 118

Shy-Drager Syndrome is

Back 118

a degenerative disease with progressive loss of neuronal cells causing autonomic dysfunction and widespread degeneration of the CNS

Front 119

Shy-Drager Syndrome is a loss of what neurotransmitter

Back 119

norepi depletion form peripheral nerve endings

Front 120

outcomes for people with Shy-Drager Syndrome

Back 120

death usually occurs within 8 years of diagnosis because of cerebral ischemia due to prolonged hypotension

Front 121

symptoms related to autonomic dysfunction of Shy-Drager Syndrome are

Back 121

orthostatic hypotension b/c vascular system won't tighten b/c baroreceptor response is inhibited
urinary retention
diminished pupillary reflex
decreased or lack of sweating
sexual dysfunction
abnormal breathing control
baroreceptor failure

Front 122

treatment for Shy-Drager Syndrome

Back 122

slow postural changes
TEDs
increased sodium diet
alpha agonist or alpha 2 antagonist
levodopa

Front 123

examples of alpha 2 antagonists

Back 123

catapres, presinex

Front 124

alpha 2 antagonists inhibit

Back 124

release of norepi? or block of receptor, or not - unsure - see slide 26 and we'll figure it out

Front 125

why do you give levodopa to people with Shy-Drager Syndrome

Back 125

levodopa is converted to dopamine which can produce vasoconstriction

Front 126

anesthetic considerations for patient with Shy-Drager Syndrome

Back 126

pt lacks ability to compensate for anesthetic induced hypotension, may need phenylephrine gtt b/c direct acting, art line monitoring, SWAN maybe, BIS b/c patient will seem more out of it than they are, blocks are controversal, treat bradycardia with atropine, thick about negative inotrope effects of gases

Front 127

most spinal cord injuries are

Back 127

traumatic and end in partial or complete transection of the cord due to fractures or dislocation of the vertebrae

Front 128

thoracic spine mechanism for spinal cord injury is

Back 128

compression or over flexion

Front 129

cervical spine mechanism of spinal cord injury is usually

Back 129

over extension

Front 130

clinical manifestations of spinal cord injury are

Back 130

dependent on level of spinal cord injury

Front 131

a spinal cord injury above what level will require vent support

Back 131

C3 - C5 because affects diaphragm

Front 132

spinal cord injury above what level will result in quadraplegia

Back 132

T1

Front 133

spinal cord injury above what level results in paraplegia

Back 133

L4

Front 134

the most common levels for spinal cord injury are

Back 134

C5-6 and T12-L1

Front 135

spinal shock occurs for how long after spinal cord injury

Back 135

1 - 3 weeks after which time reflexes begin to return (spinal hyperreflexia)

Front 136

what affects the amount of time of spinal shock

Back 136

level of break, lower the break, less of the sympathetic chain is affected

Front 137

anesthetic concerns for acute spinal cord injury

Back 137

prevent further damage
airway should be maintained with in-line cervical spine stabilization
awake fiberoptic intubations
high dose methylprednisone (30 mg/kg over 1 hour; drip of 5.4 mg/kg/hr x 23 hours),
hypotension and bradycardia, ketamine or etomidate for induction drugs to not drop HR, succs can be used for 1st 24 hours only

Front 138

how can you differentiate between spinal shock and hemorrhagic shock

Back 138

if it is spinal shock - pt will be bradycardic
hemorrhagic shock pt will be tachycardic

Front 139

treat spinal shock with

Back 139

fluids and vasopressors (may need gtt)

Front 140

treat hemorrhagic shock with

Back 140

fluids and blood

Front 141

seizures are defined as

Back 141

transient and synchronous discharges of groups of neurons in the brain

Front 142

what % of the population has had at least 1 seizure

Back 142

10 %

Front 143

common causes of seizures

Back 143

hypoglycemia, hyponatremia, drug toxicity, hypoxia, fever, increased intracranial pressure, unknown etiology

Front 144

treatment drugs for seizures

Back 144

have nasty side effects so many pts might not take the meds
most try to use only 1 drug to control seizures

Front 145

side effects of seizure medications

Back 145

sedation, depression, ataxia, diplopia, hepatic failure, aplastic anemia, hyponatremia, and many more

Front 146

what do we ask ourselves and our patients with seizures

Back 146

do our drugs stimulate or lower seizure threshhold
blood levels of drugs (dilantin)
recent seizures?
are the seizures controlled?
do we sedate them?

Front 147

good drugs for people with seizures

Back 147

versed, propofol, pentothal

Front 148

watch for other effect of seizure meds and anesthesia

Back 148

over sedation since many of patients home meds may cause sedation

Front 149

bad drugs for patients with seizures

Back 149

ketamine and etomidate - lower seizure threshold