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Adv. Health Assessment (Spring 2024) > Spring 2024 (Exam III) Neurological Diseases > Flashcards

Spring 2024 (Exam III) Neurological Diseases Flashcards

1
Q

Cerebral Blood flow is modulated by?

A

Cerebral metabolic rate
CPP (MAP-ICP)
Aterial blood CO2
Aterial blood O2
Various drugs and intracranial pathologies

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2
Q

With autoregulation CBF is approx (blank) brain tissue per minute.

Which is _____ ml/min

this is how much of CO?

A

50 mL/ 100g
750 mls/ min
15%

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3
Q

The vault is enclosed by the?

A

dura mater and bone

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4
Q

Brain tissue, intracranial CSF and Intracranial blood have a combined volume of?
what is the normal ICP at this volume?

A

1200 - 1500 mls
5-15 mmHg

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5
Q

Monro-Kellie hypothesis:

A

any increase in one component of intracranial volume must be offset by a decrease in another component to prevent an elevated ICP

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6
Q

This diagram describes what?

A

monroe-kellie hypothesis

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7
Q

the incracranial vault is considered what?

A

compartmentalized

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8
Q

this is reflection of the dura that seperates the 2 cerebral hemispheres?

A

falx cerebri

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9
Q

a reflection of dura that lies rostral to the cerebellum and marks the border btw the supratentorial and infratentorial spaces

A

tentorium cerebelli

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10
Q

______ = Herniation of hemispheric contents under _____ ; typically, compressing branches of the anterior cerebral artery , creating a _____

A

Subflacine Herniation
falx cerebri
midline shift

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11
Q

Transtentorial Herniation is herniation of the supratentorial contents past what?

A

tentorium cerebelli

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12
Q

Transtentorial herniation causes?

A

causes brainstem compression in the rostral to caudal direction

This leads to
- AMS
- defects in gaze and ocular reflexes
- hemodynamic
- respiratory compromise
- death

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13
Q

Uncas is located where?

A

medial portion of temporal lobe

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14
Q

a subtype of transtentorial herniation, where the uncus herniates over the tentorium cerebelli

A

uncal herniation

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15
Q

what are the S&S of uncal herniation

A
  • Ipsilateral oculomotor nerve dysfunction
  • pupillary dilatation
  • ptosis
  • lateral deviation of the affected eye
  • brainstem compression
  • death
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16
Q

can occur due to elevated infratentorial pressure, causing the cerebellar structures to herniate through the foramen magnum

A

herniation of the cerebellar tonsils

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17
Q

S&S of cerebellar tonsils herniation

A

medullary dysfunction, cardiorespiratory instability and subsequently death

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18
Q

label the numbers

A
  1. Subfalcine → midline shift
  2. Transtentorial -> pushing down caudally
  3. Cerebellar contents through foramen magnum -> towards the medulla
  4. Traumatic event → cause herniation out of cranial cavity
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19
Q

Tumors can increase ICP in 3 ways

A

1) directly d/t size
2) indirectly by causing edema in surrounding brain tissue
3) by obstructing CSF flow (like with tumors involving the 3rd ventricle)

Intracranial hematomas cause increased ICP similar to mass lesions

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20
Q

Blood in the CSF, as is seen in subarachnoid hemorrhage, may lead to?

A

obstruction of CSF reabsorption, and granulations can further exacerbate increased ICP

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21
Q

Infections s/a meningitis or encephalitis can lead to?

A

edema or obstruction of CSF reabsorption

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22
Q

how does Hyperosmotic drugs decrease ICP?

A

increase osmolarity, drawing fluid across BBB

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23
Q

how do corticosteroids decrease ICP?

A

decrease swelling and enhance the integrity of the BBB

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24
Q

how does cerebral vasoconstricting anesthetics like propofol decrease ICP?

A

decrease CMRO2 and CBF

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25
Q

this is a progressive, autoimmune demyelination of central nerve fibers?
onset?
characterized?

A

multiple sclerosis (MS)
- onset is 20-40
- characterized by periods of exacerbations and remissions

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26
Q

Risk factors for MS

A

Rx factors: Female, 1st deg relative w/ MS, EBV (epstein barr virus), other AI disorders, smoking

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27
Q

what triggers MS?

A

Triggers: stress, elevated temps, postpartum period

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28
Q

S&S of MS

A

progressive motor weakness
sensory disorders
visual impairment
autonomic instability.
Sx vary b/o site of demyelination

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29
Q

is there a cure for MS?

A

No, managed with corticosteroids, immune modulators and targeted antibodies

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30
Q

For MS if respiratory compromise, consider?

A

Pulmonary function test

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31
Q

LFT’s are drawn on MS only if?
what are some considerations with steroid use?

A

LFT if on Dantrolene & Azathioprine (bone marrow suppression, liver function impairment)

Close attn to glucose and electrolytes as steroids may impact levels

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32
Q

Considerations for patients with MS on long term steroids are?

A

Consider giving pre-op steroids in anyone with long-term steroid use

LT steroids cause adrenal suppression, so a stress-dose of steroids may be necessary for surgery

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33
Q

what are some anesthetic considerations for patients with MS?

A

Any increase in body temp can precipitate an exacerbation of MS sx

general and regional anesthesia, PNB’s are acceptable options
Avoid Succinylcholine as it may induce hyperkalemia
(Upregulated N-ach receptors)

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34
Q

Autoimmune; Antibodies generated against N-Ach-R’s at skeletal motor endplate

A

myasthenia Gravis (MG)

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35
Q

MG effects what kind of muslce?

A

Effects skeletal muscle, not smooth or cardiac muscle

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36
Q

Muscle weakness is worsened by what in MG?
S&S are exacerbated by what?

A

Muscle weakness, exacerbated w/exercise

Sx exacerbated by: pain, insomnia, infection, surgery

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37
Q

Cranial symptoms associated with MG

A

Ocular sx common-diplopia, ptosis
Bulbar involvement → laryngeal/pharyngeal weakness→ respiratory insufficiency, aspiration rx

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38
Q

This is common in 10% of MG cases

A

Thymic hyperplasia
(90% pts improve after thymectomy)

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39
Q

what is the treatment for MG?

A

Tx: Ach-E inhibitors (Pyridostigmine), immunosuppressive agents, steroids, plasmapheresis, IVIG

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40
Q

Preanesthetic Considerations with MG are?

A

Reduce paralytic dosage to avoid prolonged muscle weakness

If respiratory compromise -> do pulmonary function tests

Optimize respiratory function

Consider pre-op steroids in anyone with long-term steroid use

Counsel patients on the increased risk of needing post-op resp support/ventilation until fully recovered from anesthesia

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41
Q

Why are opioids used with caution in MG?

A

avoid resp compromise

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42
Q

In MG, Ach -E inhibitors may prolong what?

A

Succ’s and Ester LA’s

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43
Q

Labs for MG include?

A

Labs: CBC, BMP, +/-LFT (LFT if on Azathioprine)
Close attn to glucose and electrolytes as steroids may impact levels

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44
Q

Disorder causing the development of autoantibodies against VG Calcium Channels

A

Eaton Lambert Syndrome

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45
Q

what is the specific MOA of the Eaton Lambert Syndrome?

A

Reduce Ca++ influx into the presynaptic Ca++ channels→↓Ach release @ the NMJ

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46
Q

S&S of Eaton Lambert Syndrome

A

Sx similar to MG
Sx: progressive limb-girdle weakness, dysautonomia, oculobulbar palsy
>60% cases assoc w/ small cell lung carcinoma

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47
Q

Treatment for Eaton Lambert syndrome invovles what?

A

Selective K+ chnl blocker “3-4 diaminopyridine”
Ach-E inhibitors
immunologics (Azathioprine)
steroids
plasmapheresis
IVIG

48
Q

This represents what?

A

Lambert-Eaton syndrome

49
Q

Pre-anesthetic Considerations for Eaton Lambert Syndrome

A

Assess existing deficits
If respiratory compromise, consider pulmonary function tests

50
Q

Eaton Lambert Syndrome is very sensative to what?

A

VERY sensitive to ND-NMB & D-NMB
more sensitive to ND-NMB than MG patients

Extreme caution with paralytic and opioid dosing

Counsel on risks for needing post-op resp support until fully recovered from anesthesia

51
Q

Describe Muscular Dystrophy (MD)

A

Hereditary disorder of muscle fiber degeneration c/b breakdown of the dystrophin-glycoprotein complex
leads to myonecrosis, fibrosis, and skeletal muscle mbrn permeability.

52
Q

how many types of MD

A

6

53
Q

Most common and severe form of MD

A

Duchenne MD
occurs only in boys
onset is 2-5 yrs
wheel chair bound by 8-10 years
avg lifespan is 20-25 years d/t cardiopulmonary complications

54
Q

S&S of MD

A

progressive muscle wasting without motor/sensory abnormalities
kyphoscoliosis
long bone fragility
respiratory weakness
frequent pneumonia
EKG changes

55
Q

what labs specifically are elevated in MD?

A

Elevated serum creatine kinase c/b muscle wasting

56
Q

Preanesthetic considerations for MD

A

CBC, BMP, PFTs, consider CK

Pre-op EKG, echocardiogram. Evaluate for cardiomyopathy

Caution with ND-NMB’s, careful monitoring throughout

57
Q

Can happen when succs and volatiles are given with MD?

A

Hypermetabolic Syndrome

Avoid Succs & VA as they exacerbate instability of muscle membrane

Hypermetabolic Syndrome Can lead to: rhabdomyolysis, hyperkalemia, Vfib, cardiac arrest

58
Q

Alternative anesthetic for MD

A

Consider low dose rocuronium and TIVA for GA

Have MH cart with Dantrolene available

RA preferred over GA to avoid triggers and cardiopulmonary complications

59
Q

what are the myotonic dystrophies mentioned in class?

A

myotonic dystrophy
myotonia congenita
central core disease

60
Q

prolonged contraction after muscle stimulation
seen in several muscle disorders

A

myotonia

61
Q

most common myotonia. Onset 20-30’s

A

Myotonic Dystrophy

62
Q

Myotonic Dystrophy s/s

A

muscle wasting in face, masseter, hand, pre-tibial muscles
may also affect pharyngeal, laryngeal, diaphragmatic muscles
cardiac conduction may be affected; 20% have MVP

63
Q

Myotonia Congenita: s/s

A

Milder form, involving theskeletal muscles
smooth & cardiac muscles are spared

64
Q

describe Central Core disease

A

Rare. Core muscle cells lack mitochondrial enzymes
Sx:Proximal muscle weakness & scoliosis

65
Q

Myotonias are triggered by_____
Tx?

A

Myotonias are triggered by stress & cold temps
Tx: No cure. Sx managed w/Quinine, Procainamide, Steroids

66
Q

pre-anesthetic considerations for mytonic dystrophies

A
  • GI hypomotility-↑aspiration risk
  • High rx of endocrine abnormalities.
  • Keep patients warm to avoid flare-ups
  • Avoid Succinylcholine b/c fasciculations trigger myotonia
  • Pts are increased risk for post-op resp weakness
67
Q

3 Major Dementia Syndromes:

A

Alzheimer’s (70%),
Vascular dementia (25%),
Parkinsons (5%)

68
Q

Degeneration of dopaminergic fibers of basal ganglia

A

Parkinsons disease

69
Q

_______ regulates (inhibits excess stimulation) the extrapyramidal motor system, which is stimulated by____

A

Dopamine regulates (inhibits excess stimulation) the extrapyramidal motor system, which is stimulated by Ach

70
Q

Triad of sx in parkinsons

tx:

A

Triad of sx: skeletal muscle tremor, rigidity, akinesia (inability to voluntarily move one’s muscles and limbs)

: Levodopa (crosses BBB), anticholinergics, MAOIs (inhibit dopamine degradation), Deep brain stimulator

71
Q

avoid which drugs with parkinsons as pre-anesthetic considerations

A

Avoid Reglan, Phenothiazines, Butyrophenones
Avoid Demerol if on MAOI

72
Q

_____ must be continued to avoid unstable extreme extrapyramidal effects s/a chest wall rigidity

_______may need to be disabled to avoid interaction w/cautery

A

PO Levodopa must be continued to avoid unstable extreme extrapyramidal effects s/a chest wall rigidity

DBS may need to be disabled to avoid interaction w/cautery

73
Q

Primary tumors. Least aggressive astrocytomas

Often found in young adults w/new onset seizures

A

gliomas

74
Q

Children & young adults
Mostly benign, good outcomes if resectable

A

pilocytic astrocytoma

75
Q

Poorly differentiated
Usually evolve into Glioblastoma Multiforme

A

anaplastic astrocytomas

76
Q

Carry a high mortality
Usually requires surgical debulking & chemo
Life expectance is usually within weeks, even w/treatment

A

Glioblastoma Multiforme

77
Q

Usually benign. Arise from dura or arachnoid tissue​
Good prognosis w/surgical resection

A

meningiomas

78
Q

Noncancerous, varying subtypes
Transsphenoidalor open craniotomy for removal is usually curative

A

Pituitary Adenomas

79
Q

occlusion of ACA

A

contralateral leg weakness

80
Q

occlusion of MCA

A

contralateral hemiparesis and hemisensory deficit (face and arm more than leg)

aphasia

contralateral visual field defect

81
Q

occlusion of PCA

A

contralateral visual field defect
contralateral hemiparesis

82
Q

occlusion of penetrating arteries

A

contralateral hemiparesis
contralateral hemisensory deficits

83
Q

basilar artery occlusion

A

oculomotor deficits and/or ataxia w/ crossed sensory and motor deficits

84
Q

vertebral artery occlusion

A

lower cranial nerve deficits and/or ataxia w/ crossed sensory deficits

85
Q

Hemorrhagic stroke is 4x more likely to cause death than

A

ischemic

86
Q

The 2 most reliable predictors of outcome are:

A

Estimated blood volume & Change in LOC

87
Q

Bloodwithin the brainis called

A

An intraparenchymal hemorrhage

88
Q

Blood in the epidural, subdural, or subarachnoid spaces are referred to as

A

Blood in the epidural, subdural, or subarachnoid spaces are referred to as epidural hematoma, subdural hematoma, and subarachnoid hemorrhages, respectively

89
Q

Blood located in the ventricular system

A

Blood located in the ventricular system is an intraventricular hemorrhage, and usually occurs in conjunction with other types of hemorrhagic stroke

90
Q

New anticoagulant for thrombus=

A

New anticoagulant for thrombus=No elective cases within 3 months

91
Q

High rx pts for CVA that pause LA anticoags (Warfarin) will need ____ to bridge the gap

If RA planned, ____for sufficient time to safely perform block

A

High rx pts for CVA that pause LA anticoags (Warfarin) will need SA anticoags (LMWH, IV unfractionated heparin) to bridge the gap

If RA planned, d/c anticoagulants for sufficient time to safely perform block

92
Q

s/s of cerebral aneurysms
r/x?
dx?

A

Headache, photophobia, confusion, hemiparesis, coma

Rx: HTN, smoking, female, oral contraceptives, cocaine use

Dx: CT/angio, MRI, Lumbar puncture w/CSF analysis if rupture suspected

93
Q

Intervention should be performed within ___rupture for best outcomes

A

72 hr

94
Q

Risk for vasospasm post SAH

A

Risk for vasospasm 3-15 days post SAH

95
Q

Triple H therapy for post SAH vasospasms

A

Triple H therapy (Hypertension, Hypervolemia, Hemodilution)

96
Q

moa of post SAH vasospasms

A

Freehgbtriggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1, leading to vasoconstriction

97
Q

To avoid complications of hypervolemia, _____

A

To avoid complications of hypervolemia, HTN is the initial main treatment, and then do volemia

98
Q

2 grading scales for aneurysms

A

Hunt and Hess

GCS

99
Q

Arterial to venous connection w/o intervening capillaries
Creates an area of high flow, low resistance shunting
Believed to be congenital

A

AVM

100
Q

s/s, dx, tx of AVM

A

Sx: range from mass-effects to hemorrhage
Majority are supratentorial
Dx: Angiogram, MRI
Tx: radiation, angio-guided embolization, surgical resection (higher mortality)

101
Q

Type 1 chiari malformation

A

Type 1: downwarddisplacement ofcerebellum

102
Q

Type 2 chiari malformation

A

Arnold Chiari):downwarddisplacementofcerebellar vermis, often assoc w/myelomeningocele

103
Q

Type 3 chiari malformation

A

Rare; occipital encephalocele w/downward cerebellar displacement

104
Q

Type 4 chiari malformation

A

cerebellar hypoplasia w/o displacement of posterior fossa contents
*Not compatible with life

105
Q

chiari malformation s/s, tx

A

Sx: headache, extending to shoulders/arms,visual disturbances, ataxia

Tx: Surgical decompression

106
Q

AKA “Bourneville Disease”

Autosomal dominant disease causing benign hemartomas, angiofibromas,
and other malformations that can occur anywhere in the body’

Lesions of the brain include: cortical tumors & giant-cell astrocytomas

A

Tuberous sclerosis

107
Q

Tuberous sclerosis

Often involves co-existing tumors of ____

Presentation likely includes ___

A

Often involves co-existing tumors of face,oropharnyx, heart, lungs, liver &kidneys

Presentation likely includes mental retardation and seizure disorders

108
Q

Autosomal dominant

Benign tumors of the CNS, eyes, adrenals, pancreas and kidneys

May present w/ pheochromocytoma

A

Von Hippel-Lindau Disease

109
Q

TBI

A

Categorized: “penetrating” or “non-penetrating,” d/o breech of dura
Severity categorized by Glasco-Coma Scale
Primary injury: occurs at time of insult
Secondary injuries: neuroinflammation, cerebral edema,
hypoxia, anemia, electrolyte imbalances, and neurogenic shock
Intubation required in severe TBI (GCS <9, AW trauma, resp distress)
Mild hyperventilation to control ICP
CT of head/neck ASAP

110
Q

Neurofibromatosis

A

Autosomal dominant

3 types:
Type 1 (most common)
Type 2
Schwannomatosis (rare)

Numerous disease presentations
Anesthesia considerations account for increased ICP, airway issues, scoliosis, possibility of pheochromocytoma

Avoid NA d/t high likelihood of spinal tumors

111
Q

hydrocephalus tx:

A
  • mainly consists of diuretics (furosemide & acetazolamide decrease CSF production) although this remains controversial in children
  • Serial lumbar punctures have also been tried but only as a temporizing measure
  • The majority of cases require surgical treatment
  • VP shunt: drain placed in ventricle of the brain andempties into peritoneum
  • ETV: catheter placed into the lateral ventricle that drains into the peritoneal space, right atrium, or more rarely the pleural space
  • Shunt malfunction occurs most frequently in the first year of placement (high failure rate)
112
Q

: transient, paroxysmal, synchronous discharge of neurons in the brain
Can be c/b transient abnormalities: hypoglycemia, hyponatremia, hyperthermia, intoxication
In these cases, treating the underlying cause is curative
Epilepsy: recurrent seizures d/t congenital or acquired factors
Antiepileptic drugs decrease neuronal excitability/enhance inhibition

A

seizure disorders

113
Q

disorder of CSF accumulation, causing increased ICP, that results in ventricular dilatation

A

hydrocephalus

114
Q

can vary widely in origin &symptoms​
Outcomes are generally less favorable

A

Metastatic Carcinomas:

115
Q

Usually benign schwannomas involving the vestibular component of CN VIII within the auditory canal

Good prognosis w/resection +/- radiation

A

Acoustic Neuromas:

116
Q

Astrocytoma tumor types:

A

Gliomas
pilocytic astrocytomas
anaplastic astrocytomas
glioblastoma multiforme

Adv. Health Assessment (Spring 2024) (25 decks)

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