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Critical Care I > Misc for test 1 > Flashcards

Misc for test 1 Flashcards

1
Q

what is the key manifestation of spinal muscular atrophy

A

progressive degeneration of anterior horn cells

genetic disease

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2
Q

what is the infantile form of spinal muscular atrophy (SMA)

A

SMA type 1 (Werdnig -Hoffmann disease)

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3
Q

what is the late infantile and more slowly progressive form of spinal muscular atrophy (SMA)

A

SMA type 2 (Kugelberg-Welander syndrome)

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4
Q

what is the more chronic, juvenile form of spinal muscular atrophy (SMA)

A

SMA type 3

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5
Q

what type of disease is spinal muscular atrophy (SMA)

A

genetic

one of the most frequent autosomal recessive diseases

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6
Q

with spinal muscular atrophy (SMA), the earlier it presents the _____ the progression

A

more severe

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7
Q

what are fasciculations

A

quivering muscle movements that typically best seen on the lateral aspect of the tongue

seen easiest when child is asleep

talked about in the Spinal muscular atrophy (SMA) section

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8
Q

prognosis of SMA type 1

A

most infants with this genetic disease die within the first 2 years

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9
Q

Prognosis of SMA type 2

A

may survive to adulthood

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10
Q

Prognosis of SMA type 3

A

can initially appear normal with slower progression of weakness and a normal life expectancy

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11
Q

clinical manifestations of SMA type 1

A

severe hypotonia

generalized weakness

facial involvement

fasciculations

absent deep tendon reflexes

normal cognitive, social and language skills and sensation

with disease progression -> breathing becomes rapid, shallow, and predominantly abdominal

resp compromise leads to atelectasis, pulmonary infection and death

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12
Q

labs and diagnostic studies for spinal muscular atrophy (SMA)

A

genetic testing

creatine phosphokinase (CK) may be normal or mildly elevated

Electromyelogram (EMG) shows fasciculations, fibrillations and other signs of denervation

muscle biopsy specimens show grouped atrophy

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13
Q

treatment for Spinal muscular atrophy (SMA)

A

no specific treatment delays progression

nusinersen (antisense oligonucleotide) is being studied

symptomatic therapy is directed toward minimizing contractures, preventing scoliosis, optimizing nutrition, avoiding infections

manage resp infections aggressively - pulmonary hygiene, oxygen and abx

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14
Q

in SMA (spinal muscular atrophy) what gene is missing

A

SMN1 gene and do not produce a protein necessary for the survival of the motor cells

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15
Q

what drug has recently been approved for SMA and how does it work

A

Nusinersen - injected intrathecally and modifies mRNA from a nearly identical gene (SMN2) to increase SMN protein production.

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16
Q

an acute post-infectious demyelinating disorder of the spinal cord

A

transverse myelitis

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17
Q

how to treat transverse myelitis

A

high dose steroids

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18
Q

symptoms of an epidural abscess

A

fever
spinal pain
neurological deficits

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19
Q

lesions of the spinal cord are best seen in what imaging

A

MRI

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20
Q

flaccid, areflexic paralysis

think…

A

acute spinal cord lesions

may mimic lower motor neuron disease

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21
Q

timeline for transverse myelitis symptom progression

A

1-21 days

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22
Q

on spinal fluid - WBC normal; no OCB

neuro paralysis like symptoms

A

not inflammatory causes

Think 
infarct
dural AVF
spondylosis
tumor
check B12 level
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23
Q

On spinal fluid - increased WBC, +/- OCBs

neuro paralysis like symptoms

A

think inflammatory causes

MS
NMOSD (neuromyelitis optica spectrum disorder)
MOGAD (myelin oligodendrocyte glycoprotein antibody disorders)
infectious
sarcoid

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24
Q

on spinal fluid - markedly increased CSF protein, normal cell count

neuro paralysis like symptoms

A

Think

Spinal block (tumor/spondylosis)

Guillain - Barre

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25
Q

on spinal fluid - decreased glucose

neuro paralysis like symptoms

A

think meningomyelitis

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26
Q

what can transverse myelitis cause

A

aggressive damage to the spinal cord without warning leading to varying degrees of weakness, paralysis, loss of sensation and bladder dysfunction

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27
Q

causes of transverse myelitis

A

usually postinfectious or idiopathic

secondary transverse myelitis is caused by other autoimmune diseases (ie multiple sclerosis), infection, paraneoplastic disorders

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28
Q

clinical features of transverse myelitis

A

motor: rapidly progressing weakness of the legs (+ arms if cervical cord affected), initially flaccid
sensory: pain, dysesthesia, and paresthesia below the level of the lesion
autonomic: urinary urgency or retention, constipation, bladder or bowel incontinence

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29
Q

diagnosis for transverse myelitis

A

MRI total spine with and without contrast
-will also r/o compressive myelopathy

Lumbar Puncture
-cell count and diff, protein, glucose, VDRL, oligoclonal bands, IgG index, and cytology (looking for cancer)

-Normal CSF, or elevated CSF lymphocytosis (<100) or elevated protein level

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30
Q

what deficiencies can cause symptoms similar to transverse myelitis

A

Vit B12
Vit E
serum copper
Ceruloplasm

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31
Q

what infections can cause a similar picture to transverse myelitis

A

HIV
enterovirus
Syphilis

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32
Q

what autoimmune disease can cause transverse myelitis

A

MS

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33
Q

what disorder triggered by cancer can attack the cells in the nervous system - transverse myelitis

A

Paraneoplastic syndromes - abnormal immune system response to a neoplasm.

T cells mistakenly attack normal cells in the nervous system

(you can look at Anti-Hu and anti-CRMP5 labs)

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34
Q

a group of genetic muscle diseases characterized by progressive myofiber degeneration and the gradual replacement of muscle by fibrotic tissue

A

muscular dystrophies

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35
Q

what is the most common muscular dystrophy and one of the most common genetic disorders of childhood

A

duchenne muscular dystrophy

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36
Q

what gene for duchenne muscular dystrophy

A

X-linked disorder (Xp21) that arises from a mutation in the dystrophin gene

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37
Q

autosomal recessive disorder of the anterior horn cells in the brainstem and spinal cord

A

Spinal muscle atrophy (SMA)

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38
Q

Degenerative disease characterized by progressive denervation of the muscle, leading to progressive hypotonia and muscle weakness.

A

Spinal muscle atrophy (SMA)

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39
Q

what gender are more commonly affected in spinal muscle atrophy (SMA)

A

Males

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40
Q

SMA type one presents by what age in most cases

A

6 mos

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41
Q

Floppy infant. Unable to achieve milestones of rolling or sitting independently. Weakness is greater in proximal muscle groups vs. distal and lower extremities are more severely affected. Infants have poor head control. Demonstrate a weak cry or cough and have difficulty with feeding, swallowing, or handling oral secretions due to bulbar dysfunction. Paradoxical breathing due to intercostal muscle weakness with sparing of the diaphragm. Often have characteristic bell-shaped trunk and abdominal protrusion. When supine, assume the frog-legged position Areflexia, fine tremor (most notably in the hands), tongue fasciculations, facial weakness, and normal sensation are reported.

A

clinical manifestations of SMA type 1

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42
Q

normal development for the first 6 mos

may sit independently and demonstrate head control but never able to stand or walk independently

fine motor tremor of hands

tongue fasciculations

diaphragmatic breathing

difficulty swallowing

prone to scoliosis and contractures

A

SMA type 2

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43
Q

weakness is greater in proximal muscle groups vs distal

lower extremities more severely affected than the upper

pt typically achieve ability to walk independently but many are wheelchair bound by the 4th decade of life

A

SMA type 3

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44
Q

what does EMG show in SMA

A

acute denervation due to malfunction of motor neurons

motor and sensory conduction velocities are normal

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45
Q

serum CK in SMA vs Muscular dystrophy

A

CK in SMA may be normal or slightly elevated

Muscular dystrophy CK is classically elevated

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46
Q

what teams would be involved in an SMA pt

A 
neurology
pulmonology
orthopedics
physical and occupational therapy
genetic counseling
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47
Q

labs in SMA

A

chemistry studies - can provide info on metabolic disease, electrolyte imbalances, liver and kidney functions and drug levels

if they are on antiepileptic meds - watch liver and kidney functions

lactate - may identify resulting acidosis after prolonged seizures or in presence of septic shock in meningitis

ammonia - determine presence of metabolic disease with seizures

CBC with diff - infectious process or looking for anemia while managing increased ICP

newborn screening test - inborn errors of metabolism

infectious disease titers or levels

Looking for lyme, herpes, rubella, EBV, toxoplasmosis and other viral orgins

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48
Q

what are the anti-epileptic drugs that require drug level monitoring

A

Fosphenytoin

Phenobarbital

valproic acid

carbamazepine

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49
Q

when would you need to check levels for anti-epileptic drugs

A

initiation of drug to establish therapeutic level or range

breakthrough seizures in a previously stable pt

monitor adherence to meds

measure changes in levels with addition of second med with known interactions

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50
Q

when should you draw trough levels for antiepilepic meds

A

30 min prior to dose administration

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51
Q

goal level for phenytonin

A

total (protein and non protein bound phenytoin)

10 - 20 ug/ml

free (non protein bound)
1-2.5 ug/mL

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52
Q

calculation for correction of phenytoin level with low albumin

A

Fosphenytoin is protein bound

corrected level = measured phenytoin level/ {(albumin x 0.1) + 0.1}

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53
Q

goal level for phenobarbital

A

15-40 ug/ml

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54
Q

goal level for valproic acid

A

50-100 ug/Ml

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55
Q

goal level for carbamazepine

A

4-12 ug/mL

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56
Q

when would you order a EEG

A

evaluation of events suspected to be seizures

seizure localization

assessment of subclinical seizures

evaluation of altered LOC

Adjunct diagnostic test in the determination of brain death

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57
Q

contraindications to EEG

A

scalp infection

scalp skin breakdown

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58
Q

Hz for brain waves

A

1-3 Hz - Delta
4-7 HZ - Theta
8-12 Hz - Alpha
13-20 Hz - Beta

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59
Q

Brain wave Frequency ____ from birth to adulthood

A

increases

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60
Q

EEG - single or repetitive spikes that can be focal, multifocal or generalized

A

Epileptiform waves

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61
Q

Brain or head CT images are used in the clinical evaluation of

A

Bony abnormalities

hydrocephalus

ICH

Cerebral edema

Space occupying lesions

intracranial calcifications

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62
Q

Brain MRI is used in the clinical evaluation of

A

Ischemia or infarct

Degenerative diseases

Congenital anomalies

Arteriovenous malformations

Lesions in the posterior fossa and spinal cord

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63
Q

type of MRI that uses pulses of radio wave energy to provide images of blood vessels inside the body

A

MRA

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64
Q

MRA images are useful in the clinical evaluation of

A

reduced blood flow

aneurysm

arteriovenous malformations

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65
Q

Uses xenon-133, a radioactive dye which is injected prior to scan

A

cerebral perfusion scan

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66
Q

which imaging is more sensitive in detecting blood which makes it ideal for trauma eval

A

CT scan

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67
Q

what is the advantage of MRI

A

does not use ionizing radiation - eliminates exposure risk

higher level or gray/white differentiation

provides higher resolution detail at skull base and orbits

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68
Q

disadvantage of CT

A

radiation exposure

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69
Q

disadvantages of MRI

A

pt with metallic devices are unable to enter

longer imaging time, usually sedation required

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70
Q

cerebral perfusion scan may be considered in the clinical evaluation of

A

brain death

acute stroke

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71
Q

what does a lumbar puncture evaluate

A

can be therapeutic also

CNS infection
malignancy
autoimmune disease
inflammatory process

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72
Q

when is LP indicated

A

suspected infectious, immunologic or inflammatory process involving CNS

measure opening pressure

administration of intrathecal meds (anesthesia or chemo)

Therapeutic CSF removal to relieve increased ICP due to pseudotumor cerebri

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73
Q

contraindications for LP

A

increased ICP

platelet dysfunction

bleeding disorder

resp or hemodynamic instability

skin infection near site of entry

spinal cord trauma or compression

posterior spinal cord fusion in lumbar region

focal neuro deficit

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74
Q

Potential complications of LP

A

bleeding

infection

back pain

headache

CSF leak

Epidural or subdural spinal hematoma

Herniation (rare)

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75
Q

lab studies for LP

A

White and red blood cell counts

culture

gram stain and sensitivities

PCR and certain titers

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76
Q

what should you get prior to an LP on any pt with suspected increased ICP or suspected space occupying lesion

A

Head CT

negative CT does not completely exclude possibility of increased ICP

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77
Q

preferred device for monitoring ICP and can also be used for draining CSF

A

Ventriculostomy

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78
Q

for a ventriculostomy what is it connected to for monitoring

A

an external pressure transducer and monitor

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79
Q

what does a waveform indicate during ventriculostomy monitoring

A

resp variations and pulse pressure as well as ICP

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80
Q

Goals of ICP monitoring (ventriculostomy)

ICP and CPP numbers

A

Maintain ICP <20 -25 mmHg in older children

<15-20 in children <1 yr

Maintain CPP by maintaining adequate MAP; goal CPP >60mmHg in adolescents, >50mmHg in children and >40 mmHg in infants

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81
Q

factors to avoid that aggravate or precipitate elevated ICP

A

agitation
pain
obstruction of venous return (keep head in neutral position)
rep insufficiency such as airway obstruction, hypoxia or hypercapnia

fever
HTN
hyponatremia
anemia
seizures
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82
Q

what is anisocoria

A

unequal size of eyes pupils

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83
Q

what is the most appropriate imaging for a 3 week old to look for brain hemorrhage - unstable pt

A

Ultrasound is the most appropriate imaging modality for an unstable neonate with an open fontanel

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84
Q

6 yr old with no med history comes to ED with generalized tonic clonic seizures. what is the initial management

A

give lorazepam (ativan) to control seizure activity

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85
Q

what can you do for a intubated child to help decrease the blood flow to the brain which decreases blood volume in the cranial vault -> lowers the ICP

A

mild hyperventilation (PaCO2 32-35mmHg)

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86
Q

what diagnostic imaging is the most important technique to show an exact depiction of the AVM, its feeder vessels, nidus and draining veins

A

cerebral angiography

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87
Q

in a symptomatic, unstable pt, what diagnostic study is best to identify the presence of an AVM

A

CT - immediate viewing of the general location and will show if there is hemorrhage and edema

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88
Q

infant with a progressive, neuromuscular disease which typically presents with poor feeding, weakness, constipation, weak cry and other neurologic symptoms

A

infant botulism

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89
Q

what practice is most important to minimize infection rate in a child with a ventriculoperitoneal (VP) shunt in place

A

antibiotic prophylaxis with individually tailored specifications following a shunt placement

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90
Q

what is the most common cause of shunt failure in pediatrics

A

obstruction

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91
Q

how is a bacterial infection in CSF identified

A

Elevated WBC count (>1,000)

Elevated protein (>100mg/dL)

decreased glucose (<60% of serum glucose)

Normal WBC (0-5 cells/UL)
Normal protein (15-60 mg/dL)
Normal glucose (50-80mg/dL)
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92
Q

Disseminated encephalomyelitis often occurs following what?

A

a viral illness

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93
Q

clinical presentation for acute disseminated encephalomyelitis

A 
behavioral changes
AMS
fatigue
fever
headache
nausea
vomiting
seizures
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94
Q

Asymmetric smile on exam post ischemic stroke located in pons. What CN is affected

A

Facial nerve (CN VII)

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95
Q

what can happen if you perform an LP on a pt with increased ICP

A

can result in transtentorial herniation or herniation of the cerebellar tonsils

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96
Q

gold standard study for a child suspected of arteriovenous malformation

A

Cerebral angiography

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97
Q

at what age do most boys become symptomatic for for Duchenne muscular dystrophy, what is their clinical presentation at this age

A

2-3 years old

develop an awkward gait and inability to run properly

some may have antecedent history of mild delay in attaining motor milestones or of poor head control during infancy

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98
Q

Gower sign

A

Duchenne muscular dystrophy sign

The child arises from a lying position on the floor by using his arms to climb up his legs and body (pushing off of thighs)

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99
Q

exam finding of
firm calf hypertrophy
mild to moderate proximal leg weakness with a hyperlordotic, waddling gait

A

Duchenne muscular dystrophy

other manifestations - cardiomyopathy, scoliosis, resp decline, cognitive and behavioral dysfunction

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100
Q

in Duchenne muscular dystrophy arm weakness is evident by what age

A

6 years old

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101
Q

Duchenne muscular dystrophy most boys are wheelchair dependent by what age

A

12 years old

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102
Q

Prognosis of Duchenne muscular dystrophy

A

many live into adulthood

most die in their 20s or early 30s usually as a result of progressive resp decline or cardiac dysfunction

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103
Q

labs for Duchenne muscular dystrophy

A

serum CK - always markedly elevated (10,000-50,000 international units)

Aldolase is elevated

diagnosis - genetic testing (looking for dystrophin gene mutation)

muscle biopsy shows muscle fiber degeneration and regeneration accompanied by increased interfascicular connective tissue

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104
Q

treatment for Duchenne muscular dystrophy

A

chronic oral steroid therapy to slow pace of disease, delay motor disability and improve longevity (prednisone)

Supportive care - physical therapy, bracing, proper wheelchairs, treatment for cardiac dysfunction or pulmonary infections

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105
Q

what does the gene for dystrophin do

A

connects the contractile protein actin to the cell membrane

Duchenne muscular dystrophy

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106
Q

females and Duchenne muscular dystrophy

A

usually are asymptomatic carriers or exhibit only mild symptoms - there are rare cases of severely affected females

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107
Q

muscular dystrophies commonly present with what (gait)

A

gait disturbance due to a hip girdle weakness

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108
Q

what are some things a caregiver might report for Duchenne muscular dystrophy (early signs)

A

a child who is mildly late to learn to walk (13-18 mths)

moves more slowly than other toddlers

displays toe walking

rolling gait or waddle

large calves (pseudohypertrophy)

Gower sign (pushing off thigh when arising from the ground

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109
Q

weakness in Duchenne muscular dystrophy is progressive and starts with _____ muscles and those of the ___ and ____ ____

A

volunteer muscles

hips and pelvic girdle

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110
Q

pattern of progressive weakness in Duchenne muscular dystrophy

A

proximal leg involvement -> loss of ambulation -> arms and hands -> spinal support -> resp function

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111
Q

for Duchenne muscular dystrophy with exon 51 skipping what treatment options

A

weekly IV infusions of eteplirsen

results in small amount of dystrophin which slows progression of disease

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112
Q

Duchenne muscular dystrophy with stop codons (nonsense mutations) can be treated with

A

Ataluren - oral drug which also restores a small amount of dystrophin - results in slower weakness progression

this is only approved in European Union and still experimental in US

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113
Q

for Duchenne muscular dystrophy when should they see cardiology and obtain first echo

A

6-7 years

generally asymptomatic during first decade
may also get a cardiac MRI for greater detail

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114
Q

What cardiac problems are commonly seen developed in Duchenne muscular dystrophy

A

arrhythmias
cardiomyopathy from myocyte hypertrophy
atrophy
fibrosis

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115
Q

what cardiac meds may be considered with Duchenne muscular dystrophy

A

by age 10
ACE inhibitors or ARBS to reduce cardiac afterload and help with adding more years of normal ejection fraction before overt cardiac decline

Corticosteroids for similar and additive effect to ACE/ARB

B blockers, digoxin, furosemide and others may be required

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116
Q

As the child moves out of the plateau phase with Duchenne muscular dystrophy, what service should be consulted

A

pulmonology

progressive chest wall and paraspinal muscle weakness lead to impaired ventilator excursion, restrictive lung disease perhaps spine and chest deformities

ability to cough and clear secretions is impaired

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117
Q

common reasons for ED visits for a pt with Duchenne muscular dystrophy

A

resp insufficiency triggered by upper or lower resp infection

fractures secondary to osteopenia

Arrhythmias

heart failure

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118
Q

treating pain in a pt with Duchenne muscular dystrophy

A

be very careful in using narcotics due to resp depression in a child with a fragile ventilatory system

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119
Q

The incidence of _____ _____ is higher in those with Duchenne muscular dystrophy then with other muscle disorders

what anesthetic can cause this

A

malignant hyperthermia

succinylcholine

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120
Q

type of severe reaction that occurs in response to particular medications used during general anesthesia, among those who are susceptible

A

Malignant hyperthermia

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121
Q

symptoms of malignant hyperthermia

A 
high fever
muscle rigidity
rhabdomyolysis  
tachycardia
tachypnea
acidosis
increased Carbon dioxide production
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122
Q

drug to treat malignant hyperthermia

A

Dantrolene

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123
Q

dystrophin is present in what type of muscle

A

smooth

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124
Q

late complications for Duchenne muscular dystrophy

A

constipation
gastroesophageal reflex
gastroparesis

chewing becomes weak - gastrostomy feeding often required

Pressure ulcers

Low bone density (occurs with diseases of weakness and made worse by steroids)

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125
Q

what should be monitored for a pt with Duchenne muscular dystrophy related to bone density and what type of meds should be considered to help with this

A

monitor Calcium and vit D

Bisphosphonates

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126
Q

Xp21.2-p21.3 deletion

A

Duchenne muscular dystrophy

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127
Q

which muscular dystrophy is worse
Duchenne muscular dystrophy
or Beckers muscular Dystrophy

A

Duchenne muscular dystrophy

Duchenne is Devestating

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128
Q

Pogressive myofiber damage ->loss of dystrophin -> muscle necrosis

A

Duchenne muscular dystrophy

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129
Q

in Duchenne muscular dystrophy there is progressive ______ muscle weakness

A

proximal

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130
Q

how often should a Duchenne muscular dystrophy receive an echo

A

every 1-2 years

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131
Q

autoimmune condition where antibodies block the acetylcholine receptors (AChR) at the neuromuscular junction which decreases the number of effective receptors

A

Myasthenia Gravis

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132
Q

3 childhood varieties of Myasthenia Gravis

A

juvenile myasthenia gravis (late infancy and childhood)

Transient neonatal myasthenia

Congenital myasthenia

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133
Q

variable ptosis (drooping eye)
diplopia (double vision)
ophthalmoplegia (paralysis or weakness of the eye muscles)
facial weakness

are the presenting symptoms for what?

A

Juvenile Myasthenia

(Myasthenia Gravis)

dysphagia, poor head control and extremity weakness may occur

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134
Q

what distinguishes Myasthenia Gravis from other neuromuscular disorders with progressive worsening over the day or with repetitive activity

A

rapid fatigue of muscles

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135
Q

prognosis for Juvenile Myasthenia

A

for some it never progresses past eyes (ophthalmoplegia and ptosis - ocular myasthenia)

Others have a progressive and potentially life threatening illness that involves all musculature to include resp and wallowing

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136
Q

treatment for Juvenile Myasthenia

A

pyridostigmine (acetylcholinesterase inhibitor) and depending on severity - various forms of immunosuppression

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137
Q

what type of Myasthenia Gravis develops in the first hours to days after birth to almost all newborns whose mother has myasthenia gravis

A

Transient neonatal Myasthenia Gravis

they have maternal anti-AChR antibodies (they all have them but only 10-20% will become symptomatic)

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138
Q

signs of transient neonatal myasthenia gravis

A 
ptosis
ophthalmoplegia
weak facial movements
poor feeding
hypotonia
resp difficulty
variable extremity weakness
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139
Q

treatment for transient neonatal myasthenia gravis

A

cholinesterase inhibitors and supportive care for a few days to weeks until the weakness remits

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140
Q

Myasthenia Gravis that is due to gene mutations in the components of the neuromuscular junction

A

Congenital myasthenia gravis

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141
Q

typically present in infancy with hypotonia, ophthalmoparesis, facial diplegia and extremity weakness - can present throughout childhood.

A

Congenital myasthenia gravis

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142
Q

Prognosis for Congenital myasthenia gravis

A

lifelong disability
some might respond to pyridostigmine or other drugs that improve neuromuscular junction function

most children with MG will lead normal lives with treatment, with temporary or permanent remission

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143
Q

in autoimmune Myasthenia Gravis, the majority of individuals have antibodies to

A

AChR (Acetylcholine receptors)

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144
Q

for autoimmune Myasthenia Gravis, what med can be used for diagnostic verification?

A

administration of a cholinesterase inhibitor, edrophonium chloride can result in transient improvement in strength, particularly of ptosis, and can be used for diagnostic verification

(Tensilon test)
Edrophonium is a rapid onset (30-90 seconds) and short acting (5 min)

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145
Q

what is the bottom line problem in myasthenia gravis

A

production in of ACh is normal and the neural function is intact but there are not enough receptors on the muscle to allow for an adequate contraction

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146
Q

Myasthenic crisis is a rapid deterioration of neuromuscular and respiratory function and can occur due to

A

infection

stress

changes in medications (anticholinesterase inhibitors)

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147
Q

Diagnosis for myasthenia gravis

A

physical exam

pulmonary function tests

serological testing for AChR antibodies
EMG with repeated nerve stimulation (causing the pt to become weak)

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148
Q

Treatment for myasthenia gravis

A

mechanical ventilation

anticholinesterase meds (to inhibit breakdown of ACH) so it remains bound to the muscle and produces a sustained contraction (Pyridostigmine, neostigmine)

Immunosuppressants such as corticosteroids, azathioprine,
cyclophosphamide , cyclosporine, methotrexate, mycophenolate, and tacrolimus

IVIG

other therapies
plasmapheresis
y globulin
thymectomy (if have a thymoma, may relieve symptoms in some pt without thymoma)

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149
Q 
diaphoresis
emesis
fecal incontinence
urinary frequency
tearing
drooling
bronchorrhea
miosis
hypotension
bradycardia
weakness
tremors
paralysis
hypoventilation
dysrhythmias
A

Organophosphate poisoning (insecticide)

prevents metabolism of ACH -> leads to accumulation at muscarinic and nicotinic sites -> produces cholinergic toxicity

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150
Q

Organophosphate poisoning management

A

decontamination
supportive care
reversal of nicotinic and muscarinic effects

treat with atropine (competitive inhibitor of Ach) and pralidoxime which breaks up the organophasphate-Achase bond and restores normal Achase activity

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151
Q

chronic neuromuscular disease characterized by varying degrees of weakness and fatigability of the skeletal muscles

A

myasthenia gravis

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152
Q

myasthenia gravis that is AChR negative

A

Congenital myasthenia gravis (not autoimmune)

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153
Q

should you use immunosuppressants in congenital myasthenia gravis

A

no, it is not autoimmune so will not help

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154
Q

is pupillary response effected in ocular myasthenia gravis

A

no

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155
Q

acute inflammatory demyelinating polyradiculoneuropathy

A

Guillain-Barre Syndrome

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156
Q

post-infectious autoimmune peripheral neuropathy that can occur

A

Guillain-Barre Syndrome

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157
Q

How many days post infection does Guillain-Barre Syndrome usually present

(what type of infections)

A

about 10 days after a resp or gastrointestinal infection

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158
Q

what bacterial culprits are classic for Guillain-Barre Syndrome

A

Mycoplasma pneumonia
or
Camylobacter jejuni

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159
Q

what ages does Guillain-Barre Syndrome occur

A

all ages

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160
Q

most common cause of acute flaccid paralysis in children

A

Guillain-Barre Syndrome

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161
Q

characteristic symptoms of Guillain-Barre Syndrome

A

areflexia
flaccidity
symmetrical ascending weakness

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162
Q

areflexia
flaccidity
symmetrical ascending weakness

A

Guillain-Barre Syndrome

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163
Q

how fast does progression of Guillain-Barre Syndrome occur

A

can occur rapidly in hours or more indolently over weeks

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164
Q

typically symptoms for Guillain-Barre Syndrome start where and progress to where

A

numbness or paresthesia in hands and feet
then heavy, weak feeling in legs.

Weakness ascends to involve the arms, trunk and bulbar muscles (Tongue, pharynx, larynx)

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165
Q

deep tendon reflexes for Guillain-Barre Syndrome

A

absent even when strength is relatively preserved

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166
Q

what associated autonomic problems r/t Guillain-Barre Syndrome

A 
blood pressure changes
tachycardia
other arrhythmias
urinary retention or incontinence
stool retention
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167
Q

what key factors can help point you toward Guillain-Barre Syndrome when trying to distinguish from acute spinal cord syndrome

A

Preservation of bowel and bladder function

loss of arm reflexes

absence of a sensory level

lack of spinal tenderness

168
Q

CSF in Guillain-Barre Syndrome

A

sometimes normal early in the illness

classically shows
elevated protein levels without significant pleocytosis

169
Q

What will MRI show in Guillain-Barre Syndrome

A

MRI with gadolinium - enhancement of the spinal nerve roots

170
Q

Guillain-Barre Syndrome treated with

A

initially IVIG

plasma exchange and immunosuppressive drugs are alternatives with IVIG is unsuccessful or in rapidly progressing disease

171
Q

is Guillain-Barre Syndrome unilateral or symmetrical

A

symmetrical

172
Q

why does Guillain-Barre Syndrome occur

A

the pt has an infection such as Campylobacter jejuni or mycoplasma pneumoniae

These organisms contain protein moieties that are similar to proteins located on host myelin sheaths.

Antibodies produced to eradicate these organisms then recognize the hosts myelin and attack it like that foreign protein

173
Q

suggestive parameters for mechanical ventilation in pt with Guillain-Barre Syndrome

A

vital capacity less than 20mL/kg and a negative inspiratory force greater than -20 cm H2O

174
Q

max weakness in Guillain-Barre Syndrome usually occurs how long after onset of symptoms

A

1-2 weeks

175
Q

symptoms of Guillain-Barre Syndrome

A 
Areflexia
numbness
CN palsies
hypoventilation due to weak resp muscles
with or without altered LOC
With/without ataxia
autonomic instability can occur - fluctuations in BP, diaphoresis, vasoconstriction, pupil dilation and constriction, cardiac arrhythmias
176
Q

How does IVIG work for pt with Guillain-Barre Syndrome

A

IVIG may work via several mechanisms, including blocking macrophage receptors, inhibiting antibody production, inhibiting complement binding, and neutralizing pathologic antibodies.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 586). Wolters Kluwer Health. Kindle Edition.

177
Q

How does Plasmapheresis work with Guillain-Barre syndrome

A

Removal of circulating humoral factors (e.g., immunoglobulins and antibodies) responsible for demyelination.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 586). Wolters Kluwer Health. Kindle Edition.

178
Q

global brain dysfunction leading to an altered mental state

A

Encephalopathy

179
Q

brain requires a delicate balance of what

A 
neurotransmitters
substrates
water
electrolytes
adequate perfusion
acid base balance
temperature
180
Q

encephalopathy etiologies

A 
electrolyte imbalance
medication
environment
organ dysfunction
inborn errors of metabolism
181
Q

what type of encephalopathy occurs after an event such as cardiac arrest and why

A

hypoxic-ischemic encephalopathy

-brain is deprived of adequate perfusion or oxygenation resulting in cerebral ischemia, hypoxia and cell death

182
Q

Acute encephalopathies

A

Hypoxic-ischemic

infectious

postinfectious

vascular disorders

183
Q

what type of encephalopathy has cerebral dysfunction that is permanent and nonprogressive

A

Static encephalopathy

184
Q

what type of encephalopathy is most commonly associated with neurogenerative disorders and autoimmune disorders

A

progressive encephalopathies

185
Q

a condition of acute global cerebral dysfunction, resulting in altered consciousness, behavior changes and/or seizures not because of brain disease, TBIs or infection…This is a result of cytotoxic injury and/or neurotransmitter disruption

A

Acute toxic/metabolic encephalopathy

186
Q

what type of events can lead to hypoxic-ischemic encephalopathy

A

before, during or after birth

trauma

asphyxiation

congenital abnormality

stroke

medications

prematurity

in older pediatric pt
asphyxiation
airway obstruction with foreign body or airway edema

submersion injury

severe asthma

sepsis
low cardiac output states
chronic hypoxia from pulmonary disease
resp and cardiac arrest
systemic hemorrhage
carbon monoxide poisoning
cardiac arrhythmias
187
Q

infections that can cause encephalopathies

A 
bacterial meningitis
encephalitis
fungal meningitis
tuberculosis meningitis
parasitic infection
AIDS
HIV
ADEM (acute disseminated encephalomyelitis - lymphocytes attack myelin sheath
188
Q

immune mediated encephalopathy as a result of autoimmune most often caused by

A

anti-N-methyl-D-aspartate (Anti-NMDA) receptor encephalitis - antibodies target the subunit of the receptor

189
Q

clinical presentation in infant for encephalopathy

A

irritability
lethargy
poor feeding

190
Q

clinical presentation in child for encephalopathy

A

personality or behavioral changes

Cognitive decline

concentration problems

other symptoms: seizures, nystagmus, tremor, myoclonus, abnormal movements

191
Q

labs to order for encephalopathy workup

A

CBC with diff

CMP

LFT

Ammonia

Coagulation panel

Blood gas

blood cultures

urinalysis and urine cultures

CSF cultures

Metabolic: serum amino acids, urine organic acids, lactate, thyroid function tests

Tox screen

med drug levels

lead level

Inflammatory: CSF or oligoclonal bands, serum for antibodies (thyroid, NMDA)

look at what meds they take, could they be contributing?

192
Q

Imaging for encephalopathy workup

A

CT or MRI

EEG to look for sizures

193
Q

when should you consider steroids in enephalopathy

A

for postinfecious or autoimmune encephalopathy

194
Q

what disorders may have encephalopathies

A

Tay Sachs disease

Mucopolysaccharidosis types I and II

adrenoleukodysrophy

mitochondrial encephalopathies such as MELAS and spinocerebellar ataxia

195
Q

CBC is useful in evaluating

A

inflammation
infection
anemia
immune status

196
Q

Metabolic panel (CMP) will identify

A

electrolyte imbalance
kidney function
hydration status
serum glucose levels

197
Q

Liver function tests will show

A

enzyme activity and accumulation of toxic metabolites such as bilirubin or ammonia

198
Q

Coagulation panels will show

A

coagulopathy or hypercoagulable states

199
Q

ABG will show

A

acid-base

oxygenation/ventilation

200
Q

what can you measure on the ABG if you suspect carbon monoxide poisonings

A

Carboxyhemoglobin

201
Q

what is the first imaging study that should be ordered with encephaolopathy

A

CT

202
Q

what improves survival and neurodevelopment in newborns with moderate to severe HIE

A

hypothermia

203
Q

result of a sudden interruption of arterial or venous blood flow to a focal region of the brain

A

Cerebrovascular accidents (stroke)

204
Q

a decrease or disruption of blood flow, leading to dysfunction of brain tissue, caused by systemic hypoperfusion, embolism, thrombus, and sinus venous thrombosis

A

Ischemic stroke

205
Q

a vessel or aneurysm ruptures and leaks into the surrounding tissue and cells in the brain

A

Hemorrhagic stroke

206
Q

most common risk factors for arterial ischemic stroke in children

A

congenital and acquired heart disease

Arteriopathies (arterial dissection, moyamoya disease, vasculitis)

Sickle cell disease

Hypercoagulable conditions

207
Q

clinical presentation of neonates for ischemic stroke

A

seizures, decreased responsiveness, focal weakness

208
Q

clinical presentation of children for ischemic strokes

A

focal neurologic deficits such as hemiparesis
aphasia
visual disturbances
headhache

209
Q

clinical presentation for hemorrhagic stroke

A

signs of increased ICP such as headache and vomiting

irritability
seizures
hemiparesis

210
Q

CT for stroke

A

initial (hours after infarct) could be negative - serial imaging may be necessary

211
Q

what imaging should you order if concern for dissection

A

CTA (CT angiography)

212
Q

What imaging should you order if concerned for venous thrombosis

A

CT Venography

213
Q

supportive care for strokes

A

prevent fever
maintain normoglycemia
normovolemia to maintain adequate substrate delivery

214
Q

management of ischemic strokes

A

Heparin (unfractionated or low molecular weight) may be administered for as long as 1 week

ASA 3-5mg/kg used for ischemic stroke prophylaxis

215
Q

Management of hemorrhagic stroke

A

Neurosurgical evaluation for ICP monitoring

216
Q

when a patient presents with what symptoms should stroke be high on the differential

A

headache
seizure
focal weakness

217
Q

what is the preferred method to identify an acute stroke

A

MRI

218
Q

lab studies for stroke workup

A

coagulation panel

platelets
electrolytes
fasting cholesterol
triglycerides

if an autoimmune disorder is suspected
Protein C
Protein S
antithrombin III deficiency
anticardiolipin antibodies
antiphospholipid antibodies
219
Q

what genetic testing for stroke pt

A

factor V leiden mutation
prothrombin gene mutation (G20210A)
methylenetetrahydrofolate reductase TT677 mutation

220
Q

strokes in children with sickle cell can be due to

A 
arterial ischemia
subarachnoid or intracerebral hemorrhage 
aneurysm rupture
dissection
moyamoya syndrome
SoVT
221
Q

if your imaging studies do not identify stroke in a pt who has stroke like symptoms. What should you order?

A

EEG to evaluate for seizures

222
Q

what are the AHA class I recs for management of neonatal strokes

A

supplement coagulation factors in coag disorders

replace platelets in those with intracranial hemorrhage

ventricular drainage for those who develop hydrocephalus

treat dehydration, anemia

if they have a MTHFR mutation give folate or vit B

evacuating a hematoma that elevates ICP

223
Q

for a stroke how should head of bed be placed

A

flat to promote cerebral perfusion unless there is a concern for increased ICP or other contraindications

224
Q

for arteriopathy, idiopathic stroke or Moyamoya what drug is the drug of choice for stroke prevention. also include dosing

A

3-5mg/kg/day ASA

risk of Reye syndrome in children following viral or varicella

225
Q

for extracranial dissection or cardioembolic stroke what to use for anticoagulation

A

heparin or low molecular weight heparin (LMWH) for acute….and switch to anticoagulants or ASA for long term

226
Q

is tPA approved in children in strokes?

A

no , only clinical trials

227
Q

infections that can increase risk of arterial ischemic stroke

A

meningitis
varicella
tuberculosis

228
Q

what cardiac problems increase risk for stroke

A 
Congenital heart disease
arrhythmias
cardiomyopathy 
cardiac surgery
Kawasaki disease (KD)
Endocarditis
229
Q

a disturbance of brain function caused by paroxysmal discharges within the neuronal system

A

seizure

230
Q

Prognosis for children with a first time unprovoked seizure in about 25% of kids

A

will demonstrate a normal neuro exam and have few or no recurrent seizures

231
Q

what can cause seizures

A

genetic or abnormal cortical development

metabolic (hyponatremia, hypoglycemia)

infection (meningitis)

fever

stroke

traumatic brain injury

toxic ingestion/exposure

subtherapeutic anticonvulsant med levels for someone with h/o epilepsy

232
Q

patho for seizures

A

hypersynchronous discharges within the cortex combine with high frequency bursts of the action potentials to generate a seizure

233
Q

sustained extension or flexion of head, trunk, and extremeties

A

tonic seizure

234
Q

potential complications of status epilepticus

A

rhabdomyolysis

hyperthermia

cerebral edema

resp failure

235
Q

labs to look at in first time seizures based on individual circumstances - why would you order

A 
CBC
serum electrolytes
glucose
calcium 
magnesium

vomiting, diarrhea, dehydration, failure to return to baseline promptly

236
Q

in majority of febrile and non-febrile seizures, lab studies often show what?

A

unremarkable

237
Q

what meds can you give for persistent seizures

A

fosphenytoin or phenobarbital

238
Q

motor onset generalized seizures include:

A 
tonic
clonic
tonic-clonic
myoclonic
atonic
epileptic spasm
239
Q

non-motor onset generalized seizures include:

A

typical absence

atypical absence

myoclonic absence

absence with eyelid myoclonia

240
Q

the example given of throwing a remote across the room or dropping a plate are examples of what type of seizure

A

myoclonic

241
Q

seizure where ictal discharge occurs in a limited area of the cortex….presentation is dependent on the locus in the brain - intact recall of the event assists with diagnosing this type of seizure bc consciousness is not lost

A

focal aware seizures

242
Q

seizure - impaired consciousness and imply a larger region of spread within the cerebral cortex….usually present with automatisms (lip smacking, repetitive swallowing and clumsy motor movements)

A

focal seizures with impaired awareness

243
Q

focal or generalized onset characterized by either flexion of neck, trunk and extremities and/or abrupt extension of arms, legs, neck and trunk…..frequently occur in clusters, during sleep or just upon waking

A

epileptic spasms

244
Q

what age are epileptic spasms seen

A

typically present between 4-6 mos….most prior to 1 yr old

245
Q

epileptic spasms are associated with what

A

epileptic encephalopathy

246
Q

febrile seizures can be considered when associated with temp greater than or equal to ______ within ____ hrs of seizure without CNS infection, history of afebrile seizures, underlying epilepsy or underlying neurologic condition that predisposes the child to seizure

A

38C (100.4F)

24 hours

247
Q

what type of seizures occur at the time of systemic insult or in close temporal association with a documented brain insult

A

acute symptomatic seizures

248
Q

if there is clinical concern for meningitis in a pt under 12 mos of age what test needs to be done

A

LP

big risk factor is unvaccinated

249
Q

what age should you get labs for a seizure workup (first time, no underlying)

A

6 mos

  • electrolytes
250
Q

what age should the pt go home with a rescue med for first time unprovoked seizure

A

2 yrs and older

251
Q

meds to treat seizure

A

lorazepam (ativan) or diazepam

if lasts after 5 min -? fosphenytoin, phenobarbital, levetiracetam or valproic acid

252
Q

what is SUDEP

A

sudden unexplained death in epilepsy

rare but less likely to occur in well controlled epilepsy

253
Q

risk factors for SUDEP

A

uncontrolled generalized tonic clonic seizures

antiseizure medication polytherapy

no use of anti-seizure meds

intellectual disability

254
Q

for a ventriculostomy. where does the 0 need to line up with

A

tragus of the ear

255
Q

what happens during a drowning

A

involuntary laryngospasm as the water comes into contact with the airway after submersion - causing a conscious person to cough and inhale more water. Aspiration of water and vomitus causes further laryngospasm leading to hypoxemia and LOC.

Hypoxemia stimulates a shift in the acid base balance resulting in arrhythmias, myocardial and cardiac arrest due to metabolic or resp acidosis

256
Q

when water enters the airway, tell me about the inflammatory cascade

A

the inflammatory cascade -> causes pulmonary vasoconstriction and pulmonary edema -> surfactant is denatured and lungs become noncompliant -> difficult to ventilate with increased atelectasis -> intrapulmonary shunting with ventilation perfusion mismatching occur

257
Q

what happens in the brain in a submersion injury

A

cerebral ischemia results from inadequate blood flow to brain and if deprived of oxygen for extended time -> brain tissue begins to die (cerebral infarcts) - > injured brain begins to swell (cerebral edema) -> raises ICP -> further injury to nervous system

258
Q

submersion injury in r/t cardiac injury

A

indirect -> it is the resultant hypoxia and pulmonary injury that affect the myocardium

hypothermia and electrolyte disturbances result in arrhythmias

cardiovascular system can recover if oxygenation and acid base balance are restored

pulmonary vasoconstriction if severe enough can result in decreased R ventricular stroke volume, decreased l ventricular preload and worsened cardiac output

259
Q

asymptomatic presentation of drowning to ED - be careful…why?

A

even mild hypoxia can increase permeability of pulmonary capillaries with alveolar fluid leak and surfactant damage

resp dysfunction may take hours to manifest

children need to be observed for a prolonged time frame after submersion incident

260
Q

what should you order in a submersion injury

A

ABG values
chest x ray (looking for atelectasis, pulmonary edema, aspiration)
vital signs

261
Q

symptoms tied to a submersion injury

A 
anxiety
vomiting
cough
wheezing
hypothermia
AMS
metabolic acidosis
resp failure
cardiac arrest
262
Q

Indications for intubation post submersion

PaCO2
Pa02

A

unconscious child

peripheral arterial carbon dioxide (PaCo2) >50

inability to maintain peripheral arterial oxygen (PaO2) > 90% with supplemental Oxygen

263
Q

how to use PEEP in intubated pt for a submersion injury

A

prevent atelectasis and overcome intrapulmonary shunting

264
Q

noninvasive ventilation options in submersion injury

A

continuous positive airway pressure or

bilevel positive airway pressure

265
Q

gastric decompression in submersion injury treatment

A

via orogastric or nasogastric tubes should to minimize aspiration risk in patients with altered LOC

266
Q

common findings in submersion injury

A

hypothermia
hypoglycemia
electrolyte abnormalities

267
Q

how do you protect the pt from secondary cerebral injury post submersion injury

A

the initial cerebral ischemic injury is during the submersion

secondary occurs later from prolonged hypoxemia, cerebral edema, acidosis, hypovolemia, seizures, electrolyte imbalances

resp treatment and intervention guided by ABG values

Avoid hypercapnia (can increase cerebral HTN ->worsens cerebral edema)

Give ABX to prevent aspiration pneumonitis

normalize BP - prevent hypotension

avoid hypervolemia (may need diuretics and fluid restriction)

treat hypermetabolic states such as seizure and fever to avoid secondary brain insults

EEG should be used to detect subclinical seizures, esp if pt requires neuromuscular blocking agents

268
Q

why laryngospasm during submersion?

A

bodies way to protect you from water going into your lungs. This is to prevent that…but if your awake your coughing and choking more

269
Q

aspiration specific to fresh water

A

surfactant denaturing with subsequent alveolar collapse

intrapulmonary shunting

hypoxia

270
Q

aspiration specific to saltwater aspiration

A

large osmotic gradient with transudation of fluid from pulmonary vasculature to alveoli -> results in surfactant dilution and washout with alveolar collapse

shunting

hypoxia

271
Q

how is drowning defined?

A

resp impairment from submersion/immersion in a liquid.

The outcome can be death, morbidity, or no morbidity

avoid terms - “wet drowning, dry drowning”

instead - fatal or non-fatal drowning should be used

272
Q

drowning is the ____ leading cause of accidental death among children in the US

A

2nd leading cause

273
Q

what age group is the second peak in age distribution for drowning and why

A

adolescence

often associated with alcohol, drug use and risk-taking behavior

274
Q

Neuro classifications for submersion injuries

A

Category A - PT awake/alert, minimal brain injury

Category B - more serious asphyxial injury. Blunted to stuporous, normal pupillary response and purposeful responses to pain

Cat C - more severe injury
comatose, abnormal resp patterns (Cheyne Stokes), abnormal motor responses to pain

C1 - decorticate movements

C2 - decerebrate movements

C3 - Flaccid, apneic

275
Q

most submersion victims aspirate an average of ___ mL/kg

A

3

276
Q

for blood volume alterations to occur, what do you need to aspirate during a submersion ____mL/kg

A

11

277
Q

for electrolyte alterations to occur what do you need to aspirate during a submersion? ____mL/kg

A

22

278
Q

after submersion, pt often require supplemental oxygen or positive pressure ventilation for how long?

A

48-72 hours which is how long it takes for surfactant to reconsititute

279
Q

children who progress to ARDS after submersion injury should undergo mechanical ventilation aimed at minimizing

A

barotrauma and volutrauma

280
Q

Indications for ECMO after a submersion

A

refractory shock

refractory hypoxemia
controlled rewarming

281
Q

when should you give submersion victim abx

A

if they become febrile
increasing leukocytosis
worsening infiltrates on chest x ray
develop hemodynamic instability

282
Q

empiric steroids and submersion?

A

do not use….outcome not improved and shown to increase rates of infection

283
Q

continuous hypotension post submersion

A

inotropic support with dopamine, dobutamine, or epinephrine may be needed

284
Q

Poor neurologic outcome from a submersion injury include submersion duration greater than
what else?

A

4-5 min

warm water temp

CPR in field

CPR in field with intubation and epi administration

Continued apnea, asystole and coma after arrival to ED

285
Q

what lab values post submersion are associated with worse neurologic outcomes

A

pH < 7.1

elevated serum glucose

286
Q

what is the difference for children who drown in ice cold water

A

warrant additional consideration because they may survive prolonged cardiopulmonary arrest with a favorable neurologic outcome

287
Q

nearly all children who demonstrate significant problems in gas exchange will do so by ___ to ___ hours after submersion

A

4-6 hours

288
Q

discharge requirements post submersion from ED

A

If at the 6 hour mark they are asymptomatic and they are neurologic cat A they can be discharged from ED. No labs or x ray required

289
Q

symptomatic submersion injury patients will need what?

A

chest x ray
ABG

consider -
CBC
coags
electrolyte panel

must be admitted for obs until symptoms completely resolve

290
Q

leading cause of injury related deaths and disability for age groups newborn to 4 years old and ages 15-19 years old

A

Traumatic brain injury

291
Q

what gender is at higher risk for a TBI

A

males

292
Q

an acquired brain injury from a blow to the head or a penetrating head injury that disrupts the normal function of the brain

A

TBI

293
Q

secondary brain injury occurs as the result of

A

a cascade of biochemical, cellular and metabolic responses influenced by associated hypoxia and hypotension which affect long term outcomes

294
Q

what type of injury occurs when rapid acceleration, deceleration or rotational forces result in axonal shearing at the interface of gray and white matter?

A

Diffuse axonal injury -> leads to cell edema, damage or death - no surgical intervention available

295
Q

TBI clinical presentation

A

Altered loc

resp distress/failure

hemodynamic instability with shock

seizures

vomiting

visual disturbances

motor/sensory impairments

296
Q

diagnostic eval for TBI

A

Head CT

Head MRI

diffusion tensor imaging (if available)

297
Q

management of TBI

A

manage cerebral edema and increased ICP via external ventricular drainage

Keep ICP <20 mmHg and optimal perfusion pressure for age

mild hyperventilation

hyperosmolar therapy

hypothermia

surgical intervention if indicated

maintain hemodynamic stability with opimal oxygenation/ventilation

control seizures

pain control

sedation

neuromuscular blockade as indicated

optimize nutrition with parenteral nutrition and introduction of enteral feedings when appropriate

DVT prophylaxis

298
Q

scale to assess cognitive function and rate of disability in ABI patients

A

Rancho los Amigos scale of cognitive levels - based on cognitive and behavioral presentations as patients emerge from a coma

299
Q

anti epileptics and kids with TBI

A

young kids higher risk for seizures

use only when clinically necessary - should only be used when clinically required and at the lowest clinically effective dosage to facilitate max cognitive recovery

AEDs can interfere with a developing brain

300
Q

signs/symptoms of a concussion

A

somatic (headache)

cognitive (slowed reaction times, poor attention)

emotional (lability, irritability)

sleep disturbances (drowsiness)

physical signs (loss of consciousness, amnesia)

301
Q

what would warrant imaging in a concussion

A

increase in somnolence

headache

vomiting

302
Q

recovery time for concussion

A

majority resolve within 10 days

recovery may be slower in children

303
Q

repeated concussions, esp within a short time frame (days or weeks), carry a significant risk of permanent brain injury called

A

second impact syndrome

304
Q

symptom progression of a epidural hemorrhage

A

lucid interval following the brain injury -> decreased LOC -> then returns to normal for several hours -> then developing rapidly progressive neurological symptoms

305
Q

lens shaped extracerebral hemorrhage compressing brain

A

epidural

306
Q

crescentic extracranial hemorrhage compressing brain

A

Acute subdural

307
Q

Crescentic, low density mass on CT

A

chronic subdural

308
Q

on CTmultifocal low density areas with punctate hemorrhages

A

contusion

309
Q

Battle sign

A

bleeding over mastoid process

skull fracture

310
Q

racoon eyes

A

bleeding around orbit

skull fracture

311
Q

hemotympanum

A

bleeding behind tympanic membrane

skull fracture

312
Q

when is surgical intervention needed for depressed skull fracture

A

more than 0.5-1cm

surgical elevation
repair of associated dural tears

313
Q

Monroe-kellie Doctrine equasion

A

V of the intracranial vault (constant) = V of the brain +V of the CSF + V or the blood + V of any mass lesion

314
Q

components inside the skull and %

A

Brain 80%

CSF 10%

Blood 10%

315
Q

ICP normal values

  • in older children
  • in children < 1 year
A

<20-25cm H2O older children

<15-20 mmHg in children <1 yr

316
Q

ICP generally peaks ___ to ___ hours after a traumatic injury

A

24-72

317
Q

equation for cerebral perfusion pressure (CPP)

A

Mean Arterial pressure (MAP) - ICP = CPP

318
Q

CPP goal for infant
children
adolescents

A

infant > 40

children > 50

adolescence >60 mmHg

319
Q

Net pressure gradient supplying blood flow to brain depends on ___ and ___-

A

MAP and ICP

320
Q

Map is equal to

A

1/3 systolic BP and 2/3 diastolic BP

321
Q

CPP can be decreased from an increase in _____

A

ICP

or decrease in systemic BP

322
Q

low CPP has been associated with ___ outcomes in traumas

A

poor outcomes

323
Q

what causes increased ICP without evidence of space-occupying lesion or vascular abnormality

A

idiopathic intracranial hypertension AKA psudotumor cerebri

324
Q

Persistent increase in ICP can lead to ____ and ___

A

brain herniation and death

325
Q

Cerebral edema may be the result of

A

intracellular swelling
capillary endothelial cell dysfunction
interstitial edema

326
Q

what is the most common problem leading to increased ICP

A

traumatic brain injury

327
Q

symptoms of increased ICP

A 
LOC
Altered LOC
vomiting
increased head circumference in infant
tense fontanel in infant
seizures
status epilepticus 
coma

cushings triad

328
Q

what is cushings triad

A

sign of increased ICP

irregular resp
widening pulse pressure
bradycardia

(indicates impending herniation)

329
Q

elevations in ICP typically take ____ to ____ to peak following an injury

A

24-72 hours

330
Q

medical management of increased ICP

A

sedation

drainage of CSF

osmotic diuresis with either mannitol or hypertonic saline

Head of bed elevated and midline

mild hyperventilation is helpful in decreasing ICP with goal CO2 30-35 mmHg

if evidence of cerebral ischemia and no contraindications, consider hypothermia

331
Q

for intracranial hypertension refractory to initial medical management

A

barbiturate coma

hypothermia

decompressive craniectomy should be considered

332
Q

most common method of ICP monitoring use either

A

an intraventricular catheter

or an

intraparenchymal catheter

333
Q

contraindications to contrast

A

pregnancy

allergy to shellfish or iodinated dye

unstable vitals

impaired kidney function

before given - BUN, creatinine levels and occasionally a creatinine clearance to check kidney function

334
Q

pt may experience what with contrast

A

flushing /feeling of warmth

transient headache

salty or metallic taste in mouth

nausea

vomiting

335
Q

what is important to facilitate after contrast

A

oral or IV hydration

336
Q

what diagnostic imaging for movement disorders?

A

MRI

PET

337
Q

what uses nuclear medicine technology to primarily evaluate the nervous system through cerebral metabolism and cerebral blood flow

A

PET - Positive emission tomography

SPECT - Single-photon emission computerized tomography

338
Q

currently PET scans are most commonly used to detect and provide understanding of

A

brain disorders (tumors, memory disorders, and seizures)

Cerebrovascular disease

cerebral trauma

other CNS conditions

339
Q

in relation to glucose the PET scan reveals

A

which areas of the body are burning the most sugar

340
Q

to prep for a PET scan

A

no caffeine, alcohol, nicotine, or glucose consumed for a period up to 24 hours prior

no enteral intake for 6-12 hours prior

must be able to lay flat for 2-3 hours

341
Q

postprocedure care for PET scan

A

copious fluids to clear isotope

342
Q

SPECT scan measures

A

cerebral blood flow and perfusion

343
Q

SPECT is useful to demonstrate hypoperfusion in focal and diffuse cerebral disorders like

A

dementia
seizures
stroke
cerebral taruma

344
Q

preferred test for brain death

A

SPECT

345
Q

SPECT is helpful during acute events for

A 
stroke
seizures
dementia
amnesia
trauma
neoplasms
brain death
persistent vegetative state
Psychiatric disorders such as schizophrenia or depression
346
Q

major disadvantages for SPECT

A

high cost
IV access for isotope
must be done within 1 hr (isotope degredation)

347
Q

special prep for SPECT

A

none

348
Q

disadvantages for PET

A

high cost
limited availability for diagnostic purposes
necessity to produce short-lived isotopes which limits patient access to this imaging modality

349
Q

suicide is the ___ leading cause of death in children and adolescents in the US with higher incidence of suicide completion among ____

A

3rd

males

350
Q

more than half of male suicide occurrences involve a _____; most female suicides are caused by ___

A

males - firearm

females - poisoning

351
Q

what is a chief catalyst for suicide and suicidal thoughts

A

depression

352
Q

Risk factors for suicide pneumonic

A

IS PATH WARM

I - ideation
S- substance abuse
P - purposelessness
A- anxiety
T-trapped
H - hopelessness
W - withdrawal
A - anger
R - recklessness
M - mood changes
353
Q

what suicide risk level?

history of serious or nearly lethal attempts or planning

recently institutionalized for a psych disorder or recent psych disorder

persistent suicidal ideation, psychosis, history of aggression and impulsive acts

A

High risk

354
Q

what suicide risk level?

under medical care of a psychiatric specialist

suicidal ideation without plans or attempts

no other identified signs

A

moderate risk

355
Q

what suicide risk level

mild suicidal ideation, but without attempt

social support

no previous attemps

A

low risk

356
Q

refusal to maintain normal body weight for age and height: generally body weight <85% expected.

A

anorexia nervosa

357
Q

primary or secondary amenorrhea in postmenarchal females (eating disorder)

A

anorexia nervosa

358
Q

recurrent behaviors in an effort to avoid weight gain, including induced vomiting, abuse of laxatives, diuretics, fasting, excessive exercise

A

Bulimia nervosa

359
Q

eating disorder associated lab abnormalities

A

electrolyte abnormalities

chloride responsive metabolic alkalosis

significant hypophosphatemia

intravascular volume depletion or shock

360
Q

heart and eating disorders

A

risk for cardiac arrhythmias due to electrolyte abnormalities - depletion of total body potassium, hypomagnesemia, serum hypophosphatemia and altered acid base balance

361
Q

eating disorders and bone marrow

A

bone marrow failure may develop

362
Q

clinical presentations of anorexia nervosa and bulimia nervosa

A

emaciated body habitus

cachetic appearance

decreased body temp

bradycardia

hypotension

acrocyanosis

edema

dry skin with discoloration

cold extremeties

scalp hair loss

increased lanugo

decreased deep tendon reflexes

arrhythmias

evidence of dehydration and/or shock

363
Q

Patients with bulimia nervosa may be normal weight and body habitus with enlarged

A

parotid glands or tonsils

erosion of tooth enamel

superficial ulceration, calluses or scarring on dorsum of fingers

decreased or absent gag reflex

swelling of hands and feet r/t hypoalbuminemia

364
Q

eating disorder pt complaints

A

fatigue

muscle weakness

cramps

abd pain

constipation

easy bruising

sore throat

sleep disturbances

difficulty concentrating

increased physical activity

dizziness

fainting

365
Q

eating disorder labs and other orders

A 
CMP
carotene levels
zinc
copper
prealbumin
amylase
lipase
cholesterol
LFT
thyroid function test
estradiol levels
Urinalysis: urine electrolytes
ECG
366
Q

in diagnostic eval for eating disorders, what other problems to evaluate for

A

malignancy

inflammatory bowel disease

malabsorption syndromes such as celiac disease

Diabetes mellitus

hyperthyroidism

hypopituitarism

367
Q

management of eating disorders

A

stabilize -
correct intravascular volume depletion and normalize electrolytes

reverse hypotension, tachycardia

refer to psych

get history of anxiety, difficulty with separation from parents, peer relationships

368
Q

components to presenting a case

A

1) be organized
2) tell a story
3) one liner and impression statement
4) Present a pt, not just a disease
5) logical sequence
6) pertinent positives and pertinent negatives
7) summarize the case
8) include a differential diagnosis
9) include your management plans

369
Q

muscle weakness and fatigue are associated with

Hyperkalemia

Hypokalemia

A

Hypokalemia

370
Q

what symptoms are associated with hypokalemia and which ones are for hyperkalemia

ventricular arrhythmias
Peaked t waves
flattened t waves
decreased diastolic function
muscle weakness and fatigue
A

Hypokalemia

  • muscle weakness and fatigue
  • ventricular arrhythmias
  • flattened T waves
  • decreased diastolic function

Hyperkalemia
-peaked T waves

371
Q

critically low phosphorous levels (<1mg/dL) can result in symptoms that include

A

muscle weakness including resp muscle function

372
Q

what to do with phosphorous levels can cause laryngospasm and tetany

A

hyperphospatemia

373
Q

seizures, irritability and lethargy can be r/t hyponatremia or hypernatremia

A

both

374
Q

to restore sodium levels using hypertonic saline…how is this calculated?

A

(0.6 x (weight in kg) x (target sodium - measured sodium)) to achieve a target sodium level of 125 mEq/L

375
Q

what hormone is primarily responsible for Calcium regulation

A

PTH (regulates calcium absorption from bone and renal excretion of calcium)

376
Q

assessment of intravascular volume depletion in a 14 year old with eating disorder

A

orthostatic vital signs

377
Q

what low electrolyte can cause seizures

A

low sodium

normal is 135-145

give 3% saline solution to correct

low potassium will not cause seizures

378
Q

what serial evaluation for guillain barre will be most important for assessing resp status

A

Negative inspiratory force (NIF)

379
Q

left subdural hematoma in the frontoparietal region what impaired motor function would be anticipated

A

R hemiparesis

380
Q

after a traumatic injury, that required antiepileptic meds as prophylaxis. For how long after the injury should you keep the pt on the meds?

A

7 days after injury - switch to keppra if you still need an anticonvulsant

381
Q

rancho los amigos level?

no response to stimuli

A

Level I

382
Q

rancho los amigos level?

generalized response with inconsistent and nonpurposeful reaction to stimuli in a nonspecific manner. responses may be delayed and include physiologic changes, gross body movement and/or vocalizations

A

LevelI

383
Q

rancho los amigos level?

response to stimuli is more localized, such as withdrawal from painful stimuli or inconsistent following of simple, one step commands

A

Level III

384
Q

rancho los amigos level?

exhibits automatic but appropriate responses although “robotic-like and demonstrates decreased safety awareness and impaired judgement

A

Level VII

385
Q

what area of brain is responsible for production of speech

A

Broca area

386
Q

where is the Broca area located

A

left frontotemporal

387
Q

wernicke area is located in the

A

Parietal-temporal area

388
Q

Wernicke area is responsible for

A

language comprehension and receptive speech

389
Q

injury to Broca area may result in

A

aphasia or

dysarthria

390
Q

injury to Wernicke area may result in

A

fluent aphasia - pt may express thoughts fluently with a nonsensical speech pattern

391
Q

detailed pertinent history is collected during which portion of survey

A

secondary

392
Q

Sacral sparing is an example of an _____ spinal cord injury (SCI)

A

incomplete - some degree of sensory and/or motor function is preserved

393
Q

the most common cause of spinal cord injury in children is

A

MVC

preventative measure - use a seat belt with shoulder harness in vehicles

394
Q

what is the most sensitive test to evaluate for suspected spinal cord injury

A

MRI

395
Q

if x ray and CT are neg for fracture what would most likely be cause of paralysiss

A

SCIWORA - spinal processes remain partially cartilaginous and may not demonstrate fractures but the impact can cause partial or complete spinal cord transection

396
Q

most common chest injury in children resulting from a high energy impact injury such as a auto-ped.

A

pulmonary contusion

often has subtle symptoms and no other obvious injury to chest or chest wall

symptoms of resp distress can occur within 24-48 hours after injury

397
Q

What types of hormones do the adrenal glands produce

A

glucocorticoids
mineralocorticoids
sex hormones

398
Q

where are the adrenal glands located

A

on the kidneys

399
Q

what type of hormones are the following:
Cortisol
Corticosterone

A

Glucocorticoids

400
Q

what type of hormones maintain glucose control by affecting protein and carbohydrate metabolism

A

Glucocorticoid Hormones

produced by the adrenal glands

401
Q

what type of hormones inhibit glucose uptake in the muscle and adipose tissue

A

Glucocorticoid Hormones

402
Q

What type of hormones stimulate gluconeogenesis (particularly in the liver)

A

Glucocorticoid Hormones

403
Q

what type of hormones respond to stress by upregulating the expression of anti-inflammatory mediators and downregulating the expression of proinflammatory mediators

A

Glucocorticoid Hormones

404
Q

If you have prolonged exposure to glucocorticoids, what syndrome will develop?

A

Cushing Syndrome

405
Q

Obesity, muscle wasting/weakness, decreased glucose tolerance/hyperglycemia, buffalo hump.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 654). Wolters Kluwer Health. Kindle Edition.

A

Cushing Syndrome

406
Q

what type of hormones are the following:
aldosterone
dehydroepiandrosterone

A

Mineralocorticoid hormones

407
Q

what type of hormones maintain the balance of sodium and potassium in the body

A

Mineralocorticoid hormones

408
Q

When aldosterone is increased, ______ develops

A

aldosteronism

409
Q

Hypernatremia and hyperkalemia, resulting in hypertension.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 654-655). Wolters Kluwer Health. Kindle Edition.

A

aldosteronism

410
Q

aldosteronism

A

Hypernatremia and hyperkalemia, resulting in hypertension.

411
Q

If androgens are increased, _______ will be affected

A

sex characteristics

412
Q

What type of hormones are
Androgens
progestins
estrogens

A

sex hormones

413
Q

Disorders affecting the adrenal cortex lead to inadequate or absent production of

A

hormones

414
Q

The most common causes of acute adrenal insufficiency are

A

Waterhouse–Friderichsen syndrome, sudden withdrawal of long-term corticosteroid therapy, and stress states in patients with chronic adrenal insufficiency.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 655). Wolters Kluwer Health. Kindle Edition.

415
Q

sudden withdrawal of long-term corticosteroid therapy, and stress states in patients with chronic adrenal insufficiency

A

Waterhouse–Friderichsen syndrome

Critical Care I (27 decks)

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