Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Peds-Final > Neurology > Flashcards

Neurology Flashcards

1
Q

HA red flags that prompt further eval

A 
dramatic increase in HA severity
HA that awakens CH from sleep
change in est. HA pattern
gradually increasing frequency & severity
   suggests increasing ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

PE finding for intracranial HTN

A

papilledema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PE for HA

A

growth, HC, BP
intracranial HTN (papilledema)
focal neurologic signs
general- rhinitis, dental abscess, bruit, head trauma, hematoma, skull step-off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

red flags in hx/PE for HA may entail further investigation with what

A

head imaging (CT for hemorrhage, MRI for tumor & cerebellar imaging)
electroencephalography (EEG)
+/- sleep deprivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

tension HA

A

diffuse
symmetric
often related to fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cluster HA

A

extreme deep pain in & around one eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

migraine

A

triggered by stess
vomiting
FH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

migraine classification

A

migraine w/ aura (visual or otherwise)
“ “ w/o aura
complicated migraine (transient focal abnormality)
migraine equivelent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

paroxysmal torticollis

A

attacks of head tilt, +/- vertigo, vomiting

requires r/o posterior fossa pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

benign paroxysmal vertigo

A

attacks of unsteadiness w/ nystagmus & vomiting followed by sleep
may precede development of typical migraine
requires r/o epilepsy & CNS tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cyclic vomiting

A

protracted attacks of vomiting, 1-4x/hr, up to 5 days

requires r/o epilepsy, GI d/o, urea cycle d/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

abdominal migraine

A

attacks of migraine lasting 1-72 hrs, untreatable by other means
midline, dull, mod-severe pain
assoc. w/ anorexia, n/v, pallor
dx often by response to anti-migraine therapy
requires r/o other GI d/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

confusional migraine

A

episodic disorientation/ combativeness, sometimes followed by HA
requires r/o drug abuse, epilepsy, CNS ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Therapy for migraine acute episode

A

sleep
acute tx- acetaminophen, ibuprofen, sumatriptan, other triptans
rescue tx- NSAIDs, promethazine, metoclopramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

migraine prophylaxis

A

create mgnt plant to prevent stressors
biofeedback (stress reduction)
physical modalities (massage, PT, exercise)
meds (usu. involves a neurologist)
cyproheptadine
antihypertensives (propranolol, verapamil)
TCAs- amitriptyline, nortriptyline
anticonvulsants- valproate, topiramate, gabapentin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HA summary

A 
r/o underlying pathology
address exacerbating factors
mgnt plan
   meds (start w/ acetaminophen, ibuprofen)
   abortive agents
   daily prophylaxis (neurologist)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pseudotumor cerebri

A

increased ICP in absence of identifiable intracranial mass/ hydrocephalus
postulated to be d/t impaired CSF reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Risk factors of pseudotumor cerebri

A 
obesity
female
sinus thrombosis
head injury
chronic CO2 retention
SLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Acute S&S of intracranial HTN in pseudotumor cerebri

A 
HA
pulse synchronous tinnitus
pain behind the eye
pain w/ eye movements
transient visual obscurations
blurred vision/double vision
CN VI paresis
vomiting
macrocphaly
altered behavior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Chronic S&S of intracranial HTN in pseudotumor cerebri

A

growth impairment
optic atrophy
visual field loss
total blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diagnosing pseudotumor cerebri (one of exclusion)

A

CT- r/o hydrocephalus
MRI- r/o intracranial mass, hydrocephalus
Ophthalmologic- papilledema, optic n. changes
LP- measurement of opening pressure, normal CSF pnl & cx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Tx of pseudotumor cerebri

A

tx underlying causes- wt loss is mainstay of therapy, tx anemia
medical tx-
diuretics
acetazolamide (Diamox) causes peripheral paresthesias &
metabolic taste to carbonated soft drinks
furosemide (Lasix)
glucocorticoids
lumbar puncture
surgical tx- optic n. sheath decompression, lumboperitoneal shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Seizures

A

a sudden, transient disturbance of brain function, manifested by involuntary, motor, sensory, autonomic, or psychic phenomena, alone or in a any combo often accompanied by alteration of LOC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

epilepsy

A

repeated seizures w/o evident cause

recurrent, unprovoked seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

classification of seizures

A

symptomatic- cause is identified/ presumed

idiopathic- cause is unknown/ presumed to be genetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Examples of symptomatic seizure

A 
infxn (meningitis/encephalitis)
trauma
metabolic (hypoglycemia, hyponatremia)
hypoxic
tumor
malformation (hydrocephalus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

nonepileptic paroxysmal events

A 
benign nocturnal myoclonus
shudder attacks
tics & Tourette's syndrome
sleep orders- night terrors, sleepwalking/talking, cataplexy, narcolepsy
nightmares
migraine- BPV, paroxysmal torticollis
conversion rxn & pseudoseizure
GERD
masturbation
hypoglycemia
temper tantrums & breath-holding
syncope & vasovagal events
paroxysmal dystonia/ choreoathetosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Seizure

A 
hx- events prior, during, after
exam
lab- CBC, metabolic abnormalities
CT scan/ MRI
EEG- not sensitive or specific, may help classify seizure type to determine therapy, may reveal subclinical seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Seizure Tx

A

ABCs- protect against self-injury, airway clearance, monitor ABCs
anticonvulsants- if seizures are prolonged/hindering ABCs
education- seizure precautions, meds, daily life swimming, adequate sleep, driving, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Seizure meds

A 
abortive meds:
   benzodiazepines
      lorazepam parenterally
      diazepam orally/rectally
      midazolam nasally, PO, rectally
   phenobarbital & fosphenytoin
LT anticonvulsants- different drug classes used for different types of epilepsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

febrile seizure is a convulsion assoc. w/ a temp > than

A

38.0 C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

MC type of CH seizure

A

febrile seizure
incidence 2-5% of CH under 5 yo
peak occurrence 18-24 mo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When are febrile seizures most likely to occur (age)

A

6 mo-5yo
seizure in younger infant should concern you
some CH under 5 yo who develop febrile seizures may have persistant febrile seizures further on into CH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Febrile seizures are not d/t

A

CNS infxn/ inflammation
no acute systemic metabolic abnormality that may produce convulsions
no hx of previous febrile seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Criteria for simple febrile seizure (SFS) (65-90%)

A

duration under 15 min, total duration less than 30 min if in series
no recurrence in 24 hrs
no focal features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Complex febrile seizure (CFS)- meets 1+ criteria

A

duration > 15 mins
recur in series for total duration > 30 min or more than 1 seizure in 24 hr period
focal features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

etiology of febrile seizure

A

infxn: HSV 6 (roseola), influenza, rotavirus
immunization-related fever
predisposing factors
heredity, inhibitory NT production, maternal alcohol intake &
smoking during pregnancy raises risk 2-fold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

fever variability in febrile seizures

A

degree of fever is widely variable
ht of fever does not seem to correlate w/
onset of seizure
often the first sign of illness
simple febrile seizures MC are generalized & tonic-clonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

DDx for febrile seizure

A 
chills/rigors b/c of fever
meningitis
encephalitis
intracranial tumor
metabolic d/o
meurologic d/o (developmental delay)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

fevers in infants under 3 mo old

A

10% who appear well have a T > 38 C have a serious bacterial infxn or meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

fevers in CH 3-36 mo of age

A

2% who have a T above 39 C are found to have bacteremia

42
Q

AAP recommends strong consideration of LP in febrile seizure if

A

infant <12 mo who have had 1st seizure w/ fever

febrile seizures occurring on/after 2nd day of illness

43
Q

Diagnostic eval for febrile seizure

A

EEG no usually indicated for SFS if hx & PE benign
neuroimaging
electrolytes, glucose, Ca2+, BUN should be measured if hx & PE indicate (vomiting, diarrhea, edema, dehydration) or w/ CFS
search for underlying cause of fever: CBC, blood cx, UA, urine cx

44
Q

Febrile seizure Tx

A

ABCs
anticonvulsants if seizure >10 min, watch for respiratory compromise, drugs in office/ED- midazolam, lorazepam, fospheytoin, rectal diazepam

45
Q

Antipyresis in preventing febrile sizures

A

around the clock use not shown to be of benefit wo all CH w/ febrile seizures
unknown if some subset benefits
intermittent use warranted

46
Q

Anticonvulsant therapy for febrile seizures

A

not recommended in CH w/ 1+ SFS

47
Q

Continuous phenobarbital/ valproate reduce the risk of

A

recureent febrile seizures but have significant side effects

48
Q

SE of phenobarbital

A

transient sleep disturbances
decreased memory
reduced concentration

49
Q

SE of valproate

A

suppressed hematopoiesis
renal toxicity
pancreatitis
hepatotoxicity

50
Q

recurrence risk of febrile seizures

A 
young age at onset
hx of FS in 1st degree relative
low degree of fever while in ED
brief duration bet onset of fever & initial seizure
all 4 factors- 70% risk
0-4 factors- <1yr old
51
Q

febrile seizures & risk of epilepsy

A

2% chance (twice as high as gen. pop)

FH of FS, ethnicity, gender not risk factors

52
Q

infantile spasms

A

seizures that have characteristic clinical findings in age group 4-8 months
sudden adduction & flexion of limbs,
head & trunk
usually occurs in clusters when pt is
irritable/ fatigued

53
Q

Cryptogenic infantile spasm (40%)

A

no etiology evident, normal development before seizures

54
Q

Symptomatic infantile spasms (60%)

A

association w/ perinatal & prenatal event or other identifiable cause
have poor responses to anticonvulsants & poor intellectual prognosis

55
Q

EEG with infantile spasms

A

waking state EEG reveals chaotic high-voltage slow waves, random spikes & background disorganization

56
Q

Tx of infantile spasms

A

anticonvulsant therapy
ACTH may be helpful
ketogenic diet

57
Q

neurocutaneous d/o’s

A

d/o’s of tissue arising from neuroectoderm
skin findings
brain, spinal cord, eye manifestations
hamartomas

58
Q

hamartoma

A

nml tissue growing at abnormal sites/ abnormally rapidly

59
Q

neurofibromatosis type 1

A

NF-1>NF-2
cafe´ au lait spots
neurofibromatosis (small, rubbery, usu. on skin)
plexiform neurofibroma (diffuse thickening of n. trunk)
Lisch nodule (hamartoma located in iris)

60
Q

Complications of neurofibromas

A 
scoliosis
learning disabilities
HTN (renal artery stenosis)
d/o's of the hypothalamus
tumors- brain, eye
61
Q

neurofibromatosis type 2

A 
bilateral acoustic neuroma
unilateral 8th nerve mass
neurofibroma
meningioma
glioma
Schwannoma
juvenile posterior subcapsular lenticular opacities
62
Q

Tuberous sclerosis

A

AD (autosomal dominant) d/o characterized by proliferation of tubers from abnormal production of protein hamartin & tuberin

63
Q

Clinical manifestations of tuberous sclerosis

A

may present w/ seizures (infantile spasms)
calcified tubers in periventricular areas
mental retardation
hypopigmented skin lesions
ash leaf macules
shagreen patch
adenoma sebaceum
subungual/ periungual fibroma: commonly appear during adolescence

64
Q

ash leaf spot

A

hypopigmented macule/patch

Wood’s lamp highlights appearance

65
Q

shagreen patch

A

roughened, raised lesion w/ an orange peel, leathery texture

often located in lumbosacral region

66
Q

sebaceous adenomas

A

tiny, red, hyperpigmented nodules over the nose & cheeks

67
Q

Sturge-Weber dz

A

anomalous development of the vascular bed during early cerebral vascularization.
overlying leptomeninges richly vascularized & the brain beneath becomes atrophic & calcified

68
Q

Clinical manifestations of sturge-weber dz

A 
facial nevus (port-wine stain)
seizures
mental retardation
intracranial calcifications
hemiparesis
69
Q

CT scan findings of Sturge-Weber dz

A

cerebral atrophy

intracranial calcifications

70
Q

Guillain-Barre Syndrome
m>f
all ages, but rarely < 2 yo

A

acute idiopathic acquired inflammatory demyelinating polyradiculoneuropathy
d/o is thought to result from a post-infectious immune mediated process that predominantly affects motor nerves

71
Q

Pathophys of Guillain-Barre syndrome

A

most likely grouping of d/o’s w/ peripheral n. demyelination as a common mechanism mediated by humoral factors & cell mediated phenomenon

72
Q

In 2/3s of cases Guillain-Barre syndrome occurs after infxn with…

A 
Campylobacter sp
CMV, EBV
Haemophilus influenzae
Mycoplasma pneumoniae
viruses
73
Q

Clinical manifestations of Guillain-Barre syndrome

A 
fine paresthesias & tingling of toes & fingertips
pain may be prominent feature
ascending weakness/paralysis
   LE symmetric weakness
   ascends to arms & cranial nerves
74
Q

Guillain-Barre syndrome exam

A 
diminshed/absent DTR
paralytic ileus
poor respiratory effort
bladder dysfunction
autonomic dysregulation
   HTN, HoTN, tachycardia/bradycardia, 
   abnormal sweating
75
Q

Dx of Guillain-Barre Syndrome

A

electrophysiologic studies
mildly elevated ESR
CSF
elevated protein

76
Q

Tx of Guillain-Barre Syndrome

A

IVIG
plasmapheresis
physical therapy
watch for complications: respiratory failure, nutrition, autonomic disturbance

77
Q

transverse myelitis

A 
inflammation of the spinal cord w/ perivascular cuffing by lymphocytes
thought to have immunologic basis
pathogenesis (proposed)
   cell mediated immune response
   direct invasion of the spinal cord
   autoimmune vasculitis
78
Q

Clinical manifestations of transverse myelitis

A

BACK PAIN AT LEVEL OF LESION
ABRUPT ONSET of progressive weakness; legs weak & flaccid
areflexia
sensory disturbances in LE’s below level of spinal lesion
hx of preceding viral infxn
sphincter disturbances

79
Q

Lab findings in transverse myelitis

A 
lumbar puncture- non specific
   increased protein
   pleocytosis w/ lymphocytes
MRI (often diagnostic)
   dwelling of area of spinal cord
EMG
   normal early in dz
   may show denervation at level of lesion
80
Q

Tx of transverse myelitis

A 
meds (controversial benefit)
   corticosteroids
   IVIG
   plasmapheresis
supportive care
   physical therapy
81
Q

infant botulism

A

acute, flaccid paralytic illness caused by the neurotoxin produced by soil orgnaism Clostridium botulinum
95% of cases between 3 wks & 6 mo of age
almost 1/2 of cases are from CA

82
Q

Clostridium botulinum

A

gram + spore forming anaerobe
found in fresh & cooked agricultural products
botulinum toxin is heat labile

83
Q

forms of botulism

A

wound
food-borne
infantile

84
Q

botulism pathogenesis

A

toxin carried by blood to peripheral cholinergic synapses
binds irreversibly, blocking Ach release & causing impaired neuromuscular & autonomic transmission
loss of motor endplate function
recovery requires re-growth of terminal unmyelinated motor neurons

85
Q

Infantile botulism clinical signs

A 
symmetric, descending paralysis
cranial nerve palsies
   poor feeding
   weak suck
   feeble cry
   ptosis
   obstructive apnea
86
Q

lab confirmation of infant botulism

A

detection in serum
detection of C. botulinum in feces
CSF normal
EMG defect in neuromuscular transmission

87
Q

tx of infant botulism

A 
supportive care
   tube enteral feeding
   respiratory support
      positioning to avoid aspiration
      mechanical ventilation
botulism immune globulin (BIG)
   reduces duration of illness if given early
88
Q

tics

A

quick, repetitive, irregular, briefly suppressible movements
-facial: blinking, grimaces, twitches
-trunk & extremities: twisting, flinging
usu. last 1 mo-1yr
stress/anxiety tend to increase the amt of tics

89
Q

Tx of tics

A

teach parents natural hx
disregard
monitor for co-morbidities: school problems, ADHD, OCD, sleep difficulties

90
Q

Tourette’s syndrome is not d/t

A

direct physiological effects or a substance or a general medical condition

91
Q

Diagnostic Criteria for Tourette’s syndrome

A
  • tics occur many times a day (bouts) nearly q day/intermittently throughout a period of >1 yr (never a tic free period of >1 yr; never a tic free period of >3 consecutive mo)
  • multiple motor & 1+ vocal tics present at some time
  • onset before 18yo
92
Q

Tx of Tourette’s syndrome

A

non-pharm: counseling, adjustment of school & family members

-meds: haloperidol, fluoxetine, clonidine

93
Q

spinal muscular atrophy (SMA) types I, II, III

A

group of d/o’s characterized by degeneration of motor neurons w/ compensation from re-innervation of an adjacent motor unit
upper motor neurons NOT involved

94
Q

SMA type I

Werdnig-Hoffman dz clinical manifestations

A 
severe hypotonia
generalized weakness
thin muscle mass
involvement of the tongue (fasciculations)
perservation of extraocular muscles
95
Q

Labratory Dx of Werdnig-Hoffman dz (SMA type I)

A

serum CK may be mildly elevated (different from muscular dystorphy)
muscle bx- areas of atrophy, adjacent areas of hypertrophy
molecular genetic dx

96
Q

Tx of Werdnig-Hoffman dz (SMA type I)

A 
no tx to delay progression
funtional aids in type II or type III
supportive care
   feeding NG feeds
   respiratory support
      O2
      pulmonary toilet
97
Q

microcephaly

A

head circumference more than 2 std deviations below the mean for age

98
Q

macrocephaly

A

HC > 2 std deviations above the mean for age

99
Q

DDx for microcephaly

A 
chromosomal d/o (trisomy 13, 18, 21)
non-chromosomal genetic d/o
congenital malformation
placental insufficiency
perinatal hypoxia/trauma
metabolic
degenerative dz (Krabbe, Tay-Sachs)
toxins (fetal alcohol syndrome, meds, maternal PKU)
infxns (TORCH, toxoplasmosis, rubella, CMV, herpes, HIV)
radiation
familial
100
Q

DDx for macrocephaly

A

pseudomacrocephaly
increased ICP (w/ dilated ventricles-hydrocephalus, with mass effect-tumor, arachnoid cyst, porencephalic cyst)
benign familial macrocephaly
megalencephaly (large brain)- neurocutaneous d/o, gigantism, metabolic d/o, lysosomal storage dz, leukodystrophy- progressive white matter degeneration
thickened skull

Peds-Final (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions