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Neurological Diseases Exam > Lec 18 - SIDS > Flashcards

Lec 18 - SIDS Flashcards

1
Q

What’s the definition of SIDS

A

1989 - sudden death of infant <1, + associated with sleep unexplained after autopsy, exam of circumstances of death + clinical history review
heterogeneous entity w/characteristic epi + clin features + diverse etiological pathways

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2
Q

characterisitics of SIDS babies

A

0.5-.4/1000 live births
low SES
male
premature (low birth weight)
winter

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3
Q

characteristics of SIDS mums

A

single
smoker
high parity w/short inter-pregnancy intervals
infection in pregnancy

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4
Q

what is the respiratoy theories of SIDS

A

apparent life-threatening events
apnea > 20 seconds, cyanosis, near miss

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5
Q

what is central apnea

A

failure of inspiration
- prematurity
- seizure induced
- rem sleep

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6
Q

why does central apnea occur

A

defective:
- brainstem centres
- defective chemoreceptors
- defective stretch receptors

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7
Q

what is obstructive apnea + evidence

A

normal occurrence eg smothering -> airway blockage
small choanae
large tongue
small mandible
lack of positive distending pressure

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8
Q

what is accidental asphyxia

A

wedging
overlaying
plastic covers
water beds

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9
Q

describe gastroesophageal reflux 1

A

acid -> eso -> chemoreceptors -> brainstem -> apnea

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10
Q

describe gastroesophageal reflux II

A

acid -> bronchus -> type II pneumocyte damage -> reduced surfactant -> atelectasis -> apnea

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11
Q

describe gastroesophageal reflux III

A

acid -> eso -> chemoreceptors -> brainstem -> bradycardia

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12
Q

what are cardiac theories with SIDS

A

abberant conduction pathways
prolonged QT interval
abnormal response to autonomic control

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13
Q

what is the problem with determining cardiac theories in SIDS

A

no antemortem ECGs
lack of histologic abnormalities

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14
Q

role of infection in SIDS

A

occult infection causes or predisposes
clostridium botulinum - can cause sudden infant death but not related to SIDS
cytomegalovirus - not a problem
avon study - no difference in infection type

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15
Q

immunological hyper-reactivity in SIDS

A

house dust mites, cow’s milk protein?
no consistent findings

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16
Q

breast feeding in SIDS

A

protective = reduced DHA, inc neural maturation

17
Q

tripe risk model for SIDS

A

critical developnment period + exogenous stressors + vulnerable infant
shared sleeping = infant (young, small, premature) + parent (sedated, intoxicated, smoking, obese) + bed (multiple cosleepers, heavy covers, soft surface) some babies will die

18
Q

risk factors for SIDS

A

prone sleeping - face-down, 9x risk, airway obstruct, diaphragm splinting, reinhaling co2
cig smoke
covering head
overheating

19
Q

when does peak SIDS incidence coincide

A

with marked physiological changes in neural control of respiration, cardiac function and sleep cycles
=> generalised arousal deficit

20
Q

what are neuropath findings in SIDS

A

brainstem gliosis
arcuate nucleus receptor changes
inc neuronal dendritic spines
abnormal carotid bodies

21
Q

impact of neuropath findings

A

defective
- autonomic control
- brainstem respiratory control centres
- brainstem cardiac cc
- peripheral pulm rec
- vagal dysf
- chemo rec dysf
- arousal/sleep disturbance
- hyperpyrexia
- abnormal ntsm + brainstem receptors

22
Q

describe brainstem gliosis

A

17% cases
tegmental region in medulla, dorsal nucleus of vagus, inferior olivary nucleus, solitary nucleus, reticular nuclei
angiography - underperfused areas

23
Q

describe dendritic spines in SIDS

A

inc dendritic spines in brainstem neurons
maturational delay
effects cardiorespiratory control

24
Q

hypomyelination in SIDS

A

variable results => dec in SIDS
hypo or delayed myelination?
what is significance?

25
Q

describe decosahexenoic acid in SIDS

A

dec in SIDS
DHA related to cerebral maturation
demonstrated dec cortical levels in some SIDS infants

26
Q

arcuate nucleus hypoplasia

A

reduced size in some SIDS infants
possible cardiorespiratory effect

27
Q

ntsm abnormalities in SIDS

A

defects in medullary serotonergic network
reduced muscarininc, kainate, serotingergic receptor binding
defects in promotor region of serotonin transporter 5-HTT gene
failure to respond to autonomic challenges during sleep

28
Q

what does substance P do

A

SP is a tachykinin neuropeptide - excit + mod ntsm via tachykinin NK1R (co-transmitter with 5HT)
stim respiration
primary ntsm in carotid chemoreceptor reflex
mediates ventilatory responses

29
Q

describe role of Nk1 receptor + the relevant study

A

respiratory rhythm generation
maintenance of respiratory timing during sustatined hypoxia
arcuate nuecleus from formalin fixed paraffin stained for sub P and NK1 rec
dec in sub P immunoreactivity in arcuate nucleus in SIDS

30
Q

aim and hypothesis of bolton hunter sub p autoradiography

A

determination of NK1R binding density with sub p autoradiography in medullary 5HT system in SIDS vs controls
hypothesis: NK1R binding densirt will dec in brainstem medullary 5HT for SIDS

31
Q

what is the inferior olivary complex (IoC)

A

defecits in cerebellar systems, purkinje fiber damage, ntsm defecits in IOC = associated with SIDS
IOC - integration motor + sensory info, motor learning, control, coordination
subdivisions DAO + MAO project to diff regions cerebellum
MAO => vermis => propioception, sense spatial/positional mbm neck, shoulders, hips

32
Q

link between IOC and SIDS

A

reduction in NK1R density in DAO and MAO
neg influence on cerebellar circuitary + motor control in SIDS infants

33
Q

inc brain weight and SIDS suggestions for cause

A

cerebral swelling/oedema
agonal hypoxia/ischaemia
metabolic/toxic
megalencephaly
agonal/vascular congestion

34
Q

what is B-amyloid precursor protein

A

transmembrane glycoprotein in axons
nonspecific marker for axonal injury
hypoxia, trauma, ischaemia, toxins

35
Q

why is BAPP significnat

A

lots means difficulty control respiration => low O2 saturation
potential marker for familial central apnea
SIDS and asphyxia have similar BAPP staining patterns

Neurological Diseases Exam (14 decks)

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