Embryology of CNS & PNS Flashcards

1
Q

developing egg

A

oocyte

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2
Q

cellular process that replicates chromosomes and produces two identical nuclei in preparation for cell division

A

mitosis

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3
Q

gastrulation

A

formation of germ layers

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4
Q

formation of endoderm and ectoderm

A

by 2nd week

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5
Q

mesoderm bw/ ect and end

A

by 3rd week

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6
Q

future center where the sc and bs line up

A

notocord

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7
Q

where does the CNS form from

A

neural fold, deepens and pinches off form the outside

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8
Q

what is the neural fold made of

A

tube of ectoderm

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9
Q

creates the outer skin layers, nervous system and sense organs

A

ectoderm

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10
Q

are the outer and inner ear made of ectoderm?

A

YES

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11
Q

Makes skeletal structures, circulatory structures, meninges, notochord, reproductive organs and cartilage

A

mesoderm

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12
Q

what are the ossicles and temporal bone made of

A

mesoderm

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13
Q

what do we have in avs that uses air?

A

ET (air to nasopharynx), middle ear and mastoid air cells
air filled spaces for tubes related to our ear come from endoderm

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14
Q

makes the digestive canal and respiratory organs (viscera)

A

endoderm

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15
Q

what are the middle ear, mastoid cavities and ET made of?

A

endoderm

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16
Q

can genetic issues only affect one germ layer and not the others

A

yes

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17
Q

when is it called an embryo

A

first 8 weeks

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18
Q

when does it turn to a fetus

A

when it forms human type shape

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19
Q

what occurs in the 3rd week of CNS development

A

ectoderm neural placode, folds, then groove at dorsal midline

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20
Q

how does the neural tube fuse?

A

zips in both caudal and rostral directions

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21
Q

which end of the neural tube fuses first

A

rostral does 2 days before caudal

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22
Q

what is the superior opening of the neural tube

A

cranial/rostral neuropore

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23
Q

what is the inferior opening of the neural tube

A

caudal neuropore

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24
Q

crest cells left behind by each neural fold makes

A

form things in PNS (sensory neurons of dorsal root ganglia, some CN’s, schwann cells, etc.)

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25
what are ectodermal placodes
specialized regions of cranial ectoderm that create special sense organs and majority of the sensory neurons in the head
26
separates the neural tube into dorsal half and ventral half
sulcus limitans
27
primarily sensory
alar/dorsal plate (dorsal horns)
28
derivatives are motor
basal/ventral plate (ventral horns)
29
do alar and basal separation continue in the BS?
yes
30
sensory area of skin supplied by a single afferent spinal nerve and by afferents of cranial nerve V
dermatome
31
failure of caudal neuropore to close
spina bifida
32
spina bifida can lose
sensory and motor function at and below level of lesion
33
what is the least severe type of SB
Oculta
34
this SB is marked with a tuft of hair over it
oculta
35
is SB Oculta protected?
no, vertebrae is not covering the area just skin
36
which sb has meninges that protrude out in a saclike cavity over the defect
SB Meningocele
37
bulge of csf and dura in this SB
meningocele
38
sc and meninges protrude out in a saclike cavity over the defect
myelomeningocele sb
39
what is the difference between myelomeningocele and meningocele sb?
there is a larger gap b/w vertebrae, more CSF and dura present in the saclike cavity and the sc is also in it
40
which SB do we see the most deficit in motor and sensory function?
myelomeningocele because because they don’t transmit info properly and can get very damage being outside of the bony cavity
41
what can prevent sb?
diet and health of mom, no toxicity
42
what accomponies myelomeningocele?
arnold-chiari malformation
43
Herniation of cerebellum and caudal brainstem through the foramen magnum and may obstruct the flow of cerebrospinal fluid, producing hydrocephalus.
arnold-chiari malformation
44
what is the opening between the skin and meninges?
dural sinus, can be surgically repaired
45
how does crania bifida form
when rostral neuropore fails to close
46
can crania bifida children survive?
no, not conducive for post natal life
47
a result of this is anencephaly
crania bifida
48
are we able to detect and prevent neural deficits?
dietary supplements can reduce cases of SB and crania bifida we can detect neural tube defects through ultrasound or other prenatal tests Sufficient folic acid is needed in the maternal diet
49
this can occur before women know they are pregnant
neurulation (formation of nervous system)
50
where future bs meets future sc
cervical flexure
51
at level of future midbrain, remains as bend bw axis of brainstem and axis of cerebrum in adult CNS
cephalic flexure
52
on poster/dorsal surface in area of pons and 4th ventricle
pontine flexure
53
forebrain
prosencephalon
54
encephalon
brain
55
what are the divisions of prosencephalon
telencephalon & diencephalon
56
cerebrum/cerebral hemispheres & lateral ventricles
telencephalon
57
thalamus and surroundings and 3rd ventricle
diencephalon
58
midbrain and cerebral acqueduct
mesencephalon
59
hindbrain
rhombencephalon
60
what are divisions of thombencephalon
metencephalon and myelencephalon
61
cerebellum and pons and part of 4th ventricle
metencephalon
62
medulla and part of 4th and central canal
myelencephalon
63
no brain
anencephaly
64
how are ventricles formed
by the cavity of the neural tube
65
abnormality of cns with partial/incomplete development of prosencephalon (forebrain) and there is no separation of R and L diencephalon and telencephalon structures
holoprosencephaly
66
single midline eye abnormality
holoprosencephaly
67
is holoprosencephaly fatal?
yes
68
what is the nervous system highly impacted by
genetic changes
69
what percent do diseases increase to if neuromuscular system, eyes and ears are included
80-90%
70
single mutant gene it is transmitted from one or two people to the offspring
monogenic disorder
71
single mutant gene and there is an outside of the body environmental factor exogenous environmental factors
mutlifactorial disorder
72
Excess, lack or structural alteration of one or more of the 23 pairs of chromosomes - e.g., Down syndrome (trisomy 21)
nonmendelian chromosomal aberrations
73
alteration in mitochondrial DNA - nonmendelian; mainly maternal transmission - affects enzymes of mitochondria
mitochondrial transmission of disease
74
how do newborns nervous systems function
at the brainstem-spinal level higher centers are not yet myelinated
75
what functions do we monitor in infants?
control of respiration control of body temp regulation of thirst, fluid balance and appetite
76
what are examples of drive related behaviors
rooting, sucking, swallowing, grasping etc.
77
describe the moro reflex
called a startle reflex because it usually occurs when a baby is startled by a loud sound or movement. In response to the sound, the baby throws back his/her head, throws out his/her arms and legs, cries, then pulls his/her arms and legs back in. Sometimes, a baby's own cries can startle him/her - initiating this reflex. The Moro reflex lasts until the baby is about 5 to 6 months old
78
inability to break down ganglioside which accumulates in neurons causing them to swell, burst lysosomal storage disease
tay sachs disease
79
inability to break down sphingomyelin which accumulates in neurons causing them to swell & burst
neimann pick disease type a
80
list some symptoms of NPD Type A
seizures, hypersensitivity to touch, sudden loss of muscle tone, progressive loss of early motor skills
81
what is the survival rate for NPD T-A
death by 2-4 yrs
82
inability to metabolize cholesterol and other lipids properly * excessive lipids in the brain
NPD T-C
83
what is the survival rate for NPD T-C
mid to late teens
84
signs of NPD T-C
learning difficulties and progressive dementia seizures tremors
85
inability to metabolize phenylalanine
phenylketonuria
86
what is the survival rate of hurler syndrome
early teens due to heart disease
87
damage of hear valves and heart murmurs are common
hurler syndrome
88
is there treatment for neonatal metabolic diseases?
dietary restriction of specific amino acids * oral supplementation of specific vitamins * bone marrow transplant to supply stem cells to make missing enzyme/s
89
what is the importance or difficulty with genetic metabolic disorders? Or what makes them so severe and hard to treat?
because their at the cellular level where something like the lysosomes dont have the right enzymes to to break things down and as cells die and they cannot be replaced fast enough causing function to decrease to the point of usually not a full life past childhood.