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AUDE 5260 Human Anatomy & Neuroanatomy > Embryology of CNS & PNS > Flashcards

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
Q

what are ectodermal placodes

A

specialized regions of cranial ectoderm that create special sense organs and majority of the sensory neurons in the head

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26
Q

separates the neural tube into dorsal half and ventral half

A

sulcus limitans

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27
Q

primarily sensory

A

alar/dorsal plate (dorsal horns)

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28
Q

derivatives are motor

A

basal/ventral plate (ventral horns)

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29
Q

do alar and basal separation continue in the BS?

A

yes

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30
Q

sensory area of skin supplied by a single afferent spinal nerve and by afferents of cranial nerve V

A

dermatome

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31
Q

failure of caudal neuropore to close

A

spina bifida

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32
Q

spina bifida can lose

A

sensory and motor function at and below level of lesion

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33
Q

what is the least severe type of SB

A

Oculta

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34
Q

this SB is marked with a tuft of hair over it

A

oculta

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35
Q

is SB Oculta protected?

A

no, vertebrae is not covering the area just skin

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36
Q

which sb has meninges that protrude out in a saclike cavity over the defect

A

SB Meningocele

37
Q

bulge of csf and dura in this SB

A

meningocele

38
Q

sc and meninges protrude out in a saclike cavity over the defect

A

myelomeningocele sb

39
Q

what is the difference between myelomeningocele and meningocele sb?

A

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
Q

which SB do we see the most deficit in motor and sensory function?

A

myelomeningocele because because they don’t transmit info properly and can get very damage being outside of the bony cavity

41
Q

what can prevent sb?

A

diet and health of mom, no toxicity

42
Q

what accomponies myelomeningocele?

A

arnold-chiari malformation

43
Q

Herniation of cerebellum and caudal brainstem through the foramen magnum and may obstruct the flow of cerebrospinal fluid, producing hydrocephalus.

A

arnold-chiari malformation

44
Q

what is the opening between the skin and meninges?

A

dural sinus, can be surgically repaired

45
Q

how does crania bifida form

A

when rostral neuropore fails to close

46
Q

can crania bifida children survive?

A

no, not conducive for post natal life

47
Q

a result of this is anencephaly

A

crania bifida

48
Q

are we able to detect and prevent neural deficits?

A

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
Q

this can occur before women know they are pregnant

A

neurulation (formation of nervous system)

50
Q

where future bs meets future sc

A

cervical flexure

51
Q

at level of future midbrain, remains as bend bw axis of brainstem and axis of cerebrum in adult CNS

A

cephalic flexure

52
Q

on poster/dorsal surface in area of pons and 4th ventricle

A

pontine flexure

53
Q

forebrain

A

prosencephalon

54
Q

encephalon

A

brain

55
Q

what are the divisions of prosencephalon

A

telencephalon & diencephalon

56
Q

cerebrum/cerebral hemispheres & lateral ventricles

A

telencephalon

57
Q

thalamus and surroundings and 3rd ventricle

A

diencephalon

58
Q

midbrain and cerebral acqueduct

A

mesencephalon

59
Q

hindbrain

A

rhombencephalon

60
Q

what are divisions of thombencephalon

A

metencephalon and myelencephalon

61
Q

cerebellum and pons and part of 4th ventricle

A

metencephalon

62
Q

medulla and part of 4th and central canal

A

myelencephalon

63
Q

no brain

A

anencephaly

64
Q

how are ventricles formed

A

by the cavity of the neural tube

65
Q

abnormality of cns with partial/incomplete development of prosencephalon (forebrain) and there is no separation of R and L diencephalon and telencephalon structures

A

holoprosencephaly

66
Q

single midline eye abnormality

A

holoprosencephaly

67
Q

is holoprosencephaly fatal?

A

yes

68
Q

what is the nervous system highly impacted by

A

genetic changes

69
Q

what percent do diseases increase to if neuromuscular system, eyes and ears are included

A

80-90%

70
Q

single mutant gene
it is transmitted from one or two people to the offspring

A

monogenic disorder

71
Q

single mutant gene and there is an outside of the body environmental factor
exogenous environmental factors

A

mutlifactorial disorder

72
Q

Excess, lack or structural alteration of one or more of the 23 pairs of chromosomes
- e.g., Down syndrome (trisomy 21)

A

nonmendelian chromosomal aberrations

73
Q

alteration in mitochondrial DNA
- nonmendelian; mainly maternal transmission
- affects enzymes of mitochondria

A

mitochondrial transmission of disease

74
Q

how do newborns nervous systems function

A

at the brainstem-spinal level
higher centers are not yet myelinated

75
Q

what functions do we monitor in infants?

A

control of respiration
control of body temp
regulation of thirst, fluid balance and appetite

76
Q

what are examples of drive related behaviors

A

rooting, sucking, swallowing, grasping etc.

77
Q

describe the moro reflex

A

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
Q

inability to break down ganglioside which accumulates in neurons causing them to swell, burst
lysosomal storage disease

A

tay sachs disease

79
Q

inability to break down sphingomyelin which accumulates in neurons causing them to swell & burst

A

neimann pick disease type a

80
Q

list some symptoms of NPD Type A

A

seizures, hypersensitivity to touch, sudden loss of muscle tone, progressive loss of early motor skills

81
Q

what is the survival rate for NPD T-A

A

death by 2-4 yrs

82
Q

inability to metabolize cholesterol and other lipids properly
* excessive lipids in the brain

A

NPD T-C

83
Q

what is the survival rate for NPD T-C

A

mid to late teens

84
Q

signs of NPD T-C

A

learning difficulties and progressive dementia
seizures
tremors

85
Q

inability to metabolize phenylalanine

A

phenylketonuria

86
Q

what is the survival rate of hurler syndrome

A

early teens due to heart disease

87
Q

damage of hear valves and heart murmurs are common

A

hurler syndrome

88
Q

is there treatment for neonatal metabolic diseases?

A

dietary restriction of specific amino acids
* oral supplementation of specific vitamins
* bone marrow transplant to supply stem cells to make missing enzyme/s

89
Q

what is the importance or difficulty with genetic metabolic disorders?
Or what makes them so severe and hard to treat?

A

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.

AUDE 5260 Human Anatomy & Neuroanatomy (24 decks)

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