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פידס > Embryology > Flashcards

Embryology Flashcards

1
Q

when most susceptible to organ damage

A

3-8 weeks

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2
Q

congenital scoliosis, why susceptible to cardiac defects?

A

mesoderm

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3
Q

neural tube gives rise to ____

A

forms the CNS

hindbrain to S2

closes cranial to caudal day 28

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4
Q

syndactyly

A

bc not have the programmed cell death at APICAL RIDGE

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5
Q

congenital scoliosis

A
  1. formation failure (hemivertebrae or wedged vertebrae)

2. segmentation failure (dont separate)

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6
Q

scleretomes

form what?

A

come together to give rise to the vertebrae

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7
Q

what is

VACTERL

A

congenital spinal deformities may coexist with a syndrome such as VACTERL ( non-random co-occurrence of birth defects)

Vertebral anomalies
Anal atresia
Cardiac defects
 Tracheoesophageal fistula and/or 
Esophageal atresia
Renal 
Limb defects.
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8
Q

Pre-embryonic

when
what happens

A

first 3 weeks

fertilization to implantation, placenta formation

(dont know pregnant)

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9
Q

Embryonic

when
what happens

A

Week 3-8

organogenesis: organs develop

since new structures are developing rapidly the embryo is extremely vulnerable

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10
Q

Fetal Period

when
what happens

A

Week 8-40

maturation and growth of all structures and organs

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11
Q

Gastrulation

A

WEEK 3: cell division occurs

Trilaminar layer: 3 primary germ layers are formed

  1. Ectoderm: skin, CNS, Cranial nerves, sensory nerves, teeth
  2. Mesoderm: bone, muscle, connective tissue, blood vessels, cardiac, urogenital system
    * coexistance of congenital spine and cardiac and kidney defects with congenital bone defects
  3. Endoderm: GI, respiratory
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12
Q

Exctoderm

A

GASTRULATION: week 3

skin
CNS
sensory nerves
cranial nerves
teeth
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13
Q

Mesoderm

A

GASTRULATION: week 3

bone
connective tissue
muscles
blood vessels

kidney
cardiovascular

*co-existence of congenital spine and cardiac and kidney defects with congenital bone defects

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14
Q

Endoderm

A

GASTRULATION: week 3

Digestive
Respiratory

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15
Q

Neurulation

A

complete in 4 weeks

Neural plate: ectodermal cells thicken forming the neural plate

Neural Tube: neural plate folds forming the neural tube

Neural Crest: cells separate from the neural folds and they form the neural crest

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16
Q

Neural plate:

A

ECTODERM cells thicken forming the neural plate

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17
Q

Neural Tube

A

neural plate folds forming the neural tube

FORMS THE CNS: extends from hindbrain to S2

closes in cranial to caudal direction by DAY 28

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18
Q

Neural Crest

A

cells separate from the neural folds and they form the neural crest

FORMS PNS

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19
Q

When does neural tube close

A

closes in cranial to caudal direction by DAY 28

forms CNS, extends from hindbrain to S2

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20
Q

what forms CNS?

A

neural tube

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21
Q

what forms PNS?

A

neural crest

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22
Q

Anencephaly

A

failure of the neural tube to close cranial side

NTD

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23
Q

Spinal Bifida

A

failure of neural tube to close caudual side

thoracic or lumbar region

NTD

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24
Q

Causes of NTD

A
  1. genetic: siblings of patients with spina bifida have increased incidence of NTD
  2. nutritional: folic acid taken before/after conception reduce incidence
  3. environment: certain drugs increase risk of NTD
    - -valproic acid (anticonvulsant) causes NTD in 1%-2% of pregnant women, if given in fourth week of development when neural folds are fusing
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25
Q

NTD genetic

A

genetic: siblings of patients with spina bifida have increased incidence of NTD

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26
Q

NTD nutrition

A

genetic: siblings of patients with spina bifida have increased incidence of NTD

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27
Q

NTD environment

A

environment: certain drugs increase risk of NTD

–valproic acid (anticonvulsant) causes NTD in 1%-2% of pregnant women, if given in FOURTH WEEK of development when NEURAL FOLDS ARE FUSING

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28
Q

Endochondral ossification

A

long bone development from hyaline cartilage

*mesoderm–>mesenchymal cells–>differentiate into chondrocytes

the chondrocytes secrete collagen –form the hyaline cartilagenous embryonic skeleton

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29
Q

Appendicular Skeletal Formation

Primary Ossification Center

DIAPHYSIS

A

(chondroyctes form from the mesenchymal cells from the mesoderm)

1) chondrocytes proliferate, hypertrophy, synthesize alkaline phosphatase–>
2) this calcifies which inhibits nutrients to the chondrocytes–>
3) as a result the chondrocytes undergo APOPTOSIS–this leaves cavities for blood vessels and osteoblast invasion –>
4) osteoblasts invade causing OSTEOGENESIS!!!

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30
Q

Appendicular Skeletal Formation

Secondary Ossification Center

located at epiphyseal plate “growth plate”

A

cartilage plate separating epiphysis from diaphysis

endochondral ossification causing longitudinal bone growth

vulnerable for fracture

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31
Q

Appendicular Development

limb buds week 4

A

early stage of limb development

UPPER LIMBS grow first, lower follow two days later

APICAL ECTODERMAL RIDGE (AER) at the apex of each bud: secretes fibroblast growth factor which induces the limbs to grow

Growth occurs PROXIMAL–> DISTAL

32
Q

APICAL ECTODERMAL RIDGE

AER

A

early stage of limb development

at the apex of each bud: secretes fibroblast growth factor which induces the limbs to grow

UPPER LIMBS grow first, lower follow two days later

Growth occurs PROXIMAL–> DISTAL

33
Q

Appendicular Development

limb buds week 6

A

distal end forms a paddle like structure

Apoptosis forms space between the digits: fingers and toes are formed

34
Q

syndactyly

A

webbed fingers/toes

most common limb anomaly

webbing or fusion of fingers/toes if apoptosis doesn’t occur

35
Q

Limb bud development

What happens if there is a disturbance

4th week

A

absent limb formation

36
Q

Limb bud development

What happens if there is a disturbance

5th week

A

partial limb formed

37
Q

Limb bud development

What happens if there is a disturbance

8th week

A

after 8 weeks teratogens can not cause major limb deficiencies

38
Q

Achondroplasia

genetic basis

A

autosomal dominant

FGFR3: new mutations short (p) arm on chromosome 4

FGFR3 limits osteogenesis: mutation increases this effect and LIMITS ENDOCHONDRAL OSSIFICATION
–FGFR interferes converting cartilage to bone (especially long bones)

70% of dwarfism

39
Q

Dwarfism

A

autosomal dominant

FGFR3: new mutations short (p) arm on chromosome 4 = achondroplasia

FGFR3 limits osteogenesis: mutation increases this effect and LIMITS ENDOCHONDRAL OSSIFICATION
–FGFR interferes converting cartilage to bone (especially long bones)

responsible for 70% of dwarfism

40
Q

Clinical manifestations of Achondroplasia

A

1) cuboid shaped verebrae can cause narrow spinal canal: CORD COMPRESSION
- -20-47% frequency in neurologic complications bc spinal abnormalities

2) spinal stenosis: thoracolumbar stenosis
3) lordosis kyphosis
4) tibia vara

Infants with hypotonia and transient kyphosis
—10-15% kyphosis becomes fixed

  • –discourage early unsupported sitting and consider bracing
  • –raise the surface up for them
  • –hydrocephalus in some cases
41
Q

What mutation limits endochondral ossification?

A

The primary function of FGFR3 is to limit osteogenesis. Mutation increases this effect and therefore limits endochondral ossification

42
Q

What to do for treatment

Infants with hypotonia and transient kyphosis

A

—10-15% kyphosis becomes fixed

—discourage early unsupported sitting and consider bracing

—raise the surface up for them

43
Q

Vertebral Column Development

A

1) MESODERM cells unite to form 42-44 pairs of SOMITES
2) Week 4: somites –> Sclerotomes, myotomes, dermatomes
3) Sclerotomes migrate ventromedially on each side of the notochord to form vertebral bodies
4) vertebral bodies formed from cranial and caudal sclerotome: the union of cells from 2 adjacent scleretomes

*nucleus pulposus
notochord formed from the mesoderm cells degenerates
—>remnants of the notochord become the nucleus pulposus

*annulus fibrosis
scleretome cells form the annulus fibrosis

*vertebral arch:
vertebral body sclerotomes migrate dorsally around the neural tube to form the vertebral arch

ENDOCHONDRAL OSSIFICATION OCCURS

44
Q

nucleus pulposus

A

notochord formed from the mesoderm cells degenerates

—>remnants of the notochord become the nucleus pulposus

45
Q

vertebral arch:

A

vertebral body sclerotomes migrate dorsally around the neural tube to form the vertebral arch

46
Q

annulus fibrosis

A

scleretome cells form the annulus fibrosis

47
Q

Vertebral Anomalies

A
  1. formation failure
  2. segmentation failure
    mixed: combination of both
48
Q

Vertebral formation defects

–what are they

–cause

–types of defects

A

absence of a structural vertebral element resulting in a mis-shaped vertebrae

cause: inadequate blood supply to vertebral bodies

types of defects:
1. wedged vertebrae: unilateral partial failure of vertebral formation

  1. hemivertibrae: 1/2 vertebrae is absent
49
Q

Types of vertebral formation failure defects

A

will develop scoliosis from these!!!

  1. wedged vertebrae: unilateral partial failure of vertebral formation
  2. hemivertibrae: half of the vertebrae is absent
50
Q

Vertebral Segmentation Defects

A

Vertebra do not separate properly:
produce a bar with no growth plate or disk between vertebrae (need growth plate for the bone to lengthen)

–It is a failure of scleretome segmentation

–Segmentation failure causes the vertebra to be mis-shaped or it fuses to another vertebrae

Can develop a scoliosis
(or torticalis)

51
Q

what causes vertebral segmentation defects?

A

–It is a failure of scleretome segmentation (vertebrae therefore dont separate properly)

–Segmentation failure causes the vertebrae to be mis-shaped or it fuses to another vertebrae

52
Q

Congenital spinal deformities:

when?

causes?

A

WHEN: The failure of normal verebral development during the 4th - 6th week of gestation

CAUSES: of spinal malformation:
1) Neural tube defects

2) Vertebral formation failure
3) Segmentation failure: Vertebra do not separate properly

Location of the anaomaly on the vertebra determines the deformity
—–Lateral deformity-scoliosis most common

—–Anterior deformity-kyphosis

—–Posterior deformity: lordosis least common

  • —-Torticolis: If the defect is at the cervical or cervicothoracic region
  • -it is not just muscle issue here!!!!!
53
Q

Segmentation failure

Location of the anaomaly on the vertebra determines the deformity

A

—–Lateral deformity-scoliosis most common

—–Anterior deformity-kyphosis

—–Posterior deformity: lordosis least common

  • —-Torticolis: If the defect is at the cervical or cervicothoracic region
  • -it is not just muscle issue here!!!!!
54
Q

Congenital Scoliosis:

dx

signs of defect

A

fetal ultrasound can diagnosis it or may not be diagnosed until childhood

Signs of defect:
1) patch of hair

2) midline skin hemangioma
3) congenital heart defects
4) kidney defects
5) LLD (leg length discrepancy, mesoderm)

55
Q

what conditions can be associated with congenital spinal abnormality

A

Congenital spinal deformities may also be diagnosed during the workup of:

Either of these conditions can be associated with a congenital spinal abnormality:

Plagiocephally (flattening of the skull bones on one side) or

Torticollis: a tilted rotational position of the head

56
Q

Klippel-Feil Syndrome

A

****Segmentation failure (vertebra do not separate properly)
Congenital fusion of 2 or more cervical vertebrae

Classic clinical triad:
1) Low posterior hairline

2) Short neck
3) Cervical range of motion limitation seen in 40-50% of patients. The decrease in motion most commonly is in lateral bending and rotation

57
Q

VACTERL

A

congenital spinal deformity may co-exist with a syndrome

VACTERL association is a disorder that affects many body systems.

V= vertebral defects
A= anal atresia
C= cardiac defects
T= tracheo-esophageal fistula
R = renal anomalies
L= limb abnormalities.
58
Q

VACTERL

V

A

vertebral defects

59
Q

VACTERL

A

A

anal atresia

anus does not open to outside of the body

60
Q

VACTERL

C

A

cardiac defects

61
Q

VACTERL

T

A

tracheal abnormalities–tracheaoesophogeal fistula

62
Q

VACTERL

E

A

esophogeal atresia: esophagus does not connect to the stomach

63
Q

VACTERL

R

A

renal

64
Q

VACTERL

L

A

limb abnormalities

absent or displaced thumbs, extra fingers (polydactyly), fused fingers (syndactyly(, or a missing bone in the arm or legs

: absent or displaced thumbs, extra fingers (polydactyly) fused fingers (syndactyly), or a missing bone in the arms or legs

65
Q

Congenital Spinal Deformities

what other defects can also occur

A

Congenital heart defects occur in 30% of the patients:

a. Atrial or ventral septal defects
b. Patent Ductus Arteriosus
c. Tetrology of Fallot

Chest wall deformities: may present with multiple rib fusions, this chest wall restriction inhibits growth and development of the lungs

66
Q

Skull development

what happens

what doesnt it need

when does it occur

what happens if exposed to teratogens

A

1) Mesenchymal cells derived from NEURAL CREST and mesoderm cells encircle the brain and form the flat bones of the cranium

2) Interosseus Ossification:
Intramembranous Ossification: the mesenchyme cells differentiate directly into the osteocytes, without forming the hyaline cartilage model (DOES NOT NEED CHONDROCYTES, DOES NOT FORM HYALINE CARTILAGE!!!!)

3) 4-8 Weeks: (Note: Organ Genesis Period)
All major external and internal structures are established
By the end of this organogenetic period, all of the main organ systems have begun to develop

***Exposure of embryos to teratogens during this period may cause major congenital anomalies

67
Q

Teratogens:

what are they

what does vulnerabilty of fetus to teratogens depend on

A

Any agent affecting fetal development: birth defects

The vulnerability of the fetus to teratogens depends on:

1) Timing: Critical Periods when cellular differentiation and morphogenesis is at its peak
2) Magnitude—how much exposed to it
3) Duration of exposure
4) Ability to cross the placenta barrier

68
Q

Examples of teratogens:

A

***Drugs/chemicals

1) Alcohol: Fetal Alcohol Syndrome
2) Cocaine: prematurity congenital abnormalities

3) Prescribed drugs to threat the mother
Ie anticonvulsant: Valprocic acids = NTDs

***Infections: maternal infections that can be passed to the fetus
STORCH
•	S: syphilis
•	T: toxoplasmosis
•	O: other ie HIV
•	R: rubella
•	C: cytomegalovirus 
•	H: herpes
69
Q

STORCH

A
  • S: syphilis
  • T: toxoplasmosis
  • O: other ie HIV
  • R: rubella
  • C: cytomegalovirus
  • H: herpes

***Infections: maternal infections that can be passed to the fetus

70
Q

STORCH

S

A

syphilis

***Infections: maternal infections that can be passed to the fetus

71
Q

STORCH

T

A

taxoplasmosis

***Infections: maternal infections that can be passed to the fetus

72
Q

STORCH

O

A

other

ie hiv

***Infections: maternal infections that can be passed to the fetus

73
Q

STORCH

R

A

rubella

***Infections: maternal infections that can be passed to the fetus

74
Q

STORCH

C

A

cytomegalovirus

***Infections: maternal infections that can be passed to the fetus

75
Q

STORCH

H

A

herpes

***Infections: maternal infections that can be passed to the fetus

76
Q

Fetal Alcohol Syndrome:

A

10-20% of all cases of mental retardation

most common cause of non-genetic MR (mental retardation, the number one is Down’s syndrome)

GDD

Small size in weight in height before and after birth

Poor coordination

ADD/ADHD

Poor memory

Poor reasoning and judgment skills-FRONTAL LOBE DISORDER

Sleep and sucking problems as a baby-failure to thrive

Vision or hearing problems

Problems with the heart, kidney, or bones

Hypotonia

Learning disabilities

Speech and language delays

פידס (13 decks)

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