Embryology lecture 2 Flashcards

1
Q

Implantation

A
  • Second opportunity for cellular differentiation
  • 1.Trophoblast cells differentiate
    • Tropho means to feed , and will be its contribution to the placenta
  • 2.Embryoblast cells differentiate
    • Will be the embryo takes 6-7 days
    1. Two cavities form
      * synctiotrophoblast invade the enddometrium which is full of glucose and lipids , and get access to moms bloodstream
  • Make a cavity above the epiblast
  • In the 2nd week two layers in the inside and outside and two cavities
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2
Q

Extraembryonic(XE) Mesoderm

A
  • New layer of cells
  • Derived from epiblast(yolk sac)
  • found between inner lining of cytotrophoblast and yolk sac
  • continue to separate embryo from surrounding uterine tissue
  • New layer will be important in forming the materno-fetal interface(placenta)
  • Three layers on the inside and outside
  • add tissue outside the developing embryo,next to the cytotrophoblast
  • Put it subjacent to the cytotrophoblast
  • gives mechanical and trophic support
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3
Q

Why would an ultrasound be done in the first trimester?

A
  • Confirm a normal pregnancy
  • Determine the baby’s age
  • Look for problems such as ectopic pregnanices or the chance for a miscarriage
  • Determine the baby’s heart rate
  • Look for multiple pregnanices
  • Identify problems of hte placenta , uterus, cervix and ovaries
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4
Q

Embryonic Period

A
  • All major body systems develop
  • 2D disk to 3D cylinder
  • Folding of the embryo
  • Craniocaudal folding-CNS(occurs wehn head grows too quickly)
  • Lateral folding-annion/body wall
  • most important time is the first 3-8 weeks
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5
Q

Gastrulation

A
  • Beginning of morphogenesis(development of body form)
  • Forms a trilaminar embryonic disk
  • Process that establisehs the 3 primary germ layers endoderm, mesoderm, and ectoderm
    • These 3 layers give rise to all the tisseus and organs of the adult
  • Go from a two layer disk to a three layer disk which are your germ layers
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6
Q

Primitive streak

A
  • forms from the epiblast and creates the bakc end of hte embryo when it forms
  • Bucoopharyngeal membrane is where the mouth forms eventually
  • Future axis of embryo and marks beginning of gastrulation
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7
Q

Elongation of Primitive Streak

A
  • Forms from a proliferation of epiblast cells
  • Cells migrate to center of embryo
  • Streak elongates with cells added to caudal end
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8
Q

How do we get a notochord?

A

Primitive streak should regress and then replaced by a notochord​

  • forms in the middle fo the mesoderm
  • Migrating cells also form a median column of cells, posterior to head region
  • will becoem the notochord
  • also called chordamesoderm
  • take over the axis for the devloping embryo
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9
Q

Sacrococcygeal Teratoma

A
  • sometiems doesn’t regress and yo uget remenants of a primitive streak and get sacrococcylgeal teratoma
  • has derivative of the 3 germ layers
  • common in newborns and is a benign tumor
  • if there big enough and put a strain on the haer have to do something about the teratoma
  • Go in and uterine cavity and deliver the back end of hte baby and remove the teratoma ,put the baby back in and the babies do fine
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10
Q

Caudal Dysplasia

A
  • Germ layer disorder
  • Total or partial failure of development of the lower vertebrae, including the sacrum which results in assoicated abnormalities of the lower extremities, spine , kidneys gastrointestinal and genitourinary tracts
  • Also known as sacral agenesis , sacral regression,caudal aplasia , caudal regression sequence, sirenomelia
  • Caused by abnormal gastrulation
  • Mesoderm migration is disturbed
  • Maternal diabetes
  • In about 16% of cases
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11
Q

Classification of Caudal dysgenesis

A
  • 1.Caudal dysgenesis with complete absence of sacrum and lower vertebrae , multiple congenital anomalies, and association with maternal diabetes
  • 2.Agenesis of the distal sacral or coccygeal segments
  • 3.Hemiacral dysgenesis with presacral teratoma
  • 4.Hemisacral dysgenesis with anterior meningocele
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12
Q

Primitive Streak relates to bioethics

A
  • An important concept in bioethics,where some experts have argued that experimentation with human embryos is permissible but only before the primitive streak develops generally around 14th day of existence
  • Development of the primitive streak is taken by such bioethicists to signify the creation of a unique, human being
  • In some countries ,it is illegal to devlop a human embryo for more than 14 days outsdie a woman’s body
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13
Q

Functions of notochord

A
  • Structure-acts as a rigid axis around which the embryo develops
  • Skeletal- foundation upon which the vertebral column(vertebral bodies) will form
  • Forms part of the intervertebral discs
  • Induction-will bring about the formatino of hte neural tube(future nervous system)
  • nucleus pulposus is hte remnants of the notochord
  • the notochord will send out the frist signals to induce the formatino of the nervous system
  • Can get tumors of hte notochord , and develop from the embryonic remnants of hte notochord
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14
Q

What is a chordoma?

A
  • Primary malignant bone cancer
  • Origin:develops from remnants of embryonic notochord
  • Location:found in skull base(head) and spine
  • Incidence:1 per million per year about 300 new cases per year in US
  • Average age at diagnosis: 49 for skull base, 69 for spine
  • Age range:all ages
  • Averages survival:7 years
  • Gender distribution:affects men more frequently than women
  • Treatment options:primary sugery and radiation
  • Approved drugs:none
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15
Q

Clival Chordoma

A
  • Benign but invasive skull base tumors arise from bone and often grow through dura
    • causes problem because it compresses part of the brain
  • Most can be effectively dubulked through an endonasal approach. because of their invasiveness ,many require radiotherapy to control further growth
  • three examples of clival chordomas
  • Chordoma occurs when additional notochord cellsa re enclosed by developing bones
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16
Q

What forms the neural plate?

A
  • Notochord is the primar y inductor in the early embryo
  • Induces overlying ectoderm to form neural plate–> neural tube
  • above the notochord is the ectoderm
  • Ectoderm is goign to be one continuous sheet to two different sheets
  • The dark blue is going to be neural plate(nervous system, and hte light becomes surface ectoderm and becomes your skin)
17
Q

Induction of the Nervous system

A
  • Specific signaling molecuels are produced by cells of the notochord that elicit a response in the overlying ectoderm to begin the process of neurulation(formation of the neural tube)
  • Need to form a tube and remove any connection from the skin
18
Q

Induction

A
  • Organisms are formed by interactions between cells and tissues
  • When one group of cells/tisseus causes another set of cells/tisseus change their fate,this is called induction
  • When you have one group of cells and tissues that tell antoehr group of cells what to do
  • Inducer and responder
    • If you send it too son , responder might not be ready
    • Don’t send enough might not recognize it
    • Cut it off too son, and it won’t develop everything
  • Cross talk
    • responder needs to send a signal back basically saying it got message
19
Q

Cell-to-cell signaling

A
  • Most signaling molecules are proteins synthesized by one cell that diffuses over short distances to contact other cells
  • Growth and dfiferenetiation factors(GDFs)
  • Transcription Factor&signaling molecules
20
Q

Neurulation

A
  • Specific molecuels are prodcued by cells of the notochord that elicit a response in the overlying ectoderm to begin the process of neurulation(formation of hte neural tube)
  • will separate the ectoderm into two parts:
  • epithelial(surface) ectoderm
  • Neural ectoderm
  • Want to send the signal to start the folding process and create neural ectoderm
21
Q

Steps in Neurulation

A
  • Thickening of the neural plate
    • somite’s are big block of mesoderm at every level of the body and help with segmentation
  • Formulation of the neural folds and groove
  • Convergence of the lateral margins of hte neural plate
  • Fusion of the neural plate to form the neural tube

Neural crest migrates extensively to form a variety of strucutres throughout the body

22
Q

Derivatives of Ectoderm(surface or epithelial)

A
  • Organs and systems that maintain contact with the environment
  • Epidermis,hair,nails ,tooth enamel, cutaneous glands(sweat, oil, ceruminous) mammary glands , anterior pituitary, lens of eye,inner ear(membranous labyrinth) ,sensory nasal epithelium
23
Q

Derivatives of neuroectoderm

A
  • Derived from neural plate and neural folds
  • Neural tube-CNS(brain &spinal cord),retina, pineal body,posterior pituitary
    • Neural crest-Sensroy ganglia and nerves of PNS(cranial &spinal) ,autonomic ganglia & postganglia and postaganglionic fibers, schwann cells,adrenal medulla,pigment cells, pharyngeal arch cartilages. Components of the eye , skull,teeth, and skin
24
Q

Ectodermal Dysplasia syndromes

A
  • Group of about 150 heritable disorders that affect the ectoderm , the outer layer of tissue in developing babies. ED syndromes affect both males and females of all races and ethinic groups
  • When a child has at least two types of abnormal ectodermal features
    • Malformed teeth,extremely sparse hair etc
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Pigmentary Disorders
* Disease of melanocyte development ,function and survival * Piebaldism-charecterized by a congenital white forelock and multiple symmetrical hypopigmented or depigmented areas * Has been observed throughout history,with the first descriptions dating to early Egyptian , Greek and Roman writings * neurocrest issue
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Albinism
* Most autosomal recessive * Global reduction or absence of pigment in skin hair and eyes(oculocutaneous) or eyes only (ocular) * Eye conditions common in albinism include:nystagmus,strabismus,light sensitvity. All due to abnormal development of the eye because of lack of pigment
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Why does albinism cause nystagmus?
* Presence of melanin during ocular development is important. The fovea fails to develop proeprly if melanin is absent during development. Other areas of the retina develop normally regardless of hte presence of melanin * Additionally, neural connections between the retina and the brain are altered if melanin in the retina is absent during development * Amoung of pigment necessary for appropriate ocular development is currently unknown. More reserach needs to be completed * If not enough melanin can't focus the vision and dont' know how muh is necessary for normal development of vision
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Vitiligo
* Pigmentary disorders * Loss of melanocytes * autoimmune disorder * other support for autosomal dominat inheritance with variable expression and incomplete penetrance * possibly environmental effects * 2004-Doctors successfully transplanted melanoctyes to vitiligo affected areas.75-80% patients epxereienced repigmentation
29
Early Brain Segmentation
* Forebrain-prosencephalon * Midbrain-Mesencephalon * Hindbrain-Rhombencephalon * One long continuous cord for the spinal chord * Brain start with these areas ,and see brain bending * Once we see bend we can see the frebrain and what not
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Anencephaly(craniorachischisis)
* Forebrain doesn't develop normally which means the skull doens't develop normaly * Babies if born alive will not last long and die , no way to fix this problem
31
Iniencephalpy
* Extreme retroflexion of head * Short and almsot absent neck * Hyperextended spine * Facial skin is connected directly to the skin of the chest; the scalp is directly connected to the skin of the back
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Encephalocele
* Cranium bifida * Cranial defect with herniation of intracranial contents,most common in the occipital region * Meningoencephalocele-contains meninges and brain * Meningohydroencephalolcele-contains meninges,brain and ventricular system * encephalocele which is just meninges
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Arnold-Chiari malformation
* Herniation of cerebellar vermins or tonsils through the foramen magnum blocking the flow of CSF * Block the flow of the cerebral spinal fluid and large enoug hherniation can kill patients cuz it stops blood flow
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Failure of Closure-Caudal Neuropore
* Spina bifida-Failure of neural arches to form * S.B. occulta-arches absent , tube is normal * S.B. meningocele-dura and arachnoid also protrude * S.B. meningomyelocele-neural tissue also protrudes,also called spina bifida cystica
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Dietary and Genetic Affects on NTDs
* Dietary adn genetic causes * Daily intake of .4mg of folic acid(folate) will decrease the occurrence of neural tube defects * Prevents 70 percent of human neural tube defects(NTDs) but its mode of action is uncelar * Additional studies suggest that FA may reduce the rate of occurence of congential heart disease(CHD)
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How does folic acid prevent neural tube defects?
* Despite decades of subsequent reserach, the udnerlying mechanisms by which folic acid exerts its protective effects have remained elusive * Research on NTD pathogenesis suggests that disorders linked transformation of homocysteine to methionine * Increased homocysteine levels appear to prevent the closure of the neural tube * Significant subgroup of women who appear to be resistant to the protective effects of folic acid supplementation * May be metabolic and not exclusively dietary
37
Triple Marker Screen Test
* Measures the levels of alpha-fetoprotein(AFP), human chorionic gonadotropin(HCG), and estriol * AFP 9s produced in the fetal liver . In a fetus with an open NTD , AFP leaks across the defect into the amniotic fluid and across the placenta into the maternal serum * AFP levels in maternal blood can be measured as an indicator of open NTDs 1.AFP * Increased with neural tube defects * decreased in Trisomy 21 and Trisomy 18 Human Chorionic gonadotropin(Free bHCG) * Increased in trisomy 21 and decreased in trisomy 18 Unconjugated estriol(uE3) * decreased in trisomy 21 and trisomy 18
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