Embryology Quiz 3 Flashcards
What are the four extra embryonic layers?
Amnion Yolk Chorion Allantois
What germ layer is the Chorion from?
Part of fetal maternal interface
What germ layer is the yolk from?
Inner cell mass; hypoblast derivative
Two trophoblastic derivatives of the fetal-maternal interface?
Placenta Chorion
What germ layer is the amnion from?
Inner cell mass: epiblast derivative
Four function of the amnion
- Buffer against mechanical injury 2. Accommodate growth 3. Allow normal movement 4. Protects fetus from adhesions
What germ layer is the allantois from?
Inner cell mass; interfaces with placenta via umbilical cord
What is an excessive amount of amniotic fluid? Liquid amount? What is it associated with?
Hydramnios >2000 mL Associated with multiple pregnancies and esophageal atresia or anencephally
What does testing creatine tell you?
Fetal maturity can be determined
4 things of the Phase I of amniotic fluid formation?
- First 20 weeks 2. Free diffusion of electrolytes through fetal endoderm 3. Maternal serum 4. Secretion by amniotic membrane
What is the condition with too little amniotic fluid? Liquid amount? What is it associated with?
Oligohydramnios
What does testing A-fetoprotein tell you? What is A-fetoprotein?
High concentration in amniotic fluid is a strong indicator of a neural tube defect -A protein in CNS
3 things of Phase II of amniotic fluid formation?
- Contributions from fetal urine 2. Filtration from maternal blood vessels near the chorion leave 3. Possible filtration from fetal vessels in the umbilical cord and chorionic plate
What is the turn over rate in late pregnancy, in third trimester? At term?
Every 3 hours 500 mL/hr
What does testing Lecithin-to-sphingomyelin ratio tell you?
Fetal maturity Reflection of maturity of lungs
Possible Yolk sac functions May concentrate (2)? Relationships (2)? Traces persist as?
May concentrate -Folic acid -Vitamin A, B12, E Relationships -Site of origin of primordial germ cells -Location of blood islands Traces of yolk duct persists as Meckel’s diverticulum
Histotrophic nutrition?
The initial transfer of nutrition from maternal to embryo compared to later blood-borne nutrition (hemotrophic nutrition)
Blood islands?
Origin of initial blood cells (extra embryonic hematopolesis)
Meckel’s diverticulum?
Traces of yolk duct persist as a fibrous cord or an out pouching of the small intestine
Development of allantoic vessels and relation of allantois to the urinary bladder and median umbilical ligament?
1)Allantoic vessels develop into mesoderm of the allantois 2)Proximal part of allantois= urachus -Associated with the formation of the urinary bladder -Becomes median umbilical lig
Four stages of chorionic villi development?
Previllous embryo Primary villous Secondary villous Tertiary villous
What happens in secondary villous stage?
Mesodermal cores appear within the primary villi
What are hofbauer cells?
Are scattered among the mesenchymal cells Large Function as fetal macrophages
What tissue in the mature placenta interfaces directly with maternal uterine connective tissue?
Syncytiotrophoblast
What happens in the primary villous stage?
Solid, cytotrophoblastic ectodermal primary villi appear
Cytotrophoblastic columns? (2)
-Solid mass of cytotrophoblast -Under influence of the local hypoxic environment the cytotrophoblastic cell column expands distally and penetrates the syncytiotrophoblastic layer
Anchoring villi?
Villi that are anchored to the cytotrophoblastic shell (as opposed to floating villi)
What happens in the tertiary stage?
Characterized by the appearance of blood vessels within the mesenchymal core of the secondary villi
Chorionic plate (2)
- Bounds the chorionic cavity 2. Consists of extra embryonic mesoderm overlaid with trophoblast
What does the term “decidua” refer to?
Refers to tissues that are shed at birth
Floating villi
Unattached branches dangle freely in the maternal blood that fills the space between the chronic plate and the outer cytotrophoblastic shell
What happens in the previous embryo?
No villi have been formed on the trophoblast
Hemochorial type placenta (3)
- The villi that extend outward from the chorionic plate and their trophoblastic covering is continuous with the chorionic plate 2. The villi and outer surface of the chorionic plate are bathed in a sea of continually exchanging maternal blood 3. This is why designated hemochordial type
Decidual reaction?
Striking transformation of the stormal cells of the endometirum within days after implantation of the embryo
Cytrotrophoblastic shells (3)
- Formed by expansion of the cytotrophoblastic columns over the maternal decidual cells 2. The cytotrophoblastic cells that spread over the maternal decimal cells to form a complete cellular layer called cytotrophoblastic shell 3. Surround embryo complex
Decidual cells are what?
After stromal cells swell as a result of the accumulation of glycogen and lipid in the cytoplasm
Chorionic cavity (2)
- Embryo is suspended in this 2. Is bounded by chorionic plate
Syncytiotrophoblast, Intervillous space & villi
Surrounds a complete layer of cytotrophoblastic cells
Layers of Embryo (6)
- Chorionic cavity 2. Amnion 3. Chorionic plate 4. Syncytiotrophoblast, Intervillous space, villi 5. Outer cytotrophoblastic shell 6. Decidua capsularis
What do stromal cell swell because of?
Accumulation of glycogen and lipid in the cytoplasm
What maternal tissue is lost at childbirth?
Placenta Embryonic membranes Remainder of umbilical cord Maternal decidua
Fate of decidua capsularis?
Undergoes atrophy Fuses with decidua parietalis
Maternal blood flow
- Spiral arteries 1. Intervillous spaces (trophoblastic lacunae) 2. Exchange of materials between maternal blood in lacunae and fetal blood in capillaries 3. Returns to maternal veins in decidua basalis
Fetal blood flow
- umbicial arteries (2) within placental villi 2. Capillary beds 3. umbilical vein (1) within placental villi
How is erythroblastosis related to hydrous fetalis
The antibody causes hemolysis of erythrocytes, this release bilirubin. In severe cases, the bilirubin causes water to accumulate in the fetus (hydrous fettles)
Hydratiform mole
Noninvasive condition in which many of the chorionic villi are characterized by nodular swellings that give them the appear of grapes
Genetic analysis of hydratiform mole? (3)
1) Has been determined that hydratiform moles are the result of paternal imprinting, in which the female pronucleus does not participate in development 2) Instead chromosomal material is derived from two sperm or by duplication of single sperm pronucleus 3) Are paternally derived 46XX because 46YY embryos is not compatible with tissue survival
Placenta previa
Abnormal implantation site within the uterine cavity -mechanical obstacle covering cervical outlet -hemorrhages
3 Functions of placenta
- Diffusion of oxygen & carbon dioxide 2. Diffusion of food stuff -Faciliated diffusion of glucose via trophoblastic cells -Slower diffusion of fatty acids 3. Excretion of waste products -Urea, Uric acid, and Creatinine
Early placenta (4)
Thick perm low Small surface area Total diffusion conductance is miniscule
Late placenta (4)
Thin Perm high Large surface area Large increase in placental diffusion
Bohr effect
Hemoglobin can carry more O2 at low PCO2 -Fetal blood carries more CO2 -Excess CO2 diffuses into maternal [Maternal more acidic, fetal more alkaline] Increase capacity of fetal blood to combine with O2, decrease for maternal Shift of oxygen hemoglobin curve to right and downward forces oxygen away from hemoglobin and into tissues
Double Bohr effect
Double shift in the maternal blood and in fetal blood
Human chorionic gonadotropin Timing? Secretion? Targets (2) ? Effects (4) ?
Timing -Measureable 8-9 days -Max: 10-12th week -Lower levels: 16-20th week Secretion -Secreted by the syncytial trophoblast cells into maternal fluids Targets -Corpus luteum & testes Effects 1) Prevents involution of CL 2) Causes CL to increase secretion of progesterone and estrogen 3) Caues increased growth in CL 4) Exert interstitial cell-stimulating effect on testes of male fetus (results in production of testosterone until birth)
Estrogen Timing? Secretion? Targets? Effects (6)
Timing -Towards end of preg. secretion levels are 30x mother’s normal level Secretion - secreted by syncytotrophoblast cells of placenta -placenta estrogen formed from adrogenic steroid compounds: (formed from mother and fetal adrenal glands, converted by trophoblast cells into estradiol, estrone, estriol) Target -external genitla Effects 1) uterine enlargement 2) Breast enlargement 3) Growth of breast ductal structure 4) Enlargement of maternal ext. genitalia 5) relaxation of pelvic log 6) May affect aspects of fetal development
Progesterone Timing? Secretion? Target? Effect (4)
Timing -early by CL -Late in placenta Secretion -Secreted in small quantities by CL (early) -Secreted in large quantities by placenta (late) Targets -Decidual cells, uterus, fallopian tubes, breasts Effects 1) Causes decimal cells to develop in the endometrium 2) Decrease contractility of pregnant uterus 3) Increase secretion of fallopian tubes and uterus 4) May work with estrogen to prepare breasts for lactation
Human chorinic somatomammotropin Timing? Secretion? Target? Effect (3)?
Timing -Beginning 5th week of prey Secretion -Secreted by placenta Target -Mother Effects 1) Decrease insulin sensitivity in mother 2) Decrease utilization of glucose in mother 3) General metabolic hormone
Four theories of mother’s immune system not recognizing fetus
1) Lack of expression of major histocompatible antigens by syncytotrophoblast and cytotrophoblast 2) Paralysis of mother’s immune system 3) Decidual barrier 4) Inactivation of mother’s immune system components by molecules found on placental surface
Lack of expression of major histocompatible antigens by syncytotrophoblast and cytrophobalst
1) Some extent true 2) Syncytio and cytotropho do not express MHC ag and so do not trigger immune response 3) Ag are present on fetus and stromal tissue placenta 4) Breaks in placental barrier, fetal RBC and WBC in circulation would trigger response
Paralysis of mother immune system
Paralysis so doesn’t react to Fetal Ag, but can amount immune response to infections and foreign grafts (possibility of selective repression of immune response, but Rh incompatibility)
Decidual immune barrier
-Barrier prevents either immune recognition of fetus by mother or the reaching of competent immune cells to fetus -Evidence of barrier, but known in several cases to be breached by trauma or disease
Inactivation of mother immune system components ( T cells) by molecules on surface of placenta
Inactivation of T cells locally or paralysis of local immune response -in mice, activation of complement regulation results in rejection of fetus
Aneuploidy is? Examples
Change in chromosome number beyond 2N stage Trisomy 21, Trisomy 13, Turner, Poly-X
Euploidy is?
Addition of complete set of chromosomes in addition to the dipoid (2N) stage -Retention of polar body or two sperm -spontaneous abortion
Examples of gene mutations
Phenylketonuria Galactosemia Cystic fibrosis
Duplications and Reversal of Asymmetry
Conjoined twins Duplication is incomplete Also can have normal individual with partial or complete reversal asymmetry of internal organs situs inversus
Situs inversus
partial complete reversal asymmetry of internal organs
Faulty inductive tissue interactions
Absent of faulty induction early in development is incompatible with life, later on results in malformations -Absence of kidney or lens
Absence of Normal Cell death
Syndactyly persistence of tail
Failure of tube formation
Spina bifida anomalies, incomplete fusion of the neural tube
Disturbances in tissue resorption
tissues need to be resorbed for subsequent development Anal atresia
Failure of migration
Disturbances in migration can cause abnormalities in any structures from neural crest (thymus, outflow heart, adrenal medulla) pelvic kidneys and undescended testes
Developmental arrest
persistant structures cleft lip and palate thyroglossal duct
Destruction of formed structures
Phocomelia, damage to early structure results in missing ones later
Failure to fuse of merge
palatal shelves fail to meet, lower jaw
Hypoplasia and Hyperplasia
cell proliferation abnormal too small (hypo) too large (hyper)
Receptor defects
testicular feminization syndrome
Defective fields
disturbances of boundaries fusion of lower limbs
Secondary effects to other developmental disturbances
normal is not for another thing make it abnormal
Germ layer defect
ectodermal dysplasia, thin hair
Environmental factors
Infections Drugs and other chemicals Radiation Maternal diabetes
What causes limb defects, ear defects, and cardiovascular anomalies a) alcohol b) thalidomide c) retinoic acid
Thalidomide
Respriatory distress syndrom
Condition related to immature lungs where lungs are under inflated, alveoli partially filled with proteinaceous fluid that forms membrane over respiratory surfaces
Why Hyaline membrane disease
Membrane composed of proteins and dead cell lines that covers the alveoli making gas exchange difficult or impossible
Rh disease consequences
Jaundice (bilirubin) Low muscle tone (hypotonia) Lethargy
Kernicturus
Brain damage from excess jaundice
What causes defects involving a variety of facial structures, outflow of heart and thymus a) alcohol b) thalidomide c) retinoic acid
retinoic acid
Why no developmental insults during first 3 weeks?
Insults will either kill embryo or be compensated for by powerful regulatory properties
No major structural anomalies after week 8?
By this point, most organs have become well established
Teratology
The study of monsters, a descriptor for the newly emerging study of congenital malformations
Malformation
are primary errors of morphogensis. Usually multifactoral
What causes growth and mental retardation, microcephaly, various malformation of face and trunk a) alcohol b) thalidomide c) retinoic acid
alcohol
Deformation
disturbances in otherwise morphogenetic processes. These are typically caused by abnormal biomechanics forces such as uterine constraints Clubfoot
Teratogen
Agents that produce birth defects
Disruption
are disturbances in otherwise normal morphogenetic processes. Amniotic bands
Dysplasia
An abnormality of tissue due to an abnormal intrinsic developmental process
Association
A group of anomalies seen in more than one individual that cannot yet be attributed to a definitive causes
Syndrome
are constellations of congenital anomalies that are thought to be pathologically related but cannot be explained on the basis of a single local initiation event -often caused by single event like infection
Critical period
time period during pregnancy where embryos are more susceptible to agents or factors causing abnormal development than at other times
Sequence
is a series (cascade) of events triggered by one initiating factor Oligohydraminos
Formation of multilayered epidermis
1) Formation periderm 2) Activation of p63 by dermal mesenchyme signals 3) Progresion of single layered ectoderm to stratified 4) inactivation p63 by miR-203 5) Become 3 layered structure 6) Loss of adhesiveness to basal lamina due to loss of integrins 7) Mitosis of stem cells in basal layer to stratum spinosum 8) Kertaohyalin granules appear in stratum spinosum 9) Cell move to outer layer, lose nuclei, flattened, connected by filaggrin
Role of apoptosis
- postnatal layers of epidermis during sixth month 2. Peridermal cells undergo apoptosis
High and round velar pads result in?
Whorl
Late formation of ridge results in
Arches
Molecular basis for albinism?
Have melanocytes Lack enzyme tyrosinase to convert AA tyrosine to melanin
Melanoblasts From? Function (3)
From neural crest Migrate to dermis and then into epidermis Stain with HMB-45 Produce pigment by mid preg
Intermediate heigh volar pads result in
loop
Early formation of ridge results in
Whorls
Langerhans’ cells From? Function?
Derived from bone marrow Antigen presenting cells
Low velar pads result in
Arches
Merkel cells From? Function?
Neural crest Slow adapting mechano-receptors
Source of dermal cells in dorsal surface of body?
Mesenchyme from dermatome
Source of dermal cells in ventral and lateral surfaces of body
Mesenchyme from lateral plate mesoderm
Source of dermal cells in cranial and anterior neck?
Mesenchyme from cranial neural crest
Differentation of Dermal cells
Mesenchymal cells are induced by Wnt to dermal cells -Dermal cells express Dermo1 -Mesenchymal cells to fibroblasts
Commonalities of epidermal derivatives (4)
- development involves ectodermal-mesodermal interactions and induction 2. Begins as epidermal down growths 3. Ectoderm contributes 4. Mesenchyme contribures
Ectoderm contributes what to epidermal derivatives
Hair follicle Hair shaft Sebaceous glands Nails Eponychium Hypochium Secretory/ Duct components of mammary glands
Mesenchyme contributes what to epidermal derivatives
Hair papilla Outer hair follicle Arrector muscles
Stage where hair follicle regresses to fraction of its original length
Catagen
Wnt-1
Induced Wnt 11
Wnt 11
With FGF cause ectoderm to express Noggin
BMP
inhibits folicle development
Stage where hair stops growing
Telogen
Eda/Edar
Eda causes ectoderm to express Edar Edar with Noggin block BMP Edar stimulates expression of Shh
Noggin
With Edar block BMP
Dickkopf
Blocks Wnt
Stage where hair is actively growing
Anagen
Shh
Formation of dermal papilla below epidermal placode -With Cyclin D1 stimulate further down growth of proliferation of epidermal placodes
Induction of ectodermal placode steps (6)
- Dermal induction 2. Wnt-11 and FGF from mesoderm cause ectoderm to express noggin 3. Eda from mesoderm causes ectoderm to express Edar 4. Edar with Noggin block BMP 5. Other Wnts act through B-catenins 6. In interfollicular zones: -Dickkopf block Wnt -BMP inhibits follicle development
Stage where hair is shed
Exogen
Induction dermal papilla (2)
- Epidermal induction 2. Expression of Shh by Edar stimulates formation of dermal papilla below epidermal placode
Induction of hair germ (3)
- Dermal induction 2. Various inducers from dermal papilla along w/ Shh and Cyclin D1 in epidermal placode stimulate further down growth of proliferation of epidermal placodes 3. Final differentiation of hair primordial involves Hox genes
Milk Lines
Two bands ectodermal thickenings running along ventrolateral body walls in embryos of both genders at 6 weeks -First morphological evidence -Marked by expression of Wnts within ectodermal cells
Development of mammary glands
1) Wnt expression marks milk lines 2) Thickened milk lines -> fragmentation Rest -> primordial mammary glands 3) mammary placodes formed by inductive neuregulin-3 4) Tbx-3: marks dorsoventral location 5) PTH: increases sensitivity to BMP-4 6) BMP-4 signal to effects a. further down growth of bud b. expression Msx-2: inhibits formation hair follicle at nipple 7) Shaping of duct done by fatty component of CT
Wnts
Expression of various Wnt inside the ectodermal cells marks the milk lines
Induces individal mammary placodes to form from the aggregation and proliferation of ectodermal cells of the milk lines
Neurogluin-3
Marks the dorsoventral location of the mammary placodes
Tbx-3
Increases sensitivity of underlying mesenchymal to BMP-4
PTH
Signals within the underlying mesenchyme to stimulate further down growth of mammary bud and stimulate expression of Msx-2
BMP-4
Inhibits the formation of hair follicles in the region of the nipple
Msx-2
Mesodermal sclerotomes (of somites) is mesenchymal origin of what?
Vertebral columns Ribs Sternum
Lateral plate mesoderm is mesenchymal origin of what?
Limb bones Girdles
Head mesoderm is mesenchymal origin of what?
Calvaria and base of skull
Neural crest is mesencymal origin of what?
Facial bones
Common pathway
- Mesenchyme is induced to enter common pathway 2. Production of N-cadherins which promotes mesenchymal condensation 3. TGF-beta stimulates synthesis of fibronectin and N-CAM 4. Aggregated state of mesenchymal cells is stabilized
Membranous bone pathway
- Required transcription factors Runx-2 and Osm 2. Mesenchymal cells differentiate into osteoblasts
Permanent cartilage pathway
- Mesenchymal condensation forms chondroblasts 2. Sox-9 causes chondroblasts to secrete collagen II and cartilage matrix 3. Sox-9 is continually expressed in permanent cartilage
Endocondral bone pathway
- Runx-2, ihh, and BMP-6 induce this cartilage to undergo hypertrophy 2. Hypertrophy cartilage secrete boen proteins and vascular endothelial growth factor 3. Invading blood vessels erode the hypertrophic cartilage and bring osteoblasts in to replace cartilage with bone
Centrum derived from
Ventral and medial parts of pair sclerotomes
Neural arches derived from
Dorsal regions of sclerotomes
Costal processes/Ribs
-Proximal development depends on expression of Myf-5, Myf-6 -Distal development depends on BMP signals from somatopleural mesoderm
Retinoic acid
Cuases shifts in cranial or caudal levels in overall segmental organization if applied at critical periods
Shifts in levels (cranial or caudal) in the overall segmental organization of vertebrae
Homeotic transformations
Occipital-cervical boundary
Hox3
Cervical-thoracic boundary
Hox6
Thoracic-lumbar boundary
Hox-10
Sacral coccygeal boundary
Hox-13
Attached-floating ribs
Hox 9
Lumbar-sacral bounary
Hox11
Ribs form on lumbar and sacral
Hox10 paralog knockout
Allows sacrum to form
Hox11 knockout
Exhibits hypoplasia of clavicle delayed ossification of membrane bone (skull) and open anterior and posterior fontanelles in skull, as well as supernumerary teeth
Cleidcranial dysplasia
