VBMS 213 Embryology Quiz 1 Flashcards

Terms Definitions
ZYGOTE
fertilized eggonly one cell
EMBRYO
anything after the first division> one cell
FETUS
after formation of organs & systems
CONCEPUTUS
product of conceptionembryo or fetus plus the fetal membranes
EMBRYOGENESIS
formation of body structures and organs
ORGANOGENESIS
formation of organs
TWO REQUIREMENTS FORORGANOGENESIS
Growth - cell division - proliferationDifferntiation - cellular specialization to produce;Cell TypesExtracellular Products
WHAT DRIVES ORGANOGENESISTell me 4 things
Regulation of Gene ExpresionGene Expression depends on genetic makeupExpressed proteins COMMITS cell to behave in certain wayCellular EnvironmentIntercellular Communication
THE TWO BASIC PROCESSES OF DEVELOPMENT
Growth - proliferation, cell size and extracellular matrixDifferentiation
3 WAYS TO CONTROL GROWTH
Growth Factors - adjacent cells or transfer in bloodSpace - contraint stops growth - tf relationships to other cells importantNegative Feedback - form other cells, blood or cell itself
DIFFERENTIATION
Changes in physical and functional properties within cell
THE TWO RESULTS OF DIFFERNENTIATION
Population of daugher cells different from parentVariety of cell types within a population that was once uniform
WHICH IS FIRSTSTRUCTURE OR FUNCTIONAND THE 25 CENT WORD
Early changes tend to be functional via CHEMIODIFFERNTIATION not morphological
4 THINGS THAT CONTROL EXPRESSION AND REPRESSION OF GENES
ReceptorsPeptides, enzymes, hormonesChannels and Pumps - ionsExtra Cellular enzymes and hormones
THE 3 GENERAL CELL TYPES OF DIFFERNTIATION
Stem cells - can be anythingCommitted cells look the same but differentSpecialized cell - after many steps
MORPHOGENESIS
Development of SHAPE or FORM of whole structure or part of.reguires expression/repression of genes IN SEQUENCEregional specialization depends on morphogens
THE THREE LAYERSIN ORDER OF DEVELOPMENT
EndodermMesodermEctoderm
I SAY PRIMORDIAL AND YOU SAY
Chorda mesoderm aka THE PRIMORDIAL ORGANIZERContains segmentally arranged somites which develop from the mesodermal axis
SOMITES
Segments along the dorsumEach somite produces specific organsAll tissues that develop from them are the result of inductions in the surrounding tissues
SOMITOMERES
Somites in the head region which are NOT FULLY SEGEMENTED
TWO TYPES OF DEVELOPMENT
Instructive - via inductionPermissive - via environment
THE OPTIC VESICLE STORYA TALE OF MUTUAL INDUCTION
Optic vesicle (outpooching of the diencephalon) comes in contact with Ectoderm which INDUCES thickening of the Ectoderm producing in it the Lens Placode. The Lens Placode in turn INDUCES the optic vessicle to invaginate and form the Optic Cup which ultimately results in the Retinatf the the eye will develop wherever the optic vesicle contacts ectoderm
APOPTOSIS AND EXAMPLE
Programed cell death - important because embryo develops many structures which are absent post natallyGill Arches regress but first critical for head, neck heartDevelopment of Digits
CONGENITAL DEVELOPMENT
Failure to Regress
ONCOGENES
abnormally activated genes that regulated cell growth and cell mitosis result in cancer of the embryo or post natally but of embryological origen
MORPHOGEN
Anything that changes shape or form
DELAMINATION
Cells of epi leaving epi to form new tissue
PLACODE FORMATION
Thickening of epi - ie neural plate or optic placode
INVAGINATION
Proliferation of epi that folds and grows into the mesenchyme - ie optic cup or neural tube
MESENCHYME
Embryological connective tissue
BUDDING AND BRANCHING
complex invagination forming cords tubes and pouches
VESICULAR FORMATION
invagination that comes together, pinches off and sinks epi below the epi surface
EVAGINATION
Bulging out of epi - ie origin of optic vesicle from diencephalon
ZONA PELLUCIDA
Non cellular glycoprotein SECRETED by the oocyte
3 FUNCTIONS OF THE ZONA PELLUCIDA
Mechanical protection on the journey through the uterine tubePrevents adherence of the oocyte to the wall of the uterine tubePrevents polyspermy
TOTIPOTENT
cell that can become an individual organism - ie identical twins arise from two totipotent cells
CLEAVAGE5 QUICK FACTIODS
Occurs after fertilization, 1 - 5 days depending on speciesEach division takes about 12 hoursCell size DECREASES because no new cytoplasm is producedEach cell is a BLASTOMERECells are TOTIPOTENT up to and including the 8 cell stage
BLASTOMERE DIFFERENTIATION5 QUICK FACTIODS
After 8 divisions blastomeres differentiate into inner and outer cellsInner cells undergo COMPACTION and communicate via extensive GAP JUNCTIONSOuter cells remain in loose contact and communication, FLATTEN and form TIGHT JUNCTIONS....Outer cells become fetal membranesInner cells become embryo and fetus
MORULLA
More than 16 cells but still solid inside
BLASTULATION
Outer cells secrete fluid internally creating the blastocoel forming the BLASTOCYST
HATCHING
loss of zona pellucida as fluid in blastocoel enlarges blastocyst - essential for attachement to uterine wall
TROPHOBLAST
Outer layer of flattened cells connected by tight junctions - secretes fluid internally forming the blastocoel
GRASTULATION10 KEY WORDS THAT WILL GET YOU ONE MARK ON THE QUIZ
PROLIFERATION of the INNER CELL MASS and the DEGENERATION of the overlying TROPHOBLAST forms the EMBRYONIC DISK. Cells DELAMINATE from the developing embryonic disk form the HYPOBLAST LAYER internal to the trophoblast and the space in between is the COELUM. The chamber formed by the hypoblast is the YOLK SACK aka the primative gut. Thickening of the embryonic disk results in FORMATION OF THE EPIBLAST WHICH IS THE ORIGIN OF THE THREE EMBRYONIC LAYERS. First the PRIMITIVE STREAK forms in the epiblast initiating crainal/caudal orientation. Cells on the SURFACE of the epiblast migrate towards and then through the primative streak then spread over top of the hypoblast forming in sucession the ENDODERM, MESODERM and ECTODERM.
EPIBLAST
Origin of the 3 embryonic layers via migration through its primative streak
PRIMATIVE NODE
Forms at the crainal end of the primative streak. Epiblast cells migrate through it to form the NOTOCHORD
NOTOCHORD
Solid longitudinally oriented rod that is important in developing structures - particularly the NEURAL TUBE
NUCLEUS PULPOSIS
Residual notochord that forms the squishy bit in the centre of the intervetebral disk
TERATOLOGY
The study of the causes, mechanisms and manifestations of developmental deviations of either structural or functional nature
TERATOGENIC SUSCEPTABILITY2 PERSPECTIVES 2 MEANS
INTRINSIC - Genotype of conceptusEXTRINSIC - Enviroment including uterine
3 STAGES OF TERATOGEN SUSCEPTABILITY
PredifferentiationEarly DifferentiationAdvanced Organogenesis
2 MECHANISMS OF SPECIES DIFFERENCES FOR GENETIC TERATOGENIC SUSCEPTABILITY AND 2 EXAMPLES
Different Metabolic PathwaysDifferent PlacentasCortisone - cleft palate in mouse but not in ratThalidimide - very high LD50 in rodents but limb defects in humans on certain days of gestationTime of development of liver Smooth Endoplasmic Reticulum varies widely in species tf compounds that are metabolized to become teratogenic have vaired timing and species effects
TERATOGENIC GENERAL EFFECTSPREDIFFERENTIATION
1 - 32 CellsAll cells identicle tf LOW SUSCEPTABILITY because teratogen destroys cell but that can all be fixed with a little PROLIFERATION.Note if high dose teratogen may interfere with implantation
TERATOGENIC GENERAL EFFECTSEARLY DIFFERENTIATION
Development of Germ Layers - good old gastrulation. May just have a single differentiated cell for a given organ tf period of HIGH SUSCEPTABILITY
TERATOGENIC GENERAL EFFECTSADVANCED ORGANOGENESIS
If cells of a given organ are damaged can grow more tf LOWER SUSCEPTABILITYNote effects at this stage are more likely alter function or growth rates
ABORTIONTERATOGEN STYLE
Manifistation of ABNORMAL DEVELOPMENTNote embryo has high capacity to repair itself but declines after predifferention
THRESHOLD
NUMBER of cells a teratogen must DESTROY before it has an effect.Note teratogens destroy cells and carcinogens proliferate cells and believe it or not the right combination of the two will cancel each other out
TERATOGENIC PATHOGENESIS
Teratogens act via specific MECHANISMS on developing cells and tissues to initiate SEQUENCES of ABNORMAL EVENTS
4 KEY EVENTS ON THE TERATOGENIC PATH
MechanismPathogenesisCommon PathwayDefectNote the common pathway makes it hard to extrapolate cause from effect
QUICK!!!LIST 9TERATOGENIC MECHANISMS
MutationChromosomal AbnormalitiesMitotic InterferenceAltered DNALack of PrecursorsReduced EnergyEnzyme InihibitionOsmolar ImbalancesAltered Membranes
ABNORMAL EMBRYOGENESIS5 KEY CAUSES
Excessive Cell Death - formation of digits, loss of septal cells between organsFailure of Cell Interactions - mechanical disruption ie edemaReduced Biosynthesis - ie lack of vitaminsImpaired Morphogenic Movement - ie kidney - ureter development or contracted tendons in foals from lack of movementAltered Differentiation Schedule
4 SITES OF TERATOGENESIS
Fetus DirectPlacental-Fetal Unit - altered diffusion ratesAltered Homeostatsis of DAM - ie fever, deficiency, stressAltered Sperm - usually genetic or alkalating agents
MANIFISTATIONS OF ABNORMAL DEVELOPMENTTHE FINAL FOUR
Death - early, toxic, high doseMalformationGrowth Retardation - major but underappreciated effectPost Natal Function Deficiency - late and lower doses - immunity, behavior
ACCESS OF TERATOGENS DEPENDS ON
The physical nature of the teratogen- rate of metabolism- fat storage- protein binding
FACTORS AFFECTING FETAL DOSE8 POINTS
Maternal DoseMaternal Absorption RateMaternal MetabolismPlasma 1/2 Life of TeratogenProtein BindingPlacental Transfer Rate/RatioMolecular Weight <600 Da likely to cross - >1000 Da rarely crossCharge - neutral or fat soluble likely to cross
TIME IS UPTHE PROF IS WALKING OUT OF THE ROOM WITH THE EXAMSYOU NEED TO WRITE 2 KEY WORDS ABOUT DEGREE OF TERATOGENICITYTHEY ARE....
TimeandDose
TWO KEY DIAGNOSTIC TOOLS TO IDENTIFY TERATOGENIC ETIOLOGY GIVEN THAT THE TERATOGEN IS LONG SINCE METABOLIZED AND GONE SO NO MAGIC ANSWERS FROM THE LAB
Abnormal DevelopmentReproductive Rate
THE FOUR TERATOGENIC ETIOLOGIES
Genetic - not likely if heteroEnvironmental - lowest probabiltyInfectious - good betNutritional - also a good bet
INVESTIGATIVE STRATEGIESTHE BIG FOUR
Define the Fetal AbnormalityRecognize the Pattern - Temporal, Defects, Mortality, Geographic, Gestational age etcClassify the AbnormalityConfirm the Diagnosis & Eitiology - the lab is the last step
THE 6 PRINCIPLES OF TERATOGENOLOGY
SUSCEPTABILITY to teratogenesis depends on the genotype of the conceptus and the manner in which it interacts with adverse envionmental factorsTIME OF EXPOSURE - predifferntiation low susceptability, Early Differntiation - highest susceptability, Advanced Organogenesis - lower susceptability but functional and growth effectsTeratogenic agents act in Specific Ways (MECHANISMS)on developing cells and tissues to initiate sequences of abnormal developmental events (PATHOGENESIS)FINAL MANIFISTATIONS OF ABNORMAL DEVELOPMENT - Death, Malformation, Growth Retardation, Postnatal Functional DeficiencyPHYSICAL NATURE OF THE AGENT determines the access of adverse influences (agents) to the developing tissues (fetus)Increasing DOSE increases FREQUENCY and DEGREE of manifistations of Abnormal Development from none to lethal
CRITICAL PERIOD
Period when EACH organ is most sensitive to teratogenesis- increased sensitivity during early organogenesis
INCIDENCE OF CONGENITAL ANOMALIES...
...varies greatly amongst species
5 TYPES OF ANOMALIES
Agenesis or AplasiaExcessive FormationIncomplete DevelopmentPersistent Embryonic StructuresMalpositioning
AGENESISORAPLASIA
Lack of growhth or failure to form all or part of a structure.ie anopthalmia - no eye which would happen if opdic vesicle did not contact overlying ectoderm resulting in absence of induction
EXCESSIVE FORMATION
Organ or structure which is larger or more numerous- ie polydactyly from excessive cell death
INCOMPLETE DEVELOPMENTTHREE TYPES
Organ or structure that fails to develop completely - includes APLASIA (no growth) and HYPOPLASIA (reduced growth)INCOMPLETE GROWTH - rudimentary structure - can be morphologically abnormal ie gonalda dysplasialFAILURE TO FUSE - Cleft Palate, Heart Septal DefectsINCOMPLETE MIGRATION - organ fails to migrate to definitive location - ie cryptorchidism or Ectopic Cardis - heart in throat from non regression of the gill arches
PERSISTENT EMBRYOLOGIC STRUCTURES
Temporary structures that fail to regress - ie Uracal Diverticulum aka Persistant Uracus - failure of the uracus to close near birth tf pee out of umbilicus
MALPOSITIONING
Unilateral organ on wrong side - ie dextro positioning of heart.Note this is a MIRROR IMAGE effect not a failure to migrate and may involve more than one organ.
Dr MACHINS FOUR TERATOGENS
GENETIC - simple or multiple genes, chromasomal defects (number or structural, hereditaryENVIRONMENTAL - any external factor affecting developmentINFECTIOUSNUTRITIONAL
ABNORMAL GAMETOGENESISTELL ME A LITTLE STORY WITH 5 KEY WORDS AND PUT A LITTLE SEX INTO IT
NON DISJUNCTION of CHROMOSOMES during MEIOSIS I AND MEIOSIS II producing chromosomal abnormalities MONOSOMY and TRISOMY.Effects vary from lethal in the majority of cases to mild.
WHY DOES DISJUNCTION MORE COMMONLY OCCUR WITH SEX CHROMOSOMES
Common occurance = live animalDisjunction with sex chromosomes is less likely to be lethal because of X inactivation in females and Y does not contain vital genes so you can just inactivate extra Xs and X0 is almost as good as XY but Y0 is lethal
WHY DOES ABNORMAL GAMETOGENESIS OCCUR MORE FREQUENTLY IN FEMALES AS OPPOSED TO MALES
Ova are developed in fetus and then arrested in Mieosis I prenatally, then start up and are arrested again in Meiosis II during puberty and don't complete Meiosis II until ovulation/fertilization tf there is a long period of time for untoward events to occur. Spermatogenesis is short lived and sperm survive typically for less than 100 days tf have lower risk of meiotic malfuntions
MOST COMMON CHROMOSOMAL ABNORMALITY IN HORSES
X0 - Turners Syndrome STERILE- externally physically normal but often small in stature - often good performance horses- subdued or absent estrus may or may not let stallion mount- genital tract underdeveloped- similar symptoms in chimeric X0/XX but normal stature- chromosomal abnormalities occur in <3% of horses
THESEVEN SINSOFEQUINE TWINS
PLACENTAL INSUFFICIENCY - results in death of one or both twins depending on placental contact with uterusABORTION - death of one twin may cause infection of DAMMALFORMATION - insufficient room for musculo skeletal development and increased risk of amniotic bandsDYSTOCIAPREMATURE BIRTH - poor pulmonary developmentUNTHRIFTY - start smaller and usually not enough post natal lactationREDUCED FERTILITY IN DAM - increased risk of scar tissue from distension and dystocia
EQUINE TWINSWHAT TO DOFIVE FIXES
PINCH ONE - if less than 35 days - harder after due to huge spere of membranes - use ultra sound to identifyBALLOTMENT - the old fashioned smack to break fetal membranes - use around 35 - 40 days otherwise into fetal stage. TRANSVAGINAL ULTRASOUND GUIDED FETAL PUNCTURE - fairly risky - not recommendedSURGICAL REMOVAL - high risk to remaining fetus and mare - best done at 115 - 130 days best to use procaine penicillin because shows up on ultra sound and works intra thoracic or intra abdominal tf big target - 35% success rate on a good day you will get a mummified fetus on a bad day toxins of dying fetus affect other or kill other via vascular anastomoses which occur 40% of time in equine twins
BOVINE FREEMARTINS5 KEY WORDS AND ONE KEY PHRASE
- CHIMERIC XX/XY female with a male twin which occurs via VASCULAR ANASTOMOSES which allow the EXCHANGE OF GENETIC MATERIAL (blood cells and predetermined organ cells especially during apoptosis )between the fetuses.Females are mostly sterile, males are less affected depending on TIMING of tranfer relative to critical period of reproductive development and level of HORMONES tranfered.
SIX DIAGNOSTICS FOR FRISKY FREEMARTINS
STATISTICS - 50% chance of XX - XY twins and 80 - 95% of these will be chimeric tf ASSUME female is freemartin and feed her out.PALPATE - reproductive tract - look for reduced size and absence of uterus and or cervix.HORMONE LEVELS - <9 days presence of male produced Mullarian Inhibiting Hormone aka Antimullarian Hormone or if older presence of EstrodialKARYOTYPEGENITALIA - enlarged clitoris and tuft of hair on vulvaABSENCE of ovaries or cycling ie cysts
OVINE FREEMARTINSFOR THREE POINTS
increased incidence due to selection for increased FECUNDICITY genes - increased litter size creates more anastomosesGRADED EFFECT based on proximity within uterus to opposite sex - closer is more anastomosesFemales have more MASCULINIZATION compared to cattle - effects of timing and dose
TELL ME A DETAILED STORY ABOUT THE MECHANISMS OF FREEMARTINISM
- during development (mammalian) gonads are initially INDIFFERENT - can differentiate into ovaries or testis.- early embryo has both the female PARAMESONEPHRIC (aka Mullarian) ducts on the outside which develop into uterine tubes and uterus and MESONEPHRIC (aka Wolfian) ducts on the inside which develop into deferent ducts.The simplistic view of normal sex development is that on the Y chromosme the Sex Determining Region (Sry) is the most important of several genes for masculinization. Sry is responsible for development of testes and seminepherous tubules. In the absence of Sry the ovary develops. In the presence of Sry Mullarian Inhibiting Hormone (MIH) is produced which regresses the paramesonephric duct and allows development of the mesonephric duct tf presence of MIH = male and absence of MIH = female.But Freemartins show that gender development is complex because a female develops despite the presence of MIH from the male twin. Thinking is that there are complex XX genes that are responsible for female development as well as Autosomal DAX1.Note that the proximity of the paramesonephric and mesonephric ducts allows for a variety of fusions between female and male sex organs.
NECROTIC TIPS
Regions of no vasculature at the ends of a fetuses fetal membranes where they overlap with the fetal membranes of the adjacent fetus as the result of necosis.Absence of vasculature in the region of fetal membrane overlap prevents the formation of vasucular anastomoses and tf the transfer of genetic material which prevents the formation of freemartins
WHY ARE FREEMARTINS ARE RARE IN MOST SPECIES
Necrotic Tips
RADIATIONSEVEN STRIKES
Environmental Teratogen in HIGH LEVELSNOT SITE SPECIFICSUSCEPTABILITY - division of a single cell or critical period of an organ or systemLETHAL during preimplantation or differntiataionGrowth retardation, chromosomal fragmentation, imparied cell division, malignancy can result from exposure at ANY TIME.Radiation of Adult can effect GERM CELLS and tf the next generationX-RAYS are the most common exposure
GLUCOCORTICOIDSSIX
Hormonal Teratogens - Corticosteroid family cortisol, and synthetics prednison, dexamethasone, betamethasoneCorticosteroids are important in lung development and support of surfactant and are released during stress of birth tf Betamethasone given if premature birth is supsected - otherwise contraindicated because...High doses in 1st (mainly) and 2nd trimester result in- cleft palate- catarachs- cyclopia- interventricular septal defects- hydrodephalus- low birth weight
ASPIRINTHREE
Teratogenic Drug- cleft palate- cardio vascular defects- abortion via effect on protoglandin- dogs, cats and lab animals are most affected species
ALBENDAZOLE
Teratogenic Drug - broad spectrum antihelmintic- inhibits formation of MICROTUBULES ARRESTING MITOSIS tf affects rapidly proliferating cells.- special AFFINITY STRUCTURES SUCH AS BONE AND SOMITES which are derived from MESODERM- ventral medial aspects of somites migrate around notochord forming segmental SCLEROTOMES. - adjacent SCLEROTOMES fuse together forming a precartilagenous verterbral body but incorporate intersegmental mesenchyme between the two.- the teratogen prevents proper SEPERATION of the SCLEROTOMES - resulting in no or partial vetebral disk and FUSED VERTEBRAE- also affinity for NEURAL CREST and NEUROECTODERM tf problems with nervous system - ie prevents fusion of neural fold - SPINAL BIFIDA. - other MESDERMAL tissues- agenetic or ectopic kidney- vascular anolomies
GRISEOFULVIN
- Teratogenic Drug - antifungal agent used for ringworm- teratogenic in ALL SPECIES- Interferes with MICROTUBULE ASSOCIATED PROTEIN tf disrupts formation of MITOTIC SPINDLE tf disrupts MITOSIS- also disrupts MEIOSIS ie germ cell effects tf DO NOT HAVE TO BE PREGNANT WHEN EXPOSED.- female aneuploidy or polyploidy- male decreased SPERMATOGENESIS and NONDISJUNCTION- predifferentiation - abortion or reabsorption- affects ECTODERM and NEUROECTODERM- prevents formation and closure of neural tube- spinal bifida- ANECEPHALY- OPTIC VESICLE - anopthalmia, micropthamia, cyclopia (earlier exposure because diencephalon not yet divided)- cleft palate via facial bones affects- avoid exposure during BREEDING ie estrus and spermatogenesis are time of rapid cell division
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