VBMS 213 Embryology Quiz 1

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ZYGOTE: fertilized egg

only one cell
EMBRYO: anything after the first division

> one cell
FETUS: after formation of organs & systems
CONCEPUTUS: product of conception

embryo or fetus plus the fetal membranes
EMBRYOGENESIS: formation of body structures and organs
ORGANOGENESIS: formation of organs
TWO REQUIREMENTS FOR ORGANOGENESIS: Growth - cell division - proliferation

Differntiation - cellular specialization to produce;

Cell Types
Extracellular Products
WHAT DRIVES ORGANOGENESIS Tell me 4 things: Regulation of Gene Expresion

Gene Expression depends on genetic makeup

Expressed proteins COMMITS cell to behave in certain way

Cellular Environment

Intercellular Communication
THE TWO BASIC PROCESSES OF DEVELOPMENT: Growth - proliferation, cell size and extracellular matrix

Differentiation
3 WAYS TO CONTROL GROWTH: Growth Factors - adjacent cells or transfer in blood

Space - contraint stops growth - tf relationships to other cells important

Negative 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 parent

Variety of cell types within a population that was once uniform
WHICH IS FIRST STRUCTURE OR FUNCTION AND THE 25 CENT WORD: Early changes tend to be functional via CHEMIODIFFERNTIATION not morphological
4 THINGS THAT CONTROL EXPRESSION AND REPRESSION OF GENES: Receptors

Peptides, enzymes, hormones

Channels and Pumps - ions

Extra Cellular enzymes and hormones
THE 3 GENERAL CELL TYPES OF DIFFERNTIATION: Stem cells - can be anything

Committed cells look the same but different

Specialized cell - after many steps
MORPHOGENESIS: Development of SHAPE or FORM of whole structure or part of.

reguires expression/repression of genes IN SEQUENCE

regional specialization depends on morphogens
THE THREE LAYERS IN ORDER OF DEVELOPMENT: Endoderm
Mesoderm
Ectoderm
I SAY PRIMORDIAL AND YOU SAY: Chorda mesoderm aka THE PRIMORDIAL ORGANIZER

Contains segmentally arranged somites which develop from the mesodermal axis
SOMITES: Segments along the dorsum

Each somite produces specific organs

All 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 induction

Permissive - via environment
THE OPTIC VESICLE STORY A 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 Retina

tf 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 natally

Gill Arches regress but first critical for head, neck heart

Development 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 tube

Prevents adherence of the oocyte to the wall of the uterine tube

Prevents polyspermy
TOTIPOTENT: cell that can become an individual organism - ie identical twins arise from two totipotent cells
CLEAVAGE 5 QUICK FACTIODS: Occurs after fertilization, 1 - 5 days depending on species

Each division takes about 12 hours

Cell size DECREASES because no new cytoplasm is produced

Each cell is a BLASTOMERE

Cells are TOTIPOTENT up to and including the 8 cell stage
BLASTOMERE DIFFERENTIATION 5 QUICK FACTIODS: After 8 divisions blastomeres differentiate into inner and outer cells

Inner cells undergo COMPACTION and communicate via extensive GAP JUNCTIONS

Outer cells remain in loose contact and communication, FLATTEN and form TIGHT JUNCTIONS....

Outer cells become fetal membranes

Inner 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
GRASTULATION 10 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 SUSCEPTABILITY 2 PERSPECTIVES 2 MEANS: INTRINSIC - Genotype of conceptus

EXTRINSIC - Enviroment including uterine
3 STAGES OF TERATOGEN SUSCEPTABILITY: Predifferentiation
Early Differentiation
Advanced Organogenesis
2 MECHANISMS OF SPECIES DIFFERENCES FOR GENETIC TERATOGENIC SUSCEPTABILITY AND 2 EXAMPLES: Different Metabolic Pathways
Different Placentas

Cortisone - cleft palate in mouse but not in rat

Thalidimide - very high LD50 in rodents but limb defects in humans on certain days of gestation

Time 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 EFFECTS PREDIFFERENTIATION: 1 - 32 Cells
All 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 EFFECTS EARLY 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 EFFECTS ADVANCED ORGANOGENESIS: If cells of a given organ are damaged can grow more tf LOWER SUSCEPTABILITY

Note effects at this stage are more likely alter function or growth rates
ABORTION TERATOGEN STYLE: Manifistation of ABNORMAL DEVELOPMENT

Note 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: Mechanism
Pathogenesis
Common Pathway
Defect

Note the common pathway makes it hard to extrapolate cause from effect
QUICK!!! LIST 9 TERATOGENIC MECHANISMS: Mutation
Chromosomal Abnormalities
Mitotic Interference
Altered DNA
Lack of Precursors
Reduced Energy
Enzyme Inihibition
Osmolar Imbalances
Altered Membranes
ABNORMAL EMBRYOGENESIS 5 KEY CAUSES: Excessive Cell Death - formation of digits, loss of septal cells between organs

Failure of Cell Interactions - mechanical disruption ie edema

Reduced Biosynthesis - ie lack of vitamins

Impaired Morphogenic Movement - ie kidney - ureter development or contracted tendons in foals from lack of movement

Altered Differentiation Schedule
4 SITES OF TERATOGENESIS: Fetus Direct
Placental-Fetal Unit - altered diffusion rates
Altered Homeostatsis of DAM - ie fever, deficiency, stress
Altered Sperm - usually genetic or alkalating agents
MANIFISTATIONS OF ABNORMAL DEVELOPMENT THE FINAL FOUR: Death - early, toxic, high dose
Malformation
Growth Retardation - major but underappreciated effect
Post 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 DOSE 8 POINTS: Maternal Dose
Maternal Absorption Rate
Maternal Metabolism
Plasma 1/2 Life of Teratogen
Protein Binding
Placental Transfer Rate/Ratio
Molecular Weight <600 Da likely to cross - >1000 Da rarely cross
Charge - neutral or fat soluble likely to cross
TIME IS UP THE PROF IS WALKING OUT OF THE ROOM WITH THE EXAMS YOU NEED TO WRITE 2 KEY WORDS ABOUT DEGREE OF TERATOGENICITY THEY ARE....: Time
and
Dose
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 Development

Reproductive Rate
THE FOUR TERATOGENIC ETIOLOGIES: Genetic - not likely if hetero
Environmental - lowest probabilty
Infectious - good bet
Nutritional - also a good bet
INVESTIGATIVE STRATEGIES THE BIG FOUR: Define the Fetal Abnormality
Recognize the Pattern - Temporal, Defects, Mortality, Geographic, Gestational age etc
Classify the Abnormality
Confirm 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 factors
TIME OF EXPOSURE - predifferntiation low susceptability, Early Differntiation - highest susceptability, Advanced Organogenesis - lower susceptability but functional and growth effects
Teratogenic 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 Deficiency
PHYSICAL 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 Aplasia
Excessive Formation
Incomplete Development
Persistent Embryonic Structures
Malpositioning
AGENESIS OR APLASIA: 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 DEVELOPMENT THREE 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 dysplasial

FAILURE TO FUSE - Cleft Palate, Heart Septal Defects

INCOMPLETE 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, hereditary

ENVIRONMENTAL - any external factor affecting development

INFECTIOUS

NUTRITIONAL
ABNORMAL GAMETOGENESIS TELL 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 animal

Disjunction 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
THE SEVEN SINS OF EQUINE TWINS: PLACENTAL INSUFFICIENCY - results in death of one or both twins depending on placental contact with uterus

ABORTION - death of one twin may cause infection of DAM

MALFORMATION - insufficient room for musculo skeletal development and increased risk of amniotic bands

DYSTOCIA

PREMATURE BIRTH - poor pulmonary development

UNTHRIFTY - start smaller and usually not enough post natal lactation

REDUCED FERTILITY IN DAM - increased risk of scar tissue from distension and dystocia
EQUINE TWINS WHAT TO DO FIVE FIXES: PINCH ONE - if less than 35 days - harder after due to huge spere of membranes - use ultra sound to identify

BALLOTMENT - 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 recommended

SURGICAL 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 FREEMARTINS 5 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 Estrodial

KARYOTYPE

GENITALIA - enlarged clitoris and tuft of hair on vulva

ABSENCE of ovaries or cycling ie cysts
OVINE FREEMARTINS FOR THREE POINTS: increased incidence due to selection for increased FECUNDICITY genes - increased litter size creates more anastomoses

GRADED EFFECT based on proximity within uterus to opposite sex - closer is more anastomoses

Females 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
RADIATION SEVEN STRIKES: Environmental Teratogen in HIGH LEVELS

NOT SITE SPECIFIC

SUSCEPTABILITY - division of a single cell or critical period of an organ or system

LETHAL during preimplantation or differntiataion

Growth 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 generation

X-RAYS are the most common exposure
GLUCOCORTICOIDS SIX: Hormonal Teratogens - Corticosteroid family cortisol, and synthetics prednison, dexamethasone, betamethasone

Corticosteroids 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
ASPIRIN THREE: 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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