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111 Cards in this Set

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ZYGOTE
fertilized egg

only one cell
two gametes =
EMBRYO
anything after the first division

> one cell
at least twice as much as a zygote
FETUS
after formation of organs & systems
need some identifiable items
CONCEPUTUS
product of conception

embryo or fetus plus the fetal membranes
everything foreign to dam
EMBRYOGENESIS
formation of body structures and organs
enough of this and you become a fetus
ORGANOGENESIS
formation of organs
too easy
TWO REQUIREMENTS
FOR
ORGANOGENESIS
Growth - cell division - proliferation

Differntiation - cellular specialization to produce;

Cell Types
Extracellular Products
organs have a lot of cells

organs are different from each other
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
genes, proteins, enviro, 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
rthyms with good friday
the final frontier
good for homeostasis
DIFFERENTIATION
Changes in physical and functional properties within cell
good old form and function
THE TWO RESULTS OF DIFFERNENTIATION
Population of daugher cells different from parent

Variety of cell types within a population that was once uniform
daughters and diversions
WHICH IS FIRST

STRUCTURE OR FUNCTION

AND THE 25 CENT WORD
Early changes tend to be functional via CHEMIODIFFERNTIATION not morphological
form does not always follow function but how
4 THINGS THAT CONTROL EXPRESSION AND REPRESSION OF GENES
Receptors

Peptides, enzymes, hormones

Channels and Pumps - ions

Extra Cellular enzymes and hormones
the usual suspects think in and out of the "box"
THE 3 GENERAL CELL TYPES OF DIFFERNTIATION
Stem cells - can be anything

Committed cells look the same but different

Specialized cell - after many steps
makes the caudal part of your brain hurt

remember the chemiodifferntiation story

what are we all
MORPHOGENESIS
Formation of differentiated cells into structures
the new war museum is a _____ kind of _______
THE THREE LAYERS
IN ORDER OF DEVELOPMENT
Endoderm
Mesoderm
Ectoderm
think about how the three layers flow through the primitive streak and lay down in the coelemic space on top of the hypoblast and then take a cold shower
I SAY PRIMORDIAL AND YOU SAY
Chorda mesoderm aka THE PRIMORDIAL ORGANIZER

Contains segmentally arranged somites which develop from the mesodermal axis
a mighty middle sort of chord
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
the centipede look
SOMITOMERES
Somites in the head region which are NOT FULLY SEGEMENTED
half baked
TWO TYPES OF DEVELOPMENT
Instructive - via induction

Permissive - via environment
somebody tells you what to do

nice weather allows us to go out and play
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
scratch my back and I will scratch yours
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
i will tell you a story but first let me tell you a tale
CONGENITAL DEVELOPMENT
Failure to Regress
haven't you left yet
ONCOGENES
abnormally activated genes that regulated cell growth and cell mitosis result in cancer of the embryo or post natally but of embryological origen
dna of the big C
MORPHOGENESIS
Development of SHAPE or FORM of whole structure or part of.

reguires expression/repression of genes IN SEQUENCE

regional specialization depends on morphogens
shape form sequence
MORPHOGEN
Anything that changes shape or form
ch ch ch changes
DELAMINATION
Cells of epi leaving epi to form new tissue
coming apart
PLACODE FORMATION
Thickening of epi - ie neural plate or optic placode
what you can look forward to your middle doing about the time you are ready to buy a practice
INVAGINATION
Proliferation of epi that folds and grows into the mesenchyme - ie optic cup or neural tube
poke a balloon
MESENCHYME
Embryological connective tissue
holds the litte tyke together
BUDDING AND BRANCHING
complex invagination forming cords tubes and pouches
think histology think of complex glands - the horror the horror
VESICULAR FORMATION
invagination that comes together, pinches off and sinks epi below the epi surface
you would like to _______ into a deep sleep - deep into the mesenchyme
EVAGINATION
Bulging out of epi - ie origin of optic vesicle from diencephalon
blowing up a balloon
ZONA PELLUCIDA
Non cellular glycoprotein SECRETED by the oocyte
if it were a chicken it would be the shell
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
its a rough and tumble world with lots of sticky situations and a everybody wants to fertilize you at once
TOTIPOTENT
cell that can become an individual organism - ie identical twins arise from two totipotent cells
each of us was once one of these
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
When does it occur

How long does each division take

do cells get bigger or smaller

what is the blasted name of each cell

at the 8 cell stage cells are still _________potent
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
if you are not totipotent you have _________

pull your friends closer and what the heck share some cytoplasm

spread yourselves thin but hold tight

the big baggie and the little ball within
MORULLA
More than 16 cells but still solid inside
Sweet and inocent 16 in the mulberry patch
BLASTULATION
Outer cells secrete fluid internally creating the blastocoel forming the BLASTOCYST
like peeing in rubber underpants - you will insist to change them
HATCHING
loss of zona pellucida as fluid in blastocoel enlarges blastocyst - essential for attachement to uterine wall
kinda like the chick loosing the shell except you get to stick to something warm and nutritcious
TROPHOBLAST
Outer layer of flattened cells connected by tight junctions - secretes fluid internally forming the blastocoel
the thin bit around the fluid
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.
FORMATION OF THE EPIBLAST WHICH IS THE ORIGIN OF THE THREE EMBRYONIC LAYERS.
EPIBLAST
Origin of the 3 embryonic layers via migration through its primative streak
source of the 3 amigos which slip through the slit
PRIMATIVE NODE
Forms at the crainal end of the primative streak. Epiblast cells migrate through it to form the NOTOCHORD
Sweet chords if you strike the right node
NOTOCHORD
Solid longitudinally oriented rod that is important in developing structures - particularly the NEURAL TUBE
We would be spinless and brainless without it.
NUCLEUS PULPOSIS
Residual notochord that forms the squishy bit in the centre of the intervetebral disk
it is just like pulp fiction when that baby escapes and gives the old spinal cord a body slam right after you try and pick up that 98 lb calf
TERATOLOGY
The study of the causes, mechanisms and manifestations of developmental deviations of either structural or functional nature
the ways and means of getting the big poo when trying to develop a little structure and function.
TERATOGENIC SUSCEPTABILITY

2 PERSPECTIVES 2 MEANS
INTRINSIC - Genotype of conceptus

EXTRINSIC - Enviroment including uterine
nature or nuture indoors and outdoors
3 STAGES OF TERATOGEN SUSCEPTABILITY
Predifferentiation
Early Differentiation
Advanced Organogenesis
2 difs and a genesis
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
getting in the baggie and the goings on once in
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
small and simple can be safe - easy to make more
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
being different can be unique - hard to replace one of a kind
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
safety in numbers but will the dog hunt
ABORTION
TERATOGEN STYLE
Manifistation of ABNORMAL DEVELOPMENT

Note embryo has high capacity to repair itself but declines after predifferention
is a sign of
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
how much is too much what is basic pathology
TERATOGENIC PATHOGENESIS
Teratogens act via specific MECHANISMS on developing cells and tissues to initiate SEQUENCES of ABNORMAL EVENTS
little ways to mess up the normal order of things
4 KEY EVENTS ON THE TERATOGENIC PATH
Mechanism
Pathogenesis
Common Pathway
Defect

Note the common pathway makes it hard to extrapolate cause from effect
a way to get an effect so that all the roads lead to an unhappy Rome
QUICK!!!
LIST 9
TERATOGENIC MECHANISMS
Mutation
Chromosomal Abnormalities
Mitotic Interference
Altered DNA
Lack of Precursors
Reduced Energy
Enzyme Inihibition
Osmolar Imbalances
Altered Membranes
well with all that cell division DNA and microtubules should be popular. Regulation requires a few enzymes and petptides and you have to make all that stuff out of something an expend a little energy not to mention the whole inside outside and flow of stuff between thing use your imagination you will probably get a few marks
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
goldi locks death and just how many toes did papa bear have

iduction is a touchy feely thing

no vegimite no buildy mite

You gotta move to morph

timing is everything when you want to be different
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
being direct usually works
getting in and out of the baggie is important
having a hot mom is not a good thing
neither is having a coke head for a dad
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
caution life ends in _______
not a pretty site
wont be tipping over any scales
sorta like post traumatic stress disorder - things just aren't right
ACCESS OF TERATOGENS DEPENDS ON
The physical nature of the teratogen

- rate of metabolism
- fat storage
- protein binding
lets get ___________

how fast, storage and bondage
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
how much did mommy get and how fast did she get it and what did she do with it and how long did it last and what might influence getting into the baggy - you get the picture
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
you need to work this one yourself its fundamental
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
did it come out and what did it look like
THE FOUR TERATOGENIC ETIOLOGIES
Genetic - not likely if hetero
Environmental - lowest probabilty
Infectious - good bet
Nutritional - also a good bet
back to the basic susceptabilities and did mommy eat her vegies and stay out of the rain
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
definitions are good, as are those handy things to have when knitting a sweater, a little phylenology can go a long ways and then there is what you get paid for
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
SUSCEPTABILITY
TIME OF EXPOSURE
MECHANISMS PATHOGENESIS
FINAL MANIFISTATIONS
PHYSICAL NATURE OF THE AGENT
DOSE FREQUENCY and DEGREE
CRITICAL PERIOD
Period when EACH organ is most sensitive to teratogenesis

- increased sensitivity during early organogenesis
timing
rome was not built in a day
INCIDENCE OF CONGENITAL ANOMALIES...
...varies greatly amongst species
real doctors treat more than one _________ and you have to be smarter to be a vet because _______ ________
5 TYPES OF ANOMALIES
Agenesis or Aplasia
Excessive Formation
Incomplete Development
Persistent Embryonic Structures
Malpositioning
too much
too little
like most home improvement projects
like a drug sales rep
the side of bed you got out of this morning
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
no growth or formation two 25 cent words that start with A
EXCESSIVE FORMATION
Organ or structure which is larger or more numerous

- ie polydactyly from excessive cell death
too much death gives you better math skills like the saskatoon cat population
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
rudimentary
come on baby light my fuse already
what happens when you read the first question of the exam
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
regression is a good thing especially if you do not want to pee out of your belly button
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.
mirror mirror on the wall...
Dr MACHINS FOUR TERATOGENS
GENETIC - simple or multiple genes, chromasomal defects (number or structural, hereditary

ENVIRONMENTAL - any external factor affecting development

INFECTIOUS

NUTRITIONAL
your personal grab bag of nucleic acids
what was the weather like while you were having your amniotic bath
did your mommy stay out of the rain and avoid catching a cold
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.
think about how little gametes are made. What structures are doing the M word dance and how many times do they do it. As there often is there is a little of the goldi locks syndrom
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
women can allways have it two ways theirs and theirs and males don't contribute much anyways
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
women can allways have it two ways theirs and theirs and males don't contribute much anyways
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
girls take a long time wheras the boys are done in a jiffy
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
half a gal can be quite a gal
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
girls take a long time wheras the boys are done in a jiffy
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
insufficiency, lose one lose two, no room to move, traffic jam, dont stay long, start small, bung up mom
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
half a gal can be quite a gal
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

TRANS ABDOMINAL US GUIDED INJECTION - 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
pinch, punch, puncture, slice, inject
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
insufficiency, lose one lose two, no room to move, traffic jam, dont stay long, start small, bung up mom
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.
boy girl vasucular hook up leads to exhange of DNA and hormones
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
pinch, punch, puncture, slice, inject
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
play the odds
take feel
check the levels
a little karyoke can see if she is your type
big or small
how is the egg factory
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.
boy girl vasucular hook up leads to exhange of DNA and hormones
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
greed
distance seperates
ramier
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
play the odds
take feel
check the levels
a little karyoke can see if she is your type
big or small
how is the egg factory
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.
see pg 23 of notes
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
greed
distance seperates
ramier
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
a little rot does not get the blood flowing
WHY ARE FREEMARTINS ARE RARE IN MOST SPECIES
Necrotic Tips
No Telling
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.
see pg 23 of notes
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
pg 25
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
a little rot does not get the blood flowing
WHY ARE FREEMARTINS ARE RARE IN MOST SPECIES
Necrotic Tips
No Telling
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
pg 25
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
pg 25
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
pg 25
ASPIRIN

THREE
Teratogenic Drug

- cleft palate
- cardio vascular defects
- abortion via effect on protoglandin

- dogs, cats and lab animals are most affected species
pg 25
ASPIRIN

THREE
Teratogenic Drug

- cleft palate
- cardio vascular defects
- abortion via effect on protoglandin

- dogs, cats and lab animals are most affected species
pg 25
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
pg 26
fussy scleric fusion
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
pg 26
fussy scleric fusion
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
pg 27