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111 Cards in this Set
- Front
- Back
- 3rd side (hint)
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ZYGOTE
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fertilized egg
only one cell |
two gametes =
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EMBRYO
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anything after the first division
> one cell |
at least twice as much as a zygote
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FETUS
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after formation of organs & systems
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need some identifiable items
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CONCEPUTUS
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product of conception
embryo or fetus plus the fetal membranes |
everything foreign to dam
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EMBRYOGENESIS
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formation of body structures and organs
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enough of this and you become a fetus
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ORGANOGENESIS
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formation of organs
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too easy
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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 |
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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
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THE TWO BASIC PROCESSES OF DEVELOPMENT
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Growth - proliferation, cell size and extracellular matrix
Differentiation |
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3 WAYS TO CONTROL GROWTH
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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 |
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DIFFERENTIATION
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Changes in physical and functional properties within cell
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good old form and function
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THE TWO RESULTS OF DIFFERNENTIATION
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Population of daugher cells different from parent
Variety of cell types within a population that was once uniform |
daughters and diversions
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WHICH IS FIRST
STRUCTURE OR FUNCTION AND THE 25 CENT WORD |
Early changes tend to be functional via CHEMIODIFFERNTIATION not morphological
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form does not always follow function but how
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4 THINGS THAT CONTROL EXPRESSION AND REPRESSION OF GENES
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Receptors
Peptides, enzymes, hormones Channels and Pumps - ions Extra Cellular enzymes and hormones |
the usual suspects think in and out of the "box"
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THE 3 GENERAL CELL TYPES OF DIFFERNTIATION
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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 |
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MORPHOGENESIS
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Formation of differentiated cells into structures
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the new war museum is a _____ kind of _______
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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
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I SAY PRIMORDIAL AND YOU SAY
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Chorda mesoderm aka THE PRIMORDIAL ORGANIZER
Contains segmentally arranged somites which develop from the mesodermal axis |
a mighty middle sort of chord
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SOMITES
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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
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SOMITOMERES
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Somites in the head region which are NOT FULLY SEGEMENTED
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half baked
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TWO TYPES OF DEVELOPMENT
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Instructive - via induction
Permissive - via environment |
somebody tells you what to do
nice weather allows us to go out and play |
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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
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APOPTOSIS AND EXAMPLE
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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
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CONGENITAL DEVELOPMENT
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Failure to Regress
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haven't you left yet
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ONCOGENES
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abnormally activated genes that regulated cell growth and cell mitosis result in cancer of the embryo or post natally but of embryological origen
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dna of the big C
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MORPHOGENESIS
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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
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MORPHOGEN
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Anything that changes shape or form
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ch ch ch changes
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DELAMINATION
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Cells of epi leaving epi to form new tissue
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coming apart
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PLACODE FORMATION
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Thickening of epi - ie neural plate or optic placode
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what you can look forward to your middle doing about the time you are ready to buy a practice
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INVAGINATION
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Proliferation of epi that folds and grows into the mesenchyme - ie optic cup or neural tube
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poke a balloon
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MESENCHYME
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Embryological connective tissue
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holds the litte tyke together
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BUDDING AND BRANCHING
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complex invagination forming cords tubes and pouches
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think histology think of complex glands - the horror the horror
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VESICULAR FORMATION
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invagination that comes together, pinches off and sinks epi below the epi surface
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you would like to _______ into a deep sleep - deep into the mesenchyme
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EVAGINATION
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Bulging out of epi - ie origin of optic vesicle from diencephalon
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blowing up a balloon
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ZONA PELLUCIDA
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Non cellular glycoprotein SECRETED by the oocyte
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if it were a chicken it would be the shell
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3 FUNCTIONS OF THE ZONA PELLUCIDA
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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
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TOTIPOTENT
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cell that can become an individual organism - ie identical twins arise from two totipotent cells
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each of us was once one of these
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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 |
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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 |
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MORULLA
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More than 16 cells but still solid inside
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Sweet and inocent 16 in the mulberry patch
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BLASTULATION
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Outer cells secrete fluid internally creating the blastocoel forming the BLASTOCYST
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like peeing in rubber underpants - you will insist to change them
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HATCHING
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loss of zona pellucida as fluid in blastocoel enlarges blastocyst - essential for attachement to uterine wall
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kinda like the chick loosing the shell except you get to stick to something warm and nutritcious
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TROPHOBLAST
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Outer layer of flattened cells connected by tight junctions - secretes fluid internally forming the blastocoel
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the thin bit around the fluid
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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.
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FORMATION OF THE EPIBLAST WHICH IS THE ORIGIN OF THE THREE EMBRYONIC LAYERS.
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EPIBLAST
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Origin of the 3 embryonic layers via migration through its primative streak
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source of the 3 amigos which slip through the slit
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PRIMATIVE NODE
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Forms at the crainal end of the primative streak. Epiblast cells migrate through it to form the NOTOCHORD
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Sweet chords if you strike the right node
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NOTOCHORD
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Solid longitudinally oriented rod that is important in developing structures - particularly the NEURAL TUBE
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We would be spinless and brainless without it.
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NUCLEUS PULPOSIS
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Residual notochord that forms the squishy bit in the centre of the intervetebral disk
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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
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TERATOLOGY
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The study of the causes, mechanisms and manifestations of developmental deviations of either structural or functional nature
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the ways and means of getting the big poo when trying to develop a little structure and function.
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TERATOGENIC SUSCEPTABILITY
2 PERSPECTIVES 2 MEANS |
INTRINSIC - Genotype of conceptus
EXTRINSIC - Enviroment including uterine |
nature or nuture indoors and outdoors
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3 STAGES OF TERATOGEN SUSCEPTABILITY
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Predifferentiation
Early Differentiation Advanced Organogenesis |
2 difs and a genesis
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2 MECHANISMS OF SPECIES DIFFERENCES FOR GENETIC TERATOGENIC SUSCEPTABILITY AND 2 EXAMPLES
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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
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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
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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
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being different can be unique - hard to replace one of a kind
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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
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ABORTION
TERATOGEN STYLE |
Manifistation of ABNORMAL DEVELOPMENT
Note embryo has high capacity to repair itself but declines after predifferention |
is a sign of
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THRESHOLD
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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
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TERATOGENIC PATHOGENESIS
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Teratogens act via specific MECHANISMS on developing cells and tissues to initiate SEQUENCES of ABNORMAL EVENTS
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little ways to mess up the normal order of things
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4 KEY EVENTS ON THE TERATOGENIC PATH
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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
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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
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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 |
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4 SITES OF TERATOGENESIS
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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 |
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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 |
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ACCESS OF TERATOGENS DEPENDS ON
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The physical nature of the teratogen
- rate of metabolism - fat storage - protein binding |
lets get ___________
how fast, storage and bondage |
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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
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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
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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
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Abnormal Development
Reproductive Rate |
did it come out and what did it look like
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THE FOUR TERATOGENIC ETIOLOGIES
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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
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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
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THE 6 PRINCIPLES OF TERATOGENOLOGY
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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 |
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CRITICAL PERIOD
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Period when EACH organ is most sensitive to teratogenesis
- increased sensitivity during early organogenesis |
timing
rome was not built in a day |
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INCIDENCE OF CONGENITAL ANOMALIES...
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...varies greatly amongst species
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real doctors treat more than one _________ and you have to be smarter to be a vet because _______ ________
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5 TYPES OF ANOMALIES
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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 |
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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
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EXCESSIVE FORMATION
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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
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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 |
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PERSISTENT EMBRYOLOGIC STRUCTURES
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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
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regression is a good thing especially if you do not want to pee out of your belly button
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MALPOSITIONING
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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...
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Dr MACHINS FOUR TERATOGENS
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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 |
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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
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WHY DOES DISJUNCTION MORE COMMONLY OCCUR WITH SEX CHROMOSOMES
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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
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WHY DOES DISJUNCTION MORE COMMONLY OCCUR WITH SEX CHROMOSOMES
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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
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WHY DOES ABNORMAL GAMETOGENESIS OCCUR MORE FREQUENTLY IN FEMALES AS OPPOSED TO MALES
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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
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girls take a long time wheras the boys are done in a jiffy
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MOST COMMON CHROMOSOMAL ABNORMALITY IN HORSES
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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
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WHY DOES ABNORMAL GAMETOGENESIS OCCUR MORE FREQUENTLY IN FEMALES AS OPPOSED TO MALES
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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
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girls take a long time wheras the boys are done in a jiffy
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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
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MOST COMMON CHROMOSOMAL ABNORMALITY IN HORSES
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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
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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
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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
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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
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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
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SIX DIAGNOSTICS FOR FRISKY FREEMARTINS
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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 |
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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
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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 |
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SIX DIAGNOSTICS FOR FRISKY FREEMARTINS
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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 |
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TELL ME A DETAILED STORY ABOUT THE MECHANISMS OF FREEMARTINISM
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- 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
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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 |
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NECROTIC TIPS
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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
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WHY ARE FREEMARTINS ARE RARE IN MOST SPECIES
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Necrotic Tips
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No Telling
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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
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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
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NECROTIC TIPS
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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
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WHY ARE FREEMARTINS ARE RARE IN MOST SPECIES
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Necrotic Tips
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No Telling
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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
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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
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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
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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
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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
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ALBENDAZOLE
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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 |
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ALBENDAZOLE
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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 |
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GRISEOFULVIN
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- 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
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