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71 Cards in this Set

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SULFONAMIDES
Teratogenic drug that acts like an nutritional tertatogen

Broad spectrum antibiotic use in many species.
- espcially Equine Protozoal Myeloencephalitis
- Structural analog of ParaAminoBenzoicAcid (PABA)

PABA is required by bacteria for the synthesis of folic acid.
- Sulphonamides taken up by bacteria blocks folic acid pathway
- Most mammals get folic acid from diet
- tf sulphonamides impact bacteria and not mammals
- but RUMEN/CECUM BACTERIA ARE AN IMPORTANT SOURCE OF FOLIC ACID FOR RUMINANTS AND HORSES
- treatment with sulphonamides kills rumen/cecum bacteria

Folic acid is important in choline (membranes)and purine (DNA) synthesis
- tf FOLIC ACID IS IMPORTANT FOR RAPIDLY DIVIDING CELLS

Fetus has high number of rapidly dividing cells
- tf dam requires 5x-10x amount of folic acid

Prognosis is poor

Difficult to treat mare with Folic Acid because most sulphonamides combined with pyrimethidine which inhibits absorption of folic acid
FOLIC ACID DEFICIENCY

5 Areas
Myloid, Erythroid and Lymphoid Aplasia/Hypoplasia

- tf born with low PCV and leukopenia
- hypoplastic bone marrow
- small inactive spleen and thymus
- renal lesions, lobulated kidneys, small and sparse glomeruli via hypoxia via low PCV
- epithelial lesions ie oral ulcers, lip ulcers, skin erosions, stomach ulcers via lack of choline synthesis

Neural Tube Closure
- tf spinal bifida

Thoracic and Abdominal Wall Defects

Cleft Palate and Cleft Lip

Digit and Limb Defects

Note
- if nutritional status of dam is good there is usually enough folic acid storage in liver for 1st trimester and 2nd trimester
- NEED TO SUPPLEMENT FOLIC ACID FOR 3rd TRIMESTER
VITAMIN A
Universal Teratogen
- deficiency or excess cause congenital abnormalities
- metobolites critical for normal development

Critical for Ectoderm
- tf and structures that require induction from ectoderm

- species variation

- spermatogenesis and estrus cycling

- essential componetn of Rhodopsin (rods and cones)
HYPOVIAMINOSIS A
Abortion icluding late gestation

Still Birth

Increased Osteoblasts

Decreased Osteoclasts

Micro or anopthalmia

Optic Nevice contstricted in calves due to bony overgrowth

Rats
- eye
- cardivosculature
- drophregmalic hernieas
- hypospedia
- open ventral urethra
- cryptorchidism

Neural Tube Defects
HYPERVIAMINOSIS A
Fetal reabsorption
- lower fertility

Muskuloskeletal Defects
- extra limbs
- heart defects

Eye Defects

Urogenital defects

Gastrointestinal defects

Decreased Osteoblasts

Increased Osteoclasts

Neural Tube Defects
PLACENTA

DEFINITION

FUNCTIONS 3
Structure that forms by the apposition of fetal membranes and maternal tissues

Mediates physiological exchange (nutrients and waste) between dam and fetus

Endocrine organ required to maintain pregnancy

Protective Barrie between fetal and maternal blood
- restricts pathogens and toxins
PLACNETA CHORIONIC SURFACE

SHAPE CLASSIFICATIONS 5
Diffuse
- porcine

Microcotyledons
- equine

Cotyledons in Rows
- Bovine

Zonary
- carinivores
- bounded by marginal hematoma

Discoid
- human/rodent
FUNCTIONAL PLACENTA
Site of Exchange between fetal and maternal membranes

ie cotyledonous, zonary and dicoid placentas have areas of fetal membrane that is not part of placenta because there is no exhange in these areas
PIG

PLACNETA
Diffuse
- communication over entire surface

Gestation 114 - 115 days

Initially Pancaked shaped, becomes filamentous (up to 1') at 11 days

Travels in uterus until all fetuses distributed evenly

Formation of necrotic tips
HORSE

PLACENTA
Diffuse
- via micro cotyledons

Gestation 340 days

Conceptus initially Spherical
- wanders uterus for 25 days

Chorionic girdle develops at 25 days
- secretes mucus which adheres sphere to endometrium
- at 36 days cells invade edometruim
- mare developes immune response which forms Endometrial Cups

Endometrial Cups
- present for 2 - 3 months
- max size at 55 - 70 days
- secrete Equine Chorionic Gonadotropin which helps maintain pregnancy
- eventually mare immune system eliminates invading fetal cells
RUMINANT

PLACNETA
Cotyledons distributed in various patterns

Bovids Convex Cotyledons

Ovids Concave Cotyledons
PLACENTOME
Cotyledon + Caruncle

Cotyledon
- discrete elevations of chorioallantoic tissue of ruminant FETAL membranes that adhere intimately with the maternal caruncles.
- note can be confusing becaues real doctors refer to cotyledons as any subdivision of the human placenta

Caruncle
- fleshy masses on the wall of the UTERUS of rumminants
- much larger in pregnant animals
- point of attachement to fetal membranes
- typically about 100
CARNIVORE

PLACENTA
Zonal
- band around girth in cats and dogs
- much more invasive tf leaves scars
- breakdown of RBCs at edge of zone produces green bilirubin which may stain fetus of next pregnancy
PLACENTAL LAYERS

6 OF EM FROM BLOOD OF FETUS TO BLOOD OF DAM
FETAL LAYERS
- Edothelium aka allantoic mesoderm
- Connective Tissue aka mesoderm
- Epithelium aka chorionic ectoderm

MATERNAL LAYERS
- Epithelium
- Connective Tissue
- Endothelium
PLACENTA

4 CLASSIFICATIONS BY LAYERS

SPECIES EXAMPLES
EPITHELIOCHORIAL
- All layers intact
- Horse, Pig, Bovids (mainly)
- Caprids and Ovids (partially)

SYNEPITHELOCHORIAL aka SYNDESMOCHORIAL
- loss of maternal epithelium due to invasion of fetal membrane (trophoblasts)into endometrium
- Bovids (partially) via binucleate cells
- Carpids and Ovids (mainly)

ENDOTHELIALCHORIAL aka Deciduate
- Maternal Epithelial and Connective Tissue layers are lost as placenta develops
- Endothelium Intact
- additional maternal tissue may be lost during partuition
- Carnivores

HEMOCHORIAL
- Maternal Epithelium, Connective Tissue and Endothelium are lost as placenta develops
- Fetal placenta bathed in maternal blood
- high risk of mixing maternal and fetal blood during partuition
- rodents and primates
FETAL MEMBRANES

4
CHORION
- trophpblast contributes to

ALLANTOIS
- hypoblast contributes to
- accumulates waste

YOLK SACK
- connected BUT NOT OPEN TO gastrointestinal tract
- incorporates veins which transport nutrients
- analogous to physiological embilical hernia
- incorporated into abdominal cavity before birth especially in precosious species
- remmenent of yolk sac is Meckles Diverticulum on surface of intestine between jujunum and illeum

AMNION
- closest to fetus
- encorporates entire embryo
- creates environment exclusive of waste

Chorion and Allantois fuse in mammals to form CHORIOALLANTOIS
HYDROALLANTOIS
Inadequate fluid removal from allantois by dam

Enlarged Abdomen
- impares respiration and GI function

Horses and Cattle
DEVELOPMENT OF BODY FORM
Flat disk transitions to cylindrical shape via
- formation of head and tail processes
- lateral edges fold under embryo forming tube

Notochord induces develoment of neural plate

Mesoderm Segments into:
- Somites (aka paraxial mesoderm)
- Intermediate Mesoderm- froms gonads and reproductive system
- Lateral Mesoderm which splits into:
~ Somatic Parietal forms git
~ Splanchic forms viscera, pleura, peritoneum
- Lateral Mesoderm forms tube pulling ectoderm with it
BODY FORM

ABNORMAL DEVELOPMENT
Incomplete Fusion Along Lateral Midline
- herniation of abdominal and thoracic contents

Exact mechanisms not known

Likely happens during early post gastrulation period

likely involves lateral and intermediate mesoderm
SCHISTOSOMUS REFLUXUS

aka

FETAL MONSTER
SCHISTOSOMUS
- exposure of BOTH abdominal and thoracic viscera

REFLEXUS
- spinal inversion
- dorsal flexure sot that skull meets pelvis

Primarily seen in ruminants
- 0.01 - 1.3% of dystocia in cattle
- also humans

Usually accompanied by Ankylosis (joint fusion) of limbs due to lack of movement

Lungs and diaphrgum tend to by hypoplastic

Fetus live at term but dystocic
- tf c section or fetotomy
- if live delivery calf dies due to lack of ability to inflate lungs (open thorax)

May Feel:
- intestines
- heart beating
- abnormal flexion
- head and four limbs
- cant rearrange limbs

Fetus will secrete certain proteins which when exceptionally high indicate severe abnormalities

Genetic via two modes
- Autosomal Ressesive
- X chromosome
COELUM
Thoracic and Peritoneal cavities before division by diaphragm
PHYSIOLOGICAL HERNIA
Development of GIT external to fetus
- neccesitated by large amount of space taken by heart and liver
- hind gut retracts into enlarging abdominal cavity, then foregut
OMPHALOCELE
Portion of intestines which remain outside of abdomen via a Physiological Hernia

EXTRA CUTANEOUS
- ie covered by amnion
UMBILICAL HERNIA
Failure of UMBILICAL RING to close

Umbilical Ring is surrounded by rectus abdomenus which must fuse
- if omentum passes through umbilical ring portion of GIT becomes SUBCUTANEOUS

- if large will be subject to:
~ Strangulation
~ Twisting
~ Trauma

Genetic component is major
- tf highly heritable
UMBILICAL HERNIA

TREATEMENT
If hole SMALLER than finger
- intestine not likely to pass through defect
- may resolve over time tf wait until spay/neuter

Larger than finger requires surgery
INTRAGENIC

UMBILICAL HERNIA
Induced by Veterinarian
- excessive pulling on umbilical cord
- sever umbilical cord too close to body which pervents normal regression
- insufficient support of umbilical cords during C-Section
SEPARTATION OF PERITIONEAL AND
PLEURAL CAVITIES

3 Tissues
Formation of Diaphragm

- Septum Transversum

- Plueroperitoneal Membrane

- Somatic Mesoderm
SEPTUM TRANSVERSUM
Originates from ventral body wall

Grows dorsally

Seperates liver and heart

Results in PARTIAL seperation of abdominal and thoracic cavities

Stops growing when it meets structures in mediastinum
- ie esophagus

- blocks caudal end of "tube" formed by pleuroperitoneal membrane
PLEUROPERITIONEAL MEMBBRANE (FOLD)
Paired

Grows ventrally and medially from Dorsal and Lateral body wall

Forms longitudinal "tube"

Stops growing when it meets mediastinum
SOMATIC MESODERM
Forms later in gestation

Grows on margins of body wall

Eventually forms muscular portion of diaphragm
PLEUROPERICARDIAL MEMBRANE (FOLD)
Concurrent with lung development

Grows medially in dorsal plane from middle of thoracic wall to meet mediastinum

Lungs grow ventrally from dorsal wall which pushes pleuropericadial fold downwards until it meetus under ventral part of heart

Result is formation of Pericardium
CONGENITAL DIAPHRAGMATIC HERINIAS

NAME 3
Peritoneopericardial Herina

Pleuroperitoneal Hernia

Hiatal Hernia
PERITONEOPERICARDIAL DIAPHRAGMATIC HERNIA
Hole in Septum Transversum
- tf septum transversum does not meet pericardial fold

Allows gut to enter pericardial sac

Defect is more Ventrally located

Not likely due to trauma becauses involves two membranes

Most common diaphragmatic hernia in dogs and cats
- can go unrecognized in cats
PLEUROPERITONEAL DIAPHRAGMATIC HERNIA
Incomplete fusion of Pleuroperitioneal fold

Liver or Lung lobe becomes entraped

More Dorsally located

High mortality because organ involvement
HIATAL DIAPHRAGMATIC HERNIA
Incomplete fusion of pleuroperitoneal membrane and Mesoesophagus

Intermittent passage of gut loops

More dorsally and medially located

Small compared to pleuroperitoneal diaphrgmatic hernia
DIAPHRAGMATIC HERNIAS

4 CAUSES

DISTINGUISHING FEATURES
Autosomal Recessive
- cats 1/500 - 1/1500

Polygenic
- dogs

Teratogens
- polybrominated phenols
- nutrition
~ hypo vitamin A
~ zinc

Note will see smooth edges at expected junctions with congenital hernias
Prenatal Injury
- tearing
- trauma
- will see blood clots and ragged edges
PARVOVIRUS
Infectious Teratogen

Replicates in rapidly dividing cells
- tf GIT and bone marrow in adults

Small enough to cross placental barrier
- affects fetus
~ GIT
~ Bone Marrow
~ Lymphoid Tissue

Also increase in body temperature of DAM during infection has teratogenic effects
- tf important to treat fever in Dams
PARVO VIRUS

PIGS
1st Trimester
- resorption

2nd Trimester
- abortion, mumification

3rd Trimester
- no effect

Note because pig uterus is long those closer to blood supply have higher exposure to virus
- tf varying effects within uterus
PARVO VIRUS

DOGS
< 20 days
- resorption

20 - 35 days
- abortion

> 35 days
- live pups
- parvoviral diarrhea
- myo carditis
- poor prognosis
PARVO VIRUS

CATS
Panleukopenia (feline parvo)

Early
- resorption or fetal death

Occasionally live kittens
- brain effects
~ ataxia, exagerated stepping
~ cerebellar hypoplasia

Cerebral malformations

Hydrocephalic

Defects in eye development
- blindess
BOVINE VIRAL DIARRHEA (BVD)
Transmitted from animal to animal accross mucosal membranes

Shed in feces urine, ucus, semen of acutely or persistently infected animals

Mucosal disease
- tf replicates in mucosal surfaces

Early
- embryonic death

35 - 125 Days
- Persistently Infected Calves
- shed virus throughout lives in cycles related to stress
- ASYMTOMATIC tf high risk to herd
- may be aborted or mummified

3 - 5 Months
- Cerebellar hypoplasia
- ocular abnormalities
- skeletal abnormalities
- hypotricosis ie sparse hair, patchy coat

4 - 7 Months
- most abortions

> 180 Days
- Normal calves with precolostral antibodies
- NOT shedders
DEVELOPMENT OF FACE MOUTH AND PHARYNX
Nasal Placodes on Frontal Prominance sink to form pits forming MEDIAL AND LATERAL NASAL PROCESSES

Nose and Upper Lip
- Lateral Nasal Process
- Medial Nasal Process
- Maxillary Process

Maxillary Process and Mandibular Arch both originate form Arch One
- each side grows medially to merge
CLEFT LIP
Failure to Fuse
- more commonly where lateral nasal, medial nasal and mazillary processes meet ie bilateral
- less common is central cleft lip via maxillary processes ie unilateral

Usually defect is in underlying mesenchyme
- prevents migration of epithelium
BRACHYGNATHIA
Short Mandible aka Parrot Mouth

Common (also overbites) because not normally lethal

Cattle
- autosomal recessive

Defect in underlying mesenchyme
- bone follows form of mesenchyme
DEVELOPMENT OF THE PALATE

2 COMPONENTS
Primary
- right and left nasal processes form majority of primary palate
- incisive bone

Secondary
- derived from maxillary process via caudal half of maxillary process migrating medially
- grows above tongue to meet nasal septum
- forms palantine shelf

Fusion starts in middle of palantine shelf and progresses CAUDALLY AND CRANIALLY
- fusion incomplete forming cranial and caudal passages in palate between oral and nasal cavities
NASAL CAVITIES
Nasal Pit forms above Medial Nasal Prominance

Oronasal Membrane seperates oral and nasal cavities

Breakdown of oronasal membrane forms:
- Primitive Choana rostrally which is then obliterated by secondary palate
- Definitive Choana which is moved caudally by secondary palate
CLEFT PALATE
Most commonly failure of secondary palate to fuse anywhere along the midline

Often from Vitamin A deficiency

Failure to fuse of Primary Palate is less common

May get combination of failure to fuse of primary and secondary palates and cleft lip

Poor prognosis
- cant form suction to suckle
- aspriation of milk from nostrils
CHOANAL ATRESIA
Failure of oronasal membrane to degenerate

Obligate Nasal Breathers
- Major problem

Mouth Breathers
- loss of
~ filtering
~ warming
~ humidifying
BRANCHIAL ARCHES
aka Pharyngeal or Visceral

6 paired arches in Total
- not all present at the same time in entirety
- ie get development of paired aortic arches but not all persent at same time and some arches may not have a mesenchymal portion

Important
- head, skeletal and muscular structures
- also contribute to cranial nerves and othere structures

Formed of Endoderm and Ectoderm surrounding arch body of Mesoderm

Seperated internally by Pouches and externally opposed clefts where Endoderm and Ectoderm directly contact each other

Arches I, II and V (incorporates IV & VI) can be appreciated externally
CONTRIBUTION OF

ARCHES
Arch I
- cranial 2/3 of tongue

Arch II
- regresses then INVAGINATES (foramen cecum) forming Thyroid gland at base which then must MIGRATE to neck through THYROGLOSSAL DUCT
- failure to regress results in Extra Long Tongue in cats. Usually still get formation of thyroid gland

Arch III
- caudal 1/3 of tongue

Arch IV
- epiglotis
CONTRIBUTION OF

CLEFTS

POUCHES
Cleft I
- External Auditory Tube

Pouch I
- Internal Auditory Tube
- Tympanic membrane forms between two from endoderm and ectoderm only

Pouch II
- Palatine tonsil

Pouch III
- Thymus
- portion of Parathyroid

Pouch IV
- Parathyroid
ABNORMAL DEVELOPMENT

THYROID
Ectopic Thyroid
- failure to migrate
- rare

Thyroglossal Cyst
- failure of regression of thyroglossal duct which is lined with glandular tissue
- allways on midline unlike most other structures of neck
- can interfere with movement of neck or impinge on other structures
TEETH

6 STEPS
Thickening of ectoderm in region of jaw forms
- Labiogingival Lamina lateraly
- Dental Lamina medially

Labioginival Groove forms
- lips laterally
- gingiva medially
~ectomesenchyme forms bone
- ulitimatley becomes vestibule

Dental Lamina invaginates forming
- dental bud
- if species with decidious teeth
~2nd permanent dental bud which is arrested
Dental Bud becomes cup shaped
- Enamel Organ

Condensation of Ectomesenchyme within "cup" or bifurcation of Enamal Organ froms
- Dental Papilla
- ultimately becomes tooth pulp

Inner Layer of Epithelium lining the "cup" enamal organ and overlying the dental papilla induces overlying layer of connective tissue of the enamel organ to become ODONTOBLASTS which in turn induce the connective tissue overlying them to become AMELOBLASTS
TEETH

6 LAYERS

FROM TWO STRUCTURES
ENAMEL ORGAN
- Ameloblasts
~ Enamel
~ Dentin
- Odontoblasts

DENTAL SAC
- Cementoblasts
~ Cementum
- Peridontal Ligament
- Bone Socket
DENTIGEROUS CYSTS
Epithelial lined cavities with some form of tooth element
- ie from just dentin to whole tooth

Usually external to labial gingiva area

Most common in horses
- usually near ear
~ ie "Ear Teeth"
- fluid filled, may develop drainage tract
- can remove surgically but difficult because of high number of nerves, glands and blood vessels in area

Other species
- jaw line
- palate
SUPERNUMERY TEETH
Extra Teeth

Common in Dogs
- mainly incisors and canines
- can cause crowding and rotation
- neonates may have RETAINED DECIDUOUS TOOTH
~ permanent tooth not dragged underneath decidupus tooth
~ tf roots do not errode
~ common in toy breeds
~ remove surgically

Horses
- mainly develop in hard palate
- misplaced tissue
- platal shelves migrate dragging along ectomesynchyme with tooth potential
ANODONTIA
No Teeth
- extremely rare
- complete failure of enamel organ
- may fail to develop specific teeth
~ dogs premolars
~ cats incisors
ENAMAL HYPOPLASIA
Defective differentiation on inner layer of epithelium in Enamel Organ
- ie ameloblasts
- prenatal infection
~ dogs distemper and parvo
~ cats parvo
~ cattle BVD

- Ectomesenchymal collagen defect
~ inherited in Holstein Cows
CARDIOVASCULAR DEVELOPMENT

A FEW FACTIODS
1st functional system to develop
- required for circulation of nutrients and wastes once embryo has exceeded size of effective diffusion

Pumping Heart
- 18 days (gestation 63) dogs

Starts with Angiogenic Cell Clusters (Blood Islands)
- Coagulation leads to differentiation in edothelial lined sinusoidal spaces
- Sinusoidal Spaces coalesce and bud to form vessels

Vessels develop from Aortic Arches by budding and invaginating into underlying tissues
- cells of underlying tissues differentiate to form walls of vessesls
- vessel type (artery, vein, capillary) is determined by pressure differential

Heart starts as tube
-Dorsal aorta fuse to form descending aorta caudal to the Arches

Vascular system is dynamic
- Fusion
- Cell Death
- Invagination
- Invasion
all required to move from embryonic to adult vascular pattern
VASCULAR ANOLOMIES

TWO CAUSES
Failure to Occur

Failure to Regress
AORTIC ARCHES
6 Pairs form within Branchial Arch mesenchyme between dorsal aorta and vental aorta (aortic sac)

Not all exist at same Time !!!

Arch I and II
- minor contribution
- mainly just disappear

Arch III
- Cranial Vessels
~ common carotid

Arch IV
- Left becomes aortic arch/dorsal aorta
- Right
~ ventral portion becomes right subclavian
~ dorsal portion DEGENERATES tf DOES NOT FUSE WITH VENTRAL AORTA

Arch V
- reptiles only
- non existent in mammmals

Arch VI
- Both sides form ventrally the pulomonary trunk and pulmonary arteries (L & R)
- Left side dorsally remains open to descending aorta forming DUCTUS ARTERIOSIS
- Right side degenerates dorsally
PERSISTENT RIGHT AORTIC ARCH
aka Vascular Ring

Right aortic Arch IV persists

- forms aortic arch
- traps the trachea and esophagus between it and Left aortic arch VI (ductus arteriosis/ligamentum arteriosis
- Left aortic arch IV usually degenerates

Presentation
- small, poor body condition
- ravenous
- regurgitation and ingestion when weaned
- aspiration pneumonias
- alkalosi
- ulcers
- mega esophagus

Treatment
- cut ligmentum arteriosis
- double ligature of ligmentum arteriosis because may still be patent
PATENT DUCTUS ARTERIOSIS

WHAT IS IT

WHAT SHOULD HAPPEN

WHAT 3 THINGS FAIL
Failure of Left Aortic Arch VI to close post natally

Closure is via physiologic and anatomic mechanisms
- when animal is born INHALATION of air into lungs EXPANDS lungs OPENING blood vessels of lungs LOWERING RESISTANCE
- pO2 Increases
~ hypertrophy of Left Ventricle
- PROSTOGLANDIN decreases
- Increased pO2 and decreased Prostoglandin stimulates chemoreceptors in wall of ductus arteriosis producing
~ constricion with hours
~ fibrosis withing weeks

Failure Mechanisms
- low pO2 due to hypoxia
~ chemoreceptors are only sensitive for a short time after birth
~ hypoxia during birth due to strangulation of umbilical cord
- high level of prostoglandins or analogs
- defects in muscle or receptors of ductus arteriosis
~ patchy presence of receptors
~ defective receptors
~ insufficient muscle in wall

Also other factors such as drugs and viruses
PATENT DUCTUS ARTERIOSIS

PRESENTATION
Most common in Dogs
- 1 in 750 - 1000 puppies
- 25 - 30% of canine heart defects
- 3:1 female:male sex ratio

Also cats, horses and cattle

Excercise Intolerance

Cyanotic

Heart Murmer
- mild to grade 6 (washing machine)

Genetics
- polygenetic
- autosomal trisomys 13, 15 & 18
- translocations and deletions

Varying grades (6) depending on combined effects of
- muscular distribution
- pO2
- prostoglandin
PATENT DUCTUS ARTERIOSIS

TREATEMENT
Minor
- tie off
- ductus is friable
- place coil to induce scarring

Major
- bad surgical candidate
- if very young
~ NSAIDS (ibuprofin, aspirirn) will lower prostoglandin levels

70% die if untreated
DEVELOPMENT OF HEART TUBE

4 BEAUTEUS BULGES

NAME EM AND THEIR DESTINY
Accumulation of angiogenic clusters
- near head region
- between Splanchnic Mesoderm Layer and Endoderm
Form left and right tubes

Head Process curls ventrally dragging angiogenic clulsters/tubes with it
- heart forms between curvature of this curl, stomodeum and cranial extent of foregut

Tubes coalesce
- forms Heart tube
- bounded by
~ ventral aortae
~ vitelline veins

Heart Tube develops 4 bulges
- Bubus cordia
~ forms right ventricle
- Ventricle
~ forms left ventricle
- Atrium
~ forms left and right atria
- 2 Sinus Venosus
~ Right incorpororates into right atrium
~ Left forms cranial and caudal vena cava and has minor incorporation into left atrium
FIVE STEPS TO FOLD

THE

HEART TUBE
Breakdown of dorsal mesentary to allow
- fold
- lenghten
- twist

Bulbus cordis and Ventrical loop upon themselves to produce Right and Left ventricles respectively

Atria moves cranially and to the left becoming dorsal to the ventricle

Right Sinovenosus is incorporated into Right Atrium

Left Sinovenosus forms cranial and caudal vena cava
A-V VALVE

DEVELOPMENT
ENDOCARDIAL CUSHIONS
- proliferation of mesenchyme
- migrate across centre of ATRIOVENTRICULAR CANAL
- connect to form
~ Left and Right Atrioventricular Canals

Valves develop from PROLIFERATION of ventricular walls forming FLAPS AND LEAFLETS

Left A-V valve
- Biscupid aka mitral

Right A-V valve
- tricuspid
A-V VALVE

ABNORMALITIES
Developmental problems result in in VALVULAR DISPLASIA

Notching

Incomplete seperation from ventricles

Shortening or Thickning of leaflets

Diagnose via murmurs

Left A-V (bicuspid, mitral) is most comonly diagnosed in
- cats especially
- dogs (large breeds)

Right A-V (tricuspid)
- dogs large males
- cats
VENTRICULAR DEVELOPMENT
Division of common ventricular chamber formed by bulbus cordis and ventricle into left and right ventricles

Muscular septum grows dorsally from apex of heart towards endocardial cushion

Most dorsal portion of septum is thin and membraneous
VENTRICULAR DEVELOPMENT

DEFECTS
Membraneous portion of interventricular septum is site of most development defects
- incomplete growth and failure to reach endocardial cushions
- Sheep and Horses #1 overall heart defect
- Cattle #2 overall
- Cats and Dogs # 3 overall

Idiopathic
- Genetically linked in Hereford cattle

Displacement of Endocardial Cushions
- alters blood flow
~ affects development of other structures
~ tf usually produces other heart defects