VBMS 213 Embryology Quiz 2
Terms
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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