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46 Cards in this Set

  • Front
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ATRIAL DEVELOPMENT

5 STEPS
PRIMARY SEPTUM (Septum Primum)
- grows ventrally from dorsal wall
- effaces the ventrally located PRIMARY FORAMEM (Ostium Primum)
- contains FENESTRATIONS
~~-- allows blood flow to continue

Fenestrations coalesce to form SECONDARY FORAMEN (Osteum Secundum)
- before Primary Septum reaches Endocardial Cushions and Primary Foremen is fully effaced

SECONDARY SEPTUM (Septum Secundum)
- grows ventrally from dorsal wall
- covers Secondary Foramen
- does not extend to Endocaridal Cushions

Dorsal portion of Primay Septum degenerates leaving ventral portion

FORAMEN OVALE
- is space between remaining flap of Primary Septum and its Secondary Foramen and the flap of the Secondary Septum
FUNCTION OF FORAMEN OVALE
Acts as a valve

Left Atrial pressure is lower than right because pulmonary circulation is restricted

Blood Flow:
- from Right Atrium
- through Foramen Ovale
- between Secondary and Primary Septums
- through Secondary Foramen
- into Left Atria

Foramen Ovale closes when:
- Pulomonary Circulation Opens
- Left Atrial pressure rises above Right Atrial pressure
FORMATION

AORTA AND PULMONARY TRUNKS

6 STEPS
Occurs via positioning of TRUNKUS ATRERIOSIS

Driven by Neural Crest Cells
- tf neural crest cells must migrate to heart

4 Swellings Develop
- RIGHT SUPERIOR TRUNCUS
- RIGHT DORSAL CONUS
- LEFT INFERIOUR TRUNKUS
- LEFT VENTRAL CONUS

Swellings are oriented at 90 deg to each other

Swellings grow so that the truncus meet the conus
- twisting occurs because of 90 deg orientation

AORTICOPULMONARY SEPTUM
- develops from the TWISTING of the swellings
TWO TWISTLESS TRAGEDIES
Aorta and Pulmonary Arteries may not seperate

Form two closed circulation systems
- Right Ventricle into systemic circulation
- Left Ventricle into pulmonary circulation
- Fatal Flaw
TETRALOGY OF FALLOT
Four abnormalities, occuring coincidentally, that results in insufficiently oxygenated blood pumped to the body

Ventricular Septal Defect
- opening between left and right ventricles
- generates other 3 defects
- usually results from Endocardial Cushion Defect

Displacement of Aorta over Ventricular Septal Defect
- aka Overiding Arota

causes

Narrowing of the Pulmonary Valve which results in

Thickening of Right Ventricle Wall

May have associated Patent Ductus Arteriosis

4% of Canine Heart Defects

6% of Feline Heart Defects

Most common heart defect in horses
SEQULAE OF HYPOXIA

4
Lethargy
- a few weeks after birth when pups become active

Tachycardia

Poor Growth

Increased PVC
- polycytemia
- thicker blood
VEINS

3 BIG ONES
Vitelline
- drains yolk sac

Umbilical
- blood from placenta
- oxygenated and nutrient rich

Cardinal Veins
- drain embryo
VEINS

DEVELOPMENT STORY
Vasculature is Dynamic
- fetal and neonatal period
- many anastomeses
- degenerations

As LIVER enlarges is starts ot incorporate VITELLINE veins proximally
- forms LIVER SINUSOIDS

UMBILICAL vein regresses Proximally
- distal portion may be incorporated into LIVER SINUSOIDS

Left UMBILICAL VEIN enlarges

PORTAL VEIN develops from
- RIGHT Vitelline vein via
- distal anastomosies of VITELLINE veins
- atrophy of of LEFT Vitelline vein
- regession of Proximal Umbilical Veins
- drains gut and spleen
~~-- via mesenteric and splenic veins

DUCTUS VENOUSUS
- forms from shift of blood from Right to Left
~~-- enlargement of left Umbilical Vein
- no need to dextoxify
~~-- embryo not eating
~~-- detoxification by dam
- blood from Unbilical vein
~~-- bypasses most liver tissue
~~-- joins portal vein
~~-- drains to Vena Cava
- closes 3 - 5 days after birth
~~-- forms teres hepatis ligament
PORTOSYSTEMIC SHUNT

TWO TYPES
INTRAHEPATIC
- Ductus Venosus does not close

EXTRAHEPATIC
- External Bypasses form around liver

Normal liver functions not utilized

Idiopathic
- Intrahepatic may be due to lack of Aryl Hydrocarbon receptors required for closure

Genetics
- Autosomal variable expressivity
- purebred dogs 0.18%
- mixed breeds 0.05%
- cats higher prevalence golden or copper coloured iris

Presentation
- low growth
~~-- dont utilize nutrients from gut in liver
- lethargic
- Toxicity Problems
~~-- seizures are diagnostic if within 6 months of birth
- Jaundice
INTRAHEPATIC ATRERIOVENOUS FISTULA
Abnormal communication between hepatic artery and hepatic or portal vein

Fistula forms between artery and vein
- opening with NO CAPILLARY BED
- Tends to affect lobes or portions of lobes
- may have smaller liver due to lack of hepatic nutrition

Presentation
- similar to Portosystemic Shunt
HEPATIC MICROVASCULAR DYSPLASIA
Abnormal communication between hepatic ARTERIOLES and Hepatic or Portal VENULES

Affects whole lobes

Normal external appearance
STATE THE

3 MAJOR CHANGES OF VASCULATURE
Ductus Arteriosus closes to become Ligamentum Arteriosum

Oval Foramen closes to become Fossa Ovalis

Ductus Venosus closes to become Ligment Teres Hepatis
- note also encorporates Umbilical Vein
NEURULATION
Notochord signals overlying Ectoderm
- creates patch of NEUROECTODERM

Neuroectoderm forms CNS
- NEURAL GROOVE froms in neuroectoderm
- NEURAL FOLDS develop from enlarging Neural Groove
- cranial formation is first sign of brain development

Ectcoderm grows over top of Neural Folds

Neuroectoderm seperates from overlying Ectoderm
- NEURAL CREST forms alongside dorsal lateral edges of Neural Folds
~~ produces NUERAL CREST CELLS

Neural Folds come together forming NEURAL TUBE
TWO FATES

OF

NEURAL CREST CELLS
Form Ganglionic cells and supporting structures of PERIPHERAL NERVOUS SYSTEM

Become ECTOMESENCHYME
- migrated ventrally and Cranially
- surround pharynx and Proencephalon
- Impartanf for develoment of
~~ facial features
~~ facial skeleton
~~ facial Connective Tissue
~~ Aorticopulmonary Septum
NEURAL TUBE
Starts development in centre of embryo

Closure of Neural Folds proceeds in cranial and caudal directions from centre to from tube

Forms Brain Cranially and Spinal Cord Caudally

Carivty forms Ventricles and Spinal Canal
EARLY CNS DEVELOPMENT
Flexure and Rotation

Proencephalon
- Forebrain
~~ Telencephalon
~~-- Cerebrum
~~ Diencephalon
~~-- Thalamus Trio

Mesencephalon
- Midbrain

Rhombencephalon
- Hind Brain
~~ Metecehphalon
~~-- Cerebellum
~~-- Pons
~~ Myelencephalon
~~-- Medulla Oblaongata
CYCLOPIA
Single Medial Orbit with relatively normal rudimentary eye

Usually no vision

Various degrees of fusion of eyes

Eye development is relatively normal
HOLOPROSENCEPHALY
Failure of forebrain to divide and seperate

Results in Cyclopia

Cyclopathogenesis
- Diencephalon does not outpouch
- Mediated by defects in SHH (sonic hedge hodge) protein
~~ non utilization of cholesterol
~~ genetic chromosomal abnormality of SHH
~~ competition of plant toxins for cholesterol receptors
~~-- Jervine & Cyclopanine
~~--~~ Veratrum Californium aka Western False Hellebore

Normal Development
- cholesterol is important in signaling process for brain development
- Notochord induces cells to produce SHH
~~ directs development of forbrain and optic regions via mediation with cholesterol
- outpouching required for differentiation of telencephalon and diencephalon

Risk Period
- 14 Days Sheep, Goats and Cattle

Grieseofulvin
- only in Cats is linked to Cyclopia
HYDROCEPHALY
Alteration in Cerebral Spinal Fluid (CSF) dynmaics results in enlargement of Ventricles

Usually caused by obstruction causing improper drainage
- obstruction tends to be associated with abnormality other than ventricles
Mechanism
- Choroid Plexi continuously produce CSF
- fluid build up applies pressure to grey and white matter
~~ white matter is more affected

Presentation
- Depressed because cognition is reduced
- Domed Head
- vision deficits via ventricular pressure on optic nerves
- paralysis
- seizure
- aka Dummie Foals
~~ may not have domed head

Common in Dogs and Cats
- brachyocephalic and toy breeds
- Bermese Cats
- Siamese Cats
~~ autosomal recessive

Horses
- 3% of Births
Cows
- 4.5% especially Herefords

Congenital Hydrocephaly
- Treatmennt Futile
- Improper CNS development because most development is early
HYDROCEPHALY

3 OBSRUCTIONS

3 AGENTS
Spinal Bifida at level of spinal cord

Optic Nerve Hypoplasia at level of optic chiasm
~~ obstruction between lateral ventricles or in 3rd Ventricle

Cranial Facial Abnormalities
~~ blockage in ventricles
~~ especially Bermese Cats

Griseofulvin

Pavovirus
- Dog

Panleukopenia
SPINAL BIFIDA
Cleft in vertebral arch
- skeletal abnormality
- failure of Neural Tube to close
- dorsal spinal process is malformed in one or more vertebrae
- exposure or improper encasement of Spinal Chord

Defect is usually caudally oriented
- severity increases cranially
SPINAL BIFIDA

TWO THERIES OF CAUSE
Overgrowth of Neural Tube Cells prevents fusion of neural tube

Neural Tube fuses then later splits

Net result is skeletal abnormality
SPINAL BIFIDA

THE THREE DEGRESS
OCCULATA (Hidden)
- Defect is covered by skin
- External appearance is normal or may have pit on spine
- diagnose via radiagraph
- least severe

MENINGOCELE
- protrusion of spinal cord through vertebra
- nerve tissue remains encased in Dura Matter
~~ nerve tissue NOT exposed
- presents as bump on spine
~~ normal neural function unless trauma

MENENGOMYELOCELE
- Protrusion of Spinal Cord and membranes through defect
- neningies may or may not be intact
- skin broken by defect
- developing spinal cord damaged by exposure to proteins in Amniotic Fluid
- also physical damage
- most common
- most severe
SPINAL BIFIDA

FOUR FACTORS
Genetics
- English Bull Dogs
- Manx Cats

Sulphonamide
- decreased folic acid

Griesofulvin
- Cats

Methyl Mercury
- Cats
DERMOID SINUS
Neural Tube Defect

Incomplete seperation of Neural Tube from Overlying Ectoderm

Can occur anywhere from head to base of tail

Always on Midline

Small hole and tract
- large enough to allow infection
- particularly if drainage of CSF

Most commonly seen in Sacrococygeal Region

Mechanism
- Genitics and Folic Acid deficiency
- Rhodesiona Redge Back
~~ inverted hair stripe
- other dog breeds
- cats
DERMOID SINUS

FIVE FABULOUS CLASSES
III
- least pathalogic
- sinus extends into Connective Tissue only
- cyst

II
- sinus extends to Supraspinous Ligament
- ventral portion is closed fibrous strand
- may drain

I
- sinus extends to supraspinous ligament
- drains

IV
- sinus extends through Supraspinous Ligament and attaches to dura matter
- drains

V
- NOT OPEN TO SKIN
- sinus extends from muscle layer through to Supraspinous Ligament
MUSCULOSKELETAL SYSTEM
Paraxial Mesoderm produces Somites
- fused in head region
~~ ie SOMITOMERE

Somites produce 3 structures
- Dermatomes
~~ dorsal
~~ Dermis
- Myotome
~~ Muscle
- Sclerotome
~~ ventral
~~ migrates to fully enclose Notochord
~~ axial skeleton
~~ vertebral bodies
~~ caudal portion of one somite and cranial portion of adjacent somite form one veterbral body
~~ notchord becomes Nucleus Pulposis
-
MUSCLE
All skeletal muscle id derived from Myotome portion of Somites/Somitomeres

Myoblasts of Myotome fuse to form Multinucleate Muscle Cells

Dorsal portion of Myotome gives rise to Epaxial Muscles
- dorsal to Transverse Processes

Ventral portion of Myotomes give rise to Hypaxial muscles
- ie everything ventral to Transevers Processes

Muslsle Development requires
- Enervation
- Tension
~~ including Tendons
~~ stretched by growing bone
~~ tf abnormal bone = abnormal muscle
- most congenital muscle abnormalities are Secondary
BONE

FIVE STEPS
Most bones formed by Endochondral Osssification

Process
- Condenstation of Mesenchyme
- Differntiation of Chondroblasts
- Formation of Cartilage Model
- Cartilage Model Ossifies into Bone
- Structure of bone determined by
~~ Applied Forces
~~ Genetics
~~ tf Movement in Uterus critical
~~ most structural development takes place after birth
SKULL
Formed by 2 types of Ossification

Endochndrial
- Base of Cranium

INTRAMEMBRANOUS
- Flat Bones of Skull
- Facial Bones

Note
- Jaw has both types
- shape determined by cartilage model

Abnormalities
- normal development of skull involves interaction with many other structures of head
- eye
- brain
BLOCK VERTEBRAE
Error in RESEGEMENTAION of Somites

Partially seperated Vertebae
- may include vertebral disk malformations

Overlying vertebral body forms relatively normally
MALFORMATIONS

OF

VERTEBRAL CORD

CLINICAL SIGNS
Tend to compromise spinal cord via compression

Clinical Signs
- may occur at birth or later in life
- may have block vertebra that do not create clinical signs
- no compression = no clinical signs

Spinal Compression creates
- narrowing of spinal canal
- instability of involved segments
- animal is susceptabile to insults
~~ can be as minor trauma as a jump
- Luxation (aks dislocation)
- Fractures

Clinical Presentation
- Ataxia
- Paresis
- Paralysis
HEMIVERTEBRA

PLUS 3 QUIZ FRIENDLY TERMS
Common Cause for
- KYPHOSIS
~~ permenant FLEXION of spine
- LORDOSIS
~~ permenant EXTENSION of spine
- SCOLIOSIS
~~ permenant LATERAL DEVIATION

Wedge shaped vertebrae
- one or more

Defect in vasclar supply during develpment
~~ results in incomplete development

Abnormal Ossification
- may involve vascular deficiency

Normal in some dog breeds
- Screw Tails
~~ Bulldogs, Pugs extc

Manx Cats

Cats
- Hypervitaminosis A
ATLANTO AXIAL SUBLUXATION
Results from abnormal development of DENS

Dens normally origninates from C1
- later fuses with C2

Defects
- hypoplastic DENS most common
- absent DENS
- failure of DENS to fuse with C2
- improper development of muscles and Ligaments

Subluxation is usually Dorsal
- tf spinal cord problems

Toy breeds
MID CERVICAL SUBLUXATION
Horses
- malformation
- malarticulation
- especially C3-C4
- rapidly growing
- Thorough Breds
- aka wobblers
~~ ataxia
~~ paresis

Dogs
- C5, C6, C7
- rapid growth
~~ genetics
~~ nutrition
- Large breeds and Bassetts
OCCIPITOATLANTOAXIAL MALFORMATION

SIX SEDITIONS
Occipital Bone is Absent

Fusion of Atlas to Base of Skull

Wings of Atlas Reduced

Caudal Portion of Atlas ressembles Occipital Condyles

Dens is Hypoplastic

Axis has Transverse Processes which ressemble those of Altas
- ie wider

All Leison will be Present
- varying degrees

Produces reduced Foramen Magnum
- spinal compression

Caused by abnormal segmentation and development of Caudal Occipital and Cranial Cervical Sclerotomes

Clinical Signs
- Usually unable to get up
- if able to stand will have abnormal gait
- caudal palpation of abnormal wings
~~ Axis

Common in Arabs
- recessive
- also other breeds
OVINE HERIDITARY CHONDRODYSPLASIA
aka Spider Lamb Syndrome

Abnormal transformation of Cartilage to Bone
- defect of chonrocytes
- chondrocytes layed down in IRREGULAR PATTERN
- results in abnormal bone and bone growth during OSSIFICATION
- Abnormality may be in any part of skeleton
~~ mainly limbs and vertebrae
~~ may involve facial bones

Most common in Black Face Sheep
- 75% of occurance in Sufolk
- reduced in '60s (those were the days) to '80s via genetics
- avoid via genetic testing

Clinical Signs
- spayed legs
- kyphosis
- limb deviations
- age < 1 month
LIMB DEVELOPMENT
Initiates with development of Limb Field (bulge)
- bud stage once bud indentifiable

Ectoderm Thickens
- induces underlying mesoderm to from vascular Channel
~~ CRITICAL STEP

Apical Ridge of Bud induces underlying mesoderm to grow and differentiate
- Paddle stage
- elongation to Plate stage
- as limb nears final length
~~ Ventral Flexion
~~ Pronation
~~-- required for proper orientation of palmer/plantar surface
DIGIT DEVELOPMENT
Depends on Interdigital Necrotic Zones
- fusion or degeneration of digits occurs in species with less than 5 digits
- ie all originally develop 5 digits
JOINT DEVELOPMENT

FIVE KEY EVENTS
Movement Is Critical
- reduced or malformed joint
- abnormal development of tendons and ligaments

InterZone
- Perichondral layer of cells
- formed from Condenstation of mesochyme

Movement within INterzone leads to developmnent of Synovial Joint via
- cavitation
- production of Synovial Fluid

External portion of Interzone becomes Joint Capsule

Ligaments are formed from localized thickenings of Joint Capsule
AMELIA
Absence of one or more limbs

TBX5 Gene controls forelimbs

TBX4 Gene controls hindlimbs
ECTOPIC LIMB
Extra or Abnormaly placed Limb

Multiple expression of TBX gene
POLYDACTALY
Extra Digits

Excess interdigital necrosis

Genetic disposisiton
- Cats in Saskatoon
SYNDACTALY
Absence of Digits

Insufficient Interdigital Necrosis

Excess Fusion

Popular with Holsteins
HEMIMELIA
Missing a portion of a limb

Can result from crowded uterus

Twisted Kittens
ARTHROGRYPOSIS

WHAT IS IT

FOUR WAYS TO HAVE IT
Crooked Calf Syndrome

Contracted Limbs
- flexure most common
- also extension

Results from abnormal development
- usually displasia of muscle and tendons via
~~ Joint Defects Directly
~~ Improper Enervation to Muscle
~~ Muscle Defects Directly
~~ Insufficient Amniotic Fluid to allow proper Movement

Most Common in Cattle
- Horses
~~ Norwegian Fjiords
- Pigs
- Sheep

Multifactorial
- infections
~~ BVDV
~~ Bluetongue
- Genetics
~~ Austosomal Reccesive
~~-- Charlois
- Teratogens
~~lupines
~~ tobacco
~~ locoweed
~~ 40 -70 days cattle