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46 Cards in this Set
- Front
- Back
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 |
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FUNCTION OF FORAMEN OVALE
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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 |
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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 |
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TWO TWISTLESS TRAGEDIES
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Aorta and Pulmonary Arteries may not seperate
Form two closed circulation systems - Right Ventricle into systemic circulation - Left Ventricle into pulmonary circulation - Fatal Flaw |
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TETRALOGY OF FALLOT
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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 |
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SEQULAE OF HYPOXIA
4 |
Lethargy
- a few weeks after birth when pups become active Tachycardia Poor Growth Increased PVC - polycytemia - thicker blood |
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VEINS
3 BIG ONES |
Vitelline
- drains yolk sac Umbilical - blood from placenta - oxygenated and nutrient rich Cardinal Veins - drain embryo |
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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 |
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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 |
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INTRAHEPATIC ATRERIOVENOUS FISTULA
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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 |
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HEPATIC MICROVASCULAR DYSPLASIA
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Abnormal communication between hepatic ARTERIOLES and Hepatic or Portal VENULES
Affects whole lobes Normal external appearance |
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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 |
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NEURULATION
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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 |
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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 |
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NEURAL TUBE
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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 |
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EARLY CNS DEVELOPMENT
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Flexure and Rotation
Proencephalon - Forebrain ~~ Telencephalon ~~-- Cerebrum ~~ Diencephalon ~~-- Thalamus Trio Mesencephalon - Midbrain Rhombencephalon - Hind Brain ~~ Metecehphalon ~~-- Cerebellum ~~-- Pons ~~ Myelencephalon ~~-- Medulla Oblaongata |
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CYCLOPIA
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Single Medial Orbit with relatively normal rudimentary eye
Usually no vision Various degrees of fusion of eyes Eye development is relatively normal |
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HOLOPROSENCEPHALY
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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 |
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HYDROCEPHALY
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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 |
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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 |
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SPINAL BIFIDA
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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 |
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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 |
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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 |
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SPINAL BIFIDA
FOUR FACTORS |
Genetics
- English Bull Dogs - Manx Cats Sulphonamide - decreased folic acid Griesofulvin - Cats Methyl Mercury - Cats |
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DERMOID SINUS
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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 |
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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 |
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MUSCULOSKELETAL SYSTEM
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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 - |
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MUSCLE
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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 |
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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 |
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SKULL
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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 |
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BLOCK VERTEBRAE
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Error in RESEGEMENTAION of Somites
Partially seperated Vertebae - may include vertebral disk malformations Overlying vertebral body forms relatively normally |
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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 |
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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 |
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ATLANTO AXIAL SUBLUXATION
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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 |
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MID CERVICAL SUBLUXATION
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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 |
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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 |
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OVINE HERIDITARY CHONDRODYSPLASIA
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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 |
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LIMB DEVELOPMENT
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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 |
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DIGIT DEVELOPMENT
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Depends on Interdigital Necrotic Zones
- fusion or degeneration of digits occurs in species with less than 5 digits - ie all originally develop 5 digits |
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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 |
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AMELIA
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Absence of one or more limbs
TBX5 Gene controls forelimbs TBX4 Gene controls hindlimbs |
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ECTOPIC LIMB
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Extra or Abnormaly placed Limb
Multiple expression of TBX gene |
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POLYDACTALY
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Extra Digits
Excess interdigital necrosis Genetic disposisiton - Cats in Saskatoon |
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SYNDACTALY
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Absence of Digits
Insufficient Interdigital Necrosis Excess Fusion Popular with Holsteins |
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HEMIMELIA
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Missing a portion of a limb
Can result from crowded uterus Twisted Kittens |
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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 |