Heart Development Flashcards
Primitive hematopoietic stem cells
Make erythrocytes, megakaryocytes and macrophages
Meet immediate needs of the early embryo
Definitive hematopoietic stem cells
Programmed from hemogenic endothelial cells found in the aortic-gonadal-mesonephric (AGM) region
Appear at day 27, seed the liver at day 30
Generate full spectrum of myeloid and lymphoid cell lineages
Without AGM, you never get definitive hematopoietic stem cells
Sites of hematopoiesis
Yolk sac mesoderm- day 17-60: source of early RBCs and macrophages
Liver primordia: beginning day 23, continues to birth
AGM dorsal aorta: colonizes liver
Lymph organs
Bone marrow
AGM region vasculogenesis
Hematopoiesis is coupled to vasculogenesis, which is different from the rest of the embryo
Mesodermal cells directly turn into endothelial cells and form blood vessels in most other areas
Angiogenesis vs vasculogenesis
Vasculogenesis is de novo formation of blood vessels, while angiogenesis is the sprouting of new vessels from existing ones
Intussusception
Taking an existing blood vessel and splitting it in half
Angioma
Abnormal blood vessel and lymphatic capillary growth via vasculogenesis
Capillary hemangioma- excessive formation of capillaries
Cavernous hemangioma- excessive formation of venous sinuses
Primary heart field
Splanchnic mesoderm- precardiomyocytes
Endoderm
Endothelial precursor cells form angiogenic clusters (all though this is a vasculogenic process) which form cardiac crescent and two endocardial tubes
Endocardial tube formation
Splanchnic mesoderm consisting of precardomyocytes continue with the process of body folding and bring the two tubes towards the midline
Fuse into one single tube formed from endocardium and myocardium, and the tube dangles from dorsal mesocardium
Dorsal mesocardium must rupture so the tube can loop
Proepicardial organ
Remnants of dorsal mesocardium that are responsible for forming the epicardium- cardiovasculature, CT and visceral layer of pericardium
Primitive ventricle and proximal portion of outflow
Primitive ventricle forms left ventricle
Proximal portion of outflow forms the right ventricle
Sinus horns
Two horns come together to form sinus venosus, which expands into atrium
Lengthening of the heart tube is due to
Growth of the second heart field
Neural crest cells
Do not add to heart
Regulate GF that comes from endoderm to drive proliferation of precardiac mesenchyme/mesoderm
If NCCs do not migrate to correct place there will be problems with cardiac looping
Heterotaxia
Any symmetry anomaly
Situs inversus- total side reversal of organs
Situs ambiguous- partial reversal of organs
Visceroatrial heterotaxia - right sided heart, normal GI
Ventricular inversion- reverse cardiac looping, right sided left ventricle
Right vitelline vein and Right common cardinal vein
Right vitelline becomes inferior vena cava, right common cardinal becomes superior vena cava
Cushion tissue and separating atria and ventricles
Myocardial cells produce more extracellular matrix which pushes endocardial cells from both sides towards eachother
Endocardial cells are signaled by myocardium to undergo epithelial–>mesenchymal/mesodermal cell transition so the two sides can fuse
This is how AV septum is formed
Valves derived from what tissue
Endocardium which is derived from intraembryonic splanchnic mesoderm
Cushion tissue in outflow tract is derived from
Both endocardium (intraembryonic splanchnic mesoderm) and neural crest cells (ectoderm)
Persistent AV canal
Failure of AV septum fusion
Results in atrial septal defect and ventricular septal defect
Abnormal or agenesis of AV valves
Pulmonary hypertension, exercise intolerance, shortness of breath
Linked with downs syndrome
How does O2 rich blood entering right atrium bypass the pulmonary circuit and get into the systemic side
One-way flutter valve between atria formed by dorsal mesenchymal protrusion
Ductus arteriosus allows blood entering right atrium to travel to left atrium
Early blood flow into right atrium flows through
Goes through foramen ovale, then displaces septum primum from septum secundum and through foramen secundum
Fibrous CT of AV septum is derived from
Endocardium
Foramen primum is filled in by
Cushion tissue
AV septal defects
Excessive erosion of septum primum or inadequate development of septum secundum
Causes high atrial septal defect
Low hole septal defect caused by foramen primum defect
Septation of outflow tract
To form complete interventricular septum, there must be spiraling of the conotruncal swellings that align with the muscular portion of the IV septum as well as the AV septum
Shifting of AV canal
AV canal must shift towards the midline during development
If it does not, both the aorta and pulmonary artery exit via the right ventricle, accompanied by a ventricular septal defect
Can be caused by insufficient cardiac looping
Symptoms include cyanosis, breathlessness, murmur, poor weight gain
Cardiac NC cells
Important for sprouting of secondary heart field, lengthening/looping of the heart tube, septation of the outflow tract
Ventricular septal defects
Most common congenital heart defect
Initially there will be blood flow from left to right side, increasing blood flow to pulmonary circuit
Later after development there will be blood flow from right to left side
Persistent truncus arteriosus
There will be a ventricular septal defect involved
Cyanosis
Look into this more- not well described
Tetralogy of fallout
Small pulmonary artery
VSD
Right ventricle must work harder and hypertrophies
Over-riding aorta
(those are the four symptoms- tetra)
Causes right to left shunt at birth, causing cyanosis
Transposition of great vessels
Conotruncal ridges formed and fused but did not spiral
Right ventricle connected to the aorta, left connected to the pulmonary artery
Ductus arteriosus allows oxygenated blood to get to embryo
Pulmonary valvular atresia
Blood comes into right atria but cannot be pumped out pulmonary artery
Left ventricle does all the work and hypertrophies
Only way to get oxygenated blood is to have blood flow through foramen ovale and back through the ductus arteriosus
Aortic valvular stenosis
Left ventricle has to work harder causing hypertrophy
Aortic valvular atresia
Left ventricle has no workload so it is much smaller
Right ventricle does all the work so it hypertrophies
Bicuspid aortic valve
Initially asymptomatic but can develop left ventricular hypertrophy over time
Associated with development of aortic aneurysms
Tricuspid atresia
Tricuspid valve has no opening
No blood can enter right ventricle, so it is hypoplastic
There is a patent foramen ovale that persists and ductus arteriosus so that oxygenated blood can be distributed
Usually involves a VSD
Hypoplastic left ventricle
Mitral valve is not formed or very small
Aortic valve is not formed or very small
Ascending portion of aorta is underdeveloped
Patent ductus arteriosus and foramen ovale (or ASD)
Heart works as a uni-ventricular heart with right ventricle doing all the work
