Heart Development (Mine) Flashcards
Explain extraembryonic vasculogenesis
Occurs day 17 in the mesoderm near yolk sac endoderm
hemangioblasts aggregate, differentiate and give rise to hematopoeitic progenitor cells and endothelial precursor cells (EPC)
form blood islands that connect to form vascular network
by end of third week, yolk sac, connecting stalk, and chorionic villi are vascularized
What are the eventual sites of hematopoesis?
blood islands, yolk sac, liver, AGM, lymph organs, bone marrow
When do embryonic hematopoietic cells appear and what do they become?
day 17
move to liver around day 23
generate embryonic erythrocytes, macrophages, megakaryocytes
Definitive hematopoetic stem cells seed the liver at what day and do what?
day 30
undergo cell-cell interactions giving the embryonic hematopoetic cells full capacity to generate myeloid and lymphoid lineages
Overview of the sites of hematopoiesis
yolk sac mesoderm: day 17, done by day 60, source of early RBCs and macrophages
liver primordia: day 23, continues until birth
AGM: dorsal aorta, day 27-40, colonizes liver
lymph organs, bone marrow (10.5wks)
Describe the process of intraembryonic vasculogenesis which leads to angiogenesis and intussuception
vasculogenesis is the denovo formation of blood vessels that starts at day 18 and in the intraembryonic splanchnic mesoderm and paraxial mesoderm
angioplastic proliferation occurs via: proliferation of endothelial precursors cells, angiogenesis (budding), intussuception (splitting), and recruitment of mesoderm cells to the walls of existing vessels
CN: Angiomas
subtypes:
capillary
cavernous
hemangioma of infancy
abnormal blood vessels and lymphatic growth via vasculogenesis (from abnormal levels of angiogenic factors
excessive growth of capillary network
excessive growth of venous sinus
benign tumor, mostly of endothelial cells, can be internal and compress important structures. Typically regress with age
What is the first heart field and where is the intraembryonic coelom in relation?
formtion of EPC clusters that arrange in a horseshoe shape within a cardiogenic area of the intraembryonic splanchnic mesoderm
IE coelom lies dorsal to first heart field
How does anterior/posterior body folding affect the first heart field?
the primary heart field and coelom get folded underneath the embryo, helping to form the foregut
the first heart field now lies ventral to the foregut and dorsal to the coelom
How do the two primitive endocardial tubes form?
EPCs differentiate into endothelial cells while the first heart field is being folded under the embryo
How is the first aortic arch formed?
Lateral folding brings the cardiac tubes together
now the heart is a simple tube which sits in the future pericardial cavity
as growth occurs, the tube is pulled cervically and then into the thorax
this pulls the dorsal aorta forming the first aortic arch
What is the remnant of the dorsal mesocardium called in the adult?
proepicardial organ
originally, it suspends the heart tube but eventually ruptures
What is the primordium of the epicardium?
proepicardial cells which migrate over the myocardial surface
What forms the future right ventricle?
What forms the conus arteriosus?
What forms the truncus arteriosus?
initial outflow tract
addition of myocardium at the cranial end of the heart
distal outflow tract, forms aorta and pulmonary artery
What is required for cardiac looping to occur?
lengthening of the cardiac tube at both ends, but mostly at the cranial outflow end
this results in the formation of the second heart field which forms at the ends of the rupturing dorsal mesocardium
failure results in several defects
What are neural crest cells responsible for in the process of cardiac looping?
neural crest cell, PA mesoderm and PA endoderm interactions are necessary for maintaining cardiogenic mesoderm proliferation and proper myocardial cell specification within the second heart field
CN: Ventricular Inversion
looping anomaly
primitive ventricle fold to the side and outflow tract ends up on the left with the outcome being a right sided, left ventricle
CN: Heterotaxia
looping anomaly
any abnormal left-right development of either some or all organs, seen in immobile cilia syndrome and Kartagener syndrome
CN: Situs Inversus
Example: Visceroatrial Heterotaxia (technically, situs ambiguous)
Complete reversal of some organs
heart and GI tract are asymmetrically arranged from one another, issues with inflow and outflow tract development
What forms the coronary sinus?
What is the fate if the vitelline, umbilical and common cardinal vein?
the remnant of the left sinus horn
disappear
What forms the sinoatrial orifice?
the sinus venosus opening into the future right atrium
What type of growth makes the muscular interventricular septum and muscular atrial septum?
differential growth
requires addition of new tissue for fully closed lumen
What is endocardial cushion tissue?
it is new CT used to make the membranous portion of the atrial and ventricular septa derived from mesenchymal endocardia mesenchyme
What is the purpose of the conotruncal ridges?
part from ECT and part from NCC
make the conus arteriosus-helps blood from LV/RV go out different vessels
makes truncus arteriosus-divides into aorta and pulmonary arteries by AP septum formation
Describe the formation of the foramen ovalis
(initial division of the common atrium to the septated atrium)
The septum primum from mesenchyme and cushion tissue grows upward and then a bit of it degenerates, making the ostium secundum
septum secundum grows next to it and is much thicker and overlaps the ostium secundum. A part of the middle of it degenerates, making a hole that is overlapped by the septum primum
eventally makes the foramen ovalis which is overlapped by the septum primum making a one way valve between RA and LA
How does the foramen ovalis close?
after birth, with first breath, blood pressure increases in left atrium
RV can now pump blood into lungs so the RV and RA pressure decreases
thus the pressure is always higher on the left side of the heart even during diastole, sealing shut the foramen ovalis (within about three months)
if it stays patent, it isn’t usually a big deal
Atrial Septal Defects
result in initial left to right shunting because of increased blood flow returning from the lungs and decreased pulmonary resistance after the lungs expand
overtime, this leads to lung damage and pulmonary congestion
causes RV hypertrophy and congestive heart failiure
a right to left shunt begins and then cyanosis appears
What are the three types of ASD?
ostium secundum (high atrial spetal defects, 90%) caused by excessive absorption of septum I or large ostium II, or inadequate development of septum II
Common Atria-no septa formed
ostium primum (low atrial septal defect)-failure of up growth of AV cushion tissue from AV septum and DMP to fill in ostium primum
Describe fetal cardiac blood flow
blood entering from the IVC enters the foramen ovalis in the LA (O2) and then goes to LV and then out into fetal systemic arterial side
blood entering the RV from the RA includes less oxygenated blood from SVA and coronary sinus as well as IVC
blood leaves RV and re-enters the systemic arterial side via DA with very little passing through lungs
What is partitioning of the outflow tract?
Formation of the conus arteriosus, truncus arteriosus and aortic sac
starts with a common lumen that is divided into two tubes such that the future aorta is attached to the LV and the pulmonary artery to the RV
aortic arch VI connects the RV to the lungs and aortic arch III and IV connects the LV to the rest of the body
CN: Ventricular Septal Defects
one of the most common congenital heart defects
failure of proper closure by abnormal or inadequate fibrous tissues
starts with acyanosis (LtR shunt) but becomes cyanotic shortly after birth
RV hypertrophies and RtL shunt forms (cyanosis)
die of cardiac faiulure if untreated
What does complete closure of the ventricle septum require?
down growth of the AV septum, proper formation of the conotruncal ridges and interventricular muscular septum formation
CN: Persistent Truncus Arteriosus
Failure of contruncal ridge formation and fusion
pulmonary artery arises some distance away above the undivided truncus
causes VSD
mixing of oxygenated and unoxygenated blood
some cyanosis, pulmonary congestion, RV hypertophy, increased right ventricular pressure and worsening cyanosis
CN: Tetralogy of Fallot
conotruncal ridges from off center leading to unequal division of pulmonary trunk and aorta
VSD
pulmonary infundibular stenosis
overriding aorta
RV hypertrophies-RtL shunting (cyanosis most common initial sx)
CN: Transposition of Great Vessels
conotruncal ridges fail to spiral
Pulmonary A. connected to LV and aorta to RV
survive only because of existing shunts such as VSD, ASD, and patent DA
even with shunts, likely to die within 3yrs, unless treated
CN: Pulmonary valvular atresia
semilunar valves are fused leading to RV hypoplasia
patent foramen ovalis forms
DA remains patent
may require heart transplant depending on severity
other sx include VSD or univentricular heart
CN: Aortic valvular stenosis
leads to hypertrophy of LV and cardiac failure with pulmonary hypertension
possibly congenital, due to infection, degeneration (aging), more often in males
CN: Bicuspid aortic valve
2 leaflets instead of 3 form or three form but two are fused
regurgitation and then stenosis
asymptomatic at first, later leads to LV hypertrophy
assx with development of aortic aneurysm
CN: aortic valvular atresia
valves are completely fused, LV is hypoplastic
wide DA forms and leads to RV hypertrophy during fetal period
after birth, blood must enter atrium via ASD and then to systemic circulation via patent DA
likely need transplant, but some other surgeries have good outcomes
CN: Tricuspid Atresia
obliteration of right AV orifice
always assocaited with patent foramen ovalis, VSD, hypoplastic RV, hypertrophic LV and patent DA
can be fixed surgerically if not too severe, otherwise needs transplant
CN: Hypoplastic left ventricle
LV si developed with absent or small bicuspid and aortic valves
ascending portion of the aorta is underdeveloped and there’s a patent DA and/or patent FO
functionally a univentricular heart with RV doing all the work
surgeries help, but still high death rate at 5yrs
CN: Persistent AV canal
failure of AV septum fusion
ASD and VSD due to cushion tissue from septum contributes to fibrous portion of septa
abnormal or agenesis of AV valves
s/s: pulmonary HTN, exercise intolerance, SOB, cardiac congestion, increased risk of endocarditis
linked with Down’s Syndrome
