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CardioPulmRenal > Heart Development > Flashcards

Heart Development Flashcards

1
Q

Define vasculogenesis

A

-de novo creation of blood vessels directly from mesenchyme

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2
Q

When does extraembryonic vasculogenesis begin?

A

around day 17

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3
Q

True or False: extraembryonic vasculogenesis is coupled with hematopoeisis

A

True

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4
Q

What are hemangioblasts?

A

progenitor cells of extraembryonic vasculogenesis that can give rise to the hematopoietic lineage or to endothelial cells

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5
Q

True of False: intraembryonic vasculogenesis is couple with hematopoeisis

A

False

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6
Q

When does intraembryonic vasculogenesis begin?

A

around day 18

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7
Q

What are angioblasts?

A

a subset of cells in the intraembryonic splanchnic mesoderm that differentiate directly into endothelial precursor cells

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8
Q

Define angiogenesis

A

budding or sprouting of new vessels from existing ones

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9
Q

Define intussusception

A

splitting a blood vessels in half to make two vessels

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10
Q

How does angiogenesis happen?

A
  • tip cells “invade”
  • stalk cells follow
  • endothelial cells proliferate and migrate
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11
Q

Where do embryonic hematopoietic stem cells reside and by what day of development do they reach there?

A

in the primordial liver

by Day 23

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12
Q

What types of cells can embryonic hematopoietic stem cells become?

A

erythrocytes, macrophages, and megakaryocytes

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13
Q

What are definitive hematopoietic stem cells?

A

cells that can create the full range of myeloid and lymphoid lineages

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14
Q

What specialized cells come out of the AGM (aortic-gonadal-mesonephric) region of the dorsal aorta?

A

hemogenic endothelial cells

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15
Q

From the AGM, where do hemogenic endothelial cells go?

A

they seed the liver by day 30

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16
Q

What do the hemogenic endothelial cells do when they get to the liver?

A

cell-cell interactions with embryonic hematopoietic stem cells

give the stem cells the full capacity to generate both myeloid and lymphoid lineages

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17
Q

Where do the definitive hematopoietic stem cells go after their transformation in the liver

A

lymph organs

bone marrow

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18
Q

What are the mechanisms by which the vascular plexus expands?

A

sprouting
intussusception
cont’d proliferation of EPC’s

recruitment of new mesoderm into the walls of existing vessels

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19
Q

Pathology: Angiomas

A

-abnormal blood vessel and lymphatic capillary growth via vasculogenesis

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20
Q

What is the likely cause of angiomas?

A

abnormal levels of angiogenic factors

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21
Q

What are the two types of angiomas?

A

Capillary Angioma = excessive growth of a small capillary network

Cavernous Angioma = excessive growth of venous sinuses

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22
Q

Pathology: Hemangiomas of Infancy

A
  • benign tumors made mostly of endothelial cells
  • most regress on their own

-depending on site or degree, can lead to clinical complications

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23
Q

What germ layer gives rise to early cardiogenic precursors?

A

intraembryonic splanchnic mesoderm

has neural crest contributions

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24
Q

What do neural crest cells do in the development of the heart?

A
  • regulate the activity of the 2nd heart field
  • play a role in the separation of the outflow tracts into pulmonary A. and aorta (cushion tissue derived from neural crest cells)
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25
Q

What are some roles of endoderm during heart development?

A
  • signals the development of early blood vessels

- signals the formation of early endocardium from splanchnic mesoderm

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26
Q

What is the role of endoderm in regards to cardiac looping?

A

-signaling continual proliferation of splanchnic mesoderm (second heart field) necessary for driving cardiac looping

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27
Q

Delineate the process of forming a single cardiac tube from two primitive heart tubes.

A
  • sides of embryo move toward midline and ventrally
  • endocardial tubes are brought together and fuse
  • adjacent cardiogenic mesoderm is incorporated
  • tube sinks into the pericardial cavity
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28
Q

List the layers of the heart tube from superficial to deep.

A
  • myocardium
  • cardiac jelly
  • endocardium
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29
Q

What is myocardium?

A

mesoderm adjacent to the endocardial tubes

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30
Q

What is cardiac jelly?

A

concentration of ECM b/w endocardium and myocardium

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31
Q

What is endocardium?

A

inner epithelium continuous with blood vessels

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32
Q

Delineate the formation of endocardium.

A

mesodermal precursors
specialization of endothelial cells
endocardium

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33
Q

From what germ layer is endocardium derived?

A

intraembryonic splanchnic mesoderm

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34
Q

What is the first heart field (cardiac crescent)?

A

formation of endothelial precursor cells in clusters, plus the adjacent mesoderm

-in a horseshoe shape within a cardiogenic area of intraembryonic splanchnic mesoderm

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35
Q

How is the second heart field formed?

A

as lateral body folding occurs, the location of the second heart field is pulled farther away from the notochord and neural tube; w/o the inhibition from the notochord, the splanchnic mesoderm cells can proliferate at the cranial and caudal ends of the tube

36
Q

What does the proliferation of the cranial and caudal ends of the heart tube induce?

A

cardiac looping

37
Q

What does the left sinus horn become?

A

coronary sinus

38
Q

What does the sinus venosus become?

A

sinoatrial junction

sinus venarum

39
Q

What does the right sinus horn become?

A

superior vena cava
inferior vena cava
–from the right vitelline vein

40
Q

What forms the SA node?

A

cells in the R cardinal vein that serve as a pacemaker in the early heart stages

41
Q

Pathology: Heterotaxia

A

-any abnormal development of L-R organs

42
Q

Pathology: situs inversus

A
  • a type of heterotaxia
  • complete reverse symmetry of heart and GI
  • not fatal
  • may be asymptomatic
43
Q

Pathology: situs ambiguous

A
  • a type of heterotaxia
  • reversal of only some L-R organs
  • causes problems with inflow and outflow tracts
  • life threatening
    ex: visceroatrial heterotaxia
44
Q

Pathology: Ventricular Inversion

A
  • primitive ventricle folds to the R
  • outflow tract ends up on the L
  • -R-sided left ventricle
45
Q

What structure brings oxygenated blood back into the primitive heart?

A

umbilical vein

46
Q

What is the first structure to develop that allows blood to bypass the pulmonary circuit?

A

foramen primum

  • low in the septum primum
  • -b/w the two atria
47
Q

What is the second structure to develop that allows blood to bypass the pulmonary circuit?

A

foramen secundum

-high up in the septum primum

48
Q

What is the third structure to develop that allows blood to bypass the pulmonary circuit?

A

foramen ovalis

-in the septum secundum

49
Q

Delineate how most blood flows from R to L in a fetal heart

A
  • enters R atrium
  • through foramen ovalis
  • between septum secundum and septum primum
  • -displaces septum primum
  • flows through foramen secundum into L atrium
50
Q

Delineate a minor way that blood flows from R to L in a fetal heart.

A
  • some blood goes into R ventricle so that it gets worked
  • most shunted b/w pulmonary trunk and aorta
  • -ductus arteriosus
51
Q

How is the transverse sinus formed?

A

-the heart tube remains attached to the rest of the splanchnic mesoderm by the dorsal mesocardium

  • dorsal mesocardium ruptures and allows looping
  • makes a space separating inflow from outflow
52
Q

How is the atrioventricular canal partitioned?

A
  • myocardium signals some of the endocardial cells to delaminate (endothelium to mesenchyme)
  • mesenchymal cells migrate to fill in the ECM and the two sides fuse
53
Q

What changes in atrial blood flow occur at birth?

A
  • pressure in R atria and R ventricle decrease
  • -d/t ease of R ventricle pumping blood to lungs
  • blood flow from lungs into L atria increases pressure
  • pressure is always greater on L than R
54
Q

How are the foramina between the atria functionally closed at birth?

A

-b/c the pressure in the L side of the heart is greater than the R side, septum primum is driven up against septum secundum, resulting in a “closed” septum

55
Q

What are the germ layer(s) that contribute to the septation between the atria and ventricles?

A

-intraembryonic splanchnic mesoderm

56
Q

What are the germ layer(s) that contribute to the septation of the outflow tract?

A
  • intraembryonic splanchnic mesoderm

- neural crest (endoderm-derived)

57
Q

What are the two parts of the ventricular septum?

A
  • muscular (from the ventricle wall)

- fibrous (from the AV cushion tissue and proximal conotruncal ridges)

58
Q

How is the outflow tract partitioned?

A
  • conotruncal ridges form on R and L sides

- as ridges approach the ventricle, they come off at different angles and spiral downward

59
Q

Pathology: Persistent AV Canal

A
  • failure of AV septum fusion; abnormal or missing valve
  • normally accompanied by ASD’s and VSD’s b/c the cushion tissue from the AV septum normally contributes to the fibrous portion of the septa
60
Q

What are the symptoms of a Persistent AV Canal?

A 
pulmonary HTN
intolerance to exercise
shortness of breath
cardiac congestion
increased risk of endocarditis
61
Q

Having a Persistent AV Canal is linked with what condition?

A

Down’s Syndrome

62
Q

Pathology: Double Outlet Right Ventricle

A
  • both aorta and pulmonary trunk exit R ventricle

- VSD accompanies b/c the malalignment causes agenesis of the fibrous portion of the septum

63
Q

What is the embryological cause of Double Outlet Right Ventricle?

A

-insufficient shifting of the AV septum

or

-problem with cardiac looping

64
Q

What are the symptoms of Double Outlet Right Ventricle?

A
  • cyanosis
  • breathlessness
  • murmur
  • poor weight gain (later on)
  • occur within days of birth
65
Q

Which type of congenital heart defects are the most common?

A

VSD’s

66
Q

Pathology: Persistent Truncus Arteriosus

A
  • undivided truncus overriding both ventricles
  • causes mixing of oxygenated and deoxygenated blood

-causes a VSD b/c the fibrous portion of the septum would’ve normally come from the ridges

67
Q

What is the embryological cause of Persistent Truncus Arteriosus?

A

-failure of conotruncal ridge formation or fusion

68
Q

What are the symptoms of Persistent Truncus Arteriosus?

A
  • low degree of cyanosis
  • pulmonary congestion

-R ventricle hypertrophy d/t increased R ventricular pressure

69
Q

Pathology: Tetralogy of Fallot

A
  • unequal division of pulmonary trunk and aorta
  • pulmonary infundibular stenosis
  • overriding aorta
  • causes a VSD (missing fibrous portion)
70
Q

What are the symptoms of Tetralogy of Fallot?

A
  • fetal R ventricle hypertrophy
  • -increased R ventricle pressure causes the hypertrophy; R pressure eventually exceeds L pressure, so you get R to L shunting at birth = cyanosis of the newborn (most common cause)
71
Q

What is the embryological cause of Tetralogy of Fallot?

A

-conotruncal ridges form off-center

72
Q

Pathology: Transposition of the Great Vessels

A
  • pulmonary trunk connects to the L ventricle
  • aorta connects to the R ventricle

-survival (life expectancy approx 3 yrs) is only possible d/t existing shunts (ex: VSD, ASD, ductus arteriosus)

73
Q

What is the embryological cause of Transposition of the Great Vessels?

A

-failure of the conotruncal ridges to spiral

74
Q

Pathology: Pulmonary Valvular Atresia

A
  • pulmonary valves are fused

- -hypoplastic R ventricle

75
Q

In a patient with Pulmonary Valvular Atresia, how does blood get from the R side to the L side?

A

-patent foramen ovalis

76
Q

In a patient with Pulmonary Valvular Atresia, how does blood get into the lungs?

A

-by going into the aorta and through the ductus arteriosus

77
Q

Pathology: Aortic Valvular Stenosis

A
  • leads to L ventricle hypertrophy
  • eventual cardiac failure
  • pulmonary HTN
  • congenital, d/t infection, or degenerative
  • 4:1 male:female ratio
78
Q

Pathology: Aortic Valvular Atresia

A

-leads to hypoplastic L ventricle

79
Q

What happens in a fetal heart with Aortic Valvular Atresia?

A
  • R ventricle hypertrophy
  • wide ductus arteriosus forms during fetal stage as the only way to get oxygenated blood from the placenta into systemic circulation
80
Q

What are the abnormal features of blood flow in the heart (after birth) in a patient with Aortic Valvular Atresia?

A

-oxygenated blood flows back into R atrium through an ASD since it can’t be ejected via the aortic valve; then it gets into systemic circulation via the pulmonary trunk and a patent ductus ateriosus

81
Q

Pathology: Tricuspid Atresia

A
  • no R atrioventricular orifice
  • patent foramen ovalis and ductus arteriosus
  • VSD
  • hypoplastic R ventricle
  • hyperplastic L ventricle
82
Q

How does blood flow in a patient with tricuspid atresia?

A
  • from R atrium to L atrium through foramen ovalis
  • from L ventricle into both outflow vessels via VSD
  • -d/t location of pulmonary trunk, not much blood enters from L ventricle, and instead get to lungs via ductus arteriorsus after entering the aorta
83
Q

Pathology: Bicuspid Aortic Valve

A
  • initially asymptomatic
  • results in regurgitation and valvular stenosis
  • eventual L ventricle hypertrophy
  • often associated with aortic aneurysm
84
Q

What is the embryological cause of a Bicuspid Aortic Valve?

A

-three leaflets form, but two fuse

85
Q

Pathology: Hypoplastic Left Ventricle

A
  • small/unformed bicuspid and aortic valves
  • underdeveloped ascending aorta
  • heart works as a univentricular heart (R side)
  • high mortality
86
Q

How does blood flow if a patient has a hypoplastic left ventricle?

A
  • oxygenated blood flows back into R atrium via ASD or patent foramen ovalis
  • blood (mixed) can flow into systemic circulation via patent ductus arteriosus

CardioPulmRenal (18 decks)

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