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Cardio Pulm > Lecture 13 - Heart Development > Flashcards

Lecture 13 - Heart Development Flashcards

1
Q

Where does blood vessel formation begin? When?

A

extraembryonic splanchnic mesoderm; day 17

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2
Q

What do hemangioblasts form

A

early embryonic erythrocytes and macrophages

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3
Q

What is the early source of hematopoietic cells in the body

A

liver

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4
Q

what allows the liver to produce the full range of myeloid and lymphoid cells

A

cells from the AGM region

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5
Q

where do the AGM cells go after the liver

A

lymph organs and bone marrow

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6
Q

where are blood cells made starting at day 17

A

yolk sac mesoderm

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7
Q

when is the liver colonized so that it can make blood cells

A

23 days and continues to birth

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8
Q

when do the AGM cells go to the liver? where are they from?

A

begins day 27-40; dorsal aorta

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9
Q

when does bone marrow begin developing cells

A

10.5 weeks

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10
Q

what leads the newly forming blood vessels where they need to go

A

tip and sprout cells

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11
Q

where doe the newly forming blood veseels collect

A

extraembryonic splanchnic mesoderm and between somites (paraxial mesoderm)

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12
Q

what is intussuception

A

splitting 1 vessel into 2

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13
Q

what are angiomas

A

abnormal blood vessel and capillary growths that are usually benign

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14
Q

what can angiomas sometimes affect

A

eyesight

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15
Q

what is normally inhibiting the formation of the angiogenic clusters

A

neural cord

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16
Q

when does the primary heart field normally form

A

day 19

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17
Q

what causes the heart tubes to unite

A

lateral folding

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18
Q

what aligns the heart correctly in left/right? up/down?

A

lateral folding; cranial/caudal folding

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19
Q

what does the proepicardial organ form? what is it made of

A

visceral mesocardium; dorsal mesocardium

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20
Q

Right after the heart tubes fold, how is the heart arranged

A

artia are below the ventricles

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21
Q

what veins go into the sinus horns

A

umbilical vein - oxygenated blood from placenta
vitelline vein - yolk sac drainage
common cardinal vein - lower body/everything else

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22
Q

when do cardiac twitches occur? rhythmic contractions?

A

22; 24

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23
Q

what is at the future site of the AV node normally?

A

R sinus horn

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24
Q

what normally causes outflow anomalies

A

insufficient cardiac looping

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25
Q

what allows the secondary heart field to develop

A

lateral folding moves it farther away from neural tube’s inhibitory signals

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26
Q

what cell type modulates heart development

A

NCC with FGF8

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27
Q

what does the primary heart field form

A

l/r atrium, l vent

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28
Q

what does the secondary heart field form

A

RV and outflow trunk

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29
Q

what does the formation of primary and secondary heart fields depend on

A

retinoic acid

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30
Q

what is reverse cardiac looping called

A

ventricular inversion (LV is on the right)

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31
Q

what is situs invertus

A

total body mirroring

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32
Q

what is situs ambiguous

A

partial body mirroring

33
Q

what is visceroatrial heterotaxia

A

heart on right and normal GI

34
Q

what does the left sinus horn become

A

coronary sinus

35
Q

what does the right common cardinal vein become

A

superior vena cava

36
Q

what does the right vitelline vein become

A

inferior vena cava

37
Q

the smooth portion of the internal RA is called the

A

sinus venarum

38
Q

what is the border between the sinus venarum and the RA

A

crista terminalis

39
Q

what is the process by which the heart normally enalrges

A

differential growth

40
Q

what do the interatrial septum and interventricular septum normally get filled in by

A

they are primarily muscle but cushion tissue fills in the rest

41
Q

of what origin is cushion tissue

A

endocardial

42
Q

where do the pulmonary trunk and aorta get their cushion tissue

A

endocardial cells and ectodermal neural crest

43
Q

what happens when the cushion cells don’t form the barrier

A

persistent av canal

44
Q

what pathology would you expect with persistent av canal

A

pulmonary htn, exercise intolerance, SOB, cardiac congestion, increased risk of endocarditis

45
Q

what is persistent AV canal often linked to

A

down syndrome

46
Q

which septum forms first

A

septum primum

47
Q

what time does the septum primum form

48
Q

when does the septum secondum form

A

6th week (40 days)

49
Q

what does the foramen ovale form in

A

the septum secondum

50
Q

where are the holes in the two septa in relation to one another

A

foramen ovale (septum secondum) is lower

51
Q

what keeps the foramen ovale closed in adults

A

higher pressure in the left A

52
Q

what are the common atrial septum defects

A

excessive resorption of septum primum
diminished septum secundum
ostium primum defect

53
Q

what is a lower osteum defect

A

osteum primum defect

54
Q

what causes double outlet RV

A

insufficient shifting of AV septum or cardiac looping

55
Q

what are the symptoms of double outlet right ventricle

A

show within days

  • cyanosis
  • breathlessness
  • murmur
  • eventually, poor weight gain
56
Q

what is double outlet RV

A

pulmonary trunk and aorta both exit RV

57
Q

what does the truncus arteriosis split into

A

pulmonary trunk and aorta

58
Q

how do we ensure that we get complete septation of the outflow tract

A
  1. have the conal truncal ridges extend completely

2. downgrowth from the atrioventricular cushion tissues

59
Q

if NCC don’t migrate what effects does that have on cardiopulmonary system

A

malformation of the heart and great vessels

60
Q

craniofacial deformations and cardiac issues are both related to what

61
Q

what are the most common heart defects

62
Q

what do VSD causes

A

L-> R shunting

63
Q

what are the symptoms of VSD

A
  • pulmonary congestion
  • RV hypertonicity
  • pulmonary htn
64
Q

what is persistent truncus arteriosus

A

the pulmonary trunk and aorta don’t split

65
Q

what causes persistent truncus arteriosus

A

lack of conal truncal ridges

66
Q

what is the most common cause of cyanosis at birth

A

tetralogy of fallot

67
Q

what is the tetralogy of fallot

A

pulmonary stenosis
RV hypertrophy
overriding aorta
VSD

68
Q

what does transposition of great vessels and pulmonary valvular atresia cause

A

immediate cyanosis

69
Q

what is tranposition of great vessels

A

RV gets aorta; LV gets pulmonary trunk

70
Q

what is pulmonary valvular atresia

A

lack of formation of the pulmonary semilunar valve out of the RV

71
Q

what things cause RV hypertrophy

A

aortic valvular atresia
tetralogy of fallot
hypoplastic left ventricle

72
Q

what causes aortic valvular stenosis

A

congenital
pathological - rhematic fever
degenerative (over time)

73
Q

what cardiac defect affects males more than females

A

aortic valvular stenosis

74
Q

what heart defect is associated with the development of aortic aneurysms

A

bicuspid aortic valves

75
Q

what is bicuspid aortic valve

A

the semilunar valve leaving the LV is bicuspid instead of tricuspid; expect symptoms similar to aortic valve stenosis

76
Q

what heart defect is inheritable

A

bicuspid aortic valve

77
Q

what is tricuspid atresia

A

now way from the RV to the pulmonary trunk

78
Q

what is hypoplastic left ventricle

A 
LV is underdeveloped
Mitral valve is not formed or small
Aortic valve is not formed or small
Ascending portion of aorta is underdeveloped
heart works as a single ventricle unit

Cardio Pulm (22 decks)

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