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PBL SEM 2 > PBL 4 - cardiac embryology > Flashcards

PBL 4 - cardiac embryology Flashcards

1
Q

what is gastrulation?

A

the formation of 3 germ layers — endoderm, mesoderm and ectoderm

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2
Q

what does gastrulation enable through cell movements?

A

gets tissues and organs in correct orientation

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3
Q

what germ layer does the heart form from?

A

mesoderm

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4
Q

what happens in the 1st stage of cardiac development?

A
  • cardiac cell fate acquired

- angiotensin cells located in cardiogenic plate — cranial and lateral to neural plate

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5
Q

how many days post fertilisation do heart fields form?

A

15

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6
Q

how many heart fields are there?

A

primary and secondary heart fields

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7
Q

where does the cardiac crescent fuse and what does it form?

A

cardiac crescent fuses at mid-line to form cardiac tube

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8
Q

what do the cells in the cardiac crescent do?

A

come together and elongate a bit at the midline of the embryo, so that those regions of the cardiac crescent will fuse into a single developing heart tube (primary heart tube)

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9
Q

after how many days does the linear heart tube form?

A

21

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10
Q

where is the heart tube formed?

A

mid-line

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11
Q

what cells are incorporated in the linear heart tube?

A

primary and secondary heart field derived cells

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12
Q

where are the developing heart tubes situated in relation to the developing atria?

A

more cranial to the developing atria

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13
Q

when does cardiac looping occur?

A

23-24 days

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14
Q

why does the linear heart tube loop?

A

must loop to acquire correct anatomy to enable the adult heart to function

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15
Q

where does the looping bring the atria?

A

brings atria more upwards and behind the presumptive ventricles

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16
Q

in what direction does cardiac looping occur?

A

dextral (rightward) — C-shape loop

anti-clockwise

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17
Q

cardiac looping is the first event to establish what?

A

left-right asymmetry

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18
Q

what is the name for defects in cardiac looping?

A

heterotaxy

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19
Q

what causes Situs Inversus (SI)?

A

complete looping in wrong direction of all organs

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20
Q

what causes Left Atrial Isomerism Syndrome (LAI) and RAI?

A

disruption of the left-right axis orientation during early embryonic development

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21
Q

list 4 heterotaxy syndromes

A
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22
Q

what is cardiac chamber development?

A

when atria and ventricles move into position and acquire specific identity

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23
Q

when does septation occur?

A

weeks 4-9 post fertilisation

24
Q

atrial septation occurs in what 2 steps?

A

septum primum and septum secundum

25
Q

when does atrial septation occur?

A

occurs end of 6th-8th week post fertilisation

26
Q

what is the most common CHD to present in adulthood?

A

atrial septal defects — often asymptomatic

27
Q

where is the foramen ovale in the developing heart?

A

between atria

28
Q

what does the foramen ovale allow? what causes it to close?

A
  • allows transmission of blood between RA to LA
  • allows blood to bypass the lungs
  • pressure changes following birth pressure promotes closure
29
Q

what is a patent foramen ovale?

A
  • birth defect
  • common 10-20% of adults
  • often asymptomatic
30
Q

when does ventricular septation occur?

A

end of 7th - mid 9th week

31
Q

what accounts for up to 40% of congenital cardiac malformations?

A

ventricular septal defects

32
Q

when does AV valve formation occur?

A

mid 7th-8th week

33
Q

what are the precursors of valves?

A

endocardial cushions

34
Q

label this linear heart tube

A
35
Q

when does outflow tract (truncus arteriosus) septation occur?

A

mid 7th-8th week

36
Q

what does outflow tract (truncus arteriosus) septation do?

A

divides the truncus arteriosus into the aorta and pulmonary trunk

37
Q

what is the ridge formed down the mid-line of truncus arteriosus by?

A

truncal cushions (similar in morphology to the cushions that give rise to the valves)

38
Q

what is persistent truncus arteriosus?

A
  • brith defect
  • results from failure of septation of aorta and pulmonary artery
  • single artery arising from both ventricles
  • rare congenital defect
  • causes complex circulatory problems
39
Q

what is the name of the precursor of the epicardium?

A

proepicardium

40
Q

describe epicardium formation and how it leads to coronary vessel formation

A
  • cells from proepicardial organ (just below heart in embryo) migrate onto the developing heart tube and migrate on to form an epithelial layer on the top surface of the heart
  • they further progress during development to differentiate and move deeper into the myocardium to give rise to the coronary vessels
41
Q

what do EPDCs (epicardial derived cells) do? characteristics?

A
  • move from epicardium into myocardium
  • differentiate into other cardiac cell types
  • coronary smooth muscle, myocardial fibroblasts, vascular endothelial cells (some debate over the latter)
  • pluripotent — source of stem cells for vessel regeneration?
42
Q

by what week have major heart chambers and vessels formed by?

A

8th week

43
Q

where and what are the 3 main foetal adaptations of foetal circulation?

A
44
Q

what does the ductus arteriosus connect?

A

the pulmonary artery to aortic arch

45
Q

what does blood bypass due to the ductus arteriosus?

A

lungs

46
Q

what is formed when the ductus arteriosus closes after brith?

A

ligamentum arteriosum

47
Q

what promotes the closure of ductus arteriosus after birth?

A

increase in neonatal blood O2 content and withdrawal of maternal prostaglandins

48
Q

how common is a patent ductus arteriosus?

A

occurs 8/1000 premature births and 2/1000 full-term births

49
Q

why is a patent ductus arteriosus bad?

A

mixing of blood between aorta and pulmonary artery remains —result in abnormalities of the oxygenation of the blood due to mixing of oxygenated and deoxygenated blood

50
Q

CHD occur in how many live births (1:_)?

A

1:125

51
Q

what is the most common deletion syndrome that is an example of a CHD associated with a syndrome? 1/___ births?

A

22q11.2 deletion syndrome — 1/4000 births

52
Q

explain 22q11.2 deletion syndromes

A
  • genetic cause — TBX1 loss contributes to cardiac defect phenotypes
  • spectrum of outflow tract defects
  • TBX1, expressed in secondary heart field which gives rise to outflow tract (aorta, pulmonary artery, right ventricle)
  • animals models reveal TBX1 is needed for proliferation in secondary heart field
  • loss of TBX1 causes shorter outflow tract lacking septation
53
Q

PFO (patent foramen ovale) increases the risk of what?

A

a stroke — blood clot forms in one of vessels retuning to heart and can travel up to brain

54
Q

what % of CHD patients survive into adulthood?

A

90%

55
Q

what does the primary heart field give rise to?

A

LA, RA, LV

56
Q

what does the secondary heart field give rise to?

A

RV + outflow tract

PBL SEM 2 (44 decks)

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