101514 dev of heart Flashcards

1
Q

cardiac precursors are from?

A

splanchnic mesoderm

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2
Q

cardiogenic crescent

A

primary heart field-the U shaped region of splanchinic mesoderm that heart develops from

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3
Q

folding in the cranial caudal plane results in a

A

ventral heart

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4
Q

what can incomplete formation of the ventral wall of the thorax cause in heart dev?

A

ectopic cordia (anterior thoracic wall fails to close properly

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5
Q

what is the INITIAL primitive heart tube?

A

primitive L ventricle (at this time, has arterial and venous poles). arterial pole is superior

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6
Q

what allows for elongation of the primitive heart tube?

A

secondary heart field

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7
Q

cardiac jelly

A

expanse of ECM in primitive heart tube–it’s in btwn the myocardium and endocardium. it’s a good scaffold for later things to migrate to.

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8
Q

what does epicardium of primitive heart tube derive from?

A

proepicardial organ, a derivative of the coelomic epithelium that overlies inflow region

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9
Q

cardiogenic mesoderm forms what?

A

endocardial endothelial cell
atrial myocyte
ventricular myocyte, PUrkinje fiber

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10
Q

proepicardium forms what?

A

coronary sm musc
endothelial cell of coronary vessel
fibroblast (for visceral pericardium)

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11
Q

venous inflow enters what in the simple tubular heart?

A

sinus venosus

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12
Q

arterial outflow is originally from what?

A

primitive RV

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13
Q

looping usually going in what direction?

A

right

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14
Q

heart begins to beat when?

A

21 days

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15
Q

what tissues are used for partitioning of heart

A

cardiac muscle
cardiac mesenchyme (encocardial cushion tissue)
extracardiac mesenchyme (mesoderm origin)
neural crest mesenchyme

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16
Q

by what day does the sinus venosus (right and left horn) connect with the primitive heart tube primordial atrium?

A

22

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17
Q

what happens with regards to the sinus venosus during wks 5-8?

A

left sinus venosus becomes a tributary of the right sinus venosus

so all venous return enters the right side of heart

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18
Q

where does smooth area of right atrium come from?

A

absorption of sinus venosus (primarily the right horn)

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19
Q

where does the appendage (auricle) come from?

A

primordial atrium

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20
Q

where does endocardial cushion tissue form?

A

AV canal and outflow region (involves epithelium to mesenchyme transformationation–endocardial cells turn into cardiac mesenchyme cells which move into the cardiac jelly)

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21
Q

what subdivides the AV canal?

A

septum intermedium

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22
Q

cardiac mesenchyme contributes also to formation of what?

A

valve leaflets and chordae tendinae

fibrous skeleton of the heart

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23
Q

does the interventricular septum close?

A

no, it never does.

a secondary interventricular communication is closed by formation of membranous interventricular septum

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24
Q

what is present in the proximal and distal portions of the outflow region?

A

endocardial cushion tissue

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25
Q

aortic sac is divided by what?

A

neural crest derived mesenchyme that forms the aorticopulmonary septum

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26
Q

endocardial cushion tissue can be present in

A

division of common AV canal
proxima and distal portions of outflow region
membranous interventricular septum

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27
Q

how is o2 rich blood shunted around liver?

A

ductus venosus

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28
Q

what explains the inactivity of the pulmonary circulation?

A

high vascular resistance in lungs (fluid in lungs)

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29
Q

congenital heart disease problems can present when?

A

stillbirth
at birth
or remain undetected until later life

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30
Q

types of L to R shunt

A

ASD
VSD
AVSD
PDA

have D’s in their names
are late cyanotic

31
Q

obstruction types of congenital heart disease

A

pulmonary stenosis
aortic stenosis
coarctation

they are acyanotic

32
Q

types of R to L shunt

A
tetralogy
transposition
truncus
TV atresia
TAPVR

all start with T’s

33
Q

valvular regurgitation types of congenital heart disease

A

Ebstein

34
Q

plexogenic pulmonary HTN

A
medial hypertrophy
intimal proliferation
plexiform lesions (irreversible damage)

more severe in VSD than PDA, which are both more severe than in ASD

35
Q

majority of atrial septal defects are at what location

A

secundum

36
Q

why do less than 10% of ASD lead to pulmonary HTN?

A

b/c of the low pressure and volume of the atrium

37
Q

where is the location of 90% of VSD?

A

septum-membranous VSD

38
Q

what is the most common congenital heart anomaly

A

VSD

39
Q

VSDs are usually associated with

A

other anomalies (only 30% of them occur in isolation)

40
Q

what to do for VSD?

A

surgical closure, usually around year 1

41
Q

can ASD be asymptomatic?

A

yes, can be until adulthood

42
Q

perimembranous VSD

A

defect is usually large

43
Q

muscular VSD

A

defect is usually small
spontaneous closure by fibrous adhesions occurs in more than 60% of cases by year 1

most don’t need surgery

44
Q

what is PDA closure delayed by?

A

prostaglandin E

45
Q

when should PDA close structurally?

A

by 3 months

46
Q

classic PE finding for PDA

A

harsh, continuous, machinery like murmur

47
Q

is PDA usually seen with other anomalies or in isolation?

A

in isolation

48
Q

atrioventricular septal defect

A

deficient AV septum, associated with mitral v and tricuspid v anomalies

49
Q

what is associated with complete AVSD?

A

Down syndrome

50
Q

complete AVSD is characterized by

A

common AV valve (five leaflets)

51
Q

what causes early cyanosis

A

R to L shunts

52
Q

what can you get with R to L shunts?

A

paradoxical emboli, decompression sickness

53
Q

symptoms of R to L shunts

A

cyanosis
digital clubbing
polycythemia (too many RBCs)

54
Q

what is the most common form of cyanotic congenitcal heart dis

A

tetralogy of fallot

55
Q

tetralogy of fallot

A

anteriosuperior displacement of infundibular septum leads to-ventricular septal defect, subpulmonary stenosis, overriding aorta, R ventricular hypertrophy

56
Q

clinical outcome of tetralogy of fallot depends on

A

severity of subpulmonary stenosis–will determine how much damage lungs will incur (the more stenosis, the more protected the lungs will be)

57
Q

findings for tetralogy of fallot

A

boot shaped heart on XR due to R ventri hypertrophy

58
Q

transposition of great arteries

A

aorta arises from RV

pulmonary artery arises from LV

59
Q

sequalae of transposition of great arteries

A

separate pulmonary and systemic circulations (two separate loops)

R ventr hypertrophy
pulmonary HTN

60
Q

two types of transposition of great arteries

A

intact ventricular septum
or
with VSD

61
Q

truncus arteriosus

A

origin of aorta and pulmonary artery from truncal artery

most have large VSD

62
Q

sequalae of truncus arteriosus

A

mixing of blood

increased pulmonary blood and pulm HTN

63
Q

tricuspid atresia

A

complete occulsion of tricuspid valve orifice
results from unequal division of AV canal (mitral valve is enlarged)

needs coexisting ASD/PFO and VSD

causes R ventricular hypoplasia

symptomatic, high mortality

64
Q

total anomalous pulmonary venous return

A

pulmonary veins don’t directly drain into L atrium (L atrial hypoplasia)

connect via left innominate vein or coronary sinus

ASD/PFO allows oxygenated blood to enter systemic circulation

65
Q

aortic coarctation

A

constriction of aorta

66
Q

what are the two types of aortic coarctation

A

preductal or infantile (with PDA)

postductal or adult (w/o PDA)

67
Q

clinical presentation of aortic coarctation

A

bicuspid AV (in 50%)

preductal:
lower body cyanosis
requires surgery

postductal:
depends on degree of narrowing
upper extremity HTN
rib notching on CXR

68
Q

aortic stenosis can present with what finding

A

systolic murmur

LV hypertrophy and LA dilatation

69
Q

hypoplastic left heart syndrome

A

aortic valve atresia with intact ventricular septum

70
Q

Ebstein anomaly

A

inferiorly displace and adherent septal and posterior leaflets
reduent anterior leaflet
dilated annulus with tricuspid regurg

71
Q

primary and secondary heart fields are derived from

A

splanchnic mesoderm

72
Q

what contributres to septation of the AV canal and outflow region?

A

cardiac mesenchyme (cushion tissue)

73
Q

what is the least worrisome congenital heart defect

A

ASD