cardiac embryology Flashcards

1
Q

the two cardiogenic areas flanking the primitive streak have different growth potential, how does this relate to the final anatomy

A

situs solitus vs situs inversus

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2
Q

what are the four primitive dilations of the heart

A

bulbus cordis
primitive ventricle
primitive atrium
sinus venosus

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3
Q

what are the proximal and distal portions of the bulbus cordis called

A

distally the arterial end is the truncus arteriosus, and proximally the conus

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4
Q

at the venous end of the primitive tube the sinus venosus has two what

A

a right and left horn

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5
Q

each right and left horn of the sinus venosus receives what three veins

A

the vitelline vein (yolk sac), the umbilical vein (placenta) and the common cardinal vein (body wall)

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6
Q

fate of the truncus arteriosus

A

ascending aorta and pulmonary trunk

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7
Q

proximal portion of the bulbus cordis

A

conus that gets absorbed into the primitive ventricle

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8
Q

primitive ventricle

A

LV and RV

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9
Q

primitive atrium fate

A

RA and LA

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10
Q

sinus venosus fate

A

right horn into the right atrium, left horn regresses to form part of the coronary sinus

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11
Q

after the septum primum comes down and joins the AV cushions on what side does the second partition come down to create the flap valve of trhe foramen ovale

A

left

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12
Q

what is the smooth portion of the RA that originated from the sinus venosus

A

sinus venarum

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13
Q

from what structure does the IVC form

A

right vitelline vein

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14
Q

from what structure does the SVC form

A

right common cardinal vein

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15
Q

The right venous valve of the sinus venosus forms what structures in the RA (3)

A

Crista terminalis
Eustachian valve
Thebesian valve

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16
Q

at 30 days gestatation the LA eventrates out to create a common pulmonary vein, this joins the _____ of the lungs formerly draining into the systemic circulation

A

pulmonary venous plexus

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17
Q

The septum intermedium from the proliferation of the AV cushions contribute to which valve leaflets

A

the septal leaflets of the tricuspid valve and the anterior leaflet of the mitral valve

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18
Q

the conus develops into both outflow tracts

A

true

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19
Q

normal right looping is D or L

A

D

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20
Q

initially one primitive ventricle has connections based on right or left half, which side connects to the outflow tract and which side to the primitive atrium

A

right to the outflow tract and left to the atrium

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21
Q

from where does the primitive ventricular septum arise

A

the floor of the ventricle

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22
Q

the conal septum comes from what

A

bulbar ridges arising in the floor of the conical portion of the bulboventricular cavity give rise to the bulbar septum and grows downward to meet the primitive septum

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23
Q

the gap between the conal septum and the primitive ventricular septum is filled by what

A

proliferation of tissue from the AV cushions

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24
Q

truncus splitting occurs in its right left sequence because of what

A

spiral growth of the septum from right and left truncal swellings

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25
Q

fate of 1st arch

A

maxillary artery

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26
Q

fate of 2nd arch

A

stapedial artery

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27
Q

fate of 3rd arch

A

common and internal carotids

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28
Q

fate of 4th arch

A

subclavian on the right, distal arch on the left

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29
Q

fate of 5th arch

A

disappers

30
Q

fate of 6th arch

A

PA, ductus and artery to developing lung buds

31
Q

fate of 7th cervical intersegmental artery

A

left subclavian

32
Q

Van Praagh visceroatrial relationship

A

S, normal, I inverted, A ambiguous

33
Q

Van Praagh Ventricular Loop

A

D : RV and thus tricuspid on Right, L: RV and thus tricuspid on Left, X: indeterminate

34
Q

Van Praagh Great arteries

A

S: anterior and leftward PA
I: anterior and rightward PA
D: posterior and leftward PA
L: posterior and rightward PA

35
Q

which two shifts must occur correctly for normal looping and final ventricular morphology

A

rightward shift of the AV canal and leftward shift of the conus with disappearance of the bulboventricular flange

36
Q

Failure of establishment of connection between left aortic bud and the
epicardial arterial plexus.

A

ALCAPA

37
Q

Incomplete development of spiral septum

A

AP window

38
Q

Defect in AV cushion contribution to formation of anterior mitral valve

A

Cleft mitral valve

39
Q

Flow theory: Blood flow through cardiac chambers and great arteries during
fetal life determines their size. Coarctation occurs as a consequence of
lack of blood flow across aortic isthmus (either because of VSD or left-sided
obstructive lesions).
Ductal sling theory (Skoda): Abnormal extension of contractile ductal tissue
into the aorta. Contraction and fibrosis of this tissue at time of ductal
closure leads to coarctation

A

Coarctation of the aorta

40
Q

Failure of contribution of AV cushion towards formation of atrial and
ventricular septa

A

Common AV canal

41
Q

Common pulmonary vein gets obliterated after pulmonary systemic
connections have disappeared.

A

Common pulmonary

venous atresia

42
Q

Severe lack of ventricular septation most likely caused by total absence of
both primitive ventricular septum and component of AV cushion

A

Common ventricle

43
Q

Failure of normal development of cusps, which results in primitive
gelatinous masses guarding aortic opening

A

Congenital aortic

stenosis

44
Q

Abnormal connection between the common pulmonary vein and the LA

A

Cor triatriatum

45
Q

Persistence of the right venous valve, which results in membranous
obstruction of the tricuspid valve, RVOT or IVC.

A

Cor triatriatum dexter

46
Q

Reverse looping of the heart tube (l loop rather than d loop) with
malseptation of truncus resulting in both AV and VA discordance.

A

Corrected transposition

l-TGA

47
Q

Failure of septum to spiral in usual fashion, which results in
ventriculoarterial discordance. Alternative theory: underdevelopment of
subpulmonary conus resulting in pulmonary mitral continuity (Van Praagh)

A

d-TGA

48
Q

V Persistence of primitive arrangement where both AV valves empty into LV

A

DILV

49
Q

Rightward shifting of AV canal exceeds normal shifting resulting in both AV
valves emptying into RV.

A

DIRV

50
Q

Leftward shifting of conus exceeds the normal shifting leading to inclusion
of both conal derivatives into LVOT.

A

DOLV

51
Q

Persistence of primitive arrangement where RV empties into both outlets.
Abnormality of spiral septation such that aorta becomes dextroposed. This
is greater dextroposition than seen in TOF but lesser than TGA

A

DORV

52
Q

Failure of delamination of the septal and posterior leaflets of the tricuspid
valve resulting in downward displacement of these leaflets.

A

Ebstein’s anomaly

53
Q

Defect in AV cushion contribution to septal component of tricuspid valve,
which results in LV to RA communication

A

Gerbode defect

54
Q

Leftward displacement of septum primum deflects usual volume of blood
away from the left side of the heart, which leads to its underdevelopment
Alternative theories: 1) Premature narrowing of foramen ovale, which leads
to faulty transfer of blood from IVC to LA. 2) Severe underdevelopment of
LVOT, which leads to altered flow pattern in fetus

A

Hypoplastic left heart

syndrome

55
Q

Failure of normal contribution of AV cushion towards formation of ventricular
septum

A

Inlet VSD

56
Q

Failure of normal fusion between the various segments. Type depends
upon level of failure of fusion

A

Interrupted aortic arch

57
Q

Failure of septum primum to reach the AV cushions.

Alternate theory: Defective formation of AV cushions

A

Ostium primum defect

58
Q

Persistence of oblique valvular passage between septum primum and
secundum

A

PFO

59
Q

Failure of pulmonary valve leaflets to open resulting in decreased flow
through the tricuspid valve and RV and consequent hypoplasia. Variable
degree of RV hypoplasia depending on the stage at which fault occurs.

A

Pulmonary atresia /

intact ventricular septum

60
Q

Abnormal connection between the individual pulmonary veins and the
common pulmonary vein

A

Pulmonary vein stenosis

61
Q

Premature narrowing of foramen ovale or improper angulation of limbus
leads to hypoplasia of left-sided heart structures (flow theory)

A

Shone’s complex

62
Q

Malseptation of conal septum with primitive interventricular septum. May be
associated with posterior malaligned VSD when conal septum projects into
LVOT. Subaortic membrane develops as a result of turbulence in
abnormally shaped LVOT.

A

Subaortic stenosis

63
Q

Failure of the common pulmonary vein to connect to the pulmonary venous
plexus of the lung buds

A

TAPVR

64
Q

Classic theory: Faulty septation of bulbus cordis that results in unequal
sized great vessels (i.e., large aorta and small pulmonary trunk).
Alternative theory: Underdevelopment of subpulmonary conus with
consequent rightward and superior shift of the aortic valve.

A

TOF

65
Q

Failure of 6th arch arteries to connect with the systemic arteries carried by
the lung bud from the primitive foregut and persistence of connections from
aorta (AP collaterals). Variable degree of development of true PA depends
on stage at which defect sets in.

A

TOF / pulmonary atresia F

66
Q

Defect between the conal and primitive interventricular septum usually
associated with some degree of malalignment.

A

VSD – Conoventricular

67
Q

Defect of the endocardial AV cushion, most likely the medial cushions

A

VSD – inlet (type 3)

68
Q

Defect in the primitive interventricular septum

A

VSD – muscular (type 4)

69
Q

Defect in development of the bulbar septum

A

VSD – outlet (type 1)

70
Q

Failure of membranous septum to form completely and may occur because
of inadequacy of any of the three contributors.

A

VSD – perimembranous

type 2