deck_4452279 Flashcards

1
Q

primitive vertebrate CV plan begins.. and present by..

A

begins mid-week 3 present by week 4

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2
Q

as they migrate PHF cells specified to form left and righ t sides of heart and to form

A

atrialeft ventricle part of right ventricle

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3
Q

secondary heart field (SHF) forms

A

remainder of right ventricleoutflow tract - conus cordis and truncus arteriosus

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4
Q

the 5HT PITX2 pathway specificies .. and programs..

A

left side of bodyprograms heart cells in priamry and SHFs

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5
Q

master gene for left sidedness

A

PITX2

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6
Q

patterning of cardiac progenitor celsl occurs at the same time as

A

laterality (left-right sidedness) is established

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7
Q

circuit that supplies and drains the yolk sac ; separate from umbilical artery and vein; called the “nursery for blood vessels”

A

vitelline vein and artery

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8
Q

features of embryonic circuit

A
  • series of aortic arches connecting to dorsal aortae - d. aortae subdivides into smaller vessels to supply embryo- blood drained by anterior and posterior cardinal veins- common cardinal vein
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9
Q

bulbus cordis consists of

A

truncus arteriosusconus cordis

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10
Q

sinus venosus gives rise to

A

smooth part of right atrium (sinus venarum)coronary sinusoblique vein of left atrium

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11
Q

primitive atrium gives rise to

A

trabeculated part of right and left atria (auricles)

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12
Q

primitive ventricule gives rise to

A

trabeculated part of right and left ventricles

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13
Q

bulbus cordis gives rise to

A

conus cordis: smooth part of right ventricleaortic vestibule: smooth part of left ventricle

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14
Q

truncus arteriosus gives rise to

A

aorta, pulmonary trunk

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15
Q

blood flow in embryonic dilation

A

sinus venosus —> primitive atrium –> primitive ventricle –> bulbus cordis —> truncus arteriosus

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16
Q

more anterior structures (ventricles and outflow tract) are specified as such because of

A

lower RA concentrations

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17
Q

cardiac looping, the correct folding of heart (due to its rapid growth) is controlled by

A

PITX2 and the laterality pathwayif messed, heart could fold in different direction (could still work just fine)

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18
Q

grow the fastest during cardiac looping

A

ventricles and outflow tract

19
Q

dextrocardia caused by - presents as - can be found with - when does it occur embryologically?

A
  • heart bends to left instead of right- displaced to right with transposition of heart and great vessels- most common positional abnormality- can be found with situs inversus- during gastrulation or later during cardiac looping
20
Q

large ocmmunication between chambers that occurs when endocardial cushions fail to fuse – called? what does it result in? blood flow? treatment?

A

atrioventricular communisresults in common AV canalgiant atrial and ventricular septal defectenlarged pulmonary trunk (less resistance in pulmonary circ. vs. systemic so all blood flows through there)- Tx - put band on pulmonary artery to tie it off (lungs less congested now), then patch between right and left chambers then divide the one valve into two valves

21
Q

formation of interventricular septum

A

2 parts:muscular portion devleoping in midline on floor of the PV; growing upward towards ECC - bublar ridges growing downwards to ECC

22
Q

most VSDs occur in

A

muscular portion but close spontaneously!

23
Q

most commonly, surgically corrected VSD defects

A

membranous!

24
Q

opening between L & R ventriclesassociated shunting of blood

A

ventricular septal defects (VSDs)

25
Q

presenting baby, signs of cyanosis at 1 year check up right ventricle has hypertrophied; signs of pulmonary congestion and edemaauscultation and US shoe normal valvesdiagnosis? disease mechanism?

A

VSD!- initial lung inflation, RV pressure decreases- get left to right shunting (acyanotic) - causes increased work by RV, hypertrophy and eventual, right-to-left shunting —> cyanosis- rate depends on size of VSD

26
Q

vsd 2 facts

A

25% of congenital heart defects4 types based on position and severity

27
Q

which types of VSDs can have more significance for conudciton

A

centralproximalbasal

28
Q

valve of foramen ovale is derived from

A

septum primum

29
Q

foramen ovale upper boundary and lower boundary

A

upper: septum secundum (upper limb)lower: septum primum

30
Q

foramen ovale once fused is called

A

fossa ovalis

31
Q

RA features in terms of fossa ovale

A

limbus (septum secundum)fossa ovale( floor, septum primum)

32
Q

LA features in terms of fossa ovale

A

fossa ovale (floor, septum SECUNDUM)valve of fossa ovale (septum primum)

33
Q

ASD, stats, types of defects and what they involve

A

ASD - common, 10-15% of congenital heart defectsostium (foramen) primum defects - similar to ECC defectssecundum type - involve foramen ovale and septum primum sinus venosus - usually near opening of SVC

34
Q

ASD is a characteristic finding in this TBX5 gene mutation

A

Holt-Oram SYndrome [ H for heart!! ]- abnormality of upper extremities- can also have VSD

35
Q

in the embryo:nutritional circuits are(intra) embryonic circuits are..

A

nutritional: vitelline and umbilicalintra: cardinal veins

36
Q

connects umbilical vein with IVC

A

ductus venosus

37
Q

marks division between embryonic sinus venosus and embryonic primitive atrium (auricles)

A

crista terminalis

38
Q

SVC derived from joining

A

right anterior cardinal and common cardinal v. via brachiocephalic vein anastamosis

39
Q

embryo starts out getting drained by umbilical vein, vitelline veins and common cardinal but once sinus venosus is finished developing, we are left with these 3 vessels drianing what

A

SVC - head & neckIVC - placenta and caudal regions of embryocoronary sinus - heart itself

40
Q

partition of this forms the aortic and pulmonary semilunar valves

A

Truncus Arteriosus!

41
Q

disease pathology of eisenmenger’s syndrome; whats failed to form/ fuse? how is the blood shunting initially? later? why?

A
  • equal division of truncus, incomplete fusions of bulbar ridges inferiorly –> VSD - initial L –> R shunt, increased pulmonary blood flow and hypertension- prolif. in intima and media to narrow lumen- increased pulmonary resistance causes R to L shunt and cyanosis
42
Q

tetralogy of fallotwhat is IT?components? how/ why do they develop?

A
  • pulmonary stenosis- VSD [blood being shunted from right to left ventricle into the aorta]- overriding aorta- rt. ventricular hypertrophy [pulmonary trunk too small so ventricle hypertrophies to compensate][PS listen to H.O.V. ]
43
Q

breathing new born exhibits severe cyanosis immediately after birth and dies- boh ventricles of normal size, no A or V septal defects- lungs of normal size and well inflateddiagnosis?

A

transposition of great vessels