Embryology Flashcards

1
Q

cardiogenic mesoderm

A

gives rise to endo, epi, and myocardium

- does not form fibrous skeletal elements or valves

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2
Q

Cardiac looping

A

induced by rapid growth of ventricles

caudal end folds up and posterior –>puts venous and atrial things posterior

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3
Q

Sinus venosus

A

most caudal structure in heart tube (receives all blood form embryo)
Becomes RA
L sinus horn–>coronary sinus
R sinus horn–> sinus venarum

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4
Q

Primitive atrium

A

will become the pectinate regions of the LA and RA (i.e. auricle regions)

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5
Q

Primitive ventricle

A

will form the trabeculated portions of the LV

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6
Q

bulbus cordis

A

becomes the trabeculated portion of RV, root of ascending aorta an pulmonary trunks, outflow parts of both RV and LV

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7
Q

conus cordis

A

part of bulbous cordis that becomes smooth walled outflow of both LV and RV

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8
Q

Truncus arteriosus

A

part of bulbous cordis that becomes ascending aorta and pulmonary trunk

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9
Q

Septum Primum

A

forms first in atrial partitioning

has a small opening in inferior part called ostium primum (very short lived)

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10
Q

Osteium secundum

A

second step in atrial partitioning
forms in septum primum
allows blood to flow from RA to LA and bypass the lungs

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11
Q

Septum secundum

A

3rd step
forms laterally to primum, thicker and more muscular, will become interatrial septum
contains foramen ovale which is the definitive blood shunt (sealed at birth)
septum primum is the valve for foramen ovale

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12
Q

Patent foramen ovale

A

common, lack of fusion of foramen ovale and primum
usually asymptomatic, unless there is a pathology that increases pressure in RA, when it can open up

example of ASD (10% of all defects)

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13
Q

Neural crest cells

A

migrate into heart and form a ring of tissue around the IV septum called endocardial cushions, creating a right and left atrioventricular canal

will form the heart valves and membranous portion of ventricle wall

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14
Q

VSD (ventricular septal defect )

A

30% of all congenital defects
- holes in either muscular or membranous (more common) septa
severity depends on size
L–>R shunting of blood
sx= pulmonary hypertension, decreased systemic blood flow, LV hypertrophy

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15
Q

endocardial cushion (neural crest) disorders

A

cause persistent AV canal
ASD (ostium primum defect)
Membranous VSD

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16
Q

Aortic stenosis

A

narrowing of great vessel lumen due to stenosis of heart valve (usually semilunar)

17
Q

Tetralogy of fallot

A

caused by unequal division of truncus arteriosus

1) narrowing of pulmonary trunk
2) overriding aorta (very large)
3) Membranous VSD
4) RV hypertrophy

due to pulmonary stenosis

** common cause of cyanosis of newborn

18
Q

Transposition of great vessels

A

Aorta exits from RV, PT comes from LV

due to conotruncal ridges failing to spiral

19
Q

Persistent truncus arteriosus

A

1 artery that leaves from both RV and LV–> mix of oxygenated and deoxygenated blood to systemic circulation

from conotruncal ridges failing to form
another cause of cyanosis in the newborn

20
Q

dextrocardia

A

looping disorder that causes a right sided heart

21
Q

ectopic cordis

A

body wall defect in which there is no fusion of the thoracic wall–> heart forms externally

22
Q

DiGeorge syndrome

A
neural crest disorder--> cardiac valve defects, 
CATCH-22
Chromosome 22 deletion
abnormal face
thymic aplasia (immunocompromised), 
cleft palate
hypocalcemia (PTH defect)
23
Q

3rd Aortic arch

A
R= Common Carotid a. 
L= Common Carotid a.
24
Q

4th Aortic arch

A
R=  R Subclavian . 
L= Arch of aorta
25
Q

6th Aortic arch

A
R= Pulmonary a. 
L= Pulmonary a. and ductus arteriosus
26
Q

7th aortic arch

A
R= Subclavian a.
L= Subclavian a.
27
Q

Patent ductus arteriosus

A
ductus arteriosus does not close
L--> R blood shunt 
pulmonary overflow 
R side hypertrophy 
decreases systemic flow
28
Q

Preductal coarctation of aorta

A

Infantile, presents immediately
bypass the constriction via ductus arteriosus prenatally, but at birth there is no diversion
–> tachycardia, cyanosis of LOWER LIMBS, low femoral pulse

29
Q

Postductal coarctation of aorta

A

adolescent, present later,

during development there is no way to divert the block unless collateral circulation is developed via posterior and anterior intercostals which brings blood to descending aorta

presents as individual becomes more active
Sx= fatigue, HA, HT upper limg, weak femoral pulse, hypotension in lower limbs

30
Q

Retroesophageal R subclavian a.

A

R subclavian passes behind esophagus

can compress the esophagus–> dysphagia lucoria

31
Q

double aortic arch

A

aortic arch persists on both sides compressing the esophagus and causing dysphagia

32
Q

Tracheoesophageal Fistula

A

development of an abnormal fistula (opening) b/w trachea and esophagus due to lack of septum formation

proximal esophageal atresia

sx: infant that can’t eat (vomits immediately)
stomach become distended with air

33
Q

Fetal survivability based on lung development

A

6-16 weeks= non-survivable due to lack of lungs and surfactant

surfactant production begins at week 21, becomes survivable

preemies suffer from respiratory distress syndrome due to lack of surfactant