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CPR Exam 1 > Heart Development - Dr. Brauer > Flashcards

Heart Development - Dr. Brauer Flashcards

1
Q

Hear conditions make up how much of congenital birth defects

A

20%

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2
Q

What do Hemangioblasts give rise to what day in development

A

Become progenitor hematopoietic (RBC+ macrophage) and endothelium precursor (BV) cells
= organize into blood islands and BVs
DAY 17

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3
Q

Hematopoietic progenitor cells day 23

A

Populate in the liver = make immediate Blood cell needs for body

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4
Q

Definitive Hematopoietic stem cells (HSCs) are made by what

A

Are made from AGM homogenized endothelial cells (located in dorsal AORTA)
They go to the liver to colonize = make HSCs (can make any hematopoietic cells)

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5
Q

HSCs when made go where

A

Ones made in the liver by AGM cells ——> BM and Lymph organs

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6
Q

First hematopoietic cells are found where

A

In the yolk sac day 17 (early RBC and macrophages) from primitive HSCs

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7
Q

2nd place you see the hematopoietic cells

A 
LIVER PRIMORDIA (day 23)
The primitive HSCs go to the liver (from yolk sac) to continue making primitive RBCs and macrophages
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8
Q

3rd place you see the hematopoietic cells

A

the AGM (Aortic Gonadal Mesonephric) DORSAL AORTA makes Hemogenic endothelial cells (day 27-40)

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9
Q

4th place you see the hematopoietic cells

A

The hemogenic endothelial cells (in AGM) go to the LIVER

Liver makes DEFINITIVE HSCs from these hemogenic endothelial cells (week 5 —> birth)

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10
Q

5th place you see the hematopoietic cells

A

The Definitive HSCs go from the liver to the BM and Lymph organs (around week 10.5)

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11
Q

Major hematopoietic organ in the adult

A

BM

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12
Q

Blood vessel formation (intraembryonic vasculogenesis

A

Day 18
Endothelial precursor cells —> EPC attach with adhesion molecules into blood islands —> forms vasculogenic cords
*making BVs de novo from mesoderm

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13
Q

Blood vessels made by angiogenesis (intussusception)

A

New BVs made from existing BVs (expanding existing BV)

Intussusception = BV splits in half

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14
Q

Angiomas

A

Abnormal vasulogenesis of BV and lymphatic capillaries

  1. Capillary hemangioma (excessive capillaries)
  2. Cavernous hemangioma (excessive formation of venous sinuses
  3. Hemangiomas of infancy : this happening in neonates, and then regresses after birth
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15
Q

First Heart Field

A

the Angiogenic clusters or (EPC, endothelial progenitor cells) = forming a Cardiac Crescent in splanchnic mesoderm

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16
Q

how is the tubular heart made

A
  1. the angiogenic clusters become Endocardial tubes + Precardiomyocytes
  2. the endocardial tubes fuse
  3. tubular heart formed (Endocardium,Cardiac Jelly, Mesocardium)
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17
Q

Periepicardial Organ

A

becomes the epicardium around the heart

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18
Q

initial heart formation steps

A
  1. A is below V
  2. heart grows caudally and cranially causing it to loop
  3. V goes under A (turing counterclockwise)
  4. sinus horns –> sinus venosus —-> into A
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19
Q

what drives the lengthening of the heart development

A

secondary heart field

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20
Q

Secondary Heart Field

A

does not have initial cardiogenic markers

  • adds SM to the heart
  • DRIVES cardiac looping
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21
Q

Heterotaxia

A

any asymmetry thats abnormal

  • Situs inversus : total reversal of organs (normal physiology)
  • Situs ambiguous : partial reversal of some organs (
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22
Q

Visceroatrial heterotaxia

A

right heart, normal GI

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23
Q

Ventricular inversion

A

cardiac looping reversed

LV on right ride

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24
Q

sinoatrial growth happens most where

A

most differential expansion in the left side, causing the SA node to be located more right

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25
Q

The coronary sinus if remanent of the what

A

Left sinus horn

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26
Q

Right sinus horn incorporates to what

A

the posterior wall of future RA

27
Q

Bicuspid Aortic Valve

A

Aortic semilunar (tricuspid) valve is BICUSPID = regurgitation = LV hypertrophy or valve stenosis
can develop LV hypertrophy later in life
can cause aortic aneurism
inheritable in some cases

28
Q

Hypoplastic LV

A

underdeveloped LV + ascending aorta
small not well formed mitral valve + aortic valve
has patent ductus arteriosus + patent foramen ovale
*RV does all the work
*has patent ductus arteriosus + open FO

29
Q

Left sinus horn becomes the

A

coronary sinus

30
Q

sinus venosus opens into

A

RA in the sinoartrial orifice

31
Q

crista terminalis

A

pectinate (rough) and smoothed wall part junction in the RA

32
Q

inferior of right valvular fold

A

becomes the valve of IVC

33
Q

SA node comes from

A

right sinus horn and right common cardinal vein

34
Q

AV node comes from

A

left sinus horn

35
Q

first step in 4 chambers partitioning of heart

A

Differential growth : making muscular interventricular septum and muscular atrial septum (not closing all the way)
grows caudal –> cranial * as the heart expands up with differential expansion

36
Q

Second step in 4 chambers partitioning of heart

A

Endocardial Cushion Tissue : new CT formed in the AV region
fibrous septa formed by:
1. mesenchymal cells of endocardium (ECT)

37
Q

what separates the A and V

A

the AV region (septum fusion)

38
Q

fusion happens from

A

cushion cells

39
Q

Conotruncal ridges

A

in outflow tract

  1. Conus Arteriosus : proximal, make sure RV and LV blood are flowing separate
  2. Truncus Arteriosus : distal, dives to make aorta and pulmonary a (with aorticopulmonary septum)
40
Q

Septum primum

A

from A wall (top) to AV septum, has a hole near AV septum (OSTIUM PRIMUM)

  1. cushing cells close this hole
  2. new hole (ostium secundum or foramen secundum) forms on superior end of septum
    * RA and LA formation
41
Q

Septum Secundum

A

septum grows from A wall (top) to AV septum(NOT ALL THE WAY) also (over the foramen secundum)
* the hole formed right above the AV septum = foramen ovale

42
Q

foramen ovale how it works

A

the septum primum is the flap over it that only opens to allow blood to move RA –> LA, not the other way around
the hole is formed by the septum secundum
BLOOD GOES : RA —-(foramen ovale, foramen secundum)—-> LA

43
Q

1st breath of infant causes what

A

LA BP increases
RV and RA BP decreases
LEFT SIDE has higher P then right side= causing the septum primum into septum secundum = the close the hole

44
Q

patent foramen ovale

A

should permanently seal within 3 months

however this is when it doesn’t happen within a year

45
Q

Probe patency

A

foramen ovale doesn’t close completely only partially

46
Q

2 places cushion tissue forms

A
  1. AV setpum
  2. close the septum primum ostium primum
  3. in the conotruncal endocardial cushion tissue (when it divides the BF) + NCC cushion cells*
47
Q

Persistent AV Canal

A 
AV septum does not fuse due to failed cushion cells
AV valves degenerate 
= Pulmonary HTN
= X exercise
= SOB
= cardiac congestion (mixing blood)
= linked to down syndrome
48
Q

Atrial Septation

A 
O2 coming into RA BYPASSES pulmonary circuit in embryo (right to body system)
DUCTUS ARTERIOSUS (RV --> Descending Aorta)
49
Q

Ostium Primum Defect

A

Cushing cells dont form to close the septum primum or (foramen primum) hole

50
Q

Cyanosis

A

bluish skin due to low O2 blood saturation
due to mixing of blood, like when the shunt of foramen ovale does not close
also cause : finger clubbing, bluishs nails, lips

51
Q

Double Outlet RV

A

both pulmonery A and Aorta connect to RV
this is due to the AV canal or septum not shifting midline to allow the aorta to be in the LV
= cynosis
= murmus, SOB

52
Q 
aortic arches : 
1st 
2nd
3rd 
4th
5th
6th
A

6th aortic arch = connects to lung

3rd + 4th aortic arch = Systemic circulation to body

53
Q

the outflow tract formation

A
  1. the conotruncal ridges (swellings) spiral 180 degrees around eachother (the tubes)
  2. they fuse in the midline with the muscular septum (bottom of Vs) and the grow down from AV septum
54
Q

4 things NCC do

A
  1. help with spiraling of the outflow tract
  2. septation of the outflow tract
  3. semilunar valves cusps
  4. ANS nerves
55
Q

Ventricular septal defect

A

the ventricular septum (fibrous part) does not fuse with AV septum
CAUSE : LV –> RV pressure flow (Blood flow)
= RV works harder = RV hypertrophy and Pulmonary HTN
= Cynosis and Congestive Heart Failure (can take some months to years to see)

56
Q

in the embryo, fetus where does blood go from the RV

A

RV —-> Pulmonary trunk —-Ductus Arteriosus—-> Descending Aorta
*skips pulmonary As and lung

57
Q

Persistent Truncus Arteriosus

A

the conotruncal ridges dont form = no separation in the outflow tract of aorta and pulmonary trunk
+ Fibrous ventricular septum doesnt form
= separation happens more distally
= quick pulmonary HTN. cardiac hypertrophy, cyanosis

58
Q

part of ventricular septum usually is not developing in a septal defect

A

the fibrous part, not the muscular part

59
Q

Tetralogy of Fallot

A

outflow track divides so aorta gets more space and some gets into RV (conotruncal ridge does not from midline and therefore does not meet the muscular part the V septum)

60
Q

4 hallmarks of Tetralogy of Fallot

*most common defect that presents as cyanosis at birth

A
  1. Pulmonary Stenosis : since Pulmonary outflow is so small
  2. overriding aorta
  3. Ventricular septal defect (septa does not close)
  4. RV hypertrophy ( work hard to push blood into small pulmonary a) = cyanosis
61
Q

2 defects showing cyanosis at birth

A
  1. TOF * most common

2. Transposition of Great Vessels/ Pulmonary Valvular Atresia

62
Q
  1. Transposition of Great Vessels/ 2. Pulmonary Valvular Atresia
A
  1. the conotruncal ridges fuse with septum however dont spiral = aorta to RV and pulmonary a to LV
  2. the pulmonary semilunar valves dont form and are closed = blood cant get into pulmonary a from RV = RV hypoplasia and foramen ovale stays open*, LV hypertrophy
    * patent ductus arteriosus
63
Q

Aortic Valvular stenosis

Aortic Valvular Atresia

A
  1. partial semilunar valve of aorta, doesnt open well (small opening) = LV hypertrophy, try to get blood in to aorta
  2. X semilunar valve or opening of aorta = LV hypotrophy, RV hypertrophy, does all the work, * Patent ductus arteriosus stays*
64
Q

Tricuspid Atriesia

A

X tricuspid valve (between RA and RV), it is closed
= you have blood RA –> LA–> LV–> RV
*patent ductus arteriosus

CPR Exam 1 (20 decks)

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