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Anatomy Week 8 > Embryology III > Flashcards

Embryology III Flashcards

1
Q

When does the primative muscular heart tube begin having some contractility?

A

day 23-24

  • by the end of week 4 its a fairly functional system
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2
Q

When does heart heart development begin?

A

end of week 3

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3
Q

What are the primordial cells of heart development and what is their original location?

A
  • The cardiogenic mesoderm
  • early location is cranial to the neural tube and future mouth (these form a hollow horse-shoe shaped tube that will eventually form L and R heart tubes)
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4
Q

What causes fusion of the horseshoe shaped heart tube in the forth week?

A
  • at the end of week 3 there are series of body foldings (laterally and head to tail)
  • the amnion and 3 germ layers fold ventrally and medially to go from a mushroom shape into a ball with several infoldings
  • left and right cardiogenic tubes get closer and closer eventually fusing to a single tube as a result of lateral folding
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5
Q

At what end do the two heart tubes begin fusing into one?

A

cranial then proceeds caudally

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6
Q

What is the importance of head to tail folding in heart development?

Note: this process happens at the same time as lateral folding and results from rapid nervous system growth

A
  • it pulls the heart down into the thorax (midline mediastimum), when the heart goes into this position it brings with it its connections to CNX (parasympathetic innervation) and T1-T5 (sympathetic innervation)
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7
Q

What five divisions does the heart divide into after entering the mediastinum?

A

From cranial to caudal:

  1. Trucus arteriosus
  2. Bulbus Cordis
  3. primitive ventricle
  4. primitive atrium
  5. sinus venosus
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8
Q

What is the orientation of the heart tube in week 4 and does it have the ability to pump blood at this stage?

A

Yes, it can pump blood

Oriented vertically:

  • cranial = arterial outflow
  • caudal = venous inflow
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9
Q

What movements in week 4 reorient the heart out of its vertically orientation?

A
  1. Ventrical movement (VIL)
    - ventrally
    - inferiorly
    - Left
  2. Atrial movement (ADULR)
    - Atria
    - Dorsal
    - Upward
    - Right
  • These movements explain the orientation of the heart
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10
Q

What does the Truncus arteriosus (neural crest) give rise to?

A
  1. Aorta
  2. pulmonary trun
  3. semilunar valves
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11
Q

What does the Bulbus cordis give rise to?

A
  1. Conus Arteriosus (smooth part of the right ventricle)

2. Aortic Vestibule (smooth part of left ventricle)

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12
Q

What does the primitive ventricle give rise to?

A
  1. Trabeculated part of the right ventricle

2. Trabeculated part of the left ventricle

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13
Q

What does the primitive atrium give rise to?

A
  1. Trabeculated part of the right atrium (pectinate muscles)

2. Trabeculated part of the left atrium (pectinate muscles)

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14
Q

What is different about the sinus venosus from the other 4 parts of the primative heart tube?

A
  • its the only part that does not become subdivided by a septum, its doesnt need to do this because it is the ONLY part of the embryonic tube that consists of right and left parts
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15
Q

What does the sinus venosus give rise to?

A
  1. Sinus verarum (smooth part of the right atrium) (from Right horn)
  2. Coronary sinus and oblique vein of left atrium (from Left horn)
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16
Q

In fetal development what structures import oxygenated blood and export deoxygenated blood?

A
  • umbilical vein = oxygenated import

- umbilical arteries = deoxygenated export

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17
Q

What two major structures does fetal circulation work to bypass?

A
  1. Lungs

2. Liver

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18
Q

What does the allows fetal circulation to bypass the liver?

A

Ductus Venosus - redirects flow into the IVC

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19
Q

What is unusual about the pressure differential in fetal circulation and what causes this?

A
  • Pressure on the right side is higher than the pressure on the left
  • caused by:
    1. massive volume of blood entering the right chamber via SVC (O2 poor) and IVC (O2 rich)
  1. High pulmonary resistance due to closed pulmonary circulation
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20
Q

What structure allows fetal blood to bypass pulmonary circulation?

A
  • Foramen ovale (hole from R to L atrium, right to left shunt)
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21
Q

T or F: There is extensive mixing of blood from SVC (O2 poor) and IVC (O2 rich) in the right atrium during fetal development

A

False, while the two blood sources do enter the same chamber the flow remains laminar so that O2 rich blood from the IVC is directed through foramen ovale to systemic ciculation while O2 poor blood from SVC enters right AV valve.

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22
Q

What causes closure of the three shunts (Ductus venosus, foramen ovale, and ductus arteriosus) in the first 24-36 hours of life?

A

Foramen Ovale - closure is nearly immediate due to the pressure differential

Ductus venosus and arteriosus - results from contraction of smooth muscle in the walls of these tubes

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23
Q

What does the ligamentum arteriosum become in adult life?

A

ligament arteriosum

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24
Q

What are the 3 major cardiac septation events that transform the heart into the 4 chambered structure?

A
  1. Atrial Septation
  2. Ventricular Septation
  3. Truncal Septation (forms ascending aorta and pulmonary trunk)
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25
Q

What type of cells are responsible for a great number of the newborn cardiovascular defects?

A
  • these are mostly septation defects

- neural crest cells play a large role in septation defects

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26
Q

In order to prevent septation defects where must neural crest cells migrate?

A
  1. truncus arteriosus

2. endocardial cushions

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27
Q

What structures are formed from the truncus arteriosus and endocardial cushions?

A

(PALS up)

  • Pulmonary trunk
  • Ascending Aorta, AV valves and canals
  • Lower part of Atrial Septum
  • Semilunar valves
  • UPper part of ventricular septum
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28
Q

Why can’t the foramen ovale close until birth?

A

it allows for oxygenated blood to enter fetal circulation

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29
Q

Describe the timing and events leading to the formation of the foramen ovale.

A
  • between weeks 5 and 8
    1. Septum Primum grows down and stops before the Endocardial Cushion (EC- derived from NC cells) leaving the Foramen Primum
  1. Septum Primum grows down to EC closing of Foramen Primum but before closure a second hole (Foramen Secundum) forms
  2. Septum Septum Secundum grows down next to the Septum Primum and overlaps the foramen secundum
    * *this overlap leads to the foramen ovale with the Septum Primum acting as a one way flapper
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30
Q

What leads to the formation of the limbus in the adult heart?

A

the free edge of the septum secundum which lies on the side of the right atrium

31
Q

What type of shunting leads to non-cyanotic defects?

A

Left to right- continual cycling of oxygenated blood through the pulmonary circulation producing super saturated oxygen levels

32
Q

What type of effects does Right to Left shunting cause?

A

cyanotic defects - deoxygenated blood is pushed into peripheral circulation

33
Q

What are Atrial Septal Defects (ASDs) and what are 2 commonalities between the different types?

A
  • these occur when the atrial septum does not form properly
  • 2 types:
    1. secudum type
    2. primum type
  • Both types give rise to:
    a. Left to right shunts
    b. these are non-cyanotic
34
Q

Which of the ASDs are caused by neural crest cell defects?

A

Primum type (less common type)

35
Q

What are some characteristics of secundum type ASDs?

A
  • high on interatrial wall (above fossa ovalis)
  • more common in females
  • Most common type of ASD (~80%)
  • Less clinically significant
  • could lead to atrial fibrillation or stroke
36
Q

What are some characteristics of primum type ASDs?

A
  • involve neural crest (NC) cells (septum primum doesn’t fuse to endocardial cushion)
  • ~20% of ASDs and much more serious
  • Often implies other NC defects
  • common in kids with Down’s
37
Q

What are the two parts of the interventricular septum and what types of cells are these parts derived from?

A
  1. Muscular Portion (ventricular floor)
    - Derived from MESODERM
    - stops short of EC leaving interventricular Foramen
  2. Membranous portion
    - Derived from NEURAL
    - formed by downward growth of EC (w6-7)
38
Q

By what week is the interventricular septum fully formed?

A

Week 8

39
Q

What are the two types of Ventricular Septal Defects (VSDs) and what are the characteristics of all VSDs?

A

Two Types:

  • Membranous
  • muscular

Characteristics:

  • Right to left shunt
  • non-cyanotic at birth
40
Q

What is the most common type of newborn cardiac defects and is it neural crest dependent?

A
  • membranous VSD

- YES is it VSD dependent

41
Q

Describe the causes of membranous VSDs.

A
  • failure of membranous portion of interventricular septum to form
  • L to R shunting (non-cyanotic)
  • NC dependent
  • More common in Males
  • Results in serious problems
42
Q

What is Eisenmanger’s Complex and what is the most common cause of it?

A
  1. increased volume of blood through pulmonary trunk from VSD (L —> R shunting) causes pulmonary stenosis
  2. Pulmonary stenosis causes pulmonary hypertension and then you get R –> L shunting (cyanotic)
43
Q

When Eisenmanger Complex typically become evident?

A

kid turns blue at 9-10 months because of shunting reversal

44
Q

Patent Ductus Arteriosus, is it a septation issue?

A
  • Failure of Ductus arteriosus to close
  • NOT a septation issue
  • Left to right shunting
  • can lead to Eisenmanger Complex
45
Q

What is coarctation?

A

narrowing of the aorta

46
Q

What is more come postductal or preductal coarctation and what is the difference?

A
  • Postductal is way more common and occurs past ductus arteriosus
  • Preductal occurs proximal to ductus arteriosus
47
Q

How does the body compensate for postductal coarctation and how can postductal coarctation been detected?

A
  • body increases collateral circulation to compensate
  • detected by high right arm BP and and low leg BP
  • also can be seen on radiograph by notching of the ribs from increased size of intercostal arteries
48
Q

What defect can lead to differential cyanosis between upper and lower body?

A

Preductal coarctation

This happens because no collateral circulation develops because some blood can still reach the lower body via ductus arteriosus

49
Q

What is different about septation defects of the truncus arteriosus?

A

Septation defects here lead to cyanosis at birth because of R to L shunting

50
Q

What septum forms in the truncus arteriousus and are neural crest cells involved here?

A
  • Aorticopulmonary septum
  • This septum divides the truncus arteroisus into the aorta and pulmonary trunk

Yes, NC cells are critical to the formation of this septum

51
Q

What are three important septation defects of the truncus arteriosus?

A
  1. Tetralogy of Fallot (alignment issue)
  2. Transposition of the Great Vessels (spiraling issue)
  3. Persistent Truncus Arteriosus (no formation)
52
Q

What are the 4 classic markers of Tetralogy of Fallot ?

A
  1. Pulmonary stenosis - from pulm HTN!!!
  2. ALWAYS ACCOMPANIED BY membranous ventricular septation defect (mVSD) (therefore, must also involve NC cells)
  3. Large over-riding aorta (straddles mVSD)
  4. Hypertrophy of right ventricle

**sometimes accompanied by Patent Ductus Arteriosus

53
Q

What causes cyanosis in tetralogy of Fallot?

A
  • Septum aligns too far to the RIGHT and takes blood from BOTH R/L ventricle
  • mixing of blood from the L and R ventricles = Right to Left Shunt
54
Q

What is the issue in the transposition of the great vessels (trucus arteriosus - aorticopulmonary septation defect)?

A
  • results because spiral septum doesn’t form a spiral
  • aorta comes from the right ventricle and the pulmonary trunk comes from the left
  • Most severe of truncal defects
55
Q

What is the difference between open and closed transposition of great vessels?

A
  • open is accompanied by other ASDs, VSDs, or PDA that allow mixing of blood.
  • *This is actually better than closed
  • Closed - there are no accompaning ASDs, VSDs, or PDA
  • *very low survival rate
56
Q

Why might a physician give a baby with open transposition of great vessels prostagladins?

A
  • Prostaglanins keep the ductus arterious open (this promotes patent ductus arterious aka PDA)
57
Q

What happens in persistent truncus arteriosus (trucus arteriosus - aorticopulmonary septation defect)?

A
  • AP septum fails to form
  • single common outflow vessel of the heart
  • always accompanied by mVSD
  • Left to right shunting = cyanosis
58
Q

What are the 3 main veins of the fetus?

A
  1. Cardinal Vein
  2. Umbilical Vein
  3. Vitelline Vein
59
Q

What embryonic vein gives rise to the veins of the liver (sinusoids, hepatic portal vein, and hepatic vein)?

A

Vitelline Vein

60
Q

What embyonic vein gives rise to the SVC, IVC, brachiocephalic, azygos, and renal veins?

A

Cardinal Veins

61
Q

What vein does the umbilical vein give rise to after birth?

A

None - you don’t need it anymore

62
Q

What does the 3rd aortic arch give rise to?

A

Common carotid and first part of the internal cartotid arteries

63
Q

What do the L and R sides of the 4th aortic arch give rise to?

A

Left:
Arch of the aorta from the left common carotid to the left subclavian arteries

Right:
Right subclavian Artery (proximal portion)

64
Q

What do the L and R sides of the 6th aortic arch give rise to?

A

Left:
Ductus arteriosus

Right:
Right Pulmonary Artery

65
Q

What do the first, second, and fifth aortic arches give rise to?

A

Nothing important

66
Q

What explains the different positions of the Right recurrent laryngeal nerve and the Left recurrent laryngeal nerve?

A

adf

67
Q

When does Foramen Ovale Close?
• Ductus Arteriosus?
• Ductus Venosus?

A

• Closes with the 1st breath.

Close in 24-36 hours:
• Ductus Arteriosus
• Ductus Venosus

68
Q

In what weeks does sepatation begin and when does it end?
• What structures septate?
•Which septation event occurs first?

A

ALL septations take place simultaneously
• Truncus Arteriosus, Primative Atrium, and Primative Ventricle all Septate

• Week 5 through 8 is when this occurs

69
Q

How can kids with Tetrology of Fallot get temporary relief?

• why does this work?

A
  • They can SQUAT to get temporary relief

* Works because they get better veinous return to the lungs?

70
Q

Why does Transposition of the great vessels kill infants without concurrent defects?
• Where can oxygenated blood be found in the heart?

A
  • RIGHT side of the heart is a constant circuit into the systemic circulation - ANOXIC
  • LEFT side of the heart is a constant circuit into pulmonary circulation - HYPEROXIC
71
Q

What medication would you absolutely never want to give to someone with a transposition of the great vessels?

A
  • NSAIDs these people need prostaglandins to keep a PDA so that they can get mixing of some oxygenated blood into their systemic circulation
  • These people need PGE2 to stay high (its the drop in PGE2 after birth that leads to closure)
72
Q

What kind of Shunt does a Patent Ductus Arteriosus result in?
• how can this change?

A
  • Left to Right shunt of Higher Aortic Pressure going into the pulmonary system
  • Pulmonary Trunk stenosis can be caused by constant high pressures and Pulm Pressure may exceed systemic pressure at a point => at this time EISENMANGERs complex will happen
  • Shunt will shift Right to Left and bottom half of the body will become cyanotic
73
Q

What condition is VERY associated with diffential Cyanosis of UE and LE?

A

PRE-ductile coarctation of the aorta

•PDA remains patent and DEoxgenated blood goes into aorta but pressures are maintained so you don’t see lots of Collateral Circulation

74
Q

What condition are you likely to see RIB notching with?

A

POST-ductile coarctation of the aorta

NOT possible to maintain BP via patent pda so COLLATERALS Develope involving the:
• Left Subclavian
• Thoracic Aorta
• Left Internal Thoracic Artery
• Intercostal Artery (cause rib notches)

Can see this on CXR

Anatomy Week 8 (15 decks)

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