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year 1 flash cards > BS cardiovascular embryology > Flashcards

BS cardiovascular embryology Flashcards

1
Q

what is the meaning of vasculogenesis

A

making vessels from scratch

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2
Q

what is the meaning of angiogenesis

A

remodelling vessels

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3
Q

what is the difference between apoptosis and necrosis

A

apoptosis is programmed cell death, whereas necrosis is cell death which is a result of injury

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4
Q

during what week do we get the formation of the heart?

A

week 3, day 22(first contraction)

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5
Q

what are the 3 layers of the heart?

A
  • epicardium
  • myocardium
  • endocardium
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6
Q

what is the epicardium and what is it derived from ?

A

visceral layer of pericardium (also known as the visceral layer)
derived from visceral mesoderm

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7
Q

what is the myocardium derived from and what will it form?

A

visceral mesoderm overlying heart tube

will form the muscular wall

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8
Q

what is the endocardium derived from? and what is the advantage of having this layer

A

heart tube

makes endothelial lining less sticky

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9
Q

describe the process of vasculogensis in days 17 and 18

A

1) endoderm induces some cells overlying visceral/splanchnic mesoderm to differentiate into angioblasts
2) angioblasts differenziate into endothelial cells and form 2 tubes = endocardial tubes (vascilogensis)

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10
Q

how do we form the primitive heart tube

A

the endocardial tubes fuse in lateral folding

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11
Q

how do we get the formation of myocardium and what is the significance of this layer?

A

visceral mesoderm surrounding primitive heart tube differentiates to myocardium
- myocardium secretes thick extra cellular matrix (cardiac jelly)

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12
Q

what is cardiac jelly and why is it important?

A

gelatinous connective tissue separating the myocardium and heart tube endocardium

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13
Q

what does the epicardium cover and what will it go onto form?

A

covers outside of heart tube

outer layer responsible for formation of coronary arteries

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14
Q

by week 4 how many veins are present ? where do they drain into? how?

A

3 paired viens in caudal region

drain int tubular heart of embryo via R and L horn of sinus venous

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15
Q

by week 4 do we have any vessels at the cranial region? if so what?

A

2 dorsal aortae

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16
Q

what are the 5 dilatations that become apparent in the heart tube? name these from the caudal to cranial end

A 
sinus venous 
primitive atrium 
primitive ventricle 
conus arteriosus 
truncus arteriosus
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17
Q

what structures does the pericardial cavity refer to?

A

primative ventricle
conus arteriosus
truncus arteriosus

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18
Q

what structures does the bulbs cords refer to? what will these structures go onto form

A

truncus arteriois - will form pulmonary trunk

conus arteriosus - will form aorta

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19
Q

what happens in day 23 in the development of CV system. what is this known as?

A

heart tube folding - preparation for dividing into 4 chambers
cardiac looping

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20
Q

describe what happens in cardiac looping

A
  • bulbus cordis moves caudally, ventrally and to the R
  • primitive ventricle is displaced before moving back to midline
  • primitive atrium displaces cranially and dorsally
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21
Q

when does the sinus venous degenerate and what will it remain part of?

A

week 5
remains as part of the smooth part of the R atrium wall (R horn) = sinus vernarum
and contributes to venous drainage (L horn) of heart

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22
Q

what does the left horn form?

A

oblique vein of left atrium and coronary sinus

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23
Q

what is the coronary sinus

A

where coronary veins all drain into

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24
Q

what is the crest terminalis

A

border between the trabeculated (rough) part of the R atrium and the sinus vernarum (smooth)

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25
Q

where are pectinate muscles and what are they formed by in CV development?

A

in the trabeculated part of the atrium

formed by the primitive atrium

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26
Q

what is most of the ventricular wall formed from?

A

primitive ventricle and some of conus arterioles

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27
Q

what does the conus arterioles help form in the ventricular wall

A

smooth walls of L and R ventricles that lead inot aorta (aortic vestibule) and pulmonary trunk (conus arteriosus)

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28
Q

what does the primitive ventricle form in the ventricle wall

A

the trabeculated (rough) ventricular wall = trabeculae Carneae

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29
Q

what is the conus arteriosus also known as

A

infundibulum

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30
Q

how do we form a single pulmonary vein? what will this go onto form?

A

outgrowth of L atrial wall forms single pulmonary vein

pulmonary vein branches into L and R veins which bifurcate into 4 pulmonary veins

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31
Q

what is intussusception and when does this occur?

A

where the 4 pulmonary veins are incepted in the wall of the left atrium
happens in week 5

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32
Q

why does intussusception happen in left and not right atrium

A

left atrial wall is smoother

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33
Q

what is the majority of the atrial wall derived from?

A

primitive atrium

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34
Q

what is the septum primum and when does it form?

A

a crescent shaped outgrowth from the dorsal wall at the end of week 4

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35
Q

what is the foramen primum?

A

the diminishing connection between left and right sides of the primitive atrium as the septum primum extends

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36
Q

what are the dorsal and ventral endocardial cushions?

A

the endothelium lining the boundary between the atrium and ventricle expands, these will then fuse in the midline to form the atrioventricular septum

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37
Q

at what time does the septum primum fuse with the atrioventricular septum? what disappears as a result?

A

by week 6 - the ostium primum is obliterated

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38
Q

what occurs in the upper part of the septum primum to form the foramen secundum?

A

apoptosis

39
Q

what is the septum secuncum?

A

a second crecent shaped projection that forms in the dorsal wall of the atrium by week 6

40
Q

what is the formen ovale?

A

the opening left in the septum secundum as it does not form a complete partition?

41
Q

what is the function of the formen ovale?

A

allows blood to flow from right atrium to the left, bypassing the lungs

42
Q

how many origins does the interventricular septum have?

A

two - interventricular foramen and a membranous part

43
Q

how does the interventricular foramen form?

A

end of week 4, a muscular part that projects from the floor of primitive ventricle towards the endocardial cushions - leaving the foramen

44
Q

how does the membranous part of the interventricular septum form?

A

projects inferiorly from the endocardial cushion in week 7

45
Q

how is the truncus arteriosus septated and what does it form?

A

forms the aorta and pulmonary trunk

  • divided in two by endocardial swellings (conotruncal ridges)
  • these swellings fuse to form a septum that separates the outflow of left and right ventricles - fuses with interventricular septum
  • don’t fuse in straight line (spiral round each other) in order to connect to correct ventricle
46
Q

how do neural crests cells end up in the contruncal swellings?

A

as the neural folds elevate and fuse, cells at the lateral edge seperate and migrate laterally and ventrally

47
Q

where is blood oxygenated and detoxified in a feotus?

A

the mothers circulation - the foetal circulation shunts blood away from the lungs and liver

48
Q

where does oxygenated blood enter the feotus and circulate round the body?

A

umbilical vein - some enters the liver and the rest enters the ductus venosus and enters the inferior vena cava
then enters right atrium, passinf through foramen ovale to the left atrium, ventricle and then aorta

49
Q

why is blood in the feotal aorta not as oxygenated?

A

blood entering the right atrium from the superior vena cava is poorly oxygenated as is the blood returning from the lungs
this passes through the ductus arteriosus and reduces oxygenation in the aorta

50
Q

what does termination of the umbilical circulation cause?

A

ductus venosus closes and degenerates (becomes the ligamentum venosum in adults)

51
Q

what does the first breath after birth cause?

A

the pulmonary arteries dilate and change pressures in the atria
blood returning from the lungs increase pressure in left atrium
flimsy septum primum is pushed against sturdy septum secundum closing the foramen ovale
also causes changes in O2 saturation and the ductus venosus constricts

52
Q

what is the closed foramen ovale in adults?

A

fossa ovalis

53
Q

what is the constricted ductus venosus in adults?

A

patent ductus venous

54
Q

what is dextrocardia?

A

isolated switching of the heart

55
Q

what is dextrocardia a result of? when does this happen

A

abnormal cardiac looping

- during gastrulation: week 3 when laterality (L and R sides) determined

56
Q

what other structural defects is isolated dextrocardia associated with? why might this be a problem?

A

defects including abnormal connections with veins and arteries
abnormal separation of the heart
- deO2 blood sent to body and O2 blood sent to heart

57
Q

what is patent ductus arteriosus?

A
  • where the ductus arteriosis remains open after brith

-

58
Q

what are the consequences of patent ductus arteriosis? what can this lead to?

A
  • due to pressure gradient O2 blood travels back to lungs from the heart aorta into the pulmonary artery
  • this increases the workload of the heart to push the blood the other way
  • can lead to pulmonary hypertension, R ventricular hypertrophy and heart failure
59
Q

how do we treat patent ductus arteriosis? what’s the effect of this treatment?

A

treated with prostaglandin inhibitors

reduces the level of circulation prostoglandins allowing cells to contract and contract to close this up

60
Q

what is a patent foramen ovale? what kind of defect is this

A

caused by a failure of septum premium and secundum to fuse after birth
atrial septal defect

61
Q

why does a patent foramen ovale occur? what’s the effect of this on the blood route

A

malformations in septum primum or secundum (most commonly seccundum) such that they don’t align properly and overlap leaving a gap
blood has to take an elongated route

62
Q

normally, how do the septum primum and secundum fuse in a baby ?

A

increase amount of BP pushes septum primum and secundum together

63
Q

what are the differnt types fo patent foramen ovale? briefly describe each one

A
  • secundum ASD: secundum doesnt develop enough and so leaves a gap
  • Primum ASD: failure of fusion of primum
  • sinus venosus ASD
64
Q

how common is a probe foramen ovale

A

1 in 4

65
Q

why are most people with a probe patent foramen ovale asymptomatic

A

because septum primum and seccundum are kept together most of the time as the higher pressure in LA pushes them together- mechanically closing valve

66
Q

in what condition is a patent foramen ovale a bigger problem and why?

A

pulmonary hypertension

as RA has the higher pressure, pushing the flimsy septum primum open and allowing R to L shunt

67
Q

how is a ostium secundum defect caused

A

excessive apoptosis in septum primum
or
inadequate development of septum seccundum such as the foramen ovale and secundum (ostium) overlap
= hole is too big

68
Q

what are the consequences of a ostium secundum defect?

A

L to R shunt

can cause enlargement of RA and RV

69
Q

is a ostium secundum defect asymptomatic or symptomatic ?

A 
small defects (>5mm) - may be asymptomatic
large defects may require surgical repair
70
Q

what is a cortrilocularebiventriculare / common atrium

A

complete absence of atrial septum = one big common atrium

71
Q

how is cortrilocularebiventriculare / common atrium caused

A

failure of development of septum primum and septum seccundum

72
Q

is it common? at what point is it usually diagnosed, why is this?

A

rare

usually undiagnosed until 20-30 years of life with further compromise to CV/ respiratory system

73
Q

what is a premature closure of Foramen Ovale

A

closure of foramen ovale during prenatal life

74
Q

what are the consequences of a premature closure of Foramen Ovale? is it survivable, why?

A

results in more blood on R side and so hypertrophy of R side of the heart and underdevelopment of L side
- death usually occurs shortly after brith as the L side is important in ejecting blood around the body

75
Q

what is the most common congenital heart defect?

A

Ventricular Septal defect -‘ hole in heart’

76
Q

why do we get VSDs

A

defects in muscular or membranous part if intraventricular septum

77
Q

why are defects in muscular part of IV septum less sevre than in the membranous IV septum in a VSD?

A

defects in muscular part often resolve themselves as child grows

78
Q

what are the consequences of a VSD

A

L to R shunt due to pressure differnces

can result in pulmonary hypertension and hypertrophy of RV

79
Q

why might we get separation defects of the trunks arteriosus

A

abnormal neural crest cell development or migration can lead to number of defects in separation of trunks arteriosis in pulmonary trunk and aorta

80
Q

what are the main eparation defects of the trunks arteriosus

A
  • persistant truncus arteriosus
  • transposition of great vessels (don’t separate properly)
  • ToF
81
Q

what does a persistent truncus arteriosus lead to? how?

A

ventricular septal defect

as contruncal septum is completely absent and so cannot fuse with IV septum

82
Q

anatomically, how can a VSD lead to cyanosis

A

we create a common outflow tract as the undivided truncus is in communication with both ventricles, thereby mixing of O2 and deO2 blood

83
Q

why does transposition of the great vessels occur

A
  • conotruncal septum not form in spiral, instead straight down
  • thereby aorta arises from RV and pulmonary artery from LV
84
Q

is transposition of the great vessels compatible with life? in what cases can it be?

A

no

unless accompanying shunt such as VSD, patent foramen ovale or patent ductus ateriosis to allow mixing if blood

85
Q

how do we get formation of ToF

A

due to unequal truncus arteriosis (outflow tract), so pulmonary trunk lot larger and aorta a lot smaller, caused by anterior displacement of aorticopulmonary septum
- displacement of septum produces 4 classic defects

86
Q

what is coarctation of Aorta

A

narrowing of aorta near ductus arteriosis

87
Q

what are the 2 classifications of correction of the aorta

A

preductal (b4 patent ductus arterios) and post ductal (after patent ductus arteriosis)

88
Q

what is a preductal coarctation of aorta? what are the consequences of this? treatment? symptoms?

A
  • obliteration of patent ductus arteriosis
  • hypo perfusion of lower body
  • administration of prostaglandins to keep ductus arterosis open
  • differential cyanosis - upper body and head well perfused, lower body cyanotic
89
Q

what is post ductal correction of aorta

A
  • collateral circulation established to byapss the narrowing
90
Q

highlight the blood vessles involved in the collateral circulation of post ductal coarctation which lead to aorta

A 
blood passes through:
subclavein arteries 
to internal thoracic arteries 
to intercostal arteries 
to descending aorta
91
Q

on which vessels and what is the effect of collateral circulation in post ductal coarctation

A

internal thoracic and intercostal arteries enlarge to carry greater blood flow

92
Q

what is the ductus venosus?

A

a shunt that allows oxygenated blood into the umbilical vein that bypasses the liver. It is essential for feral circulation

93
Q

what is the remnant of the ductus arteriosus in adults?

A

ligamentum arteriosum

year 1 flash cards (23 decks)

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