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Human Development > Congenital heart disease and other abnormalities > Flashcards

Congenital heart disease and other abnormalities Flashcards

1
Q

What forms the cardiogenic mesoderm

A

Clusters of angiogenic cells

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2
Q

what arises from the cardiogenic mesoderm

A

From these arise right and left endocardial tubes.

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3
Q

what does lateral folding do

A

Lateral folding brings the tubes together and forms primitive heart tube.

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4
Q

when does lateral folding begin

A

o Occurs at day 21,

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5
Q

when is the foetal heart beat

A

beating by day 23.

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6
Q

describe the development of the heart

A

 Tube lengthens and folds further into the bulboventricular loop.
 By day 28 there is septation of the atria, ventricles and outflow tract.

 Long periods of growth and maturation over 2 nd and third trimester.

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7
Q

what does failure of septation in the atria and ventricle cause

A
  • can cause CHD
     Can be early (AVSD from endocardial cushion) OR
     Late (simple ASD or VSD).
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8
Q

Describe the parts of the primitive heart tube and what they develop into

A
  • truncus arteriosus - this develops into the proximal aorta and pulmonary artery
  • bulbs cordis - this forms the ventricular outflow tracts and right ventricle
  • primitive ventricle - left ventricle
  • primitive ratio - left and right atria
  • sinus venous - smooth part of the right atrium and coronary sinus
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9
Q

what is dextrocardia

A
  • this occurs when the heart is on the wrong side fo the chest
  • happens when cardia looping happens in the wrong direction
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10
Q

describe how the atria septum is created (wall between the two atria)

A
  • The septum starts to grow down from the top of the atria this is called the septum primum
  • As it is growing down towards the endocardial cushion the space between them is called the ostium primum
  • Before the ostium primum disappears completely a second hole forms this is called the ostium secundum
  • Once osteium secundum develops osteium primum then closes and ostium secundum develops
  • Once septum primum reaches endocardial cushions septum secundum starts to form and this goes down to the endocardial cushion
  • Septum secundum leaves a hole in it and this is the foramen ovale
  • Septum primum helps form this valve as well
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11
Q

what leaves a hole to form the foramen ovale

A
  • Septum secundum leaves a hole in it and this is the foramen ovale
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12
Q

when does the atria septum develop

A
  • Day 28/end of 4th week, two swellings of mesenchymal tissue appear from walls of the atria- endocardial cushsions
  • The endocardial cushsions grow and fuse together to divide canal into R and L
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13
Q

describe how ventricular septum develops

A
  • Has a muscular part that grows from the base of the heart to the endocardial cushions
  • And a membranous component that grows down from the endocardial cushions towards the muscular part
  • End of 4th week a muscular IVS develops from floor of primordial ventricle
  • Grows towards membranous IVS which develops from endocardial cushions
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14
Q

what is the most common type of cardiac defect

A

VSDs

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15
Q

What are the parts of fetal circulation that are different to adult circulation

A

o Foramen ovale
o Ductus arteriosus*
o Ductus venosus

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16
Q

What is the role of the parts of fetal circulation that are different to adult circulation

A

• Foramen ovale - shunts blood from RA to LA (bypassing pulmonary circulation)
• Ductus arteriosus - shunts blood from pulmonary trunk to ascending aorta (bypassing lungs)
- Ductus venosus - shunts blood from umbilical vein to IVC (bypassing liver)

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17
Q

what causes the blood not to go through pulmonary circulation in a foetus

A
  • in a foetus there is high pulmonary pressure and lower systemic pressure
  • there there is a high resistance int he lungs so it is difficult for blood to flow through
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18
Q

What is transitional circulation

A

this is when the infant is born and in its first few days it transitions from a foetal heart circulation to an adult heart circulation

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19
Q

What happens transitional circulation and why

A

 Closure of ductus arteriosus (increased oxygen levels).

 Closure of foramen ovale.
o Due to drop in pressure in pulmonary circulation/right side of heart.
 Shunting is reversed and valve closes.

 Closure of ductus venosus.
o Due to decrease in blood flow in inferior vena cava.

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20
Q

What causes the ducts arteriosus to stay open in the uterus

A

o In utero ductus is kept open under influence of PG E1.

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21
Q

What is persist pulmonary hypertension of the Newborn

A

This is when after birth in the newborn pulmonary resistance does not decrease therefore you can end up with persistent pulmonary hypertension of the newborn

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22
Q

when does persistent pulmonary hypertension of the newborn occur

A

 Occurs if problems with lungs (pneumonia, aspirate meconium).

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23
Q

describe the mechanism of action behind persistent pulmonary hypertension of the newborn

A

o There is increase pressure in PA keeping foramen ovale open.
 Shunting of deoxygenated blood into systemic circulation (baby will be cyanotic).

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24
Q

will the baby have cyanosis in persistent pulmonary hypertension of the newborn

A

baby will be cyanotic

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25
Q

what are the two groups of congenital heart disease

A

Cyanotic CHD
• Patient is blue (cyanosed)

Acyanotic CHD
• Patient is pink (not cyanosed)

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26
Q

What is the blue colour in cyanosis caused by

A

 Blue colour produced by amounts of deoxygenated Hb (g/l), not percentage saturation (SaO2).

27
Q

what are the levels of haemoglobin in the blood that can cause cyanosis

A

= deoxygenated Hb >50g/l in capillaries

= 34/l in arterial blood.

28
Q

What is the difference between CHD and lung disease

A
  • in CHD there is no problem with functioning of lungs (normal oxygenation),
  • while in lung disease there is
    limited gas exchange so body is not perfused.
29
Q

give some examples of cyanosis heart conditions

A

o Tetralogy of Fallot
o Persistent truncus arteriosus
o Transposition of the great vessels

30
Q

What happens in transposition of the great vessels

A
  • this is when the aorta is connected to the right ventricle
  • pulmonary artery is connected to the left ventricle
  • there is two separate circulations
31
Q

Why does the baby stay alive in transposition of great vessels

A

 Baby stays alive because of mixing of blood in:
o Foramen Ovale
o Ductus Arteriosus.

32
Q

what kind of heart condition is Tetralogy of Fallot and Transposition of the great arteries

A

Conotruncal malformation

33
Q

What are the 4 heart conditions in tetralogy of fallot

A

 Ventricular septal defect.
 Overriding aorta (aorta above septal defect).
 Right ventricular hypertrophy.
 Stenosis of RV (narrow outflow).

34
Q

What are other forms of cyanotic CHD

A

 Tricuspid atresia (complete valve closure)

 Pulmonary valve atresia.

 Critical pulmonary stenosis.

 Truncus arteriosus.
o Single artery arises from heart. Large ventricular septal defect below valve of trunk.

 Total anomalous pulmonary venous drainage (TAPVD)
o Pulmonary veins not connected to LA but to one of veins draining back to RA.

35
Q

What are the two major cyanotic congenital heart disease groups

A

• L→R shunts which increase pulmonary blood flow (→
pulmonary oedema/hypertension)

• Left heart outflow tract obstruction (→pulmonary oedema, impaired tissue perfusion, lactic acidosis)

36
Q

can acyanosis cause cyanosis

A
  • Cyanosis is not a fixed feature
  • Cyanosis can develop as a secondary feature

for example;
• Pulmonary oedema impairs gas exchange resulting in cyanosis
• Pulmonary hypertension causes R→L shunting resulting in cyanosis (Eisenmenger shunt)

37
Q

Name some examples of acyanosis CHD

A

o ASD - Atrial Septal Defects
o VSD - Ventricular Septal Defects
o PDA - Patent Ductus Arteriosus
- Preductal correction of the aorta

38
Q

describe a VSD

A
  • left to right shunt
39
Q

what can be used to measure how large the VSD is

A

QP;QS

- ratio of pulmonary to systemic blood flow

40
Q

What does preductal correction of the aorta cause

A

 Causes pulmonary oedema as there is increase pulmonary pressure.

41
Q

what does pre-ductal man

A

o Pre-ductal: before ductus arteriosus.

42
Q

What are other forms of acyanotic CHD

A

 Atrioventricular septal defect.

 Critical aortic stenosis.

43
Q

what are mixed cyanosis and acyanosis conditions

A
  • hypoplastic left heart

- double outlet right ventricle

44
Q

What is hypoplastic left heart

A

 No blood flowing through left ventricle to aorta.
 Patient reliant on fetal circulations to stay alive.
o Blood flows through foramen ovale into the right ventricle and then pumped to rest of body.

45
Q

what is double outlet right ventricle

A

(aorta connects to right ventricle instead of left.

46
Q

What can cause delayed presentation of CHD

A

Ductus arteriosus and foramen oval may:
 Bypass obstruction (tetralogy of fallot, pulmonary atresia, coarctation, Hypoplastic left heart).
 Allow mixing (transposition)
This delays the presentation (mild cyanosis is easily missed).

47
Q

what do the CHD signs present

A

 Symptoms only obvious once ductus closes.

48
Q

How do you re open the ducts arteriosus and Forman ovale

A
  • Re-opening ductus (prostaglandin E)

- enlarging foramen ovale (balloon septostomy transposition) = lifesaving.

49
Q

What is the treatment of CDH

A 
depends on condition.
 Monitoring.
 Diuretics for pulmonary oedema.
 Re-open ductus arteriosus with prostaglandin E
 Surgery and catheter procedures.
50
Q

how do you treat acyanotic CHD

A
  • Diuretics and ACE inhibtiors for left to right shunts

- prostaglandin E for LV outflow tract obstruction

51
Q

what is the surgical correction for

  • PDA
  • Coarction
  • VSD/ASD
A

Definitive correction
• Percutaneous catheter closure of PDA • Balloon dilatation of valvular stenosis
• Repair of coarctation
• Open heart surgery for VSD/ASD

52
Q

What are limiting factors int he treatment of CDH

A

 Anatomical: disuse atrophy
o Cannot grow new ventricles

 Functional: chronically elevated pulmonary blood flow.
o Irreversible pulmonary hypertension.

53
Q

name some examples of neural tube defects

A
  • Spina bifida occulta
  • Meningocoele
  • Myelomeningocoele (spina bifida)
  • Encephalocoele • Anencephaly
54
Q

describe examples of neural tube defects

A

 Spina Bifida Occulta = failure of one or more vertebrae in spine to form properly.
o Myelomengocoele is the most serious form (neural tissue exposed on babies back).

 Meningocoele = meninges protruding from spinal column.

 Encephalocoele = protrusion of neural tissue (brain) from head.

 Anencephaly = absence of major portion of brain, skull, and scalp.

55
Q

how do you treat myelomeningocoele and the resultant hydrocephalus

A

Hydrocephalus is common and needs a VP shunt
- the closure of the myelomeningocoele reduces the risk of infection but it does not restore normal neural function
-

56
Q

what are the neuroglocial consequences of lumbar myelomeningocele

A

 Mixed sensory, motor and autonomic problems.
o Dependent on level of lesions and degree of neural disruption.

 Loss of bladder control, faecal incontinence and loss of sensation in legs.

57
Q

what is gastrochesis

A
  • this is a full thickness small defect in abdominal wall lateral to umbilicus
58
Q

What happens in gastroschiss

A
  • bowel is free within amniotic cavity
59
Q

how do you treat gastroschesis

A
  • surgical closure possible

- bowel may take 1-3 months to start functioning normally

60
Q

what is exomphalos

A

• Wide-based defect
• Membrane covers
herniated viscera
• May be associated with other abnormalities and genetic disorders

61
Q

what does a cleft lip result from

A

Failure of fusion of maxillary and frontonasal processes

- complete surgical correction possible

62
Q

what does a cleft palate forms from

A

Failure of secondary palate (MPS) to fuse. Philtrum has formed. Due to:
o Tongue to large and stops plates from turning horizontally
o General failure of rotation

63
Q

what can a cleft palate and cleft lip affect

A
  • Eustachian tube function

- this can cause a risk of conductive hearing loss

Human Development (28 decks)

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