Congenital heart and other defects Flashcards

1
Q

Type 1 IUGR effects:

embryonic period
fetal period

A

Type 1 IUGR effects:

embryonic period
fetal period

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2
Q

The most common heart defect is ? [1]

A

Ventricle septation:
Mainly VSD but also ASD

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3
Q

Heart starts beating at day []

A

Day 22

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4
Q

Describe the structure of the heart at 22 days [5]

And what each part develops into

A

The Sinus venosus:
- Inflow, it receives the blood from the embryonic veins
- becomes the right atrium (smooth post. porton), venae cavae and the coronary sinus.

Paired primitive atria:
- become the right and left auricles, and the left atrium

Primitive ventricle:
- becomes the left ventricle eventually

Proximal 1/3rd of bulbus cordis:
- becomes the** muscular part of the right ventricle**

Other 2/3rds 1/3rd of bulbus cordis:
- will become the conus arteriosum (into pulmonary trunk) and in the left ventricle will become the aortic vestibule

Truncus arteriosus
- becomes the ascending aorta and the pulmonary trunk
- The dorsal aorta will eventually fuse together –> descending aorta

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5
Q

Describe how the partitioning of the outflow tract occurs

A

Neural crest form bulbar ridges in conus cordis
Ridges grow and twist “spiral”

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6
Q
A

Atrial septal defects can cause left to right shunting of blood. Causes R ventricular hypertrophy

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7
Q

What % people have a probe patent foramen ovale? [1]

What is a probe patent foramen ovale cause an increased risk of? [2]

A

25% of people have probe patent foramen ovale that normally causes no problems but can open and can cause increased risk of migraine and AF

Extra strain on the heart can make hole bigger.

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8
Q

What happens to large amount of muscular VSDs? [1]

A

Often spotaneously close

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9
Q

90% of VSD are in [] septum (superior and close to outflow tract) and 10% in [] septum

A

90% of VSD are in membranous septum (superior and close to outflow tract) and 10% in muscular septum

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10
Q

Explain how you close a VSD [2]

A

Ventricular septal defects are typically closed by placing a patch over the defect.

The patch may be a piece of fabric (Dacron) or the patient’s own tissue (pericardium) and it is secured with fine sutures.

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11
Q

Persistant truncus arteriosus is caused by what failing to fuse? [1]

Associated with which pathology? [1]

A

Persistent truncus arteriosus:
Truncoconal swellings fail to fuse

Associated with VSD

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12
Q

Tetralogy of Fallot is characterised by

A

Pulmonary trunk stenosis
VSD
Overriding aorta
Right ventricular hypertrophy

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12
Q

Most common cause of cyanotic heart disease in new-born is? [1]

A

Transposition of the great vessels

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13
Q

Transposition of the great vessels is caused by [] being straight and not spiralling [1]

What does this cause to occur with the great vessel positions? [1]

A

Transposition of the great vessels is caused by truncoconal spetum being straight and not spiralling [1]

Causes two parallel rather than sequential

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14
Q

Using drugs:

How do you keep PDA open? [1]
How do you close PDA? [1]

A

Open: prostaglandins
Close: NSAIDS

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15
Q

What is the difference between cleft lip and cleft palate?

A

Cleft lip:
* Failure of maxilla to fuse with medial nasal prominance

Cleft palate:
* Failure of palatal shelves to fuse (from maxillay prominences)
* Failure of ectroderm to break down to allow fusion

16
Q

What is the pathology depicted? [1]

A

Tetrallogy of Fallot - boot shaped

17
Q

Preductal – ductus arteriosus can be kept open with what drug? [1]

A

Alprostadil: prostaglandin E1

18
Q

Why would you want to keep PDA open? [1]

A

In cases of critical coarctation where there is a risk of heart failure and death shortly after birth
Prostaglandin E is used keep the ductus arteriosus open while waiting for surgery.

This allows some blood flow flow through the ductus arteriosus into the systemic circulation distal to the coarctation.

Surgery is then performed to correct the coarctation and to ligate the ductus arteriosus.