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CRRAB Week 2 > Abnormal CV Development > Flashcards

Abnormal CV Development Flashcards

1
Q

Where do most CHD defects arise?

A

Faulty embryogenesis (weeks 3-8)

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2
Q

What are the most common causes of CHD?

A 
90% - unknown
9% - genetic 
-Gene defects [ex: marfan] 2-3% familial
-Chromosome defects - 5% gametogenic, non-familial
1% - environmental 
-Rubella (patent ductus arteriosus)
-Chemical (thalidomide, ETOH)
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3
Q

What is a shunt?

A

Abnormal communications leads to blood flow diversions

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4
Q

What conditions are associated with a Left to Right shunt?

A

Cyanosis several months or years after birth [blue kids]

  1. Atrial septal defect
  2. Ventricular septal defect
  3. Patent (persistent) ductus arteriosus
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5
Q

What conditions are associated with a Right to Left shunt?

A

Cyanosis early in postnatal life [blue babies!]

  1. Tetralogy of Fallot
  2. Transposition of the great arteries/vessels (TGA)
  3. Truncus arteriosus (persistent or common trunk)
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6
Q

What shunts have cyanosis and which do not (cyanosis tradive)?

A

Right to left shunts = cyanotic

Left to right shunts = no cyanosis

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7
Q

What is cyanosis defined as?

A

Oxygen saturation below 75%

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8
Q

When do multiple or combination of defects occur in CHD?

A

-Teratogens or bc of blood flow needs
Ex: pulmonary stenosis may be associated with atrial septal defect and patent ductus arterioles or interventricular septal defect

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9
Q

What is normal pressure in the pulmonary artery vs aorta?

A

1 vs 6

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10
Q

What can shunt pressure cause?

A
  • Increased right ventricular or pulmonary artery pressure leads to pulmonary fibrosis
  • Late right ventricular failure may lead to reversed flow (ex: ventricular septal defect)
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11
Q

What causes obstructions (stenosis or atresia)?

A
  • Stressed ventricles lead to ventricular failure

- Shunts may be required for survival

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12
Q

What is an atrial septal defect (ASD)?

A

L to R

  • An abnormal opening between the right and left atria
  • Normal: flap over foramen ovale; R –> L shunt (fetus); closed adult
  • Abnormalities usually result because of incorrect development of the atrial septum.
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13
Q

What usually causes incorrect development of the atrial septum? (90% cases)

A

-Excessive resorption of the primary septum or large secondary foramen
-Incompetent foramen ovale due to hypoplastic growth of the secondary septum (large foramen ovale) and/or excessive resorption of primary septum
[Above two = 90%]

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14
Q

What usually causes incorrect development of the atrial septum? (5% cases)

A
  • Inadequate development of the primary septum producing a basal opening known as a primary foramen defect (premium anomaly) (5%)
  • Sinus venous developmental defect with high atrial septal defect (5%)
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15
Q

What generally occurs in all atrial septal defects (ASD)?

A

Left to right shunting of blood.

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16
Q

What physiology is associated with ASD?

A
  • Pulmonary blood flow may be 2-4 times normal
  • Amount of blood flow is size-dependent
  • Only large ones lead to pulmonary hypertension that leads to cyanosis tardive and cardiac failure
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17
Q

What are the complications of ASD?

A
  • RV failure

- Paradoxical embolism (and brain infarction or abscess)

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18
Q

Rx:

A

Surgery, if large (patch foramen) to close atrial septal defect

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19
Q

Which of the following is the most common form of ASD?

A

Patent foramen ovale

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20
Q

What is the most common form of congenital heart defect?

A

Interventricular septal defect!

-40% of congenital heart abnormalities

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21
Q

What is unique about VSD (ventricular septal defects)?

A
  • Size variable; symptoms = size
  • 90% involve the membranous portion of the ventricular septum; muscular septum involvement may exhibit multiple sites (Swiss-cheese septum)
  • Murmur/size (50% close spontaneously)
  • Cyanosis tardive in long-standing cases
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22
Q

What other abnormalities may be combined with VSD?

A
  • Pulmonary stenosis
  • Tetralogoy of Fallot
  • Coarctation of aorta
  • Transposition of aorta
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23
Q

What is the treatment for VSD?

A

Surgery

24
Q

What is responsible for most forms of VSDs?

A

Abnormal formation of the endocardial cushions and aorticopulmonary septum

25
Q

What is the significance of the ductus arteriosus?

A
  • It develops from the 6th aortic arch and connects the left pulmonary trunk to the aorta
  • During fetal if it serves to direct blood from the pulmonary artery to the aorta
26
Q

What is Patent (Persistent) Ductus Arteriosus (PDA)?

A
  • During fetal life this hole directs blood from the pulmonary artery to the aorta
  • Normal: flow decreases on day 1; ligamentous structure by day 30
  • -If the ductus remains patent after birth, the direction of blood flow is form the aorta to the pulmonary artery
  • -Reversed blood flow causes cardiac enlargement and increased pulmonary vascularity
27
Q

What congenital CV abnormality is associated with maternal rubella (german measles) during early pregnancy?

A

(weeks 1-8)
Patent Ductus Arteriosus.
Other defects caused by maternal rubella:
-Congenital cataracts
-Deafness due to involvement of inner ear
-Pulmonary stenosis (PS)
-Ventricular septal defect (VSD)

28
Q

What type of murmur does PDA cause?

A

“Machinery-like” murmur (thrill?)

29
Q

What are clinical complications of PDA?

A
  • Infective endocarditis common

- Pulmonary hypertension common

30
Q

What is the treatment for PDA?

A

Surgery

  • Cardiologist: catheter-placed occluder
  • Medical: Ibuprofen in pre-matures
31
Q

What four defects are associated with Tetralogy of Fallot (TF)?

A
  1. Ventricular septal defect
  2. Pulmonary stenosis
  3. Overriding (large) aorta
  4. Right ventricular hypertrophy
32
Q

What are clinical signs of TF?

A
  1. Cyanosis dependent on size of ventricular septal defect; cyanosis may be absent early
  2. Murmur due to pulmonary stenosis
33
Q

What are the complications associated with TF? How to treat TF?

A

-Paradoxical embolism (brain abscess)
-Infective endocarditis
Treatment = surgery

34
Q

What causes TGA (Transposition of the Great Arteries)?

A

It’s caused by a failure of the normal spiraling of the aorticopulmonary septum [causing straight divison of the bulbus cordis and truncus arteriosus]
-As a result, aorta originate from the right ventricle and the pulmonary artery from the left ventricle

35
Q

What shunts are common in TGA?

A
  • Atrial septal defect
  • Ventricular septal defect
  • Patent ductus arteriosus
36
Q

What is the outcome of TGA? Who gets it?

A

Outcome: incompatible with life unless an atrial and ventricular septal defect and an associated patent ductus arteriosus are present.
-M/F = 3/1; malformation particularly common in offspring of diabetic mother

37
Q

What is the best treatment for TGA?

A

Early surgery

38
Q

What is Truncus Arteriosus (Persistent)?

A

TA - A common aorticopulmonary outlet, receiving blood from both ventricles

39
Q

What causes TA?

A

Failure of the bulbar and truncal ridges (aorticopulmonary septum) to develop

40
Q

What is the pathogenesis of TA?

A

Since there is a mixing of blood from the right and left ventricles, cyanosis is present, and there is an increased pulmonary blood flow leading to irreversible pulmonary hypertension.

41
Q

What do all Right –> Left shunts involve a malformation of?

A

Aorticopulmonary septum

42
Q

Which defects involve the bulbar and truncal ridges?

A
  1. Common or persistent truncus
  2. Tetralogy of Fallot
  3. Transposition of the great arteries (TGA)
43
Q

What are three Acyanotic Obstructions?

A
  1. Coarctation of Aorta
  2. Pulmonary Stenosis and Atresia
  3. Aortic Stenosis and Atresia
44
Q

What is coarctation of the aorta?

A

Characterized by a narrowed aortic lumen (Obstructive congenital heart disease) – infolding of the aorta opposite the closed ductus arteriosus (DA)

45
Q

What do you see in Postductal (adult form) of Coarctation of the Aorta?

A
  • Common (95%); twice as common in males as females
  • BP in arms increased (normal flow to head & upper body)
  • BP in legs decreased (dec. flow to lower extremities)
  • Intercostal artery blood flow increased (notched ribs)
  • Hypertension in upper extremities; weak pulse and low bp in the lower extremities
46
Q

What complications are associated with Postductal Coarctation?

A
  • Congestive heart failure
  • Cerebrovascular accident
  • Rupture
  • Infection
47
Q

What treatments are available for Postductal Coarctation?

A

Excision, Bypass.

Experimental: Balloon angioplasty

48
Q

What is Preductal Coarctation of the Aorta?

A

(Infantile form) - 5%

  • Tubular hypoplasia of the aortic arch proximal to a patent ductus arteriosus:
  • -Early CHF (congestive heart failure)
  • -Patent ductus arteriosus
  • -Cyanosis, lower body
  • -Mortality increased
49
Q

Pulmonary/Aortic Stenosis and Atresia:

A

Aortic or pulmonary stenosis and atresia.
-Due to asymmetrical division or spiraling of the aorticopulmonary septum
(bulbar and truncal ridges)

50
Q

13 yr old boy. No femoral pulses. Increase bp in upper extremities. Enlarged intercostal vessels. What is suspected?

A

Postductal coarctation of the aorta

51
Q

What congenital defect is maternal diabetes associated with?

A

Transposition of the great arteries

52
Q

What congenital defects is DiGeorge Syndrome associated with?

A

Deletion chromosome 22q11 - involved with neural crest cells

  • Tetralogy of Fallot
  • Truncus arteriosus (Persistent)
53
Q

What is Down syndrome (trisomy 21) associated with?

A

Atrial septal defect

Ventricular septal defect

54
Q

What is Turner syndrome (45, XO) associated with?

A

Coarctation of the aorta

55
Q

What is Marfan syndrome (fibrin-1 glycoprotein abnormality, FBN1 gene; chromosomes 15q21.1 and 5q23.31) associated with?

A

Aortic stenosis

56
Q

Newborn baby becomes cyanotic over a few hours. Oxygen saturation in veins and arteries is similar. What CV abnormality is most likely responsible for the baby’s cyanosis?

A

Endocardial cushion defect

CRRAB Week 2 (9 decks)

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