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Phase 3a conditions list flashcards > Paediatrics - cardiology > Flashcards

Paediatrics - cardiology Flashcards

1
Q

Where do the umbilical arteries run between?

A

Internal iliac arteries and placenta - there are two of them

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2
Q

Where does the umbilical vein run between?

A

Placenta and portal vein

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3
Q

Where does the ductus venosus run between?

A

Umbilical vein and inferior vena cava to bypass the liver

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4
Q

Where does the ductus arteriosis connect?

A

Pulmonary artery and aorta - shunt blood from pulmonary artery

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5
Q

Does the umbilical arteries carry O2 or not?

A

No they are deoxygenated

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6
Q

Does the umbilical vein carry O2 or not?

A

Yes they are oxygenated by placenta

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7
Q

How does the foramen ovale close?

A

Alveoli open with first breath –> pulmonary BP decreases –> right atrium pressure decreases –> left atrium pushes foramen ovale inward (like a closing valve)

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8
Q

How does the ductus arteriosis close?

A

Prostaglandins needed to keep ductus arteriosis open –> oxygenated blood causes drop in prostaglandins –> ductus arteriosis closes after a few days

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9
Q

What are some examples of non-cyanotic congenital heart disease (most to least common) (6)?

A
  • VSD
  • Patent ductus arteriosus
  • ASD
  • Pulmonary stenosis
  • Aortic stenosis
  • Coarctation of the aorta
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10
Q

What is the most common form of heart defect?

A

Ventricular septal defect

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11
Q

What is the pathophysiology of the movement of blood around the heart in a ventricular septal defect?

A

Blood is shunted from the left to the right

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12
Q

What happens as a result of left to right shunting of blood in a VSD?

A

Pulmonary hypertension can occur

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13
Q

What can happen as a result of a severe VSD?

A

Eisenmenger syndrome - pulmonary pressure increases to more than systemic pressure and the shunt reverses from left to right and becomes right to left

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14
Q

What will happen to the patient as a result of eisenmenger syndrome?

A

They will become cyanotic

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15
Q

What are symptoms of a VSD (4)?

A
  • Tachypnoea
  • Dyspnoea
  • Poor feeding
  • Failure to thrive
    however often symptomless
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16
Q

When are VSD usually picked up + what sort of murmur (2)?

A
  • Sometimes visible on antenatal scanning
  • Ascultation - pansystolic murmur at lower left sternal border
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17
Q

What are some risk factors for VSD (6)?

A
  • Fam history
  • Genetic conditions e.g. Downs, Edwards, Pataus
  • Smoking
  • Maternal diabetes
  • Maternal rubella
  • Prematurity
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18
Q

How are VSDs treated (2)?

A
  • Small = left alone and monitored
  • Medication e.g. ACE-i + diuretics, open heart surgery, transvenous catheter closure
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19
Q

What are some complications of VSD (2)?

A
  • Heart failure
  • Endocarditis
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20
Q

What is the flow of blood around the heart in a patient with an atrial septal defect?

A

Shunting of blood from left to right atria

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21
Q

What complication of ASD can occur and how would the patient present?

A

Eisenmenger syndrome - patient would be cyanotic

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22
Q

What are the symptoms of an ASD (4)?

A
  • Tachy/dyspnoea
  • Poor weight gain
  • Recurrent chest infections
  • Difficulty feeding
    often asymptomatic however
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23
Q

What would be heard on auscultation of those with ASD (2)?

A
  • Soft, systolic ejection murmur
  • Fixed split S2
    these are due to more blood being forced through pulm valve
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24
Q

What are some complication of ASD (3)?

A
  • Stroke (from DVT)
  • AF
  • Pulmonary hypertension
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25
Q

How are ASDs managed (3)?

A
  • Watch and wait if small
  • Blood thinners (in adults) to prevent stroke
  • Catheter/ surgical repaire
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26
Q

What two other septal defects can occur (other than ASD and VSD)?

A
  • Patent foramen ovale (although not strictly a steal defect)
  • Atrio-ventricular septal defect
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27
Q

How would a patent ductus arteriosis present (4)?

A

Same as an ASD
* Poor feeding
* Recurrent LRTI
* Tachy/dyspnoea
* Poor weight gain

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28
Q

What would a patent ductus arteriosis sound like?

A

Continuous machinery murmur

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29
Q

How is patent ductus arteriosis managed?

A
  • Medications e.g. ibuprofen to inhibit prostaglandins
  • Surgical catheter repair if not closed by age 1
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30
Q

What is congenital pulmonary stenosis?

A

Pulmonary valve is malformed and has a narrow opening between the right ventricle and pulmonary artery

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31
Q

What does pulmonary stenosis sound like upon auscultation?

A

Ejection systolic murmur @ 2nd intercostal, left sternal border

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32
Q

What does aortic stenosis sound like?

A

Ejection systolic murmur @ second intercostal right sternal border

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33
Q

How do congenital pulmonary and aortic stenosis present?

A

Often asymptomatic, but similar to in adults

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34
Q

What is coarctation of the aorta?

A

Narrowing of the aorta, usually around the ductus arteriosis

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35
Q

What genetic syndrome is coarctation of the aorta often associated with?

A

Turners syndrome

36
Q

What are signs/ symptoms of coarctation of the aorta (5)?

A
  • Week femoral pulse
  • Ejection systolic murmur
  • Tachypnoea
  • Poor feeding
  • Grey and floppy baby
37
Q

What signs/ symptoms of coruscation of the aorta may show with development (2)?

A
  • Underdevelopment of legs/ left arm
  • Left ventricular heave
38
Q

How is coruscation of aorta treated (2)?

A
  • Surgery
  • Prostaglandin E can be used to keep the ductus arteriosus open
39
Q

What are some causes of cyanotic congenital heart disease (3)?

A
  • Tetralogy of Fallot
  • Transposition of the great arteries
  • Complete AVSD = less common
40
Q

What is transposition of the great arteries?

A

The aorta and pulmonary artery have switched place - so the aorta connects to right ventricle and pulmonary artery connects to left ventricle. This effectively creates a separate pulmonary and systemic circulation.

41
Q

What are some risk factors for these cyanotic congenital heart diseases (4)?

A
  • Rubella infection
  • Increased maternal age
  • Diabetic mother
  • Alcohol consumption
42
Q

How does transposition of the great arteries present (2)?

A
  • Sometimes picked up antenatally
  • Cyanotic baby within first day (after ovale and ductus arteriosus close)
43
Q

How is transposition of the great arteries treated?

A
  • Prostaglandin E infusion (maintains ductus arteriosus)
  • Surgery “artery switch”
44
Q

What is tetralogy of Fallot?

A
  • VSD
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy
  • Overriding aorta (aorta positioned over VSD)
45
Q

How are most cases of tetralogy of Fallot diagnosed?

A

Antenatal scans

46
Q

What is it known as when a child with tetralogy of Fallot becomes cyanotic for a brief period?

A

Tet spell

47
Q

What causes a tet spell?

A

Decrease in systemic circulation resistance / increase in pulmonary circulation resistance e.g. exertion –> increase in CO2 which reduces systemic circulation resistance

48
Q

How are congenital heart diseases investigated?

A
  • Echo
    however some picked up through antenatal scanning
49
Q

What causes heart failure in children (6)?

A
  • Congenital heart diseases
  • Cardiomyopathies
  • Arrhythmias
  • Anaemia
  • Infective endocarditis
  • Rheumatic fever
50
Q

What are the 3 main types of cardiomyopathy that may affect children?

A
  • Dilated
  • Restrictive
  • Hypertrophic
51
Q

What arrhythmias are common in children (3)?

A
  • Supraventricular tachycardia
  • Congenital heart block
  • Long QT syndrome
52
Q

What causes supraventricular tachycardia in children?

A
  • AV nodal re-entrant tachycardia
  • AV re-entrant tachycardia
  • Atrial tachycardia
53
Q

How does atrial tachycardia cause SVT?

A

Electrical signals originate in the atria somewhere other than the SA node and cause a faster heartbeat (the cause of the fast heart rate has originated in the atria)

54
Q

What is AV re-entrant tachycardia known as?

A

Wolf Parkinson’s white syndrome

55
Q

What is the re-entry point in WPW known as?

A

Bundle of Kent

56
Q

What are the symptoms of SVT (6)?

A
  • Palpitations
  • Syncope
  • Dizziness
  • SOB
  • Sweating
  • Weekness
57
Q

How is acute SVT managed in cases without life threatening features (4)?

A
  1. Vagal manoeuvres
  2. Adenosine
  3. Verapamil/ beta blocker
  4. Synchronised DC cardioversion
58
Q

What are some life threatening features of SVT (4)?

A
  • Chest pain (cardiac ischemia)
  • LOC
  • Shock
  • Severe symptoms
59
Q

What vagal manoeuvres would be used to treat SVT initially (3)?

A
  • Valsalva manoeuvre (blow against resistance)
  • Carotid sinus massage
  • Diving reflex (face in cold water)
60
Q

How do vagal manoeuvres slow heart rate?

A

Stimulate vagus nerve (PSNS)

61
Q

What is the longer term management of recurrent SVT (2)?

A
  • Radiofrequency ablation
  • Long term medication
62
Q

How do CCBs (adenosine and verapamil) and beta blockers treat SVT?

A

Slow down conduction through AV node

63
Q

Anatomically, what causes congenital heart block?

A

Underdevelopment/ malformation of the AV node

64
Q

What condition in the mother is associated with complete congenital heart block?

A

Sjogrens syndrome/ SLE

65
Q

What causes congenital heart block in those whose mother has Sjogrens/ SLE?

A

Anti-ro and Anti-la antibodies cross the placenta and cause atrophy/ fibrosis of AV node

66
Q

What might cause long-QT syndrome in children (2)?

A
  • Inherited channelopathies
  • Other similar causes to adults e.g. electrolyte imbalances, medications
67
Q

How might long-QT present in children (2)?

A
  • Usually during later childhood
  • LOC during exercise/ intense emotion
    however often symptomless
68
Q

What could long-QT be mistaken as in childhood?

A

Epilepsy (due to LOC)

69
Q

What is rheumatic fever?

A

Autoimmune condition affecting multiple systems throughout the body

70
Q

What bacteria causes rheumatic fever?

A

Group A strep (strep pyogenes)

71
Q

What is the mechanism by which the body attacks itself in rheumatic fever?

A

The antibodies on strep pyogenes are very similar to those found in the body, such as those in the myocardium, so the body ends up mistakenly attacking itself

72
Q

What type hypersensitivity is rheumatic fever?

A

Type 2

73
Q

What are the symptoms/ presentation of rheumatic fever (6)?

A
  • FEVER
  • Joint pain
  • Rash
  • SOB
  • Chorea
  • Skin nodules
  • 2-4 weeks post viral infected - ‘strep throat’
74
Q

Which joints are typically affected in rheumatic fever?

A

Larger joints

75
Q

How is the skin affected in rheumatic fever (2)?

A
  • Subcutaneous nodules (often over elbows/ extensor surfaces)
  • Erythema marginatum
76
Q

What valve is commonly affected by rheumatic fever?

A

MITRAL valve

77
Q

How is rheumatic fever investigated (3)?

A
  • Throat swab (bacterial culture)
  • Anistreptococcal (ASO) antibody titre
  • ECG/ CXR/ echo
78
Q

What criteria can be used to diagnose rheumatic fever?

A

Jones criteria

79
Q

How should rheumatic fever be managed?

A
  • NSAIDs
  • Aspirin (for carditis)
80
Q

What should be given to patients as prophylaxis follow rheumatic fever?

A

IM benzathine benzylpenicillin

81
Q

What can be done to prevent rheumatic fever from occurring in the first place?

A

Prompt treatment of strep infections with phenoxymythylpenicillin (penicillin V)

82
Q

What is a common cause of infective endocarditis in children?

A

Congenital heart disease - causing turbulent flow of blood

83
Q

What are the symptoms of infective endocarditis (5)?

A
  • Fever
  • Fatigue
  • Night sweats
  • Muscle aches
  • Anorexia
84
Q

What are some examination signs of IE (7)?

A
  • New murmur
  • Splinter haemorrhages
  • Osler nodes
  • Janeway lesions
  • Roth spots
  • Petechiae
  • Finger clubbing (if longstanding)
85
Q

What are the 2 most common bacteria in children with IE?

A
  1. Strep viridians
  2. Staph aureus
86
Q

What criteria is used to diagnose IE?

A

Dukes criteria

87
Q

How is IE treated?

A

Broad spectrum Abx (amoxicillin + gentamicin)
should be based on blood cultures

Phase 3a conditions list flashcards (29 decks)

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