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NP- Phase 3a Medicine > Paeds- Cardio > Flashcards

Paeds- Cardio Flashcards

1
Q

give some examples of congenital heart diseases (the 3 categories + examples)

A
  • holes/ connections- ASD, PDA, VSD, AVSD
  • narrowing/ stenosis- aortic coarctation, AS, PS
  • complex (right to left shunt)- transposition of great arteries, tetralogy of fallot
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2
Q

which is the only type of congenital heart disease to cause cyanosis?

A

right-to-left shunts (transposition of great arteries, tetralogy of fallot)

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3
Q

if you suspect a CHD in a patient, what features indicate that there is acute decompensation of the heart?

A

poor feeding, dyspnoea, tachycardia, hepatomegaly, cool peripheries, acidosis on ABG, pulmonary venous congestion

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4
Q

aetiology of Atrial Septal Defects

A
  • foetal alcohol syndrome
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5
Q

give 3 types of ASD

A
  • ostium secundum
  • ostium primum
  • AVSD
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6
Q

clinical features of ASD

A
  • Asymptomatic when younger
  • fixed, widely split S2
  • ejection systolic murmur in pulmonary area

in older children- arrhythmia, recurrent chest infections + wheeze

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7
Q

how would you investigate a patient with a suspected ASD?

A
  • chest radiograph

- ECG

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8
Q

what would you expect to find on a chest radiograph in a patient with an ASD?

A

CM, globular heart

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9
Q

what would you expect to find on an ECG in a patient with an ASD?

A

RVH+/- RBBB, or superior QRS axis

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10
Q

how is an ASD managed?

A
  • cardiac catheterisation

- surgical correction

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11
Q

symptoms of a patent ductus arteriosis

A
  • RARE to have symptoms- unless large defect- leads to CCF and Pulmonary HTN
  • poor feeding, failure to thrive
  • tachypnoea
  • oedema
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12
Q

clinical signs of a patient ductus arteriosis

A
  • large, bounding, collapsing pulse
  • CLASSICAL CONTINUOUS MACHINERY MURMUR IN PULMONARY AREA
  • heavy apex beat
  • left subclavicular thrill
  • loud s2
  • Gallop rhythm
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13
Q

why is an echocardiogram done in a patient with a suspected PDA?

A

to ensure that there is no duct dependant circulation- pulmonary atresia

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14
Q

how is a PDA managed?

A
  • coil/ occlusion device induced by cardiac catheter
  • ibuprofen/ indomethacin (prostaglandin inhibitors) to close
  • if persistent (>1 year), endovascular surgery
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15
Q

what is there a high risk of in VSD?

A

endocarditis

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16
Q

clinical features of a VSD

A
  • mild

if symptomatic- poor feeding, failure to thrive, tachypnoea, oedema

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17
Q

what would be found on examination of a patient with a VSD?

A
  • active pre-cordium
  • thrill
  • gallop rhythm
  • harsh loud pansystolic murmur heard on low left sternal edge
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18
Q

what would be found on a CXR in a patient with a VSD?

A

cardiomegaly

enlarged PA

pulmonary oedema

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19
Q

what would an ECG of a patient with a VSD find?

A

ventricular hypertrophy and strain

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20
Q

can a VSD close spontaneously?

A

yes- if it is small and muscular (20% close by 9 months)

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21
Q

how is a large VSD managed?

A
  • increase calorie output
  • heart failure- diuretics
  • surgery
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22
Q

in what condition are AVSD’s common?

A

Downs

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23
Q

anatomically, what is a complete AVSD?

A

5-leaflet valve between the atria and the ventricle

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24
Q

clinical features of an AVSD

A
  • presents at antenatal US scan
  • cyanosis at birth, HF at 2-3 weeks
  • no murmur
  • poor feeding, failure to thrive, tachypnoea, hepatomegaly, oedema, thrill, gallop rhythm
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25
Q

how is an AVSD managed?

A
  • treat HF medically

- surgical repair at 3-6 months

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26
Q

describe coarctation of the aorta

A

arterial duct tissue encircling the aorta at the point it inserts into duct, this consequently:

  • constricts aorta when duct closes
  • obstructs LV outflow
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27
Q

how does aortic coarctation present clinically

A
  • circulatory collapse at day 2 !!
  • weak/ absent femoral pulses
  • RF delay
  • 4 limb BP- upper and lower BP different
  • EJECTION SYSTOLIC MURMUR
  • HF and HTN
  • Metabolic acidosis
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28
Q

how does aortic coarctation present on a CXR?

A
  • CM
  • figure ‘3’ sign
  • rib notching
29
Q

how is aortic coarctation managed?

A

surgery by age of 5

30
Q

describe aortic stenosis

A

aortic valve leaflets partly fused together- restricts LV outflow

31
Q

clinical features of aortic stenosis

A
  • asymptomatic
  • ejection systolic murmur
  • carotid thrill in suprasternal region
32
Q

in aortic stenosis, where is the ejection systolic murmur heard?

A

upper right sternal edge

33
Q

how does aortic stenosis present on an ECG?

A

V2- deep S, tall R

V6- Down going T wave

34
Q

how is aortic stenosis managed?

A
  • ballon valvotomy
  • ballon dilation in older children
  • valve replacement
35
Q

describe pulmonary stenosis

A

PV leaflets partly fused together, restricting flow from the RV

36
Q

Clinical features of pulmonary stenosis

A

asymptomatic

ejection systolic murmur in ULSE

thrill

right ventricular heave

37
Q

how does pulmonary stenosis present on ECG?

A

upright T wave due to RV hypertrophy

38
Q

how is pulmonary stenosis managed?

A

transcatheter balloon dilatation

39
Q

describe transposition of the great arteries

A
  • aorta connected to RV, pulmonary artery connected to LV

- so oxygenated blood goes to lungs, deoxygenated to body- incompatible with life

40
Q

how does transposition of the great arteries present clinically?

A
  • cyanosis profound + life threatening
  • presents on day 2- ductal closure leads to reduction in mixing of saturated and desaturated blood
  • 2nd heart sound loud and single
  • acidosis
41
Q

how should a patient with suspected transposition be investigated?

A
  • check for 22q deletion

- radiography- narrow upper mediastinum- ‘egg on side’ cardiac shadow

42
Q

how is transposition managed and treated?

A
  • maintain patency of ductus arteriosus with prostagladin infusion
  • balloon atrial septostomy- hole between atria
  • surgery- arterial switch
43
Q

what 4 clinical features are present in the tetralogy of fallot?

A
  • large VSD
  • overriding aorta
  • sub-pulmonary stenosis
  • RVH
44
Q

signs and symptoms of the tetralogy of fallot?

A
  • cyanotic
  • sudden, short severe exacerbations causing distress and pallor due to hypoxia
  • breathless
  • irritability
  • easy tiring on breast feeding
45
Q

what is the tetralogy of fallot associated with?

A

Downs and 22q deletions

46
Q

what findings would be found on investigation in a patient with tetralogy of fallot?

A
  • radiograph- small heart, boot shaped apex
  • harsh ejection systolic murmur in LLSE
  • echo-cardinal features
47
Q

how is tetralogy of fallot managed?

A
  • close VSD
  • relieve RV outflow tract obstruction
  • shunt to increase pulmonary blood flow
48
Q

what is Ebstein’s abnormality?

A

posterior leaflets of the tricuspid valve are displaced anteriorly towards apex of RV

49
Q

what causes Ebstein’s abnormality?

A

lithium in pregnancy (bipolar mother)

50
Q

what are the 3 consequences of Ebsteins abnormality?

A
  • tricuspid regurg (pan-systolic murmur)
  • tricuspid stenosis (mid-diastolic murmur)
  • RA enlargement
51
Q

what is Kawasaki’s disease?

A

idiopathic self limiting systemic vasculitis

52
Q

epidemiology of Kawasaki’s

A
  • 6 months- 5 years

- asian origin

53
Q

what is the major complication of Kawasaki’s disease?

A

coronary artery aneurysm formation

54
Q

how does Kawasaki’s disease present clinically? (pneumonic)

A

MYHEART

  • My= Mucosal involvement (strawberry tongue, inflamed mucosa, mouth and lips)
  • Hand and feet swelling
  • Eyes- non - purulent bilateral conjunctivitis
  • Adenopathy (lymph)- cervical
  • Rash- truncal and polymorphic
  • Temperature/ fever
55
Q

describe the 3 phases of Kawasaki’s disease

A
  • acute febrile (1-2 weeks)- MYHEART
  • subacute (4-6) - development of coronary aneurysms
  • convalescent (6-12) - resolution of clinical signs and normalisation of inflammatory markers
56
Q

differential diagnosis of Kawasaki’s disease

A 
measles
rubella
infectious mononucleosis
parvovirus B19 
bacterial infection
57
Q

how is Kawasaki’s disease diagnosed and what tests and results are indicative of a diagnosis?

A
  • clinical
  • raised ESR, CRP, AST, A1-antitrypsin, platelets, bilirubin
  • ECG- abnormalities
  • ECHO- essential- reveals dilation and aneurysms of coronary arteries
58
Q

How is Kawasaki’s disease treated?

A
  • high dose aspirin
  • IV immunoglobulin (add prednisolone if ineffective)

aspirin and immunoglobulins used to reduce risk of coronary artery aneurysms !

59
Q

clinical signs of infective endocarditis

A 
fever 
splenomegaly
clubbing
splinter haemorrhages 
anaemia 
rash
HF
microscopic haematuria 
NEW MURMUR
60
Q

how is infective endocarditis treated?

A

BLIND- after 3 cultures- benzylpenicillin + gentamicin

61
Q

what is infective endocarditis ?

A

infection of the valves/ endocardium, causing destruction due to infective organisms forming vegetation

62
Q

how does subacute bacterial endocarditis present differently to infective endocarditis?

A

presents with more non-specific symptoms that may have lasted for more than 2 weeks

63
Q

what is rheumatic fever?

A

systemic febrile illness- cross -sensitivity reaction to group A- B- haemolytic strep

64
Q

what is the Jones diagnostic criteria (definition)?

A

used to diagnose rheumatic fever; must have 2 major or 1 major + 2 minor criteria

  • plus evidence of preceding strep infection (scarlet fever/ throat swab/ high serum ASO titre)
65
Q

what are the Major criteria in the Jones diagnostic criteria for RF?

A 
J – Joint arthritis
O – Organ inflammation, such as carditis
N – Nodules
E – Erythema marginatum rash
S – Sydenham chorea
66
Q

what are the minor criteria in the Jones diagnostic criteria for RF?

A

FEAR!
Fever
ECG Changes (prolonged PR interval) w/o carditis
Arthralgia without arthritis
Raised inflammatory markers (CRP and ESR)

67
Q

what is a MacCallum Plaque?

A

plaque found at the base of the posterior mitral leaflet in Rheumatic fever

68
Q

how is RF treated?

A
  • rest
  • aspirin
  • Benzylpenicillin then Phenoxymethylpenicillin
  • If Sydenhams Chorea present= prednisolone
69
Q

How does rheumatic fever present symptomatically?

A 
Fever
Joint pain (migratory- appears to move from joint to joint)
Rash
Shortness of breath
Chorea
Nodules

sx present 2-4 weeks after initial infection

NP- Phase 3a Medicine (22 decks)

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