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FOP/TAS > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Pathophysiology of rheumatic fever

A

Delayed immunological sequelae of Group A beta-haemolytic strep throat infection

GAS produces enzymes e.g. streptolysin O that is toxic to cardiac cells

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2
Q

Main systems that rheumatic fever affects

A

cardiac
skin
cns
joints

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3
Q

diagnostic criteria rheumatic fever

A

duckett-jones criteria
2x major OR 1x major and 2x minor

MAJOR
- migratory polyarthritis
-subcutaneous nodules
- carditis
- sydenham’s chorea
- erythema marginatum

MINOR
- arthralgia
- fever
- elevated ESR or CRP
- prolonged PR interval

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4
Q

erythema marginatum

A

non-itchy macular lesions with pale centres, normally trunk & limbs

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5
Q

Ix for rheumatic fever

A

throat swab - antistreptolysin O titres

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6
Q

Rx rheumatic fever

A

penicillin - for eradicating the infection

Carditis - aspirin
Evidence of HF - diuretics, ACEi, digoxin
Chorea - diazepam
Arthritis - aspirin & NSAID

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7
Q

Prophylaxis following rheumatic fever

A

timings depend on the presence of cardiac involvement

No cardiac -
Prophylactic penicillin for 5 years or until age 21

Cardiac -
Monthly penicillin for at least 10 years or until age 21

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8
Q

Presentation of ASD

A

Most are asymptomatic

Ejection systolic murmur at upper left sternal edge
Fixed splitting of the 2nd HS

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9
Q

Reason for murmur in ASD

A

Ejection systolic at LUSE

  • turbulence is mostly generated by blood flowing across the pulmonary valve during systole
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10
Q

why do you get splitting of the 2nd heart sound in ASD

A

equal L & R filling

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11
Q

Management ASD

A

Monitor until school age

Then surgical closure
- advised for all patients even if asymptomatic

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12
Q

Murmur in VSD

A

pansystolic murmur - LLSE +/- parasternal thrill

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13
Q

Rx VSD

A

Majority will close spontaenously
Rx medically if HF present
Rx surgically if HF severe or causing pulmonary hypertension

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14
Q

Eisenmenger syndrome

A

presence of pulmonary hypertension causes pulmonary vascular disease and cyanosis due to reversal of flow

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15
Q

Pharmacological closure of a PDA in term infants is effective T or F

A

False - only effective in preterm infants

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16
Q

Murmur aortic stenosis

A

Ejection systolic murmur RIGHT upper sternal edge - radiates to the neck/carotids

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17
Q

Mx aortic stenosis

A

most cases - conservative

If high resting pressure gradient (>60) then do balloon valvuloplasty

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18
Q

Murmur pulmonary stenosis

A

Ejection systolic murmur LUSE - radiates to back

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19
Q

Mx pulmonary stenosis

A

transvenous balloon dilatation

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20
Q

Most common congenital heart defect

A

bicuspid aortic valve

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21
Q

Pathophysiology of coarctation of the aorta

A

extension of prostaglandin sensitive tissue from the ductus arteriosus around the insertion of the aorta

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22
Q

types of coarctation of the aorta

A

Critical a.k.a pre-ductal

Non-critical a.k.a. post-ductal

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23
Q

associated cardiac defect with coarctation

A

bicuspid aortic valve

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24
Q

what GI pathology are coarctation’s at risk of

A

NEC - reduced blood flow through abdominal aorta

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25
Q

ECG signs of coarctation

A

signs of LVH

  • deep S wave V1
  • tall R wave V6
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26
Q

commonest cyanotic HD detected in 1st year of life

A

ToF

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27
Q

Pathophysiology of ToF

A

anterior displacement of the outflow tract septum that separates the single outflow tract into the aorta & pulmonary artery

> > large aorta and small pulmonary artery and VSD

> > pulmonary stenosis & RVH

> > normal systemic venous return to the R side&raquo_space; R to L shunting 2y to pulmonary stenosis through the VSD into the aorta&raquo_space; low O2 sats & cyanosis

N.B. if pulmonary stenosis and therefore RV outflow obstruction is moderate then there can be a balanced VSD and cyanosis can be mild or absent

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28
Q

Cardinal features of ToF

A

Large VSD
Overriding aorta
RV outflow obstruction
RVH

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29
Q

Murmur in ToF

A

Ejection systolic murmur LUSE (due to pulmonary stenosis)

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30
Q

ToF hypercyanotic spells underyling pathology

A

Increase in pulmonary vascular resistance, usually during activity&raquo_space; increases the R-L shunt which worsens cyanosis

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31
Q

What does Rx of ‘cyanotic spells’ in ToF aim to do

A

aims to increase pulmonary blood flow by reducing pulmonary vascular resistance and reduce systemic blood flow by increasing SVR in order to reduce the R>L shunt

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32
Q

Rx cyanotic spells in ToF

A

Knee-to-chest position
High flow O2
Pressure over femoral pulses
IV saline bolus
Morphine
B blockers

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33
Q

ECG appearance in ToF

A

Signs of RVH

Upright T wave V1
RAD
Dominant S wave in V5/6

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34
Q

most common cause of cyanotic HD in the neonatal period

A

TGA

35
Q

most common defects associated with TGA

A

VSD and pulmonary stenosis

36
Q

Rx TGA

A

PGE infusion to maintain duct patency
Maintain body temp - hypoxaemia worsens metabolic acidosis

Balloon atrial septostomy
Then definitive arterial switch in 1st 2 weeks of life

37
Q

Describe flow of blood in tricuspid atresia

A

systemic blood coming back to RA is shunted across to LA via the PFO and then travels to the LV&raquo_space; deoxygenated blood back to the systemic circulation

38
Q

Rx tricuspid atresia

A

PGE to maintain duct patency to maximise oxygenation of blue blood

BT shunt - neonatal period
Pulm artery banding (neonatal period)
Glenn shunt (6m)
Fontan procedure (preschool)

39
Q

Ebstein’s anomaly

A

inferiorly displaced tricuspid valve

more inferior&raquo_space; smaller RV&raquo_space; diminished capacity to pump&raquo_space; compromised flow to lungs&raquo_space; cyanosis at birth

40
Q

Rx hypoplastic left heart syndrome

A

PGE to maintain duct patency

  1. Norwood procedure
    then
  2. Fotann procedure
41
Q

What is a norwood procedure

A

Creation of a ‘neo-aorta’ by fusing the pulmonary artery to the atretic ascending aorta.

the main pulmonary artery is therefore disconnected from the branch pulmonary arteries

BT shunt is placed to secure pulmonary blood flow

The RV acts as the single systemic ventricle

42
Q

what is a fontan procedure

A

anastomosis of the IVC directly to the pulmonary arteries to create a passive systemic venous return to the pulmonary circulation

43
Q

how is cardiac arrest induced during a norwood procedure

A

using cardioplegia solution

  • high conc of potassium
  • increases the resting membrane potential of the myocardium
  • causes slow activation of the Na channels
  • leads to cardiac arrest in diastole
  • the solution is cold, reducing the O2 demand of the myocardium
44
Q

what is TAPVD

A

total anomalous pulmonary venous drainage

the 4 pulmonary veins drain to a confluence into the systemic circulation, instead of the L atrium

therefore all blood returning to the heart (pulm and systemic) returns to the R side of the heart

need a PFO or ASD in order to for survival

45
Q

most common causative organism infective endocarditis

A

staph aureus

46
Q

what are osler nodes and what causes them

A

painful nodes on the dorsum of hands

  • secondary to dermal immune complex deposition
47
Q

what are janeway lesions and what causes them

A

painless haemorrhagic lesions on palms and soles

  • secondary to micro abscess formation from septic emboli
48
Q

what are roth spots and what causes them

A

red spots with pale centres on fundoscopy

  • immunological phenomena of the retina
49
Q

what are splinter haemorrhages and what causes them

A

micro-emboli necrosis under the nails

50
Q

diagnostic criteria endocarditis

A

Modified Duke Criteria

2x major ; 1x major + 3x minor ; 5x minor

Major
- 2x +ve BC 12h apart
- +ve echo findings

Minor
- predisposing criteria
- fever >38
- vascular > arterial emboli/brain haemorrhage etc
- immunologic phenomena > osler nodes etc

51
Q

types of SVT

A

atrial tachycardia

AVN/junctional tachycardia

AV re-entrant tachycardia

52
Q

what is atrial tachycardia

A

an area of the atrium takes over the pacemaker activity of the heart

most common post cardiac surgery

53
Q

what is AVN/junctional tachycardia

A

abnormal re-entrant pathway within the AV node, so the AVN has pacemaker ability

54
Q

most common form of SVT > 8 years

A

AVNRT

55
Q

most common form of SVT <8 year

A

AVRT

56
Q

what is AV re-entrant tachycardia

A

there is an accessory conduction pathway joining the atria and ventricles forming a re-entry circuit e.g. WPW

57
Q

Rx SVT if shock present

A

sync DC shock 1J/kg

then

sync DC shock 2J/kg

then

continue sync at 2J/kg and consider amiodarone

58
Q

Rx sVT if no shock present

A

vagal manouevre

then

adenosine 100mcg/kg

then

adenosine 200mcg/kg

then

adenosine 300mcg/kg

59
Q

prophlyaxis SVT

A

verapamil 40mg tds

60
Q

Rx WPW

A

amiodarone

radiofrequency ablation

61
Q

causes of congenital heart block

A

maternal lupus - anti-ro or anti-la antibodies

isolated anomaly

congenital heart disease

acquired following cardiac surgery

62
Q

viral causes of myocarditis

A

coxsackie virus
adenovirus

63
Q

Rx pericarditis

A

NSAIDS
Pericardiocentesis - if causing tamponade

64
Q

size of arteries affected in kawasaki disease

A

medium sized vasculitis

65
Q

‘strawberry tongue’

A

kawasaki disease

66
Q

diagnostic criteria for kawasaki disease

A

Prolonged fever (>5 days)

+ 4 of …

  • non purulent conjunctivitis
  • oromucosal changes - strawberry tongue
  • polymorphous rash
  • cervical lymphadenopathy
  • arthritis
  • D&V
  • cough
67
Q

symptoms of atypical/incomplete kawasaki disease

A

suspect if <6m with fever >7 days and no other features

suspect if fever >5 days and 2-3 clinical features

68
Q

Rx kawasaki disease

A

IVIG + aspirin

May need 2nd dose IVIG and IVMP

69
Q

inheritance of Long QT

A

AD

70
Q

Different mutations causing HOCM

A

Troponin T mutation

Beta myosin (MYH7) in heavy chains mutation

Myosin-binding protein C mutation

Myosin light chain kinase (MYLK2) mutation

71
Q

Examination findings in HOCM

A

displaced and/or heaving apex beat

additional HS S3 + S4 - due to non compliant LV

quiet S2 with ejection systolic murmur

72
Q

What germ layer does the heart develop from

A

Mesoderm

73
Q

What weeks do the pharyngeal arches form

A

4+5

74
Q

when does cleavage of the aortic and pulmonary trunk occur

A

week 5&6

75
Q

when does the AV valves form

A

week 6&7

76
Q

what is the crista terminalis and when does it form

A

eventually forms the pathway from the SA node to the AV node

forms in week 6&7

77
Q

when do the intraventricular foramen close

A

week 7

78
Q

describe the venous systems to the primordial heart

A

Vitelline system
- returns poorly oxygenated blood from the yolk sac

Cardinal system
- carrys poorly oxygenated blood from the body of the embryo

Umbilical system
- carries well oxygenated blood from the placenta

79
Q

What does the vitelline system become after birth

A

the portal system

80
Q

what does the umbilical vein carry

A

oxygenated blood from the placenta to the baby

81
Q

when does the arterial CVS system develop

A

weeks 6-8

82
Q

list what arteries the pharyngeal arches form

A

1&2 - form some of the smaller vessels of the neck and face

3rd arches - internal carotid

4th
right - forms the right subclavian artery
left - forms the aortic arch between the L common carotid and the terminus of the ductus arteriosus

5th arches - dont form or regress completely

6th arches - form the pulmonary vasculature

83
Q

which artery can regress abnormally and form an aberrant origin

A

right subclavian artery arising from the 4th pharyngeal arch

FOP/TAS (25 decks)

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