Cardiology Flashcards

1
Q

Name some of the most common underlying congenital heart disease conditions in which IE occurs.

A

ventricular septal defects, patent ductus arteriosus, aortic valve abnormalities including bicuspid aortic valve and tetralogy of fallot

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2
Q

What is the triad of infective endocarditis?

A

endothelial damage, platelet adhesion and microbial adherence

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3
Q

Name some of the most common causative organisms of infective endocarditis.

A

Staphylococcus Aureus, Streptococcus Viridans,

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4
Q

Describe how a patient with IE would present.

A

Persistent low-grade fever, especially without another clear focus, is a concerning feature and should promote IE as a consideration. This is especially if there is a history of congenital heart disease, previous cardiac surgery or indwelling prosthetic material.

A heart murmur is almost always present formed either by turbulent flow around the vegetation or due to underlying heart disease.

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5
Q

Name some cutaneous manifestation of IE.

A

Petechiae – on skin and can be present on mucous membranes or conjunctival
Osler’s nodes – painful erythematous raised lesions on ends of fingers or toes
Janeway lesions – small, painless, erythematous, haemorrhagic raised lesions on palms or soles
Splinter haemorrhages – linear haemorrhagic streaks in the nail bed

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6
Q

Name two investigations required in suspected IE.

A

blood cultures and Echocardiography (ECHO)

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7
Q

What criteria is used for diagnosing IE?

A

Modified dukes criteria

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8
Q

In order to confirm a diagnosis of IE, how many of the modified dukes criteria need to be present?

A

In order to confirm the diagnosis there should be two major criteria, one major and three minor criteria or five minor criteria. The diagnosis is suspected if 1 major and 1 minor criteria or 3 minor criteria present.

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9
Q

What do organisms causing infective endocarditis have specific surface receptors for?

A

Fibronectin that allow the microbe to adhere to the thrombus at the outset.

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10
Q

What is acute rheumatic fever?

A

A systemic illness that occurs 2-4 weeks after pharyngitis due to cross-reactivity to streptococcus pyogenes

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11
Q

What is the gram stain of streptococcus pyogenes?

A

Gram-positive cocci

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12
Q

Name the two cytolytic toxins produced by streptococcus pyogenes.

A

Streptolysin S and O

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13
Q

Name some risk factors for developing IE.

A
Children and young people
Poverty
Overcrowded and poor hygiene places
Family history of rheumatic fever
D8/17 B cell antigen positivity
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14
Q

What is the diagnostic criteria for IE called?

A

Revised jones criteria.

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15
Q

in severe acute rheumatic failure, a heart murmur might be heard on examination, what valve is commonly affected?

A

Mitral

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16
Q

Name some investigations you’d like to do in suspected IE.

A

Bloods: ESR, CRP, FBC (WBC),
Blood cultures to exclude sepsis
Rapid Antigen Detection Test
Throat culture: may be negative by the time rheumatic fever symptoms occur
Anti-streptococcal serology: ASO and anti-DNASE B titres
ECG: prolonged PR interval
CXR if carditis is suspected: congestive heart failure may be seen in ARF due to valvular damage
Echocardiography

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17
Q

Which virulence factor causes B cells to produce a substance that cross reacts with tissues in the heart, brain, joints and skin?

A

M proetiens in the cell wall are immunogenic and stimulate B cells to make anti-M protein antibodies which cross reacts with other tissues e.g.. heart, brain, joints and skin.

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18
Q

Is ASD acyanotic or cyanotic?

A

Acyonotic

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19
Q

Name some risk factors for developing ASD.

A

Maternal smoking in 1st trimester
Maternal diabetes
Maternal rubella
Maternal drug use e.g. cocaine & alcohol

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20
Q

Name some symptoms of large ASD in paediatric patients.

A

Tachypnoea
Poor weight gain
Recurrent chest infections

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21
Q

What might be seen on an ECG of a child with an ASD?

A

Tall P wave (right atrial enlargement)
Right bundle branch block (incomplete)
Right axis deviation

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22
Q

What test is gold standard in diagnosing ASD?

A

Transthoracic echocardiogramas it provides information regarding both the size of ASD, and direction of blood flowing through the defect (using Doppler). It is also able to approximate the pulmonary artery pressure.

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23
Q

When is conservative managed of an ASD appropriate?

A

If ASD <5mm when it will spontaneously close within 12 months of birth.

24
Q

When is surgical management appropriate?

A

usually in patients with ASD > 1 cm.

25
Q

Name some complications of untreated ASD.

A

Arrhythmias (caused by atrial stretch leading to abnormal foci development)
Pulmonary hypertension
Eisenmenger syndrome (presenting with: chronic cyanosis, exertional dyspnoea, syncope, increased risk of infections, increased pulmonary vascular resistance)15
Cyanosis (only if Eisenmenger)
Peripheral oedema (if eventually leading to heart failure)
TIA / stroke

26
Q

What is the most common ASD?

A

Patent foramen ovale

27
Q

In which area will you auscultate an ASD the loudest?

A

Left upper sternal edge (pulmonary area)

28
Q

Describe the tetrad of tetrology of fallot.

A

Ventricular septal defect (VSD)
Pulmonary stenosis (PS)
Right ventricular hypertrophy (RVH)
Overriding aorta

29
Q

Name some risk factors of TOF.

A
Males
1st degree family history of CHD
Teratogens:
Alcohol (fetal alcohol syndrome)
Warfarin (fetal warfarin syndrome)
Trimethadione: antiepileptic drug used in treatment resistant epilepsy
30
Q

Describe the general examination of a paediatric patient with TOF.

A

General: central cyanosis, clubbing

Signs of congestive heart failure: sweating, pallor, tachycardia, hepatosplenomegaly, generalised oedema, bilateral basal crackles or gallop rhythm may be auscultated.

31
Q

Describe the palpation examination of a paediatric patient with TOF.

A

thrill (depends on intensity of murmur) or heave (RVH)

32
Q

Describe the auscultation examination of a paediatric patient with TOF.

A

Loud, single S2: due to closure of aortic valve in diastole with absent/reduced pulmonary valve closure (P2) depending on the degree of stenosis.
Pansystolic murmur: best auscultated either mid or upper left sternal edge (LSE). The smaller the VSD the louder the murmur and vice versa.
Ejection click4: high pitch noise which occurs at the maximal opening of semilunar (aortic or pulmonary) valves. Clicks in TOF occur due to presence of dilated aorta. Normally heart immediately after S1.
Continuous, machinery murmur: occurs in the presence of PDA with extreme forms of TOF, especially those on prostaglandin infusion. Best auscultated at the upper LSE or left infraclavicular area.
Note: the murmurs may decrease in intensity during “tet” spells due to reduced pulmonary blood flow.

33
Q

What is the gold standard for confirmation of a TOF diagnosis?

A

Echocardiogram

34
Q

Describe the medical management of TOF.

A

Squatting: Parents may observe the infants squatting or keeping their knees to their chest – this manoeuvre helps increase venous return, therefore increases systemic resistance. Parents should be advised to put child in this position whilst awaiting medical review.
Prostaglandin (PG) infusion: this helps maintain PDA in the more severe-extreme forms of TOF and must be started urgently following delivery to avoid the neonate collapsing. Depends on local practice, either PGE1 (alprostadil) or PGE2 (dinoprostone) may be used. Side effects to note include apnoeas, bradycardia and hypotension.
Beta-blockers: propranolol is commonly used in both “tet” spells and prophylaxis in moderate-severe disease. It works by reducing the heart rate thus venous return .
Morphine: reduces respiratory drive therefore also reduces hyperpnoea

35
Q

Name some genetic defects which have a high percentage of incidence of TOF.

A

CHARGE 65%, Di George 50%, Right Aortic Arch 25% and VACTERL 20%

36
Q

What gives the boot shaped heart of CXR in a patient with TOF?

A

The right ventricular hypertrophy and reduced pulmonary vascular markings give the boot-shaped heart on CXR

37
Q

What is the most common cause of cyanosis in a newborn?

A

TGA

38
Q

Name 3 common anatomic sites for mixing of oxygenated and deoxygenated blood in transposition of the great arteries to allow life to be sustained.

A

Patent foramen ovale or atrial septal defect
Ventricular septal defect
Patent ductus arteriosus

39
Q

Name some risk factors for developing TGA.

A
Age is over 40 years old
Maternal diabetes
Rubella
Poor nutrition
Alcohol consumption
40
Q

Describe the initial management of TGA.

A

Emergency prostaglandin E1 infusion to keep the ductus arteriosus patent as a temporary solution that allows mixing of blood
Correct metabolic acidosis
Emergency atrial balloon septostomy to allow for mixing

41
Q

Describe the definitive management of TGA.

A

Surgical correction, commonly arterial switch operation [ASO] is usually performed before the age of 4 weeks.
Long term follow up and counselling in the future if female patients wish to get pregnant

42
Q

What is he most common congenital heart defect?

A

VSD

43
Q

Which way do VSD’s shunt?

A

Left to right

44
Q

What is Eisenmenger’s syndrome?

A

Eisenmenger’s Syndrome is a condition where the pressure in the right ventricle exceeds that of the left ventricle and is caused by a significant gradual increase in the pulmonary vascular resistance.
It results in a shunt reversal, with deoxygenated blood flowing from the right ventricle into the left ventricle and entering the systemic circulation. This causes decreased systemic oxygen saturation and these patients become cyanotic.

45
Q

Nam some other congenital conditions that have been shown to be related to the development of a VSD.

A

Downs - trisomy 21
Trisomy 18 syndrome
Trisomy 13 syndrome
Holt-Oram Syndrome

46
Q

Describe how a patient with VSD would appear generally.

A

Undernourished: A symptom of VSD is fatigue during feeding which can cause the child to be undernourished.
Sweat on forehead: A sign of increased sympathetic activity as a compensatory mechanism for decreased cardiac output.
Increased work of breathing attributed to pulmonary congestion.
Colour: With large VSDs, patients may become cyanotic, developing a bluish complexion. A blue tinge around the lips can be misleading so it is important to check the tongue, nail beds and conjunctiva.

47
Q

Describe the murmur of a child with a VSD.

A

The murmur is either holosystolic or early systolic:

Holosystolic (Pansystolic) murmur: Starts at S1 and extends all the way to S2. This is the most likely type of murmur to be heard with VSD.
Early systolic murmur: Starts at S1 and ends in the middle or early systole. It usually occurs when there is lower than normal pressure difference between the two sides of the defect. Scenarios where this type of murmur may be heard include in a neonate with a large VSD and in children or adults with a very small VSD or a large VSD accompanied by pulmonary hypertension.

48
Q

Where can the systolic murmur od a VSD best be auscultated?

A

Lower left sternal boarder

49
Q

What long term advice should a VSD patient be given whether the defect has been repaired or not?

A
  • avoid tattoos
  • avoid piercings
  • good dental hygiene
50
Q

How do Atrioventricular Septal Defects (AVSD) develop?

A

Defects arise due to failure of endocardial cushions to fuse correctly leading to apical displacement of AV valves and causing the inlet portion of ventricular septum to be scooped out.

51
Q

Describe how individuals with Atrioventricular Septal Defects (AVSD) present.

A
Tachypnoea
Tachycardia
Poor feeding
Sweating
Failure to thrive (due to excessive metabolic cardiovascular requirements and poor caloric intake) – which in turn is due to tachypnoea.
52
Q

Describe the characteristic. findings of AVSD on an ECG.

A

Superior QRS axis with the QRS axis between -40 to -150 degrees is characteristic of the defect.
The underlying rhythm is usually sinus but may show prolonged PR interval– secondary to atrial enlargement and increased intra atrial conduction times.
P wave morphology may indicate right atrial, left atrial of bi-atrial enlargement
Right ventricular hypertrophy due to right ventricular volume overload- evident as RSR’ pattern in lead V1 may be evident.

53
Q

Describe the medical management of AVSD.

A
  • Diuretics
  • Angiotensin Converting enzymes inhibitors
  • Digoxin
  • Adequate calorie intake
54
Q

Name some complications of AVSD.

A
Failure to thrive
Recurrent lower respiratory tract infections
Congestive heart failure
Pulmonary Vascular disease
Eisenmenger’s syndrome
55
Q

How do ACE inhibitors help in AVSD?

A

ACE inhibitors reduce the systemic vascular resistance leading to afterload reduction which causes more blood to flow through the left ventricular outflow tract and subsequently reduces the amount of left to right shunt.

56
Q

Where is the ejection systolic murmur of an AVSD best auscultated?

A

Left upper sternal edge