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MRCP Part 1 > Cardiology Clinical > Flashcards

Cardiology Clinical Flashcards

1
Q

What is myocarditis?

A

Inflammation of the myocardium

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2
Q

What are the causes of myocarditis?

A
  1. viral - coxsackie B, HIV
  2. Bacterial - diphtheria, HIV
  3. Lyme disease
  4. Chagas disease, toxoplasmosis
  5. Autoimmune
  6. Doxurubicin
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3
Q

What are the indications for surgery for infective endocarditis?

A 
Severe valvular incompetence
Aortic abscess (recognised as there is lengthening of the PR interval)
Resistent infection
Cardiac failure
Recurrent emboli
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4
Q

What is a MUGA scan and when is it used?

A

Multi gated acquisition scan
Used to assess myocardial perfusion and myocardial viability (useful before and after cardiotoxic drugs to assess left ventricular ejection fraction)

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5
Q

When is a cardiac mri useful?

A

Structural images of the heart - useful in congenital heart disease, determining right and left mass and differentiating forms of cardiomyopathy

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6
Q

What is the definitive management of wolf parkinson white syndrome?

A

Radio-frequency ablation of the accessory pathway

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7
Q

What is a normal QT interval?

A

Less than 430 in males and less than 450 in females

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8
Q

What electrolyte abnormalities cause long QT syndrome?

A

Hypocalcaemia
Hypokalaemia
Hypomagnesiumemia

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9
Q

What drugs can cause long QT?

A 
Amioderone
Tricyclics (especially citalopram)
Erythromycin
Haloperidol
Ondansetron
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10
Q

Which bacteria most commonly causes endocarditis in patients with colorectal cancer?

A

Streptococcus bovis

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11
Q

What is the most common cause of infective endocarditis?

A

Staph aureus

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12
Q

What is 1st degree heart block?

A

PR interval over 0.2 seconds

Usually asymptomatic

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13
Q

What is mobitz type 1 av bock?

A

PR interval becomes progressivly longer until you get a dropped beat
May get syncope

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14
Q

What is mobitz type 2 heart block?

A

Random dropped beats with usually a ratio of 2: 1 or 3:1.

Tend to get symptoms including syncope and chest pain

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15
Q

What is third degree heart block?

A

No relationship between atria and ventricles (av node blocked completely) very low heart rate

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16
Q

What happens to the pulse in complete heart block?

A

Wide pulse pressure

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17
Q

What is the target INR for a venous thromboembolism?

A
  1. 5

3. 5 if recurrent

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18
Q

What is the target INR for atrial fibrillation?

A

2.5

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19
Q

What is the treatment for prevention of angina?

A
  1. Beta blocker or calcium channel blocker
    If not tolerated/contraindicated
  2. Long acting nitrate eg isosorbine mononitrate
  3. Nicorandil
  4. Ivabradine
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20
Q

What is the difference between paroxysmal and persistent AF?

A

Paroxysmal - 2 or more episodes that are self terminating

Persistent - 2 or more episodes that are not self terminating

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21
Q

How do statins work?

A

Inhibit HMG CoA reductase - which is the rate limiting enzyme in hepatic cholesterol synthesis

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22
Q

What is the treatment for major bleed in a patient who is taking warfarin?

A
  1. Stop warfarin
  2. IV vitamin K 5mg
  3. Prothrombin complex concentrate
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23
Q

How do thiazide diuretics work?

A

Inhibiting sodium reabsorption at the beginning of the distal convoluted tubule by blocking the Na/Cl symporter.

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24
Q

What type of pulse in associated with aortic stenosis?

A

Slow rising pulse

Narrow pulse pressure

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25
Q

What is malignant hypertension?

A

Blood pressure over 200/130. Can lead to cerebral oedema and encephalopathy as well as fibrinoid necrosis of blood vessels leading to retinal haemorrhages, exudates, proteinuria and haematuria due to renal damage.

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26
Q

What is the management of malignant hypertension?

A

Reduce diastolic BP by no lowere than 100mmHG within 12 - 24 hours. Best rest

  • Atenolol
  • IV sodium nitroprusside/labetolo if severe.
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27
Q

How do you manage aortic stenosis?

A

If asymptomatic then observe if symptomatic then valve replacement.

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28
Q

What is the definition of pulmonary hypertension?

A

Resting mean pulmonary artery pressure of 25mmHg or more

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29
Q

What is the definitive investigation for pulmonary hypertension?

A

Right heart catheterisation to measure pulmonary pressure.

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30
Q

What is the role of vasoreactivity testing in pulmonary hypertension?

A 
Vasoreactivity testing (performed with nitric oxide) helps differentiate patients. 
1. Those who respond (reduction of at least 10mmHg to less than 40mmHg without a fall in cardiac output)  may respond to long term high dose calcium channel blockers eg diltiazem
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31
Q

What is the most useful non invasive test for pulmonary hypertension?

A

Echocardiogram

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32
Q

What treatments are available for pulmonary hypertension?

A
  1. Calcium channel blockers (only in patiemts with a response to vasoreactivity testing)
  2. Postacyclin analogues eg iloprost - can be given IV/SC
  3. Endothelin recpetior antagonist eg bosentan
  4. Phosphodiesterase 5 inhibitors eg sildanefil (viagra)
  5. Heart - lung transplant
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33
Q

In STEMI what is the window for PCI?

A

120 minutes - if not possible then alteplase should be given. If a repeat ECG at 90 minutes does not show resolution then patient will need to be transferred to a PCI centre

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34
Q

What causes cannon waves on JVP?

A

The right atrium contracting against a closed tricuspid valve - can be regular or intermittent.
Regular = VT with 1: 1 ventricular atria conduction
Atrio-ventricular nodal re entry tachycardia
Irregular = Complete heart block

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35
Q

What is a cholesterol embolisation?

A

Occurs when cholesterol is released from an atherosclerotic plaque and travels as an embolism and causes an obstruction
Usually secondary to vascular surgery or angiography. Causes purpura, livido reticularis and eosinophilia as well as renal failure

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36
Q

What is brugada syndrome?

A

Inherited cardiovascular disease which may present with sudden cardiac death. Autosomal dominant.

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37
Q

What ECG changes are seen in brugada syndrome?

A

Convex ST segment elevation on over 2mm in 1 or more of V1 - V3 followed by a negative T wave
Partial right bundle branch block
(ECG changes may be more apparant following administration of flecainide)

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38
Q

What is the management of brugada syndrome?

A

Implantable cardioverter - defibrillator

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39
Q

Under what pottasium do you tend to see ECG changes consistend with hypokalaemia?

A

2.7mmol/L

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40
Q

What are the ECG changes associated with hypokalaemia?

A 
U waves 
Small T waves 
Long PR interval 
ST depression 
Long QT
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41
Q

What is the most common form of cardiomyopathy?

A

Dilated cardiomyopathy

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42
Q

When do you see pulsas alterans?

A

Left ventricular failure

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43
Q

When do you see pulsus paradoxus?

A

Severe asthma, cardiac tamponade

44
Q

When do you see a slow rising pulse?

A

Aortic stenosis

45
Q

When do you see a collapsing pulse?

A

Aortic regurgitation

Patent ductus arteriosus

46
Q

What are the features of severe aortic stenosis?

A 
Narrow pulse pressure 
Slow rising pulse 
Delayed ESM 
Soft S2
S4 
Thrill 
Long duration of murmum 
Left ventricular hypertrophy
47
Q

What are the main risk factors for aortic dissection?

A 
Hypertension 
Bicuspid aortic valve 
Trauma 
Marfans
Ehlers Danlos 
Turners 
Noonans 
Pregnancy
Syphillis
48
Q

What are the two types of artic dissection (stanford classification)

A

Type A: Ascending aorta (2/3 of cases)

Type B Descending aorta, distal to the left subclavian origin (1/3 of cases)

49
Q

What is multifocal atrial tachycardia?

A

Irregular cardiac rhythm caused by at least three different sites in the atra - seen as morphologically distinctive P waves on the ECG (more common in elderly patients)

50
Q

What is the first line treatment for pregnancy induced hypertension?

A

Labetolol

51
Q

What is the most common type of endocarditis less than 2 months post valve replacement surgery?

A

Staph epidermidis

52
Q

What is the most common cause of endocarditis?

A

Staph aureus

53
Q

What do you sue to pharmacologically cardiovert AF in those with structural heart disease ?

A

Amioderone

54
Q

What do you sue to pharmacologically cardiovert AF in those with no structural heart disease ?

A

Flecinide (or amioderone)

55
Q

What is the most common protein that is defective in HOCM?

A

Mutation in a gene encoding the beta myosin heavy chain protein or myosin binding protein C

56
Q

What are the treatment options for angina?

A
  1. Aspirin and statin (all patients)
  2. Beta blocker or rate limiting calcium channel (verapamil or diltiazem)
    If not controlled on monotherapy increase to max tolerated dose and then add in eg then add in
  3. Beta blocker _ calcium channel blocker such as nifedipine (NOT verapamil)
    If a patient on monotherapy cannot handle a second drug then consider ivabradine or nicorandil.
57
Q

After ACS (medically managed) how long should dual antiplatelet therapy be given?

A

Aspirin + ticagrelor for 12 months then aspirin alone. Clopidogrel can be given instead od ticagrelor if there is ahigh bleeding risk.

58
Q

After ACS (PCI + stenting) how long should dual antiplatelet therapy be given?

A

Aspirin + ticargrelor or prasugrel for 12 months then aspirin alone.

59
Q

Who should get an aldosterone antagonist (eg eplerenone) after an MI? When should this be started?

A

Patients with heart failure with a reduced left ventricular ejection fraction - preferably after an ACEi has been started.

60
Q

What does the murmur associated with an atrial septal defect sound like?

A

Ejection systolic murmur louder on inspiration

61
Q

No chest pain, persistent ST elevation and signs of left ventircular failure 2 weeks post MI

A

Left ventricularr aneurysm. Happens as ischaemic damage has weakened the myocardium resulting in aneurysm formation

62
Q

What is the management of atrial flutter?

A
  • Cardioversion (tends to be more sensitive than atrial fibrillation)
  • Radiofrequency ablation of the tricuspid valve isthmus is curative for most patients.
63
Q

Describe the drug treatment for heart failure with reduced ejection fraction

A
  1. ACE + Beta Blocker (one started at a time)
  2. Aldosterone antagonist (eplerenone or sprironolactone)
    Specialist review
  3. Ivabradine, sacubitril-valsartan, digoxin, hydralzine + nitrate, cardiac resynchronisation therapy
64
Q

What is the criteria for introduction of ivabradine in heart failure?

A

Sinus rhyth, over 75bpm and a left ventricular faction of less than 35%

65
Q

What is the criteria for introduction of sacubitril valsartan in heart failure?

A

Left ventricular fraction less than 35% who are symptomatic on ACEi/ARB. Should be initiated after an ACEi/ARB washout period

66
Q

What is the criteria for introduction of digoxin in heart failure?

A

Strongly indicated if there is coexistent atrial fibrillation

67
Q

What is the criteria for introduction of cardiac resynchronisation therapy in heart failure?

A

A widened QRS complex (eg LBBB)

68
Q

What group of patients may benefit from hydralazine _ nitrate in heart failure?

A

Afro-caribbean patients.

69
Q

What is the first line treatment for severe mitral stenosis?

A

Percutaneous mitral commissurotomy (also known as percutaneous mitral balloon valvotomy)

70
Q

What is the main cause of mitral stenosis?

A

Rheumatic fever

71
Q

What does the murmur of mitral stenosis sound like?

A

Mid-late diastolic murmur

72
Q

What is the most common cause of restrictive cardiomyopathy in the UK? What are the other causes

A

Amyloidosis is the most common
Haemachromatosis, lofflers syndrome, sarcoidosis, post radiation and scleroderma
Endocardial fibroelastosis cam be a cause in young children

73
Q

Does restrictive cardiomyopathy mainly affects systolic or diastolic function?

A

Diastolic

74
Q

What are the clinical signs seen in tricuspid regurgitation?

A

Pan systolic murmur, V waves in JVP, pulsatile hepatomegaly and left parasternal heave.

75
Q

What are the causes of tricuspid regurgitation?

A

Right ventricular infarction, pulmonary hypertension, rheumatic heart disease, infection endocarditis and carcinoid syndrome

76
Q

What is cholesterol embolisation?

A

A documented complication of coronary angiography - cholesterol emboli break off during the procedure and cause renal disease - The main features are eosinophillia, purpura, renal failure and livido reticularis

77
Q

What is wellens syndrome?

A

Deep T Wave Inversion in the anterior precordial leads - An ECG manifestation of critical proximal left anterior descending coronary artery stenosis in patients with unstable angina

78
Q

What is the most common gene mutation in brugada syndrome?

A

SCN5A gene mutation - this gene encodes for the myocardial sodium ion channel protein

79
Q

What ECG changes do you see in hypercalcaemia?

A

Shortened QT interval on ECG

80
Q

What is the most common ion channels abnormality associated with long QT syndrome?

A

Loss of function/Blockage of pottassium channels - l

81
Q

What are the main causes for a raised JVP?

A

Heart failure
Fluid overload
Constrictive pericarditis
Cardiac tamponade

82
Q

What vein is used to assess JVP?

A

Right internal jugular vein

83
Q

How many JVP pulses are seen per heartbeat?

A

2

84
Q

What is a normal JVP?

A

Less than 3 cm

85
Q

What are the parts of the JVP waveform?

A 
A Wave 
1st part X descent 
C Wave
2nd part X descent 
Y wave
86
Q

When does the A wave of the JVP occur?

A

Atrial contraction - causes JVP to rise

87
Q

When does the first X descent wave of the JVP occur

A

Relaxation of the atria and blood flowing back into the atrium (JVP falls)

88
Q

When does the c wave of the JVP occur?

A

Start of right ventricular contraction - causes tricuspid valve to bulge

89
Q

When does the second X descent wave of the JVP occur

A

End of right ventricular contraction - atria expands and drains blood from internal jugular vein

90
Q

When does the V wave of the JVP occur?

A

Atrial filling and therefore jugular vein filling

91
Q

When does the V wave of the JVP occur?

A

Tricuspid valve opens and emptying of the right atrium

92
Q

Why would you have absent A waves in the JVP

A

Atrial fibrillation - atria is not contracting in a normal coordinated way

93
Q

Why would you have large A waves in the JVP

A

Anything that means the atria is contracting against resistance - right ventricular hypertrophy, tricuspid stenosis

94
Q

Why would you have large V waves in the JVP

A

Triscuspid regurgitation - causes backflow of blood into internal jugular vein - also causes a loss of the x descent - increase in pressure in right atrium

95
Q

Why would you see cannon A waves in the jvp?

A

Atrial contractions against a closed tricuspid valve - seen in complete heart block, VT and single chamber cardiac pacing

Regular cannon waves - VT with 1:1 ventricular-atrial conduction

96
Q

What improvement should there be in the ST elevation 90 minutes following thrombolysis?

A

Greater than 50% resolution - otherwise rescue PCI is needed

97
Q

In asymptomatic patients, above what gradiaent would you consider surgery in aortic stenosis?

A

40mmHg and with features such as left ventricular systolic dysfunction

98
Q

What medication is given for acute SVT in asthmatics?

A

verapamil - adenosine is contraindicated

99
Q

What are the main characteristics of the murmur heard in HOCM?

A

Ejection systolic murmur - increases with the valsalva manoeuve and decreases on squatting

100
Q

What medication should be avoided in patients with HOCM?

A

ACE inhibitors - as they reduce preload they way worsen outflow obstruction

101
Q

What does the Q risk score mean?

A

Calculates the risk of developing a heart attack or stroke over the next 10 years

102
Q

Is the murmur of tricuspid regurgitation louder during inspiration or expiration?

A

Inspiration

103
Q

What does a fourth heart sound mean in the context of aortic stenosis?

A

Severe aortic stenosis

104
Q

What valvular abnormality increases the risk of aortic dissection?

A

Bicuspid aortic valve

105
Q

What medication should be given for a patient with fast atrial fibrillation and wolf parkinson white syndrome?

A

Fleccinide.

Drugs that block the AV node such as verapamil, beta blockers , digoxin and adenosine need to be avoided as the can precipitate VF.

Flecinide is a sodium channel blocker so can be safely used.

106
Q

What part of the ECG does the shock given in synchronised cardioversion correspond t?

A

The R wave

107
Q

What medication is given firs in aortic dissection?

A

IV labetolol

MRCP Part 1 (30 decks)

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