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MRCP Part 1 > Cardiology 1 > Flashcards

Cardiology 1 Flashcards

1
Q

MOA of fondaparinux?

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

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2
Q

MOA of bivalirudin?

A

Reversible direct thrombin inhibitor, given IV

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3
Q

MOA of indapamide?

A

Thiazide like diuretic

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4
Q

Stage 1 Hypertension?

A

Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg

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5
Q

Stage 2 Hypertension?

A

Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg

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6
Q

Severe Hypertension?

A

Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg

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7
Q

When should you treat stage 1 hypertension?

A

If <80 y/o and ANY of the following

  1. Target organ damage
  2. Established cardiovascular disease
  3. Renal disease
  4. Diabetes
  5. 10 year cardiovascular risk >=10%
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8
Q

When should you treat stage 2 hypertension?

A

Treat all patients, regardless of age

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9
Q

Lifestyle advice for hypertension?

A
  1. A low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg
  2. Caffeine intake should be reduced
  3. The other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight
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10
Q

NICE 2019 addition to guidelines?

A

Consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%

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11
Q

When should you get specialist review for HTN?

A

BP not controlled on 4 drugs (resistant hypertension)

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12
Q

BP not controlled on A+C+D management?

A
  1. K < 4.5 = low dose spironolactone

2. K > 4.5 = alpha or beta blocker

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13
Q

BP target for <80y/o?

A
  1. Clinic = 140/90

2. ABPM/HBPM = 135/80

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14
Q

BP target for >80 y/o?

A
  1. Clinic = 150/90

2. ABPM/HBPM = 145/85

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15
Q

New anti-hypertensive drug?

A

Direct renin inhibitor

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16
Q

Example of direct renin inhibitor?

A

Aliskiren

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17
Q

Discussion of aliskiren?

A
  1. No trials have looked at mortality data yet. Trials have only investigated fall in blood pressure.
  2. Initial trials suggest aliskiren reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists
  3. Adverse effects were uncommon in trials although diarrhoea was occasionally seen
  4. Only current role would seem to be in patients who are intolerant of more established antihypertensive drugs
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18
Q

What endocarditis is associated with colorectal cancer?

A

Streptococcus bovis (streptococcus gallolyticus subtype)

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19
Q

Greatest risk factor for developing IE?

A

Previous IE

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20
Q

Types of pts affected by IE?

A
  1. Previously normal valve (50%, usually mitral)
  2. Rheumatic (30%)
  3. Prosthetic valves
  4. Congenital heart defects
  5. IVDU (tricuspid)
  6. Recent piercings
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21
Q

Most common cause of IE?

A
  1. Staph Aureus in UK

2. Historically, it was Strep Viridans (most common in developing countries)

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22
Q

Cause of IE in pt with indwelling line?

A

CoNS e.g. Staphylococcus Epidermidis

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23
Q

Cause of IE in prosthetic valve pt after surgery?

A

CoNS e.g. Staphylococcus Epidermidis

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24
Q

Cause of IE in prosthetic valve pt >2 months after surgery?

A

Staph aureus

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25
Q

Streptococcus Viridans mushkie?

A
  1. Technically S. Viridans is a pseudotaxonomic term, referring to viridans streptococci rather than a particular organism
  2. 2 most notable viridans streptococci are: S. mitis and S. sanguinis
  3. They are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure
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26
Q

Non-infective cause of IE?

A

SLE –> Libman-Sacks endocarditis

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27
Q

Malignancy cause of IE?

A

Marantic IE

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28
Q

Culture negative causes of IE?

A
  1. Prior Abx therapy
  2. Coxiella burnetii
  3. Bartonella
  4. Brucella
  5. HACEK
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29
Q

What are the HACEK organisms?

A

Small, fastidious gram-negative bacilli

  1. Haemophilus species
  2. Aggregatibacter actinomycetemcomitans
  3. Cardiobacterium hominis 4. Eikenella corrodens
  4. Kingella kingae
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30
Q

First line management of acute pericarditis?

A

Combination of NSAID and Colchicine for 3 months

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31
Q

Features of acute pericarditis?

A
  1. Chest pain, pleuritic, relieved by sitting forwards
  2. Non-productive cough, dyspnoea, flu-like symptoms
  3. Pericardial rub
  4. Tachypnoea
  5. tachycardia
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32
Q

Causes of acute pericarditis?

A
  1. Infection = Viral (Coxsackie), TB
  2. Inflammation = CTD
  3. Malignancy
  4. Metabolic = uraemia (causes fibrinous pericarditis), hypothyroidism
  5. Post-MI (Dressler’s syndrome)
  6. Trauma
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33
Q

ECG changes in pericarditis?

A
  1. Global saddle-shaped ST elevation

2. PR depression

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34
Q

Most specific ECG marker for pericarditis?

A

PR Depression

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35
Q

Ix for all patients with acute pericarditis?

A

TTE

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36
Q

What drugs should be avoided in pts with HOCM?

A

ACE inhibitors, Nitrates, Inotropes

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37
Q

Why are ACE inhibitors C/I in HOCM with LVOT?

A

They can reduce afterload which may worsen the LVOT gradient

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38
Q

HOCM definition?

A

An autosomal dominant of muscle tissue caused by defects in the genes encoding contractile proteins

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39
Q

HOCM prevalence?

A

1 in 500

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40
Q

Management of HOCM?

A
  1. Amiodarone
  2. Beta blockers or verapamil for symptoms
  3. Cardioverter defebrillator
  4. Dual chamber pacemaker
  5. Endocarditis prophylaxis
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41
Q

Is antibiotic prophylaxis to prevent IE routinely recommended for dental procedures?

A

No

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42
Q

If person at risk of IE is given Abx for a GI/GU procedure, what should you take into account?

A

They should be given an antibiotic that covers organisms that cause IE

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43
Q

NYHA I?

A

No symptoms or limitation

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44
Q

NYHA II?

A
  1. Mild symptoms
  2. Slight limitation of physical activities = comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
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45
Q

NYHA III?

A
  1. Moderate symptoms

2. Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

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46
Q

NYHA IV?

A
  1. Severe symptoms

2. Unable to carry out any physical activity without discomfort, symptoms present at rest

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47
Q

What may a VT turn out to be?

A

SVT with aberrant conduction

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48
Q

VT with adverse signs (SBP <90, chest pain, HF, syncope) management?

A

Immediate Synchronised D/C Cardioversion

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49
Q

VT with no adverse signs?

A

Anti-arrhythmics

  1. Amiodarone ideally administered through a central line
  2. Lidocaine = use with caution in severe LV impairment
  3. Procainamide
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50
Q

What drug should NOT be used in VT?

A

Verapamil

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51
Q

VT with no adverse signs and drugs have failed?

A
  1. Electrophysiology study (EPS)

2. ICD = particularly indicated in pts with significantly impaired LV function

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52
Q

Murmur at LLSE?

A
  1. Tricuspid valve pathology
  2. VSD
  3. HOCM
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53
Q

Ejection systolic murmur louder on expiration?

A

AS and HOCM

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54
Q

Ejection systolic murmur louder on inspiration?

A

PS and ASD

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55
Q

Pansystolic murmur?

A
  1. Mitral/tricuspid regurgitation

2. VSD (harsh in nature)

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56
Q

Late systolic murmur?

A
  1. Mitral valve prolapse

2. Coarctation of the aorta

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57
Q

Early diastolic murmur?

A
  1. AR (high pitched and blowing)

2. Graham-Steel murmur (pulmonary regurgitation, also high pitched and blowing)

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58
Q

Mid-late diastolic murmur?

A
  1. Mitral stenosis (rumbling)

2. Austin-flint murmur (severe AR, also rumbling)

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59
Q

Continuous machine like murmur?

A

PDA

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60
Q

Secondary prevention of MI?

A
  1. DAPT (Aspirin + Ticagrelor/Prasugrel)
  2. ACEi
  3. Beta Blocker
  4. Statin
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61
Q

When may sexual activity resume after uncomplicated MI?

A

4 weeks

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62
Q

When can PDE5 inhibitors be used after MI?

A

6 months

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63
Q

In what patients should PDE5 inhibitors be avoided?

A

Those on nitrates/nicorandil

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64
Q

MOA of Ticagrelor/Prasugrel?

A

ADP receptor inhibitors (P2Y12 receptor antagonist that prevents ADP-mediated P2Y12 dependent platelet activation and aggregation)

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65
Q

When should ticagrelor be stopped post-MI?

A

12 months

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66
Q

When should ticagrelor be stopped post-PCI?

A

12 months

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67
Q

When should aldosterone antagonists be used post-MI?

A

Symptoms and/or signs of HF and LV systolic dysfunction, e.g. Epleronone should be initiated within 3-14 days of the MI, preferably after ACEi therapy

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68
Q

Intervention of choice for severe mitral stenosis?

A

Percutaneous mitral commissurotomy

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69
Q

Mx for severe mitral stenosis who cant tolerate PMC?

A

TMVR = transcatheter mitral valve repair

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70
Q

Causes of mitral stenosis?

A
  1. Rheumatic fever, rheumatic fever, rheumatic fever
  2. Mucopolysaccharidoses
  3. Carcinoid syndrome
  4. Endocardial fibroelastosis
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71
Q

Features of mitral stenosis?

A
  1. Mid-late diastolic murmur heard best on expiration
  2. Loud S1, opening snap
  3. Low volume pulse
  4. Malar flush
  5. AF
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72
Q

Mitral stenosis on CXR?

A

LA enlargement

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73
Q

Mitral stenosis on Echo?

A

Normal cross sectional area of mitral valve is 4-6 sq cm, tight mitral stenosis implies a cross sectional area of <1 square centimetre

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74
Q

PAH definition?

A

Resting mean pulmonary artery pressure of >= 25mmHg

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75
Q

What plays a key role in the pathogenesis of PAH?

A

Endothelin

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76
Q

PAH usually affects?

A

30-50 y/o females

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77
Q

What percentage of PAH is inherited in an AD fashion?

A

10%

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78
Q

What increases the risk of PAH?

A
  1. HIV
  2. Cocaine
  3. Anorexigens e.g. fenfluramine
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79
Q

Features of PAH?

A
  1. Progressive exertional dyspnoea
  2. Exertional syncope, exertional chest pain
  3. Peripheral oedema
  4. Cyanosis
  5. RV heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation
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80
Q

Management of PAH?

A

Acute vasodilator testing = to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide

  1. Positive response (minority) = oral CCB
  2. Negative response (majority) = Prostacyclin analogues, endothelin receptor antagonists, PDE5 inhibitors
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81
Q

Examples of prostacyclin analogues?

A

Treprostinil, Iloprost

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82
Q

Examples of endothelin receptor antagonists?

A

Bosentan, ambrisentan

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83
Q

Pt with PAH with progressive symptoms?

A

Should be considered for a heart-lung transplant

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84
Q

Normal corrected QT interval?

A
  1. <430ms in males

2. <450ms in females

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85
Q

What is LQTS?

A

Inherited condition associated with delayed repolarisation of the ventricles

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86
Q

Cause of LQTS 1 and 2?

A

Defects in the alpha subunit of the slow delayed rectifier potassium channel

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87
Q

Congenital cause of prolonged QT interval?

A
  1. LQTS 1,2,3
  2. Jervell-Lange Nielsen Syndrome
  3. Romano-Ward syndrome
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88
Q

Jervell Lange Nielsen Syndrome?

A

Includes deafness and is due to an abnormal potassium channel

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89
Q

Acquired causes of LQT?

A
  1. E- = hypokalaemia, hypocalcaemia, hypomagnesaemia
  2. Drugs
  3. Cardiac = Acute MI Myocarditis
  4. CNS = SAH and ischaemic stroke
  5. Hypothermia
  6. Malnutrition
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90
Q

Drugs that cause LQT?

A
  1. Anti-arrhythmics = Amiodarone, Sotalol, Class 1a
  2. Anti-depressants = TCAs, SSRIs (esp. citalopram)
  3. Antibiotics = erythromycin
  4. Antiemetics = ondansetron, metoclopramide, domperidone
  5. Antipsychotics = haloperidol
  6. Antipain = tramadol
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91
Q

LQT1 buzzwords?

A

Exertional syncope often swimming

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92
Q

LQT2 buzzwords?

A

Syncope following emotional stress, exercise, or auditory stimuli

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93
Q

LQT3 buzzwords?

A

Events occur at night or at rest

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94
Q

Management of LQT?

A
  1. Avoid drugs which prolong the QT interval
  2. Avoid strenuous exercise
  3. Beta blockers
  4. ICD in high risk cases
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95
Q

Usual mechanism by which drugs prolong the QT interval?

A

Blockage of potassium channels

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96
Q

How does LQTS typically present?

A

In young people, with cardiac syncope, tachyarrhythmias, palpitations, cardiac arrest

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97
Q

What is Takayasu’s arteritis?

A

Large vessel vasculitis, typically causes occlusion of the aorta

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98
Q

Takayasu’s arteritis common in?

A

Asian females

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99
Q

Features of Takayasu’s arteritis?

A
  1. Systemic vasculitis = malaise, headache
  2. Unequal BP in upper limbs
  3. Carotid bruit
  4. Intermittent claudication
  5. Aortic regurgitation (20%)
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100
Q

Association of takayasu’s arteritis?

A

Renal artery stenosis

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101
Q

Management of takayasu’s arteritis?

A

Steroids

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102
Q

Mx of haemodynamically stable pt with broad complex tachycardia?

A

IV Amiodarone

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103
Q

When is adrenaline given during VF/VT arrest?

A

Adrenaline 1mg is given once chest compressions have restarted after the third shock and then every 3-5 minutes during alternate cycles of CPR

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104
Q

Mx if cardiac arrest is witnessed in a monitored patient?

A

Up to three quick successive (stacked) shocks

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105
Q

Mx of asystole/PEA?

A

Adrenaline 1mg should be given ASAP, should be treated with 2 minutes of CPR prior to assessment of rhythm

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106
Q

O2 target following successful resuscitation?

A

94-98%

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107
Q

4Hs of reversible causes of cardiac arrest?

A
  1. Hypoxia
  2. Hypovolaemia
  3. Hypothermia
  4. Hypo/hyperkalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
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108
Q

4Ts of reversible causes of cardiac arrest?

A
  1. Tension pneumothorax
  2. Thrombus (coronary or pulmonary)
  3. Tamponade (cardiac)
  4. Toxins
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109
Q

Management of uraemic pericarditis?

A

Urgent haemodialysis

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110
Q

What extra heart sound is heard with AR?

A

S3

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111
Q

What extra heart sound is heard with AS?

A

S4

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112
Q

What extra heart sound is heard with MR?

A

S3

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113
Q

What extra heart sound is associated with TR?

A

S3

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114
Q

Features of aortic stenosis?

A
  1. Chest pain
  2. Dyspnoea
  3. Syncope
  4. Murmur = ESM radiating to the carotids, decreased following the valsalva manoeuvre
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115
Q

Features of severe aortic stenosis?

A
  1. Narrow pulse pressure
  2. Slow rising pulse
  3. Delayed ESM
  4. Soft/absent S2
  5. S4
  6. Thrill
  7. LVH/failure
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116
Q

Causes of AS?

A
  1. Supravalvular = William’s syndrome
  2. Valvular = degenerative calcification (>65y/o most common), biscuspid valve (<65/yo most common), rheumatic
  3. Subvalvular = HOCM
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117
Q

Management of AS?

A
  1. Asymptomatic = observe

2. Symptomatic = valve replacement

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118
Q

When are asymptomatic patients with AS operated on?

A

Valvular gradient >40mmHg and with features such as LV systolic dysfunction

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119
Q

Who is balloon valvuloplasty limited to?

A

Pts with critical AS who are not fit for valve replacement

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120
Q

What is Hedinger syndrome?

A

Carcinoid valvular heart disease, leads to fibrosis and subsequent pulmonary stenosis

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121
Q

What is Eisenmenger’s syndrome?

A

Reversal of a left to right shunt in a congenital heart defect due to pulmonary hypertension

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122
Q

What is Eisenmenger’s syndrome associated with?

A
  1. VSD
  2. ASD
  3. PDA
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123
Q

Features of Eisenmenger’s syndrome?

A
  1. Original murmur may disappear
  2. Cyanosis
  3. Clubbing
  4. RV failure
  5. Haemoptysis, embolism
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124
Q

Mx of Eisenmenger’s syndrome?

A

Heart-lung transplant

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125
Q

MOA of dipyridamole?

A

An antiplatelet agent, a non-specific phosphodiesterase inhibitor and decreases cellular uptake of adenosine
1. Elevates platelet cAMP levels which in turn reduce intracellular calcium levels, reduced cellular uptake of adenosine, inhibition of thromboxane synthase

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126
Q

What platelet receptor is targeted by clopidogrel?

A

P2Y12 receptor for ADP

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127
Q

What is dipyridamole used for?

A

An antiplatelet mainly used in combination with aspirin after an ischaemic stroke or TIA

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128
Q

Treatment for Prinzmetal angina?

A

Dihydropyridine calcium channel blocker e.g. felodipine

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129
Q

Management of stable angina?

A
  1. Lifestyle changes
  2. Medication
  3. PCI
  4. Surgery
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130
Q

Medications for stable angina?

A
  1. All pts should receive aspirin and a statin in the absence of any contraindication
  2. Sublingual GTN to abort angina attacks
  3. NICE recommend either a BB or CCB as first line
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131
Q

If a CCB is given for stable angina, what type should be used?

A
  1. A rate-limiting one such as verapamil or diltiazem should be used if monotherapy
  2. If used in combination with BB, then a long-acting dihydropyridine CCB e.g. nifedipine should be used
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132
Q

What should not be prescribed with verapamil and why?

A

Beta blockers, due to risk of complete heart block

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133
Q

Poor response to initial medical mx of angina?

A

Increase dose to maximum tolerated dose

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134
Q

If a patient is on monotherapy for stable angina and cannot tolerate addition of a CCB or BB?

A

Consider: LINRWhat

  1. Long acting nitrate
  2. Ivabridine
  3. Nicorandil
  4. Ranolazine
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135
Q

When should a third drug be added to BB and CCB for management of stable angina?

A

Whilst a pt is awaiting assessment for PCI or CABG

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136
Q

How can you minimise development of nitrate tolerance?

A

Pts who take standard release ISMN should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance

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137
Q

What type of ISMN dont you see nitrate tolerance in?

A

OD modified-release ISMN

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138
Q

Is temporary pacing indicated for complete heart block following an inferior MI?

A

No

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139
Q

Is temporary pacing indicated for complete heart block following an anterior MI?

A

Yes

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140
Q

When is transcutaneous pacing indicated?

A
  1. For pts who remain haemodynamically stable and bradycardic following treatment with atropine
  2. Post-anterior MI: Type 2 or complete heart block
  3. Trifascicular block prior to surgery
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141
Q

MOA of atropine?

A

Anti-muscarinic drug which can increase heart rate by inhibition of vagal tone modulating the SAN

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142
Q

Indications for temporary pacemaker?

A
  1. Symptomatic/haemodynamically unstable bradycardia, not responding to atropine
  2. Post-Anterior MI = type 2 or complete heart block
  3. Trifascicular block prior to surgery
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143
Q

What is Carvallo’s sign?

A

When the pansystolic murmur in tricuspid regurgitation becomes louder during inspiration

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144
Q

MOA of warfarin?

A

Inhibits Vitamin K epioxide reductase, stopping Vitamin K being converted to its active hydroquinone form, which in turn acts as a cofactor in the carboxylation of clotting factors 2, 7, 9,10 and Protein C

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145
Q

Can warfarin be used during breastfeeding?

A

Yes

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146
Q

Recurrent VTE INR target?

A

3.5

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147
Q

AF INR target?

A

2.5

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148
Q

How is INR calculated?

A

PT/Normal PT

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149
Q

Factors that may potentiate warfarin?

A
  1. Liver disease
  2. P450 inhibitors e.g. amiodarone, ciprofloxacin
  3. Cranberry juice
  4. Drugs which displace warfarin from plasma albumin e.g. NSAIDs
  5. Inhibit platelet function e.g. NSAIDs
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150
Q

S/e of warfarin?

A
  1. Haemorrhage
  2. Teratogenic
  3. Skin necrosis
  4. Purple toes
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151
Q

MOA of skin necrosis with warfarin?

A

When warfarin is first started, biosynthesis of protein C is reduced, resulting in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration, thrombosis may occur in venules leading to skin necrosis

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152
Q

Dentistry in warfarinised patients?

A

Check INR 72 hours before procedure, proceed if INR < 4.0

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153
Q

What medication is c/i in ventricular tachycardia?

A

Verapamil

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154
Q

What medication is c/i in irregular broad complex tachycardia?

A

Adenosine

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155
Q

Anteroseptal MI ECG and artery?

A
  1. V1-V4

2. LAD

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156
Q

Inferior MI ECG and artery?

A
  1. II, III, aVF, RCA
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157
Q

Anterolateral MI ECG and artery?

A
  1. V4-V6, I, aVL

2. LAD or Left circumflex

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158
Q

Lateral MI MI ECG and artery?

A
  1. I, aVL, V5-6

2. Left circumflex

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159
Q

Posterior MI ECG and artery?

A
  1. Tall R waves V1-V2

2. Usually left circumflex, also right coronary

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160
Q

What is VT?

A

A broad complex tachycardia originating from a ventricular ectopic focus

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161
Q

2 main types of VT?

A
  1. Monomorphic VT = most commonly caused by MI

2. Polymorphic VT = A subtype of polymorphic VT is torsades de pointes

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162
Q

What is S3 (gallop rhythm) a sign of?

A
  1. Caused by diastolic filling of the ventricle
  2. Considered normal if <30 years old and may persist in women up to 50 years old
  3. Heard in LV failure (e.g. dilated cardiomyopathy, constrictive pericarditis, mitral regurgitation)
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163
Q

Soft S1?

A

Mitral regurgitation

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164
Q

Loud S1?

A

Mitral stenosis

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165
Q

Soft S2?

A

Aortic Stenosis

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166
Q

Causes of splitting S2?

A

Normal during inspiration

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167
Q

What is S4 a sign of?

A
  1. Caused by atrial contraction against a stiff ventricle, therefore coincides with the p wave on ECG
  2. May be heard in AS, HOCM, HTN
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168
Q

Why may you feel a double apical impulse in HOCM?

A

Due to palpable S4

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169
Q

What should be avoided in pts with HOCM?

A

ACE inhibitors, Nitrates, Inotropes

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170
Q

What should be avoided in pts with WPW?

A

Verapamil as it may precipitate VT or VF

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171
Q

Deteriorating renal function with purpuric rash on feet a few days after coronary angiogram?

A

Cholesterol embolisation

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172
Q

Features of cholesterol embolisation?

A
  1. Eosinophilia
  2. Purpura
  3. Renal failure
  4. Livedo reticularis
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173
Q

How does cholesterol embolisation occur?

A
  1. Majority secondary to vascular surgery or angiography
  2. Cholesterol emboli may break off causing renal disease
  3. Other causes include severe atherosclerosis, particularly in large arteries such as the aorta
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174
Q

What is Ebstein’s anomaly?

A
  1. Congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle, a.k.a. ‘atrialisation’ of the right ventricle
  2. Septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle
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175
Q

Cause of Ebstein’s anomaly?

A

Lithium exposure in utero

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176
Q

Associations of Ebstein’s anomaly?

A
  1. PFO or ASD is seen in at least 80% of patients, resulting in a shunt between the right and left atria
  2. WPW syndrome
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177
Q

Clinical features of Ebstein’s anomaly?

A
  1. Cyanosis
  2. Prominent ‘a’ wave in the distended JVP
  3. Hepatomegaly
  4. Tricuspid regurgitation (pansystolic murmur, worse on inspiration)
  5. RBBB –> widely split S1 and S2
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178
Q

Factors favouring rate control of AF?

A
  1. Older than 65 years old

2. History of IHD

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179
Q

Factors favouring rhythm control of AF?

A
  1. Younger than 65 years old
  2. Symptomatic
  3. First presentation
  4. Lone AF or AF secondary to a corrected precipitant e.g. alcohol
  5. Congestive heart failure
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180
Q

Rate control medications for AF?

A
  1. Beta blockers
  2. Calcium channel blockers
  3. Digoxin (not considered first line as they are less effective at controlling heart rate during exercise, however they are the preferred choice if the patient has coexistent HF)
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181
Q

Rhythm control medications for AF?

A
  1. Sotalol
  2. Amiodarone
  3. Fleicanide
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182
Q

When is catheter ablation indicated for AF?

A

For those with AF who have not responded or wish to avoid anti-arrhythmic medication

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183
Q

How can tissue be ablated in AF?

A
  1. Radiofrequency (heat generated from medium frequency alternating current)
  2. Cryotherapy
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184
Q

Where is typically ablated for AF?

A

Between the pulmonary veins and the left atrum

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185
Q

Anticoagulation before ablation for AF?

A
  1. Should be used 4 weeks before and during the procedure
  2. Catheter ablation controls rhythm but does not reduce stroke risk, even if patients remain in sinus rhythm, therefor still anticoagulate as per CHA2DS2VASC
    a. 0 = 2 months anticoagulation
    b. >1 = longterm anticoagulation
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186
Q

Complications of ablation for AF?

A
  1. Cardiac tamponade
  2. Pulmonary valve stenosis
  3. Cardiac tamponade
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187
Q

Success rate of ablation for AF?

A
  1. 50% experience an early recurrence (within 3 months) of AF that often resolves spontaneously
  2. Longer term, after 3 years, around 55% of pts who have had a single procedure remain in sinus rhythm, of patients who have undergone multiple procedures around 80% are in sinus rhythm
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188
Q

Doxazosin MOA and use?

A

Alpha blocker used in refractory hypertension

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189
Q

Why are nitrates c/i on HOCM?

A

Vasodilators increase the outflow tract gradient and cause a reflex tachycardia that further worsens ventricular diastolic function

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190
Q

Why are inotropic drugs c/i in HOCM?

A

Worsen outflow tract obstruction, do not relieve the high end-diastolic pressure, and may induce arrhythmias

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191
Q

First line drug treatment for HF?

A

Both an ACEi AND a BB

  1. Generally, one drug should be started at a time, NICE advise clinical judgement when determining which one to start first
  2. BB licensed to treat HF in UK incl. bisoprolol, carvedilol, nebivolol
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192
Q

Do ACEi and BB have an effect on mortality in pts with HFpEF?

A

No

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193
Q

Second line drug treatment for HF?

A

Aldosterone antagonist

  1. E.g. spironolactone and epleronone
  2. It should be noted that both ACEi and aldosterone antagonists cause hyperkalaemia, so K should be monitored
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194
Q

Third line drug treatment for HF?

A

Should be initiated by a specialist

  1. Ivabridine = sinus rhythm >75 and LVEF <35%
  2. Sacubitril-Valsartan = LVEF <35%, for pts still symptomatic on ACEi/ARBs, should be initiated following ACEi or ARB wash out period
  3. Digoxin = not been shown to reduce mortality, may improve symptoms due to its inotropic properties
  4. Hydralazine + Nitrate = particularly indicated in Afro-Caribbean pts
  5. CRT = widened QRS (LBBB) on ECH
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195
Q

‘Other’ treatments for HF?

A
  1. Annual influenza vaccine

2. One-off pneumococcal vaccine

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196
Q

What pts require pneumococcal booster vaccine every 5 years?

A
  1. Asplenia
  2. Splenic dysfunction
  3. CKD
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197
Q

Infective endocarditis indications for surgery?

A
  1. Severe valvular incompetence
  2. Aortic root abscess (often indicated by lengthening of PR interval)
  3. Infections resistant to abx/fungal infections
  4. HF refractory to standard medical treatment
  5. Recurrent emboli after antibiotic therapy
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198
Q

Poor prognostic factors for IE?

A
  1. S. aureus infection
  2. Prosthetic valve
  3. Culture negative IE
  4. Low complement levels
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199
Q

Mortality according to organism for IE?

A
  1. Staph = 30%
  2. Bowel organism = 15%
  3. Strep = 5%
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200
Q

Initial blind therapy for IE?

A
  1. Native valve = amoxicillin, consider adding low-dose gentamicin
  2. If pen allergic/MRSA/severe sepsis = vancomycin + low dose gentamicin
  3. If prosthetic valve = vancomycin + rifampicin + low dose gentamicin
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201
Q

Native valve endocarditis caused by staph abx?

A
  1. Flucloxacillin

2. Pen allergic/MRSA = Vancomycin + rifampicin

202
Q

Prosthetic valve endocarditis caused by staph abx?

A
  1. Flucloxacillin + rifampicin + low dose gentamicin

2. If pen allergic/MRSA = vancomycin + rifampicin + low dose gentamicin

203
Q

Endocarditis caused by fully sensitive streptococci e.g. viridans abx?

A
  1. Benzylpenicillin

2. Pen allergic/MRSA = Vancomycin + low dose gentamicin

204
Q

Endocarditis caused by less sensitive streptococci?

A
  1. Benzylpenicillin + low dose gentamicin

2. If pen allergic = vancomycin + low dose gentamicin

205
Q

ARBs or ACEi preferred in african-caribbean pts?

A

ARBs

206
Q

QRISK threshold for treated stage 1 hypertension in pts <80 y/o?

A

10%

207
Q

Most common valvular abnormality in IE?

A

Tricuspid regurgitation

208
Q

Why are right sided murmurs louder during inspiration?

A

Increased venous blood return to the right side of the heartt

209
Q

When can CKD cause raised serum natriuretic petides?

A

eGFR < 60

210
Q

What is BNP?

A

Hormone produced mainly by the LV myocardium in resopnse to strain

211
Q

Effects of BNP?

A
  1. Vasodilator
  2. Diuretic and natriuretic
  3. Suppresses both sympathetic tone and the renin-angiotensin aldosterone system
212
Q

4 clinical uses of BNP?

A
  1. Diagnosing pts with acute dyspnoea = good for ruling out
  2. Prognosis in pts with chronic HF
  3. Guiding treatment in pts with chronic HF = effective treatment lowers BNP levels
  4. Screening for cardiac dysfunction = not currently recommended
213
Q

Bioprosthetic heart valve antithrombotic therapy?

A

Aspirin

214
Q

Mechanical heart valve antithrombotic therapy?

A

Warfarin + Aspirin (aspirin is only normally given in addition if there is an additional indication e.g. ischaemic heart disease)

215
Q

Most common valves which need replacing?

A

Aortic and vitral

216
Q

Options for valve replacement?

A

Biological (bioprosthetic) or mechanical

217
Q

Bioprosthetic valve mushkies?

A
  1. Usually bovine or porcine in origin
  2. Major disadvantage is structural deterioration and calcification over time (most older pts, >65 for aortic and >70 for mitral) receive a bioprosthetic valve
  3. Long term anticoagulation not usually needed, warfarin may be given for the first 3 months depending on patient factors, long term aspirin is given
218
Q

Mechanical valve muskies?

A
  1. Most common is bileaflet, ball and cage is now rare
  2. Mechanical valves have a low failure rate
  3. Major disadvantage is increased risk of thrombosis
  4. Aortic target INR = 3, mitral target INR = 3.5
219
Q

Risk of bisphosphonate infusion?

A

Can lead to hypocalcaemia

220
Q

QT interval of greater than ? is associated with ventricular arrhythmia, syncope and SCD?

A

> 0.44 seconds

221
Q

Chvostek’s sign?

A

Tapping over the facial nerve at the angle of the jaw, +ve = ipsilateral twitching of the muscles around the nose and lips

222
Q

2 scenarios where cardioversion may be used in AF?

A
  1. Electrical cardioversion as an emergency if haemodynamically unstable
  2. Electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred
223
Q

What is electrical cardioversion synchronised to?

A

To the R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced

224
Q

AF onset <48 hours management?

A
  1. Pt should be heparinised
  2. Electrical DC cardioversion OR pharmacological cardioversion (amiodarone if structural heart disease, fleicanide or amiodarone in those without structural heart disease)
  3. Pts with RFs for ischaemic stroke should be put on lifelong oral anticoagulation
  4. Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary
225
Q

AF onset >48 hours management?

A
  1. Anticoagulation should be given for at least 3 weeks prior to cardioversion
  2. Alternative is to perform a TOE to exclude a LAA thrombus, if excluded then can be heparinised and cardioverted immediately
  3. If high risk of cardioversion failure (e.g. previous failure or AF recurrence) then it is recommended to have at least 4 weeks of amiodarone or sotalol prior to electrical cardioversion
  4. Following electrical cardioversion, pts should be anticoagulated for at least 4 weeks
226
Q

Pathophysiology of HOCM?

A
  1. Most common defects involve mutation in gene encoding BMHC or MBPC
  2. Results in predominantly diastolic dysfunction (LV hypertrophy –> decreased compliance –> decreased cardiac output)
227
Q

HOCM on biopsy?

A

Myofibrillar hypertrophy with chaotic and disoarganised fashion myocytes (‘disarray’) and fibrosis

228
Q

Why may HOCM cause mitral regurgitation?

A

May impair mitral valve closure

229
Q

Associations of HOCM?

A
  1. WPW

2. Friedrich’s Ataxia

230
Q

Echo findings of HOCM?

A

MR SAM ASH

  1. Mitral regurgitation
  2. SAM of mitral valve
  3. Asymmetric hypertrophy
231
Q

ECG of HOCM?

A
  1. LVH
  2. Non-specific ST segment and T wave abnormalities, progressive T wave inversion may be seen
  3. Deep Q waves
  4. AF may occasionally be seen
232
Q

Type 1 respiratory failure in a tachycardic, tachypnoeic female with an absence of chest signs?

A

PE

233
Q

First line treatment for VTE?

A

DOAC e.g. apixaban or rivaroxaban

234
Q

VTE in active cancer management?

A

DOAC e.g. apixaban or rivaroxaban

235
Q

Is routine cancer screening recommended following a VTE diagnosis?

A

No

236
Q

How to decide what PE pts can be managed as outpatients?

A
  1. PESI score, though no formal risk stratification tool is recommended by NICE
  2. Key requirements would be haemodynamic stability, lack of comorbidities and support at home
237
Q

Treatment for PE if neither apixaban or rivaroxaban are suitable?

A
  1. LMWH followed by dabigatran or edoxaban OR

2. LMWH followed by VKA e.g. Warfarin

238
Q

PE treatment if eGFR < 15?

A

LMWH, UFH, or LMWH followed by VKA

239
Q

PE treatment in pt with antiphospholipid syndrome?

A

LMWH followed by VKA

240
Q

How long should pts with PE be anticoagulated for?

A
  1. At least 3 months

2. Continuing anticoagulation after this period is partly determined by whether VTE was provoked or unprovoked

241
Q

Provoked VTE treatment length?

A

3 months

242
Q

Active cancer VTE treatment length?

A

3-6 months

243
Q

Unprovoked VTE treatment?

A

6 months

244
Q

Mx of PE with haemodynamic instability?

A

Thrombolysis

245
Q

Mx of repeated PEs despite adequate anticoagulation?

A

IVC filter

246
Q

Treatment of torsades de pointes?

A

IV magnesium sulfate

247
Q

What is torsades de pointes?

A

A form of polymorphic VT associated with Long QT interval

248
Q

What anti-HTN increases risk of gout?

A

Thiazide-like diuretics

249
Q

Common side effect of ticagrelor?

A

Dypsnoea (in 15%) –> start on clopidogrel instead

250
Q

MOA of ticagrelor causing dyspnoea?

A

Ticagrelor inhibits adenosine clearance (by inhibiting enzyme adenosine deaminase) thereby increasing its concentration in the circulation

251
Q

Medically treated ACS antiplatelet management?

A
  1. 1st line = aspirin (lifelong) and ticagrelor (12 months)

2. 2nd line = if aspirin c/i, clopidogrel (lifelong)

252
Q

PCI antiplatelet management?

A
  1. 1st line = aspirin (lifelong) and ticagrelor/prasugrel (12 months)
  2. 2nd line = if aspirin c/i, clopidogrel (lifelong)
253
Q

TIA antiplatelet management?

A
  1. 1st line = lifelong clopidogrel

2. 2nd line = lifelong aspirin and dipyridamole

254
Q

Ischaemic stroke antiplatelet management?

A
  1. 1st line = lifelong clopidogrel

2. 2nd line = lifelong aspirin and dipyridamole

255
Q

Peripheral arterial disease antiplatelet management?

A
  1. 1st line = lifelong clopidogrel

2. 2nd line = lifelong aspirin

256
Q

Cardiac imaging techniques?

A
  1. Echo
  2. CT
  3. MRI
  4. Nuclear
257
Q

Cardiac CT mushkies?

A

Useful for assessing suspected IHD using 2 main methods, and if combined has a very high negative predictive value for IHD:

  1. Calcium score
  2. Contrast enhanced CT = allowed visualisation of coronary artery lumen
258
Q

Cardiac MRI mushkies?

A

Gold standard for structural images of the heart

  1. Assessing congenital heart disease, determining right and left ventricular mass, and differentiating forms of cardiomyopathy
  2. Myocardial perfusion can also be assessed following the administration of gadolinium
259
Q

Cardiac nuclear imaging mushkies?

A

Use radiotracers which are extracted by normal myocardium e.g. thallium, Technetium (99mTc, used in MIBI or SPECT scans), Fluorodeoxyglucose (used in PET scans)

  1. SPECT is used to assess myocardial perfusion and viability, by comparing rest images with stress images any areas of ischaemia can be classified as reversible or fixed (e.g. following MI)
  2. MUGA
260
Q

What is MUGA?

A
  1. Multi Gated Acquisition Scan
  2. Technetium-99m is injected IV, pt is placed under a gamma camera
  3. Can accurately measure LVEF, typically used before and after cardiotoxic drugs are used
261
Q

MOA of furosemide and bumetanide?

A
  1. Inhibits the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl
  2. There are 2 variants of the NKCC, loop diuretics act on NKCC2, which is more prevalent in kidneys
262
Q

Indications for loop diuretics?

A
  1. HF = acute IV, chronic oral

2. Resistant HTN, particularly in pts with renal impairment

263
Q

6 S/e of loop diuretics?

A
  1. Hypotension
  2. Hyponatraemia, hypokalaemia, hypomagnesaemia, hypocalcaemia, hypochloraemic alkalosis
  3. Ototoxicity
  4. Renal impairment
  5. Hyperglycaemia
  6. Gout
264
Q

Complication of coronary angiogram secondary to irritation of the myocardium?

A

Ventricular arrhythmia, offending catheter must be pulled back immediately to restore normal sinus rhythm

265
Q

Typical Angina?

A

All 3 of:

  1. Constricting discomfort in the front of the chest or in the neck/shoulders/jaws/arms
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN in about 5 minutes
266
Q

Atypical Angina?

A

2 of:

  1. Constricting discomfort in the front of the chest or in the neck/shoulders/jaws/arms
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN in about 5 minutes
267
Q

Non-anginal chest pain?

A

1 or none of:

  1. Constricting discomfort in the front of the chest or in the neck/shoulders/jaws/arms
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN in about 5 minutes
268
Q

Ix of pts in whom stable angina cannot be excluded by clinical assessment alone (e.g. symptoms with typical//atypical angina OR ECG changes)?

A
  1. 1st line = CTCA
  2. 2nd line = Non-invasive functional imaging
  3. 3rd line = Invasive CA
269
Q

Examples of non-invasive functional cardiac imaging?

A
  1. Myocardial perfusion scintigraphy with SPECT
  2. Stress echo
  3. First pass contrast-enhanced MR perfusion
  4. MR imaging for stress-induced WMA
270
Q

Where do HACEK organisms live?

A

On dental gums and are more common in IVDU

271
Q

What would cause pseudomonas IE?

A

When infected water enters the blood stream

272
Q

Ejection systolic murmur which increases with valsalve manoeuvre and decreases on squatting?

A

HOCM

273
Q

Management of PDA?

A
  1. Indomethacin/Ibuprofen given to the neonate, inhibits prostaglandin synthesis, closes the connection in the majority of cases
  2. If associated with another congenital heart defect amenable to surgery, then Prostaglandin E1 is used to keep duct open until after surgical repair
274
Q

PDA cyanotic or acyanotic?

A
  1. Acyanotic

2. Uncorrected, can eventually result in late cyanosis in the lower extremities, termed differential cyanosis

275
Q

PDA is between which 2 vessels?

A

Descending aorta and the pulmonary trunk

276
Q

Factors increasing PDA risk?

A
  1. Premature babies
  2. Born at high altitude
  3. Maternal rubella infection in 1st trimester
277
Q

PDA on examination?

A
  1. Left subclavicular thrill
  2. Continuous machinery murmur
  3. Large volume, bounding, collapsing pulse
  4. Wide pulse pressure
  5. Heaving apex beat
278
Q

What should amiodarone ideally be administered through?

A

A central line

279
Q

When is a non-pulsatile JVP seen?

A

SVC obstrution

280
Q

Kussmaul’s sign?

A

Paradoxical rise in JVP during inspiration, seen in constrictive pericarditis

281
Q

Parts of the JVP waveform?

A

ACX is VY

A cat’s xylophone is very yellow

282
Q

A wave of JVP?

A

Atrial contraction

  1. Large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary HTN
  2. Absent if in AF
283
Q

Canon ‘a’ waves of JVP?

A
  1. Caused by atrial contractions against a closed tricuspid valve
  2. Seen in complete heart block, VT/ectopics, nodal rhythm, single chamber ventricular pacing
284
Q

C wave of JVP?

A

Closure of tricuspid valve, not normally visible

285
Q

V wave of JVP?

A
  1. Due to passive filling of blood into the atrium against a closed tricuspid valve
  2. Giant A waves in tricuspid regurgitation
286
Q

X descent of JVP?

A

Fall in atrial pressure during ventricular systole

287
Q

Y descent of JVP?

A

Opening of tricuspid valve

288
Q

First line drug for pregnancy induced hypertension?

A

Labetalol

289
Q

Pre-eclampsia definition?

A

Condition seen after 20 weeks gestation characterised by pregnancy-induced hypertension in association with proteinuria (>0.3g/24 hours), oedema used to be the third element of the classic triad but is now often not included in the definition as it is not specific

290
Q

Pre-eclampsia pre-disposes to what conditions?

A
  1. Fetal = prematurity, IUGR
  2. Eclampsia
  3. Haemorrhage = placental abruption, intra-abdominal, intra-cerebral
  4. Cardiac failure
  5. Multi-organ failure
291
Q

High risk factors for pre-eclampsia and so should take aspirin?

A
  1. HTN in prev. pregnancy
  2. CKD
  3. AI e.g. SLE/APLS
  4. T1DM/T2DM
  5. HTN
292
Q

Moderate risk factors for pre-eclampsia?

A
  1. 1st pregnancy
  2. > 40 y/o
  3. Pregnancy interval >10 years
  4. BMI >35
  5. FHx of pre-eclampsia
  6. Multiple pregnancy
293
Q

Features of severe pre-eclampsia?

A
  1. HTN > 170/110
  2. Proteinuria
  3. Headache
  4. Visual disturbance
  5. Papilloedema
  6. RUQ/epigastric pain
  7. Hyperreflexia
  8. Plt count <100, abnormal liver enzymes or HELLP
294
Q

Management of pre-eclampsia?

A
  1. Moderate/high risk should take aspirin 75mg from 12 weeks gestation until birth
  2. Treat BP >160/110 with oral labetalol
  3. Nifedipine and hydralazine may be used if asthmatic
  4. Delivery of the baby is the most important and definitive management step
295
Q

Gold standard treatment for STEMI?

A

Primary PCI

296
Q

PESI scores and subsequent risks?

A
  1. <65 points = very low (OP)
  2. 65-85 points = low risk (OP)
  3. > 85 = IP management
297
Q

Mechanisms of BNP?

A
  1. Vasodilator
  2. Diuretic and Natriuretic
  3. Suppresses both sympathetic tone and the RAAS
298
Q

Factors which reduce BNP levels?

A

ACEi, AR2Bs and diuretics

299
Q

2 commonest causes of CKD in developed countries?

A

HTN and diabetes

300
Q

Hypertensive indications for admission?

A
  1. Severe HTN (>220/120mmHg)
  2. Grade 3-4 retinopathy
  3. Hypertensive emergencies e.g. encephalopathy, aortic dissections etc.
  4. Impending complications e.g. LVF and TIAs
301
Q

Lifestyle salt advice?

A
  1. Aim <6g a day, ideally 3g/day
  2. Average adult in the UK consumes 8-12g/day of salt
  3. Reducing salt intake by 6g/day can lower SBP by 10mmHg
302
Q

CHA2DS2-VASc score?

A
  1. Congestive heart failure = 1 point
  2. HTN = 1 point
  3. Age >75 = 2 points, Age 65-74 years = 1 point
  4. Diabetes
  5. S2 = prior stroke or TIA
  6. Vascular disease incl. IHD and peripheral arterial disease
  7. Sex (female) = 1 point
303
Q

CHADSVASC score interpretation?

A
  1. 0 = no treatmen
  2. 1 = Males = consider anticoagulation, Females = no treatment
  3. 2 or more = offer anticoagulation
304
Q

HAS BLED score (all worth 1)?

A
  1. Hypertension, uncontrolled, systolic BP >160
  2. Abnormal renal function (dialysis or creatinine >200)
  3. Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP >3 times normal)
  4. Stroke
  5. Bleeding history/tendency
  6. Labile INRs (unstable/high INRs, time in therapeutic range <60%)
  7. Elderly <65 years
  8. Drugs predisposing to bleeding (antiplatelets, NSAIDs
  9. Alcohol Use (>8 drinks/week)
305
Q

HAS BLED score interpretation?

A
  1. > = 3 indicates a ‘high risk’ of bleeding
306
Q

What can happen if cardioversion shock is delivered later in the cycle during ventricular repolarisation (T wave)?

A

Can trigger the R on T phenomenon, which invariably leads to ventricular fibrillation

307
Q

What is the R on T phenomenon?

A

Superimposition of an ectopic beat on the T wave of a preceding beat, likely to initiates sustained ventricular tachyarrhythmias

308
Q

All patients with STEMI should be given?

A
  1. Aspirin
  2. P2Y12 antagonist e.g. ticagrelor/clopidogrel, or prasugreal if they are going to have PCI
  3. UFH given for patients who will have PCI
309
Q

Choice of tPA for thrombolysis?

A

Tenecteplase (shown to be superior to alteplase)

310
Q

What should be done 90 minutes following thrombolysis?

A

ECG to assess whether there has been a greater than 50% resolution in the ST elevation

  1. If there has not been adequate resolution, then rescue PCI is superior to repeat thrombolysis
  2. For pts successfully treated with thrombolysis, PCI has been shown to be beneficial, optimal timing of this is still under investigation
311
Q

Glycaemic control in MI patients?

A

Using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to <11mmol/l

312
Q

What should a single episode of paroxysmal AF, even if provoked, prompt?

A

Consideration of anticoagulation

313
Q

Causes of tricuspic regurgitation?

A
  1. RV infarction
  2. Pulmonary HTN e.g. COPD
  3. Rheumatic heart disease
  4. IE, esp. IVDU
  5. Ebstein’s anomaly
  6. Carcinoid syndrome
314
Q

ARVC pathophysiology?

A
  1. AD inheritance pattern with variable expression
  2. RV myocardium is replaced by fatty and fibrofatty tissue
  3. 50% of pts have a mutation of genes encoding desmosomes
315
Q

What is ARVC?

A

Form of inherited cardiovascular disease which may present with syncope or SCD

316
Q

Most common causes of SCD in the young?

A
  1. HOCM

2. ARVC

317
Q

Presentation of ARVC?

A
  1. Palpitations
  2. Syncope
  3. SCD
318
Q

Investigation of ARVC?

A
  1. ECG = TWI in V1-V3, epsilon wave found in about 50% (terminal notch in the QRS complex)
  2. Echo - enlarged, hypokinetic right ventricle with a thin free wall
  3. MRI = useful for showing fibrofatty tissu
319
Q

Management of ARVC?

A
  1. Drugs = sotalol
  2. Catheter ablation to prevent VT
  3. ICD
320
Q

What is Naxos disease?

A

Autosomal recessive variant of ARVC

321
Q

Triad of Naxos disease?

A
  1. ARVC
  2. Palmoplantar keratosis
  3. Woolly hair
322
Q

Peri-arrest tachycardia - what are ‘adverse signs’ which would mean pt is unstable?

A
  1. Shock (SBP<90mmHg), pallor, sweating, cold clammy extremities, confusion or impaired consciousness
  2. Syncope
  3. MI
  4. HF

If any of these are present, then synchronised DC shocks should be given

323
Q

Management of regular narrow complex tachycardia?

A
  1. Vagal manoeuvres followed by IV adenosine

2. If unsuccessful, consider diagnosis of atrial flutter and control rate with e.g. beta blockers

324
Q

Management of irregular narrow complex tachycardia?

A
  1. Probable AF
  2. If onset <48 hours consider electrical or chemical cardioversion
  3. Rate control e.g. beta blocker or digoxin and anticoagulation
325
Q

Management of regular broad complex tachycardia?

A
  1. Assume VT (unless previously confirmed SVT with bundle branch block)
  2. Loading dose of amiodarone followed by 24 hour infusion
326
Q

Management of irregular broad complex tachycardia?

A
  1. AF with BBB = treat as for narrow complex tachycardia

2. Torsades de pointes = IV magnesium sulphate

327
Q

What should be added to CCB for black pts with HTN?

A

ARB

328
Q

3 causes of S3?

A
  1. LVF e.g. DCM
  2. Constrictive pericarditis (also called pericardial knock)
  3. Mitral regurgitation
329
Q

Side effects of sulfonylurea?

A
  1. Common = hypoglycaemia, weight gain

2. Rare = Hyponatraemia (SIADH), bone marrow suppression, hepatotoxicity, peripheral neuropathy

330
Q

Sulfonylurea MOA?

A

Bind to ATP-dependent K+ channel on the cell membrane of pancreatic beta cells, and increase pancreatic insulin secretion, only effective if functional B cells are present

331
Q

When should sulfonylureas be avoided?

A

Breastfeeding and pregnancy

332
Q

Anti-CCP?

A

Rheumatoid Arthritis

333
Q

What is Rheumatoid Factor?

A

A circulating antibody (usually IgM) which reacts with the Fc portion of the patient’s own IgG

334
Q

How can Rheumatoid factor be detected?

A
  1. Rose-Waaler Test = sheep red cell agglutination

2. Latex agglutination test = less specific

335
Q

What % of pts with RA are RF +ve?

A

70-80%

336
Q

What are high RF titre levels associated with in RA?

A

Are associated with severe progressive disease but NOT a marker of disease activity

337
Q

Conditions associated with positive positive RF?

A
  1. Felty’s = 100%
  2. Sjogren’s = 50%
  3. IE = 50%
  4. SLE = 20-30%
  5. SS = 30%
  6. General population = 5%
  7. Rarely = TB, HBV, EBV, leprosy
338
Q

What % of general population are RF positive?

A

5%

339
Q

When may anti-CCP be detected?

A

Up to 10 years before the development of rheumatoid arthritis

340
Q

Sensitivity and specificity of anti-CCP for RA?

A
  1. Sensitivity = 70%

2. Specificity = 90-95%

341
Q

Vincristine acts during what stage of mitosis?

A

Metaphase

342
Q

Vincristine is part of what class of agents and MOA?

A
  1. Vinca alkaloids, microtubule targeting agents affecting the M phase of mitosis
  2. Bind to tubulin and stop the polymerisation and assembly of microtubules, in turn disrupting spindle formation, arresting mitosis at metaphase
343
Q

Taxane MOA?

A

Enhances polymerisation of tubulin where the microtubule disassemble

344
Q

Pathophysiology of aortic dissection?

A

Tear in the tunica intima of the wall of the aorta

345
Q

Associations of aortic dissection?

A
  1. HTN
  2. Trauma
  3. Bicuspid aortic valve
  4. Collagen = Marfans, EDS
  5. Turner’s and Noonan’s
  6. Pregnancy
  7. Syphilis
346
Q

Sx of aortic dissection involving coronary arteries?

A

Angina

347
Q

Sx of aortic dissection involving spinal arteries?

A

Paraplegia

348
Q

Sx of aortic dissection involving distal aorta?

A

Limb ischaemia

349
Q

Classification of aortic dissection?

A

Stanford and DeBakey classification

350
Q

Stanford classification of aortic dissection?

A
  1. Type A = ascending aorta, 2/3 of cases

2. Type B = descending aorta, distal to left subclavian origin, 1/3 of cases

351
Q

DeBakey classification of aortic dissection?

A
  1. Type I = Originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
  2. Type II = Originates in and is confined to the ascending aorta
  3. Type III = originates in descending aorta, rarely extends proximally but will extend distally
352
Q

Hypothermia ECG changes?

A
  1. Bradycardia
  2. J wave = small hump at the end of the QRS complex
  3. 1st Degree HB
  4. Long QT interval
  5. Atrial and ventricular arrhythmias
353
Q

What is a valsalva manoeuvre?

A

A forced expiration against a closed glottis, leading to increased intrathoracic pressure which in turn has a number of effects on the cardiovascular system

354
Q

Uses of valsalva manoeuvre?

A
  1. To terminate an episode of SVT

2. To normalise middle ear pressures

355
Q

Stages of the valsalva manoeuvre?

A
  1. Increased intrathoracic pressure
  2. Resultant increase in venous and right atrial pressure reduces venous return
  3. Reduced preload lead to a fall in cardiac output (Frank-Starling mechanism)
  4. When the pressure is released there is a further slight fall in cardiac output due to increased aortic volume
  5. Return of normal cardiac output
356
Q

Most common cyanotic congenital heart disease?

A
  1. TGA most common at birth
  2. TOF most common overall
  3. Tricuspid atresia
  4. Pulmonary valve stenosis
357
Q

Most common acyanotic congenital heart diseases?

A
  1. VSD most common (30%)
  2. ASD
  3. PDA
  4. Coarctation of the aorta
  5. Aortic valve stenosis
358
Q

When does ToF typically present?

A

1-2 months after birth following the identification of a murmur or cyanosis

359
Q

What are Aschoff bodies?

A

Granulomatous nodules found in rheumatic heart fever

360
Q

What valve is most commonly affected by rheumatatic heart disease?

A

Mitral

361
Q

How do you assess exposure to group A streptococcus bacteria?

A

ASO titre

362
Q

Histology of rheumatic fever?

A
  1. Aschoff bodies (granuloma with giant cells)

2. Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus)

363
Q

Councilman bodies?

A

Hepatitis C, Yellow Fever

364
Q

Mallory Bodies?

A

Alcoholism (hepatocytes)

365
Q

Call-Exner bodies?

A

Granulosa cell tumour

366
Q

Schiller-Duval bodies?

A

Yolk Sac tumour

367
Q

What is rheumatic fever?

A

Autoimmune reaction to recent (2-6 weeks ago) S. pyogenes infection

368
Q

Pathogenesis of rheumatic fever?

A
  1. S. pyogenes infection –> activation of innate immune system leading to antigen presentation to T cells
  2. B and T cells produce IgM and IgG antibodies and CD4+ T cells are activated
  3. There is then a cross-reactive immune response (a form of Type II hypersensitivity) thought to be mediated by molecular mimicry
  4. Cell wall of S. pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries
  5. Their response leads to clinical features of rheumatic fever
369
Q

Management of rheumatic fever?

A
  1. Abx = Oral penicillin V
  2. Anti-inflammatories = NSAIDs are first line
  3. Treatment of any complications that develop e.g. heart failure
370
Q

Diagnosis of rheumatic fever?

A

Evidence of recent streptococcal throat infection accompanied by:

  1. 2 major criteria
  2. 1 major with 2 minor criteria
371
Q

Evidence of recent streptococcal throat infection for dx of rheumatic fever?

A
  1. Raised or rising streptococcal antibodies
  2. Positive throat swab
  3. Positive rapid Group A streptococcal antigen test
372
Q

Major criteria for rheumatic fever?

A

CASES

  1. Carditis (must be evidence of endocarditis in addition to pericarditis/myocarditis)
  2. Polyarthritis
  3. Sydenham’s chorea (late feature)
  4. Erythema marginatum
  5. Subcutaneous nodules
373
Q

Minor criteria for rheumatic fever?

A
  1. Raised ESR or CRP
  2. Pyrexia
  3. Arthralgia (not if arthritis a major criteria)
  4. Prolonged PR interval
374
Q

How long after stroke should you start anticoagulation?

A

2 weeks to reduce the risk of haemorrhagic transformation

375
Q

How long after TIA should you start anticoagulation?

A

In the absence of cerebral infarction or haemorrhage, anticoagulation should begin as soon as possible

376
Q

Why are loading doses of amiodarone needed?

A

Has a very long half life of 20-100 days

377
Q

What is amiodarone?

A

Class III anti-arrhythmic agent used in the treatment if atrial, nodal and ventricular tachycardias

378
Q

Main MOA of amiodarone?

A
  1. Blocks potassium channels, inhibiting repolarisation and thus prolonging the action potential
  2. Also has other actions e.g. blocking Na channels (Class I effect)
379
Q

What limits use of amiodarone?

A
  1. Very long 1/2 life = 20-100 days, so loading doses frequently used
  2. Should ideally be given into central veins (causes thrombophlebitis)
  3. Has proarrhythmic effects due to lengthening of QT interval
  4. p450 Inhibitor
  5. Numerous long-term adverse effects
380
Q

Monitoring of pts taking amiodarone?

A
  1. TFT, LFT, U&E, CXR prior to treatment

2. TFT, LFT every 6 months

381
Q

Adverse effects of amiodarone use?

A
  1. Eye = corneal deposits, photosensitivity
  2. Thyroid = hypo and hyperthyroidism
  3. Lung = pulmonary fibrosis/pneumonitis
  4. Liver = fibrosis/hepatitis
  5. Heart = Bradycardia, prolongs QT interval
  6. Veins = Thrombophlebitis and injection site reactions
  7. Skin = slate grey appearance
  8. Nerve = peripheral neuropathy, myopathy
382
Q

MOA of ACEi?

A
  1. Inhibit conversion of angiotensin I to angiotensin II

2. ACE inhibitors are activated by Phase 1 metabolism in the liver

383
Q

S/e of ACEi?

A
  1. Cough = occur in 15% of pts and may occur up to a year after starting treatment, thought to be due to increased bradykinin levels
  2. Angioedema = may occur up to a year after starting treatment
  3. Hyperkalaemia
  4. First-dose hypotension = more common in pts taking diuretics
384
Q

Cautions of ACEi?

A
  1. Pregnancy and breastfeeeding = avoid
  2. Renovascular disease = may result in renal impairment
  3. AS = may result in hypotension
  4. Hereditary/idiopathic angioedema
  5. Specialist advice should be sought before starting ACEi in pts with a potassium >=5
385
Q

Interactions of ACEi?

A

Significantly increases the risk of hypotension in pts receiving high dose diuretic therapy (>80mg Furosemide per day)

386
Q

Monitoring of ACEi?

A
  1. U&E should be checked before treatment is initiated and after increasing dose
  2. A rise in creatinine and potassium may be expected after starting ACEi
387
Q

Significant renal impairment in pt started on ACEi?

A

Undiagnosed bilateral renal artery stenosis?

388
Q

Acceptable e- changes with ACEi?

A
  1. Increase in creatinine up to 30% from baseline

2. Increase in potassium up to 5.5mmol/mol

389
Q

Most common causes of viral myocarditis?

A

Parvovirus B19 and HHV6

390
Q

Most common cardiomyopathy?

A

DCM, 90% of cases

391
Q

Causes of DCM?

A
  1. Idiopathic = most common
  2. Myocarditis = Coxsackie B, HIV, Diphtheria, Chagas disease
  3. IHD, HTN
  4. Peripartum
  5. Iatrogenic = doxorubicin
  6. Drugs = alcohol, cocaine
  7. Infiltrative = haemochromatosis, sarcoidosis
392
Q

Inherited cause of DCM?

A
  1. Either familial or syndromic e.g. DMD
  2. 1/3rd pts with DCM have genetic predisposition, many heterogeneous defects identified
  3. Most defects inherited in AD fashion
393
Q

Pathophysiology of DCM?

A
  1. Dilated heart leading to predominantly systolic dysfunction
  2. All 4 chambers are dilated but the LV more so than the RV
  3. Eccentric hypertrophy (sarcomeres added in series) is seen
394
Q

DCM findings?

A
  1. HF
  2. Systolic murmur = stretching of valves may result in mitral and tricuspid regurgitation
  3. S3
  4. Balloon appearance of the heart on the CXR
395
Q

ARB MOA?

A

Angiotensin II receptor blockers block the effects of angiotensin II at the AT1 receptor

396
Q

ARB examples?

A

Candesartan, losartan, irbesartan

397
Q

S/e of ARBS?

A
  1. Should be used with caution in pts with renovascular disease
  2. S/e = hypotension and hyperkalaemia
398
Q

Evidence base of ARBs?

A
  1. Shown to reduce progression of renal disease in pts with diabetic nephropathy
  2. Evidence base that losartan reduces CVA and IHD mortality in hypertensive patients
399
Q

Thiazide diuretic MOA?

A
  1. Inhibits Na reabsorption by blocking the NaCl symporter at the proximal part of the DCT
    2, Potassium is lost as a result of more sodium reaching the collecting ducts
400
Q

Common S/e of thiazides?

A
  1. Dehydration
  2. Postural hypotension
  3. Hyponatraemia, hypokalaemia, hypercalcaemia
  4. Gout
  5. Impaired glucose tolerance
  6. Impotence
401
Q

Rare s/e of thiazides?

A
  1. Thrombocytopenia
  2. Agranulocytosis
  3. Photosensitivity rash
  4. Pancreatitis
402
Q

Why may thiazides be helpful in treating renal stones?

A

Causes hypercalciuria

403
Q

Causes of myocarditis?

A
  1. Viral = coxsackie B, HIV
  2. Bacteria = diphtheria, clostridia
  3. Spirochaetes = Lyme
  4. Protozoa = Chagas disease, toxoplasmosis
  5. AI
  6. Drugs = doxorubicin
404
Q

Ix of Myocarditis?

A
  1. Bloods = raised inflammatory markers in 99%, raised cardiac enzymes, raised BNP
  2. ECG = tachycardia, arrhythmias, ST/T wave changes incl. ST segment elevation and TWI
405
Q

Mx of myocarditis?

A
  1. Tx of underlying cause e.g. Abx if bacterial

2. Supportive = of HF or arrhythmias

406
Q

Complications of myocarditis?

A
  1. HF
  2. Arrhythmia, possibly leading to sudden death
  3. DCM = usually a late complication
407
Q

What is CPVT?

A
  1. Chatecholaminergic polymorphic VT
  2. Inherited cardiac disease associated with SCD
  3. AD inheritance, 1:10,000
408
Q

Ambrisentan and Bosentan MOA?

A

Endothelin-1 receptor antagonist

409
Q

Endothelin and PAH pathophysiology?

A
  1. In PAH the expression of endothelin 1 is increased resulting in vasoconstriction
  2. Endothelin primarily acts upon 2 receptors ETA and ETB
  3. ETA is found in vascular smooth muscle and facilitates vasoconstriction
  4. ETB is found on the endothelium and mediates vasodilation (ambrisentan is selective for ETA receptors)
410
Q

S/e of ambrisentan?

A
  1. Peripheral oedema
  2. Sinusitis
  3. Flushing
  4. Nasal congestion
411
Q

PE triad?

A

Pleuritic chest pain, dyspnoea and haemoptysis

412
Q

Most common clinical signs of PE?

A
  1. Tachypnoea = 96%
  2. Crackles = 58%
  3. Tachycardia = 44%
  4. Fever = 43%
413
Q

What criteria could be used to rule out PE?

A
  1. PERC = Pulmonary embolism rule out criteria
  2. ALL the criteria must be absent to have a negative PERC result
  3. Negative PERC reduces probability of PE to <2%
414
Q

What score for suspected PE?

A

2-level PE Wells score

  1. PE likely >4 points
  2. PE unlikely <= 4 points
415
Q

‘Likely’ PE management?

A
  1. CTPA (if delay, treatment should be started)
  2. DOAC e.g. apixaban/rivaroxaban
  3. If CTPA -ve then consider proximal leg vein US scan if DVT is suspected
416
Q

‘Unlikely’ PE management?

A
  1. D-dimer –> if positive then CTPA

2. If negative then stop anticoagulation and consider alternative diagnosis

417
Q

CTPA diagnosis in pt with renal impairment?

A

V/Q scan

418
Q

PE ECG?

A
  1. S1Q3T3 = large S wave in Lead I, large Q wave in Lead III, Inverted T wave in Lead III (20% pts)
  2. RBBB and RAD
  3. Sinus tachycardia
419
Q

PE CXR?

A

Either normal or wedge-shaped opacification

420
Q

SVT acute management?

A
  1. Vagal manoeuvres e.g. Valsalva, carotid sinus massage
  2. IV adenosine 6mg –> 12mg –> 12mg (c/i in asthmatics, verapamil is favourable option)
  3. Electrical cardioversion
421
Q

SVT chronic management (prevention)?

A
  1. BB

2. RFA

422
Q

Why should rate-limiting CCBs be avoided in pts with AF and HFrEF?

A

Due to their negative inotropic effects

423
Q

Mx of Dressler’s syndrome?

A

NSAIDs or a prolonged course of colchicine or steroids

424
Q

When does Dressler’s syndrome occur?

A

2-6 weeks following an MI (autoimmune reaction against antigenic proteins formed as the myocardium recovers)

425
Q

Features of Dressler’s syndrome?

A
  1. Fever
  2. Pleuritic Pain
  3. Pericardial effusion
  4. Raised ESR
426
Q

Persistent ST elevation and LV failure after MI?

A

LV aneurysm

427
Q

How does LV free wall rupture present?

A
  1. Occurs in 3% MIs and occurs around 1-2 weeks afterwards

2. Present with acute failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)

428
Q

Mx of LV free wall rupture?

A

Urgent pericardiocentesis and thoracotomy

429
Q

What causes acute MR post-MI?

A

More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle

430
Q

What should be avoided in RV MI?

A

Nitrates, due to causing reduced preload

431
Q

Acute RV dysfunction triad?

A
  1. Clear lung fields
  2. JVP distension
  3. Hypotension
432
Q

RV MI occurs in what percentage of inferior MI?

A

30-50%

433
Q

Hypertension in diabetics 1st lin?

A

ACEi

434
Q

HTN aims for T1DM?

A

Intervention levels for recommending blood pressure management should be 135/85 mmHg unless the adult with type 1 diabetes has albuminuria or 2 or more features of metabolic syndrome, in which case it should be 130/80 mmHg

435
Q

ICD and HGV licence?

A

Loss of license

436
Q

Angipoplasty DVLA?

A

1 week off

437
Q

CABG DVLA?

A

4 weeks off

438
Q

ACS DVLA?

A

4 weeks off, 1 week off if succesfully treated by angioplasty

439
Q

Heart transplant DVLA?

A

6 weeks off

440
Q

ICD DVLA?

A
  1. If implanted for sustained ventricular arrhythmia: cease driving for 6 months
    if implanted prophylactically then cease driving for 1 month. 2. Having an ICD results in a permanent bar for Group 2 drivers
441
Q

Pacemaker DVLA?

A

1 week off

442
Q

Aortic aneurysm DVLA?

A
  1. > 6.5cm disqualified

2. >6cm = notify DVLA, annueal review

443
Q

SVT prophylaxis in pregnancy?

A

Metoprolol

444
Q

Following electrical cardioversion for AF, how long should pts be anticoagulated for?

A

At least 4 weeks

445
Q

Most accurate way to assess LVEF?

A

MUGA Scan

446
Q

Williams syndrome cardiac association?

A

Supravalvular aortic stenosis

447
Q

Features of complete heart block?

A
  1. Syncope
  2. HF
  3. Regular bradycardia (30-50bpm)
  4. Wide pulse pressure
  5. JVP = cannon waves in neck
  6. Variable Intensity of S1
448
Q

1st degree HB?

A

PR interval > 0.2s

449
Q

2nd degree HB?

A
  1. Type I (Mobitz I, Wenckebach) = progressive prolongation of the PR interval until a dropped beat occurs
  2. Type II (Mobitz II) = PR interval is constant but the p wave is often not followed by a QRS comples
450
Q

3rd degree HB?

A

No association between p waves and QRS complexes

451
Q

What is the J point on ECG?

A

The point at which the S wave ascends to meet the isoelectric line

452
Q

Indications for ETT?

A
  1. Assessing pts with suspected angina
  2. Risk stratifying pts following MI
  3. Assessing ET
  4. Risk stratifying pts with HOCM
453
Q

ETT S&S for IHD?

A
  1. Sensitivity = 80%

2. Specificity = 70%

454
Q

Max HR for ETT?

A
  1. 220 - patient’s age
  2. The target heart rate is at least 85% of maximum predicted to allow reasonable interpretation of test as low risk or negative
455
Q

C/I for ETT?

A
  1. MI < 7 days ago
  2. Unstable angina
  3. Uncontrolled hyper/hypotension (SBP > 180mmHg or SBP <90mmHg)
  4. AS
  5. LBBB (would make ECG difficult to interpret)
456
Q

When to stop ETT?

A
  1. exhaustion / patient request
    ‘severe’, ‘limiting’ chest pain
  2. > 3mm ST depression
  3. > 2mm ST elevation
  4. Stop if rapid ST elevation and pain
  5. Systolic blood pressure > 230 mmHg
  6. Systolic blood pressure falling > 20 mmHg
  7. Attainment of maximum predicted heart rate
  8. Heart rate falling > 20% of starting rate
  9. Arrhythmia develops
457
Q

4 ADP receptor inhibitors?

A
  1. Clopidogrel
  2. Prasugrel
  3. Ticagrelor
  4. Ticlodipine
458
Q

Why are prasugrel and ticagrelor now being used more commonly?

A

Due to its interindividual variability in antipaltelet effects

459
Q

What is NICE DAPT atm?

A

Aspirin 75mg OD and Ticagrelor 90mg BD

460
Q

Clopigrel interaction?

A
  1. With PPIs, particularly omeprazole and esomeprazole, leading to reduced antiplatelet effects
461
Q

C/I for prasugral use?

A
  1. Prior stroke or TIA
  2. High risk of bleeding
  3. Prasugrel hypersensitivity
462
Q

C/I for ticagrelor use?

A
  1. High risk of bleeding
  2. Prior intracranial haemorrhage
  3. Severe hepatic dysfunction
463
Q

Caution for ticagrelor use?

A

In Asthma and COPD, as ticagrelor-treated patients experience higher rates of dyspnoea

464
Q

Classes of drugs used to treat negative response to acute vasodilator testing PAH?

A
  1. Prostacyclin analogues = treprostinil, iloprost
  2. Endothelin receptor antagonist = bosentan, ambrisentan
  3. PDE inhibitors = sildenafil
465
Q

Features of tricuspid regurgitation?

A
  1. Pan-systolic murmur
  2. Prominent/giant V waves in JVP
  3. Pulsatile hepatomegaly
  4. Left parasternal heave
466
Q

Causes of tricuspid regurgitation?

A
  1. RV infarction
  2. Pulm HTN e.g. COPD
  3. Rheumatic heart disease
  4. IE
  5. Ebstein’s Anomaly
  6. Carcinoid syndrome
467
Q

Post-stroke AF management?

A
  1. Warfarin/DOAC should be started after 2 weeks (in the absence of haemorrhage)
  2. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed
468
Q

Most common cause of restrictive cardiomyopathy in the UK?

A

Amyloidosis secondary to myeloma

469
Q

Causes of restrictive cardiomyopathy?

A

PLEASSH

  1. Post-radiation fibrosis
  2. Loffler’s syndrome
  3. Endocardial fibroelastosis
  4. AMYLOIDOSIS
  5. Sarcoidosis
  6. Scleroderma
  7. Haemochromatosis
470
Q

What is Loffler’s syndrome?

A

Endomyocardial fibrosis with a prominent eosinophilic infiltrate

471
Q

What is endocardial fibroelastosis?

A

Thick fibroelastic tissue forms in the endocardium, most commonly seen in young chidlren

472
Q

Pathophysiology of restrictive cardiomyopathy?

A
  1. Primarily characterised by decreased compliance of the ventricular endomyocardium
  2. Causes predominantly diastolic dysfunction
473
Q

Features of restrictive cardiomyopathy?

A
  1. Similar to constrictive pericarditis

2. Low voltage ECG

474
Q

Ix for restrictive cardiomyopathy?

A
  1. Echo

2. Cardiac MRI

475
Q

Features suggesting restrictive cardiomyopathy rather than constrictive pericarditis?

A
  1. Prominent apical pulse
  2. Absence of pericardial calcification on CXR
  3. Heart may be enlarged
  4. ECG abnormalities = BBB, Q waves
476
Q

What is Eisenmenger’s syndrome?

A

Reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension

477
Q

Pathophysiology of eisenmenger’s syndrome?

A

When uncorrected left to right shunt leads to remodelling of the pulmonary vasculature, eventually causing obstruction to the pulmonary blood and pulmonary hypertension

478
Q

3 associations of eisenmenger’s syndrome?

A
  1. ASD
  2. VSD
  3. PDA
479
Q

Features of eisenmenger’s syndrome?

A
  1. Original murmur may disappear
  2. Cyanosis
  3. Clubbing
  4. RV Failure
  5. Haemoptysis, embolism
480
Q

Mx of eisenmenger’s syndrome?

A

Heart-lung transplantation is required

481
Q

Soft S2?

A

AS

482
Q

Loud S2?

A

HTN

483
Q

Fixed split S2?

A

ASD

484
Q

Reversed split S2?

A

LBBB

485
Q

Hypercalcaemia ECG abnormality?

A

Short QT interval

486
Q

Severe hypercalcaemia ECG findings?

A

Osborne (J) waves

487
Q

Features of hypercalcaemia?

A
  1. ‘Bones, stones, groans and psychic moans’
  2. Corneal calcification
  3. Shortened QT interval on ECG
  4. Hypertension
488
Q

Cannon A waves?

A

Complete heart block and atrial flutter

489
Q

Absent A waves?

A

AF

490
Q

Slow Y descent?

A

Tricuspid stenosis or cardiac tamponase

491
Q

Exaggerated X descent?

A

Constrictive pericarditis

492
Q

Abciximab MOA?

A

Glycoprotein IIb/IIIa inhibitor

493
Q

Dabigatran MOA?

A

Direct thrombin inhibitor

494
Q

Dabigatran indications?

A
  1. Prophylaxis of VTE in pts following hip or knee replacement surgery
    2 Prevention of stroke in pts with non-valvular AF who have further risk factors (CBA)
495
Q

Dabigatran s/e?

A
  1. Haemorrhage

2. Dose should be reduced in CKD and not prescribed if creatinine clearance is <30ml/min

496
Q

Rapid reversal of dabigatran?

A

Idarucizumab

497
Q

RE-ALIGN study?

A

Significantly higher bleeding and thrombotic events in patients with recent mechanical heart valve replacement using dabigatran compared with warfarin

498
Q

Pregnancy effect on BP?

A

Falls in first half of pregnancy (continues to fall until 20-24 weeks) before rising to pre-pregnancy levels before term

499
Q

Pregnancy HTN definition?

A
  1. Systolic > 140 mmHg or diastolic > 90 mmHg

2. Increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic

500
Q

Pregnancy HTN classification?

A
  1. Pre-existing hypertension
  2. Pregnancy-induced hypertension
  3. Pre-eclampsia

MRCP Part 1 (4 decks)

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