Cardiology

Question 1

Mechanism of ACEi?

Answer 1

inhibit the conversion angiotensin I to angiotensin II
ACE inhibitors are activated by phase 1 metabolism in the liver

Question 2

What are the side effects of ACEi?

Answer 2

Cough (15% - Bradykinin)
Angioedema: may occur up to a year after starting treatment
Hyperkalaemia
First-dose hypotension: more common in patients taking diuretics

Question 3

Cautions and contraindications of ACEi?

Answer 3

Pregnancy and breastfeeding - avoid
Renovascular disease (e.g. renal artery stenosis)
Aortic stenosis - may result in Hypotension
Hereditary of idiopathic angioedema
Potassium > 5

Question 4

What are acceptable U&E changes when starting ACEi?

Answer 4

Creatinine rise of 30% from baseline
Increase in potassium up to 5.5

Question 5

Outcomes of formation of coronary atheroma?

Answer 5

1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.

Question 6

What are unmodifiable risk factors for ischaemic heart disease?

Answer 6

Increasing age
Male gender
Family history

Question 7

What are modifiable risk factors for ischaemic heart disease?

Answer 7

Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity

Question 8

Stages of atheroma formation?

Answer 8

1. Initial endothelial dysfunction
2. Results in pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
3. Fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
4. Monocytes migrate from the blood and differentiate into macrophages.
   5.These macrophages then phagocytose oxidized LDL - propagate the inflammatory process.
5. Smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

Question 9

Anterior leads and artery?

Answer 9

V1-V4
LAD

Question 10

Inferior leads and artery?

Answer 10

II, III, aVF
Right coronary

Question 11

Lateral leads and artery?

Answer 11

I, V5-6
Left circumflex

Question 12

Management of STEMI?

Answer 12

Aspirin + second anti platelet
PCI

Question 13

Secondary prevention in STEMI?

Answer 13

Aspirin
Second antiplatelet if appropriate (e.g. clopidogrel)
Beta-blocker
ACE inhibitor
Statin

Question 14

ECG STEMI criteria?

Answer 14

2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)

Question 15

When should PCI be attempted?

Answer 15

1. Should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
2. If patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered

Question 16

What do patients require with PCI and radial access?

Answer 16

unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)

Question 17

What do patients require with PCI and femoral access?

Answer 17

bivalirudin with bailout GPI

Question 18

Mnx of NSTEMI?

Answer 18

Question 19

How is the grace score calculated?

Answer 19

Predicts mortality in 3 months

age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

<1.5 - low
3-6 intermediate
>9% - high

Question 20

What grace score NSTEMI patient should get a follow up PCI?

Answer 20

> 3%
Or clinically unstable

Question 21

Choice of second line antipaltelet in NSTEMI ?

Answer 21

if the patient is not at a high risk of bleeding: ticagrelor
if the patient is at a high risk of bleeding: clopidogrel

Question 22

What is the Killip risk stratification?

Answer 22

Stratifies 30 mortality risk post MI

Killip class Features 30 day mortality

I No clinical signs heart failure 6%
II Lung crackles, S3 17%
III Frank pulmonary oedema 38%
IV Cardiogenic shock 81%

Question 23

Features of acute pericarditis?

Answer 23

chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia

Question 24

Causes of pericarditis?

Answer 24

viral infections (Coxsackie)
tuberculosis
uraemia (causes ‘fibrinous’ pericarditis)
trauma
post-myocardial infarction, Dressler’s syndrome
connective tissue disease
hypothyroidism
malignancy

Question 25

ECG changes in pericarditis?

Answer 25

Global ST saddle shaped elevation

Question 26

How should pericarditis be treated?

Answer 26

Colchicine + NSAID

Question 27

In which patients should adenosine be avoided?

Answer 27

Ashtmatics - bronchospasm

Question 28

What drugs enhance adenosine? What drug reduces the effect of adenosine?

Answer 28

Enhances: dipyridamole (antiplatelet agent) Diminish: Theophylline

Question 29

What is the mechanism of action of adenosine?

Answer 29

1. Causes transient heart block in the AV node 2. Agonist of the A1 receptor in the atrioventricular node. 3. Inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux Adenosine has a very short half-life of about 8-10 seconds

Question 30

Side effects of adenosine?

Answer 30

Chest pain Bronchospasm Transient flushing Can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

Question 31

What are examples of ADP inhibitors?

Answer 31

Clopidogrel Prasugrel Ticagrelor Ticlopidine

Question 32

What is the mechanism of ADP inhibitors?

Answer 32

1. Adenosine diphosphate (ADP) is one of the main platelet activation factors, mediated by G-coupled receptors P2Y1 and P2Y12. 2. The main target of ADP receptor inhibition is the P2Y12 receptor, as it is the one which leads to sustained platelet aggregation and stabilisation of the platelet plaque. 3. Inhibitors block this

Question 33

Which ADP inhibitors should be considered in high risk patients?

Answer 33

Long term complications reduced with prasugel + aspirin rather than clopidogrel

Question 34

How long should high risk PCI patients continue DAPT for?

Answer 34

12 months post acute coronary syndrome (medically managed): add ticagrelor to aspirin, stop ticagrelor after 12 months post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months

Question 35

Side effect of ticagrelor?

Answer 35

Dyspnoea Impaired clearance of adenosine

Question 36

What are absolute contraindications for prasugrel? What should you use instead?

Answer 36

Stroke TIA High risk bleeding Ticagrelor. IF NOT THEN CLOPI

Question 37

What are contraindications for ticagrelor?

Answer 37

high risk of bleeding, those with a history of intracranial haemorrhage, and those with severe hepatic dysfunction caution in asthmatics and COPD

Question 38

What are the shockable rhythms?

Answer 38

VF Pulseless VT

Question 39

In non-shockable rhythms, when should adrenaline be given?

Answer 39

adrenaline 1 mg as soon as possible for non-shockable rhythms

Question 40

When should adrenaline be given in shockable rhythms?

Answer 40

After third shock repeat adrenaline 1mg every 3-5 minutes whilst ALS continues 1ml of 1;1000

Question 41

When should amiodarone be given in shockable rhythms?

Answer 41

300 mg After third shock 300mg after fifth shock

Question 42

When should thrombolytic drugs be considered in CPR?

Answer 42

If attempts are 60-90 mins

Question 43

What are the H's?

Answer 43

Hypoxia Hypovolaemia Hypothermia Hyperkalaemia

Question 44

What are the T's?

Answer 44

Toxins Tamponade Thrombosis Tension pneumothorax

Question 45

Mechanism of amiodarone?

Answer 45

Class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. Blocks potassium channels that inhibit repolarisation Prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)

Question 46

Issues with amiodarone?

Answer 46

- Long half life 20-100 days - Give into central veins, causes thrombophlebitis - Can be pro arrhythmic, as prolongs QT - P450 inhibitor

Question 47

Side effects of amiodarone?

Answer 47

thyroid dysfunction: both hypothyroidism and hyper-thyroidism corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity 'slate-grey' appearance thrombophlebitis and injection site reactions bradycardia lengths QT interval

Question 48

Medical management of angina?

Answer 48

1. Aspirin 2. GTN 3. Consider beta blocker or CCB first line. - If mono therapy CCB then use diltiazem / verapamil - If used with beta blocker, CCb must be dihydroperidine 4. Titrate up doses if poor response rate

Question 49

What adjunct medication can be added in for angina?

Answer 49

a long-acting nitrate ivabradine nicorandil ranolazine only add a third drug whilst a patient is awaiting assessment for PCI or CABG

Question 50

How should nitrates be prescribed?

Answer 50

asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate

Question 51

Mechanism of angiotensin receptor blockers?

Answer 51

block effects of angiotensin II at the AT1 receptor

Question 52

Treatment of anti platelets and duration in medical treated MI?

Answer 52

Aspirin (lifelong) & ticagrelor (12 months) If aspirin contraindicated, clopidogrel (lifelong)

Question 53

Treatment of anti platelets and duration in PCI?

Answer 53

Aspirin (lifelong) & prasurgrel or ticagrelor (12 months) If aspirin contraindicated, clopidogrel (lifelong)

Question 54

Treatment of anti platelets and duration in TIA?

Answer 54

1. Clopidogrel (lifelong) 2. Aspirin (lifelong) & dipyridamole (lifelong)

Question 55

Treatment of anti platelets and duration in ischaemic stroke?

Answer 55

1. Clopidogrel (lifelong) 2. Aspirin (lifelong) & dipyridamole (lifelong)

Question 56

Treatment of anti platelets and duration in peripheral vascular disease?

Answer 56

1. Aspirin 2. Clopidogrel

Question 57

Features of aortic dissection

Answer 57

Sharp tearing pain - chest pain type A - back pain type B Pulse deficit - absent brachial, carotid, femoral - > 20 mmHg drop Aortic regurgitation If involved: coronary arteries → angina spinal arteries → paraplegia distal aorta → limb ischaemia

Question 58

How are aortic dissections classified?

Answer 58

type A - ascending aorta, 2/3 of cases type B - descending aorta, distal to left subclavian origin, 1/3 of cases

Question 59

ECG changes in aortic dissection?

Answer 59

In a minority of patients, ST-segment elevation may be seen in the inferior leads

Question 60

Risk factors for aortic dissection ?

Answer 60

hypertension: the most important risk factor trauma bicuspid aortic valve collagens: Marfan's syndrome, Ehlers-Danlos syndrome Turner's and Noonan's syndrome pregnancy syphilis

Question 61

What investigations should be done for aortic dissection?

Answer 61

CXR --> widened mediastinum CT angiography of the chest, abdomen and pelvis is the investigation of choice suitable for stable patients and for planning surgery a false lumen is a key finding in diagnosing aortic dissection Transoesophageal echocardiography (TOE) more suitable for unstable patients who are too risky to take to CT scanner

Question 62

What is the management of Type A aortic dissection?

Answer 62

Surgical keep BP 100-120 - labetaolol

Question 63

Causes of aortic regurgitation due to valve disease?

Answer 63

Rheumatic fever: the most common cause in the developing world calcific valve disease Infective endocarditis Connective tissue diseases e.g. Rheumatoid arthritis/SLE Bicuspid aortic valve (affects both the valves and the aortic root)

Question 64

Causes of aortic regurgitation due to aortic root disease?

Answer 64

Bicuspid aortic valve (affects both the valves and the aortic root) Aortic dissection Spondylarthropathies (e.g. ankylosing spondylitis) Hypertension Syphilis Marfan's, Ehler-Danlos syndrome

Question 65

Clinical findings of aortic regurgitation?

Answer 65

Early diastolic murmur (increases with handgrip ) Collapsing pulse Wide pulse pressure 1. Quincke's sign (nailbed pulsation) 2. De Musset's sign (head bobbing) mid-diastolic Austin-Flint murmur in 3. severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

Question 66

What are indications for treatment of aortic regurgitation?

Answer 66

surgery: aortic valve indications include symptomatic patients with severe AR asymptomatic patients with severe AR who have LV systolic dysfunction

Question 67

Symptoms associated with aortic stenosis?

Answer 67

Chest pain Dyspnoea Syncope / presyncope (e.g. exertional dizziness) murmur an ejection systolic murmur (ESM) is classically seen in aortic stenosis classically radiates to the carotids this is decreased following the Valsalva manoeuvre

Question 68

Features of severe aortic stenosis?

Answer 68

narrow pulse pressure slow rising pulse delayed ESM soft/absent S2 S4 thrill left ventricular hypertrophy or failure Displaced apex beat

Question 69

Causes of aortic stenosis?

Answer 69

Degenerative calcification (most common cause in older patients > 65 years) Bicuspid aortic valve (most common cause in younger patients < 65 years) William's syndrome (supravalvular aortic stenosis) post-rheumatic disease subvalvular: HOCM

Question 70

When should aortic stenosis be treated?

Answer 70

If symptomatic valve replacement if asymptomatic but > 40 mmHg consider valve surgery

Question 71

What surgical options are there for aortic stenosis?

Answer 71

AVR surgical replacement in younger people CVS may be co-existant - should complete angiogram Balloon valvuloplasty used in children

Question 72

What is arrhythmogenic right ventricular cardiomyopathy (ARVC) ?

Answer 72

Autosomal dominant condition Right ventricle myocardium replaced by fatty / fibrous tissue

Question 73

What is the typical mutation in ARVC?

Answer 73

Desomosomal

Question 74

ECG changes notably seen on ARVC?

Answer 74

ECG abnormalities in V1-3, typically T wave inversion. Epsilon wave

Question 75

What echo changes as seen in ARVC?

Answer 75

- Thin walled right ventricle - Hypokinetic right ventricle -

Question 76

Best imaging for ARVC?

Answer 76

Cardiac MRI

Question 77

Management of ARVC

Answer 77

drugs: sotalol is the most widely used antiarrhythmic catheter ablation to prevent ventricular tachycardia implantable cardioverter-defibrillator

Question 78

What is Naxos disease?

Answer 78

an autosomal recessive variant of ARVC a triad of ARVC, palmoplantar keratosis, and woolly hair

Question 79

Define paroxysmal AF?

Answer 79

Self terminating episodes of AF

Question 80

Define persistent AF?

Answer 80

arrhythmia is not self-terminating > 7 days

Question 81

What is permanent AF?

Answer 81

Persistent AF - despite cardioversion

Question 82

How is AF managed?

Answer 82

Rate control - Beta blocker or diltiazem Rhythm control - Digoxin after rate control failed Then try combination of beta blocker, diltazem or digoxin Assess if anticoagulation is needed

Question 83

When can cardioverion be carried out?

Answer 83

Anticoagulated for 3 weeks prior to cardioversion AF for only 48 hours

Question 84

What is the CHAD VASC score?

Answer 84

C Congestive heart failure 1 H Hypertension (or treated hypertension) 1 A2 Age >= 75 years 2 Age 65-74 years 1 D Diabetes 1 S2 Prior Stroke, TIA or thromboembolism 2 V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1 S Sex (female) 1

Question 85

What CHAD VASC score merit anticoagulation?

Answer 85

1: If male anticoagulant. If female do not 2 or more: Anticoagulant

Question 86

How should assessment of bleeding risk be carried out?

Answer 86

ORBIT scoring system: Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females 2 Age > 74 years 1 Bleeding history (GI bleeding, intracranial bleeding or haemorrhagic stroke) 2 Renal impairment (GFR < 60 mL/min/1.73m2) 1 Treatment with antiplatelet agents 1 Provides risk of bleeding out of 100

Question 87

What type of anticoagulant should be used in AF?

Answer 87

First line: DOAC Second line: Warfarin

Question 88

Types of cardioversion and indications?

Answer 88

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

Question 89

How long should a patient be anti coagulated post cardioversion?

Answer 89

4 Weeks

Question 90

what agents can cardiovert AF?

Answer 90

Amiodarone Felcanide ( If not structural heat disease) Less effective agents beta-blockers (including sotalol) calcium channel blockers digoxin disopyramide procainamide

Question 91

When should you anticoagulant in TIA?

Answer 91

Immediately once imaging has excluded haemorrhage

Question 92

In acute stroke patients when should anticoagulation start?

Answer 92

Start after 2 weeks - anti platelet therapy should be started Large strokes may need to delay

Question 93

What does the rate of atrial flutter depend on ?

Answer 93

Degree of AV block

Question 94

What is the management of atrial flutter?

Answer 94

Same as AF - although less effective Cardioversion requires less joules Radiofrequency ablation of tricuspid valve isthmus is curative

Question 95

What are the echo findings of a atrial myxoma?

Answer 95

Auscultation: Mid-diastolic + Tumour plop pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum (Commonly left atrium)

Question 96

What is the most common congenital abnormality found in adulthood?

Answer 96

Atrial septal defect - Osmium secundum is the most common

Question 97

What is osmium secundum and osmium primum ASD?

Answer 97

Ostium primum: The septum Primus does not grow down completely Osmium secundum: The septum does not close (foramen oval valve to rostrum secundum does not close at birth)

Question 98

Murmur associated what ASD?

Answer 98

ejection systolic murmur, fixed splitting of S2

Question 99

Complications with ASD?

Answer 99

embolism may pass from venous system to left side of heart causing a stroke

Question 100

ECG changes and features of ostium Primus ASD?

Answer 100

Ostium primum present earlier than ostium secundum defects associated with abnormal AV valves ECG: RBBB with LAD, prolonged PR interval

Question 101

ECG changes and features of ostium secundum ASD?

Answer 101

Ostium secundum (70% of ASDs) associated with Holt-Oram syndrome (tri-phalangeal thumbs) ECG: RBBB with RAD

Question 102

What is atrioventricular block ?

Answer 102

atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles. There are three types

Question 103

Features of first degree heart block?

Answer 103

PR interval > 0.2 seconds asymptomatic first-degree heart block is relatively common and does not need treatment

Question 104

Types of type 2 AV node block?

Answer 104

type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

Question 105

Features of complete heart block?

Answer 105

there is no association between the P waves and QRS complexes

Question 106

Mechanism of atropine?

Answer 106

Muscarinic receptor antagonist - Used in bradycardia - Used in organophosphate poisoning

Question 107

Side effects of atropine?

Answer 107

tachycardia mydriasis atropine may trigger acute angle-closure glaucoma in susceptible patients

Question 108

What produces BNP and what is it effect?

Answer 108

Left ventricle myocardium Diuretic Suppresses renin-angiotensn system Vasodilator

Question 109

What level of BNP makes heart failures unlikely?

Answer 109

< 100

Question 110

Side effects of beta blockers?

Answer 110

bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction

Question 111

Contraindications of beta blockers?

Answer 111

uncontrolled heart failure asthma sick sinus syndrome concurrent verapamil use: may precipitate severe bradycardia

Question 112

Features of bicuspid aortic valve?

Answer 112

Normally asymptomatic in childhood Normally patients get aortic stenosis or regard

Question 113

Associations with bicuspid aortic valve

Answer 113

Left dominant coronary artery system Turner's syndrome

Question 114

Features suggesting VT rather than SVT with aberrant conduction?

Answer 114

AV dissociation fusion or capture beats positive QRS concordance in chest leads marked left axis deviation history of IHD lack of response to adenosine or carotid sinus massage QRS > 160 ms

Question 115

Inheritance in burgada syndrome? Most common mutation?

Answer 115

Autosomal dominant Mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein

Question 116

ECG features of brugada syndrome?

Answer 116

convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave partial right bundle branch block the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome

Question 117

Management in brugara?

Answer 117

Implantable cardiac defibrillator

Question 118

What is Buerger disease?

Answer 118

Middle vessel vasculitis Strong association with smoking Extremity ischaemia - intermittent claudication - ischaemic ulcers superficial thrombophlebitis Raynaud's phenomenon

Question 119

O2 saturations through cardiac circuit?

Answer 119

The right atrium (RA), right ventricle (RV) and pulmonary artery (PA) normally have oxygen saturation levels of around 70% the lungs oxygenate the blood to a level of around 98-100%. The left atrium (LA), left ventricle (LV) and aorta should all, therefore, have oxygen saturation levels of 98-100%

Question 120

How would ASD affect O2 saturations in cardiac circuit?

Answer 120

Higher O2 saturtions in RA 85%

Question 121

How would VSD affect O2 saturations in cardiac circuit?

Answer 121

High O2 saturations in RV 85%

Question 122

What cardiac markers can be used, instead of troponin ?

Answer 122

Myoglobin CK-MB CK Trop T AST LDH

Question 123

What is the first cardiac marker to rise?

Answer 123

Myoglobin

Question 124

What cardiac marker should be used if consider re-infarction?

Answer 124

CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)

Question 125

What is a SPECT scan used for in cardiac imaging?

Answer 125

assess myocardial perfusion and myocardial viability Identify areas of ischaemia

Question 126

What is MUGA used for ?

Answer 126

Multi Gated Acquisition Scan, also known as radionuclide angiography radionuclide (technetium-99m) is injected intravenously the patient is placed under a gamma camera may be performed as a stress test can accurately measure left ventricular ejection fraction. Typically used before and after cardiotoxic drugs are used

Question 127

What is a cardiac CT used for?

Answer 127

Calcium score Correlation between plaque and future ischaemic event Allow view of coronary artery lumen

Question 128

Best imaging for structural heart disease?

Answer 128

Cardiac MRI Myocardial perfusion can also be done by gadolinium

Question 129

What are the features of cardiac tamponade?

Answer 129

Classical features - Beck's triad: hypotension raised JVP muffled heart sounds an absent Y descent on the JVP - this is due to the limited right ventricular filling pulsus paradoxus - an abnormally large drop in BP during inspiration Kussmaul's sign - much debate about this ECG: electrical alternans

Question 130

Cardiac tamponade vs constrictive pericarditis?

Answer 130

Cardiac tamponade Constrictive pericarditis JVP Absent Y descent X + Y present Pulsus paradoxus Present Absent Kussmaul's sign Rare Present Characteristic features / Pericardial calcification on CXR

Question 131

Features of hypertrophic obstructive cardiomyopathy?

Answer 131

Leading cause of sudden cardiac death in young athletes Usually due to a mutation in the gene encoding β-myosin heavy chain protein Common cause of sudden death Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy

Question 132

Features of Arrhythmogenic right ventricular dysplasia?

Answer 132

Right ventricular myocardium is replaced by fatty and fibrofatty tissue Around 50% of patients have a mutation of one of the several genes which encode components of desmosome ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS comple

Question 133

Caused of dilated cardiomyopathy?

Answer 133

Classic causes include alcohol Coxsackie B virus wet beri beri doxorubicin Selenium deficiecny

Question 134

Causes of restrictive cardiomyopathy?

Answer 134

Classic causes include amyloidosis post-radiotherapy Loeffler's endocarditis

Question 135

Features of permpartum cardiomyopathy?

Answer 135

Typical develops between last month of pregnancy and 5 months post-partum More common in older women, greater parity and multiple gestations

Question 136

Features of takotsubo cardiomyopathy?

Answer 136

Stress'-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure Transient, apical ballooning of the myocardium Treatment is supportive

Question 137

Infective causes of cardiomyopathy?

Answer 137

Coxsackie B virus Chagas disease

Question 138

Infiltrative causes of cardiomyopathy?

Answer 138

Amyloidosis

Question 139

Storage causes of cardiomyopathy?

Answer 139

Haemochromatosis

Question 140

Toxicity causes of cardiomyopathy?

Answer 140

Alcohol Doxorubicin

Question 141

Inflammatory causes of cardiomyopathy?

Answer 141

Sarcoidosis

Question 142

Endocrine causes of cardiomyopathy?

Answer 142

Diabetes mellitus Thyrotoxicosis Acromegaly

Question 143

Nutritional causes of cardiomyopathy?

Answer 143

Wet Beriberi (thiamine)

Question 144

Autoimmune causes of cardiomyopathy?

Answer 144

SLE

Question 145

Features of Catecholaminergic polymorphic ventricular tachycardia

Answer 145

Autosomal dominant defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope sudden cardiac death symptoms generally develop before the age of 20 years

Question 146

Management of catecholaminergic polymorphic VT ?

Answer 146

beta-blockers implantable cardioverter-defibrillator

Question 147

Centrally acting anti-hypertensives?

Answer 147

methyldopa: used in the management of hypertension during pregnancy moxonidine: used in the management of essential hypertension when conventional antihypertensives have failed to control blood pressure clonidine: the antihypertensive effect is mediated through stimulating alpha-2 adrenoceptors in the vasomotor centre

Question 148

Chronic heart failure medication?

Answer 148

1. ACEI + Beta blocker 2. Adjunct Aldosterone antagonist Third line: Ivabradine Digoxin Sacubitril-valsartan Hydralazine Cardiac resychronisation therapy ( biventricular pacing)

Question 149

Criteria for ivabradine in heart failure?

Answer 149

criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%

Question 150

Criteria for sucubitril valsartan?

Answer 150

criteria: left ventricular fraction < 35% is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs should be initiated following ACEi or ARB wash-out period

Question 151

What vaccinations should be commenced in heart failure?

Answer 151

annual flue One off pneumococcal

Question 152

In preserved LV heart failure, do ACEI and beta blocker work?

Answer 152

No

Question 153

Features of cholesterol embolism?

Answer 153

eosinophilia purpura renal failure livedo reticularis

Question 154

Indication CRT in heart failure?

Answer 154

For patients with heart failure and wide QRS Not tolerating medical conersvative management

Question 155

NYHA classifcation of heart failure?

Answer 155

NYHA Class I no symptoms no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations NYHA Class II mild symptoms slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea NYHA Class III moderate symptoms marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms NYHA Class IV severe symptoms unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

Question 156

What drug class of clopidogrel belong to?

Answer 156

thienopyridine prasugrel ticagrelor ticlopidine

Question 157

Mechanism of action of clopiodgrel?

Answer 157

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

Question 158

Acceptable PPI use in antiplatelets?

Answer 158

Lansoprazole

Question 159

Features of coarctation of the aorta?

Answer 159

infancy: heart failure adult: hypertension radio-femoral delay mid systolic murmur, maximal over back apical click from the aortic valve notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

Question 160

Associations of coarctation?

Answer 160

Turner's syndrome bicuspid aortic valve berry aneurysms neurofibromatosis

Question 161

If a patient has an MI, and is anticoagulated. How long should they remain on anticoagulation and antiplatelet?

Answer 161

triple therapy (2 antiplatelets + 1 anticoagulant) for 4 weeks-6 months after the event and dual therapy (1 antiplatelet + 1 anticoagulant) to complete 12 months

Question 162

How to manage VTE while on DAPT?

Answer 162

an ORBIT score should be calculated. Those with a low risk of bleeding may continue antiplatelets. In patients with an intermediate or high risk of bleeding consideration should be given to stopping the antiplatelets

Question 163

Causes of constrictive pericarditis?

Answer 163

any cause of pericarditis particularly TB

Question 164

What is the eponymous sign for constrictive pericarditis?

Answer 164

Kussmaul's sign - rise in JVP on inspiration

Question 165

Features of constrictive pericarditis?

Answer 165

dyspnoea right heart failure: elevated JVP, ascites, oedema, hepatomegaly JVP shows prominent x and y descent pericardial knock - loud S3 Kussmaul's sign is positive

Question 166

Explain the coronary vasculature?

Answer 166

left aortic sinus → left coronary artery (LCA) right aortic sinus → right coronary artery (RCA) LCA → LAD + circumflex RCA → posterior descending RCA supplies SA node in 60%, AV node in 90% Coronary arteries fill in diastole

Question 167

Mechanism of dabigitran ?

Answer 167

Direct thrombin inhibitor - Cannot be used in prosthetic heart valves - Reduce dose in kidney disease - Can be used in non-valvular AF

Question 168

What is the first line anti-hypertensive and diabetes?

Answer 168

ACEI / ARB

Question 169

Features of dilated cardiomyopathy?

Answer 169

classic findings of heart failure systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation S3 'balloon' appearance of the heart on the chest x-ray

Question 170

Cannot drive for how long post angioplasty (elective)?

Answer 170

angioplasty (elective) - 1 week off driving

Question 171

CABG how long off driving?

Answer 171

CABG - 4 weeks off driving

Question 172

Acute coronary syndrome with successful angioplasty - how long off driving?

Answer 172

4 weeks off driving if no angiplasty 1 week if angioplasty

Question 173

ICD how long off driving ?

Answer 173

6 months Having an ICD results in a permanent bar for Group 2 drivers

Question 174

What is ebstein anomaly?

Answer 174

congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle - Also referred to atrialisation

Question 175

If ebstein anomaly present what other associations are likely?

Answer 175

Patent foramen ovale or ASD in 80% Wolfe parking white

Question 176

Clinical features of ebstain anomaly?

Answer 176

cyanosis prominent 'a' wave in the distended jugular venous pulse, hepatomegaly tricuspid regurgitation pansystolic murmur, worse on inspiration right bundle branch block → widely split S1 and S2

Question 177

Causes of left deviation?

Answer 177

left anterior hemiblock left bundle branch block inferior myocardial infarction Wolff-Parkinson-White syndrome* - right-sided accessory pathway hyperkalaemia congenital: ostium primum ASD, tricuspid atresia minor LAD in obese people

Question 178

Causes of right axis deviation?

Answer 178

right ventricular hypertrophy left posterior hemiblock lateral myocardial infarction chronic lung disease → cor pulmonale pulmonary embolism ostium secundum ASD Wolff-Parkinson-White syndrome* - left-sided accessory pathway normal in infant < 1 years old minor RAD in tall people

Question 179

Posterior MI changes?

Answer 179

V1-V3 changes Reciprocal changes of STEMI are typically seen: horizontal ST depression tall, broad R waves upright T waves dominant R wave in V2 Must confirm in positions V7-9

Question 180

ECG changes in digoxin toxicity?

Answer 180

down-sloping ST depression ('reverse tick', 'scooped out') flattened/inverted T waves short QT interval arrhythmias e.g. AV block, bradycardia

Question 181

ECG changes of hypokalaemia?

Answer 181

U waves small or absent T waves (occasionally inversion) prolong PR interval ST depression long QT U have no Pot and no T, but a long PR and a long QT

Question 182

ECG changes in hypothermia?

Answer 182

bradycardia 'J' wave (Osborne waves) - small hump at the end of the QRS complex first degree heart block long QT interval atrial and ventricular arrhythmias

Question 183

Causes of new LBBB?

Answer 183

myocardial infarction hypertension aortic stenosis cardiomyopathy rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

Question 184

What are sgarbossa criteria?

Answer 184

Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5) Concordant ST depression > 1 mm in V1-V3 (score 3) Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2) Score >3 - suggestive of MI

Question 185

Normal egg variations in an athlete?

Answer 185

sinus bradycardia junctional rhythm first degree heart block Mobitz type 1 (Wenckebach phenomenon)

Question 186

What is suggestive of P wave with increased amplitude?

Answer 186

Cor pulmonale

Question 187

P waves that are broad or notched? ( bifid)

Answer 187

often most pronounced in lead II a sign of left atrial enlargement, classically due to mitral stenosis

Question 188

What type of PR interval is seen in WPW?

Answer 188

Short PR interval

Question 189

Prolonged PR interval?

Answer 189

idiopathic ischaemic heart disease digoxin toxicity hypokalaemia* rheumatic fever aortic root pathology e.g. abscess secondary to endocarditis Lyme disease sarcoidosis myotonic dystrophy

Question 190

Causes of RBBB?

Answer 190

normal variant - more common with increasing age right ventricular hypertrophy chronically increased right ventricular pressure - e.g. cor pulmonale pulmonary embolism myocardial infarction atrial septal defect (ostium secundum) cardiomyopathy or myocarditis

Question 191

Causes of ST depression?

Answer 191

secondary to abnormal QRS (LVH, LBBB, RBBB) ischaemia digoxin hypokalaemia syndrome X

Question 192

ST elevation causes?

Answer 192

myocardial infarction pericarditis/myocarditis normal variant - 'high take-off' left ventricular aneurysm Prinzmetal's angina (coronary artery spasm) Takotsubo cardiomyopathy rare: subarachnoid haemorrhage

Question 193

T wave inversion?

Answer 193

myocardial ischaemia digoxin toxicity subarachnoid haemorrhage arrhythmogenic right ventricular cardiomyopathy pulmonary embolism ('S1Q3T3') Brugada syndrome

Question 194

?Peaked T waves

Answer 194

>5mm in limb leads >10mm in precordial hyperkalaemia myocardial ischaemia

Question 195

What are the features of eclampsia?

Answer 195

condition seen after 20 weeks gestation pregnancy-induced hypertension proteinuria

Question 196

Management of eclampsia?

Answer 196

Magnesium sulphate 4g over 5-10 minutes

Question 197

What is eisenmenger's syndrome?

Answer 197

reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

Question 198

Features of eisenmenger's reaction?

Answer 198

original murmur may disappear cyanosis clubbing right ventricular failure haemoptysis, embolism

Question 199

What are contraindications to exercise tolerance testing?

Answer 199

myocardial infarction less than 7 days ago unstable angina uncontrolled hypertension (systolic BP > 180 mmHg) or hypotension (systolic BP < 90 mmHg) aortic stenosis left bundle branch block: this would make the ECG very difficult to interpret

Question 200

Positive exercise tolerance test?

Answer 200

exhaustion / patient request 'severe', 'limiting' chest pain > 3mm ST depression > 2mm ST elevation.Stop if rapid ST elevation and pain systolic blood pressure > 230 mmHg systolic blood pressure falling > 20 mmHg attainment of maximum predicted heart rate heart rate falling > 20% of starting rate arrhythmia develops

Question 201

Physiological changes in exercise?

Answer 201

systolic increases, diastolic decreases leads to increased pulse pressure in healthy young people the increase in MABP is only slight increase in cardiac output may be 3-5 fold results from venous constriction, vasodilation and increased myocardial contractibility, as well as from the maintenance of right atrial pressure by an increase in venous return heart rate up to 3-fold increase stroke volume up to 1.5-fold increase

Question 202

How is heart failure define with ejection fraction?

Answer 202

Heart failure with reduced ejection fraction - < 35-40% (typically systolic dysfunction) Heart failure with preserved ejection fraction (typically diastolic dysfunction)

Question 203

Systolic dysfunction heart failure?

Answer 203

Ischaemic heart disease Dilated cardiomyopathy Myocarditis Arrhythmias

Question 204

Diastolic dysfunction heart failure?

Answer 204

Hypertrophic obstructive cardiomyopathy Restrictive cardiomyopathy Cardiac tamponade Constrictive pericarditis

Question 205

Features of left sided heart failure?

Answer 205

pulmonary oedema dyspnoea orthopnoea paroxysmal nocturnal dyspnoea bibasal fine crackles

Question 206

Features of right sided heart failure?

Answer 206

peripheral oedema ankle/sacral oedema raised jugular venous pressure hepatomegaly weight gain due to fluid retention anorexia ('cardiac cachexia')

Question 207

What does high output heart failure refer to?

Answer 207

High-output heart failure refers to a situation where a 'normal' heart is unable to pump enough blood to meet the metabolic needs of the body.

Question 208

Causes of high output heart failure?

Answer 208

anaemia arteriovenous malformation Paget's disease Pregnancy thyrotoxicosis thiamine deficiency (wet Beri-Beri)

Question 209

What causes heart sound 1 ?

Answer 209

closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis

Question 210

What causes heart sound 2 ?

Answer 210

closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal

Question 211

What causes heart sound 3?

Answer 211

caused by diastolic filling of the ventricle considered normal if < 30 years old (may persist in women up to 50 years old) heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

Question 212

What causes heart sound 4 ?

Answer 212

may be heard in aortic stenosis, HOCM, hypertension caused by atrial contraction against a stiff ventricle therefore coincides with the P wave on ECG in HOCM a double apical impulse may be felt as a result of a palpable S4

Question 213

Where should pulmonary valve be listened to?

Answer 213

Left second intercostal space, at the upper sternal border

Question 214

Where should aortic valve be listened to?

Answer 214

Right second intercostal space, at the upper sternal border

Question 215

Where should mitral valve be listened to ?

Answer 215

Left fifth intercostal space, just medial to mid clavicular line

Question 216

Where should tricuspid valve be listened to?

Answer 216

Left fourth intercostal space, at the lower left sternal border

Question 217

What causes a loud S1?

Answer 217

mitral stenosis left-to-right shunts short PR interval, atrial premature beats hyperdynamic states

Question 218

What causes a soft S1?

Answer 218

mitral regurgitation

Question 219

What causes a loud S2?

Answer 219

hypertension: systemic (loud A2) or pulmonary (loud P2) - loudest at pulmonary (P2) --> pulmonary hypertension - loudest at aortic(A2) --> systemic hypertension hyperdynamic states atrial septal defect without pulmonary hypertension

Question 220

What causes a soft S2?

Answer 220

Aortic stenosis

Question 221

What causes a split S2 ?

Answer 221

deep inspiration RBBB pulmonary stenosis severe mitral regurgitation

Question 222

Mechanism of hydralazine?

Answer 222

cGMP leading to smooth muscle relaxation in arterioles rather than veins

Question 223

Contraindicaitons for hydralazine?

Answer 223

systemic lupus erythematous ischaemic heart disease/cerebrovascular disease

Question 224

Adverse effects of hydralazine?

Answer 224

tachycardia palpitations flushing fluid retention headache drug-induced lupus

Question 225

What are the features of hypercalcaemia?

Answer 225

'bones, stones, groans and psychic moans' corneal calcification shortened QT interval on ECG hypertension

Question 226

Features and causes of eruptive xanthoma?

Answer 226

high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees) Causes of eruptive xanthoma familial hypertriglyceridaemia lipoprotein lipase deficiency

Question 227

Causes of tendon xanthoma?

Answer 227

familial hypercholesterolaemia remnant hyperlipidaemia

Question 228

When is aspirin used in pregnancy?

Answer 228

High risk pregnancies - from week 12 until birth hypertensive disease during previous pregnancies chronic kidney disease autoimmune disorders such as SLE or antiphospholipid syndrome type 1 or 2 diabetes mellitus

Question 229

Criteria for hypertension in pregnancy?

Answer 229

systolic > 140 mmHg or diastolic > 90 mmHg or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic

Question 230

Features of severe pre-eclampsia?

Answer 230

hypertension: typically > 160/110 mmHg and proteinuria as above proteinuria: dipstick ++/+++ headache visual disturbance papilloedema RUQ/epigastric pain hyperreflexia platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome

Question 231

Definition of pre-eclampsia?

Answer 231

Pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours) Oedema may occur but is now less commonly used as a criteria other organ involvement (see list below for examples): e.g. renal insufficiency (creatinine ≥ 90 umol/L), liver, neurological, haematological, uteroplacental dysfunction

Question 232

You get a high blood pressure reading... now what?

Answer 232

Question 233

What are stages of hypertension?

Answer 233

Stage 1: Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg Stage 2: Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg Stage 3: Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

Question 234

Features of phaechromocytoma?

Answer 234

labile or postural hypotension, headache, palpitations, pallor and diaphoresis

Question 235

How is a ambulatory blood pressure calculated?

Answer 235

2 blood pressures per hour Average of 14

Question 236

How should home blood pressure monitoring be completed?

Answer 236

for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated BP should be recorded twice daily, ideally in the morning and evening BP should be recorded for at least 4 days, ideally for 7 days discard the measurements taken on the first day and use the average value of all the remaining measurements

Question 237

Renal diseases that cause hypertension?

Answer 237

glomerulonephritis pyelonephritis adult polycystic kidney disease renal artery stenosis

Question 238

Endocrine causes of hypertension?

Answer 238

phaeochromocytoma Cushing's syndrome Liddle's syndrome congenital adrenal hyperplasia (11-beta hydroxylase deficiency) acromegaly

Question 239

Drug causes of hypertension?

Answer 239

steroids monoamine oxidase inhibitors the combined oral contraceptive pill NSAIDs leflunomide

Question 240

What is the pathophysiology in HOCM?

Answer 240

Autosomal dominant condition (generally) gene encoding β-myosin heavy chain protein or myosin-binding protein C results in predominantly diastolic dysfunction left ventricle hypertrophy → decreased compliance → decreased cardiac output characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes ('disarray') and fibrosis on biopsy

Question 241

Signs found in HOCM?

Answer 241

jerky pulse, large 'a' waves, double apex beat ejection systolic murmur increases with Valsalva manoeuvre and decreases on squatting hypertrophic cardiomyopathy may impair mitral valve closure, thus causing regurgitation

Question 242

What is HOCM associated with?

Answer 242

Friedreich's ataxia Wolff-Parkinson White

Question 243

Echo findings associated with HOCM?

Answer 243

MR SAM ASH mitral regurgitation (MR) systolic anterior motion (SAM) of the anterior mitral valve leaflet asymmetric hypertrophy (ASH)

Question 244

ECG changes of HOCM?

Answer 244

left ventricular hypertrophy non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen deep Q waves atrial fibrillation may occasionally be seen

Question 245

Indications for implantable defibrillators?

Answer 245

long QT syndrome hypertrophic obstructive cardiomyopathy previous cardiac arrest due to VT/VF testing and ejection fraction < 35% Brugada syndrome

Question 246

Best antihypertensive in afrocaribean diabetic firstling?

Answer 246

ARB

Question 247

How does blood pressure chain throughout pregnancy?

Answer 247

blood pressure usually falls in the first trimester (particularly the diastolic), and continues to fall until 20-24 weeks after this time the blood pressure usually increases to pre-pregnancy levels by term

Question 248

Management of HOCM?

Answer 248

Amiodarone Beta-blockers or verapamil for symptoms Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis*

Question 249

What drugs should be avoided in HOCM?

Answer 249

nitrates ACE-inhibitors inotropes ACE inhibitors can reduce afterload which may worsen the LVOT gradient. The patient in this scenario has the characteristic signs of HOCM on his echocardiogram; mitral regurgitation, systolic anterior motion of the anterior mitral valve leaflet, asymmetric hypertrophy.

Question 250

Major criteria of Dukes?

Answer 250

Cultures: - Two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or - Persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or - Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or - Positive molecular assays for specific gene targets Endocarditis: - Positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or new valvular regurgitation

Question 251

Minor Duke's criteria?

Answer 251

predisposing heart condition or intravenous drug use microbiological evidence does not meet major criteria fever > 38ºC vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots

Question 252

Duke's diagnosis criteria for infective endocarditis?

Answer 252

Infective endocarditis diagnosed if pathological criteria positive, or 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria

Question 253

Poor prognostic factors for endocarditis?

Answer 253

Staphylococcus aureus infection (see below) prosthetic valve (especially 'early', acquired during surgery) culture negative endocarditis low complement levels

Question 254

Initial blind therapy: Endocarditis + unsure what organism abx?

Answer 254

Native valve amoxicillin, consider adding low-dose gentamicin If penicillin allergic, MRSA or severe sepsis vancomycin + low-dose gentamicin If prosthetic valve vancomycin + rifampicin + low-dose gentamicin

Question 255

Native valve endocarditis + Staph?

Answer 255

Flucloxacillin If penicillin allergic or MRSA vancomycin + rifampicin

Question 256

Prosthetic valve endocarditis caused by staphylococci?

Answer 256

Flucloxacillin + rifampicin + low-dose gentamicin If penicillin allergic or MRSA vancomycin + rifampicin + low-dose gentamicin

Question 257

Endocarditis +Strep (full sensitive) ?

Answer 257

Benzylpenicillin If penicillin allergic vancomycin + low-dose gentamicin

Question 258

Endocarditis + Strep (less sensitive) ?

Answer 258

Benzylpenicillin + low-dose gentamicin If penicillin allergic vancomycin + low-dose gentamicin

Question 259

Indications for surgery?

Answer 259

severe valvular incompetence aortic abscess (often indicated by a lengthening PR interval) infections resistant to antibiotics/fungal infections cardiac failure refractory to standard medical treatment recurrent emboli after antibiotic therapy

Question 260

How to investigate arrhythmias?

Answer 260

1. ECG 2. Holter monitor 3. External loop recorder 4. Internal loop recorder

Question 261

Mechanism of ivabradine?

Answer 261

Anti-anginal acts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.

Question 262

What are the side effects of ivabradine?

Answer 262

visual effects, particular luminous phenomena, are common headache bradycardia, heart block

Question 263

What does the A wave in JVP correspond with?

Answer 263

Atrial contraction large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension absent if in atrial fibrillation

Question 264

When are cannon A waves seen in JVP and why:?

Answer 264

caused by atrial contractions against a closed tricuspid valve are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

Question 265

What causes the c wave in JVP?

Answer 265

'c' wave closure of tricuspid valve not normally visible

Question 266

What causes the V wave in jvp?

Answer 266

'v' wave due to passive filling of blood into the atrium against a closed tricuspid valve giant v waves in tricuspid regurgitation

Question 267

What causes the X wave in JVP?

Answer 267

'x' descent = fall in atrial pressure during ventricular systole

Question 268

What causes the Y wave in JVP?

Answer 268

'y' descent = opening of tricuspid valve

Question 269

Types of cannon A waves?

Answer 269

Regular cannon waves ventricular tachycardia (with 1:1 ventricular-atrial conduction) atrio-ventricular nodal re-entry tachycardia (AVNRT) Irregular cannon waves complete heart block

Question 270

Features of Kawasaki disease?

Answer 270

high-grade fever which lasts for > 5 days. Fever is characteristically resistant to antipyretics conjunctival injection bright red, cracked lips strawberry tongue cervical lymphadenopathy red palms of the hands and the soles of the feet which later peel

Question 271

Management of Kawasaki disease?

Answer 271

Management 1. high-dose aspirin - Kawasaki disease is one of the few indications for the use of aspirin in children. Due to the risk of Reye's syndrome aspirin is normally contraindicated in children 2. intravenous immunoglobulin echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms

Question 272

What is the major complication in kawaski disease?

Answer 272

Coronary artery aneurysm

Question 273

What is long Qt syndrome?

Answer 273

Delayed depolarisation of the ventricles defects in the alpha subunit of the slow delayed rectifier potassium channel

Question 274

Normal QTc?

Answer 274

< 430 females <450 males

Question 275

Congenital causes of long QT?

Answer 275

Jervell-Lange-Nielsen syndrome - includes deafness and is due to an abnormal potassium channel Romano-Ward syndrome - no deafness RomaNO deafness

Question 276

What are the three types of long QT?

Answer 276

Long QT1 - usually associated with exertional syncope, often swimming Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli Long QT3 - events often occur at night or at rest sudden cardiac death

Question 277

Management of long QT?

Answer 277

1. avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise) 2. beta-blockers*** ( sotalol can make it worse) 3. implantable cardioverter defibrillators in high risk cases

Question 278

Mechanism of loop diruretic?

Answer 278

inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.

Question 279

Adverse effects of loop diuretic?

Answer 279

hypotension hyponatraemia hypokalaemia, hypomagnesaemia hypochloraemic alkalosis ototoxicity hypocalcaemia renal impairment (from dehydration + direct toxic effect) hyperglycaemia (less common than with thiazides) gout

Question 280

What are the features of malignant hypertension?

Answer 280

classically: severe headaches, nausea/vomiting, visual disturbance however chest pain and dyspnoea common presenting symptoms papilloedema severe: encephalopathy (e.g. seizures)

Question 281

What is the pathophysiology of malignant hypertension?

Answer 281

fibrinoid necrosis of blood vessels, leading to retinal haemorrhages, exudates, and proteinuria, haematuria due to renal damage (benign nephrosclerosis). can lead to cerebral oedema → encephalopathy

Question 282

Treatment of malignant hypertension?

Answer 282

reduce diastolic no lower than 100mmHg within 12-24 hrs bed rest most patients: oral therapy e.g. atenolol if severe/encephalopathic: IV sodium nitroprusside/labetolol

Question 283

What are the associations of mitral valve prolapse?

Answer 283

congenital heart disease: PDA, ASD cardiomyopathy Turner's syndrome Marfan's syndrome, Fragile X osteogenesis imperfecta pseudoxanthoma elasticum Wolff-Parkinson White syndrome long-QT syndrome Ehlers-Danlos Syndrome polycystic kidney disease

Question 284

Features of mitral valve prolapse?

Answer 284

Complain of atypical chest pain or palpitations mid-systolic click (occurs later if patient squatting) late systolic murmur (longer if patient standing)

Question 285

What is multi-focal atrial tachycardia?

Answer 285

Irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves

Question 286

How can multi-focal atrial tachycardia be managed?

Answer 286

correction of hypoxia and electrolyte disturbances rate-limiting calcium channel blockers are often used first-line cardioversion and digoxin are not useful in the management of MAT

Question 287

Ejection systolic + Louder on expiration?

Answer 287

aortic stenosis hypertrophic obstructive cardiomyopathy

Question 288

Ejection systolic + Louder in inspiration?

Answer 288

pulmonary stenosis atrial septal defect

Question 289

Holosytolic murmur + High pitch?

Answer 289

mitral/tricuspid regurgitation (high-pitched and 'blowing' in character) tricuspid regurgitation becomes louder during inspiration, unlike mitral stenosis during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole

Question 290

Late systolic murmur?

Answer 290

mitral valve prolapse coarctation of aorta

Question 291

Early diastolic mumur + high pitch blowing?

Answer 291

aortic regurgitation (high-pitched and 'blowing' in character) Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)

Question 292

Mid-late diastolic murmur?

Answer 292

mitral stenosis ('rumbling' in character) Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)

Question 293

Myocardial infarction complications?

Answer 293

Left ventricle aneurysm - Ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. - This is typically associated with persistent ST elevation and left ventricular failure. - Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated. Left ventricle free wall rupture VSD Acute mitral regurgitation

Question 294

When can sildenafil be used after MI?

Answer 294

6 Months

Question 295

Causes of myocarditis?

Answer 295

viral: coxsackie B, HIV bacteria: diphtheria, clostridia spirochaetes: Lyme disease protozoa: Chagas' disease, toxoplasmosis autoimmune drugs: doxorubicin

Question 296

Clinical findings of myocarditis?

Answer 296

usually young patient with an acute history chest pain dyspnoea arrhythmias ↑ inflammatory markers in 99% ↑ cardiac enzymes ↑ BNP

Question 297

Complications of myocarditis?

Answer 297

heart failure arrhythmia, possibly leading to sudden death dilated cardiomyopathy: usually a late complication

Question 298

Mechanism of nicorandil?

Answer 298

potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

Question 299

Adverse effects of nicorandil?

Answer 299

headache flushing skin, mucosal and eye ulceration gastrointestinal ulcers including anal ulceration

Question 300

Mechanism of nitrates?

Answer 300

nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels

Question 301

Side effects of nitrates?

Answer 301

hypotension tachycardia headaches flushing

Question 302

Indications for temporary pacing?

Answer 302

Indications for a temporary pacemaker symptomatic/haemodynamically unstable bradycardia, not responding to atropine post-ANTERIOR MI: type 2 or complete heart block* trifascicular block prior to surgery

Question 303

Symptomatic bradycardia treatment?

Answer 303

Atropine (500mcg IV) is the first line treatment in this situation. atropine, up to maximum of 3mg transcutaneous pacing isoprenaline/adrenaline infusion titrated to response

Question 304

Management of regular broad complex tachycardia?

Answer 304

assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block) loading dose of amiodarone followed by 24 hour infusion

Question 305

Management of irregular broad complex tachycardia?

Answer 305

atrial fibrillation with bundle branch block - the most likely cause in a stable patient atrial fibrillation with ventricular pre-excitation torsade de pointes

Question 306

Management of narrow complex regular tachycardia?

Answer 306

vagal manoeuvres followed by IV adenosine if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. beta-blockers)

Question 307

Management of irregular narrow complex tachycardia?

Answer 307

probable atrial fibrillation if onset < 48 hr consider electrical or chemical cardioversion rate control: beta-blockers are usually first-line unless there is a contraindication

Question 308

Hypertension in pregnancy management?

Answer 308

1. Labetaolol Nifedipine if asthmatic Hydralazine may also be used

Question 309

Choice for treatment of PE in renal failure?

Answer 309

if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA

Question 310

PE in antiphospholipid?

Answer 310

if the patient has antiphospholipid syndrome (specifically 'triple positive' in the guidance) then LMWH followed by a VKA should be used

Question 311

Duration of anticoagulation for PE?

Answer 311

provoked: 3 months unprovoked: 6 months

Question 312

Management of PE with haemodynamic instability?

Answer 312

Thrombolysis

Question 313

Management of recurrent PE?

Answer 313

IVC filter

Question 314

What type of pulse can be associated with severe asthma?

Answer 314

Pulsus paradoxus

Question 315

Slow rising pulse?

Answer 315

aortic stenosis

Question 316

Collapsing pulse?

Answer 316

aortic regurgitation patent ductus arteriosus hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

Question 317

Jerk pulse?

Answer 317

HOCM

Question 318

Causes of restrict cardiomyopathy?

Answer 318

amyloidosis (e.g. secondary to myeloma) - most common cause in UK haemochromatosis post-radiation fibrosis Loffler's syndrome: endomyocardial fibrosis with a prominent eosinophilic infiltrate endocardial fibroelastosis: thick fibroelastic tissue forms in the endocardium; most commonly seen in young children sarcoidosis scleroderma

Question 319

Pathogenesis of rheumatic fever?

Answer 319

Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry the cell wall of Streptococcus 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 this response leads to the clinical features of rheumatic fever Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

Question 320

How is rheumatic fever diagnosed?

Answer 320

2 major criteria or 1 major with 2 minor criteria

Question 321

Major criteria for rheumatic fever?

Answer 321

erythema marginatum Sydenham's chorea: this is often a late feature polyarthritis carditis and valvulitis (eg, pancarditis) subcutaneous nodules

Question 322

Minor criteria rheumatic fever?

Answer 322

raised ESR or CRP pyrexia arthralgia (not if arthritis a major criteria) prolonged PR interval

Question 323

Mnx of rheumatic fever?

Answer 323

antibiotics: oral penicillin V anti-inflammatories: NSAIDs are first-line treatment of any complications that develop e.g. heart failure

Question 324

Management of supra ventricular tachycardia?

Answer 324

1. Valsalva 2. rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg contraindicated in asthmatics - verapamil is a preferable option 3. Electrical cardio version

Question 325

Syndrome X?

Answer 325

Features angina-like chest pain on exertion ST depression on exercise stress test but normal coronary arteries on angiography Management nitrates may be beneficial

Question 326

Contraindications of thrombolysis

Answer 326

active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension

Question 327

Stages of valsalva?

Answer 327

1. Increased intrathoracic pressure 2. Resultant increase in venous and right atrial pressure reduces venous return 3. The reduced preload leads to a fall in the 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

Question 328

Management of VT?

Answer 328

< 90 mmHg - cardiovert Drug therapy amiodarone: ideally administered through a central line lidocaine: use with caution in severe left ventricular impairment procainamide

Question 329

Management of warfarin INR 5.0-8.0 No bleeding

Answer 329

Withhold 1 or 2 doses of warfarin Reduce subsequent maintenance dose

Question 330

INR 5.0-8.0 Minor bleeding

Answer 330

Stop warfarin Give intravenous vitamin K 1-3mg Restart when INR < 5.0

Question 331

INR > 8.0 No bleeding

Answer 331

Stop warfarin Give vitamin K 1-5mg by mouth, using the intravenous preparation orally Repeat dose of vitamin K if INR still too high after 24 hours Restart when INR < 5.0

Question 332

INR > 8.0 Minor bleeding

Answer 332

Stop warfarin Give intravenous vitamin K 1-3mg Repeat dose of vitamin K if INR still too high after 24 hours Restart warfarin when INR < 5.0

Question 333

ECG changes on ?

Answer 333

short PR interval wide QRS complexes with a slurred upstroke - 'delta wave' left axis deviation if right-sided accessory pathway* right axis deviation if left-sided accessory pathway*

Question 334

Management of WPW?

Answer 334

definitive treatment: radiofrequency ablation of the accessory pathway medical therapy: sotalol***, amiodarone, flecainide sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

Question 335

Anti-biotic prophylaxis in tooth extract with valve disease?

Answer 335

Nope

Question 336

What is QRISK score?

Answer 336

Risk of stroke or heart attack in 10 years If <10 this is acceptable

Question 337

Who should primary prevention be given to?

Answer 337

QRISK score > 10% should get a statin (20 mg atorvastatin)

Question 338

What is the dose for secondary prevention ?

Answer 338

80 mg atorvastatin

Question 339

Features of tricuspid regurgitation?

Answer 339

pan-systolic murmur prominent/giant V waves in JVP pulsatile hepatomegaly left parasternal heave

Question 340

Causes of tricuspid regurgitation?

Answer 340

right ventricular infarction pulmonary hypertension e.g. COPD rheumatic heart disease infective endocarditis (especially intravenous drug users) Ebstein's anomaly carcinoid syndrome

Question 341

In complete heart block, what sign can be elicited?

Answer 341

Variable intensity of S1 Widened pulse pressure

Question 342

What is suggestive of a split fixed S2 ?

Answer 342

ASD

Question 343

AF + Old person + lots of falls = ? should you anticoagualte?

Answer 343

Assessing using the orbit score Risk of falls or old age alone is not sufficient reasoning to withhold anticoagulation

Question 344

Pathophyiology behind aortic stenosis by age?

Answer 344

Risk of falls or old age alone is not sufficient reasoning to withhold anticoagulation

Question 345

Choice of imaging for PE if renal failure?

Answer 345

VQ scan - contrast media

Question 346

What gives you pulses alternates?

Answer 346

severe lv function

Question 347

What gives a bisferiens pulse?

Answer 347

'double pulse' - two systolic peaks mixed aortic valve disease Hock

Question 348

?Target INR for mechanical aortic valve

Answer 348

3.0

Question 349

?Target INR for mechanical mitral valve

Answer 349

3.5

Question 350

Features of tetralogy of fallout?

Answer 350

ventricular septal defect (VSD) right ventricular hypertrophy right ventricular outflow tract obstruction, pulmonary stenosis overriding aorta

Question 351

Treatment of hypertension

Answer 351

Question 352

What classifies as pulmonary hypertension?

Answer 352

Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of >= 25 mmHg

Question 353

Features of pulmonary hypertension ?

Answer 353

progressive exertional dyspnoea is the classical presentation other possible features include exertional syncope, exertional chest pain and peripheral oedema cyanosis right ventricular heave, loud P2, raised JVP with prominent 'a' waves, tricuspid regurgitation

Question 354

How should treatment be guided in pulmonary hypertension

Answer 354

Acute vasodilator testing

Question 355

Pulmonary hypertension + positive vasodilator test treatment?

Answer 355

If there is a positive response to acute vasodilator testing (a minority of patients) oral calcium channel blockers

Question 356

Pulmonary hypertension + negative vasodilator testing treatment?

Answer 356

If there is a negative response to acute vasodilator testing (the vast majority of patients) prostacyclin analogues: treprostinil, iloprost endothelin receptor antagonists: bosentan, ambrisentan phosphodiesterase inhibitors: sildenafil Combination therapy helpful

Question 357

How to measure pressure in left ventricle?

Answer 357

easured is similar to that of the left atrium (normally 6-12 mmHg). balloon tipped Swan-Ganz catheter which is inserted into the pulmonary artery.

Question 358

What are the drugs cause long QT?

Answer 358

amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) methadone chloroquine terfenadine** erythromycin haloperidol ondanestron

Question 359

Dipyridamole mechanism?

Answer 359

phosphodiesterase inhibitor and decreases cellular uptake of adenosine

Question 360

Reasons to cease ACEi ?

Answer 360

A potassium above 6mmol/L should prompt cessation of ACE inhibitors in a patient with CKD

Question 361

MI long time ago + AF - not anticoagualted, on anti platelet. Management?

Answer 361

Stop antiplatelets Put on anticoagulant

Question 362

Drugs liscenced for peripheral vascular disease and mechanism?

Answer 362

Drugs licensed for use in peripheral arterial disease (PAD) include: naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life - 5HT2 antagonist cilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICE

Question 363

Features of left ventricle aneurysm?

Answer 363

Persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Question 364

Features of left ventricle free wall rupture?

Answer 364

acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

Question 365

What drug is contraindicated in broad complex tachycardia?

Answer 365

Verapamil

Question 366

Prognostic factors in HOCM?

Answer 366

syncope family history of sudden death young age at presentation non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring abnormal blood pressure changes on exercise

Question 367

Why does ticagrelor give you dyspnea?

Answer 367

Dyspnoea in ticagrelor-treated patients is due to the impaired clearance of adenosine

Question 368

Most common heart diseases at birth?

Answer 368

Congenital heart disease cyanotic: TGA most common at birth, Fallot's most common overall acyanotic: VSD most common cause

Question 369

What drug improves long term prognosis in angina?

Answer 369

Aspirin

Question 370

Mitral valve repairs?

Answer 370

Percutaneous mitral commissurotomy is the intervention of choice for severe mitral stenosis Mitral valve balloon

Question 371

Mechanism of tirofabn ?

Answer 371

GpIIa/IIIb inhibitor

Question 372

Grace score of < 1.5% management?

Answer 372

Aspirin 12 months

Question 373

Grace 1.5 - 3% ?

Answer 373

Aspirin + Clopidogrel for 12 months & outpatient perfusion/stress imaging

Question 374

Grace 3-6 % ?

Answer 374

Glycoprotein inhibitor & angiography within 96 hours

Question 375

When should 3 back to back shocks be given?

Answer 375

If already on continuing monitoring and note sudden change into VT

Question 376

In hypertension treatment, should thirazide like or thiazide diuretics be given?

Answer 376

Thiazide like - e.g. indapamide

Question 377

What heart valve issues does carcinoid syndrome cause?

Answer 377

Right heart valve stenosis

Question 378

Features of a 2 level well score? And what does this mean?

Answer 378

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3 An alternative diagnosis is less likely than PE 3 Heart rate > 100 beats per minute 1.5 Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5 Previous DVT/PE 1.5 Haemoptysis 1 Malignancy (on treatment, treated in the last 6 months, or palliative) 1 Clinical probability simplified scores PE likely - more than 4 points PE unlikely - 4 points or less

Question 379

Mechanism of heparin?

Answer 379

Activates anti-thrombin 3

Question 380

Most common cause of infective endocarditis?

Answer 380

Staphylococcus aureus now the most common cause of infective endocarditis particularly common in acute presentation and IVDUs

Question 381

Endocarditis related to dental issues?

Answer 381

Strep viridans

Question 382

Strep viridans is the name of a group, rather than the organisms. what two notable cause dental plaque endocaridits?

Answer 382

Streptococcus mitis and Streptococcus sanguinis

Question 383

Most common endocarditis post valve surgery, or from line insertions ?

Answer 383

coagulase-negative Staphylococci such as Staphylococcus epidermidis After two months post - bugs return to normal. ie. staph aureus most likely organism

Question 384

Endocariditis most commonly associated colon malignancy?

Answer 384

Strep bovis - strep gallactoganis is a type of Boris

Question 385

Culture negative endocarditis?

Answer 385

prior antibiotic therapy Coxiella burnetii Bartonella Brucella HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

Question 386

What drug can increase calcium by decreasing calcium secretion by the kidney?

Answer 386

Thiazide diuretics can cause hyponatraemia, metabolic alkalosis, hypokalaemia and hypocalciuria This doesn't improve bones

Question 387

What should target INR be if recurrent DVT 's?

Answer 387

3.5

Question 388

Congenital causes of VT?

Answer 388

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) Romano-Ward syndrome (no deafness)

Question 389

Drug causes of VT?

Answer 389

amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) methadone chloroquine terfenadine** erythromycin haloperidol ondanestron

Question 390

If high risk of cardio version failure, while anticoagulating what should also be offered?

Answer 390

Amiodarone

Question 391

Rate control should be offered to people, except?

Answer 391

whose atrial fibrillation has a reversible cause who have heart failure thought to be primarily caused by atrial fibrillation with new‑onset atrial fibrillation (< 48 hours) with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm for whom a rhythm‑control strategy would be more suitable based on clinical judgement

Question 392

Agents used to control rate in AF?

Answer 392

Beta blockers CCB Digoxin - not considered first-line anymore as they are less effective at controlling the heart rate during exercise - should only be considered if he person does no or very little physical exercise or other rate‑limiting drug options are ruled out because of comorbidities - may have a role if there is coexistent heart failure

Question 393

Agents used for rhythm control in AF?

Answer 393

beta-blockers dronedarone: second-line in patients following cardioversion amiodarone: particularly if coexisting heart failure

Question 394

Success rate of cardio version?

Answer 394

around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously longer term, after 3 years, around 55% of patients who've had a single procedure remain in sinus rhythm. Of patients who've undergone multiple procedures around 80% are in sinus rhythm

Question 395

Features of takayasu arteritis?

Answer 395

systemic features of a vasculitis e.g. malaise, headache unequal blood pressure in the upper limbs carotid bruit and tenderness absent or weak peripheral pulses upper and lower limb claudication on exertion aortic regurgitation (around 20%)

Question 396

What vessels are affected in takayasu arteritis?

Answer 396

large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse

Question 397

Imaging seen on takayasu arteritis?

Answer 397

vascular imaging of the arterial tree is required to make a diagnosis of Takayasu's arteritis either magnetic resonance angiography (MRA) or CT angiography (CTA)

Question 398

What factors may falsely elevated BNP?

Answer 398

Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis

Question 399

What factors may reduced BNP levels?

Answer 399

Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists

Question 400

Statin adverse effects?

Answer 400

myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase.

Question 401

Risk factors for rhabdomyolysis from statin?

Answer 401

female sex, low body mass index and presence of multisystem disease such as diabetes mellitus Advanced age

Question 402

What statins are more likely to give myalgia?

Answer 402

Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

Question 403

xProphylaxis in supraventricualr tachycardia?

Answer 403

Beta blocker

Question 404

Eruptive xanthomata is associated with?

Answer 404

Familial hypertriglyceridaemia

Question 405

What does a bicuspid aortic valve develop into?

Answer 405

Aortic regurgitation or stenosis

Question 406

Associations of aortic stenosis?

Answer 406

associated with a left dominant coronary circulation (the posterior descending artery arises from the circumflex instead of the right coronary artery) and Turner's syndrome around 5% of patients also have coarctation of the aorta

Question 407

Erythromycin prolongs QT by affecting what channel?

Answer 407

Potassium channels

Question 408

why is a prolonged loading regimen needed in amiodarone?

Answer 408

Amiodarone has a long half-life - it is highly lipophilic and widely absorbed by tissue, which reduces its bioavailability in serum. Therefore, a prolonged loading regime is required to achieve stable therapeutic levels

Question 409

What is the best test for a stable patient with chest pain

Answer 409

Contrast-enhanced CT coronary angiogram is the first line investigation for stable chest pain of suspected coronary artery disease aetiology Do not use stress ECG

Question 410

Loud S2?

Answer 410

Hypertension - pulmonary or systemic

Question 411

Soft S2?

Answer 411

Aortic stenosis

Question 412

Fixed split S2?

Answer 412

ASD

Question 413

Reversed split S2?

Answer 413

Pulmonary valve closes before aortic Severe aortic stenosis LBBB

Question 414

SVT + asthmatic?

Answer 414

Verapamil

Question 415

Dentistry+ warfarin?

Answer 415

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

Question 416

Patent ductus arterioles features?

Answer 416

left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat

Question 417

Complications of VSD?

Answer 417

aortic regurgitation Eisenmenger's complex Eisenmenger's complex is an indication for a heart-lung transplant right heart failure pulmonary hypertension pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortality

Question 418

How do you determine if a patient will benefit from CRT?

Answer 418

ECG - broad complex Echo - <35% ejection fraction

Question 419

What LV function bans you from driving lorries?

Answer 419

< 40%

Question 420

In thrombolysis treatment of STEMI:

Answer 420

After 90 minutes assess if greater than 50% resolution If not rescue PCI > thrombolysis

Question 421

Indications for surgery in endocarditis?

Answer 421

severe valvular incompetence aortic abscess (often indicated by a lengthening PR interval) infections resistant to antibiotics/fungal infections cardiac failure refractory to standard medical treatment recurrent emboli after antibiotic therapy

Question 422

What drug may cause ulceration in the GI tract?

Answer 422

Nicorandil

Question 423

Left ventricle aneurysm features?

Answer 423

Persistent ST elevation following recent MI, no chest pain - left ventricular aneurysm

Question 424

What should be monitored while giving magnesium IV in treatment of pre-eclampsia'?

Answer 424

urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment

Question 425

Mechanism of thiazide diuretics?

Answer 425

Thiazides/thiazide-like drugs (e.g. indapamide) - inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

Question 426

What should be monitored in endocarditis/?

Answer 426

PR interval - aortic root abscess

Question 427

What cardiovascular disease should mean pregnancy is contraindicated?

Answer 427

Pulmonary hypertension

Question 428

What causes transpoition of the great vessels?

Answer 428

Transposition of great vessels is due to the failure of the aorticopulmonary septum to spiral

Question 429

Causes of tornado dev point?

Answer 429

congenital Jervell-Lange-Nielsen syndrome Romano-Ward syndrome antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants antipsychotics chloroquine terfenadine erythromycin electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia myocarditis hypothermia subarachnoid haemorrhage

Question 430

Thiazide side effects?

Answer 430

Common adverse effects dehydration postural hypotension hyponatraemia, hypokalaemia, hypercalcaemia* gout impaired glucose tolerance impotence Rare adverse effects thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis

Question 431

What is the most common mutation in HOCM?

Answer 431

gene encoding β-myosin heavy chain protein or myosin-binding protein C

Question 432

When should statins be stopped if causing transaminitis

Answer 432

3 X the upper limits of normal

Question 433

Can warfarin be used breat feeding?

Answer 433

Yes

Question 434

Amiodarone side effects?

Answer 434

You should check if there is hypokalaemia before starting Coexistent hypokalaemia significantly increases this risk. thyroid dysfunction: both hypothyroidism and hyper-thyroidism corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity 'slate-grey' appearance thrombophlebitis and injection site reactions bradycardia lengths QT interval

Question 435

ECG changes in pericarditis

Answer 435

ECG changes the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events 'saddle-shaped' ST elevation PR depression: most specific ECG marker for pericarditis

Question 436

What test should be done for pericarditis patients?

Answer 436

Echocardiogram

Question 437

How is bleeding reversed on dabigitran?

Answer 437

idarucizumab

Question 438

If an ICD is inserted prophylactically, driving?

Answer 438

1 month

Question 439

Mechanism of sacubitril?

Answer 439

Prevents degradation of patriotic peptides BNP and ANP

Question 440

What is paradoxical embolus?

Answer 440

For a right-sided thrombus (e.g. DVT) to cause a left-sided embolism (e.g. stroke) it must obviously pass from the right-to-left side of the heart cardiac lesions may cause such events patent foramen ovale - present in around 20% of the population atrial septal defect - a much less common cause

Question 441

How should PFO be investigated?

Answer 441

Transoesphageal echo

Question 442

What should be avoided in right ventricle myocardial infarction?

Answer 442

Nitrates should be avoided in the likely diagnosis of right ventricular myocardial infarct due to causing reduced preload

Question 443

Mechanism of fondaparinux?

Answer 443

Antithrombin 3 activation

Question 444

What conditions may form eisenmengers?

Answer 444

Associated with ventricular septal defect atrial septal defect patent ductus arteriosus

Question 445

Assoications of Wolffe Parkinson white?

Answer 445

HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD

Question 446

Drugs to avoid in WPW?

Answer 446

Verapamil and digoxin should be avoided in patients with Wolff-Parkinson White as they may precipitate VT or VF

Question 447

What hsitological findings are found in rheumatic fever?

Answer 447

Aschoff bodies

Question 448

Management for uraemia pericarditis ?

Answer 448

Haemodialysis

Question 449

When should you anticoagulant a paroxysmal AF?

Answer 449

Anticoagulant for life after second episode

Question 450

Mechanism of simvastatin?

Answer 450

Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis Decreases intrinsic hepatic cholesterol synthesis

Question 451

Side effects of ivabradine?

Answer 451

Ivabradine use may be associated with visual disturbances including phosphenes and green luminescence visual effects, particular luminous phenomena, are common headache bradycardia, heart block

Question 452

Function of troponin in cardiac muscle?

Answer 452

COmponent of thin filaments

Question 453

Antithrombotic therapy in different valves?

Answer 453

Prosthetic heart valves - antithrombotic therapy: bioprosthetic: aspirin mechanical: warfarin + aspirin

Question 454

Why do thiazides cause hypokalaemia?

Answer 454

Thiazides/thiazide-like drugs (e.g. indapamide) - inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

Question 455

Why electrolyte disturbance can a bisphosphonate infusion lead to?

Answer 455

Hypocalcaemia

Question 456

In aortic dissecrtion what can be seen on CXR?

Answer 456

Widened mediastinum

Question 457

Main symptom of pulmonary hypertension?

Answer 457

Exertional dyspnoea

Question 458

Organism that causes leading cause of mortality in endocarditis?

Answer 458

Staph

Question 459

What rhythms develop from an inferior MI?

Answer 459

Atrioventricular block

Question 460

Management of aortic dissection?

Answer 460

type A - ascending aorta - control BP (IV labetalol) + surgery type B - descending aorta - control BP(IV labetalol)

Question 461

What type of shunt is there in tetralogy of fallout?

Answer 461

Right to left shunt

Question 462

What is prinzmetal angina? Treatment?

Answer 462

From the SIGN guidelines: Prinzmetal (vasospastic) angina is a rare form of angina in which pain is experienced at rest rather than during activity. It is caused by narrowing or occlusion of proximal coronary arteries due to spasm and cannot be diagnosed by coronary angiography. Beta blockers should not be used in this form of angina because they may worsen the coronary spasm. Patients with this condition may be treated effectively with a dihydropyridine derivative CCB such as amlodipine.

Question 463

Criteria for surgery for aortic stenosis

Answer 463

Gradient >40mmHg Symptoms

Question 464

STEMI + diabetes. Management?

Answer 464

Intravenous insulin

Question 465

Careful in hypertension questions, if give ejection fraction consider treatment for heart failure

Answer 465

See above