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MRCP p1 > cardiology > Flashcards

cardiology Flashcards

1
Q

what are the conditions associated with wolff parkinson white syndrome?

A

HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD

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2
Q

what is the treatment for wolff-parkinson white syndrome?

A

definitive treatment: radiofrequency ablation of the accessory pathway

medical therapy - sotalol, amiodarone and flecainide (avoid sotalol if co-existent AF as it can prolong refractory period at the AV node)

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3
Q

what are the different medications used in pulmonary hypertension?

A

prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists: bosentan, ambrisentan
phosphodiesterase inhibitors: sildenafil

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4
Q

what kinda shunt is present in patients with TOF?

A

right to left

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5
Q

what is the sign that can be noticed with third degree heart block?

A

varibale intensity of S1

lectrical impulse from the sinoatrial node is not propagated to the ventricles, resulting in incoordination between the atrium and ventricles contractions. Complete HB commonly presents with haemodynamic instability and features resultant from the associated severe bradycardia and hypotension. Common signs include a wide pulse pressure, cannon JVP waves and variable intensity of S1. This change in the first heart sound is secondary to the inconsistent blood flow volume from the atria to the ventricles.

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6
Q

what is the mode of action of dabigatran?

A

direct thrombin inhibitor

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7
Q

which antihypertensive can cause first dose hypotension?

A

ACE inhibitors

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8
Q

how long do you take anticoag in provoked PE?

A

3 months
6 months in people with active cancer

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9
Q

what is the mode of action of ticagrelor?

A

Inhibits the binding of ADP to platelets

Adenosine diphosphate (ADP) is one of the main platelet activation factors, mediated by G-coupled receptors P2Y1 and P2Y12.
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.

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10
Q

what interacts with clopidogrel to reduce antiplatelet effects?

A

A drug interaction exists between clopidogrel and proton pump inhibitors, particularly omeprazole and esomeprazole, leading to reducing antiplatelet effects.

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11
Q

what is the treatment for eclampsia?

A

IV magnesium bolus of 4g over 5-10 mins
Followed by Infusion of 1g/hr

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12
Q

how do you monitor the effect of magnesium sulphate?

A

urine output, reflexes, respiratory rate and oxygen saturations

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13
Q

how do you reverse if respiratory depresssion occurs in pateints on magensium sulphate tx for eclampsia?

A

calcium gluconate

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14
Q

what conditions are HOCM associated with?

A

Friedreich’s ataxia
Wolff-Parkinson White

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15
Q

what are the ECG changes seen in HOCM?

A

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

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16
Q

when do you consider valve replacement for aortic stenosis?

A
  • if symptomatic then valve replacement
  • if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
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17
Q

what are the options for aortic valve repalcement?

A
  • aortic valve replacement - preferred in young patients with low operative risk
  • transcatheter AVR - high operative risk
  • balloon valvuloplasty - children with no aortic valve calcification
    in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
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18
Q

what are the conditions with a right to left shunt?

A

(1)TRUNKus Arteriosus
(2) Transposition of the (two)GV
(3) TRIcuspid Atresia
(4) TETRAlogy of Fallot

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19
Q

what is the pathophysiology of HOCM? (i.e which gene affected)

A

the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C

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20
Q

You are a CT1 in Acute Medicine covering the hospital at night. You are called to the surgical ward to see a 35-year-old patient who is reporting palpitations. She is known to have Wolff-Parkinson-White syndrome. Her ECG shows fast atrial fibrillation. On examination, there is no evidence of haemodynamic instability. What is the most appropriate pharmacological management option for this patient?

A

Flecainide

In patients with accessory pathways, such as those with Wolff-Parkinson-White syndrome, AV nodal blocking drugs should be avoided in atrial fibrillation. This is because blocking the AV node may enhance the rate of conduction through the accessory pathway, causing atrial fibrillation to degenerate into ventricular fibrillation (VF).
Verapamil and beta-blockers are contraindicated

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21
Q

what is the different ECG features of type A and type B WPW

A

type A (left-sided pathway): dominant R wave in V1
type B (right-sided pathway): no dominant R wave in V1

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22
Q

what further investigation is needed if streptococcus bovis is isolated on blood cultures for infective endocarditis?

A

Colonoscopy
Strep. Bovis is associated with colorectal cancer

Strep. gallolyticus is most linked

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23
Q

what condition is eruptive xanthoma most linked with?

A

familial hypertriglycerideamia
lipoprotein lipase deficiency

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24
Q

A 65-year-old man has been started on amiodarone. He has been told he must first take higher doses and then continue on a lower maintenance dose long-term.

What is the reasoning behind this initial dose regime?

A

slow metabolism of amiodarone due to extensive lipid binding

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

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25
Q

what are some of the drawbacks of using amiodarone?

A
  1. very long half-life (20-100 days). For this reason, loading doses are frequently used
  2. should ideally be given into central veins (causes thrombophlebitis)
  3. has proarrhythmic effects due to lengthening of the QT interval
  4. interacts with drugs commonly used concurrently (p450 inhibitor) e.g. Decreases metabolism of warfarin
    numerous long-term adverse effects
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26
Q

A 65-year-old builder is seen by his general practitioner for worsening shortness of breath. This is not associated with any chest pain or cough.

Three weeks ago he was admitted and treated for an anterior ST-elevated myocardial infarction by primary percutaneous coronary intervention. He has a background of asthma and hypercholesterolaemia.

On examination his lung fields sound clear and he has a slight tachycardia of 101 beats per minute, with oxygen saturations of 96% on air and blood pressure of 145/91 mmHg. An ECG shows sinus tachycardia with anterior, concave ST-elevation in leads V1-V5 associated with deep Q waves.

What is the most likely diagnosis?

A

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

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27
Q

how long does it take for ST elevation to resolve?

A

Following a STEMI, ST segments gradually return towards normal over two weeks while Q waves persist and T waves flatten or become inverted. ST-elevation persisting for >2 weeks post-STEMI, with breathless and no chest pain, suggests the development of a left ventricular aneurysm.

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28
Q

what are some of the centrally acting anti-hypertensive medications?

A
  • 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
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29
Q

DVLA advice for MI?

A

acute coronary syndrome- 4 weeks off driving
1 week if successfully treated by angioplasty

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30
Q

what are the medications that interact with adenosine?

A

dipyridamole enhances, aminophylline reduces
DEAR

31
Q

what is the mode of action of adenosine?

A

causes transient heart block in the AV node
agonist of the A1 receptor in the atrioventricular node, which 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

32
Q

what is syndrome X?

A

angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography

Management: nitrates may be beneficial

33
Q

what are the features suggesting restrictive cardiomyopathy rather than constrictive pericarditis?

A
  • prominent apical pulse
  • absence of pericardial calcification on CXR
  • the heart may be enlarged
  • ECG abnormality - bundle branch block, Q waves
34
Q

what is the treatment of AF following stroke?

A

following a stroke or TIA it is obviously important to exclude a haemorrhage

  • following a TIA, anticoagulation for AF should start immediately once imaging has excluded haemorrhage
  • in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period (aspirin for 2 weeks) . If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed
35
Q

how do you differentiate Jervell- lange Nielsen syndrome from romano ward syndrome?

A

jervell-lange nielsen syndrome causes deafness while romano doesnt

36
Q

what is the cause of a soft S2?

A

aortic stenosis

37
Q

who should beta blockers not be the offered for in AF?

A
  • 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
38
Q

what is the protocol for DAPT post MI?

A

Most patients who’ve had an acute coronary syndrome are now given dual antiplatelet therapy (DAPT). Clopidogrel was previously the second antiplatelet of choice. Now ticagrelor and prasugrel (also ADP-receptor inhibitors) are more widely used. The NICE Clinical Knowledge Summaries now recommend:

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

this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events

39
Q

what is the treatment of broad complex ventricular tachycardia?

A

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

40
Q

what causes cannon a wave on jugular venous pressure?

A

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

Irregular cannon waves
complete heart block

41
Q

how does warfarin function?

A
  • Inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form
  • This in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.
42
Q

what drugs interact with the function of adenosine?

A

The effects of adenosine are
enhanced by dipyridamole (antiplatelet agent) and
blocked by theophyllines.

43
Q

what are the side effects of adenosine?

A
  • chest pain
  • bronchospasm
  • transient flushing
  • can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
44
Q

what juices can affect cardiac medications?

A

cranberry juice - warfarin - increases INR
grapefruit juice - potent inhibitor of the cytochrome P450 enzyme CYP3A4

45
Q

what is the notable side effect of ticagrelore?

A

ticagrelor may cause dyspnoea
due to the impaired clearance of adenosine

46
Q

what positional methods can be used to make murmurs louder?

A

Mitral & Aortic stenosis and regurgitation increase intensity of murmurs in squatting or leg raising and decrease in valsalva or standing.

whilst in HOCM & MVP increase intensity of murmurs in valsalva or standing and decrease in squatting or leg raising.

47
Q

what are the ECG changes seen in brugada syndrome?

A
  • convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
  • partial right bundle branch block
48
Q

what can be done to make ECG changes more apparent in brugada syndrome?

A

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

49
Q

what is the typical features of left ventricular aneurysm?

A

This is typically associated with persistent ST elevation and left ventricular failure.

50
Q

what is the physiological stages of valsalva manoevre?

A
  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
51
Q

what is the signs of cholesterol embolisation?

A

P: Purpura
E: Eosinophili(a)
R: Renal failure
L: Livedo reticularis

52
Q

what drugs needs to be avoided in HOCM?

A
  • Diuretic should be given with caution (Digoxin should be avoided)
  • ACE-inhibitors: should be avoided in HOCM patients with LVOT as reducing afterload can worsen the LVOT gradient.
  • Nitrates especially if the patient has an outflow tract gradient.
  • Inotrope

DANI

53
Q

what are the causes of elevated BNP?

A

Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis

54
Q

what are the causes of decreased BNP?

A

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

55
Q

what is the management of pateints with AF who have had failed electrical cardioversions in the past?

A

If high-risk of failure of cardioversion (previous failure), offer electrical cardioversion after at least 4 weeks treatment with amiodarone

amiodarone or sotalol for at least 4 weeks prior to electrical cardioversion in cases where there is a high risk of failure (recurrent AF or previous failed cardioversion attempts).

56
Q

what is bisferiens pulse and what condition is it associated with?

A

‘double pulse’ - two systolic peaks
mixed aortic valve disease

57
Q

after what time period after valve replacement can you be convinced that a particular case of endocarditis is not being caused by the prosthetic valve replacement?

A

Staphylococcus epidermidis if < 2 months post valve surgery

58
Q

what is the most common side effects of bendroflumethiazide?

A
  • impaired glucose tolerance
  • gout
  • postural hypotension
  • impotence
59
Q

what factors are affected by warfarin?

A

Vitamin K related

10, 9 , 7, 2
1972

60
Q

how long after successful cardioversion is warfarin continued on for?

A

warfarin is to be continued for at least 4 weeks after successful cardioversion

61
Q

what do you administer in pateints with PH and response to epoprostenol and NO?

A

nifedipine or diltiazem
CCB

62
Q

what is the management of a patient with HOCM who has a 24 hour ECG reveals runs of non-sustained ventricular tachycardia?

A

Implantable cardioverter defibrilator

63
Q

what is the tx of a pregnant woman with SVT?

A

metaprolol

adenosine is CI as it can decrease uterine blood flow

flecainide - foetal toxicity and hyperbilirunaemia - but can be used in tertiary centres

64
Q

what are the INR targets for warfarin in pts with DVT or AF?

A

venous thromboembolism: target INR = 2.5, if recurrent 3.5

atrial fibrillation, target INR = 2.5

65
Q

what is the tx for multifocal atrial tachycardia?

A

usually irregualr cardiac rhythm with different morphological P waves (more common in the elderly with COPD)

  • rate limiting calcium channel blocker
  • cardioversion and digoxin : not useful
66
Q

what is the subsequent tx after 6 mg adenosine is given for SVT?

A

6 mg -> 12 mg -> 18 mg

67
Q

what are the ECG signs of hypokalaemia?

A

In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

68
Q

what are the side effects of nicorandil?

A
  • headache
  • flushing
  • skin, mucosal and eye - ulceration
    :gastrointestinal ulcers including anal ulceration
69
Q

what are the signs to stop the exercise tolerance test?

A

The 23 rule

3 mm ST depression , 2 mm ST elevation, SBP more than 230 mmHg , SBP falling more than 20mmHg , HR falling more than 20%.

70
Q

what is the mx of pt’s with secondary prevention aspirin for CVD who also have AF?

A

if an indication for anticoagulant exists (for example atrial fibrillation) it is indicated that anticoagulant monotherapy is given without the addition of antiplatelets

71
Q

what is the difference is tx for the different types of aortic dissection?

A

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

type B - descending aorta - control BP(IV labetalol)

72
Q

what are the side effects of ivabradine?

A

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

73
Q

what are the available high fidelity cardiac imaging?

A

Contrast enhanced Cardiac CT - Ischemic Heart disease

Cardiac MRI - Congenital heart Disease, Left & Right ventricular mass , Cardiomyopathy

Cardiac MRI with gadolinium - Perfusion imaging of heart

Exercise ECG - least sensitive

Cardiac SPECT - Myocardial perfusion and Myocardial Viability

MUGA scan - Cardiotoxic drugs to determine LVEF

MRCP p1 (13 decks)

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