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MRCP Part 1 > Cardio > Flashcards

Cardio Flashcards

1
Q

Causes of Myocarditis

A

viral: coxsackie B, HIV

bacteria:diphtheria, clostridia

spirochaetes: Lyme disease

protozoa: Chagas’ disease, toxoplasmosis

autoimmune

drugs: doxorubicin

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2
Q

Which Coronary artery
I , V5-6

A

Lt circumflex

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3
Q

Which Coronary artery

II, III, aVF

A

RCA

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4
Q

Which Coronary artery
V1-V4

A

LAD

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5
Q

In STEMI

antiplatelet prior to PCI

A

‘dual antiplatelet therapy’, i.e. aspirin + another drug

  1. if the patient is not taking an oral anticoagulant: prasugrel
  2. if taking an oral anticoagulant: clopidogrel
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6
Q

Antiplatelets during PCI

A
  1. patients undergoing PCI with radial access:

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

  1. patients undergoing PCI with femoral access:

bivalirudin with bailout GPI

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7
Q

In stable angina
if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs:

A

a long-acting nitrate

ivabradine

nicorandil

ranolazine

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8
Q

rise in the creatinine and potassium may be expected after starting ACEi

acceptable changes

  1. increase in serum creatinine, up to ……
  2. increase in potassium up to …….
  3. decrease in eGFR of up to…….
A
  1. increase in serum creatinine, up to 30% from baselineand an
  2. increase in potassium up to 5.5 mmol/l.
  3. decrease in eGFR of up to 25%
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9
Q

Atropine is anantagonist of ……

A

Atropine is anantagonist of the muscarinic acetylcholine receptor.

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10
Q

atropine may trigger…….

A

acute angle-closure glaucomain susceptible patients

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11
Q

Effects of BNP

A
  1. vasodilator
  2. diuretic and natriuretic
  3. suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
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12
Q

Factors which reduce BNP levels include treatment with

A

ACEi,
ARBs
diuretics.

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13
Q

Beck’s triad

A
  1. hypotension
  2. raised JVP
  3. muffled heart sounds
  • Classical features of Cardiac tamponade
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14
Q

pulsus paradoxus

A

an abnormally large drop in BP during inspiration

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15
Q

eosinophilia

purpura

renal failure

livedo reticularis

Features of……?

A

Cholesterol embolisation

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16
Q

Conditions associated with Coarctation of the aorta

A

Turner’s syndrome

bicuspid aortic valve

berry aneurysms

neurofibromatosis

☆ TBBN

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17
Q

The coronary arteries fill during ………

A

diastole

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18
Q

RCA supplies SA node in ………..%, AV node in ……..%

A

RCA supplies SA node in 60%, AV node in 90%

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19
Q

The following ECG changes are considered normal variants in an athlete:
(4)

A
  1. sinus bradycardia
  2. junctional rhythm
  3. first degree heart block
  4. Mobitz type 1 (Wenckebach phenomenon)
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20
Q

Which condition is associated with Patent foramen ovale (PFO)

A

Migraine

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21
Q

4 ECG changes in PE

A
  1. S1Q3T3 ( this change is seen in no more than 20% of patients)
  2. RBBB
  3. RT axis deviation
  4. Sinus tachycardia
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22
Q

In treatment of PE
if neither apixaban or rivaroxaban are suitable then

A

if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)

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23
Q

Treatment of PE in renal Impairment

A

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

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24
Q

Comparing CTPA to V/Q scanning in pregnancy

A

CTPA slightly increases the lifetime risk ofmaternal breast cancer, Pregnancy makes breast tissue particularly sensitive to the effects of radiation

V/Q scanning carries a slightly increased risk ofchildhood cancer

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25
Q

Pathophysiology of Aortic dissection

tear in …….

A

tear in the tunica intima of the wall of the aorta

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26
Q

Aortic dissection is associated with

A

HTN
Trauma
Bicuspid aortic valve
Pregnancy
Syphilis

collagens: Marfan’s syndrome, Ehlers-Danlos syndrome

Turner’s and Noonan’s syndrome

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27
Q

ECG changes maybe seen in Aortic dissection

A

ST-segment elevation may be seen in the inferior leads

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28
Q

Stanford classification

A

type A - ascending aorta, 2/3 of cases

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

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29
Q

DeBakey classification of Aortic dissection

A
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30
Q

Aortic dissection: investigation

A
  1. Chest x-ray

widened mediastinum

  1. CT angiographyof the chest, abdomen and pelvis is the investigation of choice

suitable for stable patients and for planning surgery

  1. Transoesophageal echocardiography (TOE)

more suitable for unstable patients who are too risky to take to CT scanner

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31
Q

Management of Aortic dissection

A

Type A

surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Type B*

conservative management

bed rest

reduce blood pressure IV labetalol to prevent progression

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32
Q

Aortic dissection Complications of backward tear

A

aortic incompetence/regurgitation

MI: inferior pattern is often seen due to right coronary involvement

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33
Q

Aortic dissection Complications of a forward tear

A

unequal arm pulses and BP

stroke

renal failure

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34
Q

5 Associations of WPW

A

Secundum ASD

HOCM

thyrotoxicosis

Ebstein’s anomaly

mitral valve prolapse

*SHTEM

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35
Q

Management of WPW

A

definitive treatment: radiofrequency ablation of the accessory pathway

medical therapy: sotalol***, amiodarone, flecainide

sotalol should be avoided if there is coexistent atrial fibrillation

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36
Q

Mechanism of action of WARFARIN

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.

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37
Q

What are the risk factors for asystole. Even if there is a satisfactory response to atropine

A

complete heart block with broad complex QRS

recent asystole

Mobitz type II AV block

ventricular pause > 3 seconds

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38
Q
  • Dose of adenosine in SVT
  • Contraindication ?
A

rapid IV bolus of 6 mg → if unsuccessful give 12 mg → if unsuccessful

contraindicated in asthmatics - verapamil is a preferable option

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39
Q

Causes of long QT interval

A

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

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40
Q

A normal corrected QT interval is ……

A

A normal corrected QT interval is

< 430 ms in males and

< 450 ms in females.

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41
Q

the usual mechanism by which drugs prolong the QT interval is…….?

A

blockage of potassium channels

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42
Q

The most common variants of Long QT Syndrome (LQT1 & LQT2) are caused by defects in ……..?

A

defects in the alpha subunit of the slow delayed rectifier potassium channel.

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43
Q

Features of

  1. Long QT type 1
  2. Long QT TYPE 2
  3. LONG QT TYPE 3
A
  1. Long QT1 - usually associated with exertional syncope, often swimming
  2. Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
  3. Long QT3 - events often occur at night or at rest
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44
Q

Causes of a prolonged QT interval:
1. Congenial
2. Drugs
3. Electrolytes
4. Others

A
  1. Congenial
    - Jervell-Lange-Nielsen syndrome(includes deafness and is due to an abnormal potassium channel)
  • Romano-Ward syndrome(no deafness)
  1. Drugs
    - amiodarone,sotalol, class 1a antiarrhythmic drugs
    - SSRI & tricyclic antidepressants
    - methadone
    - chloroquine
    - terfenadine**
    - erythromycin
    - haloperidol
    - ondanestron
  2. Electrolytes : hypo Ca, k , mg
  3. Others
    - MI
    - myocarditis
    - hypothermia
    - SAH
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45
Q

Mechanism of loop diuretics that act byinhibiting …………

A

the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle,

  • reducing the absorption of NaCl.
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46
Q

Adverse effects of loop diuretics

A
  • Hypotension
  • Hypo Na , K, Mg, Ca
  • hypo chloraemic alkalosis
  • ototoxicity
  • hyperglycaemia
  • gout
  • renal impairment(from dehydration + direct toxic effect)
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47
Q

Signs of MR

A
  1. pansystolic murmur described as “blowing”
  2. S1 may be quiet as a result of incomplete closure of the valve.
  3. Severe MR may cause a widely split S2
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48
Q

Signs of Mitral stenosis

A
  1. mid-late diastolic murmur (best heard in expiration)
  2. loud S1
  3. opening snap : indicates mitral valve leaflets are still mobile
  4. low volume pulse
  5. malar flush
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49
Q

Signs of severe MS

A
  1. length of murmur increases
  2. opening snap becomes closer to S2
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50
Q

the normal cross-sectional area of the mitral valve is ……..?….. sq cm.

A ‘tight’ mitral stenosis implies a cross-sectional area of ……?….. sq cm

A

the normal cross-sectional area of the mitral valve is ( 4-6 sq cm) .

A ‘tight’ mitral stenosis implies a cross-sectional area of ( < 1 sq cm)

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51
Q

Which anticoagulant can be used in mitral stenosis

A

DOACs for mild MS

WARFARIN for moderate / severe ms

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52
Q

Management of Mitral stenosis in asymptomatic patients

A

monitored with regular echocardiograms

percutaneous/surgical management is generally not recommended

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53
Q

Management of Mitral stenosis in symptomatic patients

A

percutaneous mitral balloon valvotomy

mitral valve surgery (commissurotomy, or valve replacement)

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54
Q

Mitral valve prolapse maybe associated with

A
  1. congenital heart disease: PDA, ASD
  2. cardiomyopathy
  3. WPW syndrome
  4. Long QT Syndrome
  5. Turner’s syndrome
  6. Marfan’s syndrome, Fragile X
  7. Ehlers-Danlos Syndrome
  8. polycystic kidney disease
  9. osteogenesis imperfecta
  10. pseudoxanthoma elasticum
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55
Q

Features of severe aortic stenosis ( 8 )

A
  1. narrow pulse pressure
  2. slow rising pulse
  3. delayed ESM
  4. soft/absent S2
  5. S4
  6. thrill
  7. duration of murmur
  8. LVH or failure
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56
Q

Causes of aortic stenosis

A

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

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57
Q

Management of AS

A

if asymptomatic&raquo_space;> observe the patient is a general rule

ifsymptomatic &raquo_space;> valve replacement

if asymptomatic butvalvular gradient > 40 mmHgand with features such as left ventricular systolic dysfunction then consider surgery

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58
Q

balloon valvuloplasty in AS

A

may be used in 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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59
Q

options foraortic valve replacement (AVR)include

A
  1. surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, anangiogramis often done prior to surgery so that the procedures can be combined
  2. transcatheter AVR (TAVR) is used for patients with a high operative risk
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60
Q

Signs of AR

A

collapsing pulse

wide pulse pressure

Quincke’s sign (nailbed pulsation)

De Musset’s sign (head bobbing)

early diastolic murmur: intensity of the murmur is increased by thehandgrip manoeuvre

mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

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61
Q

In AR, aortic valve surgery indications include

A

symptomatic patients with severe AR

asymptomatic patients with severe AR who have LV systolic dysfunction

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62
Q

What is the most common type of ASD

A

Ostium secundum(70% of ASDs)

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63
Q

Signs of ASD

A

ejection systolic murmur, fixed splitting of S2

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64
Q
  1. Ostium secundum is associated with ……
  2. Ostium primum is associated with ……
A
  1. associated with Down syndrome and Holt-Oram syndrome (tri-phalangeal thumbs)
  2. associated with abnormal AV valves
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65
Q

ECG in ASD

A

Ostium secundum&raquo_space;> ECG: RBBB with RAD

Ostium primum&raquo_space;> ECG: RBBB with LAD, 1st degree AVB

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66
Q
  1. Ostium secundum is located in …….
  2. Ostium primum is located in ……
A
  1. In the mid of portion of atrial septum
  2. In the lowest portion of atrial septum
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67
Q

Complications of Bicuspid aortic valve

A

aortic stenosis/regurgitation

higher risk for aortic dissection and aneurysm formation of the ascending aorta

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68
Q

Bicuspid aortic valve is associated with

A
  1. left dominant coronary circulation (the posterior descending artery arises from the circumflex instead of the right coronary artery).
  2. Turner’s syndrome
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69
Q

Factors decrease the BNP level:

A
  1. Obesity
  2. Diuretics
  3. ACEi
  4. ARBs
  5. B blocker
  6. Aldosterone antagonists
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70
Q
  1. If BNP High, arrange ECHO within ……….
  2. If BNP raised, arrange ECHO within ……….
A
  1. Within 2 weeks
  2. Within 6 weeks
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71
Q

ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with………

A

preservedejection fraction

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72
Q

In HF, hydralazine in combination with nitrate indicated in

A

Afro-Caribbean patients

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73
Q

In HF, cardiac resynchronisation therapy is indicated in

A

widened QRS (e.g. LBBB)

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74
Q

criteria of ivabradine

A

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

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75
Q

Causes of left axis deviation (LAD)

A
  1. Lt anterior hemiblock
  2. LBBB
  3. Inferior MI
  4. WPW syndrome ( rt sided accessory pathway)
  5. HYPER K
  6. CONGENITAL: OSTIUM PRIMUM ASD , TRICUSPID ATRESIA
  7. MINOR LAD IN OBESE PEPOPLE
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76
Q

Causes of right axis deviation (RAD)

A
  1. Lt posterior hemiblock
  2. RBBB
  3. LATERAL MI
  4. Chronic lung disease
  5. PE
  6. Ostium secundum ASD
  7. WPW SYNDROME ( LT SIDED ACCESSORY PATHWAY)
  8. Normal in infant < 1 years old
  9. Minor RAD IN TALL PEOPLE
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77
Q

ECG: digoxin (4)

A

down-sloping ST depression (‘reverse tick’, ‘scooped out’)

flattened/inverted T waves

short QT interval

arrhythmias e.g.AV block,bradycardia

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78
Q

ECG features of hypokalaemia

A
  1. U waves
  2. small or absent T waves (occasionally inversion)
  3. ST depression
  4. prolong PR interval
  5. long QT
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79
Q

5 ECG changes : hypothermia

A
  1. Bradycardia
  2. atrial and ventricular arrhythmias
  3. Long QT
  4. First degree AVB
  5. Osborne wave
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80
Q

Causes of LBBB

A
  1. MI
  2. HTN
  3. Aortic stenosis
  4. Cardiomyopathy
  5. rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
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81
Q

Causes of aprolonged PR interval

A

idiopathic

ischaemic heart disease

digoxin toxicity

hypokalaemia*

rheumatic fever

aortic root pathologye.g. abscess secondary to endocarditis

Lyme disease

sarcoidosis

myotonic dystrophy

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82
Q

Causes of RBBB

A

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

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83
Q

Causes of ST depression

A

secondary to abnormal QRS (LVH, LBBB, RBBB)

ischaemia

digoxin

hypokalaemia

syndrome X

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84
Q

Causes of ST elevation

A

myocardial infarction

pericarditis/myocarditis

normal variant - ‘high take-off’

left ventricular aneurysm

Prinzmetal’s angina (coronary artery spasm)

Takotsubo cardiomyopathy

rare: subarachnoid haemorrhage

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85
Q

Causes of Peaked T waves

A

Hyper K

MI

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86
Q

Causes of Inverted T waves

A

myocardial ischaemia

digoxin toxicity

subarachnoid haemorrhage

arrhythmogenic right ventricular cardiomyopathy

pulmonary embolism(‘S1Q3T3’)

Brugada syndrome

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87
Q

During treatment with Mg So4 , you should monitor …..

A
  1. urine output
  2. RR
  3. SPO2
  4. reflexes
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88
Q

What is the first-line treatment for magnesium sulphate induced respiratory depression

A

calcium gluconate

89
Q

Causes of High-output heart failure

A

anaemia

arteriovenous malformation

Paget’s disease

Pregnancy

thyrotoxicosis

thiamine deficiency (wet Beri-Beri)

90
Q

Drug can cause HTN

A

steroids

monoamine oxidase inhibitors

the combined oral contraceptive pill

NSAIDs

leflunomide

91
Q

Causes of TR

A

right ventricular infarction

pulmonary hypertensione.g. COPD

rheumatic heart disease

infective endocarditis (especially intravenous drug users)

Ebstein’s anomaly

carcinoid syndrome

92
Q

Features of Takotsubo cardiomyopathy

A

chest pain

features of heart failure

ECG: ST-elevation

normal coronary angiogram

93
Q

7 Causes of Restrictive cardiomyopathy

A
  1. Amyloidosis
  2. Haemochromatosis
  3. Sarcoidosis
  4. Scleroderma
  5. post-radiation fibrosis
  6. endocardial fibroelastosis
  7. Loffler’s syndrome
94
Q

Features suggesting restrictive cardiomyopathy rather than constrictive pericarditis

A

prominent apical pulse

absence of pericardial calcification on CXR

the heart may be enlarged

ECG abnormalities e.g. bundle branch block, Q waves

95
Q

What is Pulsus paradoxus ?

2 Causes

A

greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration

Casuses
- severe asthma,
- cardiac tamponade

96
Q

Causes of Slow-rising/plateau

(1)

A

AS

97
Q

3 Causes of Collapsing pluse

A
  1. AR
  2. PDA
  3. hyperkinetic states(anaemia, thyrotoxic, fever, exercise/pregnancy)
98
Q

Causes of Pulsus alternans

A

Severe LVF

99
Q

What is Bisferiens pulse ?
Causes?

A

double pulse’ - two systolic peaks

  1. mixed aortic valve disease
  2. HOCM may occasionally be associated with a bisferiens pulse
100
Q

Causes of ‘Jerky’ pulse

A
  • HOCM
101
Q

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

A

a resting mean pulmonary artery pressure of >= 25 mmHg.

102
Q

In pulmonary HTN, which test can help in deciding on the appropriate management strategy.

A

acute vasodilator testing

103
Q

Treatment of pulmonary HTN, If there is apositive response to acute vasodilator testing

A

Oral CCB

104
Q

Treatment of pulmonary HTN, If there is anegative response to acute vasodilator testing

A
  1. phosphodiesterase inhibitors: sildenafil
  2. prostacyclin analogues: treprostinil, iloprost
  3. endothelin receptor antagonists
  • non-selective:bosentan
  • selective antagonist of endothelin receptor A:ambrisentan
105
Q

In pulmonary HTN, Patients with progressive symptoms should be considered for

A

heart-lung transplant.

106
Q

Target INR in mechanical valves

  • Aortic :
  • mitral :
A
  • Aortic : 3.0
  • mitral : 3.5
107
Q

Features of severe pre-eclampsia

A

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

108
Q

connection between the pulmonary trunk and descending aorta

Which condition?

A

PDA

109
Q

Management of PDA

A

indomethacin or ibuprofen
- inhibits prostaglandin synthesis

if associated with another congenital heart defect amenable to surgery thenprostaglandin E1 is useful to keep the duct openuntil after surgical repair

110
Q

angina-like chest pain on exertion

ST depression on exercise stress test

butnormal coronary arteries on angiography

Which condition?

A

Syndrome X

111
Q

Which drug is used as a first-line to control the rate in AF.

A

BB or CCB ( diltiazem )

112
Q

What to do, If one drug does not control the rate in patients with AF

A

combination therapy with any 2 of the following:

a betablocker

diltiazem

digoxin

113
Q

In AF, anticoagulation is indicated if CHA2DS2-VASc score

A

Score 1 in male
Score 2 in female

114
Q

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation

A

amiodarone

flecainide(if no structural heart disease)

others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

115
Q

If the patient has been inAF for more than 48 hours then anticoagulation should be given for…….

A

At least 3 weeks prior to CARDIOVERSION

116
Q

In AF, Following electrical cardioversion patients should be anticoagulated for

A

at least 4 weeks

117
Q

Rate control should be offered as the first‑line treatment strategy for atrial fibrillation except in people:

A
  1. New onset AF < 48 hrs
  2. Reversible cause of AF
  3. who have heart failure thought to be primarily caused by atrial fibrillation
  4. with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
  5. for whom a rhythm‑control strategy would be more suitable based on clinical judgement
118
Q

complications of catheter ablation

A

cardiac tamponade

stroke

pulmonary vein stenosis

119
Q

Features suggesting VT rather than SVT with aberrant conduction

A
  1. AV dissociation
  2. fusion or capture beats
  3. positive QRS concordance in chest leads
  4. marked left axis deviation
  5. history of IHD
  6. lack of response to adenosine or carotid sinus massage
  7. QRS > 160 ms
120
Q

Brugada syndrome

  • What type of inheritance?
  • Brugada syndrome is more common in …….
A
  • autosomal dominant
  • in Asians
121
Q

Brugada syndrome is caused by a mutation in …..

A

by amutation in the SCN5A gene which encodes the myocardial sodium ion channel protein

122
Q

ECG changes in Brugada syndrome

A

convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave

partial RBBB

123
Q

What is the investigation of choice in suspected cases of Brugada syndrome

A

the ECG changes may be more apparent following the administration of flecainide or ajmaline

124
Q

Burger disease
- It affects……. sized blood vessels.

  • strongly associated with ….
A
  • Small and medium vessel vasculitis.
  • strongly associated with smoking.
125
Q

Features of Buerger’s disease (also known as thromboangiitis obliterans)

A
  1. Raynaud’s phenomenon
  2. superficial thrombophlebitis
  3. extremity ischaemia
    - intermittent claudication
  • ischaemic ulcers
126
Q
  1. Which cardiac marker is the first to rise ?
  2. which one is useful to look for reinfarcation?
A
  1. Myoglobin
  2. CK-MB is useful to look for reinfarctionas it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)
127
Q

What are the acyanotic congenital heart diseases ?

A
  1. PDA
  2. ASD
  3. VSD
  4. COARCTATION OF AORTA
  5. AORTIC STENOSIS
128
Q

Who are at an high risk of Transposition of the great arteries (TGA)?

A

Children of diabetic mothers

129
Q

Transposition of the great arteries (TGA) is a form of cyanotic congenital heart disease. It is caused by thefailure of…………?

A

caused by thefailure of the aorticopulmonary septum to spiral during septation.

130
Q

cyanosis

tachypnoea

loud single S2

prominent right ventricular impulse

‘egg-on-side’ appearance on chest x-ray

Picture of which disease ?

A

Transposition of the great arteries

131
Q

Features of Tetralogy of Fallot

A
  1. VSD
  2. RVH
  3. Rt ventricular outflow tract obstruction, pulmonary stenosis
  4. Overriding aorta
132
Q

What is the most common cause of congenital heart disease

A

VSD

133
Q

Aetiology of VSD

A
  1. often association with chromosomal disorders
  • Down’s syndrome
  • Edward’s syndrome
  • Patau syndrome

cri-du-chat syndrome

  1. congenital infections
  2. acquired causes
    - post-myocardial infarction
134
Q

VSDs may be detected in utero during ……?

A

the routine 20 week scan.

135
Q

Investigations of Takayasu’s arteritis

A

MRA or CTA

136
Q

Treatment of Takayasu’s arteritis

A

Steroids

137
Q

Which drug is used as first-line in patients with peripheral arterial disease

A

clopidogrel should be used first-line in patients with peripheral arterial disease in preference to aspirin.

138
Q

Dressler’s syndrome tends to occur …… weeks following a MI.

A

occurs around2-6 weeks

139
Q

Dressler’s syndrome is treated with ……?

A

treated with NSAIDs.

140
Q

persistent ST elevationand left ventricular failure

Associated with Which of MI complications ?

A

Lt ventricular aneurysm

141
Q

Acute mitral regurgitation treated with….

A

treated with vasodilator therapy but often require emergency surgical repair.

142
Q

Treatment of Multifocal atrial tachycardia (MAT)

A

correction of hypoxia and electrolyte disturbances

rate-limiting calcium channel blockers are often used first-line

143
Q

Treatment of Kawasaki disease

A
  1. high-dose aspirin
  2. Iv Ig
144
Q

What is the initial screening test for coronary artery aneurysms in Kawasaki disease?

A

ECHO (rather than angiography)

145
Q

Cannon waves is Caused by …..?

A

Caused by the right atrium contracting against a closed tricuspid valve

146
Q

1- Causes of regular cannon waves

2- Causes of irregular cannon waves

A
  1. VT & atrio-ventricular nodal re-entry tachycardia (AVNRT)
  2. Complete heart block
147
Q

Causes of eruptive xanthoma

A

familial hypertriglyceridaemia

lipoprotein lipase deficiency

148
Q

Causes of Tendon xanthoma, tuberous xanthoma, xanthelasma

A

familial hypercholesterolaemia

remnant hyperlipidaemia

149
Q

Causes of Palmar xanthoma

A

remnant hyperlipidaemia

may less commonly be seen in familial hypercholesterolaemia

150
Q

Hypertension in pregnancy in usually defined as:

A

systolic > 140 mmHg or diastolic > 90 mmHg

151
Q

What is the next step, if the patient on antihypertensive (A+ C + D) and still BP uncontrolled?

A

Check potassium level

if potassium < 4.5 mmol/l add low-dose spironolactone

if potassium > 4.5 mmol/l add an alpha- or beta-blocker

152
Q

Blood pressure targets
If age < 80

A

Clinical BP : 140/90

ABPM/ HBPM : 135/ 85

  • Minus 5
153
Q

Blood pressure targets
If age > 80

A

Clinical BP : 150/90

ABPM/ HBPM : 145/ 85

  • Minus 5
154
Q

HOCM IS ASSOCIATED WITH

A

Friedreich’s ataxia

Wolff-Parkinson White

155
Q

Echo finding in HOCM

A

mnemonic - MR SAM ASH

mitral regurgitation (MR)

systolic anterior motion (SAM) of the anterior mitral valve leaflet

asymmetric hypertrophy (ASH)

156
Q

ECG findings in HOCM

A
  1. AF
  2. LVH
  3. Deep Q waves
  4. non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
157
Q

HOCM
defects involve a mutation in …….

A

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

158
Q

Drugs to avoid in HOCM

A

nitrates

ACE-inhibitors

inotropes

159
Q

Management of HOCM

A

Amiodarone

Beta-blockers or verapamil for symptoms

Cardioverter defibrillator

Dual chamber pacemaker

Endocarditis prophylaxis*

160
Q

Poor prognostic factors of HOCM

A
  1. syncope
  2. family history of sudden death
  3. young age at presentation
  4. non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring
  5. abnormal blood pressure changes on exercise
  6. increased septal wall thickness
161
Q

Eisenmenger’s syndrome

A
  1. PDA
  2. ASD
  3. VSD
162
Q

Exercise: physiological changes

Blood pressure

A

systolic increases, diastolic decreases

leads to increased pulse pressure

163
Q

Exercise: physiological changes

Cardiac output

A

stroke volume up to 1.5-fold increase

HR up to 3-fold increase

increase in cardiac output may be 3-5 fold

164
Q

Systemic vascular resistance falls in exercise due to

A

due to vasodilatation in active skeletal muscles.

165
Q

Ebstein’s anomaly may be caused by exposure to……..in utero.

A

lithium

166
Q

Ebstein’s anomaly
Associated with

A
  1. PFO
  2. ASD
  3. WPW SYNDROME
167
Q

JVP in

  1. Cardiac tamponade

Vs

  1. Constrictive pericarditis
A
  1. Absent Y descent
  2. X + Y present
168
Q

Arrhythmogenic right ventricular cardiomyopathy is inherited in an autosomal ……. pattern

A

autosomal dominant pattern

169
Q

In Arrhythmogenic right ventricular cardiomyopathy is theright ventricular myocardium is replaced by …….?

A

By fatty and fibrofatty tissue

170
Q

Management of Arrhythmogenic right ventricular cardiomyopathy

A

drugs: sotalol is the most widely used antiarrhythmic

catheter ablation to prevent ventricular tachycardia

implantable cardioverter-defibrillator

171
Q

triad of ARVC, palmoplantar keratosis, and woolly hair

A

Naxos disease

172
Q

Naxos disease is an autosomal ………….. variant of ARVC

A

autosomal recessive

173
Q

What are the ECG abnormalities in Arrhythmogenic right ventricular cardiomyopathy

A

ECG abnormalities in V1-3, typically T wave inversion

174
Q

Classic causes of Restrictive cardiomyopathy include

A

amyloidosis

post-radiotherapy

Loeffler’s endocarditis

175
Q

When can develop Peripartum cardiomyopathy ?

A

Typical develops between last month of pregnancy and 5 months post-partum

176
Q

Treatment of Takotsubo cardiomyopathy ( Stress’-induced cardiomyopathy)

A

Treatment is supportive

177
Q

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is inherited in an …….. fashion

A

autosomal dominant

178
Q

In Catecholaminergic polymorphic ventricular tachycardia,

the most common cause is a defect in ……

A

the most common cause is a defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum

179
Q

Treatment of Catecholaminergic polymorphic ventricular tachycardia

A
  1. B blocker
  2. ICD
180
Q

Aschoff bodiesdescribes the granulomatous nodules found in

A

in rheumatic heart fever

181
Q

The strongest risk factor for developing infective endocarditis is a ……..?

A

previous episodeof endocarditis

182
Q

Culture negative causes of IE

A
  1. prior antibiotic therapy
  2. Coxiella burnetii
  3. Bartonella
  4. Brucella
  5. HACEK:Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
183
Q

now the most common cause of infective endocarditis

A

Staphylococcus aureus

184
Q

endocarditis caused by organisms is linked withpoor dental hygieneor following a dental procedure

A

Streptococcus viridans

Streptococcus mitis and

Streptococcus sanguinis

185
Q

the most cause of endocarditis in patients following prosthetic valve surgery

A

coagulase-negative Staphylococci such asStaphylococcus epidermidis

186
Q

Streptococcus bovis is associated with…………….. cancer

A

colorectal cancer

187
Q

non-infective causes of IE

A

SLE (Libman-Sacks)

malignancy: marantic endocarditis

188
Q

4 Poor prognostic factors of IE

A
  1. Staphylococcus aureusinfection
  2. prosthetic valve (especially ‘early’, acquired during surgery)
  3. culture negative endocarditis
  4. low complement levels
189
Q

Mortality according to organism

staphylococci -……………%

bowel organisms - ………%

streptococci -………….. %

A

Mortality according to organism

staphylococci -30%

bowel organisms - 15%

streptococci -5%

190
Q

5 Indications for surgery in IE

A
  1. severe valvular incompetence
  2. aortic abscess (often indicated by a lengthening PR interval)
  3. infections resistant to antibiotics/fungal infections
  4. cardiac failurerefractory to standard medical treatment
  5. recurrent emboli after antibiotic therapy
191
Q

prophylaxis of Infective endocarditis

In dental procedures

A

do not require

192
Q

prophylaxis of Infective endocarditis

In upper and lower GIT procedures

A

Not require

193
Q

prophylaxis of Infective endocarditis

genitourinary tract; this includes urological, gynaecological and obstetric procedures and childbirth

A

Not require

194
Q

prophylaxis of Infective endocarditis

upper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopy

A

Not require

195
Q

Mechanism of action of WARFARIN
inhibits epoxide reductasepreventing the reduction of vitamin K to ……..?

A

its active hydroquinone form

196
Q

Factors that may potentiate warfarin

A
  1. liver disease
  2. P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
  3. cranberry juice
  4. drugs which displace warfarin from plasma albumin, e.g. NSAIDs
  5. inhibit platelet function: NSAIDs
197
Q

WARFARIN and breastfeeding

A

can be used

198
Q

INR 5.0-8.0
No bleeding

A

Withhold 1 or 2 doses of warfarin

199
Q

INR > 8
NO BLEEDING

A
  1. Stop warfarin
  2. Give oral vitamin K 1-5mg , Repeat dose of vitamin K if INR still too high after 24 hours

Restart when INR < 5.0

200
Q

INR 5.0-8.0
Minor bleeding

A
  1. Stop warfarin
  2. Give iv vitamin K 1-3mg

Restart when INR < 5.0

201
Q

INR > 8.0
Minor bleeding

A
  1. Stop warfarin
  2. Iv vitamin K 1-3mg
    Repeat dose of vitamin K if INR still too high after 24 hours

Restart warfarin when INR < 5.0

202
Q

Treatment of High INR

Major bleeding(e.g. variceal haemorrhage,intracranial haemorrhage)

A
  1. Stop warfarin
  2. Iv vitamin K 5mg
  3. Prothrombin complex concentrate - if not available then FFP
203
Q

Thiazide diuretics work byinhibiting ……..? 1……… reabsorption at the beginning of the ………2?…….. by blocking the thiazide-sensitive Na+-Cl−symporter.

A

Thiazide diuretics work byinhibiting (1. sodium ) reabsorption at the beginning of the (2. distal convoluted tubule (DCT)) by blocking the thiazide-sensitive Na+-Cl−symporter.

204
Q

7 common Side effects of thiazides

A
  1. Dehydration
  2. Postural Hypotension
  3. Hypo K , Na
  4. Hyper Ca
  5. Gout
  6. impaired glucose tolerance
  7. impotence
205
Q

4 Rare Side effects of thiazide

A
  1. thrombocytopaenia
  2. agranulocytosis
  3. photosensitivityrash
  4. pancreatitis
206
Q

Thiazide induced hypo K due to …..

A

increased delivery of sodium to the distal part of the DCT.

207
Q

Which antibiotics are contraindicated with statins ?

A

macrolides (e.g. erythromycin, clarithromycin)

Statins should be stopped until patients complete the course

208
Q

Statinsinhibit the action of …….

A

HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.

209
Q

When prescribed Statins , recommend checking LFTs at ………?

A

at baseline, 3 months and 12 months.

210
Q

When to DC statin in liver impairment

A

discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range

211
Q

Risks factors for myopathy due to statins

A
  1. advanced age,
  2. female sex,
  3. low body mass index
  4. presence of multisystem disease such as DM.
212
Q

Myopathy due to statins is more common in which preparations ?

A
  1. simvastatin
  2. atorvastatin
213
Q

Mechanism of action of hydralazine increases ……… leading to smooth muscle relaxation

A

cGMP

214
Q

6 Side effects of hydralazine

A
  1. Tachycardia
  2. Palpitations
  3. Headache
  4. Flushing
  5. Fluid retention
  6. Drug induced lupus
215
Q

Which drug can reduce the risk of developing pre eclampsia

A

Low dose aspirin

216
Q

What is the first line for pregnancy induced HTN

A

I. Labetalol

If asthmatic&raquo_space; nifedipine and hydralazine may also be used

217
Q

The specific cut-off value for defining a positive acute vasodilator test

A

decrease in mean pulmonary arterial pressure by at least 10 mmHg to a level below 40 mmHg

218
Q

What is the first line treatment of isolated systolic HTN

A

CCB

MRCP Part 1 (15 decks)

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