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Passmedicine MRCP Part 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Features suggesting VT rather than SVT with aberrant conduction

A

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

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2
Q

The strongest risk factor for developing infective endocarditis is—

A
  • a previous episode of endocarditis.
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3
Q

Brugada Syndrome is caused by which genetic change?

A

a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein

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4
Q

ECG in Brugada

A

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

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5
Q

Third Heart Sound found in

A

S3 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)
- mitral regurgitation

DCM has three letters - S3
D- Dilated Cardiomyopathy/LVF
C- Constrictive Pericarditis
M- Mitral Regurgitation

HOCM has four letters - S4

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6
Q

Fourth Heart Sound

A
  • Aortic stenosis
  • HOCM
  • Hypertension
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7
Q

HTN in pregnancy Rx

A
  • Oral labetalol is now first-line following the 2010 NICE guidelines
  • Oral nifedipine (e.g. if asthmatic)
  • Hydralazine
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8
Q

Thiazide Diuretics Causes

A

Hypotension (Postural)
Hypokalaemia
Hyponatraemia
Hypercalcaemia
Hypocalciuria
Hyperglycemia (Impaired glucose tolerance)

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9
Q

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

is the hallmark of–

A

Cardiac Syndrome X

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10
Q

Angina Rx stepwise

A

Step 1: start with BB or CCB
Step 2: increase to maximum tolerated dose
Step 3: if still poor response > add BB/CCB
(if CCB used in combination with a BB then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine)

  • if a patient is on monotherapy and cannot tolerate the addition of CCB or BB then consider one of the following drugs:
  • a long-acting nitrate
  • Ivabradine
  • Nicorandil
  • Ranolazine

Step 4: if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG

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11
Q

Sydrome X

A

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

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12
Q

Rate limiting CCB

A

Verapamil
Diltiazem

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13
Q

Poor prognostic factors for IE

A
  • Staphylococcus aureus infection
  • Prosthetic valve (especially ‘early’, acquired during surgery)
  • Culture negative endocarditis
  • Low complement levels
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14
Q

IE Rx:
Native
Prosthetic Valve
Strep B
Staph

A
  • pRosthetiG (all prosthetic valves require Rifampicin and Gent)
  • streB (all strep IEs require Benpen)
  • steF (all staph IEs require Fluclox)
  • Vallergic (all pen allergic patients receive vanc)
  • All Prosthetic valves: have to give Rifamipcin + Low dose Gent (+ other agent either Flucloxacillin or Vanc)
  • Pen allergy: Switch Penicillin to Vancomycin + low dose Gent (except in native valve staph where you give Vancomycin + Rifampicin)
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15
Q

Define Anginal Chest Pain

A
  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in about 5 minutes

patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain

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16
Q

Choice of prosthetic Heart Valves

A
  • Comparatively young (expected lifespan >15-20 years) = Mechanical (with longterm anticoagulation)
  • Old (less lifespan) = Bioprosthetic (short term anticoagulation)
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17
Q

Anticoagulation for Prosthetic Valves

A

Bioprosthetic: Aspirin
Mechanical: Warfarin

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18
Q

Target INR for Prosthetic Valves

A

Aortic: 3.0
Mitral: 3.5

AM 3:35

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19
Q

Why shouldn’t you prescribe BB with Verapamil

A

for the risk of Complete Heart Block

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20
Q

Endocrine causes of Secondary HTN

A

Primary hyperaldosteronism
Phaeochromocytoma
Cushing’s syndrome
Liddle’s syndrome
Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
Acromegaly

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21
Q

Drug Causes of Secondary HTN

A

Steroids
Monoamine oxidase inhibitors
The combined oral contraceptive pill
NSAIDs
Leflunomide

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22
Q

Poor prognostic indicator for HOCM

A

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
An increased septal wall thickness of > 3 cm

23
Q

Association of Aortic Dissection

A

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

24
Q

Classification of Aortic Dissection

A

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

DeBakey classification:
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally

25
Q

Features of severe MS

A

length of murmur increases
opening snap becomes closer to S2

26
Q

Which feature in the murmur indicates mitral valve leaflets are still mobile

A

opening snap
indicates mitral valve leaflets are still mobile

27
Q

Indications for a temporary pacemaker

A
  • Symptomatic/haemodynamically unstable bradycardia, not responding to atropine
  • post-ANTERIOR MI: type 2 or complete heart block
    (Note: post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable)
  • trifascicular block prior to surgery
28
Q

The effect of Adenosine is enhanced by

A

Dipyridamole (antiplatelet agent)

DE-AR Adinosine
Dipyradimole Elevate
Aminophylline Reduce

29
Q

The effects of adenosine is blocked by

A

Theophyllines

DE-AR Adinosine
Dipyradimole Elevate
Aminophylline Reduce

30
Q

Adenosine M/A

A

Rule of A
Agonist of A1 Receptor
of the AV Node
causes transient AV Block
inhibits **Adenylyl cyclase thus reducing cA**MP
(and causing hyperpolarization by increasing outward potassium flux)

+
DE-AR Adinosine
Dipyradimole Elevate
Aminophylline Reduce

31
Q

Mechanism, Adverse Effect and Contraindication of Nicorandil

A

Nicorandil is a vasodilatory drug used to treat angina. It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

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

Contraindications
left ventricular failure

32
Q

causes of infective endocarditis

A

Staphylococcus aureus- most common- particularly in acute presentation and IVDUs
Streptococcus viridans( Streptococcus mitis and Streptococcus sanguinis) - historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries
technically Streptococcus viridans is a pseudotaxonomic term, referring to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are
they are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure
coagulase-negative Staphylococci such as Staphylococcus epidermidis
commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination.
after 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)
Streptococcus bovis
associated with colorectal cancer
the subtype Streptococcus gallolyticus is most linked with colorectal cancer
non-infective
systemic lupus erythematosus (Libman-Sacks)
malignancy: marantic endocarditis

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

33
Q

Investigations for stable angina:

A

1st line: CT coronary angiography
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: invasive coronary angiography

Examples of non-invasive functional imaging:
myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
stress echocardiography or
first-pass contrast-enhanced magnetic resonance (MR) perfusion or
MR imaging for stress-induced wall motion abnormalities

34
Q

Verapamil should not be prescribed concurrently with

A

B Blockers (risk of CHB)

35
Q

remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)

A

verapamil (risk of complete heart block)

36
Q

Why beta-blockers should not be prescribed concurrently with verapamil

A

risk of complete heart block

37
Q

Rate Limiting CCBs

A

Verapamil
Diltiazem

38
Q

Rx of Angina

A
  • all patients should receive aspirin and a statin in the absence of any contraindication
  • sublingual glyceryl trinitrate to abort angina attacks

+
1. beta-blocker/calcium channel blocker
( if only CCB, use rate-limiting one such as verapamil or diltiazem)
2. Maximize dose
3. Add BB/CCB
(if CCB used with a BB, then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine, felodipine)
+
Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
4. If on monotherapy and cannot tolerate the other one, then consider one of the following drugs:
- a long-acting nitrate
- Ivabradine
- Nicorandil
- Ranolazine

5. if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG

39
Q

First cardiac enzyme to rise

A

Myoglobin

40
Q

Which cardiac marker is useful to look for reinfarction

A

CK-MB

41
Q

Which Cardiac Markers bind with which protein?

A

TIC - TAC
T Troponin T binds with T: Tropomyosin
I Troponin I binds with A: Actin
T Troponin C binds with C: Calcium ions

42
Q

Arrhythmogenic right ventricular cardiomyopathy

ECG Finding
Echo Finding
Clincial finding

A

the right ventricular myocardium is replaced by fatty and fibrofatty tissue

Presents with palpitations, syncope, sudden cardiac death

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 complex
echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall

Rx:
Sotalol
catheter ablation
Implantable cardioverter-defibrillator

43
Q

All Murmurs

A

Ejection systolic:
louder on expiration::
- aortic stenosis
- hypertrophic obstructive cardiomyopathy

louder on inspiration:
- pulmonary stenosis
- atrial septal defect

also: tetralogy of Fallot

Holosystolic (pansystolic):
- mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
- tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect (‘harsh’ in character)

Late systolic
mitral valve prolapse
coarctation of aorta

Early diastolic
aortic regurgitation (high-pitched and ‘blowing’ in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)

Mid-late diastolic
mitral stenosis (‘rumbling’ in character)
Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

Continuous machine-like murmur
patent ductus arteriosus

RILE
Right-sided murmur → heard best on Inspiration
Left-sided murmur → heard best on Expiration

44
Q

Ejection Systolic Murmur
:
AHPAT

A

Louder on expiration:
- aortic stenosis
- hypertrophic obstructive cardiomyopathy

louder on inspiration:
- pulmonary stenosis
- atrial septal defect

also: tetralogy of Fallot

45
Q

Late systolic Murmur

A

mitral valve prolapse
coarctation of aorta

46
Q

Early diastolic

A

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

47
Q

The examination findings of a pansystolic murmur, loudest in the mitral area and crackles on chest auscultation after MI

A

The examination findings of a pansystolic murmur, loudest in the mitral area and crackles on chest auscultation suggest a diagnosis of acute mitral regurgitation and pulmonary oedema, which is most likely to be caused by a rupture of the papillary muscle. This typically occurs 1-7 days post-infarction.

48
Q

Prinzmetal Angina

A

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, Felodipine **

49
Q

Adverse effects of amiodarone use

A

বালডা সবজায়গায় সমস্যা করে
1. Eyes: corneal deposits, photosensitivity
2. Thyroid:- thyroid dysfunction: both hypothyroidism and hyper-thyroidism
3. Heart: bradycardia, lengths QT interval
4. Lungs: pulmonary fibrosis/pneumonitis
5. Liver: liver fibrosis/hepatitis
6. Limbs; peripheral neuropathy, myopathy
7. Appearance; ‘slate-grey’ appearance
Even
thrombophlebitis and injection site reactionsl

50
Q

Monitoring of patients taking amiodarone

A

Monitoring of patients taking amiodarone
TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months

51
Q

what type of drug is amiodarone

A

Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)

52
Q

Thiazide Diuretics

A

Thiazide diuretics

Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Clˆ’ symporter. Potassium is lost as a result of more sodium reaching the collecting ducts. Thiazide diuretics have a role in the treatment of mild heart failure although loop diuretics are better for reducing overload. The main use of bendroflumethiazide was in the management of hypertension but recent NICE guidelines now recommend other thiazide-like diuretics such as indapamide and chlortalidone.

Common adverse effects:
dehydration
postural hypotension
hypokalaemia
due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions
hyponatraemia
hypercalcaemia
the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones
gout
impaired glucose tolerance
impotence

Rare adverse effects:
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

53
Q

M/A of Loop Diuretics

A

Loop diuretics

Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl. There are two variants of NKCC; loop diuretics act on NKCC2, which is more prevalent in the kidneys.

54
Q

Adverse Effects of Loop Diuretics

A

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

Passmedicine MRCP Part 1 (5 decks)

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