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Passmedicine MRCP Part 1 > Cardiology Gap > Flashcards

Cardiology Gap 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

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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

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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

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25
Q

Features of severe MS

A

length of murmur increases
opening snap becomes closer to S2

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26
Q

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

A

opening snap
indicates mitral valve leaflets are still mobile

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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
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28
Q

The effect of Adenosine is enhanced by

A

Dipyridamole (antiplatelet agent)

DE-AR Adinosine
Dipyradimole Elevate
Aminophylline Reduce

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29
Q

The effects of adenosine is blocked by

A

Theophyllines

DE-AR Adinosine
Dipyradimole Elevate
Aminophylline Reduce

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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

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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

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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)

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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

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34
Q

Verapamil should not be prescribed concurrently with

A

B Blockers (risk of CHB)

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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)

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36
Q

Why beta-blockers should not be prescribed concurrently with verapamil

A

risk of complete heart block

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37
Q

Rate Limiting CCBs

A

Verapamil
Diltiazem

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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

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39
Q

First cardiac enzyme to rise

A

Myoglobin

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40
Q

Which cardiac marker is useful to look for reinfarction

A

CK-MB

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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

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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

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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

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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

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45
Q

Late systolic Murmur

A

mitral valve prolapse
coarctation of aorta

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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)

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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.

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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 **

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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

55
Q

Indications for a temporary pacemaker

A

Indications for a temporary pacemaker
- symptomatic/haemodynamically unstable bradycardia, not responding to atropine
- post-ANTERIOR MI: type 2 or complete heart block
post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable
- trifascicular block prior to surgery

56
Q

The key diagnostic tests used to identify patients likely to benefit from cardiac resynchronization therapy is —–

A

transthoracic echocardiogram and ECG.

57
Q

Indication of Biventricular Pacing

A

Heart Failure EF < 35%
Wide QRS >120

58
Q

HOCM genetics-
mutation in

A

Autosomal Dominant

the most common defects involve a mutation in the 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

59
Q

HOCM is associated with
Neuro
Cardio

A

Friedreich’s ataxia
Wolff-Parkinson White

60
Q

Echo Findings of HOCM

A

Echo findings - mnemonic - MR SAM ASH
mitral regurgitation (MR)-
systolic anterior motion (SAM) of the anterior mitral valve leaflet- (SAM+MR causes Pansystolic Murmur)
asymmetric hypertrophy (ASH)-

61
Q

Murmurs of HOCM

A

systolic murmurs
1. ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting
2. pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation

62
Q

Drugs to avoid in HOCM

A

nitrates
ACE-inhibitors
inotropes

63
Q

Rx for HOCM

ABCDE

A

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

64
Q

Poor Prognostic feature of 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 is also associated with a poor prognosis.

65
Q

Drugs for HD Stable VT

A

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

66
Q

Which drug should not be used in VT

A

Verapamil
( due to the risk of causing significant hypotension, ventricular fibrillation and cardiac arrest. H)

67
Q

What if drug therapy fails in VT

A

EPS
ICD

68
Q

Indication of ICD in VT

A

Significantly reduced EF

69
Q

Drugs causing Prolonged QT

A

Long QT drugs: ABCDE + Hypo
A: anArrhythmic: ie Amiodrone
B: anBiotics: Macrolides, Quinolone
C: pCychotics: Haloperidol
D: antDepressant: SSRI, TCA
E: antEmetics: Ondansetron

Hypo ( hypokalemia, hypomagnesaemia, hypocalcemia)

70
Q

First Line investigations for Palpitation

A

12-lead ECG
Thyroid function tests
Urea and electrolytes
Full blood count
**
Then
Holter

Then
External loop recorder
Implantable loop recorder**

71
Q

ECG changes of Pericarditis

A

‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis

72
Q

Drugs for Pericarditis

A

NSAIDs
+
Colchicine

73
Q

‘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

A

Takotsubo

74
Q

What happens in Takotsubo

A

Transient, apical ballooning of the myocardium
Treatment is supportive

75
Q

Types of Cardiomyopathy

A
  1. Primary
    a. Genetic: HOCM, Arrhythmogenic right ventricular dysplasia
    b. Mixed: Dilated, Restrictive
    c. Acquired: Peripartum, Takotsubo
  2. Secondary:
    Infective, Infiltrative, Storage, Toxicity
    (Please check passmed)
76
Q

Dilated cardiomyopathy Classic causes include:

ABCD

A

ABCD

Alcohol
Beriberi (Wet)
Coxsackie B virus
Doxorubicin

77
Q

Restrictive Cardiomyopathy causes
SLASHER

A

SLASHER

Sarcoidosis
Lofflers
Amyloid
Scleroderma
Haemochromatosis
Eendocardial fibroelastosis
Post-Radiation fibrosis

78
Q

What happpens in Arrythmogenic Rt ventricular Dysplasia

A

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 complex

79
Q

ECG Abnormalities seen in What happpens in Arrythmogenic Rt ventricular Dysplasia

A

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

  • T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
  • Epsilon wave (most specific finding, seen in 50% of patients)
  • Localised QRS widening in V1-3 (> 110ms)
80
Q

Epsilon wave seen in

A

Arrythmogenic Rt Ventricular Dysplasia

81
Q

Inv in Cardiomyopathy

A

Echo
cMRI

82
Q

Restrictive myocarditis causes systolic/diastolic dysfn

A

causes predominately diastolic dysfunction

83
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

84
Q

PARTS OF JVP

A

A WAVE
C WAVE
V WAVE

X DESCENT
Y DESCENT

85
Q

DETAILS OF JVP

A

‘a’ wave = atrial contraction:
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in atrial fibrillation

Cannon ‘a’ waves:
caused by atrial contractions against a closed tricuspid valve. therefore can be seen in VT when atrial and ventricular contraction is not co-ordinated.
are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

‘c’ wave
closure of tricuspid valve
not normally visible

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

‘x’ descent = fall in atrial pressure during ventricular systole

‘y’ descent = opening of tricuspid valve

86
Q

Auscult of Coarc of Aorta

A

mid systolic murmur, maximal over the back
apical click from the aortic valve

87
Q

Association of Coarc of Aorta

A

TBBN

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

88
Q

Brugada Genetics

A

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

89
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

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

90
Q

Inv of Choice for Suspected Brugada

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

91
Q

Rx for Brugada

A

ICD

92
Q

Causes of Culture Neg IE

A

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

93
Q

Organisms for IE

A

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

Streptococcus viridans- common in developing countries
(Streptococcus mitis and Streptococcus sanguinis)- 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.

Streptococcus bovis- associated with colorectal cancer
the subtype Streptococcus gallolyticus is most linked with colorectal cancer

94
Q

Diagnostic Criteria of IE

A

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

95
Q

Poor prognostic factors of IE

A

Staphylococcus aureus infection
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels

96
Q

Prophylaxis for IE

A

not routinely recommended. But:

  • any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing
  • if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis
97
Q

Most common organism of IE after dental procedure

A

Viridans

(Mitis and Galactolytoicus)

98
Q

Organism of IE post valve surgery

A

Epidermidis/
Coagulase Neg

99
Q

What should you monitor when MgS04 is given?

A

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

100
Q

Types of CCBs

A

rate-limiting CCBs/Non-dihydropyridine:
Verapamil
Diltiazem

dihydropyridine CCBs:
amlodipine, nifedipine)

101
Q

4 As of Rheumatic fever
organism
blood tests
histology

A

The 4 As of rheumatic fever:
* caused by group-A-strep
* high ASO-titre
* presence of Aschoff bodies and Anitschkow cells

102
Q

Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of ———-

A

Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of >= 20 mmHg. E

103
Q

Features of Pulmonary HTN

A

Features
progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis

104
Q

Clinical signs in PH

A

right ventricular heave: indicating right ventricular hypertrophy or dilatation
**loud P2: **early in the disease reflects increased pulmonary artery pressure and may be accompanied by a palpable P2 in severe cases. With advanced PAH there may be right ventricular failure leading to a soft S2
**raised JVP with prominent ‘a’ waves: **reflects increased resistance to right atrial emptying due to elevated right ventricular end-diastolic pressure
tricuspid regurgitation

105
Q

How to decide management plan for PH?

A

acute vasodilator testing is central to deciding on the appropriate management strategy. Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide.

106
Q

What plays a key role in pathogenesis of PAH?

A

Endothelin

107
Q

Management of PAH

A

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

If there is a negative response to acute vasodilator testing (the vast majority of patients)
- prostacyclin analogues: treprostinil, iloprost
- endothelin receptor antagonists
a. non-selective: bosentan
b. selective antagonist of endothelin receptor A: ambrisentan
- phosphodiesterase inhibitors: sildenafil

Patients with progressive symptoms should be considered for a heart-lung transplant.

108
Q

Amiodarone half life

A
109
Q

Amiodarone mechanism of action

A

Amiodarone is a class III antiarrhythmic agent.*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)

110
Q

Which class is amiodarone

A

class 3

111
Q

Adverse effects of Amiodarone use

A

Adverse effects of amiodarone use
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

112
Q

Features of severe aortic stenosis

A

Narrow pulse pressure
Slow rising pulse
Delayed ESM
Soft/absent S2
S4
Thrill
Duration of murmur
Left ventricular hypertrophy or failure

113
Q

Management for Aortic Stenosis

A
  • if asymptomatic then observe the patient is a general rule
  • if symptomatic then valve replacement
  • if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery

options for aortic valve replacement (AVR) include:
- surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined
- transcatheter AVR (TAVR) is used for patients with a high operative risk

  • balloon valvuloplasty:
    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
114
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

115
Q

Commonest cause of Aortic Stenosis in Older patients

A

Degenerative Calcification

116
Q

Causes of AS in younger patients

A

Bicuspid aortic valve

117
Q

First cardiac marker to rise

A

Myoglobin

118
Q

Role of troponin in cardiac muscle

A

Component of thin filament

to remember: troponIN = thIN

119
Q

Chronic Heart Failure Management

A
120
Q

MRAs

A

Spironolactone
Eplerenone
Finerenone

Passmedicine MRCP Part 1 (8 decks)

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