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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Most common causes of the monomorphic and polymorphic VT?

A
  1. Monomorphic VT - MI
  2. Polymorphic VT - QT prolongation, which could be secondary to:
    a. drugs - Amiodarone (class III), sotalol (III & II), class 1a antiarrhythmic (Na blockers)
    TCA, SSRI - fluoxetine
    chloroquine
    terfenadine (anti-histamine)
    erythromycin
    methadone
    haloperidol, ondansetron
    b. congenital - Jervell-Lange-Nielsen syndrome (deafness and is due to an abnormal potassium channel);
    Romano-Ward syndrome (no deafness)
    c. other - electrolyte: HYPO: Ca, K, Mg
    (HYPER-k can as well but in those with structural heart disease, rare)
    acute MI, myocarditis
    hypothermia
    SAH
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2
Q

Classes of anti-arrhythmic drugs

A
  1. Sodium channel blockers:
    Ia: Quinidine, procainamide, disopyramide
    Ib: Lidocaine, phenytoin, mexiletine
  2. Beta blockers: atenolol, esmolol, propranolol, metoprolol.
  3. Potassium channel blockers: Sotalol, Amiodarone (but has I-IV features)
  4. Calcium channel blockers: Verapamil, Diltiazem, Nifedipine, amlodipine
  5. Miscellaneous: Adenosine, Mg, Digoxin

Some Block Potassium Channels

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3
Q

Management of VT

A
  1. Identify if patient is stable
    If unstable: SBP <90, syncope, chest pain, HF -> synchronised DC cardioversion

If stable -> anti-arrhythmics:
Amiodarone (III)
lidocaine (Ib - CAUTION in severe LV impairment)
procainamide (Ia)

If the drug therapy fails -> electrical cardioversion
Consider ICD in those with impaired LV

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4
Q

4 causes of raised JVP?

A

Raised JVP = raised pressure in RA (use IJV)

  1. HF
  2. Fluid overload
  3. Constrictive pericarditis
  4. Cardiac tamponade
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5
Q

JVP vs carotid pulse

A
  1. no pulsation on palpation
  2. 2 waves (pulses) per heartbeat
  3. hepatojugular reflex
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6
Q

List waves of the JVP waveform

A

A wave - atrial contraction (upward)
X descent (first) - atrial relaxation (downward)
C wave - RV contraction, TV closure and bulging into the RA (upward, not usually seen)
X descent (second) - remaining RV contraction but RA is draining blood from the IJV and is expanding (downward)
V wave - RA fill with blood and in turn the IJV is filling with blood
Y wave - TV opening and emptying of the RA

‘x’ descent = fall in atrial pressure during ventricular systole
‘y’ descent = opening of tricuspid valve

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7
Q

JVP waveform abnormalities

A
  1. Absent A waves in AF
  2. Large A waves in TS, RVH (due to PS, pulmonary hypertension), HOCM
  3. Cannon A waves - atrial contractions against a closed TV: seen in CHB, VT/ectopics, nodal rhythm, single chamber ventricular pacing
  4. Large V wave and absent X descent - TR
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8
Q

What imaging should be performed for patients in whom stable angina cannot be excluded by clinical assessment alone

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)
  • stress echocardiography
  • first-pass contrast-enhanced MR perfusion
  • MR imaging for stress-induced wall motion abnormalities
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9
Q

Definition of PAH

A

Pulmonary arterial hypertension (PAH) - resting mean pulmonary artery pressure of >= 25 mmHg.

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10
Q

Risk factors for PAH

A
  • females&raquo_space; males (30-50 years)
  • chronic lung diseases
  • HIV, cocaine and anorexigens (e.g. fenfluramine)

Around 10% of cases are AD inheritance

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11
Q

Features of PAH

A
  • progressive exertional SOB, exertional chest pain and exertional syncope
  • peripheral oedema
  • cyanosis
  • RV heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation
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12
Q

What test is key to identify an appropriate tx for PAH? What does it aim for and how is performed?

A

Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators, such as IV epoprostenol or inh nitric oxide.

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13
Q

How do you tx PAH patients with positive and negative response to acute vasodilator testing?

A
  1. Positive response (a minority of patients) - PO Ca channel blockers
  2. Negative response (the vast majority of patients)
    - prostacyclin analogues: treprostinil, iloprost
    - endothelin receptor antagonists: bosentan, ambrisentan
    - phosphodiesterase inhibitors: sildenafil

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

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14
Q

What is the advice on anticoagulation & anti-platelets in the following cases:
Stable CVD + VTE/AF
Post ACS/PCI
VTE on Anti-platelet

A

Stable CVD + VTE/AF - Anticoagulant monotherapy
Post ACS/PCI - up to 6 month triple therapy- 6 month dual therapy
VTE on Antiplatelet - calculate HAS BLED score , if low - dual, if high anticoagulant monotherapy (up to 6 months)

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15
Q

Choice of anticoagulation in the following cases of PE:

  1. Suspected and subsequently confirmed PE
  2. PE in a patient with active cancer
  3. PE in a patient with a renal impairment
  4. PE in a patient with APS
  5. PE in a haemodynamically unstable patient
  6. Recurrent PE
A
  1. apixaban or rivaroxaban once PE is suspected, with this continued if the diagnosis is confirmed.

If neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by warfarin.

  1. If the patient has active cancer - use a DOAC, unless this is contraindicated.
  2. If renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by warfarin.
  3. APS (specifically ‘triple positive’ in the guidance) then LMWH followed by warfarin
  4. Thrombolysis
  5. Consider IVC filter
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16
Q

Duration of anticoagulation for treating PE

A
  1. Provoked - 3/12, could continue up to 6/12 in total if associated with active cancer
  2. Unprovoked - 6/12
    Consider HASBLED
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17
Q

Features of severe aortic stenosis

A 
narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
LV hypertrophy or failure
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18
Q

Clinical features of symptomatic aortic stenosis

A
  • chest pain
  • dyspnoea
  • syncope
  • ESM classically radiates to the carotids; this is decreased following the Valsalva manoeuvre
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19
Q

Causes of aortic stenosis

A
  • degenerative calcification (most common cause in > 65 years)
  • bicuspid aortic valve (most common cause in < 65 years)
  • William’s syndrome (supravalvular aortic stenosis)
  • post-rheumatic disease
  • subvalvular: HOCM
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20
Q

Management of patient with AS (consider symptomatic and asymptomatic)

A
  • if asymptomatic then observe
  • if asymptomatic but valvular gradient > 40 mmHg and with features such as LVSD then consider surgery
  • if symptomatic then valve replacement

CVD may coexist -> for this reason an angiogram is often done prior to surgery so that the procedures can be combined.
Balloon valvuloplasty is limited to patients with critical AS who are not fit for valve replacement

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21
Q

Which drug should be avoided in irregular broad complex tachycardia and why?
What is this drug used for?
What condition is a CI for it?

A

Adenosine as it can precipitate VF.
Adenosine is used in narrow and regular broad complex SVT.
To be avoided in asthmatics

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22
Q

Which drug must be avoided in VT and why?

What is this drug usually used for?

A

Verapamil as it can precipitate cardiac arrest.
It should be avoided if there is any uncertainly whether this is SVT or VT.
Verapamil is an option for termination of SVT.

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23
Q
  1. What is the strongest risk factor for IE?
  2. Which is the most commonly affected valve?
  3. Which is the most typically affected valve in IVDU?
A
  1. previous episode of endocarditis.
  2. mitral valve
  3. tricuspid lesion
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24
Q
  1. What is the most common cause (organism) of IE?
  2. What is the most common cause of IE in DEVELOPING countries? Where can they be found in the body and what procedure can they be linked with?
  3. What is the most common organism causing IE in those who had undergone a surgery / prosthetic valve, have indwelling lines?
  4. What condition is the strep Bovis associated with? What is its subtype that is most associated with that condition?
  5. What are the non-infective causes of endocarditis?
  6. What are the culture negative causes of IE?
A
  1. Staphylococcus aureus
    particularly common in acute presentation and IVDUs
  2. Streptococcus viridans: Streptococcus mitis and Streptococcus sanguinis - both found in the mouth and are linked with poor dental hygiene or following a dental procedure
  3. Coagulase-negative Staphylococci: Staphylococcus epidermidis - indwelling lines, prosthetic valve surgery, perioperative contamination. After 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)
  4. Streptococcus bovis (the subtype Streptococcus gallolyticus): associated with colorectal cancer.
  5. SLE (Libman-Sacks)
    Malignancy: marantic endocarditis
6. Prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
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25
Q

What is the target INR for a patient with a:

  1. Aortic valve replacement
  2. Mitral valve replacement
A
  1. 3.0

2. 3.5

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26
Q

Bioprosthetic valve vs mechanical valve replacement - anticoagulation vs anti-platelet requirements

A 
1. Biological valve: Usually no need for anticoagulation, but warfarin may be needed for the first 3/12 depending on patient's risk factors 
Long-term anti-platelet is required 
- indications: 
> 65 years for aortic valves
> 70 years for mitral valves
  1. Mechanical: life-long anticoagulant, usually with warfarin over DOAC.
    Anti-plt depending on patient’s co-morbidities, such as IHD.
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27
Q

ECG STEMI criteria:

  1. V2-V3 changes depending on age and gender
  2. in other leads
  3. other ECG changes
A
  1. > 2.5mm STE in men <40yo OR >2.0mm STE in men >40 OR
    1.5mm STE in women
  2. > 1.0mm in other leads
  3. new LBBB
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28
Q

What are the indications for a PCI vs fibrinolysis in STEMI

A

PCI indications:

  1. Presentation within 12h and ability to deliver PCI in 2h
  2. Presentation after 12h but ongoing chest pain / cariogenic shock
  3. Failed fibrinolysis - if ECG 90min after fibrinolysis doesn’t show >50% resolution of STE

Fibrinolysis indications:
1. Presentation within 12h and inability to deliver PCI within 2h

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29
Q

Drugs used in PCI:

  1. PRIOR to PCI
  2. DURING PCI: arterial vs femoral access
  3. Other management options during PCI
A
  1. DUAT: aspirin +
    - prasugrel
    - ticagrelor if pt is at high risk of bleeding
    - clopidogrel if pt is on anticoag
    • arterial access: unfractionated heparin +/- GPI (In case of worsening / persistent thrombus
    • femoral access: Bivalirudin with GPI
3. thrombus aspiration 
complete revascularisation (for patients with multivessel CAD without cardiogenic shock)
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30
Q

List examples of GPI drugs

A 
ABCIXIMAB
tirofiban
Aggrastat
eptifibatide
Integrilin
ReoPro
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31
Q

Fibrinolysis in STEMI:

  1. What are the drugs used in fibrinolysis
  2. What should be given afterwards
  3. What should be done after the procedure
A
  1. Streptokinase, alteplase, tPA (tissues plasminogen activator), reteplase
    Those fibrinolytic drugs are also thrombolytic
  2. Ticagrelor
    - clopidogrel if patient is at high risk of bleeding
  3. ECG 60-90min after the procedure
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32
Q

Management of NSTEMI / unstable angina

  1. What at the indications for PCI
  2. What are CI to fondaparinux
  3. What alternative to fondaparinux could be used
  4. What should be given PRIOR to PCI
A
  1. PCI in NSTEMI / unstable angina if
    - Pt is unstable
    - Patient is intermediate / high GRACE risk (>3.0%):
    a. immediately if pt is unstable
    b. within 72h if pt is stable
    - Recurrent ischaemia during admission
  2. Do NOT give fondaparinux if patient is at high risk of bleeding and / or is undergoing immediate PCI / Also poor renal function
  3. Unfractionated heparin should be used if patient is undergoing immediate PCI and / or creat is >265
  4. If PCI is going ahead, then DUAT PRIOR to PCI, as with the STEMI patients undergoing PCI
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33
Q

Management of NSTEMI / unstable angina

  1. Low risk patient (GRACE =<3.0%)
  2. intermediate / high risk
A
  1. Low risk - conservative Mx:
    - DUAT: aspirin +
    ticagrelor
    if pt is high risk of bleeding / is on anticoagulant -> switch to clopidogrel
    - fondaparinux
    if not at high risk of bleeding
  2. Intermediate / high risk of bleeding:
    - DUAT: aspirin +
    prasugrel
    consider switching to ticagrelor if high risk of bleeding OR to clopi if on anticoagulant
    - unfractionated heparin
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34
Q
  1. Complications of bicuspid aortic valve

2. Syndrome / conditions associated with it

A
  1. Aortic stenosis or regurgitation;
    aortic dissection and aneurysm formation of the ascending aorta
  2. Turner’s syndrome
    coarctation of the aorta
    left dominant coronary circulation (the posterior descending artery arises from the circumflex instead of the right coronary artery)
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35
Q

Which valves are open vs closed during systole and diastole? -> murmurs

A 
Systole: 
valves open: A, P 
valves closed: M, T 
Hence -> aortic and pulmonary stenosis 
mitral and tricuspid regurgitation 
Diastole: 
valves open: M, T 
valves closed: A, P 
Hence: mitral and tricuspid stenosis 
aortic and pulmonary regurgitation

(Aortic regurgitation - Austin-Flinn murmur
Pulmonary regurgitation - Graham-Steel murmur)

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36
Q

Which murmurs get louder in inspiration vs expiration?

A

RINspiration: Right sided murmurs get louder during INspiration

LEXpiration: Left sided murmurs get louder during EXpiration

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37
Q

What the manoeuvres to increase and decrease the pre-load and after load and how would this affect the murmurs?

A
  1. Squatting / leg raise -> increases pre-load -> LOUDER murmurs (EXC HOCM, MVP)
  2. Valsalva -> decreases pre-load -> SOFTER murmurs (EXC HOCM, MVP)
  3. Hand grip -> increases after load -> LOUDER regurgitation murmurs; BUT SOFTER HOCM, MVP
  4. Amyl nitrite -> decreases after load -> LOUDER HOCM, MVP
38
Q

Aortic stenosis

  1. possible presentation
  2. features
A
  1. Presentation
    - SAD: syncope, angina, dyspnoea
    - high Ca - calcified valve
  2. ESM, radiating to carotids
39
Q

Mitral regurgitation

  1. presentation
  2. features
A
  1. rheumatic fever - rheu-mitral; associated with HTN

2. pan systolic, radiates to axilla

40
Q

Tricuspid regurgitation

  1. presentation
  2. features
A
  1. Hx of IVDU - Want to TRI new drugs?

2. pan systolic

41
Q

Mitral stenosis

  1. presentation
  2. features
A
  1. rheumatic fever - rhea-mitral; often leads to LHF

2. Opening Snap - Operating System is MicroSoft - OS is MS

42
Q

HOCM

  1. presentation
  2. murmur features - manoeuvres
  3. associated valvular abnormality
  4. inheritance
  5. What gene mutation causes it
  6. What is the pathophysiology, does it cause a systolic or diastolic dysfunction?
  7. What does the biopsy show?
A
  1. Hx of sudden cardiac death - most common cause of sudden cardiac death in the young
    Hx of syncope following an exercise - due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
  2. LOUDER with decreased pre-load and after load
    Softer with increased pre-load and after load
  3. MR
  4. AD
  5. Mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
  6. results in predominantly DIASTOLIC dysfunction: LVH → decreased compliance → decreased CO
  7. Biopsy: myofibrillar hypertrophy with chaotic and disorganised myocytes (‘disarray’) & fibrosis
43
Q

Mitral valve prolapse (MVP)

  1. presentation
  2. features
A
  1. young psych female pt
    myxomatous valve disease (usually mitral)
  2. mid / late-systolic click - to win MVP, your team needs to CLICK
44
Q

Are the following murmurs systolic or diastolic:

  1. ASD
  2. VSD
  3. HOCM
  4. CoA
  5. PDA
A
  1. ASD inspire - ASD louder on Inspiration, ESM
  2. VSD - pan systolic
  3. HOCM expire - HOCM louder on expiration, ESM
  4. Coffee Latte - CoA late systolic
  5. PDA - continuous machine like (through the systole and diastole)
45
Q

Tricuspid stenosis - usually occurs in which age group

A

usually presents in neonates

46
Q

HOCM - poor prognostic factors:
think of presentation
FH
Ix (ECG tape, ECHO, stress)

A
  • young age at presentation
  • syncope
  • FH of sudden death
  • non-sustained VT on 24 or 48h tape
  • abnormal BP changes on exercise
  • increased septal wall thickness (>3cm)
47
Q

Management of HOCM

A 
ABCDE 
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis (not for dental procedures)

Drugs to avoid:
Nitrates (reduce preload),
Inotropes (reduce preload and after load),
Ace-inhibitors (reduce after load)

48
Q

Syndromes associated with HOCM

A

Friedreich’s ataxia (AR) and Wolff-Parkinson White

49
Q

ECHO findings in HOCM

A

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

50
Q

ECG findings in HOCM:

A 
LVH
TWI 
non-specific ST segment and T-wave abnormalities, 
deep Q waves
occasionally AF
51
Q

Cyanotic vs acyanotic causes of CHD:

A 
Cyanotic: 
1. Tetralogy of Fallot - most common 
2. Transposition of great arteries 
3. Tricuspid atresia 
Fallot's is more common than TGA. However, at birth TGA is the more common lesion as patients with Fallot's generally presenting at around 1-2 months

Acyanotic:
VSD - most common
VSDs are more common than ASDs. However, in adult patients ASDs are the more common new diagnosis as they generally presents later.

52
Q

Factors favouring rate control in AF

A

> 65 years

History of IHD

53
Q

Factors favouring rhythm control

A 
< 65 years
Symptomatic
First presentation
Lone AF or AF 2' to a corrected precipitant (e.g. Alc)
CHF
54
Q

Catheter ablation in AF

  1. complications
  2. anticoagulation advice
A
  1. Complications: cardiac tamponade, stroke, PS

2. for 4/52 prior to the procedure and according to the CHADVASC after - regardless of the rhythm (even if in sinus)

55
Q

Implantable cardiac defibrillators indications

A
  • LQTS
  • HOCM
  • Brugada syndrome
  • previous cardiac arrest due to VT/VF
  • previous MI with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35%
56
Q

NYHA classes

A

I - no limitation
II - well at rest but ordinary activity results in sx
III - well at rest but less than ordinary activity results in symptoms
IV - sx at rest

57
Q

MoA of the following

  1. Thiazide diuretics
  2. K sparing diuretics
  3. amiloride and triamterene
  4. Furosemide
A
  1. Inhibit Na/Cl transporter in the distal convoluted tubule
  2. aldosterone antagonists
  3. inhibit Na channels in the collecting tubules
  4. inhibits the Na-K-Cl cotransporter (NKCC2) in the thick ascending limb of the loop of Henle
58
Q

Effects of BNP

A
  • vasodilator
  • diuretic and natriuretic
  • suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
59
Q

Tx that reduces the BNP levels

A

Tx with diuretics, ARB and ACE-i

60
Q

BNP gets secreted by the LV myocardium, hence any LV abnormality can cause raised BNP. LV abnormality such as …

A

HF, MI, valvular disease

61
Q

What are the 4 abnormalities in tetralogy of Fallot?

A
  1. VSD
  2. PS
  3. RVH
  4. Misplaced aorta
62
Q

Ebstein’s anomaly

  1. what is the anatomical anomaly in this anomaly? what are
  2. Other associated structural abnormalities and syndrome
  3. What can it be caused by?
A
  1. large atrium, small ventricle
  2. PFO, ASD is seen in at least 80% of patients
    TR
    Wolff-Parkinson White syndrome
  3. exposure to lithium in-utero.
  4. cyanosis
    hepatomegaly
    prominent ‘a’ wave in the distended JVP
    tricuspid regurgitation (pansystolic murmur, worse on inspiration) -> prominent V wave
    RBBB → widely split S1 and S2
    SVT burst on 24h tape
63
Q

Types of LQTS

A
  • LQTS1 - sx caused by exertional syncope, often swimming
  • LQTS2 - syncope occurring following emotional stress, exercise or auditory stimuli
  • LQTS3 - sx occur at night or rest (2’ to alarm / loud noise)
64
Q

Mx of LQTS

A
  1. Avoid drugs prolonging QT (see VT causes)
  2. BB, but not sotalol
  3. ICD
65
Q

Mx of atrial flutter

A

Mx is similar to that of atrial fibrillation although medication may be less effective

  • atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
  • radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
66
Q

Thiazide diuretics:

  1. MoA and site of action
  2. Indications
  3. SE + Rare ones
A
  1. inhibit Na reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the Na+-Cl− symporter. K is lost as a result of more Na reaching the collecting ducts.
  2. Thiazide diuretics have a role in the treatment of mild HF although loop diuretics are better for reducing overload. The main use of bendroflumethiazide was in the management of HTN but recent NICE guidelines now recommend other thiazide-like diuretics such as indapamide and chlortalidone.
  3. dehydration
    postural hypotension
    hyponatraemia, hypokalaemia, hypercalcaemia (the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones)
    impaired glucose tolerance
    gout
    impotence
Rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
67
Q

Eisenmenger’s syndrome

  1. What’s the medical definition of this condition?
  2. What are the associated structural abnormalities?
  3. Clinical picture
  4. Mx
A
  1. Left-to-right shunt
  2. VSD, ASD, PDA
  3. original murmur may disappear
    cyanosis, clubbing
    right ventricular failure
    haemoptysis, embolism
  4. heart-lung transplantation
68
Q

DVLA rules

  1. HTN
  2. successful catheter ablation
  3. elective angio, PPM insertion
  4. CABG, ACS
  5. heart transplant
  6. ICD
  7. Aortic aneurysm of 6cm and 6.5cm
A
  1. hypertension: no need to notify DVLA, can drive unless tx causes unacceptable side effects,
    - if Group 2 Entitlement the disqualifies from driving if resting SBP consistently >=180 mmHg and/or DBP >=100 mm Hg
  2. successful catheter ablation for an arrhythmia- 2 days off
  3. angioplasty (elective), PPM insertion - 1 week off
  4. CABG, ACS - 4 weeks off
  5. heart transplant: 6 weeks off, no need to notify DVLA
  6. ICD:
    - for sustained ventricular arrhythmia: cease for 6/12
    - prophylactically then cease driving for 1 month.
  7. aortic aneurysm of 6cm or more - notify DVLA.
    - an aortic diameter of 6.5 cm or more disqualifies patients from driving
69
Q

Rheumatic fever

  1. Organism causing it
  2. The granulomatous nodules with giant cells; vs enlarged macrophages with ovoid, wavy, rod-like nucleus found in the rheumatic heart disease
  3. Diagnostic criteria
  4. Mx
A
  1. Strep pyogenes
  2. Aschoff bodies and Anitschkow cells
    • evidence of strep infection (ASO titre indicates exposure to group A streptococcus bacteria; throat swab, raised strep antibodies)
      - 2 major
      - 1 major + 2 minor criteria
Major criteria
Carditis and valvulitis (eg, pancarditis)
Erythema marginatum
SC nodules
Polyarthritis
Sydenham's chorea: often a late feature
Minor criteria
raised ESR or CRP
pyrexia
arthralgia (not if arthritis a major criteria)
prolonged PR interval
  1. Mx:
    - PO Pen V
  2. NSAIDs
  3. Tx complications, eg HF

Mitral valve is the most common valve to be affected.

70
Q

Which conditions at the following cells / bodies associated with?

  • Councilman bodies
  • Mallory bodies
  • Call-Exner bodies
  • Schiller-Duval bodies
A

Councilman bodies -> hepatitis C, yellow fever
Mallory bodies -> alcoholism (hepatocytes)
Call-Exner bodies-> granulosa cell tumour
Schiller-Duval bodies -> yolk-sac tumour

71
Q

AVB is associated with what type of MI?

A

Inferior MI

72
Q

Complications following MI + timeline: immediate, within the first 48h, within the first week, 2 weeks, 6 weeks

A

Immediate complication - acute MR (rupture of the papillary muscle) [vs VSD]
48h - acute pericarditis
1st week - VSD (rupture of the interventricular septum) [VS acute MR]
1-2 weeks - LV free wall rupture - cardiac tamponade
2-6 weeks - Dressler syndrome
2-12 weeks - LV aneurysm - persistent STE

73
Q

Dressler syndrome:

  1. underling pathophysiology
  2. Clinical picture
  3. Mx
A
  1. autoimmune reaction against antigenic proteins formed as the myocardium recovers
  2. combination of fever, pleuritic pain, pericardial effusion and a raised ESR
  3. It is treated with NSAIDs.
74
Q

Left ventricular aneurysm

  1. Pathophysiology and when does it tend to occur?
  2. Clinical picture
  3. Complications
A
  1. The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. Usually >2 weeks, within 3 months
  2. persistent STE and features LVF
  3. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
75
Q

Left ventricular free wall rupture

  1. When does this usually occur?
  2. Clinical picture
  3. Mx
A
  1. around 1-2 weeks afterwards.
  2. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds).
  3. Urgent pericardiocentesis and thoracotomy are required.
76
Q

Ventricular septal defect

  1. When does this usually occur?
  2. Clinical picture
  3. Ix
  4. Mx
A
  1. Rupture of the interventricular septum usually occurs in the 1st week, is seen in 1-2% of patients.
  2. Features: acute heart failure associated with a pan-systolic murmur.
  3. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion.
  4. Urgent surgical correction is needed.
77
Q

Acute mitral regurgitation (as a post-MI complication)

  1. Which type of MI is it most associated with?
  2. What is the pathophysiology?
  3. Clinical picture
A
  1. infero-posterior infarction
  2. due to ischaemia or rupture of the papillary muscle.
  3. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard.
  4. Patients are treated with vasodilator therapy but often require emergency surgical repair.
78
Q

Common SE of Ticagrelor

A

SOB

79
Q

Causes of STE

A
  1. Acute MI
  2. Pericarditis / myocarditis
  3. LV aneurysm
  4. Takotsubo cardiomyopathy
  5. Prinzmetal’s angina (coronary artery spasm)
  6. normal variant - ‘high take-off’
  7. rare: subarachnoid haemorrhage
80
Q

Use of BB in tx HTN has declined sharply. Why is this?

A

Use of BB diminished due to it less likely effect on preventing stroke + potential impairment of glucose tolerance

81
Q

ACE-inhibitors:

  1. SE
  2. Caution and CI
  3. Interactions
  4. Monitoring
A
  1. cough (in around 15% of patients and may occur up to a year after starting treatment) thought to be due to increased bradykinin levels
    angioedema: up to a year after starting tx
    hyperkalaemia
    first-dose hypotension: more common in patients taking diuretics, those with AS
  2. pregnancy and breastfeeding - avoid
    renovascular disease (esp b/l renal artery stenosis) -> renal impairment
    AS - may result in hypotension
    hereditary or idiopathic angioedema
    specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0
  3. high-dose diuretic therapy (> 80mg of furosemide / day) -> significantly increased risk of hypotension
  4. U&E before tx and after increasing the dose: acceptable changes are
    - an increase in serum creatinine, up to 30% from baseline
    - an increase in potassium up to 5.5 mmol/l.
    significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
82
Q

PFO

  1. Prevalence
  2. Complications
  3. Associated condition
A
  1. 20% of the population
  2. It may allow embolus (e.g. from DVT) to pass from right side of the heart to the left side leading to a stroke - ‘a paradoxical embolus’
  3. association between migraine and PFO
    Some studies have reported improvement in migraine symptoms following closure of the PFO.
83
Q

State the classes of the following drugs:

  1. Indapamide
  2. Nifedipine
A
  1. Thiazide like diuretic

2. CCB

84
Q

Features of the aortic regurgitation

Causes of AR: valve disease and aortic root ds

A

Early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
collapsing pulse
wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

Causes (due to valve disease)
rheumatic fever
infective endocarditis
connective tissue diseases e.g. RA/SLE
bicuspid aortic valve
Causes (due to aortic root disease)
aortic dissection
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan's, Ehler-Danlos syndrome
85
Q

Atrial myxoma

  1. commonest site
  2. features
A

Atrial myxoma is the most common primary cardiac tumour.

Overview
75% occur in left atrium, most commonly attached to the fossa ovalis
more common in females

Features
systemic: SOB, fatigue, weight loss, PUO, clubbing
mid-diastolic murmur, ‘tumour plop’
emboli, AF
echo: pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum

86
Q

Indications for a temporary pacemaker

A
  1. symptomatic/haemodynamically unstable bradycardia, not responding to atropine
  2. post-ANTERIOR MI: type 2 or CHB*
  3. trifascicular block prior to surgery

*post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable

87
Q

Amiodarone:

  1. MOA
  2. Limiting factors to be considered when administering amiodarone
  3. Monitoring - before starting the tx and once started
  4. SE
A
  1. Class III - 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)
  2. The use is limited by a number of factors
    - very long half-life (20-100 days). For this reason, loading doses are frequently used
    - should ideally be given into central veins (causes thrombophlebitis)
    - lengthening of the QT interval
    - interacts with drugs commonly used concurrently (p450 inhibitor) e.g. Decreases metabolism of warfarin
    - numerous long-term adverse effects (see below)
  3. Monitoring of patients taking amiodarone
    TFT, LFT, U&E, CXR prior to treatment
    TFT, LFT every 6 months
4. 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 
QT interval prolongation
88
Q

WPW

  1. Drugs to avoid and why
  2. Tx options
A
  1. adenosine -> cardiac arrest
    digoxin, verapamil -> VT or VF
    sotalol if there is a coexisting AF -> VF
  2. Amiodarone, Flecainade, Sotalol (if no AF)
89
Q

Wolff-Parkinson White (WPW)

  1. pathophysiology
  2. ECG features
  3. Associated conditions
  4. Tx
A
  1. caused by a congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.
  2. Possible ECG features include:
    short PR interval
    wide QRS complexes with a slurred upstroke - ‘delta wave’
    LAD and no prominent R wave in V1 in right-sided accessory pathway = Type B - more common
    RAD and prominent R wave in V1 in left-sided accessory pathway = Type A
    Rare type C - delta waves are upright in leads V1-V4 but negative in leads V5-V6
3. HOCM
mitral valve prolapse
Ebstein's anomaly
thyrotoxicosis
secundum ASD
  1. definitive treatment: radiofrequency ablation of the accessory pathway
    medical therapy: sotalol (not in AF), amiodarone, flecainide
    sotalol - prolonging the refractory period at the AVN may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into VF
90
Q

Stages of atherosclerosis

A
  1. endothelial dysfunction
  2. endothelial changes
  3. Fatty infiltration of the subendothelial space by LDL
  4. Macrophages phagocytose oxidised LDL
  5. Smooth muscle proliferation and migration from the tunica media into the intima.
  6. initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
  7. this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
  8. fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
  9. monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
  10. smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

Medicine (7 decks)

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