Cardio

Question 1

Infective endocarditis risk factors

Answer 1

recent dental, endoscopic or operative procedures, valve disease (including bicuspid aortic), prosthetic valves, past rheumatic fever, heart disease/operations, IV drug use,
immunosuppression

Question 2

Signs on exam for Infect Endocarditis

Answer 2

Peripheral
Hands
 clubbing
 splinter haemorrhages
 Osler’s nodes (painful red)
 Janeway lesions (non-tender, tiny, red
palms)

Eyes
 Roth spots (red haemorrhage w white centre)
Neuro
 Signs of peripheral embolic disease forming
abscess (but embolic abscesses can form in
almost any organ)
Heart
Listening for new murmur or changed murmur.
Most often vegetations cause regurgitation
(commonly mitral)
Signs of Cardiac Failure
Source of Infection (+ temperature)

Question 3

Investigations for IE- expected bugs + abx

Answer 3

Bloods
 Cultures – strep viridians (penicillin) and staph aureus (flucloxacillin) predominantly
 FBC (raised neutrophils) and ESR (high)

Imaging
 CXR (heart failure, cardiomegaly)
 ECHO (looking for vegetations,
regurgitation, or abscess) TOE is more sensitive

Other
 MSU – for haematuria (from emboli)

Question 4

Management of IE

Answer 4

 IV antibiotics dependent on the organisms
sensitivities –at least 4 weeks but 6-8 if prosthetic valves
 Consider cardiac surgery e.g. valve replacement (if severe heart failure, valvular obstruction, abscess) - 50% require surgery
 Consider antibiotic prophylaxis (high dose, short term) for future medical/dental procedures – but this is controversial - if patient is already having antibiotics
however it is recommended to cover IE organisms

Question 5

differential diagnosis for IE

Answer 5

-Rheumatic fever
 atrial myxoma (cardiac tumour)
 other cardiac neoplasm
 SLE

Question 6

Risk factors for heart failure

Answer 6

Coronary artery disease:
 HTN, hyperlipidaemia, DM, smoking,
obesity, physical inactivity, CAD, family
history of heart disease, high alcohol intake

Dilated Cardiomyopathy:
 alcohol intake, family history or
cardiomyopathy, haemochromatosis

Question 7

Exams to do for HF

Answer 7

Cardio , resp, lying and standing BP, PVD brief

Question 8

exam findings for RHF vs LHF vs both

Answer 8

RHF - pitting oedema, JVP, ascites,
hepatomegaly (congestion)

LHF - cyanosis,cool peripheries, crackles in lung bases, stony dullness (effusion)

BOTH - murmur, conjunctival/palmar crease pallor, AF,
parasternal heave, Cheyne-stokes breathing,
displaced apex beat, S3

Look for cardiac cachexia, pacemaker

Question 9

NY HA classes of HF - 1 to 4

Answer 9

1 - Cardiac disease, but no symptoms and no limitation in ordinary physical activity,
2 - Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activitye.g. shortness of breath when walking, climbing stairs etc

3 -Comfortable only at rest. Marked limitation in activity due to symptoms, even during less-thanordinary activity, e.g. walking short distances (20–100 m).

4. Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patient

Question 10

Differentials for HF symptoms

Answer 10

Nephrotic syndrome, liver disease
(decreased albumin), if only LHF think of any lung disease (e.g. Pneumonia, COPD)

Question 11

Investigations for HF

Answer 11

Bloods
 Hb – to exclude anaemia as precipitant
 Electrolytes and Creatinine- hyperkalaemia may cause arrhythmias, hyponatraemia may indicate severe long standing cardiac failure
 BNP – elevated levels may distinguish
cardiac from non-cardiac dyspnoea. Useful for monitoring response to treatment.
 Cr and eGFR - (renal failure as a cause or as a consequence, and also make sure OK to take medications)
 TFTs (thyrotoxicosis)

Imaging
 CXR – (ABCDE) alv oedema, kurly beeline= fissure, cardiomegaly, distention of sup pul vessels, effusion. Chamber size enlarged.

Other
 Daily weights
 ECG – arrhythmia, signs of ischaemia or old infarct, LVH, LBBB

 ECHO – if the diagnosis is not already
obvious. May show regional (infarct) or global (dilated cardiomyopathy) wall motion abnormalities, estimate EF, identify valvopathy

 Coronary angiography (plus troponins and ETT) to exclude coronary artery disease
 RV biopsy to determine aetiology – rare

Question 12

how can you correct the underlying cause of HF as part of management

Answer 12

Correct Underlying Cause
 rate control arrhythmias (pacemaker or meds)
 thrombolysis for acute infarct
 CABG or angioplasty for ischaemia
 Medication review
 Control thyroid disease
 Valve replacement
 Transfusion for anaemia

Question 13

Management of acute HF

Answer 13

Manage Failure (Acute)
 Sit upright
 Morphine
 Oxygen
 GTN
 Frusemide +/- thiazide
 DO NOT GIVE BETA BLOCKERS

Question 14

Management of HF - non pharm pharm

Answer 14

Non Pharmacological
 Bed rest if unwell
 Low salt diet
 Fluid restriction (1 – 1.5L/day)
 Control CV risk factors (smoking cessation, weight loss, alcohol reduction, exercise)
 Annual influenza vaccination (increased risk)
 Educate around sx and have action plan in place for exacerbations
 ACP/ resus

Pharmacological - HFRef
1st- Furosemide initially for fluid overload
2nd- ACEI or ARB
3rd- BB once no more overload - bisoprolol titrate max dose
4th- still symptomatc spironolactone
5th-entresto –>stop the arb/ace i
5th SGLT2 inhibitor - empag -

• digoxin/anticoag for AF
  -Iv irons for anaemia
  Only use ARBs if side effect (usually cough) to ACEi

Avoid calcium channel blockers (negative inotropes) and NSAIDs (worsen renal function)

Symptom improvement = diuretics, beta blockers, ACEi, hydralazine + nitrate, digoxin, spironolactone

Increased survival = beta blockers, ACEi,
hydralazine + nitrate, spironolactone

For HFpEF its optimisation f other comorbidities

Question 15

Possible causes of HF

Answer 15

Causes =
IHD (most common), arrythmias, valvulopathy, hypertension, cardiomyopathy, myocarditis,

-chronic lung disease (cor pulmonale), pulmonary embolism,
-medications with negative inotropic properties (beta blockers and verapamil)
-high output status (anaemia,thyrotoxicosis, pregnancy etc).

Note that RVF is usually due to lung disease, LVF, or pulmonary stenosis.

Question 16

HTN important complications, 2ndary causes of htn, other aspects of hx to ask for someone with htn

Answer 16

o Stroke
o Heart failure or PVD
o Renal failure
 Symptoms of malignant hypertension (severe headache)

Potential secondary cause
o Phaeochromocytoma if paroxysmal sweating, palpitations and headache
o OSA if daytime sleepiness
o Renal artery stenosis or CKD
o Coarctation of aorta
o Adrenal tumour, conns or Cushing’s
o Meds- COC, NSAIDS
o Pregnancy
o However 95% are idiopathic/primary

 Other risk factors for vascular
disease
o Type 2 diabetes
o Hyperlipidaemia
o Family history of coronary or CVD
 Lifestyle factors
o Obesity, lack of physical activity, excessive alcohol intake, high salt
diet
o Ask about attempts and success with any of these

Question 17

Exam for HTN

Answer 17

Cardiovascular disease (look for postural BP drop, and do BP in both arms)
- Look for signs of Cushing’s (moonfaced, weight gain, purple striae, buffalo hump, proximal muscle weakness)
-Remember radio femoral delay (coarctation)

Fundoscopy (looking for hypertensive retinopathy –flame haemorrhages and cotton wool spots, AV nipping, exudates, papilledema)

Question 18

Ix for HTN - primary and secondary

Answer 18

Bloods
 U+E, creat – to look for renal disease
 ECG – to look for LVH and evidence of IHD
 CXR – to exclude cardiomegaly, LVH,CHF
 Urine analysis – looking for proteinuria
(renal failure caused by HTN. If positive can do 24 hour urine collection and work out ACR
 HBA1C and lipids – to assess for other cardiovascular risks
 Aldosterone/renin ration – to detect primary hyperaldosteronism i.e. Conns (especially if hypokalaemic and not on diuretics; high Plasma Aldosterone :Plasma Renin Activity ratio (plasma ) Also renin secreting cancers
 24 hour catecholamines if symptoms consistent with phaeochromocytoma
 Serum cortisol if investigating for Cushing’s/ dexamethasone suppression test/ ACTH stimulation test
 Renal artery Doppler study for patients with intractable hypertension renal artery stenosis
 Sleep study if considering sleep apnoea
 Ambulatory BP- at home BP record

Question 19

Dx and classes of HTN

Answer 19

Dx = BP of over 140/90 on three separate occasions a week apart (unless severe HTN with end organ MI, LVH, HF, stroke, renal damage, retinopathy)
Preferably ambulatory BP monitoring will be used at home to make diagnosis (to prevent white coat HTN)

Classes
Mild (Grade 1) 140-159/90-99
Moderate (Grade 2) 160-179/100-109
Severe (Grade 3) >180 syst +/- >110 dias

Question 20

Management of HTN based on CVD risk - basic principles (risk by gender, age, ethnicity, BP, TC/HDL ratio, smoke, DM, fam hx). Target BP?

Answer 20

CVD < 5%
o Lifestyle advise
o Discuss harms and benefits of BP lowering and statin meds
o Further assessment 5 – 10 years

 CVD 5-15%
o Individualized lifestyle advise
o Commence BP lowering +/ statin
o Further assessment 1 – 2 years

CVD > 15% and established CVD or anyone with BP 160/100
o Intensive lifestyle advise
o BP lower + statin + antiplatelet therapy
o Annual review

 Target BP
o <140/90 if >80 or significant
concern of frailty/hypotension
o <130/80 in most cases/ high risk patients

Question 21

Management of HTN - pharm + non pharm

What are some examples of the drugs (give names), and contraindication

Answer 21

Non-Pharmacological
 Diet - reduced salt, fats and sugars
 Physical activity – 30 mins a day, green prescription
 Weight – BMI < 25
 Smoking cessation – ask, brief advice and offer of help, cessation support, document
 Alcohol reduction

Pharmacological
 Recommendation to commence on a low dose of a single therapy, followed by addition of a low dose of a second medication rather than increasing the dose of the first to avoid S/E

 When choosing medication, consider previous intolerance, known contraindications, interaction with other meds, existing medical problems that favour use of a certain class.
o 1st ACEi monotherapy if young/close to target or DM,
- CCB if >55 or black
o 2nd add other ( or start w two low dose if elderly
o 3rd thiazide
o 4th add spironolactone or other medicine (bb)

 Swap ACEi for ARB- (Cilazapril for candesartan) if side effects (usually cough)
 ACEi - Not female reproductive age
 Calcium Channel Blockers
Felodipine (targets vessels) Diltiazem (targets vessels and cardiac),
Verapamil (targets cardiac tissue) Beneficial for angina

 Beta blockers. Less effective on own and not common or recommended for HTN Metoprolol, Bisoprolol, (HF)
Benefit: Angina, HF, MI
Contraindicated: asthma, DM, heart block, PVD

 Specific indications
o BPH –alpha blocker

Question 22

DIFFERENTIAL DIAGNOSIS OF IRREGULARLY
IRREGULAR BEAT

Answer 22

D Atrial fibrillation
 Ventricular ectopic beats
 Complete heart block with variable ventricular escape
 Atrial flutter

Question 23

Precipitants (for AF)

Answer 23

A- age
 T- thyrotoxicosis
 M – mitral valve disease
 I – ischaemic heart disease
 S – surgery, sleep apnoea,
smoking
 H – hypertension
 A – alcohol binge or caffeine
 P – PE
 CKD, DM, male, obesity

Question 24

exam for AF

Answer 24

 Cardiovascular exam
 Heart rate and rhythm
 Radial pulse!
 Thoracotomy scars, pacemakers, implanted
defibrillators
 Signs of cardiac failure, valvular heart disease
 Evidence of recent abdominal surgery
 Thyrotoxicosis

Question 25

Ix for AF - specific signs on most important

Answer 25

ECG
o Resting ECG
o 24 ECG Holter monitor if symptomatic
o AF specific signs
 No p waves
 Irregular QRS
 EPS (electrophysiological studies)
 Assess inducibility of
arrhythmias before and after
treatment
 ETT
 If associated symptoms or
known IHD
 ECHO
 Valve disease, cardiomyopathy,
hypertrophy, atrial size,
segmental wall abnormalities
 Bloods
 U+E, TFT’s, serial trops

Question 26

Management of symptomatic bradycardia, Ventricular tachy

Answer 26

Symptomatic brady
- atropine 1mg every 3-5 min then transcutaneous pacing or epinephrine ot dopamine infusion
- Consider permanent pacemaker if completeheart block, second degree AV block, sinus node dysfunction

VT
- Consider implanted cardioverterdefibrillators if
- VF/VT with haemodynamic
instability, contraindications to drug treatment or non-response, symptomatic long QT, persistently inducible VF/VT,VF/VT
 Works by overdrive pacing before administering DC shock

Question 27

Acute management of AF

Answer 27

Acute Management
 < 48 hours – cardioversion
o DC cardioversion if haemodynamically unstable/unconscious

o Medical cardioversion with amiodarone 5mg/kg over one hour followed by infusion 900mg over 23 hours (rule out thyrotoxicosis first)
 > 48 hours – do not cardiovert (unless TOE has proven no intracardiac thrombus). Thus rate control.

 Rate control
o BB - Metoprolol ( not if in acute HF)
o CCB - Diltiazem – short acting (15mg or 30mg) initially then long acting.
o Digoxin

 Thromboprophylaxis
o Dabigatran normally first line now
(no monitoring required)
o LMWH then commence warfarin if high risk, stop LMWH once therapeutic INR – not as common now, if dabigatran not appropriate discuss with cardio
o No anti-coagulation needed if stable sinus rhythm restored, no risk factors, and recurrence unlikely – discuss with cardio

Question 28

Chronic management of AF - rate and rhythm control methods + drugs

Answer 28

 Rate control just as good as rhythm control

 Rhythm control - Consider if symptomatic, CCF, younger, 1st presentation, or persistence despite corrected
precipitant.
o Electric cardioversion if unstable (after at least three weeks of therapeutic anticoagulation before)
o Flecainide if no structural heart disease
o Amiodarone if structural heart disease
o Note can do ‘pill in pocket’ approach with sotalol or flecainide if infrequent PAF

 Rate control
o Metoprolol or diltiazem, if that fails add digoxin (not for renal failure), if that fails try amiodarone with expert advice.

 Anticoagulation
Noacs or warfarin
o If CHA2DS2VSc score > 1

Question 29

CHA2DS2Vsc score (stroke risk) means what vs HASBLED (bleeding risk)

Answer 29

chadsvasc - stroke risk for patients w AF
C – CHF (1)
 H – HTN (1)
 A – Age (1 if 65 – 74, 2 if 75 or more)
 D – DM (1)
 S – Stroke (2), TIA (1)
 V – Vasc disease (1)
 S – Sex female (1)

Hasbled- major bleeding risk on anticoagulation
HTN
 Abnormal renal/liver fx
 Stroke hx
 prev Bleed
 Labile INR
 Elderly >65
 medication usage predisposing to bleeding, etOH >8 units a week

Question 30

Mitral stenosis causes, complications, differential dx

Answer 30

Causes
 Rheumatic heart disease 99%
 Congenital, prosthetic valve

Complications
– Pulmonary hypertension,
emboli, pressure symptoms from large LA including hoarse voice and dysphagia

Differential Diagnosis
 Atrial/ Ventricular septal defect, patent DA
 Carey coombs (A rheumatic fever)

Question 31

Ix and management of Mitral stenosis

Answer 31

Investigations
 ECG
o May be in AF
o signs of L) atrial enlargement - P mitrale if in sinus
o RVH
 CXR
o L atrial enlargement
o Pulmonary oedema
o Mitral valve calcification
 ECHO
o For diagnosis

Managements
 Medical
o If in AF, rate control + anticoagulate
o Diuretics to reduce preload and pulmonary congestion
o Long term antibiotic prophylaxis against recurrent rheumatic fever
o Short term antibiotic prophylaxis against IE for dental, GI and GU procedures may be indicated
 Surgical (if medical not controlling sx)
o Balloon valvuloplasty
o Open mitral valvotomy or valve replacement

Question 32

Signs of mitral stenosis on exam vs mitral regurgitation

Answer 32

Mitral stenosis
o Malar flush
o Low volume pulse
o AF (common)
o Loud S1 + tapping apex
o Mid diastolic murmur, heard loudest over apex in expiration on left lateral side

Mitral regurg
o +/- AF
o Displaced, hyperdynamic apex
o Pansystolic murmur, loudest over apex, radiating to the axilla, heard loudest in expiration on left lateral
side
o Soft first heart sound, possible third heart sound

Question 33

Mitral regurg causes, differential dx

Answer 33

Causes
 Functional (LV dilatation) – secondary mitral insufficiency
 Congenital
 Annular calcification
 Rheumatic fever/IE
 Papillary muscle dysfunction/rupture
 Connective tissue disorders e.g Marfan’s - Mitral valve prolapse/ruptured C.T

Differential Diagnosis
 Ventricular Septal Defect (esp if post MI), TR (V wave + pulse liver)

Question 34

Ix and management mitral stenosis

Answer 34

Investigations
 ECG
o May be in AF
o P mitrale if in sinus
o RVH

 CXR
o Enlarged LA
o Mitral valve calcification
o Pulmonary oedema
 ECHO (with Doppler)
o Diagnose and ascertain aetiology
o Size and site of regurgitant jet
o Assess LV function
 Cardiac catheterization

Management
 Rate control if in AF
 Anticoagulate if in AF, hx of embolism or additional mitral stenosis
 Diuretics or ACEi for patients with hypertension to decrease afterload
 Surgery to replace/replace the valve before LV irreversibly impaired (balloon valvuloplasty, open mitral valvotomy/ replacement
 Antibiotic prophylaxis before procedures to be considered

Question 35

What is the cause, symptoms, sign, ix and management of mitral valve prolapse

Answer 35

Causes
 Atrial Septal Defect/Patent Ductus Arteriosus, Wolf PW
 Turners/Marfan’s syndrome

Symptoms
None or atypical chest pain, palpitations
 Autonomic dysfunction (anxiety, syncope)

Signs
- Mid systolic click + late systolic murmur

Ix
 ECHO is diagnostic
 ECG may show T wave inversion

Treatment
 Surgery if severe

Question 36

Aortic stenosis causes, signs, ecg and differentials

Answer 36

Causes
 Senile calcification (most common – this is essentially a disease of older people)
 Bicuspid valve
 Rheumatic heart disease

Signs
o Slow rising pulse with narrow pulse
pressure
o P – Non displaced apex, LV heave, aortic thrill
o A – ejection systolic murmur heart
loudest at the base/left sternal edge/aortic area radiating to carotids, ejection click.

Differential Diagnosis
 Aortic Sclerosis
o Senile degeneration of valve
o Normal pulse, no radiation of murmur to carotids (elderly)

 Hypertrophic cardiomyopathy
(HCM)
o LV outflow tract obstruction due to asymmetric septal hypertrophy
o Risk of sudden death – leading cause
in the young

o May show LVH, progressive T wave
inversion and deep Q waves on inferior and lateral leads on ECG

Question 37

Ix + management for aortic stenosis

Answer 37

ECG
o P mitrale
o LVH with strain pattern
o LBBB or complete AV block

 CXR
o LVH
o Calcified aortic valve

 ECHO
o Diagnose and classify severity

 Cardiac catheterization
o Assess valve gradient, LV function, risks emboli

Management
 Prompt valve replacement
 Percutaneous valvuloplasty (TAVI) if unfit
for surgery

Question 38

Causes - acute + chronic, signs and differential for Aortic regurgitations

Answer 38

Causes
 Acute
o IE
o Ascending aortic aneurysm

 Chronic
o Rheumatic heart disease
o Connective Tissue disease (SLE, RA, Marfan’s)
o Seronegative spondyloarthritides (ank spond, psoriatic arthropathy)
o Hypertension

Signs
o Water hammer/collapsing pulse
o Wide pulse pressure
o Nailbed pulsations (Quincke’s sign)
o Carotid pulsations (Corrigan’s Sign)
o Head nodding (de Musset’s sign)
o Pulsating Uvula (Mueller’s sign)

 Cardiac
o P – thrusting displaced apex
o A – high pitched early diastolic murmur heard best in expiration with patient sitting forward

Differential MS (mid diastolic murmur

Question 39

Ix and management of Aortic regurgitations

Answer 39

Investigations
 ECG - LVH
 CXR o Cardiomegaly,
pulmonary oedema

 ECHO
o Diagnostic (TOE)

 Cardiac catheterization
o Severity of lesion, anatomy of aortic root, LV function, coronary artery disease

Managements
 Medical
o Reduce systolic hypertension (ACEi, diuretics)

 Surgical
o Indications – worsening symptoms, not responding to medical therapy,ECG changes, enlarging heart
- Replace valve before significant LV dysfunction occurs

Question 40

what are the systolic murmurs vs non systolic murmurs

Answer 40

Systolic - Aortic stenosis, mitral regurg

Diastolic - mitral stenosis, aortic regurg

Question 41

PVD - Arterial vs chronic venous insufficiency hx questions, differential dx

Answer 41

Arterial Questions
 How far can you walk? What causes relief?
How long do you need to rest for? How long
has it been this bad? When could you last…?
 Do you ever get pain at rest?
 Physical changes – cool, pale, ulcers
 CVD risk factors

Venous Questions
 Risk factors – pregnancy, past history of
trauma/fractures/surgery, hormones,
obesity, smoking
 Personal or family history of thrombophilia,
DVT, PE
 Varicose veins
 Physical changes – swelling, eczema,
pigmentation, ulcers

DIFFERENTIAL DIAGNOSIS
Arterial
 Neurogenic claudication (spinal stenosis)
 Osteoarthritis of hip/knee
 Peripheral neuropathy

Venous
 HF, liver cirrhosis, nephrotic syndrome, GI

Question 42

Exam findings arterial vs venous PVD

Answer 42

Arterial
o Pallor, mottling, gangrene
o Amputation, wasting
o Scars, hair loss
o Ulcers – ‘punched out’, peripheries,
deep, regular, painful, pale base, minimal exudate
o Onychogryphosis, onychomycosis

Venous
o Varicose veins
o Hemosiderosis (red/brown from deposition of haemosiderin from RBCs)
o Oedema
o Lipodermatosclerosis (shiny + red above ankles)
o Eczema
Ulcers – gaiter area, shallow,
irregular, painless, lots of exudate (wet)

Question 43

Ix and management of arterial and venous pvd

Answer 43

INVESTIGATIONS
 Basic bloodwork – FBC, lipids, UEC, BGLs –
for treatment/ secondary prevention

Arterial
- ABP1 - 1-1.2 normal, <0.9 arterial disease, <0.4 critical limb, >1.2 calcified
- Duplex USS
- CT - angiography/MR angiography –
if considering intervention

Venous
 Duplex ultrasound
 CT and MR venography reserved for patients with complex abnormalities.
 ABPI to rule out concurrent arterial
insufficiency before prescribing compression stockings

MANAGEMENT
Arterial
 Risk factor management – smoking cessation, regular exercise
 Antiplatelet therapy (clopidogrel 1st line)
 Statins

• Surgical
  o Revascularization
   Endovascular
   Bypass grafting
   Amputation

Venous
 Weight loss, exercise
 Compression stockings
 Education about prolonged standing and
elevating when possible
 Endovascular surgery

Question 44

Hyperlipidaemia exam findings, investigation and management

Answer 44

EXAMINATION
- Cardio exam
- Corneal arcus, xanthelasma (yellow, lipid
plaques around eyes), or xanthomata
(elsewhere eg tendons)

INVESTIGATIONS
-Lipids –normal =LDL <2, HDL >1, Triglycerides <1.7, total cholesterol <4, TC / HDL ratio <4
-Creatinine Kinase – after starting statins
-LFTs – to look for fatty liver and to look for
damage after starting statins

MANAGEMENT
- lifestyle advice (reduce BMI, reduce saturated
fats in diet, increase fresh fruit and vegetables,
increase exercise)
- treat cause if secondary

Medications:
-Who? – those with known CVD, those with
DM, those with CVD risk >20%
-1st line = Statins (eg simvastatin 40mg po
nocte). Reduce cholesterol synthesis in liver.
Side effects = myalgia (check CK), and increased LFTs

-2nd line = Fibrates (eg bezafibrate - useful in
mixed hyperlipidaemias) or Cholesterol absorption inhibitors (eg ezetimibe).
Fibrates best for hypertriglyceridemia.

Question 45

Ix for rheumatic fever

Answer 45

Bloods
 FBC, ESR, CRP
 Blood cultures if febrile
 Antistrep serology
o Anti streptolysin
o Anti-DNase B

Imaging
 CXR
 ECHO
Other
 ECG
 Throat swab

Question 46

Dx criteria for rheumatic fever

Answer 46

DIAGNOSIS (JONES CRITERIA)
1. Evidence of recent strep infection AND
2. 2 major criteria OR
3. 1 major and 2 minor criteria

Evidence of recent strep infection
- Positive throat culture (usually negative by
the time symptoms appear)
 Rapid streptococcal antigen test
 Elevated or rising streptococcal antibody
titre
 Recent scarlet fever

Major Criteria
- Joints
o Arthritis (Pain + ROM + hot), usually of large joints, Migratory polyarthritis (can be
monoarthritis in high risk
populations)

 Carditis
o Can be endocarditis, myocarditis, or
valvulitis
o Look for tachycardia, murmur,
cardiomegaly, CCF, conduction defects
o Sometimes subclinical – ECHO evidence

 Subcutaneous nodules
o Rare but highly specific
o Small, hard, mobile, painless subcutaneous nodules on extensor surfaces of joints and spine

 Erythema Marginatum
o Rare
o Blanching, circular macules with red
raised edges and clear centres.
o Trunk and proximal extremities
o Not itchy or painful

 Sydenham’s Chorea
o Jerky, uncoordinated movements
o Hands, feet, tongue, face
o Bilateral or unilateral
o Useful signs
 Milkmaids grip
 Pronator sign (arms and
palms turn outward when arms
held above head)
 Inability to maintain
protrusion of tongue

Minor Criteria
 fever
 raised ESR or CRP
 Arthralgia (not if arthritis is a major criteria)
 Prolonged PR interval (not if carditis is a major criteria)
 Previous rheumatic fever

Question 47

Acute management of Rheumatic fever

Answer 47

Acute Management
- Antibiotics
o Penicillin for 10 days (or
benzylpenicillin IM single dose)
o Erythromycin if penicillin allergy

 Anti-inflammatories
o Aspirin/NSAIDS (be wary of toxicity)

 Bed rest
o Until CRP normalized
o Gradual return to activities

 Treat any heart failure
 Surgery
o Emergency valve replacement/
repair if valve leaflet or chordae
tendineae rupture. Otherwise
deferred until active inflammation
has subsided.

 Anti-chorea meds
(Only if severe/distressing/risky)
o Carbamazepine

Question 48

Secondary prophylaxis of Rheumatic fever

Answer 48

Choice of antibiotic
 1st Line - IM benzathine penicillin every 4
weeks
 2nd Line – Oral penicillin twice daily
 3rd Line – Oral erythromycin twice daily if
allergy

Time period
 ARF + no or mild carditis
o Minimum 10 years or until 21 years old (whichever is longer)

 ARF + moderate carditis
o Minimum 10 years after most recent episode or until 30 years (whichever
is longer)

 ARF + severe carditis
o Minimum 10 years after most recent episode or until 30 years (whichever
is longer) then review by specialist to consider lifelong

Question 49

Differentials for IHD, complications of MI, Ix

Answer 49

DIFFERENTIAL DIAGNOSIS
 GORD
 Oesophageal Spasm
 MSK
 PE
 Acute pericarditis
 Pneumonia

MI Complications
 Arrhythmias
 Bradycardias
 Heart failure
 Further ischaemia

INVESTIGATIONS
- ECG – current or old changes
- Troponins – note they don’t rise until about 6hours after MI and so repeat troponin is usually done after this 6 hour period to ensure MI not missed. Can remain elevated for 2 weeks (not always specific - lots of things raise troponins)

• FBC, UEC, TFTs, Lipids, HbA1C
• CXR
• ETT – to stimulate ischaemia if needed
• ECHO – to look for valvular pathology and heart function
• Angiogram

Question 50

Immediate management of stable angina, unstable angina, STEMI and NSTEMI

Answer 50

Immediate
Stable Angina – primarily treated with GTN spray
(be careful with Sildenafil). Can add beta blockers.

Unstable angina – aspirin, GTN, consider beta
blockers. Basically all of the secondary prevention
stuff below. Consider angiogram +/- angioplasty

STEMI:
 Morphine, oxygen, short acting nitrate,
DAPT, and antiemetics - metoclopromide
 Admit to CCU for continuous ECG monitoring
 PCI/angioplasty (door to balloon in 90 mins)
o If not offered in hospital, transfer is preferable over thrombolysis if transport time is 2 – 3 hours.
o Reduced mortality compared with thrombolysis
o Can’t do if previous bypass

 Thrombolysis
o < 85 years – IV Tenecteplase (tPA,
tissue plasminogen activator). Converts plasminogen to plasmin,
initiating fibrinolysis.
o >/= 85 years – Streptokinase, unless
there is prior use, risk of reaction.
 ACEi and beta blockers - long term management

Non-STEMI
 Morphine, oxygen, short acting nitrates,
DAPT, anti-emetics - metoclopromide
 Admit to CCU for continuous ECG
monitoring
 early revascularization, not as urgent (up to 24 hours after MI)
 ACEi and beta blockers for long term management

Question 51

Secondary prevention for ischaemic heart disease

Answer 51

Non pharmacological
o Diet, physical activity, smoking cessation
o Cardiac rehabilitation programme

 Pharmacological
o BP lowering - ACE-i are the drug of choice
o Statins
- Antiplatelet - (aspirin-forever and ticagralor-12month)
o Anti-anginal
 Beta blocker
 Diltiazem
 Nitrates

 Surgical
 Patients with three vessel
disease, LV damage, L main
coronary stenosis or proximal LAD stenosis may
benefit from CABG.
 CABG not usually done in acute ACS unless angioplasty and thrombolysis have failed

Question 52

Thromboprophylaxis - drugs moa + pros and cons

Answer 52

• Dabigatran - direct thrombin inhibitor - (pros -no regular testing, antidote= idarucizumab, cons - renal excretion, GI SE).
• Rivaroxaban factor 10a inhibitor - (not easily reversed, not for severe renal disease)
• Warfarin - Vit K antagonist, target INR 2-3. Pro - effective, antidote. cons - regular INR testing, GI, IC haemarrhoage, skin necrosis, teratogenic. CI in those conditions + liver disease).