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Cardiology Flashcards

1
Q

What are the types of AF as defined by duration?

A

Paroxysmal (comes and goes - usually less than 48hrs)
Persistent (more than a week or needs cardioversion)
Long standing persistent (more than a year)
Permanent (all the time)

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2
Q

How is the need for anticoagulation determined in AF? How is it interpreted?

A 
C - congestive heart failure (1)
H - hypertension (1) - includes on current tx 
A - age over 65 (1) 
D - diabetes mellitus (1) - includes on current tx
S - previous stroke, TIA or VTE (2)
V - vascular disease (1)
A - age over 75 (1)
S - sex female (1)

0 - low risk, 1 - mod risk, >1 high risk
Don’t offer anticoagulation just off female gender, take into account bleeding risk,

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3
Q

What score is used to assess bleeding risk for anticoagulation?

A 
H - hypertension
A - abnormal liver or renal function or alcohol (1,1,1) 
S - stroke
B - bleeding history 
L - labile INR
E - elderly over 65
D - drugs (antiplatelet / NSAID)
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4
Q

What INRs should prompt the reassessment of warfarin in AF?

A

After first 6 weeks
2 higher than 5 or 1 higher than 8 in last 6 months
2 less than 1.5 in last 6 months

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5
Q

What factors should prompt for AF rhythm control over rate control?

A 
Known reversible cause
CHF due to the AF
New onset AF
Able to ablate (flutter) 
Ineffective rate control
Younger, active or symptomatic
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6
Q

What factors suggest rate control over rhythm control in AF?

A

Permanent/not responding to rhythm control

Recurrent over 65

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7
Q

What drugs can be used to control AF rate?
What should be considered in prescribing?
What can be used if drugs not effective?

A

Beta blockers
Calcium channel blockers
Digoxin (in elderly no ambulant patients only - not effective in young as high catacholamines overwhelm vagus)
Ablation of the AV with pacemaker insertion.

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8
Q

What general means can be used to achieve AF rhythm control?

A

DC cardioversion
Amiodarone
Fleccanide

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9
Q

What defines unstable AF and how should it be treated?

A

AF with MI, shock, angina or pulmonary oedema

UFH cover, DC cardiovert, 4 weeks of LMWH and anticoagulant
If CHADSVASc is >0 lifelong anticoagulant
Consider amiodarone to maintain NSR for 1 year

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10
Q

How should a case of AF that presents within 48 hours of onset be managed if rhythm control is desired?

A

UFH cover
Cardioversion
If CHADSVASc high then lifelong anticoagulants
Consider amiodarone for 1 year to maintain NSR

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11
Q

How should a stable case of AF be managed for rhythm control if it presents after 48 hours?

A

3 weeks of anticoagulation
DC cardioversion
LMWH and anticoagulation for 4 weeks
If CHADSVASc high then lifelong oral anticoagulation
Consider amiodarone before and up to a year after to maintain NSR

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12
Q

How should a stable but urgent case of AF that presents after 48 hours be managed if rhythm control desired?

A

Transosophageal ultrasound to check for clots
If absent - UFH, cardiovert, 4 weeks LMWH/anticoag
If present anticoagulate then check again after 3 weeks then proceed as for stable presentation out of 48 hours

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13
Q

What can be used for chronic rhythm control in AF?

A

Beta blocker
Flecanide
Amiodarone
Pill in pocket stratergy to be taken if symptomatic (if very low risk)

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14
Q

What are causes of atrial fibrillation?

A 
Hypertension
Heart failure
MI/ischemia
Mitral stenosis/regurgitation
Rheumatic heart disease
Alcohol
Thyrotoxicosis 
Valve surgery 
CABG 
Idiopathic
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15
Q

What are the diagnostic criteria for infective endocarditis?

A

Duke criteria
2 major, 1 major and 3 minor, 5 minor
Major - typical or persistent positive blood culture. - positive echo or confirmed regurgitation
Minor - predisposing factor. - fever. - vascular signs. - positive blood culture not meeting major. - positive echo not meeting major

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16
Q

What are risk factors for infective endocarditis?

A 
Dermatitis
IV injection / IVDU
Valve disease
Valve replacement 
Patent VSD or ductus arteriosus
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17
Q

Signs and symptoms of infective endocarditis

A 
Fever/malaise
Night sweats
Weight loss
Splenomegaly 
Clubbing
Splinter haemorrhages
New or changed murmur
Oslars nodes / janeway lesions 
Roth spots 
Abcesses
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18
Q

What are oslars nodes, janeway lesions and roth spots?

A

Oslars - vasculitis caused painful infarcts on fingers/toes
Janeways - embolic caused painless palmer or planter abcesses
Roth - vasculitis caused retinal haemorrhages with a pale centre

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19
Q

Common causes of native valve infective endocarditis?

A

Streptococcus viridans - mouth
Staphylococcus aureus - skin
Enterococcus faecalis

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20
Q

Common causes of prosthetic valve infective endocarditis within one year of surgery?

A

Coagulase -ve staphylococci

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21
Q

What fungi can be associated with infective endocarditis?

A

Candidia,

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22
Q

What examinations are required in suspected infective endocarditis?

A 
Blood cultures x3 from different sites
FBC for anaemia / neutrophilia
Urinanalysis for microscopic haematauria 
Cxr for cardiomegally 
Echo for vegitiations or regurgitations
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23
Q

Example of blind therapy for native valve infective endocarditis

A

Amoxicillin and gentamicin

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24
Q

Example of blind antibiotic therapy for prosthetic valve infective endocarditis?

A

Vancomycin, gentamicin and rifampicin

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25
Q

Signs of heart failure on CXR?

A 
Diffuse consolidation (bat wings - perihilar consolidation) 
Reticular interstitial consolidation 
Increased heart size
Kerley b lines
Bilateral pleural effusion
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26
Q

Why do you get batwing (perihilar) consolidation in heart failure? When else do you get it?

A

Better lymphatic drainage peripherally

Non cardiogenic odema

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27
Q

Causes of heart failure?

Three commonest and 4 others

A 
IHD
Dilated cardiomyopathy 
Hypertension
Non-dilated cardiomyopathy 
Valvular heart disease
Congenital heart disease
Arrhythmia 
Alcohol and drugs
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28
Q

What are the two mechanisms of heart failure? What is happening?

A

Systolic - decreased contraction strength of the heart reducing cardiac output
Diastolic - failure of the heart to appropriately relax during diastole

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29
Q

What type of heart failure would be most vulnerable to a sudden tachycardia? Why?

A

Diastolic - reduced filling time.

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30
Q

What is frank starlings law? What is frank starlings curve? How does it appear normally? Why?

A

That the higher the end diastolic volume, the greater the ventricle is stretched and the stronger the force of contraction.
The curve is a plot of ventricular performance against filling pressure. It rises initially due to starlings law then falls as the fibrous pericardium will no longer stretch and further filling compresses the arteries

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31
Q

How is starlings law effected in a systolic heart failure?

A

Decreased cardiac output causes increased end systolic volume, increased venous pressure and thus increased end diastolic volume. This would normally cause increased cardiac output back to normal however, in heart failure the starling curve is depressed thus cardiac output must be maintained by other means (e.g. Increasing pulse) .

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32
Q

What compensatory factors designed to maintain blood pressure actually end up worsening heart failure?

A

Increased afterload due to systemic vasoconstriction
Myocardial damage due to high sympathetic tone
Increased wall stretch due to high preload due to high venous return and salt/water retention

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33
Q

What physiological process that occurs during heart failure actually aids the heart long term?

A

ANP and BNP release in response to stress causing sodium and water loss with vasodilation

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34
Q

What is the classification method of heart failure?

A

Nyha classification for heart failure
1 - no limitation, normal exercise does not cause symptoms
2 - mild limitation, comfortable at rest but normal activity causes symptoms
3 - marked limitation, comfortable at rest but mild activity causes marked symptoms
4 - symptoms at rest

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35
Q

Symptoms of heart failure

A

Exertional dysponea
PND
Orthopneoa
Fatigue

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36
Q

Abdominal signs of heart failure?

A

Ascites

Hepatomegaly

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37
Q

Why does heart failure cause pulmonary oedema?

A

Pulmonary venous hypertension results in increased plural fluid production
Systemic venous hypertension results in decreased lymphatic drainage so decreased pleural fluid reabsorption

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38
Q

Primary care tests in heart failure prior to referral?

A

BNP
CXR
ECG

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39
Q

Secondary care tests for heart failure?

A

Echocardiography

Cardiac MRI

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40
Q

In mild heart failure is cardiac output reduced? What about ejection fraction?

A

CO normal due to increased preload and tachycardia

EJ decreased

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41
Q

Common causes of right heart failure?

A

Secondary to left
Cor-pulmonale
Pulmonary hypertension
Right sided valve disease or right sided ischemia

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42
Q

Non-medical management of heart failure?

A 
Low level exercise
Low salt intake
Stop alcohol 
Stop smoking
Prophylactic vaccination
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43
Q

Drug classes used in heart failure

A 
Diuretics
Ace inhibitors
Beta blockers 
Aldosterone antagonist 
Inotropic agents 
Nitrates
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44
Q

Surgical management of heart failure?

A

Biventricular pacemaker
Transplantation
Left ventricular assist device

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45
Q

If furosemide not working what options are there (confined to diuretics)?

A

Up titrate dose
Switch to bumetanide
Add a thiazide

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46
Q

What drug classes are prognosis altering in heart failure?

A

Ace inhibitors
Arbs
Beta blockers
Spironolactone

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47
Q

What drugs purely cause symptom relief in heart failure with no change to prognosis?

A

Diuretics
Inotrophs
Nitrates

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48
Q

How are beta blockers thought to work to improve heart failure prognosis?

A

Co reduces then returns to normal

Pvr decreases long term possibly due to beta 1 blockade of renin release

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49
Q

Other than social factors and directly treating the heart failure, what else should be considered in a heart failure patient?

A

Treating cause

- revasculisation, antiarrhythmics, antihypertensives

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50
Q

What management option can be considered in inpatient treatment of severe heart failure?

A

Fluid restriction

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51
Q

What aldosterone antagonist is used in heart failure? Main side effect?

A

Spironolactone - gynacomastia

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52
Q

Beta blocker for heart failure?

A

Bisoprolol

Carvediolol

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53
Q

At what point would you consider aspirin for primary prevention of cvd?

A

Qrisk2 >20

Bp

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54
Q

At what point should statins be considered for cvd primary prevention? Which? How much?

A

Qrisk2 >10
Atovastatin
20mg

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55
Q

Stage 1 hypertension thresholds

A

Clinic > 140/90

Home > 135/85

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56
Q

Stage 2 hypertension thresholds

A

Clinic 160/100

Home 150/95

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57
Q

Severe hypertension threshold

A

> 180/110

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58
Q

Treatment threshold for hypertension?

A

All stage 2

Stage 1 under 80 with - dm, ckd, cvd, qrisk2 >20%, organ damage

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59
Q

Under what age should secondary causes of htn be actively sort?

A

40

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60
Q

Secondary causes of htn?

A 
Renal artery stenosis
Fibromuscular dysplasia
Phaeochromocytoma
Cushings
Conns
OSA
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61
Q

Presentation of renal artery stenosis?

A

Refractory HTN

Deteriorating renal function worsened by ACEi

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62
Q

Treatment options for renal artery stenosis?

A

Angioplasty with stenting if:

  • bilateral
  • unilateral with only one kidney
  • effecting renal function
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63
Q

How does a phaeochromocytoma present?

A 
Refractory htn
Sweating
Palpitations
Headache
Anxiety
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64
Q

How is phaeochromocytoma tested for?

A

24 hour urine catacholamines

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65
Q

How is phaeochromocytoma diagnosed and treated? Waht needs to be considered prior to treatment?

A

Ct/mri/pet post +ve urine
Surgical removal
Load with sodium and fluids prior to surgery to prevent bp crash

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66
Q

How does cushings syndrome present in a htn capacity?

A

Refractory htn
Hypokalaemia
Central obesity, moon face, dorsocervical fat pad, purple striae, bruising, thin skin, dm, polyuria, polydipsia, hirtuism, baldness

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67
Q

How does conns syndrome present?

What metabolic abnormalities stem from the electrolyte imbalance?

A

Hypertension
Hypokalaemia
Glucose intolerance and metabolic alkalosis

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68
Q

How does conns cause hypokalaemia?

A

Aldosterone triggers

  • uptake of k into cells by na/k atpase
  • increased ENaC, ROMK and NaKATPase in principal cells of DT and CD
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69
Q

How is conns diagnosed?

A

Serum aldosterone levels

24 hr urinary aldosterone

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70
Q

What can cause conns?

A

Adrenal adenoma

Idiopathic adrenal hyperplasia

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74
Q

How is conns syndrome managed?

A

Spironolactone

Adrenalectomy (effective if adenoma cause not hyperplasia)

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75
Q

Cause of hypertrophic cardiomyopathy?

A

Genetic - dominant inheritance or spontanious

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76
Q

Symptoms of hypertrophic cardiomyopathy?

A 
Sudden death
Palpitations
Angina
Dysponea
Syncope
77
Q

Change in apex beat in hypertrophic cardiomyopathy?

A

Double tap

NOT. Displaced!

78
Q

What conditions can cause displacement of apex beat?

A 
Left ventricular dilation 
- dilated cardiomyopathy
- aortic stenosis
- severe hypertension
Mediasteinal shift
79
Q

Signs of hypertrophic cardiomyopathy?

A

Double tap apex beat
Murmur like aortic stenosis
Heart failure symptoms
Systolic thrill left sternal edge

80
Q

ECG changes in hypertrophic cardiomyopathy?

A 
LVH
AF
VT
WPW
PVCs
81
Q

Complications of hypertrophic cardiomyopathy

A

LVOT obstruction - syncope, angina

Disordered myocytes - arrhythmia, PVCs

82
Q

Treatment of hypertrophic cardiomyopathy

A 
Exercise limitation
Beta blockers
Amiodarone
Dual chamber pacing
ICD
Septal myomectomy for LVOT obstruction
83
Q

Causes of dilated cardiomyopathy?

A

Unknown but related to alcohol, htn, viruses and genetics

84
Q

Presentation of dilated cardiomyopathy

A 
Fatigue
Dysponea
LVF
AF
VT
85
Q

Signs of dilated cardiomyopathy

A

Displaced apex beat
Mitral regurgiation
CHF

86
Q

ECG in dilated cardiomyopathy

A

Poor r wave progression

87
Q

Treatment of dilated cardiomyopathy

A 
Rest
Digoxin
ACEi
Biventricular pacing
Anticoagulation
ICD
transplantation
88
Q

Causes of pericarditis?

A 
Viral
Bacterial 
Idiopathic
MI
Uraemia
Autoimmune 
Drug induced
Radiotherapy 
Tumour
89
Q

Signs of uncomplicated pericarditis?

A

Pericardial friction rub (hammonds sign)

90
Q

Cardiac enzymes in pericarditis?

A

Normal unless progresses to myocarditis

91
Q

Treatment of uncomplicated pericarditis?

A

Treat cause
Aspirin
If no response, corticosteroids

92
Q

Signs of pericardial effusion?

A 
Muffled heart sounds
Non-palpable apex beat
Dull percussion note to lower left lung
Raised JVP
Kussmauls sign 
Pulsus paradoxus
93
Q

What is kussmauls sign in pericardial effusion? Why?

A

Increased JVP on inspiration
Normally jvp falls with inspiration as decreased pressure aids return to heart. If impaired filling of heart then blood returns, but is pooled into the veins increasing jvp.

94
Q

Signs that a pericardial effusion has progressed to tamponade?

A

Haemodynamic compromise

95
Q

What is pulsus paradoxus?

A

Sbp drops on inspiration
Inspiration lowers pressure so increases venous return, dilates right ventricle, compressing left ventricle resulting in decreased blood ejected from the left!

96
Q

What is becks triad of cardiac tamponade?

A

Low bp, increased jvp, muffled heart sounds.

97
Q

Treatment of cardiac tamponade?

A

Pericardiocentesis

98
Q

How should repeated pericardial tamponades be treated?

A

Fenestrations cut into pericardium to allow drainage

99
Q

Causes of cardiac tamponade?

A

Any of pericarditis
Aortic dissection
Warfarin therapy
Trauma (inc biopsy or puncture during cardiac catheterisation)

100
Q

What is a cardiomyopathy?

A

An idiopathic myocardial disease

101
Q

How may myocarditis present?

A

Asymptomatic

Pain, fatigue, dysponea, palpitations, CHF

102
Q

What would cardiac enzymes show in a myocarditis patient?

A

Elevation

103
Q

Advice in patients with myocarditis

A

Bed rest

Avoid athletic activities for 6months at least

104
Q

Classification method of heart failure?

A

NYHA
1 - normal exercise does not produce symptoms
2 - mild limitation - normal exercise produces symptoms
3 - marked limitation - gentle exercise produces severe symptoms
4 - symptoms at rest

105
Q

Causes of raised JVP

A

Fluid overload - RVF (CHF, cor pulmonale), iatrogenic

Mechanical obstruction of SVC - cancers

106
Q

What does the JVP reflect?

A

Right atrial pressure

107
Q

Auscultation procedure of the chest in a CVS exam? What murmur are you listening for? What breathing should be performed to increase?

A

Apex beat - mitral (expiration)
Left axilla - mitral regurgitation (expiration)
Apex rolled left - mitral stenosis (expiration)
4th ICS LSE - tricuspid (inspiration)
2nd ICS LSE - pulmonary (inspiration)
2nd ICS RSE - aortic (expiration)
Neck - aortic stenosis (expiration)
4th ICS LSE leaning forward - aortic regurgitation (expiration)
Base of lungs posteriorly! Bibasal crackles

108
Q

Why would you auscultate the chest of a patient with chest pains?

A 
Extra heart sounds - heart failure
Mitral regurgitation - papillary muscle rupture post MI
VSD - post MI
Pericardial friction rub - pericarditis 
Aortic stenosis - angina
109
Q

What is the first heart sound?

A

Closure of the AV valves

110
Q

What is the second heart sound?

A

Closure of the semilunar valves

111
Q

Why may the second heart sound split?

A

Inspiration - venous return to RV increases so pulmonary closes after aortic
RBBB - delayed RV contraction
ASD - increases RV volume
LBBB - delayed LV contraction

112
Q

What is a third heart sound? Causes?

A

Sound of rapid ventricular filling in early diastole.

Normal 40 LVF

113
Q

What is a fourth heart sound? Cause?

A

End diastolic sound due to atria contracting against an incompliant ventricle
E.g. LVH,

114
Q

Which heart sound should be auscultated with the bell?

A

Mitral stenosis (leaning left at apex)

115
Q

How are heart murmurs graded?

A

1 - only heard in optimum conditions by expert
2 - heard in optimum conditions by anyone
3 - heard but no thrill
4 - heard with thrill
5 - heard with partial contact
6 - heard without stethoscope

116
Q

What is the murmur of mitral stenosis?

A

Mid diastolic murmur best heard with bell rolled to left at apex
Opening snap

117
Q

What is the murmur of mitral regurgitation?

A

Pansystolic murmur best heard at the axilla

118
Q

What is the murmur of aortic stenosis? How can cause be narrowed down by listening?

A 
Ejection systolic murmur best heard at the neck 
Ejection click (not calcified as leaflets too stiff)
119
Q

What is the usual murmur of aortic regurgitation?

A

Early diastolic murmur best heard left sternal edge when leaning forwards

120
Q

Causes of ejection systolic murmurs?

A

Aortic stenosis

LVOT obstruction

121
Q

Causes of pansystolic murmur?

A

Mitral regurgitation
Tricuspid regurgitation
VSD

122
Q

Causes of early diastolic murmurs?

A

Aortic regurgitation

Pulmonary regurgitation

123
Q

Causes of mid diastolic murmurs

A

Mitral stenosis

124
Q

Causes of continuous murmurs?

A

Patent ductus arteriosus

125
Q

Nature of pericarditis pain

A

Sharp
Worse on inspiration and swallowing
Eased by leaning forward from sitting

126
Q

How can thoracic aortic dissection be classified?

A

Type a - involving arch and aortic valve proximal to left subclavian
Type b - involving the descending thoracic aorta distal to the left subclavian artery.

127
Q

How can dissecting aortic aneurysm be diagnosed?

A

CT or transoesophageal echo

128
Q

What management should thoracic dissecting aortic aneurysms recieve?

A

Type a - antihypertensives if HTN, arch replacement surgery

Type b - medical management unless complications develop

129
Q

Which type of dissecting aortic aneurysm is more common?

A

Type a

130
Q

Complications of type a dissecting aortic aneurysms?

A

Coronary artery occlusion
Aortic incompetence
Cardiac tamponade

131
Q

What sort of replacement heart valves are there? Lifespans? Risks?

A

Manufactured - lifelong, risk of clots

Tissue - 10-20 years, no risk of clots

132
Q

Causes of aortic stenosis?

A

Senile calcification
Rheumatic heart disease
Congenital

133
Q

Symptoms of aortic stenosis?

A

Exertional dysponea
Angina
Syncope
Heart failure

134
Q

Signs of aortic stenosis?

A

Ejection systolic murmur loudest on expiration radiating to neck
Slow rising pulse
Heaving apex beat
Heart failure

135
Q

Tests that might show signs of aortic stenosis?

A

CXR - calcification
Echo - decreased flow
ECG - blocks as calcification spreads, LVH

136
Q

Causes of aortic regurgitation

A 
Infective endocarditis
Aortic dissection
Chest trauma
Rheumatic fever
Connective tissue diseases
SLE 
RA
137
Q

Symptoms of aortic regurgitation

A

Dysponea
Palpitations
Syncope
Angina

138
Q

Signs of aortic regurgitation

A

Early diastolic murmur loudest on expiration radiating to sternum
Collapsing pulse with wide pulse pressure
Carotid pulsation
Head nodding with heartbeat

139
Q

Test findings for aortic regurgitation?

A

Ecg - lvh
Cxr - lvh, pulmonary oedema
Echo - regurgitaiton

140
Q

Causes of mitral stenosis?

A

Rheumatic heart disease
Congenital
Carcinoid syndrome
Prosthetic valve

141
Q

Symptoms of mitral stenosis?

A 
Dysponea
Fatigue
Palpitations
Chest pains
Haemoptysis
Right heart failure
Systemic emboli
142
Q

Signs of mitral stenosis

A

Mid diastolic murmur loudest at apex on expiration and leaning left
Malar flush
Af
Low volume pusle

143
Q

Test findings for mitral stenosis?

A

Ecg - p mitrale, rvh, rad, af
Cxr - left atrial enlargement
Echo - low flow

144
Q

Causes of mitral regurgitation

A 
Lv dilatation
Calcification
Rheumatic fever
Infective endocarditis
Prolapse
Ruptured chordae tendinae or papillary muscle 
Congenital
145
Q

Symptoms of mitral reguritation

A

Dysponea
Fatigue
Palpitaitons

146
Q

Signs of mitral regurgitation

A

Pansystolic murmur loudest at apex radiating to axilla
Displaced hyperdynamic apex
Rv heave
Af

147
Q

Tests showing signs of mitral reguritation

A

Ecg - af, pmitrale, lvh
Cxr - lv enlargement, calcification
Echo - regurg

148
Q

How can you perform a cardiac stress test in different ways?

A

Treadmill
Beta agonist like dobutamine
Vasodilator like adenosine

149
Q

What are positive results in a cardiac stress test?

A 
Chest pains
Sob
Presyncope
St depression (significant)
Us wall motion changes
Decreased radioisotope distribution on nuclear imaging
150
Q

When does troponin begin to rise post insult? Peak? Decline?

A

3-4 hours, peak at 18-36 hours, decline in 10-14 days

151
Q

When does ckmb begin to rise post insult? Peak? Decline?

A

3-8 hours, peak at 24 hours, decline at 48-72 hours

152
Q

Causes of raised troponin?

A 
AMI
Heart surgery
PE with right ventricular strain
Pericarditis and myocarditis
Aortic dissection
Heart failure
Cardioversion
Trauma
Sepsis
End stage renal disease 
Rhabdomyolysis
153
Q

What is rheumatic fever?

A

An inflammatory disease following urti with beta haemolytic streptococcus (pyogenes) caused by antibody cross reactivity

154
Q

What is required for a diagnosis of rheumatic fever?

A

Throat culture showing strep pyogenes (rare as infection usually passed)
Blood antigen
Antibody titre
Scarlet fever

155
Q

Signs and Symptoms of rheumatic fever?

A 
Carditis - tachycadia, mit/aor regurg, ccf, cardiomegally, conduction defect 
Arthritis
Erythema marginatum
Subcutaneous nodules 
Fever 
Raised crp
156
Q

Main complication of rheumatic fever? Prevalence?

A

Rheumatic heart disease

60% of those with rheumatic fever and carditis

157
Q

Presentation of rheumatic heart disease?

A

Aortic and mitral regurgitation progressing to chronic stenosis

158
Q

Treatment for rheumatic fever?

A

Rest
Penicillin
Aspirin if carditis
Immobilise arthritic joints

159
Q

What treatments are required long term post rheumatic fever? Durations?

A

Prophylactic penicillin
If valve disease lifelong
If carditis 10 years
Otherwise 5 years

160
Q

Diagnostic criteria for infective endocarditis?

How many points needed?

A

Dukes criteria
2 major
1 major 3 minor
5 minor

161
Q

Major dukes criteria for ie

A

Positive blood culture - typical from 2 sites or atypical from 3
Evidence of endocardial involvement - vegetation, regurgitation

162
Q

Minor dukes criteria for ie?

A 
Predisposition
Fever >38
Vascular signs
Positive blood culture not meeting major
Postive echo not meeting major
163
Q

Predisposing factors for infective endocarditis

A 
Ivdu
Dental work 
Prosthetic valve
Valve disease
Structural heart disease
Previous endocarditis
164
Q

Vascular signs of infective endocarditis. What are they?

A

Roth spots - retinal haemorrhage - white centred haemorrhage
Oslars nodes - immune complex - painful, red, raised, fingers/toes
Janeway lesions - septic emboli - nonpainful, palms/soles
Splinter haemorrhages - blood clot under nail - vertical red line

165
Q

2 causative organisms of infective endocarditis?

A

Strep viridans

Staph aureus

166
Q

Signs and symptoms of ie not covered in dukes criteria?

A 
Night sweats
Weight loss
Anaemia (normochromic normocytic)
Clubbing
Long PR on ECG
Glomerulonephritis with haematuria 
Abscesses from emboli
167
Q

Key symptoms of angina

A

Constricting pain to front of chest with classic radiation
Precipitated by physical exertion
Relieved by rest or GTN

168
Q

How can angina be classified diagnostically into typical, atypical and non-anginal

A

Typical - 3?key symptoms
Atypical - 2
Non anginal - 0-1

169
Q

How should a diagnosis of angina be reached?

A

Looking at symptoms (typical vs atypical), age and risk factors (low or high) on a table derived by nice. Gives a percentage risk of coronary artery disease.

170
Q

If a patient with angina symptoms has a less than

A

Look for other causes - aortic stenosis, HCM

171
Q

If a patient has angina type symptoms and a risk of cad of >90% what should be done?

A

Make the angina diagnosis and treat

172
Q

If a patient with angina type symptoms has a risk of cad between 10 and 90% what tests are available in order from those for patients most likely to have angina to the least

A

Coronary angiography
Functional imaging
CT calcium scoring

173
Q

What is CT calcium scoring?

A

Looks for amount of calcification in the coronary arteries

174
Q

Management of angina?

A

Council re provoking factors
Short acting nitrate for symptom relief
Secondary prevention - aspirin, statin, ACEi
Reduce episodes - beta blocker, long acting nitrate
Surgery - cabg, pci

175
Q

What is cardiac functional imaging?

A

Moving MRI of the heart

176
Q

What classes as cvd for the purpose of determining if a patient should recieve 80mg atorvostatin?

A 
Mi
Angina
Stroke 
Tia
Peripheral arterial disease
177
Q

How can risk be stratified in unstable angina and NSTEMI

A

Using the GRACE score

178
Q

What component make up the grace risk score for ua and nstemi

A 
Age
Pulse
Sbp
Creatinine
Heart failure
Cardiac arrest 
St segment changes
Raised troponin
179
Q

What immediate treatments should be offered to ua and nstemi patients? What risks stratifications for each?

A
  • Aspirin - all
  • Prasugrel - all except lowest risk ua
  • Gp iib/iiia inhibitors - =/>intermediate risk going for angiography in 96 hours
  • Fondaparinux - all except renal failure or angiography in 24 hrs
  • UFH - all who cant have fondaparinux
  • Angiography - =/> intermediate risk within 96 hours
180
Q

Long term medications to add to acute treatments of ua and nstemi

A

Cardiac rehab
Acei, beta blocker, statin
Lifestyle modification advice (smoking, diet, drinking, exercise)
Consideration for stent or cabg

181
Q

Rules for driving post MI?

A

Cars - at least one month off and until dr says safe. No need to tell dvla
Trucks - tell dvla. Stop for at least 6 weeks and until dr says safe

182
Q

Non MI causes of raised troponin

A 
Myocarditis
Heart failure 
Renal failure 
PE
Septic shock
Electrical cardioversion
183
Q

Causes of raised BNP

A 
Heart failure 
Myocarditis
Renal failure
Elderly + female 
Digoxin
Hyperaldosteronism / cushings

IPE (17 decks)

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