Cardio Flashcards

1
Q

HTN Guidelines?

A

1) ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)
treat if < 80 years of age AND any of the following apply;
- target organ damage,
- established cardiovascular disease,
- renal disease,
- diabetes or
- QRISK 20% or greater

2) ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)
- drug treatment regardless of age

If <40 consider specialist to exclude secondary causes

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2
Q

HTN Stepwise Management?

A

Step 1:
- patients < 55-years-old: ACE inhibitor (A)
- patients > 55-years-old or of Afro-Caribbean origin: calcium channel blocker

Step 2:
- ACE inhibitor + calcium channel blocker (A + C)

Step 3:
- Add a thiazide diuretic (D, i.e. A + C + D)
 chlorthalidone (12.5-25.0 mg once daily) or
 indapamide (1.5 mg modified-release once daily or 2.5 mg once daily)

Step 4 (Resistant):
1) consider further diuretic treatment
- if potassium < 4.5 mmol/l add spironolactone 25mg od
- if potassium > 4.5 mmol/l add higher-dose thiazide-like diuretic treatment
2) if further diuretic therapy is not tolerated, or is contraindicated or ineffective, consider an alpha- or beta-blocker

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3
Q

BP Targets?

A
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4
Q

Allskiren?

A
  • Direct renin inhibitor
  • Inhibiting renin blocks the conversion of angiotensinogen to angiotensin I
  • Only current role would seem to be in patients who are intolerant of more established
    antihypertensive drugs
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5
Q

Features of severe pre-eclampsia?

A

 hypertension: typically > 170/110 mmHg and proteinuria as above
 proteinuria: dipstick ++/+++
 headache
 visual disturbance
 papilloedema
 RUQ/epigastric pain
 hyperreflexia
 platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome

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6
Q

Centrally acting antihypertensives?

A
  • methyldopa: used in the management of hypertension during pregnancy
  • moxonidine: used in the management of essential hypertension when conventional
    antihypertensives have failed to control blood pressure
  • clonidine: the antihypertensive effect is mediated through stimulating alpha-2 adrenoceptors in
    the vasomotor centre
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7
Q

DM HTN targets?

A

if end-organ damage (e.g. renal disease, retinopathy) < 130/80 mmHg

otherwise < 140/80 mmHg

ACEi first line due to renoprotection - if african/caribbean ACEi plus thiazide or CCB

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8
Q

HF Guidelines?

A

1) ACE-inhibitor and a beta-blocker
2) aldosterone antagonist, angiotensin II receptor
blocker or a hydralazine in combination with a nitrate
3) if symptoms persist cardiac resynchronisation therapy or digoxin

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9
Q

Drugs that exacerbate HF?

A

1) thiazolidinediones: pioglitazone is contraindicated as it causes fluid retention
2) verapamil: negative inotropic effect
3) NSAIDs/glucocorticoids: should be used with caution as they cause fluid retention
4) class I antiarrhythmics; flecainide (negative inotropic and proarrhythmic effect)

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10
Q

Adverse effects of bendroflumethiazide?

A

Common
1) dehydration
2) postural hypotension
3) hyponatraemia, hypokalaemia, hypercalcaemia
4) gout
5) impaired glucose tolerance
6) impotence

Rare
1)thrombocytopaenia
2) agranulocytosis
3) photosensitivity rash
4) pancreatitis

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11
Q

Digoxin mechanism?

A
  • decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
  • Increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump.
  • Also stimulates vagus nerve
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12
Q

Digoxin toxicity?

A

generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)

Precipitating factors
 classically: hypokalaemia* ,hypomagnesaemia
 hypercalcaemia, hypernatraemia, acidosis
 hypoalbuminaemia
 hypothermia
 hypothyroidism
 increasing age
 renal failure
 myocardial ischaemia

Precipitating Drugs:
 Amiodarone, quinidine,
 verapamil, diltiazem,
 spironolactone (competes for secretion in distal convoluted tubule therefore reduce
excretion),
 Ciclosporin.
 Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics

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13
Q

Dipyridamole mechanism?

A

inhibits phosphodiesterase, elevating platelet cAMP levels which in turn reduce
intracellular calcium levels

other actions include reducing cellular uptake of adenosine and inhibition of thromboxane
synthase

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14
Q

Arterial supply and venous drainage of heart?

A
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15
Q

ECG coronary territories?

A
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16
Q

Angina management?

A
  1. Aspirin and statin
  2. Sublingal GTN
  3. BB or CCB monotherapy
  4. Titrate up to maximum dose
  5. If still symptomatic add in CCB to BB and vice versa

(Monotherapy - rate limiting CCB, combination - dihydropyradine)

  1. If can’t tolerate combination therapy onsider long acting nitrate ivabradine, nicorandil or ranolazine
  2. if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
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17
Q

Nitrate tolerance?

A
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18
Q

Ivabradine?

A
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19
Q

IV glycoprotein IIb/IIIa receptor antagonists?

A
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20
Q

Cardiac enzymes?

A
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21
Q

Glycaemic control in ACS?

A
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22
Q

Stent thrombosis vs Restenosis?

A
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23
Q

Thrombolysis contraindications?

A
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24
Q

Dressler’s syndrome?

A
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25
Q

MI Complications ?

  • LV aneurysm
  • LV free wall rupture
  • VSD
  • Acute MR
A
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26
Q

Reasons to stop stress test?

A
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27
Q

Special situations for lipi modification?

A
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28
Q

Diagnostic criteria for familial hypercholesterolaemia?

A
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29
Q

Remnant Hyperlipidaemia?

A
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30
Q

Characteristic xanothomata from different lipid disorders?

A
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31
Q

Myocarditis causes and presentation?

A
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32
Q

Tamponade features?

A
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33
Q

Differences between cardiac tamponade and constrictive pericarditis?

A
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34
Q

Restrictive Cardiomyopathy?

A
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35
Q

Dilated cardiomyopathy?

A
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36
Q

HOCM clinical features?

A
37
Q

Echo and ECG features of HOCM?

A
38
Q

Management and drugs to avoid in HOCM?

A
39
Q

Brugada ECG changes?

A
40
Q

ECG, echo and MRI in ARVC?

A
41
Q

Catecholaminergic polymorphic VT?

A
42
Q

WPW ECG features?

A
43
Q

WPW types?

A
44
Q

WPW associations and management?

A
45
Q

Vaughan Williams Classification?

A
46
Q

When is flecainide contraindicated?

A

Post-MI

Adverse effects…
1) negativelyinotropic
2) bradycardia
3) proarrhythmic
4) oral paraesthesia
5) visual disturbances

47
Q

Amiodarone adverse effects, drug interactions and monitoring?

A
48
Q

Amiodarone induced hypothyroidism?

A
49
Q

Amiodarone induced thyrotoxicosis?

A
50
Q

Effects on adenosine by other drugs?

A
51
Q

CHADS-VASc?

A

0 - no treatment
1 - male, consider; female, no treatment
2 - offer anticoagulation

52
Q

HASBLED?

A
53
Q

Causes of prolonged QT?

A
54
Q

Features favouring VT rather than SVT with aberrant conduction?

A
55
Q

Risk of asystole in bradyarrythmias?

A
56
Q

Features and associations of coarctation of aorta?

A
57
Q

PAH - vasodilator testing?

A

Intravenous epoprostenol or inhaled nitric oxide

58
Q

PAH exam findings?

A

right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid
regurgitation

58
Q

Rheumatic fever?

A

Evidence of recent streptococcal infection with
- 2 major criteria
- 1 major with 2 mior

58
Q

IE Causes?

A
59
Q

Culture negative IE causes?

A
60
Q

IE pathological criteria?

A
61
Q

IE Major Criteria?

A
62
Q

IE Minor Criteria?

A
63
Q

Abx management for IE?

A
64
Q

IE indications for surgery?

A
65
Q

Loud S1?

A
66
Q

Quiet/soft S1?

A
67
Q

Loud S2?

A
68
Q

Soft S2?

A

Aortic stenosis

69
Q

Causes of S2 splitting?

A
70
Q

S3?

A
71
Q

S4?

A
72
Q

Mitral stenosis features?

A
73
Q

Features of severe MS?

A
74
Q

MS on echo?

A
75
Q

Mitral valve prolapse associations?

A
76
Q

Clinical features of mitral valve prolapse?

A
77
Q

AS causes?

A
78
Q

AS management?

A
79
Q

Aortic regurg features?

A
80
Q

Aortic regurg causes?

A
81
Q

Bicuspid aortic valve?

A
82
Q

Tricuspid regurg features and causes?

A
83
Q

Atrial myxoma?

A
84
Q

Systolic murmurs?

A
85
Q

Diastolic murmurs?

A
86
Q

Continuous machine-like murmur?

A

Patient ductus ateriosus