all Flashcards

1
Q

What is aortic dissection?

A

A rare but serious cause of chest pain.

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2
Q

What is the pathophysiology of aortic dissection?

A

Tear in the tunica intima of the wall of the aorta.

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3
Q

What is the most important risk factor for aortic dissection?

A

Hypertension.

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4
Q

Name two syndromes associated with aortic dissection.

A
  • Marfan’s syndrome
  • Ehlers-Danlos syndrome
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5
Q

What are some associations with aortic dissection?

A
  • Trauma
  • Bicuspid aortic valve
  • Collagens (Marfan’s syndrome, Ehlers-Danlos syndrome)
  • Turner’s syndrome
  • Noonan’s syndrome
  • Pregnancy
  • Syphilis
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6
Q

What is the typical nature of pain associated with aortic dissection?

A

Typically severe and ‘sharp’, ‘tearing’ in nature.

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7
Q

Where is the pain typically maximal in aortic dissection?

A

At onset.

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8
Q

In type A dissection, where is chest pain more common?

A

Chest pain is more common.

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9
Q

In type B dissection, where is back pain more common?

A

Upper back pain is more common.

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10
Q

What are some common features of aortic dissection?

A
  • Pulse deficit
  • Weak or absent carotid, brachial, or femoral pulse
  • Variation (>20 mmHg) in systolic blood pressure between the arms
  • Aortic regurgitation
  • Hypertension
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11
Q

What can result from the involvement of specific arteries in aortic dissection?

A
  • Coronary arteries → angina
  • Spinal arteries → paraplegia
  • Distal aorta → limb ischaemia
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12
Q

What ECG changes are typically seen in patients with aortic dissection?

A

Majority have no or non-specific changes; ST-segment elevation may be seen in a minority.

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13
Q

What are the two types in the Stanford classification of aortic dissection?

A
  • Type A - ascending aorta, 2/3 of cases
  • Type B - descending aorta, distal to left subclavian origin, 1/3 of cases
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14
Q

Describe the DeBakey classification type I.

A

Originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally.

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15
Q

Describe the DeBakey classification type II.

A

Originates in and is confined to the ascending aorta.

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16
Q

Describe the DeBakey classification type III.

A

Originates in descending aorta, rarely extends proximally but will extend distally.

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17
Q

What is the correct answer for a significant increase in blood pressure after 20 weeks of gestation without proteinuria?

A

gestational hypertension

This condition is diagnosed when there is new-onset hypertension during pregnancy without any proteinuria or features of pre-eclampsia.

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18
Q

What blood pressure reading indicates gestational hypertension?

A

≥140/90 mmHg

This threshold is used to diagnose gestational hypertension according to UK guidelines.

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19
Q

What is required for a diagnosis of gestational hypertension?

A

new-onset hypertension without proteinuria or features of pre-eclampsia

Gestational hypertension is specifically characterized by the absence of proteinuria.

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20
Q

When is gestational hypertension diagnosed during pregnancy?

A

after 20 weeks of gestation

Diagnosis occurs if hypertension develops after this point in pregnancy.

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21
Q

What does COPD stand for?

A

Chronic Obstructive Pulmonary Disease

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22
Q

Which biomarker can be falsely elevated in patients with COPD?

A

B-type natriuretic peptide (BNP)

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23
Q

Where is BNP primarily released from?

A

Ventricular myocytes

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24
Q

What triggers BNP release from ventricular myocytes?

A

Increased wall tension and volume overload

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25
Q

What complications can develop in COPD patients leading to increased BNP production?

A

Pulmonary hypertension and right ventricular strain

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26
Q

What other factors related to COPD can stimulate BNP release?

A

Hypoxia and inflammatory state

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27
Q

True or False: Elevated BNP levels in COPD patients always indicate heart failure.

A

False

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28
Q

When interpreting BNP results in COPD patients, what should clinicians consider?

A

Values may be elevated due to the underlying respiratory condition

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29
Q

What is the first-line investigation for all patients according to the updated NICE guidelines issued in 2018?

A

N-terminal pro-B-type natriuretic peptide (NT-proBNP) blood test

This test is now required regardless of previous myocardial infarction history.

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30
Q

What should be arranged if NT-proBNP levels are ‘high’?

A

Specialist assessment (including transthoracic echocardiography) within 2 weeks

High levels are defined as > 2000 pg/ml.

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31
Q

What should be arranged if NT-proBNP levels are ‘raised’?

A

Specialist assessment (including transthoracic echocardiography) within 6 weeks

Raised levels are defined as 400-2000 pg/ml.

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32
Q

What hormone is produced mainly by the left ventricular myocardium in response to strain?

A

B-type natriuretic peptide (BNP)

Very high levels of BNP are associated with a poor prognosis.

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33
Q

What are the high level thresholds for BNP and NT-proBNP?

A
  • BNP: > 400 pg/ml (116 pmol/litre)
  • NT-proBNP: > 2000 pg/ml (236 pmol/litre)

These thresholds indicate high levels of the respective peptides.

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34
Q

What are the raised level thresholds for BNP and NT-proBNP?

A
  • BNP: 100-400 pg/ml (29-116 pmol/litre)
  • NT-proBNP: 400-2000 pg/ml (47-236 pmol/litre)

These thresholds indicate raised levels of the respective peptides.

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35
Q

What are the normal level thresholds for BNP and NT-proBNP?

A
  • BNP: < 100 pg/ml (29 pmol/litre)
  • NT-proBNP: < 400 pg/ml (47 pmol/litre)

These thresholds indicate normal levels of the respective peptides.

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36
Q

List factors that can increase BNP levels.

A
  • Left ventricular hypertrophy
  • Ischaemia
  • Tachycardia
  • Right ventricular overload
  • Hypoxaemia (including pulmonary embolism)
  • GFR < 60 ml/min
  • Sepsis
  • COPD
  • Diabetes
  • Age > 70
  • Liver cirrhosis

These factors can cause elevated BNP levels.

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37
Q

List factors that can decrease BNP levels.

A
  • Obesity
  • Diuretics
  • ACE inhibitors
  • Beta-blockers
  • Angiotensin 2 receptor blockers
  • Aldosterone antagonists

These factors can cause reduced BNP levels.

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38
Q

What are the two classes of drugs used in diabetic nephropathy?

A

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs)

Examples include ramipril for ACE inhibitors and candesartan for ARBs.

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39
Q

What is the primary purpose of using ACE inhibitors and ARBs in diabetic nephropathy?

A

To reduce proteinuria and its progression

These drug classes have been shown to slow the progression of diabetic nephropathy.

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40
Q

What effect do ACE inhibitors and ARBs have on the afferent and efferent arterioles?

A

They dilate both afferent and efferent arterioles, but have a greater dilatory effect on efferent arterioles

This reduces intraglomerular pressure.

41
Q

Why do ACE inhibitors and ARBs reduce intraglomerular pressure?

A

Angiotensin II normally has a stronger vasoconstrictive effect on the efferent arteriole

By dilating the efferent arteriole, these drugs decrease mechanical stress on the glomeruli.

42
Q

What is the consequence of reduced intraglomerular pressure?

A

Decreased mechanical stress on the glomeruli and reduced protein leakage into the urine

This helps in preventing further glomerular damage.

43
Q

Who should be offered an ACE inhibitor or ARB in the context of diabetic nephropathy?

A

All diabetic patients with hypertension and diabetic nephropathy and an ACR of 3 mg/mmol or more

ACR stands for albumin-to-creatinine ratio.

44
Q

Fill in the blank: ACE inhibitors like _______ are used to treat diabetic nephropathy.

45
Q

Fill in the blank: ARBs like _______ are commonly prescribed for diabetic nephropathy.

A

candesartan

46
Q

True or False: ACE inhibitors and ARBs can prevent further glomerular damage in diabetic nephropathy.

47
Q

What are the two scenarios where cardioversion may be used in atrial fibrillation?

A
  1. Electrical cardioversion as an emergency for haemodynamically unstable patients
  2. Electrical or pharmacological cardioversion as an elective procedure for rhythm control
48
Q

What is the purpose of synchronizing electrical cardioversion to the R wave?

A

To prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced

49
Q

According to the 2014 NICE guidelines, what should be offered if the onset of atrial fibrillation is less than 48 hours?

A

Rate or rhythm control

50
Q

What should be started if atrial fibrillation onset is more than 48 hours or is uncertain?

A

Rate control

51
Q

What anticoagulation treatment should be given if atrial fibrillation onset is less than 48 hours?

A

Patients should be heparinised and those with stroke risk factors should be put on lifelong oral anticoagulation

52
Q

What are the options for cardioversion if atrial fibrillation is confirmed to be less than 48 hours?

A
  1. Electrical - ‘DC cardioversion’
  2. Pharmacological - amiodarone if structural heart disease, flecainide or amiodarone if no structural heart disease
53
Q

Is further anticoagulation necessary after electrical cardioversion if AF is confirmed as less than 48 hours duration?

A

No, further anticoagulation is unnecessary

54
Q

What should be done if the patient has been in atrial fibrillation for more than 48 hours?

A

Anticoagulation should be given for at least 3 weeks prior to cardioversion

55
Q

What alternative strategy can be performed to exclude a left atrial appendage thrombus before cardioversion?

A

Transoesophageal echo (TOE)

56
Q

What does NICE recommend for cardioversion in patients with AF for more than 48 hours?

A

Electrical cardioversion rather than pharmacological

57
Q

What should be done if there is a high risk of cardioversion failure?

A

At least 4 weeks of amiodarone or sotalol prior to electrical cardioversion

58
Q

For how long should patients be anticoagulated following electrical cardioversion?

A

At least 4 weeks

59
Q

What should be considered after 4 weeks of anticoagulation following electrical cardioversion?

A

Decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence

60
Q

What type of medication is Warfarin?

A

Oral anticoagulant

Used for managing venous thromboembolism and reducing stroke risk in patients with atrial fibrillation.

61
Q

What has largely superseded Warfarin in treatment?

A

Direct oral anticoagulants (DOACs)

DOACs do not require the same level of monitoring as Warfarin.

62
Q

What is the mechanism of action of Warfarin?

A

Inhibits epoxide reductase preventing the reduction of vitamin K

This vitamin K is essential for the carboxylation of clotting factors II, VII, IX, and X.

63
Q

Which clotting factors are affected by Warfarin?

A
  • Factor II
  • Factor VII
  • Factor IX
  • Factor X

Mnemonic for remembering these factors is 1972.

64
Q

What are the indications for Warfarin use?

A
  • Mechanical heart valves
  • Venous thromboembolism
  • Atrial fibrillation

Target INR varies based on condition and valve type.

65
Q

What is the target INR for venous thromboembolism when using Warfarin?

A

2.5, if recurrent 3.5

INR stands for International Normalised Ratio.

66
Q

What is the target INR for atrial fibrillation when using Warfarin?

A

2.5

A consistent INR is crucial for effective treatment.

67
Q

How are patients monitored while on Warfarin?

A

Using the INR (international normalised ratio)

This ratio compares the patient’s prothrombin time to the normal prothrombin time.

68
Q

What is a characteristic of Warfarin’s half-life?

A

Long half-life

Achieving a stable INR may take several days.

69
Q

What factors may potentiate the effects of Warfarin?

A
  • Liver disease
  • P450 enzyme inhibitors (e.g., amiodarone, ciprofloxacin)
  • Cranberry juice
  • NSAIDs (displace warfarin from plasma albumin and inhibit platelet function)

These factors can increase the risk of bleeding.

70
Q

What are some common side effects of Warfarin?

A
  • Haemorrhage
  • Teratogenic effects
  • Skin necrosis
  • Purple toes

Skin necrosis can occur due to a temporary procoagulant state after starting Warfarin.

71
Q

What happens to protein C biosynthesis when starting Warfarin?

A

Reduced

This can lead to a temporary procoagulant state, normally managed with concurrent heparin administration.

72
Q

True or False: Warfarin can be used in breastfeeding mothers.

A

True

Warfarin is teratogenic but can be administered during breastfeeding.

73
Q

What is pulsus paradoxus?

A

Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration, leading to faint or absent pulse in inspiration.

Associated with severe asthma and cardiac tamponade.

74
Q

What condition is characterized by a slow-rising or plateau pulse?

A

Aortic stenosis.

This pulse pattern indicates a gradual rise and fall in arterial pressure.

75
Q

What is a collapsing pulse associated with?

A

Aortic regurgitation, patent ductus arteriosus, hyperkinetic states (anemia, thyrotoxicosis, fever, exercise/pregnancy).

A collapsing pulse indicates a rapid rise and fall in arterial pressure.

76
Q

What does pulsus alternans indicate?

A

Regular alternation of the force of the arterial pulse.

Commonly associated with severe left ventricular failure.

77
Q

What is a bisferiens pulse?

A

‘Double pulse’ - two systolic peaks.

Seen in mixed aortic valve disease.

78
Q

What is a ‘jerky’ pulse indicative of?

A

Hypertrophic obstructive cardiomyopathy (HOCM).

HOCM may occasionally be associated with a bisferiens pulse.

79
Q

What does a normal apex beat indicate in aortic stenosis?

A

It indicates that the apex beat is not normally displaced.

80
Q

What does displacement of the apex beat in aortic stenosis suggest?

A

It suggests left ventricular dilatation and hence severe disease.

81
Q

What is Syndrome X?

A

A condition characterized by angina-like chest pain on exertion, ST depression on exercise stress test, but normal coronary arteries on angiography.

82
Q

What are the features of Syndrome X?

A
  • Angina-like chest pain on exertion
  • ST depression on exercise stress test
  • Normal coronary arteries on angiography
83
Q

What management options are available for Syndrome X?

A

Nitrates may be beneficial.

84
Q

True or False: Syndrome X is associated with abnormal coronary arteries.

85
Q

Fill in the blank: Syndrome X features _______ on exercise stress test.

A

ST depression

86
Q

What are the clinical features of symptomatic aortic stenosis?

A
  • chest pain
  • dyspnoea
  • syncope / presyncope (e.g. exertional dizziness)
  • murmur
  • ejection systolic murmur (ESM) radiating to the carotids
  • decreased following the Valsalva manoeuvre

The ejection systolic murmur is a key diagnostic feature of aortic stenosis, with its characteristic radiation and changes during maneuvers.

87
Q

What are the features of severe aortic stenosis?

A
  • narrow pulse pressure
  • slow rising pulse
  • delayed ESM
  • soft/absent S2
  • S4
  • thrill
  • duration of murmur
  • left ventricular hypertrophy or failure

These features indicate the severity of aortic stenosis and help in clinical assessment.

88
Q

What is the most common cause of aortic stenosis in older patients?

A

degenerative calcification

This is typically seen in patients over 65 years of age.

89
Q

What is the most common cause of aortic stenosis in younger patients?

A

bicuspid aortic valve

This condition is prevalent in patients under 65 years.

90
Q

Name a genetic syndrome associated with supravalvular aortic stenosis.

A

William’s syndrome

This syndrome is a rare cause of aortic stenosis related to genetic factors.

91
Q

What management approach is typically taken for asymptomatic aortic stenosis?

A

observe the patient

Observation is the general rule unless other clinical indicators suggest intervention.

92
Q

What is the management for symptomatic aortic stenosis?

A

valve replacement

Symptomatic patients typically require surgical intervention to replace the affected valve.

93
Q

When should surgery be considered for asymptomatic patients with aortic stenosis?

A

if valvular gradient > 40 mmHg and features like left ventricular systolic dysfunction

These criteria indicate a higher risk of adverse outcomes, warranting surgical intervention.

94
Q

What are the options for aortic valve replacement (AVR)?

A
  • surgical AVR
  • transcatheter AVR (TAVR)
  • balloon valvuloplasty

Each option is chosen based on the patient’s age, operative risk, and specific clinical circumstances.

95
Q

What is the treatment of choice for young, low/medium operative risk patients with aortic stenosis?

A

surgical AVR

This approach is preferred due to lower risks and better outcomes in suitable candidates.

96
Q

What is transcatheter AVR (TAVR) used for?

A

patients with high operative risk

TAVR is a less invasive option for patients who may not tolerate traditional surgery well.

97
Q

In what situation is balloon valvuloplasty used in adults?

A

limited to patients with critical aortic stenosis who are not fit for valve replacement

This procedure is less common and typically reserved for high-risk individuals.

98
Q

What is a common characteristic of the ejection systolic murmur (ESM) in aortic stenosis?

A

classically radiates to the carotids

This radiation is a significant clinical finding during auscultation.

99
Q

What changes occur to the ejection systolic murmur during the Valsalva manoeuvre?

A

decreased

The Valsalva manoeuvre affects the hemodynamics, altering the sound of the murmur.