Secondary Care Cardiology Flashcards

1
Q

How should unstable angina, NSTEMI and STEMI be treated and when?

A
  1. Unstable angina → Anti-anginal’s and primary prevention
  2. NSTEMI → Medical management or percutaneous coronary intervention
  3. STEMI → PCI
  4. Complex 2VD → ? Coronary Artery Bypass Graft (CABG)
  5. 3VD → CABG
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2
Q

What does the acronym MONA stand for in acute management?

A

M - Morphine
O - Oxygen
N - Nitrates
A - Antiemetics & Antiplatelets

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3
Q

What is given to target Sats in acute management?

A

Oxygen

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4
Q

What is the IV dosage range for Morphine in acute management?

A

0-10mg

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5
Q

What type of Nitrates are given in acute management?

A

IV GTN

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6
Q

What antiemetic is given in acute management?

A

IV Metoclopramide

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7
Q

Besides Aspirin, name other antiplatelets that can be administered in acute management?

A

Clopidogrel
Ticagrelor
Prasugrel

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8
Q

What is the structure of a Cardiovascular Examination?

A

End of the bed
Hands and nails
Arms
Face, eyes and mouth
Neck
Chest
Inspect
Palpate
Percussion
Auscultation

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9
Q

What factors should be considered when looking at a patient at the end of the bed?

A

Age
Cyanosis
Breathing
Pallor
Complexion
Positioning (Respiratory cross over)

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10
Q

What is one sign to look for regarding clubbing of nails?

A

Schamroth’s Window

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11
Q

What pulses should be examined on the arms and feet, and what characteristics should be noted?

A

Pulses: Radial, Brachial, Femoral, Feet pulses (Dorsalis Pedis and Posterior Tibial)
Characteristics: Rate, Rhythm, Character and volume

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12
Q

What signs should be checked for in the face and eyes?

A

Conjunctival pallor
Corneal arcus
Xanthelasma
Central Cyanosis
Angular Stomatitis
Dentition

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13
Q

How should the JVP response be assessed in the neck?

A

Palpate for liver border
Ask patient to inhale
As they do, compress the liver with side of hand
Look for JVP response

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14
Q

What should be auscultated for in the carotid arteries in the neck?

A

Bruits

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15
Q

What aspects should be inspected on the chest during a cardiovascular examination?

A

Scars
Deformities
Chest wall trauma
Symmetry
Visible pulsations
Anterior and Posterior

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16
Q

What should be palpated for on the chest during a cardiovascular examination?

A

Heaves
Thrills (Palpable murmur)
Tactile Fremitis
Apex Beat
Chest Expansions
Anterior and Posterior

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17
Q

What type of murmur is heard in Aortic Stenosis? What type of murmur is heard in Mitral stenosis? What type of murmur is heard in Aortic regurgitation? What type of murmur is heard in Mitral regurgitation?

A

Pansystolic murmur
Mid diastolic murmur
Late diastolic murmur
Systolic murmur

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18
Q

What breath sounds should be auscultated for during a chest examination?

A

Vesicular (Normal)
Reduced
Silent
Wheeze
Stridor
Crackles: Fine, Course

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19
Q

What are the aims of treatment in secondary prevention?

A

Reduce mortality
Restore blood flow
Prevent further occlusions
Determine and work to maintain LV function
Manage remaining angina symptoms

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20
Q

What are the 5 key therapies for Secondary Prevention Treatment?

A

Dual antiplatelets
Statins
ACE inhibitors
Beta-blockers
GTN

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21
Q

What is reduced and inhibited by dual anti-platelet therapy? What is protected by dual anti-platelet therapy?

A

Platelet aggregation
Stent

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22
Q

What is the lifelong dose of Aspirin?

A

75mg OD

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23
Q

What should Prasugrel be used for as 1st line if a patient had? What is the dose of Prasugrel OD if a patient is ≥75yrs?

A

PCI
5mg OD

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24
Q

What should Ticagrelor be used for as 1st line if a patient did not have? What is the dose of Ticagrelor for 12 months? What is the dose of Ticagrelor as a continuation therapy?

A

PCI
90mg BD
60mg BD

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25
Q

What can Clopidogrel be used for as 2nd line?

A

High bleeding risk and cannot tolerate ticagrelor

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26
Q

When can prasugrel be used?

A

CYP interactions

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27
Q

What does Aspirin inhibit and what is reduced? What is the STAT loading dose of Aspirin?

A

COX-1, platelet aggregation
300mg

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28
Q

What is reduced by 30% in those with acute MI by aspirin? What are contraindications for Aspirin?

A

Vascular events
Local bleeding, active PUD, haemorrhage

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29
Q

What does Ticagrelor block? What type of disease does Ticagrelor inhibit thrombus formation in?

A

ADP-mediated platelet aggregation
Atherosclerotic disease

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30
Q

What is the STAT loading dose of Ticagrelor? What is the maintenance dose of Ticagrelor? What did PLATO and RESPOND trials show in Ticagrelor use?

A

180mg
90mg BD
Reduced relative risk of MI and death from vascular causes

31
Q

What are contraindications for Ticagrelor?

A

Active bleeding, strong CYP3A4 inhibitors, Hx of intracranial haemorrhage, strong CYP3A4 inducers

32
Q

Name strong CYP3A4 inhibitors that are a contraindication for Ticagrelor

A

Simvastatin
Clarithromycin

33
Q

Name strong CYP3A4 inducers that are a contraindication for Ticagrelor

A

Phenytoin
Rifampicin

34
Q

What are S/Es of Ticagrelor?

A

Dyspnoea
GI bleed
Bradycardia

35
Q

What should be considered when prescribing Ticagrelor?

A

Increased risk of bradycardic events

36
Q

What is Clopidogrel? What does Clopidogrel inhibit? What is the STAT loading dose of Clopidogrel? What is the maintenance dose of Clopidogrel?

A

ADP receptor antagonist
Platelet aggregation
300mg
75mg

37
Q

What is reduced by Aspirin +/- clopidogrel in high-risk patients with NSTEMI?

A

End-point of CV death, stroke or MI

38
Q

What should be considered when prescribing Clopidogrel?

A

Peripheral vascular disease or history of stroke

39
Q

What does statins reduce? What benefits do statins provide in the acute period?

A

LDL-cholesterol and triglycerides
Anti-inflammatory benefits

40
Q

What are S/Es of statins?

A

Headache, nausea, abdominal cramps, muscle aches and pains

41
Q

Name lipophilic statins
Name hydrophilic statins

A

Atorvastatin, simvastatin, fluvastatin
Rosuvastatin, pravastatin

42
Q

What is less likely to be caused by a more hydrophilic statin?

A

Myopathy and myalgia

43
Q

Name a statins with a short half-life

A

Simvastatin, pravastatin, fluvastatin

44
Q

What is the target level for non-HDL (n-HDL)? What is the target level for LDL cholesterol?

A

<2.6mmol/L
<2.0mmol/L

45
Q

When should Liver Function Tests (LFTs) be monitored during lipid-lowering treatment?

A

Before, 3 months, and 12 months

46
Q

When should lipid-lowering treatment be stopped based on transaminase levels?

A

If transaminases are >3x upper limit

47
Q

When should Creatine Kinase (CK) be monitored during lipid-lowering treatment? When should lipid-lowering treatment be stopped based on CK levels?


A

Only if muscle symptoms are present
If CK is >5x upper limit of normal

48
Q

How often should cholesterol be measured after a dose change, and then after that?

A

Within 1-3 months of change, then annually

49
Q

For which condition are fibrates useful?

A

High triglycerides

50
Q

What does ezetimibe inhibit? How can ezetimibe be used in conjunction with statins?

A

Dietary absorption
Added to statin therapy

51
Q

What cardiac process do ACE inhibitors prevent post-MI? What process does Angiotensin II contribute to that leads to heart failure?

A

Cardiac remodelling
Ventricular remodelling

52
Q

What mechanical effect do ACE inhibitors have on the left ventricle? What impact do ACE inhibitors have on mortality?

A

Decreases wall stress
Decreases

53
Q

What cardiovascular events are decreased by ACE inhibitors? What is the condition of the patient when starting ACE inhibitors in secondary care?

A

Death, MI, and stroke
Haemodynamically stable

54
Q

Who completes ACE inhibitor titration? Over what time frame is ACE inhibitor titration completed?

A

GP
4-6 weeks

55
Q

What is the initial dose of Ramipril? What is the maximum daily dose of Ramipril?

A

1.25mg – 2.5mg BD
10mg

56
Q

What medication is given if ACE inhibitors are not tolerated?

57
Q

What is the starting dose of Losartan?

A

25-50mg daily

58
Q

How do beta-blockers reduce myocardial ischaemia?

A

Lowering HR and BP by reducing myocardial O2 consumption

59
Q

What did the MIAMI and ISIS-1 trials demonstrate about beta blockers?

A

Reduced risk of re-infarction and arrhythmias

60
Q

Through which mechanism do beta blockers have a slight reduction in mortality? Which cardio-selective beta blocker is recommended?

A

Reduction of negative effects of catecholamines
Bisoprolol or atenolol

61
Q

Name S/Es of beta-blockers

A

Breathlessness, sleep disturbance, cold extremities, fatigue

62
Q

What patient condition is required for starting beta-blockers in secondary care?

A

Haemodynamically stable

63
Q

How long should beta-blockers be continued post-MI in patients without LVSD or heart failure? In what patients should beta-blockers be continued indefinitely?

A

At least 12 months
LVSD

64
Q

What cardiovascular outcomes are reduced by beta-blockers?

A

Overall, coronary mortality and sudden cardiac death

65
Q

What reperfusion therapy is preferred in STEMI management?

A

Urgent PCI

66
Q

What are Glycoprotein IIb/IIIa inhibitors used for in STEMI patients intended for PCI?

A

Reduction of major cardiovascular events

67
Q

What should patients who don’t receive PCI be treated with? What route is the first dose given, followed by which route?

A

Fondaparinux
IV then SC

68
Q

What condition is Eplerenone licensed for use in following an MI?

A

Left ventricular dysfunction and heart failure

69
Q

What medication should patients with AF post-MI receive?

A

Anticoagulant

70
Q

What is the triple therapy for patients with AF post MI? Why should ticagrelor not be used in triple therapy?

A

Anticoagulant, aspirin, and clopidogrel
Bleed risk

71
Q

How does heparin reduce the risk of thrombus formation during PCI?

A

By inhibiting the coagulation cascade

72
Q

What is fondaparinux? What is the dose of fondaparinux pre PCI? What is the dose of fondaparinux post PCI? How long is it continued post-PCI?

A

Synthetic pentasaccharide
2.5mg OD
2.5mg OD
Until pain free >24 hours, up to 8 days

73
Q

What LMWH is used post-PCI?

A

Standard trust approved LMWH