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Cardiology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Aspirin MOA

A

Anti-COX - irreversibly acetylates it. Prevents production of thromboxane A2 - therefore inhibits platelet aggregation.

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2
Q

Aspirin Uses x3

A

Secondary prevention following MI and TIA/Stroke. Also for patients with angina or peripheral vascular disease.

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3
Q

Clopidogrel and prasugrel MOA - and 1x benefit

A

ADP (adenosine diphosphate) receptor antagonists - therefore also block platelet aggregation. May cause less gastric irritation

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4
Q

When clopidogrel and prasugrel used? x3

A

If aspirin intolerant, after coronary stent insertion with aspirin, ACS.

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5
Q

Tirofiban MOA and use

A

Glycoprotein IIb/IIIa antagonist - anti-platelet - unstable angina and MI - prevention of cardiovascular events

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6
Q

Warfarin MOA

A

Inhibits vitamin-k dependant synthesis of clotting factors, factor II, VII, IX and X

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7
Q

Warfarin uses x2 and complication

A

AF and mechanical valves. Needs monitoring of values

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8
Q

Apixaban MOA and Dabigatran MOA. Benefits

A

Factor Xa inhibitor and Direct thrombin inhibitor. Novel anticoagulant therapy. Don’t require therapeutic monitoring, may have a better risk:benefit ratio

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9
Q

LWH MOA and use

A

Bind to antithrombin which accelerates its inhibition of activated factor X (factor Xa) - used in ACS

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10
Q

Fondaparinux MOA and use

A

Factor Xa inhibitor - used in ACS

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11
Q

Bivalirudin MOA and use

A

Thrombin inhibitor - ACS

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12
Q

Features of angina - pathology, presentation, exacerbation and relieving factors, radiation.

A

Due to myocardial ischaemia, central tightness or heaviness, brought on by exertion and relieved by rest, radiates to arms, neck, jaw.

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13
Q

Precipitants of angina x3

A

Cold weather, emotion, heavy meals

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14
Q

Associated symptoms of angina x4

A

Dyspnoea, sweating, nausea, faintness

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15
Q

Causes of angina x6

A

Atheroma, anaemia, aortic stenosis, tachyarrhythmias, HCM, arteritis/small vessel disease

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16
Q

Types of angina x4

A

Stable (worse on exertion, better on rest),

Unstable (gradually increasing, occurs on minimal exertion or rest, greater risk of MI)

Decubitus angina (precipitated by lying flat - usually combination of CAD and heart failure)

Variant (Prinzmetal’s) angina - caused by coronary artery spasm - may coexist with fixed stenoses

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17
Q

Features of variant angina - cause, presentation, ECG, typical patient

A

Coronary artery spasm and can be in healthy coronary arteries,

Pain usually at rest rather than during activity

ECG during pain = ST elevation, resolves when pain subsides

Patients do not usually have atherosclerosis risk factors

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18
Q

Treatment of variant angina

A

Calcium channel blockers

Aspirin and B-blockers can exacerbate

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19
Q

Tests in angina x 4

A

ECG, Angiography, Functional imaging, Stress echo

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20
Q

Conservative management of angina x4

A

Stop smoking, encourage exercise and weight loss, control HTN and diabetes, decrease cholesterol with statin

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21
Q

Drugs for angina - 1st lines x 3
If b-blocker contraindicated
Extra if not controlled
One final one

A

Aspirin
B-blockers (eg. atenolol) unless contraindicated)
Nitrates

Long-acting calcium antagonists (eg. amlodipine, diltiazem)

K+ channel activator (eg. nicorandil)

Ivabradine - inhibits funny current in SA node - reduces heart rate

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22
Q

Nitrates use in angina

A

Symptoms - GTN spray or sublingual spray

Prophylaxis
Isosorbide mononitrate - need 8hour free period to avoid tolerance
Or slow release/adhesive nitrate patches, buccal pills

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23
Q

Surgical treatment of angina

Indications x4

A

Percutaneous Transluminal Coronary Angioplasty

Balloon dilatation of stenotic vessels - >70% with stent insertion

Poor response/intolerance to medical therapy, refractory not suitable for CABG, previous CABP, post-thrombolysis in patients with severe angina

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24
Q

What does ACS include? x3

A

Unstable angina, silent ischaemia, evolving MI

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25
Q

Underlying pathology of ACS

A

Plaque rupture, thrombosis and inflammation - occlusion of coronary artery

Can also get it due to emboli or coronary spasm in normal coronary arteries

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26
Q

Myocardial Infarction definition

A

Myocardial necrosis in the clinical setting of myocardial ischaemia

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27
Q

Difference between STEMI and NSTEMI

A

STEMI = full thickness damage of heart muscle due to complete occlusion of major coronary artery

NSTEMI = partial thickness damage due to occlusion of minor coronary artery or partial occlusion of a major coronary artery

Symptoms the same but ECG different

Cardiac markers usually more mild in NSTEMI

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28
Q

UK Incidence of ST elevation

A

60-70/100,000

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29
Q

Drug which increases risk of MI

A

Cocaine

30
Q

3 things which raised levels increase risk of MI

A

Fibrinogen, Insulin, Homocysteine

31
Q

2 types of trigger for MI and subtypes

A

1) Sudden shortage of myocardial oxygen supply
- Acute thrombosis on background of atherosclerosis (vigorous exercise, overeating, hot/cold - Virchow’s)
- Cardiac - unrelated to atherosclerosis (thrombo-embolism, coronary artery dissection, arteritis)
- Reduced oxygen supply (anaemia, hypoxaemia)
2) Sudden excess myocardial oxygen consumption

  • Fever
  • Thyrotoxicosis
  • Hyperadrenergic state
  • Increase LV afterload (HTN, AS)
32
Q

Symptoms of MI x5

A

Chest pain >20mins, nausea, sweating, dyspnoea, palpitations

33
Q

Silent infarct presentation of MI- when?

A

Elderly or diabetics

34
Q

1) Signs of MI x5
2) If heart failure x3
3) If papillary muscle or ventricular septum dysfunction

A

1) Distress and anxiety, pallor and sweating, tachycardia, hypotension or hypertension, 4th heart sound
2) If HF - raised JVP, 3rd heart sound, basal creps
3) Pan-systolic murmur

35
Q

Chest Xray in MI

A

Look for cardiomegaly, pulmonary oedema or diastinum (aortic rupture)

36
Q

Creatinine Kinase in MI

A

x5 1-3 days post acute MI

37
Q

CK-MB in MI

A

Isoenzyme of CK
Elevated x4
Increases within 3-12hr of onset of pain
Peak within 24 hour

38
Q

Aspartate transaminase in MI

A

Elevated x3

1-3 days after

39
Q

Lactate dehydrogenase in MI

A

Elevated x3
2-3days post
Takes 10 days to decrease to baseline

40
Q

Cardiac troponin in MI

A

x50 increase
within 2-12 hour
peak at 24-48 hr
back to baseline 5-14 days

41
Q

DDX of MI x6

A 
Angina
Pericarditis
Myocarditis
Aortic Dissection
PE
Oesophageal reflux/spasm
42
Q

Management of STEMI

- 3 aims

A

1) Restore vessel patency & reperfusion
- Primary angioplasty
- Thrombolysis/fibrinolysis

2) Reverse/prevent thrombosis
- Heparin
- GPIIb/IIa antagonists
- Clopidogrel (2-4hr onset) and prasugrel (30min onset of effect)

3) Reduce myocardial oxygen demand
- Beta-blocker
- Nitrates
- ACE-i eg. lisinopril

43
Q

Management of NSTEMI

A

Aspirin, clopidogrel, antithrombosis (fondaparinux), beta-blocker

44
Q

Use of Coronary angiogram + PCI in MI

A

Urgent if ongoing pain or ECG changes despite optimal medical therapy, HF or haemodynamic instability

Early

45
Q

Post MI management

A 
Aspirin, Clopidogrel/ticagrelor/prasugrel for 1 year 
B-blocker lifelong 
ACE-i lifelong 
Statins lifelong (even if not raised cholesterol)
Aldosterone lifelong if LVEF
46
Q

Driving after PCI

A

Wait 1 week

47
Q

Work after MI

A

May return after 2 months - unless danger occupation aka pilot, diver, airtraffic control

Heavy goods vehicles and public service drivers - return if fit criteria

48
Q

Sex after MI

A

Best avoided for 1 month

49
Q

Air travel after MI

A

Avoid for 2 months

50
Q

Peak age incidence for Rheumatic Fever

A

5-15 years

51
Q

Infective agent in rheumatic fever, presentation and in who

A

Pharyngeal infection with Lancefield group A β-haemolytic streptococci
2-4 weeks after infection rheumatic fever occurs
In susceptible 2% of population

52
Q

Pathology of rheumatic fever

A

Antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue (antigenic mimicry)

53
Q

Diagnostic criteria for rheumatic fever

A

1) Evidence of group A β-haemolytic streptococci infection

2) 2 major criteria
- carditis
- arthritis
- subcutaneous nodules
- sydenham’s chorea
- erythema marginatum

3) 1 major and 2 minor criteria
- Fever
- Raised ESR
- Arthralgia (not if arthritis is the major)
- Prolonged PR interval (not if carditis is the major)
- Previous rheumatic fever

54
Q

Evidence of group A β-haemolytic streptococci infection X4

A

1) Positive throat swab (usually -ve by time you get fever)
2) Rapid streptococcal antigen test +ve
3) Elevated or rising streptococcal antibody titre
4) Recent scarlet fever

55
Q

Evidence of carditis in rheumatic fever x6

A

Tachycardia, Murmurs (regurgitation or Carey Coombs), Pericardial rub, CCF, Cardiomegaly, Conduction defects (45-70%)

Apical systolic murmur may be the only sign

56
Q

Arthritis in rheumatic fever

A

Migratory “flitting” polyarthritis, usually only affecting the larger joints

57
Q

Subcutaneous nodules in RF

A

Small, mobile, painless nodules on extensor surfaces of joints and spine (2-20%)

58
Q

Sydenham’s chorea in RF

A

Occurs late in 10% - unilateral or bilateral

May be preceded by emotional lability and uncharacteristic behaviour

59
Q

Erythema marginatum in RF

A

Geographical type rash with red, raised edges and clear centres - mainly on trunk, thighs and arms
In 2-10%

60
Q

Management of RF

Including for carditis/arthritis and chorea

A

Bed rest until CRP normal for 2 weeks (might take 3 months)

Benzylpenicillin or erythromycin or azithromycin if allergic - for 10 days

Analgesia for carditis/arthritis - aspirin (immobilize joints in severe arthritis)

Haloperidol or diazepam for chorea

61
Q

Prognosis in RF

A

60% with carditis develop chronic rheumatic heart disease

Recurrence can occur with more infection, pregnancy and use of pill

Cardiac sequelae affects: mitral (70%), aortic (40%), tricuspid (10%) and pulmonary (2%) valves

62
Q

Prophylaxis in RF

A

Penicillin or sulfadiazine/erythromycin

If carditis + persistent valvular disease - at least until age 40 - maybe lifelong

If carditis but no valvular disease - continue for 10 years

No carditis - 5 years prophylaxis (until age of 21) is sufficient

63
Q

When are beta blockers used?

A 
Angina 
Hypertension
Disrhythmias 
Post MI 
Heart failure (with caution)
64
Q

When are loop diuretics used?

A

Heart failure

65
Q

When are thiazides diuretics used?

A

Hypertension

66
Q

Which two cardiovascular drugs can’t be combined

A

Verapamil and beta blockers

Risk of severe Bradycardia

67
Q

When are calcium antagonists used?

A

Angina and hypertension
Non-hydropyridines eg. Nifedipine and amlodipine - slow conduction at SA and AV node - therefore also used to treat dysrythmia

68
Q

Digoxin effect and use

A

Slows pulse - AF

69
Q

When does digoxin levels need to be altered or alter the level of something else?

A

If on amiodarone - half dose of digoxin

Cardio version when on digoxin - use less Energy

70
Q

How do statins work?

A

Inhibit HMG-COA reductase
Therefore inhibits de novo synthesis of cholesterol in the liver
This increases LDL receptor expression by hepatocytes leading to decreased circulating LDL cholesterol
Best given at night

71
Q

What is Dressler’s syndrome?

A 
Post MI: 1-3 weeks 
Recurrent pericarditis 
Pleural effusions 
Fever
Anaemia
Raised ESR

Treated with NSAIDs and steroids of severe

72
Q

When do you do CABG?

A

left main stem disease
Mostly - triple vessel disease or abnormal LV function

Or if PCI has failed

Cardiology (9 decks)

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