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Cardiology Flashcards

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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
Underlying pathology of ACS
Plaque rupture, thrombosis and inflammation - occlusion of coronary artery Can also get it due to emboli or coronary spasm in normal coronary arteries
26
Myocardial Infarction definition
Myocardial necrosis in the clinical setting of myocardial ischaemia
27
Difference between STEMI and NSTEMI
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
28
UK Incidence of ST elevation
60-70/100,000
29
Drug which increases risk of MI
Cocaine
30
3 things which raised levels increase risk of MI
Fibrinogen, Insulin, Homocysteine
31
2 types of trigger for MI and subtypes
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
Symptoms of MI x5
Chest pain >20mins, nausea, sweating, dyspnoea, palpitations
33
Silent infarct presentation of MI- when?
Elderly or diabetics
34
1) Signs of MI x5 2) If heart failure x3 3) If papillary muscle or ventricular septum dysfunction
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
Chest Xray in MI
Look for cardiomegaly, pulmonary oedema or diastinum (aortic rupture)
36
Creatinine Kinase in MI
x5 1-3 days post acute MI
37
CK-MB in MI
Isoenzyme of CK Elevated x4 Increases within 3-12hr of onset of pain Peak within 24 hour
38
Aspartate transaminase in MI
Elevated x3 | 1-3 days after
39
Lactate dehydrogenase in MI
Elevated x3 2-3days post Takes 10 days to decrease to baseline
40
Cardiac troponin in MI
x50 increase within 2-12 hour peak at 24-48 hr back to baseline 5-14 days
41
DDX of MI x6
``` Angina Pericarditis Myocarditis Aortic Dissection PE Oesophageal reflux/spasm ```
42
Management of STEMI | - 3 aims
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
Management of NSTEMI
Aspirin, clopidogrel, antithrombosis (fondaparinux), beta-blocker
44
Use of Coronary angiogram + PCI in MI
Urgent if ongoing pain or ECG changes despite optimal medical therapy, HF or haemodynamic instability Early
45
Post MI management
``` 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
Driving after PCI
Wait 1 week
47
Work after MI
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
Sex after MI
Best avoided for 1 month
49
Air travel after MI
Avoid for 2 months
50
Peak age incidence for Rheumatic Fever
5-15 years
51
Infective agent in rheumatic fever, presentation and in who
Pharyngeal infection with Lancefield group A β-haemolytic streptococci 2-4 weeks after infection rheumatic fever occurs In susceptible 2% of population
52
Pathology of rheumatic fever
Antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue (antigenic mimicry)
53
Diagnostic criteria for rheumatic fever
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
Evidence of group A β-haemolytic streptococci infection X4
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
Evidence of carditis in rheumatic fever x6
Tachycardia, Murmurs (regurgitation or Carey Coombs), Pericardial rub, CCF, Cardiomegaly, Conduction defects (45-70%) Apical systolic murmur may be the only sign
56
Arthritis in rheumatic fever
Migratory "flitting" polyarthritis, usually only affecting the larger joints
57
Subcutaneous nodules in RF
Small, mobile, painless nodules on extensor surfaces of joints and spine (2-20%)
58
Sydenham's chorea in RF
Occurs late in 10% - unilateral or bilateral | May be preceded by emotional lability and uncharacteristic behaviour
59
Erythema marginatum in RF
Geographical type rash with red, raised edges and clear centres - mainly on trunk, thighs and arms In 2-10%
60
Management of RF Including for carditis/arthritis and chorea
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
Prognosis in RF
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
Prophylaxis in RF
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
When are beta blockers used?
``` Angina Hypertension Disrhythmias Post MI Heart failure (with caution) ```
64
When are loop diuretics used?
Heart failure
65
When are thiazides diuretics used?
Hypertension
66
Which two cardiovascular drugs can't be combined
Verapamil and beta blockers | Risk of severe Bradycardia
67
When are calcium antagonists used?
Angina and hypertension Non-hydropyridines eg. Nifedipine and amlodipine - slow conduction at SA and AV node - therefore also used to treat dysrythmia
68
Digoxin effect and use
Slows pulse - AF
69
When does digoxin levels need to be altered or alter the level of something else?
If on amiodarone - half dose of digoxin | Cardio version when on digoxin - use less Energy
70
How do statins work?
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
What is Dressler's syndrome?
``` Post MI: 1-3 weeks Recurrent pericarditis Pleural effusions Fever Anaemia Raised ESR ``` Treated with NSAIDs and steroids of severe
72
When do you do CABG?
left main stem disease Mostly - triple vessel disease or abnormal LV function Or if PCI has failed

Cardiology (9 decks)

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