Cardiology Flashcards

1
Q

Pathophysiology of atherogenesis

A

Damage to endothelial cells → endothelium secretes chemoattractants → leukocytes migrate and accumulate in intima → foam cells/macrophages/T-lymphocytes form fatty streaks → foam cells rupture, releasing lipids + SMC migrate from media to intima → dense, fibrous cap w necrotic core formed
This plaque can partially occlude the lumen → blood flood is restricted → ischemia
Plaque can rupture → thrombus formed →lumen is fully occluded → infarction

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2
Q

Which arteries are affected most by atherogenesis?

A

LAD
Circumflex
RCA

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3
Q

Risk factors for ischaemic heart disease

A

Age
Smoking
Obesity, high serum cholesterol
Diabetes
Hypertension
Family history
M>F

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4
Q

Prinzmetal’s angina features + associations

A

Coronary artery spasms occuring at rest or at night

Cocaine and alcohol use

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5
Q

Ischaemic heart disease investigations

A

1st: Routine bloods: FBC, TFTs
ECG
Best: CT coronary angiography

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6
Q

Acute management of unstable angina/NSTEMI

A

Beta-blocker
Morphine
Oxygen if < 94%
Aspirin
Nitrate

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7
Q

Management of acute STEMI

A

PCI if within 120 minutes

Otherwise, thrombolytics: alteplase, streptokinase

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8
Q

Long term management of ischaemic heart disease

A

Dual antiplatelet: aspirin + clopidogrel
Nitrate: GTN spray
Statin: simvastatin

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9
Q

Complications post-MI

A

0-24hr post-MI: ventricular arrhythmia, HF and cardiogenic shock

1-3 days: fibrinous pericarditis

3-14 days: free wall rupture, papillary muscle rupture and LV pseudoaneurysm

2 weeks to several months: Dressler syndrome, HF, arrhythmias, mural thrombus

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10
Q

Anteroseptal ECG leads

A

V1-V4

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11
Q

Inferior ECG leads

A

II, III, aVF

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12
Q

Anterolateral ECG leads

A

V4-6, I, aVL

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13
Q

Lateral ECG leads

A

I, aVL +/- V5-6

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14
Q

Posterior ECG leads

A

V1-V2
Tall R waves

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15
Q

Anteroseptal coronary artery

A

LAD

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16
Q

Inferior coronary artery

A

Right coronary

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17
Q

Anterolateral coronary artery

A

LAD / left circumflex

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18
Q

Lateral coronary artery

A

Left circumflex

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19
Q

Posterior coronary artery

A

Left circumflex / right coronary

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20
Q

Pathophysiology of heart failure

A

Heart begins to fail, compensation occurs to maintain CO and perfusion:

[sympathetic system activation] BP falls → detected by baroreceptors → sympathetic activation → positively inotropic/chronotropic → CO increases
RAAS system

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21
Q

5 causes of heart failure

A

Ischaemic heart disease
Cardiomyopathy
Valvular heart disease (AS/MR)
Hypertension
Alcohol excess
Cor pulmonale
Anaemia, arrhythmias, hyperthyroidism

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22
Q

Types of heart failure

A

Systolic HF: inability of ventricle to contract properly

Diastolic HF: inability of ventricle to relax and fill

HF reserved ejection fraction
- systolic, EF <40%
HF preserved ejection fraction
- diastolic, EF > 40%

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23
Q

Clinical manifestations of heart failure

A

SOB
Orthopnoea
Fatigue
Ankle swelling
Pulmonary oedema
Cold peripheries

Raised JVP
End respiratory crackles

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24
Q

Heart failure CXR findings

A

Alveolar oedema
B-lines (Kerley)
Cardiomegaly
Dilated upper lobe vessels
Effusion (pleural)

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25
Investigations for heart failure
Bloods: brain natriuretic peptide (best) ECG CXR Echo (best imaging)
26
Medical management for heart failure
1st line: ACE-I + B-blocker 2nd line: ARB instead of ACEi 3rd line: Nitrate or hydralazine 4th line: Digoxin Diuretics: Furosemide (symptom relief)
27
Stage 1 hypertension values
BOTH >140/90 mmHg and ABPM >135/85
28
Stage 2 hypertension values
>160/100 or ABPM 150/95
29
Malignant hypertension values
>180/110
30
Blood pressure target < 80
< 140/90
31
Blood pressure target > 80
< 150/90
32
Management of stage 1 hypertension
QRISK to decide treatment
33
Indications for same-day admission with hypertension
Malignant hypertension + Signs of papiloedema / signs of retinal haemorrhage or Life-threatening symptoms or Suspected pheochromocytoma
34
Contraindications to use of ACE inhibitors
Pregnancy General anaesthesia
35
Anti-hypertensives stepwise management
1st: ACEi / ARB Or CCB if Afro-Caribbean / > 55 years (unless diabetic) 2nd: ACEi / ARB + CCB + thiaizide Give CCB before diuretic, unless evidence of oedema 3rd: ACEi / ARB + CCB + thiazide Resistant hypertension 4th: + spironolactone / high dose thiazide-like diuretic / alpha blocker / beta blocker
36
Causes of pericarditis
Infectious: Viral (common) - Coxsackievirus Bacterial - Mycobacterium - Tuberculosis Non-infectious Trauma (common) Uraemia, MI
37
Pericarditis clinical manifestations
Chest pain - Relieved by sittin forward - Worsened by inspiration / lying down Fever SOB Pericardial friction rub
38
Pericarditis investigations + findings
ECG: - Saddle shaped ST elevation - PR depression Diagnostic: - Echocardiogram
39
Pericarditis management + complications
NSAIDs + colchicine Cardiac tamponade
40
Cardiac tamponade symptoms
Beck's triad: Hypotension Elevated JVP Quiet heart sounds Pulsus paradoxus
41
Mechanism of cardiac tamponade reducing cardiac output
Accumulation of fluid in the pericardial space → compression of the heart chambers → decrease in venous return → decrease in filling in the heart → reducing cardiac output
42
Cardiac tamponade investigations
Gold: Echocardiogram
43
Cardiac tamponade management
Pericardiocentesis
44
Likely causative of infective endocarditis of prosthetic valve
Staph epidermis
45
Likely causative of infective endocarditis after dental procedure
Strep viridans
46
Likely causative of infective endocarditis associated with IVDU
Staph aureus
47
Infective endocarditis clinical manifestations
Fever Roth spots Osler nodes Murmur Janeway lesions Anaemia Nail-bed haemorrhage (splinter haemorrhages)
48
Difference between osler nodes and janeway lesions
Osler nodes are painful
49
Critieria for infective endocarditis
Duke's critieria: Major criteria: blood culture +ve, evidence of endocarditis on echo Minor criteria: predisposing factors, fever, vascular phenomenon, immune phenomenon, equivocal blood cultures 2 major / 1 major + 3 minor / 5 minor
50
Diagnostic investigation for infective endocarditis
Echocardiogram
51
Infective endocarditis antibiotic management
Staph: Flucloxacillin + gentamicin MRSA: vancomycin + rifampicin + gentamicin Strep: BenPen + gentamicin Not sure which organism (first line): FAG (flucloxacillin + ampilicin + gentamicin)
52
Aortic regurgitation murmur
Early diastolic descrendo
53
Aortic stenosis murmur
Ejection systolic Crescendo/decrescendo
54
Mitral stenosis murmur
Rumbling mid-diastolic Decrescendo-crescendo
55
Mitral regurgitation murmur
Holo/pan systolic radiating to left axilla
56
Miteral stenosis signs
Malar flush A fib Loud S1
57
Mitral regurgitation signs
A fib Displaced, thrusting apex Soft/absent S1
58
Aortic stenosis signs
Slow rising pulse Soft S2 Narrow pulse pressure
59
Aortic regurgitation signs
Wide pulse pressure Displaced apex Corrigan's sign: carotid pulsation De Musset's sign: head nodding with heartbeat Quincke's: capillary pulsation in nail bed
60
NYHA classification of heart failure
I - no limitation in physical activity II - slight limitation of physical activity, comfort at rest III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary). IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest
61
Management of atrial fibrillation
Rate control (rhythm control also possible) 1: B blocker 2: CCB 3: Digoxin Anticoagulation: 1: Warfarin 2: DOACs
62
Causes of atrial fibrillation
Sepsis Mitral Valve Pathology (stenosis or regurgitation) Ischemic Heart Disease Thyrotoxicosis Hypertension (Smith AF)
63
When can rhythm control be offered to people with atrial fibrillation?
Reversible cause for their AF New onset (<48 hours) AF is causing heart failure Remain symptomatic despite being effectively rate controlled
64
Rhythm control options for atrial fibrillation
Cardioversion: Pharmacological- 1: Flecanide 2: Amiodarone Electrical- Difibrillator Long term rhythm control 1: Beta blockers 2: Dronedarone 3: Amiodarone