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Cardiorespiratory > Ischaemic heart disease > Flashcards

Ischaemic heart disease Flashcards

1
Q

Which antibiotics interact with statins?

A

Macrolides e.g. clarithromycin or erythromycin.

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2
Q

What is the antiplatelet of choice in peripheral arterial disease or following an ischaemic stroke?

A

Clopidogrel

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3
Q

What is familial hypercholesterolaemia?

A

An autosomal dominant genetic condition causing very high cholesterol levels.

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4
Q

What are the 3 important features when making a clinical diagnosis of familial hypercholesterolaemia?

A

Family history of premature cardiovascular disease (e.g., myocardial infarction under 60 in a first-degree relative).
Very high cholesterol (e.g., above 7.5 mmol/L in an adult).
Tendon xanthomata (hard nodules in the tendons containing cholesterol, often on the back of the hand and Achilles).

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5
Q

What is the management of familial hypercholesterolaemia?

A

Specialist referral for genetic testing and statins.

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6
Q

What are the major side effects of GTN?

A

Headache and dizziness due to low blood pressure.

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7
Q

Why are non-dihydropyridine calcium channel blockers (e.g. verapamil or diltiazem) contraindicated with beta-blockers?

A

Due to the risk of atrioventricular block.

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8
Q

If both beta blockers and calcium channel blockers are contraindicated/not tolerated in the management of stable angina, what are the alternative options?

A

Long-acting nitrate (isosorbide mononitrate), nicorandil, ivabradine or ranolazine.

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9
Q

Describe the differentials for chest pain

A

Cardiac: angina, ACS, aortic dissection, pericarditis.
Respiratory: PE, pneumothorax, pneumonia.
GI: oesophagitis, oesophageal spasm, peptic ulcer disease.
Other: costochondritis, rib fracture, herpes zoster, depression/anxiety.

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10
Q

Stable vs. Unstable plaque

A

Stable plaque has less fat and inflammatory cells and more fibrous cells.
Unstable plaque has more fat and inflammatory cells and less fibrous cells —> more likely to rupture.

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11
Q

At what percentage stenosis of arteries does angina occur?

A

70% stenosis —> angina.

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12
Q

Does 100% occlusion of artery cause angina or MI?

A

Progressive angina. Rupture of plaque causes MI.

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13
Q

Define ischaemic penumbra

A

Tissue at risk of infarction where perfusion is inadequate to support function, but just adequate to maintain cell viability.

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14
Q

What is a +ve FHx for CVD?

A

First degree relative having MI/stoke < 60 years old.

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15
Q

Define atherosclerosis

A

Build up of atheromas in artery walls causing sclerosis (hardening/stiffening).

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16
Q

Describe the process of atherosclerosis

A
  1. Fatty streak formation from lipid deposits, due to endothelial injury.
  2. Migration of leukocytes and SM cells into vessel wall.
  3. Macrophages engulf lipids leading to foam cell formation.
  4. Fibrous cap formation (SM cell migration).
  5. Rupture of fibrous atheromatous plaque.
  6. Thrombus formation (platelet aggregation and fibrin mesh).
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17
Q

What are the 3 consequences of plaque formation?

A

Stiffening of artery walls —> hypertension.
Stenosis —> angina.
Rupture —> ischaemia —> MI.

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18
Q

List the risk factors for CVD

A

Non-modifiable: age, male, FHx.
Modifiable: raised cholesterol, smoking, alcohol, poor diet, lack of exercise, obesity, poor sleep, stress.
Co-morbidities: diabetes, hypertension, CKD, inflammatory conditions, atypical anti-psychotics.

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19
Q

What are the consequences of atherosclerosis?

A

Angina, MI, stroke/TIA, peripheral arterial disease, chronic mesenteric ischaemia.

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20
Q

Describe the primary prevention measures for CVD

A

Optimise modifiable risk factors - stop smoking, decrease alcohol, treat co-morbidities, healthy diet, excerise.
Statins.

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21
Q

Which patients should be offered statins for primary prevention of CVD?

A

QRISK3 score >10%, CKD (eGFR <60), T1D (for >10 years or are over 40).

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22
Q

What type and dose of statin should be offered to patients for primary prevention?

A

Atorvastatin 20mg

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23
Q

What is QRISK score?

A

Estimates the % risk that a patient will have a MI or stroke in next 10 years.

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24
Q

What is the MOA of statins?

A

Inhibit HMG CoA reductase, decreasing cholesterol production in the liver.

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25
Q

Why should you check LFTs 3 and 12 months after starting statins?

A

Because they can cause a transient mild rise in ALT and AST.

26
Q

What is the MOA of ezetimibe?

A

Inhibits cholesterol absorption in intestine.

27
Q

Describe the secondary prevention management principles for CVD

A

Optimise modifiable risk factors.
Anti-platelets (e.g. aspirin, clopidogrel, ticagrelor).
Atorvastatin 80mg.
Atenolol (or bisoprolol).
ACEi (ramipril).

28
Q

Define angina

A

Acute narrowing of coronary arteries by atherosclerosis causing reduced blood flow to myocardium. It occurs during times of high demand (e.g. exercise), when there’s insufficient blood supply to meet demand.

29
Q

What are the types of angina?

A

Stable angina: symptoms relieved by rest or GTN.
Unstable angina: symptoms occur at rest, considered part of ACS.

30
Q

Describe the classical clinical picture of stable angina

A

Central pressing/squeezing/constricting chest pain on exertion. Typically lasts around 10 mins and is relieved by rest or GTN within 5 mins.

31
Q

What is the gold standard investigation for angina?

A

CT coronary angiography.

32
Q

Name some other investigations for angina

A

Bloods: FBC, U&Es (prior to ACEi), LFTs (prior to statins), lipid profile, TFTs, HbA1c, fasting glucose.
ECG.
Stress Echo.
CXR (HF or lung disease).
Myocardial perfusion scan.

33
Q

What is the medical management for stable angina?

A

GTN spray (vasodilator).
Beta blocker (bisoprolol 5mg) or calcium channel blocker (amlodipine 5mg).
Secondary prevention: aspirin 75mg, atorvastatin 80mg, ACEi, beta blocker.

34
Q

What surgical options are there for stable angina?

A

Percutaneous coronary intervention (PCI) with coronary angioplasty.
Coronary artery bypass graft (CABG).

35
Q

Acute coronary syndrome (ACS) is an umbrella term for what?

A

STEMI, NSTEMI, unstable angina.

36
Q

How can you differentiate between STEMI, NSTEMI and unstable angina?

A

STEMI: ST elevation or new onset LBBB on ECG, raised troponins.
NSTEMI: no ST elevation on ECG, may be ST depression or T wave inversion, raised troponins.
Unstable angina: normal ECG and normal troponins.

37
Q

What are the 2 main branches of left coronary artery?

A

Left circumflex and left anterior descending.

38
Q

How does a MI occur?

A

Rupture of atherosclerotic plaque causing thrombus formation, leading to myocardial ischaemia and necrosis.

39
Q

Does complete occlusion of coronary arteries lead to a STEMI or NSTEMI?

A

STEMI - partial occlusion leads to NSTEMI/UA.

40
Q

Describe the clinical features of ACS

A

Central crushing/pressing chest pain, radiating to arm/neck/jaw, that continues at rest for >20 mins.
Maybe associated with N+V, sweating, SOB, palpitations.

41
Q

List the investigations for ACS

A

Troponins, ECG, CXR, echo, CT coronary angiogram.

42
Q

LAD artery supplies which heart area and is representative of which ECG leads?

A

Anteroseptal, leads V1-4.

43
Q

LCx artery supplies which heart area and is representative of which ECG leads?

A

Lateral, leads I, aVL, V5-6.

44
Q

Right coronary artery supplies which heart area and is representative of which ECG leads?

A

Inferior, leads II, III, aVF.

45
Q

What are troponins?

A

Cardiac enzymes that are used as a biomarker of myocardial necrosis.

46
Q

When should troponins be measured?

A

At baselines then 6-12 hours after onset of symptoms. A rise in troponins indicates MI.

47
Q

What is the immediate managements for suspected MI?

A

Morphine.
Oxygen in patients with sats <94% or <88% in type 2 respiratory failure.
Nitrates - sublingual GTN.
Aspirin loading dose 300mg.

48
Q

Describe the management of STEMI

A

Primary PCI if available within 2 hours of presentation.
Thrombolysis if PCI not available within 2 hours —> injecting fibrinolytic drugs e.g. streptokinase, alteplase.
Dual anti-platelet therapy continued for 12 months post-PCI —> aspirin + ticagrelor/clopidogrel.
Antithrombotic agents given during PCI —> unfractionated heparin/LMWH.

49
Q

Describe the management of NSTEMI

A

Beta blockers.
Aspirin loading dose 300mg, then 75mg,
Ticagrelor 180mg loading, then 90mg BD (clopidogrel if higher risk of bleeding).
Morphine.
Anticoagulant - fondaparinux (factor Xa inhibitor).
Nitrates - GTN.

50
Q

Describe the complications of MI

A

Death.
Rupture of heart septum or papillary muscles.
Oedema/HF.
Arrhythmias and aneurysm.
Dressler’s syndrome.

51
Q

What is Dressler’s syndrome?

A

Localised immune response to damaged myocardium/pericardium 2-3 weeks post-MI causing pericarditis.

52
Q

What can pericarditis lead to?

A

Pericardial effusion and pericardial tamponade.

53
Q

Other than atherosclerosis and thrombus formation, what other mechanisms can causes myocardial ischaemia?

A

Coronary artery spasm and spontaneous coronary artery dissection.

54
Q

A patient is admitted to the emergency department with new-onset chest pain that is radiating to their left arm. It came on shortly after performing a 5km run. The patient has a past history of angina. You perform an ECG and note the following:

ST depression in leads V1-V3
Tall R waves in leads V1-V3
Inverted T-wave in lead aVR
All other T-waves are normally oriented

What is the most likely diagnosis?

A

Posterior STEMI (posterior MI causes ST depression not elevation on a 12-lead ECG).

55
Q

When is a stress echo indicated?

A

For detecting cardiac wall motion abnormalities in patients with IHD.

56
Q

Patients with a GRACE score > 3% are indicated for what?

A

Coronary angiography within 72 hours of admission.

57
Q

What is a poor prognostic indicator in ACS?

A

Cardiogenic shock

58
Q

What is the most common cause of death following a MI?

A

VF

59
Q

Sudden heart failure, raised JVP, pulsus parodoxus and recent MI is suggestive of what complication?

A

Left ventricular free wall rupture causing cardiac tamponade.

60
Q

A patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination.

A

Ventricular septal defect

61
Q

Posterior MI ECG changes?

A

Tall, broad R waves, ST depression and tall upright T waves

Cardiorespiratory (15 decks)

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