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ELM2 - integrated cases > case 9 - chest pain > Flashcards

case 9 - chest pain Flashcards

1
Q

Which blood vessels develop atherosclerotic plaques?

A

Elastic arteries, and large/medium muscular arteries

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2
Q

What is the pathophysiological process of the formation of atherosclerotic plaques?

A

1.) endothelial cell injury increases vascular permeability, platelet adhesion and leukocyte recruitment
2.) lipoproteins, particularly oxidised LDL, seep into arterial intima
3.) cytokines released, attracts monocytes which take up LDL forming foam cells.
4.) smooth muscle cells proliferate and deposit ECM, then become foam cells. T cells are recruited.

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3
Q

What are the key gross features of an atherosclerotic plaque?

A

Fibrous cap on media of artery, underlying lipid core/necrotic centre with lipids and inflammatory cells

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4
Q

Which type of lipoprotein is associated with the development of atherosclerotic plaques?

A

(oxidised) LDL

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5
Q

What is a myocardial infarction?

A

A cardiac event in which blood flow is obstructed to a region of myocardium, causing cell death.

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6
Q

What are the key stages in the development and progression of a myocardial infarction?

A

Atherosclerotic plaque development, plaque rupture/acute plaque change, coronary artery occlusion, ischaemia, infarction, inflammatory response, fibrosis

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7
Q

Why can acute plaque change cause an MI?

A

Exposure of the necrotic centre of plaque causes coagulation, forming a thombus that can occlude the vessel.

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8
Q

What is an infarction of the heart?

A

When ischemia of the myocardium causes permanent damage, causing necrosis of the issue and the release of troponins and inflammatory mediators into the blood stream.

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9
Q

What type of necrosis occurs at a myocardial infarct?

A

Coagulative necrosis

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10
Q

What process do MIs heal through?

A

Fibrosis - forms a collagenous, fibrous scar

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11
Q

What features of a patient history may suggest MI?

A

Smoking, hypercholesterolaemia, history of MI

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12
Q

What is the most significant symptom of MI?

A

Chest pain

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13
Q

How is MI chest pain often described?

A

Crushing pain, with radiation to the mandible and left arm

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14
Q

What are the symptoms associated with MI?

A

nausea, sweating, lightheadedness, tachycardia

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15
Q

What imaging techniques can be used to diagnose MI?

A

Coronary angiography, echocardiography

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16
Q

Which cardiac biomarkers indicate probable MI?

A

troponin (CTn1), creatine kinase-MB

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17
Q

What ECG changes are present in a STEMI?

A

Significant and persistent ST segment elevation or anterior ST segment depression

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18
Q

What ECG changes are present in a NSTEMI?

A

ST segment depression or T wave inversion

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19
Q

During exercise stress testing, what does ST segment depression indicate?

A

Reversible myocardial ischaemia

20
Q

What are the ECG changes visible during symptomatic episodes of stable angina?

A

ST depression

21
Q

What are the key differences between an episode of stable angina vs a myocardial infarction?

A

Myocardial infarction:
can come on at rest, lasts longer, not relieve by nitrate sprays, troponin.ck-mb positive, ST elevation

22
Q

What are the non-modifiable risk factors for CVD?

A

Genetic predisposition, family history, increased age, male gender, history of CVD

23
Q

What are the modifiable risk factors for CVD?

A

Smoking, hypertension, LDL cholesterol, sodium intake, Diabetes Mellitus type II, stress, alcoholism, physical inactivity, obesity, inflammation

24
Q

What are the ways that hypertension increases the risk of CVD?

A

damage to endothelium causes plaques to form, increased resistance to pumping causes ventricular hypertrophy, increased risk of plaque rupture and embolism/MI, high pressure stretches arterial walls causing aneurysms

25
Q

What is the immediate treatment for stable angina?

A

Vasodilator - usually glyceryl trinitrate sublingual spray for rapid symptoms relief

26
Q

What are the short term/complication reducing treatments for stable angina?

A

Antiplatelet agent, e.g. low dose aspirin.

27
Q

What are the long term management strategies for stable angina?

A

statin, antihypertensives, dietary changes, green prescription, exercise, smoking cessation.

28
Q

What are the ratios of fuel sources used for cardiac metabolism in adults in a normal state?

A

70% carbohydrates, 30% lipid

29
Q

What is fuel utilization in cardiac metabolism modulated by?

A

Substrate availability, hormones, oxygen availability, workload/exercise

30
Q

Which hormones modulate fuel utilization in cardiac metabolism?

A

Insulin, glucagon

31
Q

Which type of metabolism does the heart usually utilise?

A

Oxidative metabolism - citric acid cycle drives the electron transport chain

32
Q

What is the main substrate of cardiac metabolism in the fed state?

A

Carbohydrates

33
Q

What is the main substrate of cardiac metabolism in the fasting state?

A

Lipids/fatty acids

34
Q

How does cardiac metabolism change in the ischemic heart?

A

Oxidative metabolism drops due to poor O2 supply, the heart relys of glycolysis (an anaerobic process using glucose)

35
Q

What are some of the classes of medicines used to ease symptoms/prevent complications in the treatment of MI?

A

nitrates for vasodilation, opioids for pain, fibrinolytics to break down thrombi, antiemetic for nausea/vomiting, anticoagulants to prevent thrombus formation

36
Q

What medicines are used to prevent further complications in MI treatment?

A

Statins, dual antiplatelet therapy

37
Q

What is the key medicine used to alter disease progression following MI?

A

ACE inhibitors - an antihypertensive

38
Q

What is the role of fibrinolytics in MI treatment?

A

Administered after MI diagnosis, help to break down clots/thrombi

39
Q

What is the basic mechanism of action of fibrinolytics?

A

They facilitate the conversion of plasminogen to plasmin, which is an enzyme that helps to break down fibrin in clots.

40
Q

Which fibrinolytic is typically used for MI treatment?

A

Tenecteplase

41
Q

Which anticoagulant (LMWH) is typically used in MI treatment?

A

Enoxaparin

42
Q

What are the trends in IHD mortality in NZ from the 1940s to present?

A

From 1940s to 1960s there was an upward trend is IHD, then afterwards there was a decline in mortality. This trend was observed in males and females, though males have a higher rate of mortality.

43
Q

Which sex has a greater prevalence of IHD mortality?

A

Male

44
Q

What are some of the reasons for declining IHD mortality since the 1960s?

A

treatment advances, emergency infrastructure, preventative medications, tobacco control, diet/exercise awareness, primary care screening

45
Q

What is a green prescription?

A

A health intervention aimed at providing individuals/whanau with tools to improve their lifestyle and health.

ELM2 - integrated cases (9 decks)

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