Session 10 Flashcards

0
Q

Describe the risk factors for coronary atheroma

A

Modifiable - hyperlipidaemia, smoking, hypertension, diabetes mellitus, exercise, obesity, stress
Non-modifiable - age (increasing), gender (male), family history

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1
Q

Identify the common causes of chest pain

A

Lungs and pleura - pneumonia, pulmonary embolism, pneumothorax
GI system - oesophagus (reflux), peptic ulcer disease, gall bladder (biliary colic, cholecystitis)
Chest wall - ribs (fractures, bone metastasis), muscles, skin
CVS heart and great vessels - myocardium (angina, MI), pericardium (pericarditis), aorta (aortic dissection)

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2
Q

What is ischaemic chest pain?

A

Any IHD can cause chest pain that is central, retrosternal or left sided.
The pain may also radiate to the shoulders and arms (left side more common) along with neck, jaw epigastrium and back.
The pain is described as tightening, heavy, crushing, constricting and pressure.

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4
Q

Describe the investigation of a patient with angina, including the principles of the exercise test

A

Clinical diagnosis is based on history. Patient may show signs related to risk factors (elevated bp, corneal arcus), evidence of atheroma elsewhere (peripheral vascular disease).
ECG - usually normal, may show signs of previous MI (pathological Q wave)
Exercise stress test - graded exercise connected to an ECG until target heart rate reached/chest pain/ECG changes/other problems. Test is positive if ECG shows ST depression > 1 mm.
A strong positive test indicates critical stenosis.

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5
Q

Describe the principles of the management of angina, including the use of some drugs in its treatment, acute myocardial infarction and unstable angina

A

Angina:
Sublingual nitrate spray/tablet (acute episodes)
B-blockers, Ca2+ channel blockers, oral nitrates (prevent episodes)
Aspirin, statins, ACE inhibitors (prevent cardiac events)
Revascularisation (long term)
Unstable angina/Acute MI:
Anti platelet agents (aspirin), anticoagulants (heparin)
Angioplasty
Coronary artery bypass graft
Pain control, oxygen, organic nitrates, B-blockers, statins, ACE inhibitors

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6
Q

Describe the pathophysiology of angina, unstable angina and myocardial infarction, and relate it to the clinical features and treatment of these conditions

A

Angina (stable):
Atheromatous plaques with a necrotic centre and fibrous cap build up in the coronary vessels, occluding more and more lumen –> ischaemia. Angina occurs when the plaque occludes more than 70% of the lumen.
Angina (unstable):
Angina worsens due to the progression of the formation of the atheromatous plaque. Increased occlusion.
Treatment - sublingual nitrate spray/tablet (acute), B-blockers, Ca2+ channel blockers, oral nitrates (prevent episodes), aspirin, statins, ACE inhibitors (prevent cardiac events), revascularisation (long term).
Myocardial infarction:
Complete occlusion of a coronary vessel, leading to an infarct of the myocardium it supplies. The fibrous cap undergoes erosion or fissuring, exposing blood to the thrombogenic material in the necrotic core. The platelet clot is followed by a fibrin thrombus which occludes the vessel or forms an embolism.

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7
Q

Understand the concept of ‘Acute Coronary Syndrome’ and explain the difference between NSTEMI and STEMI

A

Acute coronary syndrome (ACS) relates to a group of symptoms attributed to the obstruction of the coronary arteries. ACS is a result of unstable angina, NSTEMI, STEMI.
NSTEMI - non ST elevated myocardial infarction, infarct is not full thickness of myocardium
STEMI - ST elevated myocardial infarction, infarct is full thickness of myocardium
Unstable angina - partial occlusion by thrombus, no myocardial necrosis, may have ST depression, T wave inversion or normal
NSTEMI - partial occlusion by thrombus, some myocardial necrosis, no ST elevation, troponin (marker in blood)
STEMI - total occlusion by thrombus, large myocardial infarct, ST elevation, troponin (marker in blood)

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8
Q

Describe the use of an ECG in identifying the region of the heart affected from the particular groups of leads which show changes

A

Abnormalities will be seen due to the infarcted, dead myocardium. Look at which lead the abnormality is inns where that lead’s view is.

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9
Q

Understand the use of surgical treatments in coronary artery disease

A

Angiography - view vessel occlusions, consider revascularisation
Percutaneous coronary intervention (PCI) - angioplasty, stenting
Coronary bypass grafting (CBPG) - taking an artery from elsewhere in the body and grafting it to the heart

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10
Q

Describe the signs and symptoms of acute pericarditis

A

Causes - infection, post MI/cardiac surgery, autoimmune, kidney failure, malignant deposits
Symptoms - central/left sided chest pain, sharp (worse on inspiration), improved by leading forward

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11
Q

Describe the signs and symptoms of stable and unstable angina

A

Stable:
Ischaemic chest pain in brief episodes, brought on by exertion, emotion, after a meal and cold weather.
Mild –> moderate pain.
Unstable:
Ischaemic chest pain that occurs at rest or with minimal exertion. Severe pain occurring with a crescendo pattern.

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12
Q

Describe the signs and symptoms of a myocardial infarction

A

Ischaemic chest pain that is very severe, persistent at rest or with minimal exertion. It is not relieved by rest or nitrate spray. Patient may be breathless, faint and have a feeling of impending death with sweating, pallor, nausea and vomiting.

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13
Q

Describe the investigations for a myocardial infarction

A

ECG - pathological Q wave, ST elevation

Blood tests - troponin, creatine kinase

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14
Q

Describe the use of cardiac biomarkers (troponin and cardiac enzymes) in the diagnosis of MI and distinguishing between NSTEMI and unstable angina in a patient with acute coronary syndrome

A

Troponins:
Cardiac troponin I and troponin T are proteins important in actin/myosin interaction, which are released in myocyte death. It rises 3-4hrs after first onset of pain and peaks 18-36hrs. It will then decline slowly for up to 10-14 days.
Creatine kinase:
Three isoenzymes present in the skeletal muscle, brain and heart. CK-MB is the cardiac isoenzyme, rising 3-8hrs after onset and peaking at 24hrs. Levels return to normal in 48-72hrs.
The presence of either of these enzymes represents death of myocardium. It distinguishes between unstable angina and NSTEMI as there is no tissue death in unstable angina.

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