Cardio 3 CAD IE Flashcards

1
Q

What is coronary artery disease (CAD)?

A

Coronary artery disease is insufficient perfusion of the coronary arteries, often due to atherosclerosis, leading to decreased oxygen supply to the myocardium.

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2
Q

What are the causes of coronary artery disease?

A

Causes include:
β€’ Decreased supply: Atheroma, thrombosis, spasm, embolus, arteritis, anemia, hypotension.
β€’ Increased demand: Increased cardiac output (hypertension), hypertrophy from valvular stenosis or hypertension.

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3
Q

What are the pathophysiological mechanisms of atherosclerosis in CAD?

A

The process begins with endothelial injury/dysfunction, leading to the accumulation of oxidized LDL, which is taken up by macrophages, forming foam cells. This progression forms a plaque with a lipid core and fibrous cap. A thrombus may form within the plaque and cause stenosis.

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4
Q

What is the classification of coronary artery disease?

A

CAD is classified into:
β€’ Stable Angina.
β€’ Acute Coronary Syndrome (ACS): Includes unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).

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5
Q

What are the risk factors for coronary artery disease?

A

Risk factors include:
β€’ Age (men >45, women >55).
β€’ Male gender.
β€’ Family history of premature CAD.
β€’ Diabetes mellitus.
β€’ Hyperlipidemia (especially high LDL).
β€’ Hypertension.
β€’ Smoking.
β€’ Obesity and sedentary lifestyle.
β€’ Hypercoagulability.
β€’ Heavy alcohol consumption and cocaine use.

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6
Q

What is stable angina?

A

Stable angina is chest pain triggered by exertion or stress, typically relieved by rest. It occurs when oxygen demand exceeds supply and is usually associated with a fixed coronary artery obstruction.

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7
Q

What is the treatment for stable angina?

A

Treatment involves:
β€’ Anti-anginal therapy: Beta-blockers (to reduce heart rate and oxygen demand), short-acting nitrates (for immediate relief), and calcium channel blockers (if beta-blockers are contraindicated).
β€’ Secondary prevention: Aspirin and statins, along with lifestyle changes like smoking cessation, exercise, and weight control.
β€’ Revascularization: Percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) in high-risk patients.

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8
Q

What is unstable angina?

A

Unstable angina is characterized by chest pain at rest, or crescendo angina, and occurs due to reduced coronary blood flow. It may be associated with a rupture of an atherosclerotic plaque and is part of acute coronary syndrome (ACS).

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9
Q

What is the treatment for unstable angina?

A

Acute treatment: Admission to the hospital, oxygen (if oxygen saturation is less than 94%), morphine for pain control, nitrates, dual antiplatelet therapy (aspirin + clopidogrel), low-molecular-weight heparin (LMWH), and electrolyte replacement.
β€’ Revascularization: If symptoms persist after 48 hours of medical treatment or if the patient is hemodynamically unstable, angioplasty and stenting may be required.
β€’ Maintenance treatment: Continue aspirin + clopidogrel for 6-9 months, beta-blockers, nitrates, statins, and management of risk factors.

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10
Q

What is variant (Prinzmetal) angina?

A

Variant angina is caused by spontaneous episodes of angina due to severe spasm of an epicardial coronary artery, usually near an atherosclerotic lesion. This results in a transient reduction of the coronary lumen and myocardial ischemia.

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11
Q

What is the treatment for variant angina?

A

The mainstay of treatment is calcium channel blockers (CCBs) to reduce coronary spasm. Sublingual nitroglycerin may help abort episodes. Lifestyle modifications such as smoking cessation and lipid control are also important.

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12
Q

What is myocardial infarction (MI)?

A

Myocardial infarction (MI) is the necrosis of the myocardium due to occlusion of a coronary artery, typically caused by thrombosis following the rupture of an atherosclerotic plaque.

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13
Q

What are the types of myocardial infarction?

A

β€’ ST-Elevation Myocardial Infarction (STEMI): Transmural infarction involving the entire thickness of the heart wall, typically associated with ST-segment elevation on the ECG.
β€’ Non-ST-Elevation Myocardial Infarction (NSTEMI): Subendocardial infarction involving the inner third of the myocardium, typically associated with ST-segment depression or T-wave inversion on the ECG.

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14
Q

What are the clinical features of myocardial infarction?

A

β€’ Intense substernal chest pain, often described as crushing or a sensation of an elephant sitting on the chest, radiating to the neck, jaw, left arm, or back.
β€’ Diaphoresis, dyspnea, nausea, vomiting, sense of impending doom, and syncope.
β€’ In elderly or diabetic patients, MI may be asymptomatic or present with atypical symptoms.

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15
Q

How is myocardial infarction diagnosed?

A

β€’ ECG: Look for ST-segment elevation or depression, T-wave inversion, or the presence of pathological Q-waves.
β€’ Cardiac enzymes: Troponin I and T are the gold standard for detecting myocardial injury. CK-MB can be used to detect recurrent infarctions.

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16
Q

What is the treatment for myocardial infarction?

A

β€’ Initial management: Admission to the coronary care unit (CCU), oxygen (if O2 saturation <94%), dual antiplatelet therapy (aspirin + clopidogrel), morphine for pain, heparin (for anticoagulation), beta-blockers, nitrates, and statins.
β€’ Revascularization:
β€’ PCI (Percutaneous Coronary Intervention): Door-to-balloon time should be less than 90 minutes.
β€’ Thrombolytic therapy (tPA): If PCI is not available, thrombolytics should be administered within 12 hours of symptom onset, preferably within 6 hours.
β€’ Long-term treatment: ACE inhibitors, beta-blockers, statins, and antiplatelet therapy should continue indefinitely.

17
Q

What are the complications of myocardial infarction?

A

β€’ Heart failure: The most common cause of in-hospital mortality.
β€’ Arrhythmias: Especially ventricular arrhythmias, which are the leading cause of death in the first few days after MI.
β€’ Recurrent MI: Especially in patients who are not treated promptly.
β€’ Mechanical complications: Free wall rupture, interventricular septum rupture, papillary muscle rupture, ventricular aneurysm, and pericarditis.
β€’ Dressler syndrome: Occurs 1-3 weeks after MI and is characterized by a triad of fever, pericarditis, and pleuritis.

18
Q

What is the management of acute pulmonary edema after myocardial infarction?

A

β€’ Positioning: Keep the patient propped up.
β€’ Oxygen: Administer if O2 saturation is low.
β€’ Diuretics: IV furosemide to reduce fluid overload.
β€’ Morphine: For pain and venodilation.
β€’ Nitrates: IV nitrates to reduce preload and afterload.
β€’ Inotropic support: If left ventricular function is poor, consider dobutamine or dopamine.
β€’ Intra-aortic balloon pump: Used as a bridge to surgery in patients with severe heart failure or shock.

19
Q

What is rheumatic fever?

A

Rheumatic fever is an autoimmune reaction triggered by a Group A Streptococcus (GAS) infection, usually after a sore throat. It causes inflammation in various tissues, including the heart, joints, skin, and central nervous system.

20
Q

What are the major diagnostic criteria for rheumatic fever?

A

The major criteria, remembered by the mnemonic β€œJβ™₯NES,” include: Joints: Polyarthritis of large joints, which is fleeting. β™₯ (Cardiac): Carditis (murmurs, congestive heart failure, pericarditis). Nodules: Subcutaneous nodules over tendons and joints. Erythema marginatum: Transient, pink, coalescent rings on the trunk. Sydenham’s chorea: Involvement of the central nervous system.

21
Q

What are the minor criteria for diagnosing rheumatic fever?

A

Minor criteria include: Fever. Elevated ESR or CRP (acute phase reactants). History of previous rheumatic fever or rheumatic heart disease. Prolonged PR interval on ECG. Arthralgia.

22
Q

What is the treatment for rheumatic fever?

A

Bed rest, especially if carditis is present. High-dose aspirin to control arthritis, fever, and other symptoms. Penicillin to eradicate any residual streptococcal infection. Prednisolone if there is cardiac involvement. Treatment of valvular pathology if necessary.

23
Q

How is rheumatic fever prevented?

A

Prevention involves the use of penicillin (or erythromycin for penicillin-allergic patients) for the treatment of streptococcal pharyngitis, especially in patients at risk for rheumatic fever.

24
Q

What is infective endocarditis?

A

Infective endocarditis is an infection of the endocardium or the vascular endothelium of the heart, often involving the heart valves. It can be acute (rapid onset, usually caused by Staphylococcus aureus) or subacute (more gradual, caused by organisms like Streptococcus viridans).

25
What are the signs and symptoms of infective endocarditis?
Constitutional symptoms: fever, weight loss, anemia. New heart murmur and heart failure due to valve destruction. Embolization of vegetations leading to vascular phenomena like Janeway lesions (painless), splinter hemorrhages (nailbed), Roth’s spots (in retina), and Osler’s nodes (painful). Immune complex deposition causing glomerulonephritis with microscopic hematuria.
26
What investigations are needed to diagnose infective endocarditis?
Blood cultures: Three sets taken over 24 hours before antibiotics are started. Echocardiography: Transthoracic is used initially, but transesophageal echocardiography is more sensitive, especially in prosthetic valve cases. CBC: Normocytic normochromic anemia and leukocytosis. CXR: To check for heart failure or embolization. ECG: May show myocardial infarction if there is embolization to the coronary arteries. Urinalysis: Hematuria due to glomerulonephritis.
27
What is the Modified Duke Criteria for diagnosing infective endocarditis?
The modified Duke criteria include: Major criteria: 2 positive blood cultures for organisms known to cause IE or persistent bacteremia. Echocardiographic evidence of vegetation, abscess, or new valvular regurgitation. Minor criteria: Predisposing factors like cardiac lesions or IV drug use. Fever above 38Β°C. Evidence of emboli or vasculitis. Immunological features like Osler’s nodes or nephritis. Echo findings consistent with IE but not meeting major criteria.
28
What is the treatment for infective endocarditis?
IV antibiotics: Empirical therapy with penicillin and gentamicin, or vancomycin and gentamicin for suspected Staphylococcus infections. Surgical intervention: Required in cases of severe valve damage, perivalvular abscess, or prosthetic valve endocarditis. Surgery may also be necessary in cases with large vegetations or fungal infections.
29
What is the role of prophylaxis in infective endocarditis?
Prophylaxis is indicated for patients with certain cardiac conditions undergoing procedures that may lead to bacteremia, such as dental work or surgery. Cardiac conditions requiring prophylaxis: Prosthetic heart valve. History of infective endocarditis. Transplanted heart with valvular disease. Unrepaired cyanotic congenital heart disease. Repaired congenital heart disease with prosthetic material (within the first 6 months). Prophylaxis regimen: Amoxicillin is preferred; if allergic to penicillin, clindamycin or azithromycin is used.