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Cardiovascular system
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Wolff-Parkinson-White syndrome
Brugada syndrome
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Ventricular fibrillation
Ventricular tachycardia
Cardiac tumors
Shock
Arterial disease
Aneurysms
Aortic dissection
Angina pectoris
Coronary steal syndrome
Myocardial infarction
Prinzmetal angina
Stable angina
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Abetalipoproteinemia
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Coarctation of the aorta
Conn syndrome
Cushing syndrome
Hypertension
Hypertensive emergency
Pheochromocytoma
Polycystic kidney disease
Renal artery stenosis
Hypotension
Orthostatic hypotension
Lymphangioma
Lymphedema
Peripheral artery disease
Subclavian steal syndrome
Nutcracker syndrome
Superior mesenteric artery syndrome
Angiosarcomas
Human herpesvirus 8 (Kaposi sarcoma)
Vascular tumors
Behcet's disease
Kawasaki disease
Vasculitis
Chronic venous insufficiency
Deep vein thrombosis
Thrombophlebitis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
Endocarditis
0 / 19 complete
0 / 9 complete
of complete
of complete
Laboratory value | Result |
Complete Blood Count, Serum | |
Hemoglobin | 12.5 g/dL |
Hematocrit | 40.5% |
Leukocyte count | 18,100 /mm3 |
Platelet count | 250,000/mm3 |
Inflammatory Markers, Serum | |
ESR | 44 mm/hr |
CRP | 18 mg/L |
Electrolytes, Serum | |
Sodium | 131 mEq/L |
Potassium | 3.6 mEq/L |
Chloride | 94 mEq/L |
Bicarbonate | 20 mEq/L |
Calcium | 8.4 mg/dL |
2017
2016
daptomycin p. 191
presentation p. 656
Staphylococcus aureus p. 131
Streptococcus sanguinis p. 132
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
bacterial endocarditis p. 299
Endocarditis means “inflammation of the inner layer of the heart.” The heart’s wall is made up of three layers: the epicardium, the outermost layer; the myocardium; and then the endocardium, which is the layer that gets inflamed.
It turns out that most cases of endocarditis are due to a microbial infection of the endocardium, usually involving the endocardium lining the cardiac valves. Why the valves? Well, it turns out that the valves have tiny blood vessels that nourish them, even though they’re flopping around in blood all day long. This means that an infection can potentially result from a damaged valve, because it would allow microbes to escape the tiny blood vessels and invade the valve tissue, or on the flip side, microbes in the blood might enter the tiny vessels within the valve.
Either way, a microbe has to first get into the bloodstream, and that might happen if a person: has an open wound or an abscess; a dental or surgical procedure; or, an injection with an infected needle or infected substance, from using illegal drugs.
Most often, the valves on the left side — the mitral valve and the aortic valve — are affected, sometimes due to predisposing conditions, such as mitral valve prolapse and bicuspid aortic valves, but it really depends on the circumstances. Risk factors for either valve include having prosthetic valves, congenital cardiac defect involving the valves, damage to the valves from rheumatic heart disease, and intravenous drug use, which typically affects the tricuspid valve.
Now, the first step that happens in endocarditis is that the endothelial lining of the valve gets damaged. There are a number of ways this can happen, such as previous inflammation or injury. This damage exposes the underlying collagen and tissue factor, causing platelets and fibrin to adhere, which forms this tiny thrombosis or blood clot. This is called Nonbacterial Thrombotic Endocarditis, or NBTE. It’s nonbacterial because it happens even before the bacteria shows up. Now, if you add in bacteriemia, or bacteria in the blood, you’ve got yourself a recipe for infective endocarditis.
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