Rheumatic Fever and Endocarditis MCQs

(a) NBTE is characterized by the deposition of small (1 - 5 mm) sterile thrombi on the leaflets of the cardiac valves (b) Histologically, these are bland thrombi, loosely attached to the underlying valve (c) The vegetations are nondestructive and do not elicit any inflammatory reaction. (d) The local effect of the vegetations is usually trivial, they can be the source of systemic emboli that produce significant infarcts in the brain, heart, or elsewhere. Reference : Robbins 10th Ed pg 564

(a) Acute rheumatic fever can involve any or all layers of the heart. Because rheumatic fever follows group A streptococcal infections, the antihyaluronidase, anti- DNase, and antistreptolysin O (ASO) titers are often elevated. (b) The ANA level could be elevated in systemic lupus erythematosus, which is most likely to produce a serous pericarditis. (c) The strains of group A streptococci that lead to acute rheumatic fever are less likely to cause glomerulonephritis, so an elevated creatinine level is unlikely. (d) Cardiac troponins are markers for ischemic myocardial injury. Although their levels may be elevated because of the acute myocarditis that occurs in rheumatic fever,this change is not a characteristic of rheumatic heart disease. Reference : Robbins 10th Ed pg 563

Vegetations on heart valves are the classic hallmark of IE; these are friable, bulky, potentially destructive lesions containing fibrin, inflammatory cells, and bacteria or other organisms. Vegetations are prone to embolization; because the embolic fragments often contain virulent organisms, abscesses frequently develop where they lodge, leading to sequelae such as septic infarcts or mycotic aneurysms. Reference: Robin's basic pathology 10 th edition, pg 564