L6, CVS Pathology PDF - Endocarditis

Summary

These lecture notes cover Endocarditis, a condition involving inflammation of the inner lining of the heart. The document details the causes, classifications, and effects of different types of this condition. It also includes information on both acute and subacute forms of the disease.

Full Transcript

pathology - CVS endocarditis LECTURE (6) endocarditis Dr. M. Shalaby pathology - CVS endocarditis ① Endocardium. ② Myocardium. ③ Pericardium. Dr. M. Shalaby pathology - CVS end...

pathology - CVS endocarditis LECTURE (6) endocarditis Dr. M. Shalaby pathology - CVS endocarditis ① Endocardium. ② Myocardium. ③ Pericardium. Dr. M. Shalaby pathology - CVS endocarditis  Inflammation of the inner most layer of heart that lines the chambers and DEFINITION covers the heart valves. INFECTIVE NON INFECTIVE ① Infective bacterial endocarditis ① Rheumatic fever  Most common clinically seen ② SLE form. ③ Endocarditis of Carcinoid syndrome CLASSIFICATION ② T.B, syphilis, typhoid, viruses, ④ Marantic (Terminal) endocarditis. fungus and histoplasma capsulatum especially in drug addicts.  Inflammation of the endocardium, the inner lining of the heart, as well as the valves that separate the heart chambers. DEFINITION  It is primarily a disease caused by bacteria.  Infective bacterial endocarditis: Acute, Subacute & Prothetic valve.  Any patient between 35 and 65y with fever and a newly developed NB regurgitation murmur is considered infective endocarditis until prove otherwise ① Pathogens gain access to the blood stream as a result of health-care procedures, or by intravenous drug use. ② Pathogens can rapidly adhere to a mechanically injured valve surface (pre- existing valvular disease) or to an inflamed valve surface (without pre-existing valve disease). ③ Some pathogens, such as S. aureus, get access to the valve endothelium which PATHOGENESIS adds to inflammation and tissue destruction. ④ Proliferation of the pathogens on and in the endothelium leads to vegetation on the valve. ⑤ Embolization of vegetation and systemic hematogenous spreading of the pathogens often occurs, leading to complications. ⑥ Tissue injury may follow deposition of circulating immune complexes or immune responses to deposited bacterial antigens Dr. M. Shalaby pathology - CVS endocarditis Dr. M. Shalaby pathology - CVS endocarditis 1 ACUTE INFECTIVE ENDOCARDITIS  Acute suppurative inflammation. DEFINITION  Virulent microorganism + normal valve.  Causative organism: Staph. Aureus (50% of cases) ① Septic focus PREDISPOSING ② Intravenous infections in drug addicts FACTORS ③ Impaired defense mechanisms LAB.  Blood culture DIAGNOSIS  Mitral and aortic valves commonly affected and tricuspid in drug addicts only.  The valve cusps show acute suppurative inflammation. N/E  Vegetations cover the valve cusps and are large, polypoid, irregular yellow and friable  Myocardium shows abscesses  The cusps: acute suppurative inflammation with excess neutrophils M/E  Vegetations are formed of platelets, fibrin, micro-organisms and neutrophils.  Severe Valve destruction and destruction of chordae tendineae → regurge  Septic emboli are formed by breakdown of vegetations → pyemia EFFECTS &  Toxemia leading to bone marrow depression, fatty change and necrosis of PROGNOSIS parenchymatous organs.  Rapidly fatal within 8 weeks from toxic myocarditis (acute heart failure) Dr. M. Shalaby pathology - CVS endocarditis Dr. M. Shalaby pathology - CVS endocarditis  Cases of acute bacterial endocarditis (ABE) present with far more aggressive symptoms: ① Sepsis. ② Congestive heart failure. ③ Renal failure. ④ Stroke. ⑤ Septic emboli. Dr. M. Shalaby pathology - CVS endocarditis 2 SUBACUTE INFECTIVE ENDOCARDITIS  Non-suppurative inflammation. DEFINITION  Low virulence organism + diseased valve.  Causative organism: Streptococcal viridans (more than 50% of cases) ① Abnormal valves due to Rheumatic fever. PREDISPOSING ② Syphilis and congenital abnormalities. FACTORS ③ Bacteremia. ④ Impaired defense mechanisms.  Mitral and aortic together or separately  The valve cusps shows edema and hyperemia Vegetations cover the cusps and NAKED EYE are irregular, polypoid and smaller than those of acute. (N/E)  The color vary from yellowish grey to brown they are friable.  Myocardium shows cloudy swelling and fatty changes. MICROSCOPIC  The cusps are vascularised and show edema, and inflammatory cells. EXAMINATION  Vegetations are formed of fibrin, platelets and microorganism (no or few (M/E) neutrophils)  Less severe valve destruction.  Emboli (infective) leading to infarctions and mycotic aneurysms  Toxic capillaritis Skin and kidney : ① Petechial hemorrhage EFFECTS & ② Focal or diffuse glomerulonephritis. PROGNOSIS  Toxemia: leading to clubbing of fingers, fatty change, bone marrow depression and sub-acute combined degeneration of spinal cord  Untreated cases: died within 6 months to 2 years from cardiac failure, renal failure or embolic effects.  Fever, often low-grade and intermittent,  Heart murmurs, arrhythmia  These are immunologic Signs and symptoms of SBE : ① Petechiae ② Subungual (splinter) hemorrhages. DIAGNOSIS ③ Osler nodes: Tender subcutaneous nodules usually found in digits ④ Janeway lesions: Non tender maculae on the palms and soles ⑤ Roth spots: Retinal hemorrhages with small, clear centers (rare)  Signs of neurologic disease  Splenomegaly  Abdominal symptoms, such as right upper quadrant pain Dr. M. Shalaby pathology - CVS endocarditis INFECTIVE ENDOCARDITIS SIGNS ROTH SPOT IN RETINA Dr. M. Shalaby pathology - CVS endocarditis FEATURES SUBACUTE ACUTE Splenomegaly, clubbing of CLINICAL FEATURES Acute systemic infection fingers, petechial LESIONS ON VALVES Not invasive, suppurative Invasive, damaging, suppurative PREVIOUS CONDITION Previously damaged Usually previously normal VIRULENCE Less virulent Highly virulent MOST COMMON ORGANISM Streptococcus viridians Staphylococcus aureus DURATION > 6 weeks < 6 weeks  Test are done to help confirm or rule out endocarditis.  This test helps identify the causative organism in the bloodstream.  Results from this test help determine the antibiotic or combination of antibiotics to use for treatment.  Should be done before sart of antibiotic therapy  Culture-negative IE: ① Patients received antibiotics before blood cultures are taken due to systemic infection or suspected diagnosis of a bacterial infection; ② The causative microorganisms have no, or limited proliferation in conventional blood cultures, or the diagnosis of the causative microorganisms requires special media or cell culture conditions. ③ Non-infective cause of endocarditis. 3 ENDOCARDITIS ON PROSTHETIC VALVES  Staphylococcal infection (more than 50% of cases).  Occurs 2 months after surgery. ETIOLOGY  Due to intra-operative contamination with drug resistant pathogens (staph.- gram negative bacteria or fungus) Dr. M. Shalaby pathology - CVS endocarditis  Occurs in systemic lupus erythematosus (SLE)  Affects mainly the mitral valve. LIBMAN-SACKS  Vegetations are multiple , small, near the valve ring. ENDOCARDITIS  Result from immune complex mediated endocardial injury followed by thrombosis.  Intestinal carcinoid tumors with metastases to the liver ENDOCARDITIS OF  Secretion of vasoactive amines (mainly serotonin): CARCINOID SYNDROME  Secreted to hepatic vein → IVC → right side of heart → damage of endocardium which heals by fibrosis especially of the tricuspid valve NON-BACTERIAL  Known as marantic endocarditis. THROMBOTIC  Occurs in debilitated patients as those with advanced metastaic cancer ENDOCARDITIS or wasting disease. (NBTE) SUMMARY & WRAP UP  Infective endocarditis remains a major health problem.  Delayed diagnosis of the disease and culture negative IE are common.  Staphylococci are the prevalent microorganisms. Dr. M. Shalaby

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