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34 Cards in this Set
- Front
- Back
What are the prerequisites for the development of infective endocarditits?
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-Abnormal or damaged endocardium (microrganisms will only infect damaged tissue; except S. Aureus)
-HIgh flow & pressure -transient bacteremia (access to bloodstream) -Organisms with special characteristics |
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Vegatations are:
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Clot composed of meshwork of platelets and fibrin found where there was damaged endothelium; sticks to valve
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A major disadvantage of vegetations and the inflammatory response is:
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There is no inflammatory response!
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As far as flow conditions, where do vegatations typically form?
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Near areas of high flow & pressure; downstream of areas with impeded flow
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Why is infective endocarditis typically seen in insufficient valves as opposed to stenotic valves?
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Stenotic valves impede flow, and infective endocarditis typically forms in areas where there is high flow which is more likely in an area are prolapse of a valve & you have regurgitation.
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In order to develop infective endocarditis, you MUST have?
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Transient bacteremia (so bacteria have access to the bloodstream to infect the vegatation).
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What are the most common organisms seen in infective endocarditis? Why are these the most common?
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The organisms contain certain proteins that allow them to bind fibrin, fibrinogen, fibronectin, & platelets (which make up vegatations)
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Bacterial antigens may manifest as ____________?
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Immune complexes that produce rheumatologic manifestations
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What does acute vs. subacute endocarditis tell you about the virulence of the organism?
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Acute= severe, with sudden onset and short duration; highly virulent organism (S. Aureus)
-Subacute: chronic disease of long duration; avirulent organism (S. viridans or enterococci) |
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The 2 most common Strep organisms found in infective endocarditis.
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S. viridans and S. enterococci
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Alpha hemolytic
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S. viridans (green)
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Why are gram (-) organisms less likely?
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The are easily lysed when they move into the bloodstream
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Why has S. Aureus become more common cause of endocarditis than S. viridans?
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High #'s of hospitalized patients and their indwelling catherters
-IV drug abusers |
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The difference in S. Aureus and S. viridans and the tissues they infect.
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S. Aureus= infects healthy tissues
S. Viridans = only infects damaged tissue |
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A key characteristic finding in an IV drug abuser with endocarditis that distinguishes them is?
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They have endocarditis on the RIGHT side of the heart (tricuspid valve) and endocarditis is typically a disease of the LEFT side of the heart
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Clinical presentation of IV drug abuser with endocarditis.
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Fever, hemoptysis, R-sided (tricuspid valve) findings
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HACEK is?
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A group of small, fastidious gram (-) coccobacilli that live in the mouth & are associated with periodontal disease -->ONLY GRAM NEGATIVE ORGANISMS TO CAUSE INFECTIVE ENDOCARDITIS
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How is it that someone can have negative blood cultures and still have infective endocarditis?
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-Inadequate therapy just before admission
-Or infection with a fastidious organism that won't grow well; Cat scrathc; QUe fever; Whipplei |
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Portal of entry for organisms:
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S. viridans and HACEK; enter the bloodstream from the mouth after dental manipulation or poor oral hygiene
S. Aureus: through a break in the skin; IV drug abusers (with needles) Enterococci: from the gut |
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Clinical presentation of subacute infective endocarditis.
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-Symptoms non-specific (fever, malaise; fatique)
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Why are the manifestations of Subacute infective endocarditis so variable?
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Microemboli of the vegatation can involve any organ in supplied by flood flowing past the infected vegatation
-Circulating immune complexes can produce immunological responses (rheumatological, neurological) |
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Criteria used for diagnosis of Infective endocarditis
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-Positive blood Cx
-predisposing cardiac lesion -peripheral embolic phenomena (to any organ from the left heart; to the lungs to the right heart) |
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Testing for detecting a predisposing cardiac lesion?
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ECG (esp. right sided lesions of IV drug abusers)
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Peripheral manifestations of endocarditis:
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-false positive for syphillis
-positive rheumatoid factor -proliferative glomerulonephritis from the deposition of immune complexes |
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Always suspect endocarditis in a pt. who presents with:
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S. Aureus bacteremia and no obvious source (even in the absence of a heart murmmur or peripheral embolic phenomena)
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This form of infective endocarditis is more severe, but Dx is easier
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Acute
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Other lab data seen in enfective endocarditis:
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Normal WBC's
Anemia elevated sedimentation rate hyperglobunemia |
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Most important single factor in diagnosing endocarditis? What is an important characteristic of this factor?
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Positive blood culture;
-continuously positive (if not all positive, could be a non-intravascular infections) |
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Characteristics of treatment? Why?
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Must be long-term, continuous, IV, bacteriocidal therapy because there is no host defense against this disease
-measure in vitro susceptibility of the org -dose should be high enough that it will still kill if diluted 8 times or greater |
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In choice of drugs, you 2 drugs that are ? Example?
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Synergistic
penicillin and streptococci (if no penicillin resistance) penicillin +gentamycin |
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When should you administer Abx prophylaxis?
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When someone at high risk is for endocarditis undergoes a procedure that can cause transient bacteremia or someone with damaged or abnormal heart valves or congenital defects
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MCC of death involving infective endocarditis?
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HF, embolic complications (cerebral catastrophe, myocardial infarction).
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Profile of someone with endocarditis from IV drug abuse?
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Young
no heart disease R-sided endocarditis (tricuspid valve) -Mostly S. Aureus |
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Most common infecting organism in someone with prosthetic heart valves? Outcome of this infection?
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S. epidermidis (manifest in the sewing ring at time of surgery, so hospital acquired)
-valve dysfunction and surgical replacement S. Viridans manifest later and involve the working part of the prosthetic valve |