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34 Cards in this Set

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What are the prerequisites for the development of infective endocarditits?
-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
Vegatations are:
Clot composed of meshwork of platelets and fibrin found where there was damaged endothelium; sticks to valve
A major disadvantage of vegetations and the inflammatory response is:
There is no inflammatory response!
As far as flow conditions, where do vegatations typically form?
Near areas of high flow & pressure; downstream of areas with impeded flow
Why is infective endocarditis typically seen in insufficient valves as opposed to stenotic valves?
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.
In order to develop infective endocarditis, you MUST have?
Transient bacteremia (so bacteria have access to the bloodstream to infect the vegatation).
What are the most common organisms seen in infective endocarditis? Why are these the most common?
The organisms contain certain proteins that allow them to bind fibrin, fibrinogen, fibronectin, & platelets (which make up vegatations)
Bacterial antigens may manifest as ____________?
Immune complexes that produce rheumatologic manifestations
What does acute vs. subacute endocarditis tell you about the virulence of the organism?
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)
The 2 most common Strep organisms found in infective endocarditis.
S. viridans and S. enterococci
Alpha hemolytic
S. viridans (green)
Why are gram (-) organisms less likely?
The are easily lysed when they move into the bloodstream
Why has S. Aureus become more common cause of endocarditis than S. viridans?
High #'s of hospitalized patients and their indwelling catherters

-IV drug abusers
The difference in S. Aureus and S. viridans and the tissues they infect.
S. Aureus= infects healthy tissues
S. Viridans = only infects damaged tissue
A key characteristic finding in an IV drug abuser with endocarditis that distinguishes them is?
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
Clinical presentation of IV drug abuser with endocarditis.
Fever, hemoptysis, R-sided (tricuspid valve) findings
HACEK is?
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
How is it that someone can have negative blood cultures and still have infective endocarditis?
-Inadequate therapy just before admission
-Or infection with a fastidious organism that won't grow well; Cat scrathc; QUe fever; Whipplei
Portal of entry for organisms:
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
Clinical presentation of subacute infective endocarditis.
-Symptoms non-specific (fever, malaise; fatique)
Why are the manifestations of Subacute infective endocarditis so variable?
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)
Criteria used for diagnosis of Infective endocarditis
-Positive blood Cx
-predisposing cardiac lesion
-peripheral embolic phenomena (to any organ from the left heart; to the lungs to the right heart)
Testing for detecting a predisposing cardiac lesion?
ECG (esp. right sided lesions of IV drug abusers)
Peripheral manifestations of endocarditis:
-false positive for syphillis
-positive rheumatoid factor
-proliferative glomerulonephritis from the deposition of immune complexes
Always suspect endocarditis in a pt. who presents with:
S. Aureus bacteremia and no obvious source (even in the absence of a heart murmmur or peripheral embolic phenomena)
This form of infective endocarditis is more severe, but Dx is easier
Acute
Other lab data seen in enfective endocarditis:
Normal WBC's
Anemia
elevated sedimentation rate
hyperglobunemia
Most important single factor in diagnosing endocarditis? What is an important characteristic of this factor?
Positive blood culture;
-continuously positive (if not all positive, could be a non-intravascular infections)
Characteristics of treatment? Why?
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
In choice of drugs, you 2 drugs that are ? Example?
Synergistic
penicillin and streptococci (if no penicillin resistance)
penicillin +gentamycin
When should you administer Abx prophylaxis?
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
MCC of death involving infective endocarditis?
HF, embolic complications (cerebral catastrophe, myocardial infarction).
Profile of someone with endocarditis from IV drug abuse?
Young
no heart disease
R-sided endocarditis (tricuspid valve)
-Mostly S. Aureus
Most common infecting organism in someone with prosthetic heart valves? Outcome of this infection?
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