2nd Exam: Pathology of Endocarditis Flashcards Preview

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Flashcards in 2nd Exam: Pathology of Endocarditis Deck (52)
1

When talking about endocarditis we are most often talking about:

disease of the valves

2

Indicate endocarditis in slides:

Fibrin, PMNs, bacteria (not NBTE, right? More lymphos)

3

Surgical specimen of NBTE:

incompetent valves, leaflets thickened, fibrotic, covered w sterile fibrinous vegetations

4

TF? All forms of endocarditis involved inflammation of the endocardium.

F. NBTE does not

5

How to id splenic infarct:

wedge shaped palor

6

NBTE leads to:

hypercoaguability and abnormal clot formation

7

Found in area of splenic infarct:

debris, dead tissue

8

Gross appearance of spleen w infarct:

Discreet area of coagulation necrosis

9

Infective endocarditis is characterized by:

microbial invasion of heart valves or mural myocardium

10

characteristic feature of endocardidits:

vegetations

11

Ex's of vegetations:

necrotic debris, microorganisms, fibrin, inflammatory cells

12

Causes of infective endocarditis:

usually bacteria, but also fungi, Chlamydia, Coxiella, Bartonella

13

Predisposing factors to infective endocarditis:

degenerative valve disease (older pts), valve lesions at birth, IV drugs, before surgery and prosthetic valve replacement, vascular shunts/ grafts, vascular instrumentation, indwelling lines and catheters, systemic infections, poor oral health, chronic valve disease + dental procedures, neutropenia, immune suppression

14

Ex's of indwelling lines and catheters:

PADS: pacemakers, angioplasty, dialysis, stents

15

Clinical presentation of infective endocarditis:

elevated ESR and CRP, EKG abnormalities, pos blood culture (10% come back neg, septic emboli, fuo, chills, fatigue, heart murmur, known source of infection, evidence of emboli, pathologic evidence of endocarditis

16

TF? Blood cultures of a pt w IE will come back positive almost all the time.

F. some difficult to be cultured/ sequestered in valve leaflet

17

Main organism that causes IE:

staph a., over 50%, high mortality w sepsis, IV drug users, acute

18

Infective endocarditis via Staph a., effects normal or abnormal valves?

normal

19

This organism is part of the normal flora, but can cause IE:

Strep viridians (and all HACEK?)

20

Strep viridians:

subacute (prolonged course), less virulent than Staph a., damaged valve, normal oral flora,

21

Infective endocarditis via Strep v., effects normal or abnormal valves?

abnormal

22

Organisms that lead to subacute IE:

Strep v., Strep bovis (gallolyticus), HACEK organisms (usually)

23

Strep bovis (gallolyticus):

subacute IE, from GI tract, (ca, polyp IBD)

24

HACEK organisms:

usually subacute IE, about 5%, most commonly oral source

25

List HACEK organisms:

Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

26

Vegetations form here with IE:

Valves, esp. mitral and aortic

27

TF? Subacute IE agents have to be more virulent than those that cause acute.

F. vice-versa

28

What causes heart murmur in IE?

valve leaflets covered by plaque, blood flow altered

29

Complications of IE:

Local extension, embolic complications

30

Ex's of local extension of IE:

ring abscess, valve perforation, and insufficienty

31

Ex's of embolic complications of IE:

septic emboli, distant infarcts and abscesses, splinter hemmorhages, Janeway lesions, Osler nodes, conjunctival hemmorhages/ petechiae

32

non-painful, small red or bleeding macular (distinct spots) or nodular lesions on palms or soles, few mm, indicative of infective endocarditis:

Janeway lesion abscess can happen in any organ

33

small areas of bleeding under fingernails or toenails:

splinter hemmorhages

34

osler nodes:

painful, red, raised lesions found on the hands and feet

35

In which organs can abscess form (from septic emboli?)?

any

36

What type of vegetation is there on the aortic valve with IE:

destructive

37

Acute Staph a. IE of aortic valve can lead to:

valve cusp destruction, ring abscess

38

Lesions in valve and myocardium, think:

IE, septic emboli, left sided endocarditis

39

Gives rise to persistent bacteremia in endocarditis:

organisms w/in vegetations

40

What are required for subacute endocarditis:

damaged valve or abnormal endothelium

41

difference between acute and subacute endocarditis:

time frame, not amount of damage

42

Why is it normally hard to get infections in heart?

Normally smooth, insult promotes clot formation and bacteria set up

43

Pathogenic mechs for endocarditis:

bacteremia, predisposition to infection-abnormality of endothelium, virulent microorganism in body, organisms w vegetations = persistent bacteremia

44

NBTE:

row of non-infective vegetations on border of valve leaflets, more lymphos than neutrophils, not inflammation/ wall to wall w cells, bland thrombus loosely attached to valve

45

Are neg blood cultures reliable w NBTE?

no

46

Basic pathological process in heart:

thombosis, NBTE

47

Most malignancies can make you:

hypercoagulable

48

Causes of cadiac valve lesions:

hypercoagulable state, aseptic thrombi on valve

49

Symptoms of IE are similar to:

emboli-infarcts and ischemia

50

How is a spleen lesion related NBTE

Infarct attributed to embolism from valve lesion

51

Causes of systemic emboli:

mural thrombi in heart, IE, NBTE, ath plaque

52

Why is difficult to fight infection in heart?

Does have its own blood supply to get pmns to fight