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Pathology > 2nd Exam: Pathology of Endocarditis > Flashcards

2nd Exam: Pathology of Endocarditis Flashcards

1
Q

When talking about endocarditis we are most often talking about:

A

disease of the valves

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2
Q

Indicate endocarditis in slides:

A

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

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3
Q

Surgical specimen of NBTE:

A

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

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4
Q

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

A

F. NBTE does not

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5
Q

How to id splenic infarct:

A

wedge shaped palor

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6
Q

NBTE leads to:

A

hypercoaguability and abnormal clot formation

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7
Q

Found in area of splenic infarct:

A

debris, dead tissue

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8
Q

Gross appearance of spleen w infarct:

A

Discreet area of coagulation necrosis

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9
Q

Infective endocarditis is characterized by:

A

microbial invasion of heart valves or mural myocardium

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10
Q

characteristic feature of endocardidits:

A

vegetations

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11
Q

Ex’s of vegetations:

A

necrotic debris, microorganisms, fibrin, inflammatory cells

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12
Q

Causes of infective endocarditis:

A

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

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13
Q

Predisposing factors to infective endocarditis:

A

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

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14
Q

Ex’s of indwelling lines and catheters:

A

PADS: pacemakers, angioplasty, dialysis, stents

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15
Q

Clinical presentation of infective endocarditis:

A

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

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16
Q

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

A

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

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17
Q

Main organism that causes IE:

A

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

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18
Q

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

A

normal

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19
Q

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

A

Strep viridians (and all HACEK?)

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20
Q

Strep viridians:

A

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

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21
Q

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

A

abnormal

22
Q

Organisms that lead to subacute IE:

A

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

23
Q

Strep bovis (gallolyticus):

A

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

24
Q

HACEK organisms:

A

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

25
Q

List HACEK organisms:

A

Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

26
Q

Vegetations form here with IE:

A

Valves, esp. mitral and aortic

27
Q

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

A

F. vice-versa

28
Q

What causes heart murmur in IE?

A

valve leaflets covered by plaque, blood flow altered

29
Q

Complications of IE:

A

Local extension, embolic complications

30
Q

Ex’s of local extension of IE:

A

ring abscess, valve perforation, and insufficienty

31
Q

Ex’s of embolic complications of IE:

A

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

32
Q

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

A

Janeway lesion abscess can happen in any organ

33
Q

small areas of bleeding under fingernails or toenails:

A

splinter hemmorhages

34
Q

osler nodes:

A

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

35
Q

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

A

any

36
Q

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

A

destructive

37
Q

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

A

valve cusp destruction, ring abscess

38
Q

Lesions in valve and myocardium, think:

A

IE, septic emboli, left sided endocarditis

39
Q

Gives rise to persistent bacteremia in endocarditis:

A

organisms w/in vegetations

40
Q

What are required for subacute endocarditis:

A

damaged valve or abnormal endothelium

41
Q

difference between acute and subacute endocarditis:

A

time frame, not amount of damage

42
Q

Why is it normally hard to get infections in heart?

A

Normally smooth, insult promotes clot formation and bacteria set up

43
Q

Pathogenic mechs for endocarditis:

A

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

44
Q

NBTE:

A

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
Q

Are neg blood cultures reliable w NBTE?

A

no

46
Q

Basic pathological process in heart:

A

thombosis, NBTE

47
Q

Most malignancies can make you:

A

hypercoagulable

48
Q

Causes of cadiac valve lesions:

A

hypercoagulable state, aseptic thrombi on valve

49
Q

Symptoms of IE are similar to:

A

emboli-infarcts and ischemia

50
Q

How is a spleen lesion related NBTE

A

Infarct attributed to embolism from valve lesion

51
Q

Causes of systemic emboli:

A

mural thrombi in heart, IE, NBTE, ath plaque

52
Q

Why is difficult to fight infection in heart?

A

Does have its own blood supply to get pmns to fight

Pathology (23 decks)

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