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CRS > Lecture 11+12 > Flashcards

Lecture 11+12 Flashcards

1
Q

process of cardiac vegetation

A
  1. mechanical injury / endothelial injury
  2. platelet and fibrin thrombus
  3. bacterial adhesion and biofilm formation
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2
Q

clinical presentation of IE

A 
fever
heart murmur 
Embolic phenomenon 
Petechiae 
Skin manifestations  
Splenomegaly

Osler’s nodes,
Janeway lesions,
Roth spots are uncommon

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3
Q

Native valve Endocarditis

A

Staphylococcus spp.
Streptococcus spp.
Enterococcus spp.
HACEK organisms

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4
Q

Prosthetic valve Endocarditis

A

Early PVE (<1-year post-surgery, usually in first 2 months)

Coagulase Negative Staphylococcus spp. (CoNS)
S. aureus

Late PVE (>1-year post surgery)

same as NVE

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5
Q

Skin and soft tissue infections
Endocarditis
Food poisoning
Septicemia

A

staph aureus

seen:
Skin, Muscle Bone
Cardiovascular
Gastrointestinal

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6
Q

Endocarditis
Indwelling device infections
Prosthetic joint infections

A

staph epidermidis

seen:
cardio

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7
Q

Urinary tract infection

“honeymoon cystitis”

A

Staphylococcus saprophyticus

seen:
urogenital tract

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8
Q

Staphylococcus spp. and endocarditis

A

one of the most common pathogens of endocarditis

Features:
Aggressive disease

  • Increased risk of:
  • Embolism
  • Stroke
  • Persistent bacteremia
  • Death
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9
Q

Pathogenicity of S. aureus in regard to endocarditis

A

capsule: resists phagocytosis

surface adhesions:
Clumping factor A (ClfA): a fibrinogen-binding protein
Fibronectin binding protein A and B
Collagen binding protein

Hemolysins: alpha toxin: pore formation and cellular lysis

biofilm formation

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10
Q

Staphylococcus epidermidis and heart

A

coagulase negative

One of the main causes of Early PVE
Major cause of infections associated with inserted
medical devices and prostheses

usually isolated from human skin

patho:
fibrinogen binding protein
biofilm formation

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11
Q

Streptococcus mutans and Streptococcus sanguinis

A

endocarditis (cardio)

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12
Q

Viridans Streptococci

A

responsible for NVE and PVE

Members of the normal microbiota of the mouth and URT

Usually alpha-hemolytic on blood agar (but some are nonhemolytic)

Optochin resistant

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13
Q

what is a stenosis

A

Failure of a valve to open completely, obstructing
forward flow

due to primary leaflet abnormality and usually chronic (calcification or scaring)

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14
Q

what is an insufficiency

A 
Failure of a valve to close completely, thereby
allowing regurgitation (backflow) of blood

can be due to intrinsic disease or disruption of supporting structures

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15
Q

reasons for mitral stenosis

A

post inflammatory scarring

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16
Q

reasons for aortic stenosis

A

Post inflammatory scarring (rheumatic heart disease)

Senile calcific aortic stenosis

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17
Q

reasons for mitral regurgitation

A

abnormal leaflets and commissures (scarring, prolapse)

abnormal tensor apparatus (rupture or dysfunction)

abnormal LV (enlargement)

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18
Q

aortic regurgitation causes

A

intrinsic disease:
post inflammatory scarring

Aortic disease1. Degenerative aortic dilatation

  1. Syphilitic aortitis
  2. Ankylosing spondylitis
  3. Rheumatoid arthritis
  4. Marfan syndrome
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19
Q

mitral stenosis signs and symptoms

A

Dyspnea (pulmonary edema), fatigue, hematemesis

Late low pitched diastolic murmur and crepitations in
lung

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20
Q

mitral regurgitation signs and symptoms

A

Dyspnea (pulmonary edema), palpitations and fatigue

Pansystolic murmur radiating to axilla

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21
Q

aortic stenosis signs and symptoms

A

Angina, syncope, congestive heart failure

Ejection systolic murmur loudest at base and radiates to neck after S1

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22
Q

aortic regurgitation

A

Volume overload congestive heart failure

Bounding pulses, early diastolic murmur, displaced
apex beat

23
Q

Rheumatic Heart Disease (RHD)

A

acute, immunologically mediated, multisystem inflammatory disease classically occurring a few weeks after group A streptococcal infections of throat and skin

epi:
seen in developed and crowded countries
10 days to 6 weeks after group A infection
occurs mostly in ages 5 to 15

etiopath:
host immune responses to group A streptococcal
antigens that cross-react with host proteins following throat infections or sometimes skin infections

24
Q

The pathogenesis of RHD

A

type II hypersensitivity reaction

  1. Antibodies and CD4+ T cells directed against streptococcal M proteins can recognize cardiac self antigens
  2. Antibody binding can activate complement, and neutrophils and macrophages + cytokine production by the stimulated T cells = macrophage activation

Damage to heart tissue may thus be caused by a combination of antibody and T cell–mediated reactions

will have chronic fibrotic lesions

25
Q

morphology of RHD

A

deforming fibrotic valvular disease

favors the mitral valve leading to mitral stenosis

Chronic rheumatic heart disease = mostly valvular; fibrosis and calcification

26
Q

Acute rheumatic fever

A

focal lesions will be found in all three layers (pancarditis)

will have distinct lesions in the heart - Aschoff bodies

composed of immune cells = Anitschkow cells

chromatin condenses into a central, slender, wavy ribbon (caterpillar cell)

27
Q

Chronic mitral valvulitis

A

most frequent

Conspicuous irregular fibrous thickening (neovascularized) and calcification of the leaflets

Fusion of the commissures and shortening of the chordae tendineae

Fixed narrow opening (fish mouth, button hole)

Mitral stenosis

28
Q

Chronic aortic valvulitis

A

Cusps are thickened, firm and adherent to each other

Valve orifice is reduced to rigid, triangular channel

29
Q

clinical features of RF

A
  1. Migratory polyarthritis of the large joints
  2. Pancarditis (myocarditis, pericarditis, or endocarditis)
  3. Subcutaneous nodules (typically on extensor surfaces of extremities)
  4. Erythema marginatum, an irregular circinate skin rash
  5. Syndenham chorea, a neurologic disorder with involuntary rapid movements

Pharyngeal cultures for streptococci are negative by the time the illness
begins

Antibodies to one or more streptococcal enzymes, such as streptolysin O and DNase B, can be detected in the sera

Predominant clinical manifestations are carditis and arthritis, the latter more common in adults than in children

30
Q

complications of RF

A

Valvulitis murmurs

Left atrium progressively dilates → mural thrombi → embolus

congestive heart failure

Arrhythmias

Infective endocarditis

31
Q

diagnoses of RF

A

Evidence of a preceding group A streptococcal infection
Presence of two major manifestations

OR

One major and two minor manifestations (nonspecific signs and symptoms

that include:
fever, arthralgia, or elevated blood levels of acute-phase reactants)

32
Q

Calcific Aortic Stenosis

A

age-associated “wear and tear” of either anatomically normal valves or congenitally bicuspid valves

epi:
elderly population
if congenital then middle aged

etiopath:
Likely a consequence of recurrent chronic injury due to hyperlipidemia, hypertension, inflammation, and other factors similar to those implicated in atherosclerosis

Chronic progressive injury leads to valvular degeneration and incites the deposition of hydroxyapatite (the same calcium salt found in bone)

Aortic valve scarred as a result of rheumatic heart disease

33
Q

gross of CAS

A

Mounded calcified masses on the outflow surfaces of the cusps that ultimately prevent cuspal opening

Free edges of the cusps are usually not involved

34
Q

micro of CAS

A

Dystrophic calcification

Functional valve area is decreased by large nodular
calcific deposits → causes measurable outflow obstruction

Subjects the left ventricular myocardium to progressively increasing pressure overload

35
Q

clinical features of CAS

A

Angina pectoris – increased requirement of
hypertrophied myocardium

Syncope – poor perfusion of the brain

Death usually occurs due to congestive
heart failure or arrhythmias

36
Q

Myxomatous Mitral Valve

A

one or both mitral leaflets are “floppy” and prolapse—they balloon back into the left atrium during systole; also called Mitral valve prolapse (MVP)

epi:
usually women between 20-40

etiopath: 
an underlying (possibly systemic) intrinsic defect of connective tissue like in Marfan syndrome
37
Q

clinical features of MMV

A

most are asymptomatic

Palpitations, fatigue or atypical chest pain
Mid systolic click

Severe complications in about 3% of cases:
• Mitral regurgitation and congestive heart failure
• Infective endocarditis
• Ventricular arrhythmias (may lead to →SCD)
• Thromboembolic- stroke

38
Q

gross and micro for MMV

A

gross:
Soft puffed up rubbery mitral valve cusps
Ballooning of the valve leaflets into the left atrium
during systole (mid-systolic click)
Chordae tendineae which are often elongated and
fragile → may rupture in severe cases
Mitral annulus may be dilated (regurgitation)

micro:
Thinning of fibrosa layer of valve, expansion of
spongiosa layer

Excessive amounts of loose, edematous, faintly
basophilic ground substance within the middle layer
of the valve leaflets and chordae (myxomatous
degeneration)

39
Q

most common organism in deformed valves

A

Strept. viridans

40
Q

acute IE

A 
valves were previously normal 
staph aureus involved (highly virulent)
rapid progression 
lots of destruction
difficult to cure and surgery is needed
41
Q

subacute IE

A

previously deformed valves
less virulent like viridans streptococci
insidious speed.. not so much destruction
antibiotics are helpful; no surgery needed

42
Q

morphology of IE

A

Most common valves involved- mitral and
aortic valves

IV drug abuse = tricuspid valve

Classic hallmark of IE:
Vegetations on heart valves ➔ friable, bulky, potentially
destructive lesions containing fibrin, inflammatory cells, and bacteria or other organisms

can have a ring abscess

43
Q

vegetations in subacute endocarditis

A

Associated with less valvular destruction

Microscopically:
• Granulation tissue at their bases (indicative of healing)

With time, fibrosis, calcification

Chronic inflammatory infiltrate

44
Q

clinical features of subacute endocarditis (infective)

A

fever
clubbing of the fingers
splinter hemorrhage’s under nailbeds
systematic embolization

osler nodes (tender subcutaneous nodules) 
janeway lesions (nontender macule on palms and soles) 
roth spots (retinal hemorrhages)
45
Q

acute bacterial endocarditis

A

High grade fever with chills
New cardiac murmur
Features of septicemia

46
Q

subacute bacterial endocarditis

A

Low grade fever; malaise
Changing cardiac murmurs
Weight loss and splenomegaly

47
Q

diagnosis of subacute/acute endocarditis (infective)

A

Modified Duke criteria

Repeated blood cultures (for aerobic and anaerobic
organisms)

Echocardiography

48
Q

Non- Bacterial Thrombotic Endocarditis

epi? patho? comp?

A

presence of sterile thrombi on the leaflets of previously normal valves

epi:
seen in debilitated patients (cancer)

patho: 
Associated with endothelial abnormalities, 
 hypercoagulable states, adenocarcinomas
Usually asymptomatic
not really known

complications: emboli and IE

49
Q

Non- Bacterial Thrombotic Endocarditis

histo? gross?

A

gross:
most commonly seen in the mitral valve
multiple small nodules
vegetations are non-invasive

micro:
Nodules composed of eosinophilic material (fibrin) and a delicate layer of aggregated platelets
No inflammation or fibrosis
Loosely attached to the cusps

50
Q

Libman Sacks Endocarditis (LSE)

Patho?

A

small (1 to 4 mm), sterile vegetations in the setting of systemic lupus erythematosus (SLE)

patho:
Consequence of immune complex deposition + activation of complement and recruitment of Fc-receptor–bearing cells

histo:
Intense valvulitis and fibrinoid necrosis of the valve substance

location:
Vegetations can occur anywhere on the valve surface, on the chordae, or even on the atrial or ventricular endocardium

51
Q

Prosthetic Valve Disease

A 
mechanical valves: 
Thrombo-embolism
Life-long anticoagulation (hemorrhage)
Infective endocarditis
RBC destruction (hemolysis)
Inadequate healing → Paravalvular leak

Tissue valves (Bioprostheses):

Complications
less durable: matrix deterioration, rigidity, calcification→ stenosis, can perforate
Infective endocarditis
Inadequate healing → Paravalvular leak

52
Q

RHD vs IE

A

RHD = small, warty vegetations along the lines of
closure of the valve leaflets

IE = by large, irregular masses on the valve cusps that can extend onto the chordae

53
Q

NBTE vs LSE

A

NBTE = exhibits small, bland vegetations, usually attached at the line of closure

LSE = small- or medium-sized vegetations on either or both sides of the valve leaflets

CRS (16 decks)

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