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
morphology of RHD
deforming fibrotic valvular disease favors the mitral valve leading to mitral stenosis Chronic rheumatic heart disease = mostly valvular; fibrosis and calcification
26
Acute rheumatic fever
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
Chronic mitral valvulitis
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
Chronic aortic valvulitis
Cusps are thickened, firm and adherent to each other Valve orifice is reduced to rigid, triangular channel
29
clinical features of RF
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
complications of RF
Valvulitis murmurs Left atrium progressively dilates → mural thrombi → embolus congestive heart failure Arrhythmias Infective endocarditis
31
diagnoses of RF
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
Calcific Aortic Stenosis
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
gross of CAS
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
micro of CAS
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
clinical features of CAS
Angina pectoris – increased requirement of hypertrophied myocardium Syncope – poor perfusion of the brain Death usually occurs due to congestive heart failure or arrhythmias
36
Myxomatous Mitral Valve
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
clinical features of MMV
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
gross and micro for MMV
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
most common organism in deformed valves
Strept. viridans
40
acute IE
``` valves were previously normal staph aureus involved (highly virulent) rapid progression lots of destruction difficult to cure and surgery is needed ```
41
subacute IE
previously deformed valves less virulent like viridans streptococci insidious speed.. not so much destruction antibiotics are helpful; no surgery needed
42
morphology of IE
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
vegetations in subacute endocarditis
Associated with less valvular destruction Microscopically: • Granulation tissue at their bases (indicative of healing) With time, fibrosis, calcification Chronic inflammatory infiltrate
44
clinical features of subacute endocarditis (infective)
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
acute bacterial endocarditis
High grade fever with chills New cardiac murmur Features of septicemia
46
subacute bacterial endocarditis
Low grade fever; malaise Changing cardiac murmurs Weight loss and splenomegaly
47
diagnosis of subacute/acute endocarditis (infective)
Modified Duke criteria Repeated blood cultures (for aerobic and anaerobic organisms) Echocardiography
48
Non- Bacterial Thrombotic Endocarditis | epi? patho? comp?
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
Non- Bacterial Thrombotic Endocarditis | histo? gross?
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
Libman Sacks Endocarditis (LSE) | Patho?
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
Prosthetic Valve Disease
``` 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
RHD vs IE
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
NBTE vs LSE
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