Valvular and Congenital Heart Disease - Nichols and Newman Flashcards Preview

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Flashcards in Valvular and Congenital Heart Disease - Nichols and Newman Deck (48)
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What are the two forms of cardiac adaptation to valvular disease? How is this different in acute scenarios?

Concentric hypertrophy: pressure overload = STENOSIS (+ HTN) 

1. INC thickness (thich walls), but normal volume -> LV hypertrophy 

Eccentric hypertrophy: volume overload = REGURGITATION 

1. INC dilation of chamber (more volume + thin walls) -> INC output (Starling) 

Acute: no time to adapt, so pt presents severely ill 

1. Murmur heard, but no concentric or eccentric hypertrophy 

- INC pressure change with DEC structural changes in acute OR DEC pressure change with INC structural changes in chronic



Mitral valve stenosis

- Rheumatic fever 

- INC pressure behind mitral (stenosed) valve: concentric hypertrophy + dilation of LA (THROMBI), pulmonary HTN (atherosclerosis), concentric hypertrophy of RV

Presentation: shortness of breath, alveolar fluid w/fibrinous material, hemoptysis (if chronic), right heart failure, afib (stroke), dysphagia (atrium compresses back on esophagus) 

- Murmur: diastolic 


Mitral valve regurgitation

Mitral valve prolapse, LV dilation (left sided heart failure dilates mitral valve ring), rheumatic fever 

1. Prolapse: leaflets replaced by myxomatous (spongy) tissue; eccentric hypertrophy (dilation) of LA

Presentation: can be asymptomatic with murmur, sudden rise in atrial pressure, INC preload (from atrium) + DEC afterload (from venting) = INC stroke volume 

- Acute = no change in RA volume, INC pulmonary capillary wedge pressure (lg pressure buildup) 

Murmur: pansystolic 


What are the epi, patho and sign of mitral valve prolapse?

- Epi: most common valvular disease (about 2% of US population); primary or secondary 

- Pathogenesis: primary form a genetic defect in connective tissue; secondary form injury 

- Gross: redundant, billowing, ballooning, hooding, floppy leaflets, +/- elongated chordae tendineae (that can rupture) 

- Microscopic: sometimes degeneration of and attenuation of outer zona fibrosa, and expanded myxomatous inner zona spongiosa (often normal) 

- Sign: mid-systolic click  


What are 1, 2, and 3?

- Normal mitral valve 

1. Zona atrialis (sometimes also called zona fibrosa) 

2. Zona spongiosa 

3. Zona fibrosa 


What do you see?

Expanded, myxomatous zona spongiosa (e.g., in mitral valve prolapse)


What are the epi and patho of Libman-Sacks endocarditis?

- Epi: lupus 

Gross: small-medium verrucous, berry-like or flat vegetations, commonly on multiple valves (on either or both sides) 

Microscopic: necrotic debris, fibrinoid material, degenerating leukocytes, fibroblasts, and hematoxylin bodies 

- Clinically important fact: rarely embolizes


How is endocarditis related to valve pressure?

- Incidence of infection, marantic endocarditis, and rheumatic disease on a valve correlate with resting pressure on the closed valve: 

1. Mitral: 116 mm Hg 

2. Aortic: 72 mm Hg

3. Tricuspid: 24 mm Hg 

4. Pulmonic: 5 mm Hg 


Why is it really important to "catch" infective endocarditis?

100% fatal if undiagnosed/untreated, but only 20% fatal if diagnosed/treated appropriately (IV AB's, sx)


What is the pathogenesis of infective endocarditis (4)?

- Most commonly of the valves, w/vegetations -> friable masses of infecting organisms and blood clot 

1. Valvular endo injury 

2. Platelet + fibrin deposition 

3. Microbial seeding 

4. Microbial multiplication 

- NOTE: valves may be "grossly normal," but steps 1 and 2 precede 3 and 4 


What valves, etiologic agents, and portals of entry are generally involved in infective endocarditis?

- Valves: mitral > mitral + aortic = aortic > tricuspid (only 1% pulmonic) 

- Etiologic agents: staph aureus (acute) and strep viridans (sub-acute; followed by enterococcus) 



What do you see? Why is this important?

- Central venous catheterization 

- Portal of entry of bugs in infective endocarditis 


What do you see? Why is this important?

- Mouth with gingivitis, brushing teeth, chewing, dental procedures -> all portals of entry for bugs in infective endocarditis


What is the gross pathology of infective endocarditis?

Vegetations: large (up to 3cm), friable, single or multiple, tan, grey, or red brown 

1. Usually on line of valve closure (atrial side of AV valves, and ventricular side of semilunar valves) 

The larger a vegetation, the more likely it is infective 

- Destructive, and may cause: perforation of valve, adjacent abscess, fibrotic scarring, or calcification 

- Infected (septic) emboli from endocarditis commonly go to kidney, heart, spleen, brain 


What are the microscopic pathology and common symptoms/signs of infective endocarditis?

- Microscopic pathology:

1. Fibrin, platelets, masses of organisms, +/- necrosis, +/- neutrophils 

2. Later: +/- lymphos, macros, fibroblasts, fibrosis 

Symptoms: fever, chills, weakness, dyspnea

Signs: fever, heart murmur, splenomegaly, petechiae 



What do you see?

- Osler nodes in fingers: tender to the touch

- Sign of infective endocarditis 


What do you see?

- Splinter hemorrhage under fingernail (aka, subungual splinter hemorrhages)

- Sign for infective endocarditis, but not specific -> much more commonly due to trauma 


What do you see?

- Janeway lesions: hemorrhages on palms or soles (5%)

- Sign of infective endocarditis 


What do you see?

- Roth spots: retinal hemorrhages due to infective endocarditis 



What are the common lab findings and complications associated with infective endocarditis?

- Lab findings: high ESR, anemia, proteinuria (may also have Rheumatoid factor or hematuria)

Complications: heart failure, septic emboli (to kidneys, heart, spleen, brain)


What tests/procedures are helpful in diagnosing infective endocarditis? Which of these is essential?

- Transthoracic echocardiography: 60% sensitivity for vegetations 

1. Transesophageal echocardiography: >90% sensitive for vegetations 

2. Absence of vegetations on echo does not exclude endocarditis dx 

- Murmur + echo + vegetations does NOT = dx -> need BLOOD CULTURES (essential for making specific dx to guide AB therapy)

1. Continuous low-grade bacteremia characteristic of infective endocarditis: 3 sites cultures, 30-60min apart before starting AB's

2. Alert lab endocarditis suspected b/c some bac that cause endocarditis fastidious, or slow-growing, or both, so lab will use special culture media, and hold the cultures longer 


What are the pluses and minuses of surgical valve replacement?

- Can be life-saving, esp. w/acute disease 

- Immediate relief w/chronic disease, but replaces one chronic disease w/another -> mechanical valves require lifelong anti-coagulation 

- Bioprostheses deteriorate, with structural failure in up to 50% by 10 years, accelerating after that 

- Complications include: leak, thrombosis, embolism, bleeding, and endocarditis 

- Critical to make sure patients understand these risks/complications from the outset 


What do you see?

- Infective endocarditis: remember, fever + heart murmur = infective endocarditis (until proven otherwise)

- Mitral valve identifiable by chordae tendineae going to both leaflets (not aortic valve)

- Very large, extensive vegetations involving about 80% of leaflets (bigger the vegetations, the more likely they are infective) 

- NOT mitral valve prolapse b/c many cases have valves that are microscopically normal; it is just too big.  Even those with myxomatous change tend to have a normal surface -> inner zona spongiosa expanded, while outer zona fibrosa may be thinned, but is otherwise normal

- Size and extent of these very large, very extensive vegetations goes against marantic endocarditis


What is a probe-patent foramen ovale (often shortened to foramen ovale)?

- About 20% of ppl have membranous flap of tissue over foramen ovale that can be opened by pushing a probe on it

- Normally, higher pressures on left side of heart keep flap in place, maintaining separateness of left and right heart circulations

1. If pressures on right side ever rise to level higher than left, can act like probe and push open foraman ovale b/t right and left atria, letting deoxygenated blood skip passing through lungs 


What are the 4 components of tetralogy of fallot?

- Ventricular septal defect (VSD) 

- Overriding aorta 

- Pulmonic stenosis 

- RV hypertrophy 


Which congenital heart diseases are cyanotic and non-cyanotic?

- Cyanotic (all start with T, except hypoplastic left heart): tetralogy of fallot, transposition of the great vessels, truncus arteriosus, tricuspid atresia, total anomalous pulmonary venous return 

- Non-cyanotic: ventricular septal defect, atrial septal defect, patent ductus arteriosus, pulmonic stenosis, aortic stenosis 


What is the most specific diagnosis you can make from this image?

- Zone of healing tissue with bluish ground substance and a few lymphs and macs 

- Zone of basophilic debris (nuclear dust) 

- Outer layer of condensed fibrin with scattered basophilic debris 

- Central outer area of little blue dots way too small to be lymphocyte nuclei, just the right size for bacterial cocci (all bacteria are blue in H&E)

Infective endocarditis, w/bacterial cocci: probably staph or strep, since staphy cause majority of acute bac endocarditis and strep cause majority of subacute bac endocarditis


This gross pathology most likely represents...?

- Acute rheumatic valvulitis: tiny (1-2mm) verrucous (wart-like) vegetations lined up on line of valve closure

- Differential:

1. Vegetations of infective endocarditis usually much larger 

2. Vegetations of Libman-Sacks usually bigger than this (intermediate size) and rarely this numerous, nor are there features to suggest it (i.e., being on both sides of valve) 

3. Marantic a strong consideration, but so many so tiny vegetations that acute rheumatic valvulitis is just slightly more likely


Briefly describe each of these.

- Rheumatic heart disease (RHD): rheumatic fever phase marked by small, warty vegetations along lines of closure of leaflets 

- Infective endocarditis (IE): large, irregular masses on valve cusps that extend onto chordae 

- Nonbacterial thrombotic endocarditis (NBTE): typically exhibits small, bland vegetations, usually attached at line of closure (one or many may be present)

- Libman-Sacks endocarditis (LSE): small, or medium-sized vegetations on either or both sides of valve leaflets 


88-y/o hispanic male dies of a stroke, and his heart has the features in this image. The best diagnosis for this cardiac condition is...?

Infective endocarditis because it is destructive: can eat a hole in a heart valve