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89 Cards in this Set

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What is the function of normal cardiac valves?
Maintain unidirectional flow
What lines normal valves?
Endothelium
What kind of valves separate the ventricles and outflow tracts?
Semilunar Valves: Aortic and Pulmonic
What kind of valves separate the atrium and ventricles?
AV Valves: Mitral and Tricuspid
What do the AV valves attach to?
Free margins attach to ventricular walls via chordae tendinae and papillary muscles
What are the types of valvular heart disease?
- Stenosis: failure to open completely
- Insufficiency: failure to close properly, may lead to functional regurgitation
In general, what kind of processes cause stenosis?
Chronic process affecting a valve cusp; causes a failure of valve opening
In general, what kind of processes cause insufficiency?
- Valvular incompetence d/t disruption of supporting structures (eg, aortic root dilation or LV dilation)
- Intrinsic disease of valve cusps
- Causes failure to close completely
What are some valvular problems that can cause stenosis or insufficiency to the aortic valve?
- Congenital: bicuspid aortic valve (most common)
- Calcification: in old age ("senile"), causes stenosis
- Dilation of Aorta: related to HTN and aging, causes insufficiency
What are some valvular problems that can cause stenosis or insufficiency to the mitral valve?
- Rheumatic Heart Disease: causes stenosis
- Myxomatous degeneration: causes insufficiency
Which is more common: stenoses or insufficiencies?
Stenoses >> Insufficiencies
How can calcification affect cardiac valves? What valves are affected by calcification?
Dystrophic calcification:
- Damage of wear and tear complicated by deposits of calcium phosphate
- Eg, calcific aortic stenosis, mitral annular calcification
What are the risk factors for Calcific Valvular Disease?
- Hyperlipidemia
- Hypertension
- Inflammation
How does Calcific Valvular Disease compare to Atherosclerosis?
They are distinct diseases, but they share some risk factors:
- Hyperlipidemia
- Hypertension
- Inflammation
What is the most common of all valvular abnormalities?
Calcific Aortic Stenosis (AS)
Calcific Aortic Stenosis (AS)
When and to whom does Calcific Aortic Stenosis (AS) most commonly occur?
* In 40s-50s: bicuspid, unicuspid aortic valves (1-2% of population, associated w/ Notch mutation)
- Also in 70s-80s: normal valves (age-related)
* In 40s-50s: bicuspid, unicuspid aortic valves (1-2% of population, associated w/ Notch mutation)
- Also in 70s-80s: normal valves (age-related)
What mutation is associated with developing Calcific Aortic Stenosis (AS)? At what point in life?
Notch mutation; 40s-50s
Notch mutation; 40s-50s
What are the clinical effects of having Calcific Aortic Stenosis (AS)?
- Increased pressure in LV → Hypertrophy
- Angina, ischemia, and CHF
- Syncope
- Increased pressure in LV → Hypertrophy
- Angina, ischemia, and CHF
- Syncope
What is the life expectation for Calcific Aortic Stenosis (AS)?
If they have CHF, 50% will die within two years
If they have CHF, 50% will die within two years
Morphologically, what happens in Calcific Aortic Stenosis (AS)?
- Heaped up calcified masses in cusps, primarily at BASES
- Free cuspal edges NOT involved
- No fusion of commissures
- Heaped up calcified masses in cusps, primarily at BASES
- Free cuspal edges NOT involved
- No fusion of commissures
How do you treat Calcific Aortic Stenosis (AS)?
How do you treat Calcific Aortic Stenosis (AS)?
Valve Replacement
Valve Replacement
How does the type of aortic valve affect the likelihood of getting Calcific Aortic Stenosis (AS)?
- Possible w/ tricuspid aortic valve (normal)
- Much more likely with a bicuspid aortic valve (congenital defect)
- Possible w/ tricuspid aortic valve (normal)
- Much more likely with a bicuspid aortic valve (congenital defect)
What is it called when there is calcification of the mitral valve?
Mitral Annular Calcification
Morphologically, what happens in Mitral Annular Calcification?
Degenerative calcific deposits on fibrous ring, at BASE of valve
Degenerative calcific deposits on fibrous ring, at BASE of valve
When and to whom does Mitral Annular Calcification most commonly occur?
- Women >60 years old
- Increased in patients w/ myxomatous valves or elevated LV pressure
- Women >60 years old
- Increased in patients w/ myxomatous valves or elevated LV pressure
Functionally, how does Mitral Annular Calcification affect a patient?
- Usually does not affect valve function
- Calcifications are sites for thrombi / infection
What is it called when the leaflets of the mitral valve become enlarged, hooded, redundant, or floppy (myxoid)?
Myxomatous Degeneration of Mitral Valve (Prolapse)
Myxomatous Degeneration of Mitral Valve (Prolapse)
What does myxoid mean as it refers to Myxomatous Degeneration of Mitral Valve (Prolapse)?
Deposition of mucoid material in valve
(blue = collagen in trichrome stain, indicates lots of ground substance)
Deposition of mucoid material in valve
(blue = collagen in trichrome stain, indicates lots of ground substance)
When and to whom does Myxomatous Degeneration of Mitral Valve (Prolapse) most commonly occur?
- Very common (3% of adults)
- Usually affects young women
- Very common (3% of adults)
- Usually affects young women
Morphologically, what happens in Myxomatous Degeneration of Mitral Valve (Prolapse)?
- One or both leaflets are enlarged, hooded, redundant, or floppy (myxoid)
- Prolapses or balloons back into LA during systole
- One or both leaflets are enlarged, hooded, redundant, or floppy (myxoid)
- Prolapses or balloons back into LA during systole
Functionally and clinically, how does Myxomatous Degeneration of Mitral Valve (Prolapse) affect a patient?
- Usually no serious complications
- Hear mid-systolic click

- May cause regurgitation: late systolic or holosystolic murmur
- Usually no serious complications
- Hear mid-systolic click

- May cause regurgitation: late systolic or holosystolic murmur
What is the cause of Myxomatous Degeneration of Mitral Valve (Prolapse)?
- Unknown
- Could be a developmental anomaly of CT
- Feature of Marfan syndrome (fibrillin gene mutation) and other hereditary disorders
What are some possible complications of Myxomatous Degeneration of Mitral Valve (Prolapse)?
All uncommon:
- Infectious endocarditis
- Mitral insufficiency
- Thrombi on atrial surfaces leading to stroke or other systemic infarcts d/t emobli
- Arrhythmias → sudden death (most often in advanced mitral insufficiency)
What can cause thrombi to form in the LA?
Prolapse of leaflets of mitral valve causes them to rub on walls of atrium, which is irritating and can lead to thrombus formation
Prolapse of leaflets of mitral valve causes them to rub on walls of atrium, which is irritating and can lead to thrombus formation
How does Rheumatic Fever affect the heart valves?
May cause Mitral Stenosis
What is and causes Rheumatic Fever?
- Acute, immunologically mediated, multi-system, inflammatory disease w/ major cardiac manifestations
- Hypersensitivity reaction induced by Group A Streptococcal (pyogenes) pharyngitis
- Antibodies against M protein cross react w/ glycoprotein antigens in heart, joints, and other tissues
What morphological features are seen in Rheumatic Fever?
- Widely distributed inflammatory lesions
- Pancarditis
- Aschoff Body (classic lesion)
What are the features of Pancarditis seen in Rheumatic Fever?
- Pericarditis
- Myocarditis w/ Aschoff bodies**
- Endocardium and L-sided valves w/ Fibrinoid Necrosis and verrucae
- Subendocardial (MacCallum) plaques: irregular fibrous thickening of endocardium
- Pericarditis
- Myocarditis w/ Aschoff bodies**
- Endocardium and L-sided valves w/ Fibrinoid Necrosis and verrucae
- Subendocardial (MacCallum) plaques: irregular fibrous thickening of endocardium
What is the classic lesion of Rheumatic Fever?
Aschoff Body: 
- Foci of swollen eosinophilic collagen
- Surrounded by T cells, plasma cells, and macrophages
- Macrophages are plump - aka Anitschkow cells or caterpillar cells
Aschoff Body:
- Foci of swollen eosinophilic collagen
- Surrounded by T cells, plasma cells, and macrophages
- Macrophages are plump - aka Anitschkow cells or caterpillar cells
What is the special name for macrophages in Aschoff Bodies? When are these seen?
- Anitschkow cells (aka caterpillar cells)
- Seen in Rheumatic Fever
- Anitschkow cells (aka caterpillar cells)
- Seen in Rheumatic Fever
What happens to the endocardium in Rheumatic Fever?
Fibrinoid necrosis and verrucae along lines of closure of valve cusps
Fibrinoid necrosis and verrucae along lines of closure of valve cusps
What are the complications due to inflammation and fibrosis in Rheumatic Fever?
- Thickened valve leaflets
- Fusion of commissures (fishmouth or buttonhole deformities)
- Fusion / thickening of chordae tendinae
* Leads to Mitral Stenosis *
- Thickened valve leaflets
- Fusion of commissures (fishmouth or buttonhole deformities)
- Fusion / thickening of chordae tendinae
* Leads to Mitral Stenosis *
What are the complications due to Mitral Stenosis in Rheumatic Fever?
- LA dilation (sometimes thrombus formation)
- Reduced CO (mechanical obstruction prevents filling of LV)
- Pulmonary congestion, eventually RV hypertrophy, and R-sided heart failure
Which valves are affected by Rheumatic Fever and at what incidence?
- Mitral valve alone: 65-70%
- Mitral and aortic valves: 25%
- Tricuspid valve less often
- Pulmonary valve rare
Is there a genetic component to Rheumatic Fever?
Genetic susceptibility varies by individual; not all w/ Group A Strep infections develop rheumatic fever (estimate is 3%)
How do you diagnose Rheumatic Fever?
JONES Criteria:

- Preceding Group A Strep infection + 2 major manifestations OR 1 major and 2 minor

Major:
- Migratory polyarthritis (large joints)
- Carditis (pericardial friction rub, weak heart sounds, tachycardia, arrhythmia)
- Subcutaneous nodules (rare, extensor surfaces of joints)
- Erythema marginatum of skin (rare)
- Sydenham corea (involuntary, purposeless, rapid movements)

Minor (non-specific):
- Fever
- Arthralgia (joint pain)
- Elevated acute-phase reactants
What organism is responsible for causing Rheumatic Fever?
Group A (β-hemolytic) Streptococcus
Who is most likely to get Rheumatic Fever?
Children between 5 - 15 years (because they are more likely to have a Strep infxn)
How do you diagnose acute Rheumatic Fever?
- ASO (Anti-Streptolysin O) titers
- Antibodies to DNase B

- ASO and DNase B are proteins produced by Group A Strep
How long after a Group A Strep infection, does Acute Rheumatic Fever occur? Chronic Rheumatic Fever?
- Acute RF: 1-4 weeks after infection
- Chronic RF: years or decades after initial episode
What is the prognosis for Acute Rheumatic Fever?
- Good for primary attack
- Increased vulnerability to reactivation at a later date
What is the sign of Chronic Rheumatic Fever? What is the treatment?
- Valvular disease (valvulitis)
- Requires surgical repair of valves to improve outlook
What are the two types of Infective Endocarditis?
- Acute
- Subacute
- Acute
- Subacute
What kind of organism causes Acute Infective Endocarditis? How severe are the lesions? Treatment?
- Highly virulent organism
- Usually occurs on normal valve w/ 50% mortality
- Causes necrotizing ulcerative invasive infection
- Requires surgery
- Highly virulent organism
- Usually occurs on normal valve w/ 50% mortality
- Causes necrotizing ulcerative invasive infection
- Requires surgery
What kind of organism causes Sub-acute Infective Endocarditis? How severe are the lesions? Treatment?
- Low virulence organism (Strep viridans)
- Usually occurs on deformed valve (already screwed up so don't need much virulence)
- Less destructive lesions
- Responds to antibiotics
- Low virulence organism (Strep viridans)
- Usually occurs on deformed valve (already screwed up so don't need much virulence)
- Less destructive lesions
- Responds to antibiotics
In whom is Infective Endocarditis more common?
Patients w/ CV abnormalities: 
- RHD (Rhematic Fever Disease)
- Myxomatous Mitral Valve
- Calcific Valvular Stenosis
- Artificial Valves

Host Factors:
- Neutropenia
- Immunodeficiency
- Malignancy
- Diabetes
- Alcoholics
- IV drug users
Patients w/ CV abnormalities:
- RHD (Rhematic Fever Disease)
- Myxomatous Mitral Valve
- Calcific Valvular Stenosis
- Artificial Valves

Host Factors:
- Neutropenia
- Immunodeficiency
- Malignancy
- Diabetes
- Alcoholics
- IV drug users
What are some specific causes of Infective Endocarditis?
- Strep viridans (50-60% of cases w/ infected, deformed valve)
- Staph aureus (10-20% of cases overall; most common in IVDA)
- Commensal organisms of mouth
- Staph epidermidis in prosthetic valves
- Strep viridans (50-60% of cases w/ infected, deformed valve)
- Staph aureus (10-20% of cases overall; most common in IVDA)
- Commensal organisms of mouth
- Staph epidermidis in prosthetic valves
Which kind of valve problem is characterized by:
- Friable, large bulky destructive vegetations
- Fibrin, inflammatory cells and bacteria
- Eroded myocardium → ring abscesses

Which valves?
Acute and Subacute Endocarditis
- Mitral and aortic valves most common
- Tricuspid valve in IV drug users
Acute and Subacute Endocarditis
- Mitral and aortic valves most common
- Tricuspid valve in IV drug users
What are the morphological characteristics that distinguish acute from subacute endocarditis?
- Less valvular destruction
- Fibrosis and granulation tissue reaction at base of vegetation
- Less valvular destruction
- Fibrosis and granulation tissue reaction at base of vegetation
What valve is affected / damaged in infective endocarditis when patients are IV drug users? Why?
Tricuspid valve - this is the first valve that the drug comes across when the drugs are injected in the venous system
What are the histological features of Infective Endocarditis?
- Clusters of bacteria (dark blue)
- Abundant acute inflammation (neutrophils / pus)
- Clusters of bacteria (dark blue)
- Abundant acute inflammation (neutrophils / pus)
How do you diagnose Bacterial Endocarditis?
Duke Criteria:
- 2 major criteria OR
- 1 major and 3 minor criteria OR
- 5 minor criteria
What are the major criteria for Bacterial Endocarditis / Duke Criteria?
- Positive blood cultures
- Echo findings (valve-related mass / abscess)
- New valvular regurgitation (new murmur on auscultation)

(Need two major criteria, one major and three minor criteria, or five minor criteria)
What are the minor criteria for Bacterial Endocarditis / Duke Criteria?
- Predisposing heart lesion or IVDA
- Fever
- Uncommon findings from septic emboli (petechiae, splinter hemorrhages, Janeway lesions (palms, soles hemorrhagic lesions), Osler nodes (digits), Roth spots (retina))

(Need two major criteria, one major and three minor criteria, or five minor criteria)
What are the possible complications of Bacterial Endocarditis?
- Valvular insufficiency or stenosis (possible heart failure)
- Myocardial abscesses and possible perforation
- Vegetations could break-off → embolism (eg brain, kidneys, spleen, etc)
- Glomerulonephritis (immune complexes)
How do you treat Bacterial Endocarditis?
- IV antibiotics
- Valve replacement if necessary
- Prophylactic antibiotics after valve damage
What are the types of Non-Infective Vegetations?
- Non-bacterial thrombotic endocarditis
- Libman-Sacks endocarditis
What is the mechanism of non-bacterial thrombotic endocarditis?
- Depositions of small masses of fibrin, platelets, and other blood products on leaflets
- Often in debilitated patients (eg, cancer, sepsis)
- May result in emboli and infarcts
- Depositions of small masses of fibrin, platelets, and other blood products on leaflets
- Often in debilitated patients (eg, cancer, sepsis)
- May result in emboli and infarcts
What is the etiology of non-bacterial thrombotic endocarditis?
- Hyper-coaguable states
- Associated w/ mucin-producing adenocarcinomas (DVTs and Trousseau syndrome)
- Endocardial trauma - Swan-Ganz catheter
- Hyper-coaguable states
- Associated w/ mucin-producing adenocarcinomas (DVTs and Trousseau syndrome)
- Endocardial trauma - Swan-Ganz catheter
What are the morphological characteristics of non-bacterial thrombotic endocarditis?
- Sterile
- Non-destructive
- Non-inflammatory
- Small (1-5 mm)
- Along lines of closure
- Sterile
- Non-destructive
- Non-inflammatory
- Small (1-5 mm)
- Along lines of closure
What is the etiology of Libman-Sacks Endocarditis?
- Systemic Lupus Erythematosus (mitral and tricuspid valves involved; anti-phospholipid antibodies present)
- Primary Anti-Phospholipid Syndrome
- Systemic Lupus Erythematosus (mitral and tricuspid valves involved; anti-phospholipid antibodies present)
- Primary Anti-Phospholipid Syndrome
What are the morphological characteristics of Libman-Sacks Endocarditis?
- Either or both sides of leaflets
- May also be on endocardium
- 1-4 mm verrucae w/ fibrinous material 
- May have intense inflammation
- Either or both sides of leaflets
- May also be on endocardium
- 1-4 mm verrucae w/ fibrinous material
- May have intense inflammation
What is this an example of?
What is this an example of?
Rheumatic Heart Disease
Rheumatic Heart Disease
What is this an example of?
What is this an example of?
Infected Endocarditis
Infected Endocarditis
What is this an example of?
What is this an example of?
Non-Bacterial Thrombotic endocarditis
Non-Bacterial Thrombotic endocarditis
What is this an example of?
What is this an example of?
Libman-Sacks Endocarditis
Libman-Sacks Endocarditis
What are the features of Carcinoid Syndrome?
- Produces many mediators (serotonin, kallikrein, bradykinin, histamine, prostaglandins, tachykinins)
- Symptoms: flushing, cramps, nausea, vomiting, diarrhea
What mediators are released by Carcinoid Tumors?
- Serotonin
- Kalliekrein
- Bradykinin
- Histamine
- Prostaglandins
- Tachykinin
What are the symptoms of Carcinoid Syndrome?
- 50% have plaque-like fibrosis, R-heart endocardium and valves
- Flushing
- Cramps
- Nausea
- Vomiting
- Diarrhea
Why are there no symptoms at first w/ Carcinoid Syndrome?
Serotonin and bradykinin (two of the chemical mediators) are inactivated by MAO in pulmonary vasculature AND also inactivated by passage through functioning liver
On which side of the heart are the plaque-like fibroses more commonly found in Carcinoid Syndrome? Why?
- 50% of patients w/ Carcinoid Syndrome have plaque-like fibrosis of R-heart endocardium and valves
- Usually occurs on R side because o finactivation of mediators by MAO in lung
What is the cause of Carcinoid Syndrome?
- Unknown
- Related to endothelial injury caused by vasoactive agents
In what kind of patients does Carcinoid Syndrome occur in?
- Patients w/ GI carcinoids that spread to liver (hepatic mets)
- Patients w/ carcinoids outside of portal system of venous drainage
Why do patients w/ GI carcinoids w/ hepatic mets more likely to have carcinoid syndrome / heart disease?
- Normally, bioactive proteins are inactivated by liver
- With mets to liver, secretion occurs directly into hepatic vein and reaches R-side of heart
Why do patients w/ carcinoids outside of portal system of venous drainage get carcinoid syndrome / heart disease? Examples?
- Direct secretion of mediators into systemic circulation
- Eg, carcinoids arising in ovary, testes

- Very high blood levels may prevent complete inactivation by lung MAO
- Eg, primary lung carcinoid
- Direct secretion of mediators into systemic circulation
- Eg, carcinoids arising in ovary, testes

- Very high blood levels may prevent complete inactivation by lung MAO
- Eg, primary lung carcinoid
What are the characteristics of the endocardial plaque-like thickenings seen in carcinoid heart disease?
- Smooth muscle cells and collagen embedded in mucopolysaccharide matrix
- Tricuspid (insufficiency) and pulmonic (stenosis) valves equally affected
- Smooth muscle cells and collagen embedded in mucopolysaccharide matrix
- Tricuspid (insufficiency) and pulmonic (stenosis) valves equally affected
Which valves are affected by Carcinoid Syndrome?
- Tricuspid and pulmonic valves equally
- Usually tricuspid insufficiency or pulmonic stenosis
What are the potential complications of an artificial, MECHANICAL heart valve?
- Thromboembolic complications
- Infective endocarditis
- Thromboembolic complications
- Infective endocarditis
What are the potential complications of an artificial, BIOPROSTHESIS heart valve?
- Structural deterioration
- 50% need a replacement within 15 years
- Structural deterioration
- 50% need a replacement within 15 years