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CVS: Valvular Heart Disease Flashcards

1
Q

Describe the normal mitral valve.

A

Left atrium - left ventricle

Two leaflets with chordae tendinae attached to papillary muscles

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2
Q

Describe the normal tricuspid valve.

A

Right atrium - right ventricle
Three leaflets
Chordae tendinae attached to papillary muscles

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3
Q

Describe the normal aortic valve.

A

Left ventricle to aorta
Semilunar valve
3 cusps (posterior)

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4
Q

Describe the normal pulmonary valve

A

Right ventricle - pulmonary artery

Semilunar valve, 3 cusps (anterior)

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5
Q

List the valve pathology types.

A

Stenosis
Regurgitation
Both stenosis and regurgitation
Functional

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6
Q

Define stenosis of valve pathology.

A

Narrowing.

Failure of a valve to open completely leading to obstruction to blood flow (pressure overload)

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7
Q

Define regurgitation of valve pathology.

A

Incompetence

Failure of a valve to close completely leading to reversed/retrograde blood flow (volume overload).

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8
Q

Define both stenosis and regurgitation in valve pathology.

A

Both pressure and volume overload

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9
Q

Define functional issues in valve pathology.

A

Example: dilation of the right or left ventricle can pull on the papillary muscles down and outwards, preventing proper closure of structurally normal valves.

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10
Q

What murmur does mitral stenosis produce?

A

Diastolic murmur (trouble moving blood from atria to ventricles)

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11
Q

What murmur does mitral regurgitation produce?

A

Systolic murmur

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12
Q

What are the complications of valve pathology due to volume and pressure overload?

A

Chamber hypertrophy (with pressure overload), later failure and dilation
Chamber dilation (with volume overload)
Atrial fibrillation (AF) secondary to atrial dilation
AF predisposes thrombosis and embolism
Leads to HF
Susceptibility to IE

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13
Q

What are possible causes of valve disease?

A 
Congenital e.g. aortic stenosis 
Degenerative (aging) - calcific aortic stenosis 
Hereditary - mitral valve prolapse 
Immunological - RF 
Infective - IE
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14
Q

What is acute RF?

A

Acute, immunologically mediated, multisystem inflammatory disease that occurs a few weeks following a Group A Streptococcal (GAS) pharyngitis

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15
Q

How does a GAS infection cause RF?

A

Cross reactivity to group A streptococci with self antigens in the heart - molecular mimicry (forms antibodies which attack the heart)

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16
Q

What is the cardiac morphology of RF?

A

Pancarditis (inflammation of all 3 layers of the heart)

- endocarditis, myocarditis, pericarditis

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17
Q

How does RHD (chronic) occur?

A

Active phase of RF may progress over time to become chronic rheumatic disease.

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18
Q

What characterizes RHD?

A

Permanent valve deformities due to healing by fibrosis after RF

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19
Q

Which valve is most commonly affected by RHD?

A

Mitral valve with mitral stenosis
Aortic valve can be affected as well
Valve deformities lead to stenosis/regurgitation

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20
Q

Where is RF and RHD in high incidence?

A

Amongst Maori and Pasifika mostly in north island
Children aged 5-15
High frequency of recurrence unless prophylactic antibiotics given

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21
Q

What are the risk factors for rheumatic fever?

A 
Crowded housing conditions
Cold damp housing 
SE deprivation 
Barriers to primary healthcare access
Higher burden of untreated strep sore throat infections
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22
Q

Describe the pathogenesis behind RF.

A

Antibodies against M proteins of Group A beta hemolytic strep and CD4+ T cells specific for streptococcal peptides cross react with self antigens/proteins in the heart.
This leads to a combination of antibody-mediated and CD4+ T cell mediated inflammation

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23
Q

What type of hypersensitivity is antibody mediated inflammation?

24
Q

What type of hypersensitivity reaction is CD4+ T cell mediated inflammation?

A

Type IV hypersensitivity

25
Describe the antibody mediated-inflammation involved in RF.
Deposition of antibodies in tissues lead to complement activation. Complement components result in leukocyte recruitment and vasodilation and increase in vascular permeability. Release of substances from leukocytes such as lysosomal enzymes which causes tissue damage.
26
What does the CD4+ T cell mediated inflammation entail?
T cells produce cytokines that recruit and activate macrophages
27
Are streptococci still present in the throat by the time RF develops?
No | Streptococci are completely absent from the inflammatory lesions of RF!
28
How do we detect if a person had a GAS infection prior to RF?
Antibodies against streptococcal antigens can be detected in the plasma.
29
IMPORTANT TO NOTE: disease is not due to the infection of the heart by GAS bacteria! It is an immunologically mediated disease.
xxx
30
What are the clinical features of RF?
Pancarditis Migratory polyarthritis of the large joints Subcutaneous nodules Erythema marginatum of the skin Sydenham chorea ( a neurologic disorder with involuntary rapid, purposeless movements )
31
What is the morphology of endocarditis?
Inflammation of the mural and valvular endocardium on the left side of the heart.
32
What is the morphology of myocarditis?
Causes heart failure that may rarely lead to death in 1% of cases Soft and flabby myocardium leading to dilation of heart chambers Mostly left ventricle
33
What is the morphology of pericarditis?
Pericardial friction rub can be heard
34
Describe the morphology of rheumatic endocarditis.
Inflammation of the valvular endothelium (valvulitis) of the mitral and aortic valves. Results in foci of endothelial injury and necrosis within the cusps or along the chordae tendinae. Overlying these foci, small (1-2mm) platelet-fibrin thrombi form vegetations = verrucae Verrucae are sterile and adherent to lines of closure of the valves so do not embolize.
35
Describe the morphology of rheumatic myocarditis.
Foci of inflammation = Aschoff bodies. Consist of central necrosis surrounded by lymphocytes (mainly T cells), occasional plasma cells and plump activated macrophages - Antischkow cells Chromatin in the nuclei of macrophages is condensed into long, wavy ribbons = caterpillar cells
36
Describe the morphology of rheumatic pericarditis.
Inflamed pericardial surface has a shaggy fibrin rich exudate on top = bread and butter pericarditis
37
What are the outcomes of RF?
After initial attack = increased vulnerability to recurrence with subsequent GAS infections Damage to valves is cumulative (over months/years) with fibrosis increasing with every recurrent attack
38
What is the hallmark of RHD?
Valvular scarring and deformity
39
Describe the valve leaflets in RHD.
Fibrosed, thickened and distorted. Commissures are fused: "button-hole" or "fish-mouth" appearance. Chordae tendinae are thickened and shortened Leads to valve dysfunction - stenosis/regurgitation Greatly increases the risks of infection of deformed valves = IE
40
Which valve is mainly affected by RHD?
Mitral valve is affected alone in 2/3 of cases with aortic in additional 25% of cases
41
What is the characterization of IE.
A serious infection - colonization of the heart valves by an organism, usually bacteria. Leads to formation of vegetations composed of thrombotic debris, organisms and inflammatory cells. Destruction of the valve can occur. Possible break off of vegetations and embolization to distant sites.
42
What is the clinical presentation of IE?
Stormy onset with rapidly developing fever and chills.
43
What is the cause of the subacute type of IE.
Low virulence organisms can affect previously damaged valves (e.g. RHD), artificial ones, or those with congenital defects.
44
What happens in the subacute type of IE?
Endothelial injury occurs and formation of microthrombi that can easily be colonized later even by low virulence organisms should bacteremia occur. This can occur following a minor dental or surgical procedure = need prophylactic antibiotic if predisposing valve pathology is known.
45
Which valves are most commonly affected in the subacute IE?
Aortic and mitral valves.
46
What is the cause for acute IE?
High virulence organisms on previously normal valves
47
How do highly virulent organisms gain access in acute IE?
IV access (contaminated needle shared by IV drug users)
47
How do highly virulent organisms gain access in acute IE?
IV access (contaminated needle shared by IV drug users)
48
What valve is commonly affected in acute IE?
Tricuspid valve (IV injection reaching the right side of the heart)
49
Name the organisms involved in acute IE.
Staph aureus Strep pyogenes Occasionally fungi
50
Name the organisms involved in subacute IE.
Oral flora including streptococcus viridans, enterococci, haemophilus
51
Name the organisms involved in subacute IE.
Oral flora including streptococcus viridans, enterococci, haemophilus
52
List the differences between acute and subacute IE.
Acute - high virulence orgnanism, previously normal valves, destructive/rampant infection, 20-40% fatality Subacute - low virulence, diseased valve, low grade infection
53
What are the clinico-pathological features of IE.
- big, bulky, friable vegetations: containing bacteria, fibrin and inflammatory cells - ulceration/destruction of the valve - deterioration of valve function - possible embolization by septic emboli to the brain, kidneys, may cause abscesses or septic infarcts - less valvular destruction occurs in the subacute form
54
Everything in a nutshell.
GAS infection --> RF --> RHD --> IE

Pathology (8 decks)

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