13 - Cardiovascular Pathology IV Flashcards

1
Q

What are the two types of mitral valve disease?

A

Stenosis and regurgitation

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2
Q

What are the top causes of stenosis in mitral valve disease?

A
  • Rheumatic mitral disease
  • Atrial myxoma (Tumor)
  • Calcified mitral annulus
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3
Q

What are the top causes of regurgitation in mitral valve disease?

A
  • Postinflammatory scarring
  • Infective endocarditis
  • Calcified mitral annulus (“Mitral annular ring” which happens in older people)
  • Mitral valve prolapse (MOST COMMON IN THE YOUNGER POPULATION
    The problem is that it is mostly asymptomatic and it isn’t recognized until symptoms develop)
  • Drugs (fen-phen)
  • Rupture or dysfunction of papillary muscle
  • Rupture of chordae tendineae
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4
Q

Which one is the main cause of regurgitation in older people?

A

Calcified mitral annulus
“Mitral annular ring”
Happens in older people

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5
Q

Which one is the most common in the younger population?

A

Mitral valve prolapse

The problem is that it is mostly asymptomatic and it isn’t recognized until symptoms develop

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6
Q

What specific population is mitral annular calcification most common in?

A

Mitral annular calcification is most common in women over age 60.

** THINK OLDER POPULATIONS **

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7
Q

What comorbidities do we see with calcified mitral annulus?

A

Higher incidence in individuals with mitral valve prolapse or elevated left ventricular pressure as in systemic HTN, aortic stenosis, or hypertrophic cardiomyopathy.

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8
Q

How can you diagnose calcified mitral annulus (mitral annular calcification)?

A

You can see this very easily under x-ray

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9
Q

Describe what happes in calcified mitral annulus (mitral annular calcification)

A

Degenerative calcific deposits can develop in the annulus of the mitral valve.

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10
Q

What can calcified mitral annulus lead to?

A
  • Regurgitation
  • Stenosis
  • Arrhythmias
  • Embolism
  • Sudden death
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11
Q

Explain how calcified mitral annulus can lead to regurgitation

A

regurgitation by interfering with physiologic contraction of the valve ring.

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12
Q

Explain how calcified mitral annulus can lead to stenosis

A

stenosis by impairing opening of the mitral leaflets.

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13
Q

Explain how calcified mitral annulus can lead to arrhythmias, thrombosis and sudden death

A

arrhythmias and occasionally sudden death by penetration of calcium deposits to a depth sufficient to impinge on the atrioventricular conduction system.

Also a site that thrombi can embolize

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14
Q

What happens in mitral valve prolapse?

A

One or both mitral valve leaflets are “floppy” and prolapse, or balloon back, into the left atrium during systole.

You will hear it close suddenly in mid systole –> “click”
Usually an incidental finding on exam

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15
Q

What is the key histoligical change in mitral valve prolapse?

A

The key histologic change in the tissue is myxomatous degeneration.

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16
Q

How many people in the US are affected by mitral valve prolapse

A

** 3% of adults **

It is most often an incidental finding on physical examination (particularly in young women), but in a small minority of affected individuals may lead to serious complications.

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17
Q

What syndrome can mitral valve prolapse be associated with?

A

Marfan’s syndrome

Patients with Marfan syndrome usually have a more serious prolapse

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18
Q

Are most people diagnosed with mitral valve prolapse symptomatic or asymptomatic?

A

Most individuals diagnosed with MVP are asymptomatic.

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19
Q

If you hear a midsystolic click, what do you do?

A

Confirm by echocardiography

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20
Q

What symptoms will a minority of patients experience?

A

A minority of patients have chest pain mimicking angina, dyspnea, and fatigue.

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21
Q

What will a small number of mitral valve prolapse patients develop?

A
  • Infective endocarditis
  • Chordal (cordae tendinae) rupture – med emergency
  • Thromboembolism
  • Arrhythmias, both ventricular and atrial
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22
Q

How do you repair mitral valve prolapse?

A

Surgery

MVP is presently the most common cause for surgical repair or replacement of the mitral valve.

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23
Q

What is infective endocarditis?

A

Infective endocarditis is a serious infection characterized by colonization or invasion of the heart valves or endocardium of the heart by a microbe.

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24
Q

What are vegetations in infective endocarditis composed of?

A

Vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissues (sub-acute form usually).

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25
Q

What are most cases of infective carditis caused by?

A

Most cases are caused by bacterial infections (bacterial endocarditis), but other organisms can be involved ie fungi.

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26
Q

What is important when dealing with infective endocarditis?

A

Prompt diagnosis and effective treatment of IE is important.

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27
Q

Why do dentists give you antibiotics when you get dental work done?

A

So you don’t get infective endocarditis

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28
Q

What are the two types of infective endocarditis?

A

Acute and subacute

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29
Q

What bacteria causes acute infective endocarditis?

A

Staph aureus - HIGH virulence

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30
Q

What bacteria causes subacute infective endocarditis?

A

Strep viridans - LOWER virulence

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31
Q

Describe acute endocarditis

A

Remember: staph aureus

  • High virulence
  • Produces necrotizing, ulcerative, destructive lesions on normal or deformed valves
  • Difficult to cure with antibiotics and usually requires surgery
  • High mortality rate
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32
Q

Describe subacute endocarditis

A

Remember: Strep viridans

  • Lower virulence
  • Insidious infection of deformed valves that are less destructive
  • May pursue as a protracted course of weeks to months
  • Can often be cured by antibiotics (IV, long term)
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33
Q

Can an organism always be isolated in endocarditis?

A

No - in 10-15% of all cases no organism is isolated

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34
Q

Is diagnosis of infective endocarditis simple and straight forward?

A

No

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35
Q

What are the clinical criteria?

A
  • Two major
  • One major and three minor
  • Five minor
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36
Q

What are the pathologic criteria?

A

Microorganisms, demonstrated by culture or histologic examination, in a vegetation, embolus from a vegetation, or intracardiac abscess

Histologic confirmation of active endocarditis in vegetation or intracardiac abscess

37
Q

What are the major clinical criteria?

A
  • Blood culture(s) positive for a characteristic organism or persistently positive for an unusual organism
  • Echocardiographic identification of a valve-related or implant-related mass or abscess, or partial separation of artificial valve
  • New valvular regurgitaion
38
Q

What are the minor clinical criteria?

A
  • Predisposing heart lesion or intravenous drug use
  • Fever
  • Vascular lesions, including arterial petechiae, subungual/splinter hemorrhages, emboli, septic infarcts, mycotic aneurysm, intracranial hemorrhage, Janeway lesions
  • Immunological phenomena, including glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
  • Microbiologic evidence, including a single culture positive for an unusual organism
  • Echocardiographic findings consistent with but not diagnostic of endocarditis, including worsening or changing of a preexistent murmur
39
Q

What are some things you can see?

A
  • Janeway lesions on the palm of the hand
  • Osler nodes in the fingers
  • Roth spots on the retina
  • Splinter hemmorrhages in the finger nails
40
Q

What are complications that can arise from infective endocarditis?

A

1 - Septic emboli
2 - Mural endocarditis
3 - Tricuspid valve involvement

41
Q

What are septic emboli?

A

Peripheral infarcts & abscesses

Can be right or left sided…

  • Right-sided IE: pneumonic complications
  • Left-sided IE: brain, heart, spleen, kidney infarcts and/or micro abscesses
42
Q

What is mural endocarditis?

A

Mural endocarditis - infection of non-valvular endocardium. Usually in areas of injury to endocardial surface from prosthesis (catheter, pacemaker wires, jet stream)

43
Q

What population is at greatest risk of tricuspid valve involvement?

A

IV drug abusers (IVDA) increase susceptible and will have tricuspid valve involvement more often

44
Q

What types of artificial prosthetic valves exist?

A

Mechanical prostheses - caged balls, tilting disks, or hinged semicircular flaps.

45
Q

What types of tissue valves exist?

A

Tissue valves - chemically treated animal tissue, usually porcine, mounted on a prosthetic frame

46
Q

What are the complications of artificial valves?

A
  • Thrombosis/thromboembolism
  • Anticoagulant-related hemorrhage
  • Prosthetic valve endocarditis can also occur
  • Structural deterioration (intrinsic) - Wear, fracture, poppet failure in ball valves, cuspal tear, calcification
  • After about 10 years wear and tear occurs
  • Other forms of dysfunction - Inadequate healing (paravalvular leak), exuberant healing (obstruction), disproportion, hemolysis, noise
47
Q

Can you do minimally invasive valve replacement?

A

Yes

FDA approved for the aortic valve - Go in through the leg as opposed to open heart surgery

48
Q

What is myocarditis?

A

Diverse group of pathologies in which infectious microorganisms and/or an inflammatory process cause myocardial injury.

49
Q

What is the most common cause of myocarditis?

A

Viral infections are the most common cause of myocarditis - Coxsackieviruses A and B

It is Cox A or B until it is ruled out to be otherwise
MOST common – others are rare

50
Q

What do you need to clinically distinguish viral myocarditis from?

A

These disorders must be distinguished from conditions, such as ischemic heart disease, in which injuries caused by other mechanisms lead to inflammation secondarily

51
Q

What percent of myocarditis is from a viral infection?

A

50%

Can also be bacterial, fungal or parasitic

52
Q

What pathological changes will you see grossly?

A

Minimal, heart may appear normal with myocardial hemorrhages or dilated and flabby ventricles.

53
Q

What pathological changes will you see microscopically?

A

Inflammatory destruction of myocardial fibers with changes specific to a pathogen. The inflammatory lesions may be focal or patchy and eventually resolve, leaving no residual changes, or heal by progressive fibrosis.

54
Q

What is Borrelia?

A

Lyme disease

55
Q

What are the three stages of Lyme disease (Borrelia)?

A

Stage 1
Stage 2
Stage 3

56
Q

Describe stage 1 of Lyme disease

A

Stage 1: Early localized infection - flu-like symptoms and bullseye rash.

57
Q

Describe stage 2 of Lyme disease

A

Stage 2: Early disseminated infection - borrelia bacteria
may begin to spread through the bloodstream with meningitis and migratory artheritis (knees, ankles, elbows, wrist, hips, and shoulders)

58
Q

Describe stage 3 of Lyme disease

A

Stage 3: Late persistent infection - severe and chronic
symptoms that affect many parts of the body, including the
brain, nerves, eyes, joints and heart.

Chronic encephalomyelitis, which may be progressive,
can involve cognitive impairment, weakness in the legs, awkward gait, facial palsy, bladder problems, vertigo,
and back pain.

59
Q

What is Chagas (Trypanosomas cruzi)?

A

Reduviid bug

  • Bites you then poops in your wound
  • Develop a huge dilated heart
  • The infection forms amastigotes
60
Q

What is the definition of cardiomyopathy?

A

Heart disease resulting from an abnormality in the myocardium.

61
Q

What are the two forms of cardiomyopathy?

A

Primary and secondary

62
Q

Describe primary cardiomyopathy

A

cardiomyopathies are diseases predominantly confined to the heart muscle

63
Q

Describe secondary cardiomyopathy

A

cardiomyopathies have myocardial involvement as a component of a systemic or multiorgan disorder.

64
Q

Do the different etiologies present similar or different?

A

Diverse etiology may have a similar morphologic appearance.

65
Q

What are the three forms of cardiomyopathy?

A

1 - Dilated cardiomyopathy (DCM)
2 - Hypertrophic cardiomyopathy (HCM)
3 - Restrictive cardiomyopathy (RCM)

66
Q

Describe dilated cardiomyopathy

A
  • Left ventricle becomes very weak and extremely dilated

- Left atrium then becomes very dilated as well

67
Q

Describe hypertrophic cardiomyopathy

A
  • Diastolic failure because the left ventricle is hypertrophied (no space)
  • The left atrium then becomes ballooned out
68
Q

Describe restrictive cardiomyopathy

A
  • The left ventricle is the normal size, it doesn’t look much different, but it is rigid
  • The left atrium then becomes ballooned out
69
Q

What conditions are associated with heart muscle diseases?

A
  • Toxins
  • Metabolic changes
  • Neuromuscular disease
  • Storage disorders
  • Depositions
  • Infiltrative conditions
70
Q

What toxins are associated with heart muscle diseases?

A
  • Alcohol
  • Catecholamines
  • CO
  • Drugs
71
Q

What metabolic changes are associated with heart muscle diseases?

A
  • High or low thyroid hormone
  • High or low potassium
  • Nutritional deficiency
  • Hemochromatosis
72
Q

What neuromuscular diseases are associated with heart muscle diseases?

A

Muscular dystrophy

73
Q

What storage disorders are associated with heart muscle disease?

A
  • Glycogen storage disease

- Lysosomal storage disease

74
Q

What depositions are associated with heart muscle diseases?

A

Amyloidosis

75
Q

What infiltrations are associated with heart muscle diseases?

A
  • Cancer

- Radiation-induced fibrosis

76
Q

What is the clinical course of dilated cardiomyopathy?

A
  • DCM may occur at any age – most common 20-50 yrs old.

- Slowly progressive signs and symptoms of CHF such as shortness of breath, easy fatigability, and poor exertion.

77
Q

What will the ejection fraction be like in dilated cardiomyopathy?

A

Ejection fractions of less than 25%.

78
Q

What are common results of dilated cardiomyopathy?

A

Secondary mitral regurgitation and abnormal cardiac rhythms are common. Death is usually attributable to progressive cardiac failure or arrhythmia and can occur suddenly.

79
Q

What will you see in hypertrophic cardiomyopathy?

A
  • Poorly compliant left ventricular myocardium leading to abnormal diastolic filling
  • Reduced stroke volume due to impaired diastolic filling, which results from the reduced chamber size and compliance of the massively hypertrophied left ventricle.
80
Q

What is the classic pattern of hypertrophic cardiomyopathy?

A

The classic pattern is disproportionate thickening of the ventricular septum as compared with the free wall of the left ventricle (with a ratio greater than 3 : 1), frequently termed asymmetric septal hypertrophy.

“Asymmetrical hypertrophy”

81
Q

What are the symptoms of hypertrophic cardiomyopathy?

A
  • Exertional dyspnea
  • Angina
  • Atrial fib
82
Q

Describe the exertional dyspnea seen in hypertrophic cardiomyopathy

A

The limitation of cardiac output and a secondary increase in pulmonary venous pressure cause exertional dyspnea.

83
Q

Describe the angina seen in hypertrophic cardiomyopathy

A

Anginal pain is frequent because of the massive hypertrophy, high left ventricular chamber pressure, and frequently abnormal intramural arteries.

84
Q

Describe the atrial fibrillation seen in hypertrophic cardiomyopathy

A

Atrial fibrillation, mural thrombus formation leading to embolization and possible stroke, intractable cardiac failure, ventricular arrhythmias, and, not infrequently, sudden death.

It is most common causes of sudden, otherwise unexplained death in young athletes.

85
Q

What are the characteristics of restrictive cardiomyopathy?

A

Characterized by a primary decrease in ventricular compliance, resulting in impaired ventricular filling during diastole.

86
Q

What conditions can restrictive cardiomyopathy be confused with?

A

The functional abnormality can be confused with that of constrictive pericarditis or Hypertrophic cardiomyopathy.

87
Q

What causes restrictive cardiomyopathy?

A

Restrictive cardiomyopathy may be idiopathic or associated with distinct diseases or processes that affect the myocardium, principally radiation fibrosis, amyloidosis, metastatic tumors.

88
Q

What is the pathology of restrictive cardiomyopathy?

A
  • The ventricles are of approximately normal size or slightly enlarged, the cavities are not dilated, and the myocardium is firm and noncompliant.
  • Biatrial dilation is commonly observed.
89
Q

Comparing dilated, hypertrophic and restrictive cardiomyopathies, which form has a low ejection fraction?

A

Dilated