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Cardiopulm Exam 1 > Heart Part 2 > Flashcards

Heart Part 2 Flashcards

1
Q

Arrhythmias:

What kind of injury is the most common cause of rhythm disorders?

A

Ischemic injury

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2
Q

Arrhythmias:

What occurs during Sick Sinus Syndrome?

A

SA node damaged –> BRADYCARDIA

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3
Q

Arrhythmias:

Condition where myocytes depolarize independently and sporadically (atrial dilation) with variable transmission thru AV node –> IRREGULAR IRREGULAR HR

A

atrial fibrillation

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4
Q

Arrhythmias:

What is a heart block?

A

dysfunctional AV node

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5
Q

Arrhythmias:

What do you see with a First degree heart block?

A

prolonged PR interval

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6
Q

Arrhythmias:

What do you see with a Second degree heart block?

A

INTERMITTENT transmission

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7
Q

Arrhythmias:

What do you see with a Third degree heart block?

A

COMPLETE failure

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8
Q

Arrhythmias:

Hereditary conditions for Arrhythmias are dominant or recessive?

A

most autosomal dominant

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9
Q

Arrhythmias:

mutations in genes that are required for normal ion channel function
- Can be assoc with skeletal muscle disorders and diabetes also; most common isolated to heart

A

Channelopathies

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10
Q

What is the most common inherited arrhythmogenic disease?

A

Long QT syndrome

  • Function is related to K+ channel, Na+ channel, and Caveolin
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11
Q

What are some Inherited Arrhythmogenic Dzs?

A
  1. Long QT syndrome
    - Function is related to K+ channel, Na+ channel, and Caveolin
  2. Short QT syndrome
    - Function is related to K+ channels
  3. Brugada syndrome
    - Function is related to Na+ channel and Ca+ channel
  4. CPVT syndrome
    - Function is related to diastolic Ca2+ release
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12
Q

• Unexpected death from cardiac cause, either:
– WITHOUT symptoms, or
– Within 1-24 HRS of symptom onset
– 80-90% of successively resuscitated pts show NO lab or ECG change

A

Sudden cardiac death (SCD)

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13
Q

• ? disease precipitates SCD in 80-90%
– Usually >?% STENOSIS or one or more of the 3 main coronary arteries
– Unfortunately, SCD often the first manifestation of ?
– Healed remote MIs seen in about 40%

A

• Coronary artery disease

  • > 75%
  • IHD
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14
Q

What are some other causes of Sudden cardiac death (SCD) ?

A

cardiomyopathies, myocarditis, congenital abnormalities of the conduction system, myocardial hypertrophy

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15
Q

Sudden cardiac death (SCD) is due to what?

A

SCD is due to a FATAL ARRHYTHMIA MOST often arising from ISCHEMIA-INDUCED MYOCARDIAL IRRITABILITY

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16
Q

• Pressure overload results in left ventricular hypertrophy
(LVH)
- The LV wall is CONCENTRICALLY thickened (>1.5cm), weight ≥500gm

A

Left-sided (systemic) hypertensive disease

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17
Q

Left-sided (systemic) hypertensive disease:

  • Diastolic dysfunction can result in LEFT ATRIAL enlargement which can lead to?
  • May lead to ?, and is a risk factor for ?
A
  • atrial fibrillation (afib)

* CHF, … SCD

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18
Q

Right-sided (pulmonary) hypertensive disease:

– Isolated right-sided hypertensive heart disease arises in the setting of?

A
  • pulmonary hypertension
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19
Q

Right-sided (pulmonary) hypertensive disease:

• Acute COR PULMONALE may arise from what?
- Marked dilation of RV without hypertrophy

A

• a large pulmonary embolus

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20
Q

Right-sided (pulmonary) hypertensive disease:

What is the most common cause of pulmonary hypertension?

A

left-sided heart disease

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21
Q

What are some disorders predisposing to Cor Pulmonale?

A

• Diseases of the Pulmonary Parenchyma:
- Cystic fibrosis

• Diseases of the Pulmonary Vessels:

  • Recurrent pulmonary thromboembolism
  • Primary pulmonary hypertension
  • Extensive pulmonary arteritis (e.g., granulomatosis with polyangiitis)
  • Drug-, toxin-, or radiation-induced vascular obstruction
  • Extensive pulmonary tumor microembolism

• Disorders Affecting Chest Movement:
- Kyphoscoliosis

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22
Q

Pathologic changes of valves are largely of three types: ?

A

1) damage to COLLAGEN that weakens the leaflets, exemplified by MITRAL VALVE PROLAPSE
2) nodular CALCIFICATION beginning in interstitial cells, as in CALCIFIC AORTIC STENOSIS
3) FIBROTIC THICKENING, the key feature in RHEUMATIC HEART DISEASE

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23
Q

Cardiac valves:

Valvular disease can come to clinical attention due to?

A

stenosis, insufficiency

(synonyms: regurgitation or incompetence), or both

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24
Q

Cardiac valves:

What term is used to describe the incompetence of a valve stemming from an abnormality in one of its support structures, as opposed to a primary valve defect?

A

Functional regurgitation

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25
Q

Cardiac valves:

– FUNCTIONAL MITRAL VALVE REGURGITATION is particularly common and clinically
important in ?, as well as in ?

A
  • IHD,…. dilated cardiomyopathy
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26
Q

Valvular Heart Dz:

• Valve disease may present with ? and/or ?

A

• Valve disease may present with stenosis and/or insufficiency

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27
Q

Valvular Heart Dz:

• ? : valve doesn’t OPEN completely, occurs chronically
– Impedes FORWARD flow
– Chronic stenosis may cause PRESSURE overload hypertrophy –> CHF

A

• Stenosis

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28
Q

Valvular Heart Dz:

• ?: valve doesn’t close completely, may occur acutely or chronically
– Allows REVERSED flow
– Chronic insufficiency may cause VOLUME overload hypertrophy –> CHF

A

• Insufficiency

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29
Q

Etiologies of Acquired Heart Valve Dz:

Mitral Valve Disease

  1. Mitral Stenosis = ?
  2. Mitral Regurgitation= ?

Aortic Valve Disease

  1. Aortic Stenosis = ?
  2. Aortic Regurgitation = ?
A

Mitral Valve Disease
1. Mitral Stenosis = Postinflammatory scarring (rheumatic heart disease) **

  1. Mitral Regurgitation=
    - Abnormalities of Leaflets and Commissures **
    - Mitral valve prolapse **
    - Abnormalities of Tensor Apparatus
    - Abnormalities of Left Ventricle and/or Annulus

Aortic Valve Disease
1. Aortic Stenosis = Calcification of congenitally deformed valve***

  1. Aortic Regurgitation =
    - Postinflammatory scarring (RHEUMATIC heart disease) **
    - AORTIC INSUFFICIENCY : dilation of the ascending aorta, often secondary to hypertension and/or aging **
    - Syphilitic aortitis
    - Marfan syndrome
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30
Q

What is the most common valve abnormality?

A

Calcific aortic stenosis

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31
Q

Calcific aortic stenosis:
• Prevalence increases with age and usually manifests at what age?

  • “wear and tear” is associated with?
  • ? valves (BAV) show an ACCELERATED course (increased mechanical stress)
  • Affected valves contain ?-LIKE CELLS, which deposit an osteoid-like substance –> ossifies
  • ? prevent complete opening of the valve
A
  • 60-80 years
  • chronic HTN, hyperlipidemia, inflammation

• Bicuspid valves (BAV) show an accelerated course (increased mechanical stress)
- Bicuspid clinical sx 1-2 DECADES EARLIER than normal valve

  • OSTEOBLAST
  • Mounded calcifications in cusps prevent complete opening of the valve
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32
Q

What are the symptoms of Calcific aortic stenosis?

Treatment?

A

angina, CHF, or syncope

  • LEFT VENTRICULAR HYPERTROPHY (LVH) develops from increased pressure
  • Most patients with aortic stenosis will die within 5 years of developing ANGINA, within 3 years of developing syncope, and within 2 years of CHF
    onset
  • TX: surgical replacement
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33
Q

Calcific deposits occur in the FIBROUS ANNULUS

A

Mitral annular calcification

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34
Q

Mitral annular calcification:

• Normally does not affect valve function; however there are exceptions…

A
  • REGURGITATION by interfering with physiologic contraction of the valve ring
  • STENOSIS by impairing opening of the mitral leaflets
  • ARRHYTHMIAS and occasionally SUDDEN DEATH by penetration of calcium deposits to a depth sufficient to impinge on the atrioventricular conduction system
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35
Q

Mitral annular calcification:

– Nodules may become sites for?

A

thrombus formation or infective endocarditis

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36
Q

Mitral annular calcification:

Most common in what gender and age with what condition?

A
  • F > M,

- > 60 years, with Mitral valve prolapse

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37
Q

Valve leaflets prolapse back into LA during systole

A

Mitral Valve Prolapse (MVP)

“Floppy”

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38
Q

Mitral Valve Prolapse (MVP):

Most common in what gender?

A

Affects 2-3% adults in US; with a 7:1 = F:M, usually incidental (mid systolic click)

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39
Q

What syndrome is it commonly associated with?

A

Marfan syndrome: FIBRILLIN-1 (FBN-1) mutations; loss of connective tissue support in the mitral valve leaflets makes them soft and billowy, creating a so-called floppy valve

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40
Q

Mitral Valve Prolapse (MVP):

• Leaflets become thickened and rubbery, due to proteoglycan deposits (?) and elastic fiber disruption

A

MYXOMATOUS DEGENERATION

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41
Q

Mitral Valve Prolapse (MVP):

• Characteristic anatomic change in MVP is ?
of the mitral leaflets

A

interchordal ballooning (hooding)

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42
Q

What are the symptoms of Mitral Valve Prolapse?

A

• Most are ASYMPTOMATIC, a minority may experience:
– Chest pain mimicking angina (not exertional in nature)
– Dyspnea

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43
Q

What are some serious (but rare) complications of Mitral Valve Prolapse?

A

– Infective endocarditis
– Mitral insufficiency (+/- chordal rupture)
– Thromboembolism –> stroke or other systemic infarct
– Arrhythmias

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44
Q

What is a treatment for Mitral Valve Prolapse?

A

Valve repair or replacement surgery can be done for symptomatic patients or those with increased risk for significant complications; in USA, MVP is the most common cause for mitral valve surgery

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45
Q

a multisystem inflammatory disorder following pharyngeal

infection with group A streptococcus

A

Rheumatic fever

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46
Q

What is the pathogenesis of Rheumatic fever?

A

immune response to streptococcal M proteins cross reacts with cardiac (among other) self- antigens

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47
Q

What tests are used for Acute Rheumatic fever?

A

Anti-streptolysin O and anti-DNase B

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48
Q

What are the symptoms of Rheumatic fever?

A

PANCARDITIS, MIGRATORY POLYARTHRITIS (large jts), subcutaneous nodules,
RASH (ERYTHEMA MARGINATUM)
- SYDENHAM CHOREA: neurologic disorder with involuntary rapid, purposeless movements

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49
Q

What are the cardiac features of Acute RF?

A
  • PANCARDITIS, featuring ASCHOFF BODIES. Also activated macrophages called ANITSCHKOW CELLS
  • Inflammation and FIBRINOID NECROSIS of endocardium and left-sided valves, with VERRUCAE (vegetations)
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50
Q

What are the cardiac features of Chronic RF?

A

• mitral leaflet THICKENING; FUSION of commissures; with shortening, fusion and thickening of cords, –> MITRAL STENOSIS (virtually only cause of mitral stenosis)

  • LA ENLARGEMENT –> atrial fib (arrhythmias), thromboembolic events
  • pulmonary congestion/RHF; RIGHT VENTRICULAR HYPERTROPHY
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51
Q

An infection of valves or endocardium, characterized by vegetations consisting of microbes and debris, assoc with underlying tissue destruction
- Aorta, aneurysms, other blood vessels and prosthetic devices can become infected

A

Infective endocarditis (IE)

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52
Q

• ? infective endocarditis is a RAPIDLY PROGRESSING,
destructive infection of a PREVIOUSLY NORMAL valve

  • Treatment?
A

Acute

  • Requires SURGERY in addition to antibiotics
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53
Q

• ? infective endocarditis is a slower-progressing
infection of a previously deformed valve (such as in
chronic RHD)

  • Treatment?
A

Subacute

  • Can often be cured with ANTIBIOTICS alone
54
Q

What are some predisposing conditions to Infective endocarditis?

A
  1. Valvular abnormalities
    - RHD, PROSTHETIC VALVES, MV prolapse, calcific stenosis, bicuspid AV
  2. Bacteremia
    - Another site of infection
    - Dental work/surgery
    - Contaminated needle
    - Compromised epithelium
55
Q

What is a classic feature of Infective endocarditis?

A

friable, bulky, destructive valvular vegetations

56
Q

Classic features of Infective endocarditis:

  • ?-sided valves are more commonly affected
  • Right-sided valves often involved in?
  • Friability leads to? (PE if right side valve)
A
  • Left-sided
  • IV drug abusers
  • septic emboli
57
Q

What are the symptoms of Acute Endocarditis?

A

fever chills, weakness, and lassitude

58
Q

Infective endocarditis:

? are usually present (90%) with LEFT-sided lesions

A

Murmurs

59
Q

What organisms are often involved with Infective endocarditis

A

– S. viridans (valve abnormalities)

–S. aureus (normal valves, abnormal valves, IV drug abusers)

–S. epidermidis (prosthetic valves)

– HACEK (Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

60
Q

Infective Endocarditis:

Acute bacterial vs Subacute (SBE)

A

Acute Bacterial:
• <6 weeks with 50% mortality
• Highly VIRULENT organisms
• NORMAL valves
• Necrotizing, ulcerative DESTRUCTIVE lesions
• Micro: fibrin, inflammatory cells, and organisms
• RAPID onset of symptoms
• Difficult to cure; SURGERY
• Aortic and mitral valves
• Right heart valves if IV DRUG USER
• Ring abscess: vegetation erode into underlying myocardium
• EMBOLI –> septic infarcts or MYCOTIC aneurysm

Subacute (SBE):
• >6 weeks, most survive with treatment 
• Less virulent organisms; INSIDIOUS 
• ABNORMAL valves 
• Less destructive lesions 
• Micro: granulation tissue, fibrosis, CALCIFICATION, CHRONIC inflammatory cells 
• Vague FLU-LIKE symptoms 
• ANTIBIOTICS
61
Q

Important minor diagnostic criteria for Infective Endocarditis

A
  • subungual/splinter hemorrhages
  • Janeway lesions
  • Osler nodes
  • Roth spots
62
Q

• Small, STERILE thrombi on cardiac valve leaflets, along the line of closure
- Loosely attached, not invasive, do not illicit an inflammatory reaction

A

Nonbacterial Thrombotic Endocarditis (NBTE)

63
Q

Nonbacterial Thrombotic Endocarditis (NBTE):

  • May be a source of ? (produce infarcts in the brain, heart,…)
  • Associated with malignancies (especially ?), sepsis, or catheter-induced endocardial trauma
A
  • emboli

* mucinous adenocarcinomas

64
Q

a systemic disorder marked by
FLUSHING, DIARRHEA, DERMATITIS, AND BRONCHOCONSTRICTION; bioactive compounds such as SEROTONIN released by carcinoid tumors

A

Carcinoid syndrome

65
Q

Carcinoid syndrome:

  • plasma levels of serotonin and urinary excretion of the serotonin metabolite ? correlate with the severity of the cardiac lesions
A

5-hydroxyindoleacetic acid

66
Q

Carcinoid Heart Disease:

What side is usually affected?

A
  • Right endocardium and valves; left side is protected due to pulmonary vascular bed degradation of mediators
67
Q

What are the types of cardiomyopathies?

A
  • Dilated cardiomyopathy
  • Takotsubo cardiomyopathy
  • Arrhythmogenic right ventricular cardiomyopathy (ARVC)
  • Hypertrophic cardiomyopathy • Restrictive cardiomyopathy
  • Amyloid
68
Q

What is the most common and least common cardiomyopathy?

A
  • Most common: Dilated Cardiomyopathy ***(90%)

- Least common: Restrictive Cardiomyopathy

69
Q

What is a cause of phenotype associated with Dilated Cardiomyopathy?

A

Hemochromatosis

70
Q

Progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy

A

Dilated cardiomyopathy (DCM)

71
Q

Dilated cardiomyopathy (DCM) Pathogenesis:

  • Thought to be familial in 30-50% of cases (TTN mutations may account for 20% of all cases); usually autosomal ?
  • ? is strongly linked to DCM
  • Myocarditis

• Cardiotoxic drugs/substances: doxorubicin, cobalt, ? overload
- Iron overload from ? (HFE mutation) or multiple transfusions

A
  • dominant
  • Alcohol is strongly linked to DCM

• IRON
- hereditary hemochromatosis

72
Q

What is the morphology of Dilated cardiomyopathy (DCM)?

A

– dilation of all chambers
– MURAL THROMBI are common
– functional REGURGITATION of valves

73
Q

What is the presentation for Dilated cardiomyopathy (DCM)?

A

– usually manifests between ages 20-50yo

– progressive CHF –> dyspnea, exertional fatigue, Decreased EF (<25% end stage)

–ARRHYTHMIAS (SUDDEN DEATH)

–EMBOLISM

74
Q

“Broken heart syndrome”

A

Takotsubo cardiomyopathy (a dilated cardiomyopathy)

75
Q

Takotsubo cardiomyopathy (a dilated cardiomyopathy):

What is there an excess of following extreme emotional or
psychological stress?

A

catecholamines

76
Q

What is the age and gender associated with Takotsubo cardiomyopathy?

A

> 90% women, ages 58-75

77
Q

The symptoms and signs of Takotsubo cardiomyopathy are similar to what condition?

A

acute myocardial infarction

78
Q

What happens during Takotsubo cardiomyopathy?

A

APICAL BALLOONING OF THE LEFT VENTRICLE WITH abnormal wall motion and contractile dysfunction

79
Q

What molecular structures are associated with:

  1. Dilated Cardiomyopathy
  2. Hypertrophic Cardiomyopathy
  3. Dilated + Hypertrophic
A
  1. Dilated Cardiomyopathy
    - Gamma- Sarcoglycan
    - Dystrophin
    - Desmin
    - Mitochondrial proteins
    - Titin
    - Lamin A/C
  2. Hypertrophic Cardiomyopathy
    - Myosin binding protein C
    - Myosin light chains
  3. Dilated + Hypertrophic
    - Beta-Myosin heavy chain
    - Actin
    - Troponin I/T
    - alpha- Tropomyosin
80
Q

What is the percentage of genetic causes for Dilated Cardiomyopathy and Hypertrophic Cardiomyopathy ?

A
  • Dilated Cardiomyopathy = 20-50% genetic causes

- Hypertrophic Cardiomyopathy = 100% genetic causes (sarcomeric proteins)

81
Q

What is an important phenotype for Hypertrophic Cardiomyopathy?

A

Myofiber disarray

82
Q

Hypertrophic Cardiomyopathy and Dilated Cardiomyopathy have the same end points. What are they?

A

Clinical:

  • Heart failure
  • Sudden death
  • Atrial fibrillation
  • Stroke
83
Q

• Right ventricular failure and arrhythmias

– Myocardium of the RIGHT VENTRICULAR wall replaced by ADIPOSE AND FIBROSIS

– Causes ventricular tachycardia or fibrillation –> SUDDEN DEATH

A

Arrhythmogenic right ventricular cardiomyopathy ( ARVC)

84
Q

What are the genetics associated with Arrhythmogenic right ventricular cardiomyopathy ( ARVC)?

A

• Familial, AUTOSOMAL DOMINANT

– defective cell adhesion proteins in the desmosomes that link adjacent cardiac myocyte

85
Q

What syndrome is associated with Arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

• NAXOS SYNDROME: ARVC with hyperkeratosis of plantar palmar skin surfaces***

86
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC):

  • Naxos Syndrome is associated with what mutation?
A

mutations in the gene encoding the desmosome-associated protein PLAKOGLOBIN

87
Q

A genetic disorder leading to myocardial hypertrophy and diastolic dysfunction, leading to decreased stroke volume and often ventricular outflow obstruction

A

Hypertrophic cardiomyopathy

88
Q

Hypertrophic cardiomyopathy:

• Numerous mutations known, involving SARCOMERIC proteins; most commonly?

A

Most commonly Beta-myosin heavy chain (Beta-MHC)

89
Q

What is the morphology of Hypertrophic cardiomyopathy?

A

– massive myocardial hypertrophy, often with MARKED SEPTAL HYPERTROPHY (usually without dilation)

– Microscopically, MYOCYTE DISARRAY

90
Q

What are the symptoms of Hypertrophic cardiomyopathy?

A

harsh systolic ejection murmur, caused by the ventricular outflow obstruction as the anterior mitral leaflet moves toward the ventricular septum during systole

91
Q

Hypertrophic cardiomyopathy:

• What are the consequences of extensive hypertrophy?

A

– Foci of myocardial ischemia may occur

– LEFT ATRIAL DILATION and MURAL THROMBUS

– Diminished cardiac output and increased pulmonary congestion leads to exertional dyspnea

– Arrhythmias

–SUDDEN DEATH (sudden, otherwise unexplained death in young athletes)

92
Q

Decreased ventricular compliance (increased stiffness), leading to DIASTOLIC DYSFUNCTION (impaired filling), while systolic function of the LV remains normal

A

Restrictive cardiomyopathy

93
Q

Restrictive cardiomyopathy:

  • May be secondary to ? within the wall (amyloid), or increased ? (radiation)
  • Ventricles are usually of normal size, but both atria can be?
A
  • May be secondary to DEPOSITION OF MATERIAL within the wall (amyloid), or increased FIBROSIS (radiation)
  • enlarged
94
Q

Restrictive cardiomyopathy:

What is an extracellular deposition of proteins which form an insoluble Beta-pleated sheet ?

A

Amyloid

95
Q

Restrictive cardiomyopathy: Amyloid

• May be systemic (myeloma) or restricted to the heart (usually ?)

  • Certain mutated versions of transthyretin are more amyloidogenic
  • Amyloid can involve different parts of the heart, but when deposits are in the ? of the myocardium, a RESTRICTIVE cardiomyopathy results
A

• May be systemic (myeloma) or restricted to the heart (usually TRANSTHYRETIN)

  • interstitium
96
Q

What staining is involved with Amyloid restrictive cardiomyopathy?

A

Congo red stain:

apple green birefringence

97
Q

Inflammation of the myocardium, most commonly due to a virus in US

A

Myocarditis

98
Q

What viruses are most commonly associated with Myocarditis?

A

Coxsackie A and B viruses

99
Q

What are some other infectious causes of Myocarditis?

A
  1. Trypanosoma cruzi (Chagas disease)
    - 10% die during acute attack
    - May progress to cardiac insufficiency in 10-20 years
    - PARASITIZATION of scattered myofibers; MIXED INFLAMMATORY CELL INFILTRATE (PMN, lymphs, macrophages, and occ EOSINOPHILS)
  2. Various bacteria and fungi
100
Q

What are some noninfectious causes of Myocarditis?

A

Immune mediated reactions; including RF, SLE, drug hypersensitivity **

101
Q

What stain is associated with Trypanosoma cruzi (Chagas)?

A

Giemsa-stained

also look for amastigotes

102
Q

Which disease has:

• Slow accumulation fluid, <500mL asymptomatic if slow enough
– Globular enlargement of heart shadow on CXR

A

Pericardial Dz

103
Q

What condition is associated with acute Pericardial disease?

A

200-300mL rapid accumulation –> CARDIAC TAMPONADE

104
Q

What are the most common types of Pericardial disease?

A

Fibrinous and serofibrinous

105
Q

Fibrinous and serofibrinous Pericardial Disease:

What causes this?

A

AMI, POSTINFARCTION (Dressler’s), UREMIA, chest irradiation, RF, SLE, trauma…

106
Q

What symptoms are associated with Fibrinous and serofibrinous Pericardial Disease?

A

pain (sharp, pleuritic and position dependent), fever, +/- CHF

107
Q

What is the most striking feature of Fibrinous and serofibrinous Pericardial Disease?

A

Loud pericardial friction rub most striking feature

108
Q

Types of Pericarditis:

characteristically produced by noninfectious inflammatory diseases, including rheumatic fever, SLE, and scleroderma, as well as tumors and uremia

A

Serous pericarditis

109
Q

Types of Pericarditis:

active infection caused by microbial invasion of the pericardial space (direct extension, seeding from the blood, lymphatic extension, direct introduction)

A

Purulent or suppurative pericarditis

110
Q

Types of Pericarditis:

Exudate composed of blood mixed with a fibrinous
or suppurative effusion

  • What is it most commonly caused by?
A

Hemorrhagic pericarditis

– most commonly caused by the spread of a MALIGNANT NEOPLASM to the pericardial space

111
Q

Types of Pericarditis:

Tuberculous in origin; infrequently, fungal infections
evoke a similar reaction

A

Caseous pericarditis

112
Q

Types of Pericarditis:

Heart is encased in a dense, fibrous or fibrocalcific
scar that limits diastolic expansion and cardiac output, features that mimic a restrictive cardiomyopathy

A

Constrictive pericarditis

113
Q

Primary Cardiac Tumors are rare and the top 5 are all BENIGN. Examples?

A

MYXOMA, fibromas, lipomas, papillary fibroelastomas, rhabdomyomas and ANGIOSARCOMAS

114
Q

What is the most common primary cardiac tumor?

  • PEDUNCULATED (or sessile) usually in region of fossa ovalis
A

Myxoma

115
Q

Primary Cardiac Tumor:

What mutations and associated syndromes are involved with Myxoma?

A

Familial syndromes associated with myxomas have activating mutations in the GNAS1 gene, encoding a subunit of G protein (Gsα) (in association with MCCUNE-ALBRIGHT SYNDROME)

or null mutations in PRKAR1A , encoding a regulatory
subunit of a cyclic-AMP-dependent protein kinase (CARNEY COMPLEX)

116
Q

Primary Cardiac Tumor:

What do Myxomas look like?

A

**Globular hard mass, mottled with hemorrhage to soft, translucent, papillary or villous with a gelatinous appearance

117
Q

Primary Cardiac Tumor:

What are the symptoms of a Myxoma?

A

“BALL-VALVE” OBSTRUCTION, embolization or constitutional sx (fever and malaise)

  • Pedunculated form cause intermittent obstruction (position dependent) during systole of AV
    valve; or “WRECKING BALL” causing damage to the valve leaflets
  • Constitutional sx: elaboration by some myxomas of the IL-6, a major mediator of the acute-phase response
118
Q

Primary Cardiac Tumor:

What do you hear on auscultation for a Myxoma?

A

Auscultation: tumor “plop”

119
Q

Which Primary Cardiac Tumor type is this:

localized, well-circumscribed, benign tumors composed of mature fat cells; subendocardium, subepicardium, or myocardium

A

Lipoma

120
Q

Which Primary Cardiac Tumor type is this:

• Usually incidental, sea-anemone-like lesions, most often identified at autopsy; usually (>80%) located on valves

– They resemble the much smaller, usually trivial, LAMBL EXCRESCENCES that may represent remotely organized thrombus on the aortic valves of older individuals

A

Papillary Fibroelastoma

121
Q

Which Primary Cardiac Tumor type is this:

most frequent primary tumor of the PEDIATRIC heart

  • 50% sporadic mutations
  • 50% associated with tuberous sclerosis (mutations in the TSC1 (Hamartin) or TSC2
    (Tuberin) tumor suppressor gene)
A

Rhabdomyoma

122
Q

Which Primary Cardiac Tumor type is this:

malignant endothelial neoplasm that primarily affects
older adults

A

Angiosarcoma

123
Q

Cardiovascular Effects of Noncardiac Neoplasms:

What are the direct consequences of the tumor?

A
  • Pericardial and myocardial metastases
  • Large vessel obstruction
  • Pulmonary tumor emboli
124
Q

Cardiovascular Effects of Noncardiac Neoplasms:

What are the indirect consequences of the tumor (complications of circulating mediators)?

A
  • Nonbacterial thrombotic endocarditis
  • Carcinoid heart disease
  • Pheochromocytoma-associated heart disease
  • Myeloma-associated amyloidosis
125
Q

Cardiovascular Effects of Noncardiac Neoplasms:

What are the effects of tumor therapy?

A
  • Chemotherapy

* Radiation therapy

126
Q

What are the most common diseases associated with cardiac transplantation?

A

DCM and IHD are the most common

127
Q

What is a major complication of cardiac transplantation?

A

allograft rejection

- Routine endomyocardial bx to monitor

128
Q

What is the most important long term limitation to cardiac transplantation?

A

Allograft arteriopathy

129
Q

Cardiac transplantation: Allograft arteriopathy

– Late, progressive, diffusely ?

– 50% develop in 5 years, and in virtually all patients within 10 years

– Silent MI: denervated transplanted heart (NO angina)

A
  • STENOSING INTIMAL PROLIFERATION
130
Q

Cardiac transplantation:

• Needed for ? due to chronic T-cell immunosuppression

A

EBV associated B-cell lymphoma

131
Q

What is the overall survival for cardiac transplantation?

A

Overall survival: 90% at 1 year, >60% at 5 years

132
Q

What are some complications of a heart transplant?

A
  • Lymphocytic infiltrate

- Intimal thickening

Cardiopulm Exam 1 (13 decks)

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