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Pathology > Chapter 12- The Heart > Flashcards

Chapter 12- The Heart Flashcards

1
Q

What is the number one cause of worldwide mortality?

A

Cardiovascular disease

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2
Q

What is myocardium?

A

Heart muscle

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3
Q

What are the phases of heart pumping?

A

Contraction (systole) and relaxation (diastole)

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4
Q

What are the contractile components of the heart?

A

Sarcomeres

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5
Q

What is ANP secreted in response to?

A

Increased blood volume in the heart

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6
Q

What are the names for the components of AV and semilunar valves?

A

AV- leaflets

Semilunar- cusps

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7
Q

What is the pacemaker of the heart?

A

The SA node

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8
Q

Where do the conducting components of the heart lie?

A

SA node- junction if the right atrial appendage and SVC

AV node- right atrium (along septum)

Bundle of His- through the septum

Purkinje network- divisions into the right and left ventricles

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9
Q

What is the division of the Purkinje network called?

A

Arborization

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10
Q

When does blood flow to the myocardium occur?

A

Diastole

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11
Q

What are the supply vessels of the heart for each area?

A

Anterior

  • Right coronary, right marginal
  • Left coronary, left anterior descending, left marginal

Left posterior- left circumflex

Right posterior- posterior left ventricular branch

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12
Q

What are the effects of aging on the heart?

A

Sigmoid septum

Valve sclerosis and degenerative changes

Decreased myocytes and increased fibrosis

Aortic stiffness

Atherosclerosis

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13
Q

What are the causes of cardiac pathophysiology?

A

Pump failure

Flow obstruction

Regurgitant flow

Shunted flow

Abnormal conduction

Rupture of heart or major vessels

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14
Q

What is congestive heart failure?

A

End stage heart disease

Heart is unable to maintain output

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15
Q

What is forward failure vs backward failure?

A

Forward- trouble getting blood out (reduced CO and tissue perfusion)

Backward- blood pooling

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16
Q

What is the most common cause of CHF?

A

Systolic dysfunction

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17
Q

When is diastolic dysfunction seen as he cause of CHF?

A

Women over 65

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18
Q

What are two compensatory mechanisms for CHF?

A
  1. Frank-Starling mechanism (heart dilated with increased filling and enhances contraction)
  2. Myocardial hypertrophy
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19
Q

What are the three types of cardiac hypertrophy?

A
  1. Pressure overload- hypertension or stenosis (concentric increased in wall thickness)
  2. Volume overload- valvular insufficiency or ventricular dilation (no thickened wall, just bigger)
  3. Physiologic- exercise, increased mitochondria and angiogenesis
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20
Q

What are the characteristics of left sided heart failure?

A

Systolic failure

Left ventricle is hypertrophied and dilated

Secondary left atrium dilation (A-fib)

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21
Q

How does left sided heart failure manifest?

A

Pulmonary congestion and edema

Left atrial dilation

Decreased atrial perfusion (salt and water retention)

Hypoxic encephalopathy

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22
Q

What is the most common cause of right sided heart failure?

A

Left sided heart failure

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23
Q

What is right sided heart failure infrequently isolated as?

A

Cor pulmonale (alterations in structure and function due to pulmonary disorders)

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24
Q

What are the characteristics of right side heart failure?

A

Edema

Hepatomegaly with centrilobar congestion (nutmeg liver)

Congestive splenomegaly

Renal congestion

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25
Q

What is the pharmacological treatment for CHF?

A

Diuretics (relieve fluid overload)

Beta blockers (lower adrenergic tone)

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26
Q

When does most congenital heart disease occur?

A

Week 3-8

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27
Q

What are common congenital heart diseases?

A

Single gene mutations

DiGeorge

Down

Environmental factors

Lesions (obstructions and shunts

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28
Q

Left to right shunts result in what?

A

Right sided volume and pressure overload

Pulmonary hypertension

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29
Q

What is Eisenmenger syndrome?

A

Pulmonary pressure increases so much a left shunt occurs (overcorrects the left to right shunt)

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30
Q

What are the types of left to right shunts and their characteristics?

A
  1. Atrial septal defects- adults, increased distendability of the right ventricle, murmur
  2. Ventricular septal defects- membranous septum near aortic valve, right ventricular hypertrophy and pulmonary hypertension
  3. Patent ductus arteriosus- distal to left subclavian artery, ligamentum arteriosum failed to close (aorta and pulmonary artery)
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31
Q

What is the most common CHD overall?

A

Ventricular septal defects

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32
Q

What are the types of atrial septal defects?

A
  1. Primum- adjacent to mitral and tricuspid valves
  2. Secondum (90%)- deficient septum secondum formation near atrial septum

Sinus venosus- near SVC entrance

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33
Q

What is patent foramen ovale?

A

Defective sealing of fossa ovalis flap

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34
Q

What is associated with right to left shunts?

A

Tetralogy of Fallot and transposition of great arteries

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35
Q

What is tetralogy of Fallot?

A

VSD

Pulmonary stenosis with right ventricular outflow obstruction

Overriding aorta

Right ventricular hypertrophy

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36
Q

What are the “colours” of the two kinds of shunts?

A

Left to right- pink

Right to left- blue (cyanotic- skips lungs)

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37
Q

What is TGA?

A

The aorta arises from the right ventricle

Pulmonary artery arises from the left ventricle

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38
Q

What does post natal development with TGA depend on?

A

Mixing of outgoing blood (some defect- VSD, PDA, ASD or patent foramen ovale)

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39
Q

What do obstructive lesions within the heart give rise to?

A

Ventricular hypertrophy without cyanosis

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40
Q

What are the different types of obstructive lesions within the heart?

A
  1. Coarctation (constriction) of the aorta- left ventricle hypertrophy
  2. Pulmonary stenosis and atresia- right ventricle hypertrophy
  3. Aortic stenosis and atresia
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41
Q

What are the forms of aorta coarctation?

A
  1. Infantile- narrowing proximal to PDA, right to left shunting
  2. Adult- narrowing opposite the (closed) ligamentum arteriosum
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42
Q

What are the types of aortic stenosis and atresia?

A

Valvular

Hypoplastic left heart syndrome

Subaortic stenosis- ring of fibrous tissue below the cusps

Supraventricular aortic stenosis- elastin gene mutation

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43
Q

What causes ischemic heart disease?

A

Reduced coronary blood flow (atherosclerosis, vasospasm, thrombosis)

Increased myocardial demand (tachycardia and hypertrophy)

Hypoxia

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44
Q

What syndromes are associated with ischemic heart disease?

A

Angina pectoris- chest pain

Myocardial infarction- cell death (vascular occlusion)

Chronic ischemic heart disease- progressive heart failure

Sudden cardiac death- lethal arrhythmia

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45
Q

What are the types of angina pectoris?

A
  1. Stable- occurs with exertion, diminishes with rest
  2. Prinzmetal- vasospasm
  3. Unstable/crescendo- occurs with successively lesser amounts of exertion
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46
Q

What causes most myocardial infarctions?

A

Atherosclerotic plaques

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47
Q

When is complete necrosis seen in myocardial infarction?

A

After 6hrs of severe ischemia

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48
Q

What do the morphological features of acute MI depend on?

A

Location, severity, rate of obstruction development

Size of vascular bed perfused by obstructed vessels

Occlusion duration

Metabolic and oxygen needs of the myocardium

Extent of collateral blood vessels

Presence, site and severity of coronary arterial spasm

Heart rate, cardiac rhythm, blood oxygenation

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49
Q

What are the different locations of MIs and how do they affect the heart?

A
  1. Transmural- epicardium vessel occlusion, full thickness of wall involved
  2. Subendocardial/nontransmural- subendocardium is least perfused, involves inner third of ventricle wall
  3. Multifocal microinfarction- involves smaller, intramural vessels
50
Q

What are the gross changes associated with MIs and when do they occur?

A

4-12hrs- only see histo

12-24hrs- pale, cyanotic

1-3 days- yellow, defined lesions

3-7 days- dead myocytes are ingested

7-10 days- granulation tissue

> 2wks- scar

51
Q

How does reperfusion affect MIs?

A

Restores viability but remains poorly contractile

Contraction band necrosis

Additional injury (inflammation)

52
Q

What are the clinical features of MIs?

A

Chest pain, nausea, diaphoresis, dyspnea

ECG changes

CK-MB and troponin markers increase

Nearly all transmural affect the left ventricle

53
Q

When do half of all deaths due to MIs occur?

A

Within the first hour

54
Q

What is the treatment for MIs?

A

Anticoags, oxygen, beta blockers, ACE inhibitors, fibrinolytics

Angioplasty, stenting, surgical bypass

55
Q

What are the complications of MIs?

A

Ventricular rupture (free wall most common)

Papillary muscle rupture

Aneurysm

Mural thrombus

Arrhythmia

Pericarditis

CHF

Infarct expansion

56
Q

Chronic ischemic heart disease is associated with what?

A

Arrhythmias

57
Q

What is sudden cardiac death most commonly due to?

A

Lethal arrhythmia (V-fib)

58
Q

What is the most common cause of sudden cardiac death?

A

Ischemic heart disease

59
Q

What are the types of hypertensive heart disease?

A
  1. Systemic (left side)

2. Pulmonary (right side) or cor pulmonale

60
Q

What is the cause and characteristics of systemic hypertension?

A

Due to chronic elevated pressures

Concentric left ventricle hypertrophy (no other causes)

Impaired diastolic filling, increases oxygen demand

Fibrosis reduces compliance

61
Q

What is the cause of pulmonary hypertension?

A

Lung diseases cause pulmonary vascular hypertension (most often due to left sided heart failure)

62
Q

What is the difference between acute and chronic pulmonary hypertension?

A

Acute- after passive PE, only see dilation

Chronic- right ventricular pressure overload, hypertrophy

63
Q

What can cause valvular disease?

A
  1. Stenosis (failure to open)
  2. Insufficiency (failure to close, regurgitation)
  3. Functional regurgitation (abnormality in cable support structure)
64
Q

What are the major functional valvular lesions and their causes?

A

Aortic stenosis- calcification and stenosis

Aortic insufficiency- dilation of ascending aorta

Mitral stenosis- rheumatic heart disease

Mitral insufficiency- myxomatous degeneration (prolapse)

65
Q

What are the characteristics of calcification aortic valve stenosis?

A

Nodular, calcific, subendothelial masses on valve outflow

Valve fibrosis

Spares free edge of cusps

Compensatory, concentric left ventricle hypertrophy

66
Q

What are the characteristics of mitral annular calcification?

A

Calcific deposits in the fibrous annulus

Stenosis- poor leaflet movement over bulky deposits

Impingement on conducting pathways

67
Q

What are the characteristics of mitral valve prolapse?

A

Myxamatous degeneration

Enlarged leaflets, floppy

Chordae tendinae occasionaly rupture

Thrombosis behind ballooning cusps

68
Q

Mitral valve prolapse shows high frequency in what disease?

A

Marfan syndrome

69
Q

What is rheumatic fever and heart disease?

A

Acute inflammation due to GAS infection, often in children

Cardiac Ags cross react with strep Abs or T cells

70
Q

What is the only cause of acquired mitral valve stenosis?

A

Rheumatic fever/heart disease

71
Q

What are the phases of rheumatic fever?

A

Acute- Aschoff bodies, fibrinous vegetations along cusp free edge, modules of mixed mononuclear cells with necrosis

Chronic- diffuse fibrinous thickening (fishmouth/buttonhole stenoses)

72
Q

What are the characteristics of vegetations seen in rheumatic fever/heart disease?

A

Verrucous

Small, warty

Along lines of closure

73
Q

What is the diagnosis of rheumatic fever based on?

A

Skin rash (erythema marginatum)

Migratory polyarthritis of joints

Carditis

Subcutaneous nodules

Syndenham chorea (involuntary movements)

74
Q

What are the clinical implications of rheumatic fever?

A

Left atrial hypertrophy and enlargement and mural thrombi

A-fib

CHF with pulmonary congestion

Increased risk of infective endocarditis

75
Q

What are the characteristics of infective endocarditis?

A

Microbial infections of valves leading to friable vegetations

76
Q

What are the characteristics of the vegetations seen in infective endocarditis?

A

Large, irregular masses

Can extend into chordae

Friable

77
Q

What are the types of infective endocarditis and their characteristics?

A

Acute- highly virulent organisms seed normal valves

Subacute- low virulence organisms seed an abnormal or injured valve (smaller)

78
Q

What are the two forms of noninfectious vegetations?

A
  1. Nonbacterial thrombotic endocarditis

2. Endocarditis of SLE (Libman Sacks)

79
Q

What are the characteristics of vegetations seen with nonbacterial thrombotic endocarditis?

A

Small, bland

Sterile- fibrin and platelet thrombi

At line of closure

Can embolize

80
Q

What can cause nonbacterial thrombotic endocarditis?

A

Cancer

Prolonged debilitating illness with DIC

81
Q

What are the characteristics of Libman Sacks vegetations?

A

Small-medium

On either side of the leaflet

82
Q

What are the characteristics of carcinoid heart disease?

A

Release bioactive products

Extensive metastatic spread

Thickening of pulmonary and tricuspid valves (rarely involves left heart)

83
Q

What complications are associated with prosthetic valves?

A

Thromboembolic complications

Infective endocarditis

Structural deterioration

Occlusion

Hemolysis

Paravalvular leak (poor healing)

84
Q

What are cardiomyopathies?

A

Principle cardiac dysfunctions

Mechanical and/or electrical

85
Q

What are the three types of cardiomyopathies and their characteristics?

A
  1. Dilated- progressive cardiac dilation and contractile dysfunction
  2. Hypertrophic- genetic disorder resulting in poorly compliant left ventricle (asymmetrically enlarged)
  3. Reactive- reduction in ventricular compliance, impaired ventricular filling
86
Q

What are the pathways of dilated cardiomyopathy?

A

Genetics

Myocarditis

Alcohol/toxins

Peripartum cardiomyopathy

Iron overload

Supraphysiologic stress

87
Q

At what age is dilated cardiomyopathy most common?

A

20-50 years

88
Q

What types of supraphysiologic stress is associated with dilated cardiomyopathy?

A

Tachycardia, hypertension

Excess catecholamines- contraction band necrosis

Takotsubo cardiomyopathy- left ventricle contractile dysfunction following extreme stress

89
Q

What tumour can cause increased catecholamines?

A

Pheochromocytomas

90
Q

What causes death in dilated cardiomyopathies?

A

Progressive cardiac failure

Arrhythmia

91
Q

What does the heart look like in dilated cardiomyopathy?

A

Enlarged, heavy, flabby

All chambers dilated

Mural thrombi

92
Q

What are the characteristics of arrhythmogenic right ventricular cardiomyopathy?

A

Right sided ventricular failure and arrhythmia

Right ventricular wall severely thinned

93
Q

What is the heart like in hypertrophic cardiomyopathies?

A

Thick walled, heavy, hypercontracting

Asymmetrical hypertrophy (left side more enlarged) without dilation

94
Q

What are the complications of hypertrophic cardiomyopathies?

A

Abnormal diastolic filling and intermittent ventricular outflow obstruction

Reduced stroke volume

Exertional dyspnea

95
Q

What must hypertrophic cardiomyopathy be distinguished from?

A

Deposition and hypertensive diseases

96
Q

What is the primary complication of reactive cardiomyopathy?

A

Impaired ventricular filling during diastole

97
Q

What are the morphological features of reactive cardiomyopathy?

A

Ventricles normal or slightly enlarged

No dilation

Firm, noncompliant myocardium

Bilateral dilation

Patchy/diffuse interstitial fibrosis

98
Q

What can cause reactive cardiomyopathy?

A

Idiopathic or radiation fibrosis

Amyloidosis

Sarcoidosis

Metastatic tumours

Inborn errors of metabolism

99
Q

What causes myocarditis?

A

Infectious organisms and/or inflammatory processes

100
Q

What is the most common cause of myocarditis?

A

Viruses (coxsackie A and B)

101
Q

What are less common causes of myocarditis?

A

Lymphocytic (myocyte injury)

Hypersensitivity

Giant cell

102
Q

What are the characteristics of myocarditis?

A

Hypertrophy

Advanced- flabby, hemorrhagic lesions

Acute- focal necrosis, interstitial inflammatory infiltrate

103
Q

What are some other causes of cardiomyopathies?

A

Cardiotoxic drugs

Amyloidosis (restrictive)

104
Q

What is pericardial effusion?

A

Accumulation of fluid within the pericardial space (> the normal 50mL)

105
Q

What is hemopericardium?

A

Accumulation of blood within the pericardial space

106
Q

How does pericardial effusion affect the heart?

A

Slow accumulation- sac dilates to allow for extra fluid

Rapid accumulation- can compress the heart, cardiac tamponade

107
Q

What are the two types of pericarditis?

A

Acute

Chronic/healed

108
Q

What are the forms of pericarditis and their characteristics?

A
  1. Serous- noninfectious inflammatory disease
  2. Fibrinous and serofibrinous- fibrin may be lysed or organized, friction rub
  3. Purulent/suppurative- active microbial infection, constrictive
  4. Hemorrhagic- blood and fibrinous or suppurative effusion
  5. Caseous- fibrocalcific, chronic constrictive, due to Tb
109
Q

What is the most frequent type of acute pericarditis?

A

Fibrinous and serofibrinous

110
Q

What is the difference between fibrinous and serofibrinous pericarditis?

A

Fibrinous- dry with fine granular roughening

Serofibrinous- more intense inflammation, accumulation of yellow-brown turbid fluid

111
Q

What are the characteristics of chronic/healed pericarditis?

A

Plaque-like fibrous thickenings of serosal membranes

Often little/no effect on function

112
Q

What are the forms of chronic pericarditis?

A

Adhesive mediastinopericarditis- strained systole

Constrictive pericarditis- heart is encased in dense, fibrous or calcific scar

113
Q

What heart diseases are associated with rheumatologic disorders?

A

Fibrinous pericarditis

Granulomatous rheumatoid nodules

Valvulitis

114
Q

What are the types of primary cardiac tumours and their characteristics?

A

Myxomas- globular and hard or papillary and myxoid, ball valve obstruction, affect left atria

Lipomas- left ventricle, right atrium or septum

Papillary fibroelastoma- anemone-like lesions in valves

Rhabdomyomas- valvular (outflow obstruction), spider cells (artifact), grey-white, small, usually multiple, may be considered hamartomas

Angiosarcoma and rhabdomyosarcoma

115
Q

What are the most common cardiac tumours in adults and children?

A

Adults- myxomas

Children- rhabdomyomas

116
Q

What are myxomas sometimes associated with?

A

Carney syndrome

117
Q

What are rhabdomyomas sometimes associated with?

A

Tuberous sclerosis

118
Q

How do non-cardiac neoplasms spread to the heart?

A

Metastasis- venous extension (kidney, liver)

Circulating mediators

119
Q

What are the complications associated with cardiac transplantation?

A

Cellular allograft rejection

Ab mediated rejection

Graft arteriosclerosis

Opportunistic infections

120
Q

What is the one and five year survival of cardiac transplantation?

A

1- 90%

5- 60%

Pathology (25 decks)

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