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Systems Pathology > Exam 3 [Diseases Of Heart] > Flashcards

Exam 3 [Diseases Of Heart] Flashcards

1
Q

Cause of Ischemic Heart Disease

A

Usually atherosclerosis

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2
Q

Cause of Hypertension Heart Disease

A

Obesity -> Hypertension -> Atherosclerosis

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3
Q

Cause of Valvular Disease

A

May be Congenital or a Complication of other Heart Diseases

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4
Q

Heart diseases that cause Valvular disease

A
  • Rheumatic fever
  • Infective Endocarditis
  • Ischemic heart Disease
  • Cardiomyopathies
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5
Q

Major Manifestations of Heart Disease

A
  • Pain
  • Change in Size (usually enlargement)
  • Failure
  • Arrythmias
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6
Q

Hypertrophy Definition

A

Increased muscle mass of a ventricle (decreasing size of chamber)

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7
Q

Heart Dilation definition

A
  • Heart muscles becomes flabby/hypotonic
  • Ventricle stretches (enlarging the chamber)
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8
Q

Cause of Arrythmias

A
  • Ischemia
  • Myocarditis
  • Drugs
  • Electrolyte abnormalities
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9
Q

Effect of an Arrythmia

A

Decreased Cardiac Output

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10
Q

Cause of “Low Output Failure” & What is “Low Output Failure”?

A

Caused by heart disease, failure of the pump

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11
Q

Cause of “High Output Failure” & What is “High Output Failure”?

A

Caused by diseases not of the myocardium, Heart can’t pump fast enough to meet tissues needs

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12
Q

Example of Low Output Failure

A
  • Acute MI
  • Cardiac Tamponade
  • tension Pneumothorax
  • Pulmonary Embolism
  • Acute Valve failure
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13
Q

Example of High Output Failure

A
  • Anemia
  • Hyperthyroidism
  • Pregnancy
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14
Q

What is “Forward Failure”?

A

Failure of delivery of the correct amount of blood to the tissues

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15
Q

What is “Backward Failure”?

A

Congestion of blood in the venous system due to failure of heart to keep blood circulating

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16
Q

Examples of Left Ventricular Failure:

A

1) Ischemic heart Disease
2) Hypertensive Heart Disease
3) Aortic OR Mitral Valve disease
4) Myocarditis
5) Cardiomyopathy
6) Cardiac Amyloidosis
7) High Out-Put States

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17
Q

Examples of Right Ventricular Failure:

A

1) MC: Left Ventricular Failure
2) Chronic Pulmonary Disease (cor pulmonale)
3) Pulmonary OR Tricuspid Valve Stenosis
4) Congenital Heart Disease

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18
Q

What is the most common cause of isolated Right Ventricular Failure?

A

Chronic Pulmonary Disease (cor pulmonale)

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19
Q

Systemic Effects of Acute LVF (forward failure)

A

1) Hypotension
2) Syncope
3) Cardiogenic Shock
4) Sudden Death

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20
Q

Systemic Effects of Acute LVF (backward failure)

A

Pulmonary Edema

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21
Q

Systemic Effects of Chronic LVF (forward failure)

A

1) Ischemia of all organs
2) Hypoxia of Kidneys (Sodium/Fluid retention)

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22
Q

Systemic Effects of Chronic LVF (backward failure)

A

Pulmonary Congestion

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23
Q

Systemic Effects of Acute RVF (forward failure)

A

Sudden Death

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24
Q

Systemic Effects of Acute RVF (backward failure)

A

Sudden, Painful Swelling of the Liver & Increased Jugular Venous Pressure

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25
Q

Systemic Effects of Chronic RVF (forward failure)

A

No Clinical Consequences

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26
Q

Systemic Effects of Chronic RVF (backward failure)

A
  • Swelling of ankles
  • Venous Congestion of Liver “Nutmeg Liver”
  • Increased Jugular Venous Pressure
  • Hypoxia of Kidneys (Sodium/Fluid retention)
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27
Q

4 Types of Ischemic heart Disease

A

1) Angina Pectoris
2) Chronic Ischemic heart Disease
3) Myocardial infarction
4) Sudden Cardiac Death

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28
Q

When does “Typical (Stable)” Angina Pectoris become a problem?

A

When Vessel is narrowed 75% or more of the area of the Lumen

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29
Q

Cause of “Typical (Stable)” Angina Pectoris

A

Atherosclerosis

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30
Q

Symptoms of “Typical (Stable)” Angina Pectoris

A
  • Recurrent chest pain w/ activity or stress
  • Pain is limited in duration & relieved by rest
  • Pain usually Substernal OR radiates to left arm, jaw & upper abdomen
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31
Q

What medication can decrease “Typical (Stable)” Angina Pectoris Pain?

A

Sublingual Nitroglycerin (Vasodilator)

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32
Q

“Unstable” Angina Pectoris is associated with

A

Atherosclerosis

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33
Q

Cause of “Unstable” Angina Pectoris

A

Worsening symptoms of angina due to Thrombus formation over plaque of atherosclerosis

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34
Q

What brings on the symptoms of “Unstable” Angina Pectoris?

A

Exercise
- less exercise needed to bring symptoms as time passes, eventually rest can bring symptoms

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35
Q

“Unstable” Angina Pectoris is also known as:

A

Crescendo Angina because it usually ends in a Myocardial Infarction

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36
Q

Cause of “Variant (Prinzmetal)” Angina Pectoris

A
  • Unknown
  • But it is due to Vasospasm NOT ATHEROSCLEROSIS
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37
Q

When does pain occur in “Variant (Prinzmetal)” Angina Pectoris?

A

Often at rest

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38
Q

Heart Attack = ???
MI = ???

A

Heart Attack = Clinical Syndrome
MI = Autopsy Finding
“A heart attack may not be produced by an AMI”

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39
Q

Myocardial Infarction Risk Factors:

A

1) Atherosclerosis
2) Systemic Hypertetion
3) Diabetes Mellitus
4) Smoking
5) Emotional Stress/ Physical Activity
6) Hypoxia (anemia or respiratory diseases)

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40
Q

What heart layers are damaged by Myocardial Infarction?

A

Endocardium or Pericardium
+ necrosis of muscle

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41
Q

Most Myocardial Infarction’s affect what chamber of the heart?

A

Left Ventricle

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42
Q

Arteries MCly causing a Myocardial Infarction & their Percentages

A

Right Coronary Artery (30%)
Left Anterior Descending Artery (50%)
Left Circumflex Artery (20%)

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43
Q

Enzymatic Proteins in Myocardial Infarction & When they rise

A

Troponins
CPK-MB (rise in 3-6 hours, peak at 18-24 hours)
SGOT & LDH also rise

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44
Q

ECG Features in a Myocardial Infarction

A

Elevation of ST Segment + Q Waves
- T wave Inversion

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45
Q

Risk Factors of Chronic Ischemic Heart Disease (Ischemic Cardiomyopathy)

A

1) Patchy loss of muscle w/ fibrosis and inflammatory cells
2) Chronic LVF or an arrhythmia (such as a heart block)

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46
Q

What is Chronic Ischemic Heart Disease (Ischemic Cardiomyopathy)?

A
  • Multiple atherosclerotic narrowing in the blood vessels
  • Irregular chronic MI
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47
Q

Definition of Sudden Cardiac Death:

A

Unexpected death due to a lethal arrythmia such as asystole or sustained ventricular fibrilation

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48
Q

Risk Factors of Sudden Cardiac Death:

A

1) Patients w/ atherosclerosis
2) People who smoke cigarettes

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49
Q

What decreases most rapidly following cessation of smoking?

A

Risk of Sudden Cardiac Death

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50
Q

Risk factors of the development of Ischemic Heart Disease:

A

Are basically the same as for Atherosclerosis
(Incidence for CIHD is used from the measurement of incidence of atherosclerosis in a population)

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51
Q

Pathology of Hypertensive Heart Disease:

A
  • Left ventricular hypertrophy
  • Left ventricular failure (40% of deaths in hypertensive patients)
  • Ischemic heart disease
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52
Q

Cause of Acute Cor Pulmonale

A
  • Pulmonary Hypertension leading to increased pressure in R. Side of the heart
  • Massive Pulmonary Embolism
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53
Q

Cause of Chronic Cor pulmonale

A
  • COPD
  • Autoimmune Diseases
  • Blood clots in lungs
  • Cystic Fibrosis
  • Scarring of Lung tissue
  • Severe Kyphoscoliosis
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54
Q

Pathophysiology of Acute Cor Pulmonale

A
  • Increased pressure in R. Side of heart
  • R. Ventricular dilatation & failure
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55
Q

Pathophysiology of Chronic Cor Pulmonale

A
  • Increased R. Ventricular afterload
  • Preserve’s stroke volume until Myocardium fails due to Ischemia or other pathological condition
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56
Q

Etiology of Mitral Stenosis

A
  • Chronic Rheumatic heart Disease
  • Female 9:1
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57
Q

Pathophysiology of Mitral Stenosis

A
  • Increased resistance to transmittal flow
  • Thickening of valve leaflets (narrowing the valve)
58
Q

Etiology of Mitral Regurgitation

A
  • 50% due to chronic rheumatic heart disease combined with aortic stenosis
  • “Fen-Phen” induced valvular fibrosis
59
Q

Mitral Valve prolapse is seen in what population?

A

1% of young adults (mostly females)

60
Q

Mitral Valve prolapse is due to:

A

Degeneration of the valve
(A.k.a. “Floppy Valve Syndrome”)

61
Q

Rupture of what can lead to Mitral Regurgitation?

A
  • Chordate Tendinae (due to endocarditis)
  • Papillary muscles (due to MI)
62
Q

Pathophysiology of Mitral Regurgitation

A
  • Volume & pressure is transmitted backward from left atrium to the pulmonary vasculature
  • disruption of the papillary muscles, chordate tendinae or valve leaflets (chronic = L. Ventricle)
63
Q

Etiology of Aortic Stenosis

A
  • Rheumatic Aortis Stenosis
  • Congenital bicuspid valves (50% of cases)
  • Hypertrophic cardiomyopathy
64
Q

Pathophysiology of Aortic Stenosis

A
  • Ventricle can no longer compensate -> L. Ventricle enlargement
  • Reduced ejection fraction & CO
  • Lipid accumulation
  • Inflammation
  • Calcification & Fibrosis of the valve
65
Q

Etiology of Aortic Regurgitation

A
  • Rheumatic heart disease (50%) usually associated with aortic stenosis & mitral valve disease
  • Syphilitic Aneurysm
  • Valve rupture due to endocarditis
66
Q

Pathophysiology of Aortic Regurgitation

A
  • Increase in regurgitation volume in L. Ventricle
  • Poor forward flow
  • Diastolic pressure increases -> acute pulmonary edema & cardiogenic shock
67
Q

Examples of Pulmonary Valve Stenosis

A

1) Congenital
2) Tetralogy of Fallot
3) Carcinoid Syndrome

68
Q

Populations affected by Rheumatic Fever

A
  • children 5-15 years old
  • lower social economic groups
69
Q

Etiology of Rheumatic fever

A
  • Occurs 2-6 weeks following streptococcal pharyngitis
  • Group A streptococcus (streptococcus pyogenes)
70
Q

Antigen/Antibodies in Rheumatic Fever

A
  • Associated w/ HLA-B5 antigen
  • Cross reacting antibodies (hypersensitivity Type II)
71
Q

Rheumatic Fever affects what layers of the heart?

A

All of Them

72
Q

Acute vs. Chronic presentation of Rheumatic Fever

A

Acute = “acute rheumatic carditis”
Chronic = “chronic valvular deformities”

73
Q

Affect of Rheumatic Fever on the Endocardium

A

Vegetations on the heart valves

74
Q

Affect of Rheumatic Fever on the Myocardium

A

(Myocarditis)
- Becomes pale, flabby & hypotonic
- Aschoff Body = Characteristic Lesion***

75
Q

Affect of Rheumatic Fever on the Pericardium

A

(Pericarditis) Only in the most severe cases

76
Q

Clinical Features of Rheumatic Fever

A
  • Fever
  • Arthritis
  • congestive heart failure, chest pain, shortness of breath
  • fatigue
  • chorea ( uncontrollable body movements)
77
Q

What is Chronic Rheumatic Heart Disease?

A

Severe valvular scarring occurring weeks to years after acute rheumatic fever

78
Q

Most common valvular lesions

A

1) Mitral Stenosis & Mitral Incompetence
2) Aortic Valve Lesions
3) Tricuspid Valve Lesions (10%)

79
Q

Complications of Chronic Rheumatic Heart Disease

A

1) Bacterial Endocarditis
2) Mural thrombi in the Atria or Ventricles
3) Cor pulmonale
4) Congestive Heart failure
5) Adhesive Pericarditis

80
Q

Nonbacterial Thrombotic Endocarditis Pathophysiology

A
  • has vegetations
  • nondestuctive
81
Q

Libman-Sacks Endocarditis Pathophysiology

A

Immune complex sterile vegetations on heart valves

82
Q

Acute Infective Endocarditis Organisms

A

Staph Aureus OR Streptococcus Pyogenes

83
Q

Acute Infective Endocarditis Presentation

A
  • Lasts less than 6 weeks
  • May have completely normal heart
  • may produce perforation of a valve
84
Q

Subacute Infective Endocarditis Presentation

A
  • Present longer than 6 weeks
  • Patient has pre-existing cardiac abnormality
  • Rarely perforates the valve
85
Q

Subacute Infective Endocarditis Organisms

A

Staphlococcus Epidermis OR Streptococcus Viridans

86
Q

Infective Endocarditis: Populations affected

A

1) Patients w/ Cardiac Abnormalities
2) Valve replacement surgery
3) Intravenous Drug abusers

87
Q

Pathology of Infective Endocarditis

A

1) vegetations on endocardium of valves that contain organisms
2) often large, hemorrhagic & friable producing septic emboli

88
Q

Complications of Infectious Endocarditis

A

1) Valve dysfunction w/ changing murmurs
2) Septic Emboli producing mycotic aneurysyms/abscesses
3) Immune complex diseases
4) Microinfarctions from Emboli

89
Q

Causes of Infectious Myocarditis

A

1) Viral infections
2) bacterial
3) Protozoa
4) Fungi
5) helminths

90
Q

Causes of Noninfectious Myocarditis

A

1) rheumatic fever
2) systemic lupus erthematosus
3) Allergic drug reactions
4) cardiac transplantation rejection
5) sarcoidosis

91
Q

Causes of Dilated Cardiomyopathy

A

1) Post-Myocarditis
2) Alcohol Toxicity
3) Pregnancy
4) Chemical Toxicity
5) Idiopathic dilated cardiomyopathy

92
Q

Pathology of Dilated Cardiomyopathy

A
  • general enlargement/dilation
  • poor contracting -> stagnant blood leading to mural thrombi & thromboemboli
  • may produce Arrythmias
93
Q

Populations affected in Dilated Cardiomyopathy

A
  • MC 20-60 years old
  • Men > Women
  • May be familial distribution
94
Q

Clinical aspects of Dilated Cardiomyopathy

A
  • Progressive congestive cardiac failure
  • Death
95
Q

Management of Dilated Cardiomyopathy

A

Cardiac Transplant

96
Q

Peripartum Cardiomyopathy

A

Exception (50% of patients recover spontaneously after pregnancy)

97
Q

Causes of Hypertrophic Cardiomyopathy

A
  • 50% Autosomal Dominant (chromosome 14)
  • All else = Idiopathic
98
Q

Pathology of Hypertrophic Cardiomyopathy

A
  • Assymetric myocardial hypertrophy in the Interventricular Septum
  • Heart weighs > 800 mg’s
  • Ventricular outflow obstruction
  • Dilated Left Atrium
99
Q

Clinical Effects of Hypertrophic Cardiomyopathy

A
  • Sudden death
  • Dyspnea, syncope & dizziness
  • systolic ejection murmur
  • angina pain
100
Q

Risks following Hypertrophic Cardiomyopathy

A
  • Bacterial Endocarditis
  • Progressive myocardial Fibrosis produces congestive cardiac failure
101
Q

Causes of Restrictive Cardiomyopathy

A

1) Cardiac amyloidosis
2) Sarcoidosis
3) Radiation injury
4) Hemochromatosis

102
Q

Pathology of Restrictive Cardiomyopathy

A
  • ventricular muscle becomes rigid & loses compliance
  • ventricle difficult to fill, but ejection is not forceful
103
Q

Clinical Effects of Restrictive Cardiomyopathy

A
  • Fatigue, Exertional Dyspnea, Anginal pain
  • May have arrythmias (including heart blocks)
104
Q

In later stages of Restrictive Cardiomyopathy…

A

Development of Congestive Cardiac Failure

105
Q

Causes of Obliterative Cardiomyopathy

A

1) tropical endocardial fibrosis
2) eosinophilic endomyocardial fibrosis (Loffler’s Syndrome)

106
Q

Pathology of Obliterative Cardiomyopathy

A
  • Atria are normal sized
  • Thick & Opaque Endocardium
  • Thick Valves
    -Endocardium Fibrosis extends to Myocardium
  • Eosinophil Infiltration
107
Q

Clinical Features of Obliterative Cardiomyopathy

A
  • Tropical form in equatorial Africa
  • Major Fibrosis & eosinophilia of Cardiac Muscle
  • Restrictive Disease
108
Q

Obliterative Cardiomyopathy accounts for what percent of childhood Heart disease?

A

10%

109
Q

Most common congenital defect diagnosed vs. most common that is prevalent:

A

Diagnosed: VSD
Most Prevalent: ASD (not diagnosed until adulthood)

110
Q

Risk Factors of Congenital heart disease

A

1) In-Utero Infectinos
2) Chromosomal Defects
3) In-Utero Chemical Exposure (FAS)
4) In-Utero Radiation Exposure
5) Premature Delivery

111
Q

Effects of Congenital heart disease

A

1) abnormal blood flow -> murmurs
2) Shunts of blood from one side of the heart to the other
3) Short circuits of blood through circulation
4) Infective Endocarditis
5) Failure to thrive

112
Q

Presence or absence of a shunt percentages in Congenital heart disease

A

W/O: 20%
W/: 80%

113
Q

Acyanotic Congenital Heart Diseases

A

With a Shunt there is no cyanosis because direction of blood flow is Left to Right

114
Q

Cyanotic Congenital Heart Diseases

A

Right to Left shunt so it bypasses the lungs

115
Q

Small VSD (maladie de Roger) Produces:

A

1) Produces low volume shunt in systole
2) Produces pansystolic murmur

116
Q

Small VSD (maladie de Roger) Symptoms

A

-Few symptoms
- Defect decreases in size as child grows & may close spontaneously

117
Q

What is a Large VSD

A
  • Volume overload & hypertrophy of both ventricles
  • Pansystolic murmur
118
Q

What happens due to a Large VSD?

A
  • Pulmonary Hypertension from increased pulmonary blood flow
  • Thick & Narrow pulmonary vessels
  • Eventually pressure in R. atrium increases so much that shunt flow decreases in volume & reverses itself
119
Q

Patient with a LArge VSD are at risk for:

A

Infective Endocarditis

120
Q

ASD Symptoms

A

(Usually none)
Patent Foramen Ovale doesnt produce symptoms, but functionally there is no movement of blood.

121
Q

ASD Clinical features

A
  • R. Ventricular Hypertrophy
  • Delayed pulmonary valve closing (Split S2)
  • Can produce a pulmonary ejection murmur
122
Q

ASD Main Complication

A
  • Pulmonary Hypertension
  • Increased Righ side pressure
  • Eventually reversal of the shunt
123
Q

What is Patent Ductus Arteriosus

A

-Ductus Arteriosus fails to close after birth
- Premature Infants

124
Q

What medication can potentially close ductus arteriosus?

A

Indomethacin

125
Q

Patent Ductus Arteriosus Pathology

A
  • Continual blood flow from aorta to pulmonary circulation -> Pulmonary Hypertension
  • “Machinery murmur” during entire cardiac cycle
126
Q

Left to Right Shunt Defects

A

1) VSD
2) ASD
3) Patent Ductus Arteriosus

127
Q

Right to Left Shunt Defects

A

[THESE PRODUCE CYANOSIS]
1) Tetrlogy of Fallot
2) Transportation of the Great Vessels
3) Eisenmenger’s Syndrome

128
Q

Tetralogy of Fallot Components

A

1) Over-riding Aorta
2) Pulmonary Stenosis
3) Right Ventricular Hypertrophy
4) Ventricular Septal Defect

129
Q

Tetralogy of Fallot Pathology & Treatment

A
  • Pulmonary. Stenosis increases R. Ventricle pressure
  • Surgery
130
Q

Tetralogy of Fallot Characteristic Behavior

A

Children running distance would have to squat down on their heels to equilibrate pressures

131
Q

Transposition of the Great Vessels Pathology

A

-Truncus Arteriosus forms abnormally
- Pulmonary trunk arises from L. Ventricle
- Aorta arises from R. Ventricle
(2 separate circulations)

132
Q

Transposition of the Great Vessels Fatality

A

Immediately unless Foramen Ovale & Ductus Arteriosus do not close

133
Q

What is Eisenmenger’s Syndrome

A
  • A reversal of a previously acyanotic shunt that now produces cyanosis
  • Once shunt reverses -> fatal and no longer eligible for surgery
134
Q

reversal of a shunt in Eisenmenger’s Syndrome makes the individual prone to:

A

Paradoxical Emboli

135
Q

Chronic Adhesive Pericarditis

A

May occur following bacterial infection of the pericardium where there was pus formation and exudate in the pericardium

136
Q

Chronic Restrictive Pericarditis

A
  • Associated with Tuberculosis
  • Tuberculosis Pericarditis encased the heart in fibrous tissue
137
Q

Glycogen Storage Diseases that affect the heart

A

Pompe’s Disease

138
Q

Myxoma

A

[Benign tumor of the heart]
- MC Primary Heart Tumor
- MC in Left Atrium

139
Q

Pompe’s Disease “Glycogenosis Type II”: What is it?

A
  • Autosomal Recessive
  • Lysosomal storage disorder
  • Alpha-Glucosidase (DAA) Deficiency
  • cant metabolize glycogen
140
Q

Pompe’s Disease “Glycogenosis Type II”: Accumulation of Glucose Causes what?

A
  • Mental retardation
  • enlarged heart, liver & spleen
  • cardiac muscle failure

Systems Pathology (6 decks)

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