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Chapter 10 - Heart Pathology Flashcards

1
Q

Congestive Heart Failure

A

Multisystem derangement occurring when the heart is unable to eject the blood delivered to it by the venous system, “forward failure”

Caused by: Left - systemic hypertension, mitral/aortic valvular disease, ischemic heart disease, primary cardiomyopathies
Right - 2 to L heart failure, pulmonary hypertension

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2
Q

Stages of Congestive Heart Failure

A

1 - compensated failure: increased catecholamines (improve contractility), hypertrophy of myocytes and chamber dilation
2 - uncompensated failure: clinical signs of venous congestion appear (pulmonary edema, peripheral edema, congestion of abdominal viscera), cyanosis & acidosis due to decreased tissue perfusion

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3
Q

Clinical signs of Left heart failure

A 
pulmonary edema
pleural effusions
dyspnea
dyspnea lying down
"orthopnea"
fatigue, tachycardia
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4
Q

Clinical signs of Right heart failure

A 
systemic venous congestion
soft tissue edema
distended neck veins
enlarged liver
inc. deep vein thromboses/pulmonary emboli
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5
Q

Hypertensive heart disease

A

left ventricular hypertrophy in an indiv w/ history of hypertension
*Concentric ventricular thickening rather than eccentric

Clinical features: CO normal = asymptomatic
L heart failure appears with ischemia (angina pectoris)

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6
Q

Cor Pulmonale

A

R ventricular hypertrophy secondary to pulmonary arterial hypertension (lung disease, esp w/ scarring, multiple small pulmonary emboli)

Both reduce vascular bed, inc pulmonary arterial pressure

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7
Q

Congenital heart disease

A

atrial septal defects, ventricular septal defects, patent (persistent) ductus arteriosus, tetralogy of Fallot, transposition of the great arteries, coarctation of aorta

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8
Q

Shunts

A

small hole or passage which allows movement of fluids from one part of the body to another

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9
Q

Left to right shunt

A

pressure higher in left heart than in right heart, no cyanosis initially, late cyanosis when shunt reverses due to pulmonary hypertension

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10
Q

Atrial septal defect

A

*Most common congenital cardiac malformation first diagnosed in adults, no symptoms in childhood, pulmonary hypertension may reverse shunt and produce cyanosis

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11
Q

Ventricular Septal Defect (VSD)

A

Most common congenital heart disease (CHD) diagnosed at birth (most are small and close spontaneously)

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12
Q

Patent Ductus Arteriosus

A

Ductus arteriosus normally closes shortly after birth, Patent ductus arteriosus usually identified early on the corrected w/ medication or surgery, eventually shunt reverses due to pulmonary hypertension and cyanosis develops

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13
Q

Right to left shunt

A

pressure higher in right heart than in left heart
**Cyanosis initially since blood is shunted away from lungs (reduced oxygenation)

Tetralogy of Fallot

Blood is diverted from pulmonary circulation to systemic thus reducing oxygenation, cyanosis at or near birth

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14
Q

Tetralogy of Fallot

A

1 - Pulmonary Artery Stenosis
2 - Overriding aorta
3 - Ventriculoseptal defect
4 - Right ventricular hypertrophy

May also have a patent ductus which helps oxygenate the blood

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15
Q

Transposition of the Great Arteries

A

Second leading cause of congenital cyanosis

abnormal truncal septation, aorta arises from R ventricle and the pulmonary artery arises from L ventricle

*Cyanosis is the main clinical sign

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16
Q

Coarcation of Aorta

A

Abnormal narrowing of the aortic lumen (blood pressure higher in arms than legs)

Cerebral hemorrhages common due to inc intracranial arterial pressure

Weak pulses in the lower extremities with signs and symptoms of intermittent claudication (ischemic leg pain)

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17
Q

Ischemic Heart Disease

A

imbalance between myocardial supply (perfusion) and cardia demand for oxygenated blood

most common cause: atherosclerotic narrowing of coronary arteries

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18
Q

4 forms or manifestations of ischemic heart disease

A

1) angina pectoris (ischemic chest pain)
2) myocardial infarction (MI)
3) sudden cardiac death (SCD)
4) chronic ischemic heart disease w/ heart failure

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19
Q

“Acute Coronary Syndrome”

A

an umbrella term for 3 acute conditions resulting from coronary artery disease

1 - unstable angina pectoris
2 - acute myocardial infarction
3 - sudden cardiac death

**All 3 result from acute changes in the morphology of coronary atherosclerotic plaques

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20
Q

Etiology of Coronary Artery Disease

A

Hypertension, Diabetes (type I and II), Smoking, High levels of LDL, Low levels of HDL, Poorly understood hereditary factors

21
Q

Coronary Artery plaque

A

critical stenosis

> 75% luminal reduction of 1+ coronary arteries,
compensatory vasodilation is insufficient to compensate

22
Q

Acute Plaque Changes

A

abrupt changes in plaque followed by thrombosis (fissuring, hemorrhage into plaque, overt plaque rupture w/ embolization of atheromatous debris)

may occur w/ plaques less than 75% occlusive and in prev asymptomatic individuals

23
Q

Coronary Artery Thrombosis

A

1 - plaque rupture exposes thrombogenic lipids and subendothelial collagen initiating thrombosis
2 - if vessel completely occluded, infarction occurs

If vessel incompletely occluded, unstable angina or lethal ventricular arrhythmia results

24
Q

Angina Pectoris

A

Intermittent chest discomfort or pain caused by transient, reversible myocardial ischemia

25
Stable Angina Pectoris
Associated with fixed atherosclerotic narrowing of 1+ coronary arteries Discomfort in chest described as deep, poorly localized pressure, squeezing or burning sensation Produces by physical activity, emotional excitement, or physiological stress Pain relieved by rest and/or nitroglycerin or calcium channel blockers
26
Prinzmetal Angina Pectoris
Anginal pain occurring at rest or awakening patient from sleep Usually associated with coronary artery spasm often adjacent to a site of atherosclerotic plaque Mechanism underlying spasm poorly misunderstood
27
Unstable Angina Pectoris
Increased frequency of angina episodes Precipitated by progressively less exertion Described as intense pain More intense - last longer than "stable anginga" (>20 min) Induced by acute plaque change w/ a superimposed partial thrombosis or vasospasm or both
28
Myocardial Infarction
development of an area of myocardial necrosis caused by localized ischemia Risk factors are same as atherosclerosis Myocardial necrosis begins w/ 20-30 min reaching full size within 3-6 hours Begins in subendocardium extending toward epicardium Thrombolytic agents may limit size of infarct during this time frame
29
Clinical complications of Acute MI
sudden death, cardia arrhythmias, left heart failure, cardiogenic shock, myocardial rupture w/ hemopericardium and cardia tamponade, thromboembolism
30
Anatomic Complications of MI
Infarcted papillary muscle and mitral valve insufficiency External rupture of the infarct w/ cardia tamponade Mural thrombus giving rise to systemic arterial emboli Ventricular aneurysms
31
Sudden Cardiac Death
Most common cause: ischemic heart disease (coronary artery atherosclerosis) (acute "cor pulmonale" due to massive pulmonary artery thromboembolism
32
Valvular Heart Disease
Mitral valve stenosis | Regurgitation
33
Calcific Aortic Stenosis
age related degeneration, most common cause of isolated aortic stenosis in USA, L ventricular hypertrophy and dec aortic outflow lead to myocardial ischemia, death within 3-4 years unless treated
34
Mitral Valve Prolapse
results in mitral regurgitation, common cardiac disorder, prone to infective endocarditis/ arrhythmias/ emboli from L atrium *most cases are sporadic; may be seen with Marfan syndrome
35
Rheumatic Fever
acute, immunologically-mediated, multisystem inflammatory disease usually following group A streptococcal pharyngitis after an interval of a few weeks Pharyngitis severity not related to risk of developing RF Pathogenesis: Hypersensitivity reaction induced by group A streptococci, antibodies developed against "M" proteins of group A strep cross-react w/ similar epitopes in heart, joints, skin, and other, comprised of **"Anitschkow cells" Acute RF - rarely causes heart failure due to myocarditis and valvular injury Chronic RF - irreversible valvular deformity (Mitral valve 95%, Mitral+Aortic 25%)
36
Infective Endocarditis
Infection of cardiac valves or mural surfaces of endocardium Gradual onset or explosive onset depending upon the virulence of the organism (Low - low-grade fever, malaise, weight loss) (High - high ever, shaking chills, overt septicemia)
37
Acute Infective Endocarditis
Organisms of high virulence Staph aureus Often involves normal valves Intravenous drug use Often tricuspid and pulmonic valves rather than left heart valves
38
Subacute Infective Endocarditis
Organisms of low virulence 50-60% of cases of endocarditis occurring on damaged valves are caused by Strep viridans Pre-existing cardiac abnormalities, especially valvular disease (small ventriculoseptal defects, chronic rheumatic valvular disease, calcific aortic stenosis, mitral valve prolapse
39
Noninfective Endocarditis
Systemic Lupus Erythematosus: Endocarditis Usually mitral valve "Libman-Sacks disease"
40
Dilated Cardiomyopathy
4 chamber dilation and hypertrophy Idiopathic Fundamental defect is ineffective contraction: ejection fraction < than 25%. Normal = 55-70% Some association w/ alcoholism and prior viral myocarditis Occur at any age, more often in men, 20-30% due to inherited genetic disorders
41
Hypertrophic Cardiomyopathy
"Idiopathic hypertrophic subaortic stenosis" Heavy, muscular, hypercontracting heart Genetic basis of 50% of cases; AD One of most common causes of sudden unexpected death in young athletes
42
Myocarditis
Inflammatory process of the myocardium resulting in injury to cardiac myocytes Causes: viral, bacterial, parasitic, fungal, immune-mediated myocardial injury
43
Pericarditis
Inflammatory process involving the pericardium as a result of a systemic disease or a primary pericardium disorder Morphologically classified in 5 types: fibrinous, serous, purulent, hemorrhagic, caseous
44
Fibrinous Pericarditis "Bread & Butter" pericarditis
most frequent type pericardium opaque and granular associated w/ acute myocardial infarction, SLE, chest irradiation and trauma May develop a loud pericardial friction rub Can compromise cardiac output due to fluid accumulation in pericardial sac Histology shows the deposition of fibrin and leukocytic exudate
45
Bacterial (purulent) Pericarditis
Occurs by direct infection during trauma, thoracic surgery, or catheter drainage, by spread from an intrathoracic, myocardial, or subdiaphragmatic focus, and by hematogenous dissemination Frequent causes are staph, Haemophilus, and M. tuberculosis
46
Hemorrhagic pericarditis
Involves blood mixed w/ a fibrinous or suppurative effusion Most commonly caused by tuberculosis or direct neoplastic invasion Can occur in sever bacterial infections or in patients w/ a bleeding diathesis
47
Pericardial effusions
Fluid accumulation in the pericardial space Nature of fluid varies with the cause of the effusion -Serous: congestive heart failure, hypoalbuminemia -Serosanguineous (watery, blood tinged): blunt chest trauma, malignancy -Chylous (milky) mediastinal lymphatic obstruction, usually by mediastinal neoplasm Clinical features: Cardiac tamponade (heart unable to expand during diastole due to fluid in sac)
48
Hemopericardium
Ruptured infarction Penetrating cardiac trauma Cardiac tamponade results
49
Atrial Fibrillation
a disease of the heart characterized by irregular and often faster heartbeat Predisposes the patient to thromboemboli from the left heart resulting in ischemic strokes Most patients on long-term anticoagulation are being treated for this reason Clinical Features: may be asymptomatic, dizziness, light-headness, syncope, tachycardia, stroke, Treatment: Warfarin and Factor X/ Thrombin antagonists

Pathology (13 decks)

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