The Heart - Chapter 12

Question 1

List the average normal heart weight for males and females

Answer 1

Heart weight – Female 250-300 g
Heart weight – Male 300-350 g (p. 523)

Question 2

List the average normal right and left ventricular free wall thickness.

Answer 2

The expected thickness of the free wall of the right ventricle is 0.3 to 0.5 cm and that of the left ventricle is 1.3-1.5 cm. (p. 523)

Question 3

List the four cardiac valves.

Answer 3

Semilunar valves – aortic and pulmonary Atrioventricular valves – mitral and tricuspid (p. 524)

Question 4

The _____________attach the papillary muscles to the atrioventricular valve leaflets.

Answer 4

Chordae tendineae (p. 524)

Question 5

Normally, the pericardial sac contains ________ml of fluid.

Answer 5

30-50 (p. 581)

Question 6

Where do the coronary arteries originate?

Answer 6

The coronary arteries originate from the aorta immediately distal to the aortic valve. (p. 525)

Question 7

List the three major epicardial coronary arteries and describe the distribution of their blood supply.

Answer 7

LAD – left anterior descending supplies most of the apex of the heart, the anterior wall of the left ventricle, and the anterior 2/3 of the ventricular septum.
LCX – left circumflex perfuses the lateral wall of the left ventricle.
RCA – right coronary artery supplies the entire right ventricular free wall, the posterobasal wall of the left ventricle, and the posterior third of the ventricular septum. (p. 542)

Question 8

Define congestive heart failure, and list the two most frequent causes.

Answer 8

In congestive heart failure, the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only from an elevated filling pressure.
The most frequent specific causes of congestive heart disease are hypertension and ischemic heart disease. (p. 526)

Question 9

Differentiate forward congestive heart failure from backward congestive heart failure.

Answer 9

Congestive heart failure is characterized by decreased cardiac output and tissue perfusion sometimes called forward failure) or pooling of blood in the venous system (backward failure), or both. (p. 528)

google:
Backward Heart Failure: One of the ventricles fails to pump out all of its blood that comes into it. Thus, the ventricular filling pressure and systemic or pulmonary edema increase. Forward Heart Failure: The heart is not pumping out enough blood to satisfy the needs of the cells of the body.

Question 10

Two major types of congestive heart failure are_____ and ______.

Answer 10

left sided and Right sided. (p. 528)

Question 11

Define cor pulmonale.

Answer 11

Pure right-sided heart failure occurring in patients with a variety of lung disorders occurs is called cor pulmonale. Pulmonary hypertension is a common feature. (p. 530)

Question 12

Left sided heart failure is often caused by ______________.

Answer 12

Ischemic heart disease, hypertension, aortic and mitral valvular diseases, and myocardial diseases (p. 529)

Question 13

The effects of left sided heart failure in the lungs, kidneys, and brain are

Answer 13

Lungs – pulmonary congestion and edema with wet heavy lungs, producing dyspnea on exertion and orthopnea. Hemosiderin-laden macrophages (heart failure cells) denote previous episodes of pulmonary edema.
Kidneys – prerenal azotemia; retention of salt and water with consequent expansion of the interstitial fluid and blood volumes.
Brain – cerebral hypoxia may give rise to hypoxic encephalopathy with resultant irritability, loss of attention span, and restlessness which may progress to stupor and coma. (p. 529)

Question 14

The effects of right sided heart failure on the liver, spleen, kidneys, soft tissue and brain are:

Answer 14

Liver and portal drainage system – congestive hepatomegaly, passive congestion, centrilobular necrosis, cardiac sclerosis, congestive splenomegaly, and ascites.
Kidneys – congestion (more pronounced than in left sided failure).
Subcutaneous tissue – peripheral edema of dependent portions of the body; anasarca. Brain – hypoxic encephalopathy, same as in left sided failure. (p. 530)

Question 15

Right sided heart failure in the liver gives rise to ______ which is grossly characterized by ________ and may lead to ________.

Answer 15

Congestive hepatomegaly
Chronic passive congestion (nutmeg liver)
Centrilobular necrosis and cardiac sclerosis or cardiac cirrhosis (p. 530)

Question 16

Define anasarca.

Answer 16

Generalized massive edema (p. 530)

Question 17

The clinical manifestations of ischemic heart disease can be divided into what syndromes.

Answer 17

Myocardial infarction
Angina Pectoris
Chronic ischemic heart disease with heart failure Sudden cardiac death (p. 538)

Question 18

Define and differentiate the two types of myocardial infarct.

Answer 18

Most myocardial infarcts are transmural, in which the ischemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. A subendocardial infarct constitutes an area of ischemic necrosis limited to the inner 1/3 to 1⁄2 of the ventricular wall. (p. 543)

Question 19

Differentiate myocardial infarction from ischemic cardiomyopathy. Define angina pectoris.

Answer 19

The term ischemic cardiomyopathy is often used by clinicians to describe chronic ischemic heart disease. Clinically, progressive CHF may occur in patients who have had past episodes of MI or anginal attacks.
Angina pectoris is a symptom complex of ischemic heart disease characterized by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort caused by transient myocardial ischemia that falls short in inducing the myocyte necrosis. (p. 564, p. 540)

google:
Cardiac ischemia means that blood flow to the cardiac muscle tissue has decreased, which can lead to poor oxygen supply or hypoxia. Myocardial infarction means that the blood flow is completely cut off, resulting in cellular death or necrosis of the affected part of the heart muscle

Question 20

The majority of myocardial infarcts occur in the ______ ventricle.

Answer 20

Left (p. 544)

Question 21

The stain used to macroscopically differentiate ischemic vs. non-ischemic areas of the myocardium is known as ________.

Answer 21

Triphenyltetrazolium chloride (p.544)

Question 22

The most classic clinical symptoms of an acute myocardial infarction are_________.

Answer 22

Rapid, weak pulse, diaphoresis, and dyspnea (p. 547)

Question 23

The most sensitive and specific biomarkers of myocardial damage are cardiac specific proteins, _____.

Answer 23

Troponins I and T (p. 547)

Question 24

The. cause of myocardial ischemia is reduced bloodflow due to______________.

Answer 24

Atherosclerotic lesions in the coronary arteries (p. 538)

Question 25

the minimal criteria for the diagnosis of hypertensive heart disease are________and_________.

Answer 25

Left ventricular hypertrophy (usually concentric)
A history or pathologic evidence of hypertension (p. 552)

Question 26

Thickening of the left ventricular wall at the expense of left ventricular chamber volume is known as ________.

Answer 26

Pressure overload or concentric hypertrophy (p. 552)

Question 27

Describe the typical microscopic changes of hypertrophied myocardium.

Answer 27

Microscopically, the earliest change of systemic hypertensive heart disease is an increase in transverse myocyte diameters. The cellular and nuclear enlargement becomes somewhat more prominent and irregular with variation in cell size among adjacent cells and interstitial fibrosis. (p. 552)

Question 28

Define rheumatic fever and correlate it with the development of rheumatic heart disease.

Answer 28

Rheumatic fever is an acute immunologically mediated multisystem inflammatory disease that occurs a few weeks after an episode of group A streptococcal pharyngitis and often involves the heart. Acute rheumatic carditis, which complicates the active phase of rheumatic fever may progress to chronic valvular deformities. (p. 557)

Question 29

Characteristic microscopic findings in rheumatic fever are____________________.

Answer 29

Aschoff bodies and Anitschkow cells (p. 558)

Question 30

Describe the effect of acute rheumatic fever on all three layers of the heart.

Answer 30

During acute rheumatic fever, diffuse inflammation and Aschoff bodies may be found in any of the three layers of the heart – pericardium, myocardium, or endocardium – (pancarditis.) In the pericardium, they are accompanied by a fibrinous or serofibrinous pericardial exudate, described as bread and butter pericarditis, which generally resolves without sequelae. The myocardial involvement – myocarditis – takes the form of scattered Aschoff bodies within the interstitial connective tissue, often perivascular. Concominant involvement of the endocardium and the left sided valves by inflammatory foci typically results in fibrinoid necrosis within the cusps or along the tendinous cords on which sit small vegetations (verrucae) along the lines of closure. (p. 558)

Question 31

The most common valves involved in rheumatic heart disease are______________.

Answer 31

Mitral and aortic (left sided) (p. 558)

Question 32

Rheumatic vegetations are most commonly located on what part of the valve?

Answer 32

cusps (p. 558)

Question 33

after healing and scarring, the name for the most common appearance of the stenotic rheumatic mitral valve is known as ________ or ___________.

Answer 33

Fish mouth or buttonhole stenosis. (p. 559)

Question 34

The chordae tendineae in rheumatic are ___________.

Answer 34

Thickened, and fused (p. 558)

Question 35

Briefly describe the changes seen in the joints and in the skin in cases of rheumatic fever.

Answer 35

Migratory polyarthritis of the large joints and subcutaneous nodules. Erythema marginatum of the skin. (p. 559)

Question 36

The most important consequence of rheumatic fever is_____________.

Answer 36

Chronic rheumatic heart disease, characterized by deforming fibrotic valvular disease (p. 559)

Question 37

What is the most common form of congenital cardiac anomaly?

Answer 37

Ventricular septal defect (p. 531)

Question 38

Most congenital anomalies of the heart develop during what weeks of fetal life?

Answer 38

3 through 8 (Not in Robbins)

Question 39

The most common complication and/or cause of death in patients with ventricular septal defects is ___________.

Answer 39

Irreversible pulmonary vascular disease (pulmonary hypertension) (p. 535)

Question 40

The major types of atrial septal defects are ________________.

Answer 40

Secundum ASD, primum ASD, sinus venosus ASD (p. 534)

Question 41

Some of the more common complications of atrial septal defects are_________.

Answer 41

Irreversible pulmonary vascular disease, heart failure, paradoxical embolization (p. 534)

Question 42

Define transposition of the great vessels.

Answer 42

Transposition of the great vessels produces ventriculoarterial discordance; the aorta arises from the right ventricle and lies anterior and to the left of the pulmonary artery which emanates from the left ventricle. (p. 536)

Question 43

The most common form of cyanotic congenital heart disease is_________.

Answer 43

Tetralogy of Fallot (p. 535)

Question 44

The four features of Tetralogy of Fallot are____________.

Answer 44

Ventricular septal defect, subpulmonary stenosis, aorta that overrides the VSD, and right ventricular hypertrophy (p. 535)

Question 45

The ductus arteriosus is situated between which two blood vessels and is a remnant of which aortic arch?

Answer 45

Pulmonary artery and aorta
Remnant of the 6th aortic arch (Not in Robbins)

Question 46

Define and differentiate the types of coarctation of the aorta.

Answer 46

Infantile form with tubular hypoplasia of the aortic arch proximal to a patent ductus arteriosus that is often symptomatic in early childhood.
Adult form in which there is a discrete ridge like infolding of the aorta, just opposite the closed ductus arteriosus distal to the arch vessels. (p. 537)

Question 47

Define infective endocarditis and differentiate the two forms.

Answer 47

-Infective endocarditis is characterized by colonization or invasion of the heart valves, the mural endocardium, or other cardiovascular sites by a microbe, leading to the formation of vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissues.

-Acute infective endocarditis is typically caused by infection of a previously normal heart valve with a highly virulent organism that produces necrotizing, ulcerative, destructive lesions.
In contrast, infective organisms of low virulence can cause infection in a previously abnormal heart, particularly on deformed valves. In such cases, the disease may appear insidiously, and even untreated, pursue a protracted course of weeks to months (subacute endocarditis). (p. 559)

google:
Acute IE — develops suddenly and may become life threatening within days.
Subacute or chronic IE (or subacute bacterial endocarditis) — develops slowly over a period of weeks to several months.

Question 48

In contrast, infective organisms of low virulence can cause infection in a previously abnormal heart, particularly on deformed valves. In such cases, the disease may appear insidiously, and even untreated, pursue a protracted course of weeks to month

Answer 48

Streptococcus viridans (p. 559)

Question 49

Give several mechanisms for the development of infective endocarditis.

Answer 49

Obvious infection elsewhere, dental or surgical procedure that causes a bacteremia, injection of contaminated material directly into the blood stream by IV drug users or trivial breaks in the epithelial barriers of the gut, oral cavity, or skin (p. 560)

Question 50

The hallmark lesion in infective endocarditis is the_________and most frequently involves which cardiac valves?

Answer 50

Vegetation
Aortic and Mitral valves (p. 560)

Question 51

Define and differentiate the acute vs. the chronic form of cor pulmonale.

Answer 51

Acute cor pulmonale – there is marked dilation of the right ventricle without hypertrophy. Acute cor pulmonale can follow massive pulmonary embolism.
Chronic cor pulmonale results from right ventricular hypertrophy and dilation secondary to prolonged pressure overload. (p. 553)

Question 52

Define cardiac tamponade.

Answer 52

Rapidly developing fluid collections of as little as 200-300 mL may produce compression of the thin-walled atria and vena cava or the ventricles themselves, restricting cardiac filling, producing potentially fatal cardiac tamponade. (p. 573)

Question 53

Define and differentiate the five different types of acute pericarditis.

Answer 53

Serous pericarditis – characteristically produced by non-infectious inflammatory diseases such as rheumatic fever, SLE, scleroderma, tumor, or uremia; may result from an infection in the tissues contiguous to the pericardium that produces a sterile serous effusion and an inflammatory reaction in epicardial and pericardial surfaces.
Fibrinous and serofibrinous pericarditis – most frequent type of pericarditis and composed of serous fluid mixed with a fibrinous exudate.
Purulent or suppurative pericarditis – invasion of the pericardial space by microbes.
Hemorrhagic pericarditis – an exudate composed of blood mixed with a fibrinous or suppurative effusion most commonly caused by the spread of a malignant neoplasm to the pericardial space. Caseous pericarditis – Caseation within the pericardial sac. The pericardium is usually involved by direct spread from tuberculous foci within the tracheobronchial nodes. (p. 574)

Question 54

. Renal failure with associated uremia gives rise to________pericarditis.

Answer 54

Fibrinous (p.574)

Question 55

Define and differentiate the two categories of primary myocardial disease.

Answer 55

Cardiomyopathy – heart disease resulting from a primary abnormality in the myocardium Myocarditis – infectious microorganisms and/or an inflammatory process causes myocardial injury (p. 578 and 571)

Question 56

List and differentiate the three categories of cardiomyopathy.

Answer 56

Dilated cardiomyopathy – progressive cardiac hypertrophy, dilation, and contractile dysfunction

Hypertrophic cardiomyopathy – myocardial hypertrophy, abnormal diastolic filling, and intermittent left ventricular outflow obstruction

Restrictive cardiomyopathy – primary decrease in ventricular compliance resulting in impaired ventricular filling during diastole (p. 564)

Question 57

The typical gross pathologic changes in cases of cardiomyopathy are________.

Answer 57

Dilated cardiomyopathy – the heart is usually heavy, weighing 2-3 times normal, enlarged and flabby, with dilation of all chambers

Hypertrophic cardiomyopathy – massive myocardial hypertrophy without ventricular dilation - asymmetric septal hypertrophy (p. 567, 569)

Question 58

What are the most characteristic histologic features of hypertrophic cardiomyopathy?

Answer 58

1) Extensive myocyte hypertrophy
2) Myofiber disarray.
3) Interstitial and replacement fibrosis (p. 569)

Question 59

Define endocardial fibroelastosis.

Answer 59

Endocardial fibroelastosis is characterized by focal or diffuse fibroelastic thickening usually involving the mural left ventricular endocardium. Often accompanied by some form of congenital (p. 570)

Question 60

Define and differentiate the two forms of non-bacterial endocarditis.

Answer 60

Non-bacterial thrombotic endocarditis is characterized by the deposition of small sterile thrombi on the leaflets of the cardiac valves.

Libman-Sacks endocarditis – Mitral and tricuspid valvulitis with small, sterile vegetations, encountered in systemic lupus erythematosus. (p. 561-562)

Question 61

List the classic clinical features of carcinoid syndrome.

Answer 61

Flushing of the skin, cramps, nausea, vomiting, and diarrhea. (p. 562)

Question 62

The most common primary tumor of the heart in adults is the __________, which is most common in the _________ atrium.

Answer 62

Myxoma
Left atrium (left to right ratio 4:1) (p. 575)

Question 63

The most frequent primary tumor of the heart in infants and children is the________.

Answer 63

Rhabdomyoma (p. 576)

Question 64

What are the two most common causes for cardiac transplantation?

Answer 64

Dilated cardiomyopathy and ischemic heart disease (p. 577)