Heart

Front 1

What is Ischemic Heart Disease?

Back 1

1) Caused by partial or complete interruption of arterial blood flow to the myocardium.
2) Most cases, are caused by atherosclerotic narrowing of the coronary arteries, sometimes acutely aggravated by superimposed thrombosis or vasospasm.
3) May be clinically silent or manifest as angina pectoris, MI, or chronic ischmic heart disease.

Front 2

What is Angina pectoris?

Back 2

Episodic chest pain caused by inadequate oxygenation of the myocardium
2) Stable angina
3) Unstable angina
4) Prinzmetal angina

Front 3

What is stable angina?

Back 3

1) Most common form of angina
2) Pain that is precipitated by exertion and is relieved by rest or by vasodilators, such as nitroglycerin.
3) Results from severe narrowing of atherosclerotic coronary vessels, which are thus unable to supply sufficient oxygenated blood to support the increased myocardial demands of exertion.

Front 4

What is unstable angina?

Back 4

1) Prolonged or recurrent pain at rest
2) Often indicative of imminent MI

Front 5

What is prinzmetal angina?

Back 5

1) Intermittent chest pain at rest
2) Generally considered to be caused by vasospasm.

Front 6

What are the general characteristics of an MI?

Back 6

1) Most important cause of morbidity from ischemic heart disease and is one of the leading causes of death in the Western world.
2) Characterized by myocardial coagulative necrosis caused by coronary artery occlusion.
3) Marked by a series of progressive changes involving gross and microscopic appearance of the heart and release of myocardial enzymes and other proteins into the bloodstream caused by altered membrane permeability of necrotic myocardial cells.

Front 7

What are the two distinct patterns of myocardial ischemic necrosis?

Back 7

1) Transmural infarction: myocardial necrosis that traverses the entire ventricular wall from endocardium to epicardium
2) Subendocardial infarction: myocardial necrosis that is limited to the interior one third of the wall of the left ventricle.

Front 8

What are complications of an MI?

Back 8

1) Arrhythmia: most common cause of death in the first several hours following infarction
2) Myocardial (pump) failure: can lead to CHF and/or shock. The likelihood and severity are determined by the size and location of the lesion.
3) Myocardial rupture: Catastrophic complication that usually occurs within the first 4-7 days and may result in death from cardiac tamponade, a compression of the heart by hemorrhage into the pericardial space.
4) Ruptured papillary muscle
5) Mural thrombosis: thrombus formation on the endocardium overlying the infarct; may lead to left-sided embolism
6) Ventricular aneurysm

Front 9

What is Rheumatic Fever?

Back 9

1) Multisystem inflammatory disorder with cardiac manifestations and sequelae, most often affecting children betewen ages 5-15
2) Characterized by transient mild migratory polyarthritis
3) Usually occurs 1-4 weeks after an episode of tonsillitis or other infection cauesd by group A Beta-hemolytic streptococci. An elevated titer of antistreptolysin O (ASO) is evidence of a recent streptococcal infection.

Front 10

What happens 0-6 hours after an MI?

Back 10

Gross: none
Microscopic: No morphologic changes at first; vascular congestion at perimeter of lesion after the first few hours
Arrhythmia most common cause of death in early hours
CK-MB: weakly positive
Troponin I: weakly positive

Front 11

What happens 12 hours after an MI?

Back 11

Gross: none
Microscopic: First appearane of neutrophils in viable tissue adjacent to the lesion
12-16 hours:
CK-MB: strongly positive
Troponin I: strongly positive
AST: weakly positive

Front 12

What happens 12-24 hours after an MI?

Back 12

Gross: Slight swelling and change of color
Microscopic: Cytoplasm displays increasing affinity for acidophilic dyes, and striations are lost; nuclei disappear; neutrophils infiltrate the lesion
24 hours:
CK-MB: peaks
Troponin: peaks
AST: more positive

Front 13

What happens by 24 hours after an MI?

Back 13

Gross: Pale or reddish brown infarct with surrounding hyperemia
Microscopic: Well-developed changes of coagulative necrosis; progressive infiltration of neutrophils
2 days:
CK-MB: persists
Troponin I: persists
AST: peaks

Front 14

What happens by the third day after an MI?

Back 14

Gross: Increasingly yellow color of infarct
Microscopic: Replacement of neutrophils by macrophages; phagocytosis of debris begins
3 days:
CK-MB: negative
Troponin I: persists
AST: negative
LDH: peaks

Front 15

What happens from 7 days after an MI?

Back 15

Gross: Yellow infarcted area surrounded by congested red border
Microscopic: Beginning of growth of young fibroblasts and newly formed vessels into the lesion; replacement of neutrophils by macrophages and phagocytosis of debris continue
4-7 days:
Troponin: persists
LDH: persists

Front 16

What happens from 10 days after an MI?

Back 16

Gross: Red, newly formed vascular connective tissue encircles and gradually replaces yellow necrotic tissue.
Microscopic: Growth of fibrovascular tissue continues; replacement of neutrophils by macrophages and phagocytosis of debris are almost complete.

Front 17

What happens between the 2nd and 4th week post MI?

Back 17

Gross: no change
Microscopic: Progressive synthesis of collagen and other intracellular matrix proteins

Front 18

What happens from week 5 post MI?

Back 18

Gross: increasing pallor of infarct because of progressive fibrosis
Microscopic: progressive fibrosis

Front 19

What happens within 3-6 months post MI?

Back 19

Gross: well-developed gray-white scar
Microscopic: Mature fibrous tissue replaces area of infarction
Ventricular aneurysm may occur in scarred area

Front 20

What is the etiology of rheumatic fever?

Back 20

1) Apparently of immunologic origin rather than a result of direct bacterial involvement; however, the precise nature of the immune mechanism of injury remains unclear
2) Postulated to occur as a result of streptococcal antigens that elicit an antibody response reactive to streptococcal organisms as well as to human antigens in the heart and other tissues.
3) remarkably reduced in incidence in the Western World in recent years

Front 21

What are aschoff bodies?

Back 21

1) Classic lesion of rheumatic fever
2) An area of focal interstitial myocardial inflammation that is characterized by fragmented collagen and fibrinoid material, by large cells (Antischkow myocytes), and by occasional multinucleated giant cells (Aschoff cells).

Front 22

What is pancarditis in regard to rheumatic fever?

Back 22

1) Pericarditis; may result in pericardial pleural, or other serous effusions.
2) Myocarditis; may lead to cardiac failure and is the cause of most deaths occurring during the early stages of acute rheumatic fever.
3) Endocarditis; leads to valvular damage.

Front 23

What is rheumatic endocarditis?

Back 23

Usually occurs in areas subject to greatest hemodynamic stress, such as the points of valve closure and the posterior wall of the left atrium, resulting in the formation of the so-called MacCallum plaque.
The Mitral and Aortic valves, which are subjected to much greater pressure and turbulence, are more likely to be affected than are the tricuspid and pulmonaary valves

Front 24

What happens in the early stages of rheumatic endocarditis?

Back 24

Valve leaflets are red and swollen, and tiny, warty, bead-like, rubbery vegetations (verrucae) form along the lines of closure of the valve leaflet.
Small, firm verrucae of acute rheumatic fever are nonfriable and are not a source of peripheral emboli.

Front 25

What happens after fibrotic healing in regard to rheumatic endocarditis?

Back 25

Valves become thickened, fibrotic, and deformed, often with fusion of valve cusps as well as thickening of the chordae tendineae.
Calcification is often prominent
These late sequelae, which often occur many years after the episode of rheumatic fever, are grouped under the term rheumatic heart disease (RHD)

Front 26

What happens to the mitral valve in RHD?

Back 26

1) Valve that is most frequently involved in RHD
2) Only valve affected in almost 50% of cases
3) Can be affected by stenosis with fish-mouth button hole deformity, insufficiency, or a combination of both.
4) Mitral stenosis is marked by diastolic pressure higher in the left atrium than in the left ventricle

Front 27

What happens to the aortic valve in RHD?

Back 27

1) Affected most often along with the mitral valve
2) Can be affected by stenosis or insufficiency

Front 28

What happens to the tricuspid valve in RHD?

Back 28

Affected along with the mitral valve and aortic valve (trivalvular involvement) in approximately 5% of cases of RHD.

Front 29

What happens to the pulmonary valve in RHD?

Back 29

Rarely involved

Front 30

List the noncardiac manifestations of acute rheumatic fever.

Back 30

Fever
Malaise
Increased ESR
Joint involvement
Skin lesions
CNS involvement

Front 31

What are the joint manifestations of rheumatic fever?

Back 31

ARthralgia: joint pain without clinically evident inflammation
Arthritis: overt joint inflammation presenting as painful, red, swollen, hot joints, usually larger joints, esp. knees, ankles, wrists, and elbows
Migratory polyarthritis: sequential involvement of multiple joints

Front 32

What are the skin lesion manifestations of rheumatic fever?

Back 32

Small painless swellings usually over bony prominences, and erythema marginatum, a distinctive skin rash characteristic of rheumatic fever, often involving the trunk and extremities

Front 33

What is the CNS involvement of rheumatic fever?

Back 33

Involuntary, purposeless muscular movements, and bizzare grimaces, as well as emotional lability

Front 34

What is infective endocarditis?

Back 34

1) Bacterial, or sometimes fungal, infection of the endocardium, with prominent involvement of the valvular surfaces.
2) Characterized by large, soft, friable, easily detached vegatations consisting of fibrin and intermeshed inflammatory cells and bacteria
3) May be complicated by ulceration, often with perforation, of the valve cusps or rupture of one of the chordae tendineae.

Front 35

What is acute endocarditis?

Back 35

Caused by pathogens such as Staph aureus (50% of cases)

Front 36

What is subacute (bacterial) endocarditis?

Back 36

1) Caused by less virulent organisms such as strep viridans (more than 50% of cases)
2) Tends to occur in patients with congenital heart disease or preexisting valvular heart disease, often of rheumatic origin

Front 37

What are the valves involved in infective endocardits?

Back 37

1) Mitral valve is most frequently involved
2) Mitral and Aortic valves are invoved in about 40%
3) Tricuspid valve is involved in more than 50% of cases of endocarditis of intravenous drug users, in whom endocarditis is most often caused by staphylococcal infection

Front 38

What are the complications of infective endocarditis?

Back 38

1) Distal embolization occurs when vegetations fragment
2) Embolization can occur almost anywhere in the body and can result in septic infarcts in the brain or in other organs
3) Renal glomeruli may be the site of focal glomerulonephritis (focal necrotizing glomerulonephritis) caused by immune complex disease or by septic emboli.

Front 39

What is nonbacterial thrombotic endocarditis (marantic endocarditis)?

Back 39

1) Associated with debilitating disorders, such as metastatic cancer and other wasting conditions
2) Characterized by small, sterile fibrin deposits randomly arranged along the line of closure of the valve leaflets.
3) Can result in peripheral embolization but, unlike in infective endocarditis, the emboli are sterile

Front 40

What is Libmann-Sacks endocartitis?

Back 40

1) Occurs in systemic lupus erythematosus (SLE)
2) Characterized by small vegetations on either or both surfaces of the valve leaflets

Front 41

What is endocarditis of the carcinoid syndrome?

Back 41

1) Caused by the secretory products of carcinoid tumors (vasoactive peptides and amines, esp serotonin)
2) Results in thickened endocardial plaques characteristically involving the mural endocardium of the valvular cusps of the right side of the heart.
3) Rarely involves valves on the left side of the heart because serotonin and other carcinoid secretory products are detoxified in the lung

Front 42

What is valvular heart disease?

Back 42

1) Occurs often as a late result of rheumatic fever
2) May be secondary to various other inflammatory processes
3) May be congenital
4) Can occur even with prosthetic cardiac valves, which are subject to physical deterioration or can be the site of thrombus formation or infectious endocarditis. They can also cause mechanical disruption of red blood cells, resulting in hemolytic anemia with schistocyte formation.

Front 43

What is mitral valve prolapse?

Back 43

1) Most frequent valvular lesion, occurring in approximately 7% of the population, most often in young women
2) Characterized by myxoid degeneration of the ground substance of the valve (can be a component of Marfan syndrome)
3) Results in stretching of the posterior mitral valve leaflet, producing a "floppy" cusp (parachute deformity) with prolapse into the atrium during systole. These changes produce a characteristic systolic murmur with a midsystolic click.
4) Usually benign and asymptomatic but can result in mitral insufficiency
5) Often associated with a variety of arrhythmias
6) Predisposes to infective endocarditis.

Front 44

What is mitral stenosis?

Back 44

Almost always due to rheumatic heart disease

Front 45

What is mitral insufficiency?

Back 45

1) Usually a result of rheumatic heart disease
2) Can also result from mitral valve prolapse, infective endocarditis, or damage to a papillary muscle from myocardial infarction.
3) Can be secondary to left ventricular dilation, with stretching of the mitral valve ring

Front 46

What is aortic valve stenosis?

Back 46

Often presents as calcific aortic stenosis caused by calcification of:
1) An otherwide normal aortic valve as an age-related degenerative change. This condition, is the most common cause of calcific aortic stenosis in persons older than 60 years. This designation is used when the aortic valve has three cups.
2) Congenital bicuspid aortic valve
3) A valve affected by rheumatic heart disease. In this case, scarring may be evidenced by fusion of the valve commissures.

Front 47

What is aortic insufficiency?

Back 47

Can be caused by:
1) Nondissecting aortic aneurysm resulting from cystic medial necrosis
2) Rheumatic heart disease, usually in association with mitral valve disease
3) Syphilitic (luetic) aortitis (now rare) with dilation of the aortic valve ring

Front 48

What can be wrong with the tricuspid valve?

Back 48

1) Rarely involved in rheumatic heart disease, but may be involved together with the mitral and aortic valves. This trivalvular involvement accounts for approximately 5% of cases of RHD.
2) May be involved in the carcinoid syndrome.

Front 49

What can be wrong with the pulmonary valve?

Back 49

1) Most commonly affected by congenital malformations, occurring either alone or along with other congenital defects, such as in the tetralogy of Fallot.
2) Rarely involved in RHD
3) May be involved in carcinoid syndrome

Front 50

What are the chromosomal abnormalities that lead to congenital heart disease?

Back 50

Down syndrome, some of the other trisomies, Turner syndrome are often complicated by CHD.
1) Association of Turner syndrome with coarctation of the aorta is notable.
2) Endocardial cushion defects, which result in atrial and ventricular septal defects and atrioventricular valve deformities, are frequent associations of Down syndrome.

Front 51

What's up with PDA and high altitudes?

Back 51

There is an apparent increase in the incidence of PDA in patients living at high altitudes, suggesting an association with fetal oxygen deprivation.

Front 52

What is Rubella (German measles) infection?

Back 52

Prominent cause of congenital heart disease.
1) Strong evidence of a link between maternal rubella during the first trimester of pregnancy and a constellation of fetal defects, known as congenital rubella syndrome, which includes cardiovascular defects, microcephaly with mental retardation, deafness, cataracts, and growth retardation.
2) Cardiac malformations are especially frequent and commonly include PDA, aortic stenosis, ventricular septal defect, and pulmonary infundibular or valvular stenosis, sometimes occurring as part of the tetralogy of Fallot.
3) Before of during pregnancy, it is often important to determine the mother's immune status to rubella. Demonstration of anti-rubella antibodies of the IgM class indicates recent primary infection, whereas demonstration of IgG antibodies indicates either recent primary infection, past infection, or reinfection.

Front 53

What is the genetic predisposition of CHD?

Back 53

Tetralogy of Fallot can cluster in families, probably because of multifactorial inheritance.

Front 54

What is noncyanotic disease?

Back 54

1) Includes those with no shunt (aortic stenosis and coarctation of the aorta) and those with a L-R shunt (PDA, ASD, VSD).
2) In ASD, both pressure and oxygen saturation may be equalized between the two atria

Front 55

What is cyanotic disease?

Back 55

1) Transposition of the great vessels; survival depends upon the presence of a shunt between left and right ventricles
2) Malformations with R-L shunt; tetralogy of Fallot
3) Disorders in which a L-R shunt reverses to R-L because of increased pulmonary arterial pressure; late cyanosis, canosis tardive

Front 56

What is cardiomyopathy?

Back 56

1) Refers to disease of the heart muscle that are noninflammatory and are not associated with hypertension, CHD, valvular disease, or coronary artery disease.
2) Usually characterized by otherwise unexplained ventricular dysfunction; heart failure unresponsive to digitalis, ventricular enlargement ventricular arrhythmias

Front 57

What is congestive or dilated cardiomyopathy?

Back 57

1) Most common form of cardiomyopathy
2) Characterized by four-chamber hypertrophy and dilation and by both right- and left-sided intractable heart failure
3) Most often of unknown etiology
4) In some cases is related to alcoholism, thiamine deficiency, or prior myocarditis.

Front 58

What is restrictive cardiomyopathy?

Back 58

1) Caused by infiltrative processes within the myocardium that result in stiffening of the heart muscle, which interferes with pumping action
2) Is exemplified by cardiac amyloidosis, which may result in both right- and left-sided heart failure.

Front 59

What is hypertrophic cardiomyopathy?

Back 59

1) Characterized grossly by hypertrophy of all chamber walls, especially the ventricular septum (asymmetric septal hypertrophy)
2) Characterized microscopically by disoriented, tangled, and hypertrophied myocardial fibers
3) Often inherited as an autosomal dominant characteristic
4) May result in left ventricular outflow obstruction, placing the patient in danger of syncope and even sudden death, which often occurs unexpectedly in young athletes.

Front 60

What is myocarditis?

Back 60

1) Most often presents as biventricular heart failure in young persons who do not have valvular, rheumatic, or congenital heart disease.
2) Characterized morphologically by diffuse myocardial degeneration and necrosis with an inflammatory infiltrate.
3) Most often viral, and coxsackievirus is frequently the cause
4) In parts of South America, may be a component of Chagas disease, which is caused by the protozoan Trypanosoma cruzi

Front 61

What is hydropericardium?

Back 61

1) An accumulation of serous transudate in the pericardial space
2) May result from any condition causing systemic edema
3) Most often caused by congestive heart failure or by edematous conditions due to hypoproteinemia, such as the nephrotic syndrome or chronic liver disease

Front 62

What is hemopericardium?

Back 62

1) An accumulation of blood in the pericardial sack
2) Usually caused by traumatic perforation of the heart or aorta or by myocardial rupture associated with acute MI

Front 63

What is serous pericarditis?

Back 63

1) Associated with SLE, rheumatic fever, and a variety of viral infections
2) Characterized by production of a clear, straw-colored, protein-rich exudate containing small numbers of inflammatory cells

Front 64

What is Fibrinous or serofibrinous pericarditis?

Back 64

1) May be caused by uremia, myocardial infarction, or acute rheumatic fever.
2) Characterizzed by a fibrin-rich exudate

Front 65

What is purulent or suppurative pericarditis?

Back 65

1) Almost always caused by bacterial infection
2) Characterized by a grossly cloudy or frankly purulent inflammatory exudate

Front 66

What is hemorrhagic pericarditis?

Back 66

1) Usually results from tumor invasion of the pericardium.
2) Can also result form tuberculosis or other bacterial infection
3) Characterized by a bloody inflammatory exudate

Front 67

What is chronic (constrictive) pericarditis?

Back 67

1) Usually of tuberculous or pyogenic staphylococcal etiology.
2) Characterized by thickening and scarring of the pericardium with resultant loss of elasticity. This prevents the pericardium from stretching and thus interferes with cardiac action and venous return, often mimicking the sighn and symptoms of right-sided heart failure
3) Marked by proliferation of fibrous tissue with occasional small foci of calcification.

Front 68

Describe two primary tumors of the heart?

Back 68

1) Myxoma of the left atrium; most frequently occurring cardiac tumor and is found most often in adults
2) Rhabdomyoma: most common in infants and young children and is notable for its association with tuberous sclerosis

Front 69

What are the causes of left-sided heart failure?

Back 69

1) Ischemic heart disease, especially myocardial infarction
2) Hypertension
3) Aortic and mitral valvular disease
4) Myocardial diseases, such as cardiomyopathies and myocarditis

Front 70

What are the clinical manifestatins of left-sided heart failure?

Back 70

1) Dyspnea and orthopnea caused by pulmonary congestion and edema regularly occurs
2) Pleural effusion with hydrothorax often results
3) Reduction in renal perfusion, causing activation of the renin-angiotensin-aldosterone system and leading to retention of salt and water, is less frequent manifestation.
4) Cerebral anoxia is less frequent

Front 71

What are the causes of Right-sided heart failure?

Back 71

1) Left-sided heart failure; is the most common cause of right-sided heart failure
2) Left-sided lesions such as mitral stenosis
3) Pulmonary hypertensoin often caused by chronic lung disease (cor pulmonale)
4) Various types of cardiomyopathy and diffuse myocarditis
5) Tricuspid or pulmonary valvular disease

Front 72

What are the clinical manifestations of right-sided heart failure?

Back 72

1) Renal hypoxia, leading to greater fluid retention and peripheral edema than seen in left-sided failure. Edema occurs first in dependent areas and often manifests early as so-called pitting edema of the ankles.
2) Other manifestations of the fluid retention include pleural effusion and sometimes ascites
3) Hydrothorax can be a manifestation of either left-sided or right-sided heart failure.
4) Enlarged and congested liver and spleen. Chronic passive congestion of the centrilobular veins of the liver surrounded by relatively pale, sometimes fatty, peripheral regions leads to a "nutmeg" pattern.
5) Distention of the neck veins

Front 73

What is hypertrophy of the left ventricle?

Back 73

Most commonly caused by hypertension and aortic and mitral valvular disease.

Front 74

What are causes of hypertrophy of the right ventricle?

Back 74

1) Left ventricular failure
2) Chronic lung disease
3) Mitral valve disease
4) Congenital heart disease with L-R shunt.

Front 75

What is cor pulmonale?

Back 75

1) Right ventricular hypertrophy and/or dilation secondary to lung disease or primary disease of the pulmonary vasculature, such as primary pulmonary hypertension. Emphysema is a frequent cause.
2) Characterized by pulmonary arterial hypertension, the common characteristic among the entities that lead to cor pulmonale

Front 76

What is an atrial septal defects?

Back 76

1) Patent foramen ovale, usually clinically insignificant
2) Septum primum, affects lower part of septum; if large, may be associated with deformities of atrioventricular valves
3) Septum secundum, defect in the fossa ovalis
4) Sinus venosus, affects the upper part of the septum near the entrance of the superior vena cava
5) Lutembacher syndrome, atrial septal defect with mitral stenosis

Front 77

What are the clinical manifestations of ASD?

Back 77

Clinical manifestations often delayed until adult life; pulmonary hypertension and reversal of flow with resultant cyanosis are late complications; can lead to paradoxic embolism

Front 78

What is a ventricular septal defects?

Back 78

1) Vary greatly in size
2) Small defects may close spontaneously; larger defects may lead to pulmonary hypertension and eventual right-sided heart failure; reversal of flow and late cyanosis also occur

Front 79

What is tetralogy of Fallot?

Back 79

1) Pulmonary infundibular or valvular stenosis;
2) Ventricular septal defect; overriding aorta;
3) Right ventricular hypertrophy
4) Cyanosis from birth
5) Tendency of patients to assume a squatting position, presumably because of lessening of R-L shunting

Front 80

What is patent ductus arteriosus?

Back 80

1) Failure of closure of the fetal ductus arteriosus.
2) Patency maintained during fetal life by combined effects of low oxygen tension and prostaglandin synthesis
3) Can be closed surgically or pharmacologically treated with indomethacin
4) If not closed, leads eventually to pulmonary hypertension, right ventricular hypertrophy, reversal of blood flow, and late cyanosis

Front 81

What is coarctation of aorta?

Back 81

1) Narrowing of the aorta, usually distal to the origin of the subclavian arteries; extensive development of collateral circulation with dilation of intercostal arteries.
2) Hypertension limited to the upper extremities and cerebral vessels; notching of the ribs seen on x-ray

Front 82

What is Transposition of the great vessels.

Back 82

1) Aorta arises from the right ventricle, and the pulmonary artery arises from the left ventricle.
2) Compensatory anomaly such as patent ductus arteriosus necessary for survival.