XI - The Heart

Question 1

The morphologic and clinical effects of this condition primarily result from progressive damming of blood within the pulmonary circulation. The left ventricle is hypertrophied and dilated, with secondary left atrial dilation. The lungs are heavy and boggy, with perivascular and interstitial transudate, alveolar septal edema, and intra-aleolar edema. Hemosiderin-laden macrophages are present.

Answer 1

Left sided heart failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

Question 2

Hemosiderin laden macrophages are also called _______

Answer 2

Heart failure cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

Question 3

This is usually the earliest and most significant compaint of patients in Left sided HF.

Answer 3

Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

Question 4

Most common cause of right sided HF.

Answer 4

Left sided HF(TOPNOTCH)

Question 5

This is a particularly dramatic form of breathlessness, awakening patients from sleeo with attacks of extreme dyspnea bordering on suffocation.

Answer 5

Paroxysmal nocturnal dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

Question 6

Isolated right sided HF occuring in patients with intrinsic lung disease that result in chronic pulmonary hypertension.

Answer 6

Cor Pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

Question 7

Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.

Answer 7

Cardiac cirrhosis(TOPNOTCH)

Question 8

The liver is increased in size and weight, a cut section reveals congested red centers of liver lobules surrounded bybpaler, sometimes fatty peripheral regions.

Answer 8

Nutmeg liver (CPC of the liver)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

Question 9

Right-sided HF produces a tense, enlarged spleen, achieving weights of 300-500 grams. Sinusoidal dilation present.

Answer 9

Congestive splenomegaly(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

Question 10

This is a hallmark of right sided HF.

Answer 10

Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382

Question 11

Most congenital heart disease arise from faulty embryogenesis during what AOG?

Answer 11

3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382

Question 12

An abnormal communication between chambers of the heart or blood vessels.

Answer 12

Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383

Question 13

These a typically smooth-walled defects near the foramen ovale, usually without associated cardiac abnormalities. Accompanied by right atrial and ventricular dilation, right ventricular hypertrophy and dilation of the pulmonary artery.

Answer 13

Ostium secundum ASD(TOPNOTCH)

Question 14

Reversal of blood flow through a prolonged (left-to-right shunt) due to pulmonary hypertension, yielding right-sided pressures that exceed those on the left side. This causes unoxygenated blood to go into circulation, causing cyanosis.

Answer 14

Eisenmenger syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383

Question 15

These occur at the lowest part of the atrial septum and can extend to the mitral and tricuspid valves. Abnormalities of the AV Valves are usually present, forming a cleft in the anterior leaflet of the mitral valve or septal leaflet of the tricuspid valve.

Answer 15

Ostium primum ASD(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384

Question 16

Incomplete closure of the ventricular septum leading to left-to-right shunting. The right ventricle is hypertrophied and often dilated. Diameter of pulmonary artery is increased because of the increased volume by the right ventricle.

Answer 16

Ventricular Septal Defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385

Question 17

This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.

Answer 17

Ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385

Question 18

In this condition, some of the oxygenated blood flowing from the left ventricle is shunted back to the lungs. Proximal pumonary arteries, left atrium and ventricle may become dilated.

Answer 18

Patent ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385

Question 19

The most common cause of cyanotic congenital heart disease. Heart is large and “boot shaped” as a result of right ventricular hypertrophy.

Answer 19

Tetralogy of Fallot(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385

Question 20

Components of Tetralogy of Fallot.

Answer 20

Pulmonary valve stenosisOverriding of aortaRight ventricular hypertrophyVentricular septal defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386

Question 21

It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa. Right ventricular hypertrophy becomes prominent, while the left ventricle becomes somewhat atrophic.

Answer 21

Transposition of the Great Arteries(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386

Question 22

Predominant manifestation of TGA?

Answer 22

Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387

Question 23

Characterized by tubular narrowing of the aortic segment between the left subclavian artery and the ductus arteriosus. DA is usually patent and is the main source of blood to the distal aorta. RV is hypertrophied and dilated, pulmonary trunk is also dilated.

Answer 23

Preductal “infantile” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387

Question 24

Aorta is sharply constricted by a ridge of tissue at or just distal to the ligamentum arteriosum. Constricted segment is made of smooth muscle and elastic fibers that are continuous with the aortic media, and lined by thickened intima. Ductus arteriosus is closed. Proximally, the aortic arch and its vessels are dilated, LV is hypertrophic.

Answer 24

Postductal “adult” coarctation of the aorta(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387

Question 25

There is upper extremity hypertension, due to poor perfusion of the kidneys, but weak pulses and low blood pressure in the lower extremities. Claudication and coldness of the lower extremities also present. Enlarged intercostal and internal mammary arteries due to collateral circulation, seen as rib “notching” on xray.

Answer 25

Postductal coarctation of the aorta (without a PDA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 26

Left-to-right or Right-to-Left shunt?Atrial septal defect

Answer 26

Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 27

Left-to-right or Right-to-Left shunt?TOF

Answer 27

Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 28

Left-to-right or Right-to-Left shunt?VSD

Answer 28

Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 29

Left-to-right or Right-to-Left shunt?Eisenmenger syndrome

Answer 29

Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 30

Left-to-right or Right-to-Left shunt?Transposition of great arteries

Answer 30

Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 31

A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.

Answer 31

Angina pectoris(TOPNOTCH)

Question 32

A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.

Answer 32

Angina pectoris(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 33

A condition wherein the severity or duration of ischemia is enough to cause cardiac muscle death.

Answer 33

Acute Myocardial Infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 34

This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.

Answer 34

Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 35

This can result from a lethal arrythmia following myocardial ischemia.

Answer 35

Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

Question 36

How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic, in the setting of increased demand?

Answer 36

70-75% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389

Question 37

How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic at rest?

Answer 37

90%(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 389

Question 38

Episodic chest pain associated with exertion or some other form of increased myocardial oxygen demand. Pain described as crushing or squeezing substernal sensation which can radiate to left arm. Relieved by rest or vasodilators.

Answer 38

Stable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390

Question 39

Increasing frequency of pain, precipitated by progressively less exertion, episodes tend to be more intense and longer lasting.

Answer 39

Unstable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390

Question 40

Angina occuring at rest due to coronary artery spasm.

Answer 40

Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390

Question 41

Infarct involving >= 50% of the myocardial wall thickness.

Answer 41

Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391

Question 42

Most common blood vessel involved in myocardial infarction?

Answer 42

Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392

Question 43

Electron microscope findings 30 minutes after an ischemic event.

Answer 43

Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)

Question 44

An infarct can be readily identified by a reddish blue discoloration after how many hours after MI?

Answer 44

12-24 hours(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 393

Question 45

Coagulation necrosis ensues how many hours after MI?

Answer 45

4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394

Question 46

Injury to infarcts mediated in part by oxygen free radicals generated by increased number of infiltrating leukocytes facilitated by reperfusion.

Answer 46

Reperfusion injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394

Question 47

Cardiac enzymes that become detectable 2-4 hours post-infarct peaks at 48 hours and remains elevated for 7-10 days.

Answer 47

Troponin I and Troponin T(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395

Question 48

This cardiac enzyme is detectable in the blood within 2-4 hrs of MI, peaks at 24-48 hrs and returns to normal within approximately 72 hrs.

Answer 48

CKMB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395

Question 49

Myocardial rupture may occur how many days after MI?

Answer 49

3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397

Question 50

This occurs within 2-3 days of a transmural infarct and typically resolves within time. It is the epicardial manifestation of the underlying myocardial inflammation.

Answer 50

Pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397

Question 51

A late complication of MI, most commonly results from a large transmural anteroseptal infarct that heals with formation of a thin scar tissue.

Answer 51

Ventricular aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397

Question 52

This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter.

Answer 52

Concentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399

Question 53

Type of hypertrophybthat develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.

Answer 53

Eccentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399

Question 54

In this disease the left ventricle may exceed 2.0cm in thickness and the heart may weigh >500 grams. Microscopically, myocyte diameter increases, associated with irregular nuclear enlargement and hyperchromasia (“box-car nuclei”), and increased interstitial fibrosis.

Answer 54

Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399

Question 55

It is the failure of a valve to open completely, obstructing forward flow.

Answer 55

Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401

Question 56

This results from failure of a valve to close completely, thereby allowing reversed flow.

Answer 56

Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401

Question 57

The hallmark of this disease is heaped-up calcified masses on the outflow side of the cusps, which protrude intonthe sinuses of Valsalva and mechanically impede valve opening. Cusps may become secondarily fibrosed and thickened.

Answer 57

Calcific aortic stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401

Question 58

This is characterized by ballooning or hooding of the mitral leaflets. Affected leaflets are enlarged, redundant, thick and rubbery. The tendinous cords are elongated, thinned and occasionally ruptured. Histologically, there is thinning of the fibrosa layer of the valve, accompanied by expansion of the middle spongiosa layer with increased deposition of mucoid material.

Answer 58

Myxomatous degeneration of the mitral valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402

Question 59

Patients with this disease may complain of palpitations, dyspnea or atypical chest pain. Auscultation shows a midsystolic click associated with a regurgitant murmur.

Answer 59

Mitral valve prolapse(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402

Question 60

Pathognomonic sign for rheumatic fever,consisting of of a cental zone of degenerating, hypereosinophilic ECM infiltrated by lymphocytes, ocassional plasma cells and plump, activated macrophages.

Answer 60

Aschoff bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402

Question 61

These cells have abundant cytoplasm and central nuclei with chromatin arrayed in a slender, wavy ribbon (caterpillar cells) which can be found in all three layers of the heart in rheumatic fever. A component of Aschoff bodies.

Answer 61

Anitschkow cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403

Question 62

Characterized by organization and subsequent scarring, as a sequelae of rheumatic fever. The mitral (or tricuspid) valve is involved, with leaflet thickening, commisural fission and shortening, thickening and fusiong of the chordae tendinae. Fibrous bridging across valvular commisures create “fishmouth” or “ buttonhole” deformity.

Answer 62

Chronic Rheumatic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403

Question 63

Most common valve involved in RHD.

Answer 63

Mitral valve (upto 70% of cases with RHD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 405

Question 64

Major components Jones Criteria for RF.

Answer 64

CarditisMigratory polyarthritisSubcutaneous nodulesErythema marginatumSyndenham chorea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

Question 65

Minor components Jones criteria for RF

Answer 65

FeverArthralgiaElevated acute phase reactants (e.g. CRP)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

Question 66

How many major and/or minor manifestations are needed to diagnose RF?

Answer 66

Remember: 20122 major 0 minor or1 major 2 minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

Question 67

Endocarditis of previously normal valves, the most common causative agent is S. aureus.

Answer 67

Acute bacterial endocarditis(TOPNOTCH)

Question 68

Serious infection characterized by microbial invasion of heart valves or mural endocardium, often with destruction of the underlying cardiac tissues. The heart valves are friable, bulky and potentially destructive.

Answer 68

Infective endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

Question 69

Endocarditis affecting previously damaged or abnormal valves, commonly caused by viridans Streptococci.

Answer 69

Subacute bacterial endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406

Question 70

Most consistent sign of infective endocarditis.

Answer 70

Fever(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407

Question 71

Characterized by deposition of sterile, non-inflammatory, nondestructive and small (1mm) masses of fibrin, platelets and other blood components on cardiac valves, along the line of closure of leaflets or cusps.

Answer 71

Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407

Question 72

Sterile vegetations thatvcan develop on the valves of patients with SLE. These are small, granular, pinkish vegetations 1-4mm in diameter and can be located on the undersurface of AV valves, on the cords or endocardium.

Answer 72

Libman-Sacks endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408

Question 73

The lesions of this disease are distinctive, glistening white intimal plaquelike thickenings on the endocardial surfaces of the cardiac chambers and valve leaflets seen in patients with carcinoid tumors. The lesions are composed of muscle cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix.

Answer 73

Carcinoid heart disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408

Question 74

Cardiomyopathy which is characterized by progressive cardiac dilation and contractile dysfunction. The heart is characteristically enlarged and flabby, with dilation of all chambers,the ventricular thickness may be less than, equal to or greater than normal.

Answer 74

Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411

Question 75

Alcohol intake and infection with coxsackie B virus are some of the causes of this cardiomyopathy.

Answer 75

Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411

Question 76

Characterized by myocardial hypertrophy, abnormal diastolic filling and ventricular outflow obstruction. The heart is thick-walled, heavy and hypercontracting. There is an assymetrical septal hypertrophy described as “banana-like”. Histologically, there is severe myocyte hypertrophy and disarray with interstitial fibrosis.

Answer 76

Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412

Question 77

Mechanism of heart failure in hypertrophic cardiomyopathy.

Answer 77

Diastolic dysfunction (impaired compliance)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412

Question 78

A common cause of sudden death in young athlethes.

Answer 78

Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412

Question 79

The ventricles are of approximately normal size or slightly enlarged, the cavities not dilated, and the myocardium is firm. Biatrial dilation is common. Microscopically, there is interstitial fibrosis, varying from minimal to patchy to extensive and diffuse.

Answer 79

Restrictive cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413

Question 80

Mechanism of heart failure in restrictive cardiomyopathy.

Answer 80

Diastolic dysfunction or impaired compliance(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413

Question 81

Inflammation of the myocardium.

Answer 81

Myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414

Question 82

Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis.

Answer 82

Lymphocytic myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414

Question 83

Myocarditis that has interstitial and perivascular infiltrates composed of lymphocytes, macrophages and a high proportion of eosinophils.

Answer 83

Hypersensitivity myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414

Question 84

Myocarditis characterized by widespread inflammatory infiltrates containing multinucleated giant cells interspresed with lymphocytes, eosinophils and plasma cells. Poor prognosis.

Answer 84

Giant-cell myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414

Question 85

Myocarditis distinctive by virtue of parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages and occasional eosinophils.

Answer 85

Chagas myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414

Question 86

Viruses which account for most cases of myocarditis.

Answer 86

Coxsackie A and B(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414

Question 87

Type of pericarditis found in patients with uremia or viral infection. The exudate imparts an irregular apperance to the pericardial surface (bread and butter pericarditis).

Answer 87

Fibrinous pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416

Question 88

Bacterial pericarditis manifests with this type of exudate.

Answer 88

Fibrinopurulent (suppurative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416

Question 89

Heart is completely encased by dense fibrosis that it cannot expand normally during diastole.

Answer 89

Constrictive pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416

Question 90

Normal amount of pericardial fluid in pericardial sac.

Answer 90

30 - 50 mL of thin, straw-colored fluid(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417

Question 91

Serous pericardial effusion can be caused by _________

Answer 91

CHF, hypoalbuminemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417

Question 92

Chylous pericardial fluid can be caused by _______

Answer 92

Mediastinal lymphatic obstruction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417

Question 93

Rapidly developing collections of fluid within the pericardial sac can restrict diastolic cardiac filling producing this fatal sequelae.

Answer 93

Cardiac tamponade(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417

Question 94

The most common tumor of the heart.

Answer 94

Metastatic tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417

Question 95

Most common primary tumor of the adult heart.

Answer 95

Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417

Question 96

Major clinical manifestations of this cardiac tumor are due to valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms.

Answer 96

Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418

Question 97

The most frequent primary tumor of the heart in infants and children. These are generally small gray-white myocardial masses composed of a mixed population of cells, the most characteristic of which are large, rounded or polygonal cells containing numerous glycogen-laden vacuoles separated by strands of cytoplasm, so-called spider cells.

Answer 97

Rhabdomyomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418

Question 98

Serosanguinous pericardial effusion can be caused by ________

Answer 98

Blunt chest trauma, malignancy, ruptured MI, aortic dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418

Question 99

The most severe pulmonary changes in congestive heart failure

Answer 99

Accumulation of edema fluid in the alveolar spaces (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529

Question 100

Morphologic finding/telltale signs of previous episodes of pulmonary edema

Answer 100

Hemosiderin-laden macrophages (Heart failure cells) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529

Question 101

Most common underlying etiology of diastolic failure

Answer 101

Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529

Question 102

Group of congenital heart disease characterized by increase pulmonary blood flow but are not initially associated with cyanosis

Answer 102

Left-to-right shunts (ASD, VSD, PDA) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533

Question 103

Most common genetic cause of congenital heart disease

Answer 103

Trisomy 21 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533

Question 104

A 24 y/o female complained of shortness of breath and orthopnea lasting several days. The patient reported having diagnosed since childhood as having “hole in the heart.” Physical exam revealed holosystolic murmur most audible in the left parasternal area accompanied by thrill. Rales were heared in the bilateral lower lung field. The most likely cause of her condition:

Answer 104

VSD (TOPNOTCH)

Question 105

Most common cause of myocardial ischemia

Answer 105

Obstructive atherosclerotic lesions in the epicardial coronary arteries (TOPNOTCH) Robbins Basic Patholgoy, 9th ed., p. 538

Question 106

The cause of sudden cardiac death in myocardial infarction

Answer 106

Ventricular arrythmia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 539

Question 107

Irreversible cell injury in MI occur in how many minutes?

Answer 107

20-40 minutes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541

Question 108

Irreversible injury of ischemic myocytes in MI occurs first in what zone in the heart?

Answer 108

Subendocardial zone (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541

Question 109

What blood vessel supply the posterior third of the ventricular septum in majority of the individuals?

Answer 109

Right coronary artery (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541

Question 110

Pattern of infarction caused by occlusion of an epicardial vessel

Answer 110

Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543

Question 111

Pattern of infarction caused by plaque disruption or hypotension, causing circumferential myocardial damage

Answer 111

Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543

Question 112

Pattern of infarct also referred to as an “ST elevation myocardial infarct”

Answer 112

Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543

Question 113

Pattern of infarct also referred to as a “non-ST elevation infarct”

Answer 113

Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543

Question 114

The typical changes of coagulative necrosis becomes detectable in how many hours of injury?

Answer 114

First 6-12 hours(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 545

Question 115

Microscopic findings in irreversibly injured myocytes characterized by intensely eosinophilic intracellular stripes composed of closely packed sarcomeres.

Answer 115

Contraction bands(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 546

Question 116

A 62 y/o obese male had sudden onset of heaviness in the chest, associated with diaphoresis and dyspnea which started 3 hours prior to consult at the ER. The biomarkers that are most sensitive and specific of myocardial damage that you will request:

Answer 116

Troponins I and T (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 547

Question 117

A 72 y/o female experienced chest pain and hypotension. A posterior transmural infarct was suspected. Most common complications in this type of infarct

Answer 117

Conduction blocks, right ventricular involvement, or both (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549

Question 118

Free wall rupture, expansion, mural thrombi, and aneurysm are common in what type/location of infarct?

Answer 118

Anterior transmural infarct(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549

Question 119

Most common cause of rhythm disorder

Answer 119

Ischemic injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 550

Question 120

A 24 y/o female presents with history of recurrent fever and joint pains accompanied by ECG changes and increased ASO titer in the past 2 years. Physical examination reveals cardiac murmur. What is the clinical impression?

Answer 120

Rheumatic heart disease (TOPNOTCH)

Question 121

Characteristic anatomic change in MVP

Answer 121

Interchordal ballooning of mitral leaflets (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 556

Question 122

Most frequent mechanism of SCD

Answer 122

Lethal arrythmia (asystole, ventricular fibrillation) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552

Question 123

Earliest microscopic change in systemic hypertensive heart disease

Answer 123

increase in transverse diameter of myocytes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552

Question 124

Most common type of VSD

Answer 124

Membranous (Interventricular septum) VSD(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 535

Question 125

The common feature of pulmonary thromboembolism, obstructive sleep apnea, altitude disease, and parenchymal lung disease

Answer 125

Pulmonary hypertension. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 530

Question 126

A 5 wk old infant presents with tachypnea, diaphoresis, and difficulty feeding. A harsh, continuous, machinery-like murmur was noted upon auscultation. What is the most likely diagnosis?

Answer 126

Patent ductus arteriosus(TOPNOTCH)

Question 127

Presents with hypertension in the upper extremities, and manifestations of arterial insufficiency such as claudication and coldness. Produce a radiographical visible erosion (notching) of the undersurfaces of the ribs.

Answer 127

Coarctation of the aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 537

Question 128

Major cause of infective endocarditis among intravenous drug abusers

Answer 128

Staphylococcus aureus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559

Question 129

Most common cause of endocarditis of native but previously damaged or otherwise abnormal valves

Answer 129

Streptococcus viridans (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559

Question 130

Predominant manifestations of RF

Answer 130

Carditis and arthritis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559

Question 131

Classic hallmark of Infective endocarditis

Answer 131

Vegetations on heart valves(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559

Question 132

A 72 year old hypertensive female last seen apparently well 3 days ago, is found dead in her bathroom with rigor mortis and no signs of foul play. At autopsy, her heart showed left ventricular hypertrophy and a pale tan area at the anteroseptal wall. There are no thrombi in the heart chambers. The valves are unremarkable. Microscopic examination of the pale area showed well-established granulation tissue with new blood vessels and collagen deposition. Neutrophils are rare. She died of (A) an MI that occured 1 hour prior to demise (B) an MI 12 hours prior to demise (C) an MI 2 days prior to demise (D) something else entirely

Answer 132

something else entirely (evolution of morphologic changes in myocardial infarction) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 393

Question 133

In hypertensive heart disease, there is concentric thickening of the left ventricular wall. A concomitant left atrial dilatation may also be seen due to (A) volume overload from a ventricle with narrowed lumen (B) pressure overload from a ventricle with narrowed lumen (C) cytokines secreted by hypertrophic ventricular myocytes cause atrophy of atrial myocytes (D) cytokines secreted by hypertrophic ventricular myocytes cause metaplasia of atrial myocytes

Answer 133

volume overload from a ventricle with narrowed lumen (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 399

Question 134

What feature in a stenotic aortic valve suggests rheumatic valvular disease, rather than calcific aortic stenosis? (A) bicuspid valve (B) masses of calcium on the outflow side of cusps (C) fibrotic cusps (D) fusion of the commmissures

Answer 134

fusion of the commisures (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402

Question 135

A 20 year old asymptomatic female is found to have a midsystolic click on her preemployment physical examination. A 2D echo showed mitral valve prolapse. The involved leaflet would show (A) numerous fibroblasts with and dense collagen deposition (B) thinning of the fibrosa layer and myxoid expansion of the spongiosa layer (C) deposition of amorphous material that shows apple-green birefringence when stained with Congo red (D) fibrous stroma with gland-like structures secreting mucin

Answer 135

thinning of fibrosa layer and myxoid espansion of the spongiosa layer (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402

Question 136

A 5 year old male who had a sore throat 3 weeks ago develops fever and joint pains. Auscultation revealed a friction rub, and ASO titers are increased. Which of the following is expected in the patient? (A) friable vegetations on the mitral valve containing fibrin, neutrophils and gram-positive cocci (B) small vegetations on the mitral valve with abundant eosinophils (C) myocardium with circumscribed aggregates of mononuclear cells and macrophages with prominent nucleoli (D) myocardium with poorly-circumsccribed aggregates of multinucleated giant cells

Answer 136

myocardium with circumscribed aggregates of mononuclear cells and macrophages with prominent nucleoli (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 403-404

Question 137

A 19 year old football player dies suddenly during one training session. At autopsy, his heart showed myocardial hypertrophy with disproportionate thickening of the septum, and a narrowed left ventricular lumen. Microscopic examination showed myocyte hypertrophy, myofiber disarray, and interestitial fibrosis. These findings are due to (A) a mutation in one of his genes encoding sarcomeric proteins (B) a silent Coxsackie virus B infection (C) an undisclosed 3 year history of alcohol intake (D) anabolic steroids he has been taking for 6 months

Answer 137

a mutation in one of his genes encoding sarcomeric proteins (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P. 412-413

Question 138

A 34 year old female on routine checkup is found to have a diastolic murmur. 2D echo showed a pedunculated 3 cm mass in her left atrium attached to the atrial septum. She has no other known masses on workup. She undergoes heart surgery where the atrial mass is resected. Which of the following is its most likely histology? (A) stellate cells admixed with endothelial and fibroblastic cells embedded in an abundant extracellular matrix (B) sheets of large polygonal cells containing glycogen-containing vacuoles arranged around a central nucleus (C) fascicles of fibroblasts and interspersed collagen bundles (D) sheets of pleomorphic cells lining vascular spaces, some with intracytoplasmic lumens, with atypical mitoses and areas of necrosis

Answer 138

stellate cells admixed with endothelial and fibroblastic cells embedded in an abundant extracellular matrix (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 417-418