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1
Q

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.

A

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

2
Q

Hemosiderin laden macrophages are also called _______

A

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

3
Q

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

A

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

4
Q

Most common cause of right sided HF.

A

Left sided HF(TOPNOTCH)

5
Q

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

A

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

6
Q

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

A

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

7
Q

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

A

Cardiac cirrhosis(TOPNOTCH)

8
Q

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

A

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

9
Q

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

A

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

10
Q

This is a hallmark of right sided HF.

A

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

11
Q

Generalized, massive edema is called ______.

A

Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382

12
Q

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

A

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

13
Q

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

A

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

14
Q

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.

A

Ostium secundum ASD(TOPNOTCH)

15
Q

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.

A

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

16
Q

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.

A

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

17
Q

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.

A

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

18
Q

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

A

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

19
Q

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 can become dilated.

A

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

20
Q

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

A

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

21
Q

Components of Tetralogy of Fallot.

A

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

22
Q

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.

A

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

23
Q

Predominant manifestation of TGA?

A

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

24
Q

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.

A

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

25
Q

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.

A

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

26
Q

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.

A

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

27
Q

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

A

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

28
Q

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

A

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

29
Q

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

A

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

30
Q

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

A

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

31
Q

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

A

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

32
Q

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

A

Angina pectoris(TOPNOTCH)

33
Q

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

A

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

34
Q

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

A

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

35
Q

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

A

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

36
Q

This can result from a lethal arrythmia following myocardial ischemia.

A

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

37
Q

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

A

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

38
Q

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

A

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

39
Q

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.

A

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

40
Q

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

A

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

41
Q

Angina occuring at rest due to coronary artery spasm.

A

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

42
Q

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

A

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

43
Q

Most common blood vessel involved in myocardial infarction?

A

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

44
Q

Electron microscope findings 30 minutes after an ischemic event.

A

Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)

45
Q

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

A

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

46
Q

Coagulation necrosis ensues how many hours after MI?

A

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

47
Q

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

A

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

48
Q

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

A

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

49
Q

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.

A

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

50
Q

Myocardial rupture may occur how many days after MI?

A

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

51
Q

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.

A

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

52
Q

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

A

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

53
Q

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

A

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

54
Q

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

A

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

55
Q

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

A

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

56
Q

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

A

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

57
Q

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

A

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

58
Q

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.

A

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

59
Q

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.

A

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

60
Q

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

A

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

61
Q

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.

A

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

62
Q

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.

A

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

63
Q

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.

A

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

64
Q

Most common valve involved in RHD.

A

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

65
Q

Major components Jones Criteria for RF.

A

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

66
Q

Minor components Jones criteria for RF

A

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

67
Q

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

A

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

68
Q

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

A

Acute bacterial endocarditis(TOPNOTCH)

69
Q

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.

A

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

70
Q

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

A

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

71
Q

Most consistent sign of infective endocarditis.

A

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

72
Q

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.

A

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

73
Q

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.

A

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

74
Q

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.

A

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

75
Q

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.

A

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

76
Q

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

A

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

77
Q

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.

A

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

78
Q

Mechanism of heart failure in hypertrophic cardiomyopathy.

A

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

79
Q

A common cause of sudden death in young athlethes.

A

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

80
Q

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.

A

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

81
Q

Mechanism of heart failure in restrictive cardiomyopathy.

A

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

82
Q

Inflammation of the myocardium.

A

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

83
Q

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

A

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

84
Q

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

A

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

85
Q

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

A

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

86
Q

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

A

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

87
Q

Viruses which account for most cases of myocarditis.

A

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

88
Q

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).

A

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

89
Q

Bacterial pericarditis manifests with this type of exudate.

A

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

90
Q

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

A

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

91
Q

Normal amount of pericardial fluid in pericardial sac.

A

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

92
Q

Serous pericardial effusion can be caused by _________

A

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

93
Q

Chylous pericardial fluid can be caused by _______

A

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

94
Q

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

A

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

95
Q

The most common tumor of the heart.

A

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

96
Q

Most common primary tumor of the adult heart.

A

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

97
Q

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

A

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

98
Q

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.

A

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

99
Q

Serosanguinous pericardial effusion can be caused by ________

A

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