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XI - The Heart Flashcards

1
Q

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

A

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-alveolar edema. Hemosiderin-laden macrophages are present. SEE SLIDE 11.1.

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2
Q

Heart failure cells. SEE SLIDE 11.1. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381

A

Hemosiderin laden macrophages are also called _______

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3
Q

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

A

Earliest and most significant complaint of patients with left-sided heart failure

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4
Q

Left-sided HF(TOPNOTCH)

A

Most common cause of right sided HF.

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5
Q

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

A

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

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6
Q

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

A

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

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7
Q

Cardiac cirrhosis(TOPNOTCH)

A

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

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8
Q

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

A

Term used when the liver has congested centrilobular areas (due to back up of blood) surrounded by paler peripheral regions. SEE SLIDE 11.2.

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9
Q

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

A

Hallmark of right sided HF.

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10
Q

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

A

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

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11
Q

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

A

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

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12
Q

Ostium secundum ASD(TOPNOTCH) Robbins Basic Pathology, 9th Ed., p 371

A

Smooth-walled defect near the foramen ovale, usually without associated cardiac abnormalities. It comprises 90% of ASDs.

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13
Q

Accompanied by right atrial and ventricular dilation, right ventricular hypertrophy, and dilation of the pulmonary artery– reflecting chronic right-sided volume overload. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p 371

A

Chamber abnormalities seen in ASD.

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14
Q

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

A

Reversal of blood flow through a prolonged left-to-right shunt due to pulmonary hypertension, yielding a right-to-left shunt. This causes unoxygenated blood to go into circulation, causing cyanosis.

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15
Q

Ostium primum ASD. SEE SLIDE 11.3. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384

A

These occur at the lowest part of the atrial septum and can extend to the mitral (anterior leaflet) and tricuspid valves (septal leaflet).

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16
Q

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

A

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.

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17
Q

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

A

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

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18
Q

Tetralogy of Fallot. SEE SLIDE 11.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385

A

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

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19
Q

Pulmonary valve stenosis, Overriding of aorta, Right ventricular hypertrophy, Ventricular septal defect. SEE SLIDE 11.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386

A

Components of Tetralogy of Fallot.

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20
Q

Transposition of the Great Arteries. SEE 11.5 (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386

A

It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa.

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21
Q

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

A

Predominant manifestation of TGA?

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22
Q

Preductal “infantile” coarctation of the aorta. SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387

A

Characterized by circumferential 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.

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23
Q

Postductal “adult” coarctation of the aorta. SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387

A

Aorta is sharply constricted by a ridge of tissue at or just distal to the NONPATENT 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.

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24
Q

Postductal coarctation of the aorta (without a PDA). SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388

A

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.

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25
Q

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

A

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

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26
Q

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

A

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

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27
Q

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

A

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

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28
Q

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

A

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

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29
Q

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

A

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

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30
Q

Angina pectoris(TOPNOTCH)

A

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

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31
Q

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

A

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

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32
Q

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

A

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

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33
Q

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

A

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

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34
Q

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

A

This can result from a lethal arrythmia following myocardial ischemia.

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35
Q

More than 70% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 375

A

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

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36
Q

90%(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 375

A

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

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37
Q

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

A

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.

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38
Q

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

A

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

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39
Q

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

A

Angina occuring at rest due to coronary artery spasm.

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40
Q

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

A

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

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41
Q

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

A

Most common blood vessel involved in myocardial infarction?

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42
Q

Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)

A

Electron microscope findings 30 minutes after an ischemic event.

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43
Q

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

A

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

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44
Q

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

A

Coagulation necrosis ensues how many hours after MI?

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45
Q

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

A

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

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46
Q

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

A

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

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47
Q

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

A

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.

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48
Q

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

A

Myocardial rupture may occur how many days after MI?

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49
Q

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

A

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.

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50
Q

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

A

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

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51
Q

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

A

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

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52
Q

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

A

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

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53
Q

320-360 grams, 1.2-1.4 cm (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 387

A

Normal weight of heart and normal LV wall thickness

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54
Q

Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 387

A

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

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55
Q

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

A

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

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56
Q

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

A

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

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57
Q

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

A

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.

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58
Q

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

A

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.

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59
Q

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

A

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

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60
Q

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

A

Pathognomonic sign for rheumatic fever– myocardial inflammatory lesions composed of plump activated macrophages (Anitschkow cells), plasma cells, and lymphocytes. SEE SLIDE 11.7.

61
Q

TRUE. They are replaced by a fibrous scar. (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p.391

A

TRUE or FALSE: Aschoff bodies are rarely seen in chronic rheumatic heart disease

62
Q

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

A

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. SEE SLIDE 11.8.

63
Q

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

A

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. SEE SLIDE 11.9.

64
Q

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

A

Most common valve involved in RHD.

65
Q

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

A

Major components Jones Criteria for RF.

66
Q

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

A

Minor components Jones criteria for RF

67
Q

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

A

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

68
Q

Acute bacterial endocarditis(TOPNOTCH)

A

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

69
Q

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

A

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.

70
Q

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

A

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

71
Q

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

A

Most consistent sign of infective endocarditis.

72
Q

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

A

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.

73
Q

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

A

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. SEE SLIDE 11.10.

74
Q

Carcinoid heart disease. Of note, lesions that occur in fenfluramine and ergot alkaloid-induced valvulopathy look similar to this. (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 395

A

The lesions of this disease are distinctive, glistening white intimal thickenings on the endocardial surfaces of the cardiac chambers and valve leaflets. The lesions are composed of smooth muscle cells and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix. Usually right-sided (causing tricuspid insufficiency and pulmonic stenosis).

75
Q

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

A

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.

76
Q

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

A

Alcohol, myocarditis, doxorubicin, and hemochromatosis are some of the causes of this cardiomyopathy.

77
Q

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

A

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. SEE SLIDE 11.11.

78
Q

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

A

Mechanism of heart failure in hypertrophic cardiomyopathy.

79
Q

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

A

A common cause of sudden death in young athlethes.

80
Q

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

A

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.

81
Q

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

A

Mechanism of heart failure in restrictive cardiomyopathy.

82
Q

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

A

Inflammation of the myocardium.

83
Q

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

A

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

84
Q

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

A

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

85
Q

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

A

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

86
Q

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

A

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

87
Q

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

A

Viruses which account for most cases of myocarditis.

88
Q

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

A

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).

89
Q

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

A

Bacterial pericarditis manifests with this type of exudate.

90
Q

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

A

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

91
Q

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

A

Normal amount of pericardial fluid in pericardial sac.

92
Q

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

A

Serous pericardial effusion can be caused by _________

93
Q

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

A

Chylous pericardial fluid can be caused by _______

94
Q

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

A

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

95
Q

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

A

The most common tumor of the heart.

96
Q

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

A

Most common primary tumor of the adult heart.

97
Q

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

A

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

98
Q

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

A

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.

99
Q

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

A

Serosanguinous pericardial effusion can be caused by ________

100
Q

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

A

The most severe pulmonary changes in congestive heart failure

101
Q

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

A

Morphologic finding/telltale signs of previous episodes of pulmonary edema

102
Q

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

A

Most common underlying etiology of diastolic failure

103
Q

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

A

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

104
Q

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

A

Most common genetic cause of congenital heart disease

105
Q

VSD (TOPNOTCH)

A

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:

106
Q

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

A

Most common cause of myocardial ischemia

107
Q

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

A

The cause of sudden cardiac death in myocardial infarction

108
Q

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

A

Irreversible cell injury in MI occur in how many minutes?

109
Q

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

A

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

110
Q

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

A

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

111
Q

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

A

Pattern of infarction caused by occlusion of an epicardial vessel

112
Q

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

A

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

113
Q

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

A

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

114
Q

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

A

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

115
Q

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

A

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

116
Q

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

A

Microscopic findings in irreversibly injured myocytes characterized by intensely eosinophilic intracellular stripes composed of closely packed sarcomeres. SEE SLIDE 11.12.

117
Q

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

A

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:

118
Q

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

A

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

119
Q

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

A

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

120
Q

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

A

Most common cause of rhythm disorder

121
Q

Rheumatic heart disease (TOPNOTCH)

A

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?

122
Q

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

A

Characteristic anatomic change in MVP

123
Q

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

A

Most frequent mechanism of SCD

124
Q

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

A

Earliest microscopic change in systemic hypertensive heart disease

125
Q

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

A

Most common type of VSD

126
Q

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

A

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

127
Q

Patent ductus arteriosus(TOPNOTCH)

A

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?

128
Q

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

A

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.

129
Q

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

A

Major cause of infective endocarditis among intravenous drug abusers

130
Q

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

A

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

131
Q

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

A

Predominant manifestations of RF

132
Q

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

A

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

133
Q

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

A

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

134
Q

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

A

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

135
Q

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

A

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

136
Q

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

A

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

137
Q

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

A

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

138
Q

stellate cells admixed with endothelial and fibroblastic cells embedded in an abundant extracellular matrix. SEE SLIDE 11.13. (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 417-418

A

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

139
Q

30 minutes to 4 hours (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380

A

Estimated time from myocardial infarction given this morphologic change: No change grossly, with variable waviness of fibers

140
Q

4 to 24 hours. Myocardial infarcts less than 12 hours old usually are not grossly apparent. In 12 to 24 hours, there is dark mottling due to trapped blood. SEE SLIDE 11.14. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380

A

Estimated time from myocardial infarction given this morphologic change: Dark mottling grossly with microscopic evidence of coagulation necrosis

141
Q

1-3 days. SEE SLIDE 11.14 (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380

A

Estimated time from myocardial infarction given this morphologic change: Mottling with yellow-tan infarct center, prominent interstitial infiltrate of neutrophils

142
Q

3-7 days. SEE SLIDE 11.14. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380

A

Estimated time from myocardial infarction given this morphologic change: Hyperemic border with central yellow-tan softening grossly. On microscope, there is early phagocytosis of dead cells by macrophages at infarct border

143
Q

7-10 days (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380

A

Estimated time from myocardial infarction given this morphologic change: Maximally yellow-tan and soft WITH depressed red-tan margins. There is formation of GRANULATION TISSUE at the margins

144
Q

10-14 days (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380

A

Estimated time from myocardial infarction given this morphologic change: Red-gray in color, granulation tisue is well established with new blood vessels and collagen deposition

145
Q

More than 2 weeks. By 2 months, scarring is complete with a dense collagenous scar. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380

A

Estimated time from myocardial infarction given this morphologic change: Progressive graying (or scarring) of the infarcted area witn increased collagen deposition and decreased cellularity

146
Q

RHD: Usually 1-2mm vegetations called verrucae, composed mostly of fibrin, along the lines of closure; IE: Highly friable and destructive, composed of inflammatory cells, fibrin, and microorganisms. They can embolize (causing septic infarcts) and even erode the underlying myocardium, forming a ring abscess. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 394

A

Differentiate the vegetations seen in RHD and in infective endocarditis.

147
Q

5-hydroxyindoleacetic acid (5-HIAA) (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 395

A

Serotonin metabolite that correlates with the severity of right-sided heart lesions seen in carcinoid syndrome.

148
Q

Beta-myosin heavy chain. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 400

A

Sarcomeric protein most frequently affected in hypertrophic cardiomyopathy.

New Pathology TN (24 decks)

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