XI - The Heart Flashcards
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.
Left-sided heart failure(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Hemosiderin laden macrophages are also called _______
Heart failure cells. SEE SLIDE 11.1. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Earliest and most significant complaint of patients with left-sided heart failure
Dyspnea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Most common cause of right sided HF.
Left-sided HF(TOPNOTCH)
This is a particularly dramatic form of breathlessness, awakening patients from sleep with attacks of extreme dyspnea bordering on suffocation.
Paroxysmal nocturnal dyspnea (PND) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Isolated right sided HF occuring in patients with intrinsic lung disease that result in chronic pulmonary hypertension.
Cor Pulmonale(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition.
Cardiac cirrhosis(TOPNOTCH)
Term used when the liver has congested centrilobular areas (due to back up of blood) surrounded by paler peripheral regions. SEE SLIDE 11.2.
Nutmeg liver (CPC of the liver)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 381
Hallmark of right sided HF.
Pedal and pretibial edema(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
Most congenital heart disease arises from faulty embryogenesis during what AOG?
3 - 8 weeks AOG(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 382
An abnormal communication between chambers of the heart or blood vessels.
Shunt(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
Smooth-walled defect near the foramen ovale, usually without associated cardiac abnormalities. It comprises 90% of ASDs.
Ostium secundum ASD(TOPNOTCH) Robbins Basic Pathology, 9th Ed., p 371
Chamber abnormalities seen in ASD.
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
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.
Eisenmenger syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 383
These occur at the lowest part of the atrial septum and can extend to the mitral (anterior leaflet) and tricuspid valves (septal leaflet).
Ostium primum ASD. SEE SLIDE 11.3. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 384
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.
Ventricular Septal Defect(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.
Ductus arteriosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
The most common cause of cyanotic congenital heart disease. Heart is large and “boot-shaped” as a result of right ventricular hypertrophy.
Tetralogy of Fallot. SEE SLIDE 11.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 385
Components of Tetralogy of Fallot.
Pulmonary valve stenosis, Overriding of aorta, Right ventricular hypertrophy, Ventricular septal defect. SEE SLIDE 11.4. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
It is a discordant connection of the ventricles to their vascular outflow. The defect is an abnormal formation of the truncal and aortopulmonary septa.
Transposition of the Great Arteries. SEE 11.5 (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 386
Predominant manifestation of TGA?
Early cyanosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
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.
Preductal “infantile” coarctation of the aorta. SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
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.
Postductal “adult” coarctation of the aorta. SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 387
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.
Postductal coarctation of the aorta (without a PDA). SEE SLIDE 11.6. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Atrial septal defect
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?TOF
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?VSD
Left-to-right(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Eisenmenger syndrome
Right-to-Left (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
Left-to-right or Right-to-Left shunt?Transposition of great arteries
Right-to-Left(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)
A condition wherein ischemia causes pain but is insufficient to lead to death of myocardium.
Angina pectoris(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
A condition wherein the severity or duration of ischemia is enough to cause cardiac muscle death.
Acute Myocardial Infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This refers to progressive cardiac decompensation (heart failure) following myocardial infarction.
Chronic Ischemic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
This can result from a lethal arrythmia following myocardial ischemia.
Sudden Cardiac Death(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 388
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic, in the setting of increased demand?
More than 70% (critical stenosis)(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 375
How many percent should the lumen of a blood vessel be obstructed for it to be symptomatic at rest (unstable angina)?
90%(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 375
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.
Stable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Increasing frequency of pain, precipitated by progressively less exertion, episodes tend to be more intense and longer lasting.
Unstable angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Angina occuring at rest due to coronary artery spasm.
Variant or Prinzmetal angina(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 390
Infarct involving >= 50% of the myocardial wall thickness.
Transmural infarcts(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 391
Most common blood vessel involved in myocardial infarction?
Left anterior descending artery (40-50%)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 392
Electron microscope findings 30 minutes after an ischemic event.
Microfibril relaxation, glycogen loss and mitochondrial swelling(TOPNOTCH)
An infarct can be readily identified by a reddish blue discoloration after how many hours after MI?
12-24 hours(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 393
Coagulation necrosis ensues how many hours after MI?
4-12 hrs after an irreversible injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Injury to infarcts mediated in part by oxygen free radicals generated by increased number of infiltrating leukocytes facilitated by reperfusion.
Reperfusion injury(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 394
Cardiac enzymes that become detectable 2-4 hours post-infarct peaks at 48 hours and remains elevated for 7-10 days.
Troponin I and Troponin T(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
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.
CKMB(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 395
Myocardial rupture may occur how many days after MI?
3-7 days after infarction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
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.
Pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
A late complication of MI, most commonly results from a large transmural anteroseptal infarct that heals with formation of a thin scar tissue.
Ventricular aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 397
This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter.
Concentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
Type of hypertrophybthat develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.
Eccentric hypertrophy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 399
Normal weight of heart and normal LV wall thickness
320-360 grams, 1.2-1.4 cm (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 387
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.
Sytemic Hypertensive heart disease(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 387
It is the failure of a valve to open completely, obstructing forward flow.
Stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
This results from failure of a valve to close completely, thereby allowing reversed flow.
Insufficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
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.
Calcific aortic stenosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 401
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.
Myxomatous degeneration of the mitral valve(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Patients with this disease may complain of palpitations, dyspnea or atypical chest pain. Auscultation shows a midsystolic click associated with a regurgitant murmur.
Mitral valve prolapse(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
Pathognomonic sign for rheumatic fever– myocardial inflammatory lesions composed of plump activated macrophages (Anitschkow cells), plasma cells, and lymphocytes. SEE SLIDE 11.7.
Aschoff bodies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 402
TRUE or FALSE: Aschoff bodies are rarely seen in chronic rheumatic heart disease
TRUE. They are replaced by a fibrous scar. (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p.391
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.
Anitschkow cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
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.
Chronic Rheumatic Heart Disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 403
Most common valve involved in RHD.
Mitral valve (upto 70% of cases with RHD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 405
Major components Jones Criteria for RF.
CarditisMigratory polyarthritisSubcutaneous nodulesErythema marginatumSyndenham chorea(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Minor components Jones criteria for RF
FeverArthralgiaElevated acute phase reactants (e.g. CRP)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
How many major and/or minor manifestations are needed to diagnose RF?
Remember: 20122 major 0 minor or1 major 2 minor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis of previously normal valves, the most common causative agent is S. aureus.
Acute bacterial endocarditis(TOPNOTCH)
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.
Infective endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Endocarditis affecting previously damaged or abnormal valves, commonly caused by viridans Streptococci.
Subacute bacterial endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 406
Most consistent sign of infective endocarditis.
Fever(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
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.
Nonbacterial thrombotic endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 407
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.
Libman-Sacks endocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 408
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).
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
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.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
Alcohol, myocarditis, doxorubicin, and hemochromatosis are some of the causes of this cardiomyopathy.
Dilated cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 411
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.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
Mechanism of heart failure in hypertrophic cardiomyopathy.
Diastolic dysfunction (impaired compliance)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
A common cause of sudden death in young athlethes.
Hypertrophic cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 412
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.
Restrictive cardiomyopathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Mechanism of heart failure in restrictive cardiomyopathy.
Diastolic dysfunction or impaired compliance(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 413
Inflammation of the myocardium.
Myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis.
Lymphocytic myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis that has interstitial and perivascular infiltrates composed of lymphocytes, macrophages and a high proportion of eosinophils.
Hypersensitivity myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis characterized by widespread inflammatory infiltrates containing multinucleated giant cells interspresed with lymphocytes, eosinophils and plasma cells. Poor prognosis.
Giant-cell myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Myocarditis distinctive by virtue of parasitization of scattered myofibers by trypanosomes accompanied by an inflammatory infiltrate of neutrophils, lymphocytes, macrophages and occasional eosinophils.
Chagas myocarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
Viruses which account for most cases of myocarditis.
Coxsackie A and B(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 414
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).
Fibrinous pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Bacterial pericarditis manifests with this type of exudate.
Fibrinopurulent (suppurative)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Heart is completely encased by dense fibrosis that it cannot expand normally during diastole.
Constrictive pericarditis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 416
Normal amount of pericardial fluid in pericardial sac.
30 - 50 mL of thin, straw-colored fluid(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Serous pericardial effusion can be caused by _________
CHF, hypoalbuminemia(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Chylous pericardial fluid can be caused by _______
Mediastinal lymphatic obstruction(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Rapidly developing collections of fluid within the pericardial sac can restrict diastolic cardiac filling producing this fatal sequelae.
Cardiac tamponade(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
The most common tumor of the heart.
Metastatic tumor(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Most common primary tumor of the adult heart.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 417
Major clinical manifestations of this cardiac tumor are due to valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms.
Myxoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
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.
Rhabdomyomas(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
Serosanguinous pericardial effusion can be caused by ________
Blunt chest trauma, malignancy, ruptured MI, aortic dissection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 418
The most severe pulmonary changes in congestive heart failure
Accumulation of edema fluid in the alveolar spaces (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Morphologic finding/telltale signs of previous episodes of pulmonary edema
Hemosiderin-laden macrophages (Heart failure cells) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Most common underlying etiology of diastolic failure
Hypertension (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 529
Group of congenital heart disease characterized by increase pulmonary blood flow but are not initially associated with cyanosis
Left-to-right shunts (ASD, VSD, PDA) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533
Most common genetic cause of congenital heart disease
Trisomy 21 (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 533
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:
VSD (TOPNOTCH)
Most common cause of myocardial ischemia
Obstructive atherosclerotic lesions in the epicardial coronary arteries (TOPNOTCH) Robbins Basic Patholgoy, 9th ed., p. 538
The cause of sudden cardiac death in myocardial infarction
Ventricular arrythmia (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 539
Irreversible cell injury in MI occur in how many minutes?
20-40 minutes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
Irreversible injury of ischemic myocytes in MI occurs first in what zone in the heart?
Subendocardial zone (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
What blood vessel supply the posterior third of the ventricular septum in majority of the individuals?
Right coronary artery (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 541
Pattern of infarction caused by occlusion of an epicardial vessel
Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarction caused by plaque disruption or hypotension, causing circumferential myocardial damage
Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarct also referred to as an “ST elevation myocardial infarct”
Transmural infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
Pattern of infarct also referred to as a “non-ST elevation infarct”
Subendocardial infarction (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 543
The typical changes of coagulative necrosis becomes detectable in how many hours of injury?
First 6-12 hours(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 545
Microscopic findings in irreversibly injured myocytes characterized by intensely eosinophilic intracellular stripes composed of closely packed sarcomeres. SEE SLIDE 11.12.
Contraction bands(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 546
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:
Troponins I and T (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 547
A 72 y/o female experienced chest pain and hypotension. A posterior transmural infarct was suspected. Most common complications in this type of infarct
Conduction blocks, right ventricular involvement, or both (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549
Free wall rupture, expansion, mural thrombi, and aneurysm are common in what type/location of infarct?
Anterior transmural infarct(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 549
Most common cause of rhythm disorder
Ischemic injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 550
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?
Rheumatic heart disease (TOPNOTCH)
Characteristic anatomic change in MVP
Interchordal ballooning of mitral leaflets (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 556
Most frequent mechanism of SCD
Lethal arrythmia (asystole, ventricular fibrillation) (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552
Earliest microscopic change in systemic hypertensive heart disease
increase in transverse diameter of myocytes (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 552
Most common type of VSD
Membranous (Interventricular septum) VSD(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 535
The common feature of pulmonary thromboembolism, obstructive sleep apnea, altitude disease, and parenchymal lung disease
Pulmonary hypertension. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 530
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?
Patent ductus arteriosus(TOPNOTCH)
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.
Coarctation of the aorta (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 537
Major cause of infective endocarditis among intravenous drug abusers
Staphylococcus aureus (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Most common cause of endocarditis of native but previously damaged or otherwise abnormal valves
Streptococcus viridans (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
Predominant manifestations of RF
Carditis and arthritis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 559
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
something else entirely (evolution of morphologic changes in myocardial infarction) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 393
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
volume overload from a ventricle with narrowed lumen (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 399
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
fusion of the commisures (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402
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
thinning of fibrosa layer and myxoid espansion of the spongiosa layer (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P402
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
myocardium with circumscribed aggregates of mononuclear cells and macrophages with prominent nucleoli (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P 403-404
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
a mutation in one of his genes encoding sarcomeric proteins (TOPNOTCH)Robbins Basic Pathology, 8th Ed. P. 412-413
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
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
Estimated time from myocardial infarction given this morphologic change: No change grossly, with variable waviness of fibers
30 minutes to 4 hours (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380
Estimated time from myocardial infarction given this morphologic change: Dark mottling grossly with microscopic evidence of coagulation necrosis
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
Estimated time from myocardial infarction given this morphologic change: Mottling with yellow-tan infarct center, prominent interstitial infiltrate of neutrophils
1-3 days. SEE SLIDE 11.14 (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380
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
3-7 days. SEE SLIDE 11.14. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380
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
7-10 days (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380
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
10-14 days (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380
Estimated time from myocardial infarction given this morphologic change: Progressive graying (or scarring) of the infarcted area witn increased collagen deposition and decreased cellularity
More than 2 weeks. By 2 months, scarring is complete with a dense collagenous scar. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 380
Differentiate the vegetations seen in RHD and in infective endocarditis.
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
Serotonin metabolite that correlates with the severity of right-sided heart lesions seen in carcinoid syndrome.
5-hydroxyindoleacetic acid (5-HIAA) (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 395
Sarcomeric protein most frequently affected in hypertrophic cardiomyopathy.
Beta-myosin heavy chain. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 400
