cardiac pathology Flashcards
Heart failure cells (macrophages)
left sided HF
Nutmeg liver
right sided HF
Most common blood vessel involved in myocardial infarction
Left anterior descending artery
Electron microscope findings 30 minutes after an ischemic event
Microfibril relaxation, glycogen loss and mitochondrial swelling
heaped-up calcified masses
Calcific aortic stenosis
is the most prevalent heart valve disorder in developed countries
Calcific aortic stenosis
is characterized by progressive fibro-calcific remodelling and thickening of the aortic valve leaflets that, over years, evolve to cause severe obstruction to cardiac outflow
Calcific aortic stenosis
there are only two functional cusps, usually of unequal size, with the larger cusp having a midline raphe, resulting from incomplete commissural separation during development
congenitally bicuspid aortic valve
Although BAV(bicuspid aortic valve) is usually asymptomatic early in life late complications
include aortic stenosis or regurgitation, infective endocarditis, and aortic dilation and/or dissection
degenerative calcific deposits in the mitral valve typically develop in the fibrous annulus. Grossly, these appear as irregular, stony hard, occasionally ulcerated nodules (2 to 5 mm in thickness) at the base of the leaflets
Mitral Annular Calcification
Mitral Annular Calcification can lead to:
- Regurgitation by interfering with physiologic contraction of the valve ring
- Stenosis by impairing opening of the mitral leaflets
- Arrhythmias and occasionally sudden death by penetration of calcium deposits to a depth sufficient to impinge on the atrioventricular conduction system.
Because calcific nodules may also provide a site for thrombus formation
patients with mitral annular calcification have an increased risk of embolic stroke, and the calcific nodules can become a nidus for infective endocarditis.
Dilated cardiopathy:
systolic
Hypertrophic cardiopathy
diastolic
Restrictive cardiopathy
Diastolic dysfunction or impaired complianc
is the buildup of extra fluid in the space around the heart. If too much fluid builds up, it can put pressure on the heart. This can prevent it from pumping normally. A fibrous sac called the pericardium surrounds the heart. This sac consists of two thin layers.
Pericardial effusion
the presence of blood within the pericardial cavity, i.e. a sanguineous pericardial effusion. If enough blood enters the pericardial cavity, then a potentially fatal cardiac tamponade can occur.
Hemopericardium
is characteristically produced by noninfectious inflammatory diseases, including rheumatic fever, SLE, and scleroderma, as well as tumors and uremia. An infection in the tissues contiguous to the pericardium— for example, a bacterial pleuritis—may incite sufficient irritation of the parietal pericardial serosa to cause a sterile serous effusion that can progress to serofibrinous pericarditis and ultimately to a frank suppurative reaction.
Serous pericarditis
most frequent types of pericarditis
Fibrinous and serofibrinous pericarditis
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
Bacterial pericarditis manifests with this type of exudate
Fibrinopurulent
active
infection caused by microbial invasion of the pericardial
space; this can occur through
Purulent or suppurative pericarditis
pericarditis the surface is dry, with a fine granular
roughening
Fibrinous pericarditis
pericarditis a more intense inflammatory
process induces the accumulation of larger amounts of
yellow to brown turbid fluid, containing leukocytes, erythrocytes,
and fibrin. As with all inflammatory exudates, fibrin may
be lysed with resolution of the exudate, or can become organized
serofibrinous pericarditis
pericarditis has an exudate composed of
blood mixed with a fibrinous or suppurative effusion; it is
most commonly caused by the spread of a malignant neoplasm
to the pericardial space
Hemorrhagic pericarditis
Pericarditis. In some cases organization
merely produces plaque-like fibrous thickenings of
the serosal membranes (“soldier’s plaque”) or thin, delicate
adhesions that rarely cause impairment of cardiac function.
Chronic or Healed Pericarditis
may follow infectious
pericarditis, previous cardiac surgery, or mediastinal irradiation.
The pericardial sac is obliterated, and adherence
of the external aspect of the parietal layer to surrounding
structures strains cardiac function
Adhesive mediastinopericarditis
pericarditis the heart is encased in a dense,
fibrous or fibrocalcific scar that limits diastolic expansion
and cardiac output, features that mimic a restrictive cardiomyopathy.
constrictive pericarditis
Chylous pericardial fluid can be caused by
Mediastinal lymphatic obstruction
The most common tumor of the heart.
Metastatic tumor
Major clinical manifestations of this cardiac tumor are due to valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms
Myxoma
Long standing severe right-sided HF leads to fibrosis of centrilobular areas, creating this condition
cardiac cirhosis
Generalized, massive edema is called
Anasarca
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
Ostium secundum ASD
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
Ostium primium ASD
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
Eisenmenger syndrome
This arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery
Ductus arteriosus
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
Patent Ductus arteriosus
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
The four cardinal features of this defect are (1) VSD, (2) obstruction
of the right ventricular outflow tract (subpulmonary
stenosis), (3) an aorta that overrides the VSD, and (4) right
ventricular hypertrophy (Fig. 12-6A). All of these features
result embryologically from anterosuperior displacement
of the infundibular septum.
Tetralogy of Fallot
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
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
Transposition of g v
Predominant manifestation of transposition of the great arteries?
Early cyanosis
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.
Preductal “infantile” coarctation of the aorta
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
Postductal “adult” coarctation of the aorta
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
Right to left shunt
eisenmenger syndrome
reddish blue discoloration after how many hours after MI
12 24h
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
This type of hypertrophy develops in pressure-overloaded ventricles, with an increase in wall thickness, and reduced cavity diameter
Concentric hypertrophy
Type of hypertrophy that develops in patients with volume overload such as aortic valve insufficiency. Characterized by hypertrophy associated with ventricular dilation.
Eccentric hypertrophy
In this disease the left ventricle may exceed 2.0cm in thickness and the heartvmay weigh >500 grams. Microscopically, and increased interstitial fibrosismyocyte diameter increases, associated with irregular nuclear enlargement and hyperchromasia (“box-car nuclei”)
Sytemic Hypertensive heart disease
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
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
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
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
Aschoff bodies
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.
Anitschkow cells
Key pathologic features of acute RF and chronic RHD are
shown in Figure 12-23. During acute RF, focal inflammatory
lesions are found in various tissues. Distinctive lesions occur in
the heart, called
Aschoff bodies,
Key pathologic features of acute RF and chronic RHD are
shown in Figure 12-23. During acute RF, focal inflammatory
lesions are found in various tissues. Distinctive lesions occur in
the heart, called Aschoff bodies, consisting of foci of T lymphocytes,
occasional plasma cells, and plump activated macrophages
called
Anitschkow cells
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
Chronic Rheumatic Heart Diseas
Most common valve involved in RHD.
Mitral
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
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.
Libman-Sacks endocarditis
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
Carcinoid heart disease
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. Alcohol intake and infection with coxsackie B virus are some of the causes of this cardiomyopathy
Dilated cardiomyopathy systoilc
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
Hypertrophic cardiomyopathy
Mechanism of heart failure in hypertrophic cardiomyopathy *most common cause of death among young athletis
Diastolic
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 *its due Diastolic dysfunction or impaired compliance
Most common type of myocarditis wherein lymphocytes infiltrate the interstitium. This may resolve or heal by progressive fibrosis
Lymphocytic myocarditis
Myocarditis that has interstitial and perivascular infiltrates composed of lymphocytes, macrophages and a high proportion of eosinophils
Hypersensitivity myocarditis
Myocarditis characterized by widespread inflammatory infoltrates containing multinucleated giant cells interspresed with lymphocytes, eosinophils and plasma cells. Poor prognosis
Giant-cell myocarditis
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
Viruses which account for most cases of myocarditis
Coxsackie A and B
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
Bacterial pericarditis manifests with this type of exudate.
Fibrinopurulent (suppurative)
Heart is completely encased by dense fibrosis that it cannot expand normally during diastole.
constrictive pericarditis.
Serous pericardial effusion can be caused by
CHF, hypoalbuminemia
The most common tumor of the heart.
Metastatic tumor
Most common primary tumor of the adult heart * valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms, Major clinical manifestations of this cardiac tumor are due to valvular “ball-valve” obstruction, embolization or a syndrome of constitutional symptoms
Myxoma
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
the most frequent
primary tumor of the pediatric heart, and are commonly
discovered in the first years of life because of obstruction
of a valvular orifice or cardiac chamber.
Rhabdomyoma
curious, usually incidental, sea-anemone-like lesions, most
often identified at autopsy. They may embolize and thereby
become clinically important
are unusual benign neoplasms They resemble the much
smaller, usually trivial, Lambl excrescences that may represent
remotely organized thrombus on the aortic valves of
older individuals. are usually MORPHOLOGY (>80%) located on valves,
particularly the ventricular surfaces of semilunar valves and the
atrial surfaces of atrioventricular valves. Each lesion, typically 1
to 2 cm in diameter, consists of a distinctive cluster of hairlike
projections up to 1 cm in length
Papillary Fibroelastoma
Wear and tear, fibrosis and calcification, crescendo decrescando murmur is caused by
aortic stenosis
Congintial heart associted w fetal alchohol syndrom:
vsd
Congintial heart associted w down syndrom:
asd
Congintial heart associted w conginal rubella
patent ductus artierous.
Congintial heart associted w eraly cynosis:
tetraology of fallot
Congintial heart associted w maternal diabetes:
trans of great vessels
Congintial heart associted w turner syndrom:
coarcation of the aorta
Cardiomyopathy w low ekg and diminshed qrs:
restrictive.
Subendotheilial ischemia w st depp.
Stable and unstable angina
Transmural ischemia and st elvatino
prinzemtal
Transmural necrosis w first st dep and then elevation
myocardial infraction
necrosis involves the full thickness of the ventricular wall
transmural infarction
necrosis involving inner third of the ventricular wall
subendocardial infarction
pathology involving only smaller intramural vessels
occur in the setting of microembolization vasculitis or vascular spasm
eg: takotsubo cardiomyopathy “broken heart disease syndrome”
multifocal microinfarction
pancarditis
Inflammation of the endocardium and the left-sided valves typically results in fibrinoid necrosis within the cusps or tendinous cords. Overlying these necrotic foci and along the lines of closure are small (1 to 2 mm) vegetations, called
verrucae
Subendocardial lesions, perhaps exacerbated by
regurgitant jets, can induce irregular thickenings called
…………… , usually in the left atrium.
MacCallum plaques
The cardinal anatomic changes of the mitral valve in chronic RHD are
leaflet thickening, commissural fusion and shortening, and thickening and fusion of the tendinous cords
