Path images Flashcards
Arteriosclerosis, Thrombosis
- Aorta with large clot on L
- thrombus= acellular
- Atherosclerosis plaque on R
- soft core of foamy macrophages, cholesterol clefts
- cystic medial necrosis
- fibrosis
Carotid artery: Arteriosclerosis, Thrombosis
medium (carotid) artery thrombus and surrounding atherosclerosis
cystic medial necrosis: foamy macros and cholesterol clefts
Heart: Acute Myocardial Infarction with Coagulation Necrosis
Coronary Artery Thrombosis
Heart, Acute Infarction
Heart, Ischemic Heart Disease
Heart, Mural Thrombus (thrombus in contact with the endocardial lining of a cardiac chamber)
Heart, Myocardial Hypertrophy
Heart, myocardial infarction, contraction band necrosis
Heart, Rheumatic Myocarditis
Kidney, Atheromatous Emboli
Kidney, diabetic glomoerulosclerosis and HTN
Kidney, hypertension
Kidney, Infarct (Coagulation Necrosis)
Lung and Heart, Septic Emboli
Polyarteritis Nodosa
Polyarteritis Nodosa
Skin, Glomangioma
Vascular pathology in hypertension. Hyaline
arteriolosclerosis. The arteriolar wall is thickened with
increased protein deposition (hyalinized), and the lumen is
markedly narrowed.
Hyperplastic arteriolosclerosis (onion-skinning;
arrow) causing luminal obliteration (arrow; periodic acid–
Schiff stain).
Gross kidney showing granular surface consistent
with nephrosclerosis due to chronic hypertension
Heart showing left ventricular hypertrophy.
Image of fundus showing hypertensive retinopathy
with blurring of the optic disc, exudates, flame hemorrhages
and nipping of venules at the arteriovenous crossings.
Aorta (micro, H+E, low power). Early atherosclerotic
plaque. 2 components can be seen: 1) fibrous cap consisting of
dense collagen and 2) soft central core. This section also shows
fresh thrombus material overlying the atherosclerotic plaque. In
this early lesion there are mild secondary changes in the media
(atrophy).
This is a formalin-fixed abdominal
aorta with femoral vessels and attached kidneys showing moderate
atherosclerosis. The atherosclerosis typically is more severe in the
infrarenal portion and extends into the renal artery ostia and femoral
arteries. Note the sparing of the mesenteric vessels. The plaques are
somewhat raised and yellowish in color
Abdominal aortic aneurysm: Opened view, with the
location of the rupture tract indicated by a probe. The wall of the
aneurysm is exceedingly thin, and the lumen is filled by a large
quantity of layered but largely unorganized thrombus
(A) Normal aorta (photomicrograph, elastic stain). With this special stain, elastic tissue appears black. Note the closely spaced elastic lamellae in the media.
(B & C) Aorta (photomicrograph, elastic stain) demonstrating changes of cystic medial necrosis.
(B) Note the small, irregular spaces between the elastic lamellae.
(C) Aorta at higher power showing more severe changes.
Image 1. Giant-cell (temporal) arteritis. Examination of the
temporal artery of a patient with giant-cell arteritis shows a
thickened, nodular, and tender segment of a vessel on the
surface of head (arrow).
Image 2. Giant-cell (temporal) arteritis. H&E stain of
section of temporal artery showing giant cells (arrow) at
the site of the internal elastic lamina in active arteritis.
Giant-cell (temporal) arteritis.
Elastic stain of temporal artery showing
disruption/degeneration of the internal elastic
lamina. (arrow).
Image 1. Hemangioma (Gross photograph)
Typically appear as a red, well-demarcated
papule on the skin. Compare to tan-brown
freckles.
Image 2. Hemangioma (Microscopic) Note the organized, lobular
architecture. Each lobule consists of small vessels (capillaries in this case)
lined by benign endothelial cells.
Image L. Kaposi sarcoma. Gross photograph, illustrating
coalescent red-purple macules and plaques of the skin.
Image R. Kaposi sarcoma. Histologic appearance of
nodular form, demonstrating sheets of plump, proliferating
spindle cells.
Image L: Bacillary angiomatosis. Photograph of a cutaneous
lesion
Image R. Bacillary angiomatosis. Histologic appearance with acute neutrophilic inflammation and vascular (capillary) proliferation. (Inset) A modified silver (Warthin-Starry) stain demonstrates clusters of tangled
bacilli (black)
Angiosarcoma.
A, Gross photograph of angiosarcoma of the heart (right ventricle).
B, Photomicrograph of angiosarcoma with dense clumps of irregular, cells and distinct vascular lumens, many containing red blood cells.
C, Immunohistochemical staining for the endothelial cell marker CD31, demonstrating the endothelial origin of the tumor cells.
Clinical photo of the strawberry tongue and cracked, red, fissured lips. This is one of the potential diagnostic
features of Kawasaki disease.
Contrast radiograph of coronary artery aneurysms. Note that the dilated aneurysms may be separated by areas of
narrowing (stenosis). This is one of the feared complications that may develop in patients with Kawasaki disease.
Heart and lung block from a patient with
Kawasaki disease. Note the dilated left anterior
descending coronary.
Section of artery with acute inflammation. There is
necrosis and inflammation affecting the full thickness of the
vessel wall. The arterial lumen is obstructed by a thrombus.
Viewed from the right ventricle, a large ventricular
defect is present in the superior portion of the ventricular septum
Schematic of congenital left-to-right shunts.
Atrial septal defect (ASD).
Schematic of congenital left-to-right shunts.
Ventricular septal defect (VSD)
Schematic of congenital left-to-right shunts. Patent ductus arteriosus (PDA)
Aortic Valve (gross photographs, composite).
Left:Senile calcification on a tricuspid valve. Nodular calcifications
on the aortic aspect of the valve involve the sinuses of Valsalva; the ventricular surfaces are spared. Secondary fibrous
thickening of the leaflets also occurs. There is no fusion of the commissures. The valve leaflets are rigid and do not open
completely during systole resulting in obstruction to outflow. The leaflets may not close completely during diastole resulting
in some degree of aortic regurgitation.
Fig. on the right shows dystrophic calcification occurring on a bicuspid valve.
Heart (gross photograph). Concentric left
ventricular hypertrophy is the initial response to outflow
obstruction. When the ventricle can no longer completely
compensate, it begins to fail and dilates.
Calcific aortic stenosis of a previously normal
valve (viewed from aortic aspect). Nodular masses of
calcium are heaped up within the sinuses of Valsalva
(arrow). Note that the commissures are not fused, as in postrheumatic
aortic valve stenosis
Mitral Valve (gross photographs). shows the valve
opened out. Classic gross findings in mitral valve prolapse are illustrated here. There is ballooning (billowing, hooding) of
the valve leaflets and the leaflets appear elongated. The chordae tendineae are elongated and attenuated. A secondary change
in the leaflets is thickening, but there is no fusion of the commissures. Thrombi may occur on the atrial surface of the leaflets.
Mitral valve prolapse. Long axis of left ventricle
demonstrating hooding with prolapse of the posterior
mitral leaflet into the left atrium (arrow). The left ventricle
is to the right of the viewer in this four-chamber view.
Opened valve, showing pronounced hooding of the
posterior mitral leaflet with thrombotic plaques at sites of
leaflet–left atrium contact (arrows).
Mitral Valve (gross photograph) - Acute rheumatic fever. ARF is characterized by small vegetations (verrucae) along the
lines of closure of the valve leaflets. These vegetations may also involve the chordae tendineae. While the mitral valve is the most
frequently involved, aortic valve involvement is also common.
Mitral valve (gross photographs, composite) - A is viewed from atrium. B is resected mitral valve of Rheumatic heart disease - In RHD the valve shows striking chronic changes. There is diffuse fibrous thickening of the leaflets with neovascularization and fusion of the commissures. The chordae tendineae are also thickened and shortened. In extreme cases the type of “fish mouth” deformity seen on the right results. Calcification is a common secondary change. It is easy to imagine that this type of rigid valve is both stenotic and regurgitant. Mural thrombi are common, particularly in the atrium, due to interference with normal flow patterns.
Myocardium (micro, H+E) - Aschoff body. The photomicrograph illustrates the classic components of the
Aschoff body. It consists of an area of fibrinoid necrosis surrounded by lymphocytes and macrophages. Anitschkow or Aschoff cells
are modified histiocytes with plump cytoplasm and “caterpillar” nuclei. These cells may also be multinucleated. Although a classical
and pathognomic sign of RF, the Aschoff body is rarely found in adults with RHD and modern diagnosis relies upon Doppler
echocardiography.
Microscopic appearance of Aschoff body in a patient with acute rheumatic carditis. The myocardial interstitium has a
circumscribed collection of mononuclear inflammatory cells, including some large macrophages with prominent nucleoli and a
binuclear macrophage, associated with necrosis.
Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease. Small vegetations
(verrucae) are visible along the line of closure of the mitral valve leaflet (arrows). Previous episodes of rheumatic
valvulitis have caused fibrous thickening and fusion of the chordae tendineae.
chronic rheumatic heart disease
Mitral stenosis with diffuse fibrous thickening and distortion of the valve leaflets and commissural fusion
(arrows, C), and thickening of the chordae tendineae.
Aortic Valve (gross photograph) Acute infective endocarditis. This shows an aortic valve with large vegetations and an area of perforation at the arrows.
potential complications of infective endocarditis
Mitral valve vegetation (micro, H+E, low power). A
vegetation consists of a mass of fibrin and white blood cells,
although the latter may be difficult to make out at this power.
potential complications of infective endocarditis
Vegetation (micro, H+E, high power). Fibrin and
white cells are seen. The white cells are usually both
neutrophils and mononuclear cells. Probable organisms at
lower left need special stain confirmation.
complications of infective endocarditis
Vegetation (micro, tissue gram stain). A tissue gram
stain can be applied to demonstrate microorganisms.
Healed perforation of mitral valve. Remote history of
infective endocarditis.
Spleen (A) and Kidney (B) (gross photographs). A common complication of infective endocarditis is embolization to
various organs. Here pale infarcts of the spleen and kidney are obvious.
Viewed from the anterior surface note the
markedly hypertrophic ventricular septum (1) along with the
free wall of the right ventricle that is nearly as thick as the
left ventricular wall. The blue rod on the left extends from
the right ventricle into the stenotic opening of the pulmonary
artery. The rod on the right extends from the left ventricle
into the dilated aortic valve and aorta. Note that the opening
of the aorta “overrides” the ventricular septal defect
(indicated by the arrows between the rods).
PBOD 9th ed Fig 12-7
Oxygen saturation in tetralogy of Fallot
Atrial myxoma. Abundant extracellular matrix with myxoma cells.
Coronary arteries (composite gross photograph).
(A) Right: shows CA involved by atherosclerosis. Here the plaque
is much yellower reflecting high cholesterol content and probably some calcification. The red material is fresh thrombus, the
cause of the partial luminal occlusion in this case.
(B) Left: shows atherosclerotic plaque totally occluding the vessel lumen -only a slit-like orifice remains. In this case the plaque is predominantly white indicating that it is mainly fibrous. The area of
brownish discoloration at the lower left represents an area of old hemorrhage into the plaque, which resulted in rapid plaque
expansion and luminal occlusion.
Coronary artery (micro, H+E, low power). Atherosclerotic plaque causing critical (\>75%) narrowing of the CA lumen. Plaque began in the intima and has largely destroyed the media. Free cholesterol crystals are seen at the arrows. Fresh thrombus material, adjacent to an ulcerated intima (acute plaque change), has partially occluded the lumen.
This is a postmortem angiogram from a patient who died of coronary artery disease. In this technique radiopaque
dye is injected into the left and right CA systems. An x-ray is then taken to define any sites of occlusion. Note the filling
defect at the arrow in the left circumflex CA . The use of 2 different dye colors (one dye into each main coronary artery)
allows study of any collateral circulation that may have developed in response to chronic ischemia
Heart (gross photograph, transverse section). The area of recently infarcted myocardium shows pallor and slight
yellowish discoloration. The region involved is in the distribution of the left circumflex CA. This pallor, which may be very
subtle, is a gross feature of an acute (24-48 hrs.) myocardial infarction (MI) and microscopic examination may be needed to
firmly establish the diagnosis. There also are white scars anteriorly and posteriorly from old myocardial infarctions. (Note:
When looking at a cross section of a normal heart, the anterior aspect is rounded and the posterior is flattened.)
Heart (micro, H+E, mid power). Note the contrast between the normal, pale pink myocardial fibers seen at the top of
the slide and the deep pink fibers in the bottom portion, which have undergone coagulation necrosis. The normal myocardial
fibers have a pale eosinophilic, somewhat feathery-looking cytoplasm. When seen in longitudinal section, cross-striations can
be detectedand nuclei are intact. In coagulation necrosis, the myocardial fibers take on a deep eosinophilia with loss of the
feathery appearance and loss of cross-striations. Nuclei undergo karyorrhexis and karyolysis and eventually disappear.
Heart (micro, H+E, high power). At high power the cellular infiltrate can be identified as neutrophils, which are the
cell type seen in the first several days following a myocardial infarction.
Heart (micro, H+E, high power). Another lesion that may be seen in the setting of acute myocardial infarction is
referred to as contraction band necrosis. Wide, deeply eosinophilic bands run transversely across the myocardial fibers. This
apparently results from reperfusion of fibers that have been irreversibly damaged by ischemia. Reperfusion causes the fibers
to die in a maximally contracted state.
Heart (gross photograph, transverse section). Note the large discolored area in the distribution of the left anterior
descending CA. The border of the infarct that is hyperemic, reflecting the high vascularity of granulation tissue. The center
of the infarct is yellow and would be soft to the touch. This is the fully necrotic muscle remaining at the center, because
resorption and the ingrowth of granulation tissue begins at the periphery where there are viable vessels.
Myocardium (micro, H+E, mid power). Center of section shows muscle, which has undergone coagulation
necrosis with loss of cross-striations and nuclei (not seen at this magnification). The granulation tissue at the periphery is
highly vascular.
Myocardium (micro, H+E, high power). Granulation tissue is characterized by a proliferation of small blood
vessels, fibroblasts laying down young collagen and an admixture of mononuclear inflammatory cells (lymphocytes and
macrophages).
Heart (gross photograph) - Fibrinous pericarditis. This is a common reaction overlying the area of an infarct. The
pericardium appears shaggy and somewhat hemorrhagic.
Heart (gross photograph, transverse section) - Mural thrombus. This complication may occur in the area of an
infarct due to decreased contractility of the ventricular wall and resulting stasis of blood flow. The major risk of such mural
thrombi is embolization to sites such as brain and kidney.
Heart (gross photographs) Free wall rupture is a major risk of myocardial infarction, most
commonly happening 2- 4 days after the infarct; necrosis is maximal and there is not yet enough fibrous tissue to provide
tensile strength. It may lead to cardiac tamponade.
Heart (gross photographs) rupture is a major risk of myocardial infarction, most
commonly happening 2- 4 days after the infarct; necrosis is maximal and there is not yet enough fibrous tissue to provide
tensile strength. It may lead to cardiac tamponade.
Rupture of the interventricular septum (image 8) is less common and
leads to the rapid onset of congestive failure.
post MI risk:
Heart - Papillary muscle
rupture leads to congestive failure with acute
pulmonary edema and murmur.
MI
Heart (gross photograph, transverse section).
Remote, transmural infarct in the left anterior descending
CA distribution. The scar is very dense suggesting it is at
least several months old. Note the thinning of the wall in the
area of the infarct and the compensatory hypertrophy of the
opposite wall. It is easy to imagine that this ventricle does
not contract or relax efficiently.
Heart (micro, H+E, mid power). This section
shows dense, relatively acellular collagen. The degree of
vascularity is variable in old infarcts. Some residual necrotic
muscle that was never resorbed is present at the periphery of
the infarct.
Heart (gross photograph, longitudinal section) - Aneurysm. The left ventricle shows a focal area of thinning of the
lateral wall. No muscle is visible in the wall and only a thin fibrous shell remains. Such outpouchings or aneurysms do not
contract with the remainder of the ventricle during systole and, therefore, cause marked reduction in the ejection fraction
and lead to congestive failure
Heart (gross photograph, longitudinal section) - Aneurysm with thrombus. Because of the decreased contractility
in the area of the aneurysm, mural thrombus tends to accumulate due to relative stasis of blood flow. Here there is a large
apical aneurysm and almost the entire left ventricular cavity is filled with thrombus. Note the Lines of Zahn.
Brain (gross). Cerebral infarction from thrombo-emboli arising in the left side of the heart. Note the presence of
multiple infarcts.
Hypertrophic cardiomyopathy
Heart, gross photograph composite, panoramic and close-up, longitudinal section: The classical findings of
hypertrophic cardiomyopathy (HCM) includeLeft ventricle hypertrophy, most marked at the base of the interventricular
septum (Asymmetric septal hypertrophy).. Concentric hypertrophy can be seen, but is uncommon. The left ventricular
outflow tract is narrowed, and the anterior mitral leaflets are thickened from contact during ventricular systole.
In HCM, there is diastolic dysfunction.
Hypertrophic cardiomyopathy
- Left ventricular hypertrophy, usually asymmetric with disproportionate thickening of the septum compared with the free
wall of the left ventricle (asymmetric septal hypertrophy). - Enlarged left atrium.
- May have LV outflow tract obstruction.
- Normal or decreased size of LV cavity
Hypertrophic cardiomyopathy
Myocardium (micro, H+E, high power). Microscopically one sees patches with disarray of the myofibers.
Histologic features:
- Myofiber hypertrophy.
- Haphazard orientation of myofibers, myocyte disarray, not uniform throughout. Not present in all cases.
- Interstitial fibrosis.
Dilated cardiomyopathy. The overall size of the
heart is increased. There is marked dilatation of all 4 chambers, but particularly the ventricles. The walls are thinned and
flabby, and the ventricles are poorly contractive (systolic dysfunction).. Mural thrombi are common (not seen here).
Dilated cardiomyopathy. The overall size of the
heart is increased. There is marked dilatation of all 4 chambers, but particularly the ventricles. The walls are thinned and
flabby, and the ventricles are poorly contractive (systolic dysfunction).
Four-chamber dilatation and hypertrophy are evident. There is granular mural thrombus (arrow) at the apex of the left ventricle (on the right in this apical four-chamber view). The coronary arteries were patent.
Dilated Cardiomyopathy
↓LV contractility → ↓LV emptying →↑ LV and LA pressure→ ↑ pulmonary capillary pressure→pulmonary
edema, pulmonary hypertension→R CHF
↓RV contractility →↓ RV emptying →↑systemic venous pressure → peripheral edema and chronic passive
congestion in the liver CHF onset early
Hypertrophic Cardiomyopathy
↓LV compliance →↓ LV diastolic filling→ ↓ Cardiac output + ↑LA pressure± obstruction to LV outflow →
↓Cardiac output and ↑ strain on LV →→→ CHF
CHF develops more slowly than with DCM
Restrictive Cardiomyopathy
↓ LV compliance →↓ LV diastolic filling→↓ cardiac output
↓contractility →↓ cardiac output
CHF onset relatively early
Dilated cardiomyopathy. Variable myocyte
hypertrophy and interstitial fibrosis (collagen is
highlighted as blue in this Masson trichrome stain).
preductal aortic coarctation
There is a sharp constriction at, or just distal to the ligamentum arteriosum
A fetal heart with a preductal aortic coarctation
(arrowhead). Aortic outflow is obstructed, which leads to
dilation of the aortic root (arrow).
Image 2: Segment of resected aorta in patient with
postductal coarctation. Note how narrow the lumen is,
approximately 3mm.
preductal aortic coarctation
Takayasu arteritis. Aortic arch angiogram showing
narrowing of brachiocephalic, carotid, and subclavian arteries
(arrows).
Takayasu arteritis. Gross photograph of two
cross-sections of the right carotid artery taken at autopsy
of the patient shown in A, demonstrating marked intimal
thickening with minimal residual lumen.
Takayasu arteritis
Histologic view of active
Takayasu aortitis, illustrating destruction of the arterial
media by mononuclear inflammation with giant cells
(arrows).
brain infarct
post MI?
MI
