CVS-PAT 01-Aneurysm

Saccular Aneurysm of Abdominal Aorta with Atherosclerosis and Superimposed

Thrombus

• Raised yellow white atheromatous plaque over the intimal surface is seen.
• Large saccular dilation of the lower portion of the abdominal aorta just proximal to the
bifurcation. Aneurysmal sac is saccular in shape and it is totally filled with large thrombus.
• Thrombus is firmly attached to intima and is composed of laminated layers of pale layers
alternating with red brown layers (Line of Zahn).

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Saccular Aneurysm of Ascending aorta with atherosclerosis and Left ventricular
hypertrophy

• Raised yellow white atheromatous plaque over the intimal surface of the aorta and large
saccular dilation of the ascending aorta.
• Aneurysmal sac is totally filled with large thrombus. Thrombus is composed of laminated
layers of pale layers alternating with red brown layers (Line of Zahn)
• Left ventricular wall is thickened and it measures 2 cm in thickness (Normal- 1.2 to 1.5 cm).
The increase in thickness occurs circumferentially and concentrically around the LV
chamber. LV chamber is narrowed.

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Dissecting Aneurysm of Arch of Aorta

• Wall of arch of aorta shows a dissection, dividing the wall into two separate layers, and
extends downward.
• There is a false lumen within aortic wall.
• Raised yellow white atheromatous plaque over the intimal surface is seen.

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 CVS-PAT 05 - Autopsy (Hypertension)
Concentric Left Ventricular Hypertrophy

• Left ventricular wall is thickened and measures 2cm in thickness (N- 1.2 to 1.5 cm ). The
increase in thickness occurs concentrically & circumferentially around the LV chamber
and LV chamber is very much narrowed.
• Papillary muscles are hypertrophied and they look stout.
• This is the compensatory state to increased work load.
Left ventricular hypertrophy

• The histologic sections show myocardium with stratified and interconnected cardiac
myocytes.
• The left picture shows normal myocytes of normal myocardium.
• The right picture shows hypertrophied myocytes. Both cell size and nuclear size of the
myocytes increase.

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Granular contracted kidney

• Kidney is smaller than normal. Capsule is stripped with difficulty.

• Outer surface reveals fine evenly distributed granules resembling grain leather appearance
and is devoid of depressed scar.
• Inner cut surface shows irregular thinning of cortex with indistinct cortico-medullary
junction. Medullary pyramids and pelvi-calyceal system appear to be normal.
Hyaline arteriolosclerosis

• The histologic sections stained with periodic acid-Schiff stain show renal arterioles and
renal tubules.
• The arteriolar wall is thickened with increased protein deposition (hyalinized), and the
lumen is markedly narrowed.
• This finding is called hyaline arteriolosclerosis. It is strongly associated with benign
essential hypertension and it is also called benign nephrosclerosis.

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Flea Bitten Kidney

• Kidney is slightly enlarged.

• Outer cortical surface is red brown, smooth and is dotted by fine punctate petechial
hemorrhage produced by acute inflammatory rupture of glomerular capillaries.
• Inner cut surface shows similar fine punctate petechial hemorrhage distributed over cortex
and medullary pyramid. Pelvicalyceal system appears to be normal.
Hyperplastic arteriolosclerosis

• The histologic section stained with periodic acid-Schiff stain shows glomeruli, renal tubule
and renal arteriole.
• The wall of arteriole exhibits increased layers of cells and connective tissue (onion-
skinning) that narrow the vessel lumen.
• This finding is called hyperplastic arteriolosclerosis. It is associated with malignant
hypertension and it is also called malignant nephrosclerosis.

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 CVS-PAT 09 - Atherosclerosis and acute myocardial infarction
Atherosclerosis of Aorta with Left Ventricular Hypertrophy

• Aorta shows atheromatous lesions. Raised yellow white atheromatous plaques are seen over
the intimal surface of the aorta.
• Some lesions show ulcerated plaque and some show overlying thrombus.
• The heart shows thickened left ventricular wall which measures 2cm in thickness ( N- 1.2
to 1.5 cm ). The increase in thickness occurs concentrically & circumferentially around
the LV chamber and LV chamber is very much narrowed.

Coronary atherosclerosis with occlusive thrombus

• Histologic section shows atherosclerotic coronary artery The lumen of artery is occluded by
atheromatous plaque and thrombus.
• There is atheromatous plaque within tunica intima and it is composed of central lipid core
containing cholesterol clefts, lipid laden macrophages (foam cells) covered by fibrous cap.
• Rupture of fibrous cap and superimposed occlusive thrombus is seen.

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Acute myocardial infarction

• Gross photo shows acute myocardial infarct, predominantly of the postero-lateral left
ventricle.
• Non-infarcted myocardium with preserved lactate dehydrogenase activity shows brick-red
color after immersion in triphenyl-tetrazolium chloride solution.
• Area of acute myocardial infarct shows lack of staining (unstained pale zone). The anterior
scar is indicative of an old infarct.
Healed Myocardial Infarction

• The heart is enlarged. Left ventricular wall is thickened measuring about 2 cm in thickness
( Normal - 1.2 to 1.5cm ).
• There is an infarct area present in L.V wall which is paler than surrounding myocardium
and appears to be firm in consistency. It is well demarcated from surrounding myocardium.
• Overlying pericardium is dull, thickened and opaque.

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3-day-old Myocardial Infarct

• The histologic section reveals 3-day-old myocardial infarct with myocardial tissue
showing features of coagulative necrosis.
• Myocardial cells show preservation of cellular outline. There is loss of nuclei and cross
striation. The cells show increased granular eosinophilic cytoplasm.
• Dense polymorphonuclear leukocytic infiltrates are noted.
10-week-old Myocardial Infarct

• The histologic section reveals 10-week-old myocardial infarct (healed myocardial infarct)
which is highlighted with Masson’s trichrome stain.
• Necrotic tissue has been replaced by a dense collagenous scar which shows deep blue
color.
• The residual cardiac muscle cells (stained by red color) show evidence of hypertrophy.

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 CVS-PAT 14 - Valvular heart disease
Acute rheumatic heart disease

• The gross picture shows mitral valve with attached chordae tendineae.
• Small vegetations (verrucae) are visible along the line of closure of the mitral valve leaflet
(acute rheumatic valvulitis).
• Fibrous thickening and fusion of the chordae tendineae are noted and they are caused by
previous episodes of rheumatic valvulitis.
Acute rheumatic carditis

• The histologic sections show myocardium with stratified and interconnected cardiac
myocytes.
• The myocardium exhibits Aschoff body, which is a circumscribed nodule of mixed
mononuclear inflammatory cells with associated necrosis.
• Within the inflammation, large activated macrophages show chromatin condensed into
long, wavy ribbons and are called caterpillar cells.

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Mitral stenosis due to chronic rheumatic heart disease

• The gross picture shows mitral valve with two leaflets.

• There is narrowing of the valve orifice (mitral stenosis) due to diffuse fibrous thickening,
distortion of the valve leaflets and commissural fusion.
• This anatomic change, also called fish-mouth stenosis, is due to chronic rheumatic heart
disease.
Subacute infective endocarditis of mitral valve

• The gross picture shows mitral valve with two leaflets.

• There are large, irregular, friable masses (vegetations) on the valve cusps. Vegetations
extend onto the chordae.
• There is no ring abscess. These less destructive vegetations are classic findings of subacute
infective endocarditis.

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Comparison of the four major forms of vegetative endocarditis

A B C D

(A) Rheumatic fever phase of rheumatic heart disease is marked by

small, warty vegetations along the lines of closure of the valve leaflets. (B) Infective
endocarditis is characterized by large, irregular masses on the valve cusps that can
extend onto the chordae. (C) Nonbacterial thrombotic endocarditis typically
exhibits small, bland vegetations, usually attached at the line of closure. One or
many may be present. (D) Libman-Sacks endocarditis has small- or medium-sized
vegetations on either or both sides of the valve leaflets.

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 CVS-PAT 17 - Cardiomyopathy
Dilated cardiomyopathy

• The gross picture shows four-chamber view of heart.

• There is four-chamber dilatation and hypertrophy.
• There is a mural thrombus at the apex of the left ventricle.
Dilated cardiomyopathy

• The histologic section shows Masson’s trichrome stained section of myocardium with
stratified and interconnected cardiac myocytes.
• The myocardium exhibits variable myocyte hypertrophy with enlarged nuclei.
• Interstitial fibrosis (increased collagen) is evident and is highlighted as blue colour.

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 Hypertrophic cardiomyopathy

• The gross picture shows four-chamber view of heart.

• There is asymmetric septal hypertrophy. The septal muscle bulges into the left ventricular
outflow tract. The normally round-to-ovoid left ventricular cavity is compressed into a
“banana-like” configuration.
• The left atrium is enlarged.
Hypertrophic cardiomyopathy

• The histologic section shows myocardium with stratified and interconnected cardiac
myocytes.
• The myocardium exhibits extreme hypertrophy, myocyte disarray, and exaggerated
myocyte branching.
• Interstitial fibrosis is noted.

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 CVS-PAT 18 - Organ changes in heart failure
Chronic passive pulmonary congestion

• The gross picture shows enlarged lungs which appears brownish.

• The finding is due to oedema, congestion and haemosiderin deposition. The presence of
fibrosis and iron is viewed grossly as a firm, brown lung (brown induration).
• The finding occurs because of congestive heart failure which causes chronic passive
pulmonary congestion.
Chronic passive pulmonary congestion

• The histologic section shows numerous hemosiderin-laden macrophages.

• Extravasated RBCs in alveoli are phagocytosed and digested by macrophages which shows
accumulated iron stored as hemosiderin.
• This histomorphology occurs because of congestive heart failure which causes chronic
passive pulmonary congestion. Therefore, the hemosiderin-laden macrophages are also
called heart failure cells.

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Chronic passive venous congestion of liver

• The gross picture shows cut section of liver showing centrilobular regions which are red
and slightly depressed compared with the surrounding tan viable parenchyma.
• This appearance resembles the cut surface of a nutmeg (nutmeg liver pattern). The finding
is due to ischemic necrosis of centrilobular hepatocytes which exist at the distal end of the
hepatic blood supply.
• This morphology occurs because of congestive heart failure which causes chronic passive
venous congestion of liver.

Chronic passive venous congestion of liver

• The histologic section shows liver lobule with central venule and hepatocyte cell plates.
• The hepatocytes in centrilobular zone around the central venule reveal necrosis with
degenerating hepatocytes and hemorrhage. Haemosidern-laden Kupffer cells are present.
• Peripheral zones show viable hepatocytes with fatty change.

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 CVS-PAT 19 - Morphology of shock
Shock kidney

• The picture shows gross specimen of kidney with cortex, cortico-medullary junction,
medullary pyramids, and pelvi-calyceal system.
• The kidney is normal in size.
• Cut surface shows pale swollen widened cortex with dark red congested medulla. Cortico-
medullary junction is well defined.

Acute tubular necrosis

• The histologic section of kidney shows glomeruli, renal arterioles and renal tubules.
• The glomeruli look normal. The tubules show swelling and degeneration of tubular
epithelial cells.
• Some tubular epithelial cells have detached (from their basement membranes) and been
sloughed into the tubular lumens.

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