Pathology Vascular Pathology

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GIANT CELL or TAKAYASU'S ARTERITIS:
This thickening of the temporal arterial wall is associated with chronic inflammatory infiltrate centered in the media, and made of lymphocytes and occasional giant cells.

Note the moderate fibrosis of the vessel wall in both areas of acute inflammation and in uninvolved areas, indicative of both a chronic and sporadic disease process.

These histological findings are characteristic of both Giant Cell and Takayasu's arteritis, but clinical features (patient age, vessels involved) would distinguish the two.

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Back 2

GIANT CELL ARTERITIS:
One of several cross-sections from a temportal artery (do several because even correctly-done biopsies can give false negative results due to the segmental nature of the disease).

Note the narrowed vascular lumen, with thickening of the vessel wall. Elastin staining would show multiple areas of disruption of the internal elastic lamina, which is secondary to the inflammation.

These histological findings are characteristic of both Giant Cell and Takayasu's arteritis, but clinical features (patient age, vessels involved) would distinguish the two.

Front 3

:

Back 3

GIANT CELL ARTERITIS:
This thickening of the temporal arterial wall is associated with chronic inflammatory infiltrate centered in the media, and made of lymphocytes and occasional giant cells.

Note the moderate fibrosis of the vessel wall in both areas of acute inflammation and in uninvolved areas, indicative of both a chronic and sporadic disease process.

These histological findings are characteristic of both Giant Cell and Takayasu's arteritis, but clinical features (patient age, vessels involved) would distinguish the two.

Front 4

:

Back 4

GIANT CELL ARTERITIS:
This thickening of the temporal arterial wall is associated with chronic inflammatory infiltrate centered in the media, and made of lymphocytes and occasional giant cells.

Note the moderate fibrosis of the vessel wall in both areas of acute inflammation and in uninvolved areas, indicative of both a chronic and sporadic disease process.

These histological findings are characteristic of both Giant Cell and Takayasu's arteritis, but clinical features (patient age, vessels involved) would distinguish the two.

Front 5

:

Back 5

GIANT CELL ARTERITIS:
One of several cross-sections from a temportal artery (do several because even correctly-done biopsies can give false negative results due to the segmental nature of the disease).

Note the narrowed vascular lumen, with thickening of the vessel wall. Elastin staining would show multiple areas of disruption of the internal elastic lamina, which is secondary to the inflammation.

These histological findings are characteristic of both Giant Cell and Takayasu's arteritis, but clinical features (patient age, vessels involved) would distinguish the two.

Front 6

:

Back 6

GIANT CELL or TAKAYASU's ARTERITIS:
This thickening of the temporal arterial wall is associated with chronic inflammatory infiltrate centered in the media, and made of lymphocytes and occasional giant cells.

Note the moderate fibrosis of the vessel wall in both areas of acute inflammation and in uninvolved areas, indicative of both a chronic and sporadic disease process.

These histological findings are characteristic of both Giant Cell and Takayasu's arteritis, but clinical features (patient age, vessels involved) would distinguish the two.

Front 7

ID

Back 7

GIANT CELL ARTERITIS:
One of several cross-sections from a temportal artery (do several because even correctly-done biopsies can give false negative results due to the segmental nature of the disease).

Note the narrowed vascular lumen, with thickening of the vessel wall. Elastin staining would show multiple areas of disruption of the internal elastic lamina, which is secondary to the inflammation.

These histological findings are characteristic of both Giant Cell and Takayasu's arteritis, but clinical features (patient age, vessels involved) would distinguish the two.

Front 8

ID

Back 8

MALIGNANT NEPHROSCLEROSIS:
Note the "smudging" of the walls of the afferent arterioles with walls staining deep pink.

Glomeruli often contain patchy, eosinophilic fibrinoid necrosis of the tuft. Some show adhesion between the glomerular capillary and Bowman's Capsule. Some hyalinized glomeruli are also seen.

Dilated tubules are found within the cortex and contain eosinophilic (proteinaceous) material, as well as some PMNLs.

A small artery show concentric hyperplastic arteriolitis that narrows its lumen.

Front 9

ID

Back 9

MALIGNANT NEPHROSCLEROSIS:
Dilated tubules containing eosinophilic material. Increased interstitial fibrous tissue with lymphocyte infiltration

Front 10

ID

Back 10

MALIGNANT NEPHROSCLEROSIS:
ote the "smudging" of the walls of the afferent arterioles with walls staining deep pink.

Glomeruli often contain patchy, eosinophilic fibrinoid necrosis of the tuft. Some show adhesion between the glomerular capillary and Bowman's Capsule. Some hyalinized glomeruli are also seen.

Dilated tubules are found within the cortex and contain eosinophilic (proteinaceous) material, as well as some PMNLs.

A small artery show concentric hyperplastic arteriolitis that narrows its lumen.

Front 11

ID

Back 11

MALIGNANT NEPHROSCLEROSIS:
ote the "smudging" of the walls of the afferent arterioles with walls staining deep pink.

Glomeruli often contain patchy, eosinophilic fibrinoid necrosis of the tuft. Some show adhesion between the glomerular capillary and Bowman's Capsule. Some hyalinized glomeruli are also seen.

Dilated tubules are found within the cortex and contain eosinophilic (proteinaceous) material, as well as some PMNLs.

A small artery show concentric hyperplastic arteriolitis that narrows its lumen. High pressure causes medial hyperplasia, which causes concentric thickening "onion skinning". This further reduces renal blood flow and increased renin results, further increasing blood pressure. Eventually, vascular necrosis leads to interruption in blood flow and infarction. (fatal within a year)

Front 12

ID

Back 12

MALIGNANT NEPHROSCLEROSIS:
Glomeruli often contain patchy, eosinophilic fibrinoid necrosis of the tuft. Some show adhesion between the glomerular capillary and Bowman's Capsule. Some hyalinized glomeruli are also seen.

Dilated tubules are found within the cortex and contain eosinophilic (proteinaceous) material, as well as some PMNLs.

There is an increase in interstitial fibrosis with some lymphocyte infiltration.

Front 13

ID

Back 13

MALIGNANT NEPHROSCLEROSIS:
Note the "smudging" of the walls of the afferent arterioles with walls staining deep pink.

Glomeruli often contain patchy, eosinophilic fibrinoid necrosis of the tuft. Some show adhesion between the glomerular capillary and Bowman's Capsule. Some hyalinized glomeruli are also seen.

Dilated tubules are found within the cortex and contain eosinophilic (proteinaceous) material, as well as some PMNLs.

Some small arteries show concentric hyperplastic arteriolitis that narrows their lumen.

There is an increase in interstitial fibrosis with some lymphocyte infiltration.

Front 14

ID

Back 14

MALIGNANT NEPHROSCLEROSIS:
There is an increase in interstitial fibrous tissue and a slight infiltration of lymphocytes. These are responding to necrotic changes within arterioles and glomeruli and should not be confused with pyelonephritis.

Front 15

ID

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MALIGNANT NEPHROSCLEROSIS:
Capsule of the kidney is slightly thickened and infiltrated with lyphocytes. Just beneath it, there are multiple small hemorrhages.

There is an increase in interstitial fibrous tissue and a slight infiltration of lymphocytes. These are responding to necrotic changes within arterioles and glomeruli and should not be confused with pyelonephritis.

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ID

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RENAL ARTERIOSCLEROSIS:
The characteristic lesion here is hyaline thickening (deep eosinophilic material in intima or entire wall) of the afferent arteriole entering the glomeruli (arteriosclerosis). Be sure to look in the periphery for this too - recall that glomeruli are spherical, and the afferent arteriole may not have made it into the plane of section.

The hyaline thickening of the wall leads to narrowing or obliteration of the lumen.

Some glomeruli are totally hyalinized due to ischemia following obliteration of their afferent arteriole. In some cases, eosinophilic material is found in Bowman's Space around the glomerular tuft.

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ID

Back 17

RENAL ARTERIOSCLEROSIS:
Note the increase in cortical interstitial fibrosis. In the area of the cortex just beneath the capsule are numerous, dilated tubules containing eosinophilic material (proteinatious casts). A few granular and cellular casts are also found.

These tubules are draining the remaining, functioning glomeruli.

May or may not see: (In some of the tubules beneath the capsule there are numerous bacteria in colonies. Lack of cellular response to these suggests that they are a postmortem growth.)

Front 18

ID

Back 18

RENAL ARTERIOSCLEROSIS:
The characteristic lesion here is hyaline thickening (deep eosinophilic material in intima or entire wall) of the afferent arteriole entering the glomeruli (arteriosclerosis). Be sure to look in the periphery for this too - recall that glomeruli are spherical, and the afferent arteriole may not have made it into the plane of section.

The hyaline thickening of the wall leads to narrowing or obliteration of the lumen.

Interstitial fibrosis is also seen.

Front 19

ID

Back 19

RENAL ARTERIOSCLEROSIS:
The characteristic lesion here is hyaline thickening (deep eosinophilic material in intima or entire wall) of the afferent arteriole entering the glomeruli (arteriosclerosis). Be sure to look in the periphery for this too - recall that glomeruli are spherical, and the afferent arteriole may not have made it into the plane of section.

The hyaline thickening of the wall leads to narrowing or obliteration of the lumen.

Some glomeruli are totally hyalinized due to ischemia following obliteration of their afferent arteriole. In some cases, eosinophilic material is found in Bowman's Space around the glomerular tuft.

Hyalinization of the neighboring small artery as well.

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ID

Back 20

RENAL ARTERIOSCLEROSIS:
Hyaline thickening of a small renal artery with surrounding interstitial fibrosis.

Front 21

ID

Back 21

RENAL ARTERIOSCLEROSIS:
MALIGNANT NEPHROSCLEROSIS:
The characteristic lesion here is hyaline thickening (deep eosinophilic material in intima or entire wall) of the afferent arteriole entering the glomeruli (arteriosclerosis). Be sure to look in the periphery for this too - recall that glomeruli are spherical, and the afferent arteriole may not have made it into the plane of section.

The hyaline thickening of the wall leads to narrowing or obliteration of the lumen.

Some glomeruli are totally hyalinized due to ischemia following obliteration of their afferent arteriole. In some cases, eosinophilic material is found in Bowman's Space around the glomerular tuft.

Front 22

ID

Back 22

RENAL ARTERIOSCLEROSIS:
he characteristic lesion here is hyaline thickening (deep eosinophilic material in intima or entire wall) of the afferent arteriole entering the glomeruli (arteriosclerosis). Be sure to look in the periphery for this too - recall that glomeruli are spherical, and the afferent arteriole may not have made it into the plane of section.

The hyaline thickening of the wall leads to narrowing or obliteration of the lumen.

Some glomeruli are totally hyalinized due to ischemia following obliteration of their afferent arteriole. In some cases, eosinophilic material is found in Bowman's Space around the glomerular tuft.

Hyalinization of the neighboring small artery as well with interstitial fibrosis surrounding.

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ID

Back 23

WEGENER'S GRANULOMATOUS:
Acute and chronic inflammatory cells are present.


Vasculitis of medium and small vessels is seen by both acute and chronic inflammatory infiltrate in vessel walls.
Note that there is NO fibrinoid necrosis, but chronic changes like intimal and medial fibrosis ARE present.

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ID

Back 24

WEGENER'S GRANULOMATOUS:
Don't know the tissue

"Classic" example where you can see: 1) giant cells, 2) vasculitis, 3) geographic necrosis.

Deep blue is due to inflammatory infiltrate within the CT stroma. Areas of granular, basophilic material represent necrosis (necrobiosis) with no viable cells and degeneration of collagen.

The "granulomas" seen are a misnomer. These are not classic granulomas like in TB, but rather collections of histiocytes and fibroblasts with some Giant Cells.

Vasculitis of medium and small vessels is seen by both acute and chronic inflammatory infiltrate in vessel walls.
Note that there is NO fibrinoid necrosis, but chronic changes like intimal and medial fibrosis ARE present.

Front 25

ID

Back 25

WEGENER'S GRANULOMATOUS:
"Classic" example where you can see: 1) giant cells, 2) vasculitis, 3) geographic necrosis.

Admittedly difficult to ID the origin of this tissue: from mucosa or bone.

Deep blue is due to inflammatory infiltrate within the CT stroma. Areas of granular, basophilic material represent necrosis (necrobiosis) with no viable cells and degeneration of collagen.

The "granulomas" seen are a misnomer. These are not classic granulomas like in TB, but rather collections of histiocytes and fibroblasts with some Giant Cells.

Vasculitis of medium and small vessels is seen by both acute and chronic inflammatory infiltrate in vessel walls.

Front 26

ID

Back 26

WEGENER'S GRANULOMATOUS:
"Classic" example where you can see: 1) giant cells, 2) vasculitis, 3) geographic necrosis.

Admittedly difficult to ID the origin of this tissue: from mucosa or bone.

Deep blue is due to inflammatory infiltrate within the CT stroma. Areas of granular, basophilic material represent necrosis (necrobiosis) with no viable cells and degeneration of collagen.

The "granulomas" seen are a misnomer. These are not classic granulomas like in TB, but rather collections of histiocytes and fibroblasts with some Giant Cells.

Vasculitis of medium and small vessels is seen by both acute and chronic inflammatory infiltrate in vessel walls.

Front 27

ID

Back 27

WEGENER'S GRANULOMATOUS:
"Classic" example where you can see: 1) giant cells, 2) vasculitis, 3) geographic necrosis.

Admittedly difficult to ID the origin of this tissue: from mucosa or bone.

Deep blue is due to inflammatory infiltrate within the CT stroma. Areas of granular, basophilic material represent necrosis (necrobiosis) with no viable cells and degeneration of collagen.

The "granulomas" seen are a misnomer. These are not classic granulomas like in TB, but rather collections of histiocytes and fibroblasts with some Giant Cells.

Vasculitis of medium and small vessels is seen by both acute and chronic inflammatory infiltrate in vessel walls.

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Back 28

RENAL ARTERIOSCLEROSIS:
The marked narrowing of the cortex is apparent with a thickened and hyalinized renal capsule. The capsule appears adherent to the cortex and stripping it away would tear away fragments of cortical tissue.

Just beneath the capsule are numerous dilated tubules containing eosinophilic (proteinatious) casts and some granular and cellular casts.

Some of the tubules just beneath the capule contain bacteria in colonies with NO inflammatory response suggesting that this was a postmortem growth.

Front 29

:

Back 29

RENAL ARTERIOSCLEROSIS:
The marked narrowing of the cortex is apparent with a thickened and hyalinized renal capsule. The capsule appears adherent to the cortex and stripping it away would tear away fragments of cortical tissue.

Just beneath the capsule are numerous dilated tubules containing eosinophilic (proteinatious) casts and some granular and cellular casts.

Some of the tubules just beneath the capule contain bacteria in colonies with NO inflammatory response suggesting that this was a postmortem growth.