Pathology slides

By the Name of Allah,

The Most Gracious, The Most Merciful

1- cell injury

Many cells have died that

the tissue is not

recognizable. Many nuclei

have become pyknotic

(shrunken and dark) and

have then undergone

karorrhexis

(fragmentation) and

karyolysis (dissolution).

The cytoplasm and cell

borders are no longer

recognizable. In this case,

loss of the blood supply

from a major coronary

artery led to ischemia and

cell death.

Necrosis

In these images you can see this preservation of architecture: this is quite recognizably liver,

despite the absence of nuclei in the hepatocytes in the affected area. Notice the thread-like

bacteria present in the sinusoids: these are the organism causing the lesion! Darker staining

viable hepatocytes are visible around the portal regions (right) and pale, necrotic hepatocytes are

visible in the central lobular zones. Hepatocytes near the blood supply have more physiologic

reserve and will be more able to fend off the infection than those in the oxygen and nutrient-poor

central region: but in this case the "advantage" is moot.

Caseous necrosis and granulomatosis

A typical gross pathology finding in a case like this would look similar to those you see here. At left is an example of liquefactive necrosis in the brain, as seen at autopsy in a coronal section. The area of the cerebral infarct is grossly visible at the upper left, and can be highlighted by scrolling the cursor over the image. Notice also the formation of a "clear" area (arrow) visible in the gross specimen. Liquefactive necrosis of brain tissue in the infarcted area has occurred. At right you see the clear area at low magnification in an H&E slide. The region marked by the line is that which has been destroyed by cell death. The rest of the field is normal brain tissue.

Figure 7.11 Fat necrosis, ordinary type. Multinucleated histiocytic giant cells surround a

large lipid vacuole formed by fusion of destroyed adipocytes. Scattered lymphocytes and

monocytes occupy expanded spaces between cells at top.

Intracellular accumulations of a variety of materials can occur in response to cellular

injury. Here is fatty metamorphosis (fatty change) of the liver in which deranged

lipoprotein transport from injury (most often alcoholism) leads to accumulation of lipid in

the cytoplasm of hepatocytes.

• 26. Lungs: anthracotic pigment in a patient with "black lung" disease

• Note the heavy deposition of black pigment in this lung (see arrow) from a patient with coal worker s pneumoconiosis (dust-related pulmonary disease). The large spaces in the apex of this lung represent emphysema secondary to damage associated to the respiratory bronchioles from the excess anthracotic pigment. "Black lung" disease is a crippling disease and is associated with an increased incidence of TB.

Liver hemochromatosis

A Prussian blue reaction is seen in this iron stain of the liver to demonstrate large

amounts of hemosiderin that are present within the cytoplasm of the hepatocytes and

Kupffer cells. Ordinarily, only a small amount of hemosiderin would be present in the

fixed macrophage-like cells in liver, the Kupffer cells, as part of iron recycling.

Some of these skeletal muscle fibers here show atrophy, compared to normal fibers. The

number of cells is the same as before the atrophy occurred, but the size of some fibers

is reduced. This is a response to injury by "downsizing" to conserve the cell. In this case,

innervation to the small, atrophic fibers was lost. (This is a trichrome stain.)

Picture 2 : Dry gangrene on hand

2- Inflammation

Inflammatory cells.neutrophils , macrophages

,lymphocytes

The neutrophils are seen infiltrating the mucosa and

submucosa of the gallbladder in this patient with acute cholecystitis.

numerous neutrophils fill the alveoli in this case of

acute bronchopneumonia

there is marked laryngeal edema such that the airway is narrowed. This is life-

threatening. Thus, fluid collections can be serious depending upon their location.

Erythema (redness)

The arm at the botton is swollen(edematous) &

reddened(erythematous)

fibrin mesh in fluid with PMN's that has formed in the

area of acute inflammation.

PMN's that are marginated along the dilated venule wall (arrow)

are squeezing through the basement membrane (the process of

diapedesis) and spilling out into extravascular space.

Pleural effusion (serous)

Pleural

effusion(serosanguinous)

purulent exudate in pericardium

Friction blister

Serous acute inflammation

Fibrinous pericarditis

the pericardial cavity has been opened to reveal a fibrinous

pericarditis with strands of stringy pale fibrin between visceral

and parietal pericardium.

Microscopically, the fibrinous exudate is seen to

consist of pink strands of fibrin jutting from the

pericardial surface(arrows). Below this, there are a few

scattered inflammatory cells.

the yellowish fluid in this opened pericardial cavity is a

purulent exudate.

A purulent exudate is seen beneath the meninges in the brain of

this patient with acute meningitis from Streptococcus

pneumoniae infection. The exudate obscures the sulci.

extensive purulent peritonitis that resulted from rupture

of the colon. A thick yellow exudate coats the

peritoneal surfaces.

The white arrows mark areas of abscess formation in the upper

lobe of this lung. The liquefactive necrosis of an abscess is

apparent, because the purulent contents are draining out to

leave a cavity.

focal abscess in the lung. The

alveoli in that area have been

destroyed.

abscesses

One consequence of acute inflammation is ulceration.

This occurs on epithelial surfaces. Here the gastric

mucosa has been lost, or ulcerated.

Below the vocal cords in this larynx are large ulcerations. Such

subglottic ulcers are produced with prolonged endotracheal

intubation in which the cuff of the endotracheal tube fits too tight

Esophageal acute ulcer

he end result of inflammation can be scarring.

Here, the alveolar walls are thickened and filled

with pink collagen.

3- Repair

Granulation tissue

keloid

4- Neoplasia

Colonic polyps

Colonic polyps

(adenoma)

Pleomorphic adenoma

Pleomorphic adenoma (high magnification)

Fibroadenoma

Fibroadenoma

Mature teratoma

Lipoma

Lipoma

Mature adipose tissue

(lipoma)

Leiomyoma

Leiomyoma

smooth muscle bundles

Well differentiated squamous

cell carcinoma (keratin

formation-arrow)

Normal colonic mucosa vs

adenoma

Moderately differentiated

adenocarcinoma

Moderately differentiated

Liposarcoma

Anaplasia

Anaplasia

Anaplastic tumor with abnormal

mitosis

Abnormal mitotic figures highly

suggestive of malignancy

A, Carcinoma in situ. Low-power view shows the entire thickness of the epithelium is

replaced by atypical dysplastic cells. There is no orderly differentiation of squamous cells.

The basement membrane is intact, and there is no tumor in the subepithelial stroma. B,

High-power view of another region shows failure of normal differentiation, marked nuclear

and cellular pleomorphism, and numerous mitotic figures extending toward the surface.

Well encapsulated

schwannoma

Hepatic

adenoma(encapsulated)

Liver adenoma(encapsulated) low magnification

Liver adenoma(encapsulated) higher magnification

Fibroadenoma of breast encapsulated small tumor is sharply demarcated from the whiter breast

tissue.

Uterine leiomyoma

well-defined but not

encapsulated

Liver Hemangioma

Hemangioma of skin

Infiltrating breast carcinoma