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There are some muscle fibers here that show atrophy. 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 of the small fibers in the center was lost. This is a trichrome stain.

The testis at the right has undergone atrophy and is much smaller than the normal testis at the left.

This is cerebral atrophy in a patient with Alzheimer disease. The gyri are narrowed and the intervening sulci widened, particularly pronounced toward the frontal lobe region

Here is the centrilobular portion of liver next to a central vein. The cells have reduced in size or been lost from hypoxia. The pale brown-yellow pigment is lipochrome that has accumulated as the atrophic and dying cells undergo autophagocytosis.

This is cardiac hypertrophy involving the left ventricle. The number of myocardial fibers does not increase, but their size can increase in response to an increased workload, leading to the marked thickening of the left ventricle in this patient with systemic hypertension. Any increase in tissue size is not necessarily neoplasia. Here is an example of left ventricular cardiac hypertrophy in which there has been an increase in the size of the myocardial fibers in response to an increased pressure load from hypertension. With hypertrophy, the cells increase in size, but the cells do not increase in number. Except for being larger, the cells are normal in appearance. Alterations in cell growth can be physiologic (normal responses to stimuli) or pathologic. These alterations of cell growth are potentially reversible and include: Hypertrophy: an increase in cell size. Increase in skeletal muscle fiber size is a physiologic response to exercise, but the cardiac hypertrophy shown above is a pathologic response to abnormally elevated blood pressure. Hyperplasia: an increase in the number of cells. Postpartum breast lobules undergo hyperplasia for lactation, but endometrial hyperplasia in a postmenopausal woman is abnormal.

The prominent folds of endometrium in this uterus opened to reveal the endometrial cavity are an example of hyperplasia. Cells forming both the endometrial glands and the stroma have increased in number. As a result, the size of the endometrium has increased. This increase is physiologic with a normal menstrual cycle. The large fronds of endometrium seen in this uterus opened to reveal the endometrial cavity are a result of hyperplasia. This resulted from increased estrogen. With hyperplasia, there is an increase in cell numbers to produce an increase in tissue size. However, the cells are normal in appearance. Sometimes hyperplasias can be "atypical" and the cells not completely normal. Such conditions can be premalignant.

Metaplasia of the normal esophageal squamous mucosa has occurred here, with the appearance of gastric type columnar mucosa.

This is dysplasia. The normal cervical squamous epithelium has become transformed to a more disorderly growth pattern, or dysplastic epithelium. This is farther down the road toward neoplasia, but dysplasia is still a potentially reversible process.

When there is marked cellular injury, there is cell death. This microscopic appearance of myocardium is a mess because so 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 not recognizable

Here is myocardium in which the cells are dying. The nuclei of the myocardial fibers are being lost. The cytoplasm is losing its structure, because no well-defined cross-striations are seen.

The liver shows a small abscess here filled with many neutrophils. This abscess is an example of localized liquefactive necrosis.

This is liquefactive necrosis in the brain in a patient who suffered a "stroke" with focal loss of blood supply to a portion of cerebrum. This type of infarction is marked by loss of neurons and neuroglial cells and the formation of a clear space at the center left.

At high magnification, liquefactive necrosis of the brain demonstrates many macrophages at the right which are cleaning up the necrotic cellular debris. The job description of a macrophage includes janitorial services such as this, particularly when there is lipid.

Grossly, the cerebral infarction at the upper left here demonstrates liquefactive necrosis. Eventually, the removal of the dead tissue leaves behind a cavity.

As this infarct in the brain is organizing and being resolved, the liquefactive necrosis leads to resolution with cystic spaces.

This is more extensive caseous necrosis, with confluent cheesy tan granulomas in the upper portion of this lung in a patient with tuberculosis. The tissue destruction is so extensive that there are areas of cavitation (cystic spaces) being formed as the necrotic (mainly liquefied) debris drains out via the bronchi.

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.

Acute inflammation is marked by an increase in inflammatory cells. Perhaps the simplest indicator of acute inflammation is an increase in the white blood cell count in the peripheal blood, here marked by an increase in segmented neutrophils (PMN's).

Seen here is vasodilation with exudation that has led to an outpouring of fluid with fibrin into the alveolar spaces, along with PMN's. The series of events in the process of inflammation are: 1. Vasodilation: leads to greater blood flow to the area of inflammation, resulting in redness and heat.2. Vascular permeability: endothelial cells become "leaky" from either direct endothelial cell injury or via chemical mediators.3. Exudation: fluid, proteins, red blood cells, and white blood cells escape from the intravascular space as a result of increased osmotic pressure extravascularly and increased hydrostatic pressure intravascularly4. Vascular stasis: slowing of the blood in the bloodstream with vasodilation and fluid exudation to allow chemical mediators and inflammatory cells to collect and respond to the stimulus.

As in the preceding diagram, here 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.

Here is an example of the fibrin mesh in fluid with PMN's that has formed in the area of acute inflammation. It is this fluid collection that produces the "tumor" or swelling aspect of acute inflammation.

Microscopically, the extensive neutrophilic exudate of an acute abscessing pneumonia is seen here. Normal tissues are destroyed in the region of the abscess.

One consequence of acute inflammation is ulceration. This occurs on epithelial surfaces. Here the gastric mucosa has been lost, or ulcerated. A larger ulcer and several adjacent smaller ones with surrounding erythema appear at the left of center.

Chronic inflammation is more difficult to understand, because it is so variable. Seen here is chronic endometritis with lymphocytes as well as plasma cells in the endometrial stroma. In general, the inflammatory infiltrate of chronic inflammation consists mainly of mononuclear cells ("round cells"): lymphocytes, plasma cells, and macrophages.

At high magnification, granulation tissue has capillaries, fibroblasts, and a variable amount of inflammatory cells (mostly mononuclear, but with the possibility of some PMN's still being present).

The focal nature of granulomatous inflammation is demonstrated in this microscopic section of lung in which there are scattered granulomas in the parenchyma. This is why the chest radiograph with tuberculosis or other granulomatous diseases is often described as "reticulonodular". A biopsy could miss such lesions from sampling error, too.

Here are two pulmonary granulomas. Granulomatous inflammation typically consists of mixtures of cells including epithelioid macrophages, giant cells, lymphocytes, plasma cells, and fibroblasts. There may even be some neutrophils.

Granulomatous inflammation occurs in response to some agents which persist for a long time and require a more orchestrated immune response to fight them. The granuloma seen here demonstrates the typical rounded and focal nature of this type of inflammation. A couple of spherules of C. immitis are present in the giant cell in the center.

Giant cells are a "committee" of epithelioid macrophages. Seen here are two Langhans type giant cells in which the nuclei are lined up around the periphery of the cell. Additional pink epithelioid macrophages compose most of the rest of the granuloma.

These are epithelioid cells around the center of a granuloma. They get their name from the fact that they have lots of pink cytoplasm similar to squamous epithelial cells. Their nuclei tend to be long and stringy.

This is a caseating granuloma. Epithelioid cells surround a central area of necrosis that appears irregular, amorphous, and pink. Grossly, areas of caseation appear cheese-like.

Granulomas caused by tuberculosis and by pathogenic fungi such as Histoplasma capsulatum or Cryptococcus neoformans are often caseating. Here, the area of caseation is seen at the upper right.

This young woman has a malar rash (the so-called "butterfly" rash because of the shape across the cheeks). Such a rash suggests lupus. Discoid lupus erythematosus (DLE) involves mainly just the skin and is, therefore, relatively benign compared to systemic lupus erythematosus (SLE). In either case, sunlight exposure accentuates this erythematous rash ("photosensitivity"). A small number (5 to 10%) of DLE patients go on to develop SLE (usually the DLE patients with a positive ANA).

Histologically, the skin of a patient with SLE may demonstrate a vasculitis and dermal chronic inflammatory infiltrates, as seen here. Vasculitis with autoimmune disease (often related to deposition of antigen-antibody complexes) can occur in many different organs and can lead to the often confusing signs and symptoms of patients with rheumatic diseases.

Here is a more severe inflammatory skin infiltrate in the upper dermis of a patient with SLE in which the basal layer of epidermis is undergoing vacuolization and dissolution, and there is purpura with RBCs extravasated into the upper dermis (which are the reasons for the rash).

If immunofluorescence microscopy using an antibody to complement or immunoglobulin is performed, then one can see the brightly fluorescing band along the dermal epidermal junction that indicates immune complex deposits are present. A variety of immunoglobulins can be present, usually IgG, and the immune complexes trigger the "classic" complement cascade so that components such as C3 are present.

This biopsy of the lower esophagus in a patient with chronic gastroesophageal reflux disease (GERD) shows columnar metaplasia (Barrett's esophagus), and the goblet cells are typical of an intestinal type of epithelium. Squamous epithelium typical of the normal esophagus appears at the right.

This is a neoplasm. Neoplasia is uncontrolled new growth. Neoplastic cells are no longer under complete physiologic control. Note the mass of abnormal tissue on the surface of this cervix. The term "tumor" is often used synonymously with neoplasm, but a "tumor" can mean any mass effect, whether it is inflammatory, hemodynamic, or neoplastic in origin. Once a neoplasm has started, it is not reversible.

The schwannoma is seen microscopically to be composed of spindle cells (like most neoplasms of mesenchymal origin), but the cells are fairly uniform and there is plenty of pink cytoplasm.

The concept of differentiation is demonstrated by this small adenomatous polyp (tubular adenoma) of the colon. Note the difference in staining quality between the epithelial cells of the adenoma at the top and the normal glandular epithelium of the colonic mucosa below.

Here is a ventral abdominal wall defect. This defect involves the region of the umbilical cord, so this is an omphalocele. Note that there is a thin membrane covering the herniated abdominal contents (loops of bowel can be seen under the membrane). This defect would have to be repaired over a period of time. Since the bowel has mainly developed outside of the abdominal cavity, it is malrotated and the cavity is not properly formed (too small).

Examination of a stillborn fetus or neonate should consist of a careful and detailed physical examination. You must note the presence of any anomalies, as well as detail size and gestational age. The anomaly seen in this photograph, a large bilateral cleft lip, is not so subtle, but some anomalies are. Call a clinical geneticist for consultation. The presence of one anomaly suggests that additional anomalies may be present, including internal anomalies such as congenital cardiac defects that may be life-threatening.

The yellow staining in the brain of a neonate is known as kernicterus. There is a coronal section of medulla on the left and cerebral hemisphere on the right demonstrating kernicterus in deep grey matter of hemisphere and brain stem. Increased unconjugated bilirubin, which accounts for the kernicterus, is toxic to the brain tissue. Kernicterus is more likely to occur with prematurity, low birth weight, and increased bilirubin levels.

A complication of prematurity and low birth weight is neonatal necrotizing enterocolitis (NEC) in which ischemia results in focal to confluent areas of bowel necrosis, most often in the terminal ileum. Seen at autopsy here is a dark red appearance to the small intestine of a premature neonate

The clinical manifestations of neonatal necrotizing enterocolitis (NEC) in premature neonates include abdominal distension, ileus, and bloody stool at several days of age. Compared to normal bowel at the left, bowel involved by NEC at the right shows hemorrhagic necrosis, beginning in the mucosa and extending to involve the muscular wall, with the potential for perforation.

This is hyaline membrane disease due to prematurity and lack of surfactant production from type II pneumonocytes within the immature lung. Note the thick pink membranes lining the alveolar spaces.

This is anencephaly. This condition occurs when there is failure of formation of the fetal cranial vault. The brain cannot form properly when exposed to amniotic fluid. Note that this fetus died in utero--there are signs of maceration, with skin slippage and reddening.

This lobulated tan-white mass involving the kidney of a child is a Wilms tumor. It manifests most often as an abdominal mass. Over 90% of Wilms tumors are diagnosed during the first 6 years of life. About a fourth of cases are associated with hypertension.

\Wilms tumor microscopically resembles the primitive nephrogenic zone of the fetal kidney, with primitive glomeruloid structures and a cellular stroma. Wilms tumor is associated with mutations involving the WT1 tumor suppressor gene on chromosome 11. This neoplasm is very treatable with an excellent prognosis and >80% cure rate overall.

In this case, the diaphragmatic dome is missing on the left, allowing herniation of the abdominal contents into the chest cavity. The metal probe in the photograph is behind the left lung, which has been displaced by the stomach. Below the stomach is a dark spleen (at the white arrow). The white arrow overlies the left lobe of liver which is extending upward.

Agenesis refers to the absence of formation of a body part in embryogenesis. Here the kidneys are absent from the retroperitoneum, and this renal agenesis will result in oligohydramnios, because amniotic fluid is mainly derived from fetal urine. The oligohydramnios leads to deformations such as a constricted chest, diminished lung development, and pulmonary hypoplasia.

Patricia Ann O. DetabaliPathology Practical Exam 1st shift