Atrophy.

Cerebral atrophy in a patient with Alzheimer's. Gyri of the parietal and temporal lobes are narrowed and sulci are widened towards frontal pole.

Atrophy.

Right testes effected. Can occur as a result of hormonal issues, torsion, or cryptochidism (testes fails to descend).

Atrophy.

# of cells is the same as before but the size of some of the muscle fibers is reduced. Downsizing cells conserves them when injury occurs. 

In this case, innervation of the small fibers in the center was lost.

This is a trichrome stain.

Circles=myofibrils in the cross-section

Hypertrophy.

Cardiac hypertrophy in left ventricle. # of myocardial fibers does not increase, but size does. Increased workload -> thickening of left ventricle in patients with hypertension

Increased afterload ->new growth factors->cellular expansion.

Condition can cause shortness of breath, ischemia, and congestive heart failure.

Hyperplasia.

Benign prostatic hyperplasia (BPH).

Normal prostate=3 to 4cm in diameter and 20 grams, in BPH can reach 80 grams.

# of prostatic glands and stroma have increased.

Pattern is nodular, not uniform.

The increase is in response to hormonal manipulation, but NOT a normal physiologic process.

Overgrowth often occurs centrally->bladder infection and hypertrophy can occur because urethra is located centrally.

Hyperplasia.

Nodule of a hyperptastic prostate. Cells are normal, but there's too many of them.

Metaplasia.

Laryngeal respiratory epithelium in a smoker.

Chronic irritation->normal respiratory epithelium-pseudostratified columnar(right side of picture) turns to more resilient squamous epithelium(left side).

Metaplasia is NOT a normal physiologic process, may be the 1st step toward neoplasia.

Metaplasia-Barret's esophagus.

Acid reflux->normal squamous mucosa(right) turns to gastric type columnar muscoa(left), which secretes mucus to try and protect esophagial lining.

Can lead to cancers such as squamous cell carcinoma.

Coagulative Necrosis.

Dying myocardial cells-nuclei being lost, cytoplasm losing its structure(no well-defined cross-striations are seen).

Coagulative Necrosis.

Pale infarct can be seen in contrast with normal adrenal cortex.

The area just under the capsule is spared b/c of blood supply from capsular arterial branches.

This is an unusual place for an infarct.

Liquefactive Necrosis.

Cerebral infarction at the upper left. Removal of dead tissue will leave behind a cavity.

Liquefactive Necrosis.

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

Often a result of cerebrovascular injury (stroke).

Liquefactive Necrosis.

Two lung abscesses, one in the upper lobe and one in the lower lobe.

Complication of severe pneumonia, most typically virulent organisms like Staphylococcus Aureus.

Abscesses are often complications of aspiration, seen most frequently in the right posterior lung.

Consolidation by inflammatory cells occurs as a result of necrosis.

Localized liquefactive necrosis.

Liver has a small abscess filled with many neutrophils(to stop abscess from spreading)

Caseous Necrosis.

Gross appearance of caseous necrosis in a hilar lymph node(white circle in the center) in the lung infected w/ tuberculosis.

Node has a cheesy tan to white appearance.

Caseous necrosis=coagulative+liquefactive necrosis; most characteristic of granulomatous inflammation and often associated w/ TB.

Caseous Necrosis.

Extensive necrosis with confluent cheesy tan granulomas in upper portion of the lung. 

Patient has secondary TB.

Tissue destruction is so extensive that there are areas of cavitation(cystic spaces) formed as the necrotic(mainly liquefied) debris drains out via bronchi.

Caseous Necrosis.

Microscopically, it's characterized by acellular pink areas of necrosis(upper right) surrounded by a granulomatous inflammatory process(macrophages).

Gangrenous Necrosis.

Necrosis of many tissues of a body part, in this case the toes were involved in a frostbite injury. 

This is "dry" gangrene where there's mainly coagulative necrosis from the anoxic injury.

Gangrenous Necrosis.

"Wet" gangrene of the lower extremety. Called wet becaues liquefactive component from superimposed infection is present in addition to the coagulative necrosis from loss of blood supply.

Patient had diabetes mellitus.

Intracellular Accumulation.

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

Here is fatty metamorphosis of the liver where deranged lipoprotein transport from injury(alcoholism) leads to accumulation of lipid in cyoplasm of hepatocytes.

Intracellular accumulation.

Anthracotic pigment in macrophages in hilar lymph node. Caused by accumulation of carbon pigment from breathing dirty air(smoking, polution,etc).

Looks bad, but causes no major organ dysfunction.

Intracellular Accumulation.

Brown coarsely granular material in macrophages in alveolus is hemosiderin. Accumulated as a result of breakdown of RBC's and release of the iron in heme. 

Macrophages clear up the debris and it's eventually recycled.

Intracellular Accumulation.

Inthereted disorders of metabolism can lead to accumulation of storage products.

This is Gaucher's disease, a lysososmal storage disorder involving the spleen. The large pale cells contain an accumulated storage product in macrophages from lack of an enzyme.

Protein has pushed the nuclei to the periphery and caused a "tissue paper" look.

Intracellular accumulation.

Cytoplasmic organielle damage leads to injury patterns, most of which are best seen by electron microscopy. Acute injuries damage an entire ceell, so specific organelle damage doesn't really matter unless the damage accumulates over many years(like in this case). 

These are mallory bodies(red globular material)composed of cytoskeletal filaments(keratin) in liver cells chronically damaged from alcoholism.

These are a type of intermediate filament bt/w actin(thin) and myosin(thick).

Dystrophic Calcification.

Abnormal tissue with normal Ca levels.

This is in the wall of the stomach.

Left=artery w/ calcification in its wall. 

There are irregular bluish-purple deposits of calcium(normally white, but purple when stained w/ H&E) in the submucosa.

Calcium is more likely to be deposited in damaged tissue.