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A substance that has its own color.
Origin is within the patient. Ex: Melanin, bile pigments, hemosiderin, and lipofuscin are endogenous pigments.
Origin is outside the patient. Ex: Tattoos, Pneumoconiosis, and parasite derived pigments are exogenous pigments.
Appearance of melanin in an unexpected but otherwise normal tissue. Ex: Black spot on dog's tongue.
Normal post-mortem change that occurs when iron in blood stream mixes with hydrogen sulfide produced by bacteria. Typically occurs in abdomen.


Lack of melanin. Can be tyrosinase positive or tyrosinase negative.

Oxidative damage to lipids causes pigment deposit. "Aging pigment."
Brown pigment due to excess iron storage. When heme is broken down, Fe is released, but cannot be free in the body, so is stored in Ferritin. Over time, Ferritin molecules stick together and precipitate out, forming Hemosiderin.
Formation of Bile Pigments
Bile pigments are formed through the breakdown of hemoglobin. RBCs are phagocytosed and broken into heme and globin. Heme ring is opened, which releases Fe. Bilirubin (the remaining portion of the heme ring) binds to albumin in plasma and is taken to the liver where it is conjugated and excreted into the bile duct and GI tract. (Bilirubin = bile pigment)
Yellow discoloration of tissues due to excess systemic circulating bile pigments. Occurs because of excessive RBC destruction, impaired bile excretion, or a combination.
Gold brown pigmentation of tissues due to iron containing substances.
Particulate matter (pigment) in the lungs.
A type of pneumoconiosis due to carbon.
Two fundamental pathways to lethal cellular injury
1. Interference with cellular energy metabolism. (Ex: hypoxia, disruption of electron transport chain, lack of energy source.)
2. Damage to cell membrane (Ex: enzymatic disruption, physical trauma, membrane damage due to free radicals.)

3 substances that tend to become vaculated in lethally injured cells and why.

1. Water - due to lack of ATP to expell sodium from cell.
2. Glycogen - due to carbohydrate metabolism disorder.
3. Lipid - due to triglyceride build up in cytoplasm (Ex: hepatic lipidosis.)

How to identify vacuolated substance in lethally injured cells
1. Water - No distinguising features. Neither water or lipid will stain using standard processing techniques.
2. Lipid - need frozen section. Lipid in unprocessed sample will stain with Oil Red O stain.
3. Glycogen - persists in routinely processed tissue and stains with Periodic Acid Schiff's Reagent (PAS stain).
Major cellular mechanisms for generating free radicals
Intermediate products in electron transport chain, lysis of water (due to contact with metals such as Cu & Fe), cellular oxidase systems (Cytochrome P450, Xanthine oxidase, NADPH oxidase)
Means of preventing free radical mediated injury
Antioxidants (Vit E & sulfhydryl compounds allow same reaction to occur without damaging proteins). The enzyme Glutathion peroxidase makes reaction energetically favorable. Superoxide dismutase catalyzes conversion to hydrogen peroxide which can be handled by the cell.
How are cells damaged by free radicals?
- Protein strand cleavage (a membrane protein, which is expenisive to replace, isĀ  broken off)
- Disulfide linkage forms between proteins in membrane. This covalent bond prevents the proteins from moving independently.
- Lipid-lipid cross linkage in the membrane - makes the membrane more rigid.
- Fatty acid oxidation
Pathologic mechanisms for accumulation of excess lipid in cells
Generally happens in liver (Hepatic Lipidosis). Happens b/c too much Fatty Acid in, not enough Lipoprotein out. Happens when obese animal stops eating & a lot of fat is liberated for energy. Liver can't keep up. Could also happen if lipoprotein export was disrupted.
Non-physiologic cell death within a living tissue
Histologic changes in lethal cell injury
Cellular swelling & vacuolation, hyalinization of cytoplsm, pyknosis, karyorrhexis, karyolysis.
Increased eosinophilia and loss of granulation in tissue. Histologically, tissue looks uniform, glassy, and pink.
Nucleas shrinks and becomes very dark due to highly condensed chromatin.
Nucleas fragments.
Nucleas dissolves. May not see a nucleas at all, or may see a punched out area where nucleas used to be.
Coagulative Necrosis
Tissue is histologically recognizable. Grossly, tissue looks like cooked meat.
Liquefactive Necrosis
Tissue architecture is liquified. (Ex: abcess). Tissue structure is NOT recognizable.
Caseous Necrosis
Grossly looks like cottage cheese. Histologically looks like liquefactive necrosis.
Enzymatic Fat Necrosis
Destruction of adipose tissue by lipolytic enzymes. (Ex: pancreatitis).
Dystrophic Mineralization
Deposition of calcium salts in injured tissues. Systemic levels of calcium are normal. Ex: Tuberculosis lesions & white muscle disease.
Metastatic Mineralization
Deposition of calcium salts due to a disturbance in systemic levels. Ex: Primary hyperparathyroidism (PTH promotes hypercalcemia), Vitamin D intoxication, some cancers (like osteosarcoma).
Ossification vs. Mineralization
Ossification is formation of bone tissue while mineralization is deposition of calcium salts and is NOT a tissue.
Material that accumulates in tissues and has same reaction with iodine as starches. Primarily a protein deposit & has a hyaline appearance. Amyloid will stain a peach color with Congo Red Stain and when subjected to polarized light will has birefringence.
Primary Amyloidosis
AKA "Immunocytic." Disorder of antibody synthesis. Excess light chains build up and form fibrin.
Secondary Amyloidosis
AKA "Reactive." Associated with severe prolonged inflammation. Macrophages secrete Interleukin-1 during inflammation. Liver responds by producing Serum Amyloid A Protein, which builds up.
Pancreatic Islet Amyloid
May see amyloid build up in pancreatic islets in cats. Loosely linked to diabetes melatus. At first, substance was thought to be insulin, but it wasn't. So, the protein was named "Islet Associated Amyloid Polypeptide."
Paraneoplastic Syndrome
When products of a tumor do more damage than the physical presence of a tumor.
Tissue Mineralization Due to Paraneoplastic Syndrome
If a tumor produces a substance that promotes hypercalcemia, metastatic mineralization may result. Ex: primary hyperparathyroidism
Amyloidosis Due to Paraneoplastic Syndrome
If a tumor produces excess proteins, could accumulate as amyloidosis.
Neutrophil, Basophil, Eosinophil
"polymorphonuclear leukocyte" - Phagocytic, highly mobile (ameboid movement), intracellular microbicidal systems, relatively short life span in circulation, very large marginated pool of neutrophils in blood vessels, primarily along the walls of large veins.
Association with allergic response, important in parasitic infections, similar to neutrophil, but lacks lysozyme, has histaminase and other products that moderate allergic responses.
Uncommon in circulation, granules contain histamine and other vasoactive substances, has membrane receptor for IgE. Binding of antigen to surface IgE leads to degranulation.
Large cell with multiple lysosomes. Precursor to macrophage which is important in chronic inflammation.
B Lymphocyte - precursors to plasma cells which produce antibodies.

T Lymphocyte - can be regulatory or cytotoxic.
Commonly associated with blood clotting. Also plays a key role in inflammatory response. Secrete vasoactive substances when stimulated.
Plasma cells
In tissue. Derived from B lymphocytes. Produces antibodies.
In tissue. Derived from monocytes. Phagocytic. Secrete cytokines.
Epithelioid cell
Specialized secretory form of macrophage that produces and secretes cytokines and mediators of inflammation.
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