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Oncology
The medical specialty dealing with neoplasia diseases
Neoplasm
New formation or growth
Tumor
A mass or swelling of tissue
Benign
"Do little harm"

Relatively slow growing, expansile, encapsulated, closely resembles tissue of origin, and does not metastasize.
Malignant
Faster growing, less encapsulated, less resemblance to tissue of origin, my metastisize.
Anaplastic
May only vaguely resemble tissue of origin. Sign of malignancy. "Poorly differentiated."
Metastatic
Spread of viable tumor cells from original site to distant site. May occur through implantation or vascular spread.
Cancer
Malignant tumor
Hyperplasia vs. Neoplasia
Hyperplasia is an increase in cell number to meet metabolic demand. It is still limited and regulated.

Neoplasia continues even when inciting stimulas is removed. Uncontrolled cell division.
-oma
Benign tumor of mesenchymal cells or nonglandular epithelium
-adenoma
Benign tumor of glandular epithelium.
-sarcoma
Malignant tumor of mesenchymal cells.
-carcinoma
Malignant tumor of nonglandular epithelium.
-adenocarcinoma
Malignant tumor of glandular epithelium.
Cancer Naming Exceptions
Lymphoma & Melanoma - names suggest benighn, but usually malignant.
Initiation
Stable change in target cell. Rapid "one hit" inherited change in cell. Does not cause tumor, but "sets the stage."
Promotion
Allows initiated cell population to proliferate. Continuous or repeated exposure.
Oncogene
"cancer gene" - misnomer - segment of genetic material in a eukaryotic cell that carries material that is homologous to a retroviral gene.
Proto-oncogene
Eukaryotic gene that has known retroviral homologue. Often these genes have role in regulation of cell growth.
Tumor Suppressor Gene
Genes that act against the development of a neoplastic disease. Ex: Gene p53
Procarcinogen
Substanfces that are metabolized into a carcinogen
Proximate carcinogen
Active substance that is a carcinogen. Often proximate carcinogens are hepatic metabolites of procarcinogens.
Initiator
Causes a rapid, stable, inherited change in a cell. "Sets the stage" for neoplasia.
Promoter
Allows initiated cell population to proliferate. Long term/repeated event.
Physical causes of neoplasia
Ex: Radiation and trauma

Direct injury to cell. Interaction between DNA & radiation. Free radicals are generated from the interaction of ionizing radiation and water within a cell.
Viral causes of neoplasia
DNA or RNA viruses can cause neoplasia.

DNA Viruses
Integrate into host cell''s genome to cause tumors. May be productive or transforming infection
RNA Viruses


Retroviruses - reverse transcription of viral RNA genome to form DNA copy. Viral DNA copy is inserted into host genome. Transformed cells may produce more virus. Ex: FeLV
Productive Infection
Not oncogenic. DNA virus produces more of itself.
Transforming Infection
Oncogenic. Host cell transformed into a tumor cell. DNA virus does not produce more of itself.
Chemical causes of neoplasia
Chemicals may be procarcinogens or proximate carcinogens. Initiation is followed by promotion.
Paraneoplastic Syndrome
When product of tumor does more harm than physical presence of tumor. Ex: Adrenal gland tumor.
Type I Hypersensitivity
Immediate hypersensitivity - Ex: Allergic reactions & anaphylaxis

Reaginic antibody on surface of mast cell or basophil interacts with an antigen and causes the cell to degranulate. Granules contain vasoactive amines that stimulate edema and vasodilation. Aracodonic Acid metabolites are produced.
Type II Hypersensitivity
Cytotoxic Hypersensitivity - Two mechanisms.

1. Antibody mediated cytotoxicity - antibodies against cell associated substances bind and activate complement. Cell is lysed by MAC. Ex: Immune mediated hemolytic anemia and Immune mediated thrombocytopenia.

2. Antibody mimicry of a ligand - An antibody binds to cell and changes the activity of the cell. Ex: Graves disease (hyperthyroid with low TSH levels because antibody stimulates thyroid hormone production by binding to TSH receptor.) Sometimes referred to as Type V Hypersensitivity.
Type III Hypersensitivity
Immune-Complex - Circulating antibodies bind to antigens forming immune complexes. Immune complexes get deposited into tissues which activates compliment. Chemotaxis of leukocytes. Leukocytes attempt phagocytosis, but can't, resulting in "frustrated phagocytosis" - lysosomal contents are released into tissues causing tissue damage and leading to inflammation and necrosis. Ex: Serum sickness & FIP
Type IV Hypersensitivity
Delayed Hypersensitivity - Cell mediated hypersensitivity. Primarily a lymphocytic response with minimal involvement of antibodies or complement. Cytotoxic lymphocytes recognize cells as foreign based on major histocompatibility complex. CD8 lymphocytes direct cytotoxicity. Ex: TB testing & Graft rejections.
Hypersensitivities and Inflammatory Reactions
Hypersensitivities tend to illicit an inflammatory reaction.
Type I - edema & vasodilation
Type II - chemotaxis
Type III - Illicits inflammation
Type IV - More of a chronic inflammatory reponse with lymphocytes, macrophages, etc.
Ito Cells
Hepatic stellate cells - Store vitamin A and fat. Also play a role in sinusoidal blood flow.
Kupffer Cells
Macrophages in liver
Circulation of bile acids
95% of bile acids are reabsorbed through the mucosa of the small intestine.

Small intestine -> portal vein -> liver -> hepatocytes -> resecreted into bile
Hepatic Lobule
Classical hepatic unit. Central vein in center. Surrounded by portal triads. Polygonal shape.
Hepatic Acinus
Portal triad in center, surround by central vein. Diamond shape. Has 3 zones of hepatocytes.
Zone 1 Hepatocytes
Periportal - closest zone to portal triad - exposed to blood with the highest O2 and nutrient concentrations. Most active zone.
Zone 2 Hepatocytes
Midzonal - Functionally intermediate between zones 1 & 3.
Zone 3 Hepatocytes
Periascinar or Centrilobular - Closest to central vein. Exposed to blood with lowest O2 and nutrient concentrations. Most susceptible to hypoxia. Fatty acid synthesis occurs here. Highest levels of mixed function oxydase enzymes including Cytochrome P450.
Biotransformation
The metabolism of drugs, toxins, and environmental chemicals to render them harmless and facilitate their excretion from the body.
Phase I Biotransformation
Breakdown by mixed function oxidase enzymes (Cytochrome P450) into substrate for Phase II.
Phase II Biotransformation
Conjugation of Phase I metabolites.
Biotransformation & Toxicity
Biotransformation may make some parent compounds more toxic by producing highly reactive intermediate forms. Ex: metabolism of carbon tetrachloride.
Products of Liver
Plasma proteins including albumin, globulins, clotting factors, and fibrinogen.

Hepatic disease may lead to ascites and coagulopathies if production is hindered.
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