Pathology - Term1

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hypertrophy

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increase in size of cells (and organ)

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hyperplasia

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increase in # of cells

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metaplasia

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one adult cell type is replaced by another (potentially reversible)

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dysplasia

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failure of differentiation or maturation of cells

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anoxia

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inadequate oxygen in the presence of adequate blood flow

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ischaemia

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decrease in arterial flow and pressure

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infarction

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tissue necrosis as a result of reduced blood supply and anoxia

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infarct

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dead tissue

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pyknosis

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dead cells with shrunken and condensed basophilic chromatin

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karyorrhexis

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hydrolytic enzymes cause rupture of the nuclear membrane into fragments

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karyolysis

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eventually, with further hydrolysis, the chromatin basophilia fades and dissolves

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caseous necrosis

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dead tissue has a firm, dry, cheesy consistency (commonly associated with TB)

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gangrene

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necrotic tissue becomes the seat of putrefication (evil smelling gasses)

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fat necrosis

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cell death in fatty tissue (esp. following damage to pancreas - released lipases split lipid and diffuse out)

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3 stages of acute inflammatory process

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1. vasodilation and increased blood flow to damaged area
2. increased vascular permeability with leakage of plasma from microcirculation
3. migration of phagocytic leucocytes from microcirculation

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prostaglandins

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vasoactive mediators

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chemotaxis

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attraction of leucocytes to site of injury (eg. material in cell wall of pyogenic bacteria and parts of activated complement system are chemotactic for polymorphonuclear leucocytes)

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protective effects of exudate

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1. fibrinogen in plasma - conversion to fibrin to help localize and wall off injury
2. complement may be present
3. dilution of toxin
4. antibody if immune
5. antibiotics linked to plasma proteins

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main cell types in inflammatory exudate

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1. Polymorphonuclear phagocytes - predominate in earliest stages (numerous in circulation and motile)
2. Monocytes - emigrate from circulation and differentiate into mononuclear macrophages
3. Lymphocytes - may be sensitized T-lyphocytes which, on contact with antigen, release soluble lyphokines (maintain, attract, and increase activity of macrophages)

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types of exudate

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1. Serous (thin fluid) - serosal surfaces eg. peritoneum, pleura, and pericardium
2. Fibrinous - severe inflammation with marked endothelial damage
3. Catarrhal (mucus) - respiratory and GIT
4. Purulent (masses of living and dead polymorphonuclear leucocytes) - caused by pyogenic, pus stimulating bacteria
5. Diptheresis (pseudomembranous inflammation) - mixture of coagulated fibrin, necrotic epithelium and inflammatory cells; form membrane on epithelial surfaces

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abcess (basic)

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localized collection of pus produced by deep seeding pyogenic bacteria into tissue (eg. non-sterile needle)

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abcess (formation)

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a central granular acidophilic amorphous mass of debris surrounded by zone of polymorphonuclear leucocytes in an area of liquefactive necrosis;

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ulcer

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lesion of an epithelial surface in which the epithelium is destroyed, exposing the underlying tissues, and in most cases is associated with an inflammatory reaction

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cellulitis

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spreading diffuse inflammatory change in solid tissues that is sometimes purulent; not well confined (unlike abcess) and tends to spread into tissue spaces or along spaces between muscle or in subcutaneous tissues

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persistent acute inflammation

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continuation of an acute inflammatory reaction; attempts to resolve and heal lesion (eg. splinter) will occur with the formation of connective tissue (collagen) while other areas are subjected to further damage and acute inflammatory change

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persistent acute inflammation (reactions)

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1. acute inflammatory process with congestion, exudation, and polymorphonuclear leucocyte and monocyte emigration
2. healing process with fibroblasts - collagen deposition and BV proliferation
3. immunce response with lymphocytes and plasma cells

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chronic cellular inflammation

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due to bacteria of relatively low virulence but with fairly high resistance to phagocytosis and digestion; proliferative (eg. Johne's disease); eventually immune response with large number of activated macrophages

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granuloma

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central core of necrtoic debris and neutrophils surrounded by lymphocytes, plasma cells, and fibroblast - all surrounded by CT capsule

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chronic granulomatous inflammation

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nodular (or tumor-like) with central area surrounded by macrophages and giant cells, accompanied by lymphocytes, within a connective tissue capsule

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giant cell

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fusion of mature macrophages; with nuclei scatter throughout cytoplasm called 'foreign body-type'; further internal reorganization leads to nuclei in circular or horseshoe array called 'Langhan's type'

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granulomata arise as a result of what factors?

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1. phagocyte activity by mononuclear cells, reflected by presence epitheliod macrophages and multinucleated giant cells
2. presence of lymphocytes around lesion; cell mediated immunity important in granuloma develpment
3. connective tissue/collagen deposition resulting from tissue damage and attempted healing

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2 type of granuloma

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1. low turnover - long lived cells and produced by inert substances or foreign bodies; macrophages contain much phagocytosed irritant
2. high turnover - cells with short life span and only small portion contain irritant; lesion maintained by proliferation of cells and by immigration of new macrophages; produced by relatively toxic substances

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tuberculosis

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granuloma with a central area of caseous necrosis surrounded by a zone of macrophages (epitheloid cells) and giant cells, contained in a connective tissue capsule with lymphocytes

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benign tumor (mesenchymal)

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-oma; do not have ability to infiltrate surrounding normal cells and remains localized; very similar histological features to the tissue of origin (eg. fibroma, lipoma, osteoma, lymphoma, mastocytoma)

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adenoma

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benign epithelial neoplasm which is derived from glandular tissue

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papilloma

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benign tumer arising in protective epithelia (eg. squamous or transitional), usually projecting from the surface

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malignant tumor (mesenchymal)

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sarcoma (eg. fibrosarcoma, lymphosarcoma, liposarcoma, osteosarcoma, chondrosarcoma)

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malignant tumor (epithelial)

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carcinoma (eg. squamous carcinoma, basal cell carcinoma, adenocarcinoma of mammary gland)

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teratoma

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tumor containing a range of cell types (most tumors contain a single cell type) arising from totipotential cells (eg. in gonads)

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shock

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blood volume too small to fill vascular system; accompanying pathology due to inadequate perfusion of tissues that directly causes hypoxia

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types of shock

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1. cardiogenic - failure of heart pumping mechanism
2. hypovolaemic - deficiency in volume
3. vasculogenic - alterations in blood vessel resistance or size

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shock symptoms

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symptoms include lethargy, unresponsiveness, collapse, subnormal body temp, pallor of mucus membranes, rapid/weak pulse, urine not produced, loss of blood pressure

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angiogenesis (growth factors)

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VEGF (vascular endothelial factor) and FGFs (fibroblast growth factors)

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anaplasia

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lack of cell differentiation; may be characteristic of malignant neoplasia

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pleomorphism

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cells and nuclei have a great variation in shape and size; typical of malignancy

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loss of polarity

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hallmark of malignancy in which there is a disturbance in the relatinoship of the cells to each other so that they do not orient themselves properly

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space occupying lesion

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benign lesion that does damage because of pressure resulting from growth in a confined space (eg. skull)

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metastasis

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ability of malignant tumors to spread and grow in distant organs; spread in lymphatic (carcinoma) or blood stream (sarcoma) and arrive at distant organs (eg. lungs) where they may settle down, multiply and form secondary tumor deposits

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haemangiosarcoma

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malignant tumor of the vascular endothelium of the spleen; grows as a large mass in the spleen, penetrates the capsule and spreads widely over the mesentery and omentum so that it lies on the surface of other organs

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fibroma

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benign tumor of fibroblasts; may arise in great number of sites; clearly demarcated from adjacent structures so skin can be moved freely over the tumor (non-infiltrating)

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basal cell carcinoma

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skin tumor derived from basal cells of epidermis; malignancy is limited - can infiltrate locally but almost never metastasises

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coagulative necrosis

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infarcts, caseous, fat necrosis, gangrene

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liquefactive necrosis

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malacia, pus

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amyloidosis

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extracellular deposition of abnormal protein arranged in sheet structure to form fibrils

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neutrophils

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produced in bone marrow; rapid increase in acute inflammation; short life span; motile; phagocytic; granules contain proteases

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serous exudate

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early phase of most inflammatory lesions; fluid and albumin; eg. rhinitis or blisters

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fibrinous exudate

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severe injury to endothelium: leakage of fibrinogen; yellow, stringy, shaggy; forms framework to prevent spread of bacteria

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catarrhal exudate

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inflammation on a mucosa surface (respiratory and intestinal); exudate plus mucus; mucus contains antimicrobial substances

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purulent exudate

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massive neutrophil infiltration; thick grey, green, or yellow fluid; bacteria prime cause

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abcess

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defense to prevent the uncontrolled multiplication of bacteria - prevents septicaemia

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abcess (formation)

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1. neutrophils are first line of defense; engulf bacteria and release enzymes to destroy bacteria and tissues
2. forms center of pus; at edge there are scavenging cells (macrophages), plasma cells, and lymphocytes; all surrounded by a capsule

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pus

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mixture of debris, degenerative neutrophils, and bacteria

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bacteriaemia

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presence of of bacteria in blood

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toxaemia

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presence of toxins in blood

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viraemia

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presence of viruses in blood

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septicaemia

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bacteraemia or viraemia complicated by toxaemia, fever, severe illness, and often shock

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eosinophils

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less effective than neutrophils at phagocytosis; 2 tear drop nuclei with acidophilic granules; allergic rxns and parasitic infections; short life

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platelet activating factor (PAF)

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synthesized by damage endothelium

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nitric acid

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increases vascular permeability

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inflammatory mediators (vasodilation)

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histamine, prostaglandins, nitric oxide, bradykinins

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inflammatory mediators (fever)

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cytokines, prostaglandins

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mast cells and basophils

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abundant in CT (esp. skin, intestinal, and respiratory surfaces); basophilic granules contain histamin and heparin; degranulation can be induced by IgE and complement; allergic rxns

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bradykinin

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increases vascular permeability; causes pain; activated by Hageman factory (factor XII)

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cytokines

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interferon
interleukin
tumor necrosis factor
macrophage activation factor

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cytokines (function)

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stimulate neutrophils
recruit macrophages
anti-viral effects
stimulate B and T cells

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fibroblast

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produces collages (nb: fibrinogen and fibrin are a different system)

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organization, repair, and scarring

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macrophages; capillary buds grow; macrophages secrete fibrogenic and angiogenic factors; fibroblasts proliferate (collagen - thickening scar)

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granulomatous inflammation

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macrophages dominate

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chronic inflammation

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tissue damage, acute inflammation, granulation tissue, fibrosis, and immune response all take place together; macrophages, lymphocytes, and plasma cells

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macrophages

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dominant cell of chronic infllammation; derived from monocytes; voluminous cytoplasm (epitheliod); free and fixed; present antigen

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ganulomatous disorder

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tuberculosis
actinobacillosis - wooden tongue
actinomycosis - lumpy jaw
caseous lymphadenitis (sheep)

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healing and repair

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by parenchymal regeneration
by tissue replacement
restore integrity of epithelial surface
restore tensile strength of sub-epithelial tissues

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primary intention

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create wound (surgery); cleanly incised, edgees in close apposition; easily suterable

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secondary intention

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accidental wound; extensive epithelial loss such that edges don't eaily pull together; large defect filled with granulation tissue (epithelium grows over)

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granulation tissue

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perfused, fibrous connective tissue that replaces a fibrin clot; typically grows from the base of a wound and is able to fill wounds of almost any size

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healing of the sutured skin wound

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24 hrs - neutrophils at edge; fibrin center; 3 days - macrophages and granulation tissue; 7 days - BVs and fibroblasts fill wound with epithelial layer (10% strength - sutures removed); 30 days - 50%; 3 mo - 80%

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hyperaemia

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increase in blood to tissue (read appearance)
1. active - increased flow
2. passive (congestion) - decreased outflow

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haemorrhage

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-petichia (1-2mm) - minute
-purpura (2-10mm) - intermed
-ecchymoses (10mm+) - large/blotchy

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haematoma

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collection of blood in tissue spaces from trauma or vessel disease

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types of bleeding

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1. haematoma - tissue spaces (trauma)
2. haemopericardium (aorta or heart rupture)
3. haemothorax (pleura cavity)
4. haemoperitoneum (spleen or liver)
5. haemarthrosis (joint spaces)

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thrombus

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clotted mass of blood forming in the circulation composed of platelets, fibrin, and entrapped RBCs; uneven structure; laminated (stuck to wall of vessel)

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von Willebrand factor

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exposed in endothelial damage; mediates adhesion of platelets; important in coagulation cascade (soluble fibrinogen to insoluble fibrin)

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clot

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even consistency (unlike thrombus); "chicken fat" or "current jelly"

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embolism

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sudden obstruction of blood vessel; fragments of thrombi, neoplastic cells, fat globules, air bubbles, brain tissue, parasites

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anasarca

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massive generalized oedema

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ascites

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oedema of abdominal cavity (hydroperitoneum)

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causes of oedema

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1. inflammatory - increased endothelia permeability
2. non-inflammatory - increased hydrostatic pressure (rt heart failure)
3. reduced oncotic pressure (liver of kidney failure)
4. failure of lymph clearance (eg. neoplasia)

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inclusion bodies

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evidence of viruses; protein degeneration resulting in focal accumulations in either the nucleus or cytoplasm

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hamartoma

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non-neoplastic "lump"; tissue chaotically arranged; in appropriate site

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choristoma

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non-neoplastic "lump"; tissue chaotically arranged; in abnormal site

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mesenchymal tumor

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CT, fat, cartilage
endothelium
hematapoetic and lymphoid tissue
muscle

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epithelial tumor

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lining or covering of epithlelum
solid organs

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malignant neoplasia (histological signs)

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enlarges nucleus with prominent nucleolus; abnormal mitoses; multiple nuclei; bizarre cells; disorganized pleomorphic cells; spindloid cells; mitotic figures ("squashed fly")

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morphological markers of apoptosis

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1. margination of chromatin
2. condensation and fragmentation of nucleus
3. condensation of cells with preservation of organelles

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steps of tumor evolution

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1. initiation - genetic change
2. promotion - stimuli for growth
3. pogression - benign tumor becomes increasingly malignant

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tumor metastisis pathways

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1. transcoelomic - thoracic/abdomial surface
2. lymphatic - carcinomas
3. haemoatogenous - sarcomas (via BVs)

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mechanisms of metastasis

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invasion - protease degredatoin of basement membrane; desmosomes dismantled and cadherin function lost; contact with ECM components (fibronectin, lamini, collagen)

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mesenchymal vs. epithelial tumors (ECM)

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mesenchymal - produce own ECM
epithelial - surrounding mesenchymal non-neoplastic cells produce ECM (TGF stimulates fibroblast)

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angiogenesis

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required for growth of solid tumors > 1-2mm; VEGF and basic fibroblast growth factors; abnormal and disorganized compared to normal

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tissue specific antigens

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shared by tumors and normal tissue (differentiation antigens); if express in higher levels on tumor than normal funtino like tumor specific antigen

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tumor specific antigen

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expressed by tumor and limited in normal tissue; often newly expressed (oncogenic viruses, altered cell products from mutated genes)

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cachexia

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cancer related starvation

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paraneoplastic syndromes

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indirect/remote effects caused by tumor products; may ID before tumor --> useful for diagnosis

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paraneoplastic examples

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hypercalcaemia in parathyroid tumor; anaemia in bone marrow invasion; hypoglycaemia in pancreatic tumors (islet B cells)

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epigenetics

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change in gene expression of somatic cells with NO change in DNA sequence; heritable

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genetetic alterations in cancer cells

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aneuploidy
translocation
mutation
deletion
amplification

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acquired somatic mutations (intrinsic factors)

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by-products of metabolism (reactive oxygen species)

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acquired somatic mutations
(extrinsic factors)

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chemical
radiation (complete carcinogen)
viruses

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carcinogenic viruses

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retroviruses (FeLeuc, FIV)
herpesviruses (Merek's, Kaposi's sarc, Epstein-Barr)
Papovariuses (papillomaviruses)

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chemical carcinogenesis (requirements)

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need initiator and then promotor following at a suitable time; if only 1 or other then no cancer (2 stage)

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fatty degeneration (causes)

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acute toxic injury
chronic metab disease (diabetes mellitsi)
chronic hypoxia (heart failure)
long-standing elevation of blood lipids (overeating or starvation)

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dystrophic calcification

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deposition of calcium salts in tissues (dead or degenerate tissues) other than bones or teeth; serum calium levels normal

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metastatic calcification

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raised blood calcium levels (problem with systematic control); deposition in renal tubules, alveolar walls, fundic mucosa, blood vessels, skin

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amaloid and amyloidosis

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extracellular deposition of abnormal protein arranged in sheets to form fibrils; protein may be of diff source but takes on same structure; resistant to proteolytic digestion

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methaemaglobin

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red to chocoloate brown (nitrite or copper poisoning

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carboxyhaemaglobin

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red to cherry red (CO poisoning)

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oxygenated venous blood

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red (cyanide poisoning)

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billirubin

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yellow/brown or brown/green haem pigment (excreted by liver); yellow color of icterus/jaundice

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haemosiderin

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golden yellow or brown pigment; contains chemically active iron; accumulates in organs, bruises, or general in haemolytic anemia

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porphyria

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forms the haem molocule; defects result in overproduction accumulating on skin, hair, and teeth (brown); dermititis due to photosensitization

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haematins

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formalin pigment and excreta of parasites (black); no significance; fluke exhausts in Fasciola magna infections

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melanosis

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brown pigment secreted by melanocytes; brown to black spots on liver, lungs, and other tissue (common in sheep/cows/pigs); chronic injury to skin; not pathogenic

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melanophage

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macrophage filled with melanin

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lipofuschin

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yellow or light brown pigment derived from cell membranes; accumulates with age; brown in heart or kidneys of older cows

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anthracosis

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balck spots from carbon (soot)

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pneumoconiosis

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pigment from dust

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caratenoids

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stains fats yellow to yellow/orange; normally in egg yolks, adrenal cortical cells, and copus lutea

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algor mortis

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post mortem cooling; aids in estimating time of death

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rigor mortis

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stiffening 2-4 hours after death; head and neck affected first; disappears after 1-2 days

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rigor mortis (timing of death)

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1. warm and flaccid – < 3 hr
2. warm and stiff – 3-8 hr
3. cold and stiff – 8-36 hr
4. cold and flaccid – > 36 hr

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hypostatic congestion

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blood sinks in the tissue due to gravity; best seen in lungs, indicates side on which body has been laid

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post-mortem staining

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1. haemolytic staining – red
2. pseudomelanosis – green (Fe + S = FeS)
3. biliary imbibition - yellow

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autolysis

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tissue breakdown due to anoxia; no inflammation; rate enhanced by failure to cool

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emphysema (post-mortem)

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excess air in the interstitium of the lungs result from terminal gasping; common in thin and older cows

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blood splashing

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post-mortem artifact from haemorrhages in lung, muscle, and other organs; seen in sheep and pigs (electrical stunning)

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post-mortem artefacts

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Imperfect bleeding
Blood splashing
Pulmonary oedema
Splenomegaly
Emphysema
Barbiturate crystallisation
Scavenger attack

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hydropic degeneration

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swelling of organelles (esp. ER and mitochondria) from cellular damage (eg. anoxia); aka cloudy swelling

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pyogenic

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pus producing

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suppurative

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purulent inflammation (pyogenic); neutrophils dominate; eg. from Staphylococci, E. coli, and some Streptococci (S. pyogenes, S. pneumoniae)

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fibrinous inflammation

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acute inflammation where exudate has a high plasma content; fibrinogen from plasma converted to fibrin; esp. in membrane lined cavities (pleura, pericardium, peritoneum); may cause adhesions

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healing (resolution)

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complete restitution of normal architecture and function (if intact and has ability to replace specialized cells by regeneration); eg. sunburn or pneumonia

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healing (fibrosis)

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substantial damage of CT framework and/or tissue lacks ability to regenerate specialized cells; necrotic tissue and exudate removed by macrophages and fill with granulation tissue (organization) which produces collagen (scar)

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granulation tissue

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where significant damage to CT framework, mixture of proliferating capillaries (initially), fibroblasts, macrophages, lymphocytes, and plasma cells

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fibrous scar (repair from granulation tissue)

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deposition of collagen in appropriate orientation for tensile strength; fibroblasts and capillaries regress (condensed nuclei in inactive fibroblasts)

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fibrinous inflammation

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acute inflammation where exudate has a high plasma content; fibrinogen from plasma converted to fibrin; esp. in membrane lined cavities (pleura, pericardium, peritoneum); may cause adhesions

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healing (resolution)

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complete restitution of normal architecture and function (if intact and has ability to replace specialized cells by regeneration); eg. sunburn or pneumonia

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healing (fibrosis)

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substantial damage of CT framework and/or tissue lacks ability to regenerate specialized cells; necrotic tissue and exudate removed by macrophages and fill with granulation tissue (organization) which produces collagen (scar)

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granulation tissue

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where significan damage to CT framework, mixture of proliferating capillaries (initially), fibroblasts, macrophages, lymphocytes, and plasma cells

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fibrous scar (repair from granulation tissue)

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deposition of collagen in appropriate orientation for tensile strength; fibroblasts and capillaries regress (condensed nuclei in inactive fibroblasts)