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47 Cards in this Set

  • Front
  • Back
General pathology
-Defines lesions/abnormalities that may be grouped as they share common features
-Unlikely to be related to just one causal agent or one disease process
-Ex: cell degeneration/cell death, circulatory disordrs, inflammation and repair, disturbances in growth, cancer
Etiology
The cause
Pathogenesis
-Step-by-step progress in the disease
-Stages in the development of lesion or disease, from initiation to termination
Pathognomonic
Lesion or clinical sign indicative or a specific etiology
Morphological diagnosis
Based on a lesion
Etiological diagnosis
Based on a specific cause
Clinical diagnosis
Based on clinical signs
Adaptive changes
-Hypertrophy
-Hyperplasia
-Atrophy
-Metaplasia
-Dysplasia
-Aplasia and hypoplasia
Hypertrophy
Reversible increase in the size, weight, and volume of an organ

-Skeletal muscle hypertrophy due to increased workload
Hyperplasia
Reversible increase in the number of cells in an organ

-Thyroid hyperplasia due to iodine deficiency
Atrophy
Reversible acquired decrease of size of a normally developed organ due to a reduction in the size or number of cells

-Counter to hypertrophy and hyperplasia
-Atrophy of disuse, pressure atrophy, and endocrine-related atrophy
Metaplasia
Reversible replacement of one type of mature differentiated cell by a different but closely related type cell

-Respiratory irritation (chronic bronchitis): ciliated columnar to squamous epithelium
Dysplasia
Irreversible abnormal growth and development of cells

-Usually a disorder during fetal growth
-May result in organ malfunctions
Aplasia
Irreversible, complete or almost complete failure of tissue development

-Renal aplasia, segmental aplasia of gut
Hypoplasia
Failure of an organ to reach its full size due to embryological development

-May be observed at birth or develop over time
-Cerebellar hypoplasia due to in utero viral infections
Necrosis
Death of cells in the living body

-Grossly: lighter colored tissue
-Microscopically: Cytoplasmic acidophila (pink/red in the cytoplasm), pyknosis (chromatin in the nucleus), Karyorrhexis (nucleus starts breaking up), karyolysis (nucleus broken up)
Coagulative necrosis
Tissue pallor and firm
HIstologically: cell outline retained (structure), cell internal detail lost

-Toxic/hypoxic damage
LIquefactive necrosis
Tissue soft and fluidy
Histologically: cell outline and cell detail lost (structureless)

-Assoc with inflammation
-CNS more prone
Caseous necrosis
Tissue soft, friable, granular
Histologically: cell outline and detail lost (structureless) and prone to calcify

-Assoc with mycobacterium bovis (TB)!!!!!!!!!
Apoptosis
Programmed cell death of individual cells
Need energy to do it
Fat necrosis
Tissue hard, chalky white deposits
HIstologically: cholesterol clefts and calcifations
Causes release of glycerol and fatty acids, precipitations of salts, leading to soap formation
Fat deposits

-Assoc with trauma, pancreatic damage
Fibrinoid necrosis
Necrosis/fibrin deposition in walls of blood vessels

-Assoc with severe vascular injury
Things that occur after necrosis
-Inflammation
-Sequestration
-Calcification
-Putrefaction/gangrene
Rigor mortis
Temporary rigidity of muscle after death due to hypoxia, decrease ATP, and anaerobic glycolysis

-Begins in the most active, best-nourished muscles
-Gradually disappears
Hypostatic congestion
Gravitational settling of blood in dependent areas

-Tissue dark, heavy, congested and edematous
Post Mortem clots
Activation of clotting cascade by thromboplastin

-Clot is smooth, shiny, and not attached to vascular wall (easy to pull out)
Pseudomelanosis
Dark green discoloration on surface of abdominal organs/intestinal serosa

-Involves putrefactive bacteria, H2S, and Fe
Parathyroid hormone
Increases blood calcium by stimulated renal calcium absorption, osteolysis of bone and renal production of Vit D

-Produced by chief cells in parathyroid
Calcitonin
Decreases blood calcium by impairing osteoclastic bones resorption

-Responds if animal is hypercalcemic
-Produced by parafollicular cells in thyroid
Vit D
Stimulated intestinal calcium adsorption

-Activated by kidney
Dystrophic calcification
Precipitation of calcium in tissues already damaged
Metastatic calcification
Precipitation of calcium in undamaged tissue due to excess concentration in blood (hypercalcemia)

-Frequent in kidneys, lungs, stomach
-Seen on basement membranes, mitochondia, bv walls
Calcinosis circumscripta
Tumor-like masses of calcium located in the subcutis
Most commonly located over bony prominences in large dogs
Calcinosis cutis
Calcium in the dermis of dogs with hyperadrenocorticism (Cushing's disease)

-Related to collagen degeneration
Amyloid
An extracellular protein deposited as a meshwork of rigid fibrils
Very resistant to phagocytosis
Progressive accumulation --> organ dysfunction

-Grossly: severely affected tissue is pale, waxy when you cut it with a knive, lard-like stains brown with iodine
-Microscopically: homogenous eosinophilic (H&E), apple green birefringence (congo red)
-Might see in kidneys (most common), liver, blood vessels
Reactive amyloid
Results of excessive production of serum amyloid (a normal acute phase protein)
Assoc with long-standing/chronic inflammation
Immunocytic amyloid
Result from proteins derived from immunological light chains
Assoc with lymphoid tumors
Endocrine-derived local amyloid
Results from proteins derived from polypeptide hormones secreted by endocrine cells
Assoc with the pancreas of the cat
Carbon
Exogenous derived pigment
Microscopically: black granular depositis intra or extra extracellular, peribronchiolar, perivascular

-Anthracosis (black/grey mottled lungs)
Melanin
Endogenous pigment normally found in epidermis, iris, choroid, buccal mucosa, substantia nigra
Melanosis
Black pigmentation due to the presence of melanin in an abnormal location; congenital; not clinically significant
Melanoma
Tumor of melanocytes
Can be benign/malignant, pigmented/non-pigmented
Albinism
Genetically determined failure to synthesize tyrosinase leading to an absence of melanin
Leukoderma
Focal pigmentation at the site of a scar
Achromotrichia
Abnormally light hair
Reduced density of pigmentation
Lipofuscin
Intracellular golden brown pigment
Composed of breakdown products of cell membranes and membranous organelles

-Levels increase with age, "wear and tear"
Haemosiderin
Microscopically: brown, granular, intracytoplasmic in macrophages

-Seen normally in spleen, bone marrow, liver
-Seen when there is hemorrhages, congestion of lungs