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31 Cards in this Set

  • Front
  • Back
1. Etiology
Cause of disease
2. Pathogenesis
Mechanism of development of disease. It refers to the sequence of events in the response of cells or tissues to the etiologic agent from initial stimulus to expression of disease (Robbins p.4)
3. Morphologic changes
Structural alterations in cells or tissues that are either characteristic of a disease or diagnostic of an etiologic process
4. Hyperplasia
Abnormal increase in number of cells
5. Hypertrophy
Refers to an increase in the size of cells, resulting in an increaes in the size of the organ. Can be physiologic or pathologic and is caused by increased functional demand or by stimulation by hormones and growth factors. Result of increased production of cellular proteins (Robbins p.6)
6. Hypoplasia
Underdevelopment of an organ or a tissue, usually resulting from the presence of a smaller-than-normal number of cells
8. Metaplasia
Replacement of one cell type with another type. Nearly always foud in association with tissue damage, repair, and regeneration. May change to something more suited to environment (Robbins p.265)
11. Ischemia
Inadequate blood supply to a local area due to a blockage of the blood vessel to that area
13. Coagulative Necrosis
A form of necrosis in which the architecture of dead tissues is preserved for a span of at least some days. Affected issues exhibit a firm texture. The injury denatures not only structural proteins but also enzymes which can persist for weeks (Robbins p.15)
15. Reactive Oxygen Species
Chemically-reactive molecules containing oxygen, they form as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling
16. Ischemia-Reperfusion Injury
Ischemia refers to diminished blood flow to a section of body tissue. It is a counter-intuitive injury that results when blood flow is restored to the site that previously was blood-deficient. (The nutrients in the blood cause oxidative stress and inflammation)
17. Intrinsic Pathway of Apoptosis
This pathway is the result of increased mitochondrial permeability and release of pro-apoptotic molecules into the cytoplasm which initiates the suicide program of apoptosis (Robbins p. 28)
7. Atrophy
Reduced size of an organ or tissue resulting from a decrease in cell size and number. Can be physiological or pathological
9. Necrosis
Cell death characterized by denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell
10. Apoptosis
The pathway of cell death that is induced by a tightly regulated suicide program in which cells destined to die activate enzymes that degrade cells' own nuclear DNA and nuclear/cytoplasmic proteins. Death by Apoptosis is a normal phenomenon
12. Hypoxia
Refers to reduced oxygen availability OR deficiency of oxygen, which causes cell injury by reducing aerobic respiration. Caused by ischemia, inadequate oxygenatoin of blood or decreased oxygen-carrying capacity of blood
14. Mitochondrial Permeability Transition Pore
High-conductance channels in mitochondrial membrane; form upon damage to mitochondrial. Leads to loss of mitochondrial membrane potential, resulting in failure of oxidative phosporylation and progressive depletion of ATP
18. Extrinsic (Death receptor-initiated) Pathway of apoptosis
This pathway is initiated by engagement of plasma membrane death receptors (members of TNF receptor family) on a variety of cell.] Most common death receptor? [FAS which binds FAS ligand]
19a. Dystrophic calcification
When the deposition occurs locally in dying tissues; occurs despite normal serum levels in Ca and in absence of derangements of Ca metabolism
19b. Metastatic Calcification
deposition of Ca salts in otherwise normal tissues and is almost always a result from hypercalcemia secondary to some disturbance in calcium metabolism.
20. Telomere
short, repeated sequences of DNA (TTAGGG) present at the linear ends of chromosomes that are important for ensuring complete replication of chromosomal ends and for protecting chromosomal termini from fusion and degradation. When each cell replicates a small section of the telomere is not replicated]
21. Inflammation
Complex reaction in tissues that consists mainly of responses of blood vessels and leukocytes. Can be acute or chronic. Triggered by soluble factors produced by various cells or derived from plasma proteins and are generated/activated in response to inflammatory stimuli
22. Acute Inflammation
Rapid onset (minutes) and is of short duration, lasting for hours or a few days.
Characteristics:
Exudation of fluid and plasma proteins (edema) and emigration of leukocytes (neutrophils)
3 compenents:
alterations in vascular caliber that lead to an increase of blood flow, structural changes in the microvasculature that permit plasma proteins/leukocytes in, emigration of leukocytes from microcirculation
23. Chronic Inflammation
May follow acute inflammation or be insidious in onset. Longer duration. Associated with presence of lymphocytes and macrophages, the proliferation of blood vessels, fibrosis and tissue destruction
24. Exudate
extra-vascular fluid that has a high protein concentration, contains cellular debris, and has a high specific gravity. Implies increase in normal permeability of small blood vessels and thus an inflammatory response
25. Transudate
a fluid with low protein content (most of which is albumin), little or no cellular debris, and low specific gravity; essentially an ultra-filtrate of blood plasma. Results from osmotic or hydrostatic imbalance across the vessel wall w/o an increase in vascular permeability
26. Edema
denotes an excess of fluid in the interstitial tissue or serous cavities. Can be exudate or transudate
27. Transmigration (Diapedesis)
leukocyte migration through endothelium. Occurs mostly in post-capillary venules after adhesion of leukocytes to endothelium
28. Chemotaxis
Locomotion oriented along a chemical gradient. Occurs after diapedesis of leukocytes
29. Phagocytosis
An endocytotic process used by phagocytes in which cells engulf solid particles.
3 Steps:
recognition and attachment of the particle to be ingested by the phagocyte
its engulfment with subsequent formation of a phagocytic vacule
Killing/degradation of the ingested material
30. Endothelial activation
induction of expression of endothelial adhesion molecules; synthesis of chemical mediators, production of enzymes associated with matrix remodeling, and increases surface thrombogenicity of endothelium. Response to various pathophysiologic stimuli by adjusting constitutive functions and expressing inducible properties