Term
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Definition
| The branch of medicine that deals with the essential nature of disease, especially the structural and functional changes in cells, tissues, and organs that are caused by disease |
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Term
| What are 4 ways a cell can adapt to stress or injurious stimuli? |
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Definition
-hypertrophy
-hyperplasia
-atrophy
-metaplasia (he transformation of one type of one mature differentiated cell type into another mature differentiated cell type) |
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Term
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Definition
| lysosomal digestion of a cell's own components following nutrient deprivation |
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Term
| What causes hypertrophy of the Smooth ER? |
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Definition
| compensatory mechanism to toxins metabolized in the SER |
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Term
| What classifies as cytoskeletal alterations? |
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Definition
| abnormal assembly and functions of filaments, or abnormal accumulation of filaments |
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Term
| What are 6 mechanisms of cell injury? What is the most common mechanism? |
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Definition
-deletion of ATP
-damage to mitochondria
-influx of Ca (causes activation of enzymes that will damage cell components and cause apoptosis, usually)
-oxidative stress
-defects in membrane permeability (most common)
-Damage to DNA and to proteins |
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Term
| What are the hallmarks of reversible cell injury and irreversible cell injury? |
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Definition
reversible: swelling and fatty change, plasma membrane blebbing, and clumping of chromatin
irreversible: severe disturbances in mitochondrial and membrane functions |
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Term
| What is the difference in morphologic alteration between necrosis and apoptosis? |
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Definition
-Necrosis= break down of plasma and organellar membranes; leakage and enzymatic digestion of cell contents
-Apoptosis= nuclear chromatin condensation; formation of apoptotic bodies (little blobs breaking off and becoming phagocytized) |
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Term
Define these terms used when describing nuclear changes in necrosis:
-pyknosis
-karyorrhexis
-karyloysis |
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Definition
-pyknosis= condensation
-karyorrhexis= fragmentation ("nuclear dust")
-karyolysis= dissolution of nuclear structure as a result of enzymatic digestion |
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Term
| Name this type of tissue necrosis: cells are dead, but basic tissue architecture is preserved for several days; characteristic of infarcts in solid tissues except the brain |
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Definition
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Term
| Name this type of tissue necrosis: coagulative necrosis of the lower leg |
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Definition
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Term
| Name this type of tissue necrosis: seen in focal bacterial or fungal infections; inflammatory cells and leukocytes digest tissue |
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Definition
liquefactive necrosis
**also seen in the brain |
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Term
| Name this type of tissue necrosis: most often in foci of tuberculosis infection |
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Definition
| caseous necrosis (cheese-like) |
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Term
| Name this type of tissue necrosis: focal area of fat destruction often resulting from acute pancreatitis |
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Definition
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Term
| Name this type of tissue necrosis: usually seen in immune reactions involving blood vessels |
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Definition
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Term
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Definition
| programmed cell death; a highly regulated process of cell death mediated by suicide genes, which activate enzymes that degrade the cell's own DNA and proteins |
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Term
| What is physiologic apoptosis? |
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Definition
| a normal process that is important for embryonic development, and removal of cells no longer needed in adult tissues |
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Term
| What is pathologic apoptosis? |
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Definition
| eliminates cells genetically altered or injured beyond repair without eliciting a severe host reaction |
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Term
| What are 4 common causes of pathologic apoptosis? |
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Definition
-DNA mutations
-accumulation of misfolded proteins
-cell injury in certain infections
-pathologic atrophy in parenchymal organs after duct obstruction |
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Term
| What are intracellular accumulations? |
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Definition
| abnormal deposits in cells and tissues that are the result of excessive intake or defective transport or catabolism (lipids, proteins, glycogen, pigments) |
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Term
| What are the 2 most common causes associated with fatty change (steatosis) in the liver? |
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Definition
alcohol abuse
diabetes associated with obesity |
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Term
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Definition
| accumulation of blood-derived brown pigment called hemosiderin. It occurs in tissues where there is excess of iron |
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Term
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Definition
-yellow-brown pigment caused by free radical per oxidation of membrane lipids
-accumulates in many tissues (often in the heart and liver)
-normally in lysosomes
-wear and tear pigment (age spots on the hands of older people) |
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Term
| What are the two types of pathologic calcification? Describe them. |
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Definition
-Dystrophic calcification: deposition of calcium at sites of cell injury and necrosis; normal calcium metabolism
-Metastatic calcification: deposition of Ca in normal tissue; derangement in Ca metabolism; usually caused by hypercalcemia as a consequence of excessive parathyroid hormone |
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Term
| What are the three causes of cellular aging? Describe them. |
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Definition
-accumulation of DNA damage: from normal DNA replication over time, enhanced by free radicals, environmental agents
-replicative senescense: reduced ability of cells to divide because of progressive shortening of telomeres; normal cells have limited capacity for replication
-accumulation of metabolic damage= repeated environmental exposure, oxidative damage, and diminished capacity to eliminate abnormal proteins |
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Term
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Definition
| disease-causing agents such as viruses, bacteria, fungi, and parasites |
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Term
| What are the three levels of defense the body has against pathogens? |
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Definition
-skin
-inflammation (nonspecific reaction)
-immune response (specific reaction) |
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Term
| What is the difference between acute and chronic inflammation? |
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Definition
-acute: rapid onset, short duration (mins-days), fluid and plasma protein exudation (edema), PMNs (polymorphonuclear leukocyte accumulation)
-chronic: longer duration (days to years), influx of lymphocytes and macrophages, associated vascular proliferation and fibrosis |
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Term
| The main components of acute inflammation are a vascular reaction and a cellular response, describe them. |
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Definition
-vascular changes: vasodilation and increased vascular permeability (plasma proteins leave the circulation)
-cellular events: cellular recruitment and activation- emigration of leukocytes (mainly PMNs) from circulation to site of injury |
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Term
| What are 5 cardinal signs of acute inflammation? |
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Definition
-heat (calor)
-redness (rubor)
-swelling (tumor)
-pain (dolor)
-loss of function (functio laesa) |
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Term
| What are 6 stimuli for acute inflammation? |
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Definition
Infections
Trauma
Physical and chemical agents
Tissue necrosis
Foreign bodies
Immune reactions (hypersensitivity reactions) |
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Term
| Describe the two classes of mediators of inflammation |
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Definition
-plasma-derived: circulate in plasma in inactive form and must be transformed by activator
-cell-derived: produced locally by cells at the site of inflammation |
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Term
| Histamine is _________ and released from _________/_____ at site of infection or injury, and from circulating ___________ and ___________. What are some characteristics of histamine? |
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Definition
-preformed
-mast cells
-basophils
-platelets
-early response to infection, occurs quick but short acting, vasodilation, increased vascular permeability, contraction of vascular endothelial cells to form gaps |
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Term
| Bradykinin is a _________/________ derived from high molecular weight kininogen through the enzymatic action of kallikrein. It has similar actions as histamine but what is the major difference? |
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Definition
plasma protein
it induces pain |
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Term
| What is the complement system? |
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Definition
-plasma proteins that work with (complement) the immune system and also participate in the inflammatory response
-defend the body against infectious microbes
-mark microbes for destruction by phagocytes
-directly kill microbes by creating membrane-attack complexes (MACs) |
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Term
| What are membrane-attack complexes (MACs)? |
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Definition
-they are created by complement system plasma proteins
-they are large, cylindrical multi proteins that embed in the invading microbes plasma membrane, creating pores and bursting the microbe. |
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Term
| The activation of the complement cascade can occur through three pathways, what are they? Describe them. All three pathways converge toward a common terminal pathway, what is it? |
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Definition
-classical pathway= activated by antigen-antibody complexes formed in immune reactions
-alternative pathway= activated by bacterial endotoxins, fungi, snake venom, other substances
-lectin pathway= activated by the binding of plasma-binding mannose lectin to carbohydrates on bacteria
**Formation of MACs is the common terminal pathway |
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Term
| Arachidonic acid metabolites are an important group of mediators of inflammation. Arachidonic acid is derived from __________ of ________/__________ by action of phospholipase. |
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Definition
| phospholipids of cell membranes |
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Term
| What are the two pathways by which arachidonic acid is further metabolized? Describe them. |
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Definition
-lipoxygenase pathway= leukotrienes which mediates inflammation (chemotaxis, vasoconstriction, increase vascular permeability (anaphylactic shock) and lipoxins (negative regulators of leukotrines)
-cyclooxygenase pathway= prostaglandins which mediate inflammation (vasodilation, incr. vascular perm.), thromboxane (platelet aggregation, thrombosis, vasoconstriction), and prostacyclin (counteracts effects of thromboxane) |
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Term
| Define transudate and exudate |
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Definition
-transudate= plasma (no protein)
-exudate= plasma AND proteins |
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Term
| What causes the tissue edema in acute inflammation? |
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Definition
| local vasodilation leads to rise in intravascular hydrostatic pressure---> plasma and proteins move into tissues--> intravascular pressure decreases and H20 and ions outflow into tissues causing edema |
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Term
| What causes the stasis in acute inflammation? |
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Definition
| the red blood cells become more concentrated due to the outflow of water and ions into the tissues (edema), therefore blood is more viscous and circulations slows causing stasis |
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Term
| What is margination in acute inflammation? |
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Definition
| leukocytes (mainly PMNs) accumulate along endothelial walls of vessels |
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Term
| Describe the three steps of cellular events in acute inflammation regarding leukocytes |
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Definition
-leukocytes are recruited from the blood to the extravascular spaces
-they migrate to the site of infection or tissue injury
-they are activated to kill bacteria or other microbes, and eliminate necrotic tissue or foreign substances |
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Term
| Name and describe the 4 mechanisms of leukocyte migration through blood vessels |
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Definition
-margination= accumulation at periphery of vessels
-rolling= tumble along endothelial surface with transient adhesions (mediated by selectins)
-adhesion= stable attachment to endothelium (mediated by integrins)
-transmigration (diapedesis)= migration through inter-endothelial spaces (mediated by CD31) |
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Term
| What is the term used to describe the migration of leukocytes toward a site of infection or injury along a chemical gradient? |
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Definition
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Term
| What are 3 consequences of leukocyte activation? |
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Definition
-phagocytosis
-production of substances that destroy phagocytosed microbes and remove dead tissues
-production of mediators that amplify the inflammatory reaction |
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Term
| Acute inflammation generally has one of three outcomes. What are the three possible outcomes? Describe them. |
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Definition
-resolution= removal of exudate with restoration of normal tissue architecture
-progression to chronic inflammation= may follow acute inflammation if offending agent is not removed
-scarring or fibrosis= after substantial tissue destruction; abscesses usually result in scar formation |
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Term
| Loss of parenchymal cells in chronic inflammation results in what? |
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Definition
| scarring and impaired organ function |
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