Pathophys objective flash cards.txt
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What are the eight classes of cell injury?
Oxygen deprivation, Chemical Agents, Infectious agents, Immunologic reactions, genetic defects, genetic imbalances, physical agents, aging
What are three effects of reduced ATP during ischemia/hypoxia?
ATP-dependent sodium efflux pump cannot function, ATP dependent Calcium cation efflux transport cannot function, anaerobic glycolysis increases as an attempt to restore the ATP levels
What is the effect of decreased function of the ATP dependent sodium efflux pump?
increased intracellular sodium cations, decreased potassium ion concentration, influx of water, cellular swelling, decreased protein synthesis
What is the effect of decreased function of the ATP dependent calcium cation efflux?
activation of ATPases, phospholipases, proteases, endonucleases
What is the effect of increased Anaerobic glycolysis?
decreased glycogen stores, decreased pH level in the cell, decreased activity of cellular enzymes, detachment of ribosomes
How does ROS cause cellular injury?
functions as oxidizing agents
How does production of OFRs and ROS occur?
Incomplete reduction of O2 during respiration, Accepting or donating of electrons by transition metals, Absorption of X-rays, Detoxification or metabolism of chemicals in liver, Enzymes involved in inflammatory processes
What does ROS react with?
Fatty Acids, Proteins, DNA
What removes free radicals?
SOD, Glutathione peroxidases, catalase
What are the five contexts in which apoptosis occurs?
depravation of hormones or GF (menstruation), irreparable DNA damage, accumulation of misfolded proteins (alzheimer's), Immune system development, Embryogenesis (loss of vestigial tail)
increase in cell size but not number caused by increase work load, occurs by increased protein synthesis
increase in cell number but not size (breast growth)
decrease in cell size but not number caused by decreased work load, proteins degrade and protein synthesis decreases
one adult cell type is replaced by another
where does fat accumulation occur?
What causes fat accumulation?
ethanol consumption and diabetes
what is the effect of fat accumulation?
decreased liver function
what causes lipofuscin accumulation?
Damage due to ROS or OFR which indicates aging
what causes Hemosiderin accumulation?
break down of hemoglobin at sites of localized injury or hemmorrhage; associated with systemic overload of iron
What disease causes dystrophic calcification?
rheumatic heart disease, heart valve becomes sticky causing leakage
what is dystrophic calcification associated with?
accumulation of Ca associated with necrotic cells
What is metastatic calcification associated with?
pathologic bone reabsorption
What causes metastatic calcification?
What is the effect of metastatic calcification?
death of cells of the vasculature, kidneys, lungs, and gastric mucosa
What are the three factors that contribute to cellular aging?
accumulation of damage (lipofuscin, incorrectly folded proteins/ cross-linked proteins, protein glycosylation, free radical damage), incomplete replication of protein ends by telomerase, reduced regenerative capacity of stem cells
What are the 5 local signs of acute inflammation?
Heat, redness, swelling, pain, loss of function
What does changes in vascular diameter lead to?
Vasodilation, increased viscosity, margination
What causes vascular permeability?
endothelial cell contraction which leads to gaps that leak fluids, direct injury to endothelial cells, leukocyte-dependent endothelial cell damage, increased fluid flow through endothelial cells, leakage from new blood vessels that form at the site of injury
What are the effects of vascular changes?
release of transudate, release of exudate, edema
What is margination?
WBC flow along the inner wall of blood cells due to changes in blood flow
What is rolling?
leukocytes tumble along the wall
What is transmigration?
leukocyte squeezes through the gaps in edothelial cells
What on endothelial cells binds to sialyl-lewis X-modified glycoprotein on leukocytes to slow down the leukocyte?
What on Leukocytes binds to ICAM-1 and UCAM on endothelial cells to cause firm binding?
What is chemotaxis?
leukocytes follow a chemoattractant gradient composed of bacterial peptides, complement components, and cytokines to the site of an infection
What receptor on leukocytes do chemoattractants bind?
7-transmembrane G-protein coupled receptor
What mediates phagocytosis allowing for regulation?
What is a phagosome?
phagocytic vacuole containing foreign bodies
What destroys the foreign body in the phagosome?
fusing with a lysosome which contains an oxidative burst
What are examples of circulating mediators of inflammation?
complement proteins, kinins, and coagulation factors
How are circulating mediators of inflammation activated?
What cells produce histamine?
mast cells, basophils, and platelets
When is histamine released?
physical injury, immune reactions, complement binding, neuropeptides, and cytokines
What effect does histamine have?
arteriolar dialation, increased vascular permeability, endothelial cell contraction; this results in swelling, edema, and congestion
What does COX metabolize AA into?
Lipoxygenases metabolize AA into?
leukotrienes and lipoxins
What do PGs cause?
vasodilation and edema; pain and fever
What type of drugs are COX inhibitors?
What do Leukotrienes cause?
vasoconstriction and increased vascular permeability; airway constriction
What do lipoxins do?
counteract the activity of leukotrienes
What cleaves Factor XII?
What two systems are triggered by Factor XII activation?
Kinin system, Complement system
triggers assembly of MAC
C3a and C5a
trigger histamine release
chemoattractant for WBC
obsonin which aids in phagocytosis
What are the three outcomes of acute inflammation?
restoration to pre-injury state, scaring or fibrosis, chronic inflammation
What are the three main characteristics of inflammation?
infiltration by macrophages, lymphocytes and plasma cells, continuous tissue destruction by inflammatory cells, extensive tissue repair including angiogenesis and fibrosis
In what settings do chronic inflammation arise?
viral infections, persistent microbial infections, prolonged exposure to toxic agents, autoimmune diseases
What role do macrophages play in chronic inflammation?
release proteases, ROS, factors that release and promote inflammation, angiogenesis factors, growth factors stimulating infiltration and fibrosis
What role do lymphocytes play in chronic inflammation?
produce mediators which activate macrophages
What role do plasma cells play in chronic inflammation?
What role do eosinophils play in chronic inflammation?
produce major basic protein which is toxic
What role to Mast cells play in chronic inflammation?
produce histamine and AA metabolites which play a role in anaphylactic shock and allergic reactions
permanently dividing and capable of regeneration (skin and GI tract)
normally nondividing but can divide in response to injury and regenerate themselves (liver, kidney, pancrease, fibroblastic connective tissue cells, endothelial cells)
Non dividing cells that are not capable of regeneration (nerves)
What regulates the cell cycle?
cyclins binding to CDK which then become active and phorphorylate proteins to begin the cell cycle
targets the same cell that produced the factor
targets adjacent cells
specialized form of paracrine signaling
hormone functions at a site distant
EGF--> EGFR-->RAS-->MAP Kinase Cascade-->cyclin transcription
amorphous gel between connective tissue
What is the interstitial matrix composed of?
collagen, elastin, and proteoglycans
sits beneath epithelium to provide support
What is the basement membrane composed of?
type IV collagen, laminin, other adhesive glycoproteins and proteoglycans
What is the function of the basement membrane?
to define the cell orientation
What are the four general steps involved in repair by connective tissue or fibrosis?
- �Angiogenesis- Formation of new blood vessels at the site of injury (neovascularization)
- �Migration and proliferation of finroblass to the site of injury
- �Deposition of ECM by the fibroblasts
- �Maturation and remodeling of the fibrosis tissues by macrophages
What are the six steps of neovascularization?
- �Dilation and increased permeability of the preexisting blood vessel at the site of angiogenesis
- �Proteolysis of ECM to break down the basement membrane
- �Migration of endothelial cells toward a chemoattractant angiogenic stimulus a the site of injury
- �Endothelial cell proliferation just behind the leading edge of migrating cells
- �Once enough cells are present proliferation stops, lumen formation occurs and the endothelial cells self organize into tubes
- �Recruitment and organization of accessory cells to complete the mature vessel
what molecules regulate neovascularization?
Fibroblast growth factors, vascular endothelial growth factor
What are the two steps in scar formation?
- �Emigration and proliferation of fibroblasts at site of injury
- �Deposition of ECM components by fibroblast at site of injury
What factors regulate scar formation?
PDGF, FGF, TGF beta
What are the six overall steps in cutaneous wound healing?
- �Induction of acute inflammatory response by injury
- �Parenchymal cell regeneration
- �Migration and proliferation of parencymal (epithelial) and connective tissue cells
- �Synthesis of ECM proteins
- �Remodeling of parenchymal elements to restore tissue function
- �Remodeling of connective tissue to restore wound strength
What are the steps to healing by first intention?
- �Incision fills with clotted blood which forms a fibrin clot and scab
- �Neutrophils migrate to clotted blood
- oThey produce factors the stimulate epithelial cell proliferation at the wound
- oEpithelial cells advance towards eachother and secrete basement membrane componants to pinch of the clot
- oEpithelial cells meet beneath a surface of scab and form a thin layer of epithelium
- �Macrophages replace neutrophils in stromal (subcutaneous) space
- oResolve inner scab and produce factors that promote neovascularization, fibroblast migration, and ECM deposition which leads to restoration of interstitial volume
- �Epithelium (epidermal cells) proliferate and epidermis recovers its normal thickness. Surface scab falls off.
- �Inner scab is resolved and replaced by a fibrous union. Inflammatory processes are resolved.
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